Report to the California Legislature 

INDOOR AIR POLLUTION 

IN CALIFORNIA

A report submitted by: 

California Air Resources Board 

July, 2005 

Pursuant to Health and Safety Code § 39930 

(Assembly Bill 1173, Keeley, 2002) 

 Arnold Schwarzenegger 

 Governor 

California Environmental Protection Agency

Air Resources Board 
Indoor Air Pollution in California July, 2005 

 

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Indoor Air Pollution in California July, 2005 

 

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ACKNOWLEDGEMENTS 

This report was prepared with the able and dedicated support from Jacqueline Cummins, 

Marisa Bolander, Jeania Delaney, Elizabeth Byers, and Heather Choi. 

We appreciate the valuable input received from the following groups: 

• Many government agency representatives who provided information and thoughtful 

comments on draft reports, especially Jed Waldman, Sandy McNeel, Janet Macher, Feng 

Tsai, and Elizabeth Katz, Department of Health Services; Richard Lam and Bob Blaisdell, 

Office of Environmental Health Hazard Assessment; Deborah Gold and Bob Nakamura, 

Cal/OSHA; Bill Pennington and Bruce Maeda, California Energy Commission; Dana Papke 

and Kathy Frevert, California Integrated Waste Management Board; Randy Segawa, and 

Madeline Brattesani, Department of Pesticide Regulation; and many others. 

• Bill Fisk, Lawrence Berkeley National Laboratory, for assistance in assessing the costs of 

indoor pollution. 

• Susan Lum, ARB, project website management, and Chris Jakober, for general technical 

assistance. 

• Stakeholders from the public and private sectors, who attended the public workshops and 

shared their experiences and suggestions concerning indoor air quality in California. 

• The scientific peer review committee–Drs. Kirk R. Smith, S. Katharine Hammond, William W. 

Nazaroff, and Richard Sextro–who provided valuable review and comments that enhanced 

the scientific accuracy of this report. 
Indoor Air Pollution in California July, 2005 

 

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DISCLAIMER 

The mention of commercial products, their source, or their use in connection with material 

presented in this report is not to be construed as actual or implied endorsement of such 

products by the State of California. 

ALTERNATIVE FORMS OF REPORT 

If you are a person with a disability and desire to obtain this document in an alternative 

format, please contact Jacqueline Cummins at (916) 445-0753 or 

jcummins@arb.ca.gov. TTY/TDD/Speech-to-speech users may dial 7-1-1 for the 

California Relay Service. 

This report is also available electronically on ARB’s website at: 

http://www.arb.ca.gov/research/indoor/ab1173/ab1173.htm
Indoor Air Pollution in California July, 2005 

 

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APPROVED BOARD RESOLUTION 

State of California 

AIR RESOURCES BOARD 

Resolution No. 05-28 

March 17, 2005 

Agenda Item No. 05-3-3

WHEREAS, in 2002 the Legislature enacted Assembly Bill 1173 (Stats. 2002; Chapter 987) 

which requires the Air Resources Board to prepare a report on indoor air pollution in California; 

WHEREAS, Assembly Bill 1173 added section 39930 to the Health and Safety Code; 

WHEREAS, Health and Safety Code section 39930 requires the report to contain a broad scope 

of information on many aspects of indoor air pollution, including information on common indoor 

pollutants and their sources; the potential health impacts of indoor pollutants; existing 

regulations and practices; options for mitigation in schools, homes, and non-industrial 

workplaces; and state and federal efforts related to control of biological and radiological 

substances; 

WHEREAS, through three public review periods and meetings with other state agencies and 

interested stakeholders, staff have consulted with, and obtained comments from, the 

Department of Health Services, the Office of Environmental Health Hazard Assessment, the 

State Energy Resources Conservation and Development Commission, other state agencies, 

and numerous stakeholders and members of the interested public; 

 

WHEREAS, as required by Health and Safety Code section 39930(c), the report was reviewed 

by a scientific peer review panel comprised of University of California scientists, who concur that 

indoor air pollution is not currently well addressed by governments at the national, state, or local 

level; 

WHEREAS, indoor air pollution causes serious health effects, including cancer, premature 

death, asthma, and other respiratory disease; 

WHEREAS, indoor air pollution has been ranked high relative to other environmental problems 

in state and federal comparative risk assessments; this is because there are numerous sources 

of pollutants indoors that contribute to elevated indoor pollutant concentrations that pose 

significant health risks, and Californians spend an average of 87 percent of their time indoors; 

WHEREAS, indoor sources of some traditional ambient air pollutants can cause indoor 

concentrations to exceed State ambient air quality standards; 

WHEREAS, indoor sources of other pollutants such as formaldehyde, environmental tobacco 

smoke, polycyclic aromatic hydrocarbons, radon, and biological contaminants can contribute to 

indoor concentrations that can cause known adverse health effects, including cancer and 

premature death; 

WHEREAS, the cost of both fatal and non-fatal quantifiable impacts due to indoor air pollution in 

California homes, schools, and offices is estimated to total $45 billion per year; 
Indoor Air Pollution in California July, 2005 

 

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WHEREAS, although state and federal agencies have authority over some aspects of indoor air 

quality, there is no comprehensive program to protect air quality within residences, schools, or 

public buildings in California, and there are few government standards restricting emissions 

from common sources of indoor pollutants; 

WHEREAS, methods to reduce indoor air pollution include limitation of indoor sources and 

emissions, adequate ventilation, proper operation and maintenance of buildings, and public and 

professional education and outreach; 

NOW, THEREFORE, BE IT RESOLVED, that the Board concurs with the findings and 

recommendations of the report to the California Legislature entitled Indoor Air Pollution in 

California, dated February, 2005 (the “Report”). 

BE IT FURTHER RESOLVED that the Board hereby approves the Report and directs the 

Executive Officer to forward the Report to the Legislature as soon as possible. 

BE IT FURTHER RESOLVED that the Board supports an outreach and public education 

program that includes an effort focused on professionals, including health professionals, 

teachers, school facility managers, and others who must be able to identify and remedy indoor 

air quality problems. 

BE IT FURTHER RESOLVED that the Board encourages the Department of Industrial Relations 

(Cal-OSHA) to explore mechanisms to assist schools in complying with state regulations, 

especially workplace regulations related to building operation and maintenance that impact 

indoor air quality; 

BE IT FURTHER RESOLVED that the Board directs staff to promote “Best Practices” for the 

design, construction, operation, and maintenance of school facilities, state buildings, and 

general construction, in conjunction with other State agencies and relevant private sector 

groups; 

BE IT FURTHER RESOLVED that the Board supports indoor air quality research and 

technology development to answer remaining questions regarding the sources and health 

effects of indoor air pollution. 

BE IT FURTHER RESOLVED that the Board directs the Executive Officer to forward this 

resolution and the Report to those agencies whose authority and actions can affect different 

aspects of indoor air quality: the State Department of Health Services, the Office of 

Environmental Health Hazard Assessment, the State Energy Resources Conservation and 

Development Commission, the Department of Industrial Relations, and others as deemed 

appropriate. 

I hereby certify that the above is a true and correct 

copy of Resolution 05-28, as adopted by the Air 

Resources Board. 

 /s/ 

____________________________________ 

Lori Andreoni, Clerk of the Board 
Indoor Air Pollution in California July, 2005 

 

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S T A T E OF C A L I F O R N I A 

ARNOLD SCHWARZENEGGER 

Governor 

ALAN C. LLOYD, Ph.D. 

Agency Secretary 

California Environmental Protection Agency 

CALIFORNIA AIR RESOURCES BOARD

BARBARA RIORDAN, Interim Chairman 

SANDRA BERG 

DORENE D’ADAMO 

MARK J. DeSAULNIER 

HENRY GONG, Jr., M.D. 

LYDIA H. KENNARD 

RONALD O. LOVERIDGE 

BARBARA PATRICK

PATRICIA SALAS PINEDA 

RON ROBERTS 

CATHERINE WITHERSPOON 

Executive Officer 
Indoor Air Pollution in California July, 2005 

 

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AUTHORS AND REVIEWERS 

Principal Authors 

Dorothy Shimer, M.S. 

Staff Air Pollution Specialist 

Thomas J. Phillips, M.S. 

 Staff Air Pollution Specialist 

Peggy L. Jenkins, M.S., Manager 

 Indoor Exposure Assessment Section 

Contributing Authors 

Susan Lum, M.A. 

Whitney Webber, M.S. candidate 

Michael Robert, Ph.D. candidate 

Lori Miyasato, Ph.D. candidate 

Deborah Drechsler, Ph.D. 

Nancy Hughett, M.S. 

Jed Waldman, Ph.D. 

Sandra McNeel, DVM 

Report Reviewers 

Peggy Jenkins, Manager, Indoor Exposure Assessment Section 

Richard Bode, Chief, Health and Exposure Assessment Branch 

Bart Croes, P.E., Chief, Research Division 

Michael Scheible, Deputy Executive Officer 

Catherine Witherspoon, Executive Officer 

Scientific Peer Reviewers 

Kirk R. Smith, Ph.D., MPH 

School of Public Health, Environmental Health Sciences Division, University of California 

at Berkeley 

S. Katharine Hammond, Ph.D. 

School of Public Health, Environmental Health Sciences Division, University of California 

at Berkeley 

William W. Nazaroff, Ph.D. 

Civil and Environmental Engineering, University of California at Berkeley 

Richard Sextro 

Lawrence Berkeley National Laboratory, Indoor Environment Program 
Indoor Air Pollution in California July, 2005 

 

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TABLE OF CONTENTS 

ACKNOWLEDGEMENTS......................................................................................................... iii 

DISCLAIMER............................................................................................................................ iv 

APPROVED BOARD RESOLUTION......................................................................................... v 

AUTHORS AND REVIEWERS................................................................................................viii 

ACRONYMS............................................................................................................................xiii 

ABSTRACT.............................................................................................................................xvii 

EXECUTIVE SUMMARY...........................................................................................................1 

1. INTRODUCTION AND BACKGROUND ...........................................................................31 

1.1 Indoor Pollution Poses a Significant Health Risk........................................................31 

1.2 People Spend Most of Their Time Indoors .................................................................33 

1.3 Children’s Health – Vulnerability Implies Increased Indoor Air Quality Impact...........33 

1.4 Environmental Justice Considerations Relative to Indoor Air Quality.........................34 

2. HEALTH EFFECTS, SOURCES AND CONCENTRATIONS OF INDOOR AIR 

POLLUTANTS ..................................................................................................................36 

2.1 Key Health Impacts ....................................................................................................36 

2.1.1 Asthma.................................................................................................................36

2.1.2 Cancer..................................................................................................................41 

2.1.3 Irritant Effects.......................................................................................................44

2.2 Traditional (Criteria) Pollutants ...................................................................................47 

2.2.1 Particulate Matter.................................................................................................47 

2.2.2 Indoor PM Sources and Emissions......................................................................51 

2.2.3 Indoor and Personal PM Concentrations .............................................................53 

2.2.4 Carbon Monoxide.................................................................................................57 

2.2.5 Nitrogen Dioxide and Associated Acids ...............................................................60 

2.2.6 Ozone...................................................................................................................63 

2.3 Toxic Air Contaminants and Other Indoor Air Pollutants ............................................65 

2.3.1 Formaldehyde ......................................................................................................65 

2.3.2 Volatile Organic Chemicals..................................................................................70 

2.3.3 Environmental Tobacco Smoke ...........................................................................81 

2.3.4 Biological Contaminants.......................................................................................85 

2.3.5 Pesticides.............................................................................................................92

2.3.6 Lead .....................................................................................................................97 

2.3.7 Mercury ................................................................................................................99

2.3.8 Polycyclic Aromatic Hydrocarbons.....................................................................100 

2.3.9 Radon.................................................................................................................102

2.3.10 Asbestos ............................................................................................................105 

2.3.11 Polybrominated Diphenyl Ethers and Other Endocrine Disrupters ....................107 

2.4 Non-Industrial, Non-office Workplace Exposure to Air Pollutants.............................109 

2.4.1 Cal/OSHA Data on Workplace Investigations....................................................110 

2.4.2 Workplaces of Concern......................................................................................110 

2.4.3 Semiconductor Industry .....................................................................................113 

3. COSTS OF INDOOR AIR POLLUTION ..........................................................................115 

3.1 Premature Death ......................................................................................................115 

3.1.1 Deaths From CO Poisonings .............................................................................117 

3.1.2 Deaths From Volatile Organic Compounds (VOC) Exposure ............................117 

3.1.3 Deaths from Environmental Tobacco Smoke Exposure ....................................119 

3.1.4 Deaths from Radon Exposure in Homes............................................................120 

3.1.5 Deaths from Mold and Moisture-related Problems in Homes ............................120 
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3.2 Medical Costs ...........................................................................................................120

3.2.1 CO-related Hospitalization .................................................................................121 

3.2.2 VOC-related Cancer Treatment .........................................................................121 

3.2.3 ETS-related Illness and Hospitalization .............................................................121 

3.2.4 Radon-Related Cancer Treatment.....................................................................123 

3.2.5 Medical and Indirect Costs Associated with Indoor Mold and Moisture-related 

Problems in Homes............................................................................................124 

3.3 Productivity Costs of Indoor Air Pollution..................................................................126 

3.4 Summary of Estimated Costs ...................................................................................127 

3.5 Benefits of Improving Indoor Air Quality ...................................................................129 

4. EXISTING REGULATIONS, GUIDELINES, AND PRACTICES......................................131 

4.1 Standards and Regulations ......................................................................................131 

4.1.1 Workplace Air Quality Regulations.....................................................................131 

4.1.2 Ambient Air Quality Standards...........................................................................132 

4.1.3 Reference Exposure Levels for Air Toxics.........................................................132 

4.1.4 Tobacco Control in the Workplace and Public Buildings....................................133 

4.1.5 Pesticide Regulations.........................................................................................134 

4.1.6 Proposition 65 ....................................................................................................135 

4.1.7 Radon In Drinking Water....................................................................................135 

4.2 Indoor Air Quality Guidelines....................................................................................136 

4.2.1 ARB Indoor Air Quality Guidelines.....................................................................136 

4.2.2 Air Quality Guidelines For Europe......................................................................136 

4.2.3 DHS Mold Guidelines.........................................................................................136 

4.2.4 American Society of Heating, Refrigerating, and Air-Conditioning Engineers ...138 

4.2.5 U.S. EPA’s IAQ Tools For Schools Program .....................................................138 

4.3 Emission Limits.........................................................................................................139

4.3.1 Consumer Products ...........................................................................................139 

4.3.2 Appliances..........................................................................................................141 

4.3.3 Building Materials...............................................................................................147 

4.4 Building Design and Construction Standards and Guidelines ..................................151 

4.4.1 State Regulation of Design and Construction ....................................................152 

4.4.2 Federal Regulations for Building Design and Construction................................155 

4.4.3 Professional and Industry Guidelines for Design and Construction...................156 

4.5 Building Operation and Maintenance Standards ......................................................159 

4.5.1 State Standards .................................................................................................159 

4.5.2 Guidelines for Building Operation and Maintenance..........................................161 

5. METHODS TO PREVENT AND REDUCE INDOOR AIR POLLUTION..........................163 

5.1 Source Control..........................................................................................................163

5.2 Ventilation.................................................................................................................164 

5.2.1 Types of Ventilation............................................................................................164 

5.2.2 Ventilation, Health, and Comfort ........................................................................166 

5.2.3 Adequacy of Ventilation in California Buildings..................................................166 

5.3 Building Operation and Maintenance .......................................................................167 

5.4 Public and Professional Education ...........................................................................169 

5.5 Air Cleaning Devices ................................................................................................170 

6. PRIORITIZATION OF SOURCES AND POLLUTANTS BASED ON EXPOSURE AND 

ADVERSE IMPACTS......................................................................................................173 

6.1 High Ranked Source Categories ..............................................................................175 

6.2 Medium Ranked Source Categories.........................................................................178 

7. OPTIONS TO MITIGATE INDOOR AIR POLLUTION ....................................................181 

7.1 General Mitigation Options .......................................................................................181 
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7.2 Solutions for Schools................................................................................................183 

7.2.1 Problems Identified ............................................................................................184 

7.2.2 Report Recommendations .................................................................................185 

8. SUMMARY......................................................................................................................189 

9. REFERENCES................................................................................................................191 

10. GLOSSARY ....................................................................................................................245 

APPENDICES 

I. Assembly Bill 1173 Text 

II. Explanation of Indoor Cancer Risk Estimates 

III. Background for Estimates of Indoor Formaldehyde Concentrations 

IV. Responses to Comments from the Scientific Peer Review Committee 

V. Responses to Comments from the Public 

VI. Responses to Public Comments on the February 2005 Report to the Board 

LIST OF FIGURES 

ES-1: Where Californians Spend Time......................................................................................2 

ES-2: Estimated Potential Cancer Burden from Air Toxics in California by Source ..................5 

2.1: Estimated Potential Cancer Burden from Air Toxics in California by Source ................43 

2.2: Causes of CO Deaths in California................................................................................58 

2.3: Annual California CO Cases..........................................................................................59 

2.4: California Formaldehyde Levels ....................................................................................69 

2.5: Statewide Indoor and Outdoor Concentrations of VOCs ...............................................78 

5.1: Relationship of Ventilation and Indoor Air Pollutant Levels .........................................164 

LIST OF TABLES 

ES-1. Sources and Potential Health Effects of Major Indoor Air Pollutants...............................3 

ES-2. Summary of Estimated Annual Costs of Some Indoor Air Pollutants in California .......12 

ES-3.1. High Priority Source Categories for Mitigation ...............................................................19 

ES-3.2. Medium Priority Source Categories for Mitigation..........................................................23 

1.1. Average Percent of Time Californians Spend in Major Locations .................................33 

2.1. Sources and Potential Health Effects of Major Indoor Air Pollutants.............................37 

2.2. Indoor Exposures and Exacerbation of Asthma ............................................................39 

2.3. Indoor Exposures and Development of Asthma ............................................................40 

2.4. Carcinogenic Status of Selected Indoor Air Pollutants ..................................................42 

2.5. Summary of Recent Indoor PM Exposure Studies ........................................................55 

2.6. Toxic Air Contaminants Emitted From Building and Finishing Materials .......................74 

2.7. Personal, Indoor, and Outdoor VOC Concentrations from a 

 Northern California Study ..............................................................................................77 

2.8. Current Estimated Attributable Risks Associated with ETS...........................................82 

2.9 Estimates of Current California Indoor Concentrations of Nicotine and RSP ................84 

2.10. Health Outcomes and Indoor Dampness.......................................................................89 

2.11. Presence of Indoor Mold and Health Outcomes............................................................91 

2.12. Comparison of Indoor-air, Personal-air, and House-dust Levels in U.S. .......................95 
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2.13. California Portable Classrooms Study Results for Lead in Floor Dust ..........................98 

2.14. Sources of Mercury in the Residential Environment....................................................100 

2.15. Recommended Airborne Concentrations of Mercury...................................................100 

3.1. Unit Costs for Health Effects........................................................................................116 

3.2. Estimated Valuation of Mortality Attributed to Indoor Air Pollution in California ..........118 

3.3. Estimated Annual Medical Costs of Indoor Air Pollution in California..........................123 

3.4. Fraction of Asthma Attributable to Mold or Dampness in Houses ...............................125 

3.5. Updated Estimates of Annual Cost of Asthma.............................................................126 

3.6. Summary of Estimated Costs of Some Indoor Air Pollution in California ....................128 

4.1. ARB Indoor Air Quality Guidelines...............................................................................137 

4.2. Minimum Design Ventilation Rates for Nonresidential, High-Rise Residential, and 

 Hotel Buildings, 2001 Title 24 Standards.....................................................................153 

6.1. High Priority Source Categories for Mitigation.............................................................174 

6.2. Medium Priority Source Categories for Mitigation .......................................................179 
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ACRONYMS 

ACRONYM DEFINITION 

AAQS ambient air quality standards 

AB Assembly Bill 

ACM asbestos containing material 

AHERA Asbestos Hazard Emergency Response Act 

ANSI American National Standards Institute 

ARB California Air Resources Board 

ASHRAE American Society of Heating, Refrigerating, and Air-Conditioning 

Engineers 

CADR clean air delivery rate 

Cal/EPA California Environmental Protection Agency 

Cal/OSHA California Occupational Safety and Health Program, which consists of 

several agencies within the Department of Industrial Relations, including 

the Division of Occupational Safety and Health, and the Occupational 

Safety and Health Standards Board 

CCR California Code of Regulations 

CDC U.S. Centers for Disease Control and Prevention 

CDE California Department of Education 

CDFA California Department of Food and Agriculture 

CEC California Energy Commission 

CHPS Collaborative for High Performance Schools 

CIWMB California Integrated Waste Management Board 

CO carbon monoxide 

CO2 carbon dioxide 

COPD chronic obstructive pulmonary disease 

CPA Composite Panel Association 

CRI Carpet and Rug Institute 

DGS California Department of General Services 

DHS California Department of Health Services 

DOE U.S. Department of Energy 

DOF California Department of Finance 

EC elemental carbon 

EPA U.S. Environmental Protection Agency 

HAP hazardous air pollutant 

HEPA high efficiency particulate arrestance 

Hg mercury 

HSC California Health and Safety Code 

HVAC heating, ventilating, and air conditioning 

IAQ indoor air quality 

IEQ indoor environmental quality 

IESNA Illuminating Engineering Society of North America 

IREL interim (Indoor) reference exposure level 

LAUSD Los Angeles Unified School District 

LEEDTM Leadership in Energy and Environmental Design 

MCL maximum contaminant level 

MDI methylene diisocyanate 

NHEXAS National Human Exposure Assessment Survey 

NO2 nitrogen dioxide 
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NO3 particle nitrate 

NOX oxides of nitrogen 

NOEL no observable effect level 

O&M operation and maintenance 

OEHHA California Office of Environmental Health Hazard Assessment 

OP organophosphate pesticide 

OR odds ratio 

OSHA U.S. Occupational Safety and Health Administration 

PACM presumed asbestos containing material 

PAH polycyclic aromatic hydrocarbon 

PBDE polybrominated diphenyl ethers 

PBO piperonyl butoxide 

PCB polychlorinated biphenyls 

PCS Portable Classrooms Study 

PEL permissible exposure limit 

PM particulate matter 

PM2.5 particulate matter with aerodynamic diameter less than 2.5 microns 

PM10 particulate matter with aerodynamic diameter less than 10 microns 

PTEAM Particle Total Exposure Assessment Methodology 

REL reference exposure limit 

RH relative humidity 

RSP respirable suspended particulate 

SB Senate Bill 

SBS sick building syndrome 

SCSA State and Consumer Services Agency 

SO2 sulfur dioxide 

T temperature 

TVOC total volatile organic compounds 

U.S. EPA United States Environmental Protection Agency 

USD Unified School District 

VOC volatile organic compound 

WHO World Health Organization 

Units, Symbols

o

C degrees Celsius 

cfm cubic feet per minute 

CFU colony forming unit 

cm2 square centimeter 

dBA decibel (referenced to 1 ampere) 

o

F degrees Fahrenheit 

kg kilogram (one thousand grams) 

l/min liters per minute (flow rate) 

m2 square meter 

m3 cubic meter 

μg microgram (one-millionth of a gram) 

μg/g micrograms per gram (concentration) 

μg/m3

 micrograms per cubic meter (concentration) 

mg milligrams (one-thousandth of a gram) 

mg/kg milligrams per kilogram (concentration) 

ml milliliter (one-millionth of a liter) 
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ng nanogram (one-billionth of a gram) 

ng/g nanograms per gram (concentration) 

ng/cm2 nanograms per square centimeter (surface density) 

No. number 

% percent 

pCi/l picoCurie per liter (a measure of radioactivity) 

ppb parts per billion (such as one grain of sand in a billion grains of sand) 

ppm parts per million (such as one grain of sand in a million grains of sand) 

§ section 

tpd tons per day 
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Indoor Air Pollution in California July, 2005 

 

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ABSTRACT 

Indoor air pollution causes significant health effects – including respiratory illness and disease, 

asthma attacks, cancer, and premature death. This costs Californians at least $45 billion each 

year. These impacts are avoidable: preventive measures and alternatives are available, many at 

little added cost. Many agencies, professional groups, and organizations have taken actions to 

reduce indoor pollution, but these have been limited and are not sufficiently effective in 

preventing indoor air pollution. 

Significant Health Effects 

Indoor sources emit gases and particles known to trigger asthma attacks and cause cancer, 

serious heart and lung disease, and irritant effects such as eye and throat irritation. Nearly four 

million Californians now suffer from asthma; there are numerous indoor asthma and allergy 

triggers, including some chemicals previously not thought to aggravate asthma. About 230 

excess cancers are estimated to occur in California each year due to carcinogens emitted from 

indoor products and materials, such as formaldehyde from pressed wood building materials. 

This approaches the 250 estimated cancer cases per year from diesel exhaust particulate 

matter in outdoor air. Additionally, about 400 excess lung cancers are estimated to occur from 

exposure to environmental tobacco smoke. Up to 1500 excess lung cancers may occur from 

exposure to radon; however, the risk from radon is strongly associated with exposure to tobacco 

smoke, and less than one percent of California homes exceed the recommended mitigation 

level. Carbon monoxide, nitrogen dioxide, and particles are emitted from indoor combustion 

sources such as gas- and wood-burning appliances, and can cause serious respiratory and 

heart disease, sometimes resulting in premature death. Many gaseous compounds from 

building materials and consumer products occur at elevated levels indoors and exceed healthbased guideline levels. Biological contaminants, including allergens, mold, and disease 

organisms, can cause illness when indoor conditions support their growth or transmission. 

High Economic Costs 

Indoor pollution is estimated to cost California’s economy more than $45 billion each year due to 

premature deaths, medical costs, lost worker productivity, and related impacts. The total cost is 

likely much higher, because the total health impacts are not known. 

Numerous Indoor Sources of Pollutants 

There are numerous sources of pollutants in indoor environments, and because people spend 

most of their time indoors, the risk from indoor air pollution is substantial. Californians, like 

others in industrialized nations, average about 87% of their time indoors. Indoor emissions are 

partially trapped inside buildings, and people’s activities put them very near indoor sources. 

Consequently, some scientists estimate that pollutants emitted indoors are about 1,000 times 

more likely to be inhaled than comparable outdoor emissions. 

Lack of Risk Reduction Program 

Despite the high health and economic impacts and the availability of effective mitigation 

approaches, indoor pollution does not have the benefit of a focused risk reduction program at 

the state or federal level. The existing regulations that apply to indoor air quality are scattered 

across multiple agencies, and focus on workplace exposures and ventilation requirements for 

non-residential buildings. Laws such as California’s Smoke-free Workplace Law (AB 13, 1995) 

address specific sources or exposures, but leave substantial gaps in the state’s ability to reduce 
Indoor Air Pollution in California July, 2005 

 

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indoor pollution. Additionally, the resources allocated to address indoor air quality are not 

commensurate with the health risks and economic costs of indoor pollution. 

Indoor Air Pollution Can Be Prevented 

There are a variety of effective approaches for preventing or reducing indoor pollution. Source 

control, such as through emission limitations or use of alternative products or materials, is the 

most effective approach for most indoor pollutants, because emissions and harmful exposures 

are prevented. A comprehensive risk reduction program could effectively assure acceptable 

indoor air quality in California homes, schools, and public buildings. A program that stresses 

emission reductions but includes improved building codes and ventilation, public and 

professional education, and development of advisory guidelines, is recommended. Mitigation 

actions that should be taken to reduce indoor pollution include: 

• Create a comprehensive management program to assess indoor air problems, identify the 

best solutions, and develop measures to address them. 

• Establish emission limits and require emissions testing, such as for building materials and 

some consumer products, to reduce emissions from indoor sources. 

• Make children’s health in schools and homes the top priority. Implement the 

recommendations of the ARB/DHS California Portable Classrooms Study: in particular, 

ensure that schools meet workplace standards for ventilation and for the prevention and 

remediation of moisture intrusion, require low-emitting building materials and furnishings, 

and require ventilation systems to be quiet. 

• Amend building codes to assure adequate ventilation under all circumstances, and to 

address indoor combustion sources and prevent mold problems. 

• Develop indoor air quality guidelines for homes, schools, and institutional buildings, to 

identify healthful indoor pollutant levels and promote “Best Practices" for all aspects of 

building design, construction, operation, and maintenance. 

• Implement a focused outreach and education program for key professionals such as 

building managers, doctors, teachers, and others. 

• Conduct increased research on all aspects of indoor air quality, and fund indoor clean air 

technology development and commercialization projects to foster improved indoor mitigation 

technologies, such as low-noise ventilation technologies. 

Priority Sources 

High priority categories for mitigation include: indoor air cleaners that purposely emit ozone; 

building conditions that promote the growth or transmission of biological contaminants; building 

materials and furnishings; combustion appliances; environmental tobacco smoke; and radon. 

Those that are less urgent, because they are currently regulated for other purposes which yield 

benefits to indoor air, include: architectural coatings such as paints and varnishes, consumer 

products such as cleaning agents and air fresheners, household and office equipment such as 

printers and copy machines, and some pesticide products. Special priority should be paid to 

measures that reduce children’s exposures. 

Actions Are Cost-Effective 

Studies have documented the health, productivity, and economic benefits of improving indoor 

air quality. Many actions can be taken at relatively low cost that would reap large health 

benefits; others require additional authority or resources. Schools and homes are starting 

points: these require a high priority effort, because little has been done to improve those indoor 

environments, and the most sensitive members of the population – children, the elderly, and the 

infirm – spend most of their time there. 
Indoor Air Pollution in California July, 2005

 1

EXECUTIVE SUMMARY 

I. INTRODUCTION 

The California Air Resources Board (ARB, Board) staff prepared this report to the Legislature on 

indoor air pollution in response to requirements of Assembly Bill 1173 (Keeley, 2002; California 

Health and Safety Code [HSC] Section [§] 39930). This report summarizes the best scientific 

information available on indoor air pollution, including: information on common indoor pollutants 

and their sources; the potential health impacts of indoor pollutants, and associated costs; 

existing regulations and practices; options for mitigation in schools, homes, and non-industrial 

workplaces; and other information specified in the legislation. Stakeholder input was obtained 

from relevant state agencies, industries, interest groups, and the public. The report was also 

reviewed by a panel of University of California scientists with expertise in various aspects of 

indoor air quality and air pollution exposure. The Board approved the report at their March 17, 

2005 meeting (ARB Resolution no. 05-28). 

Indoor Air Pollution Poses Substantial Health Risks 

Available scientific information indicates that indoor air pollution poses substantial health risks in 

many indoor environments. In comparative risk projects that ranked environmental health 

problems in order of the risk they pose to health and the environment, both the California and 

U.S. Environmental Protection Agencies ranked indoor pollutants and sources in the high-risk 

categories. Outdoor pollution emissions from motor vehicles and stationary (industrial) sources 

were also ranked high. Indoor pollution ranked high relative to other environmental problems 

because there are numerous sources of pollutants indoors, indoor air concentrations of some 

pollutants often occur at levels that create significant health risks, and people spend most of 

their time indoors. While regulation of outdoor sources such as motor vehicles and industrial 

facilities is very extensive and has notably reduced pollutant levels in California, indoor pollution 

sources have not been addressed in a comprehensive manner. If such an effort were 

established, significant gains could be achieved in public health protection from reductions in 

indoor emissions and from other measures that might be taken to reduce indoor pollution. 

Why Indoor Sources Have Such a Significant Impact 

The total quantity of air pollutants emitted indoors is less than that emitted by outdoor sources. 

However, once emitted, indoor air pollutants are diluted much more slowly, due to the partial 

trapping effect of the building shell. Additionally, indoor emissions occur in closer proximity to 

people: Californians, like others from industrialized nations, spend most of their time indoors. As 

shown in Figure ES-1, California adults spend an average of 87 percent of their time indoors, 

and children under 12 years of age spend about 86 percent of their time indoors. Most of the 

time spent indoors is spent in the home. However, working adults spend about 25 percent of 

their time at other indoor locations such as office buildings, stores, and restaurants, primarily for 

work, and children spend about 21 percent of their time in school on a school day. Senior 

individuals spend a great deal of time in their homes. Because of these time budgets, the 

trapping effect of buildings, and people’s proximity to indoor emissions, there is a much higher 

likelihood that people will be exposed to indoor pollutants than outdoor pollutants. Investigators 

have calculated that pollutants emitted indoors have a 1000-fold greater chance of being 

inhaled than do those emitted outdoors (Smith, 1988; Bennet et al., 2002; Lai et al., 2000). 

Homes and schools are thus critical exposure microenvironments, especially for children and 

seniors. These groups are more sensitive to the adverse effects of some pollutants, and spend 
Indoor Air Pollution in California July, 2005

 2

most of their time indoors. The passenger compartments of cars and buses also are key 

exposure environments: studies have shown very high levels of vehicle exhaust pollutants 

inside cars and school buses as they travel along California roadways. However, these 

environments differ significantly from building environments and are more closely associated 

with outdoor pollution, and are not considered further in this report. 

Children Are Especially Vulnerable to Poor Indoor Air Quality 

Children are especially vulnerable to poor indoor air quality due to several factors. Children’s 

physiology and developing bodies make them more susceptible to chemicals that affect 

development and lung function. Their immune systems are not fully developed, and their 

growing organs are more easily harmed. Additionally, infants and children inhale more air 

relative to their size than do adults at a given level of activity, so that they inhale a larger relative 

dose of pollutants than do adults in the same environment. Children also tend to be more active 

than adults. These factors, combined with elevated indoor concentrations of pollutants, can lead 

to higher exposure and risk for children than adults. 

II. HEALTH EFFECTS OF INDOOR POLLUTANTS 

Indoor air pollution can cause a variety of impacts on human health, from irritant effects to 

respiratory disease, cancer, and premature death. Indoor air pollutants can be elevated to levels 

that may result in adverse health effects. The major indoor pollutants that can have a substantial 

impact on Californians’ health are listed in Table ES-1, along with their sources and associated 

health impacts. The health impacts of greatest significance include asthma, cancer, premature 

death, respiratory disease and symptoms, and irritant effects. 

Modern society includes many trade-offs, often characterized through risk/benefit analyses. 

Transportation, building materials, appliances, consumer products, plastics, and pesticides 

impart obvious benefits to society. However, the use of many beneficial or desirable products at 

times can have a down side – the emission of a variety of chemicals can have adverse impacts 

on human health. The impact on health depends on the toxicological properties of the chemical 

and the exposure and absorbed dose an individual may receive. 

OUTDOORS

 6%

INDOORS

AT HOME

62%

INDOORS OTHER

25%

ENCLOSED TRANSIT

7%

California Adults and Teens

( Population Means )

OUTDOORS

10%

INDOORS

AT HOME

76%

INDOORS OTHER

10%

ENCLOSED TRANSIT

4%

California Children

( Under 12 years old, Population Means )

Figure ES-1: Where Californians Spend Time 

(Jenkins et al., 1992a; Phillips et al., 1991) 
Indoor Air Pollution in California July, 2005

 3

Table ES-1. Sources and Potential Health Effects of Major Indoor Air Pollutants 

POLLUTANT MAJOR INDOOR 

SOURCES 

POTENTIAL HEALTH EFFECTS 

ASSOCIATED WITH ONE OR MORE 

OF THE POLLUTANTS LISTED* 

Asbestos 

Building materials in older homes 

disturbed during renovation. Naturally 

occurring in some soils. 

Lung cancer, asbestosis, 

mesothelioma 

Biological Agents 

(bacteria, fungi, viruses, 

house dust mites, animal 

dander, cockroaches, 

microbial VOCs) 

House & floor dust; bedding; poorly 

maintained air-conditioners, humidifiers, 

dehumidifiers; moist structures; insect 

infestation; building occupants; pets 

Allergic reactions; asthma; eye, nose, 

and throat irritation; humidifier fever, 

influenza, other infectious diseases 

Carbon Monoxide 

Unvented/malfunctioning gas & propane 

appliances, woodstoves, fireplaces, 

tobacco smoke, vehicles in garages 

Headache; nausea; angina; impaired 

vision and mental functioning; fatal at 

high concentrations 

Endocrine Disruptors 

(PBDEs, some phthalates, 

some pesticides) 

Flame retardants, plastics, pesticides 

Mimic or block natural effects of 

hormones (estrogen and others); 

developmental abnormalities 

Environmental Tobacco 

Smoke (ETS) Cigarettes, cigars, and pipes 

Respiratory irritation, bronchitis and 

pneumonia in children; asthma in 

preschool children; lung cancer; heart 

disease; aggravated asthma; 

decreased lung function 

Formaldehyde, 

Other Aldehydes 

Composite wood products such as 

plywood and particleboard, furnishings, 

wallpaper, durable press fabrics, paints, 

combustion appliances, tobacco smoke 

Cancer; eye, nose, and throat irritation; 

headache; allergic reactions; aggravated asthma, decreased lung function 

Lead Lead paint chips, contaminated soil Learning impairment 

Nitrogen Dioxide 

Unvented or malfunctioning gas 

appliances, other combustion 

appliances 

Aggravated asthma; decreased lung 

function; eye, nose, and throat 

irritation; increased respiratory disease 

in children 

Organic Chemicals 

(benzene, chloroform, paradichlorobenzene, methylene 

chloride, perchloroethylene, 

others) 

Solvents, glues, cleaning agents, 

pesticides, building materials, paints, 

treated water; moth repellents, drycleaned clothing, air fresheners 

Cancer; eye, nose, throat irritation; 

aggravated asthma; decreased lung 

function; at high levels: loss of coordination, damage to liver, kidney, brain 

Ozone Infiltration of outdoor air, some air 

“purifiers”, office machines 

Lung inflammation, aggravated 

asthma, cough, wheeze, chest pain 

Particulate Matter 

Cigarettes, wood stoves, fireplaces, 

cooking, candles, aerosol sprays, house 

dust 

Increased mortality and hospital 

admissions; lung cancer; irritation; 

susceptibility to sinus and respiratory 

infections; bronchitis; aggravated 

asthma; decreased lung function 

Pesticides 

Insecticides, herbicides, sanitizers, 

disinfectants used indoors, or tracked in 

or blown in from outdoors 

Neurological impairment; nausea, 

headache, dizziness; skin and eye 

irritation; hormone disruption 

Polycyclic Aromatic 

Hydrocarbons (PAH) Cigarette smoke, cooking, woodburning Cancer, gene mutation 

Radon Uranium-bearing soil under buildings, 

ground-water, construction materials Lung cancer (especially in smokers) 

* Please note that when multiple pollutants are listed in a group, each pollutant may not cause all of the health effects 

listed in the third column. 
Indoor Air Pollution in California July, 2005

 4

Asthma 

Asthma is a chronic inflammatory lung disease that results in constriction of the airways. Its 

prevalence has increased dramatically both in California and throughout the country over the 

past few decades. According to 2001 data, 11.9 percent of Californians, or 3.9 million people, 

have asthma (CHIS, 2003). Children have been especially affected; in California, asthma 

prevalence is greatest among 12 to 17 year olds. 

Indoor air pollutants exacerbate asthma symptoms, 

resulting in breathing difficulties. A recent Institute of 

Medicine (National Academy of Sciences) report, Clearing 

the Air: Asthma and Indoor Exposures (IOM, 2000), 

identified new associations between indoor air pollutants 

and asthma, in addition to the traditional indoor asthma 

triggers such as cat and dog dander, house dust mites, and 

environmental tobacco smoke (ETS). The scientists found 

sufficient evidence of an association between exacerbation 

of asthma and exposure to high levels of nitrogen dioxide 

(NO2) and other nitrogen species (NOX), and mold. They 

found limited or suggestive evidence of an association of 

asthma exacerbation with exposure to formaldehyde and 

fragrances. A more recent review of indoor pollution studies 

further identified several links between asthma symptoms 

and specific volatile organic chemicals (VOCs), especially 

formaldehyde (Delfino, 2002). Studies of workplace asthma 

have further demonstrated an association between asthma 

symptoms and VOCs, primarily from cleaning products 

(Rosenman et al., 2003). Several studies also have found 

an association of increased outdoor ozone levels with 

exacerbation of asthma, and one study recently linked 

ozone with the development of asthma in children who are 

active outdoors. Similar effects would be expected with 

exposure to ozone indoors. 

Cancer 

A substantial number of common indoor pollutants have been classified as carcinogens. 

Examples include formaldehyde, benzo(a)pyrene and other polycyclic aromatic hydrocarbons 

(PAHs), tobacco smoke, benzene, chlorinated solvents such as tetrachloroethylene, and radon 

gas. Several studies have measured indoor concentrations of carcinogenic chemicals in 

California homes. Results have shown that carcinogens, especially formaldehyde, are routinely 

found in most homes, often at higher concentrations than concurrent outdoor levels, due to the 

presence of indoor sources. These concentrations result in extended indoor exposures, which 

translate to a significant increase in cancer risk attributable to indoor pollutants, primarily those 

emitted from building materials and consumer products. As shown in Figure ES-2, ARB staff 

estimate that about 230 excess cancer cases may occur annually in California due to exposures 

from the limited number of indoor toxic air contaminants that can be quantified from residential 

and consumer sources. This estimate approaches the estimated cancer burden from outdoor 

diesel exhaust particles, which is responsible for much of the excess cancer burden associated 

with breathing ambient air in California. This indoor cancer estimate also equals about twothirds of the total burden from excess cancer resulting from outdoor air pollutant emissions. 

Asthmatic child testing her lung 

function. Three million 

Californians, including 900,000 

children, have asthma. 
Indoor Air Pollution in California July, 2005

 5

Exposure to environmental 

tobacco smoke (ETS) 

makes a significant 

contribution to the cancer 

burden from air pollution as 

well. The Office of 

Environmental Health 

Hazard Assessment 

(OEHHA) has recently 

estimated about 400 

excess lung cancer deaths 

from ETS for the year 

2004, which translates to 

about 380 excess cases for 

the year 2000, shown in 

Figure ES-2 for 

comparability (based on 

OEHHA estimates as of 

March 2005, as discussed 

in Sections 2.1.2, 2.3.3, 

and 3.1.3). This ETS risk 

level is similar to the total outdoor burden. Despite workplace restrictions and other positive 

trends, the risk from ETS remains significant, because some individuals, especially children in 

households with smokers, are still exposed to substantial levels of ETS. 

Radon, a radioactive gas, enters indoor environments from uranium-containing soil and rock 

under and near buildings, and from some domestic water obtained from groundwater and wells, 

and decays into radioactive radionuclides called radon daughters. Only an estimated 0.8 

percent of California residences have annual radon levels above 4 picoCuries per liter (pCi/l), 

the U.S. Environmental Protection Agency’s (U.S. EPA) recommended mitigation level. 

However, due to its potency and synergism with tobacco smoke, a rough, order-of-magnitude 

estimate extrapolated from national data show that radon may contribute to 1500 excess lung 

cancer deaths per year in California. However, the risk from radon cannot be fully differentiated 

from that of exposure to tobacco smoke (NRC, 1999a), and reducing exposure to tobacco 

smoke is the most effective measure to reduce the risk of lung cancer (NRC, 1999a; Mendez et 

al., 1998). Additionally, the estimated cancer deaths may be an overestimate, because 

exposure to tobacco smoke is notably lower in California than in the rest of the nation, and 

recent measurements indicate somewhat lower radon levels in the Sierra Nevada foothills than 

previously measured, indicating that statewide levels may be lower than previously estimated as 

well. In light of these factors, the actual radon risk in California is uncertain. Because elevated 

radon is found in just a few areas in California, and can vary from building to building, radon 

mitigation is not recommended in existing buildings until adequate testing has been conducted 

in each building, and preventive measures are recommended in new buildings only in areas 

where radon soil levels are elevated. 

Irritant Effects 

Many indoor pollutants cause eye, nose, throat, and respiratory tract irritation. Aldehydes, as 

well as some other VOCs and oxidants, are known mucous membrane irritants. Formaldehyde 

is the most commonly identified irritant. Acute effects of irritant chemicals can include 

respiratory and eye irritation, headache, difficulty breathing, and nausea. Some of these effects, 

Figure ES-2:

Estimated Potential Cancer Burden from Air Toxics 

in California by Source

0

50

100

150

200

250

300

350

400

Outdoor 

TAC

Sources

Indoor 

TAC Sources

Environmental 

Tobacco 

Smoke

Excess Cancers Per Year

Other Outdoor TAC

Sources

Outdoor Diesel

Exhaust (Particles)
Indoor Air Pollution in California July, 2005

 6

particularly respiratory symptoms and eye, nose, and throat irritation, can also be experienced 

with chronic exposure. Preliminary research indicates that indoor oxidants (e.g., ozone) can 

react with terpenes, such as pinene and limonene, frequently used in cleaning products for their 

favorable odor characteristics and solvent properties, to produce formaldehyde and ultrafine 

PM. Further research is needed to understand the extent and duration of exposure to reaction 

products, and the potential health effects of those exposures. 

Irritant chemicals and other factors are suspected of causing or contributing to episodes of Sick 

Building Syndrome (SBS), in which a large number of building occupants experience irritant and 

neurological effects while they are in a building. The specific causes of SBS have not yet been 

firmly identified; however, SBS episodes can affect a high number of workers, have been well 

documented, and have resulted in high costs to some businesses due to reduced productivity 

and, in some cases, legal settlements. The most common symptoms include eye irritation, 

congested nose, headache, fatigue, difficulty concentrating, and skin rash. 

Premature Death and Increased Disease 

Several pollutants for which ambient air quality standards 

have been established, occur at elevated levels indoors due 

to emissions from indoor sources. In other cases, indoor 

sources increase the exposure that occurs when high levels 

of polluted ambient air enters the indoor space. Ambient 

particulate matter (PM) has been associated with premature 

death and serious respiratory and cardiovascular (heart) 

disease in numerous studies. Carbon monoxide (CO) can 

cause death with high exposures of relatively short duration, 

and lower levels can cause flu-like symptoms and other 

health effects. Nitrogen dioxide (NO2) can harm the lungs 

and other mucous membranes, cause respiratory disease, 

and exacerbate asthma. Ozone can have similar effects at 

elevated levels; however, indoor levels are typically lower 

than outdoor levels. Indoor sources of these pollutants 

sometimes cause indoor concentrations that exceed healthbased ambient air quality standards established for outdoor 

air. 

Particulate matter 

Particulate matter (PM) is a complex mixture of very small particles and other non-gaseous 

materials suspended in the air. Indoor particle sources include combustion devices such as 

woodstoves and fireplaces, and activities such as smoking, unvented cooking, candle burning, 

and vacuuming with low performance or leaky vacuums. Indoor particles also include fibrous 

materials, pollen, mold spores and fragments, and tracked-in soil particles. Pollen and mold can 

trigger allergies and asthma. Tracked-in particles and some particles from combustion sources 

become trapped in carpets and have been shown to include a mix of toxic components such as 

polycyclic aromatic hydrocarbons (PAHs) and lead. 

A large number of major epidemiologic studies have consistently shown a strong association 

between outdoor (ambient) PM concentrations and increased mortality from cardiovascular and 

respiratory disease. They also have shown increased morbidity effects with increased PM 

levels, including increased hospitalizations and emergency room visits due to respiratory 

problems such as asthma, chronic obstructive pulmonary disease (COPD), chronic bronchitis, 

A number of indoor air pollutants 

can cause serious disease and 

premature death. 
Indoor Air Pollution in California July, 2005

 7

and pneumonia; increased respiratory symptoms such as cough and wheeze; decreased lung 

function and reduced lung function growth in children; and increased cardiovascular disease 

such as congestive heart failure, stroke, and ischemic heart disease. 

The studies documenting these effects measured outdoor particles, which are composed of a 

mix of particles from combustion sources, soil, and particles formed through chemical reactions 

in the atmosphere. Because a substantial portion of PM from indoor sources is similar to 

outdoor PM components, indoor PM emissions are highly likely to be significant contributors to 

the adverse impacts seen in the epidemiology studies, and they may also contribute to those 

effects beyond the levels quantified in the epidemiology studies. 

Reducing outdoor PM concentrations to the level of the current California ambient air quality 

standard for PM would result in significant reductions in adverse health effects, including 

approximately 6,500 deaths, 17,200 serious non-fatal illnesses, and 340,000 asthma attacks 

each year in California (ARB/OEHHA, 2002). Although current studies have not directly 

addressed the potential impacts of indoor PM on health, if consistent with outdoor PM, the 

impacts of PM of indoor origin are likely to have very large impacts on public health, potentially 

accounting for thousands of additional cases of serious illness and disease each year. 

Carbon monoxide 

Carbon monoxide (CO) is a colorless, odorless gas that causes flu-like symptoms (headache, 

nausea, lethargy) and inability to concentrate, at lower exposure levels over periods of time. At 

very high levels, CO can cause unconsciousness and even death. CO is a product of 

incomplete combustion, emitted from sources such as vehicle exhaust, gas and propane stoves 

and furnaces, woodstoves, kerosene heaters, and cigarettes. 

Very high levels of CO occur relatively infrequently indoors. However, a California study of 

death certificates showed that about 30 – 40 deaths occurred in California each year, on 

average, due to unintentional CO poisoning (Girman et al., 1998; Liu et al., 1993a, 2000). About 

two-thirds of those deaths were attributable to indoor sources. The indoor sources most 

implicated in past CO poisonings were combustion appliances, such as malfunctioning or poorly 

tuned gas or propane furnaces and stoves, and the improper use of charcoal grills and hibachis 

indoors (contrary to warnings). Motor vehicles, such 

as those unwisely left running in a garage, also have 

taken a substantial toll. The relevant literature also 

indicates that other CO health effects occur: 

hundreds of emergency room visits and thousands of 

misdiagnosed flu-like illnesses due to non-fatal CO 

poisoning are estimated to occur each year. 

Nitrogen dioxide and associated acids 

Nitrogen dioxide (NO2) is a red to dark brown gas with 

a pungent acrid odor. Adverse health effects 

attributable to NO2 include exacerbation of asthma 

(especially in children), respiratory symptoms and 

infection, lung damage, and lung disease after long 

periods of exposure. Indoor sources of NO2 include 

gas and propane appliances, wood burning stoves 

and fireplaces, kerosene heaters, charcoal grills, and 

intrusion of motor vehicle exhaust. Indoor levels can 

Unvented appliances are sources of 

nitrogen dioxide, carbon monoxide, 

and other pollutants. 
Indoor Air Pollution in California July, 2005

 8

be especially elevated from the use of older wall furnaces, when their exhaust is not vented to 

the outdoors, and from gas stoves, because people often do not use the exhaust hoods above 

them, or the exhaust is not vented to the outdoors. Several nitrogen compounds related to NO2

also are found in indoor environments, including nitrous acid (HONO) and nitric oxide (NO). 

Nitrogen dioxide is the only nitrogen oxide regulated as a pollutant in outdoor air. 

Ozone 

Ozone is a strong respiratory irritant and the main component of smog. Outdoor ozone is the 

primary source of indoor concentrations of ozone in most indoor environments, but ozone also 

is directly emitted indoors from some types of “air cleaners”, and from poorly maintained laser 

printers and other types of office equipment. Indoor levels typically range from 20 to 80 percent 

of outdoor levels, but have been shown to reach levels that exceed a Stage 1 smog alert level 

when some types of ozone-generating “air cleaners” are used. Breathing elevated 

concentrations of ozone can be harmful to health, especially for active people, including 

children. Whether inhaled indoors or outdoors, ozone can irritate the respiratory tract, which can 

cause coughing, wheezing, and pain on deep breathing. Ozone also can exacerbate asthma, 

particularly with concurrent allergen exposure. Ozone masks the odor of other indoor pollutants 

by deadening the sense of smell. It also reacts with certain indoor pollutants to produce toxic byproducts, including formaldehyde and ultrafine particles. 

Toxic Air Contaminants and Other Indoor Air Pollutants 

Other pollutants can occur at elevated levels indoors due to emissions from indoor sources. 

Some have been identified by the ARB as toxic air contaminants (TACs), air pollutants other 

than traditional (criteria) pollutants that can contribute to an increase in death or serious illness. 

 

• Volatile organic compounds (VOCs) – As mentioned above, VOCs such as formaldehyde 

and chlorinated solvents are common in indoor air, and can exacerbate asthma and cause 

cancer and irritant effects. Some of these chemicals also have reproductive, developmental, 

and neurological effects at very high levels encountered at times in non-industrial 

workplaces. Indoor levels of formaldehyde, a pungent smelling gas, nearly always exceed 

chronic health-based guideline levels and acceptable cancer risk levels. Formaldehyde is 

emitted from numerous indoor sources including building materials (especially pressed 

wood products), composite wood furnishings, personal care products, cosmetics, permanent 

pressed clothing, combustion sources, and some new carpet pads and adhesives. 

• Environmental tobacco smoke (ETS) – ETS causes cancer, heart disease, asthma 

episodes, middle ear infections in children, sudden infant death syndrome (SIDS) and other 

adverse effects. ARB and OEHHA (2005) currently estimate that exposure to ETS results in 

about 400 excess lung cancer deaths, 1,700-5,500 heart disease deaths, and more than 

31,000 asthma episodes per year in children (based on OEHHA estimates as of March 

2005; these estimates are currently under scientific peer review). These estimates would be 

expected to decrease over time, due to the substantial reductions in smoking and ETS 

exposure in California. Nonetheless, despite decreases in the percent of smokers in the 

population and the statewide prohibition of smoking in workplaces, some individuals, 

especially children, are still exposed to elevated levels of ETS in the homes and vehicles of 

smokers. 

• Polycyclic aromatic hydrocarbons (PAHs) – PAHs, emitted from combustion sources 

such as cigarettes, woodstoves and fireplaces, include a number of known or suspected 
Indoor Air Pollution in California July, 2005

 9

carcinogens. They have been found to adsorb onto particles in the air and deposit onto 

carpets, from which they can be resuspended during vacuuming or other activity. 

• Radon daughters and asbestos are other known lung carcinogens found indoors in some 

California environments. Both radon and asbestos are naturally-occurring, each emanating 

from specific types of soils. Radon levels in California are typically lower than mitigation 

guideline levels. Nonetheless, as discussed above, a rough estimate indicates that radon 

may contribute to 1,500 excess lung cancer deaths in California per year. However the risk 

from radon cannot be fully separated from that of tobacco smoke, and reduction of exposure 

to tobacco smoke remains the primary mitigation approach. Indoor asbestos is elevated only 

infrequently, typically during remodeling of older buildings. Naturally-occurring asbestos has 

been measured recently in a few areas of California, and has resulted in some mitigation 

actions. 

• Pesticides and metals – Dust from surfaces and carpets in homes and schools have been 

shown to contain numerous residues of pesticides, lead, mercury and other long-lasting 

contaminants that have originated from outdoor activities, cigarettes, fireplaces, and other 

sources. This is of special concern for very young children, who spend time on the floor, and 

put their hands in their mouths, because ingestion is often the primary route of exposure. 

Pesticides are widely used, and some can cause adverse developmental and neurological 

effects at elevated exposure levels. Many pesticides registered for use today are short lived, 

yet some are persistent in the environment, lasting 20 or 30 years or more. Recent studies 

indicate that some pesticides are more persistent in indoor environments, because they do 

not experience the effects of weather and sunlight. 

Biological Contaminants 

Biological contaminants include substances of plant, animal, or microbial origin, such as 

bacteria, viruses, mold, pollen, house dust mites, animal dander; biological toxins such as 

endotoxins and mycotoxins, and microbial volatile organic chemicals. These biological agents 

are abundant in both indoor and outdoor environments, but are considered contaminants when 

found in undesired locations or at elevated concentrations. Excessive exposure to these 

contaminants can be associated with mucous membrane irritation (which may cause symptoms 

such as itchy eyes, runny nose or sore throat) or hypersensitivity reactions such as asthma 

attacks or allergy symptoms in sensitive individuals. Some individuals in persistently damp 

buildings report a variety of symptoms such as headache, memory difficulties, vomiting, and 

diarrhea; some researchers postulate that exposure to biological toxins may induce such 

symptoms. In a recent Institute of Medicine report (IOM, 2004), scientists found a number of 

symptoms and illnesses associated with dampness in buildings and with indoor mold, although 

the scientific evidence was not yet considered sufficient to confirm a causal relationship. 

Many communicable diseases are primarily transmitted from person to person in indoor air; 

others can thrive in buildings where conditions suit them, and infect occupants. Common viral 

infections such as influenza, measles and chicken pox, as well as emerging diseases such as 

Severe Acute Respiratory Syndrome (SARS), are spread through inhalation of viruscontaminated droplets produced when an infected person coughs or sneezes, or from touching 

a surface or object contaminated with infectious droplets and then touching one’s mouth, nose, 

or eyes (CDC, 2004a). Tuberculosis is a notorious infectious disease that is transmitted in 

closely occupied spaces. Building-related illness (BRI) refers to an illness for which the specific 

cause can be identified within the building, such as bacteria in ventilation systems causing 

Legionnaires’ disease, or humidifier fever. The usual causes of BRI include viruses, bacteria, 
Indoor Air Pollution in California July, 2005

 10

and fungi. BRI impacts can be substantial, and are of increasing interest as the role of buildings 

in promoting diseases of biological contaminants becomes better understood. 

III. INDOOR CONCENTRATIONS AND PERSONAL EXPOSURES 

Indoor concentrations of many pollutants sometimes exceed health-based guideline levels or 

standards. Some pollutants, like formaldehyde, nearly always exceed recommended levels. 

Studies conducted by the ARB, the U.S. EPA, and others also have shown that indoor levels of 

VOCs and some other pollutants are often higher than outdoor levels. 

More importantly, people’s “personal exposures” to pollutants, especially to VOCs, are often 

greater than both indoor and outdoor pollutant levels. Personal exposures to some pollutants 

are elevated because people spend time very near sources of pollutants, such as when using a 

gas stove, cleaning solutions, or personal care products. During such activities, the product 

emissions are most concentrated very near the person. Pollutants become more diluted in the 

air as distance from the source increases. Consequently, for VOCs and many other pollutants, 

personal exposure levels are most closely correlated with indoor concentrations. 

Indoor – Outdoor Relationships 

There is continuous air exchange between indoor environments and the outdoors. Outdoor 

emissions readily infiltrate into indoor environments, and indoor emissions seep outdoors and 

can contribute to outdoor air pollution. For example, ozone formed outdoors and fine particles 

and other emissions from nearby motor vehicles typically penetrate indoor environments to 

varying degrees, depending on the rate of air exchange, degree of filtration, and other factors. 

For residential buildings, the main entry routes of outdoor air are open windows and doors, gaps 

in the building shell, and devices such as swamp coolers that move outdoor air indoors. For 

large public and commercial buildings, the main entry route is through the mechanical heating, 

ventilating, and air conditioning (HVAC) systems, which actively move outdoor air indoors and 

typically filter some of the particles from the air. Any pollutants in the air just outside the building 

may thus be brought into the indoor space. Indoor pollutant levels can be much higher than 

those outdoors when indoor sources are present and the air exchange rate is low. 

Similarly, indoor pollutants can flow through windows and penetrate small gaps in the building 

shell to contribute to the local outdoor burden of pollution. Emissions from certain sources used 

indoors, such as paints, consumer products, and gas and woodburning appliances contribute to 

local outdoor pollution levels, either through direct emissions or, in the case of reactive volatile 

organic chemicals, through chemical reactions. 

Environmental Justice Considerations 

ARB adopted an environmental justice policy in 2001. This policy requires the fair treatment of 

all people regardless of gender, ethnicity, and socioeconomic status. The limited research 

available indicates that some segments of the population may be disproportionately exposed to 

indoor pollutants. In California, African Americans, American Indians, and Alaska natives 

experience a higher prevalence of lifetime asthma (Meng et al., 2003). However, in general, the 

prevalence of asthma appears to be more strongly correlated with lower socioeconomic status 

than with race and ethnicity (IOM, 1993). Dust mites, cockroaches, and mold are important 

asthma triggers that are more likely to be present in locations where lower income individuals 

most often live. Additionally, research indicates that blood lead levels are higher for poor and 
Indoor Air Pollution in California July, 2005

 11

minority children in central cities. Formaldehyde levels have been highest in mobile homes, 

which are more often occupied by lower income families. 

The ARB has taken steps to address some of these issues. Special air monitoring studies have 

been conducted at schools in some communities, and a large asthma study is underway. Fact 

sheets for public outreach have been published in English and Spanish. Efforts are underway to 

limit formaldehyde emissions from composite wood products through an Air Toxics Control 

Measure. Pursuit of indoor mitigation measures can further help reduce any disparities in 

exposure and health impact that may exist among different groups of the population. 

Non-industrial Workplaces 

Non-industrial workplaces often provide 

unique situations for exposure to indoor air 

pollutants. Products and activities associated 

with non-industrial workplaces such as 

beauty salons, hospitals, dry cleaners, 

medical laboratories, jails, photocopy 

centers, aircraft cabins, indoor sports arenas, 

retail shops, copy shops, and other 

workplaces can lead to elevated levels of air 

pollutants and indoor environmental 

concerns. Despite the California 

Occupational Safety and Health Program’s 

(Cal/OSHA’s) regulations for pollutant levels 

and ventilation requirements, some workers 

in these environments experience adverse 

health effects related to indoor environmental 

quality. Additionally, many of these locations 

are regularly visited by members of the 

public. 

Cal/OSHA has various regulations to address ventilation and personal exposures, but most 

indoor air quality complaints arise in non-industrial workplaces, where preventive controls are 

not normally utilized. A review of Cal/OSHA inspection data indicates ventilation requirements 

are often not met. From 1995 through 2001, citations for ventilation violations were issued 

during 519 on-site inspections. Of these citations, the majority (260) were in services, with 114 

in schools and 33 in health care. A substantial number of citations were issued for other indoor 

air quality violations as well, but there are inconsistencies in recordkeeping, making it difficult to 

analyze for indoor air quality concerns. However, from 1997 through 1999, 849 workplace 

inspections were coded as indoor air investigations, and Cal/OSHA has indicated that the actual 

number of indoor air quality related inspections may be more than twice that number. 

IV. COSTS OF INDOOR POLLUTION 

Indoor air pollution takes a significant toll on Californians’ lives and has significant economic 

costs. Exposure to indoor pollutants results in premature death and increased disease, 

increased expenditures for health care, decreased worker productivity, and decreased learning 

by school children. Table ES-2 shows estimates of the annual costs of indoor air pollution in 

California that are currently quantifiable. It includes the valuation of health (cost of premature 

death), an estimate of the increased expenditures for health care, and an estimate of some of 

Workers who work in some non-industrial 

workplaces can experience harmful exposures 

to indoor air pollutants. 
Indoor Air Pollution in California July, 2005

 12

Table ES-2. Summary of Estimated Annual Costs of 

Some Indoor Air Pollutants in California 

Health End Point 

Health 

Valuation: 

Premature 

Death1-3 

($ Billions/yr)

Medical 

 Cost 2-4 

($ Billions/yr)

Lost 

Productivity 

Cost 2,3 

($ Billions/yr) 

Total Cost

($ Billions/yr)

CO: poisoning 0.15 <0.001 NA 0.15 

VOCs: cancer 0.73 0.011 NA 0.74 

ETS: lung cancer 2.4 0.025 NA 2.4 

ETS: heart disease 23 0.055 NA 23 

ETS: asthma episodes NA 0.0205 NA 0.020 

ETS: low birth weight NA 0.19 NA 0.19 

ETS: otitis media NA 0.0195 NA 0.019 

Radon: lung cancer 9.5 0.097 NA 9.6 

Mold and moisture: 

 asthma and allergies 0.031 0.195 NA 0.22 

Sick building syndrome NA NA 8.5 8.5 

 TOTAL6 36 0.6 8.5 45 

1. From Table 3.2. 

2. Estimates are based on average or mid-point of incidence rates of death and disease from previous tables, and 

estimates of productivity discussed in the text. Values are rounded to two significant figures. 

3. Original data were adjusted to year 2000 dollars and year 2000 population, except where noted otherwise in 

Section 3 of this report. 

4. From Table 3.3. 

5. Includes indirect costs such as lost work days, lost school days, and travel expenses. 

6. Totals are rounded to two significant figures. These totals are likely low because conservative cost estimates 

were used, and quantitative information is not readily available for many known impacts of indoor air pollution, 

such as for indoor PM and many indirect costs of health effects. 

the costs associated with reduced worker productivity. Because of the limited amount of 

information available for accurately estimating indoor pollution costs and the broad range of 

effects and resultant costs, there is considerable uncertainty in the cost estimates shown. Most 

importantly, the costs of many known or suspected indoor pollution impacts cannot currently be 

quantified due to lack of cost data and/or sufficiently quantified population exposure data. For 

example, the costs for the impacts of biological contaminants and indoor PM-related illness and 
Indoor Air Pollution in California July, 2005

 13

disease are likely to be very high, potentially in the billions of dollars, but are not yet 

quantifiable. Additionally, while ETS has been well-studied and its impacts and costs can be 

reasonably quantified, the impacts and costs for some other toxic indoor pollutants have been 

less studied and cannot be quantified at this time. 

The combined cost of both fatal and non-fatal impacts due to indoor air pollution in California 

homes, schools, and non-industrial workplaces is substantial: it is estimated to be $45 billion 

per year. As shown in Table ES-2 and discussed in Section 3 of this report, the annual 

valuation of premature deaths attributable to indoor air pollution is estimated to total about $36 

billion, with most stemming from ETS and radon. OEHHA’s ETS risk estimates from March 2005 

are currently under review by the Scientific Review Panel, and may change after this report 

becomes final. The actual total valuation of premature deaths is likely to be higher than the $36 

billion presented here, because these estimates do not include the impacts of other pollutants 

that may increase the risk of premature death, such as other carcinogens emitted from materials 

and products, and PM from cooking, wood smoke, and other indoor combustion sources. 

The quantifiable medical costs (direct and some indirect) due to indoor air pollution total more 

than $0.6 billion per year, with a large portion of the costs attributable to mold and other 

moisture-related allergens. These cost estimates for morbidity do not include the potential 

losses due to other impacts such as those from other indoor allergens, the long-term effects of 

CO poisoning, reduced student performance, lost earnings opportunity, unpaid caregivers, and 

human suffering. Finally, the cost of reduced worker productivity due to indoor air pollution 

(primarily sick building syndrome) that could be prevented is estimated to be about $8.5 billion 

per year. 

V. EXISTING REGULATIONS, GUIDELINES AND PRACTICES 

Despite the significant health effects and potential economic impacts caused by indoor sources 

of pollution, there are few government standards restricting emissions from common sources of 

indoor pollutants, and there is no comprehensive program to protect air quality within 

residences, schools, or public and private buildings. A variety of agencies and organizations 

have established standards and guidelines that can be applied to limited aspects of indoor 

environments to assist in the assessment and control of health hazards from air pollutants. 

Foremost among these are workplace standards; however, those standards are designed for 8-

hour exposures of healthy adults, are not as protective as standards set for ambient air, and are 

not designed to protect the more sensitive subgroups of the population, such as children. Other 

standards are applicable to indoor air quality, but only in a limited way. For example, ambient air 

quality standards and emission control regulations indirectly improve IAQ by improving ambient 

air quality, and Assembly Bill 13 (1995) prohibits cigarette smoking in workplaces. Although 

many of these programs have resulted directly or indirectly in improvements in indoor air quality, 

they are not adequate to ensure healthful indoor air quality. 

• Workplace Standards. The California Occupational Safety and Health Program 

(Cal/OSHA) in the Department of Industrial Relations (DIR) has authority to develop, 

promulgate, and enforce air pollutant exposure limits, ventilation regulations, and other 

standards for the workplace that directly impact indoor air quality. The California 

Occupational Safety and Health Standards Board is the unit within the Cal/OSHA program 

with authority to adopt standards and regulations to protect workers. Some of the Cal/OSHA 

standards and regulations that impact indoor air quality are the following: 
Indoor Air Pollution in California July, 2005

 14

9 Permissible Exposure Limits. The Standards Board sets permissible exposure limits 

(PELs) and other limits for airborne contaminants. The PELs are 8-hour exposure limits 

generally protective of the health of most workers. However, they are not designed to 

protect vulnerable members of the population such as infants, the elderly, or individuals 

with pre-existing heart or respiratory disease. Additionally, they are not intended to be 

protective for exposures greater than eight hours per day, five days a week, and PELs 

are not available for all indoor air contaminants. 

9 Ventilation. Cal/OSHA requires employers to maintain and operate mechanical 

ventilation systems to provide at least the quantity of outdoor air required by the State 

Building Code at the time the building permit was issued. 

9 Mold, moisture. Cal/OSHA requires that workplaces be maintained in a sanitary 

condition, and that employers correct all types of water intrusion or leakage, to reduce 

the potential for mold growth. 

• Ventilation design requirements. Minimum ventilation levels for the design quantity of 

outdoor air in new non-residential buildings, such as offices and public buildings, have been 

established by the California Energy Commission for different types of buildings and 

different types of rooms (e.g., conference rooms vs. offices). The Commission also sets 

energy efficiency standards for residences, which has resulted in reduced infiltration of 

outdoor air, or “tightening” of new homes compared to older homes. This has implications for 

indoor air quality, and the Commission is funding research to assess the need for revisions 

to the standard to assure healthful indoor air quality in homes. 

• Anti-smoking law. Cigarette smoking, a major source of indoor pollution, is prohibited in 

nearly all public buildings in California. A statewide, smoke-free workplace law passed in 

1995 (AB 13) eliminated smoking in nearly all California indoor workplaces–including 

restaurants, bars and gaming clubs–and spurred a reduction in smoking by the California 

population. The ban has been very successful in reducing worker exposure to cigarette 

smoke. In 1999, 93 percent of California’s indoor workers reported working in a smoke-free 

environment, compared to only 35 percent in 1990 (Gilpin et al., 2001). The prohibition of 

workplace smoking, along with the Department of Health Services Tobacco Control 

Program, have both had far reaching benefits. In 1994, 63 percent of Californians with 

children did not allow smoking in the house; by 2003, 77.5 percent did not allow it (DHS, 

2004b). Additionally, smoking rates among California adults declined from 26 percent to 17 

percent between 1984 and 2001 (BRFSS, 2001). 

• State and national ambient air quality standards (AAQS) and control programs, 

established by the ARB and U.S. EPA, respectively, are developed to protect the general 

public from the harmful effects of “traditional pollutants” in outdoor air, for specified 

averaging times (exposure times). California’s AAQS are often more protective than the 

national AAQS. Currently, the State AAQS are under review to ensure that they are 

protective of sensitive populations, especially infants and children (ARB/OEHHA, 2000). In 

the absence of indoor air quality standards or guidelines, the AAQS serve as useful 

guideline levels for those pollutants indoors, because they are based on specified averaging 

times and incorporate a margin of safety. Both the California and federal AAQS are listed at 

http://www.arb.ca.gov/research/aaqs/aaqs.htm. 
Indoor Air Pollution in California July, 2005

 15

• Consumer product standards. The federal Consumer 

Product Safety Commission (CPSC) has jurisdiction over 

consumer products, except for pesticides, cosmetics, tobacco 

and cigarettes, food, drugs, automobiles, and a few others. 

CPSC has authority to ban a product, establish mandatory 

safety standards, recall products for repair or replacement, 

require warning labels, or develop voluntary standards in 

conjunction with manufacturers. However, CPSC is primarily 

focused on addressing safety issues, and most often uses 

voluntary processes and labeling requirements. 

The ARB also regulates consumer products, for the purpose 

of reducing smog in California. An additional benefit is a 

reduction in the amount of certain types of VOCs that are 

released in homes and institutions. In addition to reducing the 

reactive VOC content of products, ARB has prohibited the use 

of several toxic air contaminants in 13 categories of products, 

resulting in reduced indoor emissions of those substances. 

Reducing reactive VOC emissions and toxic pollutants from 

cleaning compounds, polishes, floor finishes, cosmetics, personal care products, 

disinfectants, aerosol paints, and automotive specialty products has likely reduced personal 

exposures to those VOCs as well. 

• Pesticides. The U.S. EPA, the California Department of Pesticide Regulation (DPR), and 

county agricultural commissioners all have a role in regulating pesticides in California. The 

U.S. EPA registers, or licenses, pesticides, ensuring that the pesticide, when used 

according to label directions, can be used with a reasonable certainty of no harm to human 

health and without posing unreasonable risks to the environment. DPR provides for the 

proper, safe, and efficient use of pesticides, and for protection of the environment and 

health. To accomplish this, DPR has its own registration program and requirements, above 

those required by EPA. DPR continues to evaluate pesticides once they are registered, 

through programs to assess worker safety, water and air contamination, and pest 

management alternatives. DPR’s pest management program promotes integrated pest 

management (IPM), which is the use of preventive measures, and the use of least toxic 

pesticides when pesticides are needed. California’s 

county agricultural commissioners enforce pesticide laws 

and regulations at the local level: they issue/deny permits 

for restricted materials, taking into account local 

circumstances, and may include additional conditions on 

the permit. They also certify private applicators, conduct 

inspections, provide training, and are responsible for 

investigating pesticide-related illnesses and damage. 

• Local woodburning ordinances. Several communities 

in California have implemented woodburning ordinances 

or policies to reduce smoke emissions in their 

communities. For example, in the San Francisco Bay 

area, 24 cities have ordinances that prohibit conventional 

fireplaces in new construction. The mountain town of 

CPSC often uses labeling 

requirements to address 

product health hazards. 

Some California cities regulate 

woodburning. 
Indoor Air Pollution in California July, 2005

 16

Truckee has a more aggressive policy that states that existing unapproved wood burning 

appliances must be removed from all properties by July 15, 2006. The San Joaquin Valley 

Air Pollution Control District issues daily advisories on restrictions for residential wood 

burning. 

• Guidelines and Public Education.

9 OEHHA has developed acute and chronic reference exposure levels (RELs) as 

guidelines to prevent harm from toxic air pollution, under the Air Toxics “Hot Spots” 

Information and Assessment Act of 1987 (HSC Section 44300 et seq). Although 

established to identify healthful limits for outdoor air near industrial sources, RELs have 

been used for indoor pollutants as indicators of potential adverse health effects other 

than cancer. OEHHA has established chronic RELs for 79 air pollutants to define 

healthful levels for exposures that can last 12 years or more (OEHHA, 2003a), and acute 

RELs for 51 chemicals to define healthful levels for exposures of one hour (OEHHA, 

2000a). OEHHA also has developed an 8-hour, interim indoor REL (IREL) for 

formaldehyde of 27 ppb, specifically for indoor application. This IREL identifies the level 

below which effects such as eye, nose, and throat irritation would not be expected to 

occur during typical daytime (8-hour) occupancy of buildings. 

9 ARB’s Indoor Air Quality Guidelines have been developed to advise the public 

regarding the health effects and indoor sources of key indoor pollutants, and what the 

public can do to reduce their exposures. Some AAQS are used as recommended 

maximum exposure levels in ARB’s Supplement to the Combustion Pollutants Guideline. 

ARB’s guidelines for formaldehyde and chlorinated solvents recommend achieving as 

low a level of those pollutants as possible indoors, because they are carcinogenic, and 

there are no known levels that are absolutely safe. 

9 DHS and other agencies have developed various guidelines that can be applied to 

improve indoor environments. DHS published guidelines for reducing VOCs in new office 

buildings in 1996, played a key role in the development of Section 01350 emissions 

limits for materials used in state buildings and schools, and has been directed to develop 

guidelines to prevent and remedy mold problems in buildings. The California Energy 

Commission spearheaded the formation of the Collaborative for High Performance 

Schools (CHPS), which has developed a Best Practices Manual that include guidance 

for selecting building materials with reduced indoor pollutant emissions. The U.S. EPA 

has developed its IAQ Tools for Schools Program to provide guidance for assuring 

healthful indoor air quality in schools. All of these and ARB’s indoor air quality guidelines 

are available at no charge on the Internet. 

9 Industry and professional groups have developed numerous guidelines for improving 

indoor air quality. Examples include the building ventilation requirements of the 

American Society of Heating, Refrigerating, and Air-conditioning Engineers (ASHRAE), 

the product emissions criteria of the Carpet and Rug Institute’s (CRI) Green Label and 

Green Label Plus Programs, and voluntary formaldehyde emission limits of the 

Composite Panel Association and the Hardwood Plywood and Veneer Association. The 

industry and professional guidelines vary in their degree of IAQ protection, but are widely 

used and generally have helped reduce some indoor pollutants over the years.
Indoor Air Pollution in California July, 2005

 17

Minimizing indoor emissions is generally 

more effective than removing them after 

emission has occurred. 

T.J. Kelly, Battelle, Indoor Air Quality Symposium: Risk 

Reduction in the 21st Century, Sacramento, May, 2000 

VI. METHODS TO PREVENT AND REDUCE INDOOR AIR POLLUTION 

There are a number of methods that can be used to prevent or reduce indoor air pollution. The 

most effective approach is to remove or reduce indoor emissions by using building materials, 

consumer products, and appliances that emit little or no air pollution. Ventilation (including 

proper exhaust ducting) and public and professional education also are important components 

of a strong indoor air quality improvement program. Air cleaning devices (air filters and air 

cleaners) can be helpful in certain situations; however, their effectiveness is often limited, and 

some air cleaners actually release ozone into the indoor environment, adding to the indoor 

pollutant burden. 

• Source control is the most reliable 

approach to prevent indoor pollution 

because it does not depend on 

building maintenance or other human 

actions to assure healthful indoor air 

(NRC, 1981). Source control includes 

source substitution, source removal, 

and source modification. Reduction at 

the source is most effectively achieved through use of low- or zero-emitting products, 

materials, or appliances, or reformulation of chemical products. For example, indoor 

formaldehyde levels can be greatly reduced by using building materials that emit little or no 

formaldehyde, instead of materials made with urea-formaldehyde resins. Low emission 

product designs or reformulations can usually be accomplished by the manufacturer, with 

minimal impact on the consumer, often with only minor increased costs. 

• Ventilation is a standard engineering approach to assuring good indoor air quality and 

comfort. Ventilation removes and dilutes indoor contaminants, removes moisture from the air 

which helps to prevent mold growth, and removes body effluents such as carbon dioxide 

that lead to a stuffy environment. Natural ventilation, through open windows and doors, is 

the primary ventilation route for residences, while mechanical ventilation, using HVAC 

systems, is most common in commercial buildings. Adequate and effective ventilation, and 

ducting of exhaust from combustion appliances, are necessary for acceptable indoor air 

quality, even when known air contaminants are minimized. However, ventilation is not a 

complete solution to indoor pollution: ventilation consumes energy, and some pollutants, 

such as formaldehyde emitted from building materials, require years to off-gas and are not 

completely removed by ventilation. 

• Proper operation and maintenance of buildings is critical to achieving and maintaining 

healthful air quality in buildings. Ventilation systems should be maintained as intended and 

filters replaced routinely to prevent soiling and the growth of mold and bacteria in the 

ventilation system and in the occupied space. Roof leaks that are not repaired promptly can 

lead to moisture intrusion and mold growth. Regular cleaning of indoor spaces with proper 

cleaning methods can reduce biological contaminants, such as those associated with 

insects and pollen, as well as persistent chemicals. Inattention to proper operation and 

maintenance will not only lead to poor indoor air quality, but can also prove more costly in 

the long term due to increased costs to remedy the larger problems that result. 

• Public and professional education is a key step for reducing Californians’ exposures to 

many indoor air pollutants. People’s choices and activities have a major impact on their 
Indoor Air Pollution in California July, 2005

 18

exposures to air pollution. The use of various consumer products, and activities such as 

cigarette smoking and cooking can result in significant indoor releases of pollutants. 

Additionally, the actions of professionals in the building, healthcare, and education 

professions, for example, can have a major impact on indoor air quality and how it is 

addressed. However, education alone is not a complete solution. Some groups of the 

population cannot respond appropriately to take needed action. For example, children 

cannot read or understand all written information that is provided; elderly people living in 

group settings cannot control the products used in their facility; and low-income families may 

not be able to afford safer alternatives. 

• Air cleaning devices can also help improve indoor air quality; however, their effectiveness 

is often limited. Air cleaning devices include both central air filters and portable air cleaning 

appliances. Air filters are a normal component of mechanical HVAC systems in public and 

commercial buildings. High efficiency particulate arrestor (HEPA) filters, though not 

commonly used in 

commercial buildings, are 

most effective at removing 

particles from outdoor air as 

it is brought indoors. Air 

cleaning appliances are 

usually portable units used 

indoors to remove particles 

from the indoor air, although 

a few remove gases, and 

some remove both particles 

and gases. Mechanical air 

cleaners typically draw air through a filter while electronic air cleaners remove pollutants with 

the use of an electric charge. Electrostatic precipitators (ESPs) and ionizers are the two 

major types of electronic air cleaners on the market. 

The proper air cleaner may help control airborne particles in some situations; however, the 

limited scientific evidence available has not documented any health benefits from air 

cleaners. Most importantly, air cleaners that generate ozone intentionally should not be used 

indoors (ARB, 2005a,b; DHS, 1998; ALA, 1997). Independent studies by the U.S. EPA, the 

Consumers Union, and others have shown that these devices can emit very high amounts of 

ozone – several times the state ambient air quality standard. Additionally, ozone generators 

do not effectively destroy microbes, remove odor sources, or reduce indoor pollutants 

enough to provide any health benefits. Despite this, they are currently unregulated. ESPs 

and ionizers can produce ozone as a by-product of their technologies; proper use and 

maintenance are critical to prevent harmful levels from developing when using these 

devices, and a few such air cleaners may emit harmful levels of ozone despite proper use. 

VII. PRIORITIZATION OF INDOOR SOURCES BASED ON EXPOSURE AND 

ADVERSE IMPACTS 

Reduction of public exposure to many indoor air pollutants is most effectively achieved by 

reducing pollution at the source. Tables ES-3.1 and ES-3.2 suggest a prioritization scheme for 

implementation of mitigation measures, by source categories. The source categories have been 

ranked into two groups–high and medium priority–and are listed alphabetically within each 

ranking group. The primary factors considered in prioritizing the source categories include the 

Ozone-generating Air Cleaners 

"These machines are insidious. Marketed as a strong 

defense against indoor air pollution, they emit ozone, the 

same chemical that the ARB and U.S. EPA have been trying 

to eliminate from our air for decades." 

Barbara Riordan, interim ARB Chairperson. California Air Resources Board, 

Press Release 05-02, Sacramento, January 2005. 
Indoor Air Pollution in California July, 2005

 19

Table ES-3.1. High Priority Source Categories for Mitigation 1 

SOURCES OF POLLUTANTS2 

(listed alphabetically) 

EXAMPLES OF 

POLLUTANTS3

 EMITTED 

POTENTIAL 

APPROACH TO 

MITIGATION4

DIRECT STATE 

AUTHORITY TO 

TAKE IAQ 

MITIGATION 

ACTIONS 

Air Cleaners 

(ozone-generating) 

Ozone Emission limitations No 

Biological Contaminants

(mold, pollen, bacteria, 

viruses, house dust mites, 

cockroaches) 

Particles, allergens, asthma 

triggers, toxins 

Requirements for 

habitable spaces; 

require certification of 

mold assessors and 

mitigators 

Limited 

Building Materials & 

Furnishings 

(particle board, plywood, 

paneling, flooring, caulk, 

adhesives, new carpet 

assembly, furniture) 

Formaldehyde, 

acetaldehyde, benzene 

derivatives, acrylates, 

naphthalene, phenol, some 

other VOCs 

Emission limitations, 

product use 

restrictions, market 

incentives 

Limited (some 

indirect) 

Combustion Appliances

(unvented gas & propane 

stoves, ovens; poorly vented 

furnaces, heaters; 

woodstoves and fireplaces) 

Carbon monoxide, nitrogen 

oxides, particles, soot, 

polycyclic aromatic 

hydrocarbons 

Active exhaust 

ventilation, safety 

devices, product use 

restrictions, product redesign, improved 

venting, emission 

limitations 

No 

Environmental Tobacco 

Smoke 

(cigarettes, cigars)

Particles, polycyclic 

aromatic hydrocarbons, 

benzene, carbon 

monoxide, some other 

VOCs 

Focused parent 

education; reduce 

smoking in homes and 

vehicles 

Yes, workplaces. 

No, private 

homes and 

vehicles. 

Radon 

(soil, rock, ground water, 

building materials containing 

radium) 

Radionuclides (radon gas) Screening 

measurements, local 

building codes 

Limited 

1. Individual sources may be higher or lower than the source category ranking. 

2. All of the examples of pollutant sources may not emit all of the pollutants listed in the corresponding box in 

column two. 

3. Air pollutants may be identified as Toxic Air Contaminants (TACs) by the California Air Resources Board, and/or 

identified as Proposition 65 chemicals; or, criteria (traditional) air pollutants.

4. Public education, economic incentives, and non-regulatory approaches should also be used where appropriate. 

The actual approach taken would be determined after extensive discussions with the relevant industries, in 

consideration of costs, feasibility, and effectiveness. 

extent of the population’s exposure to the sources and their emissions, the relative reduction in 

health impacts that could be achieved with further action beyond any already undertaken, ease 

of mitigation, and trends in emissions from and use of source categories. A quantitative 

prioritization was not undertaken because such an effort is well beyond the scope of this report. 
Indoor Air Pollution in California July, 2005

 20

Such an effort would be an appropriate step prior to taking action under a comprehensive 

program to address indoor sources. Additionally, the preliminary indoor air pollution cost 

estimates provided in this report were considered, but were not weighted heavily in the 

prioritization because they primarily reflect the availability of cost information and the length of 

time a given pollutant, such as ETS and radon, has been studied, not necessarily the actual 

extent of exposure and risk in California. 

Tables ES-3.1 and ES-3.2 also suggest potential approaches for mitigating the pollutants and 

sources listed. Emission reductions should be accomplished at the manufacturing, distribution, 

or design stage. Alternatives or mitigation options are currently available for most of the sources 

listed. Emission limitations achieved at the manufacturing stage, such as reducing toxic 

contaminants in building materials, would be effectively invisible to the consumer and assure 

exposure reduction. For example, low-emitting carpets, no-formaldehyde furniture, and nontoxic cleaning products are currently sold in the marketplace. Alternative products or 

formulations must be recommended with care, however: substitutes should not result in 

increased emissions of, or exposures to, other toxic pollutants. 

Finally, Tables ES-3.1 and ES-3.2 include a column indicating whether direct authority exists at 

the state level to take the mitigation actions listed in column three. For most source categories, 

there is no state agency with clear, direct authority to take the mitigation actions indicated. In 

some categories, one or more agencies has limited authority to address a small portion of the 

sources included. For example, if needed, Cal/OSHA could impose product use restrictions or 

require other actions to reduce worker exposure to institutional cleaning product emissions. 

However, neither Cal/OSHA nor any other state agency has direct authority to restrict pollutant 

emissions from cleaning products for the purpose of reducing indoor air concentrations and 

exposures. In other cases of limited authority, the benefits to indoor air are incidental results 

from actions taken under the agency’s primary authority, or mitigation actions required to avoid 

negative impacts from regulations. 

The specific rationale for the ranking of each category is briefly discussed below. Note that 

some individual sources within the group may have a higher or lower priority. A more detailed 

assessment would be needed to prioritize specific products within these larger categories. 

High-Ranked Source Categories 

• Air cleaning devices or “air purifiers” that generate ozone can produce unhealthy levels 

of ozone in indoor environments. Some devices marketed as air cleaners purposely release 

ozone, which can result in ozone concentrations several times the State ambient standard, 

and directly harm sensitive occupants. Additionally, these air cleaners are ineffective at 

cleaning the indoor air. Many effective alternatives, such as those with high efficiency 

particle filters, are available in the marketplace. Ionizers and electrostatic precipitators emit 

ozone to varying degrees as a by-product of their function, and such emissions may need to 

be limited. The market for air cleaners has increased substantially in recent years, and is 

expected to continue to expand (Freedonia, 2004).

• Biological contaminants are a high priority because of their ubiquitous presence and their 

widespread health and fiscal effects. Animal dander, pollen, house dust mites, and 

cockroaches cause millions of sensitive individuals to experience allergy symptoms and 

asthma attacks. Indoor mold has been an increasing problem in recent years, costing 

substantial sums of money for remediation and lawsuit settlements. Bacteria such as 
Indoor Air Pollution in California July, 2005

 21

Legionella cause both serious and mild illness. Disease transmission can occur because 

infectious agents are emitted into the indoor environment. Infectious disease transmission is 

increased in indoor environments with crowded or dirty conditions and insufficient outdoor 

airflow. Mitigation actions for mold and some other biologicals might include preventive 

measures such as required annual inspections and prompt remediation in public buildings, 

group homes, and rental units, and in private homes at the time of sale. Certification 

requirements for mold assessors and remediators and other IAQ consultants would help 

assure the quality of inspections and remediation. 

• Building materials and furnishings

are a high priority for mitigation 

because they often emit multiple toxic 

air pollutants, especially when new, 

and have a high loading level in indoor 

environments, resulting in high 

exposure levels for occupants. A 

substantial percent of the population is 

exposed to such emissions due to the 

continued high rate of new building 

construction in California and the 

increasing number of home 

renovations undertaken by 

homeowners. Emission limits for pollutants emitted from building materials and furnishings 

(formaldehyde being the most predominant) would benefit all indoor environments and has 

potential for significant health benefits due to reduced incidence of asthma exacerbation, 

cancer, and eye, nose and throat irritation. 

Low-emitting alternatives are available. For example, non-wood alternatives and composite 

wood products made with phenol-formaldehyde resin have much lower formaldehyde 

emissions than composite wood products made with urea-formaldehyde resin, and could be 

substituted for some applications. In cabinets and furniture, all surfaces of these products 

can be coated or laminated to substantially reduce 

formaldehyde emissions. Building materials are 

currently available that meet Section 01350 emission 

requirements for formaldehyde and other chemicals of 

concern. A list of products for use in school construction 

projects that meet these requirements is available at 

http://www.chps.net/manual/lem_overvw.htm. These 

alternative materials are available and should be 

required in public buildings, group homes, schools, and 

other buildings. 

• Combustion appliances are also a high priority for 

mitigation, especially unvented appliances. They can 

emit carbon monoxide, nitrogen dioxide, polycyclic 

aromatic hydrocarbons, particles, and other pollutants. 

These pollutants can have severe acute health effects 

including respiratory disease and exacerbation of 

asthma, and contribute to cancer risk. Although most 

combustion appliances are used on an intermittent 

basis, they are used regularly (daily, or more often) and 

Some compressed wood materials emit 

formaldehyde. 

Cabinetry and gas appliances 

are common indoor sources that 

warrant attention. 
Indoor Air Pollution in California July, 2005

 22

are widespread throughout the building stock. Reduced exposure to pollutants from gas and 

propane appliances, whether it be through active exhaust ventilation or other measures, 

could have immediate widespread benefits for occupants in environments with such 

appliances. Precedence for mitigation of appliance emissions has been set in the state’s 

low-income weatherization program. 

Statewide measures to reduce emissions from woodstoves and fireplaces both indoors and 

outdoors also are highly desirable. Such measures could have a major impact on improving 

both community-wide indoor and outdoor air quality in many areas of the state. Emission 

limitations, product re-design, product use restrictions, and improved venting can be used 

for reducing this type of pollution. A number of local government entities have approved 

regulations restricting the use of woodstoves and fireplaces: in the San Francisco Bay area, 

24 cities have ordinances that prohibit conventional fireplaces in new construction. The 

mountain town of Truckee has a more aggressive policy that requires that existing 

unapproved wood burning appliances be removed by July 15, 2006. The San Joaquin Valley 

implemented a daily advisory for restrictions on residential fireplace or wood stove use on 

January 1, 2004. Woodsmoke especially impacts those with asthma and other respiratory 

disease. 

• Environmental tobacco smoke has been greatly reduced in California, primarily due to 

legislation that bans smoking at the workplace. However, children’s exposures remain a 

concern, because they can be highly exposed when smoking occurs in their home or in 

vehicles driven by family or friends who smoke. Actions to reduce children’s exposure–such 

as an increased focus of public education on smoking parents, and reduction of smoking 

inside vehicles and homes with children–remain a high priority. 

• Radon is ranked as a high priority due to its high estimated lung cancer risk. However, 

indoor levels in California are generally below the recommended mitigation level, and the 

need for mitigation is building- and area-specific. The risk from radon is strongly associated 

with smoking (NRC, 1999a). Mitigation might include revised building codes and 

requirements for testing and implementation of construction changes, if needed, upon the 

sale of a home or building in areas with elevated radon levels. The California Department of 

Health Services (DHS) has established a list of certified providers of radon services. 

Medium Ranked Source Categories 

The pollutant source categories included in Table ES-3.2 are lower in priority than those above, 

but nonetheless include some sources that warrant consideration for mitigation. 

• Architectural coatings, such as paints and lacquers, are available in “low VOC” versions 

due to formulation changes targeted toward reducing outdoor ozone. However, they are not 

directly regulated by the state. ARB develops Suggested Control Measures and provides 

guidance and technical assistance to air quality management districts in the state, 22 of 

which have adopted rules to reduce VOC emissions from coatings. Like building materials, 

architectural coatings are widely used and have a high loading in indoor environments when 

used, due to the large surface areas they typically cover. Additionally, some components of 

coatings can be harmful, but may not necessarily be addressed through reactive VOC 

reductions. However, because reductions have been achieved in districts that cover 95 

percent of the California population, this source category is ranked as a medium priority. 
Indoor Air Pollution in California July, 2005

 23

Table ES-3.2. Medium Priority Source Categories for Mitigation 1 

SOURCES OF POLLUTANTS2 

(listed alphabetically) 

EXAMPLES OF 

POLLUTANTS3 EMITTED 

POTENTIAL 

APPROACH TO 

MITIGATION4

DIRECT 

STATE 

AUTHORITY 

TO TAKE IAQ 

MITIGATION 

ACTIONS 

Architectural Coatings 

(e.g., paints, sealants, 

lacquers, varnishes) 

Formaldehyde, 

acetaldehyde, ethylene 

glycol, metals, others 

Emission limitations, 

chemical reformulations, 

use restrictions to reduce 

TACs & nonreactive 

VOCs with health 

impacts 

No 

Consumer Products 

(e.g., household and 

institutional cleaners, 

furniture- and floor-care 

products, air fresheners, stain 

removers, detergents) 

Personal Care Products 

(e.g., products used for hair 

and skin care) 

Methylene chloride, paradichlorobenzene, 

perchloroethylene, toluene, 

benzene, naphthalene, 

formaldehyde, 

acetaldehyde, metals, 

others 

Emission limitations, 

chemical reformulations, 

and product use 

restrictions to reduce 

TACs and nonreactive 

VOCs with health 

impacts; labeling 

program 

Limited (some 

indirect) 

Household & Office 

Equipment and Appliances 

(computers, photocopiers) 

Particles, styrene, some 

other VOCs, phthalates, 

ozone, PBDE 

Emission limitations, local 

exhaust requirements 

No 

Pesticides 

(insecticides, herbicides, 

sanitizers, disinfectants, etc., 

used indoors and outdoors; 

track-in, drift) 

Permethrin, esfenvalerate, 

chlorpyrifos5

, diazinon5, 

many others 

Integrated pest 

management; outreach; 

formulation and/or 

application changes for 

indoor use 

Limited 

1. Individual sources may be higher or lower than the source category ranking. 

2. All of the examples of pollutant sources may not emit all of the pollutants listed in the corresponding box in 

column two. 

3. Air pollutants may be identified as Toxic Air Contaminants (TACs) by the California Air Resources Board, and/or 

identified as Proposition 65 chemicals; or, criteria (traditional) air pollutants. 

4. Public education, economic incentives, and non-regulatory approaches should also be used where appropriate. 

The actual approach taken would be determined after extensive discussions with the relevant industries, in 

consideration of costs, feasibility, and effectiveness. 

5. Chlorpyrifos and diazinon are no longer sold for residential uses, except as containerized baits. Products 

purchased prior to the sales deadline may still be used. 

• Consumer products and personal care products have been regulated by ARB to reduce 

emissions of reactive VOCs in order to reduce outdoor smog formation. Reactive VOCs, and 

some toxic air contaminants, have been reduced substantially through reformulation of a 

number of product categories. For example, in reducing VOC content to comply with ARB 

regulations, manufacturers often use water-based technologies and use VOC exempt 

compounds such as acetone. To prevent increased use of TACs, ARB has prohibited the 

use of perchloroethylene, methylene chloride, and trichloroethylene in 13 categories 

including general purpose degreasers, brake cleaners, all spray paints, all aerosol 

adhesives and adhesive removers. Additionally, antiperspirants and deodorants are not 
Indoor Air Pollution in California July, 2005

 24

allowed to contain any compounds identified as TACs. The Board recently approved a rule 

to remove para-dichlorobenzene from solid air fresheners and toilet/urinal care products. 

However, despite the breadth of products addressed under ARB’s consumer products 

regulations, not all types of consumer products have been regulated. Also, due to the nature 

of some products (household cleansers, air fresheners, stain removers, etc.), the user is in 

close proximity to the release of chemicals during use, and can experience high pollutant 

exposure when using the product. Thus, there is an apparent need to reduce emissions 

from consumer products to prevent high personal exposures and risks, and to address types 

of products not currently regulated under ARB’s programs. Chemical reformulations, 

emission limitations, content limits, and/or product use restrictions of consumer products are 

mitigation approaches that could result in further significant risk reductions, especially for 

product users. Because of the ARB’s progress to date with chemically formulated products, 

some of the highest emitting consumer products have been reformulated, and therefore this 

category is ranked medium rather than high. 

• Household appliances and office equipment 

such as computers, printers, and copy machines 

can emit a variety of pollutants such as particles, 

ozone, various VOCs of concern, and PBDEs. In 

most cases, these pollutants are emitted directly into 

the living or working area, and thus are of concern. 

Additionally, more and more office equipment is 

being purchased for use in the home, increasing the 

number of people potentially exposed. Emissions 

from each type of appliance could be addressed 

through emission limitations and/or requirements for 

local exhaust of the emissions. Because emissions 

information on many specific sources in this 

category is outdated, or lacking for some pollutants, 

mitigation efforts for these products are a medium 

priority. 

• Pesticides are used indoors and around the perimeter of buildings to control household 

pests such as ants, spiders, cockroaches, rats and mice. Disinfectants and sanitizers also 

are pesticides. Pesticides can be tracked in from outdoor application and drift into the home 

after outdoor spray application. In rural areas, indoor concentrations may be greater due to 

increased use of pesticides for agricultural purposes. Levels of pesticides have been 

measured in both air samples and house dust samples. Pesticides residues are more 

persistent indoors than outdoors due to the lack of natural degradation forces such as 

ultraviolet light, high temperatures, wind, and rain. Continued research and intervention by 

the U.S. EPA and DPR, who regulate pesticides, are needed to prevent harmful exposures 

and promote the registration of less toxic pesticides for indoor use. Most importantly, the 

implementation of integrated pest management approaches should be expanded to reduce 

the need for pesticide application. 

VIII. OPTIONS TO MITIGATE INDOOR AIR POLLUTION 

This report shows that there are many sources of indoor air pollution that produce substantial 

adverse health effects, result in lost productivity, and impose substantial costs on Californians. 

Office equipment can emit ozone, 

VOCs, particles, and other pollutants. 
Indoor Air Pollution in California July, 2005

 25

Despite these facts, there is no systematic program to improve indoor air quality, there are 

relatively few regulations or standards to specifically address indoor air quality problems, and 

few resources focused on effectively addressing problems and promoting improvements. 

Current efforts to address indoor pollution are not commensurate with the scope of the risk to 

health it poses to Californians. 

General Mitigation Options 

Ambient (outdoor) air quality is protected through a comprehensive system. In California and 

under federal law, ambient air quality standards are established for traditional (criteria) 

pollutants and must be attained. Under other state authority, pollutants identified as toxic air 

contaminants must be reduced to the maximum extent feasible. The approach used to reduce 

toxic air contaminants in ambient air, in which source emissions are reduced without setting 

enforceable air quality levels, seems most applicable to indoor air, together with increased 

attention to proper building operation and maintenance. Action to reduce indoor emissions and 

exposures would assure reduction of exposure and risk from key sources, and should be a 

major component of a new effort to address indoor air. Other approaches including public 

education, product testing and labeling, improved building codes, and setting of maximum 

exposure guideline levels, should also be part of the mitigation program. The following elements 

of an indoor air pollution reduction program are recommended for consideration: 

1. Create a management system for indoor air quality that establishes a comprehensive 

program for assessing indoor health problems, identifying the actions needed to reduce the 

most significant problems, and setting guidelines, emission limits, or other requirements that 

will be effective in reducing the health impacts of indoor sources. As discussed in Sections 4 

and 6 of this report, many agencies’ actions affect indoor air quality, and a few have limited 

authority over some aspect of indoor air quality, but no state (or federal) agency has the 

authority or mandate to conduct a comprehensive indoor air pollution mitigation program. 

Such a program is needed, and should be fully coordinated with activities of other agencies 

whose actions affect indoor air. 

2. Establish emission limits, when needed, for indoor pollutant sources that pose excessive 

risks due to their indoor emissions. These might include air cleaners, building materials, 

furnishings, combustion appliances, and others. While ventilation authority exists in the 

Energy Commission and Cal/OSHA, no state agency has a direct mandate to establish 

emission limits for indoor sources for the purpose of reducing indoor exposure and risk. 

Establishment of such limits would better protect public health, and may reduce (but not 

eliminate) the amount of ventilation needed under certain circumstances in some buildings, 

thus saving energy. Compliance could be accomplished by requiring emissions testing 

through an independent laboratory certified by the state, and submittal of the data to the 

lead agency. 

3. Require manufacturers to submit building materials, furnishings, combustion 

appliances, consumer products, and other significant sources for emissions testing 

by an independent laboratory certified by the state, and to report those results to the state 

and to the public. Also, require results to be transmitted to the public via product labeling or 

accompanying materials in language consumers can understand. Implementation of a 

required test program could prove to be an effective approach, at least for reducing indoor 

pollutant levels in new buildings. A prototype emissions testing program has already been 

developed for reducing toxic VOCs from building materials and furnishings, and is designed 

to protect human health in state sustainable building projects (Section 01350, State of 
Indoor Air Pollution in California July, 2005

 26

California, 2002). A partial list of products that meet this specification is available at 

http://ciwmb.ca.gov/GreenBuilding/Specs/EastEnd/. However, there is currently no 

requirement for state agencies or others to use these guideline emission specifications, and 

only limited incentive for them to do so. Other national and international emissions test 

protocols that are widely used also are available. 

4. Make children’s health in schools, homes, and care 

institutions the top priority. Implement the 

recommendations for schools in Section 7.2 of this report. 

In schools and public daycare centers, require the use of 

building materials that are certified to be low-emitting, and 

require that schools meet workplace standards for 

ventilation and for prevention and remediation of moisture 

intrusion. Require school ventilation systems be quiet 

(under 45 decibels) and well maintained. Encourage 

school districts to adopt integrated pest management 

programs. Increase efforts to reduce children’s exposure 

to environmental tobacco smoke. Increased education 

and outreach efforts to smoking parents and caretakers 

are needed to inform them of the health dangers of 

second-hand smoke, and the actions they should be 

taking to protect children under their care from these 

dangers. 

5. Develop indoor air quality guidelines for homes, 

schools, offices, and institutional living quarters. These 

would largely identify “Best Practices” for the design, construction, operation and 

maintenance of public, commercial, school, and institutional buildings. In some cases, they 

might include the identification of healthful levels or “bright lines” for some pollutants to be 

used as goals for mitigation activities and “best practices”, but would not have an associated 

compliance program. They should also include performance measures for buildings and 

appliances, and valid certification requirements for professionals directly involved in indoor 

air quality-related occupations. Full commissioning should be required for all new public, 

commercial, and institutional residential buildings, to assure that they are constructed and 

operate as intended, and that they provide acceptable indoor air quality. ASHRAE 

Guidelines (1993, 1996) provide basic guidance for building commissioning, but state 

requirements are needed. 

6. Amend building codes to address indoor air quality, with a focus on assuring 

adequate ventilation under all circumstances. For example, unvented cook stoves, 

ovens, and other combustion appliances should not be allowed in residences: rather, they 

should be vented to the outdoors, such as through direct venting or an automatic (but quiet) 

exhaust fan that is activated when the appliance is turned on. Similarly, building codes 

should be established and enforced to prevent mold problems, residential ventilation issues, 

and others. 

7. Fund an outreach and education program focused on professionals, including health 

professionals, teachers, school facility managers, and others who must be able to identify 

and remedy indoor air quality problems. Such individuals have many obligations, yet play a 

key role through their occupation in initial identification, prevention, and mitigation of indoor 

air quality problems. Most need more in-depth information and training on indoor air quality 

Measures to reduce children's 

exposures should be a priority.
Indoor Air Pollution in California July, 2005

 27

than they typically have had. Training and technical assistance should be provided for the 

private sector to develop the skills and services needed for high-quality building 

commissioning, operation, and maintenance. 

8. Conduct more research on indoor air quality. Several high priority areas are specifically 

identified in this report for further research. Because of the known serious health impacts of 

ambient PM and recent studies showing high emissions of PM from indoor sources, 

research on the health effects of indoor PM is a high priority. The health effects of terpeneozone reaction products and the extent of people’s exposures to them, as well as other 

fragrances and indoor chemical reaction products, also are key areas warranting focused 

research. There are many new chemicals introduced into the product mix each year, yet few 

have had full health and exposure studies completed. The effects of more recently identified 

indoor chemicals, such as PBDEs, warrant further investigation. Improved methods and 

protocols to detect indoor dampness and hidden mold growth are also needed. Synergistic 

and cumulative health effects are suspected for a number of indoor pollutants with similar 

structures or properties, yet little research has been conducted in this area. Finally, 

mitigation approaches assumed to be effective have sometimes been found to be much less 

effective than anticipated; the effectiveness of recommended or required mitigation 

measures should be confirmed through appropriately designed studies to assure that the 

necessary reductions in exposure and risk will be achieved. 

9. Fund an Innovative Clean Air Technology program (ICAT) for indoor air quality to 

foster the development and commercialization of legitimate, cost effective technologies that 

can improve IAQ. For example, improved low-noise ventilation technologies, improved air 

monitors and assessment tools, and effective low-noise air cleaners are needed. ARB’s 

current ICAT program, focused on improving outdoor air quality through improved 

technology, has been very successful in bringing new technologies to commercialization in 

California, adding new options for reducing air pollution while also bringing jobs and 

investment into the state. An indoor air quality ICAT program would be expected to do the 

same. 

All of these suggested mitigation options are feasible if appropriate mandates and resources are 

provided. The degree of feasibility of individual measures, such as emission limits for a specific 

type of product, cannot be determined without substantial additional information. As discussed 

in this report, alternative products or formulations are already available for some of the indoor 

sources of current concern. However, prior to taking any regulatory action, a more detailed 

assessment of the specific remedies available, including technological and economic feasibility, 

would be needed. Additionally, like ARB’s current regulatory programs, any emission limitations 

or other mitigation measures should be developed with continuous discussion and review by 

stakeholders, the public, and other state agencies. 

Mitigating Indoor Pollution in Schools: An Urgent Need 

The Air Resources Board and the Department of Health Services recently completed a 

statewide study of kindergarten through 12th grade public schools entitled “Environmental Health 

Conditions in California’s Portable Classrooms” (ARB/DHS, 2004). Results showed there are a 

number of serious, widespread environmental health problems in California schools that need to 

be addressed. These problems were found in both portable (relocatable) and traditional (sitebuilt) classrooms. Government standards and guidelines that are designed to protect children in 

classrooms and other buildings are essentially lacking; thus, results were compared to the most 
Indoor Air Pollution in California July, 2005

 28

relevant environmental health guidelines and standards available, primarily from professional 

societies and government agencies. 

Problems in Schools 

The primary problems found include: 

• Inadequate ventilation with outdoor air during 40 percent of class hours, and seriously 

deficient ventilation 10 percent of the time. This is often due to teachers turning off HVAC 

systems because of excessive noise. 

• Formaldehyde air concentrations exceeded guideline levels for preventing acute eye, nose, 

and throat irritation in about 4 percent of the classrooms; nearly all classrooms exceeded 

guidelines for preventing long-term 

health effects, including cancer. 

• Obvious mold in about 3 percent of 

classrooms, and water stains and 

other potential mold indicators in about 

one-third of classrooms, due to 

inadequate maintenance. 

• Noise levels in all classrooms 

exceeded 35 decibels, a voluntary 

standard for classrooms; one-half of 

the classrooms also exceeded 55 

decibels, the level used for outdoor 

nuisance regulations. Excess noise 

was primarily attributable to noisy 

ventilation systems. 

Recommendations to Address the Problems Identified 

Recommendations to address the problems identified in the study were developed in 

consultation with state agencies, industries, school officials, and other interested stakeholders. 

Actions are needed at all levels. A total of 16 recommendations are discussed in the November, 

2004 Report to the Legislature. These are presented in two groups in the report: Group 1 

includes high priority, high benefit actions that can be achieved at relatively low cost and should 

be accomplished in the near term, while Group 2 recommendations will require a longer 

timeframe and/or more substantial resources to accomplish. The recommendations fall into four 

general approaches needed to remedy and prevent the problems seen. These include: 

• Direct and assist schools to comply with state regulations, especially Cal/OSHA’s workplace 

regulations related to ventilation, moisture intrusion, and other aspects of building operation 

and maintenance. Schools should conduct a self-assessment and implement an indoor air 

quality management program, like that in U.S. EPA’s IAQ Tools for Schools Program. 

• Develop and promote “Best Practices” for design, construction, operation, and maintenance 

of school facilities. The CHPS manuals provide comprehensive guidance at no charge. 

• Improve support (both funding and training) for school facilities and staff. Stable, long-term 

funding mechanisms are needed to assure adequate and timely operation and maintenance. 

Many classrooms have indoor air quality Many classrooms have formaldehyde, mold, problems 

moisture, ventilation, and noise problems. 
Indoor Air Pollution in California July, 2005

 29

Postponed maintenance often results in greater costs. Focused training programs for 

administrators, facility managers, and teachers are needed: those closest to the classroom 

are often not aware of current “best practices” for operation and maintenance of classrooms. 

• Establish guidelines and standards for school environmental health that are protective of 

children. Noise, lighting, and chemical contaminant levels appropriate for school children 

need to be identified. 

Some actions have already been taken to begin to address these problems; however, they 

constitute only a first step toward realizing actual improvements in school conditions. Only a 

small percentage of schools and districts have actively pursued the many tools that are readily 

available to them to improve the school environment. The CHPS’ Best Practices Manuals, U.S. 

EPA’s IAQ Tools for Schools Kits, and the Los Angeles Unified School District’s (LAUSD) “Safe 

School Inspection Guidebook” are all available on the Internet free of charge, yet the number of 

California schools utilizing these tools is small. A proactive effort to implement the 

recommendations of the report is needed. The complete Report to the Legislature on 

Environmental Health Conditions in California’s Portable Classrooms is available at 

http://www.arb.ca.gov/research/indoor/pcs/pcs.htm. 

IX. SUMMARY 

Indoor pollution causes substantial, avoidable illness and health effects – ranging from irritant 

effects to asthma, cancer, and premature death – and costs Californians billions of dollars each 

year. Because there are numerous sources of pollutants in indoor environments, and because 

people spend most of their time indoors, exposure and the associated risk is substantial. Many 

agencies, professional groups, and organizations have taken actions to reduce indoor pollution, 

but these have been piecemeal and are not sufficiently effective in addressing the problem. 

There are many actions that could be taken to significantly reduce indoor emissions and 

exposure. If experience in controlling sources of outdoor pollution is repeated relative to indoor 

sources, many of these measures will be low cost and will provide substantial health benefits. A 

focused risk reduction program is needed to effectively assure acceptable indoor air quality in 

California homes, schools, and public buildings. A program that stresses direct emission 

reductions and includes improved building codes and ventilation, increased public and 

professional education, product labeling, and advisory standards is recommended. Indoor air 

cleaning devices (especially ozone generators), biological contaminants, building materials and 

furnishings, combustion appliances including woodstoves and fireplaces, ETS, and radon are 

high priority source categories for mitigation. Architectural coatings, consumer products, 

household and office equipment, and pesticides are also of concern, but are a lower priority 

than the other categories identified. Special priority should be paid to measures that reduce 

children’s exposures. 

It should be noted that indoor air controls cannot be substituted for the state and national 

ambient air quality programs. As discussed above, indoor and outdoor pollution operate in 

tandem, increasing the health risk to all Californians. That means that any new initiatives to 

mitigate indoor air pollution must be accomplished alongside California’s decades-long efforts to 

improve our outdoor environment. 
Indoor Air Pollution in California July, 2005 

 30
Indoor Air Pollution in California July, 2005 

 31

1. INTRODUCTION AND BACKGROUND 

The Air Resources Board (ARB) prepared this report to the Legislature on indoor air quality in 

response to requirements of Assembly Bill 1173 (Keeley, 2002; Health and Safety Code Section 

39930; see Appendix I). As required by the legislation, this report summarizes the best scientific 

information available on indoor air pollution, including: 

• Common indoor pollutants and their sources. 

• The potential health impacts of indoor pollutants. 

• Existing regulations and current industry practices. 

• Options for mitigation in schools, non-industrial workplaces, homes, and other indoor 

locations. 

• State and federal efforts related to control of biological and radiological substances. 

In preparing the report, the ARB consulted with the Department of Health Services (DHS), the 

Office of Environmental Health Hazard Assessment (OEHHA), the California Energy 

Commission (CEC), the Department of Industrial Relations (DIR, Cal/OSHA), relevant industries 

and other stakeholders, and interested members of the public. On April 4, 2003 a public 

workshop was conducted to inform stakeholders about the report and the anticipated schedule, 

and to solicit comments from them. On June 30, 2004, another workshop was held to receive 

comments on the draft report. A website and an email list serve were established to keep 

stakeholders informed of progress on the report preparation. The website is available at 

http://www.arb.ca.gov/research/indoor/ab1173/ab1173.htm. ARB released a revised draft report 

in November 2004 for review by interested stakeholders and a University of California scientific 

peer review panel. A subsequently revised draft report was reviewed and approved by the 

Board at its March 17, 2005 Board meeting. 

This report reflects key points from the large body of knowledge that has been generated about 

indoor air quality since it became a concern in the 1970s. Researchers worldwide have made 

great progress in identifying indoor pollutants and understanding their relationship to human 

exposure and resultant health effects. Several international conferences are now held annually, 

and one journal, Indoor Air, is devoted exclusively to the field of indoor air quality. Many 

additional journals carry articles on indoor air quality. This report summarizes key findings of the 

most recent literature, with emphasis on the major trends identified by multiple investigators. 

1.1 INDOOR POLLUTION POSES A SIGNIFICANT HEALTH RISK 

State and federal comparative risk projects have repeatedly ranked indoor pollutants and 

sources in the high-risk categories of their analyses relative to other environmental health 

problems. In the 1994 California Comparative Risk Project (CCRP, 1994), the Human Health 

Committee ranked risks by two different methods: by sources and media, and by pollutant. In 

the sources and media ranking, the “residential and consumer product releases to air (indoor 

air)” category was ranked in the high risk group, along with some outdoor air pollution 

categories. In the pollutant rankings, ETS, radon, PM, and VOCs were all ranked in the high-risk 

category, and carbon monoxide and lead were ranked in the medium risk category. The results 

of the CCRP had a somewhat more substantial scientific basis than most other comparative risk 

projects, because it was based to a greater degree on actual measurement data, and used 

distributions of exposure and risk, rather than just population averages. Additionally, it was 

reviewed by an external scientific review committee. 
Indoor Air Pollution in California July, 2005 

 32

The U.S. EPA’s 1987 national comparative risk project also ranked indoor air pollution high 

relative to other environmental areas: indoor pollution other than radon was ranked fourth 

among the top thirteen national environmental problem areas assessed for cancer risk (U.S. 

EPA, 1987a). Radon was ranked first, but the risk from radon has been subsequently reexamined and reduced. A number of other states and regions have conducted comparative risk 

projects as well, with results similar to those of the U.S. EPA and California. 

The high ranking of indoor pollution relative to other environmental problems is not surprising, 

because there are numerous sources of pollutants indoors, indoor air concentrations of some 

pollutants are often high enough to pose a health risk, and people spend most of their time 

indoors. The total quantity of air pollutants emitted indoors is much less than that emitted by 

outdoor sources. However, once emitted, indoor pollutants are diluted much more slowly than 

pollutants from outdoor sources. When this factor is combined with the fact that Californians, 

like others from industrialized nations, spend most of their time indoors, there is a much higher 

likelihood that people will be exposed to pollutants emitted indoors than those emitted outdoors. 

Investigators have developed 

concepts and terms to quantify the 

portion of pollutant emissions 

actually inhaled (Bennet et al., 

2002; Lai et al., 2000). The 

inhalation transfer factor is defined 

as the pollutant mass inhaled by 

an exposed population per unit 

mass emitted from an air pollution 

source (Lai et al., 2000). Although 

more people are exposed to a pollutant released outdoors, the concentration is usually reduced 

due to wide dispersion, relative to a pollutant emitted indoors. Calculated inhalation transfer 

factors were several orders of magnitude greater for pollutants emitted indoors and in vehicles 

than those emitted outdoors, thus indicating a significantly larger fraction of pollutant is inhaled 

when it is released indoors as opposed to outdoors. 

Investigators calculate that pollutants emitted indoors have a 1000-fold greater chance of being 

inhaled than do those emitted outdoors (Smith, 1988; Bennet et al., 2002; Lai et al., 2000). 

Thus, reducing indoor emissions by a given amount might be anticipated to have a greater 

impact on reducing exposure than would reducing outdoor emissions by that same amount. 

Regulation of outdoor sources such as motor vehicles and industrial plants has notably reduced 

many outdoor pollutant levels in California. Now, there are significant gains to be achieved in 

public health protection from reductions in indoor source emissions and other measures that 

might be taken to reduce indoor concentrations and exposures. 

The health effects of indoor pollutants range from irritant effects to respiratory disease, cancer, 

and even sudden death. Indoor sources of pollutants are numerous, such as building materials, 

consumer products of all types, combustion appliances, and even some so-called “air 

fresheners”. Common indoor activities such as smoking, unvented cooking, burning candles, 

and vacuuming with low performancne or leaky vacuums also generate pollutants. The health 

effects of indoor pollutants, and indoor pollutant sources and concentrations in California, are 

discussed in Chapter 2 of this report. 

The Rule of 1000: 

A typical pollutant release indoors is 1000 times 

as effective in causing human exposure as the 

same release to urban air. 

KR Smith, in Air Pollution: Assessing Total Exposure in the United 

States, Environment, 30 (8): 10, 1988. 
Indoor Air Pollution in California July, 2005 

 33

1.2 PEOPLE SPEND MOST OF THEIR TIME INDOORS 

A key reason indoor pollution is so critical to health is that Californians, like others from 

industrialized nations, spend most of their time indoors – about 87%, on average. So, if 

pollutants are present indoors, there is a high likelihood that people will be exposed to them. As 

shown in Table 1.1, California adults spend an average of about 62% of their time in their home. 

Children spend even more time in their home; infants up to 2 years of age spend 85% of their 

time inside the home, on average. Thus, the home is a critical exposure microenvironment for 

all, and especially for children. 

Table 1.1: Average Percent of Time Californians Spend in Major Locations

AVERAGE PERCENT OF TIME 

AGE 

Inside the 

Home 

Other 

Indoors Outdoors Inside a Vehicle 

Children1

 0 - 2 

85 4 7 4 

 3 - 5 76 9 10 5 

 6 - 11 71 12 13 4 

All Children (0 - 11)1 76 10 10 4 

Adults and Teens2 62 25 6 7 

1

From: Study of Children’s Activity Patterns (Wiley et al., 1991a, ARB Contract No. A733-149; Phillips et al., 1991). 2

From: Activity Patterns of California Residents (Wiley et al., 1991b, ARB Contract No. A6-177-33; Jenkins et al., 

1992a). 

1.3 CHILDREN’S HEALTH – VULNERABILITY IMPLIES INCREASED INDOOR AIR 

QUALITY IMPACT 

In recent years there has been an increasing awareness that children may be more susceptible 

than adults to the harmful effects of air pollution. Additionally, children are more highly exposed 

to some indoor contaminants than are adults. Thus, children are likely at greater risk from indoor 

pollution than adults. 

• Children’s physiology and developing lungs and bodies make them more susceptible 

to chemicals that affect development and lung function. Children’s immune systems are 

not fully developed and their growing organs and structures are more easily harmed. For 

example, lead is more readily absorbed from the digestive tract of children, and the 

developing central nervous system is more susceptible to damage than that of an adult. 

Pollutants that cause irritation or inflammation in the airways are more likely to obstruct a 

child’s airways because they are narrower than airways of an adult. Results from the ARBfunded Children’s Health Study indicate the lungs of children in high-pollution communities 

develop more slowly and move air less efficiently than lungs of children in low-pollution 

communities (Gauderman et al., 2000). When exposed to ETS, children are at greater risk 

than adults for developing lower respiratory tract infections, bronchitis, pneumonia, fluid in 

the middle ear, and asthma symptoms (NCI, 1999). Additionally, young children appear to 
Indoor Air Pollution in California July, 2005 

 34

be more susceptible to the effects of environmental tobacco smoke (ETS) than older 

children (IOM, 2000). 

• Infants and children inhale more air relative to their size than do adults at a given level 

of activity (ARB/OEHHA, 2000; Adams, 1993). Additionally, children often breathe through 

their mouths, bypassing the filtering effect of the nose and allowing more pollutants to be 

inhaled. Thus, for the same amount of time spent in a given location/activity as an adult, a 

child will receive a greater dose of the chemicals in the air than an adult, relative to their 

body size. Children also have a larger lung surface area per unit of body weight, relative to 

adults. This contributes to a higher breathing rate/unit surface area and elevated exposure 

in children (Thurlbeck, 1988; Plopper and Thurlbeck, 1994). 

• Children’s activities bring them into close proximity to indoor sources. First, infants 

and young children spend more time indoors at home (see Table 1.1) than do adults. 

Additionally, younger children spend more time near indoor sources such as operating gas 

stoves, e.g., near the parent while cooking (Phillips et al., 1991), leading to higher 

exposures to nitrogen dioxide and other cooking emissions. 

• Also, children spend more time on floors and more frequently put fingers and objects 

into their mouth (Zartarian et al., 1998; Zartarian and Leckie, 1998). This can lead to 

additional dermal and ingestion exposure to airborne TACs deposited and adsorbed onto 

floor dust, such as lead and other toxic metals, PAHs, and pesticides. Because the 

breathing zone for an infant or small child is several inches to a foot or so above the floor, 

while that for adults is several feet above the floor, particles stirred up by activity may 

become available to be inhaled by the child but are not elevated in the breathing zone of 

adults (Bearer, 1995). 

Concerns about children’s health prompted the California Legislature to pass the Children’s 

Environmental Health Protection Act (SB 25, Escutia) in 1999. This Act requires Cal/EPA to 

specifically consider children when setting Ambient Air Quality Standards (AAQS) and reviewing 

pollutants for identification or regulation as Toxic Air Contaminants (TACs). As required by this 

legislation, ARB and OEHHA have re-evaluated the AAQS for particulate matter and are 

currently evaluating the AAQS for ozone and nitrogen dioxide. OEHHA has identified dioxin, 

lead, polycyclic organic matter, diesel exhaust particles, and acrolein as the top 5 priority TACs 

that may impact infants and children the most (OEHHA, 2001). The ARB is beginning to assess 

the adequacy of existing control measures for these compounds relative to the health of 

children. 

1.4 ENVIRONMENTAL JUSTICE CONSIDERATIONS RELATIVE TO INDOOR AIR 

QUALITY 

Senate Bill 115 (1999) directs the California Environmental Protection Agency to design an 

environmental justice mission statement for boards, departments, and offices within the agency. 

State law (California Government Code § 65040.12c) defines environmental justice as the fair 

treatment of people of all races, cultures, and incomes with respect to the development, 

adoption, implementation, and enforcement of environmental laws, regulations, and policies. In 

response to SB 115, the ARB approved Policies and Actions for Environmental Justice in 

December, 2001. This document establishes a framework for incorporating environmental 

justice into all ARB programs, policies, and regulations (ARB, 2001a). 
Indoor Air Pollution in California July, 2005 

 35

The ARB has taken several steps to directly and indirectly address environmental justice 

concerns related to indoor air quality. Special air-monitoring studies have been conducted in 

classrooms, homes, and at schools in communities located near industrial sources of pollution 

and/or heavy vehicular traffic. Preliminary results indicate pollutant levels in the selected 

communities are similar to levels in other communities. To assure that information is available to 

all stakeholders, documents designed for public education, such as fact sheets and a school 

advisory, have been published in both English and Spanish. 

Census statistics indicate that the poor are more than three times as likely (22% versus 7%) to 

have substandard-quality housing (Evans and Kantrowitz, 2002) and that blacks and lowincome persons are more likely than the general population to be in housing with severe 

physical problems (Krieger and Higgins, 2002). Children in low-income families may bear 

additional burdens because they are more likely to be in school buildings that have 

environmental problems; poor plumbing, inadequate heating, and poor indoor air quality (Evans 

and Kantrowitz, 2002). 

Research is needed to determine the complex relationship between socioeconomic status 

(SES), environmental factors, and health status, particularly as they relate to indoor air pollution. 

To date, only factors related to the prevalence of asthma have received substantial study. The 

prevalence of asthma appears to be more strongly correlated with lower socioeconomic status 

than with race and ethnicity (IOM, 1993). Yet, California data show that African Americans, 

American Indians, and Alaska Natives experience a higher prevalence of lifetime asthma than 

other groups in the population (Meng et al., 2003). Identifying the contribution of exposure to 

biological agents to poor health is difficult. The increase in asthma prevalence is greatest in 

children from lower income homes, probably due to an increase in prevalence of allergic 

conditions in their homes (Auinger et al., 2003). Dust mites and cockroaches are important 

triggers for asthmatics that are more likely to be present in urban settings (IOM, 1999). 

Reviewing data accumulated in the second National Health and Nutrition Examination Survey 

(NHANES II) and the Harvard Six Cities Study, Eggleston (2000) concluded that ethnicity, 

poverty, and residence combined to influence asthma prevalence in inner-city children in ways 

that could not be easily disentangled (IOM, 2004). 

“Economic factors [also] may encourage poor building practices. Combinations of pressure to 

build quickly and cheaply can result in poorly constructed buildings that are more likely to have 

water leaks.... Poverty combined with the lack of affordable housing may also create incentives 

to forgo or limit investment in maintenance that might help to prevent moisture problems and 

subsequent adverse impacts on the health of the occupants” (IOM, 2004). Those who live in 

substandard housing are exposed to more pests, as well as pesticides to get rid of them (Flynn 

et al., 2000). Pesticides adsorb onto particles and accumulate in the carpet, where children and 

others can be exposed to them. In an effort to improve their environment, a higher percent of 

low-income individuals use room fresheners – products that may introduce additional toxic 

chemicals to the indoor environment (Wiley et al., 1991b). 

Children living in urban areas are disproportionately exposed to lead, primarily from leadcontaining paint that has been used on older houses. Exposure to lead in both house dust and 

air takes a toll on children. Research indicates blood lead levels are higher for poor and minority 

children in central cities (IOM, 1999). 
Indoor Air Pollution in California July, 2005 

 36

2. HEALTH EFFECTS, SOURCES AND CONCENTRATIONS 

OF INDOOR AIR POLLUTANTS 

Emissions from indoor sources contribute to exposure and risk in two ways. Some pollutants are 

emitted in substantial quantities over extended periods from large surfaces, such as 

formaldehyde from composite wood products made with urea-formaldehyde resin. These 

sources contribute to elevated indoor pollutant levels in many buildings where a large portion of 

the population spends their time. Large numbers of individuals can be affected due to the large 

quantity of indoor emissions. Other products, such as aerosol sprays or solvents, emit much 

smaller quantities of pollutants, and are used by a subset of the population. However, those who 

use such products use them in such a manner that the chemicals emitted are released near the 

user’s breathing zone (area near the nose and mouth). A high concentration of the chemical 

consequently may be inhaled during product use before the chemical has a chance to dilute in 

the air. 

It is important to note that health effects are determined not only by the specific toxicology of the 

air pollutant, but also by the exposure and absorbed dose. The higher the exposure and dose, 

the higher the risk of adverse health effects. In addition, more severe effects generally occur 

with higher doses. It is not possible in this document to describe the dose-response relationship 

for all indoor air pollutants. Further information on dose-response relationships can be found on 

the OEHHA website (www.oehha.ca.gov). 

Hundreds of substances representing a range of chemical, physical, and biological species 

have been identified as indoor air pollutants. Indoor air pollutants include volatile organic 

compounds (VOCs), inorganic gases, particulate matter (PM), and complex mixtures such as 

environmental tobacco smoke (ETS). Indoor concentrations of many pollutants are often higher 

than outdoor concentrations due to the use of indoor pollutant sources in a confined space. 

Some pollutants such as formaldehyde, radon, asbestos, cigarette smoke, and mold have 

received a substantial amount of study. Other pollutants have received minimal study, and 

undoubtedly some pollutants have not yet been identified. 

Indoor air pollution can cause a variety of adverse impacts on human health, from irritant effects 

to respiratory disease, cancer, and death. The major health effects that can occur from 

exposure to common indoor pollutants are indicated in Table 2.1. These effects have a major 

impact on Californians’ health each year, and most can be readily avoided. Asthma, cancer, 

irritant effects, and sick building syndrome are discussed below. Later in this chapter the more 

common indoor pollutants, their sources, and indoor concentrations are discussed. 

2.1 KEY HEALTH IMPACTS 

2.1.1 Asthma 

Asthma is a chronic inflammatory lung disease that results in partially reversible constriction of 

the airways. It is characterized by episodes of wheezing, shortness of breath, or coughing that 

may occur at any time. Asthma is a critical health issue because of its negative impact on the 

quality of life, increased morbidity and mortality, and substantial economic impact. 
Indoor Air Pollution in California July, 2005 

 37

Table 2.1. Sources and Potential Health Effects of Major Indoor Air Pollutants 

POLLUTANT MAJOR INDOOR 

SOURCES 

POTENTIAL HEALTH EFFECTS 

ASSOCIATED WITH ONE OR MORE 

OF THE POLLUTANTS LISTED* 

Asbestos 

Building materials in older homes 

released during renovation, naturally 

occurring in some soils 

Lung cancer, asbestosis, mesothelioma 

Biological Agents 

(bacteria, fungi, viruses, 

house dust mites, animal 

dander, cockroaches, 

microbial VOCs) 

House and floor dust; bedding; poorly 

maintained air- conditioners, humidifiers, 

dehumidifiers; moist structures; insect 

infestation; building occupants; pets 

Allergic reactions; asthma, eye, nose, 

and throat irritation, humidifier fever, 

influenza, and other infectious diseases 

Carbon Monoxide 

Unvented/malfunctioning gas & propane 

appliances, wood stoves, fireplaces, 

tobacco smoke, vehicles in garages 

Headache, nausea, angina, impaired 

vision and mental functioning, fatal at 

high concentrations 

Endocrine Disruptors 

(phthalates; DDT, chlordane, 

heptachlor, o-phenylphenol, 

PBDEs)

Plastics, pesticides, flame retardants 

Mimic or block natural effects of 

hormones (estrogen and others); 

developmental abnormalities 

Environmental Tobacco 

 Smoke (ETS) Cigarettes, cigars, and pipes 

Respiratory irritation, bronchitis and 

pneumonia in children, asthma in 

preschool children, lung cancer; heart 

disease, aggravated asthma, decreased 

lung function 

Formaldehyde, Other 

Aldehydes 

Composite wood products such as 

plywood and particleboard, furnishings, 

wallpaper, durable press fabrics, paints, 

combustion appliances, tobacco smoke 

Cancer, eye, nose, and throat irritation, 

headache, allergic reactions, aggravated 

asthma, decreased lung function 

Lead Lead paint chips, contaminated soil Learning impairment 

Nitrogen Dioxide Unvented or malfunctioning gas 

appliances, other combustion appliances 

Aggravated asthma, decreased lung 

function, eye, nose, and throat irritation, 

increased respiratory disease in children 

Organic Chemicals 

 (benzene, chloroform, paradichlorobenzene, methylene 

chloride, perchloroethylene, 

others) 

Solvents; glues, cleaning agents, 

pesticides, building materials, paints, 

treated water, moth repellents; drycleaned clothing, air fresheners 

Cancer; eye, nose, throat irritation, 

aggravated asthma, decreased lung 

function; headaches, at high levels: loss 

of coordination, damage to liver, kidney 

and brain 

Ozone Infiltration of outdoor air, ozone 

generating air “purifiers”, office machines 

Lung inflammation, aggravated asthma, 

cough, wheeze, chest pain 

Particulate Matter 

Cigarettes, wood stoves, fireplaces, 

cooking, candles, aerosol sprays, house 

dust 

Increased mortality and hospital 

admissions; lung cancer; irritation; 

susceptibility to sinus and respiratory 

infections; bronchitis; aggravated 

asthma; decreased lung function 

Pesticides 

Insecticides, herbicides, sanitizers, 

disinfectants used indoors, or tracked in 

or blown in from outdoors 

Neurological impairment; nausea, 

headache, dizziness; skin & eye 

irritation; hormone disruption 

Polycyclic Aromatic 

 Hydrocarbons (PAH) Cigarette smoke, cooking, woodburning Cancer, gene mutation 

Radon Uranium-bearing soil under buildings, 

ground-water, construction materials Lung cancer (especially in smokers) 

* Please note that when multiple pollutants are listed in a group, each pollutant may not cause all of the health effects 

listed in the third column. 
Indoor Air Pollution in California July, 2005 

 38

A number of indoor pollutants can cause or exacerbate asthma and chronic bronchitis. Indoor 

biological agents are associated with these diseases (IOM, 2000); however, it is clear that 

biological agents alone cannot explain the increase in asthma over the last few decades. The 

recent rise in asthma prevalence has been too rapid to be attributed to genetic factors and 

biological allergens alone: indoor and outdoor air pollution have been identified as potentially 

important contributors to the increase of asthma (McConnell et al., 2002a,b; Platts-Mills and 

Carter, 1997; Duhme et al., 1998; Karol, 2002), although the relative contribution of these and 

other factors remains unknown. 

Over the past three decades, asthma prevalence has been on the rise in industrial nations, and 

the death rate due to this disease has doubled (Karol, 2002). The Centers for Disease Control 

and Prevention (CDC) reported that in the year 2000, asthma was responsible for 4,487 deaths 

in the U.S., as well as approximately 465,000 hospitalizations, 1.8 million emergency 

department visits, and 10.4 million visits to physicians across all age groups (CDC, 2003). 

Currently, about 7.2% of adults in the U.S. have asthma (CDC, 2003). According to 2001 data, 

11.9% of Californians, or 3.9 million people, have asthma (CHIS, 2003). California also has 

higher rates of asthma mortality than the nation as a whole. The reasons for these elevated 

rates in California are unknown at this time. Children have been particularly hard-hit; from 1980 

to 1994, there was a 160% increase in asthma prevalence in those up to 4 years of age in the 

U.S. (Mannino et al., 1998). In California, asthma prevalence is highest among children 12-17 

years of age. Asthma is one of the leading causes of school absenteeism in children, and 

results in missed workdays and lost productivity in adults. Asthma affects all races and ethnic 

groups, and both genders. Every year about 40,000 Californians are hospitalized and about 500 

Californians die because of asthma. Asthma hospitalization and death rates are higher among 

African-Americans compared to other racial groups. Further, hospitalization rates among 

children are much higher than other age groups. Although the causes for the observed increase 

in asthma prevalence, hospitalizations, and death are not fully identified, indoor air pollution has 

been identified as a contributing factor. 

In a recent report by the National Academy Institute of Medicine, entitled Clearing the Air: 

Asthma and Indoor Air Exposures (IOM, 2000), the Committee on the Assessment of Asthma 

and Indoor Air examined the scientific literature relating indoor air pollutants and other factors to 

asthma. Their key findings are shown in Tables 2.2 and 2.3. Recent reviews of the medical 

literature have also established that building dampness approximately doubles the risk for 

respiratory symptoms in building occupants and can exacerbate asthma. The agent(s) 

responsible for dampness-related increased risk for asthma exacerbation have not been 

conclusively identified but may involve some or all of the following: house dust mites, 

microbiological agents such as fungi or bacteria, or organic chemicals released during 

degradation of building materials or furnishings (Bornehag, 2001; 2004). 

The IOM committee found that, in addition to the known biological asthma triggers such as 

house dust mites, cockroaches, and animal dander, chemicals in ETS can exacerbate asthma 

in preschool children. Evidence for an association between formaldehyde exposure and 

wheezing is limited, often due to confounding factors such as exposure to multiple pollutants. 

Airway responses such as wheezing, waking with shortness of breath, and asthma attacks have 

been associated with gas stove use (Jarvis et al., 1996). Sufficient evidence exists to conclude 

that ETS can exacerbate asthma in preschool-aged children and provides an association 

between ETS exposure and the development of asthma (IOM, 2000). However, scientists found 

only limited or suggestive evidence of ETS as an asthma trigger in older children and adults, 

and insufficient evidence to consider it a causal factor in these groups (IOM, 2000). The IOM 
Indoor Air Pollution in California July, 2005 

 39

committee noted that studies have linked outdoor PM with respiratory problems, and that 

outdoor fine particles, PM2.5, readily enter the indoor environment. Studies that have addressed 

asthma specifically have found some evidence for asthma exacerbation due to outdoor PM 

exposure (IOM, 2000). 

Although the Committee on the Assessment of Asthma and Indoor Air found inadequate 

evidence to link VOCs with exacerbation of asthma, more recent studies have found an 

association between residential VOCs to asthma and its symptoms. Delfino (2002) published a 

review of the epidemiological evidence for links between air toxics and asthma. Delfino cites 

Swedish studies that showed that self-reported asthma prevalence in school children increased 

with increasing VOC levels, and asthmatic adult symptoms occurred in association with toluene, 

C8-aromatics, terpenes, formaldehyde, and limonene. Adult asthma prevalence, wheeze, and 

blood eosinophil concentrations were higher in newly painted homes, consistent with higher 

VOC levels (particularly 2,2,4-trimethyl 1,3-pentanediol diisobutyrate and formaldehyde) 

measured in such homes. In another European study cited by Delfino, elevated levels of 

benzene and styrene were associated with respiratory infections in newborns with compromised 

health. The newborns had either low birth weight or an abnormal immune response (indicated 

by high levels of IgE in cord blood). In the same study, wheezing was related to house painting 

and carpet installation during the first year of life. Delfino cautions that in these studies, the 

effects seen may be subject to confounding by other causal agents. 

Table 2.2. Indoor Exposures and Exacerbation of Asthma

Sufficient Evidence of a Causal Relationship 

• Cat 

• Cockroach, House dust mite 

• ETS (preschoolers) 

Sufficient Evidence of an Association 

• Dog 

• Fungi or molds, Rhinovirus 

• NO2, NOX (high-level exposures) 

Limited or Suggestive Evidence of an Association 

• Domestic birds 

• Chlamydia pneumonia, Mycoplasma pneumoniae, Respiratory Syncytial Virus (RSV) 

• ETS (school-aged children and adults) 

• Formaldehyde, Fragrances 

Inadequate or Insufficient Evidence to Determine Whether or Not an Association Exists 

• Cow, Horse, Rodents 

• Chlamydia trachomatis, Endotoxins 

• Houseplants, Pollen 

• Pesticides, Plasticizers, VOCs 

• Insects other than cockroaches 

 Source: IOM, 2000 
Indoor Air Pollution in California July, 2005 

 40

Delfino’s (2002) review identified several links between asthma symptoms and indoor air 

pollutants, especially formaldehyde: 

• A relationship exists between formaldehyde exposure and occupational asthma. 

• Children in homes with formaldehyde concentrations greater than 41 ppb are more often 

diagnosed with asthma and chronic bronchitis. 

• Adults show more wheeze, chronic cough, and lower peak expiratory flow in homes with 

higher formaldehyde concentrations. 

• Non-asthmatics in homes with formaldehyde levels of 50 ppb or higher have elevated levels 

of expired nitric oxide, a marker for lower airway inflammation. 

Table 2.3. Indoor Exposures and Development of Asthma 

Sufficient Evidence of a Causal Relationship 

• House dust mite 

Sufficient Evidence of an Association 

• ETS (preschoolers) 

Limited or Suggestive Evidence of an Association 

• Cockroach (preschoolers) 

• Respiratory Syncytial Virus (RSV) 

Inadequate or Insufficient Evidence to Determine Whether or Not an Association Exists 

• Cat, Cow, Horse, Dog, Domestic birds, Rodents 

• Cockroaches (except for preschoolers) 

• Fungi or mold, Chlamydia pneumoniae, Chlamydia trachomatis, Mycoplasma 

pneumoniae, Endotoxins 

• Houseplants, Pollen 

• NO2, NOX

• Pesticides, Plasticizers, VOCs, Formaldehyde, Fragrances 

• ETS (school-age and older) 

Source: IOM, 2000 

The association between VOCs and asthma is complex. Other reviews support the association 

between VOCs and symptoms of asthma (Duhme et al., 1998; Leikauf, 2002). Delfino et al.

(2003b) studied Hispanic children with mild asthma in a Los Angeles community with high VOC 

levels near major freeways. Bothersome or more severe asthma symptoms were associated 

with breath concentrations of benzene, but not other breath VOCs. On breath sample days, 

asthma symptoms were also associated with 1-hour ambient NO2 and sulfur dioxide (SO2). 

Studies conducted in the workplace also demonstrate an association between asthma 

symptoms and chemicals used indoors. Between 1993 and 1997, 12% of confirmed cases (236 

of 1,915) of work-related asthma in California, Massachusetts, Michigan, and New Jersey were 

related to exposure to cleaning products. Chlorine bleach was identified as the cleaning agent 
Indoor Air Pollution in California July, 2005 

 41

associated with the greatest number of cases. Exposures were greatest in medical settings, 

schools, and hotels (all non-industrial workplaces) with janitors, cleaners, and housekeepers 

experiencing the highest incidence of the disease (both new-onset and work-aggravated cases 

of asthma: 80% were new onset; Rosenman et al., 2003). From 1993 through mid-2003, 3,188 

cases of work-related asthma were identified from doctor’s first report of occupational injury or 

illness (DPR) in California (DHS, 2004a). These cases are not specific to cleaning products. 

2.1.2 Cancer 

Many indoor air pollutants are known or suspected carcinogens. Formaldehyde, benzo(a)pyrene 

and other polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke, benzene, 

chlorinated solvents such as tetrachloroethylene, and radon are a few of the identified 

carcinogens commonly found in indoor air, some at levels much higher than outdoor levels. 

Several technical documents provide summary data regarding the carcinogenic potential of 

these pollutants. Cancer unit risks and potency factors for 121 of the 201 carcinogenic 

substances for which emissions must be quantified in the California Air Toxics Hot Spots 

program are provided in the Technical Support Document for Describing Available Cancer 

Potency Factors (OEHHA, 2002; http://www.oehha.ca.gov/air.html). The U.S. EPA’s Integrated 

Risk Information System (IRIS) provides a similar list of cancer potency values 

(http://www.epa.gov/iris/).

Risk assessments are conducted to estimate the increased risk of health problems in people 

who are exposed to different amounts of toxic substances. Risk is dependent on the amount of 

a pollutant people actually inhale, which depends on the air concentration of the pollutant in a 

given environment, the length of time a person is in that environment, and the person’s 

breathing rate during that time. Since people spend the majority of their time indoors, moderate 

and high concentrations of indoor pollutants generally translate to elevated risk. 

Several field studies have measured indoor concentrations of carcinogenic chemicals in 

California (Wallace et al., 1988; Wallace et al., 1991a; Sheldon et al., 1992a; Avol et al., 1996; 

and others). Results of these studies indicate that carcinogens are routinely found in most 

homes, often at levels higher than outdoor levels, due to the presence of indoor sources. Table 

2.4 lists key pollutants identified in California studies, and indicates their cancer classification by 

the International Agency for Research on Cancer (IARC), a part of the World Health 

Organization. For the most recent classifications, visit the IARC website. Table 2.4 also lists the 

status of each pollutant as a California toxic air contaminant (TAC). 

ARB staff estimate that about 230 excess cancer cases occur per year in California from indoor 

sources of toxic air contaminants, not including the excess cancer from exposure to radon, 

environmental tobacco smoke (ETS), and some other indoor carcinogens. This estimate of 230 

cancer cases per year is based on risk estimates from the 1994 California Comparative Risk 

Project (CCRP, 1994), updated to reflect reduced exposure and risk from indoor formaldehyde. 

Formaldehyde levels are estimated to have decreased by about one-half since the 1980s 

studies on which the 1994 estimate was based (see Appendices II and III). The chemicals with 

the highest estimated risk in the CCRP were formaldehyde (found in many building materials 

and consumer products) and para-dichlorobenzene (used in mothballs and air fresheners). 

Other chemicals included were perchloroethylene (used in dry-cleaning), chloroform (a byproduct of water chlorination and use of chlorine in spas and washing machines), 

trichloroethylene, benzene, 1,3-butadiene, styrene, benzo(a)pyrene, and di-2-

ethylhexylphthalate (DEHP–a plasticizer). The latter organic chemicals are found in many 

different consumer products and building materials, and some also are produced by combustion 
Indoor Air Pollution in California July, 2005 

 42

processes (such as when cooking food or burning wood). (DEHP is listed as a California TAC. 

However, the International Agency for Research on Cancer (IARC) recently determined that 

there is inadequate evidence for the carcinogenicity of DEHP in humans, yet sufficient evidence 

in experimental animals for carcinogenicity (http://www-cie.iarc.fr/htdocs/monographs/vol77/77-

01.html). 

Table 2.4. Carcinogenic Status of Selected Indoor Air Pollutants 

Compound Cancer Status1 Classification of 

International Agency for Research on 

Cancer (IARC)2

Status as a California 

Toxic Air Contaminant 

Acetaldehyde Group 2B, possible human carcinogen Yes 

Asbestos Group 1, known human carcinogen Yes 

Benzene Group 1, known human carcinogen Yes 

Benzo(a)pyrene (PAHs) Group 2A, probable human carcinogen Yes 

Chloroform Group 2B, possible human carcinogen Yes 

p-Dichlorobenzene Group 2B, possible human carcinogen Yes 

Di-2-ethylhexylphthalate Group 3, not classified Yes 

Environmental Tobacco 

Smoke 

Group 1, known human carcinogen Under consideration 

Formaldehyde Group 1, known human carcinogen Yes 

Methylene chloride Group 2B, possible human carcinogen Yes 

Perchloroethylene Group 2A, probable human carcinogen Yes 

Radon Group 1, known human carcinogen Yes 

Styrene Group 2B, possible human carcinogen Yes 

Trichloroethylene Group 2A, probable human carcinogen Yes 

1

Source: OEHHA, 2002; IARC website 

2

Group 2A compounds have limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity 

in experimental animals. Group 2B compounds have limited evidence of carcinogenicity in humans and less than 

sufficient evidence of carcinogenicity in experimental animals. 

The 1994 CCRP estimates, like other cancer risk estimates, were derived using 95% upperbound cancer potency factors, combined with measured indoor exposure distributions. Cancer 

risk methodology based on upper-bound cancer potency estimates provides a common, 

protective basis for comparing risks across topic areas. However, the risk estimates should not 

be interpreted as predictions of actual disease (CCRP, 1994). The risk can be much lower, 

depending on the actual dose of the pollutant inhaled and absorbed, and other factors. 

Since the time the studies used for the CCRP were conducted, some levels of indoor pollutants 

are estimated to have decreased while others likely have increased. However, there are 

insufficient new data available to refine the 1994 estimates for those chemicals. Because 

changes likely have occurred in both directions and are likely to be relatively small, and because 

the 1994 CCRP estimates did not include all known indoor carcinogenic pollutants (methylene 

chloride and polycyclic aromatic hydrocarbons other than B(a)P were not included, for 

example), the 1994 estimates remain the best available estimates for the overall cancer risk 

posed by indoor chemical pollution in California, excluding that from radon gas, environmental 
Indoor Air Pollution in California July, 2005 

 43

tobacco smoke, and asbestos (discussed later in this document). The details of ARB’s 

assessment using the CCRP results are provided in Appendix II. 

This estimate of 230 excess cancer cases approaches the cancer burden from diesel exhaust 

particles, which is estimated to result in 260 excess cases per year in California, and exceeds 

the cancer risk for other outdoor pollutants, estimated at about 110 cancer cases per year 

(Figure 2.1). Indoor air cancer risk is also nearly two-thirds of the total cancer risk estimated for 

outdoor pollutants. It is estimated that cancer risk due to diesel exhaust particles will decrease 

75% by 2010 (ARB, 2000a), leaving indoor air as a predominant source of air pollution cancer 

risk. 

Exposure to environmental tobacco smoke (ETS) makes a significant contribution to the cancer 

burden from air pollution as well. Although smoking prevalence and exposure of non-smokers 

has decreased in California, preliminary updated exposure and risk estimates for ETS 

developed by OEHHA are similar to those estimated in 1997 (OEHHA, 1997), due to the 

increase in the California population (and thus the number of individuals exposed). Updated 

estimates, which are currently undergoing peer review, show 380 excess lung cancer cases per 

year (ARB/OEHHA, 2005). This ETS risk level is similar to the total outdoor air pollutant cancer 

burden; however, because workplace exposure has decreased to nearly zero since the mid1990s, and the prevalence of smoking has decreased substantially as well, the current cancer 

burden from ETS may be somewhat lower than shown in this graphic. Nonetheless, the 

contribution of ETS will remain significant for some time, because some individuals (including 

children) are still exposed to substantial levels of ETS. 

Payne-Sturges et al. (2004) recently calculated cancer risk associated with indoor and personal 

exposure levels of VOCs and found risk levels similar to those estimated in this report. They 

measured the personal, indoor, and outdoor concentrations of 11 VOCs for 33 non-smoking 

adults in South Baltimore, Maryland. VOC concentrations were similar to earlier reported 

measurements in the California VOC Total Exposure Assessment Methodology (TEAM) studies, 

Figure 2.1:

Estimated Potential Cancer Burden from Air Toxics 

in California by Source

0

50

100

150

200

250

300

350

400

Outdoor 

TAC

Sources

Indoor 

TAC Sources

Environmental 

Tobacco 

Smoke

Excess Cancers Per Year

Other Outdoor TAC

Sources

Outdoor Diesel

Exhaust (Particles)
Indoor Air Pollution in California July, 2005 

 44

with some variations noted both higher and lower. For personal monitoring, the highest median 

cancer risks were attributed to chloroform, benzene, and carbon tetrachloride. The authors 

assumed the cancer risks for the 11 VOCs were additive and calculated 165 lifetime cumulative 

cancer risks per 1 million based on average indoor concentrations of 11 measured VOCs, with 

formaldehyde not included. Calculations based on personal exposures and outdoor 

concentrations were 183 and 43 cumulative lifetime cancer risks per 1 million, respectively. A 

background risk (or ambient risk) was not subtracted from the indoor calculation. Applying this 

methodology to California, the estimate is comparable to the 230 excess cancer cases 

estimated in this report, based on a population of 35 million and the inclusion of formaldehyde, 

some other VOCs, and semi-volatiles such as benzo(a)pyrene, in the California estimate. 

Other recently developed risk estimates also demonstrate the carcinogenic risk posed by indoor 

pollutants present at average concentrations. In the absence of indoor standards, Hoddinott and 

Lee (2000) applied U.S. EPA Superfund risk assessment methodology to selected VOCs to 

determine if indoor concentrations produce significant risks. Indoor VOC concentrations from 

two studies completed in the 1980s (Wallace, 1987; Cohen et al., 1989) were used to determine 

the level of risk associated with VOCs measured inside residences. U.S. EPA considers 

acceptable levels of cancer risk to be one increase in lifetime cancer incidence per 10,000 to 

1,000,000 persons (U.S. EPA, 1989). Hoddinott and Lee (2000) calculated that the risk for 

adults and children, based on average levels found in homes, exceeded the acceptable risk 

level of one in a million for a number of pollutants. Those pollutants are found in dry-cleaned 

clothing, ETS, cleaning agents, glued carpet, gasoline, and degreasers. The authors concluded 

that “Chemical concentrations resulting from ‘off-gassing’ from normal household activities and 

materials can result in a health risk estimate that exceeds the benchmark used at hazardous 

waste sites”. The authors also note that “the data used in this evaluation predate changes in the 

manufacturing of indoor products. These efforts may have reduced some of the emissions in the 

average home.” 

2.1.3 Irritant Effects 

Many indoor pollutants cause eye, nose, and throat irritation (Wolkoff and Nielsen, 2001). 

Tables of irritant thresholds have been developed to provide guidance for non-irritating levels of 

pollutants at workplaces and in the home (Molhave, 1991a; Devos et al., 1990). The OEHHA 

Chronic Reference Exposure Level for formaldehyde is set at 2.4 ppb to protect against irritation 

of the eyes and upper and lower respiratory tract. Ozone, the primary ingredient in smog and a 

strong oxidant, also irritates the respiratory system, causing coughing, throat irritation, or a 

burning sensation in the airways. Ozone irritation can lead to a feeling of chest tightness, 

wheezing, and shortness of breath (ARB, 2000b). Ozone and other oxidants have been shown 

to react with other chemicals such as isoprene and terpenes, to produce irritating products such 

as formaldehyde, terpene oxides, and fine particles (Long et al., 2000; Wilkins et al., 2001). 

Further research is needed to understand the extent and duration of exposure to reaction 

products, and the potential health effects of those exposures. Some biological contaminants 

such as some types of mold are also known to cause irritant effects. 

2.1.3.1 Reaction Products 

Indoor organic chemicals react with oxidants such as ozone, hydroxyl radicals, and nitrate 

radicals to produce secondary pollutants. Weschler (2004) provides an excellent review of 

studies investigating indoor chemical reactions published since 2000. The review focuses on the 

importance of hydroxyl radicals in indoor reactions, reactions occurring on indoor surfaces, and 

the impact secondary reaction products have on building occupants. Traditional analytical 
Indoor Air Pollution in California July, 2005 

 45

methods often do not detect some of the short-lived, highly reactive compounds that are 

produced. Sensory measurements have been used to detect changes in indoor air quality 

associated with the reactions. It is thought that the ozone/terpene reactions dominate indoor 

chemistry based on the frequent presence of ozone and ubiquitous presence of terpenes in 

indoor environments (Weschler, 2004). 

Terpenes are reactive chemicals (e.g., α-pinene, d-limonene, myrcene) that are frequently used 

in cleaning products and other products for their favorable odor characteristics and solvent 

properties. In order to use less toxic ingredients in consumer products, manufacturers have 

replaced petroleum-based hydrocarbons with plant-derived compounds, such as d-limonene. 

These compounds are Generally Recognized as Safe (GRAS) by the Food and Drug 

Administration (FDA). They can be airway irritants at concentrations greater than normally 

encountered in indoor air (Wolkoff et al., 2000). However, terpenes also have been associated 

with irritation at lower levels: the irritant chemicals are hypothesized to be a product of the 

reaction of terpenes with oxidants, rather than the terpene itself (Wilkins et al., 2001; Weschler 

and Shields, 1997; Weschler and Shields, 1996; Atkinson and Arey, 2003). This is supported 

by other research that has shown that high purity d-limonene produces no allergic reaction 

when applied to the skin of guinea pigs. Alternatively, if the d-limonene is exposed to air for two 

months, then applied to the animals, they are sensitized (Karlberg et al., 1991). The authors 

concluded “if limonene is used in technical products, its handling and storage may be critical”. 

This finding may indirectly support the transformation of terpenes to more irritating compounds 

via reactive chemistry. Further work by the same investigator confirmed that air oxidation of dlimonene is essential for its sensitizing potential, and potent allergens are created (Karlberg et 

al., 1992). 

Investigators are exploring potential reactions between unsaturated hydrocarbons and oxidants 

in an effort to more positively identify the cause of sick building health effects. Several reactions, 

such as between ozone and unsaturated hydrocarbons, ozone and nitrogen oxides, and free 

radical reactions, may lead to the formation of more irritating indoor compounds. These 

reactions can lead to the production of submicron particulate matter, aldehydes (formaldehyde) 

and ketones with lower odor thresholds and greater irritancy than precursors, carboxylic acids 

such as formic acid and acetic acid, and free radicals (Weschler and Shields, 1997; Sarwar et 

al., 2004). Pollutants with reactive double bonds such as terpenes and alkenes react with ozone 

and nitrogen oxides to produce products that result in airway irritation similar to that of 

formaldehyde. Fan et al. (2003) confirmed the reaction of ozone with d-limonene and ozone with 

α-pinene under indoor conditions to generate submicron particles and other potentially irritating 

species, such as aldehydes and organic acids. To minimize these reactions, Fan et al. (2003) 

suggest “limiting use of products that emit high-reactivity alkenes during episodes when outdoor 

ozone levels are elevated”, reducing outdoor ozone levels, and minimizing the penetration of 

ozone from outdoors. 

In this growing area of research, investigators have identified an increase in fine particles 

associated with mopping floors with a pine-scented cleaning product. It is hypothesized that the 

generation of particles was the result of ambient ozone (up to 48 ppb) reacting with the terpenes 

in the cleaning product (Long et al., 2000). Sarwar et al. (2004) clearly demonstrated the indoor 

reaction between ozone and terpenes from various consumer products, leading to increases in 

fine particle mass concentrations. This area of research warrants increased effort in order to 

understand the association between indoor air pollutants and related health effects. Another 

key area of needed research is that of pollutant interactions with indoor surfaces, such as 

carpets and walls; preliminary studies have shown that such chemistry readily occurs, and can 

penetrate the surface. 
Indoor Air Pollution in California July, 2005 

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2.1.3.2 Sick Building Syndrome 

Sick Building Syndrome (SBS) is a term used to describe a collection of irritant and neurological 

effects that occur while occupants are in a building, that generally disappear when affected 

people are out of the building. Specific causes of SBS have not yet been firmly identified. The 

most common symptoms include eye irritation, congested nose, headache, fatigue, difficulty 

concentrating, and dry skin (Tenbrinke et al., 1998). SBS differs from building-related illness 

(BRI; see Biological Contaminants section) in which an identifiable factor causes a specific 

illness such as bacteria causing Legionnaires’ disease or humidifier fever. 

In an attempt to identify factors related to SBS, Seppanen and Fisk (2002) reviewed the 

literature to summarize factors associated with SBS. They found that relative to natural 

ventilation, air conditioning was consistently associated with a statistically significant increase in 

the prevalence of one or more SBS symptoms, by approximately 30-200%. This finding 

reinforces the use of ventilation as a mitigation measure for reducing indoor pollution, but still 

may not identify the primary cause. The review identifies several confounding factors that are 

not affected by the HVAC type: quantity of carpet or textile surfaces; sealed windows; building 

age; depth of the building bays; and dusty surfaces. A European review also found an 

association between ventilation and comfort and health (Wargocki et al., 2002). 

Investigators who study indoor reactive chemistry suggest that the degradation products of 

VOCs may be responsible for the reported SBS symptoms (Carslaw, 2003; Wolkoff et al., 2000; 

Wolkoff and Nielsen, 2001; Weschler, 2004). These reactions include ozone/terpene reactions 

with propagation of hydroxyl radicals and reactions on indoor surfaces such as ozone 

interacting with carpet. The impact that the products of indoor chemistry can have on building 

occupants has also been studied on a physiological level (Weschler, 2004). 

Mendell (1993) conducted a review of the epidemiological literature related to SBS. In reviewing 

32 studies, he found consistent findings for an association of SBS symptoms with airconditioning, carpets, more workers in a space, video display use, and ventilation rates at or 

below 10 liters/second/person. With specific causes unidentified, Mendell stressed the 

importance of using prudent design, operation, and maintenance practices to prevent sick 

building symptoms. 

Tenbrinke et al. (1998) reported a new approach for using VOC exposure metrics as predictors 

of SBS. These authors were able to confirm a link between exposure to low level VOCs and 

SBS symptoms. Apte and Daisey (1999) used the methodology developed by Tenbrinke to 

identify an association between mucous membrane symptoms and photocopiers. Apte and 

Daisey also identified a relationship between sore throat symptoms and fresh paint. 

Many biological agents can provoke an immunological response, which most frequently takes 

the form of allergic reactions to the agent. Common symptoms and signs are watery eyes, runny 

nose, sneezing, nasal congestion, itching, coughing, wheezing, difficulty breathing, headache, 

and fatigue. Allergic rhinitis (hay fever) and allergic asthma are examples of hypersensitive 

responses to biological contaminants. Fungal spores, microbial byproducts, dust mites, cat 

allergen, and pollens are frequently associated with allergic responses. 
Indoor Air Pollution in California July, 2005 

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2.2 Traditional (Criteria) Pollutants 

Several pollutants for which outdoor air quality standards have been established occur at 

elevated levels indoors as well, and can pose a serious health risk. Ambient PM has been 

associated with premature death and serious respiratory and cardiovascular effects in 

numerous studies. CO can cause near-term death with high exposures of relatively short 

duration. All of these pollutants can impose serious, non-fatal health impacts: NO2 from indoor 

combustion appliances can harm the lungs and other mucous membranes and cause 

respiratory disease, and ozone can have similar effects at elevated levels. The health effects, 

indoor sources, and indoor air concentrations of these traditional (criteria) pollutants are 

discussed below. 

2.2.1 Particulate Matter 

Particulate matter (PM) is broadly defined as any non-gaseous material suspended in the air. 

PM can include solid material (i.e., dust), liquid material (i.e., a sprayed aerosol), or a 

combination of solid/liquid materials (i.e., a hydrated vehicle exhaust particle). PM is generally 

classified by its size. PM2.5 refers to all suspended matter having aerodynamic diameters less 

than 2.5 microns (μm: one μm = one millionth of a meter) and is commonly referred to as ‘fine’ 

PM. PM10 refers to all suspended matter having aerodynamic diameters less than 10 μm. PM 

between 2.5 μm and 10 μm is commonly referred to as ‘coarse’ PM. Both federal and state 

ambient (outdoor) air quality standards incorporate these size distinctions. Recent studies 

suggest that PM2.5 mass may be a better indicator than PM10 mass for predicting potential 

health effects resulting from ambient (outdoor) PM exposure (Williams et al., 2000abc; Schwartz 

and Neas, 2000), although some recent studies have specifically linked health impacts to the 

coarse fraction (Lippmann et al., 2000; Mar et al., 2000; Ostro et al., 2000). 

A substantial portion of indoor particles originate outdoors from outdoor sources (Ozkaynak et 

al., 1996ab; Abt et al., 2000, Long et al., 2000; Liu and Nazaroff, 2001). Outdoor sources of PM 

that may infiltrate indoors include PM from transportation sources (i.e., gasoline and diesel 

powered highway vehicles), agricultural activities (i.e., biomass combustion emissions, fugitive 

dust emissions, pesticide sprays), biogenic emissions (i.e., forest fire smoke), and many others. 

Further reduction of these concentrations in outdoor air would likewise lower their 

concentrations in indoor environments. However, there are numerous indoor sources of PM as 

well. These include combustion devices and activities such as stoves, fireplaces, cigarette 

smoking, cooking, and candle burning, all of which can produce indoor PM with harmful 

components similar to those from outdoor air (Lofroth et al., 1991). Indoor particles also include 

fibrous materials, pollen, mold spores and fragments, and tracked-in soil particles (Wallace, 

1996a). These particles become trapped in/on building surfaces, particularly carpets, and have 

been shown to persist for a very long time, due to the lack of applying effective cleaning and 

maintenance procedures, and they may be re-suspended into the air. Some can trigger asthma 

attacks and allergy symptoms, as discussed previously. Others can have a mix of toxic 

components such as PAHs, lead, and pesticides adsorbed onto them; these components may 

contribute to serious health effects such as cancer (PAHs) and developmental effects (lead). 

Major epidemiologic studies have shown a strong association between ambient (outdoor) PM 

concentrations and increased death and disease (e.g., Dockery et al., 1993; Pope et al., 1995) 

and an increase in the rate of death from cardiovascular and respiratory disease (Samet et al., 

2000). Indoor PM, particularly from indoor combustion sources, may be similar in composition to 

outdoor PM, and might be expected to cause the same impacts as outdoor PM. However, 

research has only recently been undertaken to examine the differences in indoor and outdoor 
Indoor Air Pollution in California July, 2005 

 48

PM composition, and the relative contribution of indoor PM and outdoor PM to the total PM 

effects of death and disease have not been studied, and are high priorities for further research. 

Although considerable progress has been made in elucidating the toxicological mechanisms of 

outdoor PM toxicity, it is difficult to draw inferences between indoor and outdoor PM without 

focused studies: indoor PM could be more or less toxic than outdoor PM. However, because 

ambient PM epidemiological studies are based on particle size and include a mix of particles 

from combustion sources, soil, and other sources, the epidemiological relationships from 

ambient PM studies and their magnitude should be examined when considering the potential 

risk from indoor PM. The effects of ambient PM are summarized below, followed by a brief 

discussion of the potential impacts of indoor PM. 

2.2.1.1 Death 

Both acute and chronic ambient PM exposure have been associated with an increased risk of 

premature death, primarily in older adults with preexisting heart and/or lung disease. Studies 

conducted in California, the U.S., and in diverse cities worldwide suggest that risk of death 

increases about 0.25 to 3.5 percent with each 10 μg/m3

 increase in daily mean ambient PM2.5 

concentration (e.g., Burnett and Goldberg, 2003; Dominici et al., 2003; Fairley, 2003; Goldberg 

and Burnett, 2003; Moolgavkar, 2003; Schwartz, 2003; Ponka et al., 1998). Long-term cohort 

studies suggest that the increase in risk of death is about 4% with each 10 μg/m3

 increase in 

annual mean ambient PM2.5 concentration (Dockery et al., 1993; Krewski et al., 2000; Pope et 

al., 1995). Meta-analyses of earlier studies suggest that the effects on death are fairly consistent 

(Ostro, 1993; Dockery and Pope, 1994; Schwartz, 1994), regardless of where the study was 

performed. About 6,500 deaths occur each year in California due to outdoor particulate pollution 

levels above the State ambient air quality standards (ARB/OEHHA, 2002). 

In a recent assessment of global and regional health risks, Cohen et al. (2004) used PM2.5 

(measured or estimated) as an index for urban air pollution. They reviewed literature from all 

parts of the globe, and estimated the portion of death from specified diseases attributable to 

urban pollution (PM2.5). They estimated that pollution in urban areas worldwide causes about 

3% of death attributable to cardiopulmonary disease in adults; about 5% of death attributable to 

cancers of the trachea, bronchus, and lung; and about 1% of death attributable to acute 

respiratory infections in children. Based on a year 2000 population, this totals about 800,000 

excess deaths and 6.4 million disability-adjusted life years. The greatest burden was estimated 

to occur in the more polluted and rapidly growing cities of developing countries. The authors 

noted the universality of PM effects found worldwide, despite some differences in ambient PM 

sources and composition. This lends support to the likelihood of similarities of impacts from 

ambient and indoor PM. The authors noted that the estimates derived in their analysis are likely 

an underestimate, and that they cannot be extrapolated to smaller regions or for other purposes. 

2.2.1.2 Non-lethal Health Impacts 

Several hundred studies have been published examining the association between various 

measures of ambient PM and a variety of adverse health effects other than premature death. 

The health outcomes associated with ambient PM concentrations include hospitalization and 

emergency room visits for respiratory or cardiovascular disease; respiratory symptoms, 

including asthma symptoms; restrictions in activity and school absenteeism; and reduced lung 

function and other effects in children. Although these effects are not as serious as immediate 

death, they are serious (some can lead to death) and affect a greater proportion of the 

population, and thus have a major impact on public health. The key results from some of the 

published studies include the following: 
Indoor Air Pollution in California July, 2005 

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• Hospitalization and serious respiratory disease 

9 Studies consistently report associations between both ambient PM2.5 and PM10 and 

hospital admissions for respiratory and cardiovascular illness (e.g., Atkinson et al., 

2003; Sheppard et al., 1999; Sheppard, 2003; Ito, 2003; Zanobetti and Schwartz, 

2003; Moolgavkar, 2003; Le Terte et al., 2003). These effects have been reported 

mainly for people over age 65 who already have some form of cardiopulmonary 

disease. Respiratory causes of admission include pneumonia, chronic obstructive 

pulmonary disease (COPD) and asthma, while cardiovascular causes have included 

general cardiovascular disease, congestive heart failure, stroke, and ischemic heart 

disease. Overall, ambient PM10 has been associated with an estimated increase in 

risk of hospitalization of 1.25% - 5% per 10 μg/m3 increase in the daily mean ambient 

PM10 concentration for respiratory endpoints, and 0.3% to 2.6% for cardiovascular 

endpoints. 

9 Associations have also been reported between ambient PM10 and PM2.5 and 

emergency department visits, primarily for asthma exacerbation, which may or may 

not result in hospital admissions (e.g., Lipsett et al., 1997; Delfino et al., 1997). 

• Respiratory symptoms

9 Studies have associated ambient PM10 and PM2.5 exposure with asthma and 

respiratory symptoms, for example cough, phlegm, chest pain, or wheeze (e.g., 

Delfino et al., 2003a; Mortimer et al., 2002; Schwartz and Neas, 2000), asthma 

exacerbation (e.g., Whittemore and Korn, 1980), and use of asthma medications 

(e.g., Delfino et al., 1996; Pope et al., 1991). People with asthma retain a greater 

number of ultrafine PM particles than do healthy subjects, thus making them more 

susceptible to the health effects of air pollution Chalupa et al. (2004). 

9 Cellular level effects have also been identified. Exposure to respiratory irritants can 

result in local airway inflammation, altered epithelial cell permeability, increased 

mucus secretion, and bronchoconstriction. Disease states such as asthma and 

chronic bronchitis can adversely affect particle clearance or removal (e.g., Foster, 

1999). Also, the viability and functional integrity of cells in the lungs can be adversely 

affected by ambient PM exposures (e.g., Soukup and Becker, 2001). 

• Work loss, absenteeism, reduced productivity: 

9 Ostro (1987) and Ostro and Rothschild (1989) reported 10 to 15% reduction in 

activity due to respiratory-related causes per 10 μg/m3 of ambient PM10. 

9 Ransom and Pope (1992) reported about a 4% increase in absenteeism per 10 

μg/m3 of ambient PM10 at an elementary school in Utah.

9 Gilliland et al. (2001) reported an increase of 5.7% in total illness-related absences 

per 10 μg/m3 of ambient PM10 among 4th grade school children (ages 9-10) in 12 

southern California communities. 
Indoor Air Pollution in California July, 2005 

 50

• Effects on children 

9 Investigators with the ARB-sponsored Children’s Health Study found that, among 

children with asthma, respiratory symptoms increased with increasing ambient 

particle levels (McConnell et al., 1999). Results also suggest that children who live in 

communities with high concentrations of ambient PM may have decreased lung 

function growth compared to children living in communities with lower concentrations 

of ambient PM (Gauderman et al., 2000; Peters et al., 1999a,b). However, both of 

these results were also true for NO2 and acid vapor, and the independent effects of 

the different pollutants cannot be assessed because of high inter-pollutant 

correlations. Similar results have also been reported by Horak et al. (2002) in 

Austrian children. A recent study by Delfino et al. (2004) found clinically relevant 

decreases in lung function associated with personal PM exposure in schoolchildren 

with asthma. 

9 Several recent studies have suggested that the unborn may also be at risk of 

adverse effects from ambient PM pollution, based on statistically significant 

relationships between outdoor PM concentration and low birth weight (Ritz et al., 

2000; Bobak, 2000), premature birth (Bobak, 2000), neonatal death (Penna and 

Duchiade, 1991; Woodruff et al., 1997; Bobak and Leon, 1998), and fetal growth 

retardation (Dejmek et al., 1999). However, except for Ritz et al. (2000) and Ritz et 

al. (2002), these studies have been conducted outside the U.S., in areas with higher 

ambient PM concentrations than those typically observed in the U.S. 

The following incidences of illnesses are estimated to occur annually in California due to 

outdoor PM10 levels above the State ambient air quality standard. 

• 7,900 cases of chronic bronchitis among people age 27 or older, 

• 6,000 hospital admissions for cardiopulmonary causes among the elderly (age 65 or more), 

• 1,000 asthma-related hospital admissions among people age 64 or less, 

• 2,300 asthma-related emergency room visits among people age 64 or less, 

• 340,000 asthma attacks among all ages. 

The California ambient air quality standard for PM2.5 is 12 μg/m3 (annual mean), and the PM10 

standards are 50 μg/m3 (24-hour) and 20 μg/m3 (annual mean). There are no federal or 

California standards for indoor PM levels. The national ambient air quality standards (NAAQS) 

for PM2.5 are 65 μg/m3 (24-hour average) and 15 μg/m3 (annual mean), and for PM10 are 150 

μg/m3 (24-hour on average) and 50 μg/m3 (annual mean). These levels are often exceeded in 

California’s indoor environments, particularly when indoor sources are used or when particlegenerating activities occur. 

2.2.1.3 Potential Health Impacts of Indoor PM 

The serious adverse health impacts of certain indoor PM components are well documented. As 

discussed in other sections of this document, tobacco smoke particles, radon daughters, metals 

such as lead, semi-volatiles such as PAHs, and biological components such as pollens and 

mold all exert serious, sometimes fatal, impacts on human health. However, based on the 

serious impacts documented for outdoor PM, it is likely that indoor PM is much more than the 

sum of its parts–there are likely serious effects not yet measured, quantified, or properly 

accounted for. 
Indoor Air Pollution in California July, 2005 

 51

As indicated in the preceding section, large numbers of cases of illnesses are expected to occur 

each year in California due to outdoor particulate matter pollution levels above the State 

ambient air quality standards (ARB/OEHHA 2002). Indoor PM is comprised of varying 

proportions of PM of indoor and outdoor origin (discussed below). Because the additional PM 

burden from indoor sources is generally not well represented in epidemiology studies, indoor 

PM emissions may be significant contributors to the adverse impacts seen in the epidemiology 

studies. Additionally, indoor PM may also contribute to premature mortality, hospital admissions, 

chronic bronchitis, and other effects beyond the levels quantified in the epidemiology studies. 

Two groups have recently examined the literature to determine whether there is sufficient 

information available to permit a rough estimate of the impacts from indoor PM. The first group 

was a panel of indoor air quality and PM experts convened by ARB in February 2004 to review 

and assess what is known regarding the impacts of indoor PM on health. The panel found that 

only one study provides suggestive evidence of the health effects of indoor combustion 

emissions. In that study of rat alveolar macrophages, investigators found that indoor-generated 

particles triggered greater production of tumor necrosis factor than did a comparable amount of 

outdoor PM, suggesting that indoor-generated PM may be more bioactive than ambient 

particles (Long et al., 2001). This may be due to PM emissions from indoor combustion sources 

being relatively “fresh”, and small in size, while PM released outdoors may be more “aged” and 

potentially less toxic when inhaled. Alternatively, outdoor PM may actually be much more toxic 

than indoor PM, due to emissions from complex sources such as diesel trucks and industrial 

plants. There is considerable variability in the chemical composition, acidity, and size 

distribution of outdoor PM depending on geological conditions, traffic mix, meteorological 

conditions, proximity to major roadways, and significant stationary sources. However, the Cohen 

et al. (2004) study found that PM impacts were essentially global, with few differences across 

regions, lending support to the likelihood of similar impacts from indoor PM. The panel 

determined that available studies document the known effects of ETS particles and infectious 

and allergenic indoor biological contaminants, but that few studies have been designed to 

specifically identify effects of other types of indoor-generated PM, such as that from candles or 

woodsmoke. They concluded that research is sorely needed in this area, to determine the actual 

toxicity of indoor-generated PM, particularly from indoor combustion sources, and the relative 

toxicities of indoor and ambient PM. 

The second group that examined this issue was a European interdisciplinary group of 

researchers who reviewed the relevant literature to determine whether particle mass, surface 

area, or number concentration could be used as risk indicators for health effects in nonindustrial buildings (Schneider et al., 2003). The group concluded that the study design of most 

of the reviewed studies was not focused on finding associations between airborne PM and 

health outcomes, and consequentially, while airborne particles are likely to cause health effects 

in non-industrial environments, the scientific evidence was inadequate to permit the use of 

indoor PM mass, surface area, or number concentration as risk indicators for health effects in 

buildings. 

2.2.2 Indoor PM Sources and Emissions 

Indoor PM concentrations are typically equal to or higher than concurrently measured outdoor 

levels (see next section), depending on the sources and activities that are present indoors. 

Outdoor air infiltration and indoor combustion sources such as smoking and cooking are 

typically the greatest sources of indoor PM (Wallace, 1996a; Ozkaynak et al., 1996a,b; Brauer 

et al., 2000; Abt et al., 2000; Fortmann et al., 2001). Prominent indoor sources include 

cigarettes, woodstoves, and candles; cooking and cleaning activities (Ozkaynak et al., 1996a,b; 
Indoor Air Pollution in California July, 2005 

 52

Abt et al., 2000, 2001; Long et al., 2000); the presence and activities of occupants (Abt et al., 

2000; Rodes et al., 2001); the use of personal care products (Conner et al., 2001); and indoor 

chemical reactions (Weschler and Shields, 1997; Nazaroff and Weschler, 2004). Fibrous 

materials, pollen, mold spores and fragments, and tracked-in and blown-in soil particles are also 

components of indoor PM (Wallace, 1996a). 

The contribution of outdoor PM to indoor PM concentrations can be substantial but highly 

variable. For residential buildings, the main entry routes of outdoor air are open windows and 

doors, cracks in the building shell, and mechanical ventilation systems such as swamp coolers 

and whole house fans. Investigators of a large, population-based study in California, the Particle 

Total Exposure Assessment Methodology Study (PTEAM Study) estimated that residential 

indoor PM10, on average, is roughly comprised of about 66% outdoor PM10; 75% for PM2.5 

(Ozkaynak et al., 1996a,b). In a study of four Boston homes with air exchange rates below 1.0 

air exchange per hour (ACH), Abt et al. (2000) estimated that only 20-43 percent of indoor PM2 

to PM10 were from outdoors, while 63-92 percent of indoor PM 0.02-0.3 μm were from the 

outdoors. Abt et al. (2000) and Long et al. (2000) also found that the relative contribution of 

outdoor PM to indoor levels varied by particle size, with outdoor air generally contributing a 

majority of the smaller particles measured indoors, while indoor sources contributed more to the 

coarse (2-10 micrometers) fraction. Because these studies examined primarily older individuals 

who are less active in their homes than younger families may be, and were conducted on the 

east coast, the results of these studies may not reflect typical California proportions; however, 

they show that reductions in outdoor PM levels could have a major effect on indoor 

concentrations 

Indoor combustion source emissions, such as those from smoking and cooking, are often 

intermittent and highly variable, but emissions can be very high, resulting in exposures that can 

have significant impacts on people’s total daily exposure to PM (Long et al., 2000; Nazaroff and 

Klepeis, 2004). In the PTEAM Study homes with smokers, it was estimated that 30% of the 

PM2.5 mass and 24% of the indoor PM10 mass came from smoking. For homes in which 

cooking occurred during the monitoring period, 25% of the indoor PM2.5 and PM10 was 

estimated to come from the cooking activity (Ozkaynak, 1996b). These results are consistent 

with those of previous indoor studies that examined the impact of cigarette smoking on indoor 

PM levels, and they are consistent with subsequent studies of indoor cooking emissions that 

confirmed the high impact of cooking on indoor and personal PM levels (Abt et al., 2000; 

Wallace, 2000b; Brauer et al., 2000; Fortmann et al., 2001). 

For example, in an ARB-sponsored study, Fortmann et al. (2001) measured indoor and outdoor 

PM during 32 types of cooking activities with both gas and electric ovens and stovetops. 

Although concurrent outdoor levels reached only 20 μg/m3

, indoor PM levels during and after 

cooking often exceeded 50 μg/m3

, ARB's indoor air quality guideline level and ambient air 

quality standard for ambient PM10 for 24 hours. Kitchen PM10 levels exceeded more than 1400 

μg/m3 during frying, broiling, and baking activities with the gas stove (Fortmann et al., 2001). 

Indoor PM levels during cooking with the electric stove were generally lower; however, cooking 

with the electric stove produced much higher indoor PM levels in two cases - frying tortillas and 

stovetop stir-frying. The highest concentrations of indoor PM were produced when using the 

self-cleaning cycle of the oven for several hours. Indoor PM10 was over 3,600 μg/m3 (over 

2,000 μg/m3 PM2.5) for the gas stove, and nearly 400 μg/m3

 PM10 for the electric stove. 

Measurement of particle counts during cooking activities and oven cleaning indicated that 

particles were primarily smaller than 0.1 μm. 
Indoor Air Pollution in California July, 2005 

 53

The burning of wood, candles, and incense can also be important combustion sources of 

residential indoor PM, especially in the 2.5 μm size range and below (Wasson et al., 2002; 

Jetter et al., 2002; Brauer et al., 2000; Guo et al., 2000; Lofroth et al., 1991). Individual candles, 

for example, released 200-3600 μg/hr of PM10, and 100-1700 μg/hr of lead from the lead wick 

(Wasson et al., 2002). Another investigator found a mean lead emission rate from candles of 

770 μg/hr of lead (Van Alphen, 1999). Guo et al. (2000) modeled indoor PM2.5 concentrations 

ranging from 4.3-1173 μg/m3 based on PM emission measurements from candle burning. These 

indoor combustion sources produce PM with potentially harmful components similar to those 

from some outdoor PM combustion sources (Lofroth et al., 1991). 

Physical generation or re-suspension of particles also can contribute to airborne indoor PM 

levels. Soft or porous interior surfaces such as carpets and draperies have the potential to 

attract and re-emit particles (Thatcher and Layton, 1995; Kamens et al., 1991). Housecleaning 

can resuspend particles. When using some vacuum cleaners, resuspension can occur through 

filter leakage, leakage in the assembly of the outer vacuum shell, and from powerhead use with 

insufficient suction. In one study of several types of vacuum cleaners, including those highly 

rated for their cleaning ability, Bowser and Marshall (2003) measured peak airborne PM10 

levels ranging from about 20 μg/m3 while cleaning hard floor surfaces to nearly 140 μg/m3 while 

cleaning carpeted surfaces. Fugler (2004) noted that, during this same set of tests, “operating 

the vacuum cleaner significantly raised dust levels in the room, regardless of whether they were 

HEPA filtered or not.” Others have found substantial resuspension of cat allergens and spores 

(Woodfolk et al., 1993; Luedtke et al., 1999). Particle concentrations can be high even in homes 

where good cleaning practices are used. The particles can become re-entrained in the indoor air 

when people walk or play (Wallace, 2000a; Roberts and Dickey, 1995; Abt et al., 2000; Vette et 

al., 2001). 

Particles in house dust, such as metals, and semi-volatile chemicals such as pesticides and 

some PAHs that have their own toxic properties pose a risk to children (Rothenberg et al., 1989; 

Roberts and Dickey, 1995; Lewis et al., 1999; U.S. EPA, 1999a). Particles of house dust with 

these contaminants can be re-emitted to the air and subsequently inhaled, and may be ingested 

by children through hand-to-mouth behavior, often the primary route of exposure, or dermally 

absorbed when they spend time on the floor (Lewis et al., 1994; Zartarian et al., 1998; Zartarian 

and Leckie, 1998). For toxics such as lead, floor dust levels can be a major determinant of 

exposure. 

Biological contaminants such as fungi, bacteria, house dust mites and pollen also contribute to 

indoor particle concentrations, especially in buildings with moisture problems from flooding or 

roof leaks that have not been properly repaired. Bioallergens, such as pollen, in outdoor air can 

also penetrate indoor spaces. Re-entrained road dust may be a particularly important source of 

bioallergens in both indoor and outdoor air (Miguel et al., 1998). 

2.2.3 Indoor and Personal PM Concentrations 

Indoor PM concentrations sometimes exceed outdoor air concentrations, due to the presence of 

indoor sources of PM. For example, in one of the first comprehensive residential PM field 

studies, Spengler et al. (1981) found an increase in indoor concentrations of respirable PM of 

approximately 1 μg/m3 per cigarette smoked per day, and about a 20 μg/m3

 increase per pack. 

Other examples are discussed in the Indoor PM Sources and Emissions Section above. 

Additionally, people’s personal exposures to PM sometimes exceed both indoor and outdoor 

concentrations, primarily because people tend to spend time very near pollutant sources, such 
Indoor Air Pollution in California July, 2005 

 54

as when cooking or cleaning. This has been called the “proximity effect”, and reflects the fact 

that pollutant levels are highest near the source than farther away where emissions have 

become diluted in the air (McBride et al., 1994). A small portion of the elevated personal 

exposure levels seen across PM studies also is attributed to the existence of a “personal cloud” 

of PM surrounding a person, due to re-suspension from clothing, the use of personal care 

products (Conner et al., 2001), and skin flakes. Williams et al. (2000b) estimated a mean 

personal cloud of 3.1 μg/m3

, and Rodes et al. (2001) estimated personal clouds of 3 μg/m3 in 

two separate studies. However, Wallace (2000a) examined a breadth of studies and estimated 

an average personal PM10 cloud of 30 μg/m3

, ranging from 3-67 μg/m3. Personal PM2.5 clouds 

were estimated to range from 6-27 μg/m3

. 

Consequently, because proximity to PM-emitting sources and activities can significantly 

increase people’s actual exposures, most studies of indoor residential PM concentrations have 

included, or even focused on, measurement of occupants’ personal exposures to PM. These 

have been obtained using personal samplers worn by study participants for one or more days 

as they go about their daily routines. These measurements provide a more accurate measure of 

people’s exposure to PM, because PM levels are often higher very near people than at the 

location of indoor air sampling equipment in a room. Table 2.5 summarizes the major indoor and 

personal exposure PM studies conducted in the U.S. in recent years. Unlike earlier studies, 

there was little or no cigarette smoking in most of the studies listed in Table 2.5. 

The first major study to measure indoor, outdoor, and personal PM concentrations in California 

was the PTEAM Study. Investigators measured PM10 and PM2.5 for 12-hour daytime and 

nighttime periods in 178 homes during the fall in Riverside, California. They found 12-hour 

daytime personal PM10 concentrations to be about 50% higher than simultaneously measured 

daytime residential indoor or outdoor concentrations. Daytime personal concentrations 

averaged 150 μg/m3

, while indoor and outdoor concentrations both averaged about 95 μg/m3

(Clayton et al., 1993, Ozkaynak et al., 1996ab). Most importantly, 12-hour daytime personal 

PM10 concentrations exceeded the California 24-hour ambient air quality standard level of 50 

μg/m3

 for about 90% of the monitoring days, and exceeded the federal PM10 standard level of 

150 μg/m3

 for 25% of the monitoring days. During nighttime, personal PM10 concentrations 

decreased and were similar to concurrent indoor and outdoor concentrations (roughly 80 

μg/m3

), reflecting the influence of the proximity of people to PM sources during normal daytime 

activities in determining personal exposure concentrations. 

Studies conducted since the PTEAM study in other locations and seasons have measured 

average personal PM10 concentrations from 11-68 μg/m3

, and average personal PM2.5 

concentrations ranging from 9-34 μg/m3

. Average indoor concentrations of PM10 have ranged 

from 13-52 μg/m3

, with indoor PM2.5 concentrations from 7-34 μg/m3. However, peak indoor 

levels have been high. For example, in a seven city study, Wallace et al. (2003) found that in all 

cities, at least 2% of all 1-hour measurements exceeded 1000 μg/m3

. Long et al. (2000) 

measured indoor PM concentrations as high as 473 μg/m3

 in study homes. These elevated 

levels signify the presence of significant indoor source emissions. 

Several studies have been conducted to examine the exposure of sensitive populations to PM. 

These have reported PM10 and PM2.5 exposures for subsets of individuals with chronic 

obstructive pulmonary disease (COPD), coronary heart disease, and asthma (Liu et al., 2003; 

Williams et al., 2000a,c; Rojas-Bracho et al., 2000; Linn et al., 1999). Results from these studies 

varied based on seasonal differences, activity levels of the subjects, and other factors, but in 

most cases personal exposure was more closely associated with indoor concentrations, and 

personal exposures often exceeded both indoor and outdoor PM concentrations. Liu et al. 
Indoor Air Pollution in California July, 2005 

 55

Table 2.5. Summary of Recent Indoor PM Exposure Studies (means)1

 PM 2.5 means - μg/m3

LOCATION GROUP YEAR SEASON PERSONAL (n) INDOOR (n) OUTDOOR (n) REFERENCE 

Los Angeles, CA COPD Subjects 2001-2002 multiple 17.7 ± 11.9 91 17.6 ± 11.4 106 28.8 ± 20.4 103 Suh 2004 

Raleigh, NC African Americans 2000-2001 multiple 23.0 ± 16.1 712 19.3 ± 8.4 761 19.3 ± 8.4 761 Williams 2003 

COPD Subjects 10.5 ± 7.2 307 8.5 ± 5.1 443 9.2 ± 5.1 437

Healthy Subjects 9.3 ± 8.4 183 7.4 ± 4.8 193 9.0 ± 4.6 194

Asthmatics 13.3 ± 8.2 263 9.2 ± 6.0 276 11.3 ± 6.4 272 Seattle, WA 

Coronary Heart Dis 

2000-2001 multiple 

10.8 ± 8.4 325 9.5 ± 6.8 329 12.6 ± 7.9 323

Liu 2003 

 12.31 NR 9.01 NR Boston, MA Asthmatic Children 2000 multiple 33.82 NR 13.12 NR Brugge 2003 

2000 winter 19.6 ± 14.5 87 16.9 ± 11.7 92 13.5 ± 8.5 92 Los Angeles, CA COPD Subjects 1999 summer-fall 25.1 ± 20.8 92 18.1 ± 11.1 97 19.3 ± 9.0 96 Suh 2003 

Detroit, MI Asthmatic Children 1999-2000 multiple 34.4 ± 21.7 362 15.6 ± 8.2 NR Keeler 2002 

winter 13.3 24 9.7 24 20.5 28 Fresno, CA Retirement Facility 1999 spring 11.1 12 8.0 24 10.1 28 Evans 2000 

1999 winter 19 5.6 Baltimore, MD Elderly 1997 summer 27 25 Sarnat 2000 

1998 summer 13.0 ± 4.2 23 10.0 ± 4.7 16 22.0 ± 12.0 28 Williams 2000c Baltimore, MD Retirement Facility 1997 winter 34.4 [PM1.5] NR 17.4 NR 17.0 [PM1.5] NR Williams 2000a

1998 multiple 11.9 ± 9.6 211 11.1 ± 6.8 210 Long 2000 Boston, MA Residential Homes 1996 multiple 13.9 ± 15.2 63 11.7 ± 6.5 64 Abt 2000 

summer 18.6 ± 6.4 30 16.1 ± 9.6 30 26.5 ± 9.5 30 Birmingham, AL Residential Homes 1997-1998 winter 10.0 ± 3.3 30 11.2 ± 5.4 30 12.2 ± 5.1 30 

Lachenmyer 

2000 

Residential Homes winter 21.6 ± 15.2 93 17.2 ± 13.0 93 10.9 ± 9.2 94 

Boston, MA (people with 

COPD) 

1996-1997 summer 21.5 ± 11.9 131 17.7 ± 14.9 138 16.4 ± 13.0 138

Rojas-Bracho 

2000 

Los Angeles Elderly w/ COPD 1996-1997 winter 24 25 25 Linn 1999 

7 U.S. Cities Asthmatic Children NR NR 27.7 ± 35.9 448

0 13.6 ± 7.5 4031 Wallace 2003a

United States Office Buildings 1994-1998 summer-winter 7.2 453 14.7 453 Burton 2000 

 

 PM 10 means - μg/m3

LOCATION GROUP YEAR SEASON PERSONAL (n) INDOOR (n) OUTDOOR (n) REFERENCE 

Raleigh, NC African Americans 2000-2001 multiple 27.7 ± 19.6 761 30.4 ± 14.1 761 Williams 2003b

COPD Subjects 14.1 ± 6.6 437 14.3 ± 6.8 435

Healthy Subjects 12.6 ± 7.8 206 14.5 ± 7.0 200

Asthmatics 19.4 ± 11.1 274 16.4 ± 7.4 269 Seattle, WA 

Coronary Heart Dis 

2000-2001 multiple 

 16.2 ± 11.3 324 18.0 ± 9.0 324

Liu 2003 

2000 winter 35.0 ± 22.0 89 30.6 ± 21.2 95 36.1 ± 13.2 94 Los Angeles, CA COPD Subjects 1999 summer-fall 29.1 ± 12.8 19 29.0 ± 14.7 21 15.2 ± 8.6 21 Suh 2003 

Detroit, MI Asthmatic Children 1999-2000 multiple 68.4 ± 39.2 252 52.2 ± 30.6 363 25.8 ± 11.8 NR Keeler 2002 

winter 15.1 24 28.2 28 Fresno, CA Retirement Facility 1999 spring 37.3 12 16.7 24 28.7 28 Evans 2000 

1999 winter 28 7.5 Baltimore, MD Elderly 1997 summer 34 34 Sarnat 2000 

Baltimore, MD Retirement Facility 1998 summer 13.5 ± 5.9 15 30.0 ± 13.7 28 Williams 2000c

1998 multiple 19.4 ± 12.7 212 12.7 ± 7.5 107 Long 2000 Boston, MA Residential Homes 1996 multiple 19.6 ± 16.1 64 17.1 ± 9.1 64 Abt 2000 

Residential Homes winter 40.7 ± 26.8 93 37.3 ± 23.2 93 18.5 ± 15.9 95 

Boston, MA (people with 

COPD) 

1996-1997 summer 34.7 ± 17.5 132 28.3 ± 25.4 138 24.8 ± 21.9 137

Rojas-Bracho 

2000 

Los Angeles Elderly w/ COPD 1996-1997 winter 35 33 40 Linn 1999 

Riverside, CA Residential Homes 1996 fall 150 NR 95 NR 95 NR Ozkaynak 1996

United States Office Buildings 1994-1998 summer-winter 11.4 588 23.1 588 Burton 2000 

1 Most of these studies involved locations with little or no indoor smoking allowed. Where smoking occurs 

indoors, it makes a notable contribution to the particle concentrations. 
Indoor Air Pollution in California July, 2005 

 56

(2003) found that mean personal PM2.5 concentrations were higher than indoor and outdoor 

concentrations for each of these three sensitive groups (as well as for healthy subjects) in 

Seattle, Washington, and that PM10 indoor concentrations were higher than outdoor 

concentrations for asthmatics. Williams et al. (2000a,c) also found personal PM2.5 

concentrations higher than indoor and outdoor concentrations in a Baltimore retirement facility in 

the winter of 1997. Rojas-Bracho et al. (2000) found that mean personal PM10 and PM2.5 

concentrations were above indoor and outdoor PM10 and PM2.5 concentrations for 18 COPD 

patients in Boston. 

Linn et al. (1999) monitored 15 COPD patients for PM2.5 exposures and 15 patients for PM10 

exposures in Los Angeles during the fall and winter. Unlike other studies, this study found 

personal concentrations similar to both those indoors or outdoors. The authors suggest that the 

lack of increased personal PM in these subjects having severe COPD may be due to reduced 

personal activity, less time spent outside of the home, and other reasons. The pooled 

correlation of personal PM concentrations to ambient concentrations at a monitoring station 

were quite low. 

A recently completed study by Suh (2003) has increased our understanding of Californians’ 

exposures to PM in a sensitive subpopulation. The investigators examined the relationships 

among outdoor and indoor concentrations and personal exposures across different seasons. 

They examined daily PM exposures of a group of 15 individuals with COPD in Los Angeles over 

seven sequential days in the summer-fall and/or winter. Personal, indoor, and outdoor PM2.5, 

NO3

-

 and elemental carbon (EC) concentrations varied by season, with the exception of outdoor 

NO3

-

. For winter and summer-fall PM levels, respectively, the personal PM2.5 means (19.6, 25.1 

μg/m3

) and maxima (63.5, 137.8 μg/m3) were higher than the indoor means (16.9, 18.1 μg/m3) 

and maxima (49.5, 94.8 μg/m3

) and outdoor means (13.5, 19.3) and maxima (56.5, 53.5 μg/m3). 

For NO3

-

 and EC, higher outdoor (2.8-3.1 μg/m3), as compared to indoor (1.1-1.7 μg/m3) and 

personal (1.2-1.6 μg/m3

) levels, were found in both seasons, reflecting the fact that motor 

vehicles are their major source. In addition, the loss of NO3

-

 may occur indoors due to its 

dissociation of particulate nitrate back to gaseous form under conditions of increasing 

temperature and decreasing humidity. NO3

-

 and EC comprised a small fraction of personal, 

indoor, and outdoor PM2.5 (max. 28.5% and 17%, respectively). The indoor PM levels were low 

compared to those measured in studies of the general population, consistent with the subjects’ 

limited personal activity and very little time spent near smoking, cooking, vehicles, or other 

major PM sources. Personal PM was highly correlated with indoor PM, and indoor and outdoor 

PM correlations were significant as well. Statistical modeling results indicated that significant 

predictors of higher personal PM were time near ETS, location near a major road, higher 

population density, cooking activity, and location in an inland area (vs. coastal). 

A companion study to the above study by Suh and Koutrakis (2004) used a similar design for 16 

healthy persons in Los Angeles during the summer and/or winter. The study also involved more 

detailed characterizations of the PM levels and ventilation characteristics of the subject’s homes 

than the COPD study. Both personal and indoor PM2.5 averaged approximately 18 μg/m3

(range 2 - 68 μg/m3

). Outdoor PM2.5 levels were generally much higher (mean 29 μg/m3, range 

5 - 103 μg/m3

) than corresponding indoor and outdoor concentrations in both seasons. Outdoor 

nitrate levels averaged 11 μg/m3

 (range 0.3 - 55 μg/m3), and were also higher than indoor and 

personal levels. In contrast, outdoor EC levels were similar to corresponding indoor and 

personal levels, averaging 2 μg/m3

 (range 0 - 7 μg/m3). Personal exposures to these three 

particulate measures were more strongly associated with indoor concentrations as compared to 

outdoor concentrations, which may be attributed to the fact that the subjects spent a majority of 
Indoor Air Pollution in California July, 2005 

 57

their time indoors at home. The investigators found that indoor PM2.5 was the largest 

contributor to personal PM2.5 levels, accounting for 65-100% of daily personal PM2.5, on 

average. Significant individual and diurnal variations in all PM measurements, air exchange 

rates, and PM-generating activities such as cooking and cleaning were also observed. 

Far fewer studies have been conducted in public buildings than in residences. Indoor PM 

concentrations in public and commercial buildings appear to often be lower than ambient 

concentrations. Lower indoor PM concentrations in public and commercial buildings are due to 

the use of particle filters in mechanical ventilation systems, un-openable windows, and the lack 

of many indoor sources typically present in residences. As part of the U.S. EPA’s Building 

Assessment Survey and Evaluation (BASE) study, Burton (2000) reported PM concentrations 

from 100 randomly selected office buildings throughout the United States. Mean indoor PM2.5 

and PM10 concentrations were 7.2 μg/m3

 and 11.4 μg/m3, respectively, while outdoor levels 

were higher, at 14.7 μg/m3 and 23.1 μg/m3

, respectively. However, as with residences, the 

presence of indoor sources in public and commercial buildings can produce indoor 

concentrations that exceed concurrent ambient concentrations, especially if smoking is allowed 

in the building. For example, in a study of 38 commercial buildings in the Pacific Northwest, Turk 

et al. (1987) found that buildings where smoking was permitted had average indoor PM levels 

3.5 times higher than concurrent outdoor levels and indoor levels in buildings where smoking 

was prohibited. Sheldon et al. (1988) measured indoor PM in six buildings in the eastern U.S., 

and found indoor PM concentrations generally lower than outdoors where there was no 

smoking, but much higher indoor concentrations where smoking was allowed. 

Lillquist et al. (1998) reported indoor and outdoor PM10 measurements in three Utah hospitals 

over one winter season. Significant variability in indoor PM levels was found both among room 

types and among hospitals, and the relationship between indoor PM10 levels and outdoor levels 

was highly variable. The ICUs had significantly lower PM10 levels than other types of rooms, 

after adjusting for hospital differences. Thus, the most critically ill individuals may experience 

some protection in hospitals from ambient PM; however, in general, hospitals do not offer 

protection from ambient PM. 

2.2.4 Carbon Monoxide 

Carbon monoxide (CO) is a colorless, odorless, tasteless gas. It is a product of incomplete 

combustion, emitted from sources such as vehicles (in exhaust), gas and propane appliances, 

woodstoves, kerosene heaters, and cigarettes. CO can trigger acute health effects, even death, 

at very high levels, or flu-like symptoms and other effects at lower levels over longer periods of 

time. 

CO is regulated in the ambient environment, but not indoors. However, transient elevated 

concentrations in outdoor places such as tunnels and parking garages are not widely regulated. 

The state of California has an 8-hour average ambient air quality standard of 9.0 ppm (10 

mg/m3

) and a one-hour standard of 20 ppm (23 mg/m3). These are also ARB’s recommended 

indoor guideline levels for CO. In one large California study, about 5% of homes were found to 

have CO levels that exceeded the State 8-hour ambient air quality standard for CO (Wilson et 

al., 1993). 

2.2.4.1 Death 

The acute health effects of CO exposure have been well documented in multiple studies since 

the 1970s. Acute CO poisoning results from a lack of oxygen in the bloodstream due to 
Indoor Air Pollution in California July, 2005 

 58

formation of a CO-hemoglobin complex (carboxyhemoglobin) that prevents oxygen from binding 

to hemoglobin. Symptoms of acute poisoning include headache, nausea, lethargy and inability 

to concentrate, unconsciousness, and death at very high concentrations. An estimated 600 

deaths per year in the United States throughout the 1990s were attributable to unintentional CO 

poisoning (cited in Raub et al., 2000). 

A California study of ten 

years of death certificates 

showed that about 30 - 40 

deaths occur in California 

each year, on average, due 

to unintentional carbon 

monoxide (CO) poisoning 

(Girman et al., 1998; Liu et 

al., 1993a, 2000). About 

two-thirds of those deaths 

were attributable to indoor 

sources. As shown in 

Figure 2.2, the indoor 

sources most implicated in 

the CO poisonings were 

combustion appliances 

(usually malfunctioning or 

poorly tuned) and charcoal 

grills and hibachis used 

indoors. Together these accounted for over 50% of the deaths. The types of cooking and 

heating appliances included in the indoor combustion appliance category were wall heaters 

(37%), free-standing heaters (19%), stoves (16%), water heaters (9%), furnaces (9%), and floor 

heaters (7%). Natural gas was associated with 75% of the deaths, propane with 24%, and 

kerosene with less than 1%. Motor vehicles, such as those left running in an attached garage, 

also took a substantial toll. 

2.2.4.2 Non-lethal Health Effects 

In an examination of 1991-1994 California CO deaths and hospitalization discharge data, 

Waldman and Liu (1996) found that about 3 to 7 times as many hospitalizations for non-fatal CO 

poisoning occurred as did deaths from CO poisoning. This totals about 100-300 documented 

hospitalizations for an average year. However, uncertainties in the patient discharge database 

and the omission from the database of emergency room discharges that did not result in 

hospitalization led the investigator to conclude that the actual number of hospitalizations 

attributable to CO poisoning was at least several times higher. From the pertinent literature, 

ARB staff and Waldman estimate that five to twenty times (175-700) as many individuals as die 

from accidental CO poisoning are treated in emergency rooms or hospitalized each year due to 

serious, non-fatal CO poisonings, and that hundreds to thousands more suffer from 

undiagnosed heart problems, headache, flu-like symptoms, and other illnesses attributable to 

CO exposure (Cook et al., 1995; Mah, 2000; Kirkpatrick, 1987; CDC, 1982; Waldman, 1996). 

Figure 2.3 illustrates the likely magnitude of these non-lethal effects on the population. 

40

31

13

5

5

4

2

Indoor Combustion Appliance

Vehicle

Charcoal Grill (Used Indoors)

Fire

Small Engine

Unknown

Camping Equipment

Percent 

Figure 2.2: Causes of CO Deaths in California 
Indoor Air Pollution in California July, 2005 

 59

 30-40 

 Avoidable 

 Deaths

 175-700 

 Avoidable ER Visits 

and Hospitalizations

Hundreds to Thousands 

 of Avoidable Illnesses 

Recent studies have further documented chronic health effects following acute exposures and 

those due to prolonged exposures to CO. These chronic effects include lethargy, headaches, 

concentration problems, amnesia, dementia, psychosis, Parkinsonism, memory impairment, 

Figure 2.3: Annual California CO Cases 

personality alterations, signs of parietal dysfunction, and other minor symptoms (Townsend and 

Maynard, 2002; Mathieu-Nolf, 2002). In a study of cardiovascular hospital admission data in Los 

Angeles between 1992 and 1995, Linn et al. (2000) found that CO showed the most consistently 

significant relationship among the pollutants considered, and concluded that a wintertime 

increase in CO of 1.1 to 2.2 ppm predicted an increase of 4% in cardiovascular admissions (~20 

extra admissions per day). The elderly are especially susceptible to chronic effects of CO. 

Children are especially susceptible to harm from CO. Because they inhale more air per unit of 

body weight than do adults at similar activity levels, children will inhale a higher dose 

proportionately than adults, and will experience symptoms more quickly than adults. The unborn 

appear to be susceptible to adverse effects after exposure to CO as well. In a study of the 

relationship between ambient air pollution and low birth weight in the northeastern U.S., 

Maisonet et al. (2001) observed increased odds of low birth weight for every 1 ppm increase in 

CO during the third trimester for the entire population, and a similar increased risk in the AfricanAmerican population across all three trimesters. In an unrelated study, Ritz et al. (2000) 

estimated that the risk of pre-term birth increases by 12% per 3 ppm increase in CO averaged 

over six weeks before birth, and by 4% averaged over the first month of pregnancy. Ritz et al.

(2000) also found an increased risk of heart defects with increased ambient CO exposure during 

the second trimester of pregnancy. However, attributing the effects strictly to CO is difficult due 

to the presence of other correlated pollutants. Because these effects were seen with small 

increases in CO, the presence of indoor sources of CO in homes with pregnant women is a 

serious concern. 
Indoor Air Pollution in California July, 2005 

 60

2.2.4.3 Carbon Monoxide Emissions and Concentrations 

Most homes have relatively low CO levels, except for short intermittent elevations during use of 

an indoor source. Indoor CO concentrations can increase rapidly when a highly emitting source 

is present in an enclosed environment. For example, Jetter et al. (2002) measured CO emission 

rates from incense burning from 159-531 mg/hr, resulting in an estimated peak CO 

concentration of 9.6 mg/m3

 in a modeled typical room in a home. This is just at the California 8-

hour standard level of 9 ppm (10 mg/m3

); in combination with outdoor CO and any additional 

indoor sources, this home would have exceeded the standard. Pelham et al. (2002) reviewed 

CO levels in indoor ice arenas, stressing that U.S. and global CO exposure problems remain in 

these locations (only three U.S. states regulate CO levels in ice arenas). 

In a study of 277 Californian homes in 1992, Wilson et al. (1993) measured indoor and outdoor 

CO levels. Thirteen homes had indoor 8-hour CO concentrations above the California 8-hour 

outdoor standard and indoor air quality guideline of 9 ppm. Several homes had indoor CO 1-

hour values greater than the state standard of 20 ppm; in one case this was attributed to the 

(dangerous) use of gas burners for residential heating. In a second California study (focused on 

PAHs) of 280 homes in northern California, only two homes exceeded California CO standard 

levels, one due to use of a fireplace and the other from gas heat (Sheldon et al., 1993). 

However, in many homes, short-term excursions up to 42 ppm were observed, such as when a 

gas space heater was turned on. 

CO levels in well-maintained indoor environments where appliances are largely absent or are 

operated properly tend to be relatively low. In surveys of 136 ‘non-problem’ commercial 

buildings in New York City between 1997 and 1999, Springston et al. (2002) measured indoor 

CO concentrations ranging from 0.2 to 10.3 ppm; only 0.04% of all readings exceeded 10 ppm. 

A limited number of studies have shown that infiltration of vehicle exhaust emissions into 

residences can increase the indoor concentration of CO within those residences. Wilson et al.

(1993) found that the presence of an attached garage was a significant factor related to 

elevated indoor concentrations of CO versus outdoor concentrations. Gamage et al. (1994) 

found that the CO concentration in the bedroom located above a garage increased from less 

than 1 ppm to 17 ppm after a garaged vehicle’s engine was operated for a period of 3 minutes. 

In a detailed Canadian study, Graham et al. (2004) measured the concentration of CO inside 16 

residences over two seasons while a vehicle in the attached garage was operated under brief 

cold-start and hot-soak conditions. Significant net changes in indoor CO concentrations were 

observed to be associated with the vehicle cold start, but not the hot soak running condition. 

The infiltration of vehicle emissions is discussed further at the end of Section 2.3.2.3 of this 

report. 

2.2.5 Nitrogen Dioxide and Associated Acids 

Nitrogen dioxide (NO2) is a red to dark brown gas with a pungent acrid odor. It is emitted from 

combustion sources such as natural gas and propane-fueled appliances, wood burning stoves 

and fireplaces, kerosene heaters, charcoal grills and motor vehicles. Adverse health effects 

attributable to NO2 include exacerbation of asthma (especially in children), respiratory 

symptoms and infection, lung damage, and lung disease after long periods of exposure. Several 

nitrogen compounds related to NO2 are found in indoor environments; these include nitrous acid 

(HONO) and nitric oxide (NO). NO2 is the only nitrogen oxide regulated as a pollutant in outdoor 

air. California has a one-hour ambient air quality standard for NO2 of 0.25 ppm, not to be 

exceeded; this also serves as an indoor air quality guideline. The national ambient air quality 
Indoor Air Pollution in California July, 2005 

 61

standard is an annual mean of 100 μg/m3

 (0.053 ppm). Based on reports that 20-30% of the 

population use their gas stove (despite clear warnings against this) for space heating (Phillips et 

al., 1990), indoor NO2 is estimated to exceed the State ambient air quality standard at times in 

10-30% of California homes. 

2.2.5.1 Health Effects of Nitrogen Dioxide 

A number of studies have shown that nitrogen dioxide (NO2) exposure can result in detrimental 

effects in the lung. Investigators using human clinical studies have recently reported on NO2 and 

its effects on airway antioxidant status, inflammatory cell and mediator responses, and lung 

function (Becker and Soukup, 1999; Barck et al., 2002; Blomberg et al., 1999; Devlin et al., 

1999). Data from Devlin et al. (1999), for example, demonstrate that 2 ppm NO2 can induce a 

mild inflammatory response in the airways of healthy adults, and that NO2 may cause a mild 

impairment of lung antibacterial capacity. This study suggests that possible increases in viral 

clinical symptoms associated with NO2 may result from effects of the NO2 on host defenses that 

normally prevent the spread of virus. Data from European studies indicate that NO2 is a proinflammatory air pollutant under conditions of repeated exposure at a relatively high 

concentration of 2 ppm, 4 hours per day, for 4 days (Blomberg et al., 1999). However, brief 

exposures (less than 1 hour) to ambient concentrations of NO2 can enhance allergic 

inflammatory reaction in the airways of asthmatics (Barck et al., 2002). 

As discussed earlier, the NAS Institute of Medicine’s Committee on the Assessment of Asthma 

and Indoor Air determined that there is sufficient scientific evidence to conclude that high levels 

of indoor NO2 can exacerbate asthma (IOM, 2000). A recent epidemiology study conducted in 

Australia (Pilotto et al., 2003) supports this finding and concludes that asthma symptoms were 

reduced in primary school children after intervening to remove a high-NO2-production source at 

school 

Evidence suggests an association between exposure to NO2 and increased respiratory 

symptoms in children. Neas et al. (1991) studied the effect of indoor NO2 on respiratory 

symptoms in 1,567 children aged 7-11 in six U.S. cities from 1983 to 1988. Analysis of 

symptoms obtained through a questionnaire indicate that a 15 ppb increase in annual (average) 

indoor NO2 was associated with an increased cumulative incidence of lower respiratory 

symptoms. Girls showed a stronger association (OR = 1.7) than did boys (OR = 1.2). There was 

not an association between pulmonary function and NO2 levels. 

Chauhan et al. (2003) examined the relationships between NO2 exposure and asthma severity 

in 8-11 year old children during a respiratory viral infection. Investigators concluded that 

exposure to 7-day average NO2 levels of about 11 ppb before the start of a respiratory viral 

infection is associated with an increase in the severity of virus-induced asthma exacerbations. 

California investigators also have reported health effects of NO2 exposure on children. Peters et 

al. (1999a) studied school children to assess respiratory effects due to long-term exposure to 

four pollutants: ozone, particulate matter, acids, and NO2. Peters found NO2 significantly 

associated with reduced lung function in female children within a cohort of 3,292 school children 

in twelve Southern California communities. Increases in bronchitis symptoms of children with 

pre-existing asthma also were associated with increases in ambient NO2 levels (McConnell et 

al., 2003). It is important to note in the McConnell et al. study the annual average concentration 

of NO2 was about 19 ppb, well below the national annual average standard of 53 ppb. Within a 

cohort of 846 asthmatic children residing in eight urban areas of the U.S., Mortimer et al. (2002) 

found a 48% increase in the likelihood of asthma symptoms associated with an increase in the 
Indoor Air Pollution in California July, 2005 

 62

6-day average NO2 levels. Within a panel of 138 children in central Los Angeles, Ostro et al.

(2001) found increased odds for shortness of breath and wheezing associated with a 50 ppb 

increase in the 1-hour maximum NO2 concentrations. 

Aggregate results from numerous individual studies dealing with exposure to NO2 and 

respiratory illness in children have been inconclusive. However, Hasselblad et al. (1992) 

conducted a meta-analysis on studies with inconsistent results to conclude that children 

exposed to a long-term increase of 30 μg/m3

 NO2 (approximately 16 ppb) have about a 20% 

increase in the odds for developing respiratory illness. 

Investigators have also identified a relationship between women (age 20-44) in England who 

use gas appliances and develop asthma-like symptoms (Jarvis et al., 1996). Women who 

primarily used gas cooking appliances (known to emit NO2) had an increased risk for asthma 

attacks, wheeze, and waking with shortness of breath. The women who used a gas stove also 

had reduced lung function and increased airway obstruction compared to women who did not 

use gas stoves. These associations were not observed in men, possibly because they did not 

experience the high concentrations of pollutants near the cooking source (according to the 

authors). 

2.2.5.2 Nitrogen Dioxide Sources, Emissions, and Concentrations 

Nitrogen dioxide is emitted during combustion; sources include motor vehicles, tobacco smoke, 

and combustion appliances such as gas kitchen stoves, gas, propane, and kerosene-fueled 

heaters, wood burning stoves, fireplaces, and charcoal grills. In the absence of indoor sources, 

indoor NO2 levels are influenced by outdoor levels due to the infiltration of outdoor air (Spengler 

et al., 1994b; Weschler and Shields, 1994; Levy et al., 1998). When indoor combustion sources 

such as wall furnaces, floor furnaces, gas stoves, and unvented gas logs (not permitted in 

California) are present, they have a large influence on indoor NO2 concentrations (Spengler et 

al., 1994b; Pitts et al., 1989; Wilson et al., 1986; Wilson et al., 1993). 

Nitrogen dioxide is the most prevalent of the nitrogen oxides and has been the focus of 

numerous emission and indoor concentration studies. In an ARB-funded cooking study, 

Fortmann et al. (2001) measured indoor NO2 during various cooking protocols. Measurement 

periods varied from approximately 1 to 5 hours, representing food preparation, cooking, and 

clean-up times. Nitrogen dioxide levels increased when a gas stove was used for cooking. For 

example, while making a fried chicken dinner, average indoor NO2 levels reached 400 ppb. 

Other cooking tasks such as broiling fish, baking lasagna, frying tortillas, and stir-frying 

produced average indoor NO2 levels ranging from 30 to 170 ppb. During a cycle of automatic 

oven cleaning with a gas stove, average indoor NO2 levels exceeded 400 ppb. NO2

concentrations remained below 45 ppb during the cooking protocols performed with an electric 

stove and range. 

Indoor NO2 levels can reach unhealthy indoor levels in some situations. In the California 

Residential Indoor Air Quality Study, indoor NO2 levels were measured up to 177 ppb as 48-

hour averages (Wilson et al., 1993). At this level, it is very likely that the 250 ppb California onehour standard was exceeded for at least some portion of the time. Dennekamp et al. (2001) 

measured 5-minute peaks up to 1000 ppb NO2 when cooking with a 4-burner gas stove 

(measured at face level in front of the cook). In a Boston study, Brugge et al. (2003) found 

indoor NO2 levels were either close to or exceeded the NAAQS annual level of 53 ppb. 
Indoor Air Pollution in California July, 2005 

 63

When investigators collect samples over several days, reported concentrations are lower than 

peak concentrations measured during a distinct exposure event. For example, Lee et al. (2002) 

measured indoor NO2 and HONO levels in 119 residences in southern California over a 6-day 

sampling period. The average indoor and outdoor concentrations of NO2 were 28 and 20.1 ppb, 

respectively. Zipprich et al. (2002) collected 48-hour passive NO2 samples in Richmond, 

Virginia, in a study in which 98% of the homes had gas stoves. Mean concentrations in the 

bedrooms, living rooms, and outdoors were 18, 19, and 15 ppb, respectively. 

Spengler et al. (1994b) measured personal exposures, as well as indoor and outdoor levels of 

NO2, for about 700 individuals in the Los Angeles basin. Passive samples were collected over 

24- or 48-hour periods. The median personal and outdoor levels were 35 ppb while the median 

indoor level was 24 ppb. However, the contribution of gas appliances and gas pilot lights to total 

exposure was evident. “Personal exposures for those in homes with gas ranges with pilot lights 

average 10 ppb greater than those with electric ranges, and 4 ppb greater than those with gas 

ranges without pilot lights” (Spengler et al., 1994b). 

Levy et al. (1998) identified the use of a gas stove in a home as the most significant contributor 

to personal NO2 exposure. Their study, conducted in 15 countries found that mean personal (2-

day average) NO2 exposure was 34.8 ppb in homes with a gas stove that was used during the 

sampling period, compared to 20.5 ppb in homes without gas stove use. 

Several oxidized nitrogen compounds in addition to NO2 are emitted during combustion by gas 

appliances and/or are formed through chemical reactions. The most notable additional species, 

are nitric oxide (NO), nitrous acid (HONO), and nitric acid (HNO3) (Spicer et al., 1993). Pitts et 

al., (1985) reported direct observation of the formation of gaseous HONO from the reaction of 

NO2 (at ppm levels) with water vapor in indoor environments. Based on removal reactions, 

indoor NO2 has a lifetime of about one hour, while the lifetime for NO and HONO is several 

hours (Spicer et al., 1993). HONO can be retained on indoor surfaces for extended periods, 

then be released causing elevated concentrations after a combustion appliance is no longer in 

use (Spicer et al., 1993; Febo and Perrino, 1991). HONO concentrations in homes with gas 

appliances are typically greater indoors than outdoors and range from 10-20 ppb (Febo and 

Perrino, 1991; Spengler et al., 1993). HONO is present in indoor air as an acidic aerosol and is 

likely to be a respiratory irritant, though its respiratory toxicity has not been thoroughly 

investigated. Other important nitrogenous species include the nitrate radical (NO3), which would 

be formed indoors whenever NO2 and ozone are found together (Weschler, 2004). 

2.2.6 Ozone 

Ozone (O3), the primary component of smog, is an invisible, yet highly corrosive, odorous, and 

chemically reactive gas. Ozone is chemically unstable, and so it breaks down or reacts with 

many surfaces, liquids, and chemicals. Ozone is typically higher outdoors than indoors. It 

becomes elevated indoors most commonly from the infiltration of outdoor ozone through doors, 

windows, and swamp coolers, and sometimes from direct emissions indoors by devices such as 

certain types of copy machines, laser printers, and “air purifiers”. 

2.2.6.1 Health Effects of Ozone 

Ozone is an oxidizing pollutant and strong irritant that attacks the respiratory system, leading to 

the damage of lung tissue. Exposure to ozone damages the alveoli, the individual air sacs in the 

lung where the exchange of oxygen and carbon dioxide between the air and blood takes place 

(ARB/OEHHA, 2004). Increased occurrence of respiratory symptoms, such as cough, pain on 
Indoor Air Pollution in California July, 2005 

 64

deep breath, and difficulty taking a deep breath are associated with exposure to ozone 

(Schelegle and Adams, 1986; McDonnell et al., 1999; Kulle et al., 1985; Folinsbee et al., 

1977a,b; Seal et al., 1993). Ozone also induces cellular and biochemical changes indicative of 

lung inflammation (Devlin et al., 1991, 1996; Balmes et al., 1996; Aris et al., 1993). A major 

result from the Children’s Health Study indicates that children living in high ozone communities 

who actively participate in several sports are three times more likely to develop asthma than 

children in these communities not participating in sports or those that live in low ozone 

communities (Gauderman et al., 2000).

Epidemiological studies have found statistically significant associations between outdoor O3

concentrations and various adverse health impacts, including increased asthma symptoms 

(Whittemore and Korn, 1980; Thurston et al., 1997; Delfino et al., 1996; Mortimer et al., 2002), 

increased respiratory symptoms (e.g., Brunekreef et al., 1994), and reduced lung function 

(Brunekreef et al., 1994; Brauer et al., 1996). Some studies also report statistically significant 

associations between O3 and hospital admissions or emergency room visits, primarily for 

asthma or other respiratory causes including COPD and bronchitis (Sheppard et al., 1999; 

Schwartz, 1995; Delfino et al., 1997, 1998; Burnett et al., 1997; Anderson et al., 1997). Ozone 

has also been linked to increased school absenteeism for respiratory illnesses (Gilliland et al., 

2001), and reduced lung function growth in children (Frischer et al., 1999). 

California has an ambient air quality standard for O3 of 0.09 ppm for one hour, while the federal 

standard is 0.08 ppm averaged over eight hours. Both standards are currently under review, 

and California has proposed an 8-hour standard of 0.070 ppm (ARB/OEHHA 2005). 

2.2.6.2 Indoor Sources and Concentrations of Ozone 

Outdoor air is the most common source of indoor ozone (Weschler, 2000). Outdoor ozone (a 

component of smog; formed by the photochemical reaction of volatile organic compounds and 

nitrogen oxides emitted primarily by motor vehicles and industries) enters homes through doors, 

windows, and numerous air leaks in buildings and their ventilation systems. Studies have shown 

that indoor ozone levels generally follow the diurnal and seasonal patterns of outdoor ozone, 

with higher levels in the daytime and summer months (Liu et al., 1993b; Weschler et al., 1994; 

Liu et al., 1995; Avol et al., 1998; Geyh et al., 2000; Lee et al., 2002). Like outdoor 

concentrations, indoor ozone levels can also remain elevated for long periods of time (eight 

hours or more), and display peak variations throughout the day (Weschler et al., 1989). Indoor 

ozone levels typically range from 20 to 80% of outdoor ozone levels (Weschler, 2000). Using a 

swamp cooler or whole-house fan on a high-ozone day can increase air exchange rates enough 

to produce indoor ozone levels very close to outdoor levels for hours at a time (Avol et al., 

1996). 

The most common indoor sources of O3 are poorly maintained laser printers and photocopiers, 

and O3 generating-devices that are marketed as various types of room deodorizers and air 

cleaners. In particular, ozone generators that are marketed as “air purifiers” have been found to 

produce hazardous levels of indoor ozone. Several studies have shown that ozone at levels 

produced by ozone generators does not effectively control indoor air pollution, odors, or mold 

growth on surfaces (Boeniger, 1995; Kissel, 1993; Foarde et al., 1997). Ozone generators can 

destroy microorganisms and gases, but only at concentrations unsafe for occupied spaces. In 

addition, ozone can react with indoor surfaces–such as carpets and painted surfaces–or 

airborne chemicals, including the fragrance compounds from commercial air fresheners, to 

produce toxic and irritating byproducts such as formaldehyde (Morrison and Nazaroff, 2002; 

Kleno et al., 2001; Wainman et al., 2000; Weschler, 2000; Weschler and Shields, 1999; Moriske 
Indoor Air Pollution in California July, 2005 

 65

et al., 1998; Reiss et al., 1995ab; Weschler et al., 1992). Most importantly, these devices can 

result in levels of ozone well above health-based standards and guideline levels. For example, a 

“personal air purifier” tested for its emissions when used according to manufacturer’s directions 

resulted in ozone levels in the users breathing zone that exceeded various standard levels, 

including the California ambient air quality standard (Phillips et al., 1999). 

Other sources of indoor ozone include other types of electronic air cleaners and office 

equipment that uses electrostatic processes. Negative ion generators and electrostatic 

precipitators (ESP) and dry-process copiers, laser printers, and fax machines can generate 

significant levels of indoor ozone as a by-product (U.S. EPA, 1995; Kissel, 1993; Selway et al., 

1980; Allen et al., 1978). 

2.3 TOXIC AIR CONTAMINANTS AND OTHER INDOOR AIR POLLUTANTS 

There are a number of other important indoor pollutants that are somewhat unique in their 

exposure parameters or health effects. Toxic air contaminants (TACs) are air pollutants “which 

may cause or contribute to an increase in mortality or an increase in serious illness, or which 

may pose a present or potential hazard to human health” (HSC Section 39655). Once a 

compound is identified as a toxic air contaminant, ARB determines the need and appropriate 

degree of regulation for the compound. Regulations have been implemented to control the 

release of numerous TACs into outdoor air; however, regulations do not presently exist to 

control their release into indoor air. Foremost among these pollutants are formaldehyde, 

chloroform, p-dichlorobenzene, benzene, radon, polycyclic aromatic hydrocarbons (PAHs), and 

environmental tobacco smoke (currently in the identification process). TACs were also identified 

by the federal government as Hazardous Air Pollutants (HAPs); many are carcinogenic. Semivolatile pollutants such as pesticides, phthalates, and polybrominated diphenyl ethers can be 

released indoors, or tracked indoors from outdoors. The health effects, indoor sources, and 

indoor air concentrations of these pollutants are discussed in this section. 

2.3.1 Formaldehyde 

Formaldehyde is a pungent smelling gas emitted from numerous indoor sources. These include 

many building materials (especially pressed wood products), some new carpet assemblies, 

composite wood furnishings, consumer products, permanent pressed clothing, and combustion 

sources. Formaldehyde is listed as a TAC and a Proposition 65 substance, based on its 

carcinogenicity. It is also an upper respiratory tract irritant that produces eye, nose, and throat 

irritation. Indoor formaldehyde concentrations nearly always exceed outdoor levels due to the 

many indoor sources. Indoor and urban ambient levels typically exceed the OEHHA Chronic 

Reference Exposure Level (REL) of 2.4 parts per billion (ppb), which is based on irritant effects 

on the mucous membranes of the upper airways and eyes, and levels sometimes exceed 

OEHHA’s 8-hour REL of 27 ppb designed to protect against the same effects. Nearly all indoor 

environments also exceed the one-in-a-million cancer risk level. 

2.3.1.1 Health Effects of Formaldehyde 

A number of adverse health effects in humans have been associated with formaldehyde 

exposure. Short-term effects include eye, nose, throat and skin irritation; nausea; headache; 

and there is limited evidence for exacerbation of asthma. Dermal allergic sensitization may 

occur following relatively high occupational exposure. People vary substantially in their 

sensitivity to formaldehyde. For most individuals, effects typically occur at exposure levels 

between 0.037 and 3 ppm (ARB, 1992; U.S. EPA, 1987b). Sensitive individuals may experience 
Indoor Air Pollution in California July, 2005 

 66

acute symptoms related to irritation at lower concentrations. OEHHA has set the acute REL, 

based on a one hour exposure, at 94 μg/m3

 (75 ppb) with eye irritation as the toxicological 

endpoint (OEHHA, 2000a). The OEHHA interim REL, based on an 8-hour exposure, is 27 ppb 

designed to protect against the same effects. 

The ARB identified formaldehyde as a TAC in 1992, based on its carcinogenic potential. In 

2004, the International Agency for Research on Cancer (IARC) classified formaldehyde as a 

human carcinogen due to sufficient evidence for development of nasopharyngeal cancer in 

humans. IARC also found limited evidence that formaldehyde may cause other respiratory tract 

cancers, and a possible link with leukemia. The California Proposition 65 No Significant Risk 

Level for formaldehyde is 40 μg/day (equivalent to 1.6 ppb, based on inhaling 20 m3

/day). This 

level represents the daily intake level calculated to result in a cancer risk of one excess case of 

cancer in 100,000 individuals exposed over a 70-year lifetime (OEHHA, 2004). 

2.3.1.2 Sources of Formaldehyde 

Many materials and products emit formaldehyde. However, emissions studies have shown that 

building materials, particularly composite wood products, are likely the greatest contributors to 

formaldehyde in indoor air. Kelly et al. (1999) reported the highest emission rates for numerous 

composite wood products manufactured with urea-formaldehyde resin. These products, 

commonly used in home construction, cabinetry, and furniture, displayed formaldehyde 

emission rates ranging from 8.6 to 1,580 μg/m2

/hr. Over half of the urea-formaldehyde products 

tested had emission rates between 100 and 200 μg/m2

/hr. A covering over the wood such as a 

paper laminate, melamine laminate, or vinyl coating substantially reduced the emission rates to 

levels at or below 55 μg/m2

/hr for all products tested. Composite wood products designed for 

outdoor use are made with phenol-formaldehyde resin. When tested, these products emitted 4.1 

to 9.2 μg/m2

/hr formaldehyde, a substantial reduction from the urea-formaldehyde resin 

products. Coated products and phenol-formaldehyde resin products are preferred alternatives to 

urea-resin products. 

After numerous lawsuits in the 1970s and 1980s, the composite wood industry developed 

voluntary emission standards for medium density fiberboard (MDF) and particleboard. A 

comparison of emission rates from Pickrell et al. (1983) and Kelly et al. (1999) showed that the 

emission rates from current composite wood products averaged 49% lower than the emissions 

in the early 1980s. Industry data provided to ARB by the Composite Panel Association indicate 

that emissions of particleboard have decreased by 80% in this time frame. In response to an 

ARB survey, members of the composite wood industry responding to the survey (53%) indicated 

100% of their particleboard meets the HUD large chamber test concentration of 0.3 ppm (this 

chamber concentration is not equivalent to the concentration that would be expected in a 

home). Of the products Kelly et al. (1999) tested, all of the bare MDF products and most of the 

particleboard samples were below the industry limits. 

Formaldehyde emissions are greatest when building materials are new, and it takes years to 

complete the off-gassing. Sexton et al. (1986) carefully designed a study to measure indoor 

formaldehyde levels relative to the age of manufactured homes. Investigators found statistically 

significant higher formaldehyde concentrations in newer homes than older homes. For example, 

data collected during the summer indicated the mean concentration for houses less than four 

years old were 80 ppb, compared to houses older than four years with a mean concentration of 

61 ppb. Data from winter sampling reveal mean concentrations of 90 ppb for newer homes and 

64 ppb for older homes. Data from the study were further analyzed by the age of the mobile 

home (Sexton et al., 1989). For homes manufactured from 1980 to pre-1966, the data follow the 
Indoor Air Pollution in California July, 2005 

 67

expected pattern, with indoor values gradually decreasing with increasing age. The highest 

average concentration was in homes manufactured in 1980. Although homes manufactured in 

1981 and 1982 had maximum values greater than those from 1980, the mean concentrations 

were less. The mean for homes manufactured in 1983 continued this downward trend. 

Investigators comment that the particle board industry began introducing products with lower 

formaldehyde emission rates at this time. It is likely that these changes are reflected in the lower 

formaldehyde levels observed in mobile homes built after 1980. 

Composite wood products still release high levels of formaldehyde to the indoor environment for 

long periods of time–from months to years. Brown (1999a), an investigator in Australia, 

measured formaldehyde emission rates from particleboard, medium density fiberboard, and 

office furniture over several months. Emission rates measured in the study declined from a 

value of 300-400 μg/m2

/hr for relatively new products to 80-140 μg/m2/hr for products 5 to 10 

months old. 

In a recent study funded by the California Integrated Waste Management Board (CIWMB) and 

conducted by DHS (Alevantis, 2003), investigators identified nine products in six categories that 

emitted formaldehyde at levels high enough to exceed the California Section 01350 guideline 

level (see Section 4.3.3.2 of this report). When modeling (for use in a state office) was 

conducted independently on emissions from acoustical ceiling panels, a carpet, medium density 

fiberboard, gypsum board, resilient flooring (non-rubber based), and thermal insulation, room 

concentrations were estimated to exceed 16.5 μg/m3

 (13.5 ppb), the upper bound allowed for 

formaldehyde contribution from a single product under Section 01350 guidelines. For thermal 

insulation, products exceeding the upper limit included a standard product and a product 

marketed as formaldehyde-free. Only one of the ten standard resilient flooring samples 

exceeded the limit, while six of the samples had undetectable levels of formaldehyde. The nine 

products with elevated emissions accounted for 11% of the samples tested in this study. 

Formaldehyde was detected in 34% of the total samples tested. 

Since the creation of the Section 01350 emission guideline for building materials, many 

manufacturers have met the requirement for a variety of products. A list of these compliant 

materials is available at http://www.chps.net/manual/lem_table.htm. 

Recent studies in other states provide additional information on source contributions of indoor 

formaldehyde. In a manufactured house produced in Florida, Hodgson et al. (2002) determined 

that the greatest contributors to indoor formaldehyde levels were a particleboard cabinet case 

and passage doors, each contributing about 33% of the total house formaldehyde 

concentration. The house, which was a furnished sales model, had an indoor formaldehyde 

concentration of 77 ppb. The combined emission rate for all wood products in the house was 

approximately 10 mg/hr. The other 33% of formaldehyde was contributed by cabinet stiles, 

countertops, subflooring, and other sources. The authors recommended several techniques for 

reducing indoor residential formaldehyde levels. 

• Use vinyl coated or alternative passage doors. 

• Use fully coated particleboard in cabinet cases. 

• Use frameless cabinets. 

• Apply a laminate backing to the underside of particleboard countertops. 

Floor finishing materials such as new carpet assembly components and vinyl flooring may also 

emit formaldehyde. In a study funded by the ARB, Hodgson (1999) measured the formaldehyde 
Indoor Air Pollution in California July, 2005 

 68

emissions of several flooring products. Results for formaldehyde emissions at 24 hours showed 

the following. 

• Formaldehyde chamber concentrations were generally below the limit of detection of 1 

μg/m3

 for carpet. 

• One carpet cushion had an emission rate of 8 μg/m2

/hr. 

• Seam tape applied to carpet had an emission rate of 5 μg/m2

/hr. 

• Emissions from five different sheet vinyl flooring samples were less than or equal to 4 

μg/m2

/hr. 

• Adhesives applied to sheet flooring and cove base had emission rates ranging from 72 to 

258 μg/m2

/hr. 

• When the vinyl flooring or coving was placed on top of the adhesive, the surface product 

served as a relatively effective barrier, causing a drop in emissions. 

Paint is another building material known to emit formaldehyde. Hodgson (1999) measured 

formaldehyde emissions from 10 different paints widely used in California. As with most wet 

products, concentrations peaked initially, then declined over several hours. At 96 hours, five 

paints had emission rates greater than 10 μg/m2

/hr. To address the desire for lower-emitting 

products, many paint manufacturers are formulating low-VOC paints. These paints have 

substantially lower total VOC emissions than traditional paint; however, they may emit 

formaldehyde. Two of the paints in the study were identified as “non-VOC”, however their 

formaldehyde emissions rates at 48 hours were 43 and 12 μg/m2

/hr. Chang et al. (1999) also 

evaluated emissions from low-VOC paints. In small chamber tests, two of four low-VOC paints 

emitted formaldehyde with peak concentrations at 3.15 mg/m3 and 5.53 mg/m3

. 

2.3.1.3 Indoor Formaldehyde Concentrations 

Indoor levels of formaldehyde can reach high levels in some indoor locations despite changes in 

the manufacture of pressed wood products and changes in the construction of manufactured 

housing. Current estimated average and maximum indoor formaldehyde concentrations are 

shown in Figure 2.4 for different California environments. Figure 2.4 illustrates that 

concentrations in some homes and schools exceed OEHHA’s interim 8-hour REL of 27 ppb, 

established to identify levels above which sensitive individuals could experience acute eye, 

nose, and lung irritation. The figure also shows the relative levels of formaldehyde in different 

environments, indicating that manufactured homes are of greatest concern, while conventional 

homes and classrooms are also of concern. 

Figure 2.4 also illustrates that levels in virtually all indoor environments exceed OEHHA’s 

chronic REL (2.4 ppb) for irritant effects and OEHHA’s one-in-a-million excess lifetime cancer 

risk level (0.13 ppb) for formaldehyde. It is generally not feasible to achieve levels below these 

guideline levels because outdoor levels average about 3-5 ppb. 

Data for Figure 2.4 have been compiled from several sources. Due to the lack of more recent 

field studies that measured indoor formaldehyde levels, adjustments have been made to the 

results from older studies. Manufactured home levels are from a large, older study of 

manufactured homes (Sexton et al., 1985), with levels adjusted downward based on the 

average reduction in emissions from manufactured wood products since 1983 (Kelly et al., 

1999). The conventional home data were obtained by combining results from a 1996 study of 

southern Californian homes (Avol et al., 1996) and the National Human Exposure Assessment 

Survey (NHEXAS) exposure study in Arizona (Gordon et al., 1999). The maximum values 
Indoor Air Pollution in California July, 2005 

 69

estimated for current California manufactured and conventional homes are similar, between 

220-240 ppb, although measured values have been obtained well above these levels in some 

studies. The classroom data are taken from the California Portable Classrooms Study 

(Whitmore et al., 2003), using both Phase I and Phase II data. Concentrations in office buildings 

are from the U.S. BASE study (U.S. EPA, 2003a; Girman et al., 1999) of about 100 medium and 

large office buildings throughout the U.S., including buildings from California. The sources and 

derivations of the averages and maxima shown in Figure 2.4 are discussed in Appendix III. 

New homes built with standard construction products are likely to have unhealthy levels of 

formaldehyde. Hodgson et al. (2000) measured formaldehyde concentrations inside homes two 

months old, then continued measurements for a seven and one-half month period. The 

geometric mean concentration of formaldehyde in four manufactured homes was 34 ppb, and in 

seven site-built homes was 36 ppb. Both were substantially greater than the outdoor 

formaldehyde level of 6 ppb, and above health-based guidelines. The formaldehyde emission 

rates were fairly consistent over the seven to eight month sampling time, indicating that the off 

gassing of formaldehyde emissions from building materials in new homes extends for a long 

period of time. The author commented that these levels are approximately 50% lower than 

formaldehyde concentrations measured during the 1980s due to use of less plywood paneling in 

manufactured homes and reduced emission rates from composite wood products relative to 20 

years ago. Emission rates were calculated for these homes and found to be 45 μg/m2

/hr for the 

manufactured homes and 31 μg/m2

/hr for the site-built homes. 

Older housing stock has greatly reduced formaldehyde off-gassing rates relative to new housing 

stock. As mentioned in Section 2.3.1.2, longitudinal formaldehyde concentration studies 

extending over years do not exist and emission rates are generally not derived for older houses. 

However, the body of data on home formaldehyde concentrations indicates newer homes have 

higher levels than older homes (Hodgson et al. 2000; Gordon et al., 1999). Therefore, new 

Figure 2.4: California Formaldehyde Levels 

(ppb)

0 50 100 150 200

ppb

Maximum

Average

Manufactured 

Homes

Classrooms 

(Inside)

Conventional 

Homes

Office Buildings

Outdoor 

Statewide 

Chronic REL

(2.4 ppb)

8-hour REL

(27 ppb)

Acute REL

(76 ppb)

>200

>200
Indoor Air Pollution in California July, 2005 

 70

homes, or homes with recent remodeling are of most concern relative to formaldehyde 

exposure. 

In the most recent large-scale study of formaldehyde levels in homes (NHEXAS), conducted in 

Arizona, 25% of the homes sampled had formaldehyde levels above the 8-hour REL of 27 ppb. 

This is of concern because people are typically in their homes for longer than 8 hours a day and 

the study was designed to be representative of the general population. The formaldehyde limit 

of detection was fairly high at 10 ppb, so that formaldehyde was detectable in only 69% of the 

indoor air samples (131/189) with a median concentration of 21 μg/m3

 (17 ppb). The 75th and 

90th percentiles in residences were 34 μg/m3

 (28 ppb) and 46 μg/m3 (37 ppb), respectively, with 

a maximum value at 408 μg/m3

 (332 ppb). These investigators also commented that mean 

values are lower than those reported in the 1980s (Gordon et al., 1999). 

Although not evident in Figure 2.4, the results from Phase II of the California Portable 

Classroom Study (PCS) indicated that formaldehyde levels in at least 4% of California 

classrooms exceed OEHHA’s interim 8-hour REL of 27 ppb (Whitmore et al., 2003), the level at 

which an 8-hour exposure might result in irritant effects. This is equivalent to about 10,720 

classrooms, or at least 214,400 children (assuming 20 children per classroom...usually there 

are more) exposed to formaldehyde levels that could potentially result in irritant effects in 

sensitive individuals. Average and peak levels in the classrooms were somewhat higher than 

those measured in the U.S. EPA BASE study of public and commercial buildings, indicating 

that, during the day, school children may experience greater exposures than most adults. Data 

analyses from the PCS indicate that several factors were associated with indoor formaldehyde 

levels in classrooms including the presence of plywood and particleboard; vinyl tackboard; 

bookcases and cabinets made of pressed wood; increased temperature and humidity; and 

classroom age (higher levels in newer classrooms) (Whitmore et al., 2003). 

2.3.2 Volatile Organic Chemicals 

Volatile organic chemicals (VOCs) is a generic term for thousands of compounds with widely 

varying physical, chemical, and toxicological properties. VOCs include a variety of chemicals 

such as alkanes, alcohols, esters, ethers, and aromatic compounds. A number of specific VOCs 

are widely found in indoor environments and are known to have adverse toxicological 

properties. Potential indoor sources of VOCs include building and furnishing materials such as 

carpet, paint, and vinyl flooring; consumer products such as air fresheners, adhesives, and 

cleaning agents; water treated with chlorine; dry-cleaned clothing; environmental tobacco 

smoke; plastic products, computers, and others. 

Many of the ‘traditional’ VOCs reported in indoor air have been studied simultaneously because, 

due to their chemical properties, they are collected via the same medium and analyzed through 

the same processes. Scientific study has only touched the ‘tip of the iceberg’ in understanding 

all VOCs in indoor air. Complex compounds such as fragrances are widely used, minimally 

regulated, and an area of emerging concern for environmental impacts (Bridges, 2002). Many 

semi-volatile compounds that can be present in the gaseous phase, or adsorbed to particles 

have not been extensively studied (Rudel et al., 2003). Because the link between indoor air 

pollutants and health impacts is so complex, researchers are investigating the reaction of VOCs 

with oxidants present in indoor air and are discovering new areas for future study (Carslaw, 

2003; Weschler, 2004; Wolkoff and Nielsen, 2001; Wolkoff et al., 2000). 

Some VOCs have been identified as California TACs or federal HAPs due to their cancercausing potential. Some VOCs also cause eye, nose, and throat irritation, and neurological 
Indoor Air Pollution in California July, 2005 

 71

effects such as headache. Indoor and personal exposure levels of these VOCs are typically 

higher than concurrent outdoor levels, and may exceed acceptable cancer risk levels and other 

health-based guideline levels. Ambient VOC levels are generally considered ‘background’ levels 

for indoor pollutants due to infiltration of outdoor air, thus any additional pollutant released 

indoors results in a concentration greater than outdoors. 

2.3.2.1 Health Effects of VOCs 

The ability of organic chemicals to cause health effects varies greatly from those that are highly 

toxic, to those with no known health effect. Some of the VOCs found in indoor air in California 

have been identified as TACs based on their carcinogenic potential. Accordingly, there is no 

level of exposure to these chemicals that is known to be absolutely safe. However, health 

effects are determined not only by the specific toxicology of the air pollutant but also by the 

extent of exposure and the absorbed dose. The higher the exposure and dose, the higher the 

risk of adverse health effects. More information on dose-response can be found on the OEHHA 

website (www.oehha.ca.gov). Some of the more common carcinogenic indoor VOCs were listed 

earlier in Table 2.4. The cancer risk posed by some of the most prevalent VOCs was discussed 

above in Section 2.1.2, and a detailed discussion of those risks is provided in Appendix II. 

Many indoor VOCs also can irritate the eyes, nose, and throat (OEHHA, 2000a; OEHHA, 

2003a). They are emitted from a wide range of sources and have a variety of impacts on 

occupant health and comfort (Hodgson et al., 1994; Wolkoff, 1995; Molhave, 1991b). Hodgson 

and Levin (2003a) compared indoor VOC concentrations to odor thresholds, sensory irritation 

levels, and noncancer chronic health guidelines. “The methodology demonstrated that only a 

small number of the more than 100 reported indoor VOCs exceeded levels likely to be of 

concern with respect to the endpoints considered. The results indicated carboxylic acids and 

less volatile aldehydes and aromatic hydrocarbons are most likely to be perceived by olfaction 

and that the probability of detection is higher in residences than in offices. Although more 

consideration of the underlying toxicological data is needed, the results suggested only a few 

commonly measured VOCs, considered singly, are likely to produce serious irreversible health 

effects not associated with cancer”. The authors conclude, “For a few compounds, such as 

acrolein and formaldehyde, the evidence based on sensory irritation and chronic toxicity is 

sufficient to warrant efforts to reduce and otherwise control the sources of these compounds in 

buildings.” 

At higher concentrations (usually not encountered in homes or offices, but sometimes found in 

occupational settings), some VOCs can impact the nervous system, causing acute effects such 

as nausea, tremors, drowsiness, dizziness, and headache (OEHHA, 2000a; OEHHA, 2003a). 

Such VOCs include, most notably, aromatic hydrocarbons (such as benzene), chlorinated 

chemicals (such as perchloroethylene), and some pesticides. While concentrations that can 

trigger neurotoxic effects are not normally experienced in homes and offices, special 

circumstances can lead to elevated exposures in some specialized non-industrial workplaces. 

The nature of activities and products used in medical offices, hospitals, beauty salons, high 

production copy shops, and other non-industrial workplaces can lead to unusually high 

concentrations of some pollutants. Business parks that merge industrial and non-industrial 

businesses may also create unique situations leading to exposure to elevated levels of these 

pollutants. 

Exposure of pregnant women to organic solvents may affect the neurodevelopmental outcome 

of their children. After controlling for potential confounding factors related to maternal IQ and 

maternal education, Laslo-Baker et al. (2004) found that children exposed in utero to organic 
Indoor Air Pollution in California July, 2005 

 72

solvents obtained lower scores on subtests of intellect, language, motor, and neurobehavioral 

functioning. Many of the occupations were non-industrial and included painter, hair stylist, salon 

receptionist, and science teacher. Exposure levels were not reported. 

2.3.2.2 Sources and Emissions of VOCs 

Studies have shown that many indoor sources emit VOCs, that some indoor sources emit 

substantial amounts of VOCs, and that groups of related VOCs often have common sources. 

Exposure to VOCs is influenced by people’s activities and their proximity to sources of 

pollutants. Exposure studies indicate the greatest exposures generally result from close contact 

with specific sources, such as cleaning products. Manufacturers strive to produce products that 

meet consumers’ needs and can be used safely; however, VOCs are often required in the 

manufacture of products to impart desired properties for a given application. This results in 

trade-offs: proper use of some cleaning products, for example, can remove biological 

contaminants and some allergens and asthma triggers in the indoor environment, yet occupants 

sensitive to the odor and irritant effects of the VOC components may be affected. 

Chlorinated Solvents

Chlorinated hydrocarbons, a large group of VOCs with solvent properties, contain one or more 

chlorine atoms. Chemicals in this group have diverse sources. Levels of perchloroethylene, 

identified as a California TAC due to its carcinogenic potential, can increase when dry-cleaned 

clothes are brought into a house. Levels in a home containing recently dry-cleaned clothes can 

be 100 to 150 times greater than outdoor levels of perchloroethylene (Wallace, 2001). Levels of 

methylene chloride, another chlorinated hydrocarbon and TAC, have been greatly reduced in 

consumer products; however, it is still common in paint strippers with a label warning to use 

adequate ventilation. Short-term exposures can be significant for individuals who use paint 

strippers (Wallace, 1991). 

Para-dichlorobenzene (p-DCB), another chlorinated solvent, has been used as an “air 

freshener,” although it is listed as a TAC due to its potential carcinogenicity. Data from the U.S. 

EPA’s TEAM studies indicated that, at the time the study was conducted, about one-third of 

homes used products containing p-DCB (Wallace, 1991). In another study, the indoor air 

concentration of p-DCB increased from 1 μg/m3

 to more than 500 μg/m3 the day after a toilet 

bowl cleaner was introduced into a home (Wallace, 2001). In the NHEXAS study, the two 

highest p-DCB levels measured in Arizona homes were 3949 and 4400 μg/m3

, presumably from 

the introduction of household consumer products (Gordon et al., 1999). These examples 

illustrate the extremely high concentrations of chlorinated chemicals that can occur in 

residences. 

Chlorine is intentionally added to domestic water for public health purposes. However, chlorine 

and organic matter in the water react to produce chloroform, another compound listed as a 

California TAC. Exposure to chloroform and other trihalomethanes occurs from drinking water, 

taking showers and baths (Wallace, 2001; Gordon et al., 1998; Giardino and Andelman, 1996; 

Jo et al., 1990), and operating washing machines (Howard-Reed and Corsi, 1998) and 

dishwashers (Howard-Reed et al., 1999; Olson and Corsi, 2004). In one study, investigators 

measured chloroform concentrations while individuals actually took showers in residential 

shower stalls (Kerger et al., 2000). Average concentrations during and immediately after the 

shower ranged from 67 μg/m3

 to 265 μg/m3. The chronic REL for chloroform is 300 μg/m3

(OEHHA, 2003a). Air concentrations of trihalomethanes were about three times higher on 

average for a typical shower compared to a bath. Higher concentrations were observed with 

hotter water (Kerger et al., 2000). 
Indoor Air Pollution in California July, 2005 

 73

Chloroform can also be produced during the use of bleach and other cleaning agents that 

contain chlorine. Investigators predicted that 5.3 mg to 9.8 mg of chloroform can be released to 

indoor air during a ten-minute wash cycle when a laundry bleach containing sodium hypochlorite 

is used in a residential washing machine (Shepherd et al., 1996). If this amount of chloroform is 

released into a 10 foot by 10 foot room (22.7 m3

), the chloroform concentration would be 230 to 

430 μg/m3

, the high end of which would exceed the chronic REL. 

Benzene and Other Aromatic Hydrocarbons

Benzene, styrene, toluene, and xylene are aromatic hydrocarbons containing a hexagonal ring 

structure. In general, the major sources of these chemicals in the indoor environment are 

environmental tobacco smoke, motor vehicle exhaust, and evaporative emissions from vehicles 

in attached garages. To a lesser extent, consumer products such as solvents, adhesives, glues, 

and paint emit some of these VOCs, especially toluene (Wallace et al., 1988; Akland and 

Whitaker, 2000; Guo et al., 1999). The overwhelming source of benzene exposure for smokers 

is mainstream cigarette smoke (Wallace, 1996b); nonsmokers living with smokers may 

experience a substantial benzene exposure due to ETS as well (Wallace, 2001). For 

nonsmokers with infrequent exposure to ETS, most benzene exposure comes from auto 

exhaust, especially while traveling on busy roadways (Rodes et al., 1998), gasoline vapor 

emissions during fueling at gas stations, and in houses with an attached garage (Wallace, 

1996b). 

Some of these VOCs are also emitted from office copy machines and printers (Lee et al., 2001). 

Several investigators have studied the emission of aromatic hydrocarbons from office machines. 

Numerous VOCs, including benzene, ethylbenzene, o,m,p-xylene, and styrene were emitted 

from a dry-process photocopier studied by Brown (1999b). The author noted a 40% increase in 

VOC emission rates for double-sided operation versus single-sided operation. Leovic et al.

(1996) measured emissions from 4 dry-process photocopy machines. The compounds with the 

highest emission rates overall were ethylbenzene (highest emission at 28,000 μg/hour), o,m,pxylene, 2-ethyl-1-hexanol, and styrene (lowest emitter of these compounds at 12,000 μg/hour). 

The relative amounts of individual compounds varied with the machine. Other investigators 

(Wolkoff et al., 1993) measured emissions from toners and processed paper from office copiers 

and printers. They also report substantial variation in emissions between machines. Aromatic 

compounds such as toluene, xylenes, ethyl and propyl benzene, and styrene dominated the 

emissions. The authors concluded “a realistic estimate (assuming first order decay) of handling 

200 freshly processed copies in a 17 m3

 office room, 0.25/hour air exchange rate, and an 

emission of 6 μg/m2

hr could reach a styrene concentration, assuming complete mixing, of 12 

μg/m3

 from the processed paper.” This concentration is well below the chronic REL of 900 

μg/m3

, however results indicate total emissions including ozone and particles can have a 

significant impact on indoor air quality (Wolkoff et al., 1993; Leovic et al., 1996). 

In an unpublished study of over 100 products sold in California stores, Akland and Whitaker 

(2000) detected toluene most frequently in auto care products, glues, and personal care 

products, such as in fingernail polishes. Estimated maximum air concentrations and daily doses 

were high, up to 4000 μg/day. In the Arizona NHEXAS study, investigators measured toluene 

levels at non-smokers’ homes and found an average level of 24 μg/m3

 in homes with an 

attached garage (n=40), but only 5 μg/m3

 in homes without an attached garage (n=9) (Gordon 

et al., 1999). These concentrations are below the chronic inhalation REL for toluene of 300 

μg/m3

 (OEHHA, 2003a). 
Indoor Air Pollution in California July, 2005 

 74

VOCs from Building Materials

The pollutants discussed above are associated with one or a few predominant sources. But, 

many sources, such as building materials emit numerous VOCs. A number of studies have been 

conducted to examine VOC emissions from a variety of building materials. Most recently, a 

building material emissions testing study funded by CIWMB reported that building materials emit 

a number of VOCs that were identified as chemicals of concern (Alevantis, 2003). Several 

products in each of the categories identified below exceeded the Section 01350 guideline levels 

as follows: 

• Carpet exceeded the emission rate limits for naphthalene and acetaldehyde. 

• Fiberboard and particleboard exceeded the limits for acetaldehyde. 

• Resilient flooring products exceeded the limit for acetaldehyde, naphthalene, and phenol. 

As was mentioned in the section on formaldehyde, products meeting Section 01350 emission 

guidelines are listed at http://www.chps.net/manual/lem_table.htm. 

In a study funded by ARB, Hodgson (1999) identified 17 toxic air contaminants in the emissions 

from new carpet assembly, vinyl flooring, and latex paint. These TACs are routinely emitted to 

the indoor environment, particularly in new or recently remodeled homes and offices. Table 2.6 

contains a list of TACs identified by Hodgson in building material emissions. In addition to TACs, 

all of the bonded urethane carpet cushions emitted butylated hydroxytoluene (BHT), an irritant, 

and all carpet samples emitted 4-phenylcyclohexene (4-PC), the compound largely responsible 

for new carpet odor. The investigator tested a limited number of products on the market at the 

time. The study conducted by Alevantis (2003) contains more recent emissions data, reflective 

of current manufacturing processes. It also compares emissions to health-based guidelines. 

Table 2.6. Toxic Air Contaminants Emitted From Building and Finishing Materials 

Carpet and Cushion Paint Vinyl flooring 

Toluene m,p-Xylene Toluene 

m,p-Xylene Ethylene glycol m,p-Xylene 

o-Xylene 2-(2-Butoxyethoxy)ethanol o-Xylene 

Styrene Formaldehyde Styrene 

Ethylene glycol Acetaldehyde 1,2,4-Trimethyl benzene 

Formaldehyde Naphthalene 

Acetaldehyde Acetophenone 

Acetophenone Phenol 

2-(2-Butoxy)ethanol Formaldehyde 

Ethylbenzene Acetaldehyde 

Tetrachloroethane 

Naphthalene 

Phenol 

Emissions from polymeric building materials can be attributed to several factors (Yu and Crump, 

1998). 

• Solvent residues from the manufacturing process. 

• Unreacted monomers trapped in the product structure. 

• Secondary products from reactions of monomers. 

• Plasticizers used in production. 
Indoor Air Pollution in California July, 2005 

 75

Measurement of VOCs in new homes is another method of determining the variety of 

compounds emitted from building materials. Hodgson et al. (2000) identified α-pinene, 

formaldehyde, hexanal, and acetic acid as the predominant compounds measured in 11 new 

homes. For manufactured houses and site-built houses, the geometric mean total volatile 

organic chemicals (TVOC) emission rate was 1.7 mg/m2

-h, and 2.1 mg/m2-h, respectively. 

Individual compounds with the highest emission rates (greater than 50 μg/m2

-h) include αpinene, ethylene glycol, hexanal, acetic acid, β-pinene, and 2,2,4-trimethyl-1,3-pentanediol 

monoisobutyrate (TMPD-MIB). 

Paint not only emits numerous TACs, but emissions can continue for extended periods of time. 

Sparks et al. (1999) estimated that less than 50% of the VOCs in latex paint are emitted in the 

first year. Compounds studied include ethylene glycol, propylene glycol, Texanol®, and 

butoxyethoxyethanol. Alkyd paints contain substantially more VOCs than latex paints due to the 

use of mineral spirits as the solvent. Compounds emitted from alkyd paints include alkanes such 

as decane, nonane, octane, undecane, and aromatic compounds such as xylenes, toluene, and 

ethylbenzene (Guo et al., 1999). 

It is becoming increasingly apparent that VOCs emitted into indoor air can undergo chemical 

reactions. Morrison and Nazaroff (2002) studied the reaction of ozone with VOCs emitted by 

carpet to produce aldehydes. Of particular interest was the production of 2-nonenal, a 

compound with a low odor threshold. Investigators estimated that 2-nonenal could be generated 

from the carpet emissions at rates leading to odor detection for longer than three years. 

VOC Emissions from Consumer Products

Consumer products such as cleaning products, personal care products, art supplies, and hobby 

supplies can release pollutants to the indoor environment and cause high personal exposures to 

pollutants. Wallace et al. (1989) measured the impact of activities and product use on personal 

exposure to VOCs, several of which are carcinogens. Breath levels of VOCs were often 

significantly correlated with previous personal exposures. Use of consumer products was 

associated with a variety of increased exposures as follows: use of deodorizers (pdichlorobenzene), washing clothes and dishes (chloroform), visiting a dry cleaners (1,1,1-

trichloroethane, tetrachloroethylene), smoking (benzene, styrene), cleaning a car engine 

(xylenes, ethylbenzene, tetrachloroethylene), and painting and using paint remover (n-decane, 

n-undecane). 

During the late 1980s and early 1990s, the U.S. EPA conducted an indoor air quality research 

program to develop test protocols, determine emission factors of products, and develop 

emission models (Tichenor, 1989). During this time much was learned about emission profiles, 

sink effects, and the VOCs emitted by various consumer products. A list of organic compounds 

was identified in products such as paint, stain, adhesive, furniture polish, and caulk (Tichenor, 

1989; Tichenor and Mason, 1988). These early studies were instrumental in understanding the 

role consumer products play in indoor air quality. However, changes in product formulations 

make newer studies more appropriate for understanding current indoor air quality impacts. 

In an unpublished study, Akland and Whitaker (2000) found six products that they estimated 

would exceed the Proposition 65 no-significant-risk level for formaldehyde, including a nail 

finish, make-up, floor-cleaning spray, formica laminate, foaming tire care, and sheet flooring 

adhesive. Two products exceeded the no-significant-risk level for benzene, one product 

exceeded the level for acetaldehyde, and another product exceeded the level for 

tetrachloroethylene. The authors state “Comparison with the California levels would be 

reasonable only to the extent that the emission testing conditions represent typical indoor 
Indoor Air Pollution in California July, 2005 

 76

conditions, and that the product emissions actually resulted in exposure to the person for a 24-

hour period”. Products were applied to a glass substrate, so emissions may be different than 

would be expected in a typical situation. 

Cleaning products have been studied to assess their impact on personal exposure in indoor 

environments. Zhu et al. (2001) tested 13 cleaning products to assess the potential for human 

exposure to three glycol ethers. 2-Butoxyethanol (BE) was present in the head space samples 

of seven products, of which five were household cleaning agents. BE concentration in the 

products ranged from 0.50 to 3.72%. 2-Methoxyethanol (ME), 2-ethoxyetyhanol (EE) were not 

detected; both of these are more toxic than BE. Investigators calculated average daily inhalation 

exposure levels for an individual cleaning with these products at home. Calculations were based 

on product use scenarios developed by U.S. EPA and a “standard room”. For two all-purpose 

spray cleaners the average daily inhalation exposure for 2-butoxyethanol was 0.075 and 0.186 

mg/kg body weight/day, and for two spray glass cleaners it was 0.004 and 0.006 mg/kg body 

weight/day. The high-end exposure of 0.186 mg/kg body wt/day for a 71 kg person would be 

13.2 mg/day. This is below the U.S. EPA’s inhalation reference concentration (RfC) for BE of 13 

mg/m3

, the daily inhalation exposure that is likely to be associated with an appreciable risk of 

deleterious effects during a lifetime (U.S. EPA, 1999c). (To compare product emissions to the 

RfC, multiply the RfC by 20 m3

/day [daily breathing rate] to yield 260 mg/day, which is notably 

greater than the concentrations measured during the cleaning protocols.) 

Other investigators also have studied emissions from consumer products and personal care 

products. Cooper et al. (1995) identified ethanol, α-pinene, camphene, β-pinene, diethylene 

glycol monoethyl ether, benzaldehyde and others as components of fragrance in two colognes, 

a perfume, a soap, and an air freshener. Toxicological data indicate the compounds may be 

irritants, mutagenic, teratogenic, or carcinogenic; however, risk of these health effects may be 

low given typical use of these products. 

The impact of human occupancy and activities on VOC concentrations was documented in a 

study conducted by Shields et al. (1996). Investigators measured VOC concentrations indoors 

and outdoors at 70 offices having ranges in occupant density. The results showed that VOC 

concentrations were associated with the density of occupancy and ventilation rate. The authors 

were able to identify six compounds associated with occupant density: limonene used in 

cleaning products and air fresheners; tetrachloroethylene from dry-cleaned clothes; n-dodecane 

through n-hexadecane, probably from cosmetics, hand lotions, and shaving creams; and octaand deca-methylcyclopentasiloxanes, which are associated with underarm deodorants and 

antiperspirants. It is important to note that the compounds associated with personal care 

products were present at low concentrations and they are not TACs or on the Proposition 65 list. 

The database generated by the study can be used to identify atypical compounds or 

concentrations in office buildings. 

2.3.2.3 Indoor Concentrations of VOCs 

Several major studies of concentrations of selected toxic pollutants in California residences 

have been conducted under the sponsorship of the U.S. EPA and/or ARB. Studies of VOCs 

were conducted over different seasons in three different years (1984, 1987, and 1990) in a total 

of nearly 500 California homes (Wallace, 1991; Wallace et al., 1988; Sheldon et al., 1992a). 

Analyses of the results across these and other studies indicate that indoor VOC concentrations 

are typically two to five times higher, and sometimes many times higher, than outdoor air 

(Wallace, 1991; Wallace et al., 1988; Sheldon et al., 1992a; Ott and Roberts, 1998). Results 

also indicate that personal (actual) exposure levels are generally higher than either indoor or 
Indoor Air Pollution in California July, 2005 

 77

outdoor residential levels. These results were consistent across different seasons and different 

geographic locations. 

California Indoor VOC Studies

The average and 90th percentile personal, indoor, and outdoor concentrations of several VOCs 

measured in a northern California study are presented in Table 2.7 (Sheldon et al., 1992a). 

Personal levels are usually higher than indoor and outdoor levels due to people’s frequent use 

of, or proximity to, sources such as consumer products as they go about their daily activities. 

Table 2.7 includes a risk level for chemicals listed on the Prop 65 list. At the risk level 

presented, one excess cancer case per 100,000 individuals may be expected over a 70-year 

lifetime. The table indicates that a substantial portion of the population could be exposed to 

levels of para-dichlorobenzene, benzene, and perchloroethylene that pose an unacceptable 

excess cancer risk. 

Table 2.7. Personal, Indoor, and Outdoor VOC Concentrations 

From a Northern California Study1

(μg/m3; means and 90th percentile) 

Compound 

Cancer 

Risk Level2

Personal 

Concentration

Indoor 

Concentration 

Outdoor 

Concentration 

 mean 90 mean 90 mean 90 

paradichlorobenzene 1.0 21 88 18 36 0.30 0.94 

Benzene 0.65 5 8.9 4.7 8.3 1.2 1.9 

Perchloroethylene 0.7 1.6 3.0 1.1 2.3 0.53 0.59 

Trichloroethylene 4.0 2.3 3.4 0.68 2.0 NQ3 NQ 

Styrene Not listed 2.4 3.3 2.8 3.9 0.24 0.70 

1,1,1-

Trichloroethane Not listed 22 36 6.5 11 1.5 1.9 

m,p-xylene Not listed 9.3 18 6.3 13 1.8 2.9 

1. From Sheldon et al., 1992a. 

2. Air concentrations that should not be exceeded to meet Proposition 65. For Prop 65, the “no 

significant risk” level is defined as 1 excess case of cancer per 100,000 individuals exposed over a 

70-year lifetime. 

3. NQ = not quantifiable: below the method quantifiable limit. 

Another example of California VOC indoor and outdoor concentrations is presented in Figure 

2.5. Figure 2.5 summarizes the median levels (levels at which half of the homes are higher and 

half lower) of indoor and outdoor concentrations of selected VOCs using combined data from 

one of the California VOC TEAM studies (February and July, 1987 in Los Angeles; Pellizzari et 

al., 1989) and a study conducted in Woodland, California that was similar to the TEAM studies 

(Sheldon et al., 1992a). Figure 2.5 reflects the presence of indoor sources for all chemicals 

shown except for carbon tetrachloride, for which there are no longer indoor sources because of 

product restrictions imposed at the national level (CPSC, 1987b). Benzene concentrations 

measured in Texas homes during 1993 (Mukerjee et al., 1997a,b) were comparable to levels 

measured in the California studies. It is important to note that the indoor concentrations 

presented in Figure 2.5 are less than the corresponding chronic REL for each given pollutant by 

a factor of six, or greater. 
Indoor Air Pollution in California July, 2005 

 78

Trends 

Some spatial and temporal trends in VOC levels (not illustrated in the figure) also have been 

noted: indoor concentrations in southern California appear to be somewhat higher than indoor 

levels in northern California, and indoor levels in winter tend to be higher than indoor levels in 

summer (Jenkins et al., 1992b). 

Some additional trends found in indoor air VOC studies were identified by Brown et al. (1994) in 

their review of studies conducted between 1978 and 1990. The review encompasses 

measurements from residences, offices, schools and hospitals. Significant findings include: 

• For all compounds, indoor concentrations were greater than outdoor concentrations by a 

factor of two to 73, indicating indoor sources were present. Mean VOC and TVOC 

concentrations were generally greater in established residences than established public 

buildings. 

• New buildings had considerably higher TVOC concentrations than established buildings. For 

example, the weighted-average geometric mean TVOC concentration from 33 new 

residences was 4,500 μg/m3

, whereas it was 1,130 μg/m3 from 1,081 established buildings. 

• VOCs specific to new buildings included 2-ethoxyethylacetate, n-butanol, α-pinene, 

undecane, dodecane, tridecane, tetradecane, and 2-propanol. 

Apparent Changes in Concentrations Over Time 

Levels of some VOCs in California homes, such as benzene, have decreased since these 

studies were conducted, due to changes in some building materials and consumer products, 

and the reduced smoking rates in homes. Some studies from other locations appear to support 

this, although others indicate continued levels of concern. 

Figure 2.5:

Statewide Indoor and Outdoor Concentrations of VOCs

(medians, μg/m3

)

0 2 4 6 8 10 12 14 16

m,p-Xylene

1,1,1-Trichloroethane

Benzene

o-Xylene

Perchloroethylene

Styrene

p-Dichlorobenzene

Carbon Tetrachloride

Trichloroethylene Indoor Outdoor

μg/m3
Indoor Air Pollution in California July, 2005 

 79

In a review of 12 studies conducted in North America. Hodgson and Levin (2003b) analyzed 

residential VOC concentration data collected from 1990 through 2003. They hypothesized that 

the 1990 Clean Air Act Amendments impacted indoor VOC concentrations through reduced 

infiltration of ambient pollutants and through industry changes in consumer products and other 

materials used indoors to use less toxic compounds. Hodgson and Levin found 1,1,1-

trichloroethane concentrations to be more than three times lower than the TEAM study value. 

Benzene, 1,2-dichloroethane and tetrachloroethylene were approximately one-half an order of 

magnitude lower in the current review. The authors noted that the data were limited in a number 

of aspects. They also highlight that “despite these trends, indoor exposures to most common 

VOCs undoubtedly still dominate human exposures to these compounds”. In another study, 

VOC concentrations for five out of six VOCs measured recently in Baltimore, Maryland 

residences (Payne-Sturges et al., 2004) were somewhat lower than levels shown in Figure 2.5. 

However, there were differences in sample collection methods (passive samplers in Baltimore, 

active samplers in California) and undoubtedly differences in housing characteristics based on 

region. The focus of the Baltimore study was to estimate cancer risk. Although concentrations 

are lower than measurements taken from studies conducted during the 1980s, the authors 

estimate a cumulative indoor cancer risk of 120 per million based on the median indoor 

concentrations. 

Recent studies in other states continue to show higher levels indoors than outdoors, and indoor 

levels above health risk guidelines. For example, results from the recent Arizona National 

Human Exposure Assessment Survey (NHEXAS) indicate that indoor levels of pollutants 

continue to be greater than outdoor levels, and some are comparable to levels measured in the 

initial TEAM studies (Gordon et al., 1999). In another recent study conducted in Minneapolis/St. 

Paul, investigators confirmed the continued risk due to elevated indoor concentrations of VOCs 

(Sexton et al., 2004). Pollutant concentrations were compared to risk thresholds established in 

Minnesota. Median indoor concentrations for benzene and chloroform exceeded the level for a 

70-year lifetime cancer risk of 1 in 100,000. The 90th percentile concentrations exceeded the 

cancer risk level for benzene, chloroform, and p-dichlorobenzene. The identified pattern of 

personal VOC concentrations exceeding indoor VOC concentrations, which in turn exceed 

outdoor VOC concentrations, also was reaffirmed by this study. This relationship held for 13 of 

the 15 VOCs measured by Sexton et al. in Minneapolis/St. Paul over three seasons in 1999. 

Impacts of Attached Garages on Indoor VOC Concentrations 

Several studies have investigated the impact that attached garages have on residential indoor 

levels of VOCs. These studies implicate vehicles as well as other activities (such as storage of 

chemicals and small engines) within attached garages as the sources of these VOCs. Adgate et 

al. (2004) measured outdoor, indoor, and personal VOC exposures to children in 284 

households in Minnesota for ten VOCs. Households with attached garages had significantly 

higher concentrations of benzene, chloroform, styrene, and m/p- and o-xylene compared to 

households without an attached garage. Thomas et al. (1993) investigated the temporal 

variability of benzene exposures for residents in several New Jersey homes with attached 

garages or tobacco smoke. In homes with attached garages or ETS, mean indoor and personal 

benzene concentrations were two to five times higher than outdoor levels at all but one home. 

Measured benzene levels in four garages ranged from 3-196 μg/m3; garage source strength 

estimates ranged from 310-52,000 μg/hr. The mass transfer rate for benzene from sources in 

the garage to living areas ranged from 730-26,000 μg/hr. Material and activities inside the 

garage were the sources of the benzene. 
Indoor Air Pollution in California July, 2005 

 80

Several studies have explicitly studied VOC emissions from vehicles in attached garages. 

Gammage et al. (1984) determined that high levels of VOCs indoors in two houses were 

associated with the operation of a car in a basement garage. Tsai et al. (2000) also found 

elevated indoor concentrations of benzene, toluene, and methanol resulting from automobile 

emissions released in an attached garage. In a detailed Canadian study, Graham et al. (2004) 

measured the concentration of 175 VOCs (non-methane hydrocarbons and halogenated 

compounds) inside 16 residences over two seasons while a vehicle in the attached garage was 

operated under brief cold-start and hot-soak conditions. Positive net changes of indoor VOC 

concentrations were observed whose signatures were similar to those of the vehicle profile 

releasing the emissions. Chemical Mass Balance (CMB) modeling suggested that the infiltration 

of vehicle emissions into the house could account for between 9 and 85% of the measured 

hydrocarbon concentrations in the house during the test period. 

In a study of indoor air samples collected from 137 Anchorage homes between December 1994 

and February 1996, the Anchorage Air Pollution Control Agency determined that the presence 

of an attached garage was the factor most strongly associated with in-home benzene; indoor 

elevated benzene levels were strongly related to the use of a garage to park vehicles or store 

fuel or small engines. Other VOCs (toluene, ethylbenzene, m/p-xylene, o-xylene) were also 

higher in homes with attached garages; geometric mean concentrations were two to four times 

higher in homes without attached garages. A regression model for benzene in homes with 

attached garages revealed a significant impact of a car parked in the garage (vs. no car), 

number of trips originating from the attached garage, fuel having been opened within the last 

three days, presence of forced air furnaces (vs. hot water boilers), and living areas above the 

garage (vs. adjacent to the garage) (Schlapia and Morris,1998). 

The primary reason that attached garages contribute to elevated indoor levels of CO and VOCs 

is due to air leakage into the residence through the garage-to-residence interface. Air leakage 

rates between attached garages and homes have been measured in several different northern 

climate locales (i.e., Canada, Minnesota) throughout the last decade, with garage-to-residence 

leakage/infiltration rates ranging from 9% to 17% (CMHC/SCHL, 2001; Nelson, 2002; 

CMHC/SCHL, 2004). Garage-to-residence infiltration rates may differ in California from these 

reported values to climatic differences as well as variations in regional building codes. 

Several mitigation options may be useful in reducing leakage (Built Green of Colorado, 2004), 

including aerodynamically decoupling the garage from the house, building ductwork 10 times 

tighter than the current standard, ventilating garages with either active or passive vents, 

equipping every home with a CO sensor, testing a subset of houses in a given area to ensure 

efforts are working, and informing homeowners (Built Green of Colorado, 2004). 

VOCs in Public and Commercial Buildings

Girman et al. (1999) identified VOCs in public and private buildings, but did not associate the 

presence of VOCs with a particular source. Girman analyzed data collected at 56 office 

buildings (most with no known indoor air quality problems) across the U.S. Of the 48 VOCs 

identified in indoor air, eight were found in all of the samples, and another 26 were found in 81-

99% of the samples. Indoor concentrations of 27 VOCs were at least twice the corresponding 

outdoor concentrations. The 12 VOCs with the highest median indoor concentrations were 

acetone, toluene, d-limonene, m- and p-xylenes, 2-butoxyethanol, n-undecane; benzene, 1,1,1-

trichloroethane, n-dodecane, hexanal, nonanal, and n-hexane. Only acetone (29 μg/m3

) was 

present at a concentration above 10 μg/m3

. The study was designed to provide baseline data on 

VOCs in U.S. office buildings relative to complaint buildings. The author did not compare indoor 

concentrations to guideline levels; however, levels were below available minimum risk levels. 
Indoor Air Pollution in California July, 2005 

 81

2.3.3 Environmental Tobacco Smoke 

Environmental tobacco smoke (ETS) is the complex mixture of thousands of gaseous and 

particulate compounds emitted from the burning end of cigarettes and cigars, and in smokers’ 

exhaled breath. ETS is also called “second-hand smoke”, “passive smoke”, and “involuntary 

smoking”. Many chemicals in ETS have been identified as toxic air contaminants, and not 

surprisingly, ETS is estimated to cause thousands of deaths due to cancer and cardiac disease, 

and many thousand asthma episodes and other illnesses (ARB/OEHHA, 2005). Cigarettes are 

the most common source of ETS, but cigars and pipes are also sources. 

Passage of a statewide smoke-free workplace law in California in 1995 (AB 13, Labor Code 

6404.5, 1995) eliminated smoking in nearly all California indoor workplaces–including 

restaurants, bars and gaming clubs. In 1999, 93.4% of California’s indoor workers reported 

working in a smoke-free environment, compared to only 35% in 1990 (Gilpin et al., 2001). 

Additionally, the percentage of Californians with children under the age of 18 who do not allow 

smoking in the household has increased substantially. In 1994, 63% of Californians with 

children did not allow smoking in the house; by 2003, 77.5% did not allow it (DHS, 2004b). 

Because of such laws and trends, California has lower ETS exposures than most other states. 

2.3.3.1 Health Effects of ETS 

Exposure to ETS has been linked with a variety of adverse health effects, including heart 

disease, asthma episodes, other respiratory illness, and lung cancer (OEHHA, 1997). Primary 

tobacco smoke is an established human carcinogen for smokers (IARC, 2002; U.S. DHHS, 

1989). ETS has been identified as a cause of lung cancer in nonsmokers (U.S. DHHS, 1986; 

U.S. EPA, 1992; IARC, 2002). More recently, there is evidence from analyses of 

epidemiological studies that ETS exposure has a causal association with breast cancer 

(ARB/OEHHA, 2005). 

Table 2.8, below, provides the current estimates of the health impacts of ETS on Californians 

and Americans every year, taken from the March 2005 ARB/OEHHA draft report for the 

identification of ETS as a toxic air contaminant, which is currently in its last stage of scientific 

review (ARB/OEHHA, 2005). In addition to the large cardiac and lung impacts on adults, ETS 

has a number of serious impacts on children’s health. These include exacerbation of asthma, 

increased respiratory tract infections, increased middle ear infections, low birth weight, sudden 

infant death syndrome (SIDs), and developmental impacts (ARB/OEHHA, 2005). Children under 

18 months of age have greater tendency to suffer from bronchitis or pneumonia when their 

parents are smokers. A small reduction in birth weight has been repeatedly observed with 

mothers who are active smokers. Studies have shown fairly consistently that maternal smoking 

during pregnancy is adversely associated with measures of cognition and behavior in children 

(NCI, 1999). There is epidemiological evidence of a causal relationship between maternal 

smoking in general and risk of SIDS. 

ETS affects many tissues and organs of the body. ETS is causally associated with coronary 

heart disease in smokers and nonsmokers (NCI, 1999). Research suggests that chronic ETS 

exposure may increase the risk of stroke by about 82% (Bonita et al., 1999). ETS is estimated 

to cause about 400 excess deaths due to lung cancer each year in California (ARB/OEHHA, 

2005). In reviewing the literature on asthma and indoor air, the Institute of Medicine (2000) 

found that: 
Indoor Air Pollution in California July, 2005 

 82

“There is sufficient evidence to conclude that there is an association between ETS 

exposure and the development of asthma in younger children. [However], there is 

inadequate or insufficient evidence to determine whether an association exists between 

ETS exposure and the development of asthma in school-aged or older children, or in 

adults. There is sufficient evidence to conclude that there is a causal relationship 

between ETS exposure and exacerbations of asthma in preschool-aged children. There 

is limited or suggestive evidence of an association between chronic ETS exposure and 

exacerbations of asthma in older children and adults. Limited or suggestive evidence of 

an association between acute ETS exposure and exacerbations also exists for 

asthmatics sensitive to this exposure”. 

Table 2.8 Current Estimated Attributable Risks Associated with ETS 

(from ARB/OEHHA, 2005) 

OUTCOME EXCESS # IN CA PER YR EXCESS # IN U.S. PER YR 

Pregnancy: 

 Low Birth Weight 

 Pre-term Delivery 

1,600 

4,700 

24,3001 

71,900 

Cardiac death 

(Ischemic heart disease 

death) 

1,700 - 5,5002 22,7003 -

 69,600 

Lung Cancer Death 400 4

 3400 

Asthma episodes 

(children) > 31,000 5

 202,300 6

Otitis media visits 51,700 7

 789,700 8

SIDS 219

 43110

Breast cancer All studies: OR 1.26 (95% CI 1.10-1.45)11 

Best studies: OR 1.90 (95% CI 1.53-2.37). Approximate 

26-90% increased risk 

1 Based on adult females reporting exposure to ETS in NHANES III for 1995 (Pirkle et al., 1996) 2 Based on California Dept Health Services. 

http://www.dhs.ca.gov/hisp/chs/OHIR/vssdata/2000data/00Ch5Excel/5_9Hisp_2000.xls. Table 5-9 for yr 

2000 3

 Based on Anderson and Arias (2003). National Vital Statistics Report. Vol 51(9) Table 2 for yr 2000 

Ischemic heart diseases including AMI. 4 Assuming California exposure and death rates are similar to national rates and California population is 

12% of national population. 5 Based on number asthma attacks or episodes in previous 12 months for 0-17 year olds. Calculated from 

California Health Interview Survey for 2001 6

 Based on number asthma attacks or episodes in previous 12 months for 0-14 year olds. CDC-MMWR 

2002 51(SS01) 7 Calculated by applying national value (H6) and assuming 12% of US population lives in California 8

 Based on National Center for Health Statistics Series 13 No. 137. Ambulatory Health Care Visits by 

Children: Principal Diagnosis and Place of Visit for yrs 1993-1995. 9

 Based on California Dept Health Services. 

http://www.dhs.ca.gov/hisp/chs/OHIR/vssdata/2000data/00Ch4Excel/4_8_2000.xls. Table 4-8 for yr 2000 10 Based on National Center for Health Statistics. http://www.cdc.gov/nchs/data/nvsr/nvsr50/nvsr50_16.pdf

for yr 2000 

LBW = low birth weight; N/A = data not available. 11 OEHHA is unable at this time to calculate an attributable risk as it is not possible to account accurately for 

the portion attributable to other known risk factors. 
Indoor Air Pollution in California July, 2005 

 83

Eye and nasal irritation are the most commonly reported symptoms among adult nonsmokers 

exposed to ETS (ARB/OEHHA, 2005). 

Nazaroff and Singer (2004) estimated mean daily exposure to and inhalation intake of specific 

hazardous air pollutants found in ETS for non-smokers who live with smokers. The approach 

used a model based on cigarette consumption patterns, emission factors, residence 

characteristics, and population statistics. Results indicate “the ratio of estimated average 

exposure concentrations to reference concentrations is close to or greater than one for acrolein, 

acetaldehyde, 1,3-butadiene, and formaldehyde, indicating potential for concern regarding 

noncancer health effects from chronic exposure. In addition, lifetime cancer risks from 

residential ETS exposure are estimated to be substantial (~2 to 500 per million) for each of five 

known or probable human carcinogens: acetaldehyde, formaldehyde, benzene, acrylonitrile, 

and 1,3-butadiene.” 

2.3.3.2 ETS Sources 

The variability in emissions between brands of cigarettes is relatively low, though emissions 

from cigars and cigarettes vary in magnitude. Daisey et al. (1998) conducted a chamber study 

testing six of the most popular commercial brands in California and one reference cigarette for 

emissions of 21 different air toxics and other airborne compounds, including VOCs, nicotine, 

aldehydes, and airborne particulate matter (estimated to be PM2.5). Diluted sidestream smoke 

(produced by a smoking machine that smoked three cigarettes sequentially) was used to 

approximate ETS aging in a room-sized chamber, and a mass-balance model was used to 

generate estimates of indoor concentrations. Among the VOCs, acetaldehyde and 

formaldehyde displayed the highest emission factors (average emission factors 3,340 ng/mg 

tobacco and 2,040 ng/mg tobacco, respectively), and PM showed an emission factor of 12,400 

ng/mg. The nicotine emission factor was 1,410 ng/mg tobacco. These results suggest that ETS 

has a substantial influence on indoor concentrations of these compounds. 

Chuang et al. (1999) investigated children’s exposure to polycyclic aromatic hydrocarbons 

(PAHs) in low-income rural and inner-city areas in North Carolina. Indoor/outdoor air samplers 

and real-time PAH monitors were used to obtain measurements. The researchers determined 

that potentially carcinogenic PAH concentrations were significantly higher in smokers’ homes 

than in non-smoking homes (geometric mean: 6.14 ng/m3

 vs. 1.38 ng/m3, respectively). 

Additionally, the authors discovered that children in both rural and inner-city homes received 

higher potential doses of PAHs than adults, in part due to their lower body weights. 

2.3.3.3 ETS Concentrations 

Restrictions on smoking in California from the late 1980s to mid 1990s in workplaces and in 

public locations such as restaurants, bars, and gaming clubs have led to a substantial reduction 

in smoking in indoor environments in California, with commensurate reductions in indoor 

concentrations of ETS and non-smokers’ exposure levels. A number of studies published since 

1996 have shown that ETS constituents are present at lower concentrations in public places 

following smoking bans than they were prior to the bans (Ott et al., 1996; Hammond, 1999; 

Switzer et al., 2001; Repace, 2003), and that levels can be considerably higher in smoking 

versus comparable nonsmoking areas (Glasgow et al., 1998; Hammond, 1999; Graves et al., 

2000). 

Despite California’s workplace smoking ban, high indoor ETS concentrations still can be found 

in smokers’ homes and in private vehicles (Ott et al., 2003; Park et al., 1998; Offermann et al.,
Indoor Air Pollution in California July, 2005 

 84

2002). Children’s exposure to ETS is greatly impacted in these two environments when in the 

presence of a smoking parent or other adult. Children spend up to 85% of their time in the home 

(Wiley et al., 1991a). Thus, the potential for exposure to ETS can be extremely high when 

smoking occurs in a child’s home. In 2002, about 10% of California children 0-18 years of age 

were not protected from secondhand smoke at home (DHS, 2003b). Likewise, exposure in 

vehicles can be quite high due to the presence of a strong source in a relatively small volume of 

air. Recent residential respirable particulate matter (RSP, PM3.5) measurement is limited to a 

single study (Ott et al., 2003). A level of 300 μg/m3

 was measured in the bedroom where one 

cigarette was smoked; 5,500 μg/m3

 was the maximum bedroom level when three cigarettes 

were smoked. RSP levels ranging from 92 μg/m3

 (with ventilation) to 1,195 μg/m3 (without 

ventilation) have been measured inside a minivan (Offermann et al., 2002). 

Three comprehensive review documents summarize nicotine and RSP concentrations 

measured in smoking environments prior to 1996 (U.S. EPA, 1992; Guerin et al., 1992; NCI, 

1999). Comparison of mean nicotine concentrations from these earlier reviews with data 

published after 1995 reveals that the means have decreased in workplaces and restaurants, but 

less so in homes. In studies conducted before 1996, mean nicotine concentrations in offices and 

restaurants ranged from about 1 to 36 μg/m3

. In a more recent review, Hammond (1999) 

reported means of 2 to 8 μg/m3

 for these locations. Also, according to the Hammond review, 

nicotine levels were two- to six-times lower in indoor workplaces with smoking bans than in 

offices that allowed smoking (less than 1 μg/m3

 vs. 2-8 μg/m3, respectively). It appears that 

nationally, as smoking has become a less accepted social behavior, individuals are not smoking 

in indoor public locations as much as they did a few years earlier (in California, smoking is 

prohibited in indoor workplaces). 

Table 2.9. Estimates of Current California Indoor Concentrations 

of Nicotine and Respirable Suspended Particulates (RSP) 

(varying averaging times; from ARB/OEHHA, 2005) 

Environment Nicotine Concentration 

μg/m3

RSP Concentration 

μg/m3

Homes with smokers 

 present 

0.5 – low1 

3.0 – medium 

6.0 – high 

300-5,5003

Offices/public buildings 

 With smoking 

 Smoking prohibited 

2 – 82

<1 

56.8 – 3484

<15 

Vehicles 

 With ventilation 

 Without ventilation 

NA 

NA 

~1005

~1,200 

1. Glasgow et al., 1998 

2. Hammond, 1999 

3. Ott et al., 2003 

4. Ott et al., 1996 and Switzer et al., 2001 

5. Offermann et al., 2002 

Levels of RSP are generally comparable in both older and newer studies, but slightly lower in 

the newer studies (relative to 1996). Studies highlighted in the NCI review (1999) reported RSP 

concentrations consistent with other reviews. All measured levels tend to range from about 100 

to 400 μg/m3

 in offices and restaurants that allow smoking. Switzer et al. (2001) measured RSP 
Indoor Air Pollution in California July, 2005 

 85

levels at a church bingo site of 87 to 348 μg/m3

 above outdoor levels, and at less than 15 μg/m3

when smoking was banned. Similarly, PM3.5 concentrations at a sports tavern in California 

were 56.8 μg/m3

 with smoking, and 5.9 – 12.9 μg/m3 with smoking banned (Ott et al., 1996). 

Similar to nicotine levels, these recent RSP data from smoking locations are somewhat lower 

than the pre-1996 data. RSP levels are much lower (<15 μg/m3

) in indoor locations where 

smoking is prohibited. 

The majority of California homes are smoke-free, and would typically have a nicotine level lower 

than 0.5 μg/m3

. However, the recent body of data indicates that those who choose to smoke in 

their home have remained consistent in their smoking patterns over the years. It is important to 

note that concentrations of lower volatility ETS components such as nicotine, 3-ethenylpyridine, 

phenol, cresols, and naphthalene accumulate on surfaces to the extent that their re-emission 

(when a smoker is not present) is an important route of indirect exposure for non-smokers 

(Singer et al., 2003; Singer et al., 2002). 

Table 2.9 summarizes current estimates of indoor levels of nicotine and RSP for California. A 

more detailed discussion of indoor ETS concentrations is provided in the Draft Technical 

Support Document – Part A, Proposed Identification of Environmental Tobacco Smoke as a 

Toxic Air Contaminant (ARB/OEHHA, 2005). 

2.3.4 Biological Contaminants 

Biological contaminants are substances of plant, animal, or microbial origin. They are naturally 

abundant in the outdoor and indoor environments, but are considered contaminants when found 

in undesired locations or at elevated concentrations. They include bacteria, viruses, and fungi; 

allergens from animal dander, pollen, fungi, and the fecal particles or body fragments from 

house dust mites and cockroaches; as well as chemicals emitted by mold and bacteria such as 

endotoxins and mycotoxins. Exposure to biological contaminants may cause a variety of health 

effects, including asthma, allergy, infection, irritation, and toxic responses. Building related 

illness, or BRI, is an illness for which the specific cause–usually a virus, bacteria, or fungi–can 

be identified within the building. Examples include Legionnaire’s disease, caused by the 

Legionella bacterium, or humidifier fever. 

2.3.4.1 Health Effects of Biological Contaminants 

The health effects of biological contaminants can be grouped into three major categories: 

• Communicable disease transmission: Many infectious diseases are transmitted from person 

to person via indoor air. For example, inhalation of viruses is associated with influenza, 

measles, and chicken pox. The primary mode of transmission for the common cold virus has 

not been proven conclusively. Studies have shown transmission by both inhalation and 

direct or indirect contact between infected droplets from coughing or sneezing onto mucous 

membranes of the eyes, nose or mouth (Goldmann, 2002). Inhalation of bacteria is 

associated with tuberculosis and Legionnaire’s disease. Epidemiological studies have often 

found significantly lower prevalence of respiratory illness or surrogates for respiratory illness 

(sick leave, total absence from school) in buildings with higher ventilation rates, reduced 

office sharing, and less crowding (Fisk, 2000; Myatt et al., 2004; Shendell et al., 2004a,b). 

These and other studies indicate that a significant portion of common respiratory illness may 

be transmitted indoors by airborne particles; however, the proportion of total disease 

transmission that occurs through this route cannot be easily quantified. 
Indoor Air Pollution in California July, 2005 

 86

• Hypersensitivity reactions: Many biological agents can provoke a hypersensitivity response 

in individuals who are genetically predisposed to developing allergic disorders. Allergic 

rhinitis (hay fever) and allergic asthma are the most common examples of hypersensitive 

responses to biological contaminants. Common symptoms include watery eyes, runny nose, 

sneezing, nasal congestion, itching, coughing, wheezing, difficulty breathing, headache, and 

fatigue. Allergens from fungal spores, house dust mites, cockroaches, dog and cat dander, 

and pollen are frequently found indoors. When high concentrations of these allergens are 

present indoors they can trigger allergic responses or asthmatic exacerbation. 

Hypersensitivity pneumonitis is a rare immune-mediated lung disorder initially found in 

farmers and workers exposed to high doses of organic dusts in agricultural or industrial 

settings. A few cases of this disease have been attributed to indoor exposure to bacteria or 

mold growth. Only susceptible persons exposed to large amounts of these allergens are at 

risk of developing hypersensitivity pneumonitis (IOM, 2004). 

• Toxic responses: Many individuals in persistently damp or moldy buildings report symptoms 

such as headache, memory difficulties, vomiting, diarrhea, and increased frequency of 

cold/flu illnesses that do not appear to be caused by allergic or infectious mechanisms. The 

causes of such symptoms have not been identified. Some researchers have postulated that 

exposure to biological toxins such as endotoxins (components of the outer membrane of 

Gram-negative bacteria) and mycotoxins (secondary metabolic products of some fungi) may 

induce such symptoms. However, the health impact of inhalation exposure to biological 

toxins in indoor environments is not well understood. 

• More detailed information on the health effects of mold is discussed below in Section 

2.3.4.3. 

2.3.4.2 Sources of Biological Contaminants

Biological contaminants include allergens such as animal dander, house dust mites, 

cockroaches, and pollen; bacteria, viruses, and fungi; and chemicals emitted by mold and 

bacteria such as endotoxins and mycotoxins. 

Animal Dander

Dogs and cats are kept as pets in 32 and 27% of U.S. households, respectively (AVMA, 1997). 

Allergy to cats is reported to be about twice as common as allergy to dogs. Dog and cat 

allergens are found on small particles that can remain airborne for prolonged periods. The 

particles also adhere readily to fabrics such as clothing, upholstered furniture, and carpet and 

can easily be carried from animal–owning homes into offices, schools and day care centers 

(Custovic et al., 1998). In a recent nationally representative study, both dog and cat allergens 

were detected in all U.S. homes (Arbes, 2004). Asthmatics who are sensitive to cat allergen 

may experience allergic symptoms (congestion, runny nose, itching), asthma exacerbation and 

compromised lung function (chest tightness or wheezing) at cat allergen levels typically found in 

schools and homes without cats (Bollinger et al., 1996). 

House Dust Mites

House dust mites are microscopic relatives of spiders that feed on human skin cells and other 

organic material. Primary mite allergens are concentrated in their fecal particles and body 

fragments. These allergens are very potent, but concentrations in indoor air typically are low 

because the allergens are attached to larger particles (at least 10 μm) that settle rapidly. 

Consequently dust mite allergens are found predominantly in carpets, pillows, bedding, and 

upholstered furniture. In locations where humidity is high for most of the year, dust mites 
Indoor Air Pollution in California July, 2005 

 87

produce larger quantities of allergen (Rosenstreich et al., 1997). In contrast, mites cannot 

survive in desert or mountain (5,000 feet elevation or higher) regions where indoor humidity is 

routinely low. In a recent study of U.S. homes, mite allergens were found in all beds tested. 46 

percent of these homes had mite allergen at levels previously associated with allergic 

sensitization, while 24% had levels associated with an increased risk for asthma attacks in 

asthmatics allergic to dust mites (Arbes et al., 2003). 

Cockroaches

While many insects have been implicated as sources of inhaled allergens in small indoor 

studies, cockroaches are the only insects that have routinely been identified as a common 

source of indoor allergens (IOM, 2000). The exact part of the cockroach responsible for its 

allergens is unknown but may involve fecal particles and body parts. Like house dust mites, 

cockroach allergen is associated with particles larger than 5 μm and these particles become 

airborne only when settled dust is disturbed. Cockroach activity frequently occurs in indoor 

areas where food or standing water is available, such as kitchens and bathrooms. Cockroach 

hypersensitivity is highest among the urban poor, but the complex interrelationship between 

race, poverty and residence has been difficult to resolve (IOM, 2000). Exposure to cockroach 

allergen has been associated with almost a two-fold increased risk of wheeze in infants less 

than one year old (Belanger et al., 2003). In a recent study of southern California children, 

asthma diagnosis before five years of age was associated with exposures in the first year of life 

to cockroaches and other environmental agents (Salam et al., 2003). 

Endotoxins

Endotoxins are components of the outer membranes of Gram-negative bacterial cells. These 

bacteria occur naturally on plants and are abundant in soil and in the human intestinal tract. 

Endotoxins are released when these bacteria die or their cell membranes are damaged; thus, 

these toxins are always found in the outdoor environment. High-level exposures to airborne 

endotoxins in agricultural and waste-disposal industries contribute to acute and chronic 

bronchitis that may lead to decreased lung function (Vogelzang et al., 1998). In indoor 

environments, lower airborne endotoxin concentrations have been associated with both adverse 

health effects (increased asthma symptoms and medication use) and protective health effects 

(decreased prevalence of allergy) (IOM, 2004). Many factors appear to interact to modulate 

health effects associated with endotoxin exposure (Song et al., 2003). 

Viruses

Viruses are the smallest and simplest infectious agents, unable to survive well outside their 

plant, animal or human host. In outdoor air, viral survival depends on season, moisture content 

and temperature of the air, wind conditions, sunlight and presence of atmospheric pollutants 

(Cox, 1995). In the indoor environment, the infectivity of airborne viruses is affected by factors 

such as relative humidity and room temperature (Otten and Burge, 1999). Most viral infections 

are spread from person to person in the indoor environment. Rarely a virus such as Hantavirus 

(also known as Sin Nombre or Four Corners virus), endemic in some populations of deer mice 

in the Southwestern United States, can be transmitted to humans. Indoor air exposure to this 

virus can occur when housecleaning activities disturb dust or nests resulting in aerosolized 

mouse saliva or excreta (Mills et al., 2002). 

Damp buildings

Moisture is common in buildings, with most studies reporting signs of dampness in at least 20% 

of homes examined (IOM, 2004). Moisture problems originate from rainwater, groundwater, 

plumbing, construction, water use by occupants and condensation of water vapor. Although 

some moisture is present in all buildings, excessive dampness is more likely to occur in 
Indoor Air Pollution in California July, 2005 

 88

buildings that are older, lack central heating, are poorly insulated and overcrowded (IOM, 2004). 

The assessment of building dampness is complicated by the absence of a generally accepted 

definition of “dampness” or what constitutes a “dampness problem”. 

A recent report by the National Academy Institute of Medicine, entitled Damp Indoor Spaces 

and Health (IOM, 2004), reviewed the scientific literature regarding indoor dampness and its 

relationship to the various health outcomes that have been attributed to damp or moldy indoor 

environments. Key findings from this report are shown in Table 2.10. The report concludes that 

although many details require clarification through future research, the currently available 

scientific evidence is sufficient to regard excessive indoor dampness as a health threat to 

building occupants. 

A review of the medical literature has shown that occupants of damp buildings are twice as 

likely to experience coughing, wheezing and asthma attacks as those in dry buildings (Bornehag 

et al., 2001). The underlying causes and mechanisms of these illnesses are not completely 

understood. Some studies have associated occupant health problems with fungal or bacterial 

growth on building materials such as drywall and carpeting (Husman, 1996; Verhoeff and Burge, 

1997; Peat et al., 1998). However, building dampness is also known to increase emission of 

volatile organic compounds (VOCs) from decomposition of flooring materials, even without 

microbial growth (Pasanen et al., 1998). Damp concrete floors are known to increase the rate of 

chemical degradation of polyvinyl chloride floor coatings and glues, resulting in emissions of 

ammonia and other VOCs into the indoor air (Gustavsson and Lundgren, 1997; Wiglusz et al., 

1998; Tuomainen et al., 2004). Damp buildings also encourage the growth and allergen 

production capacity of cockroaches, house dust mites and other arthropods, as well as the 

survival of respiratory viruses. 

 

2.3.4.3 Indoor Mold 

The remainder of this section discusses indoor mold in detail, because of its apparent 

increasing occurrence at problem levels in indoor environments. 

 

Molds are simple, microscopic organisms, present virtually everywhere. Molds, along with 

mushrooms and yeasts, are fungi, which play a critical role in nature by breaking down dead 

plant and animal matter and recycling nutrients in the environment. For molds to grow and 

reproduce, they need only moisture and a food source – organic plant material, such as leaves, 

wood or paper or animal products such as leather. Because molds grow by digesting organic 

material, they gradually destroy whatever they grow on. Visible mold growth on cloth or building 

materials or furnishings, sometimes referred to as “mildew”, often has a wooly or cottony 

appearance that is frequently green, gray, brown, or black but may also be white or a range of 

other colors. Many molds that can grow indoors release countless tiny, lightweight spores that 

travel easily through the air. 

Health Effects of Mold

In recent years, media attention to indoor mold has surged, leading to rising concern about 

mold-related health effects. Because mold spores are ubiquitous in air or dust, everyone 

contacts them on a daily basis, usually without evident harm. However, persons who are allergic 

to mold and those with compromised immune systems may develop serious health problems 

from exposure to routine types and amounts of indoor mold. 
Indoor Air Pollution in California July, 2005 

 89

Table 2.10. Health Outcomes and Indoor Dampness1 

Sufficient Evidence of a Causal Relationship 

• None (the evidence was not sufficient to link dampness as a clear cause of any 

health outcome) 

Sufficient Evidence of an Association 

• Upper respiratory tract (nasal and throat) symptoms 

• Asthma symptoms in sensitized asthmatic persons 

• Wheeze 

• Cough 

Limited or Suggestive Evidence of an Association 

• Shortness of breath 

• Lower respiratory illness in otherwise healthy children 

• Asthma development 

Inadequate or Insufficient Evidence to Determine Whether an Association Exists 

• Airflow obstruction in otherwise-healthy persons 

• Skin symptoms 

• Chronic obstructive pulmonary disease 

• Mucous membrane irritation syndrome 

• Inhalation fevers (non-occupational exposures) 

• Lower respiratory illness in otherwise healthy adults 

• Rheumatologic and other immune diseases 

• Acute idiopathic pulmonary hemorrhage in infants 

• Gastrointestinal tract problems 

• Fatigue 

• Neuropsychiatric symptoms 

• Cancer 

• Reproductive effects 

1. Not applicable to immunocompromised persons, who are at increased risk for fungal infections. 

 Source: IOM, 2004 

Fungi produce a very large number of allergens, with each fungus potentially producing several 

different allergenic compounds depending on its growth pattern and environmental conditions. 

More than 80 fungal species have been associated with allergic diseases (Day and Ellis, 2001). 

Unfortunately, the limited number of standardized materials available to allergists to test patients 

for mold allergies complicates our ability to determine the frequency of mold allergy in U.S. or 

California populations. Humans are known to potentially encounter approximately 200 different 

species of fungi outdoors and perhaps 50 species indoors. Typical symptoms that mold-allergic 

persons report (alone or in combination) include: respiratory problems, such as wheezing, 

difficulty breathing and shortness of breath; nasal and sinus congestion; eye irritation (burning, 

watery or reddened eyes); dry, hacking cough; nose or throat irritation; and skin rashes. In rare 
Indoor Air Pollution in California July, 2005 

 90

instances exposures to fungi may illicit more intense immunological responses such as allergic 

bronchopulmonary aspergillosis and allergic fungal sinusitis. These conditions involve fungal 

colonization of the airways or sinuses (Storey et al., 2004). 

Serious lung infections from a few fungal groups such as Aspergillus and Fusarium species are 

common in persons being treated with high-dose cancer chemotherapy, recent solid-organ 

transplant recipients or those who are otherwise immunocompromised (Summerbell, 2001). 

Children in damp or moldy buildings sometimes report having more respiratory infections, 

including colds and ear infections (Rylander and Megevand, 2000). Some investigators have 

suggested that this increase is due to an immunosuppressive effect of exposure to indoor fungal 

growth (Johanning et al., 1996). While some fungi have been shown to cause immune 

suppression in experiments with laboratory animals, it is not yet clear if damp or moldy building 

exposures can cause significant changes in the human immune system. 

Organic dust toxic syndrome is a general term used in reference to illnesses related to 

inhalation of bacterial endotoxins or fungal toxins, typically resulting from occupational 

exposures to bioaerosols. The symptoms are similar to those of hypersensitivity pneumonitis 

(Storey et al., 2004). One other possible health outcome from exposure to mycotoxins is 

pulmonary hemorrhage (Storey et al., 2004). 

In studies of health effects associated with indoor fungal exposure, some people without 

allergies report respiratory and other symptoms similar to those experienced by mold-allergic 

individuals. In addition, occupants of moldy buildings have reported some health outcomes that 

are not usually associated with allergy (such as memory loss, depression, fatigue, mood swings, 

and “hemorrhage in the mucous membranes of the intestinal and respiratory tracts”) (IOM, 

2004). Investigators are exploring whether these effects are associated with exposure to one or 

more fungal constituents such as: 

• Fungal toxins – chemicals known to be produced under certain fungal growth conditions by 

more than 400 fungal species and capable of producing a toxic response in animals or other 

microbes. 

• Some structural components of fungi – for example, glucans (chemicals that make up all 

fungal cell walls) may affect the activity of immune cells in the lung. 

• Microbial volatile organic compounds – gaseous substances that account for the odors 

identified when mold is growing indoors. While often associated with respiratory symptoms 

in damp buildings, the specific contribution of these compounds to health complaints is still 

unclear. 

Key findings regarding indoor mold growth and health outcomes from the National Academy 

Institute of Medicine report, Damp Indoor Spaces and Health (IOM, 2004), are summarized in 

Table 2.11. The report concludes that although more research is needed to define the role of 

molds, mycotoxins and other fungal components, as well as the potential for synergistic 

interaction between molds and other microbial or chemical agents in damp buildings, the 

currently available scientific evidence is sufficient to conclude that indoor mold is associated 

with upper respiratory symptoms, cough, wheeze, asthma symptoms in sensitized asthmatic 

individuals and, rarely, hypersensitivity pneumonitis in susceptible persons. 
Indoor Air Pollution in California July, 2005 

 91

Table 2.11. Presence of Indoor Mold and Health Outcomes1 

Sufficient Evidence of Causal Relationship 

• None (the evidence was not sufficient to link mold as a clear cause of any health 

outcome) 

Sufficient Evidence of an Association 

• Upper respiratory tract (nasal and throat) symptoms 

• Asthma symptoms in sensitized asthmatic persons 

• Wheeze 

• Cough 

• Hypersensitivity pneumonitis (a rare immune-mediated lung condition) in 

susceptible persons2

Limited or Suggestive Evidence of an Association 

• Lower respiratory illness in otherwise healthy children 

Inadequate or Insufficient Evidence to Determine Whether an Association Exists 

• Shortness of breath 

• Airflow obstruction in otherwise healthy persons 

• Skin symptoms 

• Asthma development 

• Chronic obstructive pulmonary disease 

• Mucous membrane irritation syndrome 

• Inhalation fevers (non-occupational exposures) 

• Lower respiratory illness in otherwise healthy adults 

• Rheumatologic and other immune diseases 

• Acute idiopathic pulmonary hemorrhage in infants 

• Gastrointestinal tract problems 

• Fatigue 

• Neuropsychiatric symptoms 

• Cancer 

• Reproductive effects 

1. Not applicable to immunocompromised persons, who are at increased risk for fungal infections. 

2. For mold or bacteria in damp indoor environments. 

Source: IOM, 2004 

Mold Concentrations

It is common in indoor air quality investigations to find mold spores in the air and dust inside 

homes, with most of these originating outdoors. Many studies have tried to differentiate 

buildings with problem mold growth from non-moldy buildings by evaluating the type and 

concentration of indoor airborne fungal spores. The concentrations and types of mold spores in 

indoor air typically are directly related to those in outdoor air. If there is a serious mold problem 

in a building, the indoor types and concentrations of mold may, or may not, differ from those 
Indoor Air Pollution in California July, 2005 

 92

outdoors at the time of sampling. Numerous studies have found that spore concentrations vary 

widely in both outdoor and indoor air. Outdoor concentrations vary with geographical location, 

climate, season, relative humidity, wind direction and types of vegetation in the immediate area 

of the sampling device (IOM, 2004). Outdoor airborne mold spore concentrations may reach 

levels as high as 10,000 spores/m3 (Mullins, 2001). Indoor mold spore concentrations are 

usually lower than corresponding outdoor levels, but are also quite variable, ranging from 0-

10,000 colony forming units/m3

 (Shelton et al., 2002). 

Different types of molds are identified and their concentrations measured either by directly 

examining a sample under a microscope or by culturing the spores and allowing them to grow 

into colonies that are then counted. There are many reliable methods for collecting and 

analyzing fungi although no single method can identify all the fungi present in environmental 

samples (AIHA, 1996; ACGIH, 1999). Thus, different sample collection and analysis techniques 

often lead to different fungal count or concentration estimates. No standard method of mold 

identification or spore counting has been proven effective in a wide range of building 

applications or is mandated for environmental assessment by any federal or California state 

government agency. 

In a recent review of studies aimed at identifying buildings with mold problems, an expert panel 

of the Institute of Medicine concluded “...fungal counts alone provide little information about the 

microbial status of an indoor environment” (IOM, 2004). Currently, government and professional 

industry groups recommend that building investigations for mold include a thorough visual 

inspection of the premises, documentation of visibly moldy areas, and the use of professional 

judgment in determining whether mold sampling is appropriate for that particular investigation 

(U.S. EPA, 2001b; AIHA, 1996; ACGIH, 1999; Miller, 2001). 

2.3.5 Pesticides 

Pesticides can be naturally occurring or synthetic chemicals designed to control and kill insects, 

weeds, and disease carrying organisms in the home and surrounding landscaping. Ninety 

percent of American homes use pesticides (Gurunathan et al., 1998). Schools apply pesticides 

in or around the classroom (Addiss et al., 1999; Kaplan et al., 1998; Volberg et al., 1993; 

Whitmore et al., 2003). Pesticides can be tracked in on clothing or drift in from outdoors, later 

becoming resuspended in air and accumulating in dust. 

2.3.5.1 Health Effects of Pesticides 

Pesticides differ in their levels of toxicity and mechanisms of action. Some classes of 

insecticides are highly toxic, especially to the nervous system. Pesticides with relatively low 

acute toxicity are not necessarily safe, as they may have the potential to cause cancer or other 

chronic effects. Other health effects of pesticide exposure include irritation of the skin and eyes, 

and hormone or endocrine disruption. 

Two classes of widely used insecticides in the U.S. are the organophosphates and pyrethroids; 

both are neurotoxins. Pesticide workers have experienced nausea, headaches, dizziness, and 

general weakness after exposure to agricultural organophosphates. Typical indoor air 

concentrations of organophosphates previously approved for home use (i.e., chlorpyrifos and 

diazinon) generally do not result in these symptoms. In most, but not all cases, pyrethroids are 

less toxic than organophosphates. Their neurotoxic effects have not been reported for humans 

exposed to typical levels in the home. Pesticides are often measurable in house dust and carpet 

dust; levels of contamination are discussed later in this section. The effects of pesticides on 
Indoor Air Pollution in California July, 2005 

 93

children are a particular concern because their behavior can lead to greater exposure than to an 

adult. Children spend time on the floor where they contact dust that may contain pesticides. The 

hand-to-mouth behavior of young children may lead to ingesting pesticides. Furthermore, some 

studies, but not all, have shown that low-level chronic exposure to organophosphates can 

adversely affect children’s developing nervous systems (Eskenazi et al., 1999), and chronic 

exposure to pyrethroids has been linked to possible hormonal disruption (Landrigan et al., 

1999). There is insufficient evidence to determine if pesticides cause or exacerbate asthma 

(IOM, 2000). 

2.3.5.2 Sources of Pesticides 

Chlorpyrifos and diazinon, two organophosphate insecticides, previously were the most widely 

used pesticide ingredients in common household ant and roach killers and lawn-care sprays 

(U.S. EPA, 2001a; U.S. EPA, 2000d). The U.S. EPA banned the indoor use of chlorpyrifos and 

diazinon for non-agricultural settings in December 2000 and March 2001, respectively (U.S. 

EPA, 2001a; U.S. EPA, 2000d). Chlorpyrifos is persistent in some indoor environments: it has 

been observed in many indoor house dust samples since it was banned. 

Since the ban on indoor use of chlorpyrifos, a class of insecticides called pyrethroids has been 

used as substitutes for chlorpyrifos and other organophosphate pesticides. Permethrin, the most 

common pyrethroid, acts on a broad spectrum of insects, and is less persistent than chlorpyrifos 

in dust and soils. Esfenvalerate is another commonly used pyrethroid. Disinfectants and 

antimicrobials are other commonly used pesticides. 

Pesticides that are persistent in the environment and have been banned for some time include, 

DDT, and Dieldrin. DDE is a breakdown product of DDT, a widely used insecticide that was 

banned in 1972 (U.S. EPA, 2000f). Environmental sources of DDE include soil, atmospheric 

dispersion, sediment runoff, contaminated plants and animals, and improper use and disposal. 

Dieldrin was widely used from 1950 to 1974 to control insects on cotton, corn and citrus crops 

(U.S. EPA, 2000g). Also, dieldrin was used to preserve wood, control termites, and control 

locusts and mosquitoes. Most uses of dieldrin were banned in 1987. Environmental sources of 

dieldrin include soil surrounding wooden structures treated for termites; soil or sediment; 

improper use or disposal; contaminated fish and shellfish; and contaminated dairy products and 

meat. 

2.3.5.3 Pesticide Concentrations 

To date, there is little published data on indoor pesticide concentrations in California homes; 

however, several studies are currently underway. In September 1992, Bradman et al. (1997) 

measured pesticide levels in house dust samples from five farmworker homes and five nonfarmworker homes in an agricultural area south of Fresno. This study was conducted before the 

ban on indoor use of chlorpyrifos and diazinon. However, it cannot be determined if the indoor 

levels were from infiltration of outdoor air and soil track-in, or from the use of indoor pesticide. 

Of the ten pesticides detected in house dust, only chlorpyrifos and diazinon levels frequently 

exceeded 1 μg/g of dust in the homes. In general, farmworker homes had higher levels of 

chlorpyrifos and diazinon than non-farmworker homes. The highest detectable level of pesticide 

in non-farmworker homes was 2.5 μg/g of diazinon, and the highest in farmworker homes was 

169 μg/g of diazinon. 

In an ongoing California study, researchers found pesticides more frequently in house dust than 

other measured media. Diazinon, chlorpyrifos, dacthal, and cis- and trans-permethrin were 
Indoor Air Pollution in California July, 2005 

 94

detected in 95 – 100% of residential dust samples in an agricultural community (Bradman et al., 

2004). These results are part of a larger effort, a five year study of pregnant women and their 

children, called the CHAMACOS study (Center for the Health Assessment of Mothers and their 

Children of Salinas). Results indicate that pregnant women in this study have six dialkyl 

phosphate metabolites present in their urine. The 90th percentile levels are significantly higher 

than U.S. national reference data for 5 of the 6 metabolites (Bradman et al., 2002a). Forty-four 

percent of participants report the use of home pesticides, in part due to poor housing quality 

(Bradman et al., 2002b). In another current study, investigators are merging agricultural 

pesticide use reports with geographic information systems (GIS) to map annual 

organophosphate pesticide use density in the Salinas Valley, in an effort to better assess the 

association between pesticides in household dust and agricultural pesticide use. Mapped 

information will be compared to concentrations of eight pesticides measured in household dust 

(Harnly et al., 2004). Research is also underway to estimate the non-dietary exposure of young 

farm-worker children aged 6 to 26 months. An exposure model utilizes videotaped activity 

patterns and residential samples including air samples, surface wipes, and house dust samples 

to estimate inhalation, dermal, and non-dietary pesticide exposure of children. Modeled 

estimates will be compared to clothing dosimeters and urine samples (Beamer et al., 2004). 

During 2001-2002 (after the ban on indoor use of chlorpyrifos and diazinon), ARB and DHS 

funded a comprehensive statewide study of the environmental health conditions in portable 

(relocatable) and traditional classrooms. As part of the study, investigators summarized floordust pesticide concentration data for twenty different pesticides. Chlorpyrifos, cis- and transpermethrin, ortho-phenylphenol, piperonyl butoxide (PBO), and esfenvalerate were detected in 

over 80% of the classrooms. Excluding ortho-phenylphenol, these pesticides measured 95th

percentiles above 1 μg/g. Portable classrooms did not differ significantly from traditional 

classrooms in their mean pesticide concentrations (Whitmore et al., 2003). 

The pesticides detected in California and their concentrations are similar to those found in other 

studies in other areas of the U.S. A summary of the results from indoor and personal air 

concentrations and house dust levels across recent U. S. studies is presented in Table 2.12. 

The non-California studies are briefly discussed below. 

The Non-Occupational Pesticide Exposure Study (NOPES) examined inhalation exposures for 

32 different pesticides in 208 residences in Jacksonville, Florida, and 101 residences in 

Springfield/Chicopee, Massachusetts, over three different seasons from 1986 to 1988 

(Whitmore et al., 1994). Seven pesticides – chlordane, chlorpyrifos, diazinon, dichlorvos, 

heptachlor, ortho-phenylphenol, and propoxur – had the highest mean concentrations across 

seasons in Jacksonville for both indoor and personal air. Mean concentrations of all detectable 

pesticides captured in carpet ranged from 0.01 μg/g to 15.4 μg/g. The mean concentrations for 

chlorpyrifos and diazinon found captured in the carpet were 5.8 μg/g and 1.7 μg/g, respectively. 

During the 1992 spray season, Simcox et al. (1995) vacuum-sampled house dust for four 

organophosphorus (OP) insecticides, including chlorpyrifos, in 59 homes in Wenatchee, 

Washington (48 agricultural, 11 non-farming families). All four compounds were detected in 62% 

of households. Pesticide levels were significantly lower in non-farming homes than in 

agricultural homes (Table 2.12). OP levels ranged from non-detectable to 17 μg/g in agricultural 

homes and non-detectable to 0.82 μg/g in non-farming homes. Two-thirds of the agricultural 

homes contained pesticide levels above 1 μg/g for at least one OP compound. 
Indoor Air Pollution in California July, 2005 

 95

Table 2.12. Comparison of Indoor-air, Personal-air, and House-dust Levels in U.S.

Location Season Ranges and median and mean values 

 Chlorpyrifos Diazinon 

 Range Median Mean Range Median Mean

Indoor air Concentration (ng/m3) 

Minneapolis, MNa All NLb 1.742 NL NL 0.29 NL 

NHEXAS Arizonac All <3.2-3280 8 NL <2.1-20,500 4.6 NL 

Brownsville, TXd Spring 2.5-115 7.6 NL 1.6-60 1.4 NL 

 Summer 5.7-67 24 NL 2.5-78 3.5 NL 

Jacksonville, FLe Summer <2.5-2170 182 366.6 15-13,700 73 420.7 

 Spring NL NL 205.4 NL NL 109.2 

 Winter <2.5-1043 69 120.3 30-1080 21 85.7 

Springfield, MAe Spring <4.5-252 <4.5 9.8 <22-1810 <22 48.4 

 Winter <3.5-291 <3.5 5.1 <28-28 <28 2.5 

Raleigh, NCf Fall NL NL 0.08 NAg NA NA 

New Jersey areah Fall 151.2-154.2 NL NL 5.7 NL NL 

Cape Cod, MAi All <1-92 <1 NL <1-550 <1 NL 

Personal air Concentration (ng/m3) 

Minneapolis, MNa All NL 1.577 NL NL 0.275 NL 

NHEXAS Arizonac All <19-175 NL NL <15 NL NL 

Jacksonville, FLe Summer NL NL 280.4 NL NL 321.6 

 Spring NL NL 182.8 NL NL 112.7 

 Winter NL NL 118.2 NL NL 89 

Springfield, MAe Spring NL NL 7.5 NL NL 10.1 

 Winter NL NL 5.9 NL NL 1.4 

House dust Concentration (μg/g) 

Fresno, CAj Fallk 0.2-33 NL NL 0.7-169 NL NL 

 Falll <1 NL NL 0.2-2.5 NL NL 

NHEXAS Arizonac All <0.004-119 0.16 NL <0.020-66 0.13 NL 

Brownsville, TXd Spring 0.1-1.7 0.3 NL 0.1-1.8 0.06 NL 

 Summer 0.2-1.7 0.56 NL 0.1-0.8 0.07 NL 

Wenatchee, WAm Springk <0.02-3.6 0.27 0.43 NA NA NA 

 Springl <0.02-0.5 0.05 0.17 NA NA NA 

Jacksonville, FLe Winter NL 4.7 5.8 NL 0.4 1.7 

Raleigh, NCf Fall NA NA 1.6 NA NA NA 

New Jersey areah Fall 0.53-15 NL NL 0.08-0.74 NL NL 

PCSn All NL 0.308 0.607 NL 0.035 0.358 

Cape Cod, MAi All <0.2-228 <0.2 NL <0.2-51.0 <0.2 NL 

Source: Modified from Gordon et al., 1999. a

Clayton et al. , 2003. 

b

NL, not listed. 

c

Gordon et al. , 1999. 

d

Mukerjee et al. , 1997b. 

e

Whitmore et al. , 1994. 

f

Lewis et al. , 1994. 

g

NA, not applicable. 

h

Roinestad et al. , 1993. 

i

Rudel et al. , 2003. 

j

Bradman et al., 1997. 

k

Samples from agricultural family homes. 

l

Samples from non-agricultural family homes. 

mSimcox et al., 1995.

n

Whitmore et al., 2003. 
Indoor Air Pollution in California July, 2005 

 96

During May to September 1997, the Minnesota Children’s Pesticide Exposure Study (MNCPES) 

characterized indoor and personal air levels for children 3 to 12 years old in 102 homes in 

Minneapolis/St. Paul, Minnesota (Clayton et al., 2003). Although the median values for indoor 

air were slightly higher than personal air (Table 2.12), there was a highly significant correlation 

between personal air and indoor air samples for the organophosphates chlorpyrifos (0.81), 

malathion (0.51), and diazinon (0.62). Air levels for chlorpyrifos and diazinon were measurable 

for >90% and >65% of the participants, respectively. Permethrin was also detectable in air with 

a median concentration of <0.2 ng/m3

. 

In the National Human Exposure Assessment Survey (NHEXAS) performed in Arizona, Gordon 

et al. (1999) measured residential levels of chlorpyrifos and diazinon. Chlorpyrifos was found in 

dust more often than diazinon (88% vs. 53%), and had nearly the same occurrence in indoor air 

as diazinon (65% vs. 63%). There was a small association between chlorpyrifos in dust and air 

(Pearson = 0.096, Spearman = 0.773). Although the NHEXAS results are generally comparable 

to those from other studies, Gordon et al. (1999) found a higher maximum level for pesticides in 

residential samples than previously reported. 

In a recent study, Rudel et al. (2003) analyzed 39 air and 38 dust samples (collected by vacuum 

cleaner) for pesticides in 120 homes in Cape Cod, Massachusetts. Of the 23 pesticides 

detected in air and 27 detected in dust, chlorpyrifos was one of the most abundant with 90th

percentile concentrations of 12 ng/m3

 in air and 1.87 μg/g in dust. Although not as pervasive in 

dust, diazinon had one of the highest 90th percentile concentrations in air (9.0 ng/m3

). Cis- and 

trans-permethrin and PBO were also detected at relatively high levels in dust (7.04 μg/g, 16.5 

μg/g, and 15.1 μg/g, respectively). 

2.3.5.4 Safety and Other Considerations 

Pesticides can have very serious effects when used improperly, so a number of safety issues 

are associated with pesticides. The California Department of Pesticide Regulation (DPR) has 

documented infrequent, but severe, injuries and deaths due to improper use of pesticides. DPR 

maintains a Pesticide Illness Surveillance Program, which shows that, in 2002 (the most recent 

year data are available), there were over 1,000 doctor-reported illnesses associated with 

occupational and non-occupational exposure to pesticides. The use of too many pesticide 

foggers indoors at once has caused fires and explosions, because foggers typically contain 

flammable chemicals as propellants (Segawa, 2004). Also, homes undergoing fumigation have 

occasionally been broken into with serious results, although the home is locked and posted with 

warnings. 

An additional concern is the persistence of pesticides in indoor environments. Although some 

newer pesticides do not last as long as older ones, they nonetheless persist for some time, and 

persist longer indoors. A number of investigators have found pesticide residues indoors from 

prior outdoor applications, even when the outdoor levels have decreased to lower or nondetectable amounts (Lewis et al., 1994; Lewis, 2001; Lewis 2005; Whitmore et al., 1994; Simcox 

et al., 1995; Pang et al., 2002; Colt et al., 2004). This greater indoor persistence is likely due to 

the lack of weathering (rain, sun), reduced temperature extremes in indoor locations, and 

reduced microbial action (Lewis, 2001; Lewis, 2005). Also, as mentioned above, some 

breakdown products of pesticides banned years ago continue to be measured in indoor dust 

samples. 
Indoor Air Pollution in California July, 2005 

 97

2.3.6 Lead 

Lead is a toxic metal that has been used in paints, gasoline, pipes, and ceramic glazes, and to a 

lesser extent, in caulk. Lead paint chips and soil contaminated with lead pose a major hazard to 

children due to the likelihood of exposure by ingestion. Over the long term, exposure to lead can 

cause brain damage, decreased growth, hyperactivity, impaired hearing, and reproductive 

effects. 

2.3.6.1 Health Effects of Lead 

The body mistakes lead for calcium and concentrates it in the bones, where it can leach into the 

blood. Both pre-natal and post-natal exposure, and exposure during childhood results in toxicity 

to the nervous system (Thacker et al., 1992; Needleman et al., 1979). Children, especially those 

younger than five, are more susceptible to lead than adults. Chronic, low-dose exposure to lead, 

often occurring in early childhood, can lead to decreased learning ability due to brain damage. 

Acute health effects, seldom seen, include seizures, paralysis, anemia, abdominal pain, 

constipation, vomiting, and decreased appetite. Other health effects associated with chronic 

exposure to lead, such as that in adults exposed in occupational situations, may include 

increased blood pressure, impaired neurological function, anemia, kidney damage, colic, and 

male and female reproductive problems (ARB/OEHHA, 1996; ATSDR 1999a). 

Lead not only concentrates in bones–it also accumulates in the liver and kidneys. Lead has a 

half-life of 25 to 40 days in the blood and organs, and a half-life of 25 years in the bones. During 

pregnancy, lead mobilized from the bones and released into the bloodstream can pass through 

the umbilical cord and adversely affect the developing fetus. The blood lead level of concern for 

children, established by the U.S. Centers for Disease Control and Prevention in 1991, is 10 

μg/dL (CDC, 1997). Significant decreases in IQ, behavioral problems, and learning impairment 

have been documented at blood-lead levels above this threshold. Recent research showing 

health effects at levels below 10 μg/dL now supports the growing consensus that there is no 

safe level for lead exposure. 

2.3.6.2 Sources of Lead 

In the U.S., lead was eliminated from paints and gasoline in the late 1970s. Today, major 

sources of lead include old paint in homes built before 1978, lead pipes placed before the 

1930s, lead solder in copper piping installed up to 1986, and soil by busy roads. Activities that 

disturb lead-based paint, such as remodeling or paint removal, can release large amounts of 

lead-bearing particles into the air, which may later settle in dust or nearby soil. Even without 

remodeling, deteriorating lead paint can accumulate in house dust and soil Often overlooked 

sources of lead include home remedies, cosmetics, hobby materials, and foreign-made, vinyl 

mini-blinds (ATSDR, 1999a; CPSC, 1996). 

Next to resuspension of lead dust from lead-based paint, much of the lead present in indoor air 

appears to result from the infiltration of lead particles in outdoor air. Infiltrated and tracked-in 

lead dust, brought into the home from the workplace, can accumulate in carpets that can serve 

as a reservoir for lead-laden dust (U.S. EPA, 1997a). Research has shown that lead-dust 

loadings and concentrations per unit mass of dust are correlated with blood-lead levels, but no 

causal effect can be inferred from this association. Children’s mouthing behaviors and activities 

that put them in direct contact with lead-contaminated surfaces increase their probability for 

exposure to lead by ingestion. 
Indoor Air Pollution in California July, 2005 

 98

Candles containing a lead/metal core in the wick can emit lead into the air when burned. Van 

Alphen (1999) calculated the mean rate of lead release from seven candles was 770 μg/hour. In 

homes where candles are burnt once per week for several hours, lead air levels would be 

sufficient to drive the child’s blood lead levels over the CDC level of concern of 10 μg/dl. 

2.3.6.3 Lead Concentrations 

The DHS surveyed 933 older homes in Oakland, Wilmington/Compton, and Sacramento, 

California in 1987-1990 for lead concentrations in the blood of children between the ages of 12 

and 59 months (Haan et al., 1992; Sutton et al., 1995). They also measured lead concentrations 

in house paint, house dust, and soil. Blood levels of lead were greater than or equal to the 

current CDC guidelines (10 μg/dL) in 67% of the children in Oakland, 32% of those children in 

Wilmington/Compton, and 14% of those children in Sacramento. Lead concentrations in house 

dust ranged from 5 to over 9500 ppm (μg/g); median concentrations were 133 ppm in 

Wilmington/Compton and 180 ppm in Sacramento (Sutton et al., 1998). The survey estimated 

that 3 million homes in California have exterior paint levels at or above 5,000 ppm lead, the 

federal criteria for lead remediation procedures; and that 1.3 million homes have interior paint 

levels at or above 5,000 ppm lead. 

The U.S. EPA (1997a) summarized findings from a literature review on the amount of lead in 

dust within carpets, furniture, and forced air ducts. A major drawback across studies was the 

inconsistency in the methods used to collect and analyze lead. In general, the average loadings 

are lower for furniture than for floors, window components, walls, and air ducts. Furniture, 

including upholstery and window treatments, has an average loading of less than 100 μg/ft2

. 

The average loadings for forced air ducts exceed 100 μg/ft2

, and can be as high as 1,000,000 

μg/ft2

. 

Dust lead levels at schools are an important factor when determining children’s total exposure to 

lead. In a recent comprehensive study of the environmental health conditions in California 

portable (relocatable) and traditional classrooms, ARB and DHS summarized lead levels in 

floor-dust of over 200 classrooms (Whitmore et al., 2003). The median concentration and dust 

loading for lead were lower in portable classrooms than traditional classrooms, though the 

differences were not statistically significant. As stated in the report:, “Since the portable 

classrooms are generally newer, the lower concentration of lead may reflect the number of 

years’ accumulation of the particles in the classroom.” Table 2.13 reports the median and 95th

percentile concentrations for lead in the floor dust of all classrooms sampled. 

Table 2.13. California Portable Classrooms Study Results for Lead in Floor Dust 

Concentrations (μg/g) Loadings (ng/cm2 Element Room Type ) 

Median 95th Percentile Median 95th Percentile 

All 61.6 189.5 6.6 58.4 

Portable 57.5 151.6 5.8 57.9 

Lead 

Traditional 66.8 200.6 7.1 57.5 

Between 1994 and 1998, DHS surveyed the lead content in paint and soil for a random sample 

of 200 California public elementary schools and child care facilities (DHS, 1998). Results were 

used to make predictions about the lead content in all of California’s 5,000 schools. The study 

found: “As in California's housing, lead-containing paint is estimated to be in most California 
Indoor Air Pollution in California July, 2005 

 99

public elementary schools and child care facilities.” DHS estimated that one-third of schools 

contain deteriorating lead paint, and nearly 6% have soil that is contaminated with lead 

exceeding U.S. EPA Lead in Soil Guidelines. The highest levels of lead in soil were found close 

to school buildings and near buildings built prior to 1940. 

2.3.7 Mercury 

There are three types of mercury: elemental (or metallic), inorganic (or mercury salts), and 

organic. In the past, inorganic mercury was added to skin-lightening creams and medicinal 

products. Today, compounds containing inorganic mercury are used as fungicides and 

antibacterials (ATSDR, 1999b). Metallic mercury can be found in thermometers, electric 

switches, fluorescent lights, thermostats, and other products. The primary source of organic 

mercury, specifically methylmercury, is fish and other types of seafood. 

2.3.7.1 Health Effects of Mercury 

Workers exposed to mercury levels ranging from 25 to 60 μg/m3

 have experienced tremors, 

changes in personality, loss of sensation and muscle coordination, vision and hearing 

impairments, deficits in cognitive function, respiratory tract irritation, severe stomach comfort, 

skin rashes, and elevations in blood pressure and heart rate (OEHHA, 2000c). In combination 

with data from other published research, Carpi and Chen (2001) estimated that 10% of U.S. 

homes may have indoor mercury levels that exceed the U.S. EPA Reference Concentration of 

0.3 μg/m3

. Exceeding the U.S. EPA Reference Concentration may increase the likelihood of 

health impacts, but it might take years for the effects to be seen and they may not occur at all. 

Typical mercury exposures in indoor environments are not likely to produce developmental 

neurotoxicity. 

2.3.7.2 Sources of Mercury 

Indoor air is the second most common route of exposure to mercury in the general U.S. 

population (fish consumption is first) (NJ Mercury Task Force, 2002; Carpi and Chen, 2001; 

WHO, 1990). Mercury is an effective fungicide and bactericide, so it has been used as an 

intentional additive in many household products, including latex paints (interior use banned in 

1990), contact lens solutions, and nasal sprays (ATSDR, 1999b). Mercury may also be found as 

an accidental contaminant in detergents and cleansers due to its extensive use in the chloralkali industry (U.S. EPA, 1999b). Elemental mercury’s unique physical and chemical properties 

are the basis for its use in many household items. It expands uniformly with increases in 

temperature, does not cling to glass, and is liquid and can vaporize at room temperature. 

Mercury workers are exposed to greater levels of elemental mercury than the general 

population. Workers’ families are also at increased risk; workers may bring home clothing and 

shoes contaminated with mercury in the workplace (ATSDR, 1999b). Elemental mercury is also 

used in some cultural practices, either carried as a good luck charm, or sprinkled in cars and 

homes or over infants (ATSDR, 1999b). With the removal of mercury in paint and the ban on the 

sale of mercury thermometers in California (SB633, 2002), exposures to mercury in indoor air in 

California should decrease over time. Table 2.14 lists the sources of mercury in homes. 

2.3.7.3 Mercury Concentrations 

There is limited information on airborne exposures in the non-occupational environment. From 

June 2000 through March 2001, Carpi and Chen (2001) measured mercury concentrations in 

indoor air for nine residences and three businesses in the New York metropolitan area. Nearly 
Indoor Air Pollution in California July, 2005 

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all of the sites showed higher indoor levels than outdoor levels. The average indoor mercury 

concentration for all buildings was 69 ng/m3

, and was highly dependent on season. 

Table 2.14. Sources of Mercury in the Residential Environment 

Type of Mercury Sources 

Metallic Thermometers, electric switches, fluorescent lights, 

thermostats, barometers, batteries, ethnic remedies, 

spiritual practices 

Inorganic and organic Latex paints, medicines, disinfectants, detergents, 

antiseptics 

Mercury is found in many household items, but unless the mercury-containing device is broken 

or disturbed, mercury does not pollute the air. Once released, however, mercury persists in the 

indoor environment for months or years after its first release, especially if the spill is not properly 

cleaned (ATSDR, 1999b). According to the New Jersey Mercury Task Force (2002): “Exposure 

to Hg0

 (such as in certain cultural practices) can be significant with respect to health effects. As 

little as one drop (0.05 ml) of liquid Hg0

 in a sealed bedroom-sized room (assuming a room 

volume of about 33 m3

 and no air exchange) can result in an air concentration equal to the U.S. 

EPA Reference Concentration.” 

Several nationwide incidences of non-occupational exposure to mercury have been 

documented. The Ohio Department of Health, in cooperation with the federal ATSDR, analyzed 

the indoor mercury concentrations in nine school gymnasiums (ATSDR, 2002a). The highest 

detectable level of mercury in indoor air was 1.6 μg/m3

. A Morbidity and Mortality Weekly Report

summarized findings from the contamination of homes and schools with Hg0

 in Palm Beach 

County, Florida (CDC, 1995). The report illustrated how quickly mercury can spread and how 

difficult it is to contain. The local authorities evacuated 50 homes, and closed schools until 

mercury levels dropped below 10 μg/m3

. Seventeen homes contained vapor concentrations 

greater than 15 μg/m3

. Table 2.15 shows the guideline levels for mercury. 

Table 2.15. Recommended Airborne Concentrations of Mercury 

Values Mercury Vapor 

ATSDR Minimum Risk Level (MRL) 0.2 μg/m3

ATSDR recommended screening level 1 μg/m3

ATSDR action level 10 μg/m3

U.S. EPA reference concentration (RfC) 0.3 μg/m3

2.3.8 Polycyclic Aromatic Hydrocarbons 

Polycyclic aromatic hydrocarbons (PAHs) are a complex class of semi-volatile organic 

compounds and consist of two or more fused benzene rings. The larger PAH species are 

associated with fine or ultrafine particles; humans become exposed to a complex mixture of 

PAHs, not individual compounds (IARC, 1983; U.S. EPA, 1987c; Atkinson and Arey, 1989). 

Benzo(a)pyrene, a PAH with five fused benzene rings, is often considered to be the 

representative compound for PAHs (U.S. EPA, 1987c; IARC, 1983). PAHs are produced from 

incomplete combustion; indoor sources are primarily tobacco smoking, aerosols from hot 

cooking oil, woodburning, and infiltration of outdoor air. 
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2.3.8.1 Health Effects of PAHs 

Several individual PAHs are believed to be carcinogenic to humans. The U.S. Environmental 

Protection Agency (U.S. EPA) classifies benzo(a)pyrene as a possible human carcinogen; the 

International Agency for Research on Cancer (IARC) classifies benzo(a)pyrene as a probable 

human carcinogen (IARC, 1983; U.S. EPA, 1984). Other PAHs characterized by either IARC or 

U.S. EPA as possible human carcinogens include: chrysene, certain benzofluoranthenes, and 

indeno(1,2,3-cd)pyrene (IARC, 1983; U.S. EPA, 1984, ARB/OEHHA, 1994; ARB, 1994a). For 

most of the PAH species, there is currently insufficient evidence to classify these compounds as 

to their carcinogenicity. 

2.3.8.2 Sources of PAHs 

Tobacco smoking, when present, was identified as the strongest indoor source of 

benzo(a)pyrene and other PAHs indoors in a study conducted in California (Sheldon et al., 

1993; Sheldon et al., 1992b). Investigators have measured as many as 56 PAH species and 

derivatives in tobacco smoke; hundreds more may exist (Vu-Duc and Huynh, 1989; Wynder and 

Hoffman, 1964). 

Cooking activities were found to be a major contributor to PAH concentrations, along with 

infiltration of traffic-polluted outdoor air, in a small study conducted by Dubowski et al. (1999). 

These investigators also determined that candle- and incense-burning contribute to indoor 

levels of PAHs. Siegman and Sattler (1996) determined that PAH concentrations in the fumes 

from hot cooking oil ranged from 1.08 to 22.8 μg/m3

, compared to PAH concentrations found in 

a road tunnel with heavy traffic (2.6 μg/m3

) and an office with heavy cigarette smoking (1.2 

μg/m3

). However, they caution that the oil droplets may not have the same carcinogenic 

potential as PAH from combustion aerosols. 

Woodburning appliances contribute to indoor PAH levels. Fireplaces can emit soot and PAHs 

directly into the indoor air environment (Traynor et al., 1987). While newer, more efficient airtight 

stoves appear to emit less than older, leakier woodstove models, poor maintenance and certain 

practices, such as operating the woodstove with the door open, can raise indoor air PAH and 

PM levels substantially (Traynor et al., 1987; Nabinger et al., 1995; Anuszewski et al., 1998)). 

Transport of outdoor air into the home can introduce PAHs from outdoor sources such as traffic, 

diesel engines, power plants and agricultural burning (IARC, 1983; U.S. EPA, 1987c; Dubowski, 

1999). 

2.3.8.3 PAH Concentrations 

The Air Resources Board funded two large studies to characterize indoor exposures to PAHs in 

California residences. In a northern California study, investigators measured PAHs inside 280 

homes during the winter of 1992, evaluating the relationship between PAH levels and common 

indoor combustion sources (Sheldon et al., 1993). Investigators reported average 

concentrations of 2.2 ng/m3

 of benzo(a)pyrene in smoker’s homes, but only 0.83 ng/m3 in 

nonsmoker’s homes. Investigators reported that cigarette smoking significantly raised levels of 

12 of 13 PAH species when compared to levels in nonsmokers’ homes. 

In the same study, fireplace and woodstove use raised average benzo(a)pyrene levels to about 

twice the levels found in homes with no obvious combustion sources. Researchers reported 

average benzo(a)pyrene concentrations of 1.2 ng/m3

 compared to 0.83 ng/m3 measured in “no 
Indoor Air Pollution in California July, 2005 

 102

source” homes. The benzo(a)pyrene level of 0.83 ng/m3

 was primarily attributed to infiltration of 

smoke from community woodburning, a value well above the typical average outdoor levels in 

California (Atkinson and Arey, 1989). 

The second ARB-funded study was conducted in Southern California homes. In this study, 

Sheldon et al. (1992b) found polluted outdoor air to be a major source of indoor PAHs when 

other combustion sources were absent in the home. Other investigators have reported similar 

findings (Waldman et al., 1989; Lioy and Greenberg, 1990; Naumova et al., 2002). In two Los 

Angeles area communities, Naumova et al. (2002) measured PAHs in homes located near busy 

traffic areas and reported significantly lower levels of particle-bound PAHs indoors than 

outdoors. Concentrations were dominated by coronene, an indicator of motor vehicle-related 

pollution. Investigators stated that these data suggested that indoor concentrations were driven 

by outdoor PAH pollutant levels. Cigarette smoking was also a major contributor to indoor PAH 

levels in the study of southern California homes (Sheldon et al., 1992b). In smokers’ homes, 

investigators reported statistically significant increased concentrations relative to nonsmoking 

homes of nine PAH species, including benzo(a)pyrene during the daytime, and six PAH species 

during the night. 

Investigators in other states have reported substantial increases in benzo(a)pyrene indoors as a 

result of tobacco smoking in the home (Kanarek et al., 1985; Chuang et al., 1988; Turk et al., 

1987). In a study of PAH levels in 15 public buildings in the Pacific Northwest, Turk (1987) 

reported average levels of benzo(a)pyrene of 1.07 ng/m3

 smoking areas compared to 0.39 

ng/m3

 in nonsmoking areas. The mean indoor-to-outdoor ratio was 7.6. 

2.3.9 Radon 

Radon is a naturally-occurring radioactive gas derived from the decay of radium-226 (a decay 

product of uranium-238) present in small amounts in some soils, rocks, and water. Radon itself 

is relatively harmless, but its decay products, called radon daughters or radon progeny, can 

accumulate in the lung and cause cancer. A statewide survey (Liu et al., 1991) indicates that 

only 0.8% of California residences have annual radon levels above 4.0 pCi/l, U.S. EPA’s 

recommended mitigation level, and the statewide radon average is about 1 pCi/l. However, due 

to the potency of radon daughters, a rough, order-of-magnitude estimate based on an 

extrapolation from national data indicates that radon contributes to about 1500 excess cancer 

deaths per year in California. There is substantial uncertainty surrounding this estimate, 

however, in part due to its inseparability from the risk from exposure to tobacco smoke, and as 

explained further below. 

2.3.9.1 Health Effects of Radon 

Causal associations between exposure to radon and it progeny and lung cancer have been 

demonstrated in many epidemiological studies of underground miners. The National Research 

Council (NRC) Committee on the Biological Effects of Ionizing Radiations has updated 

estimates of radon potency and lung cancer deaths over a number of years, at times increasing 

or decreasing the estimated potency or deaths (NRC, 1988; NRC, 1990; NRC, 1999a). In the 

most recent assessment, NRC (1999a) estimated excess lung cancer deaths in the U.S. due to 

residential radon exposure using two different models. The results range from 15,400 to 21,800 

deaths, for the age-duration and age-concentration risk models, respectively. The U.S. EPA 

(2003c) modified the NRC models and reported 21,000 excess lung cancer deaths (90% 

confidence interval or CI: 9,000 to 50,000) due to residential radon exposure nationally. 

Concurrent exposure to radon and smoking show synergistic effects, that is, the risk of lung 
Indoor Air Pollution in California July, 2005 

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cancer is higher than predicted by adding the individual risks (NRC, 1999a). It is difficult, if not 

impossible, to separate lung cancer risk from ETS and that from radon (NRC, 1999a). 

To provide a rough estimate of the risk from radon in California for the purposes of this report, 

the first-order estimation of radon-induced lung cancer deaths in California was derived using 

simple linear extrapolation by population number, smoking prevalence, and average indoor 

radon concentrations. The national estimates (21,000 deaths/year) were multiplied by the 

fraction of the U.S. population in California (34 million out of 281 million, or 12%; U.S. Census 

2000 data); the ratio of average radon concentrations (CA: 1 pCi/l; U.S.: 1.25 pCi/l; ratio of 0.8); 

and the smoking prevalence in California (CA: 16.4%; U.S.: 22.5%, ratio of 0.73; CDC, 2004b). 

This rough calculation yields an estimate of about 1,500 (90% CI 600-2,100) excess cancer 

deaths per year in California attributable to radon exposure (Waldman, 2004; Tsai, 2005). 

However, this estimate is likely to be an over-estimate, for several reasons. First, a recent study 

in the Sierra foothills region found that the percentage of households exceeding 4 pCi/l is far 

less than the percentage found for that region in the previous statewide survey (3% vs. 25%), so 

the actual statewide radon average may be notably lower than the previous estimate of 1 pCi/l 

(Tsai and Waldman, 2005). Additionally, current indoor radon levels may be lower than the 

measurements taken 15 years ago because new construction may be more radon resistant. 

These factors would lead to a lower statewide radon average; thus the risk estimate presented 

here may be an overestimate, and should be viewed as preliminary. Finally, as discussed in an 

earlier section, smoking rates and exposure to secondhand smoke have decreased 

substantially in California as a result of state regulations and public education efforts. This may 

reduce the opportunity for synergistic effects of radon and tobacco smoke to occur, resulting in 

fewer cases of cancer. 

Although the toxicity of radon is relatively certain, based on strong epidemiological studies, 

many uncertainties associated with the estimation of exposure and risk in California remain to 

be explored. Detailed information for region-specific residential radon exposures, in combination 

with demographic data (e.g., age, gender) and smoking status (current and previous smoking; 

non-smoking) would be required to perform a more accurate radon risk assessment for 

California, but such an effort is beyond the scope of this report. Additionally, a more refined 

estimate may not be useful, for several reasons. A statewide solution in a state with such low 

average levels of radon is not useful for addressing radon. The most effective approach to 

reducing risk from radon is to avoid tobacco smoke (Mendez et al., 1998; NRC, 1999a), and 

California has aggressive state programs to promote reductions in smoking. Local building 

codes to prevent radon intrusion in regions with elevated radon are another preventive measure 

that could provide some protection. However, following the simplified estimation approach 

above, even if the statewide indoor radon average were reduced to the ambient level, 0.5 pCi/l, 

about 750 (300-1,050) lung cancer deaths would still be expected to occur per year due to 

natural radiation. 

While the majority of radon risk is associated with inhalation exposure from air, naturally 

occurring radon in water also poses a risk. About 168 cancer deaths per year are estimated to 

occur in the U.S. from radon in drinking water – 89% from lung cancer caused by breathing 

radon released from water (e.g., showering or flushing the toilet), and 11% from stomach cancer 

caused by drinking radon-containing water (NRC, 1999b). 
Indoor Air Pollution in California July, 2005 

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2.3.9.2 Sources of Radon 

Indoor radon derives from various sources in the vicinity of a building: (a) release from soils 

underneath the building (generally the most important source), (b) building materials enriched 

with uranium-238 (e.g., granite or concrete blocks used in the foundation or walls), (c) use of 

radon-enriched local well water (especially for bathing and appliance use), and (d) outdoor air. 

Elevated indoor radon levels are generally due to the combination of a rich source, a driving 

force into the building, and a relatively low dilution rate for fresh air (Eichholz, 1987). 

2.3.9.3 Radon Concentrations 

Samplers are available to test indoor radon levels at reasonable cost. Measurement techniques 

include charcoal canisters, alpha track detectors, electret ion chamber detectors or scintillation 

flasks. Radon concentrations are reported as the number of radioactive decays per time in a 

volume of either air or water, or picoCuries per liter (pCi/l). The U.S. EPA has issued 

recommendations to reduce the health risks from radon exposure in homes. Immediate 

corrective action should be pursued when indoor air radon levels are above 200 pCi/l. For radon 

levels between 20 and 200 pCi/l, corrective action should be pursued within a few months. For 

radon levels between 4 and 20 pCi/l, corrective action should be pursued within a few years 

(U.S. EPA, 2002a). 

A statewide survey in California found that only 0.8% of California residences have annual 

radon concentrations exceeding 4 pCi/l (Liu et al., 1991). This study examined annual average 

radon concentrations in over 300 homes in a population-based survey and determined that the 

average radon level in California homes is 1 pCi/l. Areas with higher than average radon levels 

include the Central Valley, the Sierra Nevada mountains and foothills, the valleys east of the 

Sierra Nevada, and Ventura and Santa Barbara counties. Surveys of California public 

elementary schools demonstrated similar geographic patterns for areas with elevated indoor 

radon (Churchill and Youngs, 1993; Zhou et al., 1998). 

The National Residential Radon Survey was conducted by the U.S. EPA in 1989-90 to assess 

annual average radon concentrations in U.S. residences (Marcinowski et al., 1994). The survey 

estimated an arithmetic annual average radon concentration in U.S. homes of 1.25 ± 0.12 pCi/L, 

and about 6.0% of homes had radon levels greater than the U.S. EPA action level of 4 pCi/l. 

Homes with elevated levels of radon are more commonly found in geographical areas with 

higher natural levels of soil radioactivity (i.e., uranium). However, predicting residential radon 

concentrations is difficult due to factors associated with home construction and operation 

(Churchill, 1997). Nonetheless, building factors, such as ventilated crawl space, and age of the 

buildings may affect the indoor radon (Tsai and Waldman, 2005). 

2.3.9.4 Activities and Policies to Address Radon in California 

The Department of Health Services’ (DHS) Environmental Management Branch, within the 

Division of Drinking Water & Environmental Management, manages the state’s Radon Program. 

The Radon Program goals are to increase the public’s awareness of the risks of radon in indoor 

air and reduce exposure by encouraging mitigation in buildings with elevated levels of radon. 

The program (ongoing for 14 years) promotes radon testing of homes, businesses, and schools 

through outreach programs and distribution of free radon test kits; maintains a statewide 

database; and is responsible for listing individuals certified to perform radon services in 
Indoor Air Pollution in California July, 2005 

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California. DHS encourages all homeowners to test their home for radon, and provides test and 

remediation information to the public. 

In addition, yearly intensive radon screening studies of selected counties identify areas with the 

potential for elevated indoor levels of radon based on short-term indoor radon measurements. 

Selection of counties and sampling sites is based primarily on geology because uranium 

occurrence is not random: it is largely influenced by geology. There are three primary benefits 

arising from the screening studies: 1) outreach and public education: approximately 25,000 

recruitment/radon information letters are sent to residents of each selected county; 2) 

identification of areas of high indoor radon potential: mitigation and construction of radon 

resistant homes are encouraged in these areas; and 3) production of detailed radon potential 

maps. To date, three such maps have been produced (Santa Barbara, Ventura and, soon to be 

released, Los Angeles) and are available through the Program’s web page at 

www.dhs.ca.gov/radon and distributed to interested city and county agencies. 

2.3.10 Asbestos 

Asbestos is a naturally occurring mineral fiber with strong commercial appeal due to its physical 

properties. It is a poor conductor, but a good insulator, and is strong, flexible, non-corrosive, and 

flame-resistant. Asbestos is a commercial term for a number of naturally-occurring minerals: 

chrysotile belongs to the serpentine group, while amosite, crocidolite, tremolite, actinolite, and 

anthophyllite are in a group called amphiboles. When inhaled, asbestos fibers penetrate deep 

into lung tissues where they cannot be expelled or destroyed by the body. Federal and 

International agencies recognize that asbestos is a carcinogen. In 1986, asbestos was identified 

as a toxic air contaminant under California’s Toxic Air Contaminants Program (AB 1807). 

Exposure to asbestos is associated with increases in non-malignant respiratory symptoms, and 

may cause asbestosis, lung cancer, and mesothelioma (ATSDR, 2001). Indoor asbestos is 

primarily found in older homes in pipe and furnace insulation, shingles, millboard, textured 

paints and other coating materials, and floor tiles. Due to the success of remediation efforts, 

asbestos concentrations are generally quite low in most buildings today. 

2.3.10.1 Health Effects of Asbestos 

Asbestos fibers are so small and thin that they can penetrate to the small alveoli in the lungs. 

Once the fibers are inside the lungs, the body's defense mechanisms attempt to break them 

down and remove them. Despite these attempts, many fibers remain in the body and are 

potential disease-causing agents. Each fiber is treated as a foreign body; inflammations develop 

as the body tries to neutralize, break down or remove the sharp, irritating fibers. Fibers longer 

than 5 μm in length tend to have the greatest health impact. These fibers and the bodies 

defense mechanisms lead to the development of the various kinds of asbestos-caused 

diseases. 

Lung cancer is the predominant asbestos-related disease, accounting for the majority of deaths 

from asbestos exposure. Asbestos workers who smoke are at greater risk of developing lung 

cancer than workers who do not smoke. Asbestosis, a diffuse fibrous scarring of the lungs 

characterized by shortness of breath, mainly arises after long-term heavy exposure to asbestos. 

Mesothelioma, a rare cancer of the lining of the chest and abdomen, does not appear to be 

influenced by smoking. A study of vermiculite miners in Libby, Montana revealed a 4.2% death 

rate due to mesothelioma (McDonald et al., 2004). Based on the high-end estimate of the 

potency of mixed asbestos fibers, breathing air that contains 100 fibers/m3

 (0.0001 fibers/ml) 
Indoor Air Pollution in California July, 2005 

 106

poses a one to two in ten thousand excess lifetime risk of cancer (ARB, 1986). Others (U.S. 

EPA, 1994) have made similar estimates. 

Non-occupational exposures are generally low compared to occupational exposures. Workers’ 

families have developed asbestos-related pulmonary disease (Whitehouse, 2000; Peipins et al., 

2003), lung cancer and mesothelioma (Magnani et al., 2001) from para-occupational exposure 

to asbestos, such as inhalation of asbestos fibers released by clothing and equipment brought 

home from job sites. People living in the vicinity of asbestos mines and factories may be at risk 

from neighborhood exposure to asbestos. Although the risk to the general population is minimal, 

no safe exposure level for asbestos has been established. 

2.3.10.2 Sources of Asbestos 

For 30 years following World War II, asbestos was extensively used in the renovation and 

construction of homes, schools, and public buildings. Asbestos was once found in nearly 3,000 

different types of commercial products, including older plastics, paper products, brake linings, 

floor tiles, textiles, sealants, cement pipe, cement sheets, and insulation (NTP, 2002). It is now 

prohibited in the manufacture, processing, and importation of most products by the 1989 

Asbestos Ban and Phase Out Rule (40 CFR 763 Subpart I, Sec. 762.160 - 763.179). Some 

asbestos paper products and asbestos-cement products remain in use today. 

Friable asbestos-containing material (ACM) can be crumbled by hand pressure when dry, 

releasing fibers to air for potential exposure by individuals. Non-friable ACM can become friable 

during abatement and maintenance activities, and with age. The three most common asbestos 

forms used in construction are amosite, crocidolite, and chrysotile (DHS, 2000). When the 

minerals are crushed, they break into tiny fibers invisible to the naked eye, but distinguishable 

under light microscope. Chrysotile fragments into curly fibers; the other types release tiny, 

needle-like fibers. 

Homes built in areas of naturally occurring asbestos may become contaminated with tracked-in 

asbestos and infiltration of fibers that are suspended in outdoor air. Once such fibers are 

indoors, they can be resuspended by normal household activities, such as vacuuming (OEHHA, 

2000b). 

2.3.10.3 Asbestos Concentrations 

For the purposes of counting asbestos fibers in samples, regulatory agencies commonly count 

as fibers those particles of asbestos minerals at least 5 μm in length and with length:width ratios 

of 3:1. For other purposes, such as detecting fibers in bulk building materials, asbestos particles 

with length:width ratios of 5:1 are counted. 

Asbestos concentrations in most buildings are quite low. Crump and Farrar (1989) examined 

indoor asbestos concentrations for 49 public buildings located in six cities across the U.S. The 

concentration of all fibers was 0.00073 f/ml, and for fibers greater than or equal to 5 μm, the 

average concentration was 0.00007 f/ml. The mean indoor concentration was 0.00020 f/ml for 

buildings with no known asbestos, 0.00059 f/ml for buildings with asbestos in good condition, 

and 0.00073 f/ml for buildings with damaged asbestos. There were no statistically significant 

differences in airborne asbestos levels among the three categories of buildings. For the 43 

buildings that contained ACM, the average indoor levels for fibers greater than or equal to 5 μm 

were 0.00005 f/ml; these levels were indistinguishable from outdoor levels (Lee et al., 1992). 
Indoor Air Pollution in California July, 2005 

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In a nationwide study conducted by Lee et al. (1992), airborne asbestos measurements were 

obtained for 315 public, commercial, residential, school, and university buildings. The mean 

indoor level was 0.02485 f/ml for total asbestos structures and 0.00013 f/ml for fibers longer 

than 5 μm. Indoor total asbestos was significantly higher than outdoor total asbestos for all 

building types. In comparing indoor and outdoor levels of fibers greater than or equal to 5 μm for 

building types, indoor levels were higher than outdoor levels only for schools (p=0.003). Only 

52% of all indoor samples contained asbestos fibers. Approximately 92% of fibers were shorter 

than 5 μm in all buildings, and 2% of fibers were amphiboles. 90% of the samples for fibers 

longer than 5 μm had levels less than 0.00071 f/ml and 0.00054 f/ml in schools and public 

buildings, respectively. 

Corn et al. (1991) reported asbestos concentrations for a portion of the study conducted by Lee 

et al. (1992) involving 71 occupied schools in eight different states. Schools from different states 

did not differ statistically in their levels of airborne asbestos. The type of asbestos-containing 

materials (ACM) present (i.e., chrysotile or amphibole) and the condition of ACM were not 

significantly correlated with levels of indoor asbestos. Most of the asbestos fibers were 

chrysotile (95%) with an average of 0.018 f/ml, and few were longer than 5 μm (7.9%). The 

mean indoor concentration of fibers over 5 μm long was 0.00024 f/ml. Total asbestos structures 

found indoors averaged 0.20 f/ml. 

2.3.11 Polybrominated Diphenyl Ethers and Other Endocrine Disrupters 

Endocrine disrupters are substances that alter the normal function(s) of the endocrine systems 

of animals and humans and adversely affect growth, development or reproduction. They can act 

like a natural hormone, bind to a receptor and prevent a normal response, or interfere with the 

way natural hormones and receptors are synthesized or controlled. Public attention has been 

drawn to endocrine disrupters that mimic or block the natural effects of female sex hormones 

(estrogens), but they can also affect male sex hormones, development and behavior. The range 

of substances that cause endocrine disruption is wide and varied, and includes both natural and 

synthetic chemicals. 

Polybrominated diphenyl ethers (PBDE), a chemical class of endocrine disrupters, are added to 

plastics and textiles to meet fire safety regulations. The PBDE class is comprised of 209 

possible congeners, differentiated by the position and number of bromine atoms on the two 

phenyl rings. U.S. EPA has classified deca-BDE as a possible human carcinogen since it has 

been linked to development of liver tumors in rats and mice. PBDEs have been identified as 

HAPs and California (TACs). 

Phthalates are another group of chemicals that have been investigated for their potential 

endocrine-disrupting activities. Some members of this group, e.g., di-butyl phthalate (DBP) and 

di-(2ethylhexyl) phthalate (DEHP), have been shown to cause severe damage in the testis (an 

endocrine organ) and interfere with testosterone production and/or function in laboratory 

animals (NTP-CERHR, 2000, 2003; Boekelheide, 2004). Many are used to provide flexibility to 

plastic products and have been used in the manufacture of many products including toys, vinyl 

upholstery, shower curtains, raincoats, garden hoses, surgical gloves, medical tubing, and blood 

storage bags. 

2.3.11.1 Health Effects of PBDEs 

Research has shown that PBDE compounds are toxic and bioaccumulate similarly to 

polychlorinated biphenyls (PCBs) and dioxins and have genotoxicity profiles similar to PCBs. 
Indoor Air Pollution in California July, 2005 

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PBDEs have similar chemical structures to PCBs and the human thyroid hormone, thyroxine 

(T4). Toxicological endpoints of PBDEs are suspected to be thyroid hormone disruption, 

neurodevelopmental deficits, and cancer (McDonald, 2002). 

Neurodevelopmental deficits have been linked to PBDE exposure (Eriksson et al., 1998, 1999; 

Viberg et al., 2000, 2001). Other results indicated deficits in brain development and possibly 

changes in the cholinergic system. Changes in the cholinergic system interfere with choline 

acetyltransferase activity and contribute to motor and mental impairments in animals. A noobservable-effects level for neurobehavioral effects has not been established for PBDEs 

(McDonald, 2002). 

Evidence shows that exposure to PBDEs can lead to disruption of endocrine function in a 

number of wildlife species. Effects suggesting endocrine disruption have been reported in 

mollusks, crustaceans, fish, reptiles, birds, and mammals in various parts of the world. There is 

limited evidence in humans that adverse endocrine-mediated effects have resulted from either 

intentional or accidental exposure to chemicals. Many of these chemicals, even at relatively low 

levels, are known to affect growth, reproduction, and development of organisms in the 

ecosystems. The impact of these substances on human health is still under investigation. 

2.3.11.2 Sources of PBDEs and Phthalates 

PBDEs are added to plastics and textiles to meet fire safety regulations. The production of 

PBDEs has steadily increased since the 1970s. Commercial forms of PBDEs include deca-, 

octa- and penta-BDE. In 1999, its use in the United States was estimated at 25,000 tons or 44% 

of the total global use (Hale et al., 2002). California is a major user of fire retardants due to strict 

regulations concerning consumer safety. 

Commercial penta-BDE is added to soft polyurethane foam cushions, upholstery textiles and 

mattresses. Commercial octa-BDE is incorporated into plastics used for hard casings of office 

equipment, fax machines, computers, telephone handsets and car trim. Commercial deca-BDE 

is utilized in high-impact plastics found in televisions, computers, stereos and other electronic 

equipment. 

Historically, DEHP has constituted approximately 50% of all the phthalate ester plasticizers 

used. In 1998, production of dioctylphthalates (which includes DEHP) was approximately 285 

million pounds (ATSDR, 2002b). DEHP is the single largest volume member of the di-octyl 

phthalates. However, in recent years the use of DEHP has declined because of health 

concerns. It is no longer used in plastic food packaging or baby teethers. Many toy 

manufacturers have discontinued its use in toys. DEHP is being replaced by linear phthalates 

and other plastomers in other applications (ATSDR, 2002b). 

2.3.11.3 PBDE and Phthalate Concentrations 

The air and dust inside U.S. homes are likely to contain a wide variety of chemicals, many of 

which are identified as endocrine disrupting substances. A recent study (Rudel et. al., 2003) 

found numerous endocrine disrupting compounds in indoor air and dust obtained from 120 

homes in Cape Cod, Massachusetts. The most abundant compounds in air included bis(2-

ethylhexyl)phthalate (DEHP), (median=77 ng/m3

, max= 1000 ng/m3); o-phenylphenol 

(disinfectant) (median=70 ng/m3

, max=590 ng/m3); 4-nonylphenol (detergent metabolite) 

(median=110 ng/m3

, max=420 ng/m3); and 4-tert-butylphenol (adhesive) (median=16 ng/m3, 

max=290 ng/m3

). The penta- and tetrabrominated diphenyl ethers used as flame retardants 
Indoor Air Pollution in California July, 2005 

 109

were frequently detected in dust. Numerous pesticides were detected in air and dusts from 

these homes, the most abundant being permethrins and the synergist piperonyl butoxide. The 

banned pesticides heptachlor, chlordane, methoxychlor, and DDT were also frequently 

detected. The median concentration of DEHP in the homes studied was 590 ng/m3

 in the air and 

4.98 μg per gram of dust collected. The authors noted that “detected concentrations exceeded 

government health-based guidelines for 15 compounds, but no guidelines are available for 28 

compounds, and existing guidelines do not consider endocrine effects.” 

PBDE congeners were quantified in samples of human breast milk collected in Sweden during 

the period from 1972 to 1997 (Noren and Meironyte, 1998). This Swedish study reported that 

levels of PBDEs in breast milk had increased 40 fold since 1972, indicating a doubling every five 

years. In a 2003 U.S. study, levels of PBDEs in women’s breast milk measured in Texas were 

10 to 100 times higher compared to levels found in Europe (Schecter et al., 2003). Two recent 

U.S. studies in California (Petreas et al., 2003) and Indiana (Mazdai et al., 2003) also report 

similar results with levels from 10 to 100 times higher than levels reported in Europe (Schecter 

et al., 2003). 

PBDEs have been found in a wide variety of environmental samples, including fish, birds, soil 

sediments, air, marine mammals, and human blood (Strandberg et al., 2001, Darnerud et al., 

2001). Penta-BDE has been detected among 89% of the fish collected from two large Virginia 

watersheds (Hale et al., 2001). An air study found that PBDE compounds were widely 

distributed and that PBDEs with lower molecular weight, such as penta-BDE (which is found 

mostly in the vapor phase), can be transported through the atmosphere to remote areas 

(Strandberg et al., 2001). 

Phthalates have been measured indoors in two California studies. In a randomly sampled 

population of 130 homes in Woodland, Sheldon et al. (1992a) measured the highest mean 

concentrations of DEHP inside automobiles (190 ng/m3

; n=8), with personal exposure levels 

next highest (86 ng/ m3

; n=9), followed by indoor levels (59 ng/m3; n=88). The mean outdoor 

concentration fell below the quantifiable limit of 57 ng/m3 for DEHP in that study (n=30). Several 

phthalates were measured in 125 homes studied as part of the Particle TEAM study conducted 

in Riverside (Sheldon et al., 1992b). DEHP and DBP were quantifiable both indoors and 

outdoors, while diethylphthalate and butylbenzylphthalate were measurable indoors but not 

outdoors. Mean Indoor daytime levels were 34 ng/m3 for butylbenzylphthalate, 110 ng/m3

 for 

DEHP, 340 ng/m3

 for diethylphthalate, and 420 ng/m3 for DBP, with outdoor levels much lower 

or not quantifiable. 

2.4 NON-INDUSTRIAL, NON-OFFICE WORKPLACE EXPOSURE TO AIR 

POLLUTANTS 

Non-industrial workplaces (other than offices) provide unique situations for exposure to indoor 

air pollutants. Products and activities associated with non-industrial workplaces such as beauty 

salons, hospitals, dry cleaners, medical laboratories, copy shops, and other workplaces can 

lead to elevated levels of air pollutants. Despite regulations for pollutant levels and ventilation 

requirements, some workers in these environments experience adverse health effects related to 

indoor environmental quality. 

Under CCR Title 8, Section 5155, the California Occupational Safety and Health Standards 

Board sets permissible exposure limits (PELs) and other requirements to limit employee 

exposure to airborne contaminants. The PELs legally apply to both industrial and non-industrial 

workplaces. The Cal/OSHA PELs include 8-hour exposure limits designed to protect healthy 
Indoor Air Pollution in California July, 2005 

 110

working adults, as well as short-term and ceiling exposure limits when they are necessary to 

prevent acute effects. However, they are not sufficient to prevent all health impacts for all 

working individuals, and they do not address possible impacts on those with asthma or 

reactions by sensitive individuals to low levels of chemicals. Cal/OSHA’s Indoor Air Quality 

Policy and Procedure (C-48) states: “Most complaints about the quality of indoor air arise from 

employees who work in non-industrial environments. Approaches using traditional industrial 

hygiene techniques usually demonstrate compliance with 8 CCR section 5155 (PELs) despite 

the persistence of IAQ complaints from the building occupants.” 

Cal/OSHA also has a regulation designed to provide adequate ventilation while workers are at 

work. Title 8, Section 5142, Mechanically Driven Heating, Ventilating and Air Conditions (HVAC) 

Systems to Provide Minimum Building Ventilation, requires HVAC systems to be operated 

during hours of occupancy to provide at least the amount of outside air required by the State 

Building Code at the time of permitting. It also contains maintenance and record-keeping 

requirements. 

2.4.1 Cal/OSHA Data on Workplace Investigations 

A review of Cal/OSHA inspection data indicates ventilation requirements are often not met. 

From 1995 through 2001, data show that citations for violations of Title 8, Section 5142 were 

issued during 514 on-site inspections (Gold, 2005). Of these citations, the majority (260) were in 

services, with 114 in schools and 33 in health care. Citations for violations of Section 5142 were 

issued in 112 inspections in Public Administration. 

Indoor air quality problems in non-industrial workplaces range beyond inadequate ventilation. A 

review of data collected by Cal/OSHA from 1997 through 1999 reveals that 849 cases were 

coded as being related to poor indoor air quality (Gold, 2005). However, because all inspections 

that included IAQ concerns were not necessarily coded as IAQ, the actual number of 

inspections involving indoor air issues may have been more than twice this number (Gold, 

2005). Of the 849 cases, 353 inspections were in service workplaces and 128 were in public 

administration (typically offices). These numbers indicate that problems exist with indoor air 

quality in these locales, but information on specific pollutants or conditions leading to the 

inspections and possible citations are not readily available. 

2.4.2 Workplaces of Concern 

In addition to the indoor air quality problems documented in Cal/OSHA records, the Hazard 

Evaluation Section and Information System (HESIS) within DHS receives many inquiries from 

individuals who are experiencing illnesses associated with poor indoor air quality (Katz, 2005). 

Problems are largely associated with several types of personal-services and communityservices environments. Typically, the individuals affected in these environments include 

employees, clients or customers, students, patients, and self-employed workers. The following 

discussion includes some non-office, non-industrial indoor environments with widespread indoor 

air problems documented by the Occupational Health Branch of DHS, the National Institute of 

Occupational Safety and Health (NIOSH) within CDC, and other scientific investigators. 

2.4.2.1 Schools, preschools, nursery schools, daycare 

Teachers and other school staff frequently report illnesses associated with poor indoor air 

quality. Often the problems contributing to those illnesses are not adequately remedied by 

school administrators for months or even years. At the request of the Legislature, ARB and DHS 
Indoor Air Pollution in California July, 2005 

 111

(2004) conducted a study of the environmental conditions in both portable and traditional 

classrooms throughout California. They found that a number of indoor air quality problems were 

widespread in California. The most serious indoor air quality problems included: 

• Inadequate ventilation with outdoor air during 40% of classroom hours, and seriously 

deficient ventilation 10% of the time, largely due to teachers turning off the ventilation 

systems due to excess noise produced by the systems. 

• Formaldehyde concentrations above guidelines for preventing acute eye, nose, and throat 

irritation in 4% of the classrooms, and exceeding guidelines for preventing long-term health 

effects. including cancer, in all classrooms. 

• Obvious mold in about 3% of classrooms, and water stains, excess wall moisture, and other 

potential mold indicators in about one-third of classrooms. 

Other studies have identified air quality problems in classrooms as well: 

• Dufresne et al., (2002) found that students in a 3-hour biology lab were exposed to average 

formaldehyde levels of 0.25 mg/m3

 (200 ppb) in one classroom, and 0.632 mg/m3 (510 ppb) 

in another classroom. These values are well above the OEHHA 8-hour guideline level of 27 

ppb. 

• In another study (Ryan et al., 2002), investigators measured personal exposures of art 

students to VOCs in a university art building. Concentrations of methylene chloride, a 

carcinogen, were elevated near the print cleaning operation, at 27.2 μg/m3

 (std. dev. 48 

μg/m3

). Concentrations were well below existing occupational limits for 40-hour exposures, 

but the elevated area exceeded the Proposition 65 no significant cancer risk level of 10 

μg/m3

. 

2.4.2.2 Photocopy centers 

Numerous VOCs are emitted during the photocopy process (see Section 2.3.2.2). Stefaniak et

al., (2000) measured VOC concentrations in three copy centers on a university campus. 38 

VOCs were detected in the personal air samples, with toluene being the highest at 690 ppb. The 

maximum area air concentration measured was 1,132 ppb toluene. The time-weighted average 

personal exposures to VOCs were 100 times less than OSHA PELs. However, the toluene 

levels exceed OEHHA’s chronic REL of 75 ppb, a guideline designed to protect against the 

effects of long-term exposure, and exceed the California Proposition 65 warning level of 172 

ppb (650 μg/m3

) for reproductive toxicity. Real-time total VOC (TVOC) concentrations ranged 

from < 71 to 21,300 ppb. The authors conclude that “even though concentrations of individual 

VOCs are well below regulatory limits, the time-weighted average TVOC concentration can be 

well above suggested levels known to cause perceived and physiological health effects in 

controlled laboratory studies”. 

2.4.2.3 Indoor sporting events 

Recreational events are attended by a wide cross section of the population, including individuals 

with heart conditions who are more susceptible to the effects of carbon monoxide (CO). Indoor 

CO levels can exceed the PEL of 25 ppm at indoor sporting events such as motocross 

competitions, tractor pulls, monster truck shows, and automobile demolition derbies, where 

internal combustion engines are operated in indoor environments (Levesque et al., 2000; 

Levesque et al., 1997; CDC, 1994). Monster truck shows and tractor pulls in Cincinnati, Ohio 

during 1992-1993 were found to have average levels of 79-140 ppm CO during events 

compared to pre-event average levels of 13-23 ppm, and a peak observation of 283 ppm 

(Boudreau et al., 1994). The authors noted that the observed concentrations varied inversely 
Indoor Air Pollution in California July, 2005 

 112

with the arena seating level (lower levels with greater height of seats). Similar CO 

concentrations were observed by Levesque et al. (2000) during monster truck shows and 

demolition derbies in Canada, and in motocross events (Levesque et al., 1997). 

Elevated CO and nitrogen dioxide (NO2) concentrations are often present in indoor ice-skating 

rinks. Pelham et al. (2002) found that, in 33 investigations of indoor skating rinks, the majority of 

the reviewed studies reported CO levels in excess of 25 ppm, and several studies reported NO2

concentrations in excess of 1 ppm, well above occupational levels (STEL = 1 ppm) and well 

above the one-hour state ambient air quality standard of 0.25 ppm. The two most identified 

causes for high CO and NO2 levels were the ice surface refinisher (Zamboni) and inadequate 

ventilation systems. 

2.4.2.4 Hair salons and nail salons 

Hair and nail products typically contain toxic and irritating chemicals, though air concentrations 

tend to be well within the applicable occupational standards (Labreche et al., 2003; Leino et al., 

1999; NIOSH, 1992). Many are highly volatile or are sprayed as aerosols, yet there is often 

inadequate ventilation to remove the airborne chemicals. Many salons are leased facilities 

where the business owner has little or no control over the ventilation system, which may 

distribute the pollutants to adjoining businesses. HESIS has received numerous inquiries from 

cosmetologists and cosmetology students about this problem. Health concerns include asthma 

and other respiratory problems, dizziness with headache, and potential effects on pregnancy. 

Because of the high number of complaints and the seriousness of the health concerns, HESIS 

has conducted several field investigations in this field of personal-service businesses (HESIS, 

2004). 

Hiipakka and Samimi (1987) measured several VOCs in personal air samples of nail salon 

operators. Reported values were below OSHA PELs; however, workers reported health 

symptoms. The incidence of throat irritation was significantly elevated relative to a control group. 

Nail sculptors consistently reported more nose and skin irritation, drowsiness, dizzy spells, and 

trembling of the hands than the control group. The mean time-weighted average concentration 

of chemicals reported were: ethyl methacrylate, 4.5 ppb; isopropyl alcohol, 15.6 ppb; butyl 

acetate, 0.4 ppb; toluene, 0.8 ppb; and polymethacrylate dust, 0.9 mg/m3

 for respirable dust. 

2.4.2.5 Other non-industrial workers/workplaces with unique exposure scenarios 

Workers in many types of workplaces and businesses are exposed to air pollutants associated 

with the type of work they perform. Large air quality studies of these businesses are lacking; 

however various small studies, complaint records, and investigations have shown that there are 

indoor air quality problems in many other types of non-industrial workplaces as well. Some of 

these workplaces or services include: 

Dry Cleaners – Residual solvents used in dry cleaning volatilize off the clean clothes leading to 

elevated levels in dry cleaner shops. Perchloroethylene has been the mostly widely used dry 

cleaning solvent; however other solvents (ethylbenzene, m,p-xylene, and o-xylene) have been 

used to some extent. In studies in New York, concentrations of perchloroethylene in 13 

apartments connected to or near dry-cleaning shops ranged from 7.6 to 23,000 μg/m3

, averaged 

5000 μg/m3

, and showed a median level of 1400 μg/m3, well above the New York Department of 

Health guideline of 100 μg/m3

 (NYS DOH, 2003) and the OEHHA chronic REL of 35 μg/m3 and 

any acceptable cancer risk levels. 
Indoor Air Pollution in California July, 2005 

 113

Janitors – Occupational asthma and other respiratory problems can be caused or aggravated 

by chemical cleaning products used inside schools, hotels, medical settings and other service 

facilities. California has nearly 400,000 people who regularly work with cleaning products. The 

Occupational Health Branch (OHB) of DHS found that the rate of work-related asthma in janitors 

is nearly double the rate in the overall workforce. Bystanders in health care and other industries 

are often indirectly exposed to cleaning chemicals as well. Nurses and nursing aides constituted 

20% of the bystanders who developed asthma in the OHB study (DHS, 2004c,d). 

Hospitals, jails, etc. – Tuberculosis, a bacteria transmitted by airborne particles, is an air 

contaminant of significant concern where high risk populations are gathered together for 

services, residence, or incarceration. These environments include hospitals, prisons, jails, 

homeless shelters, drug treatment clinics, residential facilities for HIV-infected persons (e.g., 

hospices or group housing), and residential facilities for the elderly (DIR, 1997). 

Construction workplaces – Construction workers may encounter heavy concentrations of 

plaster/wallboard dust, adhesive VOCs, lead dust from surface preparation for painting, and 

fungal particles from mold remediation or flood-damaged buildings. Several organizations have 

published detailed guidelines for the protection of mold remediation workers (U.S. EPA, 2003b). 

However, very few studies have been conducted to determine the actual effectiveness of the 

guidelines in preventing health problems among these workers. A few case reports document 

illnesses among renovation workers. 

Roofing work – Application of roofing asphalt is known to cause indoor air quality problems 

when contaminated air enters a building, often through ventilation system intake vents (Lynch 

and Kipen, 1998). Health complaints often continue well beyond the time of exposure. 

Aircraft cabins – The pesticide permethrin is routinely sprayed on some international airliner 

routes to eradicate insects inside cabins (NRC, 2002). Flight attendants have become ill due to 

the exposure to permethrin; there is also concern about passenger safety. Airlines are not 

currently required to tell passengers of pesticide use (DHS, 2003b). Aircraft exposures to 

biological contaminants and ozone also have been a concern (Nagda and Rector, 2003; 

Spengler et al., 2004; NRC, 2002; Rayman 2002). 

2.4.3 Semiconductor Industry 

Exposures experienced by workers in the semiconductor industry are included here to illustrate 

concerns regarding exposures in non-traditional industrial environments, and the suspected 

health effects of some glycol ether compounds. These same glycol ethers have been detected 

in some consumer products and residential environments. Ethylene-based glycol ethers used in 

this field have been related to reproductive problems in animal species (Eskenazi et al., 

1995a,b). Eskenazi et al. monitored reproductive activities and pregnancy rates of female 

workers in the semiconductor industry. The authors concluded that women employed in certain 

areas (fabs, dopant, and thin-film processes) have fewer pregnancies than other workers. 

Women exposed to ethylene glycol ethers had somewhat lower fecundability (probability of 

conception) than women unexposed to ethylene glycol ethers. Glycol ether levels were not 

recorded. In a similar study, glycol ethers and fluoride compounds used by workers in 

fabrication-rooms and photoresist processes accounted for increased risk of spontaneous 

abortions (Swan et al.,1995). Hammond et al. (1996) measured time-weighted average personal 

exposures for semiconductor workers. Workers that poured solvent or cleaned a coater cup 

experienced a higher exposure with a geometric mean concentration of 81 ppb of 2-
Indoor Air Pollution in California July, 2005 

 114

ethoxyethanol. Workers who loaded and unloaded cassettes experienced a lower exposure with 

a geometric mean of 14 ppb 2-ethoxyethanol. 

In summary, workplaces can pose a risk not experienced in residences or offices due to the 

nature of the activity that occurs there, or the type of sources present. While industrial 

exposures are moderated through the use of engineering controls, administrative controls, and 

personal protection gear when needed, indoor air quality problems in non-industrial workplaces 

have been less recognized and less studied. Nonetheless, some exposures in non-industrial 

workplaces have been shown to exceed guidelines for protecting the health of the general 

population, although levels of pollutants in those environments generally do not exceed 

occupational standard levels. Indoor air quality problems in non-industrial workplaces are not 

unique to California: in the past 25 years, the percentage of health evaluations that NIOSH (at 

the Centers for Disease Control and Prevention) has conducted related to indoor-air quality has 

increased from 0.5 percent of all evaluations in 1978, to 52 percent of all evaluations since 

1990. This means that in those years, the evaluations related to air quality concerns have 

increased from one of every 200 evaluations to one of every two evaluations (Office of the 

Surgeon General, 1-13-05 news release). 
Indoor Air Pollution in California July, 2005 

 115

3. COSTS OF INDOOR AIR POLLUTION 

The health effects from indoor air pollution impose large costs on society, both economic and 

personal. The loss of human life, due to indoor air pollution constitutes a large economic and 

social cost. In addition, the medical costs of increased disease due to indoor air pollution, such 

as for cancer treatments, hospitalizations, chronic respiratory disease, and emergency room 

visits for asthma attacks and CO poisoning, are substantial. Student absenteeism, reduced 

worker productivity, and associated costs also result from indoor air pollution. 

However, only very limited quantitative estimates on the costs of indoor pollution are available to 

date. Most of the available estimates are for a few specific indoor air pollutants that have been 

well studied, such as ETS and radon. There are many more indoor air pollutants that pose a 

significant health risk to the public, but the lack of cost information or other data for California 

precludes us from making even rough cost estimates here. 

Estimates of the economic costs of some aspects of indoor air pollution have been made for the 

United States (Fisk, 2000; Mendell et al., 2002). These studies allow order-of-magnitude 

estimates of the economic costs for California each year due to increased asthma symptoms 

and lost worker productivity in schools and office buildings. In addition, cost or value estimates 

can be derived for some of the health effects discussed in Chapter 2, in this report. 

This information is used below, along with national and California-specific cost estimates for 

medical treatment and other costs (where available), to estimate the annual economic costs or 

value of specific health effects from indoor pollutants in California (U.S. EPA, 2002b; Thayer et 

al., 2003). However, only the costs for selected indoor air pollutant exposures that have been 

reasonably well characterized in California are used for the final estimate. To account for 

inflation, cost estimates are adjusted to 2000 dollars using the relative increase in the urban 

consumer costs of the Consumer Price Index; for adjusting health care costs, the changes in 

medical care costs are used instead (USCB, 2002). Table 3.1 presents the unit medical costs 

(direct and indirect) and economic valuations of premature death used in the following analyses. 

3.1 PREMATURE DEATH 

Exposure to some air pollutants, primarily carbon monoxide, ETS, other carcinogens, and PM, 

can lead to near-term death or significantly increase the risk of premature death. The economic 

impact of premature death, or the value of a human life, has been estimated in the scientific 

literature and in environmental regulatory settings. The estimation methods include those based 

on: 1) an individual’s willingness to pay to avoid a health risk, 2) the additional compensation 

demanded in the labor market for riskier jobs, and 3) society’s willingness to pay to avoid a 

health or safety risk. 

U.S. EPA (2002b) reviewed 26 value-of-life studies that used either the first or second method 

above, and confirmed the finding of a previous literature review that “most of the reasonable 

estimates of the value of life are clustered in the $3.7 to $8.6 million range.” 

Based on its review and input from the scientific community, U.S. EPA selected $6 million (1999 

dollars) as a point estimate for the “value of a statistical life,” along with caveats for applying the 

study results to the general population. U.S. EPA (2000c) has used this point estimate in 

assessing the impact of regulations for diesel fuel and other pollutant sources. This point 

estimate is equivalent to $6.33 million in 2000 dollars, and is used in the following sections to 
Indoor Air Pollution in California July, 2005 

 116

estimate the annual economic valuation of excess premature deaths due to indoor air pollution. 

The estimated valuation of premature death from indoor air pollution in California is discussed 

below and summarized in Table 3.2. 

Table 3.1. Unit Costs for Health Effects 

Outcome Method1 Unit Cost in Year 2000 Dollars 2 

Premature death WTP $6,330,0003 

Cancer medical costs 

(various types, survivor only) 

COI $94,600 

Lung cancer medical costs (weighted 

average for all cases) 

COI $64,900 

Asthma patient, direct medical and 

indirect costs 

COI $6404 

Cardiovascular hospitalization COI $15,2006 

Low birth weight, lifetime COI $118,000 

Otitis media (middle ear infection) COI $3605 

Asthma, emergency room visit COI $3107 

Asthma, chronic WTP $33,0007 

Bronchitis, acute WTP $597 

Respiratory hospitalization (U.S.) COI $11,0006,7 

Acute respiratory hospitalization (CA) 

 Age < 18 

 Age ≥ 18 

COI

$11,8006,7 

$23,5006,7 

1. WTP: willingness to pay method; obtained from surveys. COI: cost of illness method; based from 

medical cost data and estimates of indirect costs such as lost workdays. 

2. Unless noted otherwise, all values are averages from Cost of Illness Handbook (U.S. EPA, 2002b), 

after adjustment to 2000 dollars using the Consumer Price Index for medical care cost. 

3. Midpoint value, adjusted for inflation using urban consumer costs. 

4. From Weiss and Sullivan (2001), including direct medial and indirect costs. The 1998 U.S. estimates 

have not been adjusted to 2000 dollars. 

5. From Gates (1996). The estimated annual U.S. cost of $5 billion per year (in 1993 dollars) was 

divided by the estimated caseload of 14 million children under 5 years of age. 

6. From a study of California costs by Thayer et al. (2003). Cost adjusted for inflation using the 

Consumer Price Index for medical care costs. 

7. These values were not used in this analysis due to inability to separate hospitalization cases from 

doctor’s visits in the literature. 

Another approach to estimating the economic cost from deaths due to indoor air pollution is to 

base the estimate on court decisions and insurance awards, such as those from CO poisoning. 

However, nearly all cases of fatal and non-fatal CO poisoning are settled out of court, and utility 
Indoor Air Pollution in California July, 2005 

 117

companies are not required to track such cases; thus, there is little reliable data available on 

these legal settlements. 

3.1.1 Deaths From CO Poisonings 

Based on the DHS review of coroners’ reports in the 1980’s, an average of 30-40 Californians 

die each year from accidental CO poisoning (Girman et al., 1998; Liu et al., 1993a, 2000). On 

average, about 2/3 of those deaths (about 20-26, or 23 average) documented in the DHS study 

were due to appliance-related causes such as faulty furnaces, gas ovens used for space 

heating, and charcoal grills used indoors. This estimate has a high degree of certainty relative to 

other pollutant risk estimates because the CO death estimates are based on coroners’ reports 

that clearly identify CO poisoning deaths. The economic value of these lost lives in California is 

estimated to be $130-160 million per year (2000 dollars), or about $150 million on average, as 

shown in Table 3.2. 

Although the rate of CO deaths in the U.S. population has declined over the years (Mott et al., 

2002; CPSC, 1997), the actual numbers of CO poisoning cases in California may have 

increased since 1990. Based on California’s population growth alone – from 30.38 million in 

1990 (USCB, 1990) to 33.87 million in 2000 (DOF, 2002a,b), a 14% increase – one might 

expect the number of deaths to have increased by a similar percentage. In addition, much of 

this population growth has occurred in the inland and foothill regions of California, which have 

longer, colder winters than coastal areas, and thus, would have a greater likelihood of CO 

poisoning due to more frequent use of combustion appliances for space heating. 

However, trends toward increased use of CO alarms and testing of combustion appliances 

could potentially have reduced the number of appliance-related CO poisonings in California 

since 1990. CO poisonings at the national level have declined (CPSC, 1997), which may be 

due to lower pollution emissions from motor vehicles and the increased heavy marketing of 

inexpensive CO alarms for use in homes, motor homes, and boats. The state’s program for 

weatherizing existing, low-income homes has required installation of CO alarms and combustion 

appliance safety testing, as discussed in Section 4.3.2. 

Overall, based on the factors in both directions discussed above, the current number of fatal CO 

poisonings in California due to appliance-related causes is assumed similar to that in 1990. It is 

likely that the risk of CO poisoning remains higher than average in older homes with older gas 

appliances, in homes with propane appliances, and in some socioeconomic groups that use 

unvented gas stoves or charcoal grills indoors more frequently. 

3.1.2 Deaths From Volatile Organic Compounds (VOC) Exposure 

As discussed in Section 2 and Appendix II, about 230 excess cancer cases due to VOCs from 

indoor exposures are estimated to occur in California each year. This estimate is based on the 

results of the California Comparative Risk Project (CCRP, 1994) that have been updated to 

reflect reductions in formaldehyde exposures and increased population growth as of the year 

2000. These are conservative estimates relative to the total cancer burden from indoor 

carcinogens, because they do not include the additional, significant cancer risk from radon, and 

the risk from many other carcinogens also found in indoor air and house dust, such as 

acetaldehyde, PAHs other than B(a)P, and asbestos. 

 
Indoor Air Pollution in California July, 2005 

 118

Table 3.2. Estimated Valuation of Annual Mortality Attributed to Indoor Air 

Pollution in California 

End Point Excess Premature Deaths

(cases/yr)1 

Valuation 

per case2

($ Million) 

Cost per Year3

($ Billion)

 Low Average High Low Average High 

CO: Poisoning4 20 23 26 6.33 0.13 0.15 0.16 

VOCs: 

Lung cancer5 115 115 115 6.33 0.73 0.73 0.73 

ETS: 

Lung cancer,7,8 3806

 3806 1,020 6.33 2.4 2.4 6.5 

ETS: 

Heart disease7,8 1,700 3,600 5,500 6.33 11 23 35 

Radon: 

Lung cancer9 600 1,500 3,500 6.33 3.8 9.5 22 

Mold and 

Moisture: 

Asthma and 

allergy10 

NA NA NA NA 0.031 0.031 0.031 

TOTAL11 18 36 64 

1. Low and high estimates are based on a range or confidence intervals, where available. Average 

estimates are based on mean values from available estimates or ranges. 

2. From Cost of Illness Handbook (USEPA, 2002b), adjusted to 2000 dollars. 

3. Costs per year are rounded to 2 significant figures. 

4. Case estimate from coroner’s data in California (Liu et al., 2000). 

5. Case estimate from average values in California Comparative Risk Project (CCRP, 1994), updated. 

See Section 2 and Appendix II of this report. 

6. From best risk estimate rather than average risk estimate; for spousal smoking only (ARB/OEHHA, 

2005). Adjusted to 2000 population total. OEHHA believes the lower end of the range is the current 

best estimate. This risk estimate is probably an overestimate because it assumes exposure and 

death rates in California are the same as those for the U.S. 

7. From ARB/OEHHA (2005). 

8. OEHHA is currently incorporating comments from the Scientific Review Panel on the ETS report. 

9. From Waldman (2004), based on USEPA (2003c), with adjustments for smaller population, lower 

average residential radon concentrations, and lower smoking prevalence rates in California. 

10. Cost estimates taken from national cost estimated by Weiss and Sullivan (2001) of $2 billion (in year 

2000 dollars), scaled to 12% for California estimate, and multiplied by fraction of asthma risk 

attributed to mold and moisture in three large epidemiology studies (0.13). 

11. These totals do not include death from exposures to other types of indoor PM, which could be 

substantial but are not currently quantifiable due to lack of appropriate studies. 
Indoor Air Pollution in California July, 2005 

 119

Half of the VOC-related cancer cases attributed to indoor air (115) per year are estimated to 

result in premature death. U.S. EPA (2002b) assumed this same fraction of fatal cases within 

five years of diagnosis when estimating the costs of typical cancer treatment. Actual premature 

death rates could be higher than one-half of the cases because cancers caused by these air 

pollutants typically result in lung, organ, or blood cancers, which are more difficult to detect and 

treat, and thus, are more deadly. The estimated value of premature deaths from the 115 excess 

cancer deaths in California totals $730 million per year, as shown in Table 3.2. This estimate 

does not explicitly include the much smaller costs of cancer treatment, which are discussed 

below. 

3.1.3 Deaths from Environmental Tobacco Smoke Exposure 

ARB/OEHHA (2005) estimate that exposure to ETS from spousal smoking in California in 2003 

produced 400 premature deaths (range 411-1,064) due to lung cancer. These estimates are 

based on the best risk estimate rather than the average risk estimate. They also are based on 

smoking prevalence rates in the U.S., and scaled down to reflect that California contained 12% 

of the U.S. population. Because these estimates do not account for the lower smoking rate and 

exposure in California relative to other states, they may overestimate the risk from ETS in 

California; however, the difference would not be expected to be large. The ETS estimates in the 

present report are based on ARB/OEHHA (2005) estimates, which are current as of March 

2005. ARB/OEHHA may further revise the ETS lung cancer and other estimates to reflect the 

comments of the external Scientific Review Panel (SRP) on breast cancer and other topics; a 

final ETS report is expected to be approved by the SRP and considered by the ARB later in 

2005. 

To adjust the ARB/OEHHA estimate back to the year 2000 population, the lung cancer risk 

estimate was multiplied by 0.96. This yields an estimated number of 380 excess lung cancer 

deaths cases per year from ETS exposures. The estimated value of premature deaths from the 

380 excess lung cancer deaths (range 380-1,020) in California totals $2.4 billion per year, as 

shown in Table 3.2. This estimate does not explicitly include the much smaller costs of cancer 

treatment, which are discussed below 

For ETS effects on ischemic heart disease, ARB/OEHHA (2004-2005) estimated that ETS 

exposure resulted in 1,700-5,500 (average = 3,600) premature deaths from heart disease. This 

estimate was based on 1999 ETS exposure data and 2000 mortality data for California. The 

estimated value of 3,600 deaths is $23 billion, as shown in Table 3.2. 

The estimated numbers of premature deaths from ETS exposure, and the morbidity effects 

discussed below, probably overestimate current risk levels for two reasons. First, ETS exposure 

is likely much lower in California compared to the U.S. The CDC (2004) found adult and 

adolescent smoking prevalence in California was about 16% in 2001, while the U.S. prevalence 

rate was 22%. In addition, per capita cigarette consumption by California adults was found to be 

about half of the U.S. average in 2001-2002 (DHS, 2002a). Secondly, the estimates include 

home and workplace exposure, but California’s workplace smoking ban has virtually eliminated 

ETS exposure in enclosed workplaces, with a few exceptions. By 1999 over 93% of indoor 

workers reported having a smoke-free workplace (DHS, 2002b). On the other hand, newer data 

on the health effects of ETS may increase the unit risk of ETS for death and disease. For 

example, ARB/OEHHA (2005) estimate that ETS increases the risk of breast cancer by about 

30%. 
Indoor Air Pollution in California July, 2005 

 120

These costs of ETS-related health effects could be prevented if people smoked only outdoors 

away from other people, or stopped smoking. However, to achieve these potential cost savings, 

further efforts are needed to change peoples’ smoking behaviors, and to improve awareness of 

and control of other indoor and outdoor asthma triggers in California (Meng et al., 2003). 

3.1.4 Deaths from Radon Exposure in Homes 

The DHS has estimated that 1,500 excess lung cancer deaths per year are attributed to the 

residential radon exposure in California (Waldman, 2004), as discussed in chapter 2. This firstorder estimate is based on the U.S. EPA’s (2003c) national estimate of 21,000 excess lung 

cancer deaths (90% CI: 9,000 to 50,000). To calculate the residential radon risk for excess lung 

cancer in California, the national estimates were multiplied by the fraction of the U.S. population 

in California (34 million out of 281 million, or 12%; U.S. Census 2000 data). The national 

estimates were also multiplied by the ratio of average radon concentrations (CA: 1 pCi/l; U.S.: 

1.25 pCi/l; ratio of 0.8) and the smoking prevalence in California (CA: 16.4%; U.S.: 22.5%, CDC, 

2004b). This yielded an estimate for the radon-induced lung cancer death in California of about 

1,500 (90% CI: 600-3,500) deaths per year. This may overestimate the excess deaths because 

recent measurements in the Sierra Nevada region indicate that this region has much lower 

radon levels than that reported from the previous statewide survey (3 vs. 25%), and that the 

statewide average may be lower than previously estimated (Tsai and Waldman, 2005). The 

estimated value of premature deaths from the 1,500 excess lung cancer deaths in California 

attributable to radon totals $9.5 billion per year, as shown in Table 3.2. 

3.1.5 Deaths from Mold and Moisture-related Problems in Homes 

Weiss and Sullivan (2001) estimated that the costs of excess death in children and adults due to 

asthma in the U.S. was $2 billion, in year 2000 dollars. Scaling this to reflect that 12% of the 

U.S. population resides in California gives an estimated cost for asthma deaths in California of 

$0.24 billion. As discussed below in the Medical Costs section, the fraction of these health 

effects attributed to mold and moisture problems in homes is 0.13. This fraction is an average of 

four large, well-conducted epidemiology studies of adults and/or children (shown in Table 3.4). 

Multiplying the estimated cost of asthma in California by this fraction yields an estimated cost of 

$31 million attributable to excess death due to residential mold and moisture problems. This 

estimate does not include other indoor allergen sources such as dust mites, pets, cockroaches, 

and chemical emissions. 

3.2 MEDICAL COSTS 

Illness and disease caused by indoor air pollution include the production of new asthma cases 

(induction), exacerbation of asthma symptoms, development of other respiratory disease and 

symptoms, and induction or exacerbation of allergies. These impacts of indoor air pollution also 

affect the quality of a person’s life in terms of reduced or limited activities, limited employment 

opportunities, and reduced productivity. 

The cost of illness and disease has been estimated in various ways. These include methods 

based on medical costs, work-related costs, education-related costs, and willingness of 

individuals to pay to avoid the anxiety, pain, suffering, and other health risks (U.S. EPA, 2002b). 

The following section uses medical costs shown in Table 3.1 to estimate the medical costs of 

indoor air pollution in California, but generally excludes the indirect costs of reduced productivity 

of individuals and employees. The estimated medical costs are summarized in 

Table 3.3. 
Indoor Air Pollution in California July, 2005 

 121

3.2.1 CO-related Hospitalization 

 

About 175-700 emergency room visits and hospitalizations (midpoint of 438) due to non-fatal 

CO poisoning are estimated to occur in California each year, on average (see Section 2.2.4.2). 

Emergency room visits cost about $442 per visit, based on costs for asthma room visits to 

emergency rooms and adjustment to 2000 dollars (U.S. EPA, 2002b). Therefore, the annual 

cost of emergency room visits due to CO poisoning in California ranges from $77,000-310,000, 

or an average of about $190,000, as shown in Table 3.3. 

The estimated number of emergency room visits due to CO is conservative because CO 

poisoning can be misdiagnosed as a viral flu illness or general fatigue. The estimated cost for 

each case of non-fatal CO poisoning is conservative because it does not include several types 

of costs that could be substantial, such as the costs for lost school and work days, hyperbaric 

oxygen treatment for severe poisoning, long-term neurological and developmental damage to 

many victims of sub-lethal CO poisoning, and the estimated hundreds to thousands more CO 

poisoning cases per year that do not result in hospitalization. 

3.2.2 VOC-related Cancer Treatment 

The number of excess cancer cases from VOC exposures was estimated above to be 230 

cases per year, and one-half of those cases (115) were assumed to survive, as discussed 

above. The average cost of medical treatment in the U.S. for the 13 most common types of 

cancer, when assuming a 50% death rate at five years and no discounting, is $82,581 in 1996 

dollars (U.S. EPA, 2002b) or $94,619 in 2000 dollars. This treatment cost estimate is 

conservative because it does not consider recent changes in cancer treatment that can be very 

expensive, such as the bone marrow transplant procedure and new pharmaceutical treatments. 

At this treatment cost per cancer case, the total cost for medical treatment for 115 cases from 

VOC exposure was estimated to be $11 million, as shown in Table 3.3. 

3.2.3 ETS-related Illness and Hospitalization 

As discussed above, ETS exposure was estimated to result in 380 excess deaths per year from 

lung cancer. To estimate the medical costs of this impact, the approach used above for VOCs 

was used, except that the average cost of medical treatment for lung cancer alone was used 

instead: $56,624 in 1996 dollars (U.S. EPA, 2002b) or $64,900 in 2000 dollars. Costs for lung 

cancer only were used because ETS exposure is primarily associated causally with lung cancer, 

while VOCs are causally associated with several other types of cancer. This cost is based on 

the total costs for non-survivors and survivors over 10 years, weighted annually for survival 

rates and discounted at 5%. The total cost of cancer treatment for the 380 cancer cases from 

ETS exposures was estimated to be $25 million (in 2000 dollars), as shown in Table 3.3. 

For estimating costs due to hospitalization for heart disease due to ETS exposure, an approach 

similar to that used above for VOCs was used. However, in this case, the average cost of 

medical treatment for heart disease ($15,200) from Table 3.1 was used. The total cost of 

hospitalization for 3,600 heart disease cases attributed to ETS exposures was estimated to be 

$55 million (in 2000 dollars), as shown in Table 3.3. 

ETS exposure in California was estimated to have resulted in at least one asthma episode in 

31,000 (range of 24,000-40,000) non-smoking children under 18 years of age over the last 12 

months (ARB/OEHHA, 2005). This estimate was based on a meta-analyses of 29 
Indoor Air Pollution in California July, 2005 

 122

epidemiological studies, and an attributable fraction based on California data for population and 

ETS exposure prevalence for 2000. The estimate includes exacerbation of asthma in both new 

and existing asthma patients in the last 12 months. These health effects were primarily 

observed in infants and older children, but they may also increase the risk of health effects later 

in life. The average unit cost for each asthma patient in the U.S. was estimated to be $640 per 

year, based on national data for 1998 (Weiss and Sullivan, 2001). This unit cost includes direct 

medical and indirect costs for all age groups, and is about twice the unit cost for asthma 

treatment in an emergency room ($310). Actual costs for asthma episodes are likely to be 

higher because the medical costs of asthma treatment are rising rapidly and the costs of upper 

and lower respiratory conditions that occur along with asthma are not included (Weiss and 

Sullivan, 2001). Multiplying the number of asthma episodes by the unit cost for asthma patients 

($640) from Table 3.1, yields an estimated cost of $19 million per year (1998 dollars) in direct 

medical costs and indirect costs, as shown in Table 3.3. 

ARB/OEHHA (2005) estimate that ETS exposure resulted in 1,600 cases of low birth weight, 

defined as a birth weight below 2,500 grams. Again, the case numbers multiplied by the unit 

medical cost shown ($118,000) in Table 3.1. OEHHA (2004) attributed a 20-100 gram 

decrement in birth weight due to ETS exposure. The estimated cost of the 1,600 cases of low 

birth weight infants was $190 million. This unit medical cost is likely to be an underestimate of 

actual costs because credible data are lacking for the first two years of life when intensive 

medical care and additional hospitalization are most likely, and for some age groups where 

costs were extrapolated from others (U.S. EPA, 2002b). In addition, cost data for non-medical 

expenses over a lifetime were lacking; these costs could be substantial as well. 

ARB/OEHHA (2005) estimated that 4,700 cases of premature delivery result from ETS 

exposure in California each year. Premature delivery is a major cause of infant mortality and 

infant medical expenses in the U.S., especially among African-Americans (MOD, 2003). 

Because the large majority of premature infants have low birth weights (Mattison et al., 2001), 

most of the medical costs of premature delivery are included in the cost estimate above for low 

birth weight due to ETS exposure. However, the increased costs of premature death, long-term 

disability, and indirect expenses due to premature delivery are not available. OEHHA is 

currently revising the report to reflect the comments of the external Scientific Review Panel on 

developmental effects and other topics, and those revised estimates will be included in this 

report at a later date. 

ARB/OEHHA (2005) also estimated that 51,700 cases of otitis media (middle ear infection) in 

children were associated with ETS exposure in California. This estimate is based on ETS 

exposure of California children in 1999, and 2000 California population data. Gates (1996) 

estimated that the direct and indirect cost of otitis media totaled $5 billion dollars per year in 

1993. Dividing this cost by the estimated caseload of 14 million children under the age of five, 

the primary patients for this diagnosis, yields a unit case cost of $360 per year (1993 dollars). 

This unit cost is an underestimate because it does not include all medical costs, the potential 

cost of impacts on children’s learning and development, and the increase in medical costs and 

consumer costs since 1993. This unit cost is relatively minor compared to, and somewhat 

redundant with, the costs estimated above for new cases of chronic asthma ($33,000); it is 

provided here to address the impacts on persons with pre-existing asthma. Multiplying the 

estimated number of cases by the unit cost ($360) yields an estimated cost of $20 million per 

year (1998 dollars), as shown in Table 3.3. 
Indoor Air Pollution in California July, 2005 

 123

Table 3.3. Estimated Annual Medical Costs of Indoor Air Pollution in California. 

Health End Point 

Average Cases 

per Year 1

(Range)

Medical Cost 

per Case1,2 

($) 

Average Cost 

per Year3

($ millions) 

CO: poisoning 438 

(175-700) 

 442 0.19 

VOCs: cancer 115 94,600 11 

ETS: lung cancer4,5 380 64,900 25 

ETS: heart disease4,5 3,600 

(1,700-5,500) 

15,200 55 

ETS: asthma episodes4,6 31,000 

(24,000-40,000) 

 640 20 

ETS: low birth weight4 1,600 118,000 190 

ETS: otitis media visits4 51,700 360 19 

Radon: lung cancer7 1,500 64,900 97 

Mold & moisture: 

 asthma and allergy8 

NA9 NA 190 

 Total10 610 

1. Original data were adjusted to 2000 dollars and 2000 population where necessary. 

2. Medical cost values were taken from Table 3.1 and do not include indirect costs, unless noted 

otherwise. Thus, cancer treatment cost does not include costs for outpatient prescription medications 

and nursing home care below the skilled level. 

3. Rounded to two significant figures. 

4. Case estimate from ARB/OEHHA (2005). 

5. Medical costs for fatal cases of cancer or heart disease also are implicitly included in death 

valuations, but are generally an insignificant amount relative to the total valuations. 

6. The case estimate is for children under 18 years of age with at least one asthma episode in the past 

12 months. 

7. From Waldman (2004), based on U.S. EPA (2003c) with adjustments for smaller population, lower 

average residential radon concentrations, and lower smoking prevalence rates in California. 

8. Cost estimates taken from national estimates for medical and indirect costs by Weiss and Sullivan 

(2001), adjusted to 2000 dollars, scaled to 12% for California estimate, and multiplied by fraction of 

asthma risk attributed to mold and moisture in four large epidemiology studies (0.13). Includes 

estimate of $60 million for indirect costs, such as lost workdays, lost school days, and reduced 

housekeeping. 

9. NA = not available. 

10. These totals do not include disease from exposures to other indoor PM, which could be substantial 

but are not currently quantifiable. 

3.2.4 Radon-Related Cancer Treatment 

As discussed above, residential exposure to radon was estimated to result in 1,500 excess 

deaths per year from lung cancer. To estimate the medical costs of this impact, the approach 
Indoor Air Pollution in California July, 2005 

 124

used above for ETS was used; $64,900 in 2000 dollars was used for the average cost of 

medical treatment for lung cancer (U.S. EPA, 2002b). Only costs for lung cancer were used 

because radon exposure is primarily associated causally with lung cancer. The total cost of 

cancer treatment for the 1,500 cancer cases attributed to indoor radon exposures was 

estimated to be $97 million (in 2000 dollars), as shown in Table 3.3. 

3.2.5 Medical and Indirect Costs Associated with Indoor Mold and Moisture-related 

Problems in Homes 

Available data demonstrate a relatively strong and consistent association of dampness and 

mold in buildings with an increase in lower respiratory symptoms that are often considered 

evidence of asthma exacerbation (IOM, 2004). The specific biological, chemical, or physical 

agent responsible for the health-relevant exposures from indoor dampness and mold are not 

fully understood. Few large studies of mold, allergens, and other biological contaminants have 

been conducted in office buildings, schools, and other non-residential buildings, so this section 

focuses on residential exposures. 

To estimate the cost of asthma attributable to dampness or mold, the fractions of asthma 

attributable to dampness or mold in apartments and homes in the U.S. and California are 

multiplied by estimates of the cost of asthma. Four large studies of the health risks of building 

dampness and mold for adults and/or children have been conducted in the U.S. and Canada, as 

shown in Table 3.4. Each of these studies controlled for the effects of many factors other than 

dampness and mold, such as housing conditions, smoking, and allergy sensitization. Most of 

the study areas have moderate or cold climates similar to California. The three studies from 

Canada or the U.S. had very similar odds ratios for dampness or mold. Similar odds ratios for 

homes with water damage and children with asthma (OR = 1.27-1.33) were found in the ARB’s 

Children’s Health Study, a large study of grade-school children in middle-income families in 

southern California (Peters et al., 1999a). In addition, McConnell et al. (2002b) reported that 

these southern California homes had mildew at rates–over 30%–similar to those reported in the 

U.S. and Canadian studies (Spengler et al., 1994a; Dales et al., 1991a,b). The association of 

dampness in buildings with asthma may be confounded by the effect of housing conditions, 

socioeconomic status, and the presence of other allergens, but large epidemiology studies that 

controlled for these factors did not find them to have a significant effect on the moisture-asthma 

relationship (Dales et al,1991a,b; Platt et al., 1989). Thus, the results of the studies shown in 

Table 3.4 can be used to make estimates for California. 

Equation 1 was used to estimate the fraction of asthma attributable (AF) to dampness and mold, 

using odds ratios (OR) and prevalence rates (p) specific to each study population: 

AF = p(OR-1) / (p(OR-1)+1) [Equation 1; Lilienfeld and Lilienfeld, 1980] 

Table 3.4 shows the calculations of attributable fraction1

 using odds ratios, rather than relative 

risks, from the results of these four major studies. The average attributable fraction of asthma 

due to dampness or mold in homes is estimated to be 0.13. 

 

1

 The attributable fraction is normally calculated using the relative risk value, but odds ratios can be used 

instead where the outcome prevalences are relatively low. For example, with prevalence rates of 11.4% 

for asthma symptoms and 16.9% for lower respiratory symptoms in the study by Spengler et al. (1994), 

the relative risks are approximately equal to the odds ratios. Thus, the attributable fraction can be 

estimated using odds ratios (ORs) in place of relative risks (RRs). 
Indoor Air Pollution in California July, 2005 

 125

Table 3.4. Fraction of Asthma Attributable to Mold or Dampness in Houses 

Study and Condition Study Population Prevalence of 

Condition (%) Asthma Symptoms 

 

Adjusted 

Odds Ratio 

(95% CI) 

Estimated 

Attributable 

Fraction 

Spengler et al. (1994), 

mold or mildew 

12,842 U.S. children 

ages 9-11 36 1.39 

(1.23-1.57) 0.12 

Dales et al. (1991a), 

dampness or mold 

13,495 Canadian 

children ages 5-8 38 1.45 

(1.23-1.71 0.15 

Dales et al. (1991b), 

dampness or mold 

14,700 Canadian 

adults 38 1.56 

(1.25 -1.95) 0.18 

Zock et al. (2002), 

mold or mildew 

last year 

19,218 adults, 

38 centers in U.S., 

Europe, Australia, 

India, New Zealand 

22 1.28 

(1.13-1.46) 0.06 

AVERAGE 0.13 

To estimate the national cost of asthma, two estimates of asthma costs (Weiss and Sullivan, 

2001; Smith et al., 1997) were reviewed. The estimates of direct costs from the two studies are 

similar. However, the estimate of medical and indirect costs based on Weiss and Sullivan 

(2001) are more recent than those from Smith et al. (1997), and they do not exclude persons in 

the military, schools, and other institutions. Thus, the Weiss and Sullivan results may better 

reflect the current costs of treatment and medications, and are used here. 

The Weiss and Sullivan estimates were adjusted to 2000 dollars and 2000 population using the 

data on population growth and medical care and general inflation. No adjustment was made for 

changes in asthma prevalence because it is not clear that asthma prevalence has changed 

since 1994 (Mannino et al., 2002). It was also assumed that the prevalence of asthma in 

California is similar to the average prevalence of asthma in the U.S. Data in IOM (2004) indicate 

that self-reported asthma prevalence in California was 7.1% versus 6.4% for the U.S.; however, 

more recent data (Rhodes et al., 2002) indicate that the prevalence of asthma in 2002 was 6.4% 

in California versus 7.5% for the full U.S. Thus, it is not clear that asthma prevalence in 

California differs from that for the U.S. at this time. 

The updated costs for the full U.S. were then multiplied by the 0.12, the percentage of U.S. 

population that resided in California in 2000. As shown in Table 3.5, the estimated premature 

death costs are $240 million, as discussed in the premature death section above. The estimated 

medical costs and indirect costs (such as lost work days and school days) of asthma in 

California are $980 million and $460 million, respectively. 

To estimate the asthma costs attributed to indoor mold and moisture problems, these costs of 

asthma in California were multiplied by 0.13, the attributable fraction of asthma from mold and 

dampness that was calculated above. This yields the estimated medical and indirect costs of 

$130 million and $60 million, respectively, for a total of $190 million, shown in Table 3.3. 
Indoor Air Pollution in California July, 2005 

 126

Table 3.5. Updated Estimates of Annual Cost of Asthma. 

Population Group Cost in U.S. ($ Billions)1 Cost in California ($ Billions)1

Death Medical Indirect2

 Total Death Medical Indirect2 Total 

Children -- -- 1.2 -- -- -- 0.14 -- 

Adults -- 2.6 -- -- -- 0.31 -- 

Both 2.0 8.2 3.8 13.9 0.24 0.98 0.46 1.7

1. In 2000 dollars. Row and column totals may not add precisely due to rounding of numbers. Source of 

U.S. estimates: Weiss and Sullivan (2001). California costs were estimated to be 12% of U.S. costs, 

based on the relative population sizes. 

2. Indirect cost elements include loss of work, loss of school, and reduced housekeeping. 

Extensive data are not available on the costs of asthma that are preventable, but a large portion 

would appear to be readily preventable. The triggers (sources or conditions) considered in this 

analysis are tobacco smoking, pets, use of gas stoves for heat, dust mites, cockroaches, and 

dampness/mold. Behavioral changes can eliminate all indoor tobacco smoking, indoor pets in 

homes of people with pet allergies, and use of gas stoves for heat in the homes of asthmatics. 

Dust mite allergen levels can be diminished by reducing indoor humidity and by surface 

cleaning; however, studies of dust mite remediation measures have had only moderate 

success. Cockroach infestations can be reduced substantially using pest management 

methods. Mold contamination in buildings can be reduced by preventing and remediating 

dampness problems. 

Many dampness problems, probably a majority of serious problems, result from water leaks that 

could be prevented through better building maintenance and improved design and construction. 

These measures would also reduce the costs of dampness-caused mold contamination and 

degradation of building materials. Better ventilation and use of dehumidifiers could reduce 

dampness problems that result from high indoor humidity. Thus, with proper measures, it is 

probably feasible to eliminate a substantial portion of the indoor particle exposures that 

contribute to asthma exacerbation. 

3.3 PRODUCTIVITY COSTS OF INDOOR AIR POLLUTION 

Sick building syndrome is a collection of non-specific symptoms such as eye, nose, skin, and 

throat irritation; headache; fatigue; and skin rash that have no known cause. Inadequate 

building ventilation, as indicated by elevated indoor CO2 concentrations, as well as elevated 

indoor levels of VOCs, elevated levels of biological contaminants, and other environmental 

stressors have been implicated as potential causes of sick building syndrome. 

Fisk (2000) estimated the economic impacts of sick building syndrome in the U.S. due to 

reductions in worker productivity. Several field and laboratory studies of office buildings and 

school buildings were reviewed; the performance reduction for specific tasks ranged from 3-5%. 

The midpoint value of 4% was reduced to 2% to estimate the overall productivity reduction 

throughout the day. Using this conservative estimate of a 2% preventable reduction in worker 

productivity due to sick building syndrome, the estimated cost savings for the U.S. in 1996 
Indoor Air Pollution in California July, 2005 

 127

dollars were $10-30 billion ($11-33 billion in 2000 dollars). An independent group of scientists 

who reviewed the literature and assessed the impacts of indoor air quality on worker health and 

productivity for the National Institute of Occupational Safety and Health estimated the same 

costs (Mendell et al., 2002). 

To estimate the costs of sick building syndrome in California, this $11-33 billion U.S. estimate by 

Fisk can be scaled to reflect California’s portion of the U.S. population, or 12%. This would yield 

a California estimate of $1.3-4.0 billion per year, for an average of $2.6 billion per year. 

Kats (2003) used the 2% preventable reduction in worker productivity estimate by Fisk (2000) to 

estimate an avoidable cost of sick building syndrome in California. Using California-specific data 

where available, Kats estimated this avoidable cost to be $9 billion per year ($6 billion in wages 

and $3 billion in worker benefits). Using only a 1% lost productivity value, Kats calculated that 

sick building syndrome reductions in State of California buildings were equivalent to a present 

value of $37-$55 per square foot of building space over 20 years, compared to average energy 

costs of $1.47 per square foot for state buildings. The avoidable cost estimate of $9 billion for 

California is much larger than the estimate derived from Fisk because it includes employee 

benefits to reflect the workers’ full market value, and it reflects the higher percentage of office 

workers and the higher salaries in California compared to the U.S. 

For estimating the costs of sick building syndrome in California’s school and office buildings, we 

use the more comprehensive and California-specific approach of Kats. We modified his 

estimate by using more recent data and conservative estimates of worker benefits costs, as 

follows. California has 7 million workers in offices or schools, and their average salary is 

$43,000 per year in 1998 dollars (Kats, 2003). Sick building syndrome symptoms are again 

conservatively estimated to cause a 2% decrease in worker productivity. Multiplying these 

values together yields a cost of about $6 billion per year. For U.S. white collar workers in 1999, 

salary accounted for 72.8% of their total compensation on average, while benefits such as 

health insurance and retirement accounted for 27.2% (USCB, 2002). Dividing this benefit 

percentage by the salary percentage yields a ratio of 0.37 as the additional fraction for 

compensation as benefits. Multiplying 0.37 by the salary estimate of $6 billion yields an 

estimated overhead cost of $2.2 billion. This is a conservative estimate because it does not 

include other overhead costs to the employer such as training, equipment, and travel. 

Combining these salary and benefit cost estimates yields a total cost estimate of $8.2 billion, or 

$8.5 billion in 2000 dollars, due to the avoidable impacts of sick building syndrome on worker 

productivity in California. 

3.4 SUMMARY OF ESTIMATED COSTS 

The combined cost of both fatal and non-fatal impacts due to indoor air pollution in California 

homes, schools, and non-industrial workplaces is substantial; it is estimated at $45 billion per 

year, as shown in Table 3.6 below. The annual valuation of premature death attributable to 

indoor air pollution is estimated to total about $36 billion. The costs attributed to ETS and radon 

dominate the total cost. However, this is not because they are necessarily the predominant 

health hazards from indoor air in California, but because those are the two pollutants out of 

many indoor air pollutants for which there are sufficient data to estimate risk and costs. The cost 

estimates in this report do not include other indoor air pollutants that can increase the risk of 

premature death, and any synergistic affects among indoor and outdoor pollutants. Examples of 

these other pollutants include: PM from wood smoke, other toxic substances emitted from 

materials and products, and biological pollutants such as mold, bacteria, pollen, and animal 
Indoor Air Pollution in California July, 2005 

 128

allergens. Therefore, the actual total valuation of death and disease costs are likely to be even 

higher than estimated here. 

Table 3.6. Summary of Estimated Annual Costs of 

Some Indoor Air Pollution in California

Health End Point 

Health 

Valuation: 

Premature 

Death1-3 

($ Billions/yr)

Medical 

Cost2-4 

($ Billions/yr)

Lost 

Productivity 

Cost2,3 

($ Billions/yr) 

Total Cost

($ Billions/yr)

CO: poisoning 0.15 <0.001 NA 0.15 

VOCs: cancer 0.73 0.011 NA 0.74 

ETS: lung cancer 2.4 0.025 NA 2.4 

ETS: heart disease 23 0.055 NA 23 

ETS: asthma episodes NA 0.0205 NA 0.020 

ETS: low birth weight NA 0.19 NA 0.19 

ETS: otitis media NA 0.0195 NA 0.019 

Radon: lung cancer 9.5 0.097 NA 9.6 

Mold and moisture: 

 asthma and allergies 0.031 0.195 NA 0.22 

Sick building syndrome NA NA 8.5 8.5 

 TOTAL6 36 0.6 8.5 45 

1. From Table 3.2. 

2. Estimates are based on average or mid-point of incidence rates of mortality and morbidity from previous tables, 

and estimates of productivity discussed in the text. Values are rounded to two significant figures. 

3. Original data were adjusted to year 2000 dollars and year 2000 population, except where noted otherwise in 

previous tables. 

4. From Table 3.3. 

5. Includes indirect costs such as lost work days, lost school days, and travel expenses. 

6. Totals are rounded to 2 significant figures. These totals are likely low because conservative cost estimates were 

used, and quantitative information is not readily available for many known impacts of indoor air pollution, such as 

for indoor PM and many indirect costs of health effects. 

The quantifiable medical costs (direct and some indirect) due to some indoor air pollutants total 

more than $0.6 billion per year, with a large portion of the costs attributable to mold and other 

moisture-related allergens and sum of all ETS-related medical costs. Again, this is certainly a 
Indoor Air Pollution in California July, 2005 

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very low estimate: the cost estimates for disease do not include of the potential losses due to 

other indoor allergens, CO poisoning’s long-term effects, reduced student performance, lost 

earnings opportunity, unpaid caregivers, and human suffering. Finally, the cost of reduced 

worker productivity due to indoor air pollution (sick building syndrome) that could be prevented 

is estimated to be $8.5 billion per year. As discussed in the next section, case studies have 

documented that measures to reduce indoor air pollution in homes and schools can have 

immediate and cost-effective benefits on human health and student performance. 

3.5 BENEFITS OF IMPROVING INDOOR AIR QUALITY 

Several case studies and demonstration programs have documented the economic, 

productivity, and health benefits that can accrue by improving IAQ. The following examples and 

other available examples provide empirical data on the benefits achieved in different types of 

buildings. 

Residential Buildings

The Seattle Healthy Home Project has found that home visits to low-income households by a 

trained community health worker can reduce asthma symptom significantly and cost-effectively 

(Takaro et al., 2004; Krieger et al., 2005). This program reduced medical costs for asthma 

treatment significantly, in both the low-intensity version (one visit over the year) and the highintensity version (multiple visits over one year). The observed marginal cost savings were 

$1,316 to $1,849 per patient over four years. These savings do not reflect the reduced number 

of emergency room visits and the reduced risk of asthma-related deaths. 

The "Healthy Neighborhoods Program" of New York State inspected over 45,000 homes for 

health and safety problems, and intervened where necessary (HUD, 1999; NYS, 1999). 

Interventions addressed lead-based paint hazards, fire safety, carbon monoxide, and asthmarelated conditions. Interventions were generally simple and low cost, such as providing working 

smoke detectors and batteries, CO detectors, and furnace filters. The program results showed 

that the visits to each home cost $132 per unit. However, the benefits for lead poisoning 

prevention, asthma reduction, and burn prevention alone were worth at least $285 per unit, 

excluding estimated benefits associated with reduced injury, CO poisoning, and fire. 

Schools

Office visits for asthma inhaler use dropped by 50% at two elementary schools in San Francisco 

Unified School District (USD) after the IAQ Tools For Schools program was pilot tested (U.S. 

EPA, 2000a). In addition, fewer asthma episodes occurred, and fewer students brought asthma 

medications or inhalers to school. 

A study of Chicago and Washington, DC schools found that better school facilities can add three 

to four percentage points to a school’s standardized test scores, even after controlling for 

demographic factors (Schneider, 2002). This and other studies reviewed by Kats (2003) and 

Fisk (2000) confirm a widely held, common sense perception that the physical quality of the 

classroom environment greatly affects how well children learn. 

An analysis of two school districts in Illinois, one small and one large, found that student 

attendance improved by 5% after incorporating cost effective indoor air quality improvements – 

regardless of school district size (Healthy Schools Campaign, 2003). 

Clovis USD near Fresno, and Everett USD near Seattle, have used the IAQ Tools for Schools

program and a rapid complaint response approach using a portable indoor air monitoring kit. 
Indoor Air Pollution in California July, 2005 

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Additional staff were not needed to implement the program. his program has quickly paid for 

equipment by reducing the number of complaints by up to 60%, and by reducing the cost for 

environmental consultants (Poytress, 2003; Jefferis, 2004). It has also greatly improved the 

credibility of the school maintenance program with school staff and parents of students. 

Indoor air quality is one of several important indoor environmental factors affecting student 

performance. In a study of over 8,000 students in third through sixth grade in Fresno, Heschong 

(2003) investigated the effect of daylight and other indoor environmental quality effects on 

student test scores over an academic year. As expected, commonly recognized factors such as 

teacher characteristics, number of computers, or attendance rates were found to be significant 

in predicting student performance. However, physical characteristics such as indoor air quality, 

ventilation, acoustics, and especially daylighting were found to be equally significant, if not more 

significant. 

The economic benefits of improved indoor air quality in schools, in terms of improved student 

productivity and health has not been estimated. The potential benefits of improved productivity, 

even assuming a slight increase in test scores and intelligence quotients (IQ), could be quite 

large. 

Office Buildings

Recent experiments in office buildings have shown that office worker performance could be 

significantly increased over the short term by removing common indoor sources of air pollution, 

such as floor coverings, used supply air filters, and personal computers (Wyon 2004). 

Alternatively, keeping these pollutant sources in place while increasing the ventilation rate from 

1.5-3 liters per second (lps) to 10-30 lps per person (3-6 cfm/person to 20-60 cfm/person) also 

increased worker performance. These short-term effects on worker performance were 

demonstrated repeatedly, even at pollutant levels that increased SBS symptoms such as 

headache and poor concentration but had no measurable effects on the occupants’ perception 

of air quality. These short-term effects have been validated recently in field intervention 

experiments in call centers in northern Europe and the tropics, and the effects were larger than 

those found in the laboratory. 

The potential benefits of these improvements in workplace indoor air quality are substantial. 

Economic calculations based on this series of experiments indicate that benefits for improving 

indoor air quality beyond the minimum level acceptable to visitors would exceed improvement 

costs by a factor of about 60 (Wargocki and Djukanovic, 2003). Typical payback periods were 

estimated to be about two years. In another study, the economic benefits of reduced employee 

sick leave in offices can be achieved by increasing ventilation rates over the minimum 

recommended rate, as shown in epidemiological research in the U.S. (Milton et al., 2000). 
Indoor Air Pollution in California July, 2005 

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4. EXISTING REGULATIONS, GUIDELINES, AND PRACTICES 

Despite the ubiquitous presence of toxic pollutants in the indoor environment, there are no 

government air quality regulations that are intended to protect the general public in residences, 

schools, or public buildings. Workplace regulations address indoor air quality, but they are 

designed for 8-hour exposures of healthy adults, and are not designed to be protective for 

longer periods nor for some of the more sensitive subgroups of the population, such as children 

and the elderly. Ambient air quality standards are focused on outdoor air quality, and are not 

designed to protect indoor air quality. Other regulations, such as California's Proposition 65, and 

AB 13, which prohibits cigarette smoking in workplaces, are applicable to indoor air quality only 

in a limited way and do not prevent indoor emissions and exposures. 

There are a few examples of government regulations for emissions from specific sources of 

indoor pollutants that are intended to protect the general public in indoor environments. In 

addition, a variety of government agencies and private organizations have established voluntary 

guidelines and practices that can be applied to indoor environments to assist in the assessment 

and control of health hazards from air pollutants. The following sections summarize the pertinent 

regulations, guidelines, and practices for the following categories: 

• Indoor and outdoor air quality in general. 

• Emission limits for consumer products, appliances, and building materials. 

• Building design. 

• Building operation and maintenance. 

4.1 STANDARDS AND REGULATIONS 

4.1.1 Workplace Air Quality Regulations 

The California Occupational Safety and Health Program (Cal/OSHA) in the Department of 

Industrial Relations (DIR) has jurisdiction over most private and public employers and 

employees in California, with the exception of U.S. government employees. Cal/OSHA has 

regulatory authority to develop, promulgate, and enforce air pollutant exposure limits, ventilation 

regulations, and other standards for the workplace that directly impact indoor air quality. The 

California Occupational Safety and Health Standards Board is the unit within the Cal/OSHA 

program with authority to adopt standards and regulations to protect workers. Labor Code 

Section 144.6 requires the Standards Board to adopt standards that “most adequately assures, 

to the extent feasible, that no employee will suffer material impairment of health or functional 

capacity even if such employee has regular exposure to a hazard regulated by such standard 

for the period of his working life.” 

Under CCR Title 8, Section 5155, the Standards Board sets permissible exposure limits (PELs) 

and other limits for airborne contaminants. The PELs legally apply to both industrial and nonindustrial workplaces. However, they are not sufficient to prevent health impacts for all working 

individuals, such as individuals with pre-existing heart or respiratory disease, and they do not 

address possible impacts on those with asthma or reactions by sensitive individuals to low 

levels of chemicals. The Cal/OSHA PELs are 8-hour exposure limits designed to protect healthy 

working adults, and may be based in part on technological and economic feasibility 

considerations (non-health related criteria). These standards are not developed to protect 

infants, the elderly, or other sensitive groups who may frequent non-industrial workplaces (such 

as public buildings and retail establishments), nor are they intended to be protective for 

exposures greater than eight hours per day, five days a week. Additionally, PELs have not been 
Indoor Air Pollution in California July, 2005 

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developed for a number of known indoor air contaminants, and they are not designed to 

evaluate the health and comfort risks posed by the complex mixtures of pollutants found in 

modern buildings such as offices, schools, and homes. Generally, lower exposure limits would 

be necessary to protect the general population. 

Both Cal/OSHA and others are aware that PELs do not fully address indoor air quality concerns 

in all workplaces. Cal/OSHA’s Indoor Air Quality Policy and Procedure (C-48) states: “Most 

complaints about the quality of indoor air arise from employees who work in non-industrial 

environments...Approaches using traditional industrial hygiene techniques usually demonstrate 

compliance with 8 CCR section 5155 (PELs) despite the persistence of IAQ complaints from the 

building occupants.” The Hazard Evaluation Section and Information Service (HESIS) within 

DHS also affirms that non-industrial workers experiencing indoor air quality problems are 

seldom exposed to contaminant levels approaching PELs. 

Cal/OSHA also has regulations concerning the operation and maintenance of HVAC systems, 

and the control of moisture, vermin, and other sanitation concerns, as discussed later in Section 

4.5. In addition, Section 3203, Illness and Injury Prevention Program, requires employers to 

have written plans for hazard identification, evaluation, and correction, for communication with 

employees, and for training. Other Cal/OSHA requirements reduce or prevent employee 

exposures to asbestos (Sections 5208, 1529), lead (Section 1532.1), and environmental 

tobacco smoke (Labor Code 6404.5, and Section 5148). 

4.1.2 Ambient Air Quality Standards 

National and State ambient air quality standards (AAQS), established by the U.S. EPA and the 

ARB, respectively, are developed to protect sensitive subpopulations from the harmful effects of 

“traditional pollutants” in outdoor air, for specified averaging times (exposure times). California’s 

AAQS are often more protective than the national AAQS. Currently, the State AAQS are under 

review to ensure that they are protective of sensitive populations, especially infants and children 

(ARB/OEHHA, 2000). In the absence of indoor air quality standards or guidelines, the AAQS 

serve as useful guidelines for indoor air quality, because they are based on specified averaging 

times and incorporate a margin of safety. Outdoor standards for PM are often exceeded in 

indoor environments, and standards for CO, NO2, and ozone are sometimes exceeded. National 

and state AAQS are available at http://www.arb.ca.gov/research/aaqs/aaqs.htm. 

4.1.3 Reference Exposure Levels for Air Toxics 

The Air Toxics “Hot Spots” Information and Assessment Act of 1987 (Assembly Bill 2588 as 

codified in Health and Safety Code Section 44300 et seq.) requires stationary sources of air 

pollutants (e.g., industrial plants) to report the types and quantities of substances their facilities 

routinely release into the air, ascertain health risks associated with the release, and notify 

nearby residents of significant risks. An amendment to the statute in 1992, SB 1731 (Calderon), 

requires OEHHA to prepare and adopt risk assessment guidelines, and requires facilities with a 

significant risk to prepare and implement risk reduction plans. Under this act, OEHHA develops 

acute and chronic reference exposure levels (RELs) as guidelines to prevent harm from toxic air 

pollution (http://www.arb.ca.gov/toxics/toxics.htm). 

RELs are used by Cal/EPA agencies as indicators of potential adverse health effects other than 

cancer. RELs are generally based on the most sensitive adverse health effect reported in the 

medical and toxicological literature. They are designed to protect the most sensitive subgroups 

of the population by the inclusion of margins of safety. Because uncertainty factors are 
Indoor Air Pollution in California July, 2005 

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incorporated into the REL, an air concentration greater than the REL does not necessarily mean 

that the exposed public will suffer adverse health impacts. The methodology and studies used to 

develop the REL health standards are detailed in two documents available on the OEHHA 

website (http://www.oehha.ca.gov/): the Air Toxics Hot Spots Program Risk Assessment 

Guidelines, Part 1: The Determination of Acute Reference Exposure Levels for Airborne 

Toxicants, March 1999 and the Air Toxics Hot Spots Program Risk Assessment Guidelines, Part 

III: The Determination of Chronic Reference Exposure Levels for Airborne Toxicants, February 

2003. 

OEHHA has established chronic RELs for approximately 71 air pollutants. Chronic RELs are 

indicators of healthy versus potentially unsafe levels resulting from long-term exposure, 

exposure lasting at least 8% of a lifetime or 12 years and possibly longer. Chronic RELs are 

intended to indicate levels that will not cause adverse health effects in individuals with high 

susceptibility for chemical injury as well as identifiable sensitive subpopulations (high-risk 

individuals). However, chronic RELs may not necessarily be indicative of safe levels in 

hypersensitive individuals. 

Acute RELs are indicators of healthy versus potentially unsafe levels of exposure for short 

periods of time, such as one hour. Because exposure is for a short time period, acute RELs are 

always higher than chronic RELs. OEHHA has established acute RELs for 51 chemicals 

(OEHHA, 2000a). OEHHA recommends that acute RELs be used to evaluate exposures that 

occur no more frequently than every two weeks in a given year. 

In addition to providing an indication of healthful versus potentially unsafe levels outdoors near 

stationary sources, the acute and chronic RELs are also being used to identify healthful versus 

unhealthful pollutant levels in indoor air. Formaldehyde is a very common indoor air contaminant 

that has both cancer and non-cancer health effects. Because of the frequent use of RELs for 

indoor application, OEHHA developed an additional REL for formaldehyde, an interim REL 

(IREL) based on an 8-hour exposure period. The IREL established for formaldehyde is 27 ppb. 

The IREL identifies the level below which irritant effects such as eye, nose, and throat irritation 

would not be expected to occur during typical daytime (8-hour) occupancy of buildings. Other 8-

hour IRELs are not yet available. Chronic RELs have been used in developing building material 

emission limits for use by DGS in specifying requirements for new state buildings and 

furnishings. These are known as Section 01350 requirements, and are discussed in detail in 

Section 4.3.3.2. 

4.1.4 Tobacco Control in the Workplace and Public Buildings 

Cigarette smoking is a major source of indoor pollution that is now prohibited in most public 

buildings in California. Passage of a statewide smoke-free workplace law in 1995 (AB 13, 

Friedman; Labor Code 6404.5, Section 5148) led to a reduction in smoking by the California 

population and eliminated smoking at nearly all California indoor workplaces, including 

restaurants, bars and gaming clubs. This statewide prohibition is primarily enforced at the local 

level. Cal/OSHA is required to respond to complaints of workplace cigarette smoke after the 

employer has been found guilty at the local level three times in the previous year. Prior to 

passage of the statewide law, numerous city and county ordinances had been implemented to 

restrict cigarette smoking. 

The smoke-free workplace law contains fourteen exceptions to the smoking ban, each with 

additional explanations and stipulations. Exclusions include some hotel/motel guest rooms, 

hotel/motel lobbies, private meeting rooms, tobacco shops, truck cabs, warehouse facilities, 
Indoor Air Pollution in California July, 2005 

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gaming and bingo clubs, bars and taverns until January, 1997, theatrical productions, medical 

research sites, private residences, patient smoking areas, employee breakrooms, and small 

businesses. Despite the exclusions, the ban has been very successful in reducing worker 

exposure to cigarette smoke. In 1999, 93.4% of California’s indoor workers reported working in 

a smoke-free environment, compared to only 45% in 1990 (Gilpin et al., 2001). 

The workplace prohibition of smoking has had far reaching benefits. The percentage of 

Californians with children under the age of 18 who do not allow smoking in the household has 

increased substantially. In 1994, 63.0% of Californians with children did not allow smoking in the 

house. By 2001, 77.9% did not allow it (Gilpin et al., 2001). Fewer Californians are smoking as a 

result of this legislation and the DHS Tobacco Control Program. Smoking rates among 

California adults have declined from 26% in 1984 to 17% in 2001 (BRFSS, 2001). Californians 

who still smoke are smoking fewer cigarettes than they did in the past (Gilpin et al., 2001). 

4.1.5 Pesticide Regulations 

Three agencies are primarily responsible for the regulation of pesticides in California: the U. S. 

EPA, the California Department of Pesticide Regulation (DPR), and county agricultural 

commissioners. Federal law requires that before selling or distributing a pesticide in the United 

States, a person or company (registrant) must obtain registration, or license, from the U. S. 

EPA. Before registering a new pesticide, the U. S. EPA must first ensure that the pesticide, 

when used according to label directions, can be used with a reasonable certainty of no harm to 

human health and without posing unreasonable risks to the environment. To make such 

determinations, U. S. EPA requires more than 100 different scientific studies and tests from 

applicants. U. S. EPA works with registrants to develop labels (legal requirements for use) that 

describe the proper storage, handling, and application for each pesticide product. U. S. EPA 

performs similar actions for older pesticides under its re-registration program. 

Under California law, DPR is responsible for providing the proper, safe, and efficient use of 

pesticides, and for protection of the environment and health. To accomplish this, DPR has its 

own registration program and study requirements, over and above those required by U.S. EPA. 

Once registered and used in California, DPR continues to evaluate pesticides, including 

programs to assess worker safety, water and air contamination, and pest management 

alternatives. DPR’s pest management program specifically focuses on solutions that incorporate 

integrated pest management (IPM), which includes the use of non-chemical practices to reduce 

pest populations, using least toxic pesticides to treat infestations above designated thresholds, 

and training relevant individuals regarding IPM approaches. The program provides: 

• DPR's IPM Innovator awards to honor California organizations that emphasize pest 

prevention, favor least-toxic pest control, and share their strategies. 

• Assistance to agricultural and urban pest managers to solve environmental problems by 

implementing IPM strategies. 

• Pest management assessments and pesticide use trends for various commodities and 

pesticides. 

• School IPM for buildings and grounds to help districts start an IPM program and fulfill 

other requirements of the Healthy Schools Act. 

DPR can issue regulations regarding sales and use of pesticides to mitigate potential health or 

environmental hazards, as well as suspend/cancel if a hazard cannot be mitigated. To ensure 

pesticides are applied properly, DPR conducts examinations and issues licenses for people who 

handle pesticides, such as applicators who use restricted pesticide materials. Restricted 
Indoor Air Pollution in California July, 2005 

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materials are those that must be applied by, or under the supervision of, a certified applicator. 

Most require a permit issued by the county agricultural commissioner before purchase and use. 

California’s county agricultural commissioners are responsible for enforcing pesticide laws and 

regulations at the local level. Agricultural commissioners evaluate and issue/deny permits for 

restricted materials, taking into account local circumstances. Agricultural commissioners may 

include additional conditions on the permit, over and above those required by the label and 

regulations. Agricultural commissioners also certify private applicators, conduct inspections, 

provide training, and are responsible for investigating pesticide-related illnesses and damage. 

4.1.6 Proposition 65 

In 1986, California voters approved Proposition 65, the Safe Drinking Water and Toxic 

Enforcement Act of 1986, an initiative to address concerns about exposure to toxic chemicals. 

Proposition 65 requires the State to publish a list of chemicals known to cause cancer, birth 

defects, or other reproductive harm. The list includes approximately 750 chemicals, many of 

which are additives or ingredients in pesticides, common household products, food, drugs, dyes, 

solvents, building materials, and other sources found indoors. Businesses are required to 

provide a “clear and reasonable” warning when their products or actions may result in a release 

of chemicals above a specified threshold level, so that members of the public are aware they 

may be exposed to harmful chemicals. Warnings have evolved to include labeling of consumer 

products, posting signs at the workplace or on new housing, and publishing notices in a 

newspaper. OEHHA develops numerical guidance levels, known as “safe harbor” levels, for 

determining whether a warning is necessary. For potential carcinogens, the Proposition 65 “no 

significant risk level” is one excess case of cancer per 100,000 individuals exposed over a 70-

year lifetime; for reproductive toxicants, the “no significant risk level” is one-thousandth of the no 

observable effect level (NOEL). Proposition 65 pollutants and safe harbor levels are available 

on the OEHHA website at http://oehha.ca.gov/prop65.html. 

4.1.7 Radon In Drinking Water 

Radon levels in typical groundwater concentrations pose higher risks than those posed by the 

other drinking water contaminants that have been subjected to regulation (e.g., disinfection byproducts). U.S. EPA was directed under the Safe Drinking Act (as amended in 1996) to attempt 

to regulate radon in drinking water. Though it has no authority to regulate indoor air radon, 

which is dominated by the soil gas infiltration, the U.S. EPA recognized that it would be far more 

cost effective to mitigate indoor air radon. The Safe Drinking Act gave U.S. EPA the latitude to 

allow higher concentrations of radon in drinking water if efforts were established to reduce 

indoor air radon to achieve risk reduction equal to or greater than the risk reduction that would 

be achieved by reducing the concentration of radon in drinking water (U.S. EPA, 1996). 

The U.S. EPA is in the process of promulgating a maximum contaminant level (MCL) for radon, 

which is the allowable concentration based only on the contaminant risk in drinking water (U.S. 

EPA, 2000e). The proposed MCL is 300 pCi/l. An alternative MCL, 4000 pCi/l for states that had 

multimedia radon mitigation programs, and would allow utilities not to treat radon concentrations 

between the MCL and AMCL. Multimedia programs would aim to reduce indoor air radon risk, 

using a combination of approaches allowed in the regulations: public education; testing; training; 

technical assistance; remediation grants, loan or incentive programs; or other regulatory or nonregulatory measures. EPA (2000e) plans to make their multimedia program regulations effective 

in December 2005. 
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4.2 INDOOR AIR QUALITY GUIDELINES 

Various governmental and private organizations issue guidelines to promote healthful indoor 

environments. Such guidelines cannot be enforced; compliance with the recommended levels is 

voluntary. Guidelines mentioned here are generally based on health or comfort endpoints. 

4.2.1 ARB Indoor Air Quality Guidelines 

The ARB has published three indoor air quality guidelines – for formaldehyde, combustion 

pollutants, and chlorinated hydrocarbons. ARB’s indoor air quality guidelines discuss the indoor 

sources and potential health effects of various pollutants, and provide information to the public 

on ways to limit or reduce their exposure to those pollutants. The guideline levels were 

developed in consultation with DHS and OEHHA, and are set to protect sensitive subgroups of 

the population. Because a number of the chemicals covered in the guidelines may cause cancer 

or other significant health problems, and no absolutely safe levels have been identified, 

recommendations are made to take action to prevent emissions of those chemicals in the home 

and to reduce exposure to the greatest extent feasible (ARB, 1991; ARB, 1994b; ARB, 2001b; 

ARB, 2004). Guidelines for traditional pollutants are based on the ambient air quality standards 

for California, because the basis of those standards is the health impacts seen at different air 

concentrations for specified exposure durations, which would be the same regardless of 

whether the individual is standing indoors or outdoors. An indoor air quality guideline for ozone 

is under development and is expected to be released in 2005. 

4.2.2 Air Quality Guidelines For Europe 

“Air Quality Guidelines for Europe” were developed by the World Health Organization’s (WHO, 

2000) Regional Office for Europe, a specialized agency of the United Nations. The guideline 

value indicates a concentration of air pollutant below which no adverse effect to human health is 

expected, based on consideration of both carcinogenic and other health effects. They are 

intended to be applicable to both indoor and outdoor air exposures. Guideline values have been 

established for 38 non-carcinogenic compounds and some carcinogens for various exposure 

periods ranging from 15 minutes to one year. They address public health and are intended to be 

protective of the entire population. Uncertainty factors are used to extrapolate from animals to 

humans and from a small group of individuals to a large population. These factors are based on 

experience, wisdom, and judgement. 

The latest edition of the WHO guidelines is more recent than the ARB indoor air quality 

guidelines. Some of the WHO guideline levels differ from the ARB guideline levels in part 

because they are based on more recent studies. For example, the current WHO NO2 guideline 

is 100 ppb for 1 hour and 20 ppb for an annual average, while ARB’s guideline is 250 ppb for 1 

hour (a guideline for an annual average is not included). The ARB guideline coincides with the 

ARB ambient air quality standard for NO2, currently under review. If a new California standard is 

adopted, the guideline value may better align with the more recent WHO guideline. 

4.2.3 DHS Mold Guidelines 

The California Department of Health Services through the Division of Environmental and 

Occupational Disease Control (DEODC) is engaged in many types of activities regarding indoor 

mold. DEODC staff members provide current information about mold health effects and 

remediation recommendations through educational outreach to the general public, health care 

professionals, city and county government staff, and private environmental assessors and mold 
Indoor Air Pollution in California July, 2005 

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remediators. Staff members also conduct research to improve understanding of how indoor 

microbial growth affects human health, especially in sensitive groups such as pregnant women, 

children, and persons with asthma. DEODC Occupational Health Branch staff conducts health 

consultations in conjunction with Cal/OSHA to prevent harmful microbial exposures in California 

workplaces. 

Table 4.1. ARB Indoor Air Quality Guidelines 

Outdoor Air Quality 

Standards Pollutant Measurement 

Period

ARB 

(2005c)

U. S. EPA

(2004a)

ARB Recommended Maximum 

Indoor Levels

Formaldehyde 

(HCHO) 

24-hour 

8-hour 

--- --- Lowest level feasible to reduce 

cancer 

< 27 ppb to avoid acute irritant 

effects 

Carbon Monoxide 8 hours 9 ppm 9 ppm 9 ppm 

(CO) 1 hour 20 ppm 35 ppm 20 ppm 

24 hours --- --- 0.08 ppm 

avoid repeated high exposures 

Nitrogen Dioxide 

(NO2) 

1 hour 0.25 ppm --- 0.25 ppm 

Particles – (PM10) 24 hours 50 μg/m3 150 μg/m3 50 μg/m3 

Particles – (PM2.5) 24 hours --- 65 μg/m3 65 μg/m3 

Polycyclic Aromatic 

Hydrocarbons (PAHs) 

--- --- --- Lowest levels feasible to avoid 

cancer risk. Avoid or minimize 

exposure. 

Chlorinated Hydrocarbons, 

e.g., chloroform 

Trichloroethylene 

p-dichlorobenzene 

methylene chloride 

perchloroethylene 

methyl chloroform 

--- --- --- Lowest levels feasible to avoid 

cancer risk. Avoid or minimize 

personal exposures. 

DHS Indoor Air Quality (IAQ) Program staff members have developed a website, 

www.dhs.ca.gov/iaq, that provides information about mold-related health effects and voluntary 

guidelines for remediation of damp/moldy buildings through fact sheets and links to other good 

sources of mold-related information. Two fact sheets, “Mold in My Home: What do I do?” and 

“Mold in My School: What do I do”, produced by DEODC staff have been used by other state 

agencies. The latter was selected by the National Clearinghouse for Educational Facilities to be 

distributed to teachers nationwide and included on the Clearinghouse website, 

www.edfacilities.org. The DHS IAQ website also posts a “Listing of Consultants Offering IAQ 

Services in California” along with guidance for hiring IAQ consultants. This listing is a service 

allowing interested individuals to contact consultants in their geographic area. Because 

California does not license, certify, or endorse mold assessment or remediation professionals, 
Indoor Air Pollution in California July, 2005 

 138

individuals seeking assistance for moldy buildings are encouraged to use these and other 

reliable web resources to learn about this topic and find experienced consultants. 

The DHS IAQ Program also provides staff to address inquiries from the public about mold and 

other indoor environmental problems through the Indoor Air Quality Telephone Assistance 

Hotline. Staff also organize and conduct meetings of the California Interagency Working Group 

on Indoor Air Quality (CIWG-IAQ), with representatives from State, Federal, local, and nongovernmental agencies having IAQ oversight or interests. The CIWG-IAQ provides a unique 

forum for discussion, collaboration, and education on issues of indoor environmental quality, 

building engineering, and related health effects among the professionals working in the field. 

The Toxic Mold Protection Act of 2001 (SB 732 Ortiz; California Health and Safety Code 

Sections 26100 et seq.) was enacted to address increasing concerns regarding health effects 

from exposure to indoor molds and to provide Californians with guidelines or standards for the 

safe and effective removal of molds from buildings. Among other tasks, this statute directs the 

California Department of Health Services (DHS) to determine the feasibility of identifying 

permissible exposure limits for indoor molds. DHS scientists have addressed this issue, and 

their conclusions are included in a report currently undergoing internal review. When approved 

for public release, this report will be posted to the DHS Indoor Air Quality website. 

DEODC staff collaborates with other nationally recognized experts in developing guidance 

documents for mold assessment or remediation professionals, including: 

• American Conference of Governmental Industrial Hygienists. Bioaerosols: Assessment and 

Control. ACGIH. Cincinnati, OH. 1999 

• American Industrial Hygiene Association. Field Guide for the Determination of Biological 

Contaminants in Environmental Samples, 2nd Edition. In production. AIHA. Fairfax, VA. 

4.2.4 American Society of Heating, Refrigerating, and Air-Conditioning Engineers 

The American Society of Heating, Refrigerating, and Air Conditioning Engineers (ASHRAE) 

provides professional guidance on minimum building ventilation rates for human health and 

comfort. While not regulatory, ASHRAE Standards, especially Standard 62, Ventilation for 

Acceptable Indoor Air Quality (ASHRAE, 2003b), and Standard 55-2004 Thermal Environmental 

Conditions for Human Occupancy (ASHRAE, 2004) are important references for California’s 

ventilation standards and recommended comfort levels for nonresidential buildings. ASHRAE 

and other groups have also developed guidelines using indoor carbon dioxide concentrations as 

an indoor air quality indicator, ranging from about 800 to 1200 parts per million (ppm) as a “not 

to exceed” level. 

4.2.5 U.S. EPA’s IAQ Tools For Schools Program

Although it does not provide indoor pollutant guideline levels, U.S. EPA’s IAQ Tools for Schools 

Program (http://www.epa.gov/iaq/schools/) provides schools with information they need to 

understand IAQ issues, prevent IAQ problems, and assure healthful indoor air quality. The 

program uses a team approach to school IEQ management and emphasizes staff and occupant 

training, communication, and improved routine operation and a district. 

In California, U.S. EPA has trained more than 2000 individuals from districts throughout the 

state. Despite the outreach, awareness and use of the IAQ Tools for Schools program among 

California schools is still relatively low: about 11% of school districts use all or part of the 
Indoor Air Pollution in California July, 2005 

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program (ARB/DHS, 2003). U.S. EPA is partnering with organizations of school officials (e.g., 

ACSA, the Association of California School Administrators, and CASBO, the California 

Association of School Business Officers) to promote increased use of this program. 

California Assembly Concurrent Resolution No. 75 (Chan), enrolled in June 2003, recognizes 

the significance of school indoor environments to the childhood asthma problem, and 

“encourages California school districts to implement the Indoor Air Quality Tools for Schools 

Program for the benefit of asthmatic children and for the health, well-being, learning, and 

productivity of the entire school population“. 

4.3 EMISSION LIMITS 

Prevention or reduction of emissions from pollutant sources is the preferred control technique 

for most pollutants. This section will discuss known regulations, guidelines, and practices for 

limiting emissions from consumer products, appliances, and building materials. 

4.3.1 Consumer Products 

4.3.1.1 Government Regulations For Consumer Products 

Consumer Product Safety Commission (CPSC)

The federal Consumer Product Safety Commission (CPSC) has broad jurisdiction over 

consumer products, which are defined as any articles which are produced or distributed for sale 

to, or use by, consumers in or around the home or in schools, recreation areas, or other nonoccupational settings. Certain products are exempted from CPSC authority, including 

pesticides, cosmetics, tobacco and cigarettes, food, drugs, automobiles, airplanes and firearms. 

In addition, houses and other buildings are specifically excluded by legislative history and 

judicial review. However, CPSC does have jurisdiction over home building materials that are 

sold or distributed as separate products to consumers. 

CPSC has the authority under certain conditions to: (1) ban a product; (2) establish mandatory 

safety standards for products; (3) recall products for repair, replacement or refund: (4) mandate 

warning labels for products; and (5) cooperate with manufacturers in the development of 

voluntary product standards. The Federal Hazardous Substances Act (FHSA), enacted in 1960 

and administered by CPSC requires labeling of “hazardous substances” if they are “intended, or 

packaged in a form suitable, for use in the household or by children”. A hazardous substance is 

further broadly defined as a “toxic” substance that may cause substantial personal injury or 

illnesses through reasonably foreseeable or customary use. In 1992, a supplemental definition 

was added to the Act to require appropriate labeling if a substance has chronic hazards of 

cancer, neurotoxicity, and developmental or reproductive toxicity. 

CPSC has made a few notable contributions in areas related to IAQ regulation and research. 

Indoor pollutants regulated to some extent by CPSC through product bans or labeling 

requirements include asbestos, vinyl chloride, and combustion pollutants from appliances. 

However, voluntary product standards, rather than product bans and mandatory standards, are 

generally preferred by CPSC for several reasons. Voluntary standards take less time to develop 

and implement and are less likely to be challenged legally, so that public protection should 

occur sooner; they tend to be less intrusive, more responsive to technological change, and 

cheaper for all concerned. 
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The CPSC has focused on regulations for safety more than for health. For example, a policy on 

methylene chloride led to labeling regulations rather than a ban on its use in household products 

(CPSC, 1987a). The mandate of the California Department of Consumer Affairs (DCA) differs 

from that of the CPSC in that the DCA does not regulate consumer products directly, but rather 

regulates services provided to consumers and those who provide them, and addresses 

consumer complaints. 

ARB Consumer Products and Architectural Coating Programs

The focus of ARB’s Consumer Products and Architectural Coating Programs is to reduce the 

amount of reactive volatile organic compounds (VOCs) that are emitted from the use of 

consumer products and architectural coatings. The driving force behind the state and local 

regulations developed under these programs is not reducing exposure to VOCs in indoor air, but 

limiting the release of VOCs that have the potential to react with other pollutants under sunlight 

to form ground-level ozone and particulate matter (PM10), the main ingredients in smog. As a 

result of these regulations, indoor air quality has improved in some situations where these 

products are used. For example, ARB prohibited the use of three TACs, perchloroethylene, 

methylene chloride, and trichloroethylene in 13 categories including general purpose 

degreasers, brake cleaners, all spray paints, all aerosol adhesives and adhesive removers. 

Additionally, antiperspirants and deodorants are not allowed to contain any compounds 

identified as TACs. Overall, these prohibitions have reduced TAC emissions in consumer 

products by over 10 tons per day (tpd). ARB performs an annual survey to determine remaining 

emissions of perchloroethylene and methylene chloride used in consumer products. The 

purpose of the survey is to determine if further mitigation measures are necessary to reduce 

potential health risks from outdoor exposures. 

State air pollution regulations define "consumer product" as a chemically formulated product 

used by household and institutional consumers, including, but not limited to, detergents; 

cleaning compounds; polishes; floor finishes; cosmetics; personal care products; home, lawn, 

and garden products; disinfectants; sanitizers; aerosol paints; and automotive specialty 

products. Excluded from this definition are architectural coatings such as other paint products 

and furniture coatings. The VOC compositions of these excluded products are regulated by the 

local air pollution control and air quality management districts (districts), although the ARB 

provides considerable technical assistance to the districts and develops Architectural Coatings 

Suggested Control Measures (i.e., model rules) for adoption by the local districts. 

The California Clean Air Act (CCAA) enacted by the Legislature in 1988 added Section 41712 to 

the California Health and Safety Code (HSC), which requires the ARB to adopt regulations to 

achieve the maximum feasible reduction in reactive organic compounds emitted by consumer 

products. In enacting Section 41712, the Legislature gave the ARB clear new authority to 

control emissions from consumer products, an area that had previously been subject to very few 

air pollution control regulations. 

To date, ARB has adopted the following regulations to fulfill the requirements of the California 

Clean Air Act as it pertains to consumer products: 

• Antiperspirants and Deodorants Regulation 

• Consumer Products Regulations 

• Alternative Control Plan 

• Aerosol Coating Products Regulation 

• Hairspray Credit Program Regulation 
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Manufacturers are given flexibility in their approach to meeting the regulations. They can modify 

their product formulas to reduce VOC content or employ innovative products that may actually 

increase the amount of “active ingredients” and change the dispenser to lower the amount of 

VOC emitted per application. An alternative control plan allows manufacturers to average their 

emissions from noncomplying products with those from products that more than meet the 

standard. Variances provide temporary relief from the VOC limits in a product regulation if a 

company cannot comply for reasons beyond their control. 

Although each consumer product may seem to be a small source of emissions, the cumulative 

use of these products by over 35 million Californians results in significant emissions. Consumer 

products accounted for approximately 267 tons per day (tpd) of VOC emissions in the year 

2000, which comprised about 8% of the total man-made VOC emissions statewide. In 2005, 

without ARB’s actions to control VOC emissions in consumer products those emissions would 

exceed 400 tpd. Even with significant reductions from control measures adopted by ARB 

factored in, due to population growth, consumer products emissions are projected to total 260 

tpd by 2010, and at that time make up about 12% of the VOC emissions projected to be emitted. 

Further reductions in VOC emissions from consumer products and other VOC sources are 

needed if ozone standards are to be achieved. 

4.3.1.2 Government Guidelines for Consumer Products 

A statewide sustainable building program can promote sustainable building concepts and 

challenge manufacturers to produce more environmentally friendly products. Recognizing this 

opportunity, Governor Davis issued Executive Order D-16-00 in August 2000. This Executive 

Order directed the Secretary of the State and Consumer Services Agency to develop a strategy 

for how the State could design, build, operate, and maintain buildings that are models of 

efficiency while providing healthy indoor environments. As part of that strategy, the Department 

of General Services (DGS) directed the development of specifications for environmentally 

preferable janitorial products for the cleaning and maintenance of state-owned buildings. Green 

Seal, a product certification organization, has recently developed a standard for cleaning 

materials (GS-37) that relies primarily on chemical content. The specification reduces emissions 

to the general work area, and reduces exposures to the individuals using the products. The 

specification is currently under revision to provide greater health protection. These 

specifications can result in reduced exposure to cleaning chemicals; however, the use of these 

products in state-owned buildings is voluntary. 

 

4.3.2 Appliances 

Indoor appliances that burn fuel (combustion appliances) or heat food but lack a venting system 

to remove combustion by-products, moisture, and odors, such as kerosene heaters, unvented 

gas logs, and unvented gas stoves, can be major sources of indoor air pollution. Wood stoves 

and fireplaces that burn gas or wood are nearly always vented by design, but they can also be a 

source of indoor air pollution due to leakage, re-entrainment of air pollutant emissions, poor 

drafting, or blockage of the flue. Building standards also require gas furnaces and gas water 

heaters to be vented, but the emissions of these appliances can sometimes leak or be drawn 

into a building due to blocked or malfunctioning vent systems. 

4.3.2.1 Government Regulations for Appliances 

The design of combustion appliances is usually regulated through product standards, outdoor 

air pollution regulations, and indirectly through energy efficiency standards for appliances and 
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buildings. The installation of combustion appliances in California is usually regulated through 

building standards that are enforced by local building officials, and through local air quality 

regulations that are implemented by local air pollution control districts. However, the 

performance testing or inspection of combustion appliances in California homes is not regulated 

unless the home is participating in a low-income weatherization (energy efficiency) program 

managed or approved by the State. These programs use a performance test method entitled the 

Combustion Appliance Safety protocol, or a modified version of it. Therefore, inspection of 

vented and unvented combustion appliances in California homes occurs mainly during home 

construction, major remodeling, and resale, but there are no emission or indoor air quality 

testing regulations for California homes unless the home is participating in certain 

weatherization programs. 

Unvented Appliances

The sale of unvented combustion heaters designed for residential use, such as kerosene 

heaters, decorative gas logs and fireplaces, and gas-fired space heaters, has been banned in 

California since the 1980s (HSC Sec. 19881[a]). These appliances are still marketed for other 

uses such as workshops and barns, and are marketed by out-of-state sellers via mail order and 

the Internet. It is not clear how effective this regulation has been in preventing the residential 

use of unvented kerosene heaters, since 1 to 3% of California households use them as primary 

or secondary heat sources (Phillips et al., 1990). 

This regulation was amended in 1997 to allow the sale and indoor use of “natural gas fueled 

unvented decorative gas logs and fireplaces,” provided a series of steps were completed (SB 

798, Haynes, HSC 19881[b-c]). The first step, the development of recommended standards by 

DHS and the Department of Housing and Community Development, was begun by funding a 

contractor study of the indoor air quality and health impacts of unvented gas logs. The 

contractor recommendations for unvented gas log standards included restrictions on emission 

rates for NO2 and CO, with adjustments for different house volumes (Traynor, 1999). DHS 

recommended not setting a California standard for these appliances, and the manufacturers of 

unvented gas logs agreed with this approach. The sale of these devices is thus still banned 

under current regulations. 

Cooking appliances that are unvented, especially gas-fired models, can also produce significant 

emissions of indoor air pollutants and water vapor, especially when malfunctioning, poorly 

maintained, or used improperly (Wilson et al., 1986; Pitts et al., 1989; Wilson et al., 1993; 

Spengler et al., 1994b; Levy et al., 1998). However, these emissions are generally not regulated 

by any government agency. In addition, California regulations do not require cook stoves or 

ovens to have exhaust ventilation, nor do they limit the flow rate of the range hood to avoid 

excessive depressurization. The State Building Standard only requires that the range hood be 

able to supply the ventilation that is required by the stove manufacturer, but installation of a 

range hood or testing of the actual air flow rate for the installed hood is not required. 

Residential building standards in some states have required that both electric and gas cook 

stoves have vented range hoods (State of Washington, 2003; MDC, 2004). In California, local 

building departments may adopt different building standards for the design and installation of 

appliances, as long as the local standards are at least equivalent to the state building standard 

code in performance, safety, and the protection of life and health (HSC 17951[d]2). For 

example, in its housing rehabilitation program, the City of Hayward (2002) requires range hoods 

to be exhausted to the outside. 
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Vented Appliances

Most of the 35 California air districts have rules governing outdoor emissions from vented gas 

appliances such as water heaters and residential central furnaces (ARB, 2003). Most of these 

rules require certification that natural gas-fired water heaters and central fan-type gas furnaces 

sold or installed in the district meet the emission limitations for NOx in South Coast Air Quality 

Management District's Rule 1121 (SCAQMD, 1983, 2004). This rule limits NOx emission to no 

more than 40 ng/J from gas water heaters and gas furnaces (the gas furnace rule does not 

apply to models for mobile homes). However, the SCAQMD emission limits for gas water 

heaters in homes will be lowered in 2006-2008 to 10 ng/J of NOx. This reduction in NOx also 

reduces the potential magnitude of indoor pollutant exposure when water heater emissions 

enter a home due to backdrafting. 

Outdoor emissions from wood burning devices have come under increasing control by local air 

pollution control districts in California. For example, in the Northern Sonoma County and San 

Luis Obispo County Air Pollution Control Districts, PM emissions from non-catalytic and catalytic 

wood fired appliances must be less than or equal to 7.5 g/hr and 4.1 g/hr, respectively. The 

districts also require U.S. EPA-Certified Phase II wood burning devices for new sales and 

installations (40 CFR, Part 60, Subpart AAA, Section 60.530 through 60.539b). State and 

federal regulations do not directly address the operation and maintenance of woodstoves to 

ensure that catalysts, door seals, and flue connections are operating properly. 

Recently the San Joaquin Valley Unified Air Pollution Control District adopted fairly stringent 

regulations for fireplaces and woodstoves. These regulations: 1) ban the installation of 

fireplaces in most new residential development, 2) require U.S. EPA Phase II wood stoves in 

any sale, supply, transfer, and installation, and 3) require the removal of older woodstoves, with 

the option to install U.S. EPA Phase II or pellet-burning wood stoves, in any real estate sale or 

transfer (SJVUAPCD, 2003). The district can also curtail wood burning in the region when 

outdoor PM levels are predicted to exceed an Air Quality Index level of 150. 

In the San Francisco Bay area, 24 cities have ordinances that prohibit conventional fireplaces in 

new construction. The mountain town of Truckee has a more aggressive policy that states that 

existing unapproved wood burning appliances must be removed from all properties by July 15, 

2006. 

California’s energy efficiency standards for new home construction have provisions aimed to 

ensure proper venting and reduce indoor emissions. These standards require vented fireplaces, 

decorative gas appliances, and gas logs to be installed with closable doors over the opening, a 

combustion air intake for outside air, and a flue damper with a readily accessible control 

(http://www.energy.ca.gov/title24/residential_manual/res_manual_chapter2.PDF , CCR, Title 24, 

Pt. 6, Sec. 150[e]). In addition, gas-fired logs, lighters, or decorative appliances must have a flue 

damper that is permanently blocked open, as required by the California Mechanical Code or the 

manufacturer. Emissions from gas fireplaces are not regulated in California or the U.S. 

However, Canada has recently adopted an energy efficiency standard for both vented and 

unvented gas fireplaces. This standard is based on an industry consensus standard of the 

Canadian Gas Association (NRCan, 2004a,b). 

Home Weatherization Programs and the Combustion Appliance Safety (CAS) Test

The California Department of Community Services Development (DCSD, 2003) manages the 

State Low-Income Home Weatherization Program, which provides insulation and air leak 

sealing for low-income homes. The program also requires completion of the Combustion 

Appliance Safety (CAS) test and appliance inspection before and after weatherization is 
Indoor Air Pollution in California July, 2005 

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completed, and cleaning and adjustment of the gas appliances to meet program specifications. 

The CAS test protocol was adopted to improve the health and safety of program participants, 

and to avoid unnecessary liability for contractors and government agencies. It is required by 

state weatherization programs in California and many other states. 

The CAS test protocol specifications in California include the following: 

• CO levels in the flue of the furnace and water heater cannot exceed 100 ppm, 100 ppm 

above the cooktop, or 225 ppm above the oven vent for both the oven and broiler burner. 

Cleaning, adjustment, and repair or replacement are required to bring the appliances within 

these limits. 

• Clothes dryers must be vented outside with metal ductwork, and CO must not exceed 100 

ppm in the exhaust vent. 

• The flue draft pressures in furnaces and water heaters appliances must meet certain 

minimums 

• House depressurization cannot exceed limits that can cause backdrafting of emissions from 

vented combustion appliances. 

• Indoor CO cannot exceed 9 ppm in the room. 

• An operable exhaust fan is required in the cooking area. 

The California Pubic Utilities Commission has recently allowed investor-owned utilities to use a 

modified CAS for their low income weatherization programs (CPUC, 2003). For example, flue 

measurements of CO and installation of CO alarms are not required, while CO concentration in 

room air must be measured. If CO levels in a particular room (or rooms) are 10 ppm or more 

above nearby outdoor levels, then the utility may (but is not required to) conduct flue tests as a 

diagnostic tool to identify the source(s) of the problem. If the incremental indoor CO levels reach 

or exceed a 35 ppm threshold, the home must be ventilated, the occupants advised to 

evacuate, and the offending appliance made inoperable pending repair/replacement. CPUC will 

issue its final decision on testing requirements in early 2005. 

4.3.2.2 Government Guidelines for Appliances 

ARB’s (1994b) Indoor Air Quality Guideline, “Combustion Pollutants in Your Home”, 

recommends actions to reduce combustion pollutants in homes, including emissions from 

combustion appliances. These actions include removing unvented combustion sources from the 

home, using and maintaining vented combustion appliances properly, and ensuring adequate 

and balanced ventilation for the whole house. Also recommended are annual inspections and 

adjustments to combustion appliances, installation of CO alarms, and testing of combustion 

appliance safety. This guideline has been widely distributed in California and other states, 

especially through low-income weatherization groups, of which many are community-based 

organizations. 

ARB (1997b) has also published a “Woodburning Handbook”, which recommends measures for 

reducing emissions and exposures from residential woodburning. These measures include 

using a gas-fired furnace or gas fireplace insert instead, increasing the efficiency of the house 

and wood stove, and improving the operation and maintenance of the wood stove. This 

handbook has been widely distributed in California, mainly through local air pollution control 

districts. 
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4.3.2.3 Professional and Industry Guidelines and Practices for Appliances 

Combustion Appliances

Gas furnaces, water heaters, gas fireplaces, and woodstoves are currently required by state 

and industry standards to have exhaust flues to the outdoors. However, gas furnaces, water 

heaters, and fireplaces typically have flues that have openings for dilution air, and are therefore 

susceptible to backdrafting. These gas appliances are also available with the direct-vent 

(sealed-combustion) feature, which uses sealed pipes for the exhaust flue and combustion air 

supply. For example, direct-vent gas furnaces and gas fireplaces have been used widely in 

California for years, and the direct-vent furnaces have been eligible for utility rebates in 

California. Direct vent gas stoves were developed by the Canadian Gas Research Institute in 

the 1990’s but have not been marketed widely. The direct-vent models are virtually zeroemitting in terms of indoor emissions, resistant to backdrafting, and very energy efficient. 

Groups of high performance home builders and remodelers currently recommend using the 

CAS test protocol discussed above to prevent indoor air quality and moisture problems from 

combustion appliances. They also recommend providing exhaust ventilation for gas cooking 

appliances, and using direct-vent or power-vented (fan-assisted) gas appliances that are 

immune to backdrafting. Examples of such building groups are the Energy Efficient Building 

Association (EEBA, 2003), the California Building Performance Contractor Association (CBPCA, 

2003a,b), the U.S. Department of Energy’s Build America program (BSC, 2003), and the 

National Association of Home Builders Green Building Program (NAHB, 2004). 

Manufacturers of gas appliances currently test gas stoves, cooktops, furnaces, and other gas 

appliances using the test standards and CO emission limits of the American National Standards 

Institute Standards Committee Z21/83. Manufacturers also use private third-party certification 

agencies that conduct complete evaluations along with factory follow-up surveillance under the 

ANSI Z21.1 test standards. A study by the Gas Research Institute (1996) found that, even in 

new homes, the ANSI/Z21/83 standard provides sufficient protection because of its high margin 

of safety incorporated into the test protocol. However, others have determined that the ANSI 

standards for CO emissions from gas stoves can allow excessive levels of indoor air pollution to 

build up in homes when gas stoves are used for extended periods without adequate venting to 

the outside (Tsongas and Hager, 1994; Tsongas, 1995; Persily, 2000). ANSI is developing a 

test method for NO2 emissions from gas stoves (Traynor, 1999). 

For testing and assessing gas stoves installed in homes, “No industry standards or uniform 

government requirements currently exist...” (American Gas Association [AGA], 2003). Some, 

California utilities have been using the CAS test protocol to test existing installations (Hosler, 

1998; see discussion of Weatherization programs above). For installing new stoves, the gas 

industry has adopted standards, but it is not clear how those standards prevent indoor air quality 

problems, how well they are incorporated into the State building standard, and how well 

contractors and homeowners comply with any such standards. 

Carbon Monoxide Alarms

The standards organizations of the United States (Underwriter's Laboratory) and Canada 

(Canadian Standards Association International) have coordinated the writing of CO standards 

and product testing for CO alarms. The standards currently prohibit showing CO levels of less 

than 30 ppm on digital displays of alarms. The new standards also require the alarm to sound at 

higher levels of CO than with previous editions of the standard. New CO alarms will not sound 

at CO concentrations up to 70 ppm, concentrations that are significantly in excess of the health-
Indoor Air Pollution in California July, 2005 

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based guidelines from ARB, WHO, and other groups. The reasoning behind these changes is to 

reduce calls to fire stations, utilities and emergency response teams when the levels of CO are 

not life-threatening. The CO alarm standards are not designed to protect the public from 

exposure to low-level, long-term exposures to CO, or from brief exposures to CO emissions 

from vehicle traffic or properly operating combustion appliances (UL, 2002). 

Detectors with a digital display and a history option can provide the true CO concentrations in a 

house. A low-level display would be useful for people with existing respiratory problems or for 

those who like to spot evolving problems, rather than having to wait for the situation to become 

serious. Low-level CO detection products are becoming commercially available. They will not be 

certified to CSA or UL standards, as these standards currently prohibit low level displays.

Air Cleaners 

The Association of Home Appliance Manufacturers (AHAM, 2004) is the standards development 

organization which is responsible for development of an American National Standard, 

ANSI/AHAM AC-1-2002, for air cleaners. This standard is the basis of a voluntary certification 

program for the performance of room air cleaners in removing tobacco smoke particles, pollen, 

and dust. Testing is conducted by a third-party independent laboratory. AHAM has recently 

developed a certification program, based on the results from Standard AC-1, that certifies the 

clean air delivery rates (CADR) of air cleaners (www.cadr.org). Manufacturers whose products 

are certified can display the AHAM seal, which confirms the CADR listed on the product. The 

ANSI standard has undergone scientific peer review, and a revised standard incorporating peer 

reviewers’ comments is expected to be released later in 2005 (Morris, 2005). AHAM also has 

recently developed a standard for testing the sound level of room air cleaners (AHAM, 2004). 

Most models of room air cleaners are effective at removing particles from the air. However, 

some emit ozone intentionally, and others (ionizers and electrostatic precipitators) can emit 

ozone as a by-product of their technology. The Underwriters Laboratory has developed a test 

protocol, UL Standard 867 (Section 37), for measuring ozone emissions from electrostatic 

precipitators. This standard is sometimes used by manufacturers of other types of air cleaners 

as well, even though not specifically designed for them. UL 867 may be revised soon to apply 

to all types of air cleaners (Morris, 2005). The performance of air cleaners is also evaluated by 

consumer research organizations (Consumers Union, 2003a). 

Vacuum Cleaners

Vacuum cleaners can be an essential tool in controlling indoor pollutants that accumulate on 

interior surfaces. They have been somewhat effective in some asthma intervention studies in 

reducing the loading of particulate asthma triggers on carpets, upholstery, and floors (Krieger et 

al., 2005; Warner et al., 2000). In recent years, vacuum cleaners have begun to include features 

such as high efficiency particle attenuation (HEPA) filters and electronic dust sensors that are 

advertised to improve the removal of allergens and dust from floors and furnishings (Consumers 

Union, 2003, 2004b). However, as discussed in Section 2.2.2, some vacuums resuspend some 

particles in the air, often to a substantial degree (Bowser and Marshall, 2003; Fugler, 2004; 

Woodfolk et al., 1993; Luedtke et al., 1999). 

Industry consensus standards have been developed for testing vacuum cleaner performance 

and durability. The ASTM International Committee F11 for Vacuum Cleaners, has developed 28 

vacuum cleaner performance standards for factors such as filtration efficiency, cleanability, 

durability and reliability (ASTMI, 2005). The Committee updates existing standards on a periodic 

basis, and also undertakes new initiatives aimed at developing standards for those performance 

characteristics not yet covered by current standards. For example, one such key new initiative is 

the development of a standard for determining the change in room air particle counts as a result 
Indoor Air Pollution in California July, 2005 

 147

of vacuum cleaning. The Carpet and Rug Institute (CRI), discussed later in Section 4.3.3.3, has 

developed a voluntary “Green Label Vacuum Cleaner” program that includes tests for soil 

removal, dust containment, and carpet appearance retention. CRI provides a list of vacuum 

cleaner models that have passed these tests and received the Green Label on their website at 

http://www.carpet-rug.com/. CRI also encourages the proper use and maintenance of vacuum 

cleaners. 

 

4.3.3 Building Materials 

Conventional building materials such as vinyl flooring, carpet, paint, cabinets, and composite 

wood products can be strong indoor sources of chemical pollutants with a major impact on 

human health. In the absence of clear regulatory authority, governmental purchasing guidelines 

are being pursued to recommend low-emitting products in new construction. Also, certain 

segments of industry have initiated voluntary programs to reduce product emissions, and label 

their products accordingly. 

4.3.3.1 Government Regulations for Building Materials 

HUD Formaldehyde Emissions in Mobile Homes

The U.S. Department of Housing and Urban Development (HUD) has set limits for 

formaldehyde emissions from plywood and particleboard used in mobile homes. HUD has 

several mandated responsibilities that directly involve indoor air quality, although its basic 

mission is to provide adequate housing, promote community and economic development of 

urban areas, and eliminate discrimination in housing markets. In 1984, HUD established 

formaldehyde emission standards for plywood and particleboard used in mobile homes: test 

chamber concentrations are not to exceed 0.2 ppm and 0.3 ppm, respectively, to maintain 

indoor air concentrations of formaldehyde in mobile homes below 0.4 ppm [24 CFR 

3280.309(a)]. CFR Title 24 Section 3280.309 also states that each new manufactured home 

shall have a health notice on formaldehyde emissions prominently displayed in the kitchen. The 

HUD mobile home standards preempt any existing or future standards of state or local 

governments that apply to the same aspect of mobile home performance (Sec. 604 [d]). 

ARB Composite Wood Control Measures

An air toxic control measure (ATCM) is under development by the ARB to reduce the release of 

formaldehyde from composite wood products such as particleboard, medium density fiberboard, 

hardwood plywood, and composite veneer. The adhesive binding systems used to manufacture 

these composite products contain urea-formaldehyde resins, which release formaldehyde to the 

air. As discussed earlier, these resins can be a strong source of formaldehyde emissions (Kelly 

et al., 1999; Hodgson et al., 2002). It is estimated that formaldehyde emissions from composite 

building materials could exceed 400 tons per year in California (ARB, 2001c). 

4.3.3.2 Government Guidelines for Building Materials 

DHS Non-Binding Guidelines

Reducing Occupant Exposure to Volatile Organic Compounds from Office Building Construction 

Materials: Non-Binding Guidelines was developed by DHS (1996), in response to California 

legislation (Ch. 1229, Statutes of 1990). The guidelines present a simple technical approach for 

evaluating, selecting, and installing building materials in order to minimize occupant exposures 

to VOCs emitted from the materials in newly constructed or remodeled office buildings. The 

guidelines recommend a five-step approach to reducing exposure to VOCs: 
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1. Evaluate and select low-VOC impact building materials and products. 

2. Pre-condition certain materials to minimize VOC emissions after installation. 

3. Install building materials and products based on their VOC emission decay rates. 

4. Ventilate a building during and after installation of new materials and products. 

5. Delay occupancy until VOC concentrations have been reduced adequately. 

These guidelines do not address individual VOCs based on their relative toxicities. However, the 

basic principles in these guidelines have been expanded more recently in manuals that describe 

“best practices” for assuring good indoor environmental quality, as described below. 

Sustainable Buildings and Section 01350

Several state agencies collaborate on task forces to develop guidelines for “green” buildings, 

also called sustainable buildings. Components of sustainable buildings include materials for 

interior surfaces and furnishings that are protective of indoor air quality and health, costeffective, durable, recyclable, and contain recycled content. Under the direction of the Secretary 

of the State and Consumer Services Agency (SCSA), interagency task forces have been 

established for Sustainable Buildings (Executive Order D-16-00) and Environmentally 

Preferable Purchasing (AB 498, Chan, 2002; Public Contract Code Section 12400-12404), to 

develop and implement guidelines for construction, renovation, and operation of state buildings, 

and procurement of state purchases. Stakeholders include members from 40 governmental 

agencies including ARB, DHS, OEHHA, Integrated Waste Management Board (CIWMB), 

Department of General Services (DGS), Division of State Architect (DSA), and the California 

Energy Commission. 

In 1999, the Legislature directed DGS to incorporate sustainable building measures into the 

design and construction of a $392 million State office building complex in Sacramento known as 

the Capitol Area East End Complex. A product of the effort is Special Environmental 

Requirements (Section 01350; State of California, 2002), which provided protocols for testing of 

emissions of VOCs from building materials and furnishings to protect human health in state 

buildings (http://ciwmb.ca.gov/GreenBuilding/Specs/Section01350/). Manufacturers can have 

their products tested at independent labs using the test protocol developed for use at the Capitol 

Area East End Complex. Under Section 01350, primary emissions from a single material or 

product are modeled to estimate a room concentration; secondary emissions resulting from 

chemical reactions are not considered. The calculated room concentration cannot exceed one 

half the health-based chronic REL (developed by OEHHA for toxic air contaminants). 

Formaldehyde is an exception; emissions from a single product cannot exceed one half the 

interim 8-hour REL for formaldehyde, as discussed elsewhere in this document. The RELs have 

undergone extensive public comments and peer review by the State’s Scientific Review Panel, 

so they are appropriate for use as an indoor guideline for this purpose. 

Section 01350 has been incorporated into the DGS standard agreement for engineering and 

architectural services. It is also used in Reference Specifications for Energy and Resource 

Efficiency (CEC, 2004) and the Collaborative for High Performance Schools (CHPS) Best 

Practices Manual (CHPS, 2001). Section 01350 has been expanded to include additional details 

for broader applications such as schools, and products used in state buildings. Most recently, 

DHS has published their “Practice for Testing of VOCs from Building Materials Using Small 

Chambers” (http://www.dhs.ca.gov/ehlb/IAQ/VOCS/Practice.htm), which updates the indoor air 

quality portions of Section 01350 . 
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Collaborative For High Performance Schools

The Collaborative for High Performance Schools (CHPS) is a California consortium of public 

agencies and energy utilities working to facilitate the design and construction of “high 

performance” schools. These are school facilities that aim to be models of energy and resource 

efficiency, as well as healthy and comfortable settings supporting quality education. CHPS uses 

a whole-building design approach, as well as providing designers with specific guidance on 

component systems, that incorporates the best of current knowledge and technologies. CHPS 

developed their own grading criteria using a point system, similar to the U.S. Green Building 

Council’s Leadership in Energy & Environmental Design (LEEDTM) rating system (U.S. Green 

Building Council, 2004). 

The CHPS Criteria include prerequisites and optional measures for low- or no-emission building 

materials, furnishings, and cleaning practices. Construction practices to minimize indoor 

pollutant buildup or dispersion are also required. The building materials requirements are based 

on the Section 01350 specifications discussed above, with adaptations for classroom 

conditions. 

Environmentally Preferable Products for School Construction

As required under SB 373 (Chapter 926, Statutes of 2001), the Division of the State Architect 

(DSA, 2004) is developing a first of its kind database of environmentally preferable products 

(EPP) for use in school construction. SB 373 defines an environmentally preferable product as a 

product that promotes healthy indoor environments for children, and demonstrates the use of 

environmentally preferable materials and systems. When compared to other similar products 

with similar functions, an environmentally preferable product has some, or all, of the following 

characteristics relative to those similar products serving similar functions: 

• Less hazardous to public health, safety, and the environment. 

• Consumes less energy in their manufacture or use. 

• Contains more, or any amount of, recycled or post-consumer material content in their 

manufacture. 

• Results in less potential waste. 

• Results in less harm to indoor air quality. 

• Consumes less water. 

• Includes features, or is manufactured from materials, that promotes recycling or reuse of the 

product. 

Development of the database is anticipated to include the following basic phases: research, 

criteria development, product screening, and database publishing. Products will be screened 

against a comprehensive set of environmental, health, and performance criteria. The indoor air 

quality criteria will be based on the requirements of Section 01350, discussed above. A 

research report looking at existing programs and resources pertinent to this project was 

completed in February, 2004 and posted on the project website 

(http://www.eppbuildingproducts.org/). Between April and July 2004, draft standards for 

composite panels, gypsum board, and fiber-based insulation were released for public comment 

and a series of public workshops was initiated. However, the Department of General Services 

has temporarily halted the project and is examining a potential change in the project approach, 

in order to ensure public participation. The criteria will be developed by working groups of state, 

federal, and local government, private and non-profit organizations and manufacturer 

representatives. 
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4.3.3.3 Professional and Industry Guidelines and Practices for Building Materials 

Several building material industries have developed voluntary emission standards and programs 

to certify products that meet those standards. The most notable are the composite wood 

products industry and the carpet and rug industry. These programs have been successful in 

reducing emissions from some products over the last few decades. 

The Composite Panel Association (CPA) is a professional organization for manufacturers of 

composite wood products. Composite wood products include pressed wood products such as 

plywood, particleboard, oriented strand board, and medium density fiberboard. The Association, 

founded in 1960, is dedicated to promoting the benefits of their products and producing products 

that meet a variety of rigid standards. Of particular note is the Grademark Certification Program 

that involves third-party certification of formaldehyde emission levels from wood panel products. 

This program uses the American National Standard Institute (ANSI) test procedures and limits 

for formaldehyde emissions from wood products. 

The ANSI standard for particleboard and medium density fiberboard (MDF) establishes product 

specifications for dimensional criteria, physical and mechanical criteria, and formaldehyde 

emissions. In some cases, the industry formaldehyde emissions criteria are more stringent than 

those established by HUD for mobile homes. Standard test method ASTM E 1333-96, 

Determining Formaldehyde Concentrations in Air and Emission Rates from Wood Products 

Using a Large Chamber, is used to simulate and measure emissions during normal product use. 

Products from each manufacturer must pass this test to bear the CPA Formaldehyde 

Grademark Program stamp. The Hardwood Plywood and Veneer Association (HPVA) also uses 

the ASTM E 1333 Large Chamber test for product evaluation. For applications for which ureaformaldehyde resin compressed wood products are needed, ARB’s guideline entitled 

Formaldehyde in the Home encourages the consumer to use composite wood products bearing 

the CPA or HPVA certification marks, because those marks confirm that the products meet 

relevant HUD and ANSI formaldehyde emission standards. 

The Carpet and Rug Institute (CRI; http://www.carpet-rug.com/) initiated a voluntary testing 

program in 1994 as a result of the U.S. EPA’s Carpet Policy Dialogue. Carpet samples are 

tested for chemical emissions by a third party laboratory according to ASTM D 5116 – Guide for 

Small-Scale Environmental Chamber Determinations of Organic Emissions from Indoor 

Materials/Products. For carpet, emissions limits were established at 0.5 mg/m2

 for TVOC; 0.05 

mg/m2

 for 4-PC (4-phenylcyclohexene, the compound most associated with “new carpet odor”); 

0.05 mg/m2

 for formaldehyde; and 0.4 mg/m2 for styrene. Most, but not all, carpet manufacturers 

participate in the CRI test program. CRI also has emission standards and labeling programs for 

carpet cushion and adhesive. Products are tested quarterly to assure continued compliance with 

the test program requirements. Carpets that meet the emission test criteria bear a green and 

white CRI Indoor Air Quality Carpet Test Program logo in carpet showrooms so that consumers 

can identify the lower emitting carpet. Despite this labeling program, new carpet may still have a 

substantial “new carpet” odor, and extensive ventilation is recommended during installation and 

immediately after installation. 

During the summer of 2004, at DHS’s urging, CRI further expanded their voluntary test program 

with the introduction of Green Label Plus (http://www.carpet-rug.com/News/040614_GLP.cfm), 

which includes some additional chemicals and emission limits from DHS’s Section 01350 test 

protocols. After a carpet product has been certified to meet the Green Label Plus criteria, it will 

be tested annually for the emission levels of 13 chemicals, and quarterly for emissions of total 

volatile organic chemicals (TVOC). The addition of some Section 01350 criteria is a major step 
Indoor Air Pollution in California July, 2005 

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toward further reducing carpet assembly emissions and assuring healthy indoor environments in 

newly carpeted areas, and addresses at least in part concerns that had continued regarding 

carpet assembly emissions. It is commendable that CRI has taken this action, and it is hoped 

that CRI will adopt any additional criteria identified in the future as necessary to assure healthful 

carpet and rug products. 

The Greenguard Environmental Institute (GEI) has established performance-based, field 

validated standards to define products and materials with low chemical and particle emissions 

for use indoors. The standards establish certification procedures, including test methods, 

allowable emission rates (or modeled indoor concentrations), product sample collection and 

handling, testing type and frequency, and program application processes and acceptance. 

Currently, over 20,000 different products are listed as certified under the Greenguard low 

emitting product standards (http://www.greenguard.org). Greenguard certification is a 

referenced standard incorporated in the U.S. Green Building Council’s LEED Program for 

commercial interiors, and is used by many municipalities and organizations across the U.S. 

Greenguard requires products to be tested on an annual basis for over 2,000 individual 

chemicals including formaldehyde, measured carcinogens and reproductive toxins, as well as 

the sum of all measured chemicals. The modeled indoor concentrations of most individual 

VOCs detected must meet the concentration criteria of less than 1/10th of the threshold limit 

values (TLVs) established by the American Conference of Government Industrial Hygienists. 

However, as in the case of OSHA’s PELs for worker health and safety, using TLV fractions is 

not protective for non-industrial workplaces and residential environments. In fact, public health 

groups and ASHRAE (1981, 2003b) have abandoned this approach based on TLVs. 

4.4 BUILDING DESIGN AND CONSTRUCTION STANDARDS AND GUIDELINES 

Unlike some states, California does not have specific building design and construction 

standards to address IAQ. Standards for the design and construction of building ventilation 

systems and appliances in California are located mainly within Title 24 of the State’s building 

energy and ventilation regulations. These standards are promulgated by the California Energy 

Commission (Commission), and are enforced by local building officials, or in the case of public 

schools, by certified inspectors and the California Division of the State Architect. 

For existing buildings, there are limited regulations or guidelines affecting indoor air quality. The 

Title 24 standards include requirements for substantial additions and alterations of buildings, 

including those for HVAC systems. Home weatherization programs operated by the State and 

some California utilities address the indoor emissions from combustion appliances and the 

building ventilation system. In addition, the Commission is beginning to consider energy 

efficiency programs for existing buildings. 

Guidelines for IAQ in building design and construction are available for the major building types, 

usually as an integral part of “green”, “healthy”, and “sustainable” building programs. In recent 

years, ARB and other State agencies have worked together, through the State Sustainable 

Building Task Force and the Collaborative for High Performance Schools, to develop IAQ 

measures to be used in sustainable buildings for the State and public schools. However, these 

IAQ measures have not yet been fully incorporated into all state building requirements, and are 

not currently required in non-State buildings, in schools, or in homes. 
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4.4.1 State Regulation of Design and Construction 

The general mandate of the Commission is to ensure a reliable energy supply in a manner 

consistent with protecting the State's environment and enhancing its economy. The Commission 

develops and periodically updates energy efficiency standards for the design and construction 

of new buildings, appliances, and insulation materials. The Commission does not directly 

regulate the operation and maintenance of buildings and appliances, factors that are among the 

most important determinants of IAQ. However, some aspects of the Title 24 standards deal with 

HVAC controls systems, building operation modes, and providing building operation, 

maintenance, and design ventilation rate information to building owners and building managers 

upon occupancy (Sec. 10-03[b]). In addition, the Title 24 standards provide the basis for HVAC 

operation and maintenance standards developed and enforced by Cal/OSHA. 

The Commission is required to routinely address indoor air quality impacts of its energy 

efficiency standards, under the authority of AB 4655 (Tanner; PRC 25402.8) and the California 

Environmental Quality Act. The Commission (CEC, 1994) prepared a report to the Legislature 

that assessed the indoor air quality impacts of its energy efficiency standards (PRC 25402.8). 

The Commission’s standards and other activities pertinent to indoor air quality and building 

design and construction standards are summarized below. 

4.4.1.1 Design Ventilation Standards: Nonresidential, High-Rise Residential, And 

Hotel Buildings 

The California Energy Commission sets minimum ventilation standards for the design and 

construction of new buildings and building additions in nonresidential buildings. The standards 

also apply to high-rise residential buildings and hotels. These standards are published under 

CCR, Title 24, Part 6, and are required to be cost-effective. Local building officials enforce these 

State standards, but for public school buildings, the California Division of the State Architect 

(DSA, 2003) reviews the building plans and certifies building inspectors, thereby replacing the 

local building official function. 

Currently, the 2001 edition of the Title 24 standards for nonresidential buildings require that 

newly constructed nonresidential buildings, and new HVAC systems in additions, be capable of 

supplying specific minimum ventilation rates for outdoor air. These minimum ventilation rates 

are typically met by a mechanical ventilation system that includes duct systems, control 

systems, and air filters. The standards require air balancing of airflows in the HVAC system, or 

airflow measurements, before occupancy in order to document that minimum ventilation rates 

are supplied. 

The minimum ventilation rate is calculated by two alternative criteria. New HVAC equipment 

must be designed and installed to be capable of providing no less than the larger of the 

following: 

• The minimum ventilation rate based on the size of the building, expressed in cubic feet per 

minute (cfm) per square foot of conditioned building floor area. Rates required for different 

types of building use are shown in Table 4.2. 

• The minimum ventilation rate based on the number of occupants: “15 cfm per person times 

the expected number of occupants.” The expected number of occupants may be specified 

by the designer. However, the expected number of occupants may not be assumed to be 

less than one half the maximum occupant load for existing purposes in Chapter 10 of the 

California Building Code. 
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Table 4.2. Minimum Design Ventilation Rates For Nonresidential, High-Rise 

Residential, and Hotel Buildings, 2001 Title 24 Standards1

Type of Use Cubic Feet per Minute per Square Foot of 

Conditioned Floor Area 

Auto repair workshops 1.50 

Barber shops 0.40 

Bars, cocktail lounges, and casinos 1.50 

Beauty shops 0.40 

Coin-operated dry cleaning 0.30 

Commercial dry cleaning 0.45 

High-rise residential (5 stories or more) Per CBC Section 12032

Hotel guest rooms (less than 500 sq. ft.) 30 cfm/guest room 

Hotel guest rooms (500 sq. ft. or greater) 0.15 

Retail stores 0.20 

Smoking Lounges 1.50 

All others 0.15 

1. Adapted from CCR, Title 24, Part 6, Sec. 121(b) 2, 

http://www.energy.ca.gov/title24/standards/index.html. 

2. Specifies minimum opening areas for operable windows, but does not require actual operation of 

window or maintenance of operability. 

These Title 24 standards also address the control of the HVAC system, which can markedly 

affect IAQ. The system and its controls must be capable of: 1) supplying the minimum 

ventilation rate at all times the building is occupied, and 2) providing one-hour pre-occupancy 

flushing at full occupancy ventilation rates, or at 3 air changes per hour or more. For spaces 

with high occupant density and at least 3,000 cfm capacity, such as auditoriums and large 

meeting rooms, the standards require “demand controlled ventilation” using a CO2 sensor to 

achieve at least 0.15 cfm per square foot and maintain indoor CO2 levels at or below 800 ppm. 

Such control systems have not been widely used in California, and it is not clear how well this 

requirement has been implemented. For the upcoming 2005 nonresidential Title 24 standards, 

the Commission required “acceptance testing” of demand control ventilation systems before 

occupancy, to ensure that the system performs as designed. 

The Title 24 nonresidential standards also include an option for natural ventilation rather than 

mechanical ventilation. Natural ventilation by windows or roof openings is allowed if the 

openings are operable, accessible to the occupants, within 20 feet of the room’s outer edge, 

and sized to be greater than 5% of the conditioned floor area (this was recently increased to 25 

feet for high-rise residential and hotel/motel guest rooms). Because there is no requirement for 

anyone to actually open the windows or to avoid nearby sources of outdoor pollutants or noise, 
Indoor Air Pollution in California July, 2005 

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the actual ventilation and IAQ provided under this option is highly variable, difficult to quantify, 

and difficult for the building owner or Cal/OSHA to verify. 

4.4.1.2 Design Ventilation Standards: Low-Rise Residential Buildings 

Unlike nonresidential buildings, most homes in California do not have outdoor air provided by 

mechanical ventilation – outdoor air is provided instead via open windows and doors and by 

unintentional air leakage in the building shell and the HVAC ductwork. In 1978, the Commission 

adopted residential building design standards that required extensive caulking, weatherstripping, and sealing to reduce air infiltration in new low-rise homes. To avoid IAQ problems for 

very tight homes in a few climate zones of California, heat recovery ventilators (air-to-air heat 

exchangers) were required to provide outdoor air ventilation for certain home designs (Maeda, 

2004), but very few builders used this option and the requirement was subsequently dropped. 

More recent Title 24 standards for low-rise residential buildings require additional reduction of 

air leakage through the sealing of HVAC ductwork. The sealing of duct work not only reduces 

natural air infiltration, but also unintentional infiltration of pollutant sources from spaces adjacent 

to the home, such as crawlspaces, garages, vehicle traffic, and local woodburning. Compliance 

credit for additional reductions in building air leakage reduction can be obtained by wrapping the 

building shell with an infiltration barrier, but this measure is optional. 

To help ensure adequate IAQ, the 2001 Title 24 standards require mechanical ventilation with 

outdoor air when the target infiltration is below a certain limit. Energy credits for “unusually tight” 

construction are not allowed unless: 1) air leakage is measured by an approved home energy 

rater using a blower door test method, 2) additional outdoor air is provided continuously by 

mechanical ventilation, and 3) combustion appliances such as furnaces and waters heaters that 

use indoor air for combustion are not installed. The mechanical system may be either an 

independent system with its own fan, filter, and ductwork, or it may be integrated with a larger 

central air system. This approach is entitled “Compliance Through Quality Construction” 

(http://www.energy.ca.gov/title24/residential_manual/res_manual_2001.PDF, p. 129). 

A few other states have already required mechanical ventilation systems for new homes. For 

example, the State of Washington (2003) adopted the Ventilation and Indoor Air Quality 

Standard as part of its energy efficiency standards for new home design and construction. This 

standard requires continuous, whole-house ventilation, and exhaust ventilation by low-noise 

fans in the bathroom and kitchen. In addition, it requires that composite wood products be lowformaldehyde (exterior grade) and that a radon removal system be installed under the 

foundation. The State of Minnesota (MDC, 2004) has promulgated a state residential ventilation 

standard that requires continuous, whole-house ventilation, and exhaust ventilation by low-noise 

fans in the bathroom and kitchen. 

4.4.1.3 Design and Performance Standards for Existing Buildings 

The Commission has begun to investigate strategies to achieve peak load reduction in existing 

buildings (mandated by AB 549, Longville). Such strategies may involve weatherization and 

duct sealing in existing buildings, which would affect the levels of indoor air pollutants produced 

by indoor pollutant sources such as combustion appliances and building materials and the 

levels of indoor moisture produced by human activities and other indoor sources. Strategies 

under consideration for non-residential buildings could affect and perhaps improve the operation 

of existing HVAC systems, e.g., retro-commissioning (performance testing) and the increased 
Indoor Air Pollution in California July, 2005 

 155

use of control systems to obtain optimum building system performance. The Commission’s 

recommendations to the Legislature are expected in October 2005. 

4.4.1.4 Standards for Home Weatherization Programs 

The California Department of Community Services Development administers the federal LowIncome Weatherization Assistance Program through trained and certified contractors (DCSD, 

2003; U.S. DOE, 2003a,b). This no-fee program installs insulation, weather-stripping, caulking, 

duct sealant, furnaces, and air conditioners as needed in low-income homes, both renter- and 

owner-occupied. To avoid IAQ and ventilation problems, the program contractors use a 

standard protocol across the state to: 

• Limit the tightening of the building shell. This minimum leakage rate is based on modeling of 

the amount of leakage typically needed to provide 0.35 air changes per hour when averaged 

over the heating season. 

• Inspect and test combustion appliances, venting systems, and ductwork, as discussed 

above under Section 4.3.2.1, Emissions Limits: Appliances. Testing requirements include 

measurements of CO emissions, vent draft pressure, and building depressurization using 

the Combustion Appliance Safety (CAS) test. 

4.4.2 Federal Regulations for Building Design and Construction 

Federal standards do not currently exist for building design, except for new federal buildings, 

manufactured housing (mobile homes), and federal public housing. New federal buildings such 

as office buildings and residential buildings must meet federal design standards for energy 

efficient design, but federal policy has been to comply with local building standards where they 

are more stringent. Although California energy efficiency standards have long been more 

stringent than federal standards, the state and federal building ventilation standards are similar, 

except that new federal standards for new single family homes include mechanical ventilation. 

Standards for manufactured housing and HUD-financed public housing are discussed below. 

4.4.2.1 Manufactured Housing 

Manufactured housing is regulated by HUD, which has developed requirements for lowformaldehyde plywood and particle board (but not medium density plywood), moisture control, 

exhaust venting, and fresh-air ventilation systems (HUD, 2002). These standards are enforced 

in California by the Manufactured Housing Section of the Department of Housing and 

Community Development. The formaldehyde emission requirements for wood products are 

discussed in Section 4.3.3. 

Earlier versions of the HUD standards gave homebuyers the option of the fresh-air ventilation 

system, but very few buyers in California selected that option. The current standard requires 

such a whole-house ventilation system and exhaust ventilation for kitchens and bathrooms. The 

whole-house ventilation system must provide 0.10 air changes per hour (ach), plus an assumed 

natural infiltration rate of 0.25 ach, for a total of 0.35 ach. However, a large study of newer 

manufactured hones in the Pacific Northwest found that many homes received much less than 

0.35 ach, and that occupants did not use the ventilation systems as they are designed to be 

used (Lubliner and Gordon, 1990). In addition, some homes with wood fireplaces that have 

loose operable access doors have been observed to "backdraft" smoke into the homes, due to 

excess negative pressures caused by the HVAC equipment (Boe, 1999). The U.S. Department 
Indoor Air Pollution in California July, 2005 

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of Energy is funding research to improve the energy and indoor air quality performance of 

manufactured housing (Lubliner and Gordon, 1990). 

4.4.2.2 Public Housing 

Federal regulations for public housing financed by HUD require that the site characteristics, 

including the neighborhood and surrounding properties, undergo environmental review. HUD 

(1996) has provided a guide for this review, which addresses site hazards such as lead, PCBs 

from transformers, fuels, and solvents that could contaminate the homes during and after 

construction. At least three public housing sites in the U.S. have been built on known hazardous 

waste sites. Other housing built by the public or private sector may undergo a similar review 

through the California Environmental Quality Assurance (CEQA) review of environmental 

impacts, but the extent of the review for CEQA appears to be much less. 

4.4.3 Professional and Industry Guidelines for Design and Construction 

Several private and public sector organizations develop recommendations that serve as 

"consensus standards” or guidelines for achieving good indoor air quality through building 

design and construction. Many of these guidelines go beyond current regulatory requirements, 

but some are eventually incorporated into the regulations of government agencies. Concern has 

sometimes been expressed regarding the validity and effectiveness of such standards in 

protecting public health and welfare. However, although they may not meet all recognized 

needs, consensus standards serve an important function by providing guidelines for 

professionals such as building designers, managers and consultants, often long before 

government rule-making procedures could provide similar guidance. Government agency staff 

often actively participate in the development of such consensus standards by serving on 

standards-development committees of the major standards organizations. 

ASHRAE has adopted a number of standards related to IAQ. These standards include those for 

ventilation and IAQ (Standard 62), air filter performance, thermal comfort, air-to-air heat 

exchanger performance, and building commissioning. These ASHRAE standards, especially 

Standard 62, have provided part of the basis for some building standards adopted by agencies 

such as HUD, CEC, and local governments. Thus, ASHRAE standards and their revisions have 

played a significant role in the previous and current State regulations for ventilation system 

design and energy-efficient building design as they relate to indoor air quality. Key guidelines 

from the public and private sector that address indoor air quality through building design, 

construction, and commissioning are summarized below. 

4.4.3.1 Guidelines for Nonresidential Buildings 

ASHRAE Standard 62, Ventilation for Acceptable Indoor Air Quality, was first adopted in 1973. It 

was based on criteria for odor perception and indoor carbon dioxide concentrations, with a 

prerequisite that all outdoor and re-circulated air meet State or federal outdoor air quality 

standards. The Standard included minimum ventilation rates for various types of rooms in 

nonresidential buildings, and specified higher recommended ventilation rates for areas with 

smoking or other indoor sources of pollutants present. In 1981, ASHRAE Standard 62-1981 

permitted lower ventilation rates in non-smoking areas, and included additional indoor air quality 

guidelines for several non-criteria pollutants such as formaldehyde and radon. The current 

version of Standard 62 for nonresidential buildings (ASHRAE, 2003a) specifies ventilation rates 

for outdoor air to adequately dilute pollutants emitted by occupants, occupant activities, and 

building materials, furnishings, and systems. For example, 15 cubic feet per minute (cfm) of 
Indoor Air Pollution in California July, 2005 

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outdoor air per person is required for most types of building occupants, and increased 

ventilation rates are specified for building areas with significant sources of indoor air pollution, 

such as bathrooms, printing and copying rooms, cooking areas, and garages. In addition, an 

appendix to the standard addresses the amount of ventilation required to reach recommended 

levels of specific indoor air pollutants. Standard 62-2001 is currently being modified under the 

continuous maintenance process; addenda to the standard are considered and undergo public 

review several times yearly. 

4.4.3.2 Guidelines for School Buildings 

Design guidelines for environmentally sustainable, healthy schools in California have been 

developed by the Collaborative for High Performance Schools (CHPS). CHPS Board Members 

include individuals from state agencies, utilities, and building professionals. CHPS (2001) has 

published the Best Practices Manual that describes such design features as selection of lowemitting materials, ventilation system specifications, and IAQ management plans. The Manual

provides a self-rating certification system and the CHPS criteria for the indoor environment and 

related building topics. School designers have latitude to incorporate practices in the manner 

that best fits the district’s application. CHPS also provides ongoing training for school facility 

staff, building designers, engineers, consultants, and manufacturers. At least ten school 

districts, including Los Angeles Unified School District and San Francisco Unified School 

District, have adopted CHPS Criteria for new school construction planning. A national version of 

CHPS has been adopted by a few other states recently. The U.S. EPA (2003b) has recently 

published “IAQ Design Tools for Schools,” which is largely based on the CHPS Best Practices 

Manual. 

CHPS recently added an Operations and Maintenance volume to the Manual, and plans further 

updates and additions in 2005. Recently, the U.S. Department of Energy adapted the CHPS 

Best Practices Manual Volume II (Design) for a national audience (U.S. DOE, 2003). Several 

school districts, notably Los Angeles Unified, have established policies to require all new 

facilities to meet the CHPS criteria, including those for emission testing of building materials. 

CHPS manuals are available free of charge on the Internet at http://www.chps.net. 

4.4.3.3 Guidelines for Residential Buildings 

For residences, ASHRAE Standard 62-73 and subsequent versions minimally addressed 

ventilation and IAQ. However, ASHRAE recently expanded Standard 62 to include ASHRAE 

Standard 62.2, which specifically addresses IAQ in low-rise residential buildings (Sherman, 

2003a; ASHRAE 2003a). This standard now includes several IAQ features, such as wholehouse mechanical ventilation with outdoor air, “local exhaust” fans in the kitchen and 

bathrooms, backdraft testing, and carbon monoxide alarms (Sherman 2003b). Ventilation rate 

requirements are 7.5 cfm/person, based on the need to remove pollutants generated by 

occupants’ indoor activities, plus 3 cfm/100 square feet of floor are, based on the need to 

remove pollutants generated by background or building-related sources. The standard also 

refers to Standard 62.1 for specific guidance in providing sufficient ventilation based on the 

pollutant emissions from the occupant activities and from the building materials and furnishings. 

This standard is for new home design, but can also be applied to existing homes. It is not a 

regulatory requirement in California, but it may help provide the basis for future State standards. 

Professional home builder and public health groups in California have developed recommended 

practices for improving the performance of new and existing homes that take a “whole-building 

approach” to address building materials, ventilation, combustion safety, moisture control, 
Indoor Air Pollution in California July, 2005 

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thermal comfort, and energy efficiency. Examples of such groups are the Energy Efficient 

Building Association (EEBA, 2003), and the California Building Performance Contractors 

Association (CBPCA, 2003ab). In addition, the National Association of Home Builders (NAHB, 

2004) is beginning to develop guidelines for “green” home building that consider the whole 

building and environmental concerns, and the Canadian Home Builders Association already has 

a green home building program (CHBA, 2004). The American Lung Association (ALA, 2004) 

has implemented the Health House Program, that includes builder guidelines, training, and 

educational information developed with a focus on preventing and reducing asthma and other 

indoor pollutant hazards. The HUD (1999) Healthy Neighborhood Program has funded several 

groups across the U.S. to use inspection and intervention to address asthma triggers, CO 

poisoning, lead poisoning, and other health and safety hazards for children in low-income 

populations. Numerous similar guidelines and programs have come into existence. 

The recommendations from these groups generally include measures such as low-VOC building 

materials, whole house mechanical ventilation, exhaust fans for high-moisture areas such as 

bathrooms and kitchens, combustion appliance safety testing, and combustion appliances that 

are resistant to backdrafting and other venting problems. However, these approaches have not 

been widely used in California – only a few custom homes or demonstration projects have used 

these approaches in California so far. 

4.4.3.4 Building Commissioning Guidelines 

Building commissioning is the process of verifying and documenting that construction, 

operation, and maintenance of a building meet the design specifications of the project. Ideally, 

commissioning is conducted by a trained, third-party inspector, begins during the design phase 

of a project, and includes the development of operation and maintenance procedures and 

related training. Through commissioning, potential problems are detected early, HVAC systems 

are precisely tuned, change orders are reduced, building operators are trained, utility and other 

costs are reduced, and a healthful and comfortable workplace is produced (ODOE, 2004). 

ASHRAE (1993, 1996) has published guidelines for commissioning HVAC and control systems 

in large buildings. The California Commissioning Collaborative (CCC, 2004), which includes 

government, utility and building services professionals, has been promoting building 

commissioning through incentives, training, research, and the development of model Requests 

for Proposals. Research funded by CCC members have found that in order to achieve building 

performance goals over the lifetime of the building, it is necessary to conduct enhanced training 

of building operators, to track building performance, and to conduct ongoing commissioning to 

meet current needs of building occupants (Friedman et al., 2003). 

Building commissioning has proven to be very cost-effective in achieving reduced use of energy 

and other resources, while providing health and safety benefits through improved indoor air 

quality. The Commission included basic commissioning requirements in earlier Title 24 

standards – air balance and flow testing of HVAC systems in nonresidential buildings 

(residential buildings do not have such requirements). The State of California has recently 

become more active in the building commissioning area. 

• With guidance from the State Sustainable Building Task Force, DGS has begun to 

incorporate building commissioning in new projects for large office buildings. DGS is also 

beginning to “re-commission” existing state buildings. 

• The Commission included HVAC commissioning requirements for HVAC control systems 

and major components in the 2001 Title 24 standards. 
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However, despite these and some related activities, formal and complete building 

commissioning is still relatively rare in California’s nonresidential buildings, and it is still in the 

methods development stage for residential applications (LBNL, 2003). 

4.5 BUILDING OPERATION AND MAINTENANCE STANDARDS 

4.5.1 State Standards 

The primary building operation and maintenance regulations in California are those of 

Cal/OSHA, which apply to most industrial and non-industrial workplaces. Non-industrial 

workplaces include beauty salons, hospitals, dry cleaners, medical laboratories, retail shops, 

copy shops, and many other workplaces that can at times have elevated levels of air pollutants 

associated with specific activities. School buildings are also subject to Cal/OSHA regulations, 

although school maintenance staff are not always aware that these workplace regulations apply. 

Residential buildings such as nursing and rest homes, daycare centers, and public housing 

used for special purposes also are subject to Cal/OSHA regulations. 

The Cal/OSHA regulations most applicable to indoor air quality are Sections 5142 and 5143 

(CCR, Title 8, http://www.dir.ca.gov/samples/search/query.htm). These regulations address the 

proper operation and maintenance of mechanical ventilation systems. Cal/OSHA enforcement 

of these standards mainly occurs when a worker files a complaint, and is therefore very limited. 

Other sections of Title 8, such as those addressing asbestos and lead, take a pro-active 

approach by requiring worker training, building assessment, and occupant notification. 

4.5.1.1 Ventilation Regulations for Workplaces 

Employers are required to maintain and operate HVAC systems to provide at least the minimum 

quantity of outdoor air required by the State Building Code (Title 24) at the time the building 

permit was issued. Section 5142, Mechanically Driven Heating, Ventilating and Air Conditioning 

(HVAC) Systems to Provide Minimum Building Ventilation, was adopted in 1987 in response to 

a labor union petition. With limited exceptions, systems must be operated during working hours, 

unless the employer can document that the outdoor air requirements are being met by nonmechanical means. Employers must perform at least annual inspections, and correct problems 

found during those inspections. This section also includes record-keeping requirements; 

employees can obtain these records on request. 

Section 5143, General Requirements of Mechanical Ventilation Systems, was adopted in 1976. 

This section requires annual performance measurement of ventilation systems that are used to 

prevent harmful exposures, such as local exhaust ventilation systems and laboratory hoods. 

This section requires contaminant-free make-up air (supply air), regular filter maintenance, and 

pressure gauge installation to indicate when filters must be cleaned or replaced. This section 

also has record-keeping requirements. 

4.5.1.2 Mold in Workplaces 

Cal/OSHA requires that workplaces be maintained in a sanitary condition. Section 3362 in CCR 

Title 8, Sanitation – General Requirements, was amended in 2002 to include new subsection (g) 

that requires employers to prevent and correct water intrusion, leakage or other uncontrolled 

accumulation because of the potential to cause mold growth. Other subsections require the 

employer to maintain the workplace in a clean, orderly, and sanitary condition; to prevent the 
Indoor Air Pollution in California July, 2005 

 160

entrance of insects, rodents or other vermin; to store putrescible wastes and garbage in covered 

cans; and to remove wastes as frequently as necessary to prevent harmful exposure. 

4.5.1.3 Construction-related Indoor Air Quality Investigations in Workplaces 

Many complaints to Cal/OSHA result from remodeling or other construction activities conducted 

in or adjacent to areas in which employees are working. In these situations, employers are 

required under Section 3203 to inspect the new operations, to evaluate hazards found, and to 

take measures to correct them in a timely manner. Section 5194 further requires employers to 

inform employees about hazardous substances in their work area, including substances being 

applied by contractors. In addition, the following Cal/OSHA sections require employers to 

control specific construction related hazards, such as asbestos, lead, and dusts. 

Section 5208, Asbestos, was filed in 1996 and amended subsequently. It requires building and 

facility owners to determine the presence, location, and quantity of installed asbestos-containing 

materials (ACM) or presumed asbestos-containing materials (PACM), and to inform employers 

or employees in that building or facility of those results. Employers are required to provide that 

information to their employees. This section further requires training for employees who perform 

janitorial or maintenance activities in areas containing ACM or PACM, and the posting of labels 

or signs on installed ACM or PACM. 

Section 1529, Asbestos, requires employers engaged in construction activities involving ACM or 

PACM to use certain control measures to protect employees in adjacent areas. Subsection (d) 

requires that asbestos contractors inform employers of employees in adjacent areas of those 

control measures, and it requires those employers to take measures to protect their employees 

from asbestos hazards and take steps on a daily basis to ensure that the control measures are 

adequately protecting their employees. 

Section 1532.1, Lead, requires employers engaged in construction activities involving lead to 

use specified control measures, to establish a regulated area where exposures exceed the PEL, 

and to inform adjacent contractors of those control measures. 

4.5.1.4 Environmental Tobacco Smoke in Workplaces 

Environmental tobacco smoke historically has been strongly correlated with poor indoor air 

quality. Since 1995, California regulations (Labor Code 6404.5, Section 5148) prohibit smoking 

in most enclosed workplaces (also discussed in Section 4.1.5). This statewide prohibition is 

primarily enforced at the local level. Cal/OSHA is not required to respond to complaints until the 

employer has been found guilty at a local level three times in the previous year 

(http://www.dir.ca.gov/dosh/dosh_publications/smoking.html). On May 29, 2003, in a Decision 

After Reconsideration (Robert D. Schultz and James A. Noll [OSHAB 01-125]), the Appeals 

Board held that the Division does not have authority to take action to enforce the Labor Code in 

the absence of a regulation promulgated by the Standards Board. Subsequently, in February 

2004, the Standards Board adopted a workplace regulation for enforcing the smoking ban. 

4.5.1.5 Indoor Air Quality Enforcement Policy & Procedures for Workplaces 

Policy and Procedure C-48 (http://www.dir.ca.gov/doshpol/p%26pc%2D48.htm) describes 

Cal/OSHA enforcement procedures for indoor air quality investigations. In general, it defines 

“serious indoor air quality complaints” as those in which there is a known or suspected buildingrelated illness, or a cluster of cancer cases or adverse birth outcomes. Non-specific complaints 
Indoor Air Pollution in California July, 2005 

 161

related to building IAQ are also considered serious when their magnitude, frequency, and their 

severity are above certain levels. “Non-serious indoor air quality complaints” are defined as 

those involving particles, HVAC systems, thermal stress, or symptoms that are not specific to a 

particular disease or pollutant. Investigations of building related illness might involve the 

Cal/OSHA medical unit, as well as support from state and local health agencies. Interview, 

inspection, monitoring, and citation procedures are also outlined. 

4.5.1.6 Standards for Nursing Homes and Public Housing 

Nursing homes, group homes, and community care facilities in California are regulated by the 

DHS Licensing and Certification Program (HSC 1265 et seq., HSC 1520 et seq.; HSC 1725 et 

seq.). The licensing requirements include provisions to protect the health and safety of clients. 

State inspectors conduct annual inspections or “surveys” and investigate complaints regarding 

the condition of the building, food preparation, and health care. They also make follow-up visits 

to assure that problems have been identified and corrected. However, it is not clear that IAQ is a 

high priority item unless there are several complaints or an outbreak of a building related illness. 

Public and Indian housing in California are funded by federal and state agencies, often through 

local public housing authorities and redevelopment agencies. Also, HUD provides funding for 

5% of U.S. homeowners and renters through programs for public, assisted, and insured housing 

as well as housing financed through HUD's formula for competitive grant programs 

(http://www.hud.gov/news/release.cfm?content=pr02-105.cfm). State agencies often provide 

additional funding. HUD has adopted regulations regarding the operation and maintenance of 

public and Indian housing that receives federal funds. Public housing authorities are required to 

annually set aside funds for building operation and maintenance. Some operation and 

maintenance activities are required to undergo environmental review (24CFR990.111). 

However, except for lead and asbestos contamination problems, public and Indian housing 

programs have not routinely addressed IAQ in their operation and maintenance programs. 

4.5.2 Guidelines for Building Operation and Maintenance 

Various guidelines for providing good indoor environmental quality through building operation 

and maintenance are available from the public and private sectors. Examples from California 

and national organizations are discussed below. Many other guidelines are available from other 

states and nations that have active programs to address indoor environmental quality. 

4.5.2.1 IAQ Tools for Schools 

The U.S. EPA’s IAQ (Indoor Air Quality) Tools for Schools Program is a program developed to 

help schools identify and prevent indoor air quality problems, using a team approach to school 

indoor environmental quality management. The program provides educational materials and 

tools for evaluating the impact of school maintenance functions and occupants’ daily activities 

on indoor air quality. U.S. EPA makes their IAQ Tools for Schools action kits available at no 

cost, and has funded numerous training workshops, including many in California. 

Implementation of this program by school districts in California and other states has not taken a 

significant amount of staff or funding, but it has yielded substantial health and economic benefits 

(see Section 3, Costs of Indoor Air Pollution). As a prerequisite for obtaining state funding for 

school operation and maintenance, the State of Minnesota has required schools to adopt an 

IAQ management plan based on the IAQ Tools For Schools program. 
Indoor Air Pollution in California July, 2005 

 162

Despite the outreach efforts for the IAQ Tools For Schools program, awareness and use of the 

program among California schools are still low: 35% of schools recently reported that they were 

familiar with the program, but only 11% of California schools reported that they use all or part of 

the program (ARB/DHS, 2003). These low levels may be due to a misperception regarding the 

level of effort required, although the program is adaptable to any level of resources. 

4.5.2.2 Large Building Air Quality Guidance 

U.S. EPA (1991) and the National Institute of Occupational Safety and Health have published 

“Building Air Quality: A Guide for Building and Facility Managers.” This document describes the 

common principles of good facility management, provides background information on topics 

related to IAQ, and recommends strategies for problem identification and resolution in large 

buildings such as office buildings. The guidance emphasizes changing how building managers 

operate and maintain their building, not increasing the amount of work or cost of maintaining the 

building. The companion document, the “Building Air Quality Action Plan”, is an easy-tounderstand, 8-step implementation path for building owners and managers (U.S. EPA, 1998). 

The U.S. EPA (1997b) has also published guidelines for occupants of office guidelines, entitled 

“An Office Building Occupant's Guide to Indoor Air Quality". Most recently, U.S. EPA is offering 

I-BEAM, an interactive software program that integrates IAQ, energy efficiency, and building 

economics into a powerful management tool. 

DHS (1995) has published guidance for occupants of large buildings with HVAC systems. 

Entitled “A ‘Do-It-Yourself’ Inspection of a Ventilation System,” this document provides 

background information and guidance to help occupants identify potential causes of IAQ 

problems in their building, and to help them ask the right questions of building managers and 

investigators. 
Indoor Air Pollution in California July, 2005 

 163

Minimizing indoor emissions is generally more 

effective than removing them after emission has 

occurred. 

T.J. Kelly, Battelle, Indoor Air Quality Symposium: 

Risk Reduction in the 21st Century, Sacramento, May, 2000

5. METHODS TO PREVENT AND REDUCE INDOOR AIR 

POLLUTION 

There are five basic approaches to indoor pollution prevention and reduction of indoor air 

pollution. The most effective and reliable approach is usually source control. Source control 

avoids, removes, or reduces the sources of indoor pollution by using building materials, 

consumer products, and appliances that emit little or no air pollution. Ventilation also is 

necessary for healthful indoor air quality and comfort. It dilutes and removes indoor air 

pollutants to help reduce exposures, but not as effectively or reliably as source reduction. 

Proper operation and regular maintenance of buildings and their ventilation systems are key to 

preventing indoor air quality problems, especially over the long term. Public and professional 

education are also key to pollution prevention; they provide the awareness and understanding 

necessary to promote informed choices about preventing and controlling indoor air quality 

problems. Finally, air cleaning devices (air filters and air cleaners) can also be helpful in certain 

situations when used along with source control and ventilation. 

An effective strategy for maintaining good indoor air quality must integrate all of these 

approaches. Many actions can be taken to prevent and reduce indoor air pollution and, in some 

cases, completely eliminate emissions of indoor air pollutants. The best approach will depend 

on the specific problem and will vary accordingly. It is important to keep in mind that, for 

pollutants that are also elevated outdoors, the pollutant concentrations indoors may not 

approach zero: indoor levels will always be influenced by outdoor pollutant levels. 

5.1 SOURCE CONTROL 

Source control is the prevention or reduction of emissions at the source. It is the most effective 

and reliable approach to reducing indoor pollution because it keeps pollutants from entering and 

spreading throughout a building. It is the most reliable approach because it does not rely on 

building maintenance, or other human actions (ARB, 1989; NRC, 1981). Source control can be 

accomplished through source substitution, source removal, and source modification. 

Source substitution involves using an alternative product that emits little or no pollutants of 

concern. For example, alternative building materials that emit little or no formaldehyde are 

generally available and can be used in place of a building material that emits formaldehyde. 

Source removal involves eliminating the 

source from the building. For example, 

having family members smoke outdoors, 

and properly disposing of old cans of paint 

stored in a closet, removes these sources 

from the home. Source modification 

involves reducing the rate at which a 

pollutant is emitted into the indoor 

environment. Source modification could 

involve a change in design, formulation, or usage of a consumer product. For example, sealing 

all surfaces of a particleboard bookshelf can greatly reduce formaldehyde emissions (Kelly et 

al., 1999; ATS, 1997; NRC, 1981). In addition, “green” cleaning products that have reduced 

levels of irritant and odorous compounds can reduce health and safety hazards for janitorial 

workers and occupants of buildings (OFEE, 2005; WRPPN, 2003). 
Indoor Air Pollution in California July, 2005 

 164

Source control typically can be accomplished at the manufacturing level without direct impact on 

people’s activities and homes. Many consumer products, for example, have been reformulated 

by manufacturers to comply with ARB’s consumer product regulations to control emissions of 

reactive VOCs to the outdoors. Gas-fired furnaces, boilers, and water heaters have also been 

re-designed to comply with air quality management district limits for nitrogen oxides emitted to 

the outdoor air, but such regulations do not exist for emissions of nitrogen oxides to the indoor 

air, which can be substantial for unvented appliances such as gas stoves. Most such product 

changes have not been noticeable to consumers, or have had minimal impact on their choices 

and activities. Appliance standards could also be improved at the manufacturing and installation 

stage to increase combustion efficiency, thereby lowering indoor and outdoor air emissions. 

Such standards might require reduced indoor nitrogen oxide emissions, automated local 

exhaust, and a clearly specified maintenance schedule. 

Standard methods for testing emission rates are available for a number of indoor pollutant 

sources, such as consumer products, paints, carpets, and other building materials. Additional 

work is needed to develop test standards for other indoor pollutant sources, e.g., ozone 

emissions from air cleaners and office equipment, and combustion product emissions from gas 

stoves and fireplaces. More importantly, consumers, architects, building and interior designers, 

and building maintenance personnel need access to accurate and reliable information on the 

emissions of toxic and irritant compounds from products and appliances. 

5.2 VENTILATION 

Building ventilation is defined as air delivered 

to a space to dilute airborne contaminants. It 

serves many purposes. Ventilation removes 

and dilutes chemical contaminants and body 

effluents (such as carbon dioxide); maintains 

comfortable levels of temperature, humidity, 

and air movement; and helps remove excess 

moisture to prevent the growth of mold, 

bacteria, and dust mites. Thus, adequate and 

effective ventilation is necessary for 

acceptable indoor air quality, even when 

known air contaminants and sources are 

minimized. For instance, the air may have 

very low levels of measured air pollutants, 

but without ventilation, exhaled carbon 

dioxide, other body effluents, and nonmeasured air pollutants will build up, 

resulting in a stuffy, uncomfortable 

environment and potentially increased levels 

of toxic and irritant compounds. The figure 

illustrates the basic principle that indoor pollutants, body effluents, humidity levels, and so on 

are generally reduced as the number of air changes with outdoor air per hour (or air exchange 

rate) increases. 

5.2.1 Types of Ventilation 

Ventilation can be “natural” or mechanical. Natural ventilation is the passive air movement 

through open doors or windows, and unintentional air infiltration through the cracks and gaps of 

Air Exchange Rate

(AER)

Figure 5.1

Relationship of Ventilation and

Indoor Air Pollutant Levels

(Simplified; IOM 2000)

Indoor Pollutant

Concentration

(relative)
Indoor Air Pollution in California July, 2005 

 165

the building envelope. Mechanical ventilation is the active movement of air through the building 

using fans to pull outdoor air in (make-up air), mix and circulate the air, and exhaust the indoor 

air to the outdoors. 

There are two types of mechanical ventilation – mixing and displacement. Mixing ventilation 

mixes “fresh” air and existing room air to uniformly dilute pollutants; this is the most common 

type of mechanical ventilation. Displacement ventilation is the introduction of “fresh” air so that 

the air around the occupants (in their breathing zone) is separated from the polluting sources. 

Displacement ventilation requires precision design and operation (Liddament, 2000). To operate 

efficiently and control air flows, mechanical ventilation systems require a relatively airtight 

building; hence, energy efficient builders commonly follow the principle of “build tight and 

ventilate right” (ESB, 1995). 

Localized mechanical ventilation is often used to remove pollutants and increase ventilation in 

special use areas. For example, ducted exhaust fans are useful in bathrooms, laundry rooms, 

and kitchens to control odors, excess moisture, and potential mold growth. Local exhaust 

ventilation can be very effective when airflow is sufficient and exhaust fans are not too noisy. 

The use of exhaust hoods (range hoods) ducted to the outdoors is especially critical when using 

gas stoves or ovens, in order to remove the emissions from the appliances and those generated 

during cooking, which can be substantial. 

For ventilating entire buildings, appliances such as heating, ventilation, and air conditioning 

(HVAC) systems are commonly used to provide mechanical ventilation, along with space 

heating and cooling. In California, these systems are used in most nonresidential buildings such 

as offices and schools, and usually include at least some minimal level of particle filtration for 

outdoor air. However, most residential buildings in California rely on natural ventilation for 

ventilating the whole building. California homes usually have a central air system, but rarely is it 

designed to bring in outdoor air or to run continuously when a building is occupied. 

Consequently, these residential systems mainly use recirculated air. They may have a small 

percentage of unfiltered outdoor air coming from unintentional leakage pathways from the 

garage, crawlspace, attic, or other areas. 

Natural ventilation has limited effectiveness and reliability because it depends on building 

occupants to routinely open windows and doors. It also relies on indoor-outdoor temperature 

differences and wind speeds sufficient to force air through windows, small cracks and other 

leakage points in a building, but these conditions are not consistently present in much of 

California. Consequently, open windows do not always provide adequate ventilation and thermal 

comfort in portable classrooms (Apte et al., 2003) and in other buildings. Natural ventilation 

does not allow for filtration of pollen and outdoor air pollutants, which can be substantially 

elevated in many parts of California. In addition, air flows from potentially contaminated areas 

such as garages and crawlspaces cannot be prevented by natural ventilation. 

Despite its advantages, mechanical ventilation nonetheless has its limitations. It often does not 

provide adequate indoor air quality and comfort because of insufficient ventilation rates, poor air 

mixing within the building, uncontrolled air flows from contaminated areas, or poor quality of 

delivered air. These problems are usually due to improper design, operation, and maintenance 

of the HVAC system and local ventilation units (U.S. EPA, 1997b). For example, HVAC systems 

can produce excessive indoor noise, which lead occupants to frequently turn off the systems, as 

shown in the California Portable Classrooms Study (ARB/DHS, 2004). Building modifications 

may occur over the years without proper modifications to the HVAC system. Ventilation systems 

themselves also can be sources of indoor air pollutants, due to buildup of dust in ductwork and 
Indoor Air Pollution in California July, 2005 

 166

filters, and mold and bacterial growth in drain pans, cooling coils, filters, and ductwork. 

Inadequate training of building operators and insufficient maintenance funding also contribute to 

poor performance of HVAC systems. 

5.2.2 Ventilation, Health, and Comfort 

The quantity and quality of the outdoor supply air plays an important role in assuring acceptable 

air quality in non-industrial buildings. A multi-disciplinary scientific consensus group recently 

reviewed over 100 peer-reviewed papers from the U.S. and Europe (Wargocki et al., 2002). This 

group concluded that increased ventilation is strongly associated with improved comfort and 

improved health (SBS symptoms, inflammation, infections, asthma, allergy, short-term sick 

leave). Increased ventilation was also associated with improved productivity of office workers. 

For residential buildings, the authors concluded that ventilation rates above 0.5 air changes per 

hour in Nordic homes were found to reduce infestation of dust mites. However, air conditioning 

systems in non-industrial buildings with mechanical systems have been associated with the 

increased prevalence of SBS symptoms, indicating the need for better design, maintenance, 

and training of building operators (Wargocki et al., 2002; Seppanen and Fisk, 2002). 

 

The conclusions above from literature reviews are relevant to buildings in the U.S. and 

California. In a study of 41 U.S. office buildings, which included some California buildings, lower 

ventilation rates per occupant (as indicated by increased indoor CO2 levels over outdoor levels) 

were significantly associated with increased SBS symptoms, increased absences, and reduced 

productivity among workers (Apte et al., 2000). These associations held after adjusting the 

statistical model for several indoor air quality and occupant characteristics of the buildings. A 

more recent study of over 400 classrooms in the Pacific Northwest examined ventilation and 

student absence rates. The researchers found that, after adjusting for socioeconomic status and 

classroom characteristics, increased indoor CO2 levels (above outdoor levels) were significantly 

associated with increased student absences (Shendell et al., 2003). 

5.2.3 Adequacy of Ventilation in California Buildings 

Information on the quantity and quality of ventilation in California's public and commercial 

buildings is very limited. Neither Cal/OSHA nor other agencies routinely inspect or track 

ventilation rates in buildings with mechanical ventilation systems. The results of a recent large 

statewide survey of K-12 classrooms in California indicated that ventilation rates were 

inadequate for about 40% of the school day, and were severely inadequate about 10% of the 

time (ARB/DHS, 2004). Similar frequencies of inadequate ventilation in classrooms have been 

found in other studies in California (Shendell et al., 2004a), in the Pacific Northwest (Shendell et 

al., 2003) and in Texas (Corsi et al., 2002). Results from a small study of California buildings 

found that average air exchange rates (in air changes per hours) were 2.24 in 14 school 

buildings, 1.35 in 22 office buildings, and 1.35 in 13 retail buildings (Grot, 1995), and ranged 

from about 0.2 to 4.7 or more. A substantial percentage of these buildings had minimum 

ventilation rates that did not meet applicable building energy and workplace regulations. 

Information on ventilation rates in California's residential buildings is also limited. A few studies 

measured air exchange rates in homes of various ages, but all of the seasons and major 

regions of California have not been well represented. ARB (1998) summarized the available 

information, estimating that average air exchange rates (in air changes per hour) for California 

homes are 0.5 to 0.9 in the winter, and 0.7 to 2.8 in the summer, with spring and fall rates falling 

between the summer and winter values. The range of reported air exchange rates was very 

wide, as indicated by the large standard deviations and the lowest values near 0.1 air change 
Indoor Air Pollution in California July, 2005 

 167

per hour. A national study of air exchange rates from a database maintained by Brookhaven 

National Lab prior to 1993 indicated an overall mean air exchange rate for California and 

Arizona homes of 1.03 air changes per hour, and a 5th – 95th percentile range of 0.22 –2.87 

(Pandian et al., 1993, 1998). 

Newer California homes are likely to have lower air exchange rates, due to the increased 

“tightness” of new homes resulting from energy efficiency requirements such as the increased 

use of water vapor barriers on exterior walls, and the mandatory sealing of HVAC ductwork. As 

homes are made tighter, there 

is an increasing risk of 

degrading indoor air quality. To 

avoid this, the California Energy 

Commission specifically 

considers IAQ when setting 

state energy efficiency 

standards for buildings and 

appliances, as discussed in 

Chapter 4. However, very little 

data on ventilation rates and 

occupant ventilation practices 

are available for new homes in 

California. To assure that air 

quality in new California homes 

is healthful, the ARB and the California Energy Commission are jointly conducting a study to 

examine the adequacy of residential air exchange rates in new homes. It is especially important 

to avoid very low ventilation rates, which have been associated with the most severe impacts on 

IAQ and human health in some studies. The incremental cost of energy to increase ventilation 

rates to acceptable levels has been found to be minimal, especially when considering the 

avoided costs of impacts on human health and productivity. 

To achieve the full benefits of building ventilation, additional work is needed to design 

mechanical ventilation systems that are quiet and easier to clean and maintain. Portable 

classrooms with quiet, efficient HVAC systems and low-noise furnishings and lighting systems 

have been shown to achieve very low noise levels that meet acoustical guidelines (Apte et al.,

2003). Low-noise exhaust fans for homes are readily available and are required by the building 

standards of some states. In addition, a convenient, inexpensive but accurate method for 

assessing ventilation rates is necessary to facilitate routine testing of ventilation systems. 

Improved awareness of, and compliance with, state regulations for operation and maintenance 

of mechanical ventilation systems in schools and other workplaces are also needed. 

Although it is necessary for adequate indoor air quality and comfort, ventilation is not a complete 

solution to indoor pollution. Ventilation consumes energy, and does not completely remove 

some pollutants, such as formaldehyde from building materials, that require years to off-gas. 

Ventilation reduces but does not completely eliminate near-source exposures when people use 

individual products in a building. Thus, it is generally preferable to remove highly toxic 

compounds from these products all together (ARB, 2000b). 

5.3 BUILDING OPERATION AND MAINTENANCE 

A well-operated building and regular maintenance is fundamental to providing good indoor air 

and a comfortable and productive indoor environment (Spengler et al., 2001; ATS, 1997). Basic 

What is needed to improve ventilation in California 

buildings? 

♦ Better commissioning and annual operational checks 

♦ Quieter systems, especially for schools 

♦ Control of building space pressures 

♦ Use of higher efficiency air filters 

♦ Better control of thermal comfort parameters 

(temperature and humidity) 

 F.J. Offermann III, Indoor Environmental Engineering, 

 Indoor Air Quality Symposium: Risk Reduction in the 21st Century, 

Sacramento, May, 2000 
Indoor Air Pollution in California July, 2005 

 168

building elements interact to affect the indoor environment. The building shell shelters the 

occupants from the elements, and at the same time may both emit and trap contaminants. The 

HVAC system conditions the air for comfort, but if not properly maintained it can add to the 

discomfort of occupants and become a source and dispersion method for mold, bacteria, dust, 

and chemical contaminants in the building (Clausen, 2004; Liddament, 2000; U.S. EPA, 1991). 

Proper building operation and maintenance (O&M) for indoor air quality are comprised of 

several key elements. First, a written plan and maintenance schedule are needed to operate 

and maintain the building as originally intended and as appropriate for the specific building 

design, and to ensure that health and safety standards are met. The plan should address not 

only the routine maintenance after occupancy, but also the control of dust, fibers, mold, and 

chemical contaminants during building construction, repairs, and renovation. Next, the building 

should be commissioned after initial construction, after major renovations, and periodically 

throughout the life of the building. As discussed in Chapter 4, commissioning involves 

performance testing and inspection of the building to ensure that it performs as intended and 

that the various building systems work together properly. For example, commissioning helps 

verify the building's energy use, ventilation rates, thermal comfort levels, and use of specified 

building materials, air filters, and other environmental features. Commissioning also includes 

completion of the O&M plan and the initial training of O&M staff before the building is occupied. 

From the energy standpoint alone, commissioning by third party agents has been shown to be 

very cost-effective. 

Another key element is training of O&M staff in the basic principles of indoor air quality and the 

proper methods to achieve good indoor air quality. Maintaining high quality indoor air requires a 

solid understanding of how buildings operate, the relationship between the HVAC equipment 

and indoor air quality, and how to achieve the design intent (Bearg, 1993). Regular cleaning 

with the proper equipment and methods can go far to eliminate some biological and dust 

contaminants. Effective cleaning, for example, involves using a vacuum cleaner with good 

filtration and efficiency, and allowing sufficient residence time of the vacuum head on the carpet 

or floor to assure good pick-up. Proper vacuuming can significantly reduce asthma and allergy 

triggers such as mold spores and animal dander in carpets, as well as pollutants that are often 

adsorbed onto floor dust, such as pesticides and PAHs. Similarly, cleaning properly with 

disinfectants and cleaning products can reduce bacteria and mold on surfaces and reduce 

exposure to potentially harmful bacteria. Training guidance is available from various sources 

mentioned throughout this report. Ongoing commissioning also is needed to assure that 

systems continue to perform as intended. 

To implement a good O&M program, adequate funding is also essential. A reasonable funding 

level can be determined based on industry norms, experience in similar buildings, and on 

manufacturer recommendations for equipment repair and replacement. However, maintenance 

programs are often the first to be cut during a budget crisis, and the maintenance budget for 

California’s public schools are especially strained (Patterson, 2000). Without adequate funding, 

maintenance programs fall further and further behind, thereby increasing the likelihood of major 

IAQ problem, structural damage, catastrophic failures, and litigation. 

A good O&M program can not only help avoid worker productivity and health impacts from poor 

indoor air quality, but it can also help reduce the potential for litigation. Several lawsuits have 

been successfully litigated for mold cases in public buildings, commercial buildings, and homes 

(Hirsch, 2005). Lawsuits over other IAQ problems such as CO poisoning, SBS, and pesticide 

poisoning have also been filed, but often end in out-of-court settlements. Litigation over IAQ has 

increased in recent years in the areas, especially in the area of mold damage (Facilities 
Indoor Air Pollution in California July, 2005 

 169

Network, 2005). This has led insurance companies to drop or limit their coverage for mold or 

water damage (Kats, 2003). It has also led to a proliferation of mold remediation companies that 

offer to inspect, test, and correct for mold problems. However, because there is no widely 

recognized licensing and training program for such companies, consumers and building owners 

are vulnerable to fraudulent practices and poor workmanship. 

Litigation and liability risks do provide an incentive for better building design, operation, and 

maintenance, but they are not an efficient approach for society. Some IAQ cases are hard to 

prove because the toxic effects are chronic and delayed long after the initial exposures. In 

addition, litigation is very expensive, and individual homeowners and small businesses rarely 

have the resources to pursue litigation against a large company. Finally, increased litigation and 

liability may affect only business practices for certain IAQ problems such as mold, and may help 

the litigants but not the population in general. 

Building O&M is effective in preventing and controlling indoor air pollution, but only to the extent 

that proper training and adequate funding are provided. O&M can help achieve good indoor air 

quality if the indoor pollutant sources are controlled and the HVAC system is properly designed 

and commissioned, but this is not always the case. 

In order to assure good O&M for buildings, additional work is needed to improve compliance 

with Cal/OSHA regulations for maintaining mechanical ventilation systems and preventing 

moisture intrusion in nonresidential buildings. For residential buildings, guidance is needed to 

improve the maintenance of the HVAC system, combustion appliances, and the building shell. 

Training of personnel in local health departments and building departments is also necessary to 

help them recognize and prevent IAQ problems in residential and nonresidential buildings and 

help enforce building and worker health standards. 

5.4 PUBLIC AND PROFESSIONAL EDUCATION 

People’s choices and behavior have a major impact on their exposures to air pollution. Human 

activities are one of the key factors in determining the condition of the indoor environment. 

Cooking, the use of various consumer products, cigarette smoking, and other activities can 

result in immediate, significant releases of pollutants indoors which are immediately inhaled 

(ARB, 1987). Also, whether people choose to clean and maintain homes and buildings properly 

can have a major impact. 

People are often not aware of the risks associated with indoor pollution and what they can do to 

protect their health. Many people assume incorrectly that any indoor air quality problem can be 

solved with an air cleaning device in their home or office, as witnessed by the recent boom in 

the sales of air cleaners. Sometimes activity pattern changes are needed, e.g., people must not 

smoke or must select different building products or consumer products to reduce their exposure 

and risk. Similarly, timely building maintenance and repair is critical to prevent mold 

development and accumulation of particles on surfaces. Even some building professionals are 

not aware of the impact of their lack of action on the building environment. Thus, increased 

awareness is a key step for reducing exposures to indoor air pollution (NRC, 1981; ATS, 1997). 

Increasing people’s awareness can be accomplished through public and professional education. 

However, public education will never be a complete solution. Some groups of the population 

cannot respond appropriately to take needed action. For example, children cannot read or 

understand all written information that is provided, elderly people living in group settings cannot 
Indoor Air Pollution in California July, 2005 

 170

control the products used in the facility, and low-income families may not be able to afford safer 

alternatives, even when they are fully aware of them. 

Additionally, public education will not always reach all members of society. The many nonEnglish speaking ethnic groups that enrich the California population pose an increased 

communication challenge. The California population contains a large number of people who 

speak a language other than English at home, as well as a large number of foreign-born 

individuals. According to the U.S. Census Bureau, the year 2000 census reported about 18% of 

the U.S. population 5 years and older spoke a language other than English at home. In 

California, that number is higher: about 40% of Californians speak a language other than 

English at home (DOF, 2002b). Also, the proportion of the California population that reported 

being foreign-born has increased from about 21% in 1990 to over 26% in 2000 (Malone et al., 

2003). 

Public education can change people’s awareness and actions, but it does so slowly and 

requires a long-term commitment with adequate funding in order to reach the desired audiences 

and compete with commercial advertising. Because of these reasons, increased public 

education and information are not adequate as a sole approach to preventing indoor pollution. 

The decisions of various persons and groups in the building, healthcare, and education 

professions can also help prevent and control indoor air pollution. Consumers and employers 

often rely on professionals to advise them on IAQ issues in their building, and perhaps to 

inspect and remediate their building. However, training for and awareness of IAQ is minimal in 

most professions involved with buildings and environmental health. Furthermore, there is no 

widely accepted training and certification program for IAQ professionals. Several groups offer 

certification as an indoor air quality expert, but the certification requirements are sometimes as 

minimal as completing a form or completing a one-day class. To change the awareness and 

actions of building owners and employers, existing training programs for building professions 

should be expanded, and adequate training on IAQ for professionals in the healthcare and 

education fields should be provided. 

5.5 AIR CLEANING DEVICES 

Air cleaning devices are available in a variety of types and sizes. Most air cleaners remove 

particles, a few remove gases, and some perform both removal processes. Air cleaners can 

remove particles from the air using a mechanical or physical barrier, or through an electronic 

device. Mechanical air cleaners draw air through a filter with different sized pores that trap the 

particles. The most common types use a flat or pleated fibrous filter that can range from low to 

high efficiency at trapping particles. Electronic air cleaners are available in three basic types: 

electrostatic precipitators (ESPs), ionizers, and mechanical-electronic hybrids. ESPs use a 

small electrical charge to charge particles, which are then collected on oppositely charged 

plates as air is drawn through the device. Ionizers, or negative ion generators, also charge 

particles, causing them to stick to surfaces near the ionizer, such as the carpet and walls. 

Hybrid devices use both mechanical and electronic devices for pollutant removal. Air cleaners 

that remove gases and odors are less common, and relatively more expensive to purchase and 

maintain. Gaseous pollutants are typically trapped or destroyed as the air is drawn through 

materials such as activated charcoal or alumina coated with potassium permanganate. 

However, the filter material can become quickly overloaded and may need to be replaced often. 

Air cleaning devices usually come as portable, stand-alone appliances, or as filters or cleaners 

in a central air system. Portable air cleaners are sometimes practical for rooms in existing 
Indoor Air Pollution in California July, 2005 

 171

homes where addition of a central air cleaner is too costly. Proper size, installation, and 

maintenance are critical for portable air cleaners to be effective. Test standards for particle 

removal by air cleaning devices have been developed by trade and engineering groups, as 

discussed above in Section 4.3.2.3. The effectiveness of some portable air cleaners in removing 

particles is rated in terms of pollutant removal efficiency or clean air delivery rate (CADR), 

measured in cubic feet per minute (cfm). A larger CADR is better. Both air flow and filter 

efficiency influence the CADR. The CADR ratings are given separately for the removal of dust, 

pollen, and environmental tobacco smoke. Standards for gas removal have not been developed. 

Portable air cleaning devices are useful for the purpose and airspace for which they are 

designed: most effectively remove particles, but are not designed to remove gaseous pollutants, 

and models that are under- or over-sized for the room or airspace to be cleaned will either be 

ineffective or will waste energy. Some models are very noisy (ARB, 2000c; ATS, 1997; 

Consumers Union, 2003a), which has been a complaint of some users. The proper type and 

size of air cleaner can be useful for some individuals with special sensitivities, such as those 

with asthma or allergies who use them in their bedrooms at night. Additionally, recent research 

has shown that in-duct ESPs can effectively reduce residential particles when the ESP is 

properly maintained (Howard-Reed et al., 2003; Wallace et al., 2004). Based on the limited 

scientific evidence that is currently available, the health benefits of air cleaners are not clear. 

Generally, it is more effective to prevent emissions rather than to try to remove them from the air 

once they are there. Nonetheless, for sensitive individuals who need an air cleaner, 

technological improvements to reduce noise and reduce the cost and need to replace filters are 

needed. 

For new homes or major remodels, "whole-house" or "fresh-air" ventilation systems that include 

some type of air cleaning device can be installed. Installed costs depend on the system size and 

the type of air cleaning device. Fresh-air ventilation systems are recommended in new, tightly 

built energy-efficient houses and for situations where the outdoor air is a major source of indoor 

pollution. To design and install any central system air cleaner, a company or contractor that is 

well experienced in designing and installing central filtration systems is important (ARB, 2005b). 

Ozone Does Not Clean the Air! 

Some air cleaning devices emit ozone, either purposely or as a by-product of the particleremoval technology used in the device. Those that generate ozone by design are often called 

‘ozone generators’. ESPs, ionizers, and hybrid models often emit ozone as an unintentional byproduct. A few studies have 

shown that some ionizers and 

ESPs, even some that meet UL 

Standard 867 (Section 37), can 

emit unhealthful levels of ozone 

(Niu et al, 2001a,b; Chen and 

Zhang, 2004). However, such 

devices typically emit ozone at 

relatively low levels, and 

research indicates that attention 

to design details and quality 

control should assure very low 

emission in these types of air cleaners (Liu et al., 2000). Emissions from purposeful ozone 

generators, on the other hand, can readily result in harmful levels of indoor ozone, and are a 

more serious concern. 

Ozone-generating Air Cleaners 

"These machines are insidious. Marketed as a strong 

defense against indoor air pollution, they emit ozone, 

the same chemical that the ARB and USEPA (U.S. 

Environmental Protection Agency) have been trying to 

eliminate from our air for decades." 

Barbara Riordan, interim ARB Chairperson. California Air Resources 

Board, Press Release 05-02, Sacramento, January 2005. 
Indoor Air Pollution in California July, 2005 

 172

Independent studies by the U.S. EPA, the Consumers Union, and others have shown that 

ozone generators can produce unsafe room levels of ozone up to several times higher than the 

state ambient air quality ozone standard of 90 ppb for one hour, reaching levels equal to a 

Stage One smog alert (200 ppb) (Mason et al., 2000; Consumers Union 1992; Chen and Zhang, 

2004). In a U.S. EPA study, ozone generators generated over 300 ppb in a test house within an 

hour or two of operation, and over 400 ppb in a chamber experiment (Mason et al., 2000). In 

another study of a variety of air cleaner models tested in a chamber under realistic conditions, 

the ozone generators were the only models to exceed the OSHA 8-hour PEL for ozone of 100 

ppb; levels again reached 300-400 ppb (Chen and Zhang, 2004). Personal air purifiers, which 

are typically small ozone-generating devices worn around the user's neck, can produce over 

100 ppb in the user's breathing zone (Phillips et al., 1999). 

In addition to the potential harm posed by excessive ozone emissions, ozone generators also 

do not effectively destroy microbes, remove odor sources, or reduce indoor pollutants enough to 

provide any health benefits as manufacturers claim (Foarde et al., 1997; Boeniger, 1995; Chen 

and Zhang, 2004; U.S. EPA, 2004b). Ozone generators are often advertised as able to kill mold 

and bacteria even at “safe” ozone levels; however, ozone in the air must reach extremely 

hazardous levels (50-100 times the state standard) to effectively kill microbes (Foarde et al., 

1997). Ozone generators also are advertised as able to remove gaseous pollutants and odors, 

but ozone only reduces one group of VOCs, alkenes (a group that includes benzene). 

Additionally, ozone deadens the sense of smell. Most importantly, ozone reacts with other 

chemicals present indoors and leads to significant increases in the indoor levels of 

formaldehyde and other aldehydes, other VOCs, and ultrafine PM (Boeniger, 1995; Weschler, 

2004). Some of these reaction products are listed as California toxic air contaminants, which 

can irritate the mucous membranes and respiratory tract or cause other health impacts. 

Current market trends indicate that the use of ozone generators in California is widespread and 

growing. In an aggressive marketing campaign for ozone-generating devices, companies have 

targeted the most vulnerable populations, such as the elderly and persons with asthma or other 

respiratory diseases. Often, the advertisements used in the marketing of these devices make 

unsubstantiated claims and use misleading terms such as "super-oxygenated," "activated 

oxygen," or "trivalent oxygen," when referring to the ozone that is emitted. 

State agencies have recommended that air cleaners that purposely generate ozone not be used 

in the home (DHS, 1997; ALA, 1997; ARB, 2005a,b). Presently, no state or federal agency has 

the direct regulatory authority to control emissions from these devices, although the Consumer 

Product Safety Commission has some authority to address products through a ban, required 

labeling, or other approaches. Efforts to restrict these devices through lawsuits, establishment of 

voluntary emission standards, cease and desist orders, and other means have all failed to 

restrict the sales and use of ozone generators. 
Indoor Air Pollution in California July, 2005 

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6. PRIORITIZATION OF SOURCES AND POLLUTANTS 

BASED ON EXPOSURE AND ADVERSE IMPACTS 

Reduction of public exposure to the many indoor air pollutants is most effectively achieved by 

reducing pollution at the source. Because exposure is dependent on the presence and use of 

sources, pollutants are best prioritized for action by source categories. Mitigation approaches 

focused on source categories would be most effective for reducing pollutant exposure, and 

would generally be feasible to implement, although the feasibility would vary by specific source. 

Tables 6.1 and 6.2 suggest a prioritization scheme for implementation of mitigation measures, 

by source categories. The source categories have been ranked into two groups – high and 

medium priority – and are listed alphabetically within each ranking group. 

The primary factors considered in prioritizing the source categories included the extent of the 

population’s exposure to the sources and their emissions, the relative reduction in health 

impacts that could be achieved with further action beyond any already undertaken, ease of 

mitigation, trends in emissions from and use of source categories, and the extent of the gap in 

reducing exposure and risk from categories of indoor sources. A quantitative prioritization was 

not undertaken because such an effort is beyond the scope of this report. Such an effort would 

be an appropriate step prior to taking action under a comprehensive program to address indoor 

sources; a detailed prioritization based on quantified criteria would be needed. Additionally, the 

preliminary indoor air pollution cost estimates provided in this report were considered, but were 

not weighted heavily in the prioritization for several reasons. Most importantly, the cost 

estimates primarily reflect the availability of cost information and the length of time a given 

pollutant, such as ETS and radon, has been studied. Because of the lack of key cost data for 

most indoor pollutants, the cost estimates do not necessarily reflect the actual extent of 

exposure and risk in California, nor does it account for current information and trends in the 

scientific literature on exposure and risk. Thus, cost information was considered but was not a 

determining factor in the prioritization of sources. 

Tables 6.1 and 6.2 also suggest potential approaches for mitigating the pollutants and sources 

listed. Emission reductions should be accomplished at the manufacturing, distribution, or 

construction stage. Alternatives or mitigation options are currently available for most of the 

sources listed. Emission limitations achieved at the manufacturing stage, such as reducing toxic 

contaminants in building materials, would be effectively invisible to the consumer and assure 

exposure reduction. Similarly, new appliance standards would reduce combustion emissions 

without reducing the range of product choices in the market place. With this approach, little or 

no change in individual behavior would be anticipated. As a result of public awareness and 

demand, there are an increasing number of “green” or low-emitting building materials, 

furnishings, and consumer products already available. Low-emitting carpets, no-formaldehyde 

furniture, and non-toxic cleaning products are currently available, and continue to grow in 

market share. 

Finally, Tables 6.1 and 6.2 includes a column indicating whether direct authority exists at the 

state level to take the actions listed in column three. For most source categories, there is no 

state agency with clear, direct authority to take the mitigation actions indicated. In some 

categories, one or more agencies has limited authority to address a small portion of the sources 

included. For example, Cal/OSHA could impose product use restrictions or require other actions 

to reduce worker exposure to institutional cleaning product emissions. However, neither 

Cal/OSHA nor any other state agency has direct authority to restrict pollutant emissions from 
Indoor Air Pollution in California July, 2005 

 174

Table 6.1. High Priority Source Categories for Mitigation: 1 

SOURCES OF 

POLLUTANTS2 

(listed alphabetically) 

EXAMPLES OF 

POLLUTANTS3

 EMITTED 

POTENTIAL 

APPROACH TO 

MITIGATION4

DIRECT 

STATE 

AUTHORITY 

TO TAKE IAQ 

MITIGATION 

ACTIONS 

Air Cleaners 

(ozone-generating) 

Ozone Emission 

limitations 

No 

Biological Contaminants

(mold, pollen, bacteria, 

viruses, house dust mites, 

cockroaches) 

Particles, allergens, 

asthma triggers, toxins 

Requirements for 

habitable spaces; 

require certification 

of mold assessors 

and mitigators 

Limited 

Building Materials & 

Furnishings 

(particle board, plywood, 

paneling, flooring, caulk, 

adhesives, new carpet 

assembly, furniture) 

Formaldehyde, 

acetaldehyde, benzene 

derivatives, acrylates, 

naphthalene, phenol, 

some other VOCs 

Emission 

limitations, product 

use restrictions, 

market incentives 

Limited (some 

indirect) 

Combustion Appliances

(unvented gas & propane 

stoves, ovens; poorly 

vented furnaces, heaters; 

woodstoves and fireplaces) 

Carbon monoxide, 

nitrogen oxides, particles, 

soot, polycyclic aromatic 

hydrocarbons 

Active exhaust 

ventilation, safety 

devices, product 

use restrictions, 

product re-design, 

improved venting, 

emission limitations 

No 

Environmental Tobacco 

Smoke 

(cigarettes, cigars) 

Particles, polycyclic 

aromatic hydrocarbons, 

benzene, carbon 

monoxide, some other 

VOCs 

Focused parent 

education; reduce 

smoking in homes 

and vehicles 

Yes, 

workplaces 

No, private 

homes and 

vehicles 

Radon 

(soil, rock, ground water, 

building materials 

containing radium) 

Radionuclides, radon gas Screening 

measurements, 

building codes 

Limited 

1. Individual sources may be higher or lower than the source category ranking. 

2. All of the examples of pollutant sources may not emit all of the pollutants listed in the corresponding box in 

column two. 

3. Air pollutants may be identified as toxic air contaminants (TACs) by the California Air Resources Board, and/or 

identified as Proposition 65 chemicals; or, criteria (traditional) air pollutants. 

4. Public education, economic incentives, and non-regulatory approaches should also be used where appropriate. 

The actual approach taken would be determined after extensive discussions with the relevant industries, in 

consideration of costs, feasibility, and effectiveness. 

cleaning products for the purpose of reducing indoor air concentrations and exposures. Also, for 

most categories, any related authority is usually indirect – the authority is not focused on 

reducing indoor pollution to protect public health, but rather is a mitigation measure to reduce 

impacts of actions taken under the primary authority, or is incidental to the primary regulatory 
Indoor Air Pollution in California July, 2005 

 175

activities. For example, one mission of the Energy Commission is to improve energy efficiency 

in California’s buildings. The Commission has been attentive to indoor air quality impacts that 

might result from their regulatory actions, and includes provisions to prevent adverse impacts on 

indoor air that might result. However, the Commission does not have authority to develop a 

regulation to address indoor air quality outside of their energy-related missions. Finally, while 

the ARB has regulatory authority over some indoor sources such as consumer products, that 

authority is targeted toward actions to reduce the impacts on outdoor air quality. Some such 

actions taken by the ARB have had positive impacts on indoor air quality as well, but those 

impacts are either incidental to the actions taken for the purpose of reducing or preventing 

outdoor air pollution, or are mitigation measures designed to reduce adverse environmental 

impacts from ARB regulations. 

The specific rationale for the ranking of each category is discussed below. Note that the 

prioritization is a ranking of the overall group of sources included in a given category: some 

individual sources within the group may have a higher or lower priority. A more detailed 

assessment would be needed to prioritize specific products within these larger categories. 

6.1 HIGH RANKED SOURCE CATEGORIES 

• Air cleaning devices or “air purifiers” that generate ozone purposely should not be used 

in occupied places, and their ozone emissions should be limited. Some devices marketed as 

air cleaners purposely release ozone, which can directly harm sensitive occupants. These 

air cleaners can produce harmful levels of indoor ozone, up to several times the state 

outdoor standard level and even a Stage 1 smog alert level. Additionally, they are ineffective 

at safe levels. Safe, effective alternatives are available in the marketplace. Ionizers and 

electrostatic precipitators, two other types of indoor air cleaners, emit ozone to varying 

degrees as a by-product of their function. These devices are effective at removing particles, 

but poor maintenance and old age can result in increased ozone emissions. Ozone 

emissions from these devices should also be limited to assure that indoor concentrations 

remain well below concentrations that may harm sensitive individuals. Consumers often 

seek advice about the type of air cleaner they should buy to meet their specific needs, but 

there are few criteria available to guide consumers in their purchase. Emission limitations 

are needed for these devices, which are currently unregulated. 

A program to reduce the use of high-ozone-emitting devices and to educate the public 

should be undertaken. Such a program might include: 

a) Development of public and professional guidance materials for indoor ozone. 

b) A public and professional outreach program to alert them to the potential harm of 

ozone generators and safe alternatives. Such a program should target medical and 

dental professionals, building managers, school administrators and facility managers, 

senior citizen organizations, public health entities, environmental organizations and 

others. 

c) Development of test protocols for air cleaners, primarily to test ozone emissions. 

d) Meetings with manufacturers and their professional organizations to facilitate actions 

to address this issue. 

• Biological contaminants are a group of both sources and pollutants. Some mold and 

bacteria can emit chemical toxins, but for the most part the organism or its parts actually 

cause the effect. Biologicals are a high priority because of their ubiquitous presence and 

their widespread health and fiscal effects. Animal dander, pollen, house dust mites, and 

cockroaches cause millions of sensitive individuals to experience allergy symptoms and 
Indoor Air Pollution in California July, 2005 

 176

asthma attacks. Indoor mold has been an increasing problem in recent years, costing 

substantial sums of money for remediation and lawsuit settlements. Bacteria such as 

Legionella cause both serious illness (for example, Legionnaire’s disease) and shorter-lived 

disease (for example, Pontiac Fever). While not emitted into the indoor environment per se, 

infectious disease transmission is increased in indoor environments with crowded or dirty 

conditions and insufficient outdoor air flow. Improved methods are needed to objectively and 

efficiently identify and quantify dampness and microbiological growth in building, especially 

within wall cavities or other areas that are difficult to access. Additional research is needed 

to develop such methods. 

The mitigation approaches for biologicals are varied. Mitigation actions for mold and some 

other biologicals might include required annual inspections and remediation in public 

buildings, group homes, and rental units, and in private homes at the time of sale. 

Certification requirements for mold assessors and remediators would help assure the quality 

of inspections and remediation. 

• Building materials and furnishings are a high priority for mitigation because they often 

emit multiple toxic air pollutants, especially when new, and have a high loading level in 

indoor environments, resulting in high exposure levels for occupants. Additionally, a 

substantial percent of the population is exposed to such emissions due to the continued high 

rate of new building construction in California and the increasing number of home 

renovations undertaken by homeowners. Emission limits for pollutants emitted from building 

materials and furnishings (formaldehyde being the most predominant) would benefit all 

indoor environments and has potential for significant health benefits due to reduced 

incidence of asthma exacerbation, cancer, and eye, nose and throat irritation. 

Low-emitting alternatives are available. Non-wood alternatives and composite wood 

products made with phenol-formaldehyde resin or methyl diisocyanate (MDI) have much 

lower formaldehyde emissions than composite wood products made with urea-formaldehyde 

resin, and could be substituted for some applications. In cabinets and furniture, all surfaces 

of these products can be coated or laminated to substantially reduce formaldehyde 

emissions. Building materials are currently available that meet Section 01350 emission 

requirements for formaldehyde and other chemicals of concern (Alevantis, 2003). Lowemitting modular office furniture was used in the Capitol Area East End Complex, and could 

be used in all future state and private offices. Numerous governmental groups focused on 

sustainable building and environmentally preferable purchasing are compiling lists of 

acceptable products that have a low impact on indoor environments. For example, a list of 

products for use in school construction projects that meet Section 01350 requirements is 

available at http://www.chps.net/manual/lem_overvw.htm. DSA is working on a similar list. 

These low- and no-emitting alternatives are available and should be required in public 

buildings, group homes, schools, and other buildings. 

• Combustion appliances are also a high priority for mitigation, especially for unvented 

appliances. Combustion appliances emit carbon monoxide, nitrogen dioxide, polycyclic 

aromatic hydrocarbons, particles, and other pollutants, depending on the appliance fuel, 

status of adjustment and maintenance, and other factors. These pollutants can have severe 

acute health effects including respiratory effects and exacerbation of asthma, and contribute 

to cancer risk. Reduced exposure to pollutants from unvented gas and propane appliances, 

whether it be through active local exhaust ventilation or other measures, could have 

immediate widespread benefits for occupants in environments with such appliances. 

Precedence for mitigation of appliance emissions has been set in the State regulations for 
Indoor Air Pollution in California July, 2005 

 177

unvented space heaters used in residences, and in the State’s low-income weatherization 

program (DCSD, 2003). Guidelines for carbon monoxide levels and venting requirements in 

this weatherization program can be expanded to statewide regulations. To prevent 

backdrafting and leakage of combustion by-products from vented combustion appliances, 

accepted measures for house-as-a-system design, such as direct-vent furnaces, limits on 

exhaust fan flows, and depressurization testing, can be required. 

Statewide measures to reduce emissions from woodstoves and fireplaces both indoors and 

outdoors also are highly desirable. Such measures could have a major impact on improving 

both community-wide indoor and outdoor air quality in many areas of the state. Emission 

limitations, product re-design, product use restrictions, and improved venting can be used 

for reducing this type of pollution. A number of local government entities have approved 

regulations restricting the use of woodstoves and fireplaces: in the San Francisco Bay area, 

24 cities have ordinances that prohibit conventional fireplaces in new construction. The 

mountain town of Truckee has a more aggressive policy that requires that existing 

unapproved wood burning appliances be removed by July 15, 2006. The San Joaquin Valley 

(http://www.valleyair.org/BurnPrograms/wood_burning.htm) implemented a daily advisory for 

restrictions on residential fireplace or wood stove use on January 1, 2004. Woodsmoke 

especially impacts those with asthma and other respiratory disease. 

• Environmental tobacco smoke has been greatly reduced in California, primarily due to 

legislation that bans smoking at the workplace. However, ETS remains the number one 

cause of lung cancer, and should be reduced to the greatest extent feasible. Children’s 

exposures remain a special concern, because they can be highly exposed when smoking 

occurs in their home or in vehicles driven by family members or friends who smoke. Actions 

to reduce children’s exposure, such as an increased focus of public education on smoking 

parents, and reduction of smoking inside vehicles and homes with children, remain a high 

priority. Additionally, some outdoor and commercial building (casino) exposures continue to 

occur, with potential for exposure reduction. 

• Radon gas and its radionuclide precursors enter indoor environments largely from uraniumbearing soil or rock under and near the building. Despite the preliminary high lung cancer 

risk from radon estimated in this report for California, the lung cancer risk from radon is 

essentially inseparable from that of smoking, making reduced exposure to tobacco smoke 

the most effective mitigation approach. Radon levels in California are relatively low, except 

in a few less populated areas such as the Sierra Nevada foothills and the Ventura 

Mountains, and recent measurements in the Sierras indicates that statewide radon levels 

may be lower than estimates derived from measurements obtained in the 1980s. Mitigation 

approaches usually include depressurizing the basement, crawl space, or sub-slab region to 

reduce infiltration. However, mitigation is not recommended until adequate testing has been 

conducted in each building, so that the expense of mitigation is avoided if not needed, or to 

assure that mitigation measures will be sufficient if they are needed. Levels in buildings very 

close to each other can vary widely. California exposure data for radon are from the late 

1980s; thus, the exposure assessment needs to be reevaluated, which may affect the 

priority level. The California Department of Health Services (DHS) has established a list of 

certified providers of radon services, in three categories: testers, mitigators, and 

laboratories. 
Indoor Air Pollution in California July, 2005 

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6.2 MEDIUM RANKED SOURCE CATEGORIES 

The pollutant source categories included in Table 6.2 are lower in priority than those above, but 

nonetheless include sources that warrant mitigation. 

• Architectural coatings, such as paints, and lacquers, are available in “low VOC” versions 

due to formulation changes targeted toward reducing outdoor ozone. However, they are not 

directly regulated by the state. ARB develops Suggested Control Measures and provides 

guidance and technical assistance to air quality management districts in the state, 22 of 

which have adopted rules to reduce VOC emissions from coatings. Like building materials, 

architectural coatings are widely used and have a high loading in indoor environments when 

used, due to the large surface areas they typically cover. Additionally, some components of 

coatings can be harmful, especially if breathed for extended times such as by painters in 

non-industrial work settings, but are not necessarily addressed through reactive VOC 

reductions. However, because reductions have been achieved in districts that cover 95% of 

the California population, this source category is ranked as a medium priority. 

• Consumer products and personal care products have been regulated by ARB to reduce 

emissions of reactive VOCs in order to reduce outdoor smog formation. Reactive VOCs, and 

in some cases toxic air contaminants, have been reduced substantially through 

reformulation of a number of product categories. In reducing VOC content to comply with 

ARB regulations, manufacturers often use water-based technologies and use VOC exempt 

compounds such as acetone. To prevent increased use of TACs, ARB has also prohibited 

the use of perchloroethylene, methylene chloride, and trichloroethylene in 13 categories. 

Antiperspirants and deodorants are not allowed to contain any compounds identified as 

TACs. Also, the Board recently approved a rule to remove para-dichlorobenzene from solid 

air fresheners and toilet/urinal care products. 

Depending on the product, zero and ultra-low VOC products are not always commercially 

and technologically feasible. Despite the breadth of products addressed under ARB’s 

consumer products regulations, not all types of consumer products are regulated. Products 

such as wallpaper and vinyl coverings or plastic products may emit chemicals, but are not 

addressed in ARB regulations. Additionally, due to the nature of some products (household 

cleansers, air fresheners, stain removers, etc.), the user is in close proximity to the release 

of chemicals during use, and experiences greater pollutant exposure than individuals who 

may be elsewhere in the room or building where the product is used. Thus, there is an 

apparent need to reduce emissions from consumer products to prevent high personal 

exposures and risks, and to address types of products not currently regulated under ARB’s 

programs. Because of the ARB’s progress to date with chemically formulated products, 

some of the highest emitters, this category is ranked medium rather than high. 

Chemical reformulations, emission limitations, content limits, and/or product use restrictions 

of consumer products are mitigation approaches that could result in further significant risk 

reductions, especially for product users. Such measures have already been taken for many 

products under ARB’s consumer product authority. 

• Household appliances and office equipment such as computers and copy machines, can 

emit a variety of pollutants such as particles, ozone, various VOCs of concern, phthalates, 

and PBDEs. Emissions from each type of appliance could be addressed through emission 

limitations and/or local exhaust requirements. Examples of a specification for local exhaust 

would be the placement of a large copy machine under a strong exhaust ventilation hood, or 
Indoor Air Pollution in California July, 2005 

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specifying a level of exhaust ventilation for a room. In most cases, these pollutants are 

emitted directly into the living or working area, and thus are of concern. Additionally, more 

and more office equipment is being purchased for use in the home, increasing the number 

of people potentially exposed in the home environment. Vacuum cleaners can be an 

effective tool in maintaining a clean indoor environment, and notable advances have been 

made in the last decade in reducing the resuspension of particles through improved filter 

bags and cleaning efficiency. However, some vacuum cleaners resuspend substantial 

amounts of particulate pollutants into the air, including cat allergen, mold and pollen spores, 

and contaminated particles from the floor. Therefore, the development of a new test protocol 

for room particle counts and an industry certification program are urgently needed.

Table 6.2. Medium Priority Source Categories for Mitigation1 

SOURCES OF 

POLLUTANTS2 

(listed alphabetically) 

EXAMPLES OF 

POLLUTANTS3

EMITTED

POTENTIAL 

APPROACH TO 

MITIGATION4

DIRECT 

STATE 

AUTHORITY 

TO TAKE IAQ 

MITIGATION 

ACTIONS 

Architectural Coatings

(e.g., paints, sealants, 

lacquers, varnishes) 

Formaldehyde, 

acetaldehyde, ethylene 

glycol, metals, others 

Emission limitations, 

reformulations, use 

restrictions to reduce 

TACs & nonreactive 

VOCs w/ health impacts 

No 

Consumer Products (e.g., 

household and institutional 

cleaners, furniture & floorcare products, air fresheners, stain removers, 

detergents) 

Personal Care Products

(e.g., products used for hair 

and skin care) 

Methylene chloride, 

para-dichlorobenzene, 

perchloroethylene, 

toluene, benzene, 

naphthalene, 

formaldehyde, 

acetaldehyde, metals, 

others 

Emission limitations, 

chemical reformu-lations, 

and product use 

restrictions to reduce 

TACs and nonreactive 

VOCs with health 

impacts; labeling program 

Limited (some 

indirect) 

Household & Office 

Equipment and Appliances 

 (computers, photocopiers) 

Particles, styrene, 

some other VOCs, 

phthalates, ozone, 

PBDEs 

Emission limitations, local 

exhaust requirements 

No 

Pesticides (insecticides, 

herbicides, disinfectants, 

sanitizers used indoors and 

outdoors; track-in, drift.) 

Permethrin, 

esfenvalerate, 

chlorpyrifos5

, 

diazinon5

, many others 

Integrated pest 

management; outreach; 

formulation or application 

changes for indoor use 

Limited 

1. Individual sources may be higher or lower than the source category ranking. 

2. All of the examples of pollutant sources may not emit all of the pollutants listed in the corresponding box in 

column two. 

3. Air pollutants may be identified as toxic air contaminants (TACs) by the California Air Resources Board, and/or 

identified as Proposition 65 chemicals; or, criteria (traditional) air pollutants. 

4. Public education, economic incentives, and non-regulatory approaches should also be used where appropriate. 

The actual approach taken would be determined after extensive discussions with the relevant industries, in 

consideration of costs, feasibility, and effectiveness. 

5. Chlorpyrifos and diazinon are no longer sold for residential uses, except as containerized baits. Products 

purchased prior to the sales deadline may still be used. 
Indoor Air Pollution in California July, 2005 

 180

Because emissions information on many specific sources in this category is outdated or 

lacking, mitigation efforts for these products are a medium priority. As further research is 

conducted on these sources, some products may become a high priority for emission 

reductions, and others may be determined not to require further attention. 

• Pesticides are used indoors and around the perimeter of buildings primarily to control 

household pests such as ants, spiders, cockroaches, rats, and mice. Some are used as 

disinfectants or sanitizers. Pesticides also can be tracked into the home from outdoor 

application and drift after outdoor spray application. In rural areas, indoor concentrations can 

be greater due to increased use of pesticides for agricultural purposes. Levels of pesticides 

can be measured in both air samples and house dust samples. Pesticide residues may be 

more persistent indoors than outdoors due to the lack of natural degradation forces such as 

ultraviolet light, high temperatures, wind, and rain. Children are often exposed through 

multiple pathways, via dermal exposure and ingestion from pesticides absorbed onto floor 

dust particles, in addition to inhalation exposure. Thus, indoor pesticide levels and 

exposures warrant further attention. However, pesticides are ranked in the medium category 

because programs are available to address them. The U.S. EPA and DPR govern the use of 

pesticides in California. The U.S. EPA banned the use of chlorpyrifos and diazinon in indoor 

environments in 2000 and 2001, respectively. Continued research and intervention by the 

U.S. EPA and DPR are needed to prevent harmful exposures and promote the registration 

of less toxic pesticides for indoor use. Most importantly, the implementation of integrated 

pest management approaches should be expanded to reduce the need for pesticide 

applications through preventive measures, and to encourage the use of the least toxic 

pesticides when chemical treatment is needed. 
Indoor Air Pollution in California July, 2005 

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7. OPTIONS TO MITIGATE INDOOR AIR POLLUTION 

This report has shown that there are many sources of indoor air pollution that produce 

substantial adverse health effects, result in lost productivity, and require considerable 

expenditures for health care. Despite these facts, there is no systematic program to improve 

indoor air quality, there are relatively few regulations, or standards to specifically address indoor 

air quality problems, and few resources focused on effectively addressing problems and 

promoting improvements. Current efforts to address indoor pollution are not commensurate with 

the scope of the risk to health it poses to Californians. 

7.1 GENERAL MITIGATION OPTIONS 

Ambient (outdoor) air quality is protected through a comprehensive system. In California and 

under federal law, ambient air quality standards are established for traditional (criteria) 

pollutants and must be attained. Under other state authority, pollutants identified as toxic air 

contaminants must be reduced to the maximum extent feasible. The approach used to reduce 

toxic air contaminants in ambient air, in which source emissions are reduced without setting 

enforceable air quality levels, seems most applicable to indoor air. Actions to reduce indoor 

emissions and exposures would assure reduction of exposure and risk from key sources, and 

should be a major component of a new effort to address indoor air. Other approaches including 

public education, product testing and labeling, and setting of maximum exposure guideline 

levels, should also be part of the mitigation program. The following elements of an indoor air 

pollution reduction program are recommended for consideration: 

1. Create a management system for indoor air quality that establishes and assigns 

authority and responsibility for assessing indoor health problems, identifying the actions 

needed to reduce the most significant problems, and setting guidelines, emissions limits, or 

other requirements that will be effective in reducing the health impacts of indoor sources. As 

discussed in Sections 4 and 6 of this report, many agencies’ actions affect indoor air quality, 

and a few have limited authority over some aspect of indoor air quality, but no state (or 

federal) agency has the authority or mandate to conduct a comprehensive indoor air 

pollution mitigation program. Such a program is needed, and should be fully coordinated 

with activities of other agencies whose actions affect indoor air. 

2. Establish emission limits, when needed, for indoor pollutant sources that pose excessive 

risks due to their indoor emissions. These might include air cleaners, building materials, 

furnishings, combustion appliances, and others. While ventilation authority exists in the 

Energy Commission and Cal/OSHA, no state agency has a direct mandate to establish 

emission limits for indoor sources for the purpose of reducing indoor exposure and risk. 

Establishment of such limits would better protect public health, and may reduce (but not 

eliminate) the amount of ventilation needed under certain circumstances in some buildings, 

thus saving energy. Compliance could be accomplished by requiring emissions testing 

through an independent laboratory certified by the state, and submittal of the data to the 

lead agency. 

3. Require manufacturers to submit building materials, furnishings, combustion 

appliances, consumer products, and other significant sources for emissions testing 

by an independent laboratory certified by the state, and to report those results to the state 

and to the public. Also, require results to be transmitted to the public via product labeling or 

accompanying materials in language consumers can understand. 
Indoor Air Pollution in California July, 2005 

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Implementation of a required test program could prove to be an effective approach, at least 

for reducing indoor pollutant levels in new buildings. A prototype emissions testing program 

has already been developed for state sustainable building projects: Section 01350 (State of 

California, 2002) is a testing and assessment protocol developed for reducing VOCs from 

building materials and furnishings, and is designed to protect human health. A partial list of 

products that meet this specification is available at 

http://ciwmb.ca.gov/GreenBuilding/Specs/EastEnd/. However, there is currently no 

requirement for state agencies or others to use these guideline emission specifications, and 

only limited incentive for them to do so. Other national and international emissions test 

protocols that are widely used also are available. ARB also has a consumer products test 

program with test methods (for VOC content) that could be adapted for a broader array of 

products. Currently, only a few laboratories have the chamber facilities and expertise to 

conduct such emissions tests. Thus, testing requirements would need to be phased in. 

However, required testing would prompt other laboratories to obtain appropriate chamber 

equipment and participate. 

4. Make children’s health in schools, homes, and care institutions the top priority. 

Implement the recommendations for schools in Section 7.2 of this report. In schools and 

public daycare centers, require the use of building materials that are certified to be lowemitting. Require that school HVAC systems be quiet (under 45 decibels) and well 

maintained. Encourage school districts to adopt integrated pest management (IPM) 

programs and send their IPM coordinators to DPR’s school IPM training classes. Increase 

efforts to reduce children’s exposure to environmental tobacco smoke. Increased education 

and outreach efforts to smoking parents and caretakers are needed to inform them of the 

health dangers of second-hand smoke, and the actions they should be taking to protect 

children under their care from these dangers. 

5. Develop indoor air quality guidelines for homes, schools, offices, and institutional living 

quarters. These would largely identify “Best Practices” for the design, construction, 

operation and maintenance of public, commercial, school, and institutional buildings. In 

some cases, they might include the identification of healthful levels or “bright lines” for some 

pollutants to be used as goals for mitigation activities and “best practices”, but would not 

have an associated compliance program. They should also include valid certification 

requirements for professionals directly involved in indoor air quality-related occupations; 

performance measures for buildings and appliances; and others. Full commissioning should 

be required for all new public, commercial, and institutional residential buildings, to assure 

that they are constructed and operate as intended, and that they provide acceptable indoor 

air quality. ASHRAE Guidelines (1993, 1996) provide basic guidance for building 

commissioning, but state requirements are needed. 

6. Amend building codes to address indoor air quality, with a focus on assuring 

adequate ventilation under all circumstances. For example, unvented cook stoves, 

ovens, and combustion appliances should not be allowed in residences: rather, they should 

be vented to the outdoors, such as through direct venting or an automatic (but quiet) 

exhaust fan that is activated when the appliance is turned on. Similarly, building codes 

should be established and enforced to prevent mold problems, residential ventilation issues, 

and other indoor air quality problems. Requirements also are needed to assure that 

adequately filtered outdoor air is provided in locales where outdoor air pollution is common. 

7. Fund an outreach and education program focused on professionals, including health 

professionals, teachers, school facility managers, and others who must be able to identify 
Indoor Air Pollution in California July, 2005 

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and remedy indoor air quality problems. Such individuals have many obligations, yet play a 

key role through their occupation in initial identification, prevention, and mitigation of indoor 

air quality problems. Most need more in-depth information and training on indoor air quality 

than they typically have had. Training and technical assistance should be provided for the 

private sector to develop the skills and services needed for high-quality building 

commissioning, operation, and maintenance. 

8. Conduct more research on indoor air quality. Several high priority areas are specifically 

identified in this report for further research. Because of the known serious health impacts of 

ambient PM and recent studies showing high emissions of PM from indoor sources, 

research on the health effects of indoor PM are a high priority. The health effects of terpeneozone reaction products and the extent of people’s exposures to them, as well as other 

fragrances and indoor chemical reaction products, also are key areas warranting focused 

research. There are many new chemicals introduced into the product mix each year, yet few 

have had full health and exposure studies completed. The effects of more recently identified 

indoor chemicals, such as PBDEs, warrants further investigation. Improved methods and 

protocols to detect indoor dampness and hidden mold growth are also needed. Synergistic 

and cumulative health effects are suspected for a number of indoor pollutants with similar 

structures or properties, yet little research has been conducted in this area. Finally, 

mitigation approaches assumed to be effective have sometimes been found to be much less 

effective than anticipated; the effectiveness of recommended or required mitigation 

measures should be confirmed through appropriately designed studies to assure that the 

necessary reductions in exposure and risk will be achieved. 

9. Fund an Innovative Clean Air Technology program (ICAT) for indoor air quality to 

foster the development and commercialization of legitimate, cost effective technologies that 

can improve IAQ. For example, improved low-noise ventilation technologies, improved air 

monitors and assessment tools, and effective low-noise air cleaners are needed. ARB’s 

current ICAT program, focused on improving outdoor air quality through improved 

technology, has been very successful in bringing new technologies to commercialization in 

California, adding new options for reducing air pollution while also bringing jobs and 

investment into the state. An indoor air quality ICAT program would be expected to do the 

same. 

All of these suggested mitigation options are feasible if appropriate mandates and resources are 

provided. The degree of feasibility of individual measures, such as emission limits for a specific 

type of product, cannot be determined without substantial additional information. As discussed 

in previous sections of this report, alternative products or formulations are already available for 

some of the indoor sources of current concern. However, prior to taking any regulatory action, a 

more detailed assessment of the specific remedies available, including technological and 

economic feasibility, would be needed. Additionally, like ARB’s current regulatory programs, any 

emission limitations or other mitigation measures would be developed with continuous 

discussion and review by stakeholders, the public, and other state agencies. 

7.2 SOLUTIONS FOR SCHOOLS 

The ARB and DHS recently completed a report on a statewide study entitled Environmental 

Health Conditions in California’s Portable Classrooms (ARB/DHS, 2004). The study was 

required by the State Legislature (AB 2872 Shelley; HSC § 39619.6) as a result of concerns 

regarding reports of mold contamination, inadequate ventilation, elevated levels of volatile 

chemicals, excessive use of some pesticides, and other problems. The study was funded to 
Indoor Air Pollution in California July, 2005 

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help identify the extent of these problems and to determine whether those problems warranted 

response by the state and/or schools and school districts. 

The study included kindergarten through 12th grade public schools. A large, representative 

sample of both portable and traditional classrooms was studied throughout the state. The 

results of this comprehensive study have been condensed into a report to the Legislature, and 

provide important information for state and local decision-makers regarding the degree to which 

California classrooms provide a safe, healthful, and productive learning environment for 

children. The report summarizes serious conditions identified in the study that need to be 

addressed at the State and local levels, and discusses options for improving conditions in both 

portable and traditional classrooms. The key results and recommendations included in the 

report are summarized below. The recommendations were developed in consultation with 

relevant state agencies, industries, school officials, and other interested stakeholders. 

7.2.1 Problems Identified 

The report identifies and addresses a number of environmental problems that were frequently 

found in classrooms throughout California. These problems were found in both portable 

(relocatable) and traditional (site-built) classrooms; however, some of the problems were found 

more frequently in portable classrooms. Government standards and guidelines that are 

designed to protect children in classrooms and other buildings are essentially lacking. Thus, in 

this study, results were compared to the most relevant environmental health guidelines and 

standards available, primarily from professional societies (such as those for ventilation and 

lighting) and government agencies, such as the Office of Environmental Health Hazard 

Assessment (OEHHA) and the California Department of Industrial Relations (Cal/OSHA). The 

primary problems found include: 

• Inadequate ventilation with outdoor air during 40% of class hours, and seriously deficient 

ventilation 10% of the time. This is due largely to teachers turning off HVAC (heating, 

ventilating, and air-conditioning) systems because of excessive noise and to other factors 

such as closed outdoor air dampers and inadequate HVAC capacity. 

• Temperature and humidity levels outside of professional standards for thermal comfort in 

about one-fourth of the classrooms. 

• Formaldehyde air concentrations above guidelines for preventing acute eye, nose, and 

throat irritation in about 4% of the classrooms; and, nearly all classrooms exceeded 

formaldehyde guidelines for preventing long-term health effects, including cancer. Elevated 

formaldehyde is due primarily to the use of formaldehyde-containing building materials and 

furnishings. 

• Noise levels in all classrooms exceeded the national voluntary acoustic standard for 

unoccupied classrooms of 35 decibels, a somewhat controversial standard that has not 

been adopted by any California agency. About one-half of the classrooms also exceeded 55 

decibels, the level used by many communities in the state for their outdoor nuisance 

regulations. Excess noise was due primarily to noisy HVAC systems. Noisy lighting and 

noise from nearby outdoor activities also contributed. Excess noise directly impacts indoor 

air quality in the classrooms: when teachers turn off the systems due to noise, classrooms 

become stuffy and indoor pollutant levels rise. 
Indoor Air Pollution in California July, 2005 

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• Lead, arsenic, and numerous pesticide residues in classroom floor dust; these residues are 

a concern because they can be inhaled, ingested, or absorbed through the skin (pesticides) 

by children, especially very young children who sit on the floor and put their hands in their 

mouths. 

• Obvious mold in about 3% of classrooms; water stains, excess wall moisture, and other 

potential mold indicators in about one-third of classrooms; musty odors reported by 69% of 

teachers. These conditions are often attributable to inadequate maintenance. 

• Lighting was inadequate in about one-third of the classrooms. 

7.2.2 Report Recommendations 

To address the breadth of problems identified and the many actions needed at all levels to 

resolve them, a total of 16 recommendations are discussed in the report to the Legislature. 

These are presented in two groups in the report. Group 1 includes high priority, high benefit 

actions that can be achieved at relatively low cost and should be accomplished in the near term, 

while Group 2 recommendations, also a priority, will require a longer timeframe and/or more 

substantial resources to accomplish. The recommendations fall into four general approaches 

needed to remedy and prevent the problems seen. The state should: 

• Direct and assist schools to comply with state regulations, especially workplace regulations 

(Cal/OSHA) related to building operation and maintenance. 

• Develop and promote “Best Practices” for design, construction, operation, and maintenance 

of school facilities. 

• Improve support (both funding and training) for school facilities and staff. 

• Establish guidelines and standards for school environmental health that are protective of 

children. 

The specific Group I recommendations are: 

• Schools, districts, and the state should assure that all school buildings meet all relevant 

state regulations, especially the Cal/OSHA workplace regulations regarding ventilation, 

sanitation and water intrusion, and illness and injury prevention. Many schools do not meet 

Cal/OSHA occupational health requirements. 

• Schools and school districts should conduct “self-assessments” of basic health and safety 

conditions, similar to the Facility Self-inspection Program undertaken by the Los Angeles 

Unified School District (LAUSD). Checklists are available on the web. 

• The state should require schools to develop indoor environmental quality management 

plans. The U.S. Environmental Protection Agency’s IAQ Tools for Schools Program (USEPA 

2003b) provides guidance and free kits to accomplish this. The kit is available free of charge 

at http://www.U.S. EPA.gov/iaq/schools/. 

• The state should establish a policy to incorporate “Best Practices” into the design, 

construction, operation, and maintenance of California schools, especially the measures 
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developed by the Collaborative for High Performance Schools (CHPS). The CHPS Best 

Practices Manual at http://www.chps.net/ provides guidance for measures that will improve 

schools while also saving energy and reducing long-term costs (CHPS, 2001). 

• State-level review by the Division of the State Architect of the designs for new schools 

should be expanded to include elements such as ventilation systems and building materials 

in addition to current elements such as fire and life-safety provisions. 

• Portable classrooms (and traditional classrooms) should be sited correctly, away from busy 

roadways and with proper drainage. 

• The state should implement an interim requirement for new classrooms of a maximum noise 

level of 45 decibels, unoccupied, until a specially-convened task force can determine an 

appropriate level for California schools (see below). 

Group 2 recommendations specify that: 

• The state and school districts should assure stable, long-term funding mechanisms and 

sources for both construction and preventive maintenance; currently, funding fluctuates from 

year to year, especially for the Deferred Maintenance Program. 

• The state should develop and offer focused training programs for school facility managers, 

custodial staff, and teachers, in cooperation with interested organizations; those closest to 

the classrooms often are not aware of current “best practices” for operation and 

maintenance of classrooms. A concerted, ongoing training program could go far to improve 

conditions in classrooms. 

• Integrated Pest Management Programs should be implemented at all schools. 

• Older portable classrooms should be retired when they become unserviceable or do not 

provide an adequate learning environment for children. 

• The state and school districts should develop and require full new building commissioning 

procedures. 

• The state should improve its database of school facilities: currently, there is no complete 

database on the condition, location, or even number, of school buildings. 

• The state should convene a task force of experts to develop a California indoor noise 

guideline or standard for K-12 schools. 

• The state should develop chemical exposure guidelines or standards for classrooms that are 

protective of children and teachers. 

• Portable classrooms should be re-designed from the ground up. Several groups are 

producing new prototypes that use an integrated “whole building” approach; these should be 

supported through the demonstration phase to evaluate design changes that provide 

substantive improvements over older portables. 

Some actions have already been taken to begin to address these problems; however, they 

constitute only a first step toward realizing actual improvements in school conditions. Only a 
Indoor Air Pollution in California July, 2005 

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small percentage of schools and districts have actively pursued the many tools that are readily 

available to them to help improve the school environment. The CHPS’ Best Practices Manual, 

U.S. EPA’s IAQ Tools for Schools Kits, and the LAUSD’s “Safe School Inspection Guidebook” 

are all available on the Internet free of charge, yet the number of California schools utilizing 

each of these tools is small. A proactive effort to implement the recommendations of the report 

is needed. 

The complete Report to the Legislature on Environmental Health Conditions in California’s 

Portable Classrooms is available at ARB’s website at 

http://www.arb.ca.gov/research/indoor/pcs/pcs.htm. 
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8. SUMMARY 

Indoor air pollution poses a significant health risk to Californians, in addition to the known risks 

from outdoor pollution. Indoor pollutant sources emit gases and particles known to trigger 

asthma attacks and cause cancer, heart and lung disease, and immediate irritant and 

neurological effects such as eye and throat irritation and headache. Indoor pollution has 

repeatedly been ranked in the “High Risk” categories in both federal and state comparative risk 

projects. Some of the known risks in California include: 

♦ Indoor air pollution includes many asthma triggers. It has been implicated by national 

scientists as a factor in the serious increase in asthma observed in recent decades. 

♦ It is estimated that about 230 excess cancers per year may occur in California due to indoor 

carcinogens from residential and consumer sources, such as formaldehyde. This 

approaches the 260 estimated excess cancer cases per year from diesel exhaust and 

equals about two-thirds of the total outdoor cancer burden. Environmental tobacco smoke 

also adds significant cancer risk. Also, rough estimates show that radon gas from certain 

soils and rock may contribute to about 1500 excess lung cancers per year. 

♦ Each year, accidental carbon monoxide poisoning from indoor sources causes about 20-26 

accidental deaths, hundreds of avoidable emergency room visits, and hundreds to 

thousands of cases of avoidable illness. 

♦ Many VOCs, especially formaldehyde, are typically found at elevated levels indoors, and 

those levels sometimes exceed health-based guideline levels, such as acceptable cancer 

risk levels. 

♦ Indoor sources of PM may be partly responsible for the large numbers of premature deaths, 

hospitalizations, emergency room visits, and increased respiratory disease associated with 

PM exposures in California each year, and may contribute to these effects beyond the levels 

quantified in the outdoor epidemiology studies. 

♦ Biological contaminants can cause communicable disease, hypersensitivity reactions, and 

even toxic responses, in addition to their widely recognized role as asthma and allergy 

triggers in indoor environments. Indoor mold problems have increased over the last decade. 

Indoor pollutants significantly impact people’s health because there are many indoor sources of 

pollutants, which often result in elevated indoor concentrations. Additionally, Californians, like 

others, spend about 87% of their time indoors, on average. Infants and young children spend 

the most time indoors, most of it in their homes. Several scientists have calculated that indoor 

emissions are about 1000 times more likely to be breathed than outdoor emissions. 

Indoor pollution is estimated to cost California’s economy $45 billion each year due to medical 

costs, lost worker productivity, loss of life, and related factors. This estimate is derived from only 

partial costs of cancer, respiratory disease, cardiovascular disease, and sick building symptoms. 

This is believed to be an underestimate; the total cost is likely much higher. 

Despite the high health and economic costs of indoor pollution, no state or federal agency has 

explicit authority to regulate indoor sources of pollution to protect building occupants from 
Indoor Air Pollution in California July, 2005 

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harmful exposures. Indoor pollution remains the only major environmental health problem that 

does not have the benefit of a focused risk reduction program. 

Many actions could be taken to reduce indoor pollution at relatively low cost that would reap 

large health benefits. Options for mitigation include the development of emission limitations for 

building materials, furnishings, consumer products, and appliances; improvements in building 

codes; focused outreach and education programs; improved technologies; and adherence to 

current “Best Practices” and other guidelines. Substitute products are available for many 

products and materials that currently emit high levels of pollutants; thus, emission reductions 

should be achievable in many products with little impact on consumers and homeowners. This 

would go far to improve indoor air quality in schools and homes, which require a focused effort 

because little has been done to improve those indoor environments. Also, the most sensitive 

members of the population–children, the elderly, and the infirm–spend most of their time there. 

Focused public education, improved appliance standards, and modified building codes would 

also foster improved indoor air quality in homes and schools. Following current “Best Practices” 

in design, construction, operation and maintenance is a non-regulatory approach that could 

yield large gains in indoor health in all types of buildings. Increased effort to publicize and 

enforce existing Cal/OSHA regulations in schools and non-industrial workplaces would also go 

far to reduce indoor pollution in those environments; those regulations are in place, but are often 

not followed. 

Perhaps most importantly, a comprehensive management system with responsibility for indoor 

air quality is needed to combine and coordinate the options indicated above into a cohesive, 

effective program. That program should include a more detailed prioritization of mitigation 

actions, careful assessment of the technical and economic feasibility of specific actions, and 

continued discussion with, and input from, interested stakeholders and members of the public. 

Such a program also should be closely coordinated with state agencies whose programs 

include some existing authority related to indoor air quality, especially Cal/OSHA and the 

Energy Commission, to assure consistency and avoid duplication of effort. 
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9. REFERENCES 

AB 13, 1995. Assembly Bill 13, author Terry Friedman, California Labor Code Section 6404.5. 

Abt E, Suh HH, Catalano P, and Koutrakis P, 2000. Characterization of indoor particle sources: 

a study conducted in the metropolitan Boston area. Environmental Health Perspectives 108(1): 

3579-3587. 

Abt E, Suh HH, Allen G, and Koutrakis P, 2001. Relative contribution of outdoor and indoor 

particle sources to indoor concentrations. Environ Science and Technol 34: 3579-3587. 

ACGIH (American Conference of Governmental Industrial Hygienists), 1999. Developing a 

Sampling Plan. In Bioaerosols: Assessment and Control. Editor: J Macher. American 

Conference of Governmental Industrial Hygienists, Cincinnati, OH. 

Adams W, 1993. Measurement of breathing rate and volume in routinely performed daily 

activities. Final Report, Air Resources Board Contract no. A033-205. 

Addiss SS, Alderman NO, Brown DR, Each CN, and Wargo J, 1999. Pest control practices in 

Connecticut public schools. North Haven, CT: Environment and Human Health, Inc. 

Adgate JL, Eberly LE, Strobebel C, Pellizzari ED and Sexton K, 2004. Personal, indoor, and 

outdoor VOC exposures in a probability sample of children. J Exposure Analysis and 

Environmental Epidemiology 14:S4-S13.

AGA (American Gas Association), 2003. Combustion Emissions from Gas Ranges. See: 

http://www.aga.org/Content/NavigationMenu/Operations_and_Engineering/Codes_and_Standar

ds1/Fact_Sheets_and_Reports/twfacts9902.pdf. 

AHAM (Association of Home Appliance Manufacturers), 2004. Clean Air Delivery Rate: 

Frequenty Asked Questions. http://www.cadr.org/consumer/faq.html. 

AIHA (American Industrial Hygiene Association), 1996. Field Guide for the Determination of 

Biological Contaminants in Environmental Samples. Editors: HK Dillon, PA Heinsohn, JD Miller. 

American Industrial Hygiene Association, Fairfax, VA, pp 37-95, 119-130. 

Akazawa M, Sindelar JL, Paltiel D, 2003. Economic costs of influenza-related work 

absenteeism, Value Health 6:107-115. 

Akland G, and Whitaker DA, 2000. Characterizing the sources of human exposure to 

proposition 65 substances. Research Triangle Institute, NC. Final report to California Public 

Health Foundation, Public Health Trust, Grant No. 543A-8803-G11299. 

ALA (American Lung Association), 1997. Residential Air cleaning Devices: Types, 

Effectiveness, and Health Impact. Available from: 

http://www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=39289. 

ALA, 2004. Health Home Program. Available from: http://www.healthhouse.org/. 
Indoor Air Pollution in California July, 2005 

 192

Alevantis L, 2003. Building material emissions study. Final Report to California Integrated Waste 

Management Board. 

http://www.ciwmb.ca.gov/GreenBuilding/Specs/Section01350/METStudy.htm. 

Allen RJ, Wadden RA, and Ross ED, 1978. Characterization of potential indoor sources of 

ozone. J Am Industrial Hygiene Assoc 39: 466-471. 

Anderson RN, Arias E, 2003. The effect of revised populations on mortality statistics for the 

United States, 2000. Natl Vital Stat Rep 51(9): 1-24. 

Anderson HR, Spix C, Medina S, Schouten JP, Castellsague J, Rossi G, Zmirou D, Touloumi G, 

Wojtyniak B, Ponka A, Bacharova L, Schwartz J, and Katsouyanni K, 1997. Air pollution and 

daily admissions for chronic obstructive pulmonary disease in 6 European cities: results from 

the APHEA project. European Respiratory Journal 10: 1064-1071. 

Anuszewski J, Larson TV, Koenig JQ, 1998. Simultaneous indoor and outdoor particle lightscattering measurements at nine homes using a portable nephelometer. J Exposure Analysis 

and Environmental Epidemiology 8(4): 483-493. 

Apte MG and Daisey JM, 1999. VOCs and “sick building syndrome”: application of a new 

statistical approach for SBS research to U.S. EPA BASE study data. Indoor Air 1: 117. 

Apte MG, Di Bartolomeo D, Hotchi T, Hodgson AT, Lee SM, Liff SM, Rainer LI, Shendell DG, 

Sullivan DP, Fisk WJ, 2003. Simultaneous Energy Savings and IEQ Improvements in 

Relocatable Classrooms. ASHRAE IAQ Applications 4 (4): 7-10. LBNL-52690. 

http://eetd.lbl.gov/IEP/pdf/LBNL-52690.pdf. 

Apte MG, Gundel LA, Dod RL, Russell ML, Singer BC, Sohn MD, Sullivan DP, Chang GM and 

Sextro RG, 2004. Indoor Measurements of Environmental Tobacco Smoke, Final Report to the 

Tobacco Related Disease Research Program. Lawrence Berkeley National Lab report LBNL49148. Berkeley, CA. March. 

ARB (California Air Resources Board), 1986. Staff Report: Initial Statement of Reasons for 

Proposed Rulemaking. Public Hearing to Consider the Adoption of a Regulatory Amendment 

Identifying Asbestos as a Toxic Air Contaminant. California Air Resources Board, agenda item 

no. 86-4-1. 

ARB, 1987. Indoor Air Quality and Personal Exposure: Briefing Paper. Research Division, 

California Air Resources Board, May 1987.

ARB, 1989. Reducing Exposures to Indoor Air Pollutants in California: Existing authorities and 

Recommended Actions. Final Report, v.1, and Appendices, v. 2. Research Division, 

Sacramento, CA. 

ARB, 1991. Formaldehyde in the Home, Indoor Air Quality Guideline no. 1. Research Division. 

ARB, 1992. Final report on the identification of formaldehyde as a toxic air contaminant, Part B, 

Health Assessment, Stationary Source Division. 
Indoor Air Pollution in California July, 2005 

 193

ARB, 1994a. Benzo(a)pyrene as a Toxic Air Contaminant, Part A. Exposure Assessment. 

Sacramento, CA. Executive Summary at: 

http://www.oehha.ca.gov/air/toxic_contaminants/html/benzo%5Ba%5Dpyrene.htm. 

ARB, 1994b. Combustion Pollutants in the Home. Indoor Air Quality Guideline no. 2, and 

Supplement. Sacramento, CA. Available from: 

http://www.arb.ca.gov/research/indoor/guidelines.htm. 

ARB, 1997a. Toxic air contaminant identification list–summaries. Stationary Source Division, 

California Air Resources Board. http://www.arb.ca.gov/toxics/tac/toctbl.htm. 

ARB, 1997b. Woodburning Handbook: How to Burn More Efficiently in Your Stove or Fireplace 

and Produce Less Air Pollution. Available from: 

http://www.arb.ca.gov/cap/handbooks/wood_burning_handbook.pdf. 

ARB, 1998. Proposed Identification of Diesel Exhaust as a Toxic Air Contaminant, Part A, 

Exposure Assessment, Appendix D, Californians’ Indoor and Total Air Exposures to Diesel 

Exhaust Particles. April. Sacramento, CA. 

ARB, 2000a. Risk reduction plan to reduce particulate matter emissions from diesel-fueled 

engines and vehicles. Stationary Source Division, California Air Resources Board, 

http://www.arb.ca.gov/diesel/documents/rrpFinal.pdf 

ARB, 2000b. Indoor Air Quality Risk Reduction in the 21st Century, Symposium Proceedings, 

Sacramento, CA May 2000. http://www.arb.ca.gov/research/indoor/proceedings.PDF

ARB, 2000c. Air Cleaning Devices for the Home: Frequently Asked Questions. Fact Sheet. 

Research Division. http://www.arb.ca.gov/research/indoor/guidelines.htm

ARB, 2001a. Policies and actions for environmental justice, approved December 13, 2001. 

California Air Resources Board. http://www.arb.ca.gov/ch/programs/ej/ej.htm.

ARB, 2001b. Chlorinated Chemicals in Your Home, Indoor Air Quality Guideline no. 3. Research 

Division. http://www.arb.ca.gov/research/indoor/guidelines.htm

ARB, 2001c. Composite Wood Products, Fact Sheet. Available from: 

http://www.arb.ca.gov/ch/factsheets/formaldehyde.pdf. 

ARB, 2003. List of the Current Rules in Each of the 35 Air Districts. Available from: 

http://www.arb.ca.gov/drdb/drdbltxt.htm. 

ARB, 2004. Formaldehyde in the Home (Updated). Indoor Air Quality Guideline no. 1. 

http://www.arb.ca.gov/research/indoor/guidelines.htm. 

ARB, 2005a. News release, January 20, 2005, ARB Warns, Danger from Popular "Air Purifying" 

Machines. http://www.arb.ca.gov/newsrel/nr012005.htm. 

ARB, 2005b. Air Cleaning Devices For the Home: Frequently Asked Questions. Fact sheet, 

updated February 4, 2005. http://www.arb.ca.gov/research/indoor/acdsumm.pdf. 
Indoor Air Pollution in California July, 2005 

 194

ARB, 2005c. California Ambient Air Quality Standards. 

http://www.arb.ca.gov/research/aaqs/caaqs/caaqs.htm. 

ARB/DHS (California Air Resources Board and Department of Health Services), 2004. Report to 

the Legislature: Environmental Health Conditions in California’s Portable Classrooms, Nov. 

2003. http://www.arb.ca.gov/research/indoor/pcs/pcs.htm. 

Arbes SJ Jr, Cohn RD, Yin M, Muilenberg ML, Burge HA, Friedman W, Zeldin DC, 2003. House 

dust mite allergen in US beds: results from the First National Survey or Lead and Allergens in 

Housing. J Allergy Clin Immunol 111(2): 408-414. 

Arbes SJ Jr, Cohn RD, Yin M, Muilenberg ML, Friedman W, Zeldin D, 2004. Dog allergen (Can 

f1) and cat allergen (Fel d1) in US homes: results from the National Survey of Lead and 

Allergens in Housing. J Allergy Clin Immunol 114(1): 111-117. 

ARB/OEHHA (California Air Resources Board and Office of Environmental Health Hazard 

Assessment), 1994. Benzo(a)pyrene as a toxic air contaminant. Approved by the Scientific 

Review Panel. 

ARB/OEHHA. 1996. Proposed Identification of Inorganic Lead as a Toxic Air Contaminant. 

http://www.arb.ca.gov/toxics/summary/leadsum.pdf. 

ARB/OEHHA, 2000. Staff Report, Adequacy of California Ambient Air Quality Standards: 

Children’s Environmental Health Protection Act. December. 

ARB/OEHHA, 2002. Staff Report: Public Hearing to Consider Amendments to the Ambient Air 

Quality Standards for Particulate Matter and Sulfates. Air Resources Board and Office of 

Environmental health Hazard Assessment, Sacramento, CA. 

ARB/OEHHA, 2003. Proposed Identification of Environmental Tobacco Smoke as a Toxic Air 

Contaminant. (Draft Report, Parts A and B). Available from: 

http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm. 

ARB/OEHHA, 2004. Draft Report on the Ozone Ambient Air Quality Standard. 

http://www.arb.ca.gov/research/aaqs/ozone-rs/ozone-draft-rpt.htm . 

ARB/OEHHA, 2005. Proposed Identification of Environmental Tobacco Smoke as a Toxic Air 

Contaminant – March 2005, Parts A and B. http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm.

Aris RM, Christian D, Hearne PQ, Kerr K, Finkbeiner WE, and Balmes JR, 1993. Ozoneinduced airway inflammation in human subjects as determined by airway lavage and biopsy. 

American Review of Respiratory Diseases 148: 1363-1372. 

ASHRAE (American Society of Heating, Refrigerating, and Air-conditioning Engineers), 1981. 

Ventilation for Acceptable Indoor Air Quality. ASHRAE Standard 62-1981. American Society of 

Heating Refrigerating and Air-conditioning Engineers, Atlanta, GA. 

ASHRAE, 1993. Guideline 4-1993 -- Preparation of Operating and Maintenance Documentation 

for Building Systems. Atlanta, GA. 

ASHRAE, 1996. Guideline 1-1996. The HVAC Commissioning Process. Atlanta, GA. 
Indoor Air Pollution in California July, 2005 

 195

ASHRAE, 2003a. Standard 62.2-2003, Ventilation and Acceptable Indoor Air Quality in LowRise Residential Buildings. Atlanta, GA. http://www.ashrae.org. 

ASHRAE, 2003b. Standard 62-2001, "Ventilation for Acceptable Indoor Air Quality", plus 

Addenda approved by ASHRAE’s Board of Directors since the 2001 adoption. Atlanta, GA. 

ASHRAE, 2004. Standard 55-2004, “Thermal Environmental Conditions for Human Occupancy”, 

supersedes ASHRAE Standard 55-1992. Atlanta, GA. 

ASTMI (American Society for Testing and Materials International), 2005. Committee F11 on 

Vacuum Cleaners. West Conshohocken, PA. 

http://www.astm.org/COMMIT/COMMITTEE/F11.htm. 

Atkinson R, and Arey J, 1989. Atmospheric lifetime and fate of benzo(a)pyrene. In: Lifetimes 

and Fates of Toxic Air Contaminants in California’s Atmosphere, Final Report, Contract No. 

A732-107, California Air Resources Board. 

Atkinson RW, Anderson HR, Sunyer J, Ayres J, Baccini M, Vonk JM, Boumghar A, Forastiere F, 

Forsberg B, Touloumi G, Schwartz J, and Katsouyanni K, 2003. Acute Effects of Particulate Air 

Pollution on Respiratory Admissions, In: Health Effects Institute Special Report: Revised 

Analyses of Time-Series Studies of Air Pollution and Health. 

Atkinson R, and Arey J, 2003. Gas-phase tropospheric chemistry of biogenic volatile organic 

compounds: a review. Atmospheric Environment 37 Supplement No. 2: S197-S1219. 

ATS (American Thoracic Society), 1997. Achieving Healthy Indoor Air. American J Respiratory 

and Critical Care Medicine 156: s33-s64. 

ATS, 2003a. American Thoracic Society Statement: Occupational Contribution to the Burden of 

Airway Disease. American J Respiratory and Critical Care Medicine 167: 787-797. 

ATS, 2003b. Workshop on Lung Disease and the Environment: Where Do We Go from Here? 

American J Respiratory and Critical Care Medicine 168: 250-254. 

ATSDR, 1999a. Toxicological profile for lead. Atlanta, GA: U.S. Department of Health and 

Human Services, Public Health Service. Available from: 

http://www.atsdr.cdc.gov/toxprofiles/tp13.html. 

ATSDR (Agency for Toxic Substances and Disease Registry), 1999a. Toxicological profile for 

lead. Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. 

Available from: http://www.atsdr.cdc.gov/toxprofiles/tp13.html. 

ATSDR, 1999b. Toxicological profile for mercury. Atlanta, GA: U.S. Department of Health and 

Human Services, Public Health Service. Available from: 

http://www.atsdr.cdc.gov/toxprofiles/tp46.html. 

ATSDR, 2001. Toxicological profile for asbestos. Atlanta, GA: U.S. Department of Health and 

Human Services, Public Health Service. Available from: 

http://www.atsdr.cdc.gov/toxprofiles/tp61.html. 
Indoor Air Pollution in California July, 2005 

 196

ATSDR, 2002a. Health Consultation: Mercury Exposures from 3M Tartan Brand Floors. 

Available from: http://www.atsdr.cdc.gov/HAC/PHA/westerville/wes_p1.html. 

ATSDR, 2002b. Toxicological Profile for di(2-ethylhexyl) phthalate (DEHP). Atlanta, GA: U.S. 

Department of Health and Human Services, Public Health Service. Available from: 

http://www.atsdr.cdc.gov/toxprofiles/tp9.html. 

Auinger P, Lanphear BP, Kalkwarf HJ, and Mansour ME, 2003. Trends in otitis media among 

children in the United States. Pediatrics 112(3 Pt 1): 514-20. 

AVMA (American Veterinary Medical Association), 1997. Results of the AVMA survey of US petowning households on companion animal ownership. American Veterinary Medical Association, 

Schaumberg, IL. 

Avol E, Colome S, Estes M, Navidi W, Rappaport E, Lurmann F, Hering S, 1996. Residential 

Microenvironmental and Personal Sampling Project for Exposure Classification, Final Report for 

ARB Contract no. 92-317, University of Southern California, July 1996. 

Avol EL, Navidi WC, and Colome SD, 1998. Modeling ozone levels in and around Southern 

California homes. Environ Sci Technol 32: 463-468. 

Balmes JR, Chen LL, Sannell C, Tager I, Christian D, Hearne PQ, Kelly T, and Aris RM, 1996. 

Ozone-induced decrements in FEV and FVC do not correlate with measures of inflammation. 

American J Respiratory and Critical Care Medicine 153: 904-909. 

Barck C, Sandstrom T, Lundahl J, Hallden G, Svartengren M, Strand V, Rak S, and Bylin G, 

2002. Ambient level of NO2 augments the inflammatory response to inhaled allergen in 

asthmatics. Respiratory Medicine 96: 907-917. 

Beamer P, Canales RA, Ferguson AC, AuYeung W, Leckie JO, Bradman A, and Eskenazi B, 

2004. Estimates of non-dietary exposure of young farm-worker children using micro-level 

activity time series and the CASE model. 14th Annual Meeting of the International Society of 

Exposure Analysis, 2004, Abstracts. 

Bearer C, 1995. How are children different from adults? Environmental Health Perspectives

103 (Supplement 6): 7-12. 

Bearg DW, 1993. Indoor Air Quality and HVAC Systems. Lewis Publishers, Boca Raton. 

Chapter 1. 

Becker S, and Soukup JM, 1999. Effect of nitrogen dioxide on respiratory viral infection in 

airway epithelial cells. Environmental Research 81:159-166. 

Belanger K, Beckett W, Triche E, Bracken MB, Holford T, Ren P, McSharry JE, Gold DR, PlattsMills TA, Leaderer BP, 2003. Symptoms of wheeze and persistent cough in the first year of life: 

associations with indoor allergens, air contaminants and maternal history of asthma. Amer J 

Epidemiology 158(3):195-202. 

Bennet DH, McKone TE, Evans JS, Nazaroff WW, Margni MD, Jolliet O, and Smith KR, 2002. 

Defining intake fraction. Environmental Science and Technology May 1, 2002: 207A-211A. 
Indoor Air Pollution in California July, 2005 

 197

Blomberg A, Krishna MT, Helleday R, Soderberg M, Ledin M, Kelly FJ, Frew AJ, Holgate ST, 

and Sandstrom T, 1999. Persistent airway inflammation but accomodated antioxidant and lung 

function responses after repeated daily exposure to nitrogen dioxide. Amer J Respiratory and 

Critical Care Medicine 159: 536-543. 

Bobak M, 2000. Outdoor air pollution, low birth weight, and prematurity. Environmental Health 

Perspectives 108(2):173-176. 

Bobak M, and Leon DA, 1998. Air pollution and infant mortality: the effects are specific for 

respiratory causes in the post-neonatal period. Epidemiology 9: S58. 

Boe AB, 1999. Field observations from SGC/NC homes in Oregon. Oregon State University 

Energy Extension Program. 1997-99. As cited in Lubliner and Gordon, 1990. 

Boekelheide K (2004). Cracking the nut. Toxicol Sci 81, 1-2. 

Boeniger MF, 1995. Use of ozone generating devices to improve indoor air quality. J American 

Industrial Hygiene Association 56: 590-598. 

Bollinger ME, Eggleston PA, Flanagan E, Wood RA, 1996. Cat antigen in homes with and 

without cats may induce allergic symptoms. Journal of Allergy and Clinical Immunology 97(4): 

907-914. 

Bonita R, Duncan J, Truelsen T, Jackson RT, and Beaglehole R, 1999. Passive smoking as well 

as active smoking increases the risk of acute stroke. Tobacco Control 8(2): 156-160. 

Bornehag CG, Blomquist G, Gyntelberg F, Järvhom B, Malmberg P, Nordvall L, Nielsen A, 

Pershagen G, Sundell J, 2001. Dampness in buildings and health. Nordic interdisciplinary 

review of the scientific evidence on associations to “dampness” in guildings and health effects 

(NORDDAMP). Indoor Air 11:72-86. 

Bornehag, CG, Sundell J, Bonini S, Custovic A, Malmber P, Skerfving S, Sigsgaard T, and 

Verhoeff A, 2004. Dampness in buildings as a risk factor for health effects, EUROEXPO: a 

multidisciplinary review of the literature (1998-2000) on dampness and mite exposure in 

buildings and health effects. Indoor Air 14(4): 243-257. 

Boudreau DR, Spadafora MP, Wolf LR, and Siegel E, 1994. Carbon monoxide levels during 

indoor sporting events-Cincinnati, 1992-1993. MMWR available at 

http://www.cdc.gov/mmwr/preview/mmwrhtml/00023631.htm . 

Boutin-Forzano S, Adel N, Gratecos L, Jullian H, Garnier JM, Ramadour M, Lanteaume A, 

Hamon M, Lafay V, and Charpin D, 2004. Visits to the emergency room for asthma attacks and 

short-term variations in air pollution. Respiration 71: 134-137. 

Bradman MA, Harnly ME, Draper W, Seidel S, Teran S, Wakeham D, and Neutra R, 1997. 

Pesticide exposures to children from California's Central Valley: results of a pilot study. J 

Exposure Analysis and Environmental Epidemiology. 7(2): 217-234. 

Bradman A, Eskenazi B, McKone T, Castorina R, Harnly M, and Barr D, 2002a. 

Organophosphate pesticide exposures to pregnant women living in an agricultural community. 

Presented at the joint conference of the International Society of Exposure Analysis and 
Indoor Air Pollution in California July, 2005 

 198

International Society for Environmental Epidemiology, Final Program and Abstracts, August 11-

15, 2002, Vancouver, BC, Canada. 

Bradman A, Hernandez R, McKone T, Harnly M, Chavira R, Tager I, Lipsett M, Macher J, 

Castorina R, Cabrera E, Vargas A and Cam J, 2002b. Home Environmental Health 

Assessment for Epidemiological and Exposure Studies, Center for the Health Assessment of 

Mothers and Children of Salinas. Presented at a joint conference of the International Society of 

Exposure Analysis and International Society for Environmental Epidemiology, Final Program 

and Abstracts, August 11-15, 2002, Vancouver, BC, Canada. 

Bradman A, Castorina R, Claus B, Mckone T, Eskenazi B, Whitaker D, Morgan J, Sheldon L, 

Nishioka M, Barr D, and Harnly M, 2004. Quantitative pesticde exposure assessment of 

children living in an agricultural community. Presented at the 14th Annual Conference of the 

International Society of Exposure Analysis, October 17-21 2004, Philadelphia. 

Bramley TJ, Lerner D, and Sarnes M, 2002. Productivity losses related to the common cold. J 

Occup Environ Med 44:822-829. 

Brauer M, Blair J, and Vedal S, 1996. Effect of ambient ozone exposure on lung function in farm 

workers. J Respiratory and Critical Care Medicine 154: 981-987. 

Brauer M, Hirtle R, Lang B, and Ott W, 2000. Assessment of indoor fine aerosol contributions 

from environmental tobacco smoke and cooking with a portable nephelometer. J Exposure 

Analysis and Environmental Epidemiology 10: 136-144. 

Bridges, B, 2002. Fragrance: emerging health and environmental concerns. Flavour and 

Fragrance Journal 17: 361-371. 

BRFSS (Behavior Risk Factor Surveillance System), 2001. Behavior Related Factors Survey. 

California Department of Health Services, Cancer Surveillance Section. 

Brown SK, 1999a. Chamber assessment of formaldehyde and voc emissions from wood-based 

panels. Indoor Air 9: 209-215. 

Brown, SK, 1999b. Assessment of pollutant emissions from dry-process photocopiers. Indoor 

Air (9): 259-267. 

Brown SK, Sim MR, Abramson MJ, and Gray CN, 1994. Concentrations of volatile organic 

compounds in indoor air-a review. Indoor Air 4: 123-134. 

Brugge D, Vallarino J, Ascolillo L, Osgood N-D, Steinbach S, and Spengler J, 2003. 

Comparison of multiple environmental factors for asthmatic children in public housing. Indoor Air

13: 18-27. 

Brunekreef B, Hoek G, Breugelmans O, and Leentvaar M, 1994. Respiratory effects of low-level 

photochemical air pollution in amateur cyclists. J Respiratory and Critical Care Medicine 150: 

962-966. 

BSC (Building Science Corporation), 2003. BSC Building America Performance Criteria. 

Westford, MA. Available from: http://www.buildingscience.com/buildingamerica/targets.htm. 
Indoor Air Pollution in California July, 2005 

 199

Built Green of Colorado, 2004. The garage-to-house issue: controlling the dangers of carbon 

monoxide. May. 

Burnett RT, Brook JR, Yung WT, Dales RE, and Krewski D, 1997. Association between ozone 

and hospitalization for respiratory diseases in 16 Canadian cities. Environmental Research 72: 

24-31. 

Burnett RT, and Goldberg MS, 2003. Size-fractionated particulate mass and daily mortality in 

eight Canadian cities in Health Effects Institute Special Report: Revised Analyses of TimeSeries Studies of Air Pollution and Health. 

Burton LE, Girman JR, Womble SE, 2000. Airborne particulate matter within 100 randomly 

selected office buildings in the United States (BASE). Proceedings of Healthy Building 2000, 

1:157-162. 

Cal/EPA (California Environmental Protection Agency), 1994. A guide for reviewing 

environmental policy studies, Moss S, McCann R, Feldman M. A Handbook for the California 

Environmental Protection Agency. 

Carpi A, and Chen YF, 2001. Gaseous Elemental Mercury as an Indoor Air Pollutant. 

Environmental Science and Technology 35: 4170-4173. 

Carslaw N, 2003. New directions: where next with indoor air measurements? Atmospheric 

Environment 37: 5645-5646. 

CBPCA (California Building Performance Contractor Association), 2003a. California Home 

Performance UPDATE, September/October. San Francisco, CA. Available from: 

http://www.calhomeperformance.org/pdfs/newslettersep-oct03.pdf. 

CBPCA, 2003b. PY 2002 - 2003 CPUC Energy Efficiency Programs Quarterly Report Narrative. 

Available from: http://www.cbpca.org/reports/CBPCA_172-02_Q3_2003.doc. 

CCC (California Commissioning Collaborative), 2004. Mission Statement. Sacramento, CA. 

Available from: http://www.cacx.org/. 

CCRP (California Comparative Risk Project), 1994. Toward the 21st Century: Planning for the 

Protection of California's Environment. Berkeley, CA: Office of Environmental Health Hazard 

Assessment. Available from: http://www.oehha.ca.gov/multimedia/comprisk.html. 

CDC (U.S. Centers for Disease Control and Prevention), 1982. Perspectives in Disease 

Prevention and Health Promotion Carbon Monoxide Intoxication – A Preventable Environmental 

Health Hazard. MMWR 31(39): 529-531. 

CDC, 1994. Carbon monoxide levels during indoor sporting events – Cincinnati, 1992-1993. 

MMWR 43(02): 21-23. 

CDC, 1995. Mercury Exposure in a Residential Community – Florida, 1994. MMWR 44(23): 

436-437, 443. Available from: http://www.cdc.gov/mmwr/preview/mmwrhtml/00037313.htm. 

CDC, 1997. Screening young children for lead poisoning: guidance for state and local public 

health officials. Atlanta: US Department of Health and Human Services, CDC Childhood Lead 
Indoor Air Pollution in California July, 2005 

 200

Poisoning Prevention Program. Available from URL: 

http://www.cdc.gov/nceh/lead/guide/guide97.htm. 

CDC, 2000. Pulmonary hemorrhage/hemosiderosis among infants – Cleveland, Ohio, 1993-

1996. MMWR 49: 180-184. 

CDC, 2002. Surveillance for asthma – United States, 1980-1999. MMWR 51.

CDC, 2003. Self-reported asthma prevalence and control among adults – United States, 2001. 

MMWR 52: 381-384. 

CDC, 2004a. Basic information about SARS. Fact Sheet. 

http://www.cdc.gov/ncidod/sars/factsheet.htm.

CDC, 2004b. Adult Cigarette Smoking in the United States: Current Estimates. Fact Sheet. 

May. Office on Smoking and Health National Center for Chronic Disease Prevention and Health 

Promotion. Atlanta, GA. Available at: 

http://www.cdc.gov/tobacco/factsheets/AdultCigaretteSmoking_FactSheet.htm.

CEC (California Energy Commission), 1994. California's Energy Efficiency Standards and 

Indoor Air Quality, Publication P400-94-003. Sacramento, CA. 

CEC, 2004. Reference Specifications for Energy and Resource Efficiency, Contract Number 

500-98-027. San Francisco, CA: Eley Associates. Available from: 

http://www.energy.ca.gov/reports/2004-05-24_500-04-015.PDF. 

Chalupa DC, Morrow PE, Oberdorster G, Utell MJ, and Frampton MW, 2004. Ultrafine particle 

desposition in subjects with asthma. Environmental Health Perspectives 112(8): 879-882. 

Chang JCS, Fortmann R, Roache N, and Lao H, 1999. Evaluation of low-VOC latex paints. 

Indoor Air 9: 253-258. 

Chauhan AJ, Inskip HM, Linaker CH, Smith S, Schreiber J, Lohnston SL, and Holgate ST, 2003. 

Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in 

children. Lancet 361: 1939-1944. 

CHBA (Canadian Home Builders Association), 2004. The R-2000 Program. 

http://r2000.chba.ca/What_is_R2000/R2000_program.php. 

Chen W and Zhang JS, 2004. Effectiveness of portable room air cleaners for control of volatile 

organic compounds in indoor air, presented at CIB World Building Congress 2004, Toronto, 

Canada, May 2-7, 2004. 

CHIS, 2001. California Health Information Survey, 2001. Data available at http://chis.ucla.edu/. 

CHIS, 2003. Asthma in California: Findings from the 2001 California Health Interview Survey. 

Available from: http://www.healthpolicy.ucla.edu. 

CHPS (Collaborative for High Performance Schools), 2001-2005. Best Practices Manual, Vols 

1-4. Available from: www.chps.net. 
Indoor Air Pollution in California July, 2005 

 201

Chuang JC, Mack GA, Stockrahm JW, Hannan SW, Bridges C and Kuhlman MR, 1988. Field 

evaluation of sampling and analysis for organic pollutants in indoor air. Prepared by Batelle 

Columbus Laboratories for the U.S. EPA, EPA Report No. 600/4-88/028. 

Chuang JC, Callahan PJ, Lyu CW, and Wilson NK, 1999. Polycyclic aromatic hydrocarbon 

exposures of children in low-income families. J Exposure Analysis and Environmental 

Epidemiology 2: 85-98. 

Churchill R, 1997. Radon mapping – Santa Barbara and Ventura Counties. California Geology

50(6): 167-177. 

Churchill RK, and Youngs LG, 1993. The Department of Health Services Elementary School 

Radon Survey: Relationship between geology, soil and indoor radon. California Department of 

Conservation. 

City of Hayward, 2002. General Plan, Appendix O: Opportunities for Energy Conservation in 

Residential Development. http://www.ci.hayward.ca.us/about/generalplan/xAppendix-O.pdf. 

Clausen G. 2004. Ventilation filters and indoor air quality: a review of research 

from the International Centre for Indoor Environment and Energy. Indoor Air 14: Suppl 7:202-7. 

Clayton JC, Perritt RL, Pellizzari ED, Thomas KM, Whitmore RW, Wallace LA, Ozkaynak H, and 

Spengler JD, 1993. Particle total exposure assessment methodology (PTEAM) Study: 

distribution of aerosol and elemental concentrations in person, indoor, and outdoor air samples 

in a Southern California community. J Exposure Anal and Environ Epidem 3(2): 227-250. 

Clayton AC, Pellizzari ED, Whitmore RW, Quackenboss JJ, Adgate J, and Sefton K, 2003. 

Distributions, associations, and partial aggregate exposure of pesticides and polynuclear 

aromatic hydrocarbons in the Minnesota Children's Pesticide Exposure Study (MNCPES). J 

Exposure Anal and Environ Epidem 13(2): 100-111. 

CMHC/SCHL (Canadian Mortgage and Housing Corporation), 2004. Garage Performance 

Testing, Research Highlights, Technical Series 04-108, April.

CMHC/SCHL, 2001. Air Infiltration from Attached Garages in Canadian Houses, Research 

Highlights, Technical Series 01-122.

Cohen MA, Ryan PB, Yanagisawa Y, Spengler JD, Ozkaynak H, and Epstein PS, 1989. 

Indoor/outdoor measurements of volatile organic compounds in the Kanawha Valley of West 

Virginia. J Air Pollution Control Assoc 39: 1086-1093. 

Cohen AJ, Anderson HR, Ostro B, Pandey KD, Krzyzanowski M, Kuenzli N, Gutschmidt K, 

Pope CA, Romieu I, Samet JM, and Smith KR, 2004. Mortality Impacts of Urban Air Pollution, in 

Ezzati M, Rodgers AD, Lopez AD, Murray CJL (eds) Comparative Quantification of Health 

Risks: Global and Regional Burden of Disease due to Selected Major Risk Factors. Geneva: 

World Health Organization, Vol 2 of 3, pp.1353-1433. 

Colt JS, Lubin J, Camann D, Davis S, Cerhan J, Severson RK, Cozen W, Hartge P. 2004. 

Comparison of pesticide levels in carpet dust and self-reported pest treatment practices in four 

US sites. J. Exposure Anal and Environ Epidem, 14, 74-83. 
Indoor Air Pollution in California July, 2005 

 202

Conner TL, Norris GA, Landis MS, and Williams RW, 2001. Individual particle analysis of indoor, 

outdoor, and community samples from the 1998 Baltimore particulate matter study. Atmospheric 

Environment 35: 3935-3946. 

Consumers Union, 2003a. Air cleaners: behind the hype. Consumer Reports, October, p.26-29. 

Consumers Union, 2003b. Vacuum cleaners: when more isn’t better. Consumer Reports, 

November. 

Consumers Union, 2004. Cannister vacuum cleaners. Consumer Reports. May. 

Cook M, Simon PA, and Hoffman RE, 1995. Unintentional carbon monoxide poisoning in 

Colorado, 1986 through 1991. Amer J Public Health 85(7): 988-990. 

Cooper SD, Raymer JH, Pellizzari ED, and Thomas KW, 1995. The identification of polar 

organic compounds found in consumer products and their toxicological properties. J Exposure 

Anal and Environ Epidem 5(1): 57. 

Corn M, Crump K, Farrar DB, Lee RJ, and McFee DR, 1991. Airborne concentrations of 

asbestos in 71 school buildings. Regulatory Toxicology and Pharmacology 13(1): 99-114. 

Corsi RL, Torres VM, Sanders M, Kinney KA, 2002. Carbon dioxide levels and dynamics in 

elementary schools: results of the TESIAS study. Proceedings: Indoor Air 2002. 

http://www.chps.net/info/iaq_papers/PaperIV.4.pdf. 

Cothern CR, 1987. Environmental Radon. Environmental Science Research Series 35: 1-28. 

Cox CS, 1995. Stability of airborne microbes and allergens. Bioaerosols Handbook, Eds., Cox 

and Wathes, Lewis Publishers, Boca Raton, FL. 

Cox DH, 2002. Heart Disease Deaths in California, 1999. Data Summary No. DS02. 

CPSC (U.S. Consumer Product Safety Commission), 1987a. Statement of enforcement policy 

concerning household products containing methylene chloride. Fed Register 52: 34698. 

CPSC, 1987b. Commercial Practices, Code of Federal Regulations, 16CFR1500.17A2, 

Washington DC, 1987. 

CPSC, 1996. Report on Lead in Vinyl Miniblinds. Available from: 

http://www.cpsc.gov/LIBRARY/FOIA/FOIA97/OS/BP971.PDF. 

CPSC, 1997. Estimates of Non-fire Carbon Monoxide Poisoning Deaths and Injuries. 

Memorandum from Kimberly Ault to Elizabeth Leland, December 17. Epidemiology and Health 

Sciences. Washington, D.C. http://www.cpsc.gov/library/foia/foia98/brief/3512c1f.pdf. 

CPSC, 2003. Non-fire carbon monoxide deaths associated with the use of consumer products: 

1999 and 2000 annual estimates. Available from: http://www.cpsc.gov/LIBRARY/co03.pdf. 

CPUC (California Public Utilities Commission), 2003. Draft Decision of ALJ Gottstein. Interim 

Opinion: Phase 4 Standardization Results for Low-Income Energy Efficiency Measure Cost-
Indoor Air Pollution in California July, 2005 

 203

Effectiveness and Natural Gas Appliance Testing. November 11. San Francisco, CA. Available 

at: http://www.cpuc.ca.gov/Published/Agenda_decision/31319.htm. 

Crump KS, and Farrar DB, 1989. Statistical analysis of data on airborne asbestos levels 

collected in an EPA survey of public buildings. Regulatory Toxicology and Pharmacology 10: 

51-62.

Custovic A, Fletcher A, Pickering CA, Francis HC, Green R, Smith A, Chapman M, Woodcock 

A, 1998. Domestic allergens in public places. III: house dust mite, cat, dog and cockroach 

allergens in British hospitals. Clinical and Experimental Allergy 28(1): 53-59. 

Daisey JM, Mahanama KRR, and Hodgson AT, 1998. Toxic volatile organic compounds in 

simulated environmental tobacco smoke: emission factors for exposure assessment. Journal of 

Exposure Analysis and Environmental Epidemiology 8: 313-334. 

Dales RE, Zwanenburg H, Burnett R, and Franklin CA, 1991a. Respiratory health effects of 

home dampness and molds among Canadian children. Amer J Epidemiol 134(2): 196-203. 

Dales RE, Burnett R, and Zwaneburg H, 1991b. Adverse health effects among adults exposed 

to home dampness and molds. American Review of Respiratory Disease 143(3): 505-509. 

Darnerud PO, Eriksen GS, Hohannesson T, Larsen PB, and Viluksela M, 2001. Polybrominated 

Diphenyl Ethers: Occurrence, Dietary Exposure and Toxicology. Environmental Health 

Perspectives 109(s1): 49-68. 

Day JH, Ellis AK, 2001. Allergenic microorganisms and hypersensitivity. In: Microorganisms in 

Home and Indoor Work Environments. Editors: B Flannigan, RA Samson, JD Miller. Taylor & 

Francis. New York, NY. 

DCSD (California Department of Community Services Development), 2003. California LowIncome Home Energy Assistance Program (CAL LIHEAP). Sacramento, CA. Available from: 

http://www.csd.ca.gov/liheap.html. 

Dejmek J, Selevan SG, Benes I, Solansky I, and Sram RJ, 1999. Fetal growth and maternal 

exposure to particulate matter during pregnancy. Environmental Health Perspectives 107(6): 

475-480. 

Delfino RJ, Coate BD, Zeiger RS, Seltzer JM, Street DH, and Koutrakis P, 1996. Daily asthma 

severity in relation to personal ozone exposure and outdoor fungal spores. Amer J Respiratory 

and Critical Care Medicine 154: 633-641. 

Delfino RJ, Murphy-Moulton AM, Burnett RT, Brook JR, and Becklake MR, 1997. Effects of air 

pollution on emergency room visits for respiratory illnesses in Montreal, Quebec. Amer J 

Respiratory and Critical Care Medicine 155: 568-576. 

Delfino RJ, Murphy-Moulton AM, and Becklake MR, 1998. Emergency room visits for respiratory 

illnesses among the elderly in Montreal: association with low level ozone exposure. 

Environmental Research 76: 67-77. 
Indoor Air Pollution in California July, 2005 

 204

Delfino RJ, 2002. Epidemiological evidence for asthma and exposure to air toxics: linkages 

between occupational, indoor, and community air pollution research. Asthma Occurrence 110 

(s4): 573-589. 

Delfino RJ, Gong H, Jr., Linn WS, Pellizzari ED, and Hu Y, 2003a. Asthma symptoms in 

Hispanic children and daily ambient exposures to toxic and criteria air pollutants. Environmental 

Health Perspectives 111: 647-656. 

Delfino RJ, Gong H, Linn WS, Hu Y, and Pellizzari ED, 2003b. Respiratory symptoms and peak 

expiratory flow in children with asthma in relation to volatile organic compounds in exhaled 

breath and ambient air. J Exposure Analysis and Environmental Epidemiology 13(5): 348-363. 

Delfino RH, Quintana PJE, Flora J, Gastanaga VM, Samimi BS, Kleinman MT, Liu S, Bualino C, 

Wu CF, McLaren, CE, 2004. Association of FEV1 in asthmatic children with personal and 

microenvironmental exposure to airborne particulate matter. Environmental Health Perspectives

112(8): 932-941. 

Dennekamp M, Howarth S, Dick CAJ, Cherrie JW, Donaldson K, and Seaton A, 2001. Ultrafine

particles and nitrogen oxides generated by gas and electric cooking. Occupational and 

Environmental Medicine 58: 511-516. 

Devlin RB, McDonnell WF, Mann R, Becker S, House DE, Schreinemachers D, and Koren HS, 

1991. Exposure of humans to ambient levels of ozone for 6.6 hours causes cellular and 

biochemical changes in the lung. American Journal of Respiratory Cell and Molecular Biology 4: 

72-81. 

Devlin RB, McDonnell WF, Mann R, Becker S, Madden MC, McGee MP, Perez R, Hatch G, 

House DE, and Koren HS, 1996. Time-dependent changes of inflammation mediators in the 

lungs of humans exposed to 0.4 ppm ozone for 2 hr: A comparison of mediators found I 

bronchoalveolar lavage fluid 1 and 18 hr after exposure. Toxicology and Applied Pharmacology

138: 176-185. 

Devlin RB, Horstman DP, Gerrity TR, Becker S, and Madden MC, 1999. Inflammatory response 

in humans exposed to 2.0 ppm nitrogen dioxide. Inhalation Toxicology 11: 89-109. 

Devos M, Patte F, Rouault J et al., 1990. Standardized Human Olfactory Thresholds. New York, 

Oxford University Press.

DHS (California Department of Health Services), 1995. A "Do -it-yourself" Inspection of a 

Ventilation System. Air and Industrial Hygiene Laboratory, Berkeley CA.

DHS, 1996. Reducing Occupant Exposure to Volatile Organic compounds from office building 

construction materals: Non-binding guidelines. Available from: http://www.cal-iaq.org/VOC/. 

DHS, 1997. State Warns Against Ozone Air Cleaners. News releases (April 1997) available at 

http://www.applications.dhs.ca.gov/pressreleases/store/pressreleases/27-97.html. 

DHS, 1998. Lead Hazards in California's Public Elementary Schools and Child Care Facilities: 

Report to the California State Legislature. Available from: 

http://www.dhs.cahwnet.gov/childlead/schools/opening.htm. 
Indoor Air Pollution in California July, 2005 

 205

DHS, 2000. IAQ Info Sheet: Asbestos in the Home and Workplace. Available at: http://www.caliaq.org/asb00-03.htm. 

DHS, 2002a. California Tobacco Control Update. Tobacco Control Section, Sacramento, CA. 

Available at: http://www.dhs.ca.gov/tobacco/documents/TCSupdate.PDF. 

DHS, 2002b. Indoor and Outdoor Secondhand Smoke Exposure. Tobacco Control Section. 

Sacramento, CA. http://www.dhs.ca.gov/ps/cdic/ccb/tcs/documents/secondhandsmoke.pdf, 

http://www.dhs.ca.gov/tobacco. 

DHS, 2003a. Tobacco Control Successes in California: A Focus on Young People, Results 

from the California Tobacco Surveys, 1990-2002. Final Report. California Department of Health 

Services Tobacco Control Section. October 2003. 

DHS, 2003b. Occupational illness among flight attendants due to aircraft disinfection. Full report 

by Occupational Health Branch, October 23, 2003. 

http://www.dhs.ca.gov/ohb/OHSEP/disinsection.pdf . 

DHS, 2004a. California Asthma Facts, August 2004: Work-Related Asthma. Prepared by the 

Environmental Health Investigations Branch, available at http://www.californiabreathing.org/. 

DHS, 2004b. TCS Update 2004. California Department of Health Services, Tobacco Control 

Section, Sacramento. 

DHS, 2004c. California Asthma Facts, Volume 2, Issue 2. California Dept. of Health Services, 

Environmental Health Investigations Branch. 

http://www.ehib.org/cma/papers/California_Asthma_Facts_WRA.pdf. 

DHS, 2004d. Cleaning Products Can Trigger Work-Related Asthma. Occupational Health 

Watch, Summer 2004. California Dept. of Health Services, Occupational Health Branch. 

http://www.dhs.ca.gov/ohb/ohw3.pdf. 

Diamond M, 2001. IAQ and the Law. In: Spengler JD, Samet JM, and McCarthy JF, eds. Indoor 

Air Quality Handbook. San Francisco, CA: McGraw-Hill, pp. 71.1-71.10. 

DIR (California Department of Industrial Relations), 1997. Interim Tuberculosis Control 

Enforcement Guidelines. Policy & Procedures Manual, P&P C-47. California Dept. of Industrial 

Relations, Division of Occupational Safety and Health. 

http://www.dir.ca.gov/DOSHPol/P&PC-47.HTM

Dockery DW, Pope C, Xu X, Spengler JD, Ware JH, Fay M, Ferris BG, and Speizer FE, 1993. 

An association between air pollution and mortality in six U.S. cities. The New England J 

Medicine 329(24): 25-74. 

Dockery DW, and Pope C, 1994. Acute respiratory effects of particulate air pollution. Annual 

Review of Public Health 15: 107-132. 

DOF (California Department of Finance), 2002a. E-4 Revised Historical City, County and State 

Population Estimates, 1991-2000, with 1990 and 2000 Census Counts. Available from: 

http://www.dof.ca.gov/HTML/DEMOGRAP/E-4text2.htm. 
Indoor Air Pollution in California July, 2005 

 206

DOF, 2002b. Census 2000 California Profile. Available from: 

http://www.dof.ca.gov/HTML/DEMOGRAP/Census_2000_CA_Profile.htm. 

Dominici F, Samet JM, and Zeger SL, 2003. Combining evidence on air pollution and daily 

mortality from the 20 largest U.S. cities: a hierarchical modeling strategy. J Royal Statistical 

Society 163(3): 263-302. 

DSA (California Division of the State Architect), 2003. The DSA Project Submittal and Plan 

Review Process. Sacramento, CA: Department of General Services. Available from: 

http://www.dsa.dgs.ca.gov/ProjectSubmittalProcess/default.htm. 

DSA, 2004. EPP Database Project. Sacramento, CA. http://www.eppbuildingproducts.org/ . 

Dubowski SD, Wallace LA, and Buckley TJ, 1999. The contribution of traffic to indoor 

concentrations of polycyclic aromatic hydrocarbons. J Exposure Analysis and Environmental 

Epidemiology 9: 312-321. 

Dufresne A, Rivard CI, Malo JL, and Gautrin D, 2002. Exposure to formaldehyde among animal 

health students. American Industrial Hygiene Association Journal 63: 647-650. 

Duhme H, Weiland SK, and Keil U, 1998. Epidemiological analyses of the relationship between 

environmental pollution and asthma. Toxicology Letters 102-103: 307-316. 

EEBA (Energy Efficient Building Association), 2003. EEBA Criteria. Bloomington, MN. Available 

from: http://www.eeba.org/technology/criteria.htm. 

Eggleston PA, 2000. Environmental causes of asthma in inner city children; the National 

Cooperative Inner City Asthlma Study. Clinical Reviews in Allergy & Immunology 18(3):311-324. 

Eichholz GG, 1987. Environmental Radon. Environmental Science Research Series 35: 157-

172. 

Eriksson P, Jokobsson E, and Fredriksson A, 1998. Developmental neurotoxicity of brominated 

flame-retardants polybrominated diphenyl ethers and tetrabromo-bisphenol A. Organohalogen 

Compounds 35: 375-377. 

Eriksson P, Viberg H, Jakobsson E, Orn U, and Fredriksson A, 1999. PBDE, 2,2,4,4,5-

pentabromodiphenyl ether, causes permanent neurotixic effects during defined period of 

neurotoxic effects. Organohalogen Compounds 40: 330-335. 

ESB (Energy Source Builder), 1995. Build Tight, Ventilate Right. April 1995, # 37. 

http://oikos.com/esb/index.html#37. 

Eskenazi B, Gold EB, Samuels SJ, Wight S, Lasley BL, Hammond SK, Rasor MO, and 

Schenker MB, 1995a. Prospective assessment of fecundability of female semiconductor 

workers. American Journal of Industrial Medicine 28: 817-831. 

Eskenazi B, Gold EB, Lasley BL, Samuels S, Hammond SK, Wight S, Rasor MON, Hines CJ, 

and Schenker MB, 1995b. Prospective monitoring of early fetal loss and clinical spontaneous 

abortion among female semiconductor workers. Amer J Industrial Medicine 28:833-846. 
Indoor Air Pollution in California July, 2005 

 207

Eskenazi B, Bradman A, and Castorina R, 1999. Exposures to children to organophosphate 

pesticides and their potential adverse health effects. Environmental Health Perspectives, 

107(S3): 409-419. Available from: http://ehp.niehs.nih.gov/members/1999/suppl-3/409-

419eskenazi/eskenazi-full.html. 

Evans GF, Highsmith RV, Sheldon LS, Suggs JC, Williams RW, Zweidinger RB, Creason JP, 

Walsh D, Rodes CE, and Lawless PA, 2000. The 1999 Fresno particulate matter exposure 

studies: comparison of community, outdoor, and residential PM mass measurements. Journal of 

Air and Waste Management Association 50: 1887-1896. 

Evans GW, Kantrowitz E, 2002. Socioeconomic status and health: the potential role of 

environmental risk exposure. Annual Review of Public Health 23:303-331. 

Facilities Net, 2005. Risks, Lawsuits Linked to Mold Are Growing. 

http://www.facilitiesnet.com/news/Jan05news2.shtml. 

Fairley D, 2003. Mortality and air pollution for Santa Clara County, California, 1989-1996 in 

Health Effects Institute Special Report: Revised Analyses of Time-Series Studies of Air Pollution 

and Health. 

Fan Z, Lioy P, Weschler C, Fiedler N, Kipen H, and Zhang J, 2003. Ozone-initiated reactions 

with mixtures of volatile organic compounds under simulated indoor conditions. Environmental 

Science and Technology 37: 1811-1827. 

Febo A, and Perrino C, 1991. Prediction and experimental evidence for high air concentration of 

nitrous acid in indoor environments. Atmospheric Environment 25A (5/6): 1055-1061. 

Fisk WJ, 2000. Health and productivity gains from better indoor environments and their 

relationship with building energy efficiency. Ann Rev. Energy Environ 25: 537-566. 

Fisk, WJ, Faulkner D, Palone J, and Seppanen O (2002). Performance and cost of particle air 

filtration technologies. Indoor Air 12(4):223-234. LBNL-47833. 

http://eetd.lbl.gov/IED/viaq/pubs/LBNL-47833.pdf. 

Flynn E, Matz P, Woolf A and Wright R, 2000. Indoor Air Pollutants Affecting Child Health. Alan 

Woolf, editor. A project of the American College of Medical Toxicology funded by the U.S. 

Agency for Toxic Substances and Disease Registry. 

Foarde K., van Osdell D, and Steiber R.1997. Investigation of Gas-Phase Ozone as a 

Potential Biocide. Applied Occupational Environmental Hygiene. 12(8): 535-542. 

Folinsbee LJ, Silverman F, and Shephard RJ, 1977a. Decrease of maximum work performance 

following ozone exposure. J Applied Physiology 42(4): 531-536. 

Folinsbee LJ, Horvath SM, Raven PB, Bedi JF, Morton AR, Drinkwater BL, Bolduan NW, and 

Gliner JA, 1977b. Influence of exercise and heat stress pulmonary function during ozone 

exposure. J Applied Physiology 43(3): 409-413. 

Fortmann, R, Kariher, P, and Clayton, R, 2001. Indoor Air Quality: Residential Cooking 

Exposures. Final Report. ARCADIS Geraghty & Miller, Inc., Research Triangle Park, NC. 
Indoor Air Pollution in California July, 2005 

 208

Prepared for ARB, Research Division, Sacramento, CA. Contract Number 97-330. 

http://www.arb.ca.gov/research/indoor/cooking/cooking.htm. 

Foster WM, 1999. Deposition and clearance of inhaled particles. In: Holgate ST, Samet JM, 

Koren HS, Maynard RL, eds. Air pollution and health. San Diego: Academic Press, 295-324. 

Freedonia Group, 2004. Consumer Water Purification and Air Cleaning Systems to 2008 – 

Market Size, Market Share, Market Leaders, Demand Forecast and Sales, Report no. 1829. 

The Freedonia Group, Cleveland, Ohio. http://www.freedoniagroup.com. 

Friedman H., Potter, A, Haasl T., Claridge D, and Cho S, 2003. Guide: Strategies for Improving 

the Persistence of Building Performance. Portland Energy Conservation, Inc., and Texas A&M 

University Prepared for the California Commissioning Collaborative (CCC), 2004. Mission 

Statement. Sacramento, CA. 

http://es57055.easystreet.com/news/NewsBriefDetails.aspx?id=32.

Frischer T, Studnicka M, Gartner C, Tauber E, Horak F, Veiter A, Spengler J, Kuhr J, and 

Urbanek R, 1999. Lung function growth and ambient ozone. Amer J Respiratory and Critical 

Care Medicine 160: 390-396. 

Gammage RB, Hawthorne AR, and Dudney CS, 1984. Parameters affecting air leakage in East 

Tennessee homes. Health Physics 47(1): 204-204. 

Gates GA, 1996. Cost –effectiveness considerations in otitis media treatment. Otolaryngol Head 

Neck Surg 14: 525-30. 

Gauderman WJ, McConnell R, Gilliland F, London S, Thomas D, Avol E, Vora H, Berhane K, 

Rappaport EB, Lurmann F, and Margolis HG, 2000. Association between air pollution and lung 

function growth in Southern California children. Am J Respir Crit Care Med 162: 1383-1390. 

Geyh AS, Xue J, Ozkaynak H, and Spengler JD, 2000. The Harvard Southern California 

Chronic Ozone Exposure Study: assessing ozone exposure of grade-school-age children in two 

southern California communities. Environ Health Perspect 108(3): 265-70. 

Giardino NJ and Andelman JB, 1996. Characterization of the emissions of trichloroethylene, 

chloroform, and 1,2-dibromo-3-chloropropane in a full-size, experimental shower. J. Expos Anal 

Environ Epidemiol 6(4): 413-423 (Oct-Dec). 

Gilliland FD, Berhane K, Rappaport EB, Thomas DC, Avol E, Gauderman WJ, London SJ, 

Margolis HG, McConnell R, Islam KT, and Peters JM, 2001. The effects of ambient air pollution 

on school absenteeism due to respiratory illnesses. Epidemiology 12(1): 43-54. 

Gilpin E, Emery S, Farkas A, Distefan J, White M, and Pierce J, 2001. Cancer prevention and 

control program, University of California, San Diego. The California Tobacco Control Program; a 

decade of progress, results from the California tobacco survey, 1990-1999. California Dept. 

Health Services. 

Girman JR, Chang Y-L., Hayward SB, and Liu K-S, 1998. Causes of Unintentional Deaths from 

Carbon Monoxide Poisonings in California. West J Med 168(3): 158-165. 
Indoor Air Pollution in California July, 2005 

 209

Girman JR, Hadwen GE, Burton LE, Womble SE, and McCarthy JF, 1999. Individual volatile 

organic compound prevalence and concentrations in 56 buildings of the building assessment 

survey and evaluation (BASE) study. Indoor Air 2: 460-465. 

Glasgow RE, Foster LS, Lee ME, Hammond SK, Lichtenstein E, and Andrews JA, 1998. 

Developing a brief measure of smoking in the home: description and preliminary evaluation. 

Addict Behav 23: 567-571. 

Gold, 2005. Personal communication, Deborah Gold, Cal/OSHA, to Peggy Jenkins, 2005. 

Goldberg MS, and Burnett RT, 2003. Revised analysis of the Montreal time-series study in 

Health Effects Institute Special Report: Revised Analyses of Time-Series Studies of Air Pollution 

and Health. 

Goldmann DA, 2001. Epidemiology and prevention of pediatric viral respiratory infections in 

health-care institutions. Emerging Infectious Diseases. April 7(2): 249-253. 

Gordon SM, Wallace LA, Callahan PJ, Kenny DV, and Brinkman MC, 1998. Effect of water 

temperature on dermal exposure to chloroform. Environ Health Perspect 106(6): 337-345. 

Gordon SM, Callahan PJ, Nishioka MG, Brinkman MC, O’Rourke MK, Lebowitz MD, and 

Moschandreas DJ, 1999. Residential environmental measurements in the National Human 

Exposure Assessment Survey (NHEXAS) pilot study in Arizona: preliminary results for 

pesticides and VOCs. J Expo Anal Environ Epidemiol 9: 456-470. 

Graham LA, Noseworthy L, Fugler D, O’Leary K, Karman D and Grande C 2004. Contribution 

of Vehicle Emissions from an Attached Garage to Residential Indoor Air Pollution Levels. J Air 

and Waste Management Association 54:563-584. 

Graves CG, Ginevan ME, Jenkins RA, and Tardiff RG, 2000. Doses and lung burdens of 

environmental tobacco smoke constituents in nonsmoking workplaces. J Expo Anal Environ 

Epidemiol 10: 365-377. 

Grot RA, 1995. Air Change Rates in Non-residential Buildings in California. Lagus Applied 

Technology, Escondido, CA. Prepared for the California Energy Commission, Report P400-91-

034BCN. Sacramento, CA. 

Guerin MR, Jenkins RA, and Tomkins BA, 1992. The chemistry of environmental tobacco 

smoke: Composition and measurement. Lewis Publishers, Boca Raton. 

Guo Z, Chang JCS, Sparks LE, and Fortman RC, 1999. Atmos Environ 33: 1205-1215. 

Guo Z, Mosley R, McBrian J, and Fortmann R, 2000. Fine particulate matter emissions from 

candles. Engineering Solutions to Indoor Air Quality Problems VIP-98: 211-225. 

Gurunathan S, Robson M, Freeman N, Buckley B, Roy A, Meyer R, Bukowski J, and Lioy PJ, 

1998. Accumulation of chlorpyrifos on residential surfaces and toys accessible to children. 

Environ Health Perspect 106: 9-16. 
Indoor Air Pollution in California July, 2005 

 210

Gustavsson H, Lundgren B, 1997. Off-gassing from building materials: a survey of case studies. 

In: Brune D, Gerhardsson G, Crockford GW, Dáuria D, editors: The Workplace, volume 1. 

Fundamentals of health, safety and welfare. International Labor Office, Geneva, 533-555. 

Haan M, Zahler L, Athanasoulis M, Broadwin R, Mann J, Goldman LR, Sutton P, Schlag R, 

McLaughlin R, Flessel P, Guirguis G, 1992. Blood Lead Levels Among Children in High-Risk 

Areas -- California, 1987-1990. MMWR 41(17):291-294. 

http://www.cdc.gov/mmwr/preview/mmwrhtml/00016606.htm. 

Hale RC, La Guardia MJ, Harvey EP, Mainor TM, Duff WH, and Gaylor MO, 2001. 

Polybrominated Diphenyl Ether Flame Retardants in Virginia Freshwater Fishes (USA). Environ 

Sci Technol 35(23): 4585-4591. 

Hale RC, La Guardia MJ, Harvey E, and Mainor TM, 2002. Potential role of fire retardant-treated 

polyurethane form as a source of brominated diphenyl ethers to the US environment. 

Chemosphere 46: 729-735. 

Hammond SK, Hines CJ, Hallock MF, Woskie SR, Kenyon EM, and Schenker MB, 1996. 

Exposures to glycol ethers in the semiconductor industry. Occupational Hygiene (2): 355-366. 

Hammond SK, 1999. Exposure of U.S. workers to environmental tobacco smoke. Environ 

Health Perspect 107(Supplement 2): 329-340. 

Harnly M, McLaughlin R, Bradman A, McKone T, Eskenazki B and Nishioka M, 2004. 

Improving spatial precision of agricultural pesticide use indices. Presented at the 14th Annual 

Conference of the International Society of Exposure Analysis, October 17-21, 2004. Abstract 

Book. 

Hasselblad V, Eddy DM, and Kotchmar D, 1992. Synthesis of environmental evidence: nitrogen 

dioxide epidemiology studies. J. Air Waste Manage. Assoc. 42: 622-671. 

Hayden S, 2004. Natural Resources Canada, CANMET Advanced Combustion Technologies 

Group. Ottawa, Ontario, Canada. Personal communication. 

Healthy Schools Campaign, 2003. Apparently Size Doesn’t Matter: Two Illinois School Districts 

Show Successful IAQ Management. School Health Watch:The Newsletter of the Illinois Healthy 

Schools Campaign, 2(2). Available from: 

http://www.healthyschoolscampaign.org/news/newsletter/2003-summer_HSC-newsletter.pdf. 

Hedge A, 1995. In defense of “the sick building syndrome.” Indoor Environment 4: 251-253. 

HEI (Health Effects Institute), 2003. Revised analyses of time-series studies of air pollution and 

health. HEI Special report. 

Henderson KA, Matthews IP, Adisesh A and Hutchings AD, 2003. Occupational exposure of 

midwives to nitrous oxide on delivery suites. Occup Environ Med 60: 958-961. 

Heschong L, 2003. Windows and Classrooms: A Study of Student Performance and the 

Indoor Environment. (P500-03-082-A-7). California Energy Commission. 

Available from: http://h-m-g.com/downloads/Daylighting/day_registration_form.htm. 
Indoor Air Pollution in California July, 2005 

 211

HESIS (California Hazard Evaluation System and Information Service), 2004. Site investigation 

of student health complaints at Federico’s beauty College, Bakersfield, California. Letter dated 

December 22, 2004. 

Hiipakka D, and Samimi B, 1987. Exposure of acrylic fingernail sculptors to organic vapors and 

methacrylate dusts. Am. Ind. Hyg. Assoc. J. 48(3): 230-237. 

Hoddinott KB, and Lee AP, 2000. The use of environmental risk assessment methodologies for 

an indoor air quality investigation. Chemosphere 41: 77-84. 

Hodgson AT, 1999. Common Indoor Sources of Volatile Organic Compounds: Emission Rates 

and Techniques for Reducing Consumer Exposures. Final report under contract no. 95-302. 

Sacramento, CA, California Environmental Protection Agency, Air Resources Board. 

Hodgson AT, Rudd AF, Beal D, and Chandra S, 2000. Volatile organic compound 

concentrations and emission rates in new manufactured and site-built houses. Indoor Air 10: 

178-192. 

Hodgson AT, Beal D, and McIlvaine JER, 2002. Sources of formaldehyde, other aldehydes and 

terpenes in a new manufactured house. Indoor Air 12: 235-242. 

Hodgson AT and Levin H, 2003a. Classification of measured indoor volatile organic compounds 

based on noncancer health and comfort considerations. Lawrence Berkeley National Laboratory 

Report – 53308, September 2003. 

Hodgson AT and Levin H, 2003b. Volatile organic compounds in indoor air: a review of 

concentrations measured in North America since 1990. Lawrence Berkeley National Laboratory 

Report – 51715, April 21, 2003. 

Hodgson, M, Levin, H, and Wolkoff,P, 1994. Volatile organic compounds in indoor air. Journal of 

Allergy and Clinical Immunology 94, 296-303. 

Horak F, Studnicka M, Gartner C, Spengler JD, Tauber E, Urbanek R, Veiter A, and Frischer T, 

2002. Particulate matter and lung function growth in children: a 3-yr follow-up study in Austrian 

schoolchildren. Eur Respir J 19: 838-845. 

Hosler DL, 1998. Personal communication, Southern California Gas Company, Los Angeles, 

CA. As cited in Traynor (1999). 

Howard-Reed C and Corsi RL, 1998. Volatilization of hazardous contaminants from drinnking 

water to indoor air: the role of residential washing machines. J. Air & Waste Mgmt Assoc 48(10):

907-914. 

Howard-Reed C, Corsi RL, and Moya J, 1999. Volatilization of hazardous chemicals from 

drinking water to indoor air: the role of residential dishwashers, Environ Sci & Technol 33(13): 

2266-2272. 

Howard-Reed C, Wallace LA, and Emmerich SJ, 2003. Effect of ventilation systems and air 

filters on decay rates of particles produced by indoor sources in an occupied townhouse. 

Atmospheric Environment 37: 5295-5306. 
Indoor Air Pollution in California July, 2005 

 212

HUD (U.S. Department of Housing and Urban Development), 1996. Environmental Assessment 

Guide For Public Housing. Washington, DC. Prepared by Steven Winter Associates, Inc., 

Norwalk, CT. October 30. http://www.huduser.org/publications/pubasst/enviro.html. 

HUD, 1999. The Healthy Homes Initiative: A Preliminary Plan (Full Report), Office of Lead 

Hazard Control, Washington, DC. April. http://www.hud.gov/offices/lead/reports/HHIFull.pdf. 

HUD, 2002. Manufactured Home Construction and Safety Standards, 24 CFR 3280. 

http://www.hud.gov/offices/hsg/sfh/mhs/mhshome.cfm. 

Husman H, 1996. Health effects of indoor-air microorganisms. Scandinavian Journal of Work, 

Environment and Health 22:5-13. 

IARC (International Agency for Research on Cancer), 1983. IARC Monographs on the 

Evaluation of the Carcinogenic Risk of Chemicals to Humans: Certain Polycyclic Aromatic 

Hydrocarbons and Heterocyclic Compounds, Volume 32. Available from: 

http://www-cie.iarc.fr/monoeval/allmonos.html. 

IARC (International Agency for Research on Cancer), 2002. IARC monographs on the 

evaluation of the carcinogenic risk of chemicals to humans: tobacco smoke and involuntary 

smoking 83. 

IOM (Institute of Medicine), 1993. Indoor Allergens: Assessing and Controlling Adverse Heallth 

Effects. Washington D.C: National Academy Press. 

http://books.nap.edu/books/0309048311/html/. 

IOM (Institute of Medicine), 1999. Toward environmental justice research, education, and health 

policy needs. Washington D.C: National Academy Press. 

http://books.nap.edu/books/0309064074/html/. 

IOM (Institute of Medicine), 2000. Clearing the air: asthma and indoor air exposures. National 

Academy of Sciences, Washington DC: National Academy Press. 

http://www.nap.edu/books/0309064961/html/. 

IOM (Institute of Medicine), 2004. Damp indoor spaces and health. National Academy of 

Sciences. Washington D.C: National Academy Press. 

http://www.nap.edu/books/0309091934/html/. 

Ito K, 2003. Associations of particulate matter components with daily mortality and morbidity in 

Detroit, Michigan in Health Effects Institute Special Report: Revised Analyses of Time-Series 

Studies of Air Pollution and Health. 

Jarvis D, Chinn S. Luczynska C, and Burney P, 1996. Association of respiratory symptoms and 

lung function in young adults with use of domestic gas appliances. Lancet 347: 426-431. 

Jefferis G, 2004. Maintenance and Operations, Everett Unified School District, Everett, WA. 

Personal communication, January 7. See also: 

http://www.enterprisenewspapers.com/archive/2003/8/8/2003861629365.cfm. 

Jenkins PL, Phillips TJ, Mulberg EJ, and Hui SP, 1992a. Activity patterns of Californians: use of 

and proximity to indoor pollutant sources. Atmos Environ 26A(12): 2141-2148. 
Indoor Air Pollution in California July, 2005 

 213

Jenkins PL, Hui SP, Phillips TJ, and Lum SB, 1992b. Toxic Air Pollutants in California 

Residences. Presentation. Current Issues in Air Toxics, Proceedings of the Third Annual West 

Coast Regional Air and Waste Management Association Conference, November 1992, 

Sacramento, CA. 

Jetter JJ, Guo Z, McBrian JA, and Flynn MR, 2002. Characterization of emissions from burning 

incense. Sci Total Environ 295(1-3): 51-67. 

Jo WK, Weisel CP, Lioy PJ, 1990. Chloroform exposure and the health risk associated with 

multiple uses of chlorinated tap water. Risk Analysis 10: 581-585. 

Jo WK, and Kim SH, 2001. Worker exposure to aromatic volatile organic compounds in dry 

cleaning stores. Amer Industrial Hygiene Assoc J 62, 4: 466-471. 

Johanning E, Biagini R, Hull D, Morey P, Jarvis B, Landsbergis P, 1996. Health and 

immunology study following exposure to toxigenic fungi (Stachybotrys chartarum) in a waterdamaged office environment. In Arch Occup Environ Health 68:207-218. 

Kamens R, Lee C, Wiener R, and Leith D, 1991. A study to characterize indoor particles in three 

non-smoking homes. Atmos Environ 25(5/6): 939-948. 

Kanarek M, Quackenboss JJ, Kaarakka P, Duffy C, and Rohrer KM, 1985. Energy conservation 

through weatherization and indoor air quality. Final Report May 16, 1985. Performed by the 

University of Wisconsin for Wisconsin Power and Light Co. 

Kaplan J, Marquardt S, and Barber W, 1998. Failing Health: Pesticide Use in California Schools. 

San Francisco, CA: CALPIRG Charitable Trust. 

Karlberg, AT, Boman, and Melin B, 1991. Animal experiments on the allergenicity of d-limonene 

– the citrus solvent. Ann. Occup. Hyg. 35(4): 419-426. 

Karlberg AT, Magnusson K, and Nilsson U, 1992. Air oxidation of d-limonene (the citrus solvent) 

creates potent allergens. Contact Dermatitis 26: 332-340. 

Karol MH, 2002. Respiratory allergy: what are the uncertainties? Toxicology 181-182: 305-310. 

Kats G, 2003. The Costs and Financial Benefits of Green Buildings. A Report to California’s 

Sustainable Building Task Force. P. 66. 

http://WWW.CIWMB.CA.GOV/GreenBuilding/Design/CostBenefit/Report.pdf. 

Katz, 2005. Personal communication from Elizabeth Katz, HESIS, DHS, to Peggy Jenkins, 

ARB, February 16. 

Keeler GJ, Dvonch T, Yip FY, Parker EA, Isreal BA, Marsik FJ, Morishita M, Barres JA, Robins 

TG, Brakefield-Caldwell W, and Sam M, 2002. Assessment of personal and community-level 

exposures to particulate matter among children with asthma in Detroit, Michigan, as part of 

Community Action Against Asthma (CAAA). Environ Health Perspect 110 Suppl 2:173-81. 

Kelly TJ, Smith DL, and Satola J, 1999. Emission rates of formaldehyde from materials and 

consumer products found in California homes. Environ Sci Technol 33: 81-88. 
Indoor Air Pollution in California July, 2005 

 214

Kelly TJ, Battelle, May 2000, Indoor Air Quality Symposium: Risk Reduction in the 21st Century, 

Sacramento, CA. 

Kerger BD, Schmidt CE, and Paustenbach DJ, 2000. Assessment of airborne exposure to 

trihalomethanes from tap water in residential showers and baths. Risk Anal 20(5): 637-651. 

Kirkpatrick JN, 1987. Occult carbon monoxide poisoning. West J Med 146(1): 52-56. 

Kissel JC, 1993. Potential impact of deliberately introduced ozone on indoor air quality. J Expo 

Anal Environ Epidemiol 3(2): 155-64. 

Kleno JG, Clausen PA, Weschler CJ, and Wolkoff P, 2001. Determination of ozone removal 

rates by selected building products using the FLEC emission cell. Environ Sci Technol 35: 2548-

2553. 

Krewski, D.; Burnett, R.; Goldberg, M.; Hoover, K.; Siemiatycki, J.; Jerrett, M.; Abrahamovicz, 

M.; White, W. Reanalysis of the Harvard Six Cities Study and the American Cancer Society 

Study of Particulate Air Pollution and Mortality; Health Effects Institute: Cambridge, MA, 2000. 

Krieger J, Higgins DL, 2002. Housing and health: time again for public health action. Am J 

Public Health 92(5): 758-768. 

Krieger JW, Takaro TK, Song L, Weaver M, 2005. The Seattle-King County Healthy Homes 

Project: A Randomized, Controlled Trial of a Community Health Worker Intervention to 

Decrease Exposure to Indoor Asthma Triggers. American Journal of Public Health 95(4): 652-

659. 

Kulle TJ, Sauder LR, Hebel JR, Chatham MD, 1985. Ozone response relationships in healthy 

nonsmokers. Am Rev Respir Dis 132: 36-41. 

Labreche F, Forest J, Trottier M, Lalonde M Simard R, 2003. Characterization of chemical 

exposures in hair dressing salons. Applied Occupational and Environmental Hygiene 18: 1014-

1021. 

Lachenmyer C and Hidy GM, 2000. Urban measurements of outdoor-indoor PM25 

concentrations and personal exposure in the deep south. Part I. Pilot study of mass 

concentrations for nonsmoking subjects. Aerosol Science & Technol. 32(1): 34-51. 

Lai ACK, Thatcher TL, Nazaroff WW, 2000. Inhalation transfer factors for air pollution health risk 

assessment. Journal of the Air and Waste Management Association 50: 1688-1699. 

Landrigan PJ, Claudio L, Markowitz SB, Berkowitz GS, Brenner BL, Romero H, Wetmur JG, 

Matte TD, Gore AC, Godbold JH, Wolff MS, 1999. Pesticides and Inner-City Children: 

Exposures, Risks, and Prevention. Environ Health Perspect 107(S3): 431-437. Available from: 

http://ehp.niehs.nih.gov/members/1999/supp-3/431-437landrigan/landrigan-full.html. 

Laslo-Baker D, Barrera M, Knittel-Keren D, Kozer E, Wolpin J, Khattak S, Hackman R, Rovet J, 

Koren G, 2004. Child neurodevelopmental outcome and maternal occupational exposure to 

solvents. Arch Pediatr Adolesc Med 158: 956-961. 
Indoor Air Pollution in California July, 2005 

 215

LBNL (Lawrence Berkeley National Laboratory), 2003. Residential Commissioning Project. 

Indoor Environment Department, Environmental Energy Technology Division. Berkeley, CA. 

http://epb1.lbl.gov/EPB/commissioning/index.html. 

LBNL, 2004. Sick Building Syndrome. Indoor Environmental Program. Berkeley, CA. 

http://eetd.lbl.gov/IED/viaq/v_syndrome_1.html. 

Lee K, Xue J, Geyh AS, Ozkaynak H, Leaderer BP, Weschler CJ, Spengler JD, 2002. Nitrous 

acid, nitrogen dioxide, and ozone concentrations in residential environments. Environ Health 

Perspect 110(2): 145-50. 

Lee RJ, Van Orden DR, Corn M, and Crump KS, 1992. Exposure to airborne asbestos in 

buildings. Regul Toxicol Pharmacol 16: 93-107. 

Lee SC, Lam S, Fai HK, 2001. Characterization of VOCs, ozone, and PM10 emissions from 

office equipment in an environmental chamber. Building and Environment 36: 837-842. 

Leech JA, Raizenne M, and Gusdorf J, 2004. Health in occupants of energy efficient new 

homes. Indoor Air 3: 169-173. 

Leikauf GD, 2002. Hazardous air pollutants and asthma. Environ Health Perspect

110(Supplement 4): 505-526. 

Leino T, Kahkonen E, Saarinen L, Eckerman MLH, and Paakkulainen H, 1999. Working 

conditions and health in hairdressing salons. Applied Occupational and Environmental Hygiene

14: 26-33. 

Leovic, KW, Sheldon, LS, Whitaker, DA, Hetes, RG, Calcagni, JA, and Baskir, JN, 1996. 

Measurement of indoor air emissions from dry-process photocopy machines. Journal of Air & 

Waste Management Association 46: 821-829. 

Levesque B, Allaire S, Prud’homme H, Rhainds M, Lebel G, Bellemarre D, and Dupuis K, 1997. 

Indoor motocross competitions: air quality evaluation. American Industrial Hygiene Association 

Journal 58: 286-290. 

Levesque B, Allaire S, Prud’homme H, Dupuis K and Bellemare D, 2000. Air quality monitoring 

during indoor monster truck and car demolition shows. J Exposure Anal and Environ Epidemiol

10: 58-65. 

Levy JI et al., 1998. Impact of residential nitrogen dioxide exposure on personal exposure: an 

international study. J. Air & Waste Manage. Assoc. 48: 553-560. 

Lewis RG, 2001. Chapter 35, Pesticides. In Indoor Air Quality Handbook, eds. Spengler JD, 

Samet JM, and McCarthy JF, 2001.. McGraw-Hill. New York. 

Lewis RG, 2005. Chapter 3: Residential Post-Application Pesticide Exposure Monitoring, in 

Occupational and Incidental Residential Exposure Assessment, C. A. Franklin and J. P. 

Worgan, eds., John Wiley & Sons, Ltd., Sussex, 2005, pp. 71-128. 
Indoor Air Pollution in California July, 2005 

 216

Lewis R, Fortmann R, and Camann D, 1994. Evaluation of methods for monitoring the potential 

exposure of small children to pesticides in the residential environment. Arch Environ Contam 

Toxicol 26: 37-46. 

Lewis R, Fortune C, Willis R, Camann D, and Antley J, 1999. Distribution of pesticides and 

polycyclic aromatic hydrocarbons in house dust as a function of particle size. Environ Health 

Perspect 107: 721-726. 

Liddament MW, 2000. A Review of Ventilation and the Quality of Ventilation Air. Indoor Air 10: 

193-199. 

Lilienfeld AM, and Lilienfeld DE, 1980. Foundations of Epidemiology (2nd Edition). New York: 

Oxford University Press. 

Lillquist DR, Lee JS, Ramsay JR, Boucher KM, Walton ZL, and Lyon JI, 1998. A comparison of 

indoor/outdoor PM10 concentrations measured at three hospitals and a centrally located 

monitor in Utah. Appl Occup Environ Hyg 13(6): 409-415. 

Linn WS, Gong, Jr H, Clark KW, and Anderson KR, 1999. Day-to-day particulate exposure and 

health changes in Los Angeles area residents with severe lung disease. J Air Waste Manag 

Assoc 49: 108-115. 

Linn WS, Szlachcic Y, Gong H, Kinney PL, and Berhane KT, 2000. Air pollution and daily 

hospital admissions in metropolitan Los Angeles. Environ Health Perspect 108: 427-434. 

Lioy PJ, and Greenberg A, 1990. Factors associated with human exposures to polycyclic 

aromatic hydrocarbons. Toxicol Ind Health 6(2): 209-223. 

Lippmann M et al., 2000. Association of particulate matter components with daily mortality and 

morbidity in urban populations. Research Report / Health Effects Institute 56(95): p. 5-72, 

discussion 73-82. 

Lipsett M, Hurley S, and Ostro B, 1997. Air pollution and emergency room visits for asthma in 

Santa Clara County, California. Environ Health Perspect 105(2): 216-222. 

Liu DL, and Nazaroff WW, 2001. Modeling pollutant penetration across building envelopes. 

Atmospheric Environment 35: 4451-4462. 

Liu KS, Hayward SB, Girman JR, Moed BA, and Huang FY, 1991. Annual average radon 

concentrations in California residences. J Air Waste Manag Assoc 41(9): 1207-1212. 

Liu KS, Girman JR, Hayward SB, Shusterman D, and Chang YL, 1993. Unintentional carbon 

monoxide deaths in California from charcoal grills and hibachis. J Expo Anal Environ Epidemiol

3(Suppl 1): 143-51. 

Liu KS, Paz MK, Flessel P, Waldman J, and Girman J, 2000. Unintentional carbon monoxide 

deaths in California from residential and other nonvehicular sources. Arch Environ Health 55(6): 

375-381. 

Liu L, Guo J, Li J, and Sheng L, 2000. The effect of wire heating and configuration on ozone 

emission in a negative ion generator, J. Electrostatics, 48: 81-91. 
Indoor Air Pollution in California July, 2005 

 217

Liu LJ, Koutrakis P, Suh HH, Mulik JD, and Burton RM, 1993b. Use of personal measurements 

for ozone exposure assessment: a pilot study. Environ Health Perspect 101(4): 318-24. 

Liu LJ, Koutrakis P, Leech J, and Broder I, 1995. Assessment of ozone exposures in the greater 

metropolitan Toronto area. J Air Waste Manag Assoc 45(4): 223-34. 

Liu LJS, Box M, Kalman D, Kaufman J, Koenig, Larson T, Lumley T, Sheppard L, and Wallace 

L, 2003. Exposure assessment of particulate matter for susceptible populations in Seattle. 

Environ Health Perspect 222(7): 908-918. 

Lofroth G, Stensman C, Brandhorst-Satzkorn M, 1991. Indoor sources of mutagenic aerosol 

particulate matter: smoking, cooking and incense burning. Mutat Res 261(1): 21-28. 

Long CM, Suh HH, and Koutrakis P, 2000. Characterization of indoor particle sources using 

continuous mass and size monitors. J Air Waste Manag Assoc 50: 1236-1250. 

Long CM, Suh HH, Kobzik L, Catalano PJ, Ning YY, and Koutrakis P, 2001. A pilot investigation 

of the relative toxicity of indoor and outdoor fine particles: in vitro effects of endotoxin and other 

particulate properties. Environ Health Perspect 109(10): 1019-26. 

Lubliner M, and Gordon A, 1990. Ventilation in US Manufactured Homes: Requirements, Issues 

and Recommendations. Presented at the 21st Annual Air Infiltration and Ventilation Centre 

Conference, The Hague, Netherlands, September 26 –29. Washington State University Energy 

Extension Program. http://www.fsec.ucf.edu/Bldg/baihp/pubs/wsu-aivc/index.htm . 

Lynch RM, and Kipen H, 1998. Building-related illness and employee lost time following 

application of hot asphalt roof: A call for prevention. Toxicology and Industrial Health, 14(6):

857-868. 

Maeda, B, 2004. Personal communication. Building and Appliance Standards Office, California 

Energy Commission, Sacramento, CA. 

Magnani C, Dalmasso P, Biggeri A, Ivaldi C, Mirabelli D, Terracini B, and 2001. Increased risk 

of malignant mesothelioma of the pleura after residential or domestic exposure 

to asbestos: a case-control study in Casale Monferrato, Italy. Environ Health Perspect 109:915–

919. 

Mah JC, 2000. Non-Fire Carbon Monoxide Deaths and Injuries Associated with the Use of 

Consumer Products: Annual Estimates. U.S. Consumer Product Safety Commission, 

Directorate for Epidemiology, Division of Hazard Analysis, Bethesda, MD 20814, October 2000. 

http://www.cpsc.gov/library/co00.pdf. 

Maisonet M, Bush TJ, Correa A, and Jaakkola JJK, 2001. Relation between ambient air 

pollution and low birth weight in the Northeastern United States. Environl Health Perspect 

109(3): 351-356. 

Malone N, Baluja KF, Costanzo JM, and Davis CJ, 2003. The Foreign-Born Population: 2000, 

Census 2000 Brief, US Census Bureau, Washington, DC. 
Indoor Air Pollution in California July, 2005 

 218

Mannino DM, Homa DM, Pertowski CA, Ashizawa A, Nixon LL, Johnson CA, Ball LB, Elizabeth 

J, and Kang DS, 1998. Surveillance for asthma: United States, 1960-1995. MMWR 47: 1-28. 

Mannino DM, Homa DM, Akinbami LJ, Moorman JE, Gwynn C, and Redd SC, 2002. 

Surveillance for asthma – United States, 1980-1999. MMWR 51(SS01): 1-13. 

Mar TF, Norris GA, Koenig JQ, Larson TV, 2000. Associations between Air Pollution and 

Mortality in Phoenix, 1995-1997. Environmental Health Perspectives 108(4): 347-353. 

Marcinowski F, Lucas RM, and Yeager WM, 1994. National and regional distributions of 

airborne radon concentrations in U.S. homes. Health Phys 66(6): 699-706. 

Marr LC, Morrison GC, Nazaroff WW, and Harley RA, 1998. Reducing the risk of accidental 

death due to vehicle-related carbon monoxide poisoning. Journal of the Air and Waste 

Management Association 48, 899-906. 

Mason MA, Sparks LE, Moore SA, Dolgov I, and Perry RB, 2000. Characterization of ozone 

emissions from air cleaners equipped with ozone generators and sensor and feedback control 

circuitry. 

Mathieu-Nolf M, 2002. Poisons in the air: a cause of chronic disease in children. J Toxicol Clin 

Toxicol 40: 483-489. 

Mattison DR, Damus K, Fiore E, Petrini J, Alter C, 2001. Preterm delivery:a public health 

perspective. Pediatric Perinat Epidemiol. Suppl 2:7-16. 

http://www.marchofdimes.com/files/Preterm_delivery.pdf.

Mazdai A, Dodder NG, Abernathy MP, and Hites RA, 2003. Polybrominated diphenyl ethers in 

maternal and fetal blood samples. Environ Health Perspect 111: 1249-1252. 

McBride DE, Koenig JQ, Luchtel DL, Williams PV, and Henderson WR, 1994. Inflammatory 

effects of ozone in the upper airways of subjects with asthma. Am J Respir Crit Care Med 149: 

1192-1197. 

McConnell R, Berhane K, Gilliland F, London SJ, Vora H, Avol E, Gauderman WJ, Margolis HG, 

Lurmann F, Thomas DC, and Peters JM, 1999. Air pollution and bronchitic symptoms in 

Southern California children with asthma. Environ Health Perspect 107(9):757-60. 

McConnell R, Berhane K, Gilliland F, London SJ, Islam T, Gauderman WJ, Avol E, Margolis SG, 

and Peters JM, 2002a. Asthma in exercising children exposed to ozone: a cohort study. Lancet

359:386-91. 

McConnell R, Berhane K, Gilliland F, Islam T, Gauderman WJ, London SJ, Avol E, Rappaport 

EB, Margolis HG, Peters JM, 2002b. Indoor risk factors for asthma in a prospective study of 

adolescents. Epidemiology13(3): 288-295. 

McConnell R, Berhane K, Gilliland F, Molitor J, Thomas D, Lurmann F, Avol E, Gauderman WJ, 

and Peters JM, 2003. Prospective study of air pollution and bronchitic symptoms in children with 

asthma. Am J Respir Crit Care Med 168: 790-797. 
Indoor Air Pollution in California July, 2005 

 219

McDonald JC, Harris J, and Armstrong B, 2004. Mortality in a cohort of vermiculite miners 

exposed to fibrous amphibole in Libby, Montana. Occup Environ Med 61: 363-366. 

McDonald TA, 2002. A perspective on the potential health risks of PBDEs. Chemosphere 46: 

745-755. 

McDonnell WF, Stewart PW, Smith MV, Pan WK, and Pan J, 1999. Ozone-induced respiratory 

symptoms: exposure-response models and association with lung function. Eur Respir J 14: 

845-853. 

MDC (Minnesota Department of Commerce), 2004. Minnesota Energy Code, Chapter 7672 

Detached Single-Family and Two-Family Dwellings. Effective April 15, 2000. 

Mendell MJ, 1993. Non-specific symptoms in office workers: a review and summary of the 

epidemiologic literature. Indoor Air 3: 227-236. 

Mendell MJ, Fisk WJ, Deddens JA et al. 1996. Elevated symptom prevalence associated with 

ventilation type in office buildings. Epidemiology 7: 583-589. 

Mendell MJ, Fisk WJ, Kreiss K, Levin H, Alexander D, Cain WS, Girman JR, Hines CJ, Jensen 

PA, Milton DK, Rexroat LP, and Wallingford KM, 2002. Improving the Health of Workers in 

Indoor Environments: Priority Research Needs for a National Occupational Research Agenda. 

Am J Public Health 92 1430–1440. 

Mendez D, Warner KE, and Courant PN, 1998. Effects of Radon Mitigatoin vs. Smoking 

Cessation in Reducing Radon-Related Risk of Lung Cancer. Amer J Public Health 88(5): 811-

812. 

Meng Y, Babey SH, Malcolm E, Brown ER, Chawla N, 2003. Asthma in California: Findings 

from the 2001 California Health Interview Survey. UCLA Center for Health Policy Research, 

University of California, Los Angeles, CA. 

http://www.healthpolicy.ucla.edu/pubs/publication.asp?pubID=83. 

Menzies D et al., 1994. The “sick building” – a misleading term that should be abandoned. 

Indoor Air Quality 37-48. 

Menzies D, and Bourbeau J, 1997. Building-related illnesses. N Engl J Med 337: 1524-1531. 

Miguel AG, Cass GR, Glovsky MM, and Weiss J, 1998. Allergens in paved road dust and 

airborne particles, Final Report to the California Air Resources Board contract No. 95-312, 

August 1998. 

Miller JD, 2001. Mycological investigations of indoor environments. in Microorganisms in Home 

and Indoor Work Environments. Editors: B Flannigan, RA Samson, JD Miller. Taylor & Francis. 

New York, NY. 

Mills JN, Corneli A, Young JC, Garrison LE, Khan AS, and Ksiazek TG, 2002. Hantavirus 

pulmonary syndrome--United States: updated recommendations for risk 

reduction. Centers for Disease Control and Prevention. MMWR Recomm Rep. 2002 Jul 

26;51(RR-9):1-12. 
Indoor Air Pollution in California July, 2005 

 220

Milton D, Glencross P, and Walters M, 2000. Risk of sick leave associated with outdoor air 

supply rate, humidification, and occupants’ complaints. Indoor Air 10, 212-221. 

MOD (March of Dimes Birth Defects Foundation), 2003. PeriStats: Born Too Soon and Too 

Small in the United States. White Plains, NY. 

http://www.marchofdimes.com/peristats/prematurity.aspx?reg=99. 

Molhave L, 1991a. Indoor Climate, Air Pollution, and Human Comfort. J Expo Anal Environ 

Epidemiol 1(1): 63-81. 

Molhave L., 1991b. Volatile organic compounds, indoor air quality and health. Indoor Air (4): 

357-376. 

Molhave L, 2003. Organic compounds as indicators of air pollution. Indoor Air 13(Suppl. 6): 12-

19. 

Moolgavkar SH, 2003. Air pollution and daily deaths and hospital admissions in Los Angeles 

and Cook Counties in Health Effects Institute Special Report: Revised Analyses of Time-Series 

Studies of Air Pollution and Health. 

Moriske HJ, Ebert G, Konieczny L, Menk G, and Schondube M, 1998. Concentrations and 

decay rates of ozone in indoor air in dependence on building and surface materials. Toxicol Lett

96-97: 319-323. 

Morris, 2005. Personal communication, Wayne Morris, Vice President, Association of Home 

Appliance Manufacturers, to ARB staff, April 6, 2005. 

Morrison GC, and Nazaroff WW, 2002. Ozone interactions with carpet: secondary emissions of 

aldehydes. Environmental Science and Technology 36: 2185-2192. 

Mortimer KM, Neas LM, Dockery DW, Redline S, and Tager IB, 2002. The effect of air pollution 

on inner-city children with asthma. Eur Respir J 19(4): 699-705. 

Mott JA, Wolfe MI, Alverson C et al., 2002. National vehicle emissions policies and practices 

and declining US carbon monoxide-related mortality. JAMA 288, 988-995. 

Mukerjee S, Ellenson WD, Lewis RG, Stevens RK, Somerville MC, and Shadwick DS, 1997a. 

An environmental scoping study in the Lower Rio Grande Valley of Texas – I. Comparative 

assessement of air sampling methods. Environ Int 23(5): 611-628. 

Mukerjee S, Ellenson WD, Lewis RG, Stevens RK, Somerville MC, Shadwick DS, and Willis RD. 

1997b. An environmental scoping study in the Lower Rio Grande Valley of Texas – III. 

Residential microenvironmental monitoring for air, house dust, and soil. Environ Int 23(5): 657-

673. 

Mullins J, 2001. Microorganisms in outdoor air. In: Microorganisms in Home and Indoor Work 

Environments. Editors: B Flannigan, RA Samson, JD Miller. Taylor & Francis. New York, NY. 

Myatt TA, Johnston SL, Zuo Z, Wand M, Kebadze T, Rudnick S, and Milton DK, 2004. 

Detection of airborne rhinovirus and its relation to outdoor air supply in office environments. Am 

J Respir Crit Care Med. Jun 1;169(11):1187-90. 
Indoor Air Pollution in California July, 2005 

 221

Nabinger SJ, Persily AK, Sharpless KS, Wise SA, 1995. Measurements of Indoor Pollutant 

Emissions from EPA Phase II Wood Stoves. NISTIR 5575. National Institute of Standards and 

Technology, Building and Fire Research Laboratory, Gaithersburg, MD. 

http://fire.nist.gov/bfrlpubs/build95/art059.html. 

Nagda NL, and Rector HE, 2003. A critical review of reported air concentrations of organic 

compounds in aircraft cabins. Indoor Air 13(3): 292-301. 

NAS (National Academy of Sciences), 1999. Health Effects of Exposure to Radon: BEIR VI. 

Committee on Health Risks of Exposure to Radon, National Research Council. 

http://www.epa.gov/radon/beirvi.html. 

NAHB (National Association of Home Builders), 2004. Model Green Home Building Guidelines 

Initiative Launched At the 2004 International Builders' Show. Upper Marlboro, MD. 

http://www.nahb.org/news_details.aspx?newsID=724, 

http://www.nahbrc.org/green3.asp?CategoryID=1891. 

Naumova YY, Eisenreich SJ, Turpin BJ, Weisel CP, Morandi MT, Colome SD, Totten LA, Stock 

TH, Winer AM, Alimokhtari S, Kwon J, Shendell D, Jones J, Maberti S, and Wall SJ, 2002. 

Polycyclic aromatic hydrocarbons in the indoor and outdoor air of three cities in the U.S. Environ 

Sci Technol 36: 2552-2559. 

Nazaroff WW, and Weschler CJ, 2004. Cleaning products and air fresheners: exposure to 

primary and secondary air pollutants. Atmos Environ 38: 2841–2865. 

Nazaroff WW, and Singer BC, 2004. Inhalation of hazardous air pollutants from environmental 

tobacco smoke in U.S. residences. J Exposure Analysis and Environmental Epidemiology 14: 

S71-S77. 

Nazaroff WW, and Klepeis NE, 2004. Environmental tobacco smoke particles. Indoor 

Environment: Airborne Particles and Settled Dust, Morawska L, and Salthammer T (Eds.), 

Wiley-VCH, Weinheim, Germany, 2004, pp. 245-274. 

NCI (National Cancer Institute), 1999. Health effects of exposure to environmental tobacco 

smoke: The report of the California Environmental Protection Agency. Smoking and Tobacco 

Control Monograph no. 10. Bethesda, MD. U.S. Department of Health and Human Services, 

National Institutes of Health, National Cancer Institute, NIH Pub. No. 99-4645. 

Neas LM, Dockery DW, Ware JH, Spengler JD, Speizer FE, and Ferris BG, Jr., 1991. 

Association of indoor nitrogen dioxide with respiratory symptoms and pulmonary function in 

children. Amer J Epidemiol 134 (2): 204-218. 

Needleman HL, Gunnoe C, Leviton A, Reed R, Peresie H, Maher C, and Barrett P, 1979. 

Deficits in psychologic and classroom performance of children with elevated dentine levels. N 

Engl J Med 100: 689-695. 

Nelson BD, 2002. Evaluation of Homes Built to the New Minnesota Energy Code, Minnesota 

Energy Office. 
Indoor Air Pollution in California July, 2005 

 222

New Jersey Mercury Task Force, 2002. Volume II: Impacts of Mercury in New Jersey. Available 

from: http://www.state.nj.us/dep/dsr/mercury_task_force.htm. 

Nguyen TTL, Pentikäinen T, Rissanen P, Vahteristo M, Husman T, Nevalainen A, 1998. Health 

related costs of moisture and mold in dwellings. Publication of the National Public Health 

Institute, B13, Kuopio University Printing Office, Finland. 

NIOSH (National Institute for Occupational Safety and Health), 1992. NIOSH Health Hazard 

Evaluation, Chapple Hair Styling Salon. HETA 89-138-2215. NIOSH HC 28. 

NIOSH Pocket Guide to Chemical Hazards, February 2004, printed edition NIOSH Publication 

Number 97-140, available at http://www.cdc.gov/niosh/npg/npgd0293.html. 

Niu J, Tung TCW, and Burnett J, 2001a. Ozone emission rate testing and ranking method using 

environmental chamber, Atmos Environ 35: 2143-2151. 

Niu JL, Tung TCW, and Burnett J, 2001b. Quantification of dust removal and ozone emission of 

ionizer air-cleaners by chamber testing, J. Electrostatics, 51-52: 20-24. 

Noren K, and Meironyte D, 1998. Contaminants in Swedish human milk. Decreasing levels of 

organochlorine and increasing levels of organobromine compounds. Organohalogen 

Compounds 40: 1111-1123. 

NRC (National Research Council), 1981. Indoor Pollutants. National Academy Press, 

Washington, D.C. 

NRC, 1988. Health Risks of Radon and Other Internally Deposited Alpha-Emitters, Committee 

on the Biological Effects of Ionizing Radiations (BEIR IV). National Academy Press, 

Washington, D.C. 

NRC, 1990. Health Effects of Exposure to Low Levels of Ionizing Radiation. Committee on the 

Biological Effects of Ionizing Radiations (BEIR V). National Academy Press, Washington, D.C. 

NRC, 1999a. Biological effects of ionizing radiation (BEIR) VI report: The health effects of 

exposure to indoor radon. Committee on Health Risks of Exposure to Radon. National Academy 

Press: Washington DC. 

NRC, 1999b. Risk assessment of radon in drinking water. Committee on risk assessment of 

exposure to radon in drinking water. National Academy Press: Washington DC. 

NRC, 2002. The Airliner Cabin Environment and the Health of Passengers and Crew. Board 

on Environmental Studies and Toxicology. National Academy Press, Washington, D.C. 

NRCan (Natural Resources Canada), 2004a. All About Gas Fireplaces. Ottawa, Ontario, 

Canada. http://oee.nrcan.gc.ca/Publications/infosource/Pub/home/all_about_gas_fireplaces.pdf. 

NRCan, 2004b. Breathe Easier With Healthy Ventilation and Fewer Pollutants. Ottawa, Ontario, 

Canada. http://oee.nrcan.gc.ca/Publications/infosource/pub/r2000/BreatheFactEng.cfm. 

October 20. 
Indoor Air Pollution in California July, 2005 

 223

NTP (National Toxicology Program), December 2002. Report on Carcinogens, Tenth Edition. 

Available from: http://ehp.niehs.nih.gov/roc/toc10.html. 

NTP-CERHR (National Toxicology Program-Center for the Evaluation of Risks to Human 

Reproduction), 2000. NTP-CERHR Expert Panel Report on Di (2-ethylhexyl) Phthalate. National 

Toxicology Program, U.S. Department of Helath and Human Services, Research Triangle Park, 

NC, October. 

NTP-CERHR, 2003. National Toxicology Program – Center for the Evaluation of Risks to 

Human Reproduction. NTP-CERHR Monograph on the Potential Human Reproductive and 

Developmental Effects of Di-n-Butyl Phthalate (DBP). NIH Publication No. 03-4486. 

NYS (New York State), 1999. Assisting Communities to Improve Public Health. (Annual Report, 

1999-2000). Albany, NY: Center for Community Health, Department of Health. 

NYS DOH (New York State, Department of Health), 2003. Fact Sheet: Tetrachloroethylene 

(perc) in indoor air and outdoor air, May, 2003. Available from: 

http://www.health.state.ny.us/nysdoh/environ/btsa/fs_perc.pdf. 

ODOE (Oregon Department of Energy), 2004. Commissioning for Better Buildings in Oregon. 

Salem, OR. http://www.energy.state.or.us/bus/comm/bldgcx.htm. 

OEHHA (Office of Environmental Health Hazard Assessment), 1997. Health Effects of Exposure 

to Environmental Tobacco Smoke. Final Report. Available from: 

http://www.oehha.org/air/environmental_tobacco/finalets.html. 

OEHHA, 2000a. Acute reference exposure levels (RELs), averaging times, and toxicologic 

endpoints. Available from: http://www.oehha.ca.gov/air/acute_rels/allAcRELs.html. 

OEHHA, 2000b. Asbestos fact sheet available from 

http://www.oehha.ca.gov/public_info/facts/index.html. 

OEHHA, 2000c. Air Toxics Hot Spots Program Risk Assessment Guidelines Part III Technical 

Support document for the Determination of noncancer Chronic Reference exposure levels. 

Office of Environmental Health Hazard Assessment, California Environmental Protection 

Agency, April 2000. 

OEHHA, 2001. Prioritization of toxic air contaminants under the children’s environmental health 

protection act. OEHHA, Cal/U.S. EPA. October 2001. Available from: 

http://www.oehha.ca.gov/air/toxic_contaminants/SB25finalreport.html. 

OEHHA, 2002. Air toxics hot spots program risk assessment guidelines part two: technical 

support document for describing available cancer potency factors. OEHHA, Cal/U.S. EPA. April, 

1999. Available from: http://www.oehha.ca.gov/air/hot_spots/pdf/TSDNov2002.pdf. 

OEHHA, 2003a. All Chronic Reference Exposure Levels Adopted by OEHHA as of August 

2003. Available from: http://www.oehha.ca.gov/air/chronic_rels/AllChrels.html. 

OEHHA, 2003b. Proposed Identification of Environmental Tobacco Smoke as a Toxic Air 

Contaminant, Part B: Health Effects. November 2003. Public Review Draft. See also: Errata 

Page, March 3, 2004. http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm. 
Indoor Air Pollution in California July, 2005 

 224

OEHHA, 2004. Proposition 65 status report safe harbor levels: no significant risk levels for 

carcinogens and maximum allowable dose levels for chemicals causing reproductive toxicity. 

Available from: http://oehha.ca.gov/prop65/pdf/Jan2005StatusReport.pdf. 

OFEE (Office of the Federal Environmental Executive), 2005. Green Janitorial Products and 

Services. Washington, DC. http://www.ofee.gov/gp/greenjanitorial.html. 

Offermann FJ, May 2000, Indoor Air Quality Symposium: Risk Reduction in the 21st Century, 

Sacramento, CA. 

Offermann FJ, Colfer R, Radzinski P, and Robertson J, 2002. Exposure to environmental 

tobacco smoke in an automobile. Proc. Indoor Air. 506-511. 

Ostro BD, 1987. Air pollution and morbidity revisited: a specification test. J of Environmental 

Economics and Management 14: 87-98. 

Ostro BD, 1993. The association of air pollution and mortality: examining the case for inference. 

Arch Environ Health 48(5): 336-342. 

Ostro BD, and Rothschild S, 1989. Air pollution and acute respiratory morbidity: an 

observational study of multiple pollutants. Environ Res 50: 238-247. 

Ostro BD, Broadwin R, and Lipsett MJ, 2000. Coarse and fine particles and daily mortality in the 

Coachella Valley, California: a follow-up study. J Expos Analysis and Environ Epidemiology, 10: 

412-419. 

Ostro B, Lipsett M, Mann J, Braxton-Owens H, and White M, 2001. Air pollution and 

exacerbation of asthma in African-American children in Los Angeles. Epidemiol 12(2): 200-8. 

Ott W, Switzer P, and Robinson J, 1996. Particle concentrations inside a tavern before and after 

prohibition of smoking: Evaluating the performance of an indoor air quality model. J Air Waste 

Manag Assoc 46:1120-1134. 

Ott WR, and Roberts JW, 1998. Everyday Exposure to Toxic Pollutants. Sci Am February 1998: 

86-91. 

Ott W, Wallace L, and Mage D, 2000. Predicting particulate (PM10) personal exposure 

distributions using a random component superposition statistical model. JAir & Waste 

Management Assoc 50: 1390-1406. 

Ott WR, Klepeis NE, and Switzer P, 2003. Analytical solutions to compartmental indoor air 

quality models with application to environmental tobacco smoke concentrations measured in a 

house. J Air Waste Manag Assoc 53(8): 918-36. 

Otten JA, Burge HA, 1999. Viruses. Bioaerosols: Assessment and Control, ed. J. Macher, 

American Conference of Governmental Industrial Hygienists, Cincinnati, OH. 

Ozkaynak H, Xue J, Spengler J, Wallace L, Pellizzari E, Jenkins P, 1996a. Personal exposure 

to airborne particles and metals: results from the Particle TEAM study in Riverside, California. J 

Expo Anal Environ Epidemiol 6: 57-77. 
Indoor Air Pollution in California July, 2005 

 225

Ozkaynak H, Xue J, Weker R, Butler D, Koutrakis P, and Spengler J, 1996b. The Particle TEAM 

(PTEAM) study: analysis of the data. Report to the U.S. EPA, Volume III of Final Report. 

Pandian MD, Ott WR, Behar JV, 1993. Residential air change rates for use in indoor air and 

exposure modeling studies. J Expo Anal Environ Epidemiol 3(4): 407-16. 

Pandian MD, Behar JV, Ott WR, Wallace LA, Wilson AL, Colome SD, Koontz M, 1998. 

Correcting errors in the nationwide database of residential air change rates. J Expo Anal 

Environ Epidemiol (8)4: 577-586. 

Pang Y, MacIntosh DL, Camann DE, Ryan PB. 2002. Analysis of aggregate exposure to 

chlorpyrifos in the NHEXAS-Maryland investigation. Environ. Health Perspect. 110:235-240. 

Park J, Spengler JD, Yoon D, Dumyahn T, Lee K, and Ozkaynak H, 1998. Measurement of air 

exchange rate of stationary vehicles and estimation of in-vehicle exposure. J Expo Anal Environ 

Epidemiol 8: 1-9; 65-78. 

Pasanen A-L, Korpi J-P, Pasanen P, 1998. Critical aspects on the significance of microbial 

volatile metabolites as indoor air pollutants. Environment International 24: 703-712. 

Payne-Sturges DC, Burke TA, Breysse P, Diener-West M, and Buckley TJ, 2004. Personal 

exposure meets risk assessment: a comparison of measured and modeled exposures and risks 

in an urban community. Environmental Health Perspectives 112(5): 589-598. 

Peat JK, Dickerson J, Li J, 1998. Effects of damp and mould in the home on respiratory health: 

a review of the literature. Allergy 53:120-128. 

Peipins LA, Lewin M, Campolucci S, Lybarger JA, Miller A, Middleton D, Weis C, Spence M, 

Black B, and Kapil V, 2003. Radiographic abnormalities and exposure to asbestoscontaminated vermiculite in the community of Libby, Montana, USA. Environ Health Perspect

111(14): 1753-9. 

Pelham TW, Holt LE, and Moss MA, 2001. Exposure to carbon monoxide and nitrogen dioxide 

in enclosed ice areanas. Occup Environ Med 59: 224-233. 

Pelham TW, Holt LE, and Moss MA, 2002. Exposure to carbon monoxide and nitrogen dioxide 

in enclosed ice arenas. Occup Environ Med 59: 224-310. 

Pellizzari ED, Michael LC, Perritt K., Smith DJ, Hartwell TD, and Sebastik J, 1989. Development 

and Implementation of Exposure Assessment Procedures for Toxic Air Pollutants in Several Los 

Angeles County, CA Communities. Final report, ARB Contract No. A5-174-33. 

Penna MLF, and Duchiade MP, 1991. Air pollution and infant mortality from pneumonia in the 

Rio de Janeiro metropolitan area. Bulletin of PAHO 25: 47-54. 

Persily A, 2000. Estimation of indoor carbon monoxide levels due to emissions from residential 

gas ovens. Letter report to U.S. Consumer Product Safety Commission, December 12. 

Buildings and Fire Research Laboratory, National Institute of Standards and Technology, 

Gaithersburg, MD. 
Indoor Air Pollution in California July, 2005 

 226

Peters JM, Avol E, Navidi W, London SJ, Gauderman WJ, Lurmann F, Linn WS, Margolis H, 

Rappaport E, Gong H, and Thomas DC, 1999a. A study of twelve Southern California 

communities with differing levels and types of air pollution. I. Prevalence of respiratory 

morbidity. Am J Respir Crit Care Med 159(3):760-7. 

Peters JM, Avol E, Gauderman WJ, Linn WS, Navidi W, London SJ, Margolis H, Rappaport E, 

Vora H, Gong H Jr, and Thomas DC, 1999b. A study of twelve Southern California communities 

with differing levels and types of air pollution. II. Effects on pulmonary function. Am J Respir Crit 

Care Med 159(3): 768-75. 

Petreas M, She J, Brown FR, Winkler J, Windham G, Rogers E, Zhao G, Bhatia R, and Charles 

MJ, 2003. High body burdens of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in California 

women. Environ Health Perspect 111(9): 1175-9. 

Phillips TJ, Mulberg EJ, and Jenkins PL, 1990. Activity Patterns of California adults and 

adolescents: Appliance use, ventilation practices, and building occupancy. Proceedings, 

ACEEE 1990 Summer Study of Energy Efficiency in Buildings, Environment 4: 4.187-4.196. 

American Council for an Energy-Efficient Economy, Washington, DC. 

Phillips TJ, Jenkins PL, and Mulberg EJ, 1991. Children in California: activity patterns and 

presence of pollutant sources. Proceedings of the 84th Annual Meeting and Exhibition, Air & 

Waste Management Association, (17) Paper no. 91-172.5, June 1991. 

Phillips TJ, Bloudoff DP, Jenkins PL, and Stroud KR, 1999. Ozone emissions from a "personal 

air purifier". J Expo Anal Environ Epidemiol 9(6): 594-601. 

Pickrell J, Mokler B, Griffis L, Hobbs C, and Bathija A, 1983. Formaldehyde Release Rate 

Coefficients from Selected Consumer Products. Environ Sci Technol 17(12): 753-757. 

Pilotto LS, Nitschke M, Smith BJ, Pisaniello D, Ruffin RE, EcElroy HJ, Martin J, and Hiller JE, 

2003. Randomized controlled trial of unflued gas heater replacement on respiratory health of 

asthmatic school children. International Journal of Epidemiology. 33: 208-214. 

Pirkle JL, Flegal KM, Bernert JT, Brody DJ, Etzel RA, Maurer KR, 1996. Exposure of the US 

population to environmental tobacco smoke: the Third National Health and Nutrition 

Examination Survey, 1988 to 1991. JAMA 275(16): 1233-40. 

Pitts JN, Wallington TJ, Biermann HW, and Winer AM, 1985. Identification and measurement of 

nitrous acid in an indoor environment. Atmospheric Environment 19(5): 763-767. 

Pitts JN, Biermann HW, Tuazon EC, Green M, Long WE, and Winer AM, 1989. Time-resolved 

identification and measurement of indoor air pollutants by spectroscopic techniques: gaseous 

nitrous acid, methanol, formaldehyde and formic acid. JAPCA 39: 1344-1347. 

Platt SD, Martin CJ, Hunt SM, Lewis CW, 1989. Damp housing, mould growth, and 

symptomatic health state. BMJ. 298(6689): 1673-1678. As cited in Spengler et al., 1994. 

Platts-Mills TAE, and Carter MC, 1997. Asthma and indoor exposure to allergens. N Engl J Med 

336: 1382-1384. 
Indoor Air Pollution in California July, 2005 

 227

Plopper CG, and Thurlbeck WM, 1994. Growth, Aging, and Adaptation. Textbook of Respiratory 

Medicine, 2nd Edition. Eds., Murray and Nadel. W.B. Saunders, Philadelphia. 

Ponka A, Savela M, and VirtanenM, 1998. Mortality and air pollution in Helsinki. Arch Environ 

Health 53(4): 281-286. 

Pope CA, Dockery DW, Spengler JD, and Raizenne ME, 1991. Respiratory health and PM10

pollution. Am Rev Respir Dis 144: 668-674. 

Pope CA, Thun MJ, Namboodiri MM, Dockery DW, Evans JS, Speizer FE, and Heath CW, 

1995. Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults. 

Am J Respir Crit Care Med 151: 669-674. 

Poytress J, 2003. Maintenance and Operations, Clovis Unified School District, Clovis, CA. 

Personal communications. November 14. 

Ransom MR, Pope CA III, 1992. Elementary school absences and PM10 pollution in Utah 

Valley. Environ Res 58: 204-219. 

Raub JA, Mathieu-Nolf M, Hampson NB, and Thom SR, 2000. Carbon monoxide poisoning – a 

public health perspective. Toxicology 145: 1-14. 

Rayman RB, 2002. Cabin air quality. Aviat Space environ Med 73(3): 211-5, March 2002. 

Reiss R, Ryan PB, Koutrakis P, and Tibbetts SJ, 1995a. Ozone reactive chemistry on interior 

latex paint. Environ Sci Technol 29(8): 1906-12. 

Reiss R, Ryan PB, Tibbetts SJ, and Koutrakis P, 1995b. Measurement of organic acids, 

aldehydes, and ketones in residential environments and their relation to ozone. J Air Waste 

Manag Assoc 45(10): 811-22. 

Repace JL, 2003. An air quality survey of respirable particles and particulate carcinogens in 

Delaware hospitality venues before and after a smoking ban. Repace Associates, Inc., Bowie 

MD. 

Repair Clinic, 2004. Answers To Common Questions About Range Vent Hoods. 

http://www.repairclinic.com/0088_7_4.asp. 

Rhodes L, Bailey CM, and Moorman JE, 2002. Asthma prevalence and control characteristics 

by race/ethnicity. MMWR 53(07): 145-148. 

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5307a1.htm. 

Riley WJ, McKone TE, Lai ACK, and Nazaroff WW, 2002. Indoor particulate matter of outdoor 

origin: Importance of size-dependent removal mechanisms. Environ Sci & Technol 36: 200-207. 

[See errata on p. 1868.] 

Ritz B, Yu F, Chapa G, and Fruin S, 2000. Effect of air pollution on preterm birth among children 

born in Southern California between 1989 and 1993. Epidemiology 11(5): 502-511. 

Ritz, B., Yu, F., Fruin, S., Chapa, G., Shaw, G., Harris, J. (2002). Ambient air pollution and risk 

of birth defects in Southern California. Am. J. of Epidemiology. 1:17-25. 
Indoor Air Pollution in California July, 2005 

 228

Roberts JW, and Dickey P, 1995. Exposure of children to pollutants in house dust and indoor 

air. Rev Environ Contam Toxicol 143: 60-77. 

Rodes C, Sheldon L, Whitaker D, Clayton A, Fitzgerald K, Flanagan J, DiGenova F, Hering S, 

and Frazier C, 1998. Measuring concentrations of selected air pollutants inside California 

vehicles. Final Report to the California Air Resources Board, Contract no. 95-339, Sacramento, 

CA. 

Rodes CE, Lawless PA, Evans GF, Sheldon LS, Williams RW, Vette AF, Creason JP, and 

Walsh D, 2001. The relationships between personal PM exposures for elderly populations and 

indoor and outdoor concentrations for three retirement center scenarios. J Expo Anal Environ 

Epidemiol 11(2): 103-115. 

Roinestad KS, Louis JB, and Rosen JD, 1993. Determination of pesticides in indoor air and 

dust. J AOAC Int 76: 1121-1126. 

Rojas-Bracho L, Suh HH, and Koutrakis P, 2000. Relationships among personal, indoor, and 

outdoor fine and coarse particle concentrations for individuals with COPD. J Expo Anal Environ 

Epidemiol 10: 294-306. 

Rosenfeld AH, 1999. The Art of Energy Efficiency: Protecting the Environment with Better 

Technology. Ann Rev Energy Environ 24: 33-82. 

Rosenman KD, Reilly MJ, Schill DP, Valiante D, Flattery J, Harrison R, Reinisch F, Pechter E, 

Davis L, Tumpowsky CM, and Filios M, 2003. Cleaning products and work-related asthma. J 

Occup Environ Med 45: 556-563. 

Rosenstreich DL, Eggleston P, Kattan M, Baker D, Slavin RG, Gergen P, Mitchell H, McNiffMortimer K, Lynn H, Ownby D, Malveaux F, 1997. The role of cockroach allergy and exposure 

to cockroach allergen in causing morbidity among inner-city children with asthma. N Engl J Med 

336: 1356-13634. 

Rothenberg S, Nagy P, Pickrell J, and Hobbs C, 1989. Surface area, adsorption, and desorption 

studies on indoor dust samples. Am Ind Hyg Assoc J 50(1): 15-23. 

Rudel RA, Camann DE, Spengler JD, Korn LE, and Brody JG, 2003. Phthalates, alkylphenols, 

pesticides, polybrominated diphenyl ethers, and other endocrine-disrupting compounds in 

indoor air and dust. Environ Sci Technol 37(20): 4543-4553. 

Ryan TJ, Hart EM, and Kappler LL, 2002. VOC exposures in a mixed-use university art building. 

American Industrial Hygiene Association Journal 63: 703-708. 

Rylander R, Megevand T, 2000. Environmental risk factors for respiratory infections. Archives of 

Environ Health. 55(5):300-303. 

Salam MT, Li Y-F, Langholz B, Gilliland FD, 2003. Early-life environmental risk factors for 

asthma: findings from the Children’s Health Study. Environ Health Perspect 112(6): 760-765. 

Samet JM, Dominici F, Curriero FC, Coursac MS, and Zeger SL, 2000. Fine particulate air 

pollution and mortality in 20 U.S. cities 1987-1994. N Engl J Med 343(24): 1742-1749. 
Indoor Air Pollution in California July, 2005 

 229

Sarnat JA. Koutrakis P. and Suh HH. 2000. Assessing the relationship between personal 

particulate and gaseous exposures of senior citizens living in Baltimore, MD. J Air & Waste 

Management Assoc. 50(7):1184-1198. 

Sarpong SB, Wood RA, and Eggleston PA, 1996. Short-term effects of extermination and 

cleaning on cockroach allergen Bla g 2 in settled dust. Ann Allergy Asthma Immunol. Mar76(3):

257-60. 

Sarwar G, Olson DA, Corsi RL, and Weschler CJ, 2004. Indoor fine particles: the role of terpene 

emissions from consumer products. J Air and Waste Management Association 54: 367-377. 

SCAQMD (South Coast Air Quality Management District), 1983. RULE 1111. NOx Emissions 

From Natural-Gas-Fired, Fan-Type Central Furnaces. July 8. Diamond Bar, CA. 

http://www.aqmd.gov/rules/reg/reg11/r1111.pdf.

SCAQMD, 2004. Rule 1121 - Control Of Nitrogen Oxides From Residential Type, Natural GasFired Water Heaters. Rule 1121 Control Of Nitrogen Oxides From Residential Type, Natural 

Gas-Fired Water Heaters. Amended September 4. Diamond Bar, CA. 

http://www.aqmd.gov/rules/reg/reg11/r1121.pdf.

Schecter A, Pavuk M, PapkeO, Ryan JJ, Birnbaum L, and Rosen R, 2003. Polybrominated 

Diphenyl Ethers (PBDEs) in U.S. Mothers’ Milk. Environ Health Perspect 111(14): 1723-1729. 

Schelegle ES, and Adams WC, 1986. Reduced exercise time in competitive simulations 

consequent to low level ozone exposure. Med Sci Sports Exerc 18(4): 408-414. 

Schlapia A and Morris SS, 1998. Architectural, Behavioral and Environmental Factors 

Associated with VOCs in Anchorage Homes 98-A504, Anchorage Air Pollution Control Agency. 

Schneider M, 2002. Public School Facilities and Teaching: Washington, DC and Chicago. 

November 2002. A Report Prepared for the Neighborhood Capital Budget Group (NCBG). 

Available from: http://www.ncbg.org/press/press111302.htm. 

Schneider T, Sundell J, Bischof W, Bohgard M, Cherrie JW, Clausen PA, Dreborg S, Kildese J, 

Kjaergaard SK, Lovik M, Pasanen P, and Skyberg K, 2003. Europart. Airborne particles in the 

indoor environment. A European interdisciplinary review of scientific evidence on associations 

between exposure to particles in buildings and health effects. Indoor Air 13 (1): 38-48. 

Schwartz J, 1994. Air pollution and daily mortality: a review and meta analysis. Environ Res 64: 

36-52. 

Schwartz J, 1995. Air pollution and hospital admissions for cardiovascular disease in Detroit, 

Michigan. Am J Epidemiol 142(1):23-35. 

Schwartz J, 2003. Daily deaths associated with air pollution in six US cities and short-term 

mortality displacement in Boston in Health Effects Institute Special Report: Revised Analyses of 

Time-Series Studies of Air Pollution and Health. 

Schwartz J, and Neas M, 2000. Fine particles are more strongly associated than coarse 

particles with acute respiratory health effects in schoolchildren. Epidemiology 11(1): 6-10. 
Indoor Air Pollution in California July, 2005 

 230

Seal E, McDonnell WF, House DE, Salaam SA, Dewitt PJ, Butler SO, Green J, and Raggio L, 

1993. The pulmonary response of white and black adults to six concentrations of ozone. Am 

Rev Respir Dis 147: 804-810. 

Segawa, R, 2004. Personal communication to Peggy Jenkins, ARB, February 27, 2004. 

Segawa, R, 2005. Personal communication to Peggy Jenkins, ARB, March 28, 2005. 

Selway MD, Allen RJ, and Wadden RA, 1980. Ozone production from photocopying machines. 

Am Ind Hyg Assoc J 41(6): 455-9. 

Seppanen O, and Fisk WJ. 2002. Association of system with SBS symptoms in office workers. 

Indoor Air. 12(2): 98-112. 

Sexton K, Petreas MX, Liu KS, and Kulasingam GC, 1985. Formaldehyde concentrations 

measured in California mobile homes. For Presentation at the 78th Annual Meeting of the Air 

Pollution Control Association. 

Sexton K, Liu KS, and Petreas MX, 1986. Formaldehyde concentrations inside private 

residences: a mail-out approach to indoor air monitoring. Journal of the Air Pollution Control 

Association 36(6): 698-704. 

Sexton K, Adgate SJ, Ramachandran G, Pratt GC, Mongin SJ, Stock TH, and Morandi MT, 

2004. Comparison of personal, indoor, and outdoor exposures to hazardous air pollutants in 

three urban communities. Environ Sci Technol 38: 423-430. 

Sheldon LS, Handy RW, Hartwell TD, Whitmore RW, Zelon HS, and Pellizzari ED, 1988. Indoor 

air quality in public buildings: volume 1. U.S. EPA, Washington DC; U.S. EPA 600/6-88/009a. 

NTIS PB89-102503/AS. 

Sheldon L, Clayton A, Jones B, Keever J, Perritt R, Smith D, Whitaker D, and Whitmore R, 

1992a. Indoor Pollutant Concentrations and Exposures. Final report to ARB Contract No. A833-

156. 

Sheldon LS, Clayton CA, Keever J, Perritt RL, and Whitaker DA, 1992b. PTEAM: Monitoring of 

Phthalates and PAHs in Indoor and Outdoor Air Samples in Riverside, California - Volume 2. 

Final report to ARB, Contract No. A933-144. 

Sheldon LS, Clayton CA, Keever J, Perritt RL, and Whitaker DA, 1993. Indoor concentrations of 

polycyclic aromatic hydrocarbons in California Residences, ARB Contract No. A033-132. 

Shelton BG, Kirkland KH, Flanders WD, Morris GK, 2002. Profiles of airborne fungi in buildings 

and outdoor environments in the United States. Applied and Environmental Microbiology 

68(4):1743-1753. 

Shendell DG, Prill RP, Fisk WJ, Apte MG, Blake D, Faulkner D, 2003. Associations between 

classroom CO2 concentrations and student attendance. Indoor Air, 14 (5): 333-341. LBNL54413. Lawrence Berkeley National Laboratory. Berkeley, CA. 

http://eetd.lbl.gov/ied/pdf/LBNL-54413.pdf. 
Indoor Air Pollution in California July, 2005 

 231

Shendell DG, Winer AM, Weker R, Colome SD, 2004a. Evidence of inadequate ventilation in 

portable classrooms: results of a pilot study in Los Angeles County. 

Indoor Air 14(3):154-8. 

Shendell DG, Barnett C, and Boese, 2004b. Science-based recommendations to prevent or 

reduce potential exposures to biological, chemical, and physical agents in schools. J. School 

Health 74(10): 390-396. Also available as extended complete final report in PDF at: 

http://www.healthyschools.org/documents/HPSchlsWhtPpr.pdf 

Shepherd JL, Corsi RL, and Kemp J, 1996. Chloroform in Indoor Air and Wastewater: The Role 

of Residential Washing Machines. J Air Waste Manage Assoc 46(7): 631-642. 

Sheppard L, 2003. Ambient air pollution and non-elderly asthma hospital admissions in Seattle, 

Washington, 1987-1994 in Health Effects Institute Special Report: Revised Analyses of TimeSeries Studies of Air Pollution and Health. 

Sheppard L, Levy D, Norris G, Larson TV, and Koenig JQ, 1999. Effects of ambient air pollution 

on non-elderly asthma hospital admissions in Seattle, Washington. Epidemiology 10(1): 23-30. 

Sherman, M, 2003a. ASHRAE & Residential Ventilation. LBNL Report Number 53776, October. 

Energy Performance of Buildings Group, Indoor Environment Department, Environmental 

Energy Technology Division, Lawrence Berkeley National Laboratory. 

http://epb.lbl.gov/Publications/lbnl-53776.pdf. 

Sherman, M, 2003b. ASHRAE’s First Residential Ventilation Standard. LBNL Report Number 

54331. Energy Performance of Buildings Group, Indoor Environment Department, 

Environmental Energy Technology Division, Lawrence Berkeley National Laboratory. Berkeley, 

CA. http://epb.lbl.gov/Publications/lbnl-54331.pdf, 

Shields HC, Fleischer DM, and Weschler CJ, 1996. Comparisons among VOCs measured in 

three types of U.S. commercial buildings with different occupant densities. Indoor Air 6: 2-17. 

Siegmann K, and Sattler K, 1996. Aerosol from hot cooking oil, a possible health hazard. J 

Aerosol Science 27, Supplement 1: S493-S494. 

Simcox JJ, Fenske RA, Wolz SA, Lee IC, and Kalman D, 1995. Pesticides in household dust 

and soil: Exposure pathways for children of agricultural families. Environ Health Perspect 103: 

1126-1134. 

Singer BC, Hodgson, AT, Guevarra KS, Hawley KL, and Nazaroff WW, 2002. Gas-phase 

organics in environmental tobacco smoke. 1. Effects of smoking rate, ventilation, and furnishing 

level on emission factors. Environmental Science and Technology 35(5): 846-853. 

Singer BC, Hodgson AT and Nazaroff WW, 2003. Gas-phase organics in environmental tobacco 

smoke: 2. Exposure-relevant emission factors and indirect exposures from habitual smoking. 

Atmospheric Environment 37: 5551-5561. 

SJVUAPCD (San Joaquin Valley Unified Air Pollution Control District), 2003. Rule 4901 - Wood 

Burning Fireplaces And Wood Burning Heaters. 

http://www.arb.ca.gov/drdb/sju/curhtml/r4901.pdf. Fresno, CA. 
Indoor Air Pollution in California July, 2005 

 232

Smith DH, Malone DC, Lawson KA, Okamoto LJ, Battista C, and Saunders WB, 1997. A 

national estimate of the economic cost of asthma. Am J Respir Crit Care Med 156: 787-793. 

Smith K, 1988. Air Pollution: Assessing Total Exposure in the United States. Environment 30(8): 

10-38. 

Song BJ, Liu AH, 2003. Metropolitan endotoxin exposure, allergy and asthma. Curr Opin Allergy 

Clin Immunol 3:331-335. 

Soukup JM, and Becker S, 2001. Human alveolar macrophage responses to air pollution 

particulates are associated with insoluble components of coarse material, including particulate 

endotoxin. Toxicol Appl Pharmacol 171(1): 20-26. 

Sparks LE, Guo Z, Change JC, and Tichenor BA, 1999. Volatile organic compound emissions 

from latex paint-part 1. Chamber experiments and source model development. Indoor Air 9:10-

17. 

Spengler JD, Dockery DW, Turner WA, Wolfson JM, Ferris BG, 1981. Long-term measurements 

of respirable sulfates and particles inside and outside homes. Atmos Environ. 15:23-30. 

Spengler J, Brauer M, Samet JM, and Lambert WE, 1993. Nitrous acid in Albuquerque, New 

Mexico homes. Environ. Sci. Technol. 27: 841-845. 

Spengler J, Neas L, Nakai S, Dockery D, Speizer F, Ware J, and Raizenne M, 1994a. 

Respiratory symptoms and housing characteristics. Indoor Air 4: 72-82. 

Spengler J, Schwat M, Billick I, Colome S, Wilson A L, and Becker E, 1994b. Personal exposure 

to nitrogen dioxide in the Los Angeles Basin. J. Air Waste Manage. Assoc. 44: 39-47. 

Spengler JD, and Chen Q, 2000. Indoor Air Quality Factors in Designing a Health Building. Ann 

Rev Energy Environ 25: 567-601. 

Spengler JD, Samet JM, and McCarthy JF, 2001. Indoor Air Quality Handbook. McGraw-Hill. 

New York. 

Spengler JD, Ludwig S, Weker RA, 2004. Ozone exposures during trans-continental and transPacific flights. Indoor Air 14 (Suppl) 7: 67-73. 

Spicer CW, Kenny DV, Ward, GF, and Billick IH, 1993. Transformations, lifetimes, and sources 

of NO2, HONO, and HNO3 in indoor environments. J. Air Waste Manage. Assoc. 43: 1479-1485. 

Springston JP, Esposito WA, and Cleversey KW, 2002. Baseline indoor air quality 

measurements collected from 136 metropolitan New York region commercial office buildings 

between 1997-1999. Am Ind Hyg Assoc J 63(3): 354-60. 

State of California, 2002. Exhibit c: energy efficiency and sustainable building measures tiers 

one and two. State of California standard agreement, STD 2 RESD. July 2001. Available from: 

http://www.ciwmb.ca.gov/greenbuilding/design/Tiers.pdf. 
Indoor Air Pollution in California July, 2005 

 233

State of Washington, 2003. Washington State Ventilation and Indoor Air Quality Code (2003 

Edition), Section 51-13. Washington State Building Code Council, Olympia, WA. 

ftp://198.147.238.10/energy.wsu.edu/pubs/code/2003VIAQ.pdf. 

Stefaniak AB, Breysse PN, Murray PM, Rooney BC, and Schaefer J, 2000. An evaluation of 

employee exposure to volatile organic compounds in three photocopy centers. Environmental 

Research Section A 83:162-173. 

Storey E, Dangman KH, Schenck P, DeBernardo RL, Yang CS, Bracker A and Hodgson MJ, 

2004. Guidance for Clinicians on the Recognition and Management of Health Effects Related to 

Mold Exposure and Moisture Indoors. Farmington, CT, Center for Indoor Environments and 

Health at UConn Health Center. http://www.oehc.uchc.edu/clinser/MOLD%20GUIDE.pdf. 

Strandberg B, Dodder NG, Basu I, and Hites RA, 2001. Concentrations and spatial variations of 

polybrominated diphenyl ethers and other organohalogen compounds in Great Lakes air. 

Environ Sci Technol 35(6):1078-83. 

Stratton J, April 1997, Press Release 27-97, California Department of Health Services, 

Sacramento, CA. 

Suh H, 2003. Characterization of the composition of personal, indoor, and outdoor particulate 

matter exposures. Final report to ARB for contract number 98-330. 

Suh H, Koutrakis P, 2004. Detailed characterization of indoor and personal particulate matter 

concentrations. Final report to ARB for contract number 00-302. 

Summerbell RC, 2001. Respiratory tract infections caused by indoor fungi. In: Microorganisms 

in Home and Indoor Work Environments. Editors: B Flannigan, RA Samson, JD Miller. Taylor & 

Francis. New York, NY. 

Sutton PM, Athanasoulis M, Flessel P, Guirguis G, Haan M, Schlag R, Goldman LR, 1995. 

Lead levels in the household environment of children in high-risk communities in California. 

Environ Res. 68(1):45-57. 

Swan SH, Beaumont JJ, Hammond SK, VonBehren J, Green RS, Hallock MF, Woskie SR, 

Hines CJ, and Schenker MB, 1995. Historical cohort study of spontaneous abortion among 

fabrication workers in the semiconductor health study: agent-level analysis. American J 

Industrial Medicine 28: 751-769. 

Switzer P, Klepeis N, and Ott W, 2001. Quantification of population exposure to secondhand 

smoke. Final Report (Grant 6RT-0118) submitted to the Tobacco-Related Disease Research 

Program of the University of California. 

Takaro TK, Krieger JW, and Song L, 2004. Effect of environmental interventions to reduce 

exposure to asthma triggers children in Seattle. J Expo Anal Environ Epidemiol 14(Suppl1): 

s133-43. 

Tenbrinke JT, Selvin S, Hodgson AT, Fisk WJ, Mendell MJ, Koshland CP, and Daisey JM, 

1998. Development of new volatile organic compound (voc) exposure metrics and their 

relationship to “Sick Building Syndrome” symptoms. Indoor Air 8: 140-152. 
Indoor Air Pollution in California July, 2005 

 234

Thacker SB, Hoffman DA, Smith J, Steinberg K, and Zack M, 1992. Effect of low-level body 

burdens of lead on the mental development of children: limitations of meta-analysis in a review 

of longitudinal data. Arch Environ Health 47(5):336-46. 

Thatcher TL, and Layton DW, 1995. Deposition, resuspension, and penetrations of particles 

within a residence. Atmos Environ 29(13): 1487-1497. 

Thayer MA, Chestnut LG, Laza JK, and Van Den Eeden SK, 2003. The economic value of 

respiratory and cardiovascular hospitalizations. San Diego State University. Report prepared for 

the California Air Resources Board and California Environmental Protection Agency. 

ftp://ftp.arb.ca.gov/carbis/research/apr/past/99-329.pdf. 

Thomas KW, Pellizzari ED, Clayton CA, Perritt RL, Dietz RN, Goodrich RW, Nelson WC and 

Thomas LA, 1993. Temporal variability of benzene exposures for residents in several New 

Jersey homes with attached garages or tobacco smoke. J Exposure Analysis and 

Environmental Epidemiology 3(1):49-73. 

Thompson WW, Shay DK, Weintraub E, Brammer L, Cox N, Anderson LJ, Fukuda K, 2003. 

Mortality associated with influenza and respiratory syncytial virus in the United States. J Am 

Med Assoc 289: 179-186. 

Thurlbeck WM, 1988. Growth, Aging, and Adaptation. In: Murray, JF, Nadel JA, editors: 

Textbook of Respiratory Medicine, Philadelphia, 1988. W.B. Saunders Company, 37-46. 

Thurston GD, Lippmann M, Scott MB, and Fine JM, 1997. Summertime haze air pollution and 

children with asthma. Am J Respir Crit Care Med 155: 654-660. 

Tichenor, BA, 1989. Measurement of organic compound emissions using small test chambers. 

Environment International (15): 389-396. 

Tichenor, BA, and Mason, MA, 1988. Organic emissions from consumer products and building 

materials to the indoor environment. Journal of the Air Pollution Control Association 38: 264-

268. 

Townsend CL, and Maynard RL, 2002. Effects on health of prolonged exposure to low 

concentrations of carbon monoxide. Occup Environ Med 59: 708-714. 

Traynor GW, 1999. Evaluation of technical literature, indoor air pollution modeling, options for 

California standards, and recommended standards. Implementation of SB 798: development of 

standards for unvented gas logs and decorative fireplaces. T. Marshall Associated, Ltd., 

Pleasanton, CA. Prepared for the California Department of Health Services, Indoor Air Quality 

Section, Berkeley, CA. 

 

Traynor GW, Apte MG, Carruthers AR, Dillworth JF, Grimsrud DT, and Gundel LA, 1987. Indoor 

air pollution due to emissions from woodburning stoves. Environ Sci Technol 21(7): 691-697. 

Tsai FC, 2005. Submittal to Peggy Jenkins, ARB, AB1173 Radon (DHS), February 16, 2005. 

Tsai FC, and Waldman JM, 2005. The California Sierra Radon Study. Environmental Health 

Laboratory Report CA/DHS/EHLB/R-173. CA Department of Health Services. 850 Marina Bay 

Parkway. Richmond, CA 94804. 
Indoor Air Pollution in California July, 2005 

 235

Tsai PY and Weisel CP, 2000. Penetration of evaporative emissions into a home from an M85-

fueled vehicle parked in an attached garage. J Air and Waste Management Association 50(3):

371-377. 

Tsongas G, Hager WD, 1994. Field monitoring of elevated carbon monoxide production from 

residential gas ovens. In: Proceedings of the American Society of Heating, Refrigerating, and 

Air-Conditioning Engineers, Inc, Indoor Air Quality ‘94 Conference. Atlanta, Georgia: American 

Society of Heating, Refrigerating, and Air-Conditioning Engineers, Inc, 1994. 

Tsongas G, 1995. Carbon Monoxide from Ovens: A Serious IAQ Problem. Home Energy 

Magazine, September/October. Available at: http://hem.dis.anl.gov/eehem/95/950907.html. 

Tuomainen A, Seuri M, Sieppi A, 2004. Indoor air quality and health problems associated with 

damp floor coverings. Int Arch Occup Environ Health 77:222-226. 

Turk BH, Brown JT, Geisling-Sobotka K, Froehlich DA, Grimsrud DT, Harrison J, Koonce JF, 

Prill RJ, and Revsan KL, 1987. Indoor air quality and ventilation measurements in 38 Pacific 

Northwest commercial buildings. Volume I: measurement results and interpretation. Lawrence 

Berkeley Laboratory; Final report, LBL-22315. 

UL (Underwriters Laboratory), 2002. Standard 2034, Standard for Single and Multiple Station 

Carbon Monoxide Alarms, ANSI Approved. Northbrook, IL. 

USCB (U.S. Census Bureau), 1990. American Fact Finder: 1990 Summary Tape File 1 (STF 1) 

- 100-Percent data. http://factfinder.census.gov/metadoc/1990stf1td.pdf. 

USCB (U.S. Census Bureau), 2002. Statistical abstract of the United States. 

http://www.census.gov/prod/www/statistical-abstract-04.html. 

USCB (U.S. Census Bureau), 2002. The American Housing Survey. 

http://www.census.gov/hhes/www/ahs.html. 

USCB, 2003. California: 2000. Summary Social, Economic, and Housing Characteristics, 2000 

Census of Population and Housing. March 2003. PHC-2-6. 

http://www.census.gov/census2000/states/ca.html. 

U.S. DHHS (Department of Health and Human Services), 1986. The health consequences of 

Involuntary smoking: A report of the Surgeon General. U.S. DHHS, Public Health Service, 

Centers for Disease Control. DHHS Publication No. (CDC) 87-8398. 

U.S. DHHS, 1989. Reducing the health consequences of smoking. 25 years of progress: A 

report of the Surgeon General. U.S. DHHS, Centers for Disease Control, Center for Chronic 

Disease Prevention and Health Promotion, Office on Smoking and Health. DHHS Publication 

No. (CDC) 89-8411. 

U.S. DOE (Department of Energy), 2003a. California weatherization and low-income energy 

programs. Washington, DC. 

http://www.eere.energy.gov/weatherization/cfm/index.cfm/state_abbr=ca. 
Indoor Air Pollution in California July, 2005 

 236

U.S. DOE, 2003b. Weatherization Assistance Program Guidelines & Procedures. Washington, 

DC. http://www.eere.energy.gov/weatherization/prog_guide.html. 

U.S. EPA (Environmental Protection Agency), 1984. Health effects assessment for 

benzo(a)pyrene, Cincinnati, OH: Environmental Criteria and Assessment Office, EPA 540/1-86-

022, PB86-134335. 

U.S. EPA, 1987a. Unfinished Business: A Comparative Assessment of Environmental Problems 

(Overview report and 4 volumes), US Environmental Protection Agency, Office of Policy 

analysis, Office of Policy, Planning and Evaluation, Washington DC, February 1987. 

U.S. EPA, 1987b. Assessment of health risks to garment workers and certain home residents 

from exposure to formaldehyde. Office of Pesticides and Toxic Substances. 

U.S. EPA, 1987c. Locating and estimating air emissions from sources of polycyclic organic 

matter (POM). EPA 540/1-86-022, PB86-134335. 

U.S. EPA, 1989. Risk assessment guidance for Superfund Human Health Evaluation Manual 1

(U.S. EPA/540/1-89/002). 

U.S. EPA, 1991. Building Air Quality: A Guide for Building and Facility Managers. Washington, 

DC. http://www.epa.gov/iaq/largebldgs/baqtoc.html. 

U.S. EPA, 1992. Respiratory health effects of passive smoking: Lung cancer and other 

disorders. U.S. EPA/600/6-90/006F. U.S. EPA Office of Research and Development, 

Washington, DC. 

U.S. EPA, 1994. Health effects notebook for hazardous air pollutants. Available at 

http://www.epa.gov/ttn/atw/hapindex.html. Air Risk Information Support Center (Air RISC), 

Research Triangle Park, North Carolina. Contract No. 68-D2-0065. 

U.S. EPA, 1995. Office equipment: design, indoor air emissions, and pollution prevention 

opportunities. Washington, DC: Office of Research and Development; 1995. Report no. 

EPA/600/R-95/045. 

U.S. EPA, 1996. Safe Drinking Water Act: Amendments of 1996. 

Available from: http://www.U.S. EPA.gov/safewater/sdwa/sdwa.html. 

U.S. EPA, 1997a. Summary and assessment of published information on determining lead 

exposures and mitigating lead hazards associated with dust and soil in residential carpets, 

furniture, and forced air ducts. Washington, D.C.: Office of Pollution Prevention and Toxics, 

USEPA. EPA 747-S-97-001. 

U.S. EPA, 1997b. An Office Building Occupant's Guide to Indoor Air Quality. Washington, DC. 

http://www.epa.gov/iaq/pubs/occupgd.html. 

U.S. EPA, 1998. Building Air Quality (BAQ) Action Plan. (EPA/402-K-98-001, DHHS (NIOSH) 

Pub. No. 98-123). Available from: http://www.epa.gov/iaq/largebldgs/actionpl.html. 
Indoor Air Pollution in California July, 2005 

 237

U.S. EPA, 1999a. Transport of Lawn-Applied 2,4-D from turf to home: Assessing the relative 

importance of transport mechanisms and exposure pathways. U.S. EPA 600-R-99-040. 

Research Triangle Park, NC. 

U.S. EPA, 1999b. Reducing Mercury Use in Healthcare: Promoting a Healthier Environment. 

Available at http://www.epa.gov/glnpo/bnsdocs/merchealth/. 

U.S. EPA, 1999c. Integrated Risk Information System, Ethylene glycol monobutyl ether 

(EGBE)(2-Butoxyethanol) (CASRN 111-76-2), http://www.epa.gov/iris/subst/0500.htm#refinhal. 

U.S. EPA, 2000a. Case Studies - G.W. Carver and Charles Drew Elementary Schools. U.S. 

EPA 402-F-00-010A. August 2000. http://www.epa.gov/iaq/schools/pdf_files/gwcarver.pdf. 

U.S. EPA, 2000b. Case Study: Little Harbour School, Portsmouth School Department, 

Portsmouth, New Hampshire. http://www.epa.gov/cgi-bin/claritgw?opDisplay&document=clserv:OAR:0038;&rank=4&template=epa. 

U.S. EPA, 2000c. Final Rulemaking Documents and Fact Sheets. Control of air pollution from 

new motor vehicles: Heavy-duty engine and vehicle standards and highway diesel fuel sulfur 

control Requirements. Regulatory Impact Analysis (U.S. EPA420-R-00-026), Chapter VII: 

Benefit-Cost Analysis. http://www.epa.gov/otaq/diesel.htm#documents. P. VII-50. 

U.S. EPA, 2000d. Chlorpyrifos Revised Risk Assessment and Agreement with Registrants. 

Available from: http://www.epa.gov/pesticides/op/chlorpyrifos/agreement.pdf. 

U.S. EPA, 2000e. Proposed Radon in Drinking Water Rule. U.S. EPA 815-F-99-009. Available 

from: http://www.U.S. EPA.gov/safewater/radon/proposal.html. 

U.S. EPA, 2000f. DDT. Persistent bioaccumulative and toxic (PHT) chemical program, 

http://www.epa.gov/pbt/ddt.htm. 

U.S. EPA, 2000g. Aldrin/Dieldrin. Persistent bioaccumulative and toxic (PBT) chemical program, 

http://www.epa.gov/pbt/aldrin.htm. 

U.S. EPA, 2001a. Diazinon Revised Risk Assessment and Agreement with Registrants. 

Available from: http://www.epa.gov/pesticides/op/diazinon/agreement.pdf. 

U.S. EPA, 2001b. Mold Remediation in Schools and Commercial Buildings. (U.S. EPA/402/K01/001) Washington, DC. Available at http://www.epa.gov/mold/images/moldremediation.pdf. 

U.S. EPA, 2002a. A Citizen's Guide to Radon: The Guide to Protecting Yourself and Your 

Family From Radon (4th edition). U.S. EPA 402-K02-006. Available from: 

http://www.U.S. EPA.gov/iaq/radon/pubs/citguide.html. 

U.S. EPA, 2002b. Cost of Illness Handbook; U.S. Environmental Protection Agency, 

http://www.epa.gov/oppt/coi/toc.html. 

U.S. EPA, 2003a. Building Assessment Survey and Evaluation (BASE) Study. Available from: 

http://www.epa.gov/iaq/largebldgs/base/base_publications.html. 
Indoor Air Pollution in California July, 2005 

 238

U.S. EPA, 2003b. IAQ Design Tools for Schools. Available from: 

http://www.epa.gov/iaq/schooldesign/.

U.S. EPA, 2003c. EPA Assessment of Risks from Radon in Home. EPA 402-R-03-003. Office of 

Air and Radiation. Washington, D.C. http://www.epa.gov/radon/risk_assessment.html. 

U. S. EPA, 2004a. National Ambient Air Quality Standards. Available at: 

http://www.epa.gov/air/criteria.html. 

U.S. EPA, 2004b. Ozone Generators that are Sold as Air Cleaners: An Assessment of 

Effectiveness and Health Consequences. http://www.epa.gov/iaq/pubs/ozonegen.html.

U.S. Green Building Council, 2004. Green Building Rating System: For Existing Buildings 

Operations and Upgrades (LEED-EB). Available from: 

http://www.usgbc.org/Docs/LEEDdocs/PublicCommentDraftLEED-EB20040223.pdf. 

Van Alphen, 1999. Emission testing and inhalational exposure-based risk assessment for 

candles having Pb metal wick cores. The Science of the Total Environment 243/244: 53-65. 

Verhoeff AP, Burge HA, 1997. Health risk assessment of fungi in home environments. Ann 

Allergy Asthma Immunol 78: 544-556. 

Vette A, Rea A, Lawless P, Rodes C, Evans G, Highsmith R, and Sheldon L, 2001. 

Characterization of indoor-outdoor aerosol concentration relationships during the Fresno PM 

exposure studies. Aerosol Sci Technol 34: 118-126. 

Viberg H, Fredriksson A, and Jakobsson E, 2000. Developmental neurotoxic effects of 

2,2,4,4,5-pentabromodiphenyl ether (PBDE 99) in the neonatal mouse. Toxicologist 54: 1360. 

Viberg H, Fredrikkson A, Jakobsson E, Ohrn U, and Eriksson P, 2001. Brominated flameretardant: uptake, retention and developmental nurotoxic effects of decabromo-diphenyl ether 

(PBDE 209) in the neonatal. Toxicologist 61: 1034 (abstract). 

Vogelzang PFJ, Joost WJ, van der Gulden J, Fogering H, Kolk JJ, Heederik D, Preller L, Tielen 

MHM, van Schyck CP, 1998. Endotoxin exposure as a major determinant of lung function 

decline in pig farmers. Amer J Resp Crit Care Med 157: 15-18. 

Volberg DI, Surgan MH, Jaffe S, Hamer D, and Sevinsky JA, 1993. Pesticides in Schools: 

Reducing the Risks. New York, NY: New York Office of the Attorney General. 

Vu-Duc T, and Huynh C, 1989. Sidestream tobacco smoke constituents in indoor air modeled in 

an experimental chamber – polycyclic aromatic hydrocarbons. Environ Int 15: 57-64. 

Wainman T, Zhang J, Weschler CJ, and Lioy PJ, 2000. Ozone and limonene in indoor air: a 

source of submicron particle exposure. Environ Health Perspect 108(12): 1139-45. 

Waldman J, 2004. Submittal to Peggy Jenkins, ARB, AB1173-Section on Rn Risk, oCTOBER 

26, 2004. 

 
Indoor Air Pollution in California July, 2005 

 239

Waldman JM, Buckley TJ, and Lioy PJ, 1989. Indoor and outdoor levels of benzo(a)pyrene in a 

community of older homes. For presentation at the 82nd annual meeting, Air and Waste 

Management Association, Anaheim, CA, June 25-30, 1989. 

Waldman JM, and Liu KS, 1996. Unintentional Carbon Monoxide Poisoning in California: 

Determining Risk Factors for Deaths and Hospitalization. Presented at the 6th annual 

conference of the International Society of Exposure Analysis, New Orleans. 

Wallace LA, 1987. The Total Exposure Assessment Methodology (TEAM) Study, Project 

Summary, EPA/600/S6-87/002. U.S. Environmental Protection Agency, Washington, D.C. 

Wallace L, 1991. Comparison of risks from outdoor and indoor exposure to toxic chemicals. 

Environ Health Perspect 95: 7-13. 

Wallace L, 1993. A decade of studies of human exposure: what have we learned? Risk Anal 

13(2): 135-139. 

Wallace L, 1996a. Indoor particles: a review. J Air Waste Manage Assoc 46: 98-126. 

Wallace L, 1996b. Environmental Exposure to Benzene: An Update. Environ Health Perspect

104(6): 1129- 1136. 

Wallace L, 2000a. Correlations of personal exposure to particles with outdoor air 

measurements: a review of recent studies. Aerosol Sci Technol 32: 15-25. 

Wallace LA, 2000b. Real-time monitoring of particles, PAH, and CO in an occupied townhouse. 

Appl Occup Environ Hyp 15: 39-47. 

Wallace LA, 2001. Human exposure to volatile organic pollutants: implications for indoor air 

studies. Ann Rev Energy Environ 26: 269-301. 

Wallace L, Pellizzari E, Hartwell TD, Sparacino C, Whitmore R, Sheldon L, Zelon H, and Perritt 

R, 1987a. The TEAM study: personal exposures to toxic substances in air, drinking, water, and 

breath of 400 residents of New Jersey, North Carolina, and North Dakota. Environ Res 43: 290-

307. 

Wallace L, Pellizzari E, Leaderer B, Zelon H, and Sheldon L, 1987b. Emissions of volatile 

organic compounds from building materials and consumer products. Atmos Environ 21(2): 385-

393. 

Wallace L, Pellizzari E, Hartwell TD, Whitmore R, Zelon H, Perritt R, and Sheldon L, 1988. The 

California team study: breath concentrations and personal exposures to 26 volatile compounds 

in air and drinking water of 188 residents of Los Angeles, Antioch, and Pittsburgh, CA. Atmos 

Environ 22(10): 2141-2163. 

Wallace LA, Pellizzari ED, Hartwell TD, Davis V, Michael LC, and Whitmore RW, 1989. The 

influence of personal activities on exposure to volatile organic compounds. Environmental 

Research 50: 37-55. 
Indoor Air Pollution in California July, 2005 

 240

Wallace L, Nelson WC, Ziegenfus R, and Pellizzari E, 1991a. The Los Angeles TEAM study: 

personal exposures, indoor-outdoor air concentrations and breath concentrations of 25 volatile 

organic compounds. J Expo Anal Environ Epidemiol 1: 37-72. 

Wallace, LA, William N, Ziegenfus R, Pellizzari ED, Michael LC, Zelon H, Hartwell T, Perritt R, 

and Westerdahl D, 1991c. The Los Angeles TEAM study: Personal exposures, indoor-outdoor 

air concentrations, and breath concentrations of 25 volatile organic compounds. J Expo Anal 

Environ Epidemiol 1(2): 157-192. 

Wallace LA, Mitchell H, O’Connor GT, Neas L, Lippmann M, Kattan M, Koenig J, Stout JW, 

Vaughan BJ, Wallace D, Walter M, Adams K, and Liu L-JS, 2003. Particle concentrations in 

inner-city homes of children with asthma: the effect of smoking, cooking, and outdoor pollution. 

Environ Health Perspect 111: 1265-1272. 

Wallace LA, Emmerich SJ, and Howard-Reed C, 2004. Effect of central fans and in-duct filters 

on deposition rates of ultrafine and fine particles in an occupied townhouse. Atmospheric 

Environment, 38(4): 405-413. 

Wargocki P, Wyon DP, Yong KB, Clausen G, and Fanger PO, 1999. Perceived Air Quality, Sick 

Building Syndrome (SBS) Symptoms and Productivity in an Office with Two Different Pollution 

Loads. Indoor Air 9: 165-179. 

Wargocki P, Sundell J, Bischof W, Brundrett G, Fanger PO, Gyntelberg F, Hanssen SO, 

Harrison P, Pickering A, Seppanen O, and Wouters P, 2002. Ventilation and health in nonindustrial indoor environments: report from a European Multidisciplinary Scientific Consensus 

Meeting (EUROVEN). Indoor Air 12: 113-128. 

Wargocki P, and Djukanovic R, 2003. Estimate of an economic benefit from investment in 

improved indoor air quality in an office building. Proceedings of the Healthy Buildings 2003 

Conference, Singapore 3: 382-387. Singapore, NUS. 

Warner JA, Frederick JM, Bryant TN, Weich C, Raw GJ, Hunter C, Stephen FR, McIntyre DA, 

Warner JO, 2000. Mechanical ventilation and high-efficiency vacuum cleaning: A combined 

strategy of mite and mite allergen reduction in the control of mite-sensitive asthma. School of 

Medicine Allergy and Inflammation Sciences Division (Child Health), University of Southampton, 

United Kingdom. J Allergy Clin Immunol 105(1 Pt 1): 75-82. 

Washington DOH, 1995. School Indoor Air Quality Best Management Practices Manual. 

Washington State Department of Health, Community Environmental Health Programs, Olympia. 

Wasson SJ, Guo Z, McBrian JA, and Beach LO, 2002. Lead in candle emissions. Sci Total 

Environ 296: 159-174. 

Weiss KB, and Sullivan SD, 2001. The health economics of asthma and rhinitis: I, assessing the 

economic impact. J Allergy Clin Immunol 107(1): 3-8. 

Weschler CJ, 2000. Ozone in indoor environments: concentration and chemistry. Indoor Air. 

10(4): 269-88. 

Weschler CJ, 2004. Chemical reactions among indoor pollutants: what we’ve learned in the new 

millennium. Indoor Air 14 (Supplement 7): 184-194. 
Indoor Air Pollution in California July, 2005 

 241

Weschler CJ and Shields HC, 1994. Indoor chemistry involving O3, NO, and NO2 as evidenced 

by 14 months of measurements at a site in southern California. Environ. Sci. Technol. 28: 2120-

2132. 

Weschler CJ, and Shields HC, 1996. Production of the hydroxyl radical in indoor air. 

Environmental Science and Technology 30: 3250-3258. 

Weschler CJ, and Shields HC, 1997. Potential reactions among indoor pollutants. Atmos 

Environ 31(21): 3487-3495. 

Weschler CJ, and Shields HC, 1999. Indoor ozone/terpene reactions as a source of indoor 

particles. Atmos Environ 33: 2301-2312. 

Weschler CJ, Shields HC, and Naik DV, 1989. Indoor ozone exposures. J Air Pollut Control 

Assoc 39(12): 1562-8. 

Weschler, CJ, Hodgson, AT, and Wooley, JD, 1992. Indoor chemistry: ozone, volatile organic 

compounds and carpets. Environ Sci Technol 26: 2371-2377. 

Weschler, CJ, Shields HC, and Naik DV, 1994. Indoor chemistry involving O3, NO, and NO2 as 

evidenced by 14 months of measurements at a site in Southern California. Environ Sci Technol

28: 2120-2132. 

Whitehouse A, 2000. Asbestos-related disease in the community of Libby. Presented at the 

Libby Asbestos Exposure Scientific Council Meeting, 22 February 2000, Cincinnati, OH. 

Whitmore RW, Immerman FW, Camann DE, Bond AE, Lewis RG, and Schaum JL, 1994. Nonoccupational exposures to pesticides for residents of two U.S. cities. Arch Environ Contam 

Toxicol 26(1): 47-59. 

Whitmore RW, Clayton A, Phillips M, Akland G, 2003. California Portable Classrooms Study, 

Final Report. 3 Vols. Prepared by Research Triangle Institute. Final Report to ARB for Contract 

No. 00-317. : http://www.arb.ca.gov/research/indoor/pcs/pcs-fr/pcs-fr.htm. 

Whittemore AS, and Korn EL, 1980. Asthma and air pollution in the Los Angeles area. Am J 

Public Health 70(7): 687-696. 

WHO (World Health Organization), 1990. Environmental Health Criteria 101. Methylmercury. 

Available at http://www.inchem.org/documents/ehc/ehc/ehc101.htm, December 29, 2003. 

WHO, 2000. Air Quality Guidelines for Europe. WHO Regional Publications, European Series, 

No. 91. Copenhagen, Denmark. http://www.euro.who.int/air/Activities/20020620_1. 

WHO, 2002. The World Health Report 2002, Reducing Risks, Promoting Healthy Life, World 

Health Organization, Geneva, Switzerland. 

Wiglusz R, Igielska B, Sitko E, Nikel G, Jarnuszkiewicz I, 1998. Emission of volatile organic 

compounds (VOCs) from PVC flooring coverings. Bull Inst Marit Trop Med 49: 101-107. 
Indoor Air Pollution in California July, 2005 

 242

Wiley JA, Robinson JP, Cheng YT, Piazza T, Stork L, and Pladsen K, 1991a. Study of 

Children’s Activity Patterns. Final report, ARB Contract No. A733-149. 

Wiley JA, Robinson JP, Piazza T, Garrett K, Cirksena K, and Martin G, 1991b. Activity Patterns 

of California Residents. Final report, ARB Contract No. A6-177-33. 

Wilkins CK, Clausen PA, Wolkoff P, Larsen ST, Hammer M, Larsen K, Hansen V, and Nielsen 

GD, 2001. Formation of strong airway irritants in mixtures of isoprene/ozone and 

isoprene/ozone/nitrogen dioxide. Environ Health Perspect 109(9): 937-941. 

Williams R, Suggs J, Evans G, Creason J, Kwok R, Rodes C, Lawless P, and Sheldon L, 

2000a. Indoor, outdoor, and personal exposure monitoring of particulate air pollution: The 

Baltimore elderly epidemiology-exposure pilot study. Atmos Environ 34: 4193-4204. 

Williams R, Suggs J, Evans G, Creason J, Kwok R, Rodes C, Lawless P, and Sheldon L, 

2000b. The 1998 Baltimore particulate matter epidemiology-exposure study: part 1. Comparison 

of ambient, residential outdoor, indoor and apartment particulate matter monitoring. J Expo Anal 

Environ Epidemiol 46(10): 518-532. 

Williams R, Creason J, Zweidinger R, Watts, R, Sheldon L, and Shy C, 2000c. The 1998 

Baltimore particulate matter epidemiology-exposure study: part 2. Personal exposure 

assessment associated with an elderly study population. J Expo Anal Environ Epidemiol 10: 

533-543. 

Williams R, Suggs J, Rea A, Leovic K, Vette A, Croghan C, Sheldon L, Rodes C, Thornburg J, 

Ejire A, Herbst M, and Sanders Jr. W, 2003. The Research Triangle Park particulate matter 

panel study: modeling ambient source contribution to personal and residential PM mass 

contributions. Atmospheric Environment 37: 5365-5378. 

Wilson AL, Colome SD, Baker PE, and Becker EW, 1986. Residential Indoor Air Quality 

Characterization Study of Nitrogen Dioxide, Phase I, vol. 2, final report for Southern California 

Gas Company. 

Wilson AL, Colome SD, and Tian Y, 1993. California residential indoor air quality study, volume 

1: Methodology and descriptive statistics, prepared for the Gas Research Institute, Pacific Gas 

and Electric Company, San Diego Gas and Electric Company, and Southern California Gas 

Company. 

Wolkoff, P, 1995. Volatile organic compounds – sources, measurements, emissions, and the 

impaact on indoor air quality. Indoor Air (Suppl. 3/95) 9-73. 

Wolkoff P, Wilkins CK, Clausen PA, and Larsen K, 1993. Comparison of volatile organic 

compounds from processed paper and toners from office copiers and printers: methods, 

emission rates, and modeled concentrations. Indoor Air (3): 113-123. 

Wolkoff P, Clausen PA, Wilkins CK, and Nielsen GD, 2000. Formation of strong airway irritants 

in terpene/ozone mixtures. Indoor Air 10:82-91. 

Wolkoff P, and Nielsen GD, 2001. Organic compounds in indoor air – their relevance for 

perceived indoor air quality? Atmos Environ 35: 4407-4417. 
Indoor Air Pollution in California July, 2005 

 243

Woodruff TJ, Grillo J, and Schoendorf KC, 1997. The relationship between selected causes of 

postneonatal infant mortality and particulate air pollution in the United States. Environ Health 

Perspect 105: 608-612. 

WRPPN (Western Regional Pollution Prevention Network), 2003. Janitorial Products Prevention 

Project. Reno, NV. http://www.wrppn.org/Janitorial/jp4.cfm. 

Wynder EL, and Hoffman D, 1964. Polycyclic aromatic hydrocarbons. Advances in Cancer 

Research 8 U.S. Environmental Protection Agency (U.S. EPA), 1987: 312-322.

Wyon DP, 2004. The effects of indoor air quality on performance and productivity. Indoor Air

14(s7): 92-101. 

Yu C, and Crump D, 1998. A review of the Emission of VOCs from Polymeric materials used in 

buildings. Building and Environment 33(6): 357-374. 

Zanobetti A, and Schwartz J, 2003. Airborne particles and hospital admissions for heart and 

lung disease in Health Effects Institute Special Report: Revised Analyses of Time-Series 

Studies of Air Pollution and Health. 

Zartarian VG, Ferguson AC, and Leckie JO, 1998. Quantified mouthing activity data from a fourchild pilot field study. J Expo Anal Environ Epidemiol 8(4): 543-553. 

Zartarian VG, and Leckie JO, 1998. Feature Article—Dermal Exposure: The Missing Link. 

Environ Sci Technol 3(3): 134A-137A. 

Zhou JY, Liu KS, and Waldman JM, 1998. Survey of indoor radon concentrations in California 

elementary schools. California Department of Health Services, Environmental Health Laboratory 

Branch. Report EHLB/R-400, May 1998. Available from: http://www.caliaq.org/RadonInCalSchools99.html. 

Zhu J, Cao X, and Beauchamp R, 2001. Determination of 2-butoxyethanol emissions from 

selected consumer products and its application in assessment of inhalation exposure 

associated with cleaning tasks. Environ Int 26: 589-597. 

Zipprich JL, Harris SA, Fox JC, and Borzelleca JF, 2002. An analysis of factors that influence 

personal exposure to nitrogen oxides in residents of Richmond, Virginia. J Expo Anal Environ 

Epidemiol 12: 273-285. 

Zock JP, Jarvis D, Luczynska C, Dunyer J, and Burney P, 2002. Housing characteristics, 

reported mold exposure, and asthma in the European Community Respiratory Health Survey. 

Journal of Allergy and Clinical Immunology 110: 285-292. 
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Indoor Air Pollution in California July, 2005 

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10. GLOSSARY 

TERM DEFINITION 

Active/Passive Sampling Active sampling depends on a mechanical process like pumping 

to collect the sample at a known rate; this is used for VOC and 

aldehyde sample collection. Passive sampling involves nonmechanical processes, usually diffusion, in which the air is 

sampled at whatever rate it passes across a badge surface or 

tube opening. 

Air Changes per Hour ACH, the volume of air moved in one hour. One air change per 

hour in a room, home, or building means that the equivalent of the 

volume of air in that space will be replaced in one hour. 

Air Cleaners These are devices designed to remove pollutants from a room. Air 

cleaners can be portable, or part of a central air system. Air 

cleaners can be mechanical, employing a filter to remove 

pollutants, or electronic using a small electrical charge to collect 

particles from air pulled through a device. 

Air Fresheners These devices are promoted to neutralize odors rather than 

remove pollutants. Products often emit a fragrance which diffuses 

into the air. Some styles can spray fragrances and be 

programmed for fragrance dispersion. 

Air Flow Rate The rate at which air moves into a space. Expressed in units of air 

changes per hour or cubic feet per minute. 

Air Handling Unit HVAC (heating, ventilation and air conditioning) unit. Refers to 

equipment that includes a blower or fan, heating and/or cooling 

coils, and related equipment such as controls, condensate drain 

pans, and air filters. Does not include ductwork, registers, or 

grilles, or boilers and chillers. 

Allergen A chemical or biological substance (e.g., pollen, animal dander, or 

house dust mite proteins) that induces an allergic response, 

characterized by hypersensitivity. 

Ambient Air Quality State (ARB) and federal (U.S. EPA) enforceable 

Standards (AAQS) regulations designed to protect the public from the harmful effects 

of traditional pollutants in outdoor air. 

Asthma A chronic disease of lung tissue which involves inflamed airways, 

breathing difficulty, and an increased sensitivity to allergens and 

contaminants in the air. 

Biological Contaminants Agents derived from or that are living organisms (e.g., viruses, 

bacteria, fungi, and mammal, arthropod, and bird antigens) that 

can be inhaled and can cause many types of health effects 
Indoor Air Pollution in California July, 2005 

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including allergic reactions, respiratory disorders, hypersensitivity 

diseases, and infectious diseases. Also referred to as biological 

agents. 

Comfort Measures Factors that determine human perception of thermal comfort, 

including temperature, relative humidity, and draft 

Commissioning Testing the important building systems before occupancy to 

ensure that they operate the way the designers expect and that 

they serve the needs of the building occupants. Systems that can 

be tested include HVAC, electrical, energy management, 

plumbing, etc. 

Fungi A group of organisms that lack chlorophyll, including molds, 

mildews, yeasts, mushrooms. 

Integrated Pest A pest management strategy that focuses on long-term prevention 

Management (IPM) or suppression of pest problems through a combination of 

techniques such as monitoring for pest presence and establishing 

treatment threshold levels, using non-chemical practices to make 

the habitat less conducive to pest development, improving 

sanitation, and employing mechanical and physical controls. 

Pesticides that pose the least possible hazard and are effective in 

a manner that minimizes risks to people, property, and the 

environment, are used only after careful monitoring indicates they 

are needed according to pre-established guidelines and treatment 

thresholds. 

Micron A unit of length equal to one millionth of a meter; a micrometer. 

Microorganism A microscopic organism, usually a bacterium, fungus, or 

protozoan. 

Natural Ventilation The movement of outdoor air into a space through intentionally 

provided openings, such as windows and doors, or through nonmechanical ventilators, by wind, air pressure differences, or other 

natural, non-mechanical means. 

Permissible Exposure Enforceable pollutant exposure limits determined by 

Limits (PELs) OSHA that are designed to protect healthy adult workers in 

industrial environments from adverse health effects associated 

with pollutant exposure. None of these limits are targeted toward 

protecting children. 

Pesticides A pesticide is any substance or mixture of substances intended to 

prevent, destroy, repel, or mitigate any pest. Though often 

misunderstood to refer only to insecticides, the term pesticide also 

applies to herbicides, fungicides, disinfectants, and antimicrobials. 

Under U. S. law, a pesticide is also any substance or mixture of 

substances intended for use as a plant regulator, defoliant, or 

desiccant. 
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Polycyclic Aromatic A class of stable organic molecules comprised of only carbon and 

Hydrocarbons (PAHs) hydrogen. They are a common product of combustion from 

automobiles, airplanes, woodburning, cigarettes, and some types 

of cooking. Many of these molecules are highly carcinogenic and 

very common. 

Portable Classrooms Classrooms that are designed and constructed to be moveable 

and transportable over public streets, also known as temporary or 

relocatable classrooms. 

Quality Control (QC) Internal checks on the operation of sample collection and/or 

sample analysis. Methods for determining the operation include 

blanks, spiked samples, flow checks, and duplicate samples. QC 

measures can be used to determine accuracy, bias, and precision 

of the data reported. 

Real-time Monitoring This type of environmental measurement gives instantaneous 

information at the point of sampling; measurements are recorded 

as often as every minute, every second, or in fractions of a 

second. 

Reference Exposure The concentration level at or below which no adverse 

Level (REL) health effects are anticipated for a specified exposure duration. 

RELs are based on the most relevant, adverse health effect 

reported in the medical and toxicological literature for the 

population group known to be most sensitive to the chemical. 

RELs are designed to protect the most sensitive individuals in the 

population by the inclusion of margins of safety. Since margins of 

safety are incorporated to address data gaps and uncertainties, 

exceeding the REL does not automatically indicate an adverse 

health impact will occur. OEHHA provides acute (1-hour) and 

chronic (lifetime, non-cancer), RELs for a number of chemicals, 

and has developed an 8-hour “indoor” REL for formaldehyde. 

Relative Humidity The measure of moisture in the atmosphere, expressed as a 

percent of the maximum moisture the air can hold at a given 

temperature. 

Return Air Air removed from a space by the HVAC system to be recirculated 

or exhausted. 

Sick Building Syndrome A set of symptoms (including headache, fatigue, and eye irritation) 

typically affecting workers in modern airtight office buildings, 

believed to be caused by indoor pollutants (such as formaldehyde 

fumes or microorganisms). 

Supply Air Air delivered to the conditioned space by the HVAC system and 

used for ventilation, heating, cooling, humidification, or 

dehumidification. It is usually a combination of outdoor air and 

return air. 
Indoor Air Pollution in California July, 2005 

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Traditional Classrooms Classrooms in permanent, site-built school buildings. 

Variable Air Volume Air handling system that conditions the air to a 

System temperature using a varying amount of outside airflow based 

essentially on the outdoor temperature. 

Ventilation The process of intentionally supplying and removing air by natural 

or mechanical means to and from any space. 

Volatile Organic Compounds that evaporate quickly from the many 

Compounds (VOCs) housekeeping, maintenance, and building products made with 

organic chemicals. These compounds are released from products 

that are being used and that are in storage. Many are 

carcinogenic, neurotoxins, or mucous membrane irritants. 
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APPENDIX I

HEALTH AND SAFETY CODE § 39930

The legislative mandate for the report to the legislature on Indoor Air Quality is

contained in the Health & Safety Code amendment contained in Section 2 of Assembly

Bill 1173 (Keeley, 2002):

39930. (a) The State board shall, not later than January 1, 2004, in consultation

with the State Department of health Services, the Office of Environmental Health

Hazard Assessment, the State Energy Resources Conservation and Development

Commission, any other state agency the state board determines is appropriate, affected

indoor emissions sources, and interested members of the public, provide a report to the

Legislature summarizing all of the following:

(1) The best scientific information available including, but not limited to, the most

recent empirical data, on indoor air pollution including, but not limited to, air

contaminants that have been identified as toxic air contaminants pursuant to Sections

39655, 39657, or 39660, or air contaminants for which the state board has adopted

ambient air quality standards.

(2) The potential adverse effects of indoor air pollution exposure on public health in

the state, including, but not limited to, vulnerable populations, including, but not limited

to, elderly persons, infants, and children, based upon the information described in

paragraph (1).

(3) Readily available information about the effects of existing regulations and current

industry practices in mitigating those exposures.

(4) A listing that references work performed by other state or federal entities

regarding biological and radiological substances, including a summary of activities

conducted by the State Department of health Services pursuant to Chapter 18

(commencing with Section 26100) of Division 20.

(b) The report described in subdivision (a) shall include all of the following:

(1) A list of indoor air pollutants that are described in the summaries provided

pursuant to paragraphs (1) and (4) of subdivision (a).

(2) A list of indoor air pollutants, as defined in Section 39013, ranked in groups

designated as high, medium, and lower priorities, that the state board has determined,

based upon empirical data or other scientific information, are likely to have the most

significant adverse impacts on human health through exposures in schools, nonindustrial workplaces, homes, and other indoor locations, and the probable source

categories for these pollutants.

(3) An analysis of the indoor emissions, indoor exposures, and potential health effects

from the indoor source categories described in paragraph (1), and options for mitigating

those health effects in schools, non-industrial workplaces, homes, and other indoor

locations, including, but not limited to, a discussion of the feasibility and public health

effects of implementing each option.
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(4) A description of options for schools and school districts to improve indoor air

quality in public schools. The state board shall develop these options in consultation

with representatives from school district facility departments, school district

maintenance departments, and statewide educational organizations.

(c) (1) The state board shall enter into an agreement with the National Academy of

Sciences, the University of California, the California State University, or a similar

institution of higher learning that has scientific expertise, any combination of those

entities, or with a scientist or group of scientists of comparable stature and qualifications

that is recommended by the president of the University of California, to conduct an

external scientific peer review of the scientific basis for the report described in

subdivision (a).

(2) The state board may not submit the report to the Legislature until all of the

following conditions are met:

(A) The draft report is submitted to the external scientific peer review entity described

in paragraph (1) for evaluation.

(B) The external scientific peer review entity, within the timeframe agreed upon by the

board and the external scientific peer review entity, prepares written comments that

contain an evaluation of the scientific basis for the draft report. If the state board

disagrees with any aspect of the findings of the external scientific peer review entity, the

state board shall include as part of the final report, an explanation of its basis for arriving

at the determination, including, but not limited to, the reasons that the state board

determined that the report was based on sound scientific knowledge, methods, and

practices.

(d) The state board shall present and review the content of the report described in

subdivision (a) at a public meeting prior to providing the report to the Legislature.
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APPENDIX II

 Explanation Of Indoor Cancer Risk Estimates

February, 2005

Summary: The toxic air contaminant (TAC)-related cancer risk estimates presented in this

report are based on results of the California Comparative Risk Project (CCRP), Final Report,

May 1994, for indoor indicator pollutants–excluding radon, environmental tobacco smoke (ETS),

and asbestos–with adjustments (downward) based on changes in current exposure levels of

formaldehyde relative to those from studies used in the CCRP assessment. This information is

the best information available for California, and the indoor air concentrations on which these

estimates are based are supported by more recent studies from other states. Background

information on the estimates developed in the CCRP is discussed below, followed by a detailed

discussion of how the cancer risk estimates for this report (AB1173) were developed.

BACKGROUND: the California Comparative Risk Project (report available at

http://www.oehha.ca.gov/multimedia/comprisk.html.

• The CCRP estimated about 268 excess annual cancer cases from indoor residential

and consumer product sources for the 10 indicator chemicals included in the estimate.

The majority of that risk was from formaldehyde and p-dichlorobenzene. The excess annual

cancer cases were taken from the table “Residential and Consumer Product Sources: II.

Human Health Risk Assessment Results for Indicator Chemicals” from the CCRP. The 10

chemicals are:

formaldehyde p-dichlorobenzene

benzene benzo(a)pyrene

1,3-butadiene chloroform

di-2-ethylhexylphthalate (DEHP) styrene

tetrachloroethylene (perchloroethylene) trichloroethylene

• The risk is that which was attributable only to the emissions from the indoor sources.

In the CCRP Project, the outdoor contribution to the indoor concentrations was subtracted

from the indoor levels, with the remainder attributable to indoor sources.

• The cancer risks estimated are ANNUAL excess cancer cases. This is somewhat

different from the expression we typically use for outdoor air, expressed as cancer risk from

70 years of exposure per million people exposed, but the two can be roughly converted for

comparison (see below).

• The risk from residential and consumer products was ranked in the High Risk

category with a high level of confidence based on the extensive contribution to both

cancer and non-cancer risks, the widespread exposure throughout the population, and the

consistency of monitoring results across many studies.

• Like other source and media categories in the CCRP, the estimates developed for the

Indoor (residential and consumer product) category do not include risk posed by other

known carcinogens that occur indoors from indoor sources. Thus, the cancer risk
II - 2

estimated for the 10 indicator chemicals is likely to be an underestimate of the actual

cancer risk from indoor sources other than ETS, radon, and asbestos.

• Notes regarding the CCRP estimates:

1. They are based on exposure distributions developed from the best available studies at

the time, with greater weight given to California studies. Generally, 3-4 California studies

of large numbers of homes in both northern and southern California (totaling about 600-

800 homes) were available; these covered a range of seasons, income levels, etc. and

were randomly selected using census tract information. For some pollutants,

measurements from public buildings, offices, etc. in other studies were also available.

2. Indoor concentrations tend to be log-normally distributed, meaning a small but

decreasing portion of the population experiences particularly high exposures well above

the mean. In the CCRP, indoor concentration distributions for a few pollutants appeared

to be potentially bi-modal (having a group in the population with especially high indoor

concentrations because their house contains large sources of a given pollutant, such as

mothballs/p-dichlorobenzene...e.g., either the household uses mothballs, or they do not,

and if they do, their levels are quite high and that group in the population has distinctly

greater indoor concentrations than others). Because of this, concentration distributions

(rather than means) were used to develop exposure estimates to achieve more accurate

risk estimates.

3. Although distributions were used to estimate risk, the resulting average individual risk

was used to estimate annual cancer cases, and thus these may be conservative

estimates, since the average does not necessarily fully capture those at very high risk.

Additionally, only the population with an exposure level above the one in ten thousand

risk level was included in the risk estimation; thus, those with lower cancer risks were not

counted, effectively reducing the total count relative to the population estimate that

would be derived if those with lower cancer risks had also been included.

CURRENT ESTIMATE for AB 1173 report:

• We reviewed the estimates for the 10 chemicals and performed a quick literature search

to identify more recent data that might indicate that an adjustment is needed to better

reflect current indoor exposure levels.

• Formaldehyde is the only one of the 10 indicator chemicals for which there are sufficient

new data to develop a more current exposure distribution. Recent emissions studies

(e.g., Kelly et al., 1999; Hodgson et al., 2000; Hodgson et al., 2002; Hodgson, 1999)

show that indoor formaldehyde emissions from many materials and products have

decreased by an average of 49% since the earlier Pickrell emissions study (1983).

These and other studies indicate that indoor exposure concentrations have decreased

by about 50% since the early to mid-1980s, when the majority of the studies used in the

CCRP project were conducted. This was not surprising, since several industry initiatives

and some known product changes had occurred since the mid-80s. Thus, for our new

estimate, we assumed that the current formaldehyde risk would be about half of

that estimated in the CCRP Project, or about 62 excess cancer cases per year.
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• Recent studies show that levels of some of the other indicator indoor pollutants

attributable to indoor sources, such as chloroform and styrene, may have increased in

recent years, but there are no new indoor California studies in the last decade that would

document this, and information obtained regarding changes in the known sources is

mixed. For others, such as benzene, there is reason to believe that indoor levels from

indoor sources have decreased somewhat since the earlier studies, due to product

composition changes and reduced indoor smoking, but there are no readily available

data to support a revised calculation.

In the CCRP, DEHP was included in the list of chemicals used to develop the cancer

estimates. However, IARC recently concluded that DEHP is not a human carcinogen,

and downgraded its classification to Group 3 (not classified as a human carcinogen, due

to inadequate evidence for human carcinogenicity). In the CCRP, DEHP accounted for

one cancer case, so the total cancers estimated from CCRP was decreased by one for

the current estimate. Thus, the current total risk posed by the indicators other than

formaldehyde and DEHP remains a reasonable estimate of cancer risk.

• Our current estimate is thus calculated as follows:

268 minus 63 (1/2 the previous formaldehyde estimate, and minus one for DEHP) = 205

excess cancer cases per year, times 34/30 (or 1.13) to adjust the original CCRP

estimates to the year 2000 California population of 34 million, for a total of 232 excess

cancer cases per year due to emissions from indoor sources of the chemicals. This

rounds to 230. However, 230 is likely an underestimate due to: a) the conservative

nature of the original estimate; b) the fact that there are other indoor carcinogens that

are known but not included in the estimate (see bullet below); and c) the uncertainty of

the risk estimation process, which is best addressed by using a range where possible.

Thus, at least 230 excess cancers per year are estimated.

• There are a number of additional carcinogens known to be emitted from indoor

sources that were not included in the indicator chemicals list for the CCRP Project

due to a lack of sufficient indoor data to estimate an exposure level. For example, other

PAHs, acetaldehyde and other aldehydes, and asbestos are carcinogenic and have

been measured indoors and as emissions from products. Persistent chemicals such as

PCBs have been found in house dust, and various toxic metals have been measured at

higher levels in both indoor air and house dust. However, the data are not sufficient to

estimate population exposure. Others like acrolein are just beginning to be studied in

the indoor air. Thus, the adjusted estimate above is assuredly an underestimate of

the actual cancer risk posed by toxic chemicals emitted or produced by indoor

sources.

Comparison to Outdoor Risk Levels (Fig. 2.1 in the report).

• Using the excess cancer cases per million per 70 years in Table 7 of ARB’s October 2000

diesel risk reduction plan and the year 2000 California population of 34 million, current

estimated ANNUAL excess cancer cases from diesel exhaust particles total 262

(540/million X 34 / 70), or about 260 excess cancers per year. This figure does not account

for recently implemented or planned regulations, but those changes would have little impact

on the 70 year lifetime exposures of most adults in the population, and thus this estimate

remains reasonable.
II - 4

• Using the same table, the non-diesel risk from other outdoor sources is calculated to

total 106 excess cancers (218/million X 34 / 70= 106), or about 110 excess cancers per

year.

• The total excess cancer cases per year from different sources of air pollutants are thus

estimated to be:

Residential and Consumer Product Sources: 230 /year

Diesel exhaust PM10: 260 /year

Other outdoor sources: 110 /year

Figure 2.1 in the AB 1173 report reflect these numbers.

Note: OEHHA has indicated previously that conversion of the outdoor risk estimates to

annual cancer cases to allow comparison of the CCRP indoor annual excess cancer

estimates is acceptable for this type of general comparison.

RADON, ETS, AND ASBESTOS

Radon and ETS: the exposure and risk estimates have been updated and are included in

the text.

Asbestos has not been widely measured in California indoor environments, and there are

many measurement difficulties for this set of fibers. There are insufficient data on which to

base an indoor asbestos risk estimate (from indoor sources) at this time, just as there was at

the time of the CCRP project.
III - 1

APPENDIX III

Background for Estimates on Indoor Formaldehyde Concentrations

February, 2005

Figure 2.4 is intended to give a general indication of current estimates of indoor formaldehyde

levels in several California environments, and to illustrate relative levels among those

environments. Data on formaldehyde levels in homes, schools, and offices were obtained from

several information sources. A description of the sources used for each category follows. Please

note that these estimates were derived only for the illustration provided in Figure 2.4: they were

not used for the cancer risk estimates discussed in this report. As discussed in Appendix II, the

cancer risk estimates for formaldehyde were based on the estimates from the 1994 California

Comparative Risk Project and reduced based on a more recent emissions study.

Manufactured homes

Estimated Average: 37 ppb, Maximum: 227 ppb

Formaldehyde levels in manufactured homes are based on measurements made in California

manufactured homes during the early 1980s, reduced by a factor representative of the reduction

in formaldehyde emissions in new composite wood products since that time. The resultant value

is consistent with recent limited measurements in manufactured homes.

The California Department of Health Services measured formaldehyde levels in approximately

600 mobile homes in 1984 and 1985. Investigators obtained integrated one-week

measurements for approximately 600 mobile homes. The geometric mean formaldehyde

concentration measured in the summer was 72 ppb (arithmetic mean 91 ppb), and 78 ppb

(arithmetic mean 91 ppb) in the winter (Sexton et al., 1985). The maximum value was 464 ppb

measured in the summer.

Formaldehyde emissions from new composite wood products are lower today than they were in

the early 1980’s due to changes in manufacturing procedures. A comparison of emission rates

from Pickrell (1983) and Kelly (1999) indicate formaldehyde emission rates from these products

have decreased an average of about 49% over the last 20 years. Comparison of data from the

two investigators indicate particleboard emissions are 92% of what they were in 1983, interior

plywood emissions are 15% of 1983 values, and paneling emissions are 39% of 1983

emissions. An unweighted average of these reductions in emissions yields a gross average

estimate that emissions today are 49% of what they were in 1983.

The estimate of an average formaldehyde concentration of 37 ppb in manufactured homes is

based on the average of the winter and summer geometric means determined by Sexton, then

reduced by 49% to reflect changes in manufacturing practices. The maximum value measured

by Sexton (464 ppb) was also reduced by 49% to reflect manufacturing changes.

Hodgson et al. (2002) measured formaldehyde levels inside four new manufactured homes in

humid climates of the southeastern U.S. The homes were furnished but not occupied (sales

models) and had a geometric mean formaldehyde concentration of 34 ppb. Over extended time

periods, this level would be reduced as the emissions from building materials decline. However,

human activities tend to elevate formaldehyde concentrations due to use of combustion

appliances and products that emit formaldehyde, which would offset the decline from building

materials. Thus, the level measured by Hodgson is consistent with the concentration estimated

above.
III - 2

Sexton K, Liu K, and Petreas M. (1986), Formaldehyde Concentrations Inside Private

Residences: A Mail-Out Approach to Indoor Air Monitoring, JAPCA 36: 698-704.

Pickrell J, Mokler B, Griffis L, Hobbs C, and Bathija A. (1983), Formaldehyde Release Rate

Coefficients from Selected Consumer Products, Environmental Science and Technology 17(12):

753-757.

Kelly T, Smith DL, and Satola J. (1999). Emission Rates of Formaldehyde from Materials and

Consumer Products Found in California Homes, Environmental Science and Technology 33(1):

81-88.

Hodgson AT, Rudd AF, Beal D, and Chandra S. (2000) Volatile organic compound

concentrations and emission rates in new manufactured and site-built houses, Indoor Air 10:

178-192.

Classrooms (Inside)

Estimated Average: 18 ppb, Maximum: 110 ppb

The California Portable Classrooms Study (PCS) data from 2001 and 2002 were used to

estimate school-year average and maximum concentrations of formaldehyde in California’s K12 classrooms. This is a large, representative statewide data set of formaldehyde

measurements obtained across four seasons using both active and passive sampling methods.

School-Year Average Concentration

Because indoor formaldehyde levels increase with increased temperature and humidity, we

combined PCS formaldehyde data from Phase I (warmer seasons) and Phase II (cooler

seasons) to estimate school-year average concentrations. We excluded most of July and all of

August in estimating the school-year average, although 22 % of California’s K-12 students

attend year-round schools or summer school (CDE, 2002). Therefore, our estimate of schoolyear average concentration for formaldehyde is likely a conservative estimate for the state.

We used field study data from the PCS Phase II to estimate classroom formaldehyde levels in

the 6 months of cooler weather, October – March. In Phase II, formaldehyde was measured

using the DNPH method with active sampling over 6-8 classroom hours from October 2001 to

early March 2002. The mean concentration for this period was 13 ppb, and the geometric mean

was 12 ppb. Monthly breakdowns of Phase II formaldehyde concentrations were not readily

available, but they would be limited to only two time periods because of the limited sample size

(201 classrooms) in Phase II. Phase II data provide reasonably accurate estimates of classroom

concentrations of formaldehyde for the fall and winter seasons when monitoring occurred.

Mail survey data from the PCS Phase I were used to estimate classroom formaldehyde levels in

the 6 months of warmer weather (April through September). In Phase I, formaldehyde was

measured using a passive monitor deployed for 7-10 days, including nights and weekends, in

April to early July 2001. The mean concentration for this period was 27 ppb (geometric mean of

22 ppb).

As expected, both the means and 95th percentile concentrations were notably higher in Phase I

compared to Phase II (ARB-DHS, 2003). The higher indoor levels in Phase I were expected

because the Phase I sampling was conducted during warmer weather when indoor
III - 3

formaldehyde levels are usually higher, and because the sample size was substantially larger,

increasing the probability of including classrooms with more extreme levels in the sample.

Phase I also included nights and one or two weekends in the sampling period, during which the

classrooms were probably not ventilated, which could result in higher formaldehyde levels. Also,

in Phase II sampling, technicians operated the ventilation system to make flow measurements,

which might have reduced formaldehyde levels relative to what they might have been under

normal operation conditions.

Phase I measurements confirm that there was a positive bias associated with the weekend

sampling included in the 7 to 10 day measurement. The weekend bias was determined by

comparing data from classrooms with >25% of the sample days on weekends (2 weekends) vs.

those with < 25% weekend days (1 weekend). The first group had mean formaldehyde levels of

30 ppb vs. 25 ppb in the second group, or a difference of 5 ppb due to an additional weekend of

sampling in these seasons. These results are from analyses using weighted data.

To estimate the overall effect of the weekend bias on the Phase I mean, we calculated a

weighted average of the weekend bias. About half of the sample (52%) included one weekend,

and about half of the sample (48%) included two weekends. The weighted average was

calculated as follows:

(0.52 of sample x 1 x weekend bias) + (0.48 of sample x 2 x weekend bias)

= 1.48 x weekend bias = 1.48 x 5 ppb = 7 ppb positive bias on Phase I mean

Therefore, the positive bias in the Phase I mean for estimating the mean schoolday (weekday)

concentrations was estimated to be 7 ppb. Additional positive bias may have occurred due to

sampling overnight, but data are not available to quantify the magnitude of this bias. However,

the magnitude of the overnight bias is expected to be much less than that for the weekend bias

because the nighttime period is usually much cooler, which would result in reduced

formaldehyde concentrations relative to weekend concentrations.

The Phase I data were also adjusted for the lack of data for September. To estimate

formaldehyde levels during the warmer season (April – September), the Phase I data were

extrapolated to estimate what concentrations would likely be in September, and the 4 month

average was then calculated. The monthly means for April, May, and June-early July were 18,

29, and 36 ppb, respectively. July and August were considered to be mostly a vacation period

for schools. The monthly mean for September was assumed to be the same as that for June –

early July. The average for April, May, June, and September was calculated, and the weekend

bias then subtracted, as follows:

(18 ppb + 29 ppb + 36 ppb + 36 ppb) / 4 - (7 ppb for weekend bias in means)

= 30 ppb – 7 ppb weekend bias

= 23 ppb for warmer season, excluding summer vacation

To estimate the school-year average concentrations of classroom formaldehyde in California,

we then averaged the estimated concentrations for the warmer seasons and the measured

concentration for the cooler season:

(23 ppb in warmer season + 13 ppb in cooler season) / 2

= 18 ppb school-year average estimate
III - 4

In conclusion, the school-year average concentration of formaldehyde in California K-12

classrooms was estimated to be 18 ppb, after adjustment for weekend bias and the lack of

September data. This value is slightly lower than the unadjusted average of the Phase I and

Phase II data (20 ppb).

School-Year Maximum Concentration

To estimate school-year maximum concentrations of formaldehyde in California’s K-12

classrooms, data from PCS Phase I, PCS Phase II, and case studies in California were

considered. The maximum formaldehyde level measured among 199 classrooms in PCS Phase

II was 71 ppb (Whitmore, 2003). Because these measurements were made in the fall and

winter, and because extreme values are not easily measured with such a small sample size, this

value assuredly underestimates the maximum formaldehyde concentration.

In the Phase I mail survey during the spring and early summer, the maximum formaldehyde

level measured among 911 classrooms was 138 ppb (Whitmore et al., 2003). However, this

value overestimates the maximum because the passive sampler measurement for 7-10 days

includes weekends and nights. The highest percentile values reported with statistical confidence

were the 95th percentile values for portable classrooms, so these values were used to estimate

the weekend bias. The portables subsample with 2 weekends had a 95th percentile of 78 ppb,

vs. 62 ppb for the portables subsample with one weekend, a difference of 16 ppb. Using the

same approach used above to adjust the average concentrations for weekend bias, a weighted

average of 24 ppb is estimated for the weekend bias in the 95th percentile (1.48 x 16 ppb).

Subtracting this bias from the maximum value of 138 ppb yields an estimated maximum of 114

ppb. This value may be an overestimate of the maximum concentration because the bias due to

overnight sampling is not included. Rounding down, the statewide maximum is estimated to be

about 110 ppb.

Although higher than the 71 ppb maximum obtained in the Phase II field study, this value is

supported by data from case studies of California schools, which include a maximum of 98 ppb

for 6-8 hours. These studies employed active sampling using the DNPH method measurements

in 90 classrooms in August, September, or October of 1999 and 2000. Selected classrooms in

five school districts, including the Saugus and Beverly Hills districts, were examined.

Because each of these data sets represents a small sample size relative to the total population

of classrooms in California, one would not expect the classrooms with the very highest

formaldehyde levels to be included in the sample. Samples tend to reflect the mean but not the

extreme values existent in the actual population being studied. Thus, the statewide maximum is

estimated to be at least 110 ppb, and probably higher.

For more information on the Portable Classroom study, please see:

ARB and DHS, (November 2003) Environmental Health Conditions in California’s Portable

Classrooms, Report to the California Legislature.

http://www.arb.ca.gov/research/indoor/pcs/leg_rpt/pcs_r2l.pdf, p. 53 et seq.

California Department of Education (CDE). Year-Round Education, 2002-03 Statistics. Based

on 2002 CBEDS. Sacramento, CA. http://www.cde.ca.gov/facilities/yearround/yrstat02.htm.

Whitmore R, Clayton A, Phillips M, and Akland G. (2003). California Portable Classrooms Study:

Phase I-Mailed Survey and Phase II-Main Study, Final report to ARB for Contract no, 00-317.
III - 5

Whitmore, R, 2003. Personal communication, February 24. Research Triangle Institute,

Research Triangle Park, NC.

Conventional Homes

Estimated Average: 14 ppb, Maximum: 232 ppb.

Formaldehyde levels measured in the National Human Exposure Assessment Survey

(NHEXAS) in Arizona and a southern California study were used to estimate current

concentrations in Californian homes. The NHEXAS study was conducted from October 1993

through September 1998. Investigators used a probability-based sampling scheme to obtain

results that are representative of the entire state of Arizona. Sampling was conducted over

different seasons and included 189 homes. Passive sampling tubes with a sodium bisulfiteimpregnated disk were used to collect formaldehyde for a 6 - 7 day period. Construction

practices, climate, and ventilation practices are assumed to be reasonably similar in California

and Arizona. Results from the NHEXAS study indicate the average formaldehyde level for all

homes was 17 ppb. The maximum formaldehyde concentration was 331 ppb. Although

unusually high, this value is considered a valid result by the authors. They report it is within a

factor of 2 of maximum levels measured by other investigators.

Data are also available from a study sponsored by ARB, in which investigators measured

formaldehyde levels in approximately 70 homes in limited areas of southern California (Avol et

al, 1996). Investigators used the 2,4-dinitrophenylhydrazine method with active monitors. The

results are lower than expected for a sample representative of the entire California population of

homes for two reasons: sampling was conducted during the summer only with doors and

windows open much of the time, and most of the homes were notably older homes, and not new

homes. The mean concentration in this study was 9.1 ppb, and the maximum was 31.3 ppb.

Results from both of the above studies were used to estimate indoor concentrations in

conventional California homes. The NHEXAS study has great credibility since it used a

probability-based sampling scheme for a statewide study conducted in a neighboring state. The

southern California study represents the portion of Californians who live in a mild southern

California climate in homes that are not new, during under one set of conditions. Results from

the two studies are weighted approximately by sample size of the two studies to obtain a current

estimate for conventional California homes. The NHEXAS mean and maximum were weighted

by a factor of .67, while the California data were weighted by a factor of .33.

Average: 0.67 (17) ppb + 0.33 (9) = 11 + 3 = 14 ppb.

Maximum: 0.67 (331) + 0.33 (31) = 222 + 10 = 232.

Avol, E. (1996), “Residential Microenvironmental and Personal Sampling Project for Exposure

Classification", final report to ARB, Contract no. 92-317.

Gordon SM, Callahan PJ, Nishioka MG, Brinkman MC, O’Rourke MK, Lebowitz, MD,

Moschandreas DJ. (1999). Residential environmental measurements in the National Human

Exposure Assessment Survey (NHEXAS) pilot study in Arizona: preliminary results for

pesticides and VOCs, Journal of Exposure Analysis and Environmental Epidemiology 9, 456-

470.
III - 6

Office Buildings

Estimated Average: 13 ppb, Maximum: 26 ppb

The U.S. EPA Building Assessment Survey and Evaluation (BASE) Study examined pollutant

levels inside 100 non-problematic office buildings in the U.S. Formaldehyde data from this

study has not yet been fully analyzed or published. However, preliminary formaldehyde data

were presented in an addendum to a U.S. EPA draft report; “Ranking Risks from Air Toxics

Indoors” prepared for Pauline Johnston, U.S. EPA, Indoor Environments Division. Preliminary

data available in the addendum were used to estimate formaldehyde levels in office buildings.

When analyses of the BASE study data are completed, the final results will be used to represent

California office buildings. The value of 26 ppb is likely lower than the maximum.

Source: U.S. EPA Building Assessment Survey and Evaluation (BASE) Study. More

information on the U.S. EPA BASE Study can be found at

http://www.epa.gov/iaq/largebldgs/index.html.

Outdoor levels

Estimated Average: 3 ppb, Maximum: 15 ppb

Outdoor formaldehyde concentrations are from the air toxics sampling network that was

designed to produce a statewide annual average for individual toxic air contaminants. Data from

the most recent five years (1998 - 2002) for which data are available were averaged to negate

any effects due to global weather influences. Data from the Toxics Network is available at

http://www.arb.ca.gov/aqd/toxics/statesubstance.html.
IV - 1

APPENDIX IV

ARB Responses to Comments of the

Scientific Peer Review Committee

Report to the California Legislature

Indoor Air Pollution in California

California Air Resources Board

November 2004

The ARB wishes to extend its deep appreciation to the scientific peer review committee

for their extensive review of the November 2004 draft Report. The members of the

committee included Drs. S. Katharine Hammond, William W. Nazaroff, and Kirk R.

Smith, all from the University of California at Berkeley, and Mr. Richard Sextro, from the

Lawrence Berkeley National Laboratory. We especially thank Dr. Smith for serving as

the Chair of the committee. The committee’s comments have improved the Report

notably, and will help guide future assessments and actions that may be taken as a

result of the report.

COMMENTS:

I. To begin, we commend the California Legislature for commissioning this work.

Indoor air quality is an important issue for the health and well being of Californians and

the state government can play a significant role in helping to ensure good indoor air

quality in both public and private spaces. The topic is not currently well addressed by

governments at the national, state, or local level. Consequently, an effort to summarize

the state of knowledge and to explore the potential for governmental action is

appropriate. California has a proud tradition of leading the country on matters of

environmental health, including in the area of indoor air quality.

II. The Air Resources Board has prepared a good draft report. The document assembles

a large and diverse body of literature and presents it in a coherent, well-organized, and

well-written manner. Particularly impressive are the extensive scope of the pollutant-bypollutant summaries and the compilation of existing regulations and guidelines.

III. As is generally the case in a scientific peer review, this commentary focuses on

aspects of the report that could be improved, rather than discussing the portions that are

already in good shape.

IV. In looking over our complete review, below, however, we are concerned that it may

be a rather large effort by ARB staff to fully respond. We worry that this would lead to a

significant delay in moving forward with efforts in the state to deal with the aspects of

indoor air pollution that are well-documented and worthy of action. We recommend,

therefore, that the state consider dividing indoor air issues into phases or tiers. In this

way, appropriate policy actions can proceed with a first tier, i.e., those pollutants and

indoor environments where the evidence is already adequate as a basis for action.

Further analysis, needed measurements and other research can be initiated for
IV - 2

contaminants and environments in a second tier. Such division could be made according

to judgments of the importance of remaining uncertainties in 1) exposure-response

relationships, 2) exposure patterns in California, and 3) effectiveness of available control

measures. We would be happy to work with ARB staff in making such judgments or

reviewing those made by others.

Response: We agree with the Committee’s intent to avoid any considerable

delay in moving forward. Consequently, our responses fall into three general

categories: 1) immediate changes were made (or will be made in the final

version of the report), 2) future research is needed, and 3) comment requires

intensive analysis that will not change the report recommendation, but should be

carried out in the future.

We start by discussing each of the major pollutants, principally with regard to

presentations in Chapter 2 and 3 and then comment on other issues in the executive

summary and chapter by chapter. Minor points are collected at the end.

Radon

For the most part, the report relies on the various surveys conducted in CA to assess

exposures and to estimate the annual number of lung cancer deaths associated with

radon exposure. The overall health effect estimates for CA (p. 90) are done in

proportion to the U.S. EPA estimates, adjusting for lower average radon concentrations

in the state compared with the US average and correcting for the prevalence of smoking

in CA vs. the US as a whole. This latter ‘correction’ must be done with some care, as

the BEIR VI report on which the EPA risk assessment is based only provided risk

estimates for two smoking categories - never smokers and ever smokers. Depending

upon how many current non-smokers in CA are former smokers, the validity of this

adjustment is unclear.

Response: ARB staff consulted with the Department of Health Services, the

lead state agency for addressing radon, in preparing these responses to

comments on radon. The California radon risk estimate was characterized as

preliminary and order-of-magnitude. It was based on an approximate adjustment

for different smoking rates in California in recent years. The text was revised to

stress the importance of the smoking-radon interaction, and that a truly more

accurate assessment would require resources and data not currently available.

In the same paragraph on p. 90, there is a discussion about the estimates being ‘worstcase’ because “elevated radon regions in California are less populated”. The distribution

of indoor radon concentrations is irrelevant here, as the risk assessment is based on the

average radon concentration, not the underlying concentration distribution. On the other

hand, given that only 0.8% of the measured indoor concentrations are above 4 pCi/L in

CA, compared with 7% nationwide, the task of determining which regions (and thus

populations) are at potentially greatest risk is tractable. To some extent, this has already

been done by virtue of the studies in the Sierra Nevada foothills and the Santa BarbaraVentura counties Rincon.

Response: The text concerning "worst-case" was removed. However,

explanation was added to clarify that this estimate is nonetheless very likely an
IV - 3

overestimate, due to more recent data showing substantially lower levels in the

Sierras (3% now vs. 25% previously estimated as above the 4 piC/l

recommended mitigation level), and other factors as discussed in the revised

text.

The report also notes, at p. 90 (3rd para.), that radon in drinking water contributes to the

overall risk. However, the report should note that the estimated 168 annual cancer

deaths is for the nation as a whole. Furthermore, based on the assessments of radonin-drinking-water concentrations in CA, one would expect very few of these cases to

occur in CA due to the low dissolved Rn concentrations. Note also that these cases are

based on public water systems, not wells serving individual homes.

Response: Clarification was added that the 168 is a national estimate.

It is interesting to note that if the overall risk assessment approach were applied to

average outdoor concentrations (0.4 pCi/L – which represents the ‘lower limit’ to radon

risk reduction), the expected annual cancer death rate is still ~800 for CA (~600 if the

smoking prevalence adjustment is made). According to the EPA radon risk assessment

report (EPA 2003c in the ref. List), the estimated lung cancer deaths among neversmokers is 2900 nationwide or ~350 in CA. Adjusting this for the outdoor air

concentration (0.4/1.25), the number of lung cancer deaths per annum in CA among

never-smokers due to exposures equivalent to those outdoors is ~100.

Response: The text was revised to include an estimate of deaths if indoor

radon levels were reduced to outdoor radon levels. It illustrates that, because

radon is naturally-occurring and occurs indoors and out, there is a substantial

background risk that cannot reasonably be mitigated, other than through

reduction of exposure to tobacco smoke.

Finally, with respect to radon risk estimates, there are several places in the report

narrative (p. 5, para. 2; p. 28, para. 1; p II-4) that state that radon risks have been

reduced and that it is closely associated with smoking. The EPA risk assessment has, if

anything, increased the risks associated with radon exposures. The previous risk

assessment (circa 1992) yielded a central estimate of ~13,000 lung cancer deaths per

year – the current estimate is ~21,000 and the relative risk estimate for never smokers

has increased (see Pawel and Puskin 2004). With respect to never smokers, the

estimated radon-related lung cancer death rate is 350 per year for CA, which is on par

with the estimates for ETS-associated lung cancer. Finally, while there is uncertainty in

all risk estimates for exposures to contaminants, radon is the least uncertain. There

have been statewide and regional surveys, so the distribution of exposures can be

reasonably estimated. The dose-response information is largely based on human

exposures – uranium and hard-rock miners at high exposure levels and residential

studies at the low end.

Response: As indicated above, ARB consulted with DHS on the responses to

comments on radon. The NRC estimates for radon potency (and estimated

deaths), on which EPA bases their estimates, have oscillated over the years.

Between 1980 and 1987 (NRC’s BEIR IV and BEIR V reports), the estimated risk

and numbers of deaths were reduced, based on the NRC’s reconsideration of

differences between uranium miners and the general public, and other factors.
IV - 4

Subsequently, estimates increased, for various reasons. The point is that,

despite the agreement that radon is a potent carcinogen, the most

knowledgeable scientists have decreased and increased their estimates for

radon over the years. Additionally, the estimates for number of deaths in the

U.S. has also increased because of improved exposure estimates in high radon

states, which is where EPA has focused much of its attention...but California has

much lower levels of radon. EPA has changed their interpretation of the BEIR

results over the years as well. It is important to note, though, that the majority of

the risk accrues to active smokers; it is not spread across the population evenly.

Thus, the risk numbers must be considered in light of other factors, such as the

inseparability of the risk between smoking and radon, as noted by the NRC in its

various BEIR reports. As the panel correctly notes, the risk to never smokers in

California is much lower: 350 cancer deaths based on EPA’s estimates. Most

recently, the NRC (p. 19, BEIR VI report, Health Effects of Exposure to Radon,

1999a) stated that:

1) the deaths from radon-attributable lung cancer in smokers could most

efficiently be reduced through tobacco-control measures, in that most of the

radon-related deaths among smokers would not have occurred if the victims

had not smoked;

2) the committee’s...approach to assessing lung-cancer risks posed by indoor

radon and cigarette smoking are subject to considerable uncertainty because

of gaps in our scientific knowledge of effects at low levels of exposure; and

3) the attributable risk for smoking, the leading cause of lung cancer, is far

greater than for radon, the second leading cause.

Specific comments

1. p. 5, middle paragraph. Better to refer to “radium-containing” rock and soil as the

source of radon. (Uranium is the ultimate progenitor, but geochemistry can cause

separation between uranium and radium, the immediate parent.)

Response: The text was revised.

2. p.20. The cancer risk from lifetime radon exposure, even at 1 pCi/L is remarkably

high in comparison with the 1/100,000 used as the NSRL for Prop 65.

Response: Comment noted.

3. p.20. The State of California has frequently developed its own environmental quality

standards and guidelines, and these are often more stringent than the federal ones. It is

curious that the federal 4 pCi/L guideline has not been seriously scrutinized by CA

agencies.

Response: Comment noted.

4. §2.3.9. Radon-222 emanates from the decay of radium-226 (not uranium-238).

Radon is not directly a carcinogenic hazard; rather it is its short-lived radioactive decay

products that accumulate in the lungs and irradiate epithelial cells.
IV - 5

Response: Text changed.

5. Based on the discussion above, the characterization of the risk estimate as

“preliminary” on p 160 is unwarranted.

Response: The text was revised to characterize the estimate as a rough, orderof-magnitude estimate.

6. The radon discussion in Appendix II (p. II-4) is inconsistent with the exposure and risk

estimates performed elsewhere in the report.

Response: The Appendix was revised.

Volatile organic chemicals

Formaldehyde

Appendix III presents a method for estimating HCHO concentrations in the current

building stock. For manufactured homes, an overall reduction factor of 49% is applied

to the concentrations measured in the 1980s, on the grounds that manufacturing

processes have reduced average emission rates by this amount. However, this

reduction applies to new manufactured homes and not to the existing manufactured

home stock. A better (more defensible) basis for estimating the changes in indoor

HCHO concentrations in these residences would be to estimate the annual rate of new

manufactured home construction since the Sexton, et al. survey and combine these with

the concentrations in the existing stock. The 49% likely didn’t occur all at once, so some

sort ‘phased’ reduction factor should be derived. Some accounting for the removal of

older manufactured housing is also necessary, assuming the data are available on

which to base an estimate.

The application of the 49% reduction to the peak concentration doesn’t appear to be

legitimate. Given that the 49% reduction applies to new construction, it is still possible

to have high concentrations in older manufactured homes. In addition, since the 49% is

an average, there are still likely to be new homes in which low-emitting products were

not always used, etc. A better way to estimate the 90 or 95th percentile peak

concentrations (not the highest) would be to use the concentration distribution given by

the data from Sexton (GM and GSD) and add in an estimated distribution for new

manufactured homes. This could be done year by year with the GM adjusted downward

to account for the emission changes. As a first estimate, keeping the GSD the same is

reasonable. In the end, there will be a new distribution of HCHO concentrations updated

to 2000, from which one can derive an estimate for the 90 or 95th percentile peak

concentration.

Response: New homes, not older homes, are the primary concern for exposure

to formaldehyde. A more complex calculation that takes into consideration

reductions associated with the percentage of older homes in California is not

considered necessary, because most building materials have completed their

majority of off-gassing after about five years. The changes in composite wood

manufacturing processes occurred in the early 1980s; as a result, decreased

initial off-gassing rates did occur substantially at one time. Manufacturers have
IV - 6

continued to change their processes to a lesser extent, so emissions have

declined a small amount since the 1980s, but not enough to warrant a more

complex mathematical approach associated with varying ages of housing stock.

For the same reasons, a 49% reduction of the peak values measured by Sexton

should be representative of today’s high-end formaldehyde concentrations. An

older house will not have high concentrations of formaldehyde as a result of

composite wood materials that had a high initial emission rate 20 years ago.

One issue not addressed by the report directly is how much HCHO concentrations

decline with building age due to out-gassing, etc. Some discussion of the aging effect is

necessary, hopefully with some quantitative estimate of the decline in HCHO with age.

The discussion on p. III-1, para. 6 – that human activities generating HCHO offset the

aging effect – is incorrect on its face, unless there has been an increase in such

activities with time. Besides, if such activities are important, they deserve their own set

of exposure estimates.

Response: A paragraph has been added to describe the observed decrease in

home formaldehyde levels during the first five years in new manufactured homes

(Sexton et al., 1986). An old (1980s) analysis of a small number of Oak Ridge,

TN homes showed a distinct drop from years 1-5, relative to formaldehyde levels

in older homes; however, while we have the slide based on that study, we could

not locate the reference, and so have not yet included that study in the revised

report. The report also contains other references to chamber studies and

measurements in test homes taken eight to ten months after an initial

measurement.

As building materials age and formaldehyde emissions decrease, people’s

activities have a more significant impact on indoor formaldehyde concentrations.

For example, cigarette smoking, use of combustion appliances, the introduction

of new clothing and fabrics, and the result of indoor air chemistry will become the

major formaldehyde sources (not the building materials). Older homes can also

experience substantial increases in their formaldehyde levels when new

bookcases or furnishings are purchased, or when remodeling occurs.

Appendix III also presents an estimate for HCHO concentrations in conventional homes,

which is based on a sample-size weighted average of two studies. Given the different

natures of the two studies, this averaging is not justified. The report notes the limitations

of the study conducted in southern CA – limited by the fact that it was summer only with

potentially high ventilation rates due to doors and windows being open. The only

legitimate comparison that can be made with these data are with data collected under

similar conditions in the AZ study – either as a reality check or possibly to add the data

from the two studies together for the same seasonal conditions. The AZ study also has

its limitations with respect to its application to CA housing and these need to be

discussed. While it appears reasonable to argue that construction practices and

ventilation conditions may be similar (enough), a probability based sample for AZ will be

heavily biased toward houses in Phoenix and Tucson, whose climates may be similar to

some areas in southern CA, but not likely the coastal population centers like San Diego,

LA and especially the SF Bay Area. Given that both temperature and humidity affect

HCHO emission rates, these issues deserve further discussion in the report – perhaps

with some emission-rate-based adjustments.
IV - 7

Response: In essence, this comment highlights the lack of recent California

data for this topic. Reasons for including the two studies follow. The Arizona

study is a recent study, and it is weighted to be representative of the entire

Arizona population. To the extent new homes are included, the study includes

accurate indoor concentrations for newly constructed homes. It is possible that

differences in temperature, humidity, and ventilation considerations relative to

California would lead to different indoor formaldehyde levels in California.

However, those values are certainly within the same order of magnitude, and

probably are within a factor of 2 of the Arizona homes. As far as we know, the

study conducted in Southern California is the most recent California study. We

felt it should be included, despite its shortcomings as to older housing stock and

only summer sampling. As you mention, these facts are explained in the

appendix, then a weighted combined estimate is calculated.

With respect to the peak concentration, there is certainly no good basis for adjusting the

peak measurement from the AZ study. However, the report is inconsistent in its

derivation and use of peak concentrations/exposures throughout. In those cases where

sufficient measurements have been made, it is best to use a 90 or 95th percentile

approach, which can be estimated directly from the data (if there are sufficient numbers

of measurements) or from a cumulative distribution plot. Such an approach reduces the

impact of an extreme measurement and provides a more statistically sound means of

describing elevated concentrations.

Response: Your comment is well taken. We could leave the Arizona peak result

unadjusted. However, not knowing the conditions surrounding that

measurement, for consistency we adjusted it slightly downward by a weighted

measurement from southern California. The net effect is that we report a peak

of 232 ppb instead of 331 ppb (which industry has commented is much too high).

Peak concentrations are used in Figure 2.4 to illustrate maximum levels that

have been measured; they are used in Figure 2.4 because 90th or 95th percentile

values are not available for most of the categories shown. In Table 2.7, on the

other hand, 90th percentile concentrations for VOCs were available and are

presented. Each is clearly identified.

In the end, given the potential importance of HCHO to indoor contaminant exposures

and risks, a well-defined statewide survey of HCHO concentrations would be the best

way to resolve these questions.

Response: Although we agree that a well-defined statewide survey of

formaldehyde concentrations would provide the best results, such an effort is

outside the scope of this report. The California Portable Classroom Study was

recently completed, and provides a recent, statewide, comprehensive study of

indoor formaldehyde levels. The results are disturbing and compelling: using just

the field study results, which were the most conservative measurements, we

found that over 4% of the classrooms had formaldehyde levels above OEHHA’s

acute REL for irritant effects, and all classrooms exceeded the acceptable

cancer risk guideline. While a new residential statewide survey of formaldehyde

concentrations would undoubtedly be enlightening, the body of knowledge

associated with formaldehyde, along with cancer risk estimates, indicate that
IV - 8

formaldehyde is a chemical of major concern in the indoor environment and

warrants prompt reduction.

Other VOC/TAC

The review of VOC and TAC is quite extensive in the report. In many respects, however,

it presents an undiscriminating treatment of VOCs, even though it is clear that the

authors recognize the strongly varying potency among different compounds. In addition

to being careful to discriminate among the different compounds that have been

measured, it is also essential to point out that many potentially important compounds for

human health and comfort are not routinely measured. Carslaw (2003) presents a nice

(brief) summary of this issue. Weschler (2004) is also a good source for the latest

information on indoor air chemistry and its relationship to human health and comfort.

(He has referred to this issue under the heading of “stealth chemicals.”) Overall, the

sections on sources, emissions and concentrations of various VOCs need context,

which is provided by health information, and the levels at which health effects occur. In

some cases there are reports of emissions that have been measured on VOCs for which

no toxicologic or health data are reported; the report should either restrict itself to

compounds for which adverse health effects are known or strongly suspected, or at

least clearly separate these from compounds with known health effects, so the reader is

clear.

Response: The VOC section is complex due to the many pollutants, sources,

and health effects that are included within the category. Statements have been

added to clarify that many compounds in indoor air are not routinely measured,

and reactive chemistry is a new field of research. The report states that by

definition there is no safe exposure level to carcinogens; it discusses the concept

of exposure and dose, and refers the reader to the OEHHA website for specific

information. The report quotes work by Hodgson and Levin (2003) stating that in

most cases indoor levels of most VOCs are below health benchmarks such as

chronic Reference Exposure Levels, odor thresholds, and irritancy levels

(Section 2.3.2.1). However, as noted, some are frequently above acceptable

cancer risk levels, and as noted by the panel members, there are many

potentially harmful chemicals that are not routinely measured.

The risk estimates for these materials include HCHO, which is already discussed above.

For the remaining chemicals, the concentrations and exposures are considerably less

certain. The report notes, for example, that with the changes in smoking habits, some of

these exposures (e.g., benzene) may be much smaller than that found in the 1992 study

(Sheldon et al., 1992a). The overall risk estimate (annual cancer deaths) presented in

Table 3.2 (p. 99) of 115 has large uncertainties associated with it (as acknowledged in

the report) yet no estimates are provided for either the low or high case – implying a

much greater precision on the central estimate than is warranted. At a minimum, one

could use formaldehyde exposure as the limiting case (assuming these exposures are

more ubiquitous than are exposures to other chemicals).

Response: As indicated in the report and Appendix II, the risk estimates are

taken from the Comparative Risk Project. That document did not present the full

breadth of information developed during the project, including confidence

intervals or other measures of variability for each carcinogen, although such

uncertainty was stressed in the text of that report. However, the panel’s comment
IV - 9

is noted, and caveats were added in the report and the appendix to emphasize

that the values used are estimates with potentially substantial uncertainty.

Specific comments

1. p 20, “architectural coatings.” The “low VOC” products were developed to minimize

ambient ozone forming potential. This is a very different goal than minimizing toxicity

associated with exposure to primary or secondary emissions indoors. The

presumption in this document is that these low VOC products have yielded benefits

in improved indoor air quality. That presumption requires scientific support, or else it

should be presented as speculation or inference.

Response: Specific information was added regarding ARB restrictions against

using certain toxic air contaminants in consumer products.

2. Missing from the discussion in this section are two source categories that seem

important: outdoor air pollution and attached garages (and their contents). The only

place attached garages are mentioned is on p. 65, second paragraph.

Response: A discussion of information regarding attached garages was added

for both the CO and VOC sections of the report. Some additional information

regarding outdoor pollution was added as well; however, the focus of this report

is on indoor pollution.

3. Health Effects of Formaldehyde (pp. 58-59). Given the large number of people

exposed over the guidelines, as given later, and OEHHA calculations, compare the

estimate the number of cancer deaths from formaldehyde with the actual # of

nasopharyngeal cancer deaths in CA (shouldn’t exceed)

Response: Between 1998-2002 there was an average of 98 nasopharyngeal

cancer deaths per year in California. Our estimate of 62 cancer deaths due to

formaldehyde per year compares very well with this figure. The remaining

cancers are most likely attributable to occupational formaldehyde exposures. We

will add this information to the final version of the report.

4. Indoor Formaldehyde Concentrations (pp 60-61). End of first paragraph: Classrooms

and offices should be of nearly equal concern as homes, given the distributions

shown in Figure 2.4.

Response: Text was adjusted in the report to indicate that classrooms and

conventional homes also are a concern. However, offices have lower

formaldehyde levels as would be expected, due to the different materials used.

5. Page 60, first bullet in 2

nd list. Should not equate “emissions” with “concentrations.”

What does it mean to have “carpet emissions were generally below the limit of

detection of 1 μg/m3?”

Response: Text was changed, thank you.

6. p. 67, last paragraph What levels of 2-methoxyethanol and 2-ethoxyethanol were

found in these cleaning products? These are the solvents associated with
IV - 10

spontaneous abortion in the semiconductor health study (Swan et al., 1995;

Eskenazi et al., 1995); these effects were observed at quite low levels, well under 1

ppm (Hammond et al., 1996). Note that 2-ethoxyethanol is mentioned again on

p.70, 3rd bullet; once again, given its demonstrated toxicity, report levels

Response: Only 2-butoxyethanol was found in the cleaning products. Text was

clarified and the concentration in the cleaning products was added. On page 70,

the compound is 2-ethoxyethylacetate. The reader should refer to the citation for

additional information.

Biological Agents

The treatment of “biological agents” in the Executive Summary effectively states the

main points. Here are a few items that should be considered in revision:

• The list of biological contaminants (p 9) should also include microbial VOCs and

SVOCs, which are often associated with unpleasant odors. (Although the link

between odor and health is not strongly established, odor has well-accepted

historical legitimacy as a basis for air pollution control measures.)

Response: Although firm data associating indoor microbial VOC exposures with

human health effects is not available, the reviewer’s comments relative to

malodors, especially considering individual variation in sensitivity to odors, are

reasonable. MVOCs will be added to the list of biological contaminants.

However, evidence for potential health effects from microbial SVOCs is too

preliminary to include in this document.

• Transmission of infectious disease and exposure to pathogens from poorly

maintained ventilation systems merit attention, as noted. In addition to the points

made in the executive summary (p 9), it might be worth noting concerns about

indoor air transmission of emerging infectious agents, as evidenced by the recent

SARS outbreak. The broader relationship to security concerns and possible

exposure to biological agents (e.g. anthrax spores) may also be worth mentioning.

Response: Added SARS as an example of an emerging infectious agent. A

broader discussion of indoor exposure to bioterrorism agents is beyond the

scope of this document.

• Table ES-2 (p 11) lists the total costs associated with “ETS: asthma episodes” as

0.001 billion $/y and associated with “mold and moisture: asthma and allergies” as

0.22 billion $/y. It is not credible that the cost of mold and moisture-induced asthma

is 200 times that of ETS-induced asthma. See further discussion below.

Response: The medical costs for ETS-induced asthma were revised upward.

Additional detail will be added in the future to include the explanation discussed

below regarding potential underestimates.

Because of differences in the types of data available, the original cost estimates

in Section 3 and Table ES-2 for asthma due to ETS exposure and to moldmoisture exposure were calculated using different methods. The medical cost

estimates for ETS used a unit cost for a doctor’s visit ($42) multiplied by the
IV - 11

number of children with an asthma episode due to ETS exposure. The ETS

estimate does not include adults, and does not include mortality, because such

data are not available. Mortality cost estimates were not made for ETS-induced

asthma because the ARB/OEHHA (2004-2005) risk assessment did not include

premature deaths in its summary table for health. For the mold-moisture

estimates, the medical and mortality costs were derived by taking a fraction of

the total U.S. costs (direct and indirect) for asthma, and multiplying that by the

fractions of asthma attributed to mold and moisture.

In the revised estimate, the medical cost estimates for ETS-induced asthma

were revised upward using a unit cost of $640 (1990 dollars), the per capita cost

of asthma in the U.S. (direct and indirect) cited by Weiss and Sullivan (2001).

The mold-moisture estimate is now 10 times greater than the cost of ETSinduced asthma episodes. This remaining difference between the ETS and moldmoisture total estimates for the medical cost of asthma is due to the following:

• The attributable fraction of asthma due to mold-moisture is higher than that

for asthma due to ETS (13% vs. 3.5%). The ETS value is taken from

ARB/OEHHA (2004-2005).

• The ETS estimate is for children's cases only, so it does not include the

substantial indirect costs for lost work days, as shown in the cost estimates

by Weiss and Sullivan (2001).

• The direct cost for treating children is not fully reflected in the ETS estimate;

the unit cost is based on the population average cost in the U.S., but children

may require more medical care than adults.

• The unit cost used for the ETS estimate has not been adjusted from 1990 to

2000 dollars.

Biological Agents: Chapter 2

• In Table 2.1 (p 33), consider adding “building occupants” to the “major indoor

sources” column for “biological agents.” Certainly this is the major source category

for infectious disease transmission. Another important source is “infestations” by

cockroaches.

Response: The recommended additions were made.

• The underlying reason for the increase in asthma is not well understood. It is

misleading to suggest that indoor and outdoor air pollution are understood to be

important causes. The opening paragraph on p 34 creates an inaccurate impression.

Response: No change was made relative to this comment. The sentence in

question (last sentence in the paragraph) was worded carefully, is already

qualified, and is well-supported by literature citations. We believe the panel may

have misinterpreted the statement, which reads “...indoor and outdoor air

pollution have been identified as potentially important contributors to the increase

of asthma.” Nonetheless, we will clarify this statement in the final version.

• Care should be taken to distinguish information on asthma initiation (becoming an

asthmatic) from information on asthma exacerbation (attacks in asthmatics).

Different pollutants have different impacts, which in turn have different implications
IV - 12

for age distributions, burdens, and policy. If a study being examined does not

provide information allowing us to tell whether the effect was on initiation or

exacerbation, it should be so stated in the discussion.

Response: We agree with the panel’s preference, and that is why both Tables

2.2 and 2.3 (from IOM 2000) are included in the report. Due to time constraints,

we were not able to revisit all papers throughout the report that discuss asthma,

but will make edits accordingly in the final version of the report.

• The specific reference to Tables 2.2 and 2.3 from the IOM report is appropriate.

However, it is important to note that the IOM report only found sufficient evidence of

a causal relationship for several factors: house dust mite (for development and

exacerbation), ETS (for exacerbation among preschoolers), and cat and cockroach

(exacerbation). The text on p 34 overstates the case of causality: “The committee

found that, in addition to the known biological asthma triggers such as mold, house

dust mites, and animal dander, chemicals such as ... can exacerbate asthma in

sensitive individuals.” (Emphasis added here.) This sentence strongly suggests

causality, but for molds scientific evidence only supported a finding of an

association, rather than causality.

Response: The original sentence combined the results of several categories in

a summary sentence, as the first sentence in a paragraph, followed by a specific

discussion of each trigger, which is very explicit. The first sentence has been

revised. Molds were included in the introductory sentence because the focus of

that clause was biologicals vs. chemicals.

• In addition to the IOM, a large review was recently published in the EU related to this

topic (Bornehag et al., 2004). A key conclusion: “Dampness in buildings is a risk

factor for health effects among atopics and non-atopics both in domestic and in

public environments. However, the literature is not conclusive in respect of causative

agents, e.g. mites, microbiological agents and organic chemicals from degraded

building materials.” (Emphasis added here.) Given the existence of authoritative

reviews by scholarly committees such as this EU review and also the IOM reports in

2000 and 2004, it seems inappropriate to give comparable weight to the review

findings of a single scientist (Delfino, 2002) (p 35-36).

Response: Reference to the Bornehag review was added, including the

absence of an identified specific causative agent in damp buildings. The

EuroExpo review (basis for the Bornehag et al. article, 2004) specifically sought

studies that evaluated building dampness and health effects. Thus their

conclusions that damp buildings increased the risk for respiratory symptoms in

non-atopics and asthma exacerbation, but the underlying agent in damp was not

identified. The Delfino review included a different population of studies looking

at the relationship between indoor airborne chemicals and asthma regardless of

moisture problems in the building.

• The discussion of Sick Building Syndrome (SBS) relies on relatively old literature of

limited scope (p 41). More recent investigations that add substantially to the

literature include Mendell et al. (2002), Seppanen and Fisk (2002), and Wargocki et

al. (2002). While the causal connections with pollutants have not been elucidated,
IV - 13

Mendell et al. summarize the state of understanding for biologically plausible

connections. All three of these papers make a strong case for associations between

ventilation system deficiencies and SBS symptoms. The present review should

incorporate some of this more recent evidence.

Response: The suggested references were added to the discussion of Sick

Building Syndrome.

• Section 2.3.4 begins by listing biological contaminants (p 74). Properly, one should

refer to fragments or excreta from house dust mites and cockroaches, rather than

the entire organism. (Also applies at bottom of p 75.)

Response: This additional detail has been added.

• The discussion of health effects of biological contaminants (p 74-81) relies heavily

and appropriately on the recent IOM (2004) review. Overall, this section makes its

major points effectively and accurately. It could be further improved in some specific

details, as described here:

? It is stated (p 75) that “colds are more often transmitted by direct contact.” In

our reading of the literature, the mode of transmission of rhinovirus is not

well known. The statement should be supported by a reference to an

authoritative source, or removed.

Response: Text was changed to acknowledge that the mode of rhinovirus

transmission is not fully understood.

? A conference paper by Myatt et al (2002) is cited in relation to communicable

disease transmission (p 75). A recent peer-reviewed journal article by the

same investigators is a more scientifically compelling source (Myatt et al.,

2004).

Response: Updated reference included.

? In discussing toxic responses to “damp or moldy” buildings (p 75), endotoxins

and mycotoxins are listed as possible causative agents. This presentation

leaves the impression that the problem is clearly of biological origin. The

literature leaves open the possibility that the underlying cause of health

problems in damp buildings is chemical, rather than biological. This point

should not be lost in the presentation of evidence. (This is done well in a

paragraph on p 77.)

Response: The text states that exposure to toxic bacterial and/or fungal

elements in indoor environments is controversial and not proven to be linked to

human health effects.

? Section 2.3.4.2 (p 75-77) discusses “sources” of biological contaminants.

The subsection on house dust mites should note that the allergens are

carried on excreta and body fragments that may become resuspended by

simple indoor activities such as walking and cleaning. The discussion of

cockroaches does not present information about sources. The review should
IV - 14

briefly explain what is allergenic about cockroaches and how exposure might

occur. Similarly, the discussion of viruses does not say anything about

sources of viruses.

Response: Clarification of mite excreta and body fragments as source of

allergen has been added. Comment on potential for mite allergen resuspension

is not included due to the rapid resettling rate and the large size of resuspended

particles (IOM, 2000, p 139). Additions to text were made to augment sections

on cockroach and viral exposure.

? On p 79, a statement is made that “healthy children in damp or moldy

buildings sometimes report having more respiratory infections....” This

statement requires a reference to an appropriate study; otherwise, it is

inappropriate in a scientific review.

Response: Sentence revised and literature citation added.

? Unless you really think pulmonary hemorrhage is a concern (in which case

more support is needed), drop the sentence appearing at the end of the 3

rd

paragraph, p 79.

Response: The sentence will be dropped or additional support added in the

final version of the report.

• Section 2.3.4.3 (p 77) opens with the statement that indoor mold is experiencing

“increasing occurrence at problem levels.” This statement requires supporting

evidence.

Response: It is based on the great demand for mold inspection and remediation

services that did not exist 10-15 years ago, and the increasing number of calls

received from the public by state agencies regarding very serious mold problems

(extensive visible or hidden mold) in homes in California. Mold was hardly

mentioned at ARB’s 1994 indoor air quality symposium, yet at a similar

symposium in 2000, it was the unintended focus of discussion. However, we will

revise the sentence in the final version.

• The discussion of “mold concentrations” (p 80-81) makes the important point that

objective measures of moldy indoor conditions that would pose health problems are

lacking. If indoor mold is deemed a high priority issue (as listed in Table 6.1, p 147),

then research is likely warranted on methods of diagnosis.

Response: The need for additional research in mold environmental assessment

methods was added to the recommendation for further research.

Biological Agents: Chapter 3

• The review determines that 13% of asthma cases are attributable to residential mold

and moisture-problems/dampness. The basis for this determination is an analysis of

four large studies, as summarized in Table 3.4 (p 105). This 13% finding is important

in the context of this review, as it drives the estimates of cost associated with
IV - 15

mortality (Table 3.2, p 99) and morbidity (Table 3.3, p 103). Several concerns arise

that should be considered in revising the draft:

? The estimated asthma costs for ETS is $1.3 million per year, less than 1% of

the estimated cost of asthma for mold & moisture ($190 million per year). It

simply seems implausible that the true difference in costs could be so large,

given these facts. (1) Epidemiology is the basis for both ETS and

mold/moisture to be investigated as “causes” of asthma. (2) The prevalence

of ETS exposure (e.g. in one’s residence) and mold/moisture exposure is

comparable in magnitude (~ 10-30%). (3) The odds ratio for asthma to be

associated with mold/moisture is small in epidemiological terms (1.3-1.6).

The differences should be reviewed and either the estimates revised or the

differences explained.

Response: See the response above, under Biological Agents.

? In presenting cost estimates for mold/moisture, the implication is that there is

a causal association. (This is what is implied in the term “attributable.”) Yet

IOM (2000) could only conclude that there is an association between

exposures to fungi/mold and exacerbation of asthma (Table 2.2, p 35).

Response: Subsequent studies have strengthened the link between

mold/moisture and asthma. Clarification of any causal association will be

added to the report at a later date.

? The studies cited in Table 3.4 are not specific to California. Are construction

and climate conditions sufficiently similar to justify the direct application of

these studies to estimate conditions in California? Even if so, a caution

should be added.

Response: The text was modified to explain the applicability of these studies

to California conditions.

? The presentation states (p 106) that the estimate “does not include the costs

of other indoor allergen sources...” Please confirm that there was careful

control in all of these studies on all other allergenic agents. Mold and

moisture would tend to indicate poor operation and maintenance and this

would likely correlate with the prevalence and levels of other allergenic

agents.

Response: Due to time constraints, those studies will be reviewed in the

future and the report will be revised if needed to add any necessary

clarification.

? At the top of p 106, the figure $24 million should be $240 million.

Response: Thank you, the text was changed.

• The discussion of the potential for control of moisture and mold problems (p. 106) is

inappropriately simplistic. Yes, of course, in principle mold and moisture problems

can be controlled. We can also build a fleet of motor vehicles that don’t emit
IV - 16

excessive pollutants, and we can eliminate smoking-related diseases by having

everyone quit smoking. But these feasible solutions are very challenging to

implement in part because they rely on informed action by large segments of the

population. Any discussion of control should acknowledge the real and substantial

challenges. Specifically, the statement that it is “probably feasible to eliminate at

least 50% of the particle exposures that contribute to asthma” (p 107) is

unsupported speculation and should be removed.

Response: We did not intend to be overly simplistic, but rather, brief. However,

we do believe that preventive maintenance and proper attention to building

operation and maintenance are more readily achievable than some other

resolutions to indoor pollution that require new technologies, for example. The

examples cited above...smoking cessation (where people are addicted), and a

new fleet of low-emitting cars (where new technologies, and actions by both

manufacturers and the public must all be implemented) would in our view be in a

different, more long-term category, because they are more difficult to achieve.

• There is not sound scientific evidence to support the claim that biological particles

are the dominant source of the adverse health effects associated with dampness

and mold. (Furthermore, that statement is not necessary in the discussion here.) (p

104)

Response: One paragraph was revised to remove reference to biological

particles. Other similar references in the document will similarly be revised

before the report is finalized.

Environmental Tobacco Smoke

Health Effects of ETS

The report has properly listed some of the most well known effects of ETS, e.g., lung

cancer and heart disease, but some of the others are dealt with less systematically;

some, e.g. SIDS, asthma induction, are mentioned in one section, but are not included

in the calculations of the Costs of Indoor Air Pollution (Chapter 3). The California EPA

has produced two excellent reviews of the health effects of ETS, Health Effects of

Exposure to Environmental Tobacco Smoke, 1997, and the recent update, Proposed

Identification of Environmental Tobacco Smoke as a Toxic Air Contaminant SRP

Version, October 2004. The information in these reports should be incorporated into

this report, at least as a complete summary and with references to the report. We

suggest a table of these health effects, including the estimated number of Californians

affected by each disease (with upper and lower confidence estimates where available);

this has already been done in the Cal/EPA report on Proposed Identification of ETS as a

TAC, October, 2004. This document on Indoor Air Pollution should be congruent with

the two documents cited above. Note that the effect of ETS on heart disease has a very

profound public health impact, which deserves more attention than has been given in

this report.

Response: The report summarized and cited the information from the October

2004 Part B report by OEHHA. This information has been updated using the

more recent OEHHA estimates, and a table with OEHHA’s case estimates

attributed to ETS exposure has been added to the ETS Health Effects section.
IV - 17

The text and estimates will be further revised as appropriate after the Scientific

Review Panel has approved the ARB/OEHHA ETS document.

Exposure to ETS

Environmental tobacco smoke is a major indoor contaminant/risk factor in CA for which

the exposure estimates currently are substantially uncertain. The report notes this, but

spends considerable time describing studies conducted before smoking was

banned/reduced (pp 71-74). For the most part, these studies have little quantitative

relevance today. Not only have workplace and public (e.g., bars and restaurants) ETS

exposures been reduced to essentially zero, surveys indicate that smoking behavior in

homes is being changed to reduce ETS exposures to non-smoking members of the

household. ETS exposures of nonsmokers should also be adjusted to account for the

observation that cigarette consumption in CA is about half that of the US.

Response: We concur that smoking is nearly gone from California’s public

buildings, and that fewer people are allowing smoking in their homes.

Nonetheless, there are still significant exposures to ETS in some buildings in

California. Older studies and studies of ETS in casinos and bingo parlors were

included in the report for completeness, because some California environments

continue to allow smoking. Some new casinos in the state allow smoking, and

there remains a percentage of homes and other environments where smoking is

allowed. Children are especially at risk of being exposed in homes and cars if an

adult in their family smokes and does not avoid smoking around the children.

It is unclear how the panel’s comment on ETS relates to the pages indicated,

which discuss VOC levels in homes, not ETS. However, if the concern is that the

VOC levels are outdated, cigarettes are not the primary indoor source of most of

the VOCs discussed. Only the benzene measurements (and to a lessor extent

xylene and toluene) would be expected to be substantially different in homes

now. Additionally, the VOC study indicated was the last large, population-based

indoor/personal VOC study to be conducted in the state, and thus warrants

discussion. The Energy Commission is funding, and ARB is managing, a study

of indoor air quality, including VOCs, in new California homes, which should

provide more current information.

ETS: Chapter 3

Table 3.1 of the report lists the Unit Costs for Health Effects; these have been treated

unevenly. At the very least, the costs of visits to physicians should be included, as these

have been well studied. As an example, Table 6.11 of the document Proposed

Identification of Environmental Tobacco Smoke as a Toxic Air Contaminant reports that

there are over 50,000 ETS attributable office visits for otitis media for children under the

age of 3; even at $100 per office visit this comes to a cost of over $5 million. There are

ways to incorporate also the lost work time due to having to take the child to a doctor.

Similarly, Table 6.09 lists doctor consultations for respiratory symptoms, and reports a

15% increase if a smoker is in the household, and a 38% increase if two or more

smokers are present. More seriously, young children have over twice the risk of

developing bronchitis or wheezing if they are exposed to a pack or more a day (Table

6.08).
IV - 18

Response: The text and tables have been revised to include unit costs and total

cost estimates for all but one of the health outcomes with estimated case

numbers from Table ES-2 of the OEHHA ETS risk assessment. Otitis media

(middle ear infection) was added. The unit cost for asthma cases has been

increased to $640 per year, based on national per capita averages, as discussed

above. Respiratory symptoms and bronchitis are not included in this table, so

cost estimates were not developed. SIDS was not included in the cost estimate

because cost estimates were not available. Assuming that each case of

premature death from SIDS would have a valuation of $6.3 million, the cost

would total about $130 million. This amount would not significantly affect the total

cost estimate for ETS (over $25 billion in Table 3.6).

The cost of premature delivery was not estimated separately because it overlaps

with the costs of low birth weight to a large degree. Caveats were added to the

text for the additional costs of premature delivery that could not be quantified

currently.

How was the cost for low birth weight children ($118,000 per case) derived? How low

birth weight? Most ETS related low birth weights are small decrements in birth weight—

are these the number of cases of babies born with a weight under a given weight, or

with a statistically significant lower birth weight?

Response: The cost is based on U.S. EPA’s Cost of Illness report, as

summarized in Section 3. U.S. EPA compared the costs for low birth weight

infants (less than 2,500 g) vs. other infants. OEHHA (2004) attributed a 20-100

g decrement in birth weight due to ETS exposure, and a downward shift in the

distribution of birth weights. The final report will clarify this discussion.

Parts of Table 3.3 seem inconsistent. For example, the medical cost for ETS asthma

episodes is estimated at $42 each, yielding an estimated cost per year of $1.3 million,

while asthma costs related to mold and moisture are estimated over 100 times greater--

$190 million. Does this really make sense? What about emergency room visits for

asthma attacks? Different methodologies may have been used to derive these numbers

(see page 106), but they need to be reconciled when they are compared and

contrasted, as in this table.

Response: The text and tables have been revised, as discussed above.

ETS risk assessment

The basis for the risk estimate in this report (p. 100) is from OEHHA, based only on

spousal smoking (incorrectly referred to as 2004 – should be 2003c), although this has

apparently not yet been peer reviewed by the external review panel for OEHHA.

Response: The text and tables have been revised to reflect the latest OEHHA

risk assessment, which has been revised in response to the panel comments

and is still under review.

The risk estimate given on p. 100 is based on estimated US lung cancer rates, re-scaled

for the CA population fraction, corrected to the year 2000. No correction was made for
IV - 19

the differences in smoking rates, although the data are discussed in para. 5 and the

same data are used to correct the risk estimates for radon (described earlier). This

would reduce the central estimate to ~ 275, based on the estimated number of smokers.

An even lower estimate would result from the observation that cigarette consumption in

CA is about half that of the US.

Response: Changes, clarifications and caveats will be to added to the report at

a later date to reflect the latest OEHHA risk estimates and with the radon

approach.

Table 3.2 (p. 99) surprisingly does not provide upper or lower bound estimates for

annual lung cancer cases associated with ETS. Clearly such bounds are necessary, as

the current estimates are misleading as to the precision of the central estimate. At the

lower end, it is possible that behavior modification by smokers in their homes has

reduced non-smoker exposures. At the upper end, estimates of ETS exposure based

on nicotine measurements may be underestimated, based on recent work reported by

Apte, et al (2004). This work demonstrated that for situations where the interior surfaces

are not chronically exposed to ETS, nicotine sorbs to these surfaces more rapidly, thus

leading to lower measured nicotine concentrations in the air (and hence, lower ETSRSP exposure estimates).

Response: The text was revised to show the range in the latest OEHHA

estimates. OEHHA used the lower bound because it was based on the best

study available.

Particles (PM)

We were concerned that the health effects of indoor PM were not discussed in detail.

Although PM epi has not been done with indoor-generated PM (IPM) per se, there is

little reason to think that IPM is somehow not a health hazard, given its sources

(combustion, for example). And, if less hazardous than outdoor PM, it is unlikely to be

so by a large factor. Extrapolating from outdoor PM to IPM is less uncertain than

extrapolating, e.g., from high dose-rate studies to low dose-rate environmental

conditions, or from animal studies to humans.

This raises a variant of the drunk-looking-under-the-streetlamp principle, i.e., it is a bit of

an anomaly that we have such excellent and extensive work on outdoor epi. It is simply

because, unlike most risk factors, a small number (often just 1) of existing measurement

stations can be used to characterize reasonably well the changes in exposure to huge

populations with reasonably good health records for important outcomes. The area

illuminated by this strong streetlamp, however, should not be confused with the area

where the biggest impacts from PM exist (which include different locations, populations,

and diseases). With appropriate care, we should attempt to extrapolate the results to

the darker parts of the street (e.g., indoor PM, vulnerable populations, and, even, end

points not usually examined, childhood pneumonia, for example, as done in the WHO

Comparative Risk Assessment (Cohen et al., 2004). Such kinds of extrapolations are

already accepted as necessary and useful from occupational settings and animal

studies to indoor environments, arguably larger stretches than from outdoor PM to IPM.
IV - 20

If CARB were to extrapolate outdoor PM epi to indoor concentrations from indoor

sources, even if there were to be some discounting due to different particle mixes, the

results are likely to be much larger than the relatively small contributions to frank health

risks from VOCs. Given that it is based on epi with similar populations and exposure

levels (and not animals and high-exposure occupational settings), it would likely be more

convincing as well to most observers.

Response: We agree that indoor PM assuredly has large impacts on health.

Accordingly, the November 2004 report included a full three-page discussion of

the health effects of ambient PM (more than any other pollutant in the report),

because there is no such body of information for indoor PM. That was followed

by a discussion of the likelihood that indoor PM has similar effects. In response

to the panel’s comments, we have added additional studies and text to bolster

those sections of the report. However, as discussed in the report, ARB convened

a panel of expert scientists in indoor PM in February 2004 to advise us regarding

the conclusions that can be drawn at this time regarding the health impacts of

indoor PM. They concluded that there is insufficient information on which to base

any type of quantitative estimate of the health impact of indoor PM. Additionally,

a European group conducted a similar assessment, and came to a similar

conclusion (Schneider et al., 2003). We also consulted with the OEHHA’s PM

staff, who concurred with those conclusions. Thus, we are not able to include a

quantitative estimate in this report. However, ARB is in the process of funding

research into the health impacts of indoor-generated PM, beginning with indoor

combustion emissions, and we hope to begin to shed some light on this critical

area very soon. We encourage others to pursue this area of research as well.

Indoor and Personal PM Concentrations

The report overstates the similarity between indoor and personal PM, especially if one

examines CA data as presented in Table 2.5. Thus, the third line of the report

inaccurately states that personal exposures “often exceed both indoor and outdoor

concentrations.” However, examination of Table 2.5 for PM2.5 reveals that while this is

true for studies in Boston, Detroit, and Baltimore (Midwest and east coast), it is less true

for studies in California. In the Suh 2004 and the Linn 1999 studies in LA and the Evans

2000 study in Fresno, the personal exposures were less or comparable to the outdoor

concentrations; only the Suh 2003 study of COPD subjects in LA found personal

exposures greater than outdoor concentrations. Similarly, the report should note that,

while Boston and Detroit had higher indoor than outdoor concentrations of both PM10

and PM2.5, California cities generally had lower indoor concentrations for PM10 and

PM2.5 than ambient concentrations.

Response: Changes were made to the text to clarify these relationships, and

additional edits may be made in the final version of the report. However, the

statement that personal exposure levels are often higher than both indoor and

outdoor concentrations is correct, for the general population and for certain

seasons. Additionally, personal exposures are more often correlated with indoor

concentrations than outdoor, particularly in population-based studies, although a

few studies have found stronger correlations with outdoor PM. Study design,

season, and study population are all key characteristics that affect the PM levels

measured. The PTEAM study, a large population-based study of the general
IV - 21

population conducted in Riverside, found a much higher personal PM exposure

levels relative to indoor and outdoor levels, which were similar. Since PTEAM,

most studies have improved the study design (by using a longitudinal rather than

cross-sectional design), but have focused on sensitive populations (many elderly

or with compromised health), rather than the general population. Members of

sensitive groups often have different activity patterns than the general

population: they may be less active, and conduct fewer activities that generate

indoor PM, and they may operate their homes differently (more or less windowopening), resulting in lower personal exposures and indoor concentrations than

healthy families with active children and pets might generate. There are also

distinct seasonal differences in the relationship among indoor, outdoor, and

personal concentrations, and also differences between PM2.5 relationships and

PM10 relationships: these are both reflected in the Fresno data, for example.

Finally, it should be noted that the Suh studies (2003 and 2004) both involved

very small sample sizes...about a dozen homes in each (the sample size

indicated is the number of daily measurements...this will be clarified in the final

report).

We have several suggestions for Table 2.5

• The values reported should be geometric means or medians, not means, which

can be elevated by one or two high values.

Response: Some studies did not report geometric means, so arithmetic means

are shown. Additionally, the arithmetic mean is more reflective of the entire

distribution, including the high end values that may represent the most impacted

portion of the population.

• The entries should be grouped first by regions of the country

• All studies in one city (e.g., LA, Boston) should be grouped together to ease

comparisons

Response: We are not attempting to compare indoor concentrations by region

of the country. Season, urban vs. rural location, subject type (COPD, etc) and

activity level, and several other factors are at least as important, if not more so,

in determining indoor PM concentrations. Regional groupings might be easier for

identifying California studies, and may be provided in the final version of the

report; however, studies of indoor PM are sufficiently new that studies in other

regions of the country remain very informative.

• Some measure of the dispersion of the data should be included (e.g., SD, GSD)

• The number of samples should be reported

Response: Done.

• Residential data should be separated from office building data

• Include the other office building data mentioned on page 50

Response: The office building data from the BASE study are now shown at the

bottom of each table. The other two studies are not included in the table because

they were conducted in the early to mid-80s, in buildings where substantial
IV - 22

smoking occurred, and are not particularly relevant to current conditions in

California.

• Where possible, report data separately for buildings where smoking did and did

not occur during the sample collection

Response: Clarification has been added in the text that most of the studies

shown in the table are from homes or buildings where little or no smoking

occurred, most often because of the health problems of the participants. One

exception is the PTEAM study, in which a very small percentage of homes were

smoking homes. A footnote will be added to the table in the future.

Other points:

? p. 49 top: Spengler et al. reported measurements of personal, indoor,

and outdoor PM sampling long before the PTEAM study—we think it was

the 6 City data reported in the 1980s

? p. 49 3

rd paragraph, 6th line:, rather than “for each of the three groups,”

actually,, for 3 of the 4 groups for outdoors, and all groups for indoors

? p. 49, 3

rd paragraph, 6th and 7th lines: the data on PM10 personal are

missing from the Tab le—please include

? p. 50 2nd line: 19.6 here but 19.5 in table—reconcile

? p. 50, 8th and 9th lines: a percentage is missing

Response: Corrections and additions have been made, thank you.

? p. 50, 2

nd paragraph: The data discussed here are quite different from

other comparable data, where the personal exposures were comparable

to the indoor, and less than the outdoor; the discussion is therefore

misleading

Response: Comment noted.

? p. 50 3

rd paragraph, line 8; the indoor concentrations reported should be

compared to outdoor concentrations. Did the BASE study uniformly

exclude buildings with smoking (we think it did not)? This should be

considered in it evaluation here.

? Do we have data on smoking for any of the home studies reported? If so,

report whether smoking occurred during sampling, and separate reports

from homes with smoking from those without smoking and place on

adjacent lines

? The last two points may lead to an observation along the lines that

smoking is a major contributor to indoor PM. The Spengler study alluded

to earlier also provides data on this point, and estimates an increase in

PM of about 1 ug/m3 per cigarette smoked per day, or 20 ug/m3 per pack.

Response: Information from Spengler et al was added in the PM source

emissions section. Where smoking occurs, it is indeed the greatest contributor

to indoor PM, as shown in many earlier indoor PM studies not included in Table

2.5. However, as mentioned above, most of the studies in Table 2.5 had little or

no smoking in the homes during monitoring. We will review these studies and
IV - 23

determine whether there is sufficient additional information to warrant separation

of smoking and non-smoking locations in this table.

Carbon Monoxide (CO)

• Page 52. It seems unlikely that the epidemiological studies cited here determined

CO exposures with a high degree of accuracy.

• Owing to indoor sources and also variable proximity to vehicular emissions, one

doubts that ambient CO is a good proxy for CO inhalation exposure.

Response: The California CO study was a study of death certificates, not an

epidemiology study, where CO poisoning was the known cause of death.

Ambient CO was not measured or discussed in this study. Rather, blood CO

levels and the decedents’ immediate history were used to assign a cause of CO

poisoning in the death certificates.

• First two lines on p. 52 state natural gas, propane and kerosene fuels add to >

99%, but motor vehicles “also took a substantial toll” (31% in figure 2.2)

Response: The summed percents relate to the preceding sentences, which

discuss the percent of the indoor deaths attributable to the different types of

indoor sources. Those indoor sources contributed about 50% of the total deaths

due to accidental CO poisoning, as stated in the preceding sentences. Additional

clarification will be added to the final version of the report.

• How many homes had indoor CO greater than the state standard of 20 ppm?

Response: It is unclear which study this comment is referring to. The CO

mortality study did not involve measured data, as indicated above. In the Wilson

et al study, several homes had levels over 20 ppm; we will insert the actual

number of homes in the final report.

• Page 53, §2.2.4.3. The first line (“most homes have relatively low CO levels”)

begs for support. CO levels in the wintertime may often be persistently elevated

owing to high ambient levels (e.g. in Los Angeles) and to the use of improperly

vented heating devices (e.g. in the mountains).

Response: Our statement is correct and well-supported. In the two large

California studies cited (Wilson et al 1993 and Sheldon et al 1993), both of which

included winter data and sample sizes of 277 and 280 homes, respectively,

neither showed more than a few homes with CO levels above health-based

standards. Ambient CO levels have decreased sufficiently in Los Angeles that

there are very few winter excursions above the ambient standards.

• Perhaps move figure 2.2 and the discussion of types of appliances to section

2.2.4.3, Emissions.

Response: We believe it fits best with the discussion of the results of the

mortality study, but the information from that study could be split as suggested.
IV - 24

• The paragraph that refers to Springston et al. (2002) should point out that these

were commercial buildings (in which combustion appliances might have been

absent altogether).

Response: We will check that for the final version of the report.

• Related to vehicle emissions, probably more important than CO in ice rinks is

accidental poisoning deaths associated with idling motor vehicles in attached

garages. See Marr et al. (1998).

Response: We have added a section on attached garages to the report.

• Page 98, §3.1.1. We see no rationale for excluding CO poisoning deaths from

motor vehicle emissions as many of these occur in indoor spaces. See Marr et

al., 1998.

• Page 98, middle. A better reference (than CPSC, 1997) to the recent state of

accidental CO poisoning deaths nationwide is Mott et al., 2002.

Response: In the California CO mortality study, vehicle-related CO deaths often

occurred outdoors, under circumstances such as individuals trying to warm up

the car (using the heater while idling a long time), and many were associated

with alcohol use. The statistics on the number of deaths that occurred in an

attached garage were not readily available, and would likely add very little to the

total CO mortality estimate.

Pesticides

Pesticides are substantially discussed in the report, but notably absent from either the

“high priority” or “medium priority” source lists for mitigation. The omission seems

inappropriate. The underlying reason for the omission is unclear.

Response: Pesticides were added to the medium priority sources for mitigation.

Health effects section (p. 81, para 5 ff) on pesticides is weak. More CA data on pesticide

concentrations should be available now from the ongoing studies by Pat Buffler and

Brenda Eskenazi at UC Berkeley, however.

Response: Information was added to the pesticide health effects section.

However, time did not permit consulting with the investigators suggested above.

Non-industrial Workplace Exposures

With respect to workplace exposures, the report focuses mostly on office exposures,

and these are treated well. However, there are other non-industrial workplace exposures

that should be addressed. Brief mention is a made of a few of these occupations

(janitors, barbers, and beauticians), however, a more systematic effort is needed to

address the exposures of these workers, and to evaluate other non-industrial

occupations with important exposures, e.g., auto repair shops, indoor construction work.

This would be, however, an enormous task, and perhaps the scope of the report should
IV - 25

actually be restricted to home and office exposures, although the original charge to ARB

was broader. A clear statement is needed at the start of what is covered.

Response: We realize the information on non-industrial workplaces was weak.

Thank you for acknowledging that inclusion of this information could be “an

enormous task”. We have included a section, 2.4, to highlight some of the

exposure information that is known regarding non-office, non-industrial

workplaces. While not a robust assessment, the new section provides a

reasonable handle on the scope of the many indoor air quality issues that arise

in non-industrial workplaces in California. Additional information may be added

to the final report.

COMMENTS BY SECTION

Executive Summary

As the summary stands now, a reader cannot get a good overview of either the health

outcomes or of the sources.

The report contains a large amount of data on a very broad topic. However, it does not

synthesize the data well. Thus the second bullet states 230 excess cancers occur from

indoor carcinogens, yet that excludes those from ETS, radon. The authors should

choose a template to summarize the data, either by health outcome or by source—

currently it is mixed, and not all the data are presented. To the degree possible,

numbers should be presented for all of the outcomes for all of the relevant exposures

(e.g., numbers of lung cancers attributable to VOCs and radon, but not ETS, are

presented; no numbers are presented for the number of coronary heart disease deaths

and cases attributed to indoor air problems, yet this is likely to be a much larger

number).

Response: It has been a challenging task to organize the information in this

report. We have attempted to organize information by pollutant with Table ES-1

serving as a summary for what is known about the pollutants, sources, and

associated health effects. Methods for mitigation are organized by source

categories (Table ES 3.1 and 3.2) because manufacturing changes have the

potential to address multiple pollutants (if more than one is present) associated

with a given product. The numerical estimates for the major health endpoints

were specified throughout the summary.

Page 6, penultimate paragraph. The reference to ambient PM mortality should not refer

to an association with “exposures” but rather with “concentrations.” (It is very important

to be precise in distinguishing among all of the parameters of concern.)

Response: Statement corrected, thank you.

Page 8, first paragraph. Worth mentioning here that ozone produces PM as a byproduct

as well.

Response: Text now includes PM.
IV - 26

Chapter 4 Existing Regulations

The discussion of current regulations, guidelines and practices seems very complete

and the review committee did not identify any major omissions. As a general observation

however, the discussion presented in this chapter is not always careful to note that

many of these regulations, etc. are explicitly focused on outdoor air quality and only

secondarily – if then – on indoor air quality.

Response: The text was revised.

Transference of standards based on outdoor epi to indoor air should be done with

caution. Outdoor epi is done by looking at changes in health based on changes in

outdoor levels, not changes in exposure. Since most people spend most of their time

indoors and the indoor concentrations of outdoor pollutants is less than they are

outdoors, the real impact per unit exposure is higher. Consider, for example, that a

change of 50 ug/m3 of PM causes so much ill-health in the outdoor epi. If the

penetration level is 80%, however, it is actually showing the effect for only a 40 ug/m3

change in exposure. Indoor levels are much more closely related to real exposure,

however, and so, arguably the same amount of ill-health represented by 50 ug/m3 of

outdoor PM would occur with a 40 ug/m3 of indoor pollution (from indoor sources).

Standards should be modified accordingly. All this of course does not take into account

the different populations that may exist in certain indoor environments (more vulnerable)

or different toxicities of indoor and outdoor particles.

Put another way, having a less stringent standard for indoor than outdoor air does not

meet the “laugh test” for protecting public health. Would then an appropriate approach

for pollution control be to ban chimneys and other methods of taking pollutants out of

buildings where people spend time? To the extent that indoor environments can be

considered a public good (and there is a substantial basis for doing so to a significant

degree), the only possible reason to have less stringent standards indoors would be

because it has been shown that IPM is less unhealthy than outdoor PM because of its

chemical/physical characteristics. Arguments about population vulnerability and less

than 100% penetration from outdoors to indoors only argue for more strict standards

indoors.

Response: Ambient air quality standards were used as approximate

benchmarks in our indoor air quality guidelines, similar to what was done for the

WHO guidelines for indoor and outdoor air quality. Ambient air quality standards

are comprised of two parts: a concentration and an exposure duration, or

averaging time, that are relatively safe, with a margin of safety. A person

exposed to a certain level of PM for one hour would experience the same health

impact whether he/she is standing indoors or outdoors. As long as the

averaging time is specified, there is no need to adjust an indoor guideline

level....the level is set based on the duration of exposure, or averaging time, and

the concentration. Also, to clarify, this section discusses indoor air quality

guidelines, not standards: there are no indoor air quality standards.
IV - 27

Specific comments

1. Page 111. The limitations of workplace regulations are more severe than those

listed. They do not apply to indoor environments that are not workplaces. Also, they

have been developed from an industrial hygiene perspective in which one or a few

key chemicals dominate exposure. They seem entirely ill designed to serve as a

basis for evaluating the health and comfort risks posed by the complex mixtures

found in, e.g., modern office buildings.

Response: There are few buildings that are not workplaces covered by

Cal/OSHA’s regulations. Unlike federal OSHA, Cal/OSHA’s rules apply

regardless of the number of employees. Only federal buildings are not covered

by state regulations. As indicated in our text, Cal/OSHA has not only PELs,

which we agree (and have stated in the report) are inadequate to protect many

people, but they also have other regulations such as the Minimum Building

Ventilation Standard, which applies broadly, and is protective of, or provides

benefits to, any person in the building.

2. Page 113. Have the radon in drinking water regulations been promulgated and

finalized?

Response: Not yet. Will clarify in final report.

3. §4.3 Emission Limits. Much of this section is far from the issue indoor air pollution

(e.g. the discussion of ARB’s consumer products and architectural coatings

programs). Note the earlier comment on whether the coating program has a positive

impact on indoor air.

Response: Language has been added regarding the impact on indoor air (ARB

has prohibited some TACs in certain products, for example).

4. p. 125. The section on “DHS non-binding guidelines” does not discriminate among

VOC emissions based on toxicity. Nor does it consider the possibility of secondary

emissions caused by oxidation (e.g. owing to ozone exposure) of materials.

5. Page 126, first full paragraph. This sentence doesn’t make sense as written:

“emissions from a single material or product cannot exceed one half the chronic

REL.” Emissions would be expressed in mass per time. The REL is expressed in

mass per volume. They cannot be directly compared.

6. Page 127, §4.3.3.3. This statement requires substantiation: “These programs have

been successful in reducing emissions from their products over the last few

decades.”

7. Page 128, bottom. As in comment 64, the discussion of the GEI emissions criteria

mixes measures. The implication is that emissions are to be limited so that

individual VOCs “must meet the criteria of less than 1/10th of the threshold limit

values....” In addition to the problem of equating emissions to concentrations, this

also seems like an ineffective criterion for ensuring good indoor air quality. (An

indoor environment in which multiple chemicals approached 1/10th of their

respective TLVs would not be healthful for general occupancy.)

8. Page 131, lower half. The citation Maeda, 2004 does not appear in the reference

list. (The committee did not audit the concordance between citations and

references in general.)
IV - 28

9. Page 132, §4.4.1.3. Weatherization and duct sealing would affect not only indoor

levels produced by combustion appliances, but from other sources, too.

Response: Text was revised for most of these comments; remainder will be

made in final version.

Chapter 5 Methods to Prevent and Reduce Indoor Air Pollution

In a document that is painstakingly detailed with respect to regulations and guidelines

(30 pages), it is disappointing to find control and mitigation so thinly discussed (5 pages

in the main report, plus 2 in the executive summary). The major themes are more or less

correct: source control, ventilation, public education, air cleaning devices, and building

operation and maintenance. But the level of treatment of these topics is superficial to

the point of being simplistic. This section is the weakest part of the report.

Response: We agree that the section needed work, and have revised and

expanded the entire section.

Detailed critique is provided below for the first two topics.

• Source Control (p 15 and 141)

? “There are many actions that can be taken to reduce indoor air pollution and,

in some cases, completely eliminate sources.” The problem of source control

is much more complex and challenging to implement than acknowledged in

this section.

?

Response: Text was revised.

? Actions taken to “completely eliminate sources” are only pertinent for indoor

emissions, and only for a subset of pollutants. When sources are outdoor air

or the occupants themselves, then complete elimination is not an alternative.

?

Response: Section was revised, but it was never stated that all sources could

be eliminated.

? “The most effective preventive measure is to use building materials,

consumer products, and appliances that emit little or no air pollution.” This

might be a practical alternative for some indoor air quality problems, but only

if such information were widely available, which is not the case. Specifying

reliable and practical test methods that work across the many diverse source

categories is but one of many challenges.

Response: Several available methods are mentioned in the options for

mitigation section, but we agree that others are needed.

? Reformulation of manufactured products and processes to eliminate certain

toxic compounds and minimize overall emissions is an appropriate strategy.

The report should acknowledge that not all indoor air problems are of the sort

that can be controlled by this means (e.g., SBS, for which the causative

agents are not yet known). It should also acknowledge that emitted species
IV - 29

vary markedly in their toxicity and so it is the composition of what is emitted

in addition to the total amount that matters. Third, it should acknowledge the

potential significance of secondary emissions, occurring because of reactions

among the constituents or because of degradation/oxidation with time

following installation or use.

Response: Some revisions have been made, and additional clarification will be

added in the future. A more detailed assessment of potential risk reduction

measures would be conducted before specific product reformulation is

recommended.

• Ventilation. (p 15, p 142-143) Ventilation and its role in influencing indoor air quality

is a much richer subject than can be adequately addressed in the brief treatment it

receives in this report. Overall, relative to its importance, the document undervalues

ventilation as a part of the overall indoor air pollution issue, particularly in office

buildings and other structures with mechanical ventilation. While source control is an

important part of an overall IAQ management strategy, so is the reliable provision of

an adequate supply of good quality ventilation air to indoor spaces. Emissions

control is clearly most important to avoid extreme problems (e.g., CO poisonings).

But emissions will never be reduced to zero. Ventilation has an important role

affecting IAQ in typical indoor environments. Important elements of the ventilation

dimension of the IAQ issue that are inadequately discussed in this report include the

following:

? Data on current ventilation rates in the California building stock and trends.

? Relationship between ventilation and indoor pollutant levels.

? Challenges of providing adequate ventilation in the new residential building

stock, given tighter construction practices.

? Tensions between reducing ventilation for energy efficiency (CEC’s focus)

and the need for adequate ventilation to ensure good IAQ (and the technical

potential for improving ventilation efficiency or effectiveness).

? Challenge of providing good quality ventilation air when ambient air is

unacceptably polluted, a common condition in California.

Response: Information and Figure 5.1 were added. Some additional information

may be added in the final version.

? Consideration of “ambient air” as either a “high priority” or “medium priority”

source category for mitigation.

Response: The mitigation of pollution in ambient air is already a high priority...it

is the reason for ARB’s existence. However, it is not the focus of this report.

Improved air filtration was included in recommendations for improved building

operation and maintenance and indoor clean air technology development.

? (p 22-23) Ensuring adequate ventilation in the building stock is glaringly

absent from the 9 recommended “elements of an indoor air pollution

reduction program.” (Brief mention of proper venting of combustion sources

under point 6, and low-noise fans under point 9 are not commensurate with

the importance of this issue.)
IV - 30

Response: Recommendation No. 7 was revised to specify ventilation as a high

priority. However, ventilation problems are largely ones of enforcement and

diligence, not lack of laws or regulations. The Energy Commission has authority

to establish minimum levels of outdoor air, and Cal/OSHA has authority over

HVAC operation and maintenance.

• Litigation. Needed here also is a section discussing the history of litigation and its

threat as an intervention for IAQ, which is referred to several places in the text, but

never discussed directly. One of the arguments for keeping the government out of

IAQ is that the courts work well enough to keep us safe. Clearly, there have been

successes, which should be acknowledged, but also there are failures. It would also

be good to examine how well this can be expected to work in future and whether

there might be legislation that could make it work better.

Response: Such information was added to the text.

Chapter 6 Prioritization of Sources and Pollutants

The criteria for choosing priorities need to be made a bit more clear as well as how they

were applied. Indeed, it is the committee’s view that there are really two (or possibly

more) tiers – Tier 1 – where the indoor exposures for which the contaminant

concentration or exposure distributions are fairly certain and the exposure-health-risk

relationships are reasonably well understood and Tier 2, where there are uncertainties in

these characterizations that would prevent informed actions (based on current

knowledge). Within these tiers, prioritization criteria could be defined and applied.

Response: We believe that the two tiers of prioritization by source is the best

approach, because then multiple pollutants emitted from a single source can be

addressed at once. It is unclear where the panel believes the known health

effects to be less certain.

• The EPA has done some interesting graphs showing the result of multiplying the

range of exposures to a substance times the range of potencies expected to derive

a range of impact. Can CARB do something similar?

Response: Such an effort would take substantial time. (EPA spent two years

on such an assessment for indoor pollutants, which has not yet been released.)

This approach would be a useful approach for a comprehensive program.

• Are there (hidden) criteria of cost-effectiveness, i.e. are some things left off because

they are considered undoable at reasonable cost?

• Are there (hidden) criteria of political feasibility, i.e. are there some things left off

(e.g., candles, incense) because they would not be acceptable?

Response: No, nothing is hidden. This analysis was not intended to be as

detailed as indicating all sources in a category that might be addressed.

• What happened to lead? It is clearly important, but perhaps A) it was determined

not to be an air issue because most exposure is by other routes or B) it was felt that

it is being handled already. Explanation needed.
IV - 31

• Mercury, although perhaps less important, raises the same questions.

Response: DHS manages the lead health program for the state. Mercury is

handled by DHS and some local health departments.

• Pesticides are conspicuous by their absence on either the high or medium list of

priorities.

• What happened to attached garages? And the related issue of gasoline vapor

exposures? Nasty stuff, gasoline.

Response: Both were added as suggested in the revised report.

How would all the proposed activities be organized and coordinated within the state?

This seems like an extremely important but unaddressed issue.

Response: An agency in charge of a comprehensive program would clearly

need to routinely coordinate with other agencies and interested parties. For state

agencies, the California Indoor Air Quality Interagency Working Group serves as

a good example of how such coordination might be accomplished. That group

meets quarterly and is coordinated by DHS to foster communication and

collaboration among agencies in addressing indoor air issues. Additionally, ARB

has convened state agency review groups for this report and for the Portable

Classrooms Study report, and received excellent input and suggestions on both

reports. Finally, the state Sustainable Building Task Force and other interagency

groups have successfully involved all agencies needed to assess specific issues

or to provide input on various projects, and serve as successful prototypes for

effective interagency communication and coordination.

Chapter 7 Options to Mitigate Indoor Air Pollution

(Pages 22-25 and 153-159) This portion of the report advances recommendations about

actions that can be taken to improve indoor air quality in general, and in schools in

particular. These recommendations are consistent with underlying science, to the extent

that it is currently understood. A few observations about this section are worth

considering during final revision of the report.

• (p 153) An effective overall management system for indoor air quality requires not

only knowledge of pollutant sources, behavior, and consequences, but also strong

expertise in building sciences. Part of the difficulty in effectively responding to the

indoor air pollution problem is not only because of a lack of clear authority for the

issue within any state agency, but also because of fragmented and incomplete

relevant expertise.

Response: Comment noted.

• (p 156-157) The emphasis on source control throughout this report should be

tempered by the findings reported here for schools. Take note that the key problems

reported in schools could not be addressed merely by effective source control. In

addition, effective (and quiet) ventilation systems and proper maintenance are

reported to be of importance.
IV - 32

Response: Our report did not indicate that source control would handle all

indoor air problems. The report indicates throughout that ventilation, public

education, and other measures are all part of an effective, comprehensive

program to reduce indoor pollution. The text has been edited to emphasize this.

Also, regarding schools, one of the most important problems identified was the

elevated levels of formaldehyde, which require source control for effective risk

reduction.

• (p 22 & 153) This sentence, which appears in both the executive summary and in

the main report should be reconsidered: “The approach used to reduce toxic air

contaminants in ambient air, in which source emissions are reduced without setting

enforceable air quality levels, seems most applicable to indoor air.” his statement

seems to reflect an ARB-centered perspective in which only policy tools that have

been developed for ambient air pollution control can be employed. The indoor

environment shares some attributes with ambient air pollution, but it is sufficiently

distinct to invite fundamental rethinking of policy approaches, rather than an effort to

find the best fit from the current portfolio.

Response: This statement was intended to differentiate from an approach more

like the criteria standard-setting approach, in which strict standards are

established and must be met. Instead, our TACs program allows identification of

exposures and risks, with mitigation based on best available technology, not

meeting a pre-set standard. Thus, as technology improves, additional reductions

can be implemented.

Other Points

Methodological issues: When discussing mortality impacts, it is a bit misleading to sum

simple deaths across diseases and risk factors. The disturbing issue about exposures to

pollution or other risk factors, of course, is actually the premature mortality they cause.

Thus, at the least, the term “premature” morality (or deaths) should be the wording.

Response: Text was revised.

As everyone dies, however, the degree of prematurity is critical, which is why lost-lifeyear measures are becoming more widely used. It would not seem possible that ARB

can change the favored metric in one report, but it would seem worthwhile to offer a lostlife-year evaluation in parallel to the simple mortality tabulation, which requires

knowledge/ assumption about the age distribution of the premature mortality. Even

better, of course, would be a combined measure (QALY, DALY, etc) that combines lost

years due to premature mortality with those due to illness/injury. The committee

recognizes that doing so is probably beyond the resources and time available for this

report, however.

Response: Comment noted. However, adding such an approach is beyond the

time and resources available for this report.

There seems to be no discussion of “counterfactual” (CF) values in the assessments,

but rather an implication that the entire pollutant level is up for grabs. Is it a reasonable
IV - 33

assumption that it would be possible to achieve zero concentrations of pollutants indoors

with any conceivable set of interventions? We think not as there is no indoor

environment in the world that has ever achieved it, bar perhaps Level 5 laboratories or

some such. Just as it is inaccurate and misleading to account 100% of outdoor

concentrations to “air pollution”, so it is for indoor pollution (even not accounting for the

outdoor pollution going indoors). The WHO Outdoor Air Comparative Risk Assessment

(CRA), for example, used 7.5 μg/m3 PM2.5 as the counterfactual level for outdoor air

pollution (Cohen et al., 2004). It also did a sensitivity analysis that showed that changing

the CF up or down has a big effect on the resulting overall estimate of burden, as you

might expect. Zero, however, would be clearly wrong and misleading.)

The best CF to use would be one actually demonstrated in real interventions, preferably

determined as a shift in the exposure distribution as it would be in the real world (also

done in the CRA for some risk factors). In lieu of that, you could take the current 10%

level or some such as the CF level with the assumption that it would be possible to

reach that level with feasible interventions.

Response: We did not mean to imply that risk can be reduced 100%. Clearly,

the level of a pollutant outdoors will limit the levels that can be achieved indoors,

in many cases. We have added some information reflective of a “counterfactual”,

such as the estimate of the remaining risk if indoor levels of radon were

decreased to the ambient level, and will add additional information in the final

report.

Section 2.1 The Key Health Impacts identified are asthma and cancer, and both are in

fact very important; two others are cited, irritant effects and sick building syndrome

(which is not itself a health effect). However, there are some other very important health

impacts that should be carefully considered: heart disease, reproductive effects and

diseases of the immune and nervous systems. Asthma and heart disease deserve more

attention, given the large numbers of people affected, and therefore the public health

impact of these diseases. Where there is uncertainty about the effects of indoor air

pollutants on these other diseases, but some evidence exists, the uncertainty should be

acknowledged.

Response: Additional information was other impacts was added to the text.

The committee is also worried about Section 2.1.2, which seems to conflate chemicals

with quite different levels of IARC carcinogenic status (table 2.4, p. 38) without noting

the uncertainty in doing so.

Response: Table 2.4 is simply to inform the reader regarding the IARC status of

some common indoor air pollutants.

Mercury: It has been shown that the concentration can reach nearly 20 mg/m3 indoors

where liquid mercury has been spilled, and the Threshold Limit Value is 0.025 mg/m

3

for elemental mercury. Clearly seriously high levels of mercury are possible if elemental

mercury is left in place, e.g., from a broken thermometer.

Response: This is an accidental situation, and is currently being addressed

through a program in the state to collect old mercury thermometers.
IV - 34

Risk perception: You may want to explore at bit more the anomaly that we heavily

control hazardous waste dumps/leaking gas tanks/etc. and yet allow the very same

chemicals almost free rein inside our houses within easy access of our young children,

and so on. There is a natural tendency to be more concerned with uncontrolled “waste”

but we are fooling ourselves if we act as if the material in our house is really under our

control or somehow safer because we are still using it. This stretches a bit past IAQ per

se, but is an important aspect of the risk perceptions related to it

Response: We agree with the statement and the public’s (and decisionmakers’)

lack of information on indoor air quality or their perception that it does not

present a problem. However, public concern is growing as the public becomes

more aware of the problem. This is evident in the number of public phone calls

we receive from those seeking information, and the large and increasing number

of visits to our indoor air quality website.

A double solidus should be avoided, as it can be ambiguous. Instead of g/m2/h, for

example, use g/(m2-h), which has no ambiguity. (One could use g m-2 h-1, of course, but

this might be too technical-looking for the intended audience.)

Response: The representation of units was not changed. We felt this would be

more understandable by the lay audience.

The word “data” is used as plural in some places and as singular in others.

Response: We try to treat “data” as a plural term, and will edit the final version

carefully.

Minor comments on Executive Summary

• Page 1, 1

st paragraph. Not clear what is meant by “will be considered by the

California Air Resources Board.”

Response: The report will be discussed by our Board at their March meeting, to

receive Board member comments before it will be finalized and sent to the

Legislature.

• Page 1, final paragraph. Rather than “much less diluted,” it is better to say that

indoor emissions are “diluted much more slowly”. (Also, P 28, first full paragraph.)

Response: Change was made.

• Page 1, final paragraph. Smith’s “rule of 1000” has been substantiated by other

investigators. The point made has much broader support than “one investigator has

calculated.” Sample references: Bennett et al., 2002; Lai et al., 2000. (Also, P 28,

middle.)

Response: Additional support by other investigators was noted.
IV - 35

• Page 2, Figure ES-1 (and elsewhere). Please provide references for figures and

tables that display published data.

Response: Some notations were added to figures, and more will be cleaned up

for the final version.

• Page 3, Table ES-1. Another major source of carbon monoxide is attached garages.

Another major source of “formaldehyde and other aldehydes” is environmental

tobacco smoke.

Response: Suggestions were added to table.

• Page 5, Figure ES-2. Apparently the basis for this figure is detailed in the main

report. The executive summary should point to the main body of the report where

the estimates are developed.

Response: So noted.

• Page 5, middle paragraph. Better to refer to “radium-containing” rock and soil as the

source of radon. (Uranium is the ultimate progenitor, but geochemistry can cause

separation between uranium and radium, the immediate parent.)

Response: Some changes were made, but text remains uranium in some places

for ease of understanding by lay readers.

• Page 8, first paragraph. Worth mentioning here that ozone produces PM as a

byproduct as well.

Response: PM was added to text.

• Page 9, final paragraph. To the best of my knowledge, swamp coolers are relatively

uncommon in California. Better to focus on the main ventilation processes:

infiltration, natural ventilation, and flow induced by fans (central air, and local

exhaust).

Response: Swamp coolers are fairly common in some parts of the state. An

ARB-sponsored study specifically identified swamp coolers as a factor in moving

the outdoor air (and ozone) to the indoors. Swamp coolers have also been

associated with increased levels of dust mite allergen in homes.

• Page 10, final paragraph. Specify a time period when referring to IAQ costs as

“potentially in the billions of dollars” (per year?).

Response: Yes, per year. Will clarify here and throughout the report in the final

version.

• Page 12, first paragraph under V. Should point out that workplace standards also

don’t apply to where children spend most of their time.
IV - 36

Response: Workplace standards in California do apply in schools and in publicly

operated day care centers. They of course do not apply in homes, where

children spend most of their time.

• Page 13. Proposition 65 is not mentioned in this list, although it seems that it has

had a salutary effect on air pollutant exposure associated with certain consumer

products, such as the elimination of TCE from “White-Out.”

Response: Prop 65 is discussed later in the report. We agree that is can have

substantial positive impacts on indoor air, although it was not intended to

address indoor air.

• Page 15, “reduction at the source”. Control through source reduction is not so simple

as reducing total mass emission rates. Toxicity can vary by orders of magnitude

among species, and so the toxicity of emissions needs to be factored into any

source-control strategy.

Response: We agree. We would add that the percent of the population affected

and the typical duration of exposure are also important considerations in

determining an appropriate source control strategy.

• Page 16, “air cleaning devices”. The discussion in the executive summary could also

acknowledge the potential for future improvements in air cleaner technology (as

discussed on p. 155 (ICAT for IAQ).

Response: We will add a statement to that section in the final version of the

report. Mitigation option no. 9 (indoor ICAT) includes a statement regarding the

need for effective, low noise air cleaners.

• Page 17. Groundwater is also an important source of radon. Building materials are

potential sources when they contain elevated levels of radium (not “radon gas”).

Response: Both suggestions were included in the tables.

• Page 18, first paragraph. Meaning of phrase is unclear: “the gap in reducing

exposure and risk from categories of indoor sources.”

Response: That phrasing was deleted.

• Page 19, first paragraph. Contrary to what is stated, disease transmission can

certainly occur because infectious agents are “emitted into the indoor environment

per se.”

Response: Text has been corrected.

• Page 23, point 8. Good to mention the importance of indoor chemical reactions, in

particular the importance of pollutant-surface interactions as an area in need of

further study (e.g. ozone-carpet).
IV - 37

Response: We agree that pollutant surface interactions are an aspect of indoor

chemistry that needs further research. However, we believe that is a fine point

not appropriate for the executive summary.

Minor comments, Chapter 1

• Page 27, middle. There are not “several journals” that are “devoted exclusively” to

the field of indoor air quality. Only one is first-rate: Indoor Air. Other journals carry

IAQ articles, but are not devoted to it.

Response: Text was adjusted accordingly.

• Page 29, bottom. Careful: Children do not “inhale a greater quantity” in an absolute

sense (although they do per unit body weight).

Response: Text indicates their increased inhalation is relative to body weight.

• Page 30, “children’s activities”. Reference group is unclear for “younger children

spend more time near indoor sources....”

Response: We will recheck and clarify in the final version.

Minor comments, Chapter 2

• Page 32, second sentence. Not clear what the antecedent is of “some.”

Response: Corrected.

• Page 32, third paragraph. Not clear what the basis is for the statement “only a

fraction of indoor pollutants have been identified.”

Response: Clarification made.

• p. 32, para 3, end. This is quite misleading. With our growing analytic capability

we are approaching a stage where we can essentially measure just about

anything just about everywhere. This is not an indication of concern, however, for

it is dose and toxicity that drive risk, not occurrence.

Response: Indeed dose and toxicity drive risk and that point is made elsewhere

in Chapter 2. However, to the extent that any toxic air contaminant is introduced

into an indoor environment, especially one with children present, it provides the

potential for exposure, and contributes to whatever burden may already exist in

that environment.

• 34, line 3: asthma increase called “tremendous” before any discussion of it.

Response: “Tremendous” was removed.
IV - 38

• p. 34, para 2: Careful, increase in simple asthma prevalence does not track

directly to increases in asthma burden, which is driven by severe asthma attacks

and deaths.

Response: We remain concerned about the rise in asthma prevalence,

however, for all of the reasons discussed.

• Page 39. On the theme of ETS exposure, it may be worth noting the estimates

that have been made of population intake to specific hazardous air pollutants

from residential ETS (Nazaroff and Singer, 2004).

Response: Such information was added to the ETS discussion in section

2.3.3.1.

• Page 40. Not sure that isoprene does not react rapidly with ozone, in comparison

with air-exchange rates. (See Atkinson and Arey, 2003, for confirmation.)

Response: The mention of isoprene relates to the work of Wilkins et al., (2001)

who studied its reactive chemistry.

• 40, last line: What terpene?

Response: The point is that at room concentrations the reactivity products are

probably more irritating than the precursors. The ‘terpene’ refers to those

generally studied, pinene, limonene, etc.

• Page 41. In addition to forming formaldehyde, and secondary PM, the ozoneterpene reaction system generates the OH radical, which is a major story line for

indoor air chemistry. This was an important aspect of the Fan et al. (2003) paper.

The seminal paper on this topic is Weschler and Shields (1996).

Response: Comment noted.

• p. 42, para 2, end: need citations here.

Response: Several citations were added.

• Page 42, bottom. Worth noting is another key difference between indoor PM and

outdoor PM: age of aerosol. Particles with organic content often tend to be

emitted with the carbon in a chemically reduced form. As particles age in the

atmosphere, the carbon is slowly oxidized. This changes the polarity and water

solubility of the organic surface of the particle and could conceivably affect the

toxicity. In this way, a typical indoor combustion particle might be quite different

than a typical outdoor combustion particle.

Response: Good point, will incorporate in final revision.

• Page 45, lower third. The statement that NAAQS for PM are “often exceeded in

California’s indoor environments” is not well supported by evidence presented. If

true, then the current empirical basis is limited, since there are not too many
IV - 39

indoor PM measurements in California. (The PTEAM study is a noteworthy

exception to this statement; however, that is a special case since the

measurements were made during the autumn in Riverside, conditions that would

tend to produce higher indoor PM levels than typical for California as a whole.)

Response: The studies shown in Table 2.5 for California do support that

statement. All of the Los Angeles studies of indoor PM2.5 show indoor averages

that exceed the California standard for PM2.5, annual average of 12 μg/m3.

Similarly, the indoor averages of all of the studies of PM10 conducted in Los

Angeles (not just PTEAM) exceed the state PM10 annual standard of 20 μg/m3.

Finally, as indicated in the statement, homes with indoor sources would be

especially likely to exceed the standards, based on the very high indoor PM

emissions measured in the studies discussed in section 2.2.2.

• Page 45, §2.2.2. Is this line justifiable from existing data? “Indoor PM

concentrations are typically equal to or higher than concurrently measured

outdoor levels.” Evidence suggests that residential PM levels are comparable

between outdoors and indoors (lower without smoking; higher with smoking), but

that in commercial buildings w/o smoking, indoor PM levels are systematically

lower than those outdoors.

Response: See response in earlier responses on PM.

• Page 46, first full paragraph. There are a few recent papers on indoor particles

of outdoor origin that provide a stronger basis for the discussion than those

papers cited here. See, for example, Riley et al., 2002; and Ott et al., 2000.

Response: We will add these citations in the final version of the report.

• Page 46, first full paragraph. The discussion of residential ventilation here is a

bit skewed. Dominating are infiltration, natural ventilation (windows), and

mechanical flow induced by central air systems, exhaust fans, and vented

combustion devices (e.g., fireplaces). Swamp coolers and whole house fans are

rather less common (although perhaps not in Riverside).

Response: There are few fireplaces in southern California. Swamp coolers and

whole house fans are listed as examples of mechanical ventilation devices in

homes that would influence indoor-outdoor relationships.

• Page 46 and elsewhere. No mention is made of the degree to which pollutants

penetrate from outdoors to indoors along with infiltration air. Several papers have

been published on this topic since the mid 1990s, among them being Liu and

Nazaroff (2001).

Response: Information will be added.

• Page 46, 2nd full paragraph. A thorough review of the role of ETS as a source of

indoor PM can be found in Nazaroff and Klepeis (2004).

Response: Thank you. Citation will be added.
IV - 40

• Page 55. Missing from the discussion of nitrogen oxides is the potentially

important chemistry involving the nitrate radical (NO3), which would be formed

indoors whenever NO2 and O3 are found together. See Weschler (2004).

Response: Revisions will be added to the text.

• Page 56, §2.2.6. Reference to “swamp coolers” seems misplaced here, as it

would seem to be a relatively uncommon configuration for the California housing

stock.

Response: The number of homes with swamp coolers is not insignificant, and

the Energy Commission previously encouraged their use, because they are more

energy efficient than refrigerant coolers. Also, in the USC study Children’s Health

Microenvironmental Study, Steve Colome found that homes with swamp coolers

in use had ozone nearly as high as outdoor levels on high ozone days.

• Page 57. Suggest updating the reference of Weschler et al. 1989 to Weschler,

2000.

Response: We will update this and others in the final version of the report.

• Page 57, last paragraph. Ozone from any source can react with indoor surfaces

(not only ozone from ozone generators), including carpets (Weschler et al.,

1992, as cited; and Morrison and Nazaroff, 2002).

Response: Will clarify in final version.

• Page 60, first bullet in 2

nd list. Should not equate “emissions” with

“concentrations.” What does it mean to have “carpet emissions were generally

below the limit of detection of 1 μg/m3?”

Response: Correction made.

• p. 65, para 2: this seems to have about the only mention of attached garages,

which we understood to actually be a major source of exposure. Is this not so?

Response: A section has been added on attached garages.

• Page 72, first paragraph. The result cited from Gilpin et al. (2001) is reported

here differently than on the next page. Here it says that 78% of households with

children didn’t permit indoor smoking in 2001. (Implication: 22% of all households

with children permit indoor smoking.) On the next page, it says that 22% of

smoking parents still allowed smoking inside the home.

Response: Will be corrected in the final version.

• Page 72, bottom. Substantially more detail on ETS emission factors of toxic air

contaminants is now available in the papers by Singer et al. (2002, 2003).
IV - 41

Response: Thank you.

• 72, para 3: Not clear why there is a discussion in this report about active

smoking in pregnant women. Will lead to confusion.

Response: The one sentence about smoking during pregnancy serves to

illustrate health effects associated with ETS.

• p. 74, Table 2.8: what are the averaging times?

Response: Nicotine and RSP concentrations in this table represent different

averaging times because they are from multiple studies. The ETS document

prepared by ARB to identify ETS as a TAC has a full summary of the averaging

times.

• Page 75, first bullet. The statement that “colds are more often transmitted by

direct contact” should be supported with a reference. My understanding is that

the mode of transmission of rhinovirus is largely unknown.

Response: Text was changed.

• Page 85, §2.3.6.2. Should also mention candles with metal wicks as a source of

lead exposure. (Van Alphen, 1999)

Response: This was added to the report.

• Page 88, §2.3.8. Cooking (hot oils) should also be mentioned as a potentially

important source of PAHs (it is in §2.3.8.2, but not in the opening paragraph).

(Reference: Siegmann and Sattler, 1996).

Response: Cooking oils were added to opening paragraph. Citation was

included in source discussion.

• Page 91, Asbestos: This section should first explain the relevance of asbestos

fibers >5 microns long. Explain the standards and the restriction to biologically

relevant fibers. Keep the units constant, e.g., fibers/ml or per m3.

Response: Text was modified to discuss the impact of fiber length and the use

of fiber length for standard setting. The units are the same as those used by the

authors of various papers.

• Page 93 Health effects of PBDEs: Even if NOELs are not available, give LOELs.

Again, some context is needed to understand other exposures.

Response: Additional information will be added to the final version of the report.

A statement from Rudel et al. (2003) was added in the concentration section that

indicates 15 compounds measured in her study exceeded guideline levels. Dr.

Rudel also notes that existing guidelines do not consider endocrine effects.
IV - 42

• Page 94 Sources of PBDE: Should explain why PBDE is added to these

materials (fire retardant). PBDE Concentrations: Concentrations should be given

here, and contextualized with health data/standards/health studies.

Response: Text has been added to the source section to indicate PBDEs are

fire retardants. Concentration data were added and contextualized with a

statement about guideline levels.

Minor comments, Chapter 3

• Page 98, §3.1.1. Why exclude CO poisoning deaths from motor vehicle

emissions, as many of these occur in indoor spaces? See Marr et al., 1998.

Response: See previous response.

• Page 98, middle. A better reference (than CPSC, 1997) to the recent state of

accidental CO poisoning deaths nationwide is Mott et al., 2002.

Response: Thank you, we will incorporate this.

• Page 100, middle. “In addition, cigarette consumption by California adults was

found to be about half of the US average....” On what basis? Per smoker? Per

adult?

Response: We will clarify in the final version.

• Page 106-107. Where is this statement substantiated?: “with proper measures,

it is probably feasible to eliminate at least 50% of the particle exposures that

contribute to asthma exacerbation, and likely more.”

Response: See earlier response; however, this statement will be removed.

• Page 107. At a few points in this discussion, it is suggested that the 2%

productivity reduction owing to SBS is “conservative.” Is the evidence sufficiently

strong to conclude whether this is a conservative estimate or not.

Response: The estimate was based on a mid-point value, so it is a conservative

estimate in that context. Subsequent studies (summarized in Wyon 2004)

suggest that even greater worker performance improvements, on the order of 5-

10%, are achievable. This more recent information has been included in the text.

• Page 110. The last sentence on this page seems speculative, especially

regarding IQ effects. Improved IAQ in schools will lead to higher intelligence

quotients among students?!

Response: Yes, the sentence does refer to “potential benefits.” There are

studies that indicate students have higher test scores when in more comfortable

environmental conditions. Lead exposure, which would be reduced by improved
IV - 43

building maintenance and dust control in schools and homes with lead present,

has specifically been associated with decrements in children’s IQ’s.

Minor comments, Chapter 4

• Page 111. The limitations of workplace regulations are more severe than those

listed. They do not apply to indoor environments that are not workplaces. Also,

they have been developed from an industrial hygiene perspective in which one or

a few key chemicals dominate exposure. They seem entirely ill designed to serve

as a basis for evaluating the health and comfort risks posed by the complex

mixtures found in, e.g., modern office buildings.

Response: The second and third paragraphs in this section discuss the

shortcomings of Cal/OSHA regulations relative to full protection of workers.

• Page 111-112. I’m pleased to see the discussion of Prop 65 and the new EPA

radon in water regulations in this section. (Have the radon in water regs

progressed since 2000; update?)

Response: The regulations have not been promulgated yet.

• §4.3 Emission Limits. Much of this section is far from the issue indoor air

pollution (e.g. the discussion of ARB’s consumer products and architectural

coatings programs).

Response: These two ARB programs do limit emissions from products. They

serve as examples of how the agency can work with industry to derive products

with less adverse environmental impacts. Additionally, ARB has restricted the

use of several TACs in certain types of products.

• Page 126, first full paragraph. This sentence doesn’t make sense as written:

“emissions from a single material or product cannot exceed one half the chronic

REL.” Emissions would be expressed in mass per time. The REL is expressed in

mass per volume. They cannot be directly compared.

Response: Text was changed to indicate the emissions are put through a

modeling process to estimate a room concentration.

• Page 127, §4.3.3.3. This statement requires substantiation: “These programs

have been successful in reducing emissions from their products over the last few

decades.”

Response: Text was changed.

• Page 128, bottom. As in comment 64, the discussion of the GEI emissions

criteria mixes measures. The implication is that emissions are to be limited so

that individual VOCs “must meet the criteria of less than 1/10th of the threshold

limit values....” In addition to the problem of equating emissions to

concentrations, this also seems like an ineffective criterion for ensuring good
IV - 44

indoor air quality. (An indoor environment in which multiple chemicals

approached 1/10th of their respective TLVs would not be healthful for general

occupancy.)

Response: Text was changed.

• Page 132, §4.4.1.3. Weatherization and duct sealing would affect not only indoor

levels produced by combustion appliances, but from other sources, too.

Response: text was changed.

Minor comments, Summary

• Page 160, near bottom. The underlying reason for the “rule of 1000” is not

because of the factors cited, but rather because the rate of ventilation provided

to buildings per occupant is about 1000 times less than the amount of windsupplied “ventilation” to an urban area, per inhabitant.

Response: Text has been changed to reflect this correction.

Additional references that might be used in the report: most cited above.

Apte, M.G., Gundel, L.A., Dod, R.L., Russell, M.L., Singer, B.C., Sohn, M.D., Sullivan,

D.P., Chang, G-M, and Sextro, R.G., Indoor Measurements of Environmental

Tobacco Smoke, Final Report to the Tobacco Related Disease Research Program,

Lawrence Berkeley National Lab report LBNL-49148, Berkeley, CA, March 2004.

Atkinson R., Arey J. Gas-phase tropospheric chemistry of biogenic volatile organic

compounds: A review. Atmospheric Environment 37 (supplement 2), 197-219,

2003.

Bennett D.H., McKone T.E., Evans J.S., Nazaroff W.W., Margni, M.D., Jolliet O., Smith

K.R., Defining intake fraction, Environmental Science & Technology 36, 206A-211A,

2002.

Bornehag CG, Sundell J, Bonini S, Custovic A, Malmberg P, Skerfving S, Sigsgaard T,

Verhoeff A, Dampness in buildings as a risk factor for health effects, EUROEXPO: a

multidisciplinary review of the literature (1998-2000) on dampness and mite

exposure in buildings and health effects, Indoor Air 14, 243-257, 2004.

Carslaw N., New directions: Where next with indoor air measurements? Atmospheric

Environment 37, 5645-5646, 2003.

Cohen AJ, Anderson HR, Ostro B, Pandey KD, Krzyzanowski M, Kuenzli N,

Gutschmidt K, Pope CA, Romieu I, Samet JM, Smith KR, Mortality Impacts of Urban

Air Pollution, in Ezzati M, Rodgers AD, Lopez AD, Murray CJL (eds) Comparative

Quantification of Health Risks: Global and Regional Burden of Disease due to

Selected Major Risk Factors, Geneva: World Health Organization, Vol 2 of 3,

pp.1353-1433, 2004.

Eskenazi, B., Gold, E.B., Lasley, B.L., Samuels, S., Hammond, S.K., Wight, S., Rasor,

M.O'N., Hines, C.J., Schenker, M.B. Prospective monitoring of early fetal loss and

clinical spontaneous abortion among female semiconductor workers. American

Journal of Industrial Medicine, 28:833-846, 1995.
IV - 45

Hammond, S.K., Hines, C.J., Hallock, M.F., Woskie, S.R., Kenyon, E., and Schenker,

M.B. Glycol ether exposures in the semiconductor industry. Occupational Hygiene

2:355-366, 1996.

Lai A.C.K., Thatcher T.L., and Nazaroff W.W., Inhalation transfer factors for air pollution

health-risk assessments, Journal of the Air & Waste Management Association 50,

1688-1699, 2000.

Liu DL, Nazaroff WW, Modeling pollutant penetration across building envelopes,

Atmospheric Environment 35, 4451-4462, 2001.

Marr L.C., Morrison G.C., Nazaroff W.W., and Harley R.A., Reducing the risk of

accidental death due to vehicle-related carbon monoxide poisoning, Journal of the

Air and Waste Management Association, 48, 899-906, 1998.

Mendell MJ, Fisk WJ, Kreiss K, Levin H, Alexander D, Cain WS, Girman JR, Hines CJ,

Jensen PA, Milton DK, Rexroat LP, Wallingford KM, Improving the health of workers

in indoor environments: Priority research needs for a national occupational research

agenda, American Journal of Public Health 92, 1430-1440, 2002.

Morrison G.C., and Nazaroff W.W., Ozone interactions with carpet: Secondary

emissions of aldehydes, Environmental Science & Technology, 36, 2185-2192,

2002.

Mott J.A., Wolfe M.I., Alverson C.J., et al., National vehicle emissions policies and

practices and declining US carbon monoxide-related mortality, JAMA 288, 988-995,

2002.

Myatt TA, Johnston SL, Zuo ZF, Wand M, Kebadze T, Rudnick S, Milton DK, Detection

of airborne rhinovirus and its relation to outdoor air supply in office environments,

American Journal of Respiratory and Critical Care Medicine 169, 1187-1190, 2004.

Nazaroff W.W. and Singer B.C., Inhalation of hazardous air pollutants from

environmental tobacco smoke in US residences, Journal of Exposure Analysis and

Environmental Epidemiology, 14, S71-S77, 2004.

Nazaroff W.W., and Klepeis N.E., Environmental tobacco smoke particles, Indoor

Environment: Airborne Particles and Settled Dust, Morawska L. and Salthammer T.

(Eds.), Wiley-VCH, Weinheim, Germany, 2004, pp. 245-274.

Ott W, Wallace L, Mage D, Predicting particulate (PM10) personal exposure distributions

using a random component superposition statistical model, Journal of the Air &

Waste Management Association 50, 1390-1406, 2000.

Riley W.J., McKone T.E., Lai A.C.K., and Nazaroff W.W., Indoor particulate matter of

outdoor origin: Importance of size-dependent removal mechanisms, Environmental

Science & Technology, 36, 200-207, 2002. [See errata on p. 1868.]

Seppanen O, Fisk WJ, Association of ventilation system type with SBS symptoms in

office workers, Indoor Air 12, 98-112, 2002.

Siegmann K. and Sattler K, Aerosol from hot cooking oil, a possible health hazard,

Journal of Aerosol Science 27 suppl. 1, S493-S494, 1996.

Singer B.C., Hodgson A.T., Guevarra K.S., Hawley E.L., and Nazaroff W.W., Gasphase organics in environmental tobacco smoke: 1. Effects of smoking rate,

ventilation, and furnishing level on emission factors, Environmental Science &

Technology, 36, 846-853, 2002.

Singer B.C., Hodgson A.T. and Nazaroff W.W., Gas-phase organics in environmental

tobacco smoke: 2. Exposure-relevant emission factors and indirect exposures from

habitual smoking, Atmospheric Environment, 37, 5551-5561, 2003.

Swan, S.H., Beaumont, J. Hammond, S.K., Von Behren, J., Green, R.S., Hallock, M.,

Woskie, S.R., Hines, C.J., Schenker, M.B. Historical cohort study of spontaneous
IV - 46

abortion among fabrication workers in the semiconductor health study: Agentspecific analysis. American Journal of Industrial Medicine, 28:751-769, 1995.

Van Alphen M. Emission testing and inhalational exposure-based risk assessment for

candles having Pb metal wick cores, The Science of the Total Environment 244, 53-

65, 1999.

Wargocki P, Sundell J, Bischof W, Brundrett G, Fanger PO, Gyntelberg F, Hanssen SO,

Harrison P, Pickering A, Seppanen O, Wouters P, Ventilation and health in nonindustrial indoor environments: report from a European Multidisciplinary Scientific

Consensus Meeting (EUROVEN), Indoor Air 12, 113-128, 2002.

Weschler C.J. and Shields H.C., Production of the hydroxyl radical in indoor air,

Environmental Science & Technology 30, 3250-3258, 1996.

Weschler C.J., Chemical reactions among indoor pollutants: What we’ve learned in the

new millennium, Indoor Air 14 (Suppl 7), 184-194, 2004.
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APPENDIX V

RESPONSES TO PUBLIC COMMENTS 

on the 

NOVEMBER 2004 REPORT 

We appreciated the comments received on the November 2004 draft report. They have helped

further refine the content and strength of the report.

ACCESS BUSINESS GROUP

Comment: ARB continues to cite consumer products as a source of TACs without considering

the abundance of evidence obtained in the VOC reduction program for ambient air quality.

Exposure of consumers to TACs is unlikely due to a variety of US product safety regulations

and voluntary efforts of manufacturers. ARB has focused reformulation on the highest use

products.

Response: Based on information available, the report accurately characterizes sources

of these compounds and uses caveats such as “at the time the study was conducted”.

“Consumer products” is a broad term, and, as noted in the comment, not all types of

consumer products are regulated by ARB. Additionally, the U.S. product safety

regulations referred to are generally labeling requirements or other requirements that do

not require removal of potential TACs from the product. 

We acknowledge in the report the achievements at eliminating TACs in consumer

products. However, accessing the ARB database of solvents that can be used in

consumer products, we find well over 100 solvents of varying properties and health

effects are listed in the database. The database also indicates the mass emissions of

various VOCs from consumer and commercial products. Data indicate that tons of VOCs

are released on a daily basis, with spray hair styling products being the highest emitter

of pounds of VOCs.

Comment: Table ES-1 is a confusing collection of data. Endocrine disruptors are listed as

pollutants without much evidence that they are found in indoor air. DDT has been discontinued

as a chemical in US commerce for many years. “Organic chemicals” seems misleading since

most of the products listed do not contain the listed pollutants. 

Response: Table ES-1 is designed to give the reader a quick overview of the many

categories of indoor air pollutants. ARB believes it has highlighted the categories of

pollutants most often discussed and studied in the scientific literature. To meet the

intended purpose of the table, pollutants, sources, and potential health effects have

been grouped together. A footnote was previously added that explains that each

pollutant may not cause all of the health effects listed in the third column. A good

summary of concentrations of endocrine disruptors in indoor air and on house dust is

provided by Rudel et al. (2003). Although the sale of DDT was prohibited many years

ago, it is detected in house dust in virtually every study that analyzes for it. It is

extremely persistent in the environment.
V - 2

Comment: The listing of personal care products and cosmetics as a source of formaldehyde is

speculative. Such use has largely been discontinued. When it was present, emissions were

trivial.

Response: Fingernail products were very high emitters of formaldehyde in the Kelly et

al study of formaldehyde emissions funded by the ARB and completed in 1996. In an

unpublished study of products purchased from California retail stores, Akland and

Whitaker (2000) found formaldehyde in several fingernail products and a few other

personal care products as well. Emissions were not necessarily trivial, and most

importantly, personal exposures of the users of the products clearly could be quite high.

Comment: The report states, “Low emission product designs or reformulations can usually be

accomplished by the manufacturer, with minimal impact on the consumer, often with only minor

increased costs.” This is not likely to be true if further reductions in consumer product emissions

above those already achieved in the ambient air VOC emissions reductions. Further reductions

at each phase of regulations have been more difficult and more costly. 

Response: We agree that as regulated products are further regulated, the incremental

reductions are more costly per unit of pollutant reduction. However, ARB regulates only

a limited number of consumer product categories; there is room for emissions reductions

in categories that are not currently regulated. There may also be opportunity for further

reductions in building materials and appliances.

Comment: In Section 1.4 “Environmental Justice Considerations Relative to Indoor Air Quality”,

the citation of pesticide residues in carpeting and room freshener use seem unnecessarily

critical. It seems appropriate to encourage those who live in substandard housing to use

appropriate consumer products to deal with pests and malodors.

Response: Data relating indoor air quality to environmental justice issues are scarce.

The two citations provided on pesticide and air freshener use are appropriate to include

in this section. The Department of Health Services and private organizations participate

in asthma intervention programs to educate low-income individuals to improve their

environment by reducing asthma triggers. Proper use of cleaning products is

undoubtedly part of the educational curriculum. However, preventive measures are

preferred over pesticide use. 

Comment: Section 2.3.3, “Volatile Organic Compounds”, seems confusing as VOCs are cited

when specific toxic or irritant VOCs are intended. Most VOCs have no adverse health effects at

the levels found in indoor air.

Response: VOCs studied by the scientific community in indoor air are reported in this

section. In many cases indoor concentrations are below health benchmark levels.

However, studies indicate that those homes at the high end of distributions may

experience unsafe levels of specific VOCs. Additionally, those with carcinogenic

potential are sometimes elevated above one in a million or one in a hundred thousand

risk levels. . 

Comment: The section on VOC emissions from consumer products has many examples of

misinformation. For example, chloroform is cited as a consequence of laundry and dish washing

when neither would be a likely source, absent chlorine bleaching. Instead the use of municipally

treated water is the likely cause of ambient chloroform. ARB has the opportunity to use the
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survey information on VOC from the consumer products ambient air program to correct these

errors.

Response: The release of chloroform from the use of chlorine-containing cleaning

agents during wash cycles does indeed occur and the report provides appropriate

citations. Prior to discussing this source, the report discusses the release of chloroform

from treated domestic water, particularly during showers. Additional citations will be

added to the report.

AMERICAN CHEMISTRY COUNCIL, PHTHALATE ESTERS PANEL

ARB Comment regarding phthalate esters: The Office of Environmental Health Hazard

Assessment, reviews and assesses the toxicity of chemicals and conducts risk assessments.

Questions related to the toxicity of DEHP and other phthalate esters have been referred to

OEHHA for response. OEHHA has not been able to respond to all of ACC’s detailed comments

on phthalates. Additionally, many of those detailed comments go beyond the scope of this

report. ARB has corrected the IARC classification of DEHP and made other edits accordingly.

Responses to some key comments are provided here. Following OEHHA’s response to other

comments, the final report will be revised as appropriate. 

Comment: The report is technically correct in stating that DEHP is in IARC Group 3, not

classifiable as to human carcinogenicity. The summary fails to present the heart of the IARC’s

conclusion – that “the mechanism by which di(2-ethylhexyl phthalate increases the incidence of

hepatocellular tumours in rats and mice is not relevant to humans” (IARC, 2000). Suggested

alternate wording for the report is provided.

Response: OEHHA has not responded to the comment on mechanism. Based on the

IARC assessment of phthalates, it is correct to say that there is inadequate evidence of

carcinogenicity of DEHP in humans, but that there is sufficient evidence in experimental

animals for carcinogenicity. This information is included in the report on pages 38-39. 

Comment: The final report should not indicate that other phthalates are carcinogenic. Three

pages in the report are identified where it is implied that phthalates are carcinogenic. 

Response: The reference to other phthalates as potential carcinogens was removed

from Appendix II, but the text of the main report was inadvertently left as before. We will

review the final version of the report for those statements and correct as needed. Also,

based on the IARC reclassification of DEHP to Group 3, the one case of cancer from

DEHP in the Comparative Risk Project was subtracted from the indoor cancer risk

estimate, leaving a total of 232, instead of 233, estimated cancers. Because of rounding,

this change did not affect the estimate of 230 excess cancers per year used in the main

report. 

Comment: It is misleading to refer to all phthalates as endocrine disrupters. Comments provided

in June indicate the weight of evidence demonstrates that phthalates neither mimic nor interfere

with estrogen and androgen; some, but not all, phthalates have been shown to cause lowered

testosterone levels when administered to rodents at very high doses. 

Response: We will change the wording to reflect this in the final version of the report. 
V - 4

Comment: Measured levels of phthalates in indoor air are far below animal effect levels. A

previous ARB response indicates that a complete evaluation of their prevalence in indoor air

would be undertaken prior to any recommendations regarding these chemicals. The levels are

so low, they are a very low priority, consideration should be given to removing phthalates

entirely from the report.

Response: We agree that a complete evaluation would be undertaken prior to any

recommendations specific to phthalates. However, because DEHP and other phthalates

may act as endocrine disruptors, phthalates should remain in the report. 

AMERICAN CHEMISTRY COUNCIL, SOLVENTS COUNCIL

Comment: The draft report still fails to adequately assess potential health risks because it fails

to compare indoor air VOC concentrations to relevant health benchmarks. The mere inclusion of

benchmarks with no additional discussion to put these benchmarks into perspective does little to

help the reader accurately assess the potential risk, if any, posed by exposure to indoor air.

The comment then lists five specific chemicals and requests additional discussion of those

chemicals relative to the benchmarks identified for them. 

• Response: The appropriate benchmark comparison for a 1 in 100,000 cancer risk level was

provided for VOCs in Table 2.7. Additionally, the benchmarks for formaldehyde are included

in the text, and comparison to Figure 2.4 is made simple because the benchmarks are

included in the figure. Benchmarks were included in the text for other chemicals as well, as

noted in the commentor’s comments. When benchmarks are presented in the text, it is

assumed the reader can determine if the relevant concentration is above or below the

benchmark. We do not believe that the additional detailed discussion requested for each

chemical is appropriate for this report. The report also states that there is no level of

exposure that is known to be absolutely safe for carcinogens. Thus, for those compounds

identified as carcinogens, any elevated concentration above the concurrent outdoor levels is

undesirable, and indicates the presence of one or more indoor sources. Whether such

sources need to be, or should be, mitigated, depends on many factors. 

Comment: The report presents a misleading impression of VOC health risks because it lumps

“VOCs” together in a single, undifferentiated group. For example, the reference to “VOCs:

cancer” in Table ES-2 should be changed to “Selected Known or Suspected Carcinogens,” and

a footnote added to explain the cost estimate is the sum of cost estimates derived for a certain

number of compounds. The mention that indoor and outdoor air pollution have been identified

as contributors to an increase of asthma is overly broad and undefined. More discussion should

be included on the Institute of Medicine report regarding pollutants and asthma.

Response: The report reflects that VOCs are comprised of a large number of chemicals.

The heading “VOCs: cancer” is explained in the health and cost sections, and is more

informative and specific than the heading suggested. Appendix II clearly lists the

chemicals that were included in the cancer risk estimate. Tables 2.2 and 2.3 are copied

from the Institute of Medicine (IOM) report, with the citation provided and accompanying

discussion in the text. If a reader needs to further explore indoor exposures and

exacerbation or development of asthma they should read the IOM report.

Comment: The prioritization scheme is improved but still fails to represent accurately the

relatively minor risks and costs associated with indoor air VOC exposure. Products should be
V - 5

listed as “high” priority only if it can be demonstrated that exposures exceed or can be

reasonably anticipated to exceed relevant health benchmarks. Hodgson and Levin (2003)

conclude that “for a very few compounds, such as acrolein and formaldehyde, the evidence

based on sensory irritation and chronic toxicity is sufficient to warrant efforts to reduce and

otherwise control the sources of these compounds in buildings.” A quantitative prioritization is

needed to determine whether a “comprehensive program” is required.

Response: The purpose of the report was to provide an overview of sources and health

effects of indoor pollutants, list existing regulations and practices for mitigating

exposures, and describe options and recommendations to improve indoor air quality. A

quantitative prioritization is needed if a comprehensive program is implemented, but that

work is outside the scope of this report. The statement by Hodgson and Levin (2003) is

based on sensory irritation and chronic toxicity, but does not address carcinogenicity.

As mentioned above, for carcinogens, there is no level of exposure that is known to be

absolutely safe. 

Comment: The report still fails to explain adequately that its estimate of excess cancer cases

from indoor air VOCs is very conservative and probably greatly overestimates actual risks,

which could be zero. The report should include more detailed discussion of the uncertainties

inherent in estimating potential excess cancers and the highly conservative nature of its upperbound excess cancer estimates. The report should include more discussion of Wallace (1991)

which states that the risk may be zero.

Response: The VOC cancer risk estimate is based on risk calculations in the

Comparative Risk Project (CCRP), and only the excess cancers for the population

estimated to be exposed above a one in 10,000 risk level were counted. The procedures

used in the CCRP were peer-reviewed, and represent standard practice in health risk

assessment. Additionally, as stated in Appendix II, the CCRP estimate does not include

all VOCs and semi-volatile chemicals that are known or suspected carcinogens. For

example, PAHs other than B(a)P, and aldehydes other than formaldehyde, are not

included, yet there are known indoor sources of those compounds. 

Comment: The report does not demonstrate a need for new legislative authority to regulate

VOCs. The majority of VOCs, when compared to health benchmarks present little or no health

risk. Focusing on VOCs will divert resources away from more hazardous air pollutants, such as

ETS and radon. 

Response: The report does not focus on VOCs. In the high priority group, only building

materials are sources of VOCs. However, as indicated in the report, while indoor VOC

levels typically do not exceed non-cancer health benchmarks, a number of them have

been measured indoors at levels above their respective cancer risk levels of concern. 

ASSOCIATION OF HOME APPLIANCE MANUFACTURERS (AHAM)

Comment: AHAM disagrees with the prioritization of sources. Air cleaners and combustion

appliances should not be on the high priority list and vacuum cleaners should not be on the

medium priority list.

Response: The focus of the air-cleaners category is on those air cleaners that generate

ozone, especially those that generate ozone purposely, to supposedly clean the air
V - 6

(stated in the table). Vacuum cleaners are included in the group of household appliances

and office equipment, although the focus of the group is computers, copy machines, and

printers, which can be sources of pollutant emissions. While the group is medium

priority, vacuum cleaners were included, since they can sometimes re-suspend

substantial amounts of particles. There are some very good vacuum cleaners on the

market; vacuum cleaners would be a low priority in this group. The report also

recommends the development of innovative clean air technologies for indoor air, which

could include improved air cleaner, vacuum cleaner, and combustion appliance

technologies. 

Comment: AHAM believes there is disagreement regarding the validity of activity pattern study

data from the 1980s and 1990s, and recommends further research and discussion with

stakeholders to update information on time spent indoors. 

Response: We are unaware of studies showing any substantially different results from

the early activity pattern studies, in terms of time spent indoors and outdoors.

Subsequent to ARB’s studies, a large national surveys and local field studies have

replicated the general findings on time spent indoors. We believe that the other areas

indicated in the report warrant higher priority for research. 

Comment: The ARB response to an earlier comment indicates that recommended mitigation

options for improved public education and professional training would address the misuse of

outdoor cooking appliances. However, the draft report still does not clearly reflect this important

point. As another example, the public should be educated to follow industry-recommended

cleaning guidelines for humidifiers. Consumers must bear some responsibility for maintaining

their appliances.

Response: The text was revised to include more discussion of public and professional

education and outreach strategies. However, we believe it is largely industry’s

responsibility to educate their customers regarding recommended cleaning and use of

appliances. 

Comment: The report fails to mention, by definition, the combustion of natural gas creates byproducts and therefore, zero-emitting gas appliances are not technologically feasible. A recent

study by the Gas Research Institute found the ANSI/Z21/83 standards have such a high margin

of safety that they do not need to be changed. (Citation provided)

Response: Direct-vented (sealed-combustion) appliances are virtually zero-emitting in

terms of indoor emissions. For example, direct-vent gas furnaces and gas fireplaces are

very energy efficient, are resistant to backdrafting, and have been used widely for years.

Direct vent gas stoves were developed by the Canadian Gas Research Institute in the

1990’s but have not been marketed widely. The report will be revised to clarify this topic.

It is not clear that the ANSI/Z21/83 standards would assure healthful levels of indoor

NO2 and aldehydes as well as CO, especially over the lifetime of the appliance with

typical maintenance levels. 

Comment: Two letters are provided from the Consumer Product Safety Commissions regarding

studies conducted at NIST. These studies state that the current ANSI Z21.1 standards for

emission contain sufficient safety margins. CPSC concluded that no changes are necessary to
V - 7

the voluntary safety standards. AHAM believes a full survey of homes and buildings is needed

to develop a baseline data set.

Response: While the standards may be sufficient for safety (prevention or death)

purposes, we believe they are not sufficient to adequately protect health. The referenced

modeling studies address indoor CO, and, in fact, show that the ARB’s IAQ guideline

and state ambient air quality standard would be exceeded. For example, the 1-hour and

8-hour guideline level would be exceeded in the baking scenarios with smaller kitchen

volumes and lower air exchange rates. The medium and lower air exchange rates used

in the modeling are not as low as those are for some new or weatherized homes in

California. This modeling estimate does not include the contributions of outdoor CO

levels, which can be substantial at times. Further, these studies do not address what is

typically the limiting factor for combustion appliances: indoor NO2. 

A full statewide survey of gas appliances in homes and other buildings is not necessary.

Rather, testing, development, training, and verification are needed to improve the

design, operation, and maintenance of combustion appliances and their venting

systems.

Comment: AHAM objects to most of the proposals in Section 7, “Options to Mitigate Indoor Air

Pollution”. Establishing emission limits specifically for California is not justified. Stakeholders

participate in standard development groups such as ANSI and ASTM, which are designed to

ensure products do not diminish indoor air quality. ARB staff are encouraged to participate with

these standards development groups.

Response: We commend those working on ASTM and ANSI standards that include

consideration of indoor air quality. However, ANSI and ASTM standards are not based

on California housing and environmental factors, and may not adequately protect our

citizens’ health. Additionally, they are not required to be met by all manufacturers. ARB

actively participated in the development of UL/ANSI standards for indoor products in the

past, but unfortunately did not result in standards; we will participate in the future as

resources allow. 

Comment: The report utilizes incorrect data and assumptions. Specifically, it states that there

are no industry consensus standards for vacuum cleaners. ASTM International has a technical

committee, ASTM Committee F11 for Vacuum Cleaners (established in 1972). This committee

has 28 industry consensus standards for vacuum cleaner performance. The committee

undertakes new initiatives. Currently under review is a standard for determining the change in

room air particle counts as a result of vacuum cleaning.

Response: The upcoming standard for airborne particles appears to be the only

standard that addresses IAQ directly. The final report will be revised to incorporate

information on any existing performance standards that protect indoor air quality at that

time.

Comment: The ASTM F11 committee members undertake new initiatives aimed at developing

standards for those performance characteristics not yet covered by the current standards. One

of those....is the development of new standards for determining “the change in room air particle

counts as a result of vacuum cleaning.” The lack of such basic information (about the initiatives)

in the report indicates the ARB should work with stakeholders to gather current and accurate

information rather than seek authority for emission standards. As an example, ARB should
V - 8

work with industry to get more reliable data on usage patterns of range hoods in homes before

making any recommendation.

Response: We commend the ASTM F11 committee for moving forward in this area.

However, development of consensus test methods is different from developing limits that

must be met. Such information is not “basic information” on indoor air quality that

negates the scientific findings in the report. Regarding the specific example given, there

is sufficient information available to conclude that range hood use and design are often

inadequate. The ARB activity pattern studies and other studies confirm that range hood

use in homes is very limited. Additionally, the ARB residential cooking study and other

studies show that range hoods are not always very effective. New and existing

information on this topic would be considered in developing a risk reduction strategy. 

CalAG, LLC

Comment: CalAg, LLC has developed a patented technology for the production of MDF from

California rice straw. The product uses a formaldehyde-free polyurethane resin in the binding

process. Panelboard product will be on the market by early 2007. MDF made with agricultural

fibers and MDI resin will have no off-gassing and will be a substitute for any application that

currently uses wood based MDF. Laminates could be applied for decorative purposes, but

would not be needed to reduce off-gassing. 

Response: Thank you for providing panelboard products that do not emit formaldehyde

for consumers. The report mentions some alternatives currently available, thereby

indicating it is feasible to produce low-emitting products. Your products further

substantiate that alternatives are available. 

CALIFORNIA WOOD INDUSTRY COALITION (by Venable)

Comment: Please explain the Chemical Industry Institute of Toxicology (CIIT) risk assessment

from 1999 in the final report. The CIIT report’s quantitative results should be expressed in

addition to and in distinction to those of OEHHA and its acceptance by other national and

international governmental bodies be acknowledged.

Response: In November 2002, ARB and OEHHA denied a petition to formally review

the CIIT formaldehyde risk assessment. The petition was based in part on the potency

estimate change associated with the CIIT 1999 report. OEHHA determined that the

report was a new analysis of old evidence rather than new evidence. OEHHA stated

that more information is needed to evaluate the risk assessment model used by CIIT,

and that it needs to be peer-reviewed and validated. In the future, if formaldehyde risk

assessments are reevaluated, information stemming from this work may be considered. 

Comment: Recommend removal of the point estimates of risk, or if used, put them into context

by also referencing the Maximum Likelihood Estimate (MLE) expression of the California model

and the CIIT results in close proximity. Although statements are included regarding 95% Upper

Confidence Limit, they are not carried throughout the report. Appendix II discussion reflects the

CRP report as a basis of point estimate of risk, a practice the CRP authors considered

Inappropriate. The Appendix does not even mention the fact that a statistical UCL expression

was used.
V - 9

Response: In the CCRP, the cancer potency value used to estimate risk was the 95th

percentile value, which is standard practice in cancer risk assessments. The CCRP

methods and procedures were reviewed and approved by a peer review committee.

However, the full distribution of exposure values were used for the calculation (not a high

end value), and only the portion of the population with estimated risk above the 1 in

10,000 level were included in the calculation of estimated cancer cases. Had cases with

less than a 1 in 10,000 risk level been included, the estimate would have been much

higher. In reviewing available data on formaldehyde and other carcinogens, ARB staff

found that the CCRP provided the most robust, California-specific analysis of indoor

exposure and risk, and that is why the CCRP estimates were used as a starting point.

The formaldehyde estimate was cut in half, as described in Appendix III, based on

reductions in emissions quantified by an ARB-funded study that showed that emissions

from the most common formaldehyde-emitting products and materials had decreased by

49%. The resulting estimate of 62 excess cancers per year compares very well with the

98 nasopharyngeal cancers per year (average of reported cancers from 1998-2002)

reported by the California Department of Health Services’ cancer registry. The remaining

nasopharyngeal cancer deaths are likely the result of occupational exposures to

formaldehyde, which may at times be higher than residential exposures. However,

workplace users of formaldehyde typically have the benefit of engineering,

administrative, and personal protection controls not used by occupants of new mobile

homes, classrooms, or other buildings. Thus, some new building occupants can

experience higher exposures to formaldehyde over a longer period of time (more hours

per day, and more days per week) than would many workers who use formaldehyde in

their workplace. 

We will review our discussions further and include additional caveats regarding the

uncertainty in any such estimates in the final version of the report. However, we will not

remove the formaldehyde estimates provided, because, as explained below, they are

relatively robust, and supported by current nasopharyngeal death rates.

Comment: Regarding independent laboratory testing for emissions, it is not practical to test a

complex product such as furniture. Pieces vary considerably by size, composition, construction

techniques, etc. It would be impossible to develop a test protocol that would capture meaningful

information on consumer furnishings, per se.

Response: Multiple protocols may be needed to test all types of furniture, but this is not

an impossible task. Some types of furniture have already been tested for emissions.

Precedent has been set for emissions testing of modular office panels and furniture for

the Capitol East End Project. These pieces were purchased in a very large order and

manufactured under controlled conditions. We acknowledge other types of furniture may

have more variety in the components and are manufactured under a variety of

conditions. This topic has been discussed related to the formaldehyde Air Toxics Control

Measure. ARB will pursue continued discussions with industry if the recommendation to

develop an emissions testing procedure is implemented. 

Comment: We are curious as to why some references to the ongoing ARB ATCM proceeding

have been eliminated (pages 26 and 104 of June draft report). The Coalition is proud of the

cooperative effort that is underway in working with ARB staff over the last four years.
V - 10

Response: ARB appreciates the cooperative attitude the composite wood industry has

maintained in working on the formaldehyde ATCM. Reference to the effort was removed

from the Executive Summary because the ATCM is not yet in effect, and the specific

timeline is uncertain. It is still included in the body of the report in Section 4.3.3.1.

Comment: Thank you for adding results of the ARB survey in context of the ATCM proceeding

on page 60. The results are of a chamber concentration, and could be mistakenly interpreted as

the ambient level in a home. Please clarify.

Response: A statement was added to the report to clarify that chamber concentration

does not equal the level in the interior of a home.

Comment: There is one inaccuracy regarding industry standards. The CPA lowered the large

chamber emission limits for certain particleboard products, thus they are not identical to HUD

standard for mobile homes.

Response: Wording was appropriately adjusted in the report.

CLOROX

Comment: The correlation between asthma and bleach (page 37) is inaccurate. The Rosenman

et al study cited in the report lacks scientific rigor.

Response: Authors of the Rosenman et al. (2003) study examined a database of workrelated asthma cases associated with cleaning products, reported primarily by

physicians between 1993 and 1997. The article discusses limitations of the database:

limited documentation of pulmonary function; identification of the causal agent is based

on history; and the database contains only a minority of the work-related asthma cases

for the study states. However, the paper provides further citations for new-onset workrelated asthma occurring after a documented exposure to cleaning products, and more

citations for exacerbation of pre-existing asthma from such exposures. The large

number of cases reported would indicate an association exists between asthma, bleach,

and other cleaning products. 

Comment: Cleaning products when used in the manner directed are part of the solution and not

the cause of asthma. The report fails to recognize the benefits of cleaning products to mitigate

the effects of asthma. Two citations provided.

Response: The role of cleaning properly with spray and liquid disinfectants and other

cleaning products is included in Section 5.5, Building Operation and Maintenance, and

highlighted in the Executive Summary. Cleaning products can reduce bacteria and mold

on surfaces, and reduce exposure to them. Despite this benefit, some can influence

indoor air quality in a manner that requires attention to proper use and potential tradeoffs. Thus, preventive measures that reduce the need for cleaning products are highly

desirable. 
V - 11

CONSUMER SPECIALTY PRODUCTS ASSOCIATION

Comment: CSPA continues to be concerned about the undue emphasis on indoor emissions

that present little or no health risks while failing to highlight more significant risks. ARB fails to

fully appreciate the rigorous federal product safety regulations that govern formulated consumer

products as well as the efforts of manufacturers of those products to assure product safety. The

report understates the regulations affecting products used indoors. The Executive Summary

dismisses U.S. Consumer Product Safety Commission (CPSC) regulations.

Response: It is not clear which indoor emissions CSPA believes are insignificant. We

believe that all indoor emissions of carcinogenic compounds and irritant compounds are

potentially significant, and must be considered in light of other factors such as the

presence of multiple indoor sources, extent of infiltration from outdoors, length of

duration of exposure, and so on. A brief synopsis of the jurisdiction CPSC has over

consumer products is presented in the Executive Summary. More detail is provided in

Section 4.3.1.1 including information on the Federal Hazardous Substances Act. This

Act provides guidelines for determining if a substance is “toxic”, and has labeling

requirements including the use of specific signal words. However, CPSC’s actions are

focused more on safety than health, and CPSC only infrequently prohibits a specific

component in a product. 

Comment: The report fails to adequately consider the public health and indoor air quality

benefits of many of the formulated consumer products, articulated in Attachment C to our

previous comments. Please include Attachment C and A to the website and in the next version

of the report.

Response: The report acknowledges that many consumer products have beneficial

effects. Section 5.5 “Building operation and maintenance” discusses the need for regular

building maintenance, as well as the beneficial aspects of regular and effective cleaning.

Attachments A and C were added to the Clorox comments on our website. 

Comment: Table ES-1 improperly aggregates large classes of pollutants with a wide range of

properties, toxicity, sources, and health effects. Only the most toxic pollutants likely to be

present indoors should be listed and individually paired with its sources and effects. The

category of “Organic Chemicals” is particularly misleading. Issue is taken with air fresheners

and cleaning agents, aerosol sprays, candles, and endocrine disrupters.

Response: Table ES-1 is designed to give the reader a quick overview of the many

categories of indoor air pollutants. ARB believes it has highlighted the categories of

pollutants most often discussed and studied in the scientific literature. To meet the

intended purpose of the table, pollutants, sources, and potential health effects have

been grouped together. The footnote explains that each pollutant may not cause all of

the health effects listed in the third column. The table contents are supported by

information presented in the rest of the report. Research has shown that “air fresheners”

contain VOCs and can have irritating effects on some members of the population.

Candle smoke and aerosol sprays contribute to particulate matter. Further information

on these sources and on endocrine disruptors, including citations, is in the relevant

sections of the report.

Comment: Results of the Rosenman et al. (2003) study and Delfino (2002) review have not

been accurately characterized in the Draft Report. There is no clear evidence that these VOCs
V - 12

are associated in any causative way with asthma. Epidemiological studies such as this are

often subject to confounding factors that mask actual causes.

Response: The report does not indicate that these studies purport a causal relationship,

but rather an association with asthma symptoms (in individuals with asthma), or

exacerbation. See the response to comment submitted by Clorox, above, for further

information on the Rosenman et al study as well.

Comment: The report is correct to note that the specific causes of SBS have not yet been firmly

identified. However, it is contradictory and speculative in implying that “irritant chemicals” are

suspected (Executive Summary).

Response: Refer to Section 2.1.3.2 for a more complete discussion of SBS. Irritation of

the eyes, nose, and skin is generally associated with factors such as low ventilation rate,

recent renovation or remodeling, and sources such as photocopiers. These factors lead

the scientific community to conclude that some component of gaseous or particulate

pollution is the source of the irritation.

Comment: The report lists candle burning as a potential source of harmful PM. It is not clear

what size particles are being discussed. In the Executive Summary, the report does not analyze

the differences in the physics and chemistry of particles outdoors and indoors, including the

greater tendency indoors for particles to agglomerate and fall out, and to be captured in sinks

such as fabrics and carpeting. Studies have shown that particulates from candles are above the

one micron range, and therefore are not considered respirable.

Response: The information requested is discussed in the body of the report in Section

2.2.1. PM from indoor sources, including that from combustion sources, is emitted in a

variety of size ranges, including sizes above and below one micron, all of which can

contribute to health impacts, as described in the report. 

Comment: The term “Pesticides” is a broad term. Pesticides are regulated by state and federal

agencies. They undergo numerous tests and are not capable of producing “adverse

developmental and neurological effects”. Pesticides used indoors do not persist for long in the

environment...synthetic pyrethroids last only six to seven weeks before degrading. 

Response: In Section 2.3.5, the report briefly discusses different categories of

pesticides and their concentrations measured in air and house dust. Indeed, pesticides

are extensively regulated and the results of many types of toxicity tests are required to

register a pesticide. Nonetheless, they can cause adverse effects on humans when

exposure is elevated. The California Department of Pesticide Registration maintains a

Pesticide Illness Surveillance Program. In 2002 (the most recent year data is available),

there were over 1,000 doctor-reported illnesses associated with occupational and nonoccupational exposure to pesticides. Although some newer pesticides do not last as

long as some older ones, they nonetheless persist for some time, and that time may be

longer in real homes than anticipated. At the 2004 annual meeting of the International

Society of Exposure Analysis, several speakers noted their findings that some pesticides

appear to last longer indoors than previously estimated, possibly due to the lack of

weathering (rain, sun) and temperature extremes in indoor locations. 

Comment: Expand the review of biological contaminants in the Executive Summary.
V - 13

Response: We believe the discussion of biological contaminants in the Executive

Summary is an appropriate length.

Comment: The discussion of environmental justice properly notes that many biological asthma

triggers are likely to be present in locations where lower income individuals most often live.

Unfortunately, by stigmatizing cleaning products that eliminate many biological contaminants,

ARB is reducing the likelihood of mitigating these pests.

Response: Environmental justice issues associated with asthma triggers are far more

complex than indicated here. Spengler and others have shown that preventive measures

are most effective in reducing asthma triggers and preventing exposure to them in low

income households. Asthma intervention programs managed by the Department of

Health Services and private organizations are working to educate low-income individuals

to improve their environment by reducing asthma triggers. We do not believe we have

stigmatized cleaning products in our report, nor do we believe that low income

households will throw away their cleaning supplies due to the content of this report. 

Comment: Table ES-2 and Table 3.6 show that the vast majority of estimated costs are

associated with ETS and radon. It is unfortunate that cost estimates for biological contaminants

such as infectious diseases were not included. The CDC estimates that infectious diseases

result in Americans spending more than $950 billion on direct medical costs.

Response: We acknowledge the magnitude of the health impacts and costs of infectious

disease in the U.S. However, infectious diseases can be transmitted through routes such

as personal contact, and shared food and utensils among families. It is not feasible in

this document to identify the portion of infectious disease that is solely attributable to

indoor air quality. 

Comment: Table ES-2 implies that all VOCs cause cancer. The few VOCs contributing to this

alleged risk should be specified here.

Response: The Executive Summary relays the highlights of the major findings in the

report. Please refer to Section 3.1.2, “Deaths From Volatile Organic Compounds (VOC)

Exposure” for details on the cancer calculation. Appendix II clearly lists the chemicals

included in the cancer calculation. However, as noted in Appendix II, not all VOCs that

are carcinogens were accounted for in the estimate. 

Comment: In the Executive Summary, it is stated that low-emission product designs or

reformulations can usually be accomplished by the manufacturer, with minimal impact on the

consumer, often with only minor increased costs. This statement is patently false. Industry’s

experience working with ARB regulations indicates it is difficult to maintain product efficacy

during reformulations. Costs in many categories have been substantial.

Response: That sentence refers to the increased costs to the consumer, which typically

are minimal. Costs for reformulations and product changes vary by industry, by facility,

and by other factors, such as whether the changes can be implemented as part of other

planned modernization or other product changes. In the ARB regulatory framework, ARB

conducts economic analyses for proposed regulations. A full analysis would be

conducted if regulatory changes were implemented. It should be noted that, in a review

of the estimated vs. actual costs of implementing mobile source rules, US EPA found

that the actual costs of changes required by rules were much less than those estimated
V - 14

by the relevant stakeholders, and even less than those estimated by EPA (JF Anderson

and T Sherwood, 2002, Comparison of EPA and Other Estimates of Mobile Source Rule

Costs to Actual Price Changes, Presentation at the SAE Government Industry Meeting,

Washington, DC, May 14, 2002.) 

Comment: CSPA likes the segregation of sources into high and medium priority tables. The

high priority source categories are well-documented and should be the focus of any state

activities for the remainder of the decade. 

Response: We are glad you are in agreement with our prioritization. 

Comment: The report states that “non-toxic cleaning products are currently sold in the

marketplace.” Unfortunately, that viewpoint does not take efficacy into account. The legitimacy

of “non-toxic” claims is questionable.

Response: Websites for environmentally friendly products and sensitive populations tout

“non-toxic” alternatives to many products. The message is that alternatives to standard

products are available to do the intended job, though they may take more abrasive

action, a period of contact before removing, etc. We agree with your question about

legitimacy. A self-proclaimed statement about safety carries little weight. That is why

we are promoting several recommendations to mitigate indoor air pollution through

emission limits, emission testing, and a comprehensive management system for indoor

air quality. 

Comment: Table ES-3.2 and Table 6.2 should be edited because very few of the consumer

products listed emit the pollutants listed as examples. Also, the table does not acknowledge the

comprehensive federal regulatory system in place. 

Response: The CPSC has regulated some products, but usually they have used

labeling requirements instead of emission limits or content limits, although some such

actions have been taken. Many products are not regulated for their impact on indoor air

quality. Therefore, federal regulatory efforts have not been adequate for indoor air

quality concerns.

Comment: We do not need a management system for indoor air quality nor need to require

consumer products to be tested for emissions. 

Response: Noted. Our reasons for our recommendations are spelled out in the report.

Introduction and Background

Comment: We are uncertain which “room fresheners” are described on page 32 when referring

to Wiley et al. (1991).

Response: In this case, room fresheners included any of several products such as

aerosol, plug-in devices, or those that work through evaporative diffusion. 
V - 15

Health Impacts, ETS

Comment: It is not true that a high concentration of an aerosol spray is inhaled during product

use. The spray from these products is highly directional to provide product to the intended

target.

Response: The report states that “a high concentration of the chemicals consequently

may be inhaled during product use before the chemical has a chance to become more

dilute in the air”. Despite the fact that the spray is directional, solvent is released into the

air in the vicinity of the user, where it is likely that some fraction of it will be inhaled.

People also move around when using some aerosol sprays, such as when washing

windows, thus increasing the likelihood of inhaling the aerosol. 

Comment: CDC data indicate that the rate of Americans experiencing an asthma attack in a 12-

month period has declined in the last few years.

Response: The rate of asthma attacks may have gone down due to efforts to use

preventative medicines to manage asthma. Asthma treatment is not the focus of this

report.

Comment: Tables 2.2 and 2.3 indicate asthma is associated primarily with agents of biological

origin. There should be more focus on biological contaminants in this discussion.

Response: There is substantial discussion of biologicals in the report.

Comment: Discussion based on the 10-year-old CCRP is of limited relevance because many

product reformulations have occurred. Consumer products have very limited amounts of

formaldehyde, greatly reduced para-dichlorobenzene, and no trichloroethylene. An updated

study should be a condition for any new initiative on indoor air pollution.

Response: As discussed above and in the report, the CCRP estimates were adjusted

(down) where new data are available. Some products used in homes and public

buildings still contain toxic air contaminants, so we believe our estimates are

appropriate. However, as stated in the document, development of a comprehensive

program would include collection of additional information and further assessment. 

Comment: The referenced study by Fan et al. (2003) is described in a very misleading manner.

The authors conclude that the best strategy to reduce indoor reactivity would be to lower

outdoor ozone levels.

Response: The report lists the conclusions of Fan et al. (2003) in the same order that

the author lists them. The first suggested method for mitigation states “it is prudent to

limit the use of products that emit high-reactivity alkenes during episodes when outdoor

ozone levels are elevated”. 

Comment: The section on particulate matter contains only a single paragraph on biological

contaminants. o provide an accurate and balanced perspective, a more thorough review of

biologicals should be provided here.

Response: Biological contaminants are discussed fully in Section 2.3.4, hence they are

given cursory treatment in the PM section.
V - 16

Comment: It is inaccurate to say that consumer products are a source of formaldehyde. Some

coatings and adhesives may emit formaldehyde, but most of our industry’s formulated

household consumer specialty products to not.

Response: Some types of coatings, sealants, caulks, adhesives, cosmetics, and

wallpaper can all emit formaldehyde. Whether or not formaldehyde is an ingredient in a

consumer product, it also can be produced through reaction of some emitted chemicals

with other chemicals present in the indoor environment. 

Comment: Use of the broad term “Volatile Organic Compounds” to represent a very narrow

class of chemicals that may present health concerns is misleading. “Sources and Emissions of

VOCs” contains dated or inaccurate information. Some chemicals such as benzene, toluene,

and para-dichlorobenzene have been greatly decreased in consumer products since the 1991

EPA TEAM studies were conducted. 

Response: Based on information available, the report accurately characterizes sources

of these compounds and uses caveats such as “at the time the study was conducted”.

The report cites more recent studies than the TEAM studies for all chemicals. The

paragraph on para-dichlorobenzene includes citations from Wallace, 2001 and Gordon

et al., 1999. The paragraph on benzene states that the overwhelming source of benzene

exposure for smokers is mainstream cigarette smoke, as well as exposure from auto

exhaust and gasoline vapor emissions. Akland and Whitaker (200) detected toluene

most frequently in auto care products, glues, and personal care products, such as in

fingernail polishes. 

Comment: The section on VOCs is grossly misleading because it fails to acknowledge that the

mere existence of a VOC in indoor air does not mean there is a risk of adverse health impacts.

Many VOCs are not Toxic Air Contaminants and do not present health impacts at the levels at

which they exist in indoor air.

Response: The report does not state that all VOCs are harmful. The report highlights

the chemicals that have been studied in indoor air and are considered by the general

scientific community to be indoor air pollutants. In some cases, chronic RELs or other

health benchmarks are included so the reader can compare reported concentrations to

levels that are expected to be free of adverse health impacts. However, if a chemical is

a carcinogen, there is no known safe exposure level. For a full review of levels

associated with health impacts, please search the OEHHA website.

Comment: Issue is taken with results reported from several studies cited in the report (Akland

and Whitaker, 2000; Zhu et al., 2001; Cooper et al, 1995). 

Response: The report reflects findings from those studies that were conducted on

products available at the time. Akland and Whitaker (2000) was included because,

although not published, all data were obtained from products purchased in retail stores

in California. 

 

Costs

Comment: Data in Table 3.2 are highly misleading. In some cases cost data are given where

etiology has been reasonably established. In other cases, the costs are less certain (ETS
V - 17

cancer and heart disease). The estimate for VOC lung cancer is even more uncertain. It is

misleading and grossly inaccurate to present the same value for “low”, “average”, and “high”

estimates.

Table 3.3 suffers from the same problems as Table 3.2, as it mixes cost estimates of very

different types. “VOCs: cancer” is not a diagnosable health end point. Suggestions are provided

for a better column heading and replacement term for “VOCs: cancer”.

Response: The tables in Section 3 are intended to provide an overall estimate of the

known costs of indoor pollution. The costs for ETS cancer and heart disease are fairly

robust; they are based on estimates published in an EPA document in which all

immediate medical costs are summed. The text in Sections 2 and 3, and Appendix II,

describes the meaning of the word “cancer” in the VOC risk estimates. The range or

confidence intervals in the health risk estimates are discussed in detail in the risk

assessment for ETS by OEHHA. Those values will be finalized after the ARB Scientific

Review Panel has completed their review of OEHHA’s estimates. The confidence

intervals for VOC carcinogens are not provided in the final Comparative Risk report; that

is why the same values are shown in all columns. In the final report, we will delete the

VOC estimate in the high and low columns and use a “not available” designation. 

Methods to prevent and reduce, to the end

Comment: In Section 5.2 “Ventilation”, ARB fails to distinguish between ASHRAE Standard 62.1

for commercial and high-rise residential spaces and 62.2 for all other residential spaces. We

would like to issue caution regarding addendum “n” to 62-2001. Addendum “n” reduces the

prescribed minimum ventilation rates for many spaces, based on low-emitting European

buildings. We urge California to not adopt those lowered ventilation rates and potentially

jeopardize the health of many Californians.

Response: The two ASHRAE ventilation standards are discussed in Section 4, see

Residential Guidelines and Nonresidential Guidelines.

In setting ventilation standards, the California Energy Commission must consider

protection of IAQ. ASHRAE standards along with other information are considered in

developing these ventilation standards; stakeholder input is encouraged.

Thank you for mentioning the low-emitting buildings in Europe. Such buildings highlight

the fact that low-emitting alternatives are available and that other countries give indoor

air quality a higher priority than the U.S. 

Comment: Mitigation options should include recommendations for biological contaminants

because they present the greatest health risks and costs in California. We are concerned that

consumer products are included among materials requiring emissions testing and labeling.

Response: Mitigation options for biological contaminants are being addressed by the

Department of Health Services, federal agencies, and local agencies. Consumer

products are one of several types of products that are recommended for emissions

testing; however, they are in the medium, not high, priority group.
V - 18

DEL ORO

Comment: Remove negative statements about the health effects of d-Limonene and citrus

terpenes. These misleading conclusions will have a negative effect on the American citrus

community.

Response: The June 2004 draft report included some poor wording regarding the

effects associated with terpenes. Language was improved in the November 2004 draft

and is no longer misleading.

DURAFLAME (Cline & Duplissea)

Comment: Manufactured firelogs are not a contributor to indoor pollution. Banning fireplaces in

new construction is overkill. Suggest that consideration be given to middle-ground solutions that

have scant controversy and easy public acceptance. Indoor Air Quality standards would create

a large, intrusive and potentially expensive bureaucracy with scant health benefits. Mandates

that impact personal habits are difficult to enforce. Recommendations for ICAT should include

new and existing products that are clean-burning, such as manufactured firelogs.

Response: We appreciate your development of a lower-emitting product. Such middle

ground options would be considered in the development of any comprehensive program,

or any regulations. It is not our intent to enlarge bureaucracy, nor to impose mandates

that impact people’s choices. Rather, as indicated in the report, changes can be made

at the manufacturing stage, or in the design and construction of buildings, that would

greatly improve indoor air quality.

FLORIDA CHEMICAL COMPANY, INC.

Comment: We would like ARB to remove a statement on page 36 regarding the reporting by

Delfino of a self-reported asthma prevalence associated with several chemicals including

terpenes and limonene. The statement is misleading and will lead to false conclusions.

Scientific literature reports that d-limonene and other terpenes are used to alleviate asthmatic

and respiratory symptoms. 

Response: The results of the study cited by Delfino are pertinent to the report. The

report also contains a caveat that the effects seen may be subject to confounding by

other causal agents.

Comment: Several arguments are made to change language in the report regarding the

reactivity of terpenes with oxidants to produce formaldehyde and ultrafine PM. Generally, the

comment suggests that the word “terpene” be removed from the report. It is pointed out that

conditions used to demonstrate reactions have been laboratory experiments with levels greater

than normally observed indoors. Wilkins et al.(2001) conducted studies on isoprene, rather than

terpenes. 

Response: The important message is that several investigators are confirming that

these chemicals with double bonds react with oxidants present in indoor air to produce

irritating compounds. The paper by Long et al. (2000) clearly shows the generation of
V - 19

ultrafine PM as a result of cleaning with a product containing terpenes under typical

household conditions. This paper measured the production of particles from various

typical indoor activities. Particle production from mopping was exceeded by particle

production from frying and burning food. It is true that the Wilkins study investigated the

reactivity of isoprene. However, other studies cited, in addition to Wilkins, were

conducted with terpenes.

Comment: Scientific literature is not fully quoted, resulting in an inaccurate relaying of

information. Test conditions should be included in the report.

Response: We believe that the report as written accurately relays the authors’ findings

and conclusions. The test conditions of the studies cited are typical, accepted

approaches for identifying reactions and health impacts. 

FORMALDEHYDE COUNCIL

Comment: The costs attributable to VOCs (2% of total indoor air costs) do not justify the

emphasis on VOC reduction in indoor air. A quantitative prioritization, while apparently beyond

the scope of this project, is a necessary step prior to taking action under a comprehensive

program to address indoor sources.

Response: The cost estimates do not necessarily reflect the full extent of exposure and

risk in California. As stated in the report, cost estimates reflect the availability of cost

information and the length of time a given pollutant has been studied. We do not believe

that there is an undue emphasis on reduction of indoor VOCs in the report. The high

priority source categories emit a variety of pollutants, including criteria pollutants,

allergens, radon, and VOCs. As stated in the previous responses to comments, a

detailed prioritization based on quantified criteria would be an appropriate step prior to

taking action under a comprehensive program. 

Comment: The cancer risk assessment methodology developed by the CIIT Centers for Health

Research should be referenced in the final report. Eleven papers have been published over the

past four years on this work. It has undergone extensive review by U.S. EPA, Health Canada,

and has been used by other agencies around the world. Other efforts to refine the

understanding of risk associated with exposure to formaldehyde are anticipated (IRIS and NCI

epidemiology study). The report should acknowledge these forthcoming developments because

they may validate the CIIT approach. Recommendations in the report may not be implemented

for many years, additional information may be available at that time.

Response: In November 2002, ARB and OEHHA denied a petition to formally review

the CIIT formaldehyde risk assessment. The petition was based in part on the potency

estimate change associated with the CIIT 1999 report. OEHHA determined that the

report was a new analysis of old evidence rather than new evidence. OEHHA stated

that more information is needed to evaluate the risk assessment model used by CIIT,

and that it needs to be peer-reviewed and validated. In the future, if formaldehyde risk

assessments are reevaluated, information stemming from this work may be considered. 

Comment: ARB should reconsider mitigation strategies associated with formaldehyde,

particularly the relationship between outdoor and indoor exposure levels. With outdoor levels

above the guideline level, consider the feasibility of a strategy that would seek to make indoor
V - 20

exposure levels lower than outdoor levels. Also consider that in schools, adequate ventilation,

and uncomfortable temperature and humidity levels are also problems of concern. The draft

Report gives an extremely misleading impression that the problem of elevated formaldehyde in

classrooms must be corrected immediately. Outdoor formaldehyde levels also so not meet the

chronic REL guideline.

Response: Indoor formaldehyde levels are several times greater than outdoor levels;

thus, there is a great deal of room for improvement in indoor formaldehyde

concentrations. Reduction of formaldehyde levels in schools with elevated indoor

concentrations is indeed considered a very high priority by ARB, because in some

classrooms the levels are many times the levels considered acceptable even for

prevention of acute effects, and the occupants are children. If regulations are developed

to reduce formaldehyde levels in indoor air, the ambient air concentration will certainly

be taken into account: we would not expect indoor levels to be lower than outdoor levels.

However, we do not agree with the rationale suggested, which is that nothing should be

done indoors because outdoor levels also exceed guidelines (to a much lessor degree).

The majority of the exposure and risk is from the elevated indoor concentrations, which

are several times higher than outdoor levels. 

Comment: Misleading statements about formaldehyde levels in indoor air abound. Two

examples are provided. Include statements (caveats) about the feasibility of meeting health

guidelines based on outdoor levels.

Response: The statements you quoted from the report are correct as written.

Formaldehyde levels nearly always do exceed chronic health-based guideline levels and

acceptable cancer risk levels. It is also true that it is generally not feasible to achieve

levels below these guideline levels because outdoor levels average about 3-5 ppb. If

regulations are developed to reduce formaldehyde levels in indoor air, the ambient air

concentration will certainly be taken into account. No further discussion is needed

regarding ambient formaldehyde concentrations.

FRAGRANCED PRODUCTS INFORMATION NEWORK

Comment: Fragrances are intentionally added to numerous products such as cosmetics,

detergents, candles, cleaners, etc. By definition, fragrances are volatile organic chemicals. The

fragrance industry is primarily self-regulated with little oversight. Of 54 fragrance materials that

are used at 1 million pounds or more annually only 2 have a full set of basic toxicity data.

Scientific literature includes citations that fragrances can be a sensory irritant, a lower airway

irritant, and trigger for asthma. 

There is a limited awareness about the fragrance issue in the general population or the medical

and scientific communities. Thus far, the industry has not adequately addressed concerns

regarding the impact of multiple sources of fragrance on indoor air quality and health. There is

an immediate need for regulatory agencies to educate on the impact of scented consumer

products on sensitive populations. Research is needed to determine mechanisms by which

fragrance negatively impacts respiratory health. There is a need for a cooperative process with

industry to determine problematic materials and find suitable substitutes.

Response: We appreciate the information provided by the Network. We share the

Network’s concern regarding fragranced products, and agree that further research in this
V - 21

area is needed. Some information was added to the report, and we will include

fragranced products in the list of area of research needs in the final report. 

GAS APPLIANCES MANUFACTURERS ASSOCIATION (GAMA)

Comment: On page 150, vented and unvented combustion appliances are combined into one

category without distinction. Vented products meet national performance standards that do not

allow combustion products to be emitted into the living space. Readers need to know this piece

of information.

Response: The text will be revised at a later date to reflect the report’s preceding

discussions of the risks from unvented or poorly vented combustion appliances. As

discussed above (under AHAM comments), vented products other than direct-vent

models can emit pollutants into the living space.

Comment: Page 122- SCAQMD emission limits for gas water heaters in homes will be

postponed until 2006, not 2005 as stated in the report.

Response: Thank you, this will be updated in the final version of the report. 

Comment: The statement that design changes for appliances can be made with minor increased

costs are not correct. Industry expenditures to develop water heater systems that meet new

NOx limits total many millions of dollars, ultimately to be borne by the consumer. The discussion

of the porous insert technology does not include costs to incorporate this feature into a complete

gas appliance system (gas stove).

Response: Costs for design changes for appliance vary by industry, by facility, by

appliance, and by other factors, such as whether the changes can be implemented as

part of other planned facility modernization or appliance changes. In the ARB regulatory

framework, ARB conducts economic analyses for proposed regulations. A full analysis

would be conducted if regulatory changes were implemented. It should be noted that, in

a review of the estimated vs. actual costs of implementing mobile source rules, US EPA

found that the actual costs of changes required by rules were much less than those

estimated by the relevant stakeholders, and even less than those estimated by EPA (JF

Anderson and T Sherwood, 2002, Comparison of EPA and Other Estimates of Mobile

Source Rule Costs to Actual Price Changes, Presentation at the SAE Government

Industry Meeting, Washington, DC, May 14, 2002.) 

The text will be revised in the final report to add a caveat concerning the system design

for incorporating the porous insert.

HEARTH, PATIO, AND BARBECUE ASSOCIATION

Comment: The draft report does not distinguish between conventional and certified wood

stoves, and in so doing overestimates the emissions of wood stoves. Since 1992 all wood

stoves have to be certified which results in a reduction of PM and PAH emissions. Additionally,

they must operate with their gasketed doors firmly closed. As a result, certified stoves cannot

leak pollutants into the indoor environment. It would be appropriate to recommend that

conventional wood stoves be replaced with certified wood stoves.
V - 22

Response: The report mentions the U.S. EPA emission standards for certified

woodstoves. Those standards are for emissions to the outdoors; such stoves may have

lower emissions to the indoors, but those emissions can still be substantial. The federal

standards do not require door seals or the catalyst to be maintained over the life of the

stove, nor do they prevent woodstoves from being operated with leaky doors. Any stove

can leak into the room while the stove is being stoked. 

Comment: The report fails to establish a direct link between emission to the ambient

atmosphere and decreased indoor air quality for hearth products. Examples are provided of

local air districts that require limited wood stove emissions to the ambient air, but their impact on

indoor air quality is not stated. The report also mentions energy efficiency standards for certain

hearth products and requirements for a permanently open flue damper for certain applications.

The discussion assumes, without any supporting information, that a more efficient appliance will

benefit indoor air quality. A strong causal connection must be made between these

recommended control measures and an improvement in indoor air quality.

Response: As stated in our responses to this comment on the previous draft report, the

large study in two California cities by Sheldon et al. documented the infiltration of

outdoor PAHs from neighborhood woodburning on indoor PAH levels. In addition,

several studies have shown that a major part of outdoor PM can penetrate into homes,

as discussed in Section 2. Finally, ARB and air districts receive a number of complaints

each winter from citizens who live in neighborhoods with woodburning who are bothered

by woodsmoke entering their home from outdoors.

Comment: The report imprecisely concludes that fireplaces are a significant source of carbon

monoxide. The report cites a study by Sheldon et al., in which “a fireplace” – presumably one

unit in one home – caused a violation of a CO standard. It is important to identify if this was a

wood or gas log fireplace. It would be extremely unlikely for a woodburning fireplace to cause a

violation because the occupants of a home would quickly detect improper venting. Gas

fireplaces are designed and tested to minimize CO generation and leakage. Such incidents are

generally due to improper installation and/or operation. It appears the significance of one

fireplace has been exaggerated in the report. Please remove fireplaces from Tables ES-1 and

2.1 unless a clearer and stronger discussion of fireplaces as a source of CO can be provided.

Response: Fireplace emissions of PM, PAHs, aldehydes, and other pollutants in

addition to CO are also a health concern. It was not specified whether the one home with

a fireplace that exceeded the CO standard had a gas or woodburning fireplace.

However, Sheldon et al. also found that several homes had CO levels between 5 and 9

ppm that exceeded ambient levels, indicating a significant indoor source of CO. A

smoldering fire that produces a high level of CO may not necessarily produce enough

smoke to alert the occupants, especially if they are sleeping at night, which is a

documented scenario for CO poisoning. Additionally, backdrafting can occur, bringing

CO and other combustion pollutants back into the living area. We recognize that this is

not usually die to fault design, but rather to other factors; however, it needs to be

considered in assessing fireplaces (and other combustion devices) in terms of their

potential impact on indoor air quality. 

Comment: The report has placed wood stoves and fireplaces too high on the ranked list of

pollution sources for mitigation. Hearth products when properly installed and maintained will not

significantly contribute to contaminants in indoor air. Industry is working with U.S. EPA, under
V - 23

the auspices of ASTM International, to develop standards for a wood-fueled fireplace that will

emit fewer particles. ARB must consider the benefits of potential mitigation approaches, whether

effects will be direct or indirect, how significant the improvements will be, and the size of the

population that will benefit.

Response: The category of “combustion appliances” remains in the high priority group

because one or more combustion appliances are present in virtually every home, and

because gas stoves and some other devices are unvented, leading to a high potential for

emission and exposure. However, this does not mean that every device would warrant

changes. A full analysis would be conducted if measures are to be pursued to address

indoor combustion appliances. For its existing regulatory programs, ARB conducts

economic analyses prior to taking action. 

INSTITUTE OF MEDICINE

Comment: Several corrections or improvements were recommended, with specific language

changes provided. Suggested wording changes are subtle, but make statements align perfectly

with IOM reports.

Response: Thank you, the suggested changes were implemented.

MANUFACTURED HOUSING RESEARCH ALLIANCE

Comment: There have been changes in manufactured homes construction that result in overall

reduction in formaldehyde levels. Specifically, there has been a dramatic reduction in the use of

UF-bonded wood products. This was not addressed in the revised report. The response to

comments that 4 homes in Florida is representative of California is flawed.

Response: Hodgson et al. (2000) state that the formaldehyde levels in manufactured

homes are approximately 50 percent of what they were two decades ago. He attributes

this to construction changes, such as less paneling, and reduced emissions from the

products relative to 20 years ago. This is consistent with conclusions from a

formaldehyde emissions study conducted by Tom Kelly at Battelle (1996). These

statements are included in the report. ARB acknowledges that conditions in Florida may

not be representative of conditions in California, but there are some areas of California

that are similar to Florida, and there is no published data countering these results. It is

important to note that there are other sources of formaldehyde besides building

materials in a new home. Examples include wallpaper, draperies, furniture, and gas

appliance use. We would agree that a study of new manufactured homes would provide

useful information. 

DAVID MORALEZ, Davis, CA

Comment: Gratitude is expressed for the long overdue report. Support is offered for the

recommendations listed to make meaningful progress to protect the public from unhealthy

indoor air. Ideally the recommendations would be supported with funding.

Response: Thank you, we appreciate your positive comments.
V - 24

NATIONAL PROPANE GAS ASSOCIATION

Comment: Statements related to low- or zero-emitting appliances are misleading for several

reasons. Appliances are specifically designed to exhaust all of the combustion products to the

outdoor air, therefore no exhaust can enter the living space when equipment is properly

installed. The recommendation for zero-emitting appliances implies one should use electric

appliances, which shifts the pollutants to another site (where the power plant is located).

Response: Direct-vented (sealed-combustion) appliances are virtually zero-emitting in

terms of indoor emissions. For example, direct-vent gas furnaces and gas fireplaces are

very energy efficient, are resistant to backdrafting, and have been used widely for years.

Direct vent gas stoves were developed by the Canadian Gas Research Institute in the

1990’s but have not been marketed widely. The report will be revised to clarify this topic.

The report also discussed the need for proper, effective, and well-maintained venting of

combustion appliances and for cooking appliances, both electric and gas. 

Comment: ARB recommends active exhaust ventilation to reduce pollutants from combustion

appliances. This would have no impact on the appliance if the venting system is properly

installed because all pollutants would be vented to the outside. Active exhaust ventilation is

required to achieve the requisite number of air changes per hour in homes with tight new

construction. Active exhaust could also lead to backdrafting problems.

Response: Our intention is to recommend active local exhaust ventilation, with

installation specifications that assure adequate flow and low noise levels. Such a

provision would be provided if the operation of a range hood were linked to the operation

of a gas kitchen stove. To prevent backdrafting, accepted measures for house-as-asystem design should be used, such as direct-vent gas furnaces, limits on flow rates for

range hoods and other exhaust devices, and depressurization testing.

Comment: On page 23 of the report, an option is suggested to require manufacturers to have a

third party conduct emissions testing on appliances. Appliances already receive testing during

the certification process. Adding a label with results would confuse the general public. They

would interpret it to mean the emissions that are deposited within the living space, which would

not occur with a properly installed vent.

Response: Our focus is on unvented appliances, such as gas stoves, which typically

are not vented, and can emit pollutants directly to the indoor space. Because all

products on the market may meet certain emission performance criteria, consumers and

builders need labels and accessible information to identify low-emitting products.. This

approach would be developed with input from the public, consumer groups, and other

stakeholders.

PEACE RIVER CITRUS PRODUCTS

Comment: Remove negative statements about the health effects of d-Limonene and citrus

terpenes. These misleading conclusions will have a negative effect on the American citrus

community.
V - 25

Response: The June 2004 draft report included a misstatement regarding the health

effects associated with terpenes. Language was revised in the November 2004 draft,

and information from recent scientific studies and related information was included. We

believe that the information we provided in the November 2004 report is correct. 

REGAL AIR QUALITY, INC.

Comment: We need a vehicle to identify the population that is currently at risk but don’t know it

and provide proper education and information for them. The report should include a

recommendation that seniors be provided with monetary assistance to implement procedures to

retrofit their homes for improved indoor air quality. Specifically, HVAC duct insulation can emit

formaldehyde in areas with high temperatures such as Arizona. Improvements to the HVAC

system and/or insulation can improve the occupant’s health, but monetary assistance is

sometimes needed.

Response: We agree that there is increased education needed. In California, our

approach to address cost issues might be to recommend low-emitting formaldehyde duct

insulation in state and utility weatherization programs for low-income households. We

are not yet certain, however, whether the duct insulation used by California builders also

emits formaldehyde as does the type used in Arizona. Accordingly, we have included

limited measurements to be made in residential ventilation systems in a study of new

homes in California, which we expect to start later this year. 

RESILIENT FLOOR COVERING INSTITUTE

Comment: In October, 2004, the DHS determined that the Section 01350 limit for acetaldehyde

should be something other than one-half the OEHHA chronic REL. This should be reflected in

the report. Alternate wording is provided for a couple of places in report.

Response: We did not concur with DHS on this matter, but will add the information to

the final report if it is accurate at that time. Our concern is that it would allow a single

product to potentially contribute sufficient amounts of the chemical to exceed OEHHA’s

chronic REL guideline value (which for acetaldehyde is 9 ug/m3

). 

SEMPRA ENERGY

Comment: They expect their comments to be shared with the scientific review panel.

Response: All of the comments received from the public on the June 2004 draft report

were provided to the peer review panel when they reviewed the November 2004

document, so that they could see the comments received and how we responded to

them. The peer review panel has completed their review, so will not be sent the current

comments. However, if any peer review member requests them, we certainly would

provide them. 

Comment: Banning gas stove use would have a profound economic and social impact on the

state. A study would probably show that electrocution death rates from electric cooking

appliances are nearly equal to death rates from CO poisoning from gas cooking appliances.
V - 26

Response: The report does not recommend banning gas stoves from homes, but rather

to use alternatives such as direct vent appliances, or to improve their local exhaust and

reduce their emissions. In addition to concerns regarding CO poisoning, ARB is

concerned about NO2 emissions and other emissions from combustion appliances. A

revision to the building standards would require a detailed analysis and public review.

Comment: An attached report (2000) conducted by the CPSC with assistance from NIST looked

at CO emissions from the misuse of natural gas ranges. The CPSC declined to take any further

action on setting new CO emission standards based on their studies.

Response: While the standards may be sufficient for safety purposes (prevention of lifethreatening effects or death), we believe they are not sufficient to adequately protect

health. The referenced modeling studies address indoor CO, and, in fact, show that the

ARB’s IAQ guideline and state ambient air quality standard would be exceeded. For

example, the 1-hour and 8-hour guideline level would be exceeded in the baking

scenarios with smaller kitchen volumes and lower air exchange rates. The medium and

lower air exchange rates used in the modeling are not as low as those are for some new

or weatherized homes in California. This modeling estimate does not include the

contributions of outdoor CO levels, which can be substantial at times. Further, these

studies do not address what is typically the limiting factor for combustion appliances:

indoor NO2. 

Comment: The foods cooked and specific type of cooking activity are more important to IAQ

than the energy source of the cooking appliance. For example, PAHs are emitted during

cooking with electricity or gas.

Response: That is true for most PM emissions, although PM emissions (especially

ulftrafine PM) are generally higher when using a gas stove. In addition, NO2, CO, and

aldehydes are always higher when using a gas stove.

SOAP AND DETERGENT ASSOCIATION

Comment: Add references to the Executive Summary for the production of formaldehyde and

ultrafine PM from the reaction of terpenes and oxidants (page 5). Also, add a reference to the

paragraph about VOCs on page 8.

Response: Numerous facts are presented in the Executive Summary, most of them

widely accepted in the field of indoor air quality. Please refer to the body of the report to

find extended discussion with references. 

Comment: Household and institutional cleaners are listed as a source of several VOCs in

Tables ES-3.2 (and 6.2). However, these ingredients are not intentionally added to water

soluble, surfactant-based products. Therefore, these chemicals should be absent or at de

minimus levels in the water soluble, surfactant-based products. 

Response: Thank you for this information. We do not feel clarification is needed in the

text because footnotes indicate all of the pollutant sources may not emit all of the

pollutants listed in the corresponding box. However, such information would clearly be

important in developing mitigation approaches for specific products. 
V - 27

Comment: The paragraph describing the types and uses of mercury does not detail the products

with inorganic mercury. We recommend their inclusion.

Response: The sources of inorganic mercury are listed in Table 2.13; this is sufficient.

Comment: According to the U.S. EPA report, “Reducing Mercury Use in Healthcare: Promoting

a Healthier Environment”, mercury can be a contaminant in detergents and cleansers when the

mercury-cell process is used to manufacture some cleaning product ingredients. This should be

statedThe products mentioned in the U.S. EPA report are down-the-drain products.

Recognizing this, one would not expect any mercury that may be in a product to become air

borne. Moreover, there are no validated methodologies for testing cleaning product for mercury.

Therefore, reported test findings may not be actual mercury concentrations.

Response: Our report adequately states the findings from the 1999 EPA report. In fact,

if we consider the statement from the EPA report that "many forms of mercury circulate

in the environment, moving from land or water to air and back again," the comment to

not expect any mercury in a [down-the-drain] product to become airborne does not

necessarily hold true. More importantly, any mercury in products used indoors that are

released to the indoor environment, even as splash droplets, will persist. Also, it may be

the case that there are no validated methodologies for testing cleaning products, but the

concentrations in the AB 1173 report are not being reported for cleaning products.

Comment: Add a description of the DGS EPP task force to page 120-121.

Response: The Environmentally Preferable Purchasing (EPP) Task 

Force is discussed in Section 4.3.3.2 under the subheading “Sustainable Buildings and

Section 01350”. EPP is also discussed in the same section under the subheading

“Environmentally Preferable Products for School Construction”.

SOUTHERN GARDENS CITRUS (two commentors: Liddle and Chapman) 

Comment (same comment from both commentors): Remove negative statements about the

health effects of d-Limonene and citrus terpenes. These misleading conclusions will have a

negative effect on the American citrus community.

Response: The June 2004 draft report included a misstatement regarding the health

effects associated with terpenes. Language was revised in the November 2004 draft,

and information from recent scientific studies and related information was included. The

information we provided in the November 2004 report is correct. 

TREATT

Comment: Remove negative statements about the health effects of d-limonene and citrus

terpenes. Technical arguments will be made by others in the citrus industry.

Response: The June 2004 draft report included a misstatement regarding the health

effects associated with terpenes. Language was revised in the November 2004 draft,
V - 28

and information from recent scientific studies and related information was included. We

believe that the information we provided in the November 2004 report is correct.

UNITED STATES DEPARTMENT OF AGRICULTURE

Comment: The report states a major objection to the use of d-limonene and other terpenes in

cleaning products is due to the reaction products formed between terpenes and oxidants in the

air. These compounds cause irritation without any terpenes being present. Before banning

terpenes, the actual levels of formed irritants should be determined and alternatives for safe

cleaning chemicals investigated. Numerous agencies do not categorize terpenes as posing

health risks.

Response: We do not suggest banning terpenes: rather, we indicate that further

research is needed. ARB certainly acknowledges that formaldehyde and PM are

irritants, regardless of their source. However, if terpenes introduced to indoor air in

cleaning products lead to significant increased levels of these irritants in indoor air, then

mitigation would be warranted. Several investigators around the country and the world

are studying the reaction of terpenes and oxidants to determine potential impacts on

indoor air quality.
VI - 1 

APPENDIX VI 

Responses to Public Comments 

on the 

February 2005 Draft Report for Board Review 

Eleven individuals and organizations commented on the February 2005 report that was 

considered by the Board. Comments are arranged in alphabetical order of the commenting 

organization and have been paraphrased by ARB staff. 

ASSOCIATION OF HOME APPLIANCE MANUFACTURERS 

Comment: The report makes substantial errors in equating air cleaners that purposely emit 

ozone with the vast majority of air cleaners. The report should differentiate between air cleaners 

that generate trace amounts of ozone and those primarily designed to generate ozone. The 

majority of air cleaning devices that comply with existing U.S. national safety standards for 

ozone emissions should not be listed in the “high priority” category. 

Response: The February draft report clearly distinguishes between these types of air 

cleaners in Section 5.5 and Section 6.1, and does not imply that the vast majority of air 

cleaners emit ozone. Ozone-generating air cleaners are included as a high-priority 

source in Table 6.1; and the supporting text in Section 6.1 emphasizes that devices that 

purposely emit ozone are the primary concern. The report also states that air cleaners 

based on different technologies may or may not emit ozone as a by-product, thus 

causing some concern. 

Comment: It should be pointed out that Underwriters’ Laboratory (UL) has a safety standard 

related to ozone output for air cleaning devices; air cleaning devices that meet this standard 

should be exempt from regulation. The standard is 50 ppb ozone; one reference in the report to 

a 100 ppb UL standard on p. 139 should be corrected. 

Response: The voluntary UL standard is discussed in Section 4.3.2.3; the ozone limit 

has been corrected. Section 4.3.2.3 of the report was revised to include substantial 

information provided by AHAM on AHAM’s and ANSI’s role in testing and certifying air 

cleaners reflect the 50 ppb standard, and to reflect the planned revisions to the UL 

according to AHAM. However, not all air cleaners are certified to meet this standard. In 

addition, Niu et al., 2001a,b found that some ionizers and electrostatic precipitators that 

meet the UL standard can still emit unhealthful levels of ozone; Section 5.5 was revised 

to reflect this information. It is our view that a health-based protocol and standard that is 

protective of sensitive individuals would need to be more protective than a safety 

standard such as the UL standard, and that the UL test protocol needs some refinement 

to assure safe levels of ozone. 

Comment: The report makes a value judgment regarding the effectiveness of air cleaners. 

Response: The statement regarding the effectiveness of air cleaners is supported with 

three citations, one of which is the Consumers Union, which publishes Consumer 

Reports. 
VI - 2 

Comment: It is incorrect to state that no state or federal agency has direct regulatory authority 

to control emissions from these devices. Los Angeles County requires that such products meet 

the UL Standard 867, Section 37 that limits emissions to 50 ppb ozone. 

Response: Our statement is correct. Los Angeles County is a local agency rather than 

a state agency, and does not directly regulate emissions. However, we are encouraged 

to see that Los Angeles is providing some guidance in this area and taking whatever 

actions they are able to take to address ozone emissions from air cleaners. 

Comment: The Report does not recognize that gas cooking products are used on an 

intermittent basis. Nor does it recognize the recent review by the U.S. Consumer Products 

Safety Commission on the adequacy of the present CO emission limit under the ANSI Z21.1 

standards. 

Response: The intermittent use of gas stoves was added to the Executive Summary. 

However, as indicated in the report, the majority of the population has gas appliances in 

their homes, and they are designed to be used for hours at a time, for example for 

baking, roasting, and simmering. Indoor pollutant concentrations during cooking 

activities can exceed ambient air standards, as indicated in the report. We have added 

information regarding the ANSI/Z21 standard, but it is not clear this would assure 

healthful levels of indoor NO2, and aldehydes, and CO, over the lifetime of the appliance. 

We reference modeling studies that indicate that the ARB’s IAQ guideline and state 

ambient air quality standards would be exceeded under some conditions. 

Comment: The Report does not adequately explain the issue of CO deaths. It appears to 

overstate the number of deaths relative to the January 2005 National Fire Protection 

Association report that indicates the national average of non-fire related CO deaths involving 

home cooking equipment totals 22. The CPSC indicates that in 1996, 217 people died due to 

CO poisoning in the entire country. 

Response: Several recent sources of national and California data are cited in Section 

2.2.4.1. The California study is considered most accurate because it reviewed ten years 

of death certificates. The cited body of literature would indicate the numbers from the 

Fire Association are low; this is likely due to the fact that those figures do not include all 

CO-related deaths, only those that are suspected as CO deaths at the time of the event.. 

Comment: The report lumps together all combustion appliances including gas stoves/ ovens, 

furnaces, heaters, wood stoves, and fireplaces in Table 6.1. We do not believe that any of the 

listed/certified gas appliances cause significant IAQ issues, especially cooking appliances. 

Response: The February draft report discusses CO mortality, by type of indoor 

combustion appliance, in Section 2.2.4.1, and emphasizes the increased risks of CO and 

NO2 from unvented and poorly vented combustion appliances (Sections 2.2.4–2.2.5, ). 

As stated previously, based on modeling results, it is not clear that certified appliances 

would assure healthful levels of indoor NO2 and aldehydes as well as CO, especially 

over the lifetime of the appliance with typical maintenance levels. Although combustion 

appliances are grouped together at this time, every device may not warrant changes. A 

full analysis would be conducted if measures are to be pursued to address indoor 

combustion appliances, and unvented appliances would be the primary focus, as stated. 

Comment: The Report fails to mention that zero-emitting gas appliances are not technologically 

feasible. However, appliances do conform to standards set by the ANSI/Z21/83 committee. The 
VI - 3 

report fails to mention the recent Gas Research Institute study which found that the standards 

have a high margin of safety and they do not need to be changed. CPSC also concluded that no 

changes are necessary to the voluntary safety standards. These ANSI standards are developed 

by a consensus of pubic and private groups, and testing is done by third-party agencies. 

Response: Direct-vented (sealed-combustion) appliances are virtually zero-emitting in 

terms of indoor emissions. For example, direct-vent gas furnaces and gas fireplaces are 

very energy efficient, are resistant to backdrafting, and have been used widely for years. 

Direct vent gas stoves were developed by the Canadian Gas Research Institute in the 

1990s but have not been marketed widely. Such options are included in the report for 

completeness; any emission reduction or exposure reduction measures pursued in the 

future would fully consider the technical and economic feasibility at that time. 

Regarding the adequacy of the ANSI standards, and CPSC’s findings, etc., we have 

included additional information in the report as requested by AHAM. However, ANSI and 

CPSC both are safety oriented, and do not use health measures as protective as those 

used in California for identifying acceptable vs. potentially unhealthful pollutant levels. 

Comment: The report should reference the CPSC guide for emergency response personnel, 

“Responding to Residential Carbon Monoxide Incidents”. 

Response: The CPSC guide for emergency personnel (July 2002) has useful safety 

information, but it does not recommend any further investigation if CO levels are below 

30 ppm. This level is based on their benchmark of false alarm resistance and the 

protection of healthy adults. However, this benchmark level is less protective than 

California’s ambient air quality standard for CO, which is designed to protect sensitive 

subgroups such as heart disease patients and children. In addition, an indoor reading of 

30 ppm usually indicates the presence of an indoor source of CO, one that often needs 

to be addressed. Further, the guide does not include testing for backdrafting, a common 

cause of elevated CO when exhaust fans or HVAC systems are operating. 

Comment: In Section 4, the report discusses emission levels from unvented appliances, without 

discussing any evidence for health effects at expected CO or NOx emissions from properly 

installed and maintained gas appliances. Table 4.1 recommends 20 ppm as a maximum 1-hour 

exposure to CO. There is no basis for this level that is lower than the U.S. EPA 35 ppm level. 

Response: The report summarizes clinical, epidemiological, and exposure studies in 

Section 2.2.4 and 2.2.5, supporting the concern for health risks due to indoor CO and 

NO2 exposures that have been observed in homes. The increased exposures and health 

risks linked to combustion appliances are discussed. Data indicate that indoor levels can 

exceed ambient air quality standards for CO and NO2, sometimes due to poor appliance 

venting by design, and sometimes due to improper installation or maintenance. 

California has an ambient air quality standard of 20 ppm CO, based on an 1-hour 

exposure duration. This standard was widely reviewed and approved by notable 

scientists, and is the basis of the indoor guideline level. 

Comment: AHAM objects to most of the proposals in Section 7, “Options to Mitigate Indoor Air 

Pollution”. Establishing emission limits specifically for California is not justified. ARB should 

work within existing safety standard processes rather than establishing emission limits and 

testing requirements specific for California. 
VI - 4 

Response: ANSI and ASTM standards are safety standards, are not based on 

California housing and environmental factors, and may not adequately protect our 

citizens’ health. Additionally, they are not required to be met by all manufacturers. We 

believe that emission limits are needed for some sources, but as indicated in the report, 

a more detailed assessment would be conducted prior to the development of emission 

limits for any specific type of product. ARB actively participated in the attempted 

development of UL/ANSI standards for indoor products in the past, but unfortunately the 

process did not result in standards. We will participate in the future as resources allow. 

Comment: The Executive Summary states that vacuuming the house contributes to indoor air 

pollution. This is not based on fact. 

Response: Several references were added to Section 2.2.2, Indoor PM Sources and 

Emissions, that indicate vacuuming can be a source of elevated indoor particulate matter 

levels. 

Comment: The report incorrectly states that there are no consensus standards for testing and 

performance of vacuum cleaners. 

Response: Section 4.3.2.2 of the report was revised to reflect the ASTM performance 

standards, and that an industry standard to address PM emissions from vacuum 

cleaners is under development. 

Comment: There is no evidence in the report to support the statement that household 

appliances and office equipment such as computers, copy machines, and vacuum cleaners can 

emit a variety of pollutants such as particles, ozone, various VOC’s of concern, phthalates, and 

PBDE’s. 

Response: These sources are discussed under several pollutants in Chapter 2. 

Emissions from office machines also are discussed in Section 2.3.12, “Non-Industrial 

Workplaces” in the subsection titled “Photocopy Centers”. Citations for vacuum cleaner 

studies were added, as indicated above. 

Comment: ARB has not made a strong case for the regulation of vacuum cleaners. They 

should be removed from the Section 6 prioritization. 

Response: Vacuum cleaners were removed from the prioritization tables. Much 

progress has been made in improving vacuum cleaner performance and emission limits. 

However, as indicated in the new citations that show emissions of high levels of PM 

during vacuuming, some models of vacuums may be a cause for concern and should be 

addressed. ARB encourages the industry to complete the development of a standard to 

address particle emissions during vacuuming, and to develop a robust certification 

program to eliminate this concern. We are willing to participate as resources allow. 

Comment: ARB should continue to support educational and outreach programs. Cleaning 

guidelines for appliances are included with appliances. Consumers must bear some 

responsibility for maintaining their appliances in a proper manner. AHAM believes that 

consumer education would be more effective than added regulation. 

Response: Both public education and source reduction are needed for reducing indoor 

emissions to acceptable levels. The report text was previously revised to include more 

discussion of public and professional education and outreach strategies. However, we 
VI - 5 

believe it is also industry’s responsibility, and it is more effective for industry to fully 

educate their customers regarding recommended cleaning and use of appliances. 

Comment: AHAM continues to disagree with the Report that many actions can be taken to 

reduce indoor air pollution at relatively low cost, including the development of emissions 

limitations for...appliances. 

Response: We believe there are a number of actions that can be immediately taken to 

reduce indoor air pollution at low cost. Although there would be costs for emission 

limitations, costs for design changes for appliance vary by industry, by facility, by 

appliance, and by other factors, such as whether the changes can be implemented as 

part of other planned facility modernization or appliance changes. 

THE CENTER FOR SCHOOL MOLD HELP 

Comment: The critical importance of addressing mold issues within schools is paramount for 

this organization. Aggressively addressing the issues of mold in schools will ultimately be more 

cost effective than not dealing with these issues. School mold is a national health problem. 

The recommendations presented in the report are not strong enough; strong regulations are 

needed.Guidelines become just another state document with inadequate clout. 

Recommendations presented in the report should include enforced mandates and tough 

sanctions, the requirement of “Best Practices”, and mandatory training relative to indoor air 

quality issues. 

Speakers offered many suggestions for mandating the mitigation of mold in classrooms. 

Examples include minimum exposure standards for mold, biological toxins and their interplay 

with chemical toxins. School districts could use unannounced facility inspections, issue an 

environmental report card, and regional agencies could issue a stiff penalty for inadequate 

conditions. School funding should be contingent upon following good air quality standards. 

Speakers recommended that the state conduct research on the systemic health effects of longterm exposures to biological toxins in order to set minimum exposure standards for children and 

adults. The state should create a “Child Environmental Protection Agency”. The state should 

fund SB732 to set mold standards for school buildings and institute mandatory regulations 

related to mold and water intrusion promptly. 

Witnesses provided testimony of personal experience in severely water damaged classrooms 

with resulting illness and the loss of their quality years of life. School districts meet their 

complaints with the three Ds – defensiveness, denial, and discrediting. 

Response: Thank you for your support of our report. We agree with most of the 

suggestions you offer; however, there is a lack of regulatory authority to enforce existing 

guidelines and “Best Practices”. As indicated in Section 4.2.3 of the report, the 

Department of Health Services (DHS) is the lead state agency for addressing mold 

issues. They have a draft report undergoing internal review regarding the feasibility of 

identifying permissible exposure limits for indoor mold, pursuant to SB 732. DHS is also 

conducting research on how indoor microbial growth affects human health. The Centers 

for Disease Control (CDC) just started a large project to investigate how microbial 

growth affects human health. We agree that more actions should be taken, and are 

working cooperatively with nonregulatory programs such as the EPA Tools for Schools 
VI - 6 

program, and school environmental health departments to implement recommendations 

from the California Portable Classroom Study. 

CONSUMER SPECIALTY PRODUCTS ASSOCIATION 

Comment: CSPA is concerned that the report presents undue emphasis on indoor emissions 

that present little or no health risks while failing to highlight more significant risks. The review of 

biological contaminants is cursory and greatly under-represents the serious health risks 

associated with this pollutant category. 

Response: It is not clear which indoor emissions CSPA believes are insignificant. We 

believe that all indoor emissions of carcinogenic compounds and irritant compounds are 

potentially significant, and must be considered in light of other factors such as the 

presence of multiple indoor sources, extent of infiltration from outdoors, duration of 

exposure, and so on. For all pollutants, the report describes sources and health risks 

associated with the pollutant. We previously expanded Section 2.3.4 on biological 

contaminants, and it is one of the longest pollutant sections. 

Comment: Dozens of studies provide clear evidence that biological contaminants contribute to 

serious public health problems. CSPA specifically mentions a study that indicates cockroach 

allergens play a predominant role in the exacerbation of asthma symptoms. The report is flawed 

by not mentioning the many benefits of formulated consumer products. 

Response: The report cites many recent studies that identify links between biological 

contaminants and adverse health effects. We acknowledge that many more are 

available in the literature that were not included in our report. Relative to cockroaches 

being an allergen, three recent citations were provided. The report acknowledges that 

many consumer products have beneficial effects. Also, section 5.3 “Building operation 

and maintenance” discusses the need for regular building maintenance, as well as the 

beneficial aspects of regular and effective cleaning. 

Comment: The Report still fails to appreciate fully the rigorous federal product safety 

regulations that govern formulated consumer products as well as the efforts of manufacturers of 

those products to assure product safety that go beyond mere regulatory compliance. 

Response: A brief synopsis of the jurisdiction of the Consumer Product Safety 

Commission (CPSC) over consumer products is presented in the Executive Summary, 

with more detail provided in Section 4.3.1.1. However, CPSC’s actions are focused more 

on immediate safety (actions to prevent immediate death or life-threatening illness) than 

health, and CPSC only infrequently prohibits a specific component in a product. The 

section also includes information on the benefits of voluntary (industry) standards. 

DANIELS, LEE 

Comment: Please provide just one reproducible scientific study that has proven second hand 

smoke causes cancer. It is a fact that second hand smoke has never been shown to be a 

causative factor in lung cancer. 

Response: Section 2.3.3 provides several citations that link environmental tobacco 

smoke (ETS) with various health effects, and many others are provided in a report that 

specifically examines the research on ETS. That draft report, prepared by ARB and 
VI - 7 

OEHHA staff, for the identification of ETS as a toxic air contaminant, contains a much 

more complete discussion of this topic. It is cited in the indoor air pollution report and is 

available on the ARB website at http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm. 

ENVIRONMENTAL HEALTH SCIENCES AND EDUCATION; COMMUNITY ACTION TO 

FIGHT ASTHMA 

Comment: Many references pertaining to studies conducted in California schools were not 

included in the report. These studies have been provided to ARB. 

Response: The report includes several of these references; some were cited under the 

primary author’s name, or a more recent version was cited. The report did not include 

the ARB study of children’s school bus exposures and the CDE study of school sound 

levels because these issues were not the primary focus of the AB 1173 report. The 

report did not include the Daisey et al. review, the Shendell et al. (2003 a,b) pilot study of 

VOCs in portable classrooms, and the Hodgson et al. 2003 study of VOCs in four 

portable classrooms because they were included in the California Portable Classroom 

Study (PCS) report, which is summarized in the report. The results of the PCS,, based 

on a large, statewide, representative sample for California, provided the most 

substantive basis for the report’s conclusions. 

The AB 1173 draft report has been revised to include information from some additional 

studies: the Apte et al. 2003, Shendell et al. 2003c, and Shendell 2004 references were 

included in Section 5.2; the DHS study of lead blood levels and lead dust concentrations 

in older homes was included in Section 2.3.6.3. 

Comment: Recommendations for mitigating indoor pollution in schools should be updated and 

include an attached reference (Shendell et al., 2004). It is a paper that reviews about 300 

scientific citations and offers 18 recommended best practices to reduce or prevent potential 

occupant exposures to biological, chemical, and physical agents of concern in American school 

facilities. 

Response: This article was already included in the February 2005 draft report. The 

recommended best practices in the article are consistent with those of the ARB/DHS 

report on the California Portable Classroom Study (summarized in Section 7.2 of the 

draft report), and with other references cited in the February 2005 draft report, such as 

documents from CHPS and U.S. EPA. 

FLORIDA CHEMICAL COMPANY, INC. 

Comment: There is insufficient data to support the concerns raised about d-limonene and/or 

terpenes in general. ARB has stepped outside the bounds of today’s accepted science in regard 

to potential reactions of terpenes. We presented multiple studies to ARB and have not seen any 

response to those studies. The presence of terpenes cannot be equated to public risk. The 

report fails to consider the indoor air quality benefits associated with cleaning products 

formulated with citrus terpenes. 

Response: At your request, we have added information from two of the three studies

you provided with A.T. Karlberg as lead author. As you know, these papers deal with 

auto oxidation of d-limonene to create compounds with sensitizing and allergenic 

potential. When terpenes react with ozone in air, they produce irritating compounds such 
VI - 8 

as formaldehyde and ultrafine particles, which may pose a public risk. The Report 

includes multiple citations from highly respected scientists documenting these reactions, 

indicating ARB is not “outside the bounds of today’s acceptable science”. However, 

more research is needed to fully understand these reactions, resultant levels of 

products, exposures, and associated health impacts, and this is included in our 

recommendation regarding further research. 

GROCERY MANUFACTURERS OF AMERICA 

Comment: The Report fails to adequately consider public health and indoor air quality benefits 

that accrue with the use of many consumer products. Many consumer products play an 

important role in reducing indoor exposures to biological contaminants. Considering products 

only as air pollutants without giving equal attention to benefits does not adequately inform the 

debate. 

Response: This comment has been made by industry during each comment period. As 

a result, we have attempted to provide greater balance to the report. General discussion 

deals with the trade-offs of modern society. Consumer products impart obvious benefits 

to society; however, these desirable products at times have a down side – the emission 

of a variety of chemicals. Section 5.3 “Building Operation and Maintenance” also 

recognizes that regular cleaning of indoor spaces with proper cleaning methods can 

reduce biological contaminants. 

LEWIS, J. 

Comment: How may I obtain a copy of test procedures and results? The association between 

breast cancer and environmental tobacco smoke is hard to believe and I don’t believe the 

results. 

Response: The information on exposure to environmental tobacco smoke and breast 

cancer indicates that exposure to environmental tobacco smoke can increase the risk of 

breast cancer. However, this information is currently under review by the Scientific 

Review Panel, an external scientific peer review panel who will make the final 

determination. For complete details of this topic and references, please refer to the 

document Proposed Identification of Environmental Tobacco Smoke as a Toxic Air 

Contaminant, available at http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm. 

MAYTAG 

Comment: Combustion appliances should not be listed as a high priority category. Excessive 

exposures are due to consumer misuse and the appliances are only used on an intermittent 

basis. The Consumer Product Safety Commission, California Energy Commission, and the U.S. 

Department of Energy have studied appliance emissions and concluded that carbon monoxide 

and nitrogen oxide emissions from gas ranges are insignificant due to the nature of product use. 

Response: The category of “combustion appliances” remains in the high priority group 

because one or more combustion appliances are present in virtually every home, and 

because gas stoves and some other devices are unvented, leading at times to high 

emission and exposure. Studies cited in the report indicate that under normal stove and 

range operation, indoor nitrogen dioxide levels can exceed the 1-hr ambient air quality 
VI - 9 

standard. However, this does not mean that every device would warrant changes. A full 

analysis would be conducted if measures are to be pursued to address indoor 

combustion appliances. For its existing regulatory programs, ARB conducts economic 

analyses prior to taking action. 

Regarding other agencies’ assessments of the risk posed by unvented gas appliances, 

as explained above, we use a more protective health basis for assessment than do 

those groups. 

Comment: The fact that adults stay inside the home 62% of the time on average, is 

questionable and appears to be high. 

Response: We are unaware of studies showing any substantially different results from 

the early activity pattern studies, in terms of time spent indoors and outdoors. 

Subsequent to ARB’s studies, large national surveys and local field studies have 

replicated the general findings on time spent indoors. 

Comment: The incidence of California CO poisoning-caused deaths due to indoor sources 

seems high. The January 2005 National Fire Protection Association report indicates that the 

1997 – 2001 national average of non-fire related CO deaths involving home cooking equipment 

totals 22. 

Response: Several recent sources for national and California data are cited in Section 

2.2.4.1. The California study is considered most accurate because it reviewed ten years 

of death certificates where the cause of death due to CO poisoning was absolutely 

certain. See additional information in response to AHAM, above. 

Comment: Appliances are not differentiated in the report as to water heaters, furnaces, 

charcoal grills, and gas ranges and ovens. These should be differentiated to accurately portray 

the danger of CO poisoning from each type of appliance. Maytag believes a very small number 

of deaths were attributable to gas ranges. 

Response: The contribution of these categories of appliances to CO deaths in California 

is provided in Section 2.2.4.1. An updated collection and analysis of data, as you 

suggest, would be a first step should we be directed to control emissions from 

combustion appliances.

Comment: Vacuum cleaners should be removed from the list of medium priority source 

categories. There is no substantial information in the report that vacuum cleaners release 

harmful emissions. The report should state that there are industry consensus standards for 

testing the performance of vacuum cleaners. 

Response: Vacuum cleaners were removed from the prioritization tables; however, as 

indicated in the new citations that show emissions of high levels of PM during 

vacuuming, they can produce PM levels of health concern, and those vacuums should 

be addressed. ARB encourages the industry to complete the development of a standard 

to address emissions during vacuuming, and to develop a robust certification program to 

eliminate this concern. 

Comment: We object to proposed emissions limits. ARB should work with existing standards 

organizations such as ANSI and ASTM to ensure that products are safe and effective. 
VI - 10 

Response: We commend those working on ASTM and ANSI standards that include 

consideration of indoor air quality. However, ANSI and ASTM standards are not based 

on California housing and environmental factors, and may not adequately protect our 

citizens’ health. Additionally, they are not required to be met by all manufacturers. ARB 

actively participated in the development of UL/ANSI standards for indoor products in the 

past, but unfortunately the work did not result in standards; we will participate in the 

future as resources allow. 

THE SOAP AND DETERGENT ASSOCIATION 

Comment: We recommend clarification for the term “consumer product”. Many types of 

products are included under this broad term, from thousands of household and institutional 

cleaners to imprecisely defined personal care products. It would be beneficial to carry a detailed 

description of “consumer product” throughout the report. The report should explicitly list which 

consumer products are associated with the listed chemical substances. 

Response: As you indicate, many types of products are mentioned in the report as 

consumer products. Consumer product has been defined and categorized somewhat by 

the ARB Consumer Products Program. The report adequately describes the types of 

products that are discussed. If further action is taken on this source category, more effort 

would be placed on definitions, before proceeding with mitigation efforts. In regards to 

specifically listing chemicals associated with specific products, this would be an 

overwhelming task outside the scope of this report. As you indicate, there are thousands 

of products. Many ingredients are protected by confidentiality laws. 

Comment: SDA recommends that all tables and text lists be placed in alphabetical order. 

Response: Tables that list pollutants or source categories are in alphabetical order. In 

Chapter 2, criteria pollutants are discussed first, followed by other indoor air pollutants, 

with more significant ones discussed first. 

Comment: We recommend working with established programs to implement emission limits 

rather than create new systems. Due to pre-existing regulations on consumer products, a 

requirement to submit consumer products for emission testing would be an unwarranted step for 

manufacturers to take. We recommend that this option be omitted for consumer products. 

Response: Working with established programs makes sense. However, the existing 

ARB programs focus on smog precursors in consumer products, and does not fully 

address all potential emissions of concern, nor does it address all consumer products. If 

implemented, emissions testing would first be initiated for the high priority categories. 

Comment: We recommend that discussion of the development of asthma precede the 

exacerbation of asthma. The Rosenman et al. (2003) study has several limitations that should 

be included in the report to put it in proper perspective based on shortcomings of data collection 

and reporting. 

Response: Asthma exacerbation is the more frequent effect, and thus is appropriately 

discussed first. As we have stated previously, the authors of the Rosenmann et al. 

(2003) study examined a database of work-related asthma cases associated with 

cleaning products, reported primarily by physicians between 1993 and 1997. The article 

discusses limitations of the database: limited documentation of pulmonary function; 
VI - 11 

identification of the causal agent is based on history; and the database contains only a 

minority of the work-related asthma cases for the study states. However, the paper 

provides further citations for new-onset work-related asthma occurring after a 

documented exposure to cleaning products, and more citations for exacerbation of preexisting asthma from such exposures. The large number of cases reported would 

indicate an association exists between asthma, bleach, and other cleaning products. 

Comment: We are concerned with the use of the California Comparative Risk Project (CCRP), 

particularly the various definitions of “consumer product”. The CCRP website is incomplete, 

missing some tables, etc. 

Response: Calculations of cancer risk were based on indoor concentrations (minus 

outdoor concentrations) of specific TACs. These TACs were routinely found in indoor 

environments in residential studies in California, and were associated with known indoor 

sources. Calculations were based on distributions of indoor concentrations from multiple 

field studies. We have notified OEHHA regarding the tables missing from their website. 

If the problem is not resolved soon, we can provide copies of the needed tables to those 

interested. 

VICKI 

Comment: I disagree with the link between smoking and breast cancer. I am 54 years old, grew 

up with two parents who smoked in vehicles as well as in the home, my husband is a smoker, 

and I just had a clear mammogram. Think twice before cutting the rights of smokers. 

Response: Thank you for your comments. We hope that you continue to experience 

good health. This topic is currently under review by the Scientific Review Panel (SRP), 

an external scientific peer review panel, as part of a separate action to list ETS as a toxic 

air contaminant. The SRP will make the final determination regarding an association 

between environmental tobacco smoke and breast cancer. For complete details of this 

topic and references, please refer to the document Proposed Identification of 

Environmental Tobacco Smoke as a Toxic Air Contaminant, available at 

http://www.arb.ca.gov/toxics/ets/dreport/dreport.htm.