# FINAL 2007 AQMP APPENDIX I

HEALTH EFFECTS

JUNE 2007SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT GOVERNING BOARD
Chairman: WILLIAM A. BURKE, Ed.D. Speaker of the Assembly Appointee
Vice Chairman: S. ROY WILSON, Ed.D. Supervisor, Fourth District Riverside County Representative

MEMBERS :

MICHAEL D. ANTONOVICH Supervisor, Fifth District Los Angeles County Representative

BILL CAMPBELL Supervisor, Third District Orange County Representative

JANE W. CARNEY Senate Rules Committee Appointee

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

GARY OVITT Supervisor, Fourth District San Bernardino Coun ty Representative

JAN PERRY Councilmember, City of Los Angeles Cities Representative, Los Ange les County, Western Region

MIGUEL A. PULIDO Mayor, City of Santa Ana Cities Representativ e, Orange County

TONIA REYES URANGA Councilmember, City of Long Beach Cities Representative, Los An geles County, Eastern Region

VACANT Governor’s Appointee

DENNIS YATES Mayor, City of Chino Cities Representative, Sa n Bernardino County

EXECUTIVE OFFICER:
BARRY R. WALLERSTEIN, D.Env.

### CONTRIBUTORS

South Coast Air Quality Management District

Elaine Chang, Dr. P.H. Deputy Executive Officer Planning, Rule Development, and Area Sources

Laki Tisopulos, Ph.D., P.E. Assistant Deputy Executive Officer Planning, Rule Development, and Area Sources

Author Jean Ospital, Dr. P.H. Health Effects 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 Lo ng-Term Exposure Effects..................................................................... I-13 Ultrafine Particles ........................................................................................... I-15 Carbon Mon oxide ........................................................................................... I-15 N itrogen Dioxide............................................................................................. I-16 Sulfur Dioxide................................................................................................. I-17 Sulfates............................................................................................................ I -18 Toxi c Air Contaminants.................................................................................. I-19



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



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



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



### ATTACHMENT 2 ................................................................................................ I-32

### APPENDIX 1 HEALTH EFFECTS

Health Effects of Air Pollution Ozone Particulate Matter Carbon Monoxide Nitrogen Dioxide Sulfur Dioxide Sulfates Toxic Air ContaminantsHealth Effects of Air Pollution

I-1 

### INTRODUCTION

This document presents a summary of scie ntific findings on the health effects of ambient air pollutants. The California He alth and Safety Co de Section 40471(b) requires that the South Coast Air Quality Ma nagement District pr epare a report on the health impacts of particulate matter in the South Coast Air Basin, in conjunction with the preparation of the Air Quality Manageme nt Plan revisions. This document, which was prepared to satisfy that requirement, al so includes the effect s of the other major pollutants.



### HEALTH EFFECTS OF AIR POLLUTION

Ambient air pollution is a major public health concern. Ex cess deaths and increases in illnesses associated with high air pollution levels have been doc umented in several episodes as early as 1930 in Meuse Valley, Belgium; 1948 in Do nora, Pennsylvania; and 1952 in London. Although levels of pollutants th at occurred during these acute episodes are now unlikely in the United States, ambient ai r pollution continues to be linked to increases in respiratory illness (morbidity) and increases in death rates (mortality).

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

• Increased mortality

• Increased health care utilization (hos pitalization, 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 e ffects to air pollutants is derived from population-based observational and field studies (epidemiological ) as well as controlled laboratory studies involving human subjects and animals. Th ere have been an increasing number of studies focusing on the mechan isms (that is, on learning how specific organs, cell types,Final 2007 AQMP Appendix I: Health Effects

I-2 and biochemicals are involved in the huma n body’s response to air pollution) and specific pollutants responsible for individual effects. Yet the underlying biological pathways for these effects are not always clearly understood.

Although individuals inhale pollutants as a mixture under ambient conditions, the regulatory framework and the c ontrol measures developed are mostly pollutant-specific. This is appropriate, in that different pollutant s 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 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 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). Thes e plans examine multiple pollu tants, cumulative impacts, and transport issues related to attaining he althful air quality. A brief overview of the effects observed and attributed to various air pollutants is presented in this document.

This summary is drawn substantially from reviews presented previously (SCAQMD, 1996 and 2003), a nd from reviews on the effects of air pollution by the American Thoracic Society (ATS, 1996), the U.S. EP A reviews for ozone (U.S. EPA, 2006 ), Carbon Monoxide (U.S. EPA, 2000), and Pa rticulate Matter (U.S. EPA, 2004), from a published review of the health effects of air pollution (Brunekree f and Holgate, 2002), and from reviews prepared by the California EPA Office of the Environmental Health Hazard Assessment for Particulate Matter (C al EPA, 2002) and fo r Ozone (Cal EPA, 2005) . More detailed citations and discu ssions on air pollution health effects can be found in these references. 1



### OZONE

Ozone is a highly reactive co mpound, 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 pe netrate into the gas exchange region of the deep lung.

The EPA primary standard for ozone is 0.08 ppm averaged over eight hours. The California Air Resources Board (CARB) has established standards of 0.09 ppm averaged over one hour and at 0. 070 ppm averaged over eight hours.

The major subgroups of the population consid ered to be at incr eased risk from ozone exposure are outdoor exercising individua ls including childre n and people with preexisting respiratory disease(s) such as asth ma. The data base identifying the former

1 Most of the studies referred to in this appendix are cited in the above sources. Only more recent specific references will be cited in this summary.Health Effects of Air Pollution

I-3 group as being at increased risk to oz one exposure is much stronger and more quantitative than that for the latter group, probably becau se of a larger number of studies conducted with health y individuals. The adverse effects reported with shortterm ozone exposure are greater with incr eased activity because activity increases the breathing rate and the volume of air reaching the lungs, resu lting in an increased amount of ozone reaching the lu ngs. Children may be a particul arly vulnerable population to air pollution effects because they spend more tim e outdoors, are genera lly 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, dama ge to cells of the respiratory tract, decreases in lung function, increased su sceptibility to respirat ory infection, and increased risk of hospitalization.

The Children’s Health Study, conducted by researchers at the University of Southern California, followed a cohort of children that live in 12 comm unities in southern California with differing levels of air pollu tion for several years. A publication from this study found that school absences in f ourth graders for respiratory illnesses were associated with ambient ozone levels. An increase of 20 ppb ozone was associated with an 83% increase in illness relate d absence rates (Gilliland, 2001).

The number of hospital admissions and emerge ncy room visits for all respiratory causes (infections, respiratory failure, chronic bronchitis, etc.) incl uding asthma show a consistent increase as ambient ozone leve ls increase in a co mmunity. These excess hospital admissions and emergency room visits are observed when hourly ozone concentrations are as low as 0.08 to 0.10 ppm.

Numerous recent studies have found positive associations between increases in ozone levels and excess risk of mortality. These as sociations persist even when other variables including season and levels of particulate matter are accounted for. This indicates that ozone mortality effects ar e independent of other po llutants (Bell, 2004).

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-matched hea lthy 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 respirati on-compromised individuals. Since the respirationcompromised group may have lower lung func tion to begin with, the same degree of change may represent a substantially greater adverse effect overall.Final 2007 AQMP Appendix I: Health Effects

I-4 A recent publication from the Children’s Hea lth Study focused on children and outdoor exercise. In communities wi th high ozone concentrati ons, 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 childr en are associated with heavy exercise in communities with high levels of ozone. Wh ile it has long been kno wn that air pollution can exacerbate symptoms in indi viduals with respiratory diseas e, 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 wi de range of effects induced or associated with ambient ozone exposure. Thes e 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 a ppears that while functional changes may exhibit adaptation, biochemical and cellula r changes which may be associated with episodic and chronic exposure effects may not exhibit similar adaptation. That is, internal damage to the respiratory system ma y continue with repeated ozone exposures, even if externally observable effects (che st 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 vari ous 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 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 biochemical changes associated w ith 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 inflammatory cha nges can be observed 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.Health Effects of Air Pollution

I-5 Some animal studies show results that indicate possible chronic effects including functional and structural changes of the l ung. These changes indicate that repeated inflammation associated with ozone exposure over a lifetime may result in sufficient damage to respiratory tissue such that indivi duals later in life may experience a reduced quality of life in terms of respiratory functi on 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.

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 pregna ncy (Ritz et al., 2002). This is the first study linking ambient air pollutants to birth defects in humans. Confirmation by further studies is needed.Final 2007 AQMP Appendix I: Health Effects

I-6 TABLE 1 Adverse Health Effects of Ozone (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, decr eased 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 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, el asticity, and biochemistry in laboratory an imals that are indicative of airway irritation and inflamma tion with possible development of chronic lung disease Increased susceptibility to bact erial respiratory infections in laboratory animals From: SCAQMD, 1996

In summary, acute adverse effects associat ed with ozone exposures have been well documented, although the sp ecific causal mechanism is still somewhat unclear. Additional research efforts are required to ev aluate the long-term ef fects of air pollution and to determine the role of ozon e in influencing chronic effects.Health Effects of Air Pollution

I-7 

### PARTICULATE MATTER

Airborne particulates are a co mplex group of pollutants that vary in source, size and composition, depending on lo cation and time. The comp onents include nitrates, sulfates, elemental carbon, or ganic carbon compounds, acid aerosols, trace metals, and material from the earth’s crust. Substanc es of biological origin, such as pollen and spores, may also be present.

Until several years ago, the health effects of particulates were focused on those sized 10
μ m (micrometers) aerodynamic diameter and sm aller. These can be inhaled through the upper airways and deposited in the lower airway s and gas exchange tissues in the lung. These particles are referred to as PM10. EPA initially pr omulgated ambient air quality standards for PM10 of 150 μ g/m 3 averaged over a 24-hour period, and 50 μ g/m 3 for an annual average. EPA has ve ry recently rescinded the annual PM10 standard, but kept the 24-hour standard.

In recent years additional focu s has been placed on partic les having an aerodynamic diameter of 2.5 μ m or less (PM2.5). A greater faction of particles in this size range can penetrate and deposit deep in the lungs. The EPA recently lo wered the air quality standards for PM2.5 to 35 μ g/m 3 for a 24-hour average and reaffirmed 15 μ g/m 3 for an annual average standard. Th ere was considerable controve rsy and debate surrounding the review of particulate matter health ef fects and the consideration of ambient air quality standards (Kaiser, 1997; Vedal, 19 97) when the EPA pr omulgated the initial PM2.5 standards in 1997.

Since that time, numerous studies have been published and some of the key studies were closely scrutinized and analyses repeated. The result is that ther e are now substantial data confirming the adverse health effects of PM2.5 exposures.

There are also differences in the composition and sources of particles in the different size ranges that may have implications for hea lth effects. The par ticles larger than 2.5
μ m (often referred to as the coarse fract ion) are mostly pr oduced by mechanical processes. These include au tomobile 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, particle s smaller than 2.5 μ m are mostly derived from combustion sources, such as automobiles, trucks, and other ve hicle 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.

Attention to another range of very small par ticles has been increasing over the last few years. These are generally referred to as “ultrafine” particles, with diameters of 0.1 μ mFinal 2007 AQMP Appendix I: Health Effects

I-8 or less. These particles are mainly from fresh emissions of combustion sources, but are also formed in the atmosphere from photoche mical reactions. Ultrafine particles have relatively short half lives (minutes to hours) and rapidly grow through condensation and coagulation process into larger particles within the PM2.5 size range. These particles are garnering interest since laboratory studies indicate that their toxicity may be higher on a mass basis than larger particles, and ther e is evidence that th ese small particles can translocate from the lung to the blood and to other organs of the body.

The health effects of ambient particulate matter have been recently reviewed (ATS, 1996; U.S. EPA, 2004, Brunekr eef, 2002). In addition, the California Air Resources Board (CARB) and the Office of Envi ronmental Health and Hazard Assessment (OEHHA) have reviewed the adequacy of the California Air Quality Standards for Particulate Matter (Cal EPA, 2002).

The major types of effects associated with particulate matter include:

• Increased mortality

• Exacerbation of respir atory disease and of cardiova scular disease as evidenced by increases in:

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

-School absences -Work loss days

• Effects on lung function

• Changes in lung morphology

The U.S. EPA has recently lowe red the short-term ambient ai r quality standard for fine particles (PM2.5) and has rescinded the annual standard for PM10. Th e current federal and California standards are listed below:Health Effects of Air Pollution

I-9 Standard Federal California

PM10 24-Hour average 150 μ g/m 3 50 μ g/m 3

PM10 Annual Average -- 20 μ g/m 3

PM 2.5 24-Hour Average 35 μ g/m 3
--
PM 2.5 Annual Average 15 μ g/m 3 12 μ g/m 3



### Short-Term Exposure Effects

Epidemiological studies have provided conti nued and consistent evidence for most of the effects listed above. An association be tween increased daily or several-day-average concentrations of PM10 and excess mortality and morbidity is consistently reported from studies involving commun ities across the U.S. as well as in Europe, Asia, and South America. A review an d analysis of epidemiologica l literature for acute adverse effects was undertaken by Dockery and Po pe to estimate these effects as percent increase in mortality asso ciated with each incr emental increase of PM10 by 10 μg/m 3

. The estimates are presented in Table 2. It appears that individuals who are elderly or have preexistent lung or hear t disease are more susceptible than others to the adverse effects of PM10.Final 2007 AQMP Appendix I: Health Effects

I-10 TABLE 2

Combined Effect Estim ates of Daily Mean Particulate Pollution

% Change in Health Indicator per each 10 μg/m 3 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 ex cess 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 μ g/m 3 increase in PM10 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 μ g/m 3 increase in PM10 (Samet, 2000a). This study also analyzed the effects of gaseous co-pollutants. The results indicated that the a ssociation of PM10 and mortality were not confounded by the presence of the gase ous pollutants. When the gaseous pollutants were included in the anal yses, the significance of the PM10 estimates remained. The PM10 effects were reduced somewhat when O 3 was also considered andHealth Effects of Air Pollution

I-11 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 2000 b) was one that used a fl awed statistical software package. The investigators have reanalyzed their data using corrected settings for the software (Dominici, 2002a, Dominici 2002b ). When the estimates for the 90 cities in the study were recalculated, the estimate changed from 0.41 percent increase in mortality for a 10 μ g/m 3 increase in PM10 to a 0.27 per cent increase. Th ere remained a strong positive association between acute expo sure to PM10 and mortality. Thus while the quantitative estimate is reduced, the ma jor 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 μ g/m 3
increase in 24-hour PM2.5 leve ls. The estimates for cardi ovascular related mortality range from 3.0 to 7.0% per 25 μ g/m 3 24-hour PM2.5, and for respiratory mortality estimates range from 2.0 to 7.0% per 25 μ g/m 3 24-hour PM2.5.

Several studies have attempted to assess the relative importance of pa rticles smaller than 2.5 μ m and those between 2.5 μ m and 10 μ m (PM10-2.5). While some studies report that PM2.5 levels are better pred ictors of mortality effects, others suggest that PM10-2.5 is also important. Most of the studies fo und higher mortality a ssociated with PM2.5 levels than with PM10-2.5. For example, a study of six c ities in the U.S. found that particulate matter less than 2.5 μ m were associated with incr eased 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 μ g/m 3 24-hour average.

The relative importance of both PM2.5 and PM10-2.5 may vary in different regions depending on the relative concentrations a nd components, which can also vary by season. More research is needed to better assess the relative effect s of fine (PM2.5) and coarse (PM10-2.5) fractions of particulate matter on mortality.

A number of studies have evaluated the asso ciation between partic ulate matter exposure and indices of morbidity such as hospit al admissions, emergency room visits or physician office visits for respiratory and car diovascular diseases. The effects estimates are generally higher than the effects for mo rtality. 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, largerFinal 2007 AQMP Appendix I: Health Effects

I-12 numbers experience milder effects, which may re late either to the coarse or to the fine fraction of airborne particulate matter.

In the NMMAPS study, hospital admissions for those 65 years or older were assessed in 14 cities. Hospital admissions for these i ndividuals showed an increase of 6% for cardiovascular diseases and a 10% increase for respiratory disease admissions, per 50
μ g/m 3 increase in PM10. The ex cess risk for cardiovascular disease ranges from 3-10% per 50 μ g/m 3 PM10 and from 4-10% per 25 μ g/m 3 PM2.5 or PM10-2.5.

Similarly, school absences, lost workdays an d 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 delaye d impact on these parameters following elevated particulate matter exposures. Thes e 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 respir atory symptoms (increased sputum, chest pain and wheeze). The severity of these effect s is widely varied and is dependent on the population studied, such as adults or children with and without asthma. Sensitive individuals, such as thos e with asthma or pre-existing respiratory disease, may have increased or aggravated symptoms associated with short-term particulate matter exposures. Several st udies have followed th e number of medical visits associated with polluta nt exposures. A range of increases from 3% to 42% for medical visits for respiratory illne sses was found corresponding to a 50 μ g/m 3 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 particulat e matter can produce health effects are being investigated in laboratory studies. Inflammatory response s in the respiratory system in humans and animals exposed to concentrated 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 inflammatory proce ss. The effects of particulate matter may be mediated in part through the production of reactive oxygen species during the inflammatory process. Recent reviews disc uss mechanistic studies in more detail (Brunekreef, 2002; Brook, 2004).Health Effects of Air Pollution

I-13 

### Long-Term Exposure Effects

While most studies have evaluated the acute effects, some studies specifically focused on evaluating the effects of chronic expos ure to PM10 and PM2.5. Studies have analyzed the mortality of adu lts living in different U.S. cities. After adjusting for important risk factors, these studies found a consistent positive asso ciation of deaths and exposure to particulate matt er. A similar association wa s observable in both total number of deaths and deaths du e to cardiorespiratory causes. A shortening of lifespan was also reported in these studies.

Significant associations for PM2.5 for bot h total mortality and cardiorespiratory mortality were reported in a study using datafrom the American Cancer Society. A reanalysis of the data from this study c onfirmed the finding (Krewski, 2000). The Harvard Six Cities Study eval uated several size ranges of particulate matter and reported significant associations with PM15, PM 2.5, sulfates, and non-sulfate particles, but not with coarse particle s (PM15 – PM2.5). An extens ion of the Harvard Six Cities Cohort confirmed the association of morta lity with PM2.5 levels (Laden, 2006). These studies provide evidence that the fine partic les, as measured by PM2.5, may be more strongly associated with mortality effects from long-term partic ulate 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 researcher s 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 effect s is larger in the long-term studies than in the short-term investigatio ns. An analysis of the American Cancer Society Cohort from the Los Angeles area us ed a more detailed estimate of long-term PM2.5 exposures and found that the risk of mortality was up to three times higher than estimated with the national co hort (Jerrett, 2005). These findings indicate that longterm exposures may be more important in terms of overall health effects.

Recent studies report evidence indicating that particulate matter exposure early in pregnancy may be associated with lowered birth weights (Bobak, 1999). Other studies from the U.S., the Czech Republic and Mexico City have reported that neonatal and early postnatal exposure to particulate matter may lead to increased infant mortality. A more recent study in Southern California found increased risks for infant deaths associated with exposures to particulates and other po llutants (Ritz, 2006). These results suggest that infants may be a subgrou p affected by particulate matter exposures.

In addition, some long-term effect studies ha ve reported an increased risk of mortality from lung cancer associ ated with particulate matter exposures. A study involving California Seventh Day Adve ntists (very few of whom smoke) has reported an association of lung cancer mort ality with PM10 levels. It is not clear from these studiesFinal 2007 AQMP Appendix I: Health Effects

I-14 whether the association relate s to causation of disease, or whether individuals with cancer are more susceptible to other effect s of particles leadi ng to the observed mortality association. A recent study that followed a large number of individuals living in the largest U.S. cities found elevated lung cancer risk associat ed with long term average PM2.5 levels (Pope, 2002).

Several studies have assessed the effects of long-term particulate matter exposure on respiratory symptoms and lung function change s. Associations have been found with symptoms of chronic bronchitis and decrea sed 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 NO 2 and acid vapor levels.

A cohort of fourth graders from the Southe rn California communities was followed over a period of four years by the Children’s Health Study. A lower rate of growth in lung function was found in children living in areas with higher levels of particulate pollution (Gauderman, 2000). Decreases in lung function growth we re associated with PM10, PM2.5, PM10-2.5, acid vapor, and NO 2 . There was no associa tion 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 ch ildren confirmed the findings that decreased lung function growth was associated with particulates, nitric oxides, and elemental carbon levels (Gauderman, 2002). Elementa l carbon is often 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 function growth ra te (Avol, 2001). By the time the fourth graders graduated from high sch ool, a significant number showed lower lung function. The risk of lower lung function wa s about five times higher in children with the highest PM2.5 exposure when compared to the lowest exposure communities (Gauderman, 2004). These deficits are likely to persist since the children were at the end of their growth period.

Despite data gaps, the extens ive body of epidemiological studies has both qualitative and quantitative consistency s uggestive of causality. A cons iderable body of evidence from these studies suggests that ambient par ticulate matter, alone or in combination with other coexisting pollutants, is associated with significa nt increases in mortality and morbidity in a community.

In summary, the scientific litera ture indicates that an increased risk of mortality and morbidity is associated with particulate matter at ambien t levels. The evidence for particulate matter effects is mostly deri ved from population studies with supportive evidence from clinical and animal studies. A lthough most of the e ffects are attributable to particulate matter, co-pollu tant effects cannot be ruled out on the basis of existing studies. The difficulty of separating the effect s may be due to the fact that particulateHealth Effects of Air Pollution

I-15 levels co-vary with other combustion source pollutants. That is, the particle measurements serve as an i ndex of overall exposure to combustion-related pollution, and some component(s) of combustion polluti on other than particles might be at least partly responsible for the observed health effects.



### ULTRAFINE PARTICLES

As noted above, numerous studies have foun d association of particulate matter levels with adverse effects, includi ng mortality, hospital admissi ons, and respiratory disease symptoms. The vast majority of these studies used particle mass of PM10 or PM2.5 as the measure of exposure. So me researchers have postulat ed, however, that ultrafine particles may be responsible for some of th e observed associations of particulate matter and health outcomes (Oberdorster, et al, 1995; Seaton, et al, 1995). Ultrafine particles are generally classified of 0.1 μ m and small diameter. Several potential mechanisms have been brought forward to suggest that the ultrafine portion may be important in de termining the toxicity of am bient particulates, some of which are discussed below. For a given mass concentratio n, ultrafine particles have much higher numbers and surface area compared to larger particles. Pa rticles can act as carriers for other adsorbed agents, such as trace metals and organic co mpounds; and the larger surface area may transport more of such toxic agen ts than larger particles.

Smaller particles can also be inhaled deep into the lungs. As much as 50% of 0.02 μ m diameter particles are estimated to be deposited in the alveolar region of the lung.



### CARBON MONOXIDE

The high affinity of carbon monoxide (CO) to bond with oxyg en-carrying proteins (hemoglobin and myoglobin) results in reduc ed oxygen supply in the bloodstream of exposed individuals. The reduced oxygen supp ly is responsible for the toxic effects of CO which are typically manife sted in the oxygen-sensitive or gan systems. The effects have been studied in contro lled laboratory environments in volving exposu re of humans and animals to CO, as well as in populatio n-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 fo r 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 (U.S . EPA, 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 inFinal 2007 AQMP Appendix I: Health Effects

I-16 terms of COHb levels in blood measured as percentage of total hemoglobin bound to CO. COHb levels in non-smokers range between 0.3 and 0.7% and 5 to 10% in smokers. COHb levels in excess of 1. 5% in a significant proportion of urban nonsmoking populations can be considered as evidence of widespread exposure to environmental CO. Under controlled laboratory conditions, 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 w ith coronary artery disease who engaged in exercise duri ng CO exposures have shown th at COHb levels as low as 2.4% can lead to earlier onset of electrocar diograph 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, a nd 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 pregnancy to increase s in pre-term births. (Ritz, 2000). However, the results were not consistent in different areas studied. The increase in the pre-term births was also associated with PM10 levels. Another study found increased risks for cardiac related birth defe cts with carbon monoxide exposure in the second month of pregnancy (Ritz, 2002). Further study is needed to confirm these observations.



### NITROGEN DIOXIDE

The California EPA is currently reviewing th e health effects of nitrogen dioxide (Cal EPA, 2006). Evidence for lo w-level nitrogen dioxide (NO 2) exposure effects is derived from laboratory studies of asthmatics and from 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 sympto ms, respiratory illness, decreased lung function, increased emergency room visits for asthma, and cardio pulmonary mortality. However, since NO 2 exposure generally occu rs in the presence of other pollutants, such as particulate matter, these studies are ofte n unable to determine th e specific role of NO 2 in causing effects. The Children’s Health Study in Southern Calif ornia found associations of air pollution, including NO 2 , PM10, and PM2.5, with respir atory symptoms in asthmatics (McConnell, 1999). Particles and NO 2 were correlated, and effects of individualHealth Effects of Air Pollution

I-17 pollutants could not be discerne d. A subsequent analysis indicated a stronger role for NO2 (McConnell, 2002).

Ambient levels of NO 2 were also associated with a decr ease in lung function growth in a group of children followed for ei ght years. In addition to NO 2 , the decreased growth was also associated with particulate matte r and airborne acids. The study authors postulated that these may be a measure of a package of pollutants from traffic sources. (Gauderman, 2004). Results from controlled exposure studies of asthmatics demonstrate an increase in the tendency of airways to contract in resp onse to a chemical stimulus (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 ppm). Mixed results have been reported when people with chronic obstructive lung disease 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 co mbination 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 th e immune system. Non-specific changes in cells involved in maintaining immune functi ons (cytotoxic T cells and natural killer cells) have been observed in humans after repe ated exposure (4-6 da ys) to >0.6 ppm of NO 2 (20 min. - 2 hours). All these change s collectively support the observation reported both in population and animal studies of increased susceptibility to infections, as a result of NO 2 exposure.



### SULFUR DIOXIDE

Controlled laboratory studies involving hum an 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 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 SO 2 inhalation is observable within 2 minutes of exposure, increases further w ith continuing exposure up to 5 minutes then remain s relatively steady as exposure continues. SO 2 exposure is generally not associated with any delayed reactions or repetitive asthmatic attacks.Final 2007 AQMP Appendix I: Health Effects

I-18 No significant changes have been reported from studies, which have evaluated the effects of exposure to co-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 chr onic toxicity in animals 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 guin ea pigs repeatedly exposed to high levels (72 ppm) of SO 2 . This effect needs furthe r evaluation in clinical and population studies to identify any chronic exposure impact on both asthma tic incidence and attacks in a population.

Some epidemiological studies indicate th at the mortality an d morbidity effects associated with the fine fraction of partic les show a similar association with ambient SO 2 levels. In these studies, efforts to separate 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 genera ted from similar combustion sources they represent the same pollution inde x for the observed effects.



### SULFATES Based on a level determined necessary to protect the most sensitive individuals, the California Air Resources Board in 19 76 adopted a standard of 25 μg/m 3 (24-hour average) for sulfates.

In recent years, a vast majority of effects (m ortality and morbidity) associated with fine particles (PM2.5) and sulfur dioxide have 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, ha ving been emitted from common sources; and the effects observed may be due to the combina tion 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 susceptib le population subgroup with some changes in lung function ob served with exposu res below 100 μg/m 3 . In general, however, laboratory exposures of human volunteers to su lfates at or near ambient levels have not found significant change s in lung function.

Results from animal studies involving exposur es to sulfuric acid aerosol, ammonium bisulfate and ammonium sulfate indicate that acidic particles (former two) are more toxic than non-acidic particles (latter). In a ddition, the severity or magnitude of both mortality and morbidity effect s is relatively higher in popu lation studies of the eastern United States and Canada where sulfate c oncentrations are hi gher than for thoseHealth Effects of Air Pollution

I-19 observed in the western United States. Mixe d results have been reported from studies which attempted to ascertain the role of aci dity 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 s ubstances that may pose a risk of adverse health effects. These effects are usually an increased risk fo r cancer or adverse 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 estimat e the additional cancer risk from ambient levels of toxics. This esti mate represents 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 canc er cases per million people exposed.

The SCAQMD conducted a study on the ambi ent concentrations and estimated the potential health risks from air toxics (SQAQMD, 2000). A one year monitoring program was undertaken at 12 sites through out the SCAB. Over 30 substances were measured, and annual average levels were ca lculated. 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 cont ributor to this risk was diesel exhaust, accounting for 71% of the air toxics risk. A breakdown of the major contributors to the air toxics risk is shown in the following graph.Final 2007 AQMP Appendix I: Health Effects

I-20 

### Basinwide Cancer Risk ~1,400 in one million

71% 8%

7% 3% 11%



### Diesel Exhaust 1,3-Butadiene Benzene Carbonyls Others

FIGURE 1 Major pollutants contributing to Air Toxics Cancer Risk in the South Coast Air Basin

For non-cancer health effect s, OEHHA has developed acu te and chronic Reference Exposure Levels (RELs). RELs are concen trations in the air below which adverse health effects are not likely to occur. Ac ute RELs refer to short-term exposures, generally of one-hour duration. Chronic RELs refer to l ong-term exposures of several years. The ratio of ambient concentratio n to the appropriate REL can be used to calculate a Hazard Index. A Hazard Index of less than one would not be expected to result in adverse effects.

The key air toxics contributing to risk fro m 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 TrichloroethyleneHealth Effects of Air Pollution

I-21 

### CONCLUSION

The vast body of scientific evidence shows that the adverse impacts of air pollution in human and animal health are clear. A cons iderable number of population-based and laboratory studies have esta blished a link between increas ed morbidity and in some instances, earlier morta lity and air pollution.REFERENCESReferences

I-22 

### References American Thoracic Society, Committee of th e Environmental and Occupational Health Assembly of the American Thoracic Society. (1996). “Health E ffects of Outdoor Air Pollution.” American J ournal Respiratory and Critical Care Medicine, Parts 1 and 2. 153:3- 50 and 153:477-498.

Avol EL, Gauderman JW, Tan SM, London SJ, Peters JM. (2001) . “Respiratory Effects of Relocating to Areas of Differing Air Polluti on Levels.” Am J Respir Crit Care Med, 164:11:2067-2072.

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

Bobak M, Leon DA. (1999). “Pregnancy Ou tcomes and Outdoor Air Pollution: An Ecological Study in Districts of the Czech Repu blic 1986-8.” Occup. and Environ. Med. 56:539-543.

Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Lipsett M, Leupker R, Mittleman M, Samet J, Smith SC Jr., Tager I. (2004). “Air Pollution and Cardiova scular Disease: A Statement for Healthcare Professionals from the Expert Panel on Population and Prevention Science of the American Heart Associ ation.” Circulation, 109:2655-2671

Brunekreef, B and ST Holgat e. (2002). “Air Pollution and Health.” The Lancet, 360(9341):1233-42, http://www.thelancet.com/journa l/vol360/iss9341/full/llan.360.9 341.editorial_and_review.2 2808.1

California Environmental Protec tion Agency, California Air Res ources Board, and Office of Environmental Health Hazard Assessment. (2002). "Public Hearing to Consider Amendments to the Ambient Ai r Quality Standards for Partic ulate Matter and Sulfates.” http://arbis.arb.ca.gov/research/aaqs/ std-rs/pm-final/pm-final.htm#Summary

California Environmental Protecti on Agency, Air Resources Board. (2005). “Review of the California Ambient Air Quality Standard for Ozone.”

California Environmental Protec tion Agency, California Air Res ources Board and Office of Health Hazard Assessment. (2006). “Rev iew of the California Ambient Air Quality Standard for Nitrogen Dioxide.” Draft Staff Report.

Dominici F, McDermott A, Zeger SL, Samet JM. (2002.) “On the use of Generalized Additive Models in Time-Serie s Studies of Air Pollution and Health.” Am J Epidemiol., 156:193-203.Final 2007 AQMP Appendi x I: Health Effects

I-23 Dominici F, McDermott A, Zeger SL, Samet JM. (2002). A Report to the Health Effects Institute: Reanalyses of the NMMAPS Database. http://www.biostat.jhsph.edu/ ~fdominic/HEI/nmmaps.html

Gauderman JW, McConnell R, Gilliland F, London S, Thomas D, Avol E, Vora H, Berhane K, Rappaport EB, Lurmann F, Margolis HG, Pe ters J. (2000). “Association between Air Pollution and Lung Function Growth in Southe rn California Children.” Am J Respir Crit Care Med, 162(4):1383-1390.

Gauderman JW, Gilliland F, Vora H, Avol E, Stram D, McConnell R, Thomas D, Lurmann F, Margolis HG, Rappaport EB, Berhane K, Peters J. (2002). . “Association between Air Pollution and Lung Function Growth in Sout hern California Children. Results from a Second Cohort.” Am J Respir Crit Care Med, 166:76-84.

Gauderman JW, Avol E, Gilliland F, Vora H, Thomas D, Berhane K, McConnell R, Kuenzli N, Lurmann F, Rappaport E, Margolis H, Bates D, Peters J. (2004). “The Effect of Air Pollution on Lung Development from 10 to 18 Years of Age.” N Engl J Med, 351(11):1057-1067.

Gilliland FD, Berhane K, Rappaport EB, Thomas DC, Avol E, Gaude rman WJ, London SJ, Margolis HG, McConnell R, Islam KT, Peters JM . (2001). “The Effects of Ambient Air Pollution on School Absenteeism Due to Respiratory Illnesse s.” Epidemiology, 12(1):43- 54.

Jerrett M, Burnett RT, Ma R, Pope CA III, Kr ewski D, Newbold KB, Thurston G, Shi Y, Finkelstein N, Calle EE, Thun MJ. (2005). “Spatial Analysis of Ai r Pollution and Mortality in Los Angeles. Epidem iology, 15(6):727-736.

Krewski D, Burnett RT, Goldbe rg MS, Hoover K, Siemiatyck i J, Abrahamowicz M, White WH, et al. (2000). “Reanalysis of the Harv ard Six Cities Study and the American Cancer Society Study of Partic ulate Air Pollution and Mortality. A Special Report of the Institute’s Particle Epidemiology Reanalysis Pr oject.” Health Effects Institute.

Laden F, Schwartz J, Speizer FE, Dockery DW . (2006). “Reduction in Fine Particulate Air Pollution and Mortality.” Am J Respir Crit Care Med, 173:667-672.

McConnell R, Berhane K, Gilliland F, Lond on SJ, Islam T, Gaud erman WJ, Avol E, Margolis HG, Peters JM. (2002). “Asthma in exercising children exposed to ozone: a cohort study.” Lancet, 359:386-91.References

I-24 McConnell R, Berhane K, Gilliland F, Lond on SJ, Vora H, Avol E, Gauderman WJ, Margolis HG, Lurman F, Thomas DC, Peters JM. (1999). “Air Pollution and Bronchitic Symptoms in Southern California Children with Asthma.” EHP, 107(9):757-760.

McConnell R, Berhane K, Gilliland F, Molitor J, Thomas D, Lurmann F, Avol E, Gauderman WJ, Peters JM. (2003). “Prosp ective Study of Air Po llution and Bronchitic Symptoms in Children with Asthma.” Am J Respir Crit Care Med, 168:790-797.

National Research Council. (1998). “Research Priorities for Airborne Particulate Matter I: Immediate Priorities and a Long Range Resear ch Portfolio.” Washington, DC, National Academy Press.

Oberdorster G, et al. (1995). “Association of Particulate Air Pollution and Acut e Mortality: Involvement of Ultra-Fine Particle s.” Inhalation Toxicol 7:111-124.

Peters J, et al. (1997). “Children’s Health Study.” http://www.arb.ca.gov/research/chs/chs.htm

. Pope III CA, Burnett RT, Thun MJ, Calle E, Kr ewski D, Kazuhiko I, Thurston G. (2002). “Lung Cancer, Cardiopulmonary Mortality, and Long-Term Exposure to Fine Particulate Air Pollution.” JAMA, 287:1132-1141.

Pope III CA, Dockery DW. (2006). “Health E ffects of Fine Particulate Air Pollution: Lines that Connect.” JAWMA, Critical Review. 56(6):709-742.

Ritz B, Yu F, Chapa G, Frui n S. (2000). “Effect of Air Pollution on Preterm Birth Among Children Born in Southern California betwee n 1989 and 1993.” Epidemiology, 11(5)502- 11.

Ritz B, Yu F, Fruin S. Chap a G, Shaw GM, Harris JA. (2002 ). “Ambient Air Pollution and Risk of Birth Defects in Southern Calif ornia.” Am J Epidemiol, 155(1):17-25.

Ritz B, Wilhelm M, Zhao, Y. (2006). “A ir Pollution and Infant Death in Southern California, 1989-2000.” Pediatrics. 118(2):493-502

Samet JM, Dominici F, Curriero FC, Coursac I, Zeger SL. (2000). “Fine Particulate Air Pollution and Mortality in 20 U.S. Cities, 1987–1994.” N Engl J Med, 343(24):1742-9.

Samet JM, Zeger SL, Dominici F, Curriero F, Coursac I, Dockery DW, Schwartz J, Zanobetti A. (2000). “The National Morbidity , Mortality, and Air Po llution Study Part II: Morbidity and Mortality from Air Pollution in the United Stat es.” Res Rep Health Eff Inst, 94Final 2007 AQMP Appendi x I: Health Effects

I-25 SCAQMD. (2000). Multiple Ai r Toxics Exposure Study in th e South Coast Air Basin. MATES II. South Coast Air Qua lity Management District. http://www.aqmd.gov/mate siidf/matestoc.htm

Seaton A, et al. (1995). “Particulate Air Po llution and Acute Health Effects.” Lancet 345:176-178.

United States Environmental Prot ection Agency. (2000). “Air Quality Criteria for Carbon Monoxide.” EPA 600/P-99/001F.

United States Environmental Protection Agen cy. (2004). “Air Quality Criteria for Particulate Matter.” EPA 600/P-99/002aB.

United States Environmental Pr otection Agency. (2006). “A ir Quality Criteria of Ozone and Other Photochemical Oxidants .” EPA 600/R-05/004aF-CF.

Vedal S. (1997). “Critical Review. Ambient Particles and Health: Li nes that Divide.” JAMA, 47(5):551-581.ATTACHMENT 1 COMMENTS RECEIVED ON DRAFT APPENDIX I FROM SCAQMD ADVISORY COUNCIL

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

Staff responses to comments are in Attachment 2.Attachment 1

I-26Final 2007 AQMP Appendi x I: Health Effects

I-27Attachment 1

I-28Final 2007 AQMP Appendi x I: Health Effects

I-29Attachment 1

I-30Final 2007 AQMP Appendi x I: Health Effects

I-31ATTACHMENT 2 STAFF RESPONSES TO COMMENTS RECEIVEDFinal 2007 AQMP Appendi x I: Health Effects

I-32 Comment:

Citations missing in References section.

Response:

The missing citations are below.

Oberdorster G, et al. 1995. “Associati on of Particulate Air Pollution and Acute Mortality: Involvement of Ultra-Fine Pa rticles.” Inhalation Toxicol 7:111-124.

Seaton A, et al. 1995. “Particulate Air Po llution and Acute Health Effects.” Lancet 345:176-178.

Comment:

Include an explanation of how oxidizing agents a ffect biological tissue.

Response:

Oxidants such as ozone can read ily react with biochemicals in tissues to alter their chemical structure and affect their biochemical functioning.

Comment:

Are percent changes in h ealth indicators for PM 2.5 the same as for PM 10 ? Include a table for percentage change for PM 2.5 indicators as was done for PM 2.5 .

Response:

The table for PM 10 was used to provide a brief summary of information related to daily changes in PM levels with various health in dicators, and was taken from a previous review paper. The discussion for PM 2.5 associated outcomes includes a brief description of some of the more recent studies of health effects, whic h does include percenta ge changes associated with changes in ambient expo sures. The discussion show s that the relative changes associated with PM 2.5 levels are not the same as those with PM 10 . The discussion also points out that some studies indicate the effects from PM 10 exposures may be attributed to the PM 2.5 component, whereas other studies indicate that the fraction of PM 10 larger than 2.5 μm diameter also contribute. The relative contribution of the diffe rent fractions of PM 10 to health outcomes is an o ngoing area of research.Attachment 2

I-33 Comment:

Ultrafine particles may affect cellular AT P production, and this could explain why particulate matter might exacerbate diabetic conditions.

Response:

Studies have indeed shown that ultrafine part icles can penetrate into cell mitochondria and result in cell death. The m echanism is thought to include oxidative injury to cellular components. While ther e are studies that indicate indivi duals with diabetes may be more sensitive to the effects of air pollutants, staff opinion is that there are not sufficient data available to determine whether particulat e exposures exacerbate diabetic conditions.

Comment:

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

Response:

Sulfur dioxide (SO 2 ) occurs as a gas in the atmosphere, whereas sulfat es (referring to the ion SO 4 -2 ) are generally found as a com ponent of particulate matter.

Comment:

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

Response:

Staff assessment of the benefits of implem enting the AQMP and attaining the ambient air quality standards is included in the Socioeconomic Report.

Comment:

Some clarification should be co nsidered in the AQMP that acute and chronic effects of toxic air pollutants should take priority, as far as regulations are concerned, over carcinogenic effects.

Response:

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

I-34 Comment:

A check should be done of all th e District monitoring stations to confirm that they are not impacted by unusual site conditions.

Response:

This is beyond the scope of Appendix I. Th e air quality monitoring network stations are sited in conformance with federal and state gui delines to be at locations representative of regional air quality.

Comment:

An analysis of indoor air quality and PM 2.5 should be included.

Response:

There are few studies on the health effects on indoor PM 2.5 exposures. The study cited by the commenter did not provide in formation on health effects.