FINAL 

2003 AQMP APPENDIX I 

HEALTH EFFECTS 

AUGUST 2003 
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: 

FRED AGUIAR 

Supervisor, Fourth District 

San Bernardino County Representative 

MICHAEL D. ANTONOVICH 

Supervisor, Fifth District 

Los Angeles County Representative 

HAL BERNSON 

Councilmember, City of Los Angeles 

Cities Representative, Los Angeles County, Western Region 

JANE W. CARNEY 

Senate Rules Committee Appointee 

WILLIAM S. CRAYCRAFT 

Councilmember, City of Mission Viejo 

Cities Representative, Orange County 

BEATRICE J.S. LAPISTO-KIRTLEY 

Councilmember, City of Bradbury 

Cities Representative, Los Angeles County, Eastern Region 

RONALD O. LOVERIDGE 

Mayor, City of Riverside 

Cities Representative, Riverside County 

LEONARD PAULITZ 

Councilmember, City of Montclair 

Cities Representative, San Bernardino County 

JAMES W. SILVA 

Supervisor, Second District 

Orange County Representative 

CYNTHIA VERDUGO-PERALTA 

Governor’s Appointee 

EXECUTIVE OFFICER:

BARRY R. WALLERSTEIN, D.Env. 
CONTRIBUTORS 

South Coast Air Quality Management District 

Elaine Chang, DrPH 

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 

 Carbon Monoxide I-15 

 Nitrogen Dioxide I-16 

 Sulfur Dioxide I-17 

 Sulfates I-17 

 Toxic Air Contaminants I-18 

CONCLUSION I-20

REFERENCES R-1 

ATTACHMENT 1 

 Comments Received 

ATTACHMENT 2 

 Responses to Comments 
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 slight increase 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, and 

biochemicals are involved in the human body’s response to air pollution) and specific 
Final - Appendix I: Health Effects 

I-2 

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 a review presented previously (SCAQMD, 

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

(ATS, 1996), the USEPA reviews for ozone (USEPA, 1996), Carbon Monoxide 

(USEPA, 2000), and Particulate Matter (USEPA, 2002), and from a recent published 

review of the health effects of air pollution (Brunekreef and Holgate, 2002) 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 standards for ozone are 0.12 ppm averaged over 1 hour, and 0.08 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 

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 

 

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 

conducted with healthy individuals. The adverse effects reported with short-term 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, has been following a cohort of children that live in 12 communities in 

southern California with differing levels of air pollution for several years. A recent 

publication from this study has 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 for all respiratory causes (infections, respiratory 

failure, chronic bronchitis, etc.) including asthma show a consistent increase as ambient 

ozone, sulfate or sulfur dioxide 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. However, limitations in the study designs preclude 

attributing the effects solely to ambient ozone concentrations. 

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 respiration-compromised group 

may have lower lung function to begin with, the same degree of change may represent a 

substantially greater adverse effect overall. 

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 
Final - Appendix I: Health Effects 

I-4 

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. 

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. 
Health Effects of Air Pollution 

I-5 

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 - 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 

A few studies have suggested that population exposure to community air pollution, 

including ozone and particulate matter is related to genetic toxicity and increased 

incidence of cancer. In recent years, an increase in daily mortality has also been 

reported to be associated with ozone levels. Because of limitations in study design in a 

number of studies, as well as assumptions involved and coexisting pollutants, the 

severity of chronic effects associated with ozone exposure alone cannot be ascertained 

from these studies. 
Health Effects of Air Pollution 

I-7 

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. 

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. 

The health effects of particulates are 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 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. 

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 set air quality standards for PM2.5 at 

65 μg/m3

 for a 24-hour average and 15 μg/m3 for an annual average. Although 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), the EPA promulgated the revised standards in 1997. A long term research 

program was also established to analyze health effects related to particulate air pollution 

(NRC, 1998). The new standards were challenged by industry groups, but were 

ultimately upheld by the U.S. Supreme Court. 

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. 
Final - Appendix I: Health Effects 

I-8 

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

1996; EPA, 2002, 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 (CARB, 2002). This is being done as a requirement of the Children’s 

Environmental Health Protection Act (Senate Bill 25). 

As part of this review, CARB and OEHHA staffs recommended that the California 

Ambient Air Quality Standards for particulate matter be revised as follows: 

PM10 Annual Average: 20 μg/m3 

PM10 24-Hour Average: 50 μg/m3 

PM2.5 Annual Average: 12 μg/m3 

PM2.5 24-Hour Average 25 μg/m3

The proposed standards were reviewed by the State Air Quality Advisory Committee 

and were considered at the CARB May, 2002 meeting. 

The CARB adopted the proposed annual average standards. The 24-hour average 

standards consideration was postponed. The postponement was due to a recently 

discovered flaw in a statistical software package widely used in recent analyses of shortterm effects of particulate air pollutants. This flaw may result in inaccurate calculations 

of the magnitude of associations of health effects with pollutant levels. The studies of 

short-term effects are being reanalyzed with appropriate corrections to the software and 

are being reviewed by CARB and EPA staff. The software flaw does not affect the 

results of long term studies using annual average levels of particulate matter. This is 

discussed further under the short term exposure effects section below. 

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 
Health Effects of Air Pollution 

I-9 

• Effects on lung function 

• Changes in lung morphology 

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 - 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 
Health Effects of Air Pollution 

I-11 

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 

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 the flawed statistical software 

package noted previously. 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 PM 2.5 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 determine 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 numbers 
Final - Appendix I: Health Effects 

I-12 

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

airborne particulate matter. 

In the recent 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 . A recent review discusses mechanistic studies in more detail 

(Brunekreef, 2002). 
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 recent 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). These studies provide evidence that the fine particles, as 

measured by PM2.5, may be more strongly associated with mortality effects from longterm 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-tern investigations. These findings indicate that long-term 

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. 

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 

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. Other studies of populations in the U.S. have not found significant 

association of lung cancer mortality with particulate matter levels. 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). 
Final - Appendix I: Health Effects 

I-14 

Evaluating mortality effects in a public health context is a complex task and requires 

information regarding the extent of life shortening or prematurity of death associated 

with particulate matter exposures. The relative risk estimates vary considerably 

depending on the type of study (acute vs. chronic) and also among studies within each 

group. Some attempts have been made in a broad sense to calculate the number of 

deaths associated with PM10 exposure by applying different statistical methods using the 

relative risk estimates of specific studies. However, U.S. EPA has concluded that 

although a substantial portion of deaths associated with long-term PM10 exposure may be 

independent of the daily deaths associated with recent PM10, quantification of the extent 

of life- shortening or the number of deaths directly associated with PM10 exposure from 

either type of studies is difficult. 

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 4th graders from the Southern California communities were 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). These 

findings indicate that cleaning the air can result in improvements in children’s health. 

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 
Health Effects of Air Pollution 

I-15 

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 

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. 

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 (USEPA, 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 

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, 
Final - Appendix I: Health Effects 

I-16 

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 

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, and decreased 

lung function. 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 pollutants could not 

be discerned. 

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

group of children followed for four years. In addition to NO2, the decreased growth was 

also associated with particulate matter and airborne acids. 

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 
Health Effects of Air Pollution 

I-17 

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. 

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. 
Final - Appendix I: Health Effects 

I-18 

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 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 
Health Effects of Air Pollution 

I-19 

the air toxics risk. A breakdown of the major contributors to the air toxics risk is shown 

in the following graph. 

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 Hazarad 

Index. A Hazard Index of less than one would not be expected to result in adverse 

effects. 
Final - Appendix I: Health Effects 

I-20 

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 

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 

R - 1 

References 

American Thoracic Society, Committee of the Environmental and Occupational 

Health Assembly of the American Thoracic Society. “Health Effects of Outdoor 

Air Pollution.” Parts 1 and 2. American Journal Respiratory and Critical Care 

Medicine,,, Vol. 153, pp. 3-50 and pp. 477-498, 1996. 

Avol, Gauderman, Tan, London, and Peters. “Respiratory Effects of Relocating to 

Areas of Differing Air Pollution Levels.” American Journal Respiratory and 

Critical Care Medicine, Vol. 164, pp.2067-2072, 2001. 

Bobak and Leon. “Pregnancy Outcomes and Outdoor Air Pollution: an 

Ecological Study in Districts of the Czech Republic 1986-8.” Occupational and 

Environmental Medicine, Vol. 56, pp539-43, 1999. 

Brunekreef, B. and S.T. Holgate. “Air Pollution and Health.” The Lancet, Vol. 

360, pp. 1233-42, 2002. 

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

_review.22808.1 

California Air Resources Board. “"Public Hearing To Consider Amendments To 

The Ambient Air Quality Standards For Particulate Matter And Sulfates.” May 3, 

2002. http://arbis.arb.ca.gov/research/aaqs/std-rs/pm-final/pmfinal.htm#Summary

Dominici, McDermott, Zeger, and Samet. “On the use of Generalized Additive 

Models in Time-Series Studies of Air Pollution and Health.” American Journal of 

Epidemiology, Vol. 156, pp. 193-203, 2002 

Dominici, McDermott, Daniels, Seger and Samet. A Report to the Health Effects 

Institute: Reanalyses of the NMMAPS Database. October 31, 2002. 

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

Gilliland, Berhane, Rappaport, Thomas, Avol, Gauderman, London, Margolis, 

McConnell, Islam, Peters. “The Effects of Ambient Air Pollution on School 

Absenteeism Due to Respiratory Illness.” Epidemiology, Vol. 12, No. 1, 

pp. 43-54, January 2001. 

Gauderman, McConnell, Gilliland, London, Thomas, Avol, Vora, Berhane, 

Rappaport, Lurmann, Margolis, Peters. “Association between Air Pollution and 
Appendix I: Health Effects 

R -2 

Lung Function Growth in Southern California Children.” American Journal 

Respiratory and Critical Care Medicine, Vol. 162, pp. 1383-1390, 2000. 

Gauderman, Gilliland, Vora, Avol, Stram, McConnell, Thomas, Lurmann, 

Margolis, Rappaport, Berhane, and Peters. “Association between Air Pollution 

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

Second Cohort.” American Journal Respiratory and Critical Care Medicine, Vol. 

166, pp.76-84, 2002. 

Krewski, Burnett, Goldberg, Koover, Siemiatycki, Jerrett et al. “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, July, 2002. 

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

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

National Academy Press, 1998. 

McConnell, Berhane, Gilliland, London, Islam, Gauderman, Avol, 

Margolis, Peters. “Asthma in exercising children exposed to ozone: a cohort 

study.” Lancet Vol. 359, pp.386–91, 2002. 

Pope, Burnett, Thun, Calle, Krewski, Kazuhiko. And Thurston. “Lung Cancer, 

Cardiopulmonary Mortality, and Long-Term Exposure to Fine Particulate Air 

Pollution.” JAMA, Vol. 287, pp. 1132-41, 2002. 

Ritz, Yu, Chapa, Fruin. “Effect of Air Pollution on Preterm Birth Among 

Children Born in Southern California between 1989 and 1993.”Epidemiology Vol. 

11, No. 5, 2000. 

Ritz, Yu, Fruin, Chapa, Shaw and Harris. “Ambient Air Pollution and Risk of 

Birth Defects in Southern California.” American Journal of Epidemiology Vol. 

155, No. 1, pp.1-9, 2002. 

Samet, Dominici, Curriero, Coursac, and Zeger, “Fine Particulate Air Pollution 

and Mortality in 20 U.S. Cities, 1987–1994.” New England Journal of Medicine. 

Vol. 343, pp.1742-9, 2000. 

Samet, Zeger, Dominici, Curriero, Coursac, Dockery, Schwartz and Zanobetti. 

“The National Morbidity, Mortality, and Air Pollution Study Part II: Morbidity 

and Mortality from Air Pollution in the United States.” Health Effects Institute 

Research Report Number, 94 Part II, June, 2000. 

http://healtheffects.org/pubs/samet2.pdf 
References 

R - 3 

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

MATES II. South Coast Air Quality Management District, March 2000. 

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

United States Environmental Protection Agency. “Air Quality Criteria for O3 and 

Other Photochemical Oxidants.” EPA 600/P–93–004aF through EPA/600/ P–93–

004cF, July 1996. 

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

Monoxide.” EPA 600/P-99/001F, June 2000. 

United States Environmental Protection Agency. Third External Review Draft. 

“Air Quality Criteria for Particulate Matter.” Vol. I-II, EPA 600/P-99/002aB, 

002bB, April 2002. 

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

and Other Photochemical Oxidants.” EPA 600/P–93–004aF through EPA/600/ P–

93–004cF, July 1996. 

Vedal. “Critical Review. Ambient Particles and Health: Lines that Divide.” 

Journal of the Air and Waste Management Association, Vol. 47, No. 5, pp.551-

581, 1997. 

Attachment 1 

Attachment 1 - 1 

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 2 

Attachment 2 - 1 

ATTACHMENT 2 

STAFF RESPONSES TO COMMENTS RECEIVED

Comment: 

Include more extensive referencing. 

Response: 

Additional references for recent studies have been added. 

Comment: 

Include a summary of the history of health effects research for PM2.5 including 

the controversy over EPA’s PM2.5 standard. 

Response: 

References to the controversy regarding the particulate matter standards and the 

health research plan have been added. 

Comment: 

Address health effects of air toxics to some degree. 

Response: 

A brief discussion of air toxics has been added. 
Appendix I: Health Effects 

Attachment 2 -2 

Comment: 

Include recent studies of air pollution effects on pregnancy outcomes and lung 

growth retardation effects in children. 

Response: 

These have been included. 

Comment: 

Tabulate those control measure that are envisioned to bring the District into 

compliance with national and state air quality standards. 

Response: 

These are addressed in other sections of the AQMP. 

Comment: 

Present current PM10 and PM2.5 levels and emissions in various regions of the 

SCAB. 

Response: 

Current air quality and emissions sources are presented in other sections of the 

AQMP. 

Comment: 

Provide detailed and specific information regarding the scientific study of the 

health effects of air pollution with citations to valid scientific studies. 

Response: 

Additional citations have been included. 

Comment: 
Attachment 2 

Attachment 2 - 3 

Include a detailed discussion of the recent CARB review of health impact of 

particulate matter and of its impact on proposed AQMP control measures. 

Response: 

Proposed measures to attain ambient air quality standards are provided in other 

sections of the AQMP. 

Comment: 

It would be helpful to relate what is known about the health effects of air pollution 

to potential health effects in the SCAB based on existing ambient levels. 

Response: 

The purpose of this appendix is to provide an overview of air pollution health 

effects, rather than to provide estimates of health risk from current ambient levels 

of pollutants in specific areas of the SCAB. The AQMP provides a plan to attain 

healthful air quality by meeting ambient air quality standards in all parts of the 

SCAB.