# FINAL 2003 AQMP APPENDIX I

HEALTH EFFECTS

AUGUST 2003SOUTH 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 Ange les County, Western Region

JANE W. CARNEY Senate Rules Committee Appointee

WILLIAM S. CRAYCRAFT Councilmember, City of Mission Viejo Cities Representativ e, Orange County

BEATRICE J.S. LAPISTO-KIRTLEY Councilmember, City of Bradbury Cities Representative, Los Ange les County, Eastern Region

RONALD O. LOVERIDGE Mayor, City of Riverside Cities Representative, Riverside County

LEONARD PAULITZ Councilmember, City of Montclair Cities Representative, Sa n 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 OfficerTable 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 ContaminantsHealth Effects of Air Pollution

I-1 

### INTRODUCTION

This document presents a summary of scientif ic findings on the health effects of ambient air pollutants. The California Health and Safe ty Code Section 40471(b ) requires that the South Coast Air Quality Manage ment District prepare a repor t on the health impacts of particulate matter in the South Coast Air Basi n, in conjunction with the preparation of the Air Quality Management Plan revisions. This document, which was prepared to satisfy that requirement, also includes th e 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 w ith high air pollution levels have been documented in several episodes as early as 1930 in Meuse Valley, Be lgium; 1948 in Donora, Pennsylvania; and 1952 in London. Alth ough levels of pollutants that occurred during these acute episodes are now unlikely in the United States, ambien t air pollution continues to be linked to increases in respiratory illness (morbidity) a nd slight increase in death rates (mortality).

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

• Increased mortality

• Increased health care utilization (hosp italization, physic ian 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 anim als. There have been an increasing number of studies focusing on the mechanisms (t hat is, on learning how specif ic organs, cell types, and biochemicals are involved in the human body’s response to air pollution) and specificFinal - 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 am bient conditions, the regulatory framework and the control measures developed are mostly pollutant-specific. This is appropriate, in that di fferent 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 pollutant s, from the same or different sources, may sometimes act together to harm health mo re than they would acting separately. Nevertheless, as a practical matter, health sc ientists, 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 th e air quality standards, comprehensive plans are developed such as the Air Quality Mana gement Plan (AQMP) and the Air Toxics Control Plan (ATCP). These plans examine multiple pollutants, cumulative impacts, and transport issues related to attaining healthfu l air quality. A brief overview of the effects observed and attributed to various air pollu tants 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 Ameri can Thoracic Society (ATS, 1996), the USEPA reviews for oz one (USEPA, 1996), Carbon Monoxide (USEPA, 2000), and Particulate Matter (USE PA, 2002), and from a recent published review of the health effects of air pollu tion (Brunekreef and Holgate, 2002) More detailed citations and discussi ons on air pollution health effe cts can be found in these references. 1



### OZONE

Ozone is a highly reactive compound, and is a strong oxi dizing 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 pene trate into the gas exchan ge region of the deep lung.

The EPA standards for ozone are 0.12 pp m averaged over 1 hour, and 0.08 ppm averaged over eight hours.

The major subgroups of the population consid ered to be at incr eased 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 ozon e exposure is much stronger and more quantitative than that for the la tter 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 indivi duals. The adverse effects reported with short-term ozone exposure are greater with incr eased activity because activity increases the breathing rate and the volume of air reachi ng the lungs, resulting in an increased amount of ozone reaching the lungs. Children may be a particul arly vulnerable population to air pollution effects because they spend more time outdoor s, are generally more active, and have a higher ventilation rate than adults.

A number of adverse health effects associat ed with ambient ozone levels have been identified from laboratory and epidemiological studies (EPA, 1996; ATS, 1996). These include increased respiratory symptoms, da mage to cells of the respiratory tract, decreases in lung function, incr eased susceptibility to respiratory infection, and increased risk of hospitalization.

The Children’s Health Study, conducted by re searchers 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 asso ciated with ambient ozone le vels. An increase of 20 ppb ozone was associated with an 83% increase in illness re lated absence rates (Gilliland, 2001).

The number of hospital admissions for all re spiratory causes (infections, respiratory failure, chronic bronchitis, etc.) including asth ma 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 ho urly ozone concentrations are as low as 0.08 to 0.10 ppm. However, limitations in the stud y 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 incr eased hospitalizations and emergency room visits. Laboratory studies have attempted to compare the degree of lung function change seen in age and gender-match ed healthy individuals versus asthmatics and those with chronic obstructive pulmonary disease. Whil e the degree of change evidenced did not differ significantly, that finding may not accurate ly reflect the true im pact 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 concen trations, the relative risk of developing asthma in children playing thre e or more sports was found to be over three times higher than in children play ing no sports (McConnell, 2002). These findings i ndicate that new cases of asthma in children ar e associated with heavy exerci se in communitie s with high levels of ozone. While it has long been known that air pollution can exacerbateFinal - Appendix I: Health Effects

I-4 symptoms in individuals with respiratory di sease, this is among the first studies that indicate ozone exposure may be causally linked to asthma.

In addition, human and animal studies invo lving both short-term (few hours) and longterm (months to years) exposures indicate a wide range of effects induced or associated with ambient ozone exposure. Thes e are summarized in Table 1.

Some lung function responses (volume and ai rway 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 th e observed shift in resp onse 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 repe ated ozone exposures, even if externally observable effects (chest symptoms a nd 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 vari ous measures such as respiratory volumes, airway resistance and reactiv ity, irritative cough and ches t 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 a nd children under ambient expo sure conditions (0.10 - 0.15 ppm). The responses reported are indicative of decreased breathing capacity and are reversible.

In laboratory studies, cellular and biochemica l changes associated with respiratory tract inflammation have also been consistently reported in the airway lining after low level exposure to ozone. These ch anges include an increase in specific cell types and in the concentration of biochemical mediators of inflammation and injury such as cytokines and fibronectin. These infla mmatory changes can be observe d in healthy adults exposed to ozone in the range of 0.08 to 0.10 ppm.

The susceptibility to ozone ob served under ambient conditio ns could be due to the combination of pollutants that coexist in the atmosphere or ozone may actually sensitize these subgroups to the eff ects of other pollutants.

Some animal studies show re sults that indicate possibl e chronic effects including functional and structural changes of the lu ng. These changes i ndicate that repeated inflammation associated with ozone exposure over a life time may result in sufficient damage to respiratory tissue such that indi viduals later in life may experience a reduced quality of life in terms of respiratory functio n and activity level achi evable. An autopsy study involving Los Angeles County resident s 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 pu lmonary 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 (O 3 ) (Summary of Key Studies)

0 3 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 0 3 outdoors Exacerbation of respiratory symptoms (e.g., cough, chest pain) in individuals with pr eexisting 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 (redu ced ability to take a deep breath), increased respiratory symptoms (cough, shortness of breath, pain upon deep inspiration), increased airway responsiveness and increased airw ay 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 le ss reproducible changes in lung function Attenuation of response with repeated exposure

≥ 0.12 with prolonged, repeated exposure (chamber exposures) Changes in lung structure, func tion, elasticity, and biochemistry in laboratory animals that are indicative of airway irritation and inflammation with possible develo pment of chronic lung disease Increased susceptibility to bacterial respiratory infections in laboratory animals From: SCAQMD, 1996

A few studies have suggested that populat ion exposure to community air pollution, including ozone and particulate matter is related to genetic toxicity and increased incidence of cancer. In recent years, an in crease 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 as sociated 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 ev aluate the long-term effects of air pollution and to determine the role of ozon e 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, aci d aerosols, trace metals, and material from the earth’s crust. Substances of biol ogical 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 PM 10 . EPA promulgated ambient air quality standards for PM 10 of 150 μg/m 3 averaged over a 24-ho ur period, and 50 μg/m 3 for an annual average.

In recent years additional focu s has been placed on partic les having an aerodynamic diameter of 2.5 μm or less (PM 2.5 ). A greater faction of partic les in this size range can penetrate and deposit deep in the lungs. The EPA set air quality standards for PM 2.5 at 65 μg/m 3 for a 24-hour average and 15 μg/m 3 for an annual averag e. Although there was considerable controversy and debate surroundin g the review of particulate matter health effects and the consideration of ambient ai r quality standards (Kaiser, 1997; Vedal, 1997), the EPA promulgated the revised sta ndards in 1997. A lo ng 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 a nd 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 su ch as cutting and grinding, and resuspension of particles from the gr ound or road surfaces by wind and human activities.

In contrast, particles smalle r than 2.5 μm are mostly derived from combustion sources, such as automobiles, trucks, and other vehi cle 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. Com ponents 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, Brun ekreef, 2002). In addition, th e California Air Resources Board (CARB) and the Office of Environmental He alth and Hazard Assessment ( OEHHA) have reviewed the adequacy of the Califor nia Air Quality Standards for Particulate Matter (CARB, 2002). This is being do ne 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 partic ulate matter be revised as follows:

PM 10 Annual Average: 20 μg/m 3

PM 10 24-Hour Average: 50 μg/m 3

PM 2.5 Annual Average: 12 μg/m 3

PM 2.5 24-Hour Average 25 μg/m 3

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 propos ed annual average standard s. The 24-hour average standards consideration was postponed. Th e postponement was due to a recently discovered flaw in a statistical software packag e widely used in recent analyses of shortterm effects of particulate air pollutants. Th is flaw may result in inaccurate calculations of the magnitude of associations of health effects with pollu tant 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 aver age levels of particulate matter. This is discussed further under the short te rm exposure effects section below.

The major types of effects associated with particulate matter include:

• Increased mortality

• Exacerbation of respiratory di sease and of cardiovascular disease as evidenced by increases in:

-Respiratory symptoms -Hospital admissions and emergency room visits -Physician office visits

-School absences -Work loss daysHealth Effects of Air Pollution

I-9 • Effects on lung function

• Changes in lung morphology



### Short-Term Exposure Effects

Epidemiological studies have pr ovided continued and consistent evidence for most of the effects listed above. An association between increase d daily or several-day-average concentrations of PM 10 and excess mortality and morbidity is consistently reported from studies involving communities across the U.S. as well as in Eur ope, Asia, and South America. A review and analys is of epidemiological literat ure for acute adverse effects was undertaken by Dockery and Pope to estim ate these effects as percent increase in mortality associated with each incremental increase of PM 10 by 10 μ g/m 3 . The estimates are presented in Table 2. It appears that in dividuals who are elderl y or have preexistent lung or heart disease are mo re susceptible than others to the adverse effects of PM 10 .Final - Appendix I: Health Effects

I-10 TABLE 2

Combined Effect Estim ates of Daily Mean Particulate Pollution

% Change in Health Indicator per each 10 μ g/m 3 Increase in PM 10 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 a nd Critical Care Medicine , Vol. 153, 113-50, 1996)

Many recent studies have confirmed that ex cess mortality and morb idity are associated with particulate matter levels. Estimates of mortality effects fro m these studies range from 0.3 to 1.7% increase for a 10 μg/m 3 increase in PM 10 levels. The National Morbidity, Mortality, and Air Pollution Study (NMMAPS), a recent study of the largest U.S. cities, determined a co mbined risk estimate of abou t a 0.5% increase in total mortality for a 10 μg/m 3 increase in PM 10 (Samet, 2000a). This study also analyzed the effects of gaseous co-pollutants. The re sults indicated that the association of PM 10 and mortality were not confounded by the presence of the ga seous pollutants. When theHealth Effects of Air Pollution

I-11 gaseous pollutants were included in the analyses, the significance of the PM 10 estimates remained. The PM 10 effects were reduced somewhat when O 3 was also considered and tended to be variably decreased when NO 2 , CO, and SO 2 were added to the analysis. These results argue that the effects are likel y 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 st atistical 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/m 3 increase in PM 10 to a 0.27 percent increase. There remained a strong positive associat ion between acute exposure to PM 10 and mortality. Thus while the quantitative estimate is reduc ed, the major findings of the study did not change.

Studies of PM 2.5 also find associations with elevat ed mortality. The estimates for PM 2.5 generally are in the range of 2.0 to 8. 5% increase in total deaths per 25 μg/m 3 increase in 24-hour PM 2.5 levels. The estimates for cardiovas cular related mortality range from 3.0 to 7.0% per 25 μg/m 3 24-hour PM 2.5 , and for respiratory mort ality estimates range from 2.0 to 7.0% per 25 μg/m 3 24-hour PM 2.5 . Several studies have attempted to assess the re lative importance of particles smaller than 2.5 μm and those between 2.5 μm and 10 μm (PM 10-2.5 ). While some studies report that PM 2.5 levels are better predictors of mort ality effects, others suggest that PM 10-2.5 is also important. Most of the studies found higher mortality a ssociated with PM 2.5 levels than with PM 10-2.5 . For example, a study of six cities in the U.S. found that particulate matter less than 2.5 μm were associated with increa sed mortality, but that the larger particles were not. Other studies in Mexico C ity and Santiago, Chile reported that PM 10-2.5 was as important as PM 2.5 . Overall effects estimates for PM 10-2.5 fall in the range of 0.5 to 6.0 % excess mortality per 25 μg/m 3 24-hour average.

The relative importance of both PM 2.5 and PM 10-2.5 may vary in different regions depending on the relative concentrations and components, which can also vary by season. More research is needed to de termine the relative effects of fine (PM 2.5 ) and coarse (PM 10-2.5 ) fractions of particulate matter on mortality.

A number of studies have evaluated the asso ciation between particulate matter exposure and indices of morbidity such as hospita l admissions, emergency room visits or physician office visits for resp iratory and cardiovascular dise ases. The effects estimates are generally higher than the effects for mo rtality. The effects are associated with measures of PM 10 and PM 2.5 . Effects are also associated with PM 10-2.5 . Thus, it appears that when a relatively small number of people experience severe effects, larger numbersFinal - Appendix I: Health Effects

I-12 experience milder effects, which may relate eith er to the coarse or to the fine fraction of airborne particulate matter.

In the recent NMMAPS study, hospital admiss ions 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% in crease for respiratory disease admissions, per 50 μg/m 3 increase in PM 10 . The excess risk for cardi ovascular disease ranges from 3-10% per 50 μg/m 3 PM 10 and from 4-10% per 25 μg/m 3 PM 2.5 or PM 10-2.5 . Similarly, school absences, lost workdays a nd 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 dela yed impact on these parameters following elevated particulate matter exposures. Thes e observations are consistent with the hypothesis that increas ed susceptibility to infection follows particulate matter exposures.

Some studies have reported that short-term pa rticulate matter exposure is associated with changes in lung function (lung capacity and breathing volume); upper respiratory symptoms (hoarseness and sore throat); and lower respir atory 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 childre n with and without asthma. Sensitive individuals, such as those with asthma or pre-exis ting respiratory disease, may have increased or aggravated symptoms asso ciated with short-term particulate matter exposures. Several studies have followed th e number of medical visits associated with pollutant exposures. A range of increase s from 3% to 42% for medical visits for respiratory illnesses was found corresponding to a 50 μg/m 3 change in PM 10 . A limited number of studies also l ooked at levels of PM 2.5 or PM 10-2.5. The findings suggest that both the fine and coarse fractions may ha ve associations with some respiratory symptoms.
The biological mechanisms by which particul ate matter can produce health effects are being investigated in laboratory studies. Inflammatory response s in the respiratory system in humans and animals exposed to co ncentrated ambient particles have been measured. These include effects such as in creases in neutrophils in the lungs. Other changes reported include incr eased release of cytokines and interleukins, chemicals released as part of the infla mmatory process. The effects of particulate matter may be mediated in part through the production of reactiv e oxygen species during the inflammatory process . A recent review di scusses 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 PM 10 and PM 2.5 . Studies have analyzed the mortality of adults living in different U.S. cities. After adjusting for important risk factors, these studies found a consistent pos itive association of de aths and exposure to particulate matter. A similar association wa s observable in both total number of deaths and deaths due to cardiorespiratory causes. A shortening of lifespa n was also reported in these studies.

Significant associations for PM 2.5 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 confirme d the finding (Krewski, 2000). The Harvard Six Cities Study evaluated several size ra nges of particulate matter and reported significant associations with PM 15 , PM 2.5 , sulfates, and non-sulfate particles, but not with coarse particles (PM 15 – PM 2.5 ). These studies provide evidence that the fine particles, as measured by PM 2.5 , may be more strongly associated with mortality effects from longterm particulate matter exposure s than are coarse compounds.

A follow-up study of the American Cancer Society cohort confirmed and extended the findings in the initial study. The research ers 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 ca rdiopulmonary 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 investigatio ns. These findings indicate that long-term exposures may be more important in terms of overall health effects.

Recent studies report evidence indicating that particulat e 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 ha ve reported an increased risk of mortality from lung cancer associated with partic ulate matter exposures. A study involving California Seventh Day Adve ntists (very few of whom smoke) has reported an association of lung can cer mortality with PM 10 levels. It is not clear from these studies whether the association relates to causation of disease, or whet her 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 mo rtality with particulate matter levels. A recent study that followed a large number of in dividuals living in the larges t 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 prem aturity of death associated with particulate matter expo sures. The relative risk es timates vary considerably depending on the type of study (acute vs. ch ronic) and also among studies within each group. Some attempts have been made in a broad sense to calculate the number of deaths associated with PM 10 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 de aths associated with long-term PM 10 exposure may be independent of the daily deaths associated with recent PM 10 , quantification of the extent of life- shortening or the number of deaths directly associated with PM 10 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 change s. 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 significan t association of particulate matter with bronchitis or phleg m in children with asthma. These effects were also associated with NO 2 and acid vapor levels.

A cohort of 4 th graders from the Southe rn 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 PM 10 , PM 2.5 , PM 10-2.5 , acid vapor, and NO 2 . There was no associati on with ozone levels. The investigators were not able to identify independent effects of the pollutants, but noted that motor vehicle emissions are a ma jor source of the pollutants.

A follow-up study on a second cohort of ch ildren confirmed the findings that decreased lung function growth was asso ciated with particulates, n itric oxides, and elemental carbon levels (Gauderman, 2 002). Elemental carbon is of ten used as a measure for diesel particulate. Additionally, childre n who moved to areas with less air pollution were found to regain some of the lung f unction growth rate (Avol, 2001). These findings indicate that cleaning the air can re sult in improvements in children’s health.

Despite data gaps, the extens ive body of epidemiological studies has both qualitative and quantitative consistency suggestiv e of causality. A consider able body of evidence from these studies suggests that ambient particulat e matter, alone or in co mbination with other coexisting pollutants, is associ ated with significant increase s in mortality and morbidity in a community.

In summary, the scientific litera ture indicates that an incr eased risk of mortality and morbidity is associated with particulate matter at ambien t levels. The evidence forHealth Effects of Air Pollution

I-15 particulate matter effects is mostly derive d from population studie s with supportive evidence from clinical and anim al studies. Although most of the effects are attributable to particulate matter, co-pollutant effects ca nnot be ruled out on the basis of existing studies. The difficulty of separating the effect s 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 myog lobin) results in reduced oxyge n supply in the bloodstream of exposed individuals. The reduced oxygen supply is responsible for the toxic effects of CO which are typically manife sted in the oxygen -sensitive organ systems. The effects have been studied in contro lled 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 suscep tible to the effects of CO. Protectio n of this group is the basis of the existing National Ambient Air Qua lity Standards for CO at 35 ppm for one hour and 9 ppm averaged over ei ght 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 tran sport 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 bloo d measured as percentage of total hemoglobin bound to CO. COHb levels in non-s mokers range between 0.3 an d 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, healt hy 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 electrocardi ograph 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 Ca lifornia have indicated an association with CO exposure during pregna ncy to increases in pr e-term births. (Ritz,Final - Appendix I: Health Effects

I-16 2000). However, the results were not consistent in different areas st udied. The increase in the pre-term births wa s also associated with PM 10 levels. Another study found increased risks for cardiac related birth def ects with carbon monoxide exposure in the second month of pregnancy (Rit z, 2002). Further study is needed to confirm these observations.



### NITROGEN DIOXIDE

Evidence for low-level nitrogen dioxide (NO 2) exposure effects is derived from laboratory studies of asthmatics and fro m epidemiological studies. Additional supportive evidence is deri ved from animal studies. Epidemiological studies using the presence of an unvented gas stove as a surrogate for indoor NO 2 exposures suggest an increased inci dence of respiratory infections or symptoms in children.

Recent studies related to out door exposure have found hea lth effects associated with ambient NO 2 levels, including respiratory symptoms , respiratory illness, and decreased lung function. However, since NO 2 exposure generally occurs in the presence of other pollutants, such as particul ate matter, these studies are of ten unable to determine the specific role of NO 2 in causing effects. The Children’s Health Study in Southern California found a ssociations of air pollution, including NO 2 , PM 10 , and PM 2.5 , with respiratory symptoms in asthmatics (McConnell, 1999). Particles and NO 2 were correlated, and effects of individual pollutants could not be discerned.

Ambient levels of NO 2 were also associated with a decr ease in lung function growth in a group of children followed for f our years. In addition to NO 2 , the decreased growth was also associated with particul ate matter and airborne acids. Results from controlled exposure studies of as thmatics demonstrate an increase in the tendency of airways to contract in response to a chemical stim ulus (bronchial reactivity). Effects were observed with an exposure to 0.3 ppm NO 2 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 pp m). Mixed results have been reported when people with chronic obstructive lung di sease are exposed to low levels of NO 2 . Short-term controlled studies of animals exposed to NO 2 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 observe d after relatively high levels of short-term ozone exposure is observed to increase when animals are exposed to a combination of ozone and NO 2 . 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 inHealth Effects of Air Pollution

I-17 cells involved in maintaining immune functi ons (cytotoxic T cells and natural killer cells) have been observed in humans after repeated exposure (4-6 days ) to >0.6 ppm of NO 2 (20 min. - 2 hours). All these changes collectively support the observation reported both in population and animal st udies of increased susceptibility to infections, as a result of NO 2 exposure.



### SULFUR DIOXIDE

Controlled laboratory studies involving human volunteers have clearly identified asthmatics as the most sensitiv e group to the effects of ambient sulfur dioxide (SO 2) exposures. Healthy subjects have failed to demonstrate any short-term respiratory functional changes at exposure le vels up to 1.0 ppm over 1-3 hours.

In asthmatics, brief exposure (10 minutes) to SO 2 at levels as low as 0.25 ppm can result in significant alteration of lung function, su ch as increases in ai rway resistance and decreases in breathing capacity. In some, th e exposure can result in severe symptoms necessitating the use of medicati on for relief. The response to SO 2 inhalation is observable within 2 minutes of exposure, incr eases further with continuing exposure up to 5 minutes then remains relatively steady as exposure continues. SO 2 exposure is generally not associated with any delayed reactions or repetitive asthmatic attacks.

No significant changes have been reporte d from studies, which have evaluated the effects of exposure to co-p ollutants (ozone or nitrogen dioxide), prior to or in conjunction with SO 2 exposure.

Animal studies have shown that despite SO 2 being a respiratory irritant, it does not cause substantial acute or chronic toxicity in an imals exposed at ambient concentrations. However, relatively high exposures (10 ppm of SO 2 for 72 hours) in mice can lead to tissue damage, fluid accumulati on and sloughing of re spiratory lining. Sensitization to allergies is observable in guinea pigs rep eatedly exposed to high levels (72 ppm) of SO 2 . This effect needs further evaluation in clin ical and population studies to identify any chronic exposure impact on both asthmatic incidence and attacks in a population.

Some epidemiological studies i ndicate that the mortality and morbidity effects associated with the fine fraction of particles show a similar association with ambient SO 2 levels. In these studies, efforts to se parate the effects of SO 2 from fine particles have not been successful. Thus, it is not clear whether the two pollutants act synergistically, or whether being generated from similar com bustion 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 μ g/m 3 (24-hour average) for sulfates.Final - Appendix I: Health Effects

I-18 In recent years, a vast major ity of effects (mortality and mo rbidity) associat ed with fine particles (PM 2.5 ) and sulfur dioxide ha ve shown a similar association with ambient sulfate levels in some population studies. Th e efforts to fully sepa rate 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 combin ation of pollutants, rather than a single pollutant.

A clinical study involving exposure of human s ubjects 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 μ g/m 3 . In general, however, laboratory exposures of human vo lunteers to sulfates at or near ambient levels have not found significant change s in lung function.

Results from animal studies in volving exposures to sulfuric acid aerosol, ammonium bisulfate and ammonium sulfate indicate that acidic particles (former two) are more toxic than non-acidic particles (latte r). 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 sulfat e concentrations are higher th an for those observed in the western United States. Mixed results have been reported from st udies 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 Ai r 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 in creased risk for cancer or a dverse birth outcome. After review by the state Scientific Review Pa nel, the CARB holds a public hearing on whether to formally list substa nces that may pose a significant risk to public health as a Toxic Air Contaminant.

CARB and OEHHA also establish potency factor s for air toxics that are carcinogenic. The potency factors can be used to estim ate the additional cance r risk from ambient levels of toxics. This estimate represen ts the chance of contracting cancer in an individual over a lifetime exposure to a give n level of an air toxic and is usually expressed in terms of additional can cer cases per million people exposed.

The SCAQMD conducted a study on the ambien t concentrations and estimated the potential health risks from air toxics (SQAQM D, 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 contribut or to this risk was diesel exhaust, accounting for 71% ofHealth 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 effect s, OEHHA has developed ac ute and chronic Reference Exposure Levels (RELs). RELs are concentra tions 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 lo ng-term exposures of several years. The ratio of ambient concentration to the appropri ate REL can be used to calculate a Hazarad Index. A Hazard Index of le ss than one would not be expe cted 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 cons iderable number of population-based and laboratory studies have esta blished a link between increased morbidity and in some instances, earlier morta lity and air pollution.REFERENCESReferences

R - 1 

### References American Thoracic Society, Committee of the Environmental and Occupational Health Assembly of the American Thoraci c 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 Effect s of Relocating to Areas of Differing Air Pollu tion 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, Vo l. 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/jour nal/vol360/iss9341/full/lla n.360.9341.editorial_and _review.22808.1

California Air Resources Board. “"Public Hearing To Consider Amendments To The Ambient Air Quality Stan dards For Particulate Matter And Sulfates.” May 3, 2002. http://arbis.arb.ca.gov/res earch/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 Pollu tion 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 NMMA PS 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 Effe cts of Ambient Air Pollution on School Absenteeism Due to Respiratory Illness. ” Epidemiology, Vol. 12, No. 1, pp. 43-54, January 2001.

Gauderman, McConnell, Gilliland, Lond on, Thomas, Avol, Vora, Berhane, Rappaport, Lurmann, Margolis, Peters. “Association between Air Pollution andAppendix I: Health Effects

R -2 Lung Function Growth in Southern Ca lifornia Children.” American Journal Respiratory and Critical Care Medici ne, Vol. 162, pp. 1383-1390, 2000.

Gauderman, Gilliland, Vora, Avol, Stra m, McConnell, Thomas, Lurmann, Margolis, Rappaport, Berh ane, and Peters. “Associ ation between Air Pollution and Lung Function Growth in Southern California Children. Results from a Second Cohort.” American J ournal Respiratory and Critic al Care Medicine, Vol. 166, pp.76-84, 2002.

Krewski, Burnett, Goldberg, Koover, Siemiatycki, Jerrett et al. “Reanalysis of the Harvard Six Cities St udy and the American Cancer Society Study of Particulate Air Pollution and Mortality. A Special Report of the Institute’s Particle Epidemiology Reanalysis Project.” He alth Effects Inst itute, July, 2002.

National Research Council. “Research Prior ities for Airborne Particulate Matter I: Immediate Priorities and a Long Range Re search Portfolio.” Washington, DC, National Academy Press, 1998.

McConnell, Berhane, Gilliland, Lo ndon, Islam, Gauderman, Avol, Margolis, Peters. “Asthma in exercisi ng children exposed to ozone: a cohort study.” Lancet Vol. 359, pp.386–91, 2002.

Pope, Burnett, Thun, Calle, Krewski, K azuhiko. And Thurston. “Lung Cancer, Cardiopulmonary Mortality, and Long-Ter m 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 be tween 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, a nd Zeger, “Fine Par ticulate 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, Cours ac, Dockery, Schwartz and Zanobetti. “The National Morbidity, Mortality, and Air Pollution Study Part II: Morbidity and Mortality from Air Polluti on in the United States.” Health Effects Institute Research Report Number, 94 Part II, June, 2000. http://healtheffects.org/pubs/samet2.pdfReferences

R - 3 SCAQMD. Multiple Air Toxics Exposure Study in the South Coast Air Basin. MATES II. South Coast Air Quality Ma nagement District, March 2000. http://www.aqmd.gov/mate siidf/matestoc.htm

United States Environmental Protection Agen cy. “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 Agen cy. “Air Quality Cr iteria for Carbon Monoxide.” EPA 600/P- 99/001F, June 2000.

United States Environmental Protection Ag ency. Third External Review Draft. “Air Quality Criteria for Particulate Ma tter.” Vol. I-II, EP A 600/P-99/002aB, 002bB, April 2002.

United States Environmental Protection Agen cy. “Air Quality Criteria of Ozone and Other Photochemical Ox idants.” EPA 600/P–93 –004aF through EPA/600/ P– 93–004cF, July 1996.

Vedal. “Critical Review. Ambient Par ticles 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 DRAF T APPENDIX I FROM SCAQMD ADVISORY COUNCIL

The letter requesting comments and a c opy 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 recen t studies have been added.

Comment:

Include a summary of the history of hea lth 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 othe r 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 emissi ons 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 po llution 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 kn own about the health effects of air pollution to potential health effe cts in the SCAB based on existing ambient levels.

Response:

The purpose of this appendix is to pr ovide 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 ai r quality standards in all parts of the SCAB.