FINAL

APPENDIX I

HEALTH EFFECTS

NOVEMBER 1996
SOUTH COAST AIR QUALITY MANAGEMENT DISTRICT

GOVERNING BOARD 

Chairman: JON D. MIKELS

San Bernardino

County Representative

Vice Chairman: WILLIAM A. BURKE, Ed.D.

Speaker of the Assembly Appointee

MEMBERS:

MICHAEL D. ANTONOVICH

Los Angeles County Representative

MARVIN BRAUDE

Cities Representative, Los Angeles County, Western Region

CANDACE HAGGARD

Cities Representative, Orange County

MEE HAE LEE

Senate Rules Committee Appointee

RONALD O. LOVERIDGE

Cities Representative, Riverside County

LEONARD PAULITZ

Cities Representative, San Bernardino County

JAMES SILVA

Orange County Representative

NELL SOTO

Cities Representative, Los Angeles County, Eastern Region

S. ROY WILSON, Ed.D.

Riverside County Representative

VACANT

Governor's Appointee

EXECUTIVE OFFICER

JAMES M. LENTS, Ph.D.
CONTRIBUTORS

South Coast Air Quality Management District

Barry R. Wallerstein, D.Env.

Deputy Executive Officer

Planning, Transportation, and Information Management

Mel Zeldin

Director of Planning

Cindy Greenwald

Planning Manager

Mike Nazemi

Manager

Technology Advancement

Author

Dr. Shankar Prasad

Health Effects Officer


Table of Contents

i

Table of Contents

HEALTH EFFECTS OF AIR POLLUTION

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

Particulate Matter (PM10).......................................................................................I-5

Short-Term Exposure Effects .....................................................................I-6

Long-Term Exposure Effects......................................................................I-7

Effects Associated with Fine and Coarse Fraction .....................................I-8

Carbon Monoxide (CO) .........................................................................................I-9

Nitrogen Dioxide (NO2).......................................................................................I-10

Sulfur Dioxide (SO2)............................................................................................I-11

Sulfates.................................................................................................................I-11

CONCLUSION.....................................................................................................I-12

ATTACHMENT 1

State Of The Art - Health Effects Of Outdoor Air Pollution

APPENDIX I

HEALTH EFFECTS

Health Effects of Air Pollution

Ozone

Particulate Matter (PM10)

Carbon Monoxide (CO)

Nitrogen Dioxide (NO2)

Sulfur Dioxide (SO2)

Sulfates

Health Effects of Air Pollution

I - 1

HEALTH EFFECTS OF AIR POLLUTION

Ambient air pollution is a major public health concern. Excess deaths associated with air 

pollution episodes have been documented as early as 1930 in Meuse Valley, Belgium; 

1948 in Donora, Pennsylvania; and 1952 in London. Although acute air pollution 

episodes associated with such readily-evident excess deaths are now unlikely in the 

United States, air pollution continues to be linked as a cause of respiratory illness 

(morbidity) and slight increase in death rates (mortality).

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

a) Increased health care utilization (hospitalization, physician and emergency room 

visits)

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

c) Reduction in life-span

d) Potential increased risk of developing cancer

e) Decreased breathing capacity 

f) Lung inflammation

g) Potential immunological changes

h) 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

i) A decreased tolerance for exercise.

The evidence linking these general effects to air pollution, and specific effects to a 

specific pollutant(s) is derived from population-based observational and field studies 

(epidemiological) as well as controlled laboratory studies involving human subjects and 

animals. There have been an increasing number of studies focusing on the mechanisms 

and specific pollutant(s) responsible for individual effects, yet these effects are not 

always clearly understood. Long-term effects of exposure, being more difficult to 

identify and measure, require further research and evaluation.

Although individuals inhale pollutants as a mixture under ambient conditions, a focus on 

specific pollutants occurs because the regulatory framework and the control measures 

developed therefrom are mostly pollutant-specific. Results from recent studies have 

raised doubts about the adequacy of the existing National Ambient Air Quality Standards 
APPENDIX I: Health Effects

I - 2

(NAAQS) for ozone and PM10 in protecting public health. Hence, U.S. EPA recently 

reviewed these NAAQS and recommended revised NAAQS for ozone and PM10. A brief

overview of the effects observed and attributed to various air pollutants is presented in 

this document.

The summary presented is drawn from: (1) a two-part article: “State of the Art: Health 

Effects of Outdoor Air Pollution” prepared by a committee of the Environmental and 

Occupational Health Assembly of the American Thoracic Society (presented as an 

appendix to this document); (2) draft versions of U.S. EPA’s Staff Paper on the review 

of NAAQS for ozone(1995) and PM10 (1996); and (3) a report to the Health Effects 

Institute on Phase 1B: Particle Epidemiology Evaluation Project (1995).1

OZONE

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

exposure are outdoor exercising individuals including children and people with 

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

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

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

conducted with healthy individuals. The adverse effects reported with short-term ozone 

exposure are greater with increased activity because activity increases the volume of air 

reaching the lungs, resulting in an increased amount of ozone reaching the lungs.

The number of hospital admissions for all respiratory causes (infections, respiratory 

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

ozone, sulfate or sulfur dioxide levels increase in a community. These excess hospital 

admissions and emergency room visits are observed when hourly ozone concentrations 

are as low as 0.08 to 0.10 ppm. However, limitations in the study designs preclude 

attributing the effects solely to ambient ozone concentrations.

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

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

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

seen in age and gender matched healthy individuals versus asthmatics and those with 

chronic obstructive pulmonary disease. While the degree of change evidenced did not 

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

these respiration-compromised individuals. Since the respiration-compromised group 

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

substantially greater adverse effect overall.

 

1 All of the studies referred to in this Appendix are cited in the above noted sources. Specific references to individual 

studies will not be made in this summary.
Health Effects of Air Pollution

I - 3

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

with ambient ozone exposure (Table 1). The effects reported include decreased 

breathing capacity and exercise performance; increased airway resistance and 

responsiveness (indicative of involvement of both smaller distal and larger proximal 

airways); impaired host defenses; excess hospital admissions and emergency room visits; 

acute inflammation of the lung tissue; and respiratory cell damage.

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 phenomena, 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.

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

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

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

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

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

observed in adults and children under ambient exposure conditions (0.10 - 0.15 ppm)2. 

The responses reported are indicative of decreased breathing capacity and are reversible.

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

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

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

the concentration of biochemical mediators of inflammation and injury such as cytokines 

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

to ozone in the range of 0.08 to 0.10 ppm.

Finally, the lack of consistency between population and laboratory studies also suggests 

that the susceptibility observed under ambient conditions could be due to the 

combination of pollutants (not ozone alone) which co-exist in the atmosphere, or that 

ozone may actually sensitize these subgroups to the effect(s) of other pollutants.

Some animal studies show results which indicate possible chronic effects including 

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

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

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

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

 

2

Federal Standard .12 ppm, 1-hour average. State Standard .09 ppm, 1-hour average.
APPENDIX I: Health Effects

I - 4

study involving Los Angeles County residents provided supportive evidence of lung 

tissue damage (structural changes) attributable to air pollution.

TABLE 1

Adverse Health Effects of Ozone (O3)

(Summary of Recent Key Studies)

03 Concentration and Exposure Hr, 

ppm

Health Effect

Ambient air containing 0.10 - 0.15 

daily 1-h max over days to weeks

Decreased breathing capacity), in children, 

adolescents, and adults exposed to 03 outdoors

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

chest pain) in individuals with preexisting disease 

(e.g., asthma) with low ambient exposure, decreased 

temperature, and other environmental factors resulting 

in increased summertime hospital admissions and 

emergency department visits for respiratory causes

0.12 (1-3h)

0.08 (6.6h)

(chamber exposures)

Decrements in lung function (reduced ability to take a 

deep breath), increased respiratory symptoms (cough, 

shortness of breath, pain upon deep inspiration), 

increased airway responsiveness and increased airway 

inflammation in exercising adults

0.12 (1-3 h)

0.08 (6.6h)

(chamber exposures)

Effects are similar in individuals with preexisting 

disease except for a greater increase in airway 

responsiveness for asthmatic and allergic subjects

0.12 (1-3h)

0.08 (6.6h)

(chamber exposures)

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

reproducible changes in lung function

Attenuation of response with repeated exposure

0.12 with prolonged, repeated 

exposure 

(chamber exposures)

Changes in lung structure, function, elasticity, and 

biochemistry in laboratory animals that are indicative 

of airway irritation and inflammation with possible 

development of chronic lung disease

Increased susceptibility to bacterial respiratory 

infections in laboratory animals
Health Effects of Air Pollution

I - 5

A few studies have suggested that population exposures to community air pollution 

(ozone and particulate matter), are related to genetic toxicity and increased incidence of 

cancer. In recent years, an increase in daily mortality has also been reported from studies 

involving Southern California’s population. Because of limitations in study design in a 

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

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

from these studies.

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

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

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

and to determine the role of ozone in influencing chronic effects.

PARTICULATE MATTER (PM10)

Inhalability and deposition characteristics of particles less than 10 micrometers in size, 

which could potentially damage the lower respiratory tract and the gas-exchange region 

of the lung were the driving force to set the NAAQS for PM10.

3

 U.S. EPA in its recent 

PM10 NAAQS review has concluded that the difference in exposure relationships, and 

the strong likelihood of the fine mode fraction of PM10 being significant contributors to 

PM-related health effects in sensitive populations, are sufficient to justify the 

consideration of fine and coarse mode particles in PM10 as separate classes of pollutants. 

The major categories of adverse health effects associated with PM10 include:

a) Increased mortality (acute and chronic)

b) Exacerbation of preexisting respiratory and cardiovascular diseases leading to 

an increase in hospital admissions, emergency room visits, school absences, lost 

work days and restricted activity days

c) Changes in lung function and structure

d) Altered defense mechanisms

e) Increased risk of developing cancer

Short-Term Exposure Effects

Epidemiological studies have provided continued and consistent evidence for most of the 

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

 

3

Federal Standard 50 μg/m3, annual arithmetic mean; 150 μg/m3, 24-hour average. State Standard 30 μg/m3, annual 

geometric mean; 50 μg/m3, 24-hour average.
APPENDIX I: Health Effects

I - 6

concentrations of PM10 (measured or estimated) and excess mortality as well as 

morbidity is consistently reported from studies involving communities across the U.S. as 

well as in Europe and South America. A review and analysis of recent epidemiological 

literature for acute adverse effects was undertaken by Dockery and Pope to estimate 

these effects as percent increase in mortality associated with each incremental increase 

of PM10 by 10 μg/m3. The estimates are presented in Table 2. It appears that individuals 

who are elderly or have preexistent lung or heart disease are more susceptible than others 

to the adverse effects of PM10.

TABLE 2

Combined Effect Estimates of Daily Mean

Particulate Pollution

% Change in Health Indicator

per each 10 μg/m3Increase 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)

A positive association between short-term exposures to PM and hospital admissions for 

respiratory or cardiac diseases is reported in several studies. When results from many 

epidemiological studies are viewed together, the observed greater effect on admissions 

for chronic obstructive respiratory disease is consistent with the observation from 

mortality studies -- suggesting stronger associations between respiratory related mortality 

and PM exposure.
Health Effects of Air Pollution

I - 7

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

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

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

elevated PM exposures. These observations are consistent with the hypothesis that 

increased susceptibility to infection follows PM exposures.

Some studies have reported that short-term PM exposure is associated with changes in 

lung function (lung capacity and breathing volume); upper respiratory symptoms 

(hoarseness and sore throat); and lower respiratory symptoms (increased sputum, chest 

pain and wheeze). The severity of these effects is widely varied and is dependent on the 

population studied, such as adults or children with and without asthma.

In contrast to the availability of data from population based studies, data from laboratory 

studies (human and animal) is insufficient to fully explain the potential causal 

mechanism associated with the severity of effects related to an incremental increase of 

10 μg/m3of PM10. In addition, most of the population-based studies suggest a linear 

relationship between morbidity and mortality versus ambient PM10 levels. However, the 

expected severity of effects is not always observable in areas with high ambient PM10

levels. This may be due to the fact that pollutant sources, as well as the concentration 

and combination of pollutants, vary significantly among different geographical areas.

Long-Term Exposure Effects

While many studies have evaluated the acute effects, two studies specifically focused on 

evaluating the effects of chronic exposure to PM10 and PM2.5. These studies have 

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

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

exposure to fine particles. A similar association was observable in both total number of 

deaths and deaths due to cardiorespiratory causes. A shortening of lifespan was also 

reported in these studies. The estimated range of relative risk of dying from long-term 

exposure to PM10 in U.S. cities is 17 to 37 percent. This estimate is substantially higher 

than the 3 to 20 percent estimated from acute effects studies.

In addition, long-term effects studies have reported an increased risk of mortality from 

lung cancer associated with PM exposures. A study involving Seventh Day Adventists 

has reported an association of cancer in females with increased particulate matter (total 

suspended particles) exposure. It is not clear from these studies whether the association 

relates to causation of disease, or whether individuals with cancer are more susceptible to 

other effects of particles leading to the observed mortality association.

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

information regarding the extent of life shortening or prematurity of death associated 
APPENDIX I: Health Effects

I - 8

with PM exposures. The relative risk estimates vary considerably depending on the type 

of study (acute vs. chronic) and also among studies within each group. Some attempts 

have been made in a broad sense to calculate the number of deaths associated with PM10

exposure by applying different statistical methods using the relative risk estimates of 

specific studies. However, U.S. EPA has concluded that although a substantial portion 

of deaths associated with long-term PM10 exposure may be independent of the daily 

deaths, quantification of the extent of life- shortening or the number of deaths directly 

associated with PM10 exposure from either types of studies is difficult.

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

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

from these studies suggests that ambient particulate matter, in concentrations below the 

current NAAQS alone or in combination with other coexisting pollutants is associated 

with significant increases in mortality and morbidity in a community.

Effects Associated with Fine and Coarse Fraction

The data to compare the adverse impact of fine versus coarse particles is quite limited in 

comparison to that of PM10 (which contains both coarse and fine mode fractions). 

However, multiple indicators of fine fraction ( PM2.5, sulfate, coefficient of haze, black 

smoke, carbonaceous material and hydrogen ion levels) are associated with short-term 

effects in over 15 cities located in different parts of the world. The health outcomes 

studied include mortality in sensitive population subgroups, increased hospitalization, 

respiratory symptoms and decreased lung function. In a long-term effects study 

involving over 500,000 people living in 151 U.S. cities, the mortality association was 

statistically more significant with fine particles and sulfates than with coarse particles.

In addition, controlled laboratory studies involving exposure of humans and animals to 

high levels of pollutants suggest: a) a higher percentage of fine fraction particle 

deposition in the lungs than of coarse fractions; b) a relative increase in cellular and 

immunological toxicity with fine fraction particle exposure (ammonium sulfate and 

nitrate) than with the coarse fraction (road dust); c) a wide range of short and long-term 

toxic effects with exposures to acid aerosols which are present in the fine fraction; and d) 

possible additive or synergistic effects when exposures include fine particles and other 

pollutants such as ozone, nitrogen dioxide or acids either in aerosol or vapor phase. 

Further research is required to evaluate whether the reported asthmatic effects are more 

closely associated with the coarse fraction of particles. Evidence is accumulating to 

indicate that fine particles are probably more toxic than coarse particles and that the fine 

fraction is responsible for most of the reported PM effects. In view of these observations, 

U.S. EPA has opted to consider the two fractions in PM10 as separate classes of 

pollutants and has recommended the development of a PM2.5 NAAQS which will assist 

in developing future controls to regulate this class of pollutants.
Health Effects of Air Pollution

I - 9

In summary, the scientific community concurs that: a) an increased risk of mortality and 

morbidity is associated with PM10 at levels below the current NAAQS; b) the evidence 

for PM effects is mostly derived from population studies; c) there are data gaps of 

supportive evidence from clinical and animal studies; d) although most of the effects are 

attributable to PM2.5, co-pollutant effects cannot be ruled out on the basis of existing 

studies; and e) the difficulty of separating the effects may be due to the fact that PM2.5

levels may co-vary with other combustion source pollutants, and hence, may serve as an 

index of air pollution from these sources instead of a separate pollutant by itself.

CARBON MONOXIDE (CO)

The high affinity of CO to bond with oxygen-carrying proteins (hemoglobin and 

myoglobin) results in reduced oxygen supply in the bloodstream of exposed individuals. 

It is that reduced oxygen supply which appears to be responsible for the toxic effects of 

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

have been studied in controlled laboratory environments involving exposure of humans 

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

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

known to be susceptible to the effects of CO, and protection of this group is the basis of 

the existing NAAQS for CO.4

Inhaled CO has no direct toxic effect on lungs but rather appears to exert its effects by 

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

chemical complex of CO and hemoglobin). Exposure to CO is often evaluated in terms 

of COHb levels in blood measured as percentage of total Hb bound to CO. COHb levels 

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

excess of 1.5% in a significant proportion of urban nonsmoking populations can be 

considered as evidence of widespread exposure to environmental CO.

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

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

consumption of oxygen. Studies involving subjects with ischemic heart disease who 

engaged in exercise during CO exposures have shown that COHb levels as low as 2.2% 

can lead to: a) earlier onset of electrocardiograph changes indicative of increased 

deficiency of oxygen supply to the heart; b) earlier onset of chest pain; c) increase in the 

duration of chest pain; and d) 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. These changes, 

however, are unlikely at observed ambient CO levels.

 

4

Federal Standard 9 ppm, 8-hour average; 35 ppm, 1-hour average. State Standard 9 ppm, 8-hour average; 20 ppm, 1-

hour average.
APPENDIX I: Health Effects

I - 10

NITROGEN DIOXIDE (NO2)

Evidence for low-level NO2 exposure effects is derived from laboratory studies of 

asthmatics and indoor population-based studies of homes with gas stoves as the exposure 

source. Additional supportive evidence is derived from animal studies.

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

NO2 exposures suggest an increased incidence of respiratory infections or symptoms in 

children. The same results have not been seen in similarly exposed adults. These studies 

have provided the basis for the consideration of the margin of safety provided by 

California’s short-term standard (0.25 ppm with a one hour averaging period).

Collectively, results from controlled exposure studies of asthmatics demonstrate an 

increase in the tendency of airways to contract in response to a chemical stimulus 

(bronchial reactivity) on exposure to <0.3 ppm NO2 for a period ranging from 30 minutes 

to 3 hours. A similar response is reported in some studies with healthy subjects at higher 

levels of exposure (1.5 - 2.0 ppm). Mixed results have been reported when people with 

chronic obstructive lung disease are exposed to low levels of NO2.

Short-term controlled studies of animals exposed to <0.3 ppm of NO2 over a period of 

three hours indicate cellular changes associated with allergic and inflammatory response 

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

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

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

ozone and NO2.

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

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

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

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

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

both in population and animal studies of increased susceptibility to infections, as a result 

of NO2 exposure.

SULFUR DIOXIDE (SO2)

Controlled laboratory studies involving human volunteers have clearly identified 

asthmatics as the most sensitive group to the effects of ambient SO2 exposures. Healthy 

subjects have failed to demonstrate any short-term respiratory functional changes at 

exposure levels up to 1.0 ppm over 1-3 hours.
Health Effects of Air Pollution

I - 11

In asthmatics, brief (10 minutes) exposure to SO2 at levels as low as 0.255ppm can result 

in significant increases in airway resistance as well as decreases in breathing capacity. In 

some, the exposure can result in severe symptoms necessitating the use of medication for 

relief. The response to SO2 inhalation is observable within 2 minutes of exposure, 

increases further with continuing exposure up to 5 minutes then remains relatively steady 

as exposure continues. SO2 exposure is generally not associated with any delayed 

reactions or repetitive asthmatic attacks.

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

of exposure to co-pollutants (ozone or nitrogen dioxide) prior to or in conjunction with 

SO2 exposure.

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

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

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

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

allergies is observable in guinea pigs repeatedly exposed to high levels (72 ppm) of SO2. 

This effect needs further evaluation in clinical and population studies to identity the 

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

Some epidemiological studies indicate that the mortality and morbidity effects associated 

with the fine fraction of particles show a similar association with ambient SO2 levels. In 

these studies, efforts to separate the effects of SO2 from fine particles have not been 

successful. Thus, it is not clear whether the two pollutants act synergistically, or whether 

being generated from similar combustion sources they represent the same pollution index 

for the observed effects.

SULFATES

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

California Air Resources Board in 1976 adopted a standard of 25 μg/m3(24-hour 

average) for sulfates. In addition, U.S. EPA has concluded that 24-hour average sulfate 

concentrations of 8-10 μg/m3can aggravate symptoms in people with respiratory 

disease(s) and can affect lung function in children.

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

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

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

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

the fact that these pollutants co-vary under ambient conditions having been emitted from 

 

5

Federal Standard .03 ppm, annual average; .14 ppm, 24-hour average. State Standard .05 ppm, 24-hour average; .25 

ppm, 1-hour average.
APPENDIX I: Health Effects

I - 12

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

rather than a single pollutant.

Clinical studies involving exposure of human subjects to sulfuric acid aerosol (<100 

μg/m3) have indicated that adolescent asthmatics may be a susceptible population 

subgroup. Lung function changes (volume and resistance to air flow) are observable in 

this subgroup as well as in people with chronic obstructive lung disease such as chronic 

bronchitis and emphysema.

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

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

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

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

States and Canada where sulfate concentrations are higher than for those observed in the 

western United States. Mixed results have been reported from studies which attempted 

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

CONCLUSION

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

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

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

instances, earlier mortality and air pollution.
ATTACHMENT 1

STATE OF THE ART - HEALTH EFFECTS OF 

OUTDOOR AIR POLLUTION

Reprinted with permission from the editor of

American Journal of Respiratory and Critical Care Medicine

Note: Copies of this attachment are not available on electronic media.

For a copy, contact:

Public Information Center

South Coast Air Quality Management District

21865 E. Copley Drive

Diamond Bar, CA 91765