FINAL 2007 AQMP 

APPENDIX I 

HEALTH EFFECTS 

JUNE 2007 
SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT 

GOVERNING BOARD

Chairman: WILLIAM A. BURKE, Ed.D. 

 Speaker of the Assembly Appointee 

Vice Chairman: S. ROY WILSON, Ed.D. 

Supervisor, Fourth District 

Riverside County Representative

MEMBERS: 

MICHAEL D. ANTONOVICH 

Supervisor, Fifth District 

Los Angeles County Representative 

BILL CAMPBELL

Supervisor, Third District 

Orange County Representative 

JANE W. CARNEY 

Senate Rules Committee Appointee 

RONALD O. LOVERIDGE 

Mayor, City of Riverside 

Cities Representative, Riverside County 

GARY OVITT 

Supervisor, Fourth District 

San Bernardino County Representative 

JAN PERRY 

Councilmember, City of Los Angeles 

Cities Representative, Los Angeles County, Western Region 

MIGUEL A. PULIDO 

Mayor, City of Santa Ana 

Cities Representative, Orange County 

TONIA REYES URANGA 

Councilmember, City of Long Beach 

Cities Representative, Los Angeles County, Eastern Region 

VACANT 

Governor’s Appointee 

DENNIS YATES 

Mayor, City of Chino 

Cities Representative, San Bernardino County 

EXECUTIVE OFFICER:

BARRY R. WALLERSTEIN, D.Env.
 

CONTRIBUTORS 

South Coast Air Quality Management District 

Elaine Chang, Dr. P.H. 

Deputy Executive Officer 

Planning, Rule Development, and Area Sources 

Laki Tisopulos, Ph.D., P.E. 

Assistant Deputy Executive Officer 

Planning, Rule Development, and Area Sources 

Author

Jean Ospital, Dr. P.H. 

Health Effects Officer
Table of Contents 

 i 

Table of Contents 

INTRODUCTION............................................................................................I-1 

HEALTH EFFECTS OF AIR POLLUTION................................................I-1

 Ozone ................................................................................................................ I-2 

 Particulate Matter.............................................................................................. I-7 

 Short-Term Exposure Effects ...................................................................... I-9 

 Long-Term Exposure Effects..................................................................... I-13 

 Ultrafine Particles ........................................................................................... I-15 

 Carbon Monoxide ........................................................................................... I-15 

 Nitrogen Dioxide............................................................................................. I-16 

 Sulfur Dioxide................................................................................................. I-17 

 Sulfates............................................................................................................ I-18 

 Toxic Air Contaminants.................................................................................. I-19 

CONCLUSION ..................................................................................................... I-21

REFERENCES...................................................................................................... I-22 

ATTACHMENT 1 ................................................................................................ I-26 

ATTACHMENT 2 ................................................................................................ I-32 
APPENDIX 1 

HEALTH EFFECTS

 Health Effects of Air Pollution 

 Ozone 

 Particulate Matter 

 Carbon Monoxide 

 Nitrogen Dioxide 

 Sulfur Dioxide 

 Sulfates 

 Toxic Air Contaminants 
Health Effects of Air Pollution 

I-1 

INTRODUCTION 

This document presents a summary of scientific findings on the health effects of 

ambient air pollutants. The California Health and Safety Code Section 40471(b) 

requires that the South Coast Air Quality Management District prepare a report on the 

health impacts of particulate matter in the South Coast Air Basin, in conjunction with 

the preparation of the Air Quality Management Plan revisions. This document, which 

was prepared to satisfy that requirement, also includes the effects of the other major 

pollutants. 

HEALTH EFFECTS OF AIR POLLUTION 

Ambient air pollution is a major public health concern. Excess deaths and increases in 

illnesses associated with high air pollution levels have been documented in several 

episodes as early as 1930 in Meuse Valley, Belgium; 1948 in Donora, Pennsylvania; 

and 1952 in London. Although levels of pollutants that occurred during these acute 

episodes are now unlikely in the United States, ambient air pollution continues to be 

linked to increases in respiratory illness (morbidity) and increases in death rates 

(mortality). 

The adverse health effects associated with air pollution are diverse and include: 

• Increased mortality 

• Increased health care utilization (hospitalization, physician and emergency 

room visits) 

• Increased respiratory illness (symptoms, infections, and asthma exacerbation) 

• Decreased lung function (breathing capacity) 

• Lung inflammation 

• Potential immunological changes 

• Increased airway reactivity to a known chemical exposure - a method used in 

laboratories to evaluate the tendency of airways to have an increased 

possibility of developing an asthmatic response 

• A decreased tolerance for exercise. 

The evidence linking these effects to air pollutants is derived from population-based 

observational and field studies (epidemiological) as well as controlled laboratory studies 

involving human subjects and animals. There have been an increasing number of 

studies focusing on the mechanisms (that is, on learning how specific organs, cell types, 
Final 2007 AQMP Appendix I: Health Effects 

I-2 

and biochemicals are involved in the human body’s response to air pollution) and 

specific pollutants responsible for individual effects. Yet the underlying biological 

pathways for these effects are not always clearly understood. 

Although individuals inhale pollutants as a mixture under ambient conditions, the 

regulatory framework and the control measures developed are mostly pollutant-specific. 

This is appropriate, in that different pollutants usually differ in their sources, their times 

and places of occurrence, the kinds of health effects they may cause, and their overall 

levels of health risk. Different pollutants, from the same or different sources, may 

sometimes act together to harm health more than they would acting separately. 

Nevertheless, as a practical matter, health scientists, as well as regulatory officials, 

usually must deal with one pollutant at a time in determining health effects and in 

adopting air quality standards. To meet the air quality standards, comprehensive plans 

are developed such as the Air Quality Management Plan (AQMP) and the Air Toxics 

Control Plan (ATCP). These plans examine multiple pollutants, cumulative impacts, 

and transport issues related to attaining healthful air quality. A brief overview of the 

effects observed and attributed to various air pollutants is presented in this document. 

This summary is drawn substantially from reviews presented previously (SCAQMD, 

1996 and 2003), and from reviews on the effects of air pollution by the American 

Thoracic Society (ATS, 1996), the U.S. EPA reviews for ozone (U.S. EPA, 2006 ), 

Carbon Monoxide (U.S. EPA, 2000), and Particulate Matter (U.S. EPA, 2004), from a 

published review of the health effects of air pollution (Brunekreef and Holgate, 2002), 

and from reviews prepared by the California EPA Office of the Environmental Health 

Hazard Assessment for Particulate Matter (Cal EPA, 2002) and for Ozone (Cal EPA, 

2005) . More detailed citations and discussions on air pollution health effects can be 

found in these references.1

OZONE 

Ozone is a highly reactive compound, and is a strong oxidizing agent. When ozone 

comes into contact with the respiratory tract, it can react with tissues and cause damage 

in the airways. Since it is a gas, it can penetrate into the gas exchange region of the 

deep lung. 

The EPA primary standard for ozone is 0.08 ppm averaged over eight hours. The 

California Air Resources Board (CARB) has established standards of 0.09 ppm 

averaged over one hour and at 0.070 ppm averaged over eight hours. 

The major subgroups of the population considered to be at increased risk from ozone 

exposure are outdoor exercising individuals including children and people with 

preexisting respiratory disease(s) such as asthma. The data base identifying the former 

 

1

 Most of the studies referred to in this appendix are cited in the above sources. Only more recent specific references 

will be cited in this summary. 
 Health Effects of Air Pollution 

I-3 

group as being at increased risk to ozone exposure is much stronger and more 

quantitative than that for the latter group, probably because of a larger number of 

studies conducted with healthy individuals. The adverse effects reported with shortterm ozone exposure are greater with increased activity because activity increases the 

breathing rate and the volume of air reaching the lungs, resulting in an increased amount 

of ozone reaching the lungs. Children may be a particularly vulnerable population to air 

pollution effects because they spend more time outdoors, are generally more active, and 

have a higher ventilation rate than adults. 

A number of adverse health effects associated with ambient ozone levels have been 

identified from laboratory and epidemiological studies (EPA, 1996; ATS, 1996). These 

include increased respiratory symptoms, damage to cells of the respiratory tract, 

decreases in lung function, increased susceptibility to respiratory infection, and 

increased risk of hospitalization. 

The Children’s Health Study, conducted by researchers at the University of Southern 

California, followed a cohort of children that live in 12 communities in southern 

California with differing levels of air pollution for several years. A publication from 

this study found that school absences in fourth graders for respiratory illnesses were 

associated with ambient ozone levels. An increase of 20 ppb ozone was associated with 

an 83% increase in illness related absence rates (Gilliland, 2001). 

The number of hospital admissions and emergency room visits for all respiratory causes 

(infections, respiratory failure, chronic bronchitis, etc.) including asthma show a 

consistent increase as ambient ozone levels increase in a community. These excess 

hospital admissions and emergency room visits are observed when hourly ozone 

concentrations are as low as 0.08 to 0.10 ppm. 

Numerous recent studies have found positive associations between increases in ozone 

levels and excess risk of mortality. These associations persist even when other variables 

including season and levels of particulate matter are accounted for. This indicates that 

ozone mortality effects are independent of other pollutants (Bell, 2004). 

Several population-based studies suggest that asthmatics are more adversely affected by 

ambient ozone levels, as evidenced by increased hospitalizations and emergency room 

visits. Laboratory studies have attempted to compare the degree of lung function 

change seen in age and gender-matched healthy individuals versus asthmatics and those 

with chronic obstructive pulmonary disease. While the degree of change evidenced did 

not differ significantly, that finding may not accurately reflect the true impact of 

exposure on these respiration-compromised individuals. Since the respirationcompromised group may have lower lung function to begin with, the same degree of 

change may represent a substantially greater adverse effect overall. 
Final 2007 AQMP Appendix I: Health Effects 

I-4 

A recent publication from the Children’s Health Study focused on children and outdoor 

exercise. In communities with high ozone concentrations, the relative risk of 

developing asthma in children playing three or more sports was found to be over three 

times higher than in children playing no sports (McConnell, 2002). These findings 

indicate that new cases of asthma in children are associated with heavy exercise in 

communities with high levels of ozone. While it has long been known that air pollution 

can exacerbate symptoms in individuals with respiratory disease, this is among the first 

studies that indicate ozone exposure may be causally linked to asthma. 

In addition, human and animal studies involving both short-term (few hours) and longterm (months to years) exposures indicate a wide range of effects induced or associated 

with ambient ozone exposure. These are summarized in Table 1. 

Some lung function responses (volume and airway resistance changes) observed after a 

single exposure to ozone exhibit attenuation or a reduction in magnitude with repeated 

exposures. Although it has been argued that the observed shift in response is evidence 

of a probable adaptation phenomenon, it appears that while functional changes may 

exhibit adaptation, biochemical and cellular changes which may be associated with 

episodic and chronic exposure effects may not exhibit similar adaptation. That is, 

internal damage to the respiratory system may continue with repeated ozone exposures, 

even if externally observable effects (chest symptoms and reduced lung function) 

disappear. 

In a laboratory, exposure of human subjects to low levels of ozone causes reversible 

decrease in lung function as assessed by various measures such as respiratory volumes, 

airway resistance and reactivity, irritative cough and chest discomfort. Lung function 

changes have been observed with ozone exposure as low as 0.08 to 0.12 ppm for 6-8 

hours under moderate exercising conditions. Similar lung volume changes have also 

been observed in adults and children under ambient exposure conditions (0.10 - 0.15 

ppm). The responses reported are indicative of decreased breathing capacity and are 

reversible. 

In laboratory studies, cellular and biochemical changes associated with respiratory tract 

inflammation have also been consistently reported in the airway lining after low level 

exposure to ozone. These changes include an increase in specific cell types and in the 

concentration of biochemical mediators of inflammation and injury such as cytokines 

and fibronectin. These inflammatory changes can be observed in healthy adults 

exposed to ozone in the range of 0.08 to 0.10 ppm. 

The susceptibility to ozone observed under ambient conditions could be due to the 

combination of pollutants that coexist in the atmosphere or ozone may actually sensitize 

these subgroups to the effects of other pollutants. 
 Health Effects of Air Pollution 

I-5 

Some animal studies show results that indicate possible chronic effects including 

functional and structural changes of the lung. These changes indicate that repeated 

inflammation associated with ozone exposure over a lifetime may result in sufficient 

damage to respiratory tissue such that individuals later in life may experience a reduced 

quality of life in terms of respiratory function and activity level achievable. An autopsy 

study involving Los Angeles County residents provided supportive evidence of lung 

tissue damage (structural changes) attributable to air pollution. 

A recent study of birth outcomes in southern California found an increased risk for birth 

defects in the aortic and pulmonary arteries associated with ozone exposure in the 

second month of pregnancy (Ritz et al., 2002). This is the first study linking ambient air 

pollutants to birth defects in humans. Confirmation by further studies is needed. 
Final 2007 AQMP Appendix I: Health Effects 

I-6 

TABLE 1 

Adverse Health Effects of Ozone (O3) 

(Summary of Key Studies) 

03 Concentration and Exposure Hr, ppm Health Effect 

Ambient air containing 0.10 - 0.15 daily 1-h 

max over days to weeks 

Decreased breathing capacity, in children, adolescents, and 

adults exposed to 03 outdoors 

Exacerbation of respiratory symptoms (e.g., cough, chest 

pain) in individuals with preexisting disease (e.g., asthma) 

with low ambient exposure, decreased temperature, and other 

environmental factors resulting in increased summertime 

hospital admissions and emergency department visits for 

respiratory causes 

≥0.12 (1-3h) 

≥0.08 (6.6h) 

(chamber exposures) 

Decrements in lung function (reduced ability to take a deep 

breath), increased respiratory symptoms (cough, shortness of 

breath, pain upon deep inspiration), increased airway 

responsiveness and increased airway inflammation in 

exercising adults 

Effects are similar in individuals with preexisting disease 

except for a greater increase in airway responsiveness for 

asthmatic and allergic subjects 

Older subjects (>50 yrs old) have smaller and less 

reproducible changes in lung function 

Attenuation of response with repeated exposure 

≥0.12 with prolonged, repeated exposure 

(chamber exposures) 

Changes in lung structure, function, elasticity, and 

biochemistry in laboratory animals that are indicative of 

airway irritation and inflammation with possible development 

of chronic lung disease 

Increased susceptibility to bacterial respiratory infections in 

laboratory animals 

From: SCAQMD, 1996 

In summary, acute adverse effects associated with ozone exposures have been well 

documented, although the specific causal mechanism is still somewhat unclear. 

Additional research efforts are required to evaluate the long-term effects of air pollution 

and to determine the role of ozone in influencing chronic effects. 
 Health Effects of Air Pollution 

I-7 

PARTICULATE MATTER 

Airborne particulates are a complex group of pollutants that vary in source, size and 

composition, depending on location and time. The components include nitrates, 

sulfates, elemental carbon, organic carbon compounds, acid aerosols, trace metals, and 

material from the earth’s crust. Substances of biological origin, such as pollen and 

spores, may also be present. 

Until several years ago, the health effects of particulates were focused on those sized 10 

μm (micrometers) aerodynamic diameter and smaller. These can be inhaled through the 

upper airways and deposited in the lower airways and gas exchange tissues in the lung. 

These particles are referred to as PM10. EPA initially promulgated ambient air quality 

standards for PM10 of 150 μg/m3

 averaged over a 24-hour period, and 50 μg/m3 for an 

annual average. EPA has very recently rescinded the annual PM10 standard, but kept 

the 24-hour standard. 

In recent years additional focus has been placed on particles having an aerodynamic 

diameter of 2.5 μm or less (PM2.5). A greater faction of particles in this size range can 

penetrate and deposit deep in the lungs. The EPA recently lowered the air quality 

standards for PM2.5 to 35 μg/m3

 for a 24-hour average and reaffirmed 15 μg/m3 for an 

annual average standard. There was considerable controversy and debate surrounding 

the review of particulate matter health effects and the consideration of ambient air 

quality standards (Kaiser, 1997; Vedal, 1997) when the EPA promulgated the initial 

PM2.5 standards in 1997. 

Since that time, numerous studies have been published and some of the key studies were 

closely scrutinized and analyses repeated. The result is that there are now substantial 

data confirming the adverse health effects of PM2.5 exposures. 

There are also differences in the composition and sources of particles in the different 

size ranges that may have implications for health effects. The particles larger than 2.5 

μm (often referred to as the coarse fraction) are mostly produced by mechanical 

processes. These include automobile tire wear, industrial processes such as cutting and 

grinding, and resuspension of particles from the ground or road surfaces by wind and 

human activities. 

In contrast, particles smaller than 2.5 μm are mostly derived from combustion sources, 

such as automobiles, trucks, and other vehicle exhaust, as well as from stationary 

combustion sources. The particles are either directly emitted or are formed in the 

atmosphere from gases that are emitted. Components from material in the earth’s crust, 

such as dust, are also present, with the amount varying in different locations. 

Attention to another range of very small particles has been increasing over the last few 

years. These are generally referred to as “ultrafine” particles, with diameters of 0.1 μm 
Final 2007 AQMP Appendix I: Health Effects 

I-8 

or less. These particles are mainly from fresh emissions of combustion sources, but are 

also formed in the atmosphere from photochemical reactions. Ultrafine particles have 

relatively short half lives (minutes to hours) and rapidly grow through condensation and 

coagulation process into larger particles within the PM2.5 size range. These particles 

are garnering interest since laboratory studies indicate that their toxicity may be higher 

on a mass basis than larger particles, and there is evidence that these small particles can 

translocate from the lung to the blood and to other organs of the body. 

The health effects of ambient particulate matter have been recently reviewed (ATS, 

1996; U.S. EPA, 2004, Brunekreef, 2002). In addition, the California Air Resources 

Board (CARB) and the Office of Environmental Health and Hazard Assessment 

(OEHHA) have reviewed the adequacy of the California Air Quality Standards for 

Particulate Matter (Cal EPA, 2002). 

The major types of effects associated with particulate matter include: 

• Increased mortality 

• Exacerbation of respiratory disease and of cardiovascular disease as evidenced 

by increases in: 

-Respiratory symptoms 

-Hospital admissions and emergency room visits 

-Physician office visits 

-School absences 

-Work loss days 

• Effects on lung function 

• Changes in lung morphology 

The U.S. EPA has recently lowered the short-term ambient air quality standard for fine 

particles (PM2.5) and has rescinded the annual standard for PM10. The current federal and 

California standards are listed below: 
 Health Effects of Air Pollution 

I-9 

Standard Federal California

PM10 24-Hour average 150 μg/m3

 50 μg/m3

PM10 Annual Average -- 20 μg/m3

PM 2.5 24-Hour Average 35 μg/m3 -- 

PM 2.5 Annual Average 15 μg/m3

 12 μg/m3

Short-Term Exposure Effects 

Epidemiological studies have provided continued and consistent evidence for most of 

the effects listed above. An association between increased daily or several-day-average 

concentrations of PM10 and excess mortality and morbidity is consistently reported 

from studies involving communities across the U.S. as well as in Europe, Asia, and 

South America. A review and analysis of epidemiological literature for acute adverse 

effects was undertaken by Dockery and Pope to estimate these effects as percent 

increase in mortality associated with each incremental increase of PM10 by 10 μg/m3

. 

The estimates are presented in Table 2. It appears that individuals who are elderly or 

have preexistent lung or heart disease are more susceptible than others to the adverse 

effects of PM10. 
Final 2007 AQMP Appendix I: Health Effects 

I-10 

TABLE 2 

Combined Effect Estimates of Daily Mean 

Particulate Pollution 

 % Change in Health Indicator 

per each 10 μg/m3

 Increase in PM10

Increase in daily mortality 

Total deaths 1.0 

Respiratory deaths 3.4 

Cardiovascular deaths 1.4 

Increase in hospital usage (all respiratory 

diagnoses) 

Admissions 1.4 

Emergency department visits 0.9 

Exacerbation of asthma 

Asthmatic attacks 3.0 

Bronchodilator use 12.2 

Emergency department visits* 3.4 

Hospital admissions 1.9 

Increase in respiratory symptom reports 

Lower respiratory 3.0 

Upper respiratory 0.7 

Cough 2.5 

Decrease in lung function 

Forced expiratory volume 0.15 

Peak expiratory flow 0.08 

* One study only 

(Source: American Journal of Respiratory and Critical Care Medicine, Vol. 153, 113-

50, 1996) 

Many recent studies have confirmed that excess mortality and morbidity are associated 

with particulate matter levels. Estimates of mortality effects from these studies range 

from 0.3 to 1.7% increase for a 10 μg/m3

 increase in PM10 levels. The National 

Morbidity, Mortality, and Air Pollution Study (NMMAPS), a recent study of the largest 

U.S. cities, determined a combined risk estimate of about a 0.5% increase in total 

mortality for a 10 μg/m3

 increase in PM10 (Samet, 2000a). This study also analyzed the 

effects of gaseous co-pollutants. The results indicated that the association of PM10 and 

mortality were not confounded by the presence of the gaseous pollutants. When the 

gaseous pollutants were included in the analyses, the significance of the PM10 estimates 

remained. The PM10 effects were reduced somewhat when O3 was also considered and 
 Health Effects of Air Pollution 

I-11 

tended to be variably decreased when NO2, CO, and SO2 were added to the analysis. 

These results argue that the effects are likely due to the particulate exposures; they 

cannot readily be explained by coexisting weather stresses or other pollutants. 

The NMMAPS study (Samet 2000b) was one that used a flawed statistical software 

package. The investigators have reanalyzed their data using corrected settings for the 

software (Dominici, 2002a, Dominici 2002b). When the estimates for the 90 cities in 

the study were recalculated, the estimate changed from 0.41 percent increase in 

mortality for a 10 μg/m3

 increase in PM10 to a 0.27 percent increase. There remained a 

strong positive association between acute exposure to PM10 and mortality. Thus while 

the quantitative estimate is reduced, the major findings of the study did not change. 

Studies of PM2.5 also find associations with elevated mortality. The estimates for 

PM2.5 generally are in the range of 2.0 to 8.5% increase in total deaths per 25 μg/m3

increase in 24-hour PM2.5 levels. The estimates for cardiovascular related mortality 

range from 3.0 to 7.0% per 25 μg/m3

 24-hour PM2.5, and for respiratory mortality 

estimates range from 2.0 to 7.0% per 25 μg/m3 24-hour PM2.5. 

Several studies have attempted to assess the relative importance of particles smaller than 

2.5 μm and those between 2.5 μm and 10 μm (PM10-2.5). While some studies report 

that PM2.5 levels are better predictors of mortality effects, others suggest that PM10-2.5 

is also important. Most of the studies found higher mortality associated with PM2.5 

levels than with PM10-2.5. For example, a study of six cities in the U.S. found that 

particulate matter less than 2.5 μm were associated with increased mortality, but that the 

larger particles were not. Other studies in Mexico City and Santiago, Chile reported 

that PM10-2.5 was as important as PM2.5. Overall effects estimates for PM10-2.5 fall 

in the range of 0.5 to 6.0 % excess mortality per 25 μg/m3

 24-hour average. 

The relative importance of both PM2.5 and PM10-2.5 may vary in different regions 

depending on the relative concentrations and components, which can also vary by 

season. More research is needed to better assess the relative effects of fine (PM2.5) and 

coarse (PM10-2.5) fractions of particulate matter on mortality. 

A number of studies have evaluated the association between particulate matter exposure 

and indices of morbidity such as hospital admissions, emergency room visits or 

physician office visits for respiratory and cardiovascular diseases. The effects estimates 

are generally higher than the effects for mortality. The effects are associated with 

measures of PM10 and PM2.5. Effects are also associated with PM10-2.5. Thus, it 

appears that when a relatively small number of people experience severe effects, larger 
Final 2007 AQMP Appendix I: Health Effects 

I-12 

numbers experience milder effects, which may relate either to the coarse or to the fine 

fraction of airborne particulate matter. 

In the NMMAPS study, hospital admissions for those 65 years or older were assessed in 

14 cities. Hospital admissions for these individuals showed an increase of 6% for 

cardiovascular diseases and a 10% increase for respiratory disease admissions, per 50 

μg/m3

 increase in PM10. The excess risk for cardiovascular disease ranges from 3-10% 

per 50 μg/m3

 PM10 and from 4-10% per 25 μg/m3 PM2.5 or PM10-2.5. 

Similarly, school absences, lost workdays and restricted activity days have also been 

used in some studies as indirect indicators of acute respiratory conditions. The results 

are suggestive of both immediate and delayed impact on these parameters following 

elevated particulate matter exposures. These observations are consistent with the 

hypothesis that increased susceptibility to infection follows particulate matter 

exposures. 

Some studies have reported that short-term particulate matter exposure is associated 

with changes in lung function (lung capacity and breathing volume); upper respiratory 

symptoms (hoarseness and sore throat); and lower respiratory symptoms (increased 

sputum, chest pain and wheeze). The severity of these effects is widely varied and is 

dependent on the population studied, such as adults or children with and without 

asthma. Sensitive individuals, such as those with asthma or pre-existing respiratory 

disease, may have increased or aggravated symptoms associated with short-term 

particulate matter exposures. Several studies have followed the number of medical 

visits associated with pollutant exposures. A range of increases from 3% to 42% for 

medical visits for respiratory illnesses was found corresponding to a 50 μg/m3

 change in 

PM10. A limited number of studies also looked at levels of PM2.5 or PM10-2.5. The 

findings suggest that both the fine and coarse fractions may have associations with some 

respiratory symptoms. 

The biological mechanisms by which particulate matter can produce health effects are 

being investigated in laboratory studies. Inflammatory responses in the respiratory 

system in humans and animals exposed to concentrated ambient particles have been 

measured. These include effects such as increases in neutrophils in the lungs. Other 

changes reported include increased release of cytokines and interleukins, chemicals 

released as part of the inflammatory process. The effects of particulate matter may be 

mediated in part through the production of reactive oxygen species during the 

inflammatory process. Recent reviews discuss mechanistic studies in more detail 

(Brunekreef, 2002; Brook, 2004). 
 Health Effects of Air Pollution 

I-13 

Long-Term Exposure Effects 

While most studies have evaluated the acute effects, some studies specifically focused 

on evaluating the effects of chronic exposure to PM10 and PM2.5. Studies have 

analyzed the mortality of adults living in different U.S. cities. After adjusting for 

important risk factors, these studies found a consistent positive association of deaths and 

exposure to particulate matter. A similar association was observable in both total 

number of deaths and deaths due to cardiorespiratory causes. A shortening of lifespan 

was also reported in these studies. 

Significant associations for PM2.5 for both total mortality and cardiorespiratory 

mortality were reported in a study using data from the American Cancer Society. A reanalysis of the data from this study confirmed the finding (Krewski, 2000). The 

Harvard Six Cities Study evaluated several size ranges of particulate matter and 

reported significant associations with PM15, PM2.5, sulfates, and non-sulfate particles, 

but not with coarse particles (PM15 – PM2.5). An extension of the Harvard Six Cities 

Cohort confirmed the association of mortality with PM2.5 levels (Laden, 2006). These 

studies provide evidence that the fine particles, as measured by PM2.5, may be more 

strongly associated with mortality effects from long-term particulate matter exposures 

than are coarse compounds. 

A follow-up study of the American Cancer Society cohort confirmed and extended the 

findings in the initial study. The researchers estimated that, on average, a 10ug/m3 

increase in fine particulates was associated with approximately a 4% increase in total 

mortality, a 6% increase in cardiopulmonary mortality, and an 8% increase risk of lung 

cancer mortality (Pope, 2002). The magnitude of effects is larger in the long-term 

studies than in the short-term investigations. An analysis of the American Cancer 

Society Cohort from the Los Angeles area used a more detailed estimate of long-term 

PM2.5 exposures and found that the risk of mortality was up to three times higher than 

estimated with the national cohort (Jerrett, 2005). These findings indicate that longterm exposures may be more important in terms of overall health effects. 

Recent studies report evidence indicating that particulate matter exposure early in 

pregnancy may be associated with lowered birth weights (Bobak, 1999). Other studies 

from the U.S., the Czech Republic and Mexico City have reported that neonatal and 

early postnatal exposure to particulate matter may lead to increased infant mortality. A 

more recent study in Southern California found increased risks for infant deaths 

associated with exposures to particulates and other pollutants (Ritz, 2006). These 

results suggest that infants may be a subgroup affected by particulate matter exposures. 

In addition, some long-term effect studies have reported an increased risk of mortality 

from lung cancer associated with particulate matter exposures. A study involving 

California Seventh Day Adventists (very few of whom smoke) has reported an 

association of lung cancer mortality with PM10 levels. It is not clear from these studies 
Final 2007 AQMP Appendix I: Health Effects 

I-14 

whether the association relates to causation of disease, or whether individuals with 

cancer are more susceptible to other effects of particles leading to the observed 

mortality association. A recent study that followed a large number of individuals living 

in the largest U.S. cities found elevated lung cancer risk associated with long term 

average PM2.5 levels (Pope, 2002). 

Several studies have assessed the effects of long-term particulate matter exposure on 

respiratory symptoms and lung function changes. Associations have been found with 

symptoms of chronic bronchitis and decreased lung function. A study of school 

children in 12 communities in Southern California showed significant association of 

particulate matter with bronchitis or phlegm in children with asthma. These effects 

were also associated with NO2 and acid vapor levels. 

A cohort of fourth graders from the Southern California communities was followed over 

a period of four years by the Children’s Health Study. A lower rate of growth in lung 

function was found in children living in areas with higher levels of particulate pollution 

(Gauderman, 2000). Decreases in lung function growth were associated with PM10, 

PM2.5, PM10-2.5, acid vapor, and NO2. There was no association with ozone levels. 

The investigators were not able to identify independent effects of the pollutants, but 

noted that motor vehicle emissions are a major source of the pollutants. 

A follow-up study on a second cohort of children confirmed the findings that decreased 

lung function growth was associated with particulates, nitric oxides, and elemental 

carbon levels (Gauderman, 2002). Elemental carbon is often used as a measure for 

diesel particulate. Additionally, children who moved to areas with less air pollution 

were found to regain some of the lung function growth rate (Avol, 2001). By the time 

the fourth graders graduated from high school, a significant number showed lower lung 

function. The risk of lower lung function was about five times higher in children with 

the highest PM2.5 exposure when compared to the lowest exposure communities 

(Gauderman, 2004). These deficits are likely to persist since the children were at the 

end of their growth period. 

Despite data gaps, the extensive body of epidemiological studies has both qualitative 

and quantitative consistency suggestive of causality. A considerable body of evidence 

from these studies suggests that ambient particulate matter, alone or in combination 

with other coexisting pollutants, is associated with significant increases in mortality and 

morbidity in a community. 

In summary, the scientific literature indicates that an increased risk of mortality and 

morbidity is associated with particulate matter at ambient levels. The evidence for 

particulate matter effects is mostly derived from population studies with supportive 

evidence from clinical and animal studies. Although most of the effects are attributable 

to particulate matter, co-pollutant effects cannot be ruled out on the basis of existing 

studies. The difficulty of separating the effects may be due to the fact that particulate 
 Health Effects of Air Pollution 

I-15 

levels co-vary with other combustion source pollutants. That is, the particle 

measurements serve as an index of overall exposure to combustion-related pollution, 

and some component(s) of combustion pollution other than particles might be at least 

partly responsible for the observed health effects. 

ULTRAFINE PARTICLES 

As noted above, numerous studies have found association of particulate matter levels 

with adverse effects, including mortality, hospital admissions, and respiratory disease 

symptoms. The vast majority of these studies used particle mass of PM10 or PM2.5 as 

the measure of exposure. Some researchers have postulated, however, that ultrafine 

particles may be responsible for some of the observed associations of particulate matter 

and health outcomes (Oberdorster, et al, 1995; Seaton, et al, 1995). Ultrafine particles 

are generally classified of 0.1 μm and small diameter. 

Several potential mechanisms have been brought forward to suggest that the ultrafine 

portion may be important in determining the toxicity of ambient particulates, some of 

which are discussed below. 

For a given mass concentration, ultrafine particles have much higher numbers and 

surface area compared to larger particles. Particles can act as carriers for other adsorbed 

agents, such as trace metals and organic compounds; and the larger surface area may 

transport more of such toxic agents than larger particles. 

Smaller particles can also be inhaled deep into the lungs. As much as 50% of 0.02 μm 

diameter particles are estimated to be deposited in the alveolar region of the lung. 

CARBON MONOXIDE 

The high affinity of carbon monoxide (CO) to bond with oxygen-carrying proteins 

(hemoglobin and myoglobin) results in reduced oxygen supply in the bloodstream of 

exposed individuals. The reduced oxygen supply is responsible for the toxic effects of 

CO which are typically manifested in the oxygen-sensitive organ systems. The effects 

have been studied in controlled laboratory environments involving exposure of humans 

and animals to CO, as well as in population-based studies of ambient CO exposure 

effects. People with deficient blood supply to the heart (ischemic heart disease) are 

known to be susceptible to the effects of CO. Protection of this group is the basis of the 

existing National Ambient Air Quality Standards for CO at 35 ppm for one hour and 

9 ppm averaged over eight hours. The health effects of ambient CO have been recently 

reviewed (U.S. EPA, 2000). 

Inhaled CO has no known direct toxic effect on lungs but rather exerts its effects by 

interfering with oxygen transport through the formation of carboxyhemoglobin (COHb, 

a chemical complex of CO and hemoglobin). Exposure to CO is often evaluated in 
Final 2007 AQMP Appendix I: Health Effects 

I-16 

terms of COHb levels in blood measured as percentage of total hemoglobin bound to 

CO. COHb levels in non-smokers range between 0.3 and 0.7% and 5 to 10% in 

smokers. COHb levels in excess of 1.5% in a significant proportion of urban 

nonsmoking populations can be considered as evidence of widespread exposure to 

environmental CO. 

Under controlled laboratory conditions, healthy subjects exposed to CO sufficient to 

result in 5% COHb levels exhibited reduced duration of maximal exercise performance 

and consumption of oxygen. Studies involving subjects with coronary artery disease 

who engaged in exercise during CO exposures have shown that COHb levels as low as 

2.4% can lead to earlier onset of electrocardiograph changes indicative of deficiency of 

oxygen supply to the heart. Other effects include an earlier onset of chest pain, an 

increase in the duration of chest pain, and a decrease in oxygen consumption. 

Animal studies associated with long-term exposure to CO resulting in COHb levels that 

are equivalent to those observed in smokers have shown indication of reduction in birth 

weight and impaired neurobehavior in the offspring of exposed animals. 

Recent epidemiological studies conducted in Southern California have indicated an 

association with CO exposure during pregnancy to increases in pre-term births. (Ritz, 

2000). However, the results were not consistent in different areas studied. The increase 

in the pre-term births was also associated with PM10 levels. Another study found 

increased risks for cardiac related birth defects with carbon monoxide exposure in the 

second month of pregnancy (Ritz, 2002). Further study is needed to confirm these 

observations. 

NITROGEN DIOXIDE 

The California EPA is currently reviewing the health effects of nitrogen dioxide (Cal 

EPA, 2006). Evidence for low-level nitrogen dioxide (NO2) exposure effects is derived 

from laboratory studies of asthmatics and from epidemiological studies. Additional 

supportive evidence is derived from animal studies. 

Epidemiological studies using the presence of an unvented gas stove as a surrogate for 

indoor NO2 exposures suggest an increased incidence of respiratory infections or 

symptoms in children. 

Recent studies related to outdoor exposure have found health effects associated with 

ambient NO2 levels, including respiratory symptoms, respiratory illness, decreased lung 

function, increased emergency room visits for asthma, and cardiopulmonary mortality. 

However, since NO2 exposure generally occurs in the presence of other pollutants, such 

as particulate matter, these studies are often unable to determine the specific role of NO2

in causing effects. 

The Children’s Health Study in Southern California found associations of air pollution, 

including NO2, PM10, and PM2.5, with respiratory symptoms in asthmatics 

(McConnell, 1999). Particles and NO2 were correlated, and effects of individual 
 Health Effects of Air Pollution 

I-17 

pollutants could not be discerned. A subsequent analysis indicated a stronger role for 

NO2 (McConnell, 2002). 

Ambient levels of NO2 were also associated with a decrease in lung function growth in 

a group of children followed for eight years. In addition to NO2, the decreased growth 

was also associated with particulate matter and airborne acids. The study authors 

postulated that these may be a measure of a package of pollutants from traffic sources. 

(Gauderman, 2004). 

Results from controlled exposure studies of asthmatics demonstrate an increase in the 

tendency of airways to contract in response to a chemical stimulus (bronchial 

reactivity). Effects were observed with an exposure to 0.3 ppm NO2 for a period 

ranging from 30 minutes to 3 hours. A similar response is reported in some studies with 

healthy subjects at higher levels of exposure (1.5 - 2.0 ppm). Mixed results have been 

reported when people with chronic obstructive lung disease are exposed to low levels of 

NO2. 

Short-term controlled studies of animals exposed to NO2 over a period of several hours 

indicate cellular changes associated with allergic and inflammatory response and 

interference with detoxification processes in the liver. In some animal studies the 

severity of the lung structural damage observed after relatively high levels of short-term 

ozone exposure is observed to increase when animals are exposed to a combination of 

ozone and NO2. 

In animals, longer-term (3-6 months) repeated exposures at 0.25 ppm appear to decrease 

one of the essential cell-types (T-cells) of the immune system. Non-specific changes in 

cells involved in maintaining immune functions (cytotoxic T cells and natural killer 

cells) have been observed in humans after repeated exposure (4-6 days) to >0.6 ppm of 

NO2 (20 min. - 2 hours). All these changes collectively support the observation 

reported both in population and animal studies of increased susceptibility to infections, 

as a result of NO2 exposure. 

SULFUR DIOXIDE 

Controlled laboratory studies involving human volunteers have clearly identified 

asthmatics as the most sensitive group to the effects of ambient sulfur dioxide (SO2)

exposures. Healthy subjects have failed to demonstrate any short-term respiratory 

functional changes at exposure levels up to 1.0 ppm over 1-3 hours. 

In asthmatics, brief exposure (10 minutes) to SO2 at levels as low as 0.25 ppm can result 

in significant alteration of lung function, such as increases in airway resistance and 

decreases in breathing capacity. In some, the exposure can result in severe symptoms 

necessitating the use of medication for relief. The response to SO2 inhalation is 

observable within 2 minutes of exposure, increases further with continuing exposure up 

to 5 minutes then remains relatively steady as exposure continues. SO2 exposure is 

generally not associated with any delayed reactions or repetitive asthmatic attacks. 
Final 2007 AQMP Appendix I: Health Effects 

I-18 

No significant changes have been reported from studies, which have evaluated the 

effects of exposure to co-pollutants (ozone or nitrogen dioxide), prior to or in 

conjunction with SO2 exposure. 

Animal studies have shown that despite SO2 being a respiratory irritant, it does not 

cause substantial acute or chronic toxicity in animals exposed at ambient concentrations. 

However, relatively high exposures (10 ppm of SO2 for 72 hours) in mice can lead to 

tissue damage, fluid accumulation and sloughing of respiratory lining. Sensitization to 

allergies is observable in guinea pigs repeatedly exposed to high levels (72 ppm) of 

SO2. This effect needs further evaluation in clinical and population studies to identify 

any chronic exposure impact on both asthmatic incidence and attacks in a population. 

Some epidemiological studies indicate that the mortality and morbidity effects 

associated with the fine fraction of particles show a similar association with ambient 

SO2 levels. In these studies, efforts to separate the effects of SO2 from fine particles 

have not been successful. Thus, it is not clear whether the two pollutants act 

synergistically, or whether being generated from similar combustion sources they 

represent the same pollution index for the observed effects. 

SULFATES 

Based on a level determined necessary to protect the most sensitive individuals, the 

California Air Resources Board in 1976 adopted a standard of 25 μg/m3

 (24-hour 

average) for sulfates. 

In recent years, a vast majority of effects (mortality and morbidity) associated with fine 

particles (PM2.5) and sulfur dioxide have shown a similar association with ambient 

sulfate levels in some population studies. The efforts to fully separate the effects of 

sulfates from other coexisting pollutants have not been successful. This may be due to 

the fact that these pollutants covary under ambient conditions, having been emitted from 

common sources; and the effects observed may be due to the combination of pollutants, 

rather than a single pollutant. 

A clinical study involving exposure of human subjects to sulfuric acid aerosol indicated 

that adolescent asthmatics may be a susceptible population subgroup with some changes 

in lung function observed with exposures below 100 μg/m3

. In general, however, 

laboratory exposures of human volunteers to sulfates at or near ambient levels have not 

found significant changes in lung function. 

Results from animal studies involving exposures to sulfuric acid aerosol, ammonium 

bisulfate and ammonium sulfate indicate that acidic particles (former two) are more 

toxic than non-acidic particles (latter). In addition, the severity or magnitude of both 

mortality and morbidity effects is relatively higher in population studies of the eastern 

United States and Canada where sulfate concentrations are higher than for those 
 Health Effects of Air Pollution 

I-19 

observed in the western United States. Mixed results have been reported from studies 

which attempted to ascertain the role of acidity in determining the observed toxicity. 

TOXIC AIR CONTAMINANTS 

Toxic air contaminants are pollutants for which there generally are no ambient air 

quality standards. Under California’s Air Toxics Program, CARB staff and OEHHA 

assess the health effects of substances that may pose a risk of adverse health effects. 

These effects are usually an increased risk for cancer or adverse birth outcome. After 

review by the state Scientific Review Panel, the CARB holds a public hearing on 

whether to formally list substances that may pose a significant risk to public health as a 

Toxic Air Contaminant. 

CARB and OEHHA also establish potency factors for air toxics that are carcinogenic. 

The potency factors can be used to estimate the additional cancer risk from ambient 

levels of toxics. This estimate represents the chance of contracting cancer in an 

individual over a lifetime exposure to a given level of an air toxic and is usually 

expressed in terms of additional cancer cases per million people exposed. 

The SCAQMD conducted a study on the ambient concentrations and estimated the 

potential health risks from air toxics (SQAQMD, 2000). A one year monitoring 

program was undertaken at 12 sites throughout the SCAB. Over 30 substances were 

measured, and annual average levels were calculated. The results showed that the 

overall risk for excess cancer from a lifetime exposure to ambient levels of air toxics 

was about 1,400 in a million. The largest contributor to this risk was diesel exhaust, 

accounting for 71% of the air toxics risk. A breakdown of the major contributors to the 

air toxics risk is shown in the following graph. 
Final 2007 AQMP Appendix I: Health Effects 

I-20 

Basinwide Cancer Risk ~1,400 in one million

71%

8%

7%

3%

11%

Diesel Exhaust

1,3-Butadiene

Benzene

Carbonyls

Others

FIGURE 1 

Major pollutants contributing to Air Toxics Cancer Risk in the South Coast Air Basin 

For non-cancer health effects, OEHHA has developed acute and chronic Reference 

Exposure Levels (RELs). RELs are concentrations in the air below which adverse 

health effects are not likely to occur. Acute RELs refer to short-term exposures, 

generally of one-hour duration. Chronic RELs refer to long-term exposures of several 

years. The ratio of ambient concentration to the appropriate REL can be used to 

calculate a Hazard Index. A Hazard Index of less than one would not be expected to 

result in adverse effects. 

The key air toxics contributing to risk from mobile and stationary sources are listed 

below. 

TABLE 3 

Key Air Toxic Air Contaminants in the SCAB 

Mobile Sources Stationary Sources 

Acetaldehyde Hexavalent Chromium 

Benzene Methylene Chloride 

1,3 Butadiene Nickel 

Diesel Exhaust Perchloroethylene 

Formaldehyde Trichloroethylene 
 Health Effects of Air Pollution 

I-21 

CONCLUSION 

The vast body of scientific evidence shows that the adverse impacts of air pollution in 

human and animal health are clear. A considerable number of population-based and 

laboratory studies have established a link between increased morbidity and in some 

instances, earlier mortality and air pollution. 
REFERENCES
References 

I-22 

References 

American Thoracic Society, Committee of the Environmental and Occupational Health 

Assembly of the American Thoracic Society. (1996). “Health Effects of Outdoor Air 

Pollution.” American Journal Respiratory and Critical Care Medicine, Parts 1 and 2. 153:3-

50 and 153:477-498. 

Avol EL, Gauderman JW, Tan SM, London SJ, Peters JM. (2001). “Respiratory Effects of 

Relocating to Areas of Differing Air Pollution Levels.” Am J Respir Crit Care Med, 

164:11:2067-2072. 

Bell ML, McDermott A, Zeger SL, Samet, JM, Dominici, F. (2004). “Ozone and ShortTerm Mortality in 95 US Urban Communities, 1987-2000.” JAMA 292:2372-2378. 

Bobak M, Leon DA. (1999). “Pregnancy Outcomes and Outdoor Air Pollution: An 

Ecological Study in Districts of the Czech Republic 1986-8.” Occup. and Environ. Med. 

56:539-543. 

Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Lipsett M, Leupker R, Mittleman M, 

Samet J, Smith SC Jr., Tager I. (2004). “Air Pollution and Cardiovascular Disease: A 

Statement for Healthcare Professionals from the Expert Panel on Population and Prevention 

Science of the American Heart Association.” Circulation, 109:2655-2671 

Brunekreef, B and ST Holgate. (2002). “Air Pollution and Health.” The Lancet, 

360(9341):1233-42, 

http://www.thelancet.com/journal/vol360/iss9341/full/llan.360.9341.editorial_and_review.2

2808.1

California Environmental Protection Agency, California Air Resources Board, and Office of 

Environmental Health Hazard Assessment. (2002). "Public Hearing to Consider 

Amendments to the Ambient Air Quality Standards for Particulate Matter and Sulfates.” 

http://arbis.arb.ca.gov/research/aaqs/std-rs/pm-final/pm-final.htm#Summary

California Environmental Protection Agency, Air Resources Board. (2005). “Review of the 

California Ambient Air Quality Standard for Ozone.” 

California Environmental Protection Agency, California Air Resources Board and Office of 

Health Hazard Assessment. (2006). “Review of the California Ambient Air Quality 

Standard for Nitrogen Dioxide.” Draft Staff Report. 

Dominici F, McDermott A, Zeger SL, Samet JM. (2002.) “On the use of Generalized 

Additive Models in Time-Series Studies of Air Pollution and Health.” Am J Epidemiol., 

156:193-203. 
Final 2007 AQMP Appendix I: Health Effects 

I-23 

Dominici F, McDermott A, Zeger SL, Samet JM. (2002). A Report to the Health Effects 

Institute: Reanalyses of the NMMAPS Database. 

http://www.biostat.jhsph.edu/~fdominic/HEI/nmmaps.html

Gauderman JW, McConnell R, Gilliland F, London S, Thomas D, Avol E, Vora H, Berhane 

K, Rappaport EB, Lurmann F, Margolis HG, Peters J. (2000). “Association between Air 

Pollution and Lung Function Growth in Southern California Children.” Am J Respir Crit 

Care Med, 162(4):1383-1390. 

Gauderman JW, Gilliland F, Vora H, Avol E, Stram D, McConnell R, Thomas D, Lurmann 

F, Margolis HG, Rappaport EB, Berhane K, Peters J. (2002). . “Association between Air 

Pollution and Lung Function Growth in Southern California Children. Results from a 

Second Cohort.” Am J Respir Crit Care Med, 166:76-84. 

Gauderman JW, Avol E, Gilliland F, Vora H, Thomas D, Berhane K, McConnell R, Kuenzli 

N, Lurmann F, Rappaport E, Margolis H, Bates D, Peters J. (2004). “The Effect of Air 

Pollution on Lung Development from 10 to 18 Years of Age.” N Engl J Med, 

351(11):1057-1067. 

Gilliland FD, Berhane K, Rappaport EB, Thomas DC, Avol E, Gauderman WJ, London SJ, 

Margolis HG, McConnell R, Islam KT, Peters JM. (2001). “The Effects of Ambient Air 

Pollution on School Absenteeism Due to Respiratory Illnesses.” Epidemiology, 12(1):43-

54. 

Jerrett M, Burnett RT, Ma R, Pope CA III, Krewski D, Newbold KB, Thurston G, Shi Y, 

Finkelstein N, Calle EE, Thun MJ. (2005). “Spatial Analysis of Air Pollution and Mortality 

in Los Angeles. Epidemiology, 15(6):727-736. 

Krewski D, Burnett RT, Goldberg MS, Hoover K, Siemiatycki J, Abrahamowicz M, White 

WH, et al. (2000). “Reanalysis of the Harvard Six Cities Study and the American Cancer 

Society Study of Particulate Air Pollution and Mortality. A Special Report of the Institute’s 

Particle Epidemiology Reanalysis Project.” Health Effects Institute. 

Laden F, Schwartz J, Speizer FE, Dockery DW. (2006). “Reduction in Fine Particulate Air 

Pollution and Mortality.” Am J Respir Crit Care Med, 173:667-672. 

McConnell R, Berhane K, Gilliland F, London SJ, Islam T, Gauderman WJ, Avol E, 

Margolis HG, Peters JM. (2002). “Asthma in exercising children exposed to ozone: a 

cohort study.” Lancet, 359:386-91. 
References 

I-24 

McConnell R, Berhane K, Gilliland F, London SJ, Vora H, Avol E, Gauderman WJ, 

Margolis HG, Lurman F, Thomas DC, Peters JM. (1999). “Air Pollution and Bronchitic 

Symptoms in Southern California Children with Asthma.” EHP, 107(9):757-760. 

McConnell R, Berhane K, Gilliland F, Molitor J, Thomas D, Lurmann F, Avol E, 

Gauderman WJ, Peters JM. (2003). “Prospective Study of Air Pollution and Bronchitic 

Symptoms in Children with Asthma.” Am J Respir Crit Care Med, 168:790-797. 

National Research Council. (1998). “Research Priorities for Airborne Particulate Matter I: 

Immediate Priorities and a Long Range Research Portfolio.” Washington, DC, National 

Academy Press. 

Oberdorster G, et al. (1995). “Association of Particulate Air Pollution and Acute Mortality: 

Involvement of Ultra-Fine Particles.” Inhalation Toxicol 7:111-124. 

Peters J, et al. (1997). “Children’s Health Study.” 

http://www.arb.ca.gov/research/chs/chs.htm. 

Pope III CA, Burnett RT, Thun MJ, Calle E, Krewski D, Kazuhiko I, Thurston G. (2002). 

“Lung Cancer, Cardiopulmonary Mortality, and Long-Term Exposure to Fine Particulate 

Air Pollution.” JAMA, 287:1132-1141. 

Pope III CA, Dockery DW. (2006). “Health Effects of Fine Particulate Air Pollution: 

Lines that Connect.” JAWMA, Critical Review. 56(6):709-742. 

Ritz B, Yu F, Chapa G, Fruin S. (2000). “Effect of Air Pollution on Preterm Birth Among 

Children Born in Southern California between 1989 and 1993.” Epidemiology, 11(5)502-

11. 

Ritz B, Yu F, Fruin S. Chapa G, Shaw GM, Harris JA. (2002). “Ambient Air Pollution and 

Risk of Birth Defects in Southern California.” Am J Epidemiol, 155(1):17-25. 

Ritz B, Wilhelm M, Zhao, Y. (2006). “Air Pollution and Infant Death in Southern 

California, 1989-2000.” Pediatrics. 118(2):493-502 

Samet JM, Dominici F, Curriero FC, Coursac I, Zeger SL. (2000). “Fine Particulate Air 

Pollution and Mortality in 20 U.S. Cities, 1987–1994.” N Engl J Med, 343(24):1742-9. 

Samet JM, Zeger SL, Dominici F, Curriero F, Coursac I, Dockery DW, Schwartz J, 

Zanobetti A. (2000). “The National Morbidity, Mortality, and Air Pollution Study Part II: 

Morbidity and Mortality from Air Pollution in the United States.” Res Rep Health Eff Inst, 

94 
Final 2007 AQMP Appendix I: Health Effects 

I-25 

SCAQMD. (2000). Multiple Air Toxics Exposure Study in the South Coast Air Basin. 

MATES II. South Coast Air Quality Management District. 

http://www.aqmd.gov/matesiidf/matestoc.htm

Seaton A, et al. (1995). “Particulate Air Pollution and Acute Health Effects.” Lancet 

345:176-178. 

United States Environmental Protection Agency. (2000). “Air Quality Criteria for Carbon 

Monoxide.” EPA 600/P-99/001F. 

United States Environmental Protection Agency. (2004). “Air Quality Criteria for 

Particulate Matter.” EPA 600/P-99/002aB. 

United States Environmental Protection Agency. (2006). “Air Quality Criteria of Ozone 

and Other Photochemical Oxidants.” EPA 600/R-05/004aF-CF. 

Vedal S. (1997). “Critical Review. Ambient Particles and Health: Lines that Divide.” 

JAMA, 47(5):551-581. 
 

ATTACHMENT 1 

COMMENTS RECEIVED ON DRAFT APPENDIX I FROM SCAQMD ADVISORY 

COUNCIL

The letter requesting comments and a copy of comments received follow. 

Staff responses to comments are in Attachment 2. 
Attachment 1 

I-26 
Final 2007 AQMP Appendix I: Health Effects 

I-27 
Attachment 1 

I-28 
Final 2007 AQMP Appendix I: Health Effects 

I-29 
Attachment 1 

I-30 
Final 2007 AQMP Appendix I: Health Effects 

I-31 
ATTACHMENT 2 

STAFF RESPONSES TO COMMENTS RECEIVED
Final 2007 AQMP Appendix I: Health Effects 

I-32 

Comment: 

Citations missing in References section. 

Response: 

The missing citations are below. 

Oberdorster G, et al. 1995. “Association of Particulate Air Pollution and Acute 

Mortality: Involvement of Ultra-Fine Particles.” Inhalation Toxicol 7:111-124. 

Seaton A, et al. 1995. “Particulate Air Pollution and Acute Health Effects.” Lancet 

345:176-178. 

Comment: 

Include an explanation of how oxidizing agents affect biological tissue. 

Response: 

Oxidants such as ozone can readily react with biochemicals in tissues to alter their chemical 

structure and affect their biochemical functioning. 

Comment: 

Are percent changes in health indicators for PM2.5 the same as for PM10? Include a table for 

percentage change for PM2.5 indicators as was done for PM2.5. 

Response: 

The table for PM10 was used to provide a brief summary of information related to daily 

changes in PM levels with various health indicators, and was taken from a previous review 

paper. The discussion for PM2.5 associated outcomes includes a brief description of some of 

the more recent studies of health effects, which does include percentage changes associated 

with changes in ambient exposures. The discussion shows that the relative changes 

associated with PM2.5 levels are not the same as those with PM10. The discussion also points 

out that some studies indicate the effects from PM10 exposures may be attributed to the 

PM2.5 component, whereas other studies indicate that the fraction of PM10 larger than 2.5 

μm diameter also contribute. The relative contribution of the different fractions of PM10 to 

health outcomes is an ongoing area of research. 
Attachment 2 

I-33 

Comment: 

Ultrafine particles may affect cellular ATP production, and this could explain why 

particulate matter might exacerbate diabetic conditions. 

Response: 

Studies have indeed shown that ultrafine particles can penetrate into cell mitochondria and 

result in cell death. The mechanism is thought to include oxidative injury to cellular 

components. While there are studies that indicate individuals with diabetes may be more 

sensitive to the effects of air pollutants, staff opinion is that there are not sufficient data 

available to determine whether particulate exposures exacerbate diabetic conditions. 

Comment: 

Include a definition of the differences between sulfur dioxide and sulfates. 

Response: 

Sulfur dioxide (SO2) occurs as a gas in the atmosphere, whereas sulfates (referring to the ion 

SO4

-2) are generally found as a component of particulate matter. 

Comment: 

Add a discussion on how the AQMP would reduce health effects. 

Response: 

Staff assessment of the benefits of implementing the AQMP and attaining the ambient air 

quality standards is included in the Socioeconomic Report. 

Comment: 

Some clarification should be considered in the AQMP that acute and chronic effects of toxic 

air pollutants should take priority, as far as regulations are concerned, over carcinogenic 

effects. 

Response: 

Staff position is that all adverse effects are important. 
Final 2007 AQMP Appendix I: Health Effects 

I-34 

Comment: 

A check should be done of all the District monitoring stations to confirm that they are not 

impacted by unusual site conditions. 

Response: 

This is beyond the scope of Appendix I. The air quality monitoring network stations are 

sited in conformance with federal and state guidelines to be at locations representative of 

regional air quality. 

Comment: 

An analysis of indoor air quality and PM2.5 should be included. 

Response: 

There are few studies on the health effects on indoor PM2.5 exposures. The study cited by 

the commenter did not provide information on health effects.