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Woodward-Clyde Consultants 

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TABLE OF CONTENTS 

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Chapter 1, INTRODUCTION 

1.1 The Ambient Carbon Monoxide Problem 

1.2 Organization of the Report 

Chapter 2. HEALTH EFFECTS OF LOW-LEVEL EXPOSURE TO CO:' 

SUMMARY OF EMPIRICAL AND EPIDEMIOLOGICAL FINDINGS 

2.3 

2.4 

Health Effects on Cardiovascular Patients 

Health Effects on Chronic Obstructive Pulmonary 

Disease Patients 

Health Effects on Fetuses and Young Children 

Health Effects on General Populace 

11 

11 

14 

Chapter 3. STRUCTURE OF RISK ASSESSMENT MODEL 16 

3.1 Overview of the Risk Assessment Model 

3.2 Components of the Risk Assessment Model 

16 

17 

Chapter 4. EXPOSURE TO CARBON MONOXIDE 22 

4.1 Ambient CO Quality 

4.2 Human Exposure to CO 

4.3 Physiological Response to CO 

22 

23 

24 

Chapter 5. EXPERTS' RISK ASSESSMENTS OF HEALTH EFFECTS FROM 

LOW-LEVEL EXPOSURE TO CARBON MONOXIDE 27 

5.1 Selection of Health Experts and Interview Style 

5.2 The Health Effects Assessment Procedure 

5.3 Summary of Health Effects and Risk Measures 

5.4 Synopsis of the Health Effects Assessments 

28 

29 

33 

36 

Chapter 6. DOSE-RESPONSE RELATIONSHIPS RELATING COHb 

LEVELS TO HEALTH EFFECTS 46 

6.1 Dose-Response Relationships for Major Health Effects 

6.2 Dose-Response Relationships for Other Health Effects 

48 

51 
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Chapter 7. ESTIMATES OF RISK 

7.1 Combination of Exposure Data and Dose-Exposure 

Relationships 

7.2 Risk Estimates for Four Cities 

7.3 Analysis for Sensitive Groups 

7.4 Analysis for Special Exposure Group 

7.5 Risk Estimates for the U.S. Urban Population 

7.6 Sensitivity Analysis 

55 

55 

65 

68 

70 

71 

72 

r\ 

Chapter 8. SUMMARY AND DISCUSSION 

8.1 Summary of the Analysis 

8.2 Discussion of the Results 

8.3 Potential Refinements of the Analysis 

74 

74 

78 

79 

APPENDIX A. Representative interviews with experts. 

REFERENCES 

FIGURES and TABLES 

83 

96 

102 
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:v+ Chapter 1. INTRODUCTION 

It is well known that exposure to air pollution can have adverse 

health effects on some members of the public. Recognizing this, Congress 

passed the Clean Air Act Amendments of 1970 and 1977, which require the 

Administrator of The Environmental Protection Agency (EPA) to set primary 

national ambient air quality standards to protect the public health with an 

adequate margin of safety. However, the problem of determining an appropriate standard for any particular pollutant is difficult for several 

reasons: 

1. there are usually several different health effects attributable 

to exposure to a pollutant, 

2. there are many experts knowledgeable about the particular health 

effects of a pollutant, perhaps with differing views, 

3. the best available data relating exposure to health effects has 

numerous shortcomings: it is extrapolated from small control 

groups observed under laboratory conditions, inferred from 

laboratory studies involving animals, or observed from actual 

societal circumstances (e.g., during a smog alert) where numerous 

possible "extraneous" effects can not be controlled, 

4. there is significant uncertainty about the relationship between 

proposed standards and resulting human exposure since this 

depends on factors such as the meteorology which dilutes and 

distributes the pollutants and activity patterns and locations of 

humans, 
if' 

5. many different types of alternative standards are available 

including combinations which limit the concentration of the 

pollutant, specify the time period over which concentration is 

measured, and indicate the number of times the limit can be 

exceeded before the standard is violated, 

6. the need to utilize value judgments in deciding which health 

effects are categorized as adverse and the relative importance of 

the different types of health effects. 

The complexity of appraising alternative standards is clearly sufficient to 

rule out the possibility that a reasonable selection can occur without the 

insights that can be provided by a thorough analysis. In addition, such an 

analysis can be useful in documenting and justifying the appropriateness of 

the alternative chosen. 

The purpose of this report is to demonstrate the development and presentation of an analysis of possible ambient air quality standards for one 

major pollutant, carbon monoxide (CO). The analysis is conducted to 

address explicitly the six complexities inherent in such standard-setting 

problems and to illustrate a methodology, not to develop an analysis which 

is to be used in standard setting at this time. Specifically, we develop a 

risk assessment model to relate adverse health effects to alternative 

carbon monoxide standards. The problem is decomposed into manageable 

portions, corresponding to fields of expertise. The risk assessment 

involves a blend of information gathering and modeling to quantify and 

synthesize all the available information, including the professional 

judgments of several experts as well as experimental data. Quantitative 

estimates are obtained for selected summary measures of adverse health 
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».^ effects,'and uncertainty is recognized formally in terms of probability 

distributions. 

1.1 The Ambient Carbon Monoxide Problem 

This section briefly outlines the problem addressed by specifying the 

objectives chosen for the analysis and the alternative standards examined. 

Based on the available information about exposure to carbon monoxide, 

the major health effects appear to be the possibility of increased angina 

attacks and increased heart attacks (i.e., myocardial infarction), some of 

which may be fatal. In addition, other effects include the aggravation of 

angina, peripheral vascular disease (PVD), chronic obstructive pulmonary 

disease (COPD), vigilance impairment, and increased health effects for 

newborns when mothers were exposed. The objective for the problem was to 

provide a risk assessment for these health effects associated with exposure 

to carbon monoxide. In this risk assessment, we develop quantitative 

estimates (including probabilities) of the occurrence of each health effect 

for each proposed standard. 

There were eight alternative standards analyzed in the study. The 

standards, which were specified by the EPA, were defined in terms of three 

parameters: the minimum allowable quality of air (i.e., daily maximum 

allowable pollution concentration) indicated by parts per million of CO 

averaged over time, the time period (i.e., the averaging time) over which 

this level must be obtained, and the expected number of exceedances allowed 

per year. The eight alternatives are summarized in Table 1.1. Alternative 
J. 

1, the status quo as of 1981, represents not just a standard, but the ^ 

overall air quality situation associated with 1981 standards, regulations 

concerning emission reductions, enforcement programs, and so on. 

1.2 Organization of the Report 

This report is organized as follows. Background information concerning the health effects of exposure to CO is summarized in Chapter 2. The 

overall structure of the risk assessment model is presented in Chapter 3 

with emphasis on the decomposition of the problem into manageable component 

models. Chapter 4 summarizes the exposure model used to relate CO standards to actual person-exposure measures. The gathering of information 

about adverse health effects and the choice'of final risk output measures 

is discussed in Chapter 5. The dose-response curves relating such measures 

to the level of exposure are developed in Chapter 6. The risk estimates 

for each standard are given in Chapter 7, and Chapter 8 contains a brief 

summary and some concluding comments. 
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Chapter 2. HEALTH EFFECTS OF LOW-LEVEL EXPOSURE TO CO: SUMMARY OF 

EMPIRICAL AND EPIDEMIOLOGICAL FINDINGS 

The mechanism by which exposure to CO results in health effects is 

succinctly described in U.S. EPA [1980] as follows: 

"EPA interprets the existing health effects evidence to indicate that 

the principal mechanism of CO toxicity is through hypoxemia (deficient 

oxygenation of the blood). This mechanism suggests that adverse 

effects on the body result from the strong affinity of blood 

hemoglobin for CO (over 200 times greater than for oxygen), which 

results in the formation of carboxyhemoglobin (COHb). Thus, the 

oxygen-carrying capacity of the blood is reduced since hemoglobin that 

has combined with CO in this manner is not available to transport 

oxygen; furthermore, the presence of COHb inhibits the release of 

oxygen from the remaining hemoglobin. Effects on the cardiovascular, 

central nervous, pulmonary, and other systems are directly related to 

this reduction in the ability of the blood to deliver oxygen to these 

systems." 

The EPA Criteria Document for Carbon Monoxide (EPA [1979]) provides a 

detailed review and scientific assessment of the effects of CO exposure on 

COHb level and on health. The groups of individuals that appear most 

sensitive to CO exposure are cardiovascular patients, chronic obstructive 

pulmonary disease patients, and pregnant women with their fetuses. This 

section summarizes empirical and epidemiological evidence on the effects of 

low-level CO exposure to members of these sensitive groups, although 
effects on individuals not in these groups are also mentioned. For a much 

more detailed review of the effects of CO exposure on COHb level (measured 

as the percent of concentration in the blood) and on health, see the 

Criteria Document (EPA [1979]). A shorter review is provided by Goldsmith 

and Landaw [1968]. 

Before proceeding, it is important to mention that the group with the 

highest levels of COHb in the blood is smokers. The levels caused by smoking generally exceed those resulting from exposure to air pollution. Thus, 

the contribution of air pollution to COHb levels in a smoker is usually 

much less than the contribution attributable to smoking. Because of this 

circumstance and the fact that smoking is a voluntary activity, the EPA 

directed that this study not address CO-related health effects for smokers. 

The health effects of concern relate to low-level CO exposure due to air 

pollution. 

2.1 Health Effects on Cardiovascular Patients 

U.S. EPA [1979] review the effects of CO on cardiovascular patients. 

Major health effects include aggravation of angina pectoris and peripheral 

vascular disease, and possible increased mortality from heart attacks 

(i.e., myocardial infarction). Angina pectoris is a cardiovascular disease 

in which mild exercise or excitement produces symptoms of pressure and pain 

in the chest because of insufficient oxygen supply to the heart muscle. 

Available health effects data indicate that persons with angina and other 

types of coronary heart disease probably incur the greatest risk from 

low-level ambient exposures to CO. Angina patients who have been exposed 
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to low levels of CO while resting have subsequently exhibited, during 

exercise, reduced time to onset of angina and increased duration of angina 

attacks. 

Aggravation of angina may be the first in a series of progressively 

more serious symptoms that accompany cardiovascular disease. Coronary 

insufficiency is a more serious symptom that occurs at greater levels of 

oxygen deprivation. The most serious symptom in this series is myocardial 

infarction (i.e., a heart attack), which may result in longer and more 

intense pain and irreversible heart damage or possibly death. Categorized 

as peripheral vascular disease are a number of different diseases, the 

major type being arteriosclerosis. Low-level CO exposure aggravates 

peripheral vascular disease by decreasing the time to onset of pain. These 

effects are discussed in U.S. EPA [1980]. 

Aggravation of Angina Pectoris. Several experiments have exposed individuals to CO. Aronow [1981], Aronow and Isbell [1973], and Anderson et al. 

[1973] directly exposed subjects to CO in laboratory settings. Aronow 

[1978] put subjects in ventilated or unventilated rooms filled with tobacco 

smoke containing CO and other pollutants. Finally, Aronow et al. [1972] 

had subjects breathe air while riding in an open car on Los Angeles freeways. These experiments have shown that angina pectoris patients, upon 

exposure to CO, experience a decrease in the amount of time they are able 

to exercise before the onset of anginal pain. The degree of time-reduction 

until onset of angina is positively related to the COHb level. 
.< The data for the subjects in the above experiments are summarized in 

Table 2.1. Excluding Aronow's [1978] tobacco smoke study, these data are 

plotted in Figure 2.1. Using linear regression, the best-fitting representation of the percent decrease in time until anginal pain (PDEC) as a 

function of the COHb concentration is 

PDEC = 2.56 + 4.63 (COHb) 

for COHb levels ranging from 1.3 to 8 percent. Thus, for each percentage 

increase in the COHb level, the time until onset of pain decreases an 

average of 4.63 percent. Note that there is considerable deviation among 

individual patients from this model, as evidenced by the data points in 

Figure 2.1. This regression line was fitted by us. The value of the 

2 

correlation coefficient (R ) was 0.166 - undoubtedly a low value. 

Subsequently, we do not use this relationship in our risk assessment. 

Aggravation of Peripheral Vascular Disease. Aronow et al. [1974] studied 

the effect of CO exposure on men with intermittent claudication of the calf 

or thigh due to occlusive arterial disease. After CO exposure, the mean 

COHb level was 2.77 percent and there was a 17 percent decrease in time 

until exercise-induced onset of pain. Studies relating other COHb levels 

to decreased time until pain have not been reported. 

Increased Risk of Death by Myocardial Infarction. Epidemiological studies 

suggest that there may be an increased risk of death by myocardial infarction (MI) as the CO in ambient air is increased. In a study by Kurt et al. 

[1978, 1979] in Denver, a positive relationship was observed between the 

ambient CO levels and the number of respiratory and cardiovascular complaints. The specific health effect which has been reported is decreased 
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exercise performance. Cohen et al. [1969] found a significantly higher 

fatality rate among hospital admissions for myocardial infarctions in 

"more-polluted" Los Angeles areas. This association only held for the 13 

weeks during 1958 which had the highest overall weekly mean CO pollution 

levels in the range 7.7-14 ppm. For the less-polluted weeks of that year, 

the fatality rates were similar in both the "more-polluted" and "lesspolluted" areas. A study in Baltimore (Kuller et al. [1975]) at lower 

ambient CO levels did not detect an increased mortality rate. Radford 

[1975] found MI patients' diagnoses to be consistent with the effects of CO 

on the myocardium, though the effects could not definitely be attributed to 

CO exposure. 

In support of Cohen et al., Hexter and Goldsmith [1971] built a multiple linear regression model which related daily mortality in 1962-1965 

for Los Angeles County to the logarithm of the daily mean CO concentration 

and other independent variables including temperature and day of year to 

adjust for cyclical variations. The result indicated 

(Total deaths/day) = (all other factors) + 24.94 log(CO), 

where CO is measured in parts per million. Note that when the CO level 

changes from 7.3 ppm to 20.2 ppm, there is an increase of 24.94 (log 20.2-

log 7.3) = 11 in total deaths per day. Using this model, there would be an 

estimated 11 more deaths/day if the CO level changed from the minimum 

observed level of 7.3 daily mean ppm to the maximum of 20.2 daily mean ppm. 

10 
2.2 Health Effects on Chronic Obstructive Pulmonary Disease Patients * 

There is little information available on the effects of CO on chronic 

obstructive pulmonary disease patients. Aronow et al. [1977] conducted an 

experiment in which chronic obstructive pulmonary disease patients were 

exposed to CO. The.mean COHb level after CO exposure was 4.08 percent. 

Compared to before exposure there was a 33 percent reduction in time until 

marked exercise-induced dyspnea after CO exposure. The authors indicated 

that they believe this significant reduction in exercise performance is due 

to cardiovascular limitations. 

2.3 Health Effects on Fetuses and Young Children 

U.S. EPA [1979, 1980] and the Surgeon General's 1979 report on 

"Smoking and Health" and the 1980 report on the "Health Consequences of 

Smoking for Women" summarized the effects of CO-containing tobacco smoke on 

fetuses and young children. Longo [1977] reviewed studies of the effects 

of CO on pregnant animals and humans. Major health effects include 

increased perinatal mortality, increased congenital abnormalities, and 

below-normal birth weights. 

Increased Perinatal Mortality. In a laboratory experiment, Astrup et al. 

[1972] observed increased neonatal mortality rates among pregnant rabbits 

exposed to moderate amounts of CO. Obvious ethical considerations make it 

impossible to conduct a similar experiment for human females. However, 

epidemiological studies of pregnant women who voluntarily expose themselves 

to CO in tobacco smoke have been conducted. Though CO is combined with 

11 
P.15 

other substances in tobacco smoke, the experimental mammalian studies 

strongly suggest that the CO in smoke is, at least in part, responsible for 

the infants' deleterious health effects. 

The perinatal (i.e., late fetal and early neonatal) mortality rate has 

been shown to increase as the number of cigarettes smoked daily increases. 

Meyer et al. [1976] report Ontario (Canada) perinatal mortality rates 

(after adjusting for other factors) for nonsmokers, daily smokers of less 

than a pack, and for smokers of a pack or more a day. Light smokers' 

(daily smokers of less than a pack) babies had a 20 percent greater chance 

of death. Heavy smoking led to a 35 percent greater chance of death 

among the heavy smokers' babies. Meyer et al. [1975] described the similar 

results of a collaborative perinatal study for twelve United States centers 

for black and white women. Finally, Rantakallio [1969] reported perinatal 

mortality rates for smoking and nonsmoking mothers in North Finland. Each 

study used different definitions for light and heavy smokers, so only an 

approximate comparison of the observed'mortality rates is possible as shown 

in Figure 2.2. 

Though these studies linked maternal smoking level to the perinatal 

mortality rate, they did not identify the maternal COHb levels corresponding to various smoking levels or mortality rates. According to Longo's 

[1977] review, the COHb concentration in normal nonsmoking pregnant women 

is usally 0.5 to 1.0 percent. Smoking mothers' COHb levels at time of 

birth have ranged from 2 to 14 percent, though these may be lower than the 

average COHb during the pregnancy. Haddon et al. [1961] observed a mean 

COHb level of 6.2 percent when at least one cigarette was smoked within an 

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hour of delivery. When at least one cigarette was smoked 1 to 24 hours 

prior to delivery, a mean COHb of 3.6 percent was observed. 

Increased Congenital Abnormalities. In laboratory experiments, upon maternal CO exposure, mice and rabbits developed minor skeletal alterations 

(Schwetz et al. [1975]), and rabbits had limb deformities (Astrup et al. 

[1972]). Human smoking studies suggest that these CO-related health 

effects in animals may also occur in humans. Andrews [1972] reported that 

2.37 percent of nonsmokers' children have congenital abnormalities, which 

increased to 2.73 percent for smokers' offspring. Himmelberger [1978] 

presented the risk of these abnormalities for different smoking and age 

levels, as shown in Figure 2.3. 

Below-Normal Birth Weight. In laboratory experiments, moderate maternal CO 

exposure led to decreased infant birth weights among rabbits (Astrup et al. 

[1972]) and rats (FeChter and Annau [1976]). Human smoking studies suggest 

that this CO-related event may also occur in humans exposed to ambient CO 

levels. 

Increasing levels of maternal smoking are linked with lower birth 

weights (Meredith [1975]) and greater risks of prematurity (Meyer [1977]). 

During childhood, progeny of smoking mothers in Finland were hospitalized 

more often and had more doctor's visits, as shown in Table 2.2 (Rantakallio 

[1969]). 

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2.4 Health Effects on the General Populace 

The major health effects of moderate CO exposure on the general 

populace are decrements in vigilance and limitations on work capacity. 

Decrements in Vigilance. Many effects of CO on the central nervous system 

have been studied, including altered sleep patterns (O'Donnell et al. 

[1971], Groll-Knapp et al. [1978], and Haider et al. [1976]), time discrimination (Beard and Wertheim [1967]), eye-hand coordination (Johnson et al. 

[1974]), and driving tasks (Wright et al. [1973]). The studies of decrements in vigilance will be summarized here as representative of central 

nervous system health effects. Six studies of the relationship of moderate 

CO exposure with vigilance performance are listed in Table 2.3. Four 

studies report decrements in vigilance, though two studies found no change. 

Horvath et al. [1971] exposed subjects to 0, 26, and 111 pp'm CO for 

over two hours. During exposure, performance on a visual vigilance task 

was monitored. When exposed to 111 ppm CO, initially there was a significant decrement in vigilance performance, but this began improving after 

approximately 37 minutes. Figure 2.4 from O'Hanlon [1972] shows the vigilance performance and Table 2.4 from Horvath et al. [1971] contains the mean 

COHb levels with their ranges. Fodor and Winneke [1972] and Groll-Knapp et 

al. [1972] observed decrements in vigilance though they did not report actual COHb levels. Beard and Grandstaff [1975] found that end-of-vigilancetest mean COHb values of 1.8, 5.2, and 7.5 percent were associated with 

decreases in correct numbers of responses of 14, 16, and 8 percent respectively. 

14 
Decrement in Work Capacity. Moderate CO exposure impairs exercise performance (as measured by maximal aerobic power, V MAX) in healthy people. 

Horvath et al. [1975] observed statistically significant decreases in 

maximal aerobic power when COHb levels exceeded a threshold of 4.3 percent. 

The relationship between COHb level and decrement in nonsmokers' maximum 

aerobic power (PDEC=percent decrease in power) is modeled by 

PDEC = 2.2 + 0.91 (COHb), 

where COHb is indicated in percent. This linear relationship is plotted in 

Figure 2.5 and is reproduced from U.S. EPA [1979]. It represents the data 

from Horvath's group and other similar studies. As stated in U.S. EPA 

[1979],the relationship does not apply to smokers in Horvath's series, who 

had COHb levels in excess of 4 to 5 percent with no decrement in their 

respective V MAX values. As can be seen from Figure 2.5, the linear fit 

is not accurate indicating a considerable deviation among individual 

patients from this model. Weiser et al. [1978] report a similar model 

based on their study and others. This model is 

PDEC = 0.35 + 1.08(COHb). 

15 
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Chapter 3. STRUCTURE OF RISK ASSESSMENT MODEL 

A risk assessment model for an air pollutant is intended to relate air 

quality standards to risk output measures. To evaluate alternative standards, the key information is the relationship between a standard and the 

health effects that the public may experience if this standard is established. Simply stated, we would like to know for each alternative CO 

standard, how many people are expected to suffer health effects and what is 

the magnitude or seriousness of these health effects. 

3.1 Overview of the Risk Assessment Model 

As indicated in Figure 3.1, the basic input to the risk assessment 

model is an alternative standard for ambient CO. The eight specific standards evaluated in this study are listed in Table 1.1. The status quo 

refers to the air quality as it currently exists. The other standards are 

defined by three parameters indicating the standard level in parts per 

million (ppm), the time period over which concentrations should be averaged 

to examine compliance, and the expected number of exceedances allowed per 

year. Thus, for instance, one standard examined in this study was 9 ppm 

using an 8 hour average with allowable exceedances occurring on at most 5 

days per year on the average. This means that a pollution incident is 

recorded whenever the daily maximum 8-hour average ambient CO level exceeds 

9 ppm. If the expected number of incidents in a year is six or more, then 

the standard is violated. 

16 
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The output measures for the risk assessment model estimate the number 

of cases that may occur (including information regarding the likelihood of 

occurrence) due to elevated ambient CO levels for the following health 

effects: angina attacks, nonfatal heart attacks, fatal heart attacks, 

premature births, vigilance impairment, and aggravation of angina, chronic 

obstructive pulmonary disease, and peripheral vascular disease. Some 

background information concerning these health effects as a result of 

exposure to CO was presented in Chapter 2, and a detailed discussion of 

such health effects, including the development of the specific risk output 

measures, is found in Chapter 5. This section presents the overall 

structure of the risk assessment model. More details about specific 

portions of the model are provided in Chapters 4 through 7. 

3.2 Components of the Risk Assessment Model 

The relationship between a specific ambient CO standard and risk 

output measures involving adverse health effects is obviously a very 

complex relationship. For example, consider a typical question about this 

relationship: How many additional angina attacks might be expected to 

occur under a CO standard of 35 ppm using a 1 hour average with 1 expected 

exceedance per year than under a CO standard of 25 ppm using a 1 hour 

average with 1 expected exceedance per year? No data bearing directly on 

this question are available, and no expert could be expected to be able to 

provide a reliable answer to the question. Information (i.e., data, 

expertise) from several fields such as meteorology, physiology, and 

medicine would be relevant. Thus, we need to decompose the problem into 

more manageable components corresponding to specific types of information. 

17 
P.21 

These components are then analyzed and logically integrated to gain insight 

and information about the overall problem. 

The decomposition of a complex problem into more manageable parts is 

based on the "divide and conquer" spirit of decision analysis (see Raiffa 

[1968]). The nature of this decomposition is what we refer to as the 

structure of the risk assessment model. It is dictated to a large extent 

by the types of information that are both useful and obtainable. The 

decomposition, shown in Figure 3.2, illustrates component models to 

consider the following: 

1. the relationship between a CO standard and the ambient 

air quality in terms of ambient CO levels, 

2. The relationship between ambient CO levels and the degree of 

exposure of people to different CO levels, 

3. the physiological responses of people to their exposure to CO, 

4. the adverse health effects related to physiological responses, 

5. the relationship between individual adverse health effects and 

specific risk output measures. 

Admittedly these relationships are not simple, but when considered individually they are obviously less complex than the overall relationship between 

standards and risk measures shown in Figure 3.1. Collectively they provide 

a reasonable manner to characterize the overall relationship. We will 

briefly describe each component model in this section; more details concerning components 1-3 are given in Chapter 4 and more details concerning 

components 4 and 5 are found in Chapters 5 and 6. 

18 
The first component model involves the relationship between a CO 

standard and the ambient levels of CO. The standard is simple (e.g., 35 

ppm, 1 hour average, 1 expected exceedance per year) and is not sufficient 

to indicate how often various levels of CO below the standard will occur. 

For example, how often will the 1 hour average exceed 20 ppm for a specific 

standard? The air quality at a given location depends not just on the 

standard, but on meteorological conditions and the nature of the location. 

For example, the level of CO near a busy street is usually higher than in 

the middle of a large park. The basic output from the component model 1 is 

a set of distributions of CO levels for different types of locations at 

different times. 

Given distributions of ambient CO levels, the exposure of individuals 

will still vary. An individual's exposure depends on his or her activities 

and movement from location to location at different times. Thus, the 

second component model depends on the activity patterns within the population of interest. Someone who commutes across a city daily will have a 

different distribution of exposure than someone who stays at home most of 

the time. The output of the component model 2 is a distribution of CO 

exposure levels among the members of a population over time. 

What happens when a person is exposed to a high concentration of CO in 

the air? The primary physiological response is an increase in the level of 

carboxyhemoglobin (COHb) in the blood. Component model 3 relates COHb 

levels to CO exposure. This provides a distribution of COHb levels across 

people and across time. 

19 
P.23 

In the fourth component model we are finally ready to consider health 

effects. An elevation in COHb level in the blood may lead to the adverse 

health effects indicated in Chapter 2. For example, increased COHb tends 

to reduce the time until the onset of an angina attack and may cause decrements in performance for people doing tasks that require vigilance. Component model 4 concerns the 'relationship between increased COHb levels and 

various adverse health effects. For example, if the COHb level is increased from its "normal" value to a particular higher-than-normal level, what 

percentage of angina patients will have additional attacks? Component 

model 4 can be thought of in terms of probabilistic dose-response relationships. The COHb level represents the dose, and the response is measured in 

terms of the probability of various health effects to an individual. 

Finally, the fifth component model translates individual health 

effects into specific risk output measures. Combining information from the 

earlier components with data regarding the number of people suffering from 

angina will enable us to estimate the additional number of angina patients 

having additional attacks, using probabilities as well as point estimates. 

The structure of the risk assessment model shown in Figure 3.2 represents the decomposition of the risk assessment that seems most appropriate 

to examine alternative ambient CO standards. It is possible to obtain 

information necessary for the component models in this decomposition using 

expertise most pertinent to each component. Fortunately, EPA had previously collected and integrated the information necessary for the first three 

component models into an overall exposure model. This enabled us to expend 

more time and effort on the other components. Models corresponding to com20 
ponents 4 and 5 necessary to relate COHb levels to the number of CO-induced 

health effects were not previsouly available. We found that medical 

experts could provide useful information about health effects associated 

with different COHb levels. Thus, for each portion of the risk assessment 

model, we were able to obtain the most reliable information available given 

the cost and time constraints of this study. 

After the individual components of the risk assessment model are 

investigated, it is necessary to combine them to provide insights and 

understanding about the relative impacts of different standards. Briefly, 

this means that a standard results in a distribution of CO levels in the 

air, which can be combined with component model 2 to yield a distribution 

of CO exposure levels in a 'population. This, in turn, can be combined with 

component model 3 to provide an overall distribution of COHb levels, which 

is then used as an input to component models 4 and 5. This provides the 

desired information in terms of the selected risk output measures. By 

going through this process for different standards, we can relate the 

number of cases of health effects to the standards, which is the intent of 

the risk assessment model. 

Having provided an overview of the general structure of the risk 

assessment model, we turn to more detailed discussions of the individual 

components. The standard/air quality/exposure/physiological response 

portion of the model (i.e., components 1, 2, and 3) is discussed in Chapter 

4, information about health effects is described in Chapter 5, and the 

development of dose-response relationships is covered in Chapter 6. 

21 
Chapter 4. EXPOSURE TO CARBON MONOXIDE 

The Office of Air Quality Planning and Standards (OAQPS) of the EPA 

has developed a general "National Ambient Air Quality Standard (NAAQS) 

Exposure Model" (NEM) to estimate population exposures associated with 

possible standards. The structure of this model corresponds to the first 

three components of the risk assessment model presented in Chapter 3. 

Details about the NAAQS exposure model are found in Biller et al. [1981] 

and Johnson and Paul [1981], Our study used the output of NEM to generate 

exposure estimates associated with the various CO standards under considerion. Hence, the general approach taken in NEM and the nature of its output 

are discussed briefly in this chapter. The discussion addresses the first 

three components of the risk assessment model in Figure 3.2 in order. 

4.1 Ambient CO Quality 

The first component involves the relationship between a standard for 

CO and the distribution of CO levels in the air. Of course, it is not 

feasible to measure distributions of CO levels under various hypothetical 

standards. Actual measurements involve the air quality "as is," and such 

data have been collected at selected monitoring sites. The.sites were 

chosen to represent specific "neighborhood types." In addition to the data 

collection stage, some emphasis was given to data validation, including the 

use of time series models to fill in gaps in data sets. 

Since the air quality data represent the CO levels "as is," adjustments are necessary to determine the air quality that would be expected 

22 
P.26 

under alternative CO standards. This is accomplished by NEM with a 

so-called "rollback model," which adjusts CO levels in relation to 

background CO by proportionally adjusting CO levels above a background 

level so that the most polluted monitor (neighborhood type) just attains 

the standard. Parameters of the rollback model were estimated by EPA to 

simulate the air quality expected under different standards. This provides 

a distribution of CO levels at different types of locations (e.g. 

center-city residential, suburban commercial, center-city industrial) at 

different times. For purposes of the risk assessment, it is assumed that 

the respective standard is just met. Thus, if 5 exceedances are allowed, 

it is assumed that exactly 5 exceedances occur. 

4.2 Human Exposure to CO 

The next step is to translate air quality data into exposure data. We 

may know how often a certain CO level tends tfo occur at different loca--

tions, but the relevant question for a health risk assessment is how often 

people are actually exposed to that level of CO. The answer to this 

question requires considerable information about the activity patterns of 

members of the population of interest. Such information is provided by a 

human activities data base (Roddin et al. [1979]) developed for OAQPS. The 

data on activity patterns was used to separate the population into cohort 

groups, which are groups of people who live in the same type of neighborhood, work in the same type of neighborhood, are members of the same 

age-occupation class, and have similar activity patterns. A single cohort 

can then be used to represent an entire group. The cohort is assigned (on 

an hourly basis) to a neighborhood type, a microenvironment (e.g., indoors 

23 
P.27 

at work, in a vehicle, outdoors), and an activity level (low, medium, or 

high). The information on activity level does not actually influence 

exposure, but is necessary to estimate the physiological response to that 

exposure as indicated in the next subsection. 

The exposure model simulates typical movements of cohorts and the 

distribution of CO levels at different types of locations at different 

times. These are combined to produce an overall distribution of human 

exposure to CO. This exposure is measured in several ways (e.g., pollutant 

encounters, number of people exposed, number of people at peak exposure) 

for different averaging times (e.g., one-hour, eight-hour). Examples of 

the output of the exposure model for CO are given in Tables 4.1-4.3. 

4.3 Physiological Response to CO 

As discussed in Chapter 2, exposure to CO leads to increased COHb 

levels in the blood. "The primary factors determining the final level of 

COHb in individuals are the following: concentration of CO inhaled, 

duration of exposure, alveolar ventilation rates (which depend on the level 

of activity), initial COHb level, endogenous CO production, blood volume, 

hemoglobin concentration, relative affinity constant of hemoglobin for CO 

and oxygen (0„) barometric pressure, and relative diffusive capability of 

the lungs" (U.S. EPA [1980]). 

"When individuals inhale air containing a constant concentration of 

CO, several hours are required for them to reach a state of equilibrium, at 

which point the COHb level in the body no longer increases. For a given CO 

24 
P.28 

level, the time required to reach equilibrium is influenced by a number of 

factors, the most important for normal individuals being the level of 

activity as measured by the alveolar ventilation rate (V ). At low levels 

of activity (rest/intermittent light activity, V =5-10 L/min), approximately 8-12 hours are needed for equilibrium to be achieved. For moderate 

exercise (equivalent to 3 mph walking on level ground or light industry or 

housework), V =20 L/min, and the equilibrium level of COHb may be reached 

in half that time" (U.S. EPA [1980]). 

Normally, individuals are not exposed to constant concentrations for 

long periods of time. The Coburn model (Coburn et al. [1965]) permits the 

calculation of COHb concentration as a function of time, with the physiological factors previously mentioned considered. EPA believes the Coburn 

model predicts with reasonable accuracy the typical COHb levels resulting 

from specified CO exposures for non-equilibrium situations. Thus, the 

Coburn model allows one to obtain information on COHb levels resulting from 

short-term CO exposures. 

The final step performed as part of the "exposure analysis" converts 

the data regarding CO exposure to data regarding COHb exposure using the 

Coburn model. Examples of the output of the exposure model for COHb are 

given in Tables 4.4-4.6 and Figures 4.1-4.2. In words, the primary 

measures of interest are: 

1. The annual number of person-hours with a COHb level greater 

than x, for various values of x. 

2. The annual number of person-days with at least one hour of a 

COHb level greater than x, for various values of x. 

25 
P.29 

3. The annual number of person-years with at least one hour of 

a COHb level greater than x, for various values of x. 

These measures were determined for all of the standards under consideration 

and for four cities (Los Angeles, Philadelphia, Chicago, and St. Louis). 

In an additional analysis (called Special Group), a particular subset 

of the population of each city was considered. This subset is intended to 

represent individuals with restricted activities. Parameters were chosen 

to limit the cohorts to those with the characteristics such as chronic 

obstructive pulmonary disease. The same type of exposure analysis run for 

the entire population was run for this special group. 

Disclaimer: After completing the illustrative analysis in this report, we 

were informed by the EPA that the exposure estimates which were provided to 

us systematically overestimated CO exposures. This results in overestimates of the estimated health effects associated with various standards. 

It does not affect the methdology, which could utilize updated exposure 

estimates when they became available. 

26 
P.30 

Chapter 5. EXPERTS' RISK ASSESSMENTS OF HEALTH EFFECTS FROM LOW-LEVEL 

EXPOSURE TO CARBON MONOXIDE 

The problem of relating COHb levels to specific health effects is 

exceedingly complex. It is not possible to gather data directly on the 

health effects of CO exposure in the real world for several reasons. The 

CO exposure is of course mixed up with exposure to other air pollutants. 

Health effects related to air pollution are probably affected by numerous 

other factors such as stress. Data in the laboratory can be controlled to 

provide useful information, but then must be "extrapolated" to yield estimated real world effects. And some experiments would simply be ruled out 

because of ethical (and common sense) considerations such as subjecting 

heart patients to prolonged high CO exposure to observe when heart attacks 

occur. 

As indicated in Chapter 2, there is a significant collection of data 

concerning the health effects of CO exposure. To interpret the relevance 

of this for determining the possible health effects of CO exposure, the 

professional judgments of medical and health experts are essential. This 

section describes the results of the interviews with several health experts 

conducted to assess their estimates of health risks from low-level CO 

exposures. The focus of our discussions is on sensitive groups, since the 

health effects on other people is considered to be minimal by most experts. 

27 
P.31 

5.1 Selection of Health Experts and Interview Style 

A list of 20 experts was compiled in consultation with the EPA to 

represent a crosssection of various specialties in the health effects of 

CO. Fourteen of these experts, listed in Table 5.1, were actually interviewed. The length of interviews ranged from 30 minutes to two hours. 

Some experts were personally interviewed two or three times while only 

phone conversations were held with others. The experts' knowledge and 

experience pertaining to the health risk assessment, willingness to cooperate, potential travel costs involved to conduct some personal interviews, 

and timing considerations were the main factors causing variability in the 

length and depth of interviews. The travel cost and time constraints 

placed serious restrictions on our interviewing of experts. However, we 

feel that these interviews provided valuable information for the purposes 

of this study: to develop the methodology and illustrate its use with the 

health risk assessment. 

Preserving independence of opinion and permitting ventilation of 

diverse opinion is important in the early stages of risk assessment. Thus, 

each expert was interviewed independently. However, needless to say, these 

experts share information through publications, scientific meetings, etc., 

and thus their responses are not completely independent. We merely wish to 

point out that our risk assessment process did not involve dialogue and 

direct sharing of information. 

It is our opinion that a reasonable degree of agreement among experts 

exists on the major health effects of CO. However, the magnitude of each 

28 
P.32 

health effect and the levels of exposures at which these effects begin 

differ somewhat from expert to expert. Hence, if a complete risk 

assessment were to be conducted in support of standard setting, it would be 

desirable to have repeated interviews with experts, providing feedback 

regarding the previous iteration of the risk assessment model. It would 

also be desirable to have more in-depth interviews to reduce further the 

likelihood and the effect of motivational or hueristic bias on the 

resulting assessments. Cost and time constraints made these important 

extensions infeasible in this study. In addition, we feel that it would be 

desirable to design a structured group meeting in which experts interact 

with one another in the risk assessment process. Our results, which 

attempt to integrate the collective expert judgments, could provide one 

focal point for productive discussion of the health effects of CO exposure. 

5.2 The Health Effects Assessment Procedure 

Each interview began with a brief description of the project and the 

need for experts' opinions in health-risk assessment. The expert was asked 

to qualitatively identify the health effects of low-level CO exposures. A 

description of these health effects is given in Section 5.3. Subsequently, 

for a specified health effect the expert was asked to provide specific 

information about health effects associated with various COHb levels. For 

example, consider reduced time to onset of pain in angina patients as a 

health effect. The expert was asked what percentage of angina patients 

would be expected to experience this health effect at a COHb level of 2 

percent. The question was repeated for several different levels of COHb 

(e.g., 1.5, 2.5 and 3 percent). Several alternative questioning formats 

29 
P.33 

were used to elicit this information. Assuming a large population, 

sampling fluctuations will be negligible, and a percentage figure given by 

an expert can be interpreted as a subjective probability that a randomly 

selected individual from the population will suffer the health effect. We 

feel that it is easier for the experts to interpret the questions if they 

are phrased in terms of percentages. 

The following is a sample dialogue in which the COHb level is 

specified and an expert's estimate of the percentage of the population 

suffering the health effect (i.e., of the probability that an individual in 

the population will suffer the health effect) is elicited. 

Analyst: EPA has determined that angina patients constitute a sensitive 

group that must be protected from the adverse health effects of 

CO. Suppose an experiment is conducted on 1000 angina patients. 

These patients are representative of the population of angina 

patients in terms of severity of the condition, age, sex, general 

health status, and so on. A study is performed on these patients 

to evaluate the effect of breathing CO, sufficient to raise, the 

COHb to 2 percent within two to four hours. Let us define 

aggravation of angina to mean there is a decrease of at least 10 

percent in exercise duration until onset of an angina attack. In 

your professional scientific judgment, how many patients will 

experience aggravation of their condition in this hypothetical 

experiment? Will it be less than or greater than 500? 

Expert: Answer (assume it is greater than 500) 

Analyst: Will it be less than or greater than 750? 

30 
P.34 

Expert: Answer (assume it is less than 750) 

Analyst: What is your best guess (i.e., median) about the number of 

patients that will experience aggravation? That is, if you guess 

650, you should feel equally comfortable in taking a bet that it 

will be above 650 or below 650? In other words, if I bet on it 

being below 650, and you bet on it being above 650 (neither of us 

know what the true value is until the results of the experiment 

are known), it is a fair bet? 

Expert: Answer 

The general question is then repeated for other levels of COHb. 

An alternative question to determine the. expert's estimate of the 

level of COHb that will cause the specified percentage of the population to 

experience a health effect (i.e., the level of COHb that will cause a 

specified probability of suffering the health effect) is as follows. 

Analyst: EPA has determined that angina patients constitute a sensitive 

group who must be protected from the adverse health effects of 

CO. Based on your professional scientific opinion, what level of 

COHb would protect 99 percent of the angina patients and cause no 

more than one in a hundred to suffer aggravation of the 

condition? Will it be less than 5 percent COHb? 

Expert: Answer (assume yes) 

Analyst: Will it be less than 3 percent COHb? 

Expert: Answer (assume yes). It will probably be around 1.8 percent 

COHb. 

31 
P.35 

Similar questions are then posed concerning the level of COHb 

necessary to protect other percentages of angina patients from aggravation 

of the condition. It should be emphasized that all of these questions 

elicit experts' subjective probabilities, even though they are not phrased 

specifically in terms of probability. 

Because of the complexity of the problem, it is useful as indicated to 

elicit the same information from different perspectives. This produces redundant information and sometimes indicates inconsistencies in the expert's 

responses. These inconsistencies are easy to detect. They are pointed out 

to the expert and reasons for them are solicited. Assessments are then 

revised to produce consistent judgments. Procedures for and information 

about the assessment and quantification of professional judgment can be 

found in many sources including Winkler [1967, 1969, 1981], Tversky and 

Kahneman [1974], Spetzler and StaSl von Holstein [1975], Sarin [1978], and 

Wallsten and Budescu [1980]. 

In a majority of cases, the experts initially hesitated when providing 

numerical estimates. As the interview progressed, they became increasingly 

willing to quantify their judgments. In fact, checks at the time of the 

interview revealed remarkable consistency in the responses. In some cases 

the same expert was again interviewed at another date and it was found that 

the responses remained stable. (Similar evidence for stability and consistency is provided in Wallsten, Forsyth, and Budescu, [1982]).This shows 

that while scientists are often reluctant to quantify their judgments, a 

proper interrogation procedure helps in this quantification. Furthermore, 

when their judgments are based on professional information, they reveal 

remarkable stability and consistency. 

32 
P.36 

5.3 Summary of Health Effects and Risk Measures 

Based on the survey of empirical findings reported in Chapter 2 and 

the interviews with experts, several possible health effects associated 

with low-level CO exposure have been identified. These health effects are 

divided into two categories: major and other. We consider cases of major 

health effects to be more serious than cases of other health effects. 

Combined with the number of cases of each of these health effects induced 

by exposure to CO, the major effects would appear more significant for 

appraising appropriate ambient CO standards. Our estimates of CO risks in 

Chapters 6 and 7 include both major and other health effects, although the 

uncertainties about the probabilitistic estimates (i.e., second-order 

probabilities) are only investigated for the major effects. 

There are three major health effects of exposure to CO. These are 

additional angina attacks, additional heart attacks, and additional deaths 

from heart attacks. These are defined and measured in the resulting risk 

assessments as follows: 

Additional Angina Attacks: CO exposure reduces the exercise time to the 

onset of an angina attack in angina patients. It is therefore believed 

that a larger number of angina attacks occur when angina patients are 

exposed to CO. Patients who exercise and barely avoid an angina attack 

(not necessarily consciously) in "normal air" would have a reduced threshold and therefore an attack in air with a higher CO level. As CO levels 

increase, the time to onset of an attack is further reduced and a larger 

number of patients will have CO-induced attacks. Thus, one major health 

33 
effect measure is the annual number of angina patients suffering additional 

attacks as a result of CO exposure. 

Additional Heart Attacks: By reducing the oxygen-carrying capacity of the 

blood, CO increases the discrepancy between oxygen demand and supply to 

heart muscle. Thus, when exposed to CO, some patients with cardiovascular 

disease may have heart attacks that would not have occurred without the CO 

exposure. Hence, a second major health effect measure is the annual number 

of additional heart attacks suffered by heart patients as a result of CO 

exposure. 

Deaths from Heart Attacks: Two separate circumstances may result in more 

deaths from heart attacks in higher CO environments. First, simply because 

there are more heart attacks, one would expect more deaths if the likelihood of dying given a heart attack remained constant. In addition, however, some patients suffering a heart attack may die if CO levels are high, 

whereas they would not die under low CO levels. The last major health 

effect measure is the annual number of additional heart attack deaths as a 

result of CO exposure. 

To interpret the meaning of the major health effects, it is important 

to recognize the following. An individual may have a heart attack induced 

by CO and die as a result. With the measures defined above, this event is 

counted both as an additional CO-induced heart attack and as an additional 

CO-induced death. We chose these measures since they correspond to the 

progression of the severity of health effects which medical experts consider. For evaluation of alternatives, it may be necessary to distinguish 

34 
P.38 

between fatal and nonfatal heart attacks to avoid the double counting of 

effects. In this case, it is easy to determine the additional number of 

nonfatal heart attacks induced by CO by subtracting the number of additional deaths from the number of additional heart attacks. 

In addition to the major health effects, the following five health 

effects are also quantified in our risk assessment. Since these health 

effects have been described in Chapter 2, only their measures for the risk 

assessment are given here. 

Aggravation of Angina: This health effect is measured by the annual number 

of angina patients who experience at least a 10 percent reduction in time 

to onset of angina attacks. 

Aggravation of Chronic Obstructive Pulmonary Disease (COPD): This health 

effect is measured by the annual number of COPD patients who will have a 10 

percent or more reduction in the time to onset of marked dyspnea during 

exercise. 

Aggravation of Peripheral Vascular Disease: This health effect is measured 

by the annual number of peripheral vascular patients who experience at 

least a 10 percent reduction in time to onset of vascular attacks. 

Impairment of Vigilance: This health effect is measured by the annual 

number of people who experience some vigilance impairment due to CO 

exposure. 

Incidence of Prematurity: This health effect is measured by the additional 

annual number of babies born prematurely due to frequent CO exposures 

during pregnancy. 

35 
P.39 

It is critical to recognize that all of our health effects measures 

indicate the number of additional cases annually relative to what is 

expected given background CO levels. For most of the alternative standards 

considered, the number of additional cases is less than that associated 

with the "status quo" alternative. Thus, we would expect fewer cases of 

the health effects induced by CO if the corresponding standard were 

established. 

5.4 Synopsis of the Health Effects Assessments 

This subsection provides an overview of the health effects indicated 

by the experts. In Appendix A, details of interviews with Dr. Aronow and 

Dr. Kurt are given in order to indicate the manner of the assessments. 

Kindly note that there is no reporting of responses from Dr. Tashkin and 

Dr. Friedlander. Dr. Tashkin provided only general information and Dr. 

Friedlander was primarily consulted for the air-quality considerations. 

Patients with Cardiovascular Disease 

Angina. All experts agreed that angina patients will suffer aggravation of 

their condition at low levels of CO exposure. All experts commenting on 

the number of angina attacks felt more attacks would occur at higher CO 

levels. The percentages can be interpreted as probabilities. For example, 

at a COHb level of 2 percent, the probability that an angina patient will 

suffer aggravation of angina is 0.90. 

36 
P.40 

Aronow: Aggravation of angina 

Final COHb(percent) Patients with aggravation of angina (percent) 

(10% or more reduction in time to onset of pain) 

1.0 5 

1.5 20 

2.0 >90 

2.5 99 

CO-Induced Angina Attacks 

Final COHb(percent) Patients with CO-induced angina attacks (percent) 

1.0 0-5 (2% median) 

1.5 5-20 (10% median) 

2.0 10-40 (25% median) 

2.5 40 (median) 

4.0 60 (median) 

5.0 80 (median) 

Kurt: CO-Induced Angina Attacks 

Final COHb(percent) Patients with CO-induced angina attacks (percent) 

1.5 Some effect but statistically undetectable 

2.0 20 

2.5 30 

Mustafa: At 2 percent final COHb, there would be 10-20 percent additional 

angina attacks. 

This level indicates the final COHb after one to four hours of exposure 

to CO. It is assumed that the patients are engaged in some exercise and 

are not at rest. 

37 
P.41 

Rokaw: Expect 10-15 percent more angina attacks if COHb level is 

elevated by 2 percent. 

Collier: More angina attacks at 2-3 percent final COHb level than at lower 

COHb levels. 

Horvath: At 2 percent final COHb, one should expect 100 percent of 

patients to have aggravation of angina based on the Aronow study. 

Peripheral Vascular Disease. The mechanism inducing both angina and 

peripheral vascular attacks is identical. The difference is that angina 

involves chest pain and a peripheral vascular attack involves leg pain. 

Hence, the responses of Drs. Aronow, Kurt, Mustafa, Rokaw, and Collier were 

the same as those reported for angina and therefore are not repeated. 

Heart Attacks. All experts agreed that CO exposure would cause an increase 

in the likelihood of a heart attack among those who already have heart 

disease. 

Aronow: Heart Attacks 

Final COHb(percent) Patients with CO-induced Heart Attacks (percent) 

1.5 1 

2.0 5 

3.0 10 

4.0 15 

5.0 20 

38 
P.42 

Ayres: At 3 percent final COHb, there may be a 5 percent increase in 

heart attacks. 

Kurt: At 2 percent final COHb, there might be a 20 percent increase in 

heart attacks. 

Mustafa: At 2 percent final COHb, there would be a 10-20 percent increase 

in heart attacks. 

Rokaw: We might expect a 1-2 percent increase in heart attacks if the 

COHb level is elevated by 2 percent. 

Coulson: If an individual is about to have a heart attack, CO can tip him 

to a heart attack. 

Benignus: Exposure to CO can cause an increased probability of heart 

attack. 

Horvath: It is theoretically possible that the probability of heart attack 

will increase with greater exposure to CO. 

Additional Deaths. Most experts believed that CO exposure will cause a 

higher death rate among those who are having a heart attack. 

39 
P.43 

Aronow: Fatal Heart Attacks 

Final COHb(percent) Increase in Deaths from Heart Attacks (percent) 

1.5 1 

2.0 5 

3.0 10 

4.0 ' 15 

5.0 20 

Ayres: There may be a 3-5 percent increase in death rate at a 3 percent 

final COHb. 

Kurt: More deaths will occur because CO will precipitate more heart 

attacks. But, the percentage of deaths amongst those who have 

heart attacks will remain about the same. 

Mustafa: The increase in deaths from heart attacks might be 5 percent at a 

COHb of 2 percent. 

Rokaw: The probability of death given a heart attack will increase by 

10-15 percent if the COHb level is elevated by 2 percent. 

Benignus: Higher COHb levels would increase the probability of death given 

that a heart attack occurs and could increase the expected 

severity of the attack. 

Beard: The presence of higher COHb levels impairs the chances of 

survival given one does have a heart attack*. 

40 
P.44 

Progression of Disease. Some experts believed that CO exposure causes an 

increase in the rate of progression of cardiovascular disease among those 

who already have the disease. 

Aronow: Low levels of CO precipitate anginal pain, myocardial 

infarctions, and even death. The following judgments relate to 

the increase in the probability that an individual with stable 

angina will die by the end of 1, 5, or 10 years due to COHb 

levels higher than the background level of less than 1 percent 

COHb. 

Chance of death (percent) when 

exposed to CO resulting in 

By end of Final C0Hb<l%(background) Final COHb = 2% Final COHb = 5% 

Year 1 5 6 15-20 

Year 5 25 30 

Year 10 50 60 

Collier: There is every reason to suspect that the progression of 

cardiovascular disease will be accelerated by CO exposure. 

Patients with COPD 

Most experts believe that low-level CO exposure on a chronic basis 

does not increase the prevalence of respiratory disease but it does 

increase incidences of aggravation of the pre-existing condition. 

41 
P.45 

Aronow: Aggravation of COPD 

Final COHb(percent) Patients with aggravation of COPD (percent) 

1.0 5 

1.5 20 

2.0 90 

3.0 99 

Ayres: Seriously ill pulmonary patients will experience health effects 

between 2-4 percent final COHb. 

Kurt: At a 2 percent final COHb level, CO will precipitate dyspnea but 

will not cause chronic bronchitis. Similarly, it will not precipitate an asthma attack but will aggravate it if an attack is 

already taking place. For example, in an otherwise mild attack, 

CO could cause worsening of the symptoms to medium and a medium 

attack could become a -serious attack in the presence of CO. 

Collier: A 2 percent final COHb level will adversely affect the patients 

by limiting their activity. There is no study linking CO as the 

cause of COPD. 

Mustafa: Ten to twenty percent of emphysema patients will have a 20-50 

percent reduction in activity at 2 percent final COHb. Five to 

ten percent of bronchitis patients will have a 20-50 percent 

reduction in activity at 2 percent final COHb. The chance of 

dying during a serious asthma attack will increase by 5-10 

percent at 2 percent final COHb. 

42 
P.46 

Rokaw: Severe emphysema patients are most vulnerable to CO. Lung 

disease probably will not respond (e.g., not more mucous 

formation) to CO. Presence of low levels of CO during an asthma 

attack will not aggravate the breathing problem. 

Crandall: COPD patients may already have low blood oxygen content, and if 

CO reduces the oxygen carrying capacity, then aggravation of 

their condition may result. It is unlikely that severe widespread effects will be seen below 2.5 percent final COHb during 

short-term exposures. 

Pregnant Women with their Fetuses 

Most experts believed that frequent CO exposure during pregnancy could 

result in a lower weight of the baby at birth. Since there is a higher 

death rate among lower weight babies, CO may indirectly cause a higher 

death rate among new born babies. Dr Longo was the only expert who was 

willing to provide quantitative estimates relating COHb with incidences of 

prematurity. These estimates like other health effect estimates are based 

on his professional judgment. 

43 
P.47 

•^p^p^^rLongo: Premature Births 

Final COHb(percent) Incidences of Prematurity (percent) 

1-2 Difficult to detect an increase over 

normal level of 7 percent 

3-4 ' 10 

5 30 

10 60 

Horvath: A smaller growth of fetus will be observed at low levels of CO 

exposure. 

Kurt: CO will cause lower weight of the babies at birth. 

Other Health Effects 

Vigilance effects 

Beard: At 2-3 percent final COHb, impairment of the ability to 

distinguish the length of short time segments, impairment of 

visual acuity under low illumination, reduction of performance 

regarding critical flicker fusion frequency, and increased 

reaction time to stimulus in the field of vision occur. 

Benignus: At 4 percent final COHb, 50 percent of population of healthy 

young people who are at the limit of vigilance will be affected 

in a vigilance sense (i.e., they will not be able to perform an 

assigned task in a suitable fashion). 

44 
P.48 

Aronow: At 2-4 percent final COHb, there is a reduction in maximal 

exercise time. I would also be concerned about special groups 

such as pilots and drivers, because of a decrease in vigilance. 

Mustafa: At a 2-3 percent final COHb, there is an adverse effect on the 

ability to do arithmatic, memory, and the ocular system for 5 

percent of people. At 5 percent final COHb, the percentage of individuals 

affected increases to 20 percent. At 2-3 percent final COHb, 5 

percent of people are affected by headaches causing bother but 

not requiring-rest. At 2-3 percent final COHb, there may be a 1-5 

percent increase in traffic accidents over final COHb levels of 1 

percent. An adaptation may occur if the motorists are facing the 

higher COHb levels every day. 

Atherosclerosis 

Kurt: Long term exposure to low levels of CO (2-3 percent final COHb) 

causes atherosclerosis. This level of exposure could cause a 20 

percent increase in the prevalence of coronary heart disease in 

1-20 years. 

Rokaw: CO as a co-factor in addition to diet, heredity effects, etc., 

which causes atherosclerosis. 

45 
P.49 

Chapter 6. DOSE-RESPONSE RELATIONSHIPS RELATING COHb LEVELS TO HEALTH 

EFFECTS 

The EPA exposure model for CO provides distributions of COHb levels 

within the population, as indicated in Chapter 4. To investigate quantitatively the resulting health effects we need to relate COHb levels to our 

risk output measures. This major step in this is to develop dose-response 

relationships, with the COHb level representing the dose and the likelihood 

of various health effects representing the responses. 

Ideally, we would like to have data from carefully controlled experiments with the health effects indicated by the risk output measures 

recorded for various COHb levels. Such data could provide numerous points 

from which dose-response curves could be estimated. However, experimental 

data of this nature are not available. Various epidemiological and clinical studies provide useful information for our study of CO-related health 

effects but do not directly yield points on a dose-response curve. The 

information gathered from experts concerning CO-related health effects uses 

the information from those epidemiological and clinical studies as well as 

professional experience and judgments to provide the link necessary for 

modeling of the dose-response relationships of interest. 

Assessments of the experts give the data points to which an expected 

dose-response relationship can be fit and provide quantitative information 

about the degree of uncertainty about the relationship. The points suggest 

potential models that could be used to represent the dose-response curve. 

For each of the three major health effects (i.e., angina attacks, 

46 
P.50 

heart attacks, and heart attack deaths), we develop probability distributions on the responses associated with different COHb levels, as well as an 

expected dose-response curve. The expected dose-response curve can be 

interpreted in terms of probabilities, and the probability distributions on 

the responses can therefore be thought of as second-order probabilities. 

For the other health effects, only expected dose-response'curves (i.e., 

first-order probabilities) are developed. 

As indicated in Chapter 5, the responses of interest are the number of 

additional cases of the different health effects. Our dose-response functions below relate COHb levels to the percentage of additional cases of the 

health effect for the population of interest. This percentage is, of 

course, simply multiplied by the population of the appropriate groups to 

provide the additional number of cases. Percentage of cases, rather than 

number, is used in the dose-response relationships for several reasons: 

• Medical experts think in terms of the studies they have conducted 

or read and patients they have seen. They think about the percentages of these experiencing health effects, rather than the 

implied number of individuals in society experiencing these 

effects. 

• Partially as a result of the above, the experts' judgments in 

Chapter 5 provided percentages experiencing effects at different 

COHb levels. 

• Two separate factors, percentage of the population with the 

effect and size of the population, determine the number of cases 

of a health effect. There can be uncertainties about each. 

47 
P.51 

Keeping these factors separate during the analysis should improve 

the quality of information, facilitate professional review and 

appraisal, and provide for more interesting sensitivity analysis. 

6.1 Dose-Response Relationships for Major Health Effects 

First, consider angina attacks. The dose is the COHb level in the 

blood, expressed as a percentage. The response, denoted by P , is the 

percentage of angina patients suffering additional attacks due to the COHb 

level. Dose-response points aggregated from expert assessments are given 

in Table 6.1 and illustrated in Figure 6.1. The assessments of the experts 

which directly provided information for this relationship are also shown in 

Table 6.1 As can be seen, for the P level associated with a COHb level, 

we took the mean response when more than one expert provided information. 

This is reasonable given the similarity of the professional judgments. 

A linear relationship could be used as a model for the data in Figure 

6.1, although a model linear in transformed variables provided a better 

fit. The dose was expressed in logarithmic terms, and the response was 

expressed in log-odds terms. The resulting model for the expected 

dose-response curve is 

ln( 2_-) = -3.65+3.11 ln(COHb), (6-1) 

100-PA A 

where COHb is measured in percent and the logarithms are natural 

logarithms. The correlation coefficient for this model is 0.99, implying 

2 

an R =0.98, which indicates an excellent fit. An alternative way to 

express the model is 

48 
P.52 

P A = 100 

• 0.026(COHb)3,U "" 

. l+0.026(COHb)3'

U 

(6-2) 

The relationship expressed alternately by (6-1) and (6-2) is the median 

dose-response curve. However, it would also be useful to model the uncertainty concerning the dose-response curve for additional angina attacks. 

One advantage of using log-odds for the dependent variable in (6-1) is 

that, in this case, a constant standard deviation is consistent with the 

available information. Conditional on any COHb level, we chose to use a 

normal probability distribution to represent the uncertainty. Thus, 

p 

we take the log-odds, ln, A >, to be normally distributed with a mean of 

UOO-PJ! 

(-3.65+3.11 ln(COHb)) and standard deviation 0.50. This standard deviation is reasonably consistent with the quantitative estimates of Aronow and 

the qualitative expressions of other professionals about the uncertainty of 

the angina dose-response relationship. 

The dose-response model for additional angina attacks implies that at 

a COHb level of 3.5 percent, the log-odds term is normally distributed with 

mean 0.246 and standard deviation 0.50. In terms of P , we expect 56.1 

percent of angina patients to suffer additional attacks, and a 95 percent 

credible interval ranges from 32.1 percent to 77.7 percent of angina 

patients. The median dose-response curve and the curves of upper and lower 

limits for 95 percent credible intervals are shown in Figure 6.1. Of 

course, curves could be generated for any fractiles of P.; the three curves 

in Figure 6.1 are the 0.025, 0.50, and 0.975 fractiles. 

The second major health effect is the incidence of additional heart 

attacks among those with heart disease. As before, the dose is the COHb 

49 
P.53 

level in the blood, expressed as a percentage. The response, denoted by 

P , is the percentage increase in total heart attacks, fatal and nonfatal. 

Dose-response points obtained through expert assessment, are given in Table 

6.2 and Figure 6.2. Here a linear model provides a perfect fit 

except for the first point, and we will use such a model for the median 

dose-response curve, 

f -5 + 5« 

I 0, 

_, ., • .(COHb), for COHb^l, 

HA 

1 " for C0Hb<l, (6-3) 

which is illustrated in Figure 6.2. 

It should be noted that only Dr. Aronow expressed judgments about the 

relationship between additional heart attacks and COHb for several different levels. Hence, the curve in Figure 6.2 is based upon this judgment. 

However, as indicated in Chapter 5, the other experts expressed judgments 

about the percentage increase in heart attacks at a 2 percent level of 

COHb. Dr. Kurt estimated this increase at 20 percent, Dr. Mustafa suggested 10-20 percent, and Dr. Rokaw thought a 1-2 percent increase might be 

observed. These judgments are reasonably consistent with the median estimate in Figure 6.2 (i.e., some estimates fall both above and below the 

median). Furthermore, they indicate something about the degree of uncertainty concerning additional heart attacks. 

The information available from experts suggests that the variability 

of the response increases as the dose increases. For example, the standard 

deviation of the percentage increase in heart attacks is greater at a COHb 

level of 4 percent than at a COHb level of 2 percent. To model this shift 

50 
P.54 

in variability, we represent the 0.025 fractile of the dose-response 

relationship by the line 

f -2.5 + 2.5(COHb), for C0Hb_>l, 

H A \ 0, for C0Hb<l, (6-4) 

and the 0.975 fractile by the line 

p = f -10 + 10(COHb), for COHb^.1, 

"

 H A

 \ 0, for COHb<l, (6-5) 

The median dose-response curve and the curves of upper and lower limits for 

95 percent credible intervals are shown in Figure 6.2. 

The third major health effect involves deaths associated with heart 

attacks. If we let P denote the probability of death for those who are 

having a heart attack, the available probabilistic information in Chapter 5 

provided by Dr. Aronow indicates that the dose-response curve is 

approximately 

pj?[l+0.05(C0Hb-l)], for COHb _>1, 

P D= { p £ for COHb <1, (6'6) 

where P is the probability that a heart attack is fatal in air with 

background levels of CO (which corresponds to C0Hb<l). It is worth 

mentioning that the other experts' judgments, not used in constructing the 

dose-response curve of (6-6), about the increasing rate of fatalities from 

heart attacks were reasonably consistent with the curve. 

6.2 Dose-Response Relationships for Other Health Effects 

This subsection develops expected dose-response relationships for the 

aggravation of angina, COPD, and PVD and for vigilance effects and prema51 
P.55 

ture births. The manner in which this is done is similar to that for the 

major health effects so details are omitted. Also, because these effects 

are felt to be less important than the major effects, no models of the 

uncertainty are developed, although the procedures to do this would correspond to that for major effects. 

The limited experimental evidence concerning COHb and angina involves 

reduction in the time until the onset of an angina attack. Thus, experts 

seem to feel more comfortable with this concept than with the percentage of 

angina patients suffering additional attacks. Some points are presented in 

Table 6.3 and Figure 6.3, and the figure also includes the expected 

dose-response curve that resulted from our modeling: 

100-P^ 

0.00019e' 

' AA 

ln( •£•£-) = -8.556 + 5.242(COHb), (6-7) 

AA 

o r - 5.242(COHb) 

PAA " 10° l+0.00019e5-

242(C0Hb) 

(6-8) 

where the COHb level is indicated in percent and P represents the perAA 

centage of angina patients with an aggravated condition defined as at least 

a ten percent reduction in time to the onset of pain. From (6-7), one sees 

that the chosen model is linear when P.. is transformed to log-odds. 

Another health effect involves aggravation of chronic obstructive 

pulmonary disease (COPD). As indicated in Chapter 5, we define an 

aggravated condition of COPD as a significant reduction (20 percent or 

more) in the time to onset of marked dyspnea during exercise. If we denote 

the percentage of patients with aggravated COPD as P , the information 

from the experts indicates that the dose-response curve is the same as the 

52 
P.56 

dose-response curve for reduction in time until the onset of an angina 

attack. Thus, 

100-P, 

0.00019e" 

ropn ln( ^£i^) = _8.556 + 5.242(COHb), (6-9) 

COPD 

°

r " 5.242(COHb) 

PC0PD = 10° l+0.00019e5'

242(COHb) 

(6-10) 

The dose-response rate for the percentage (Ppvn) of peripheral 

vascular patients who will have reduced time to the onset of a vascular 

attack is also identical to the dose-response curve for reduction in time 

until the onset of an angina attack. This seems reasonable, since the 

underlying mechanism is the same in the two cases, with the location of 

pain differing. Thus, 

PPVD = 10° 

0.00019e5-

242(COHb) 

l+0.00019e5-

242(COHb) 

(6-11) 

where the COHb level is in percent. 

The health effect measure relating to vigilance is defined as the 

percentage of individuals who will experience some impairment in vigilance 

(i.e., inability to perform an assigned task suitably). Denoting this 

measure by P^, we estimated the following dose-response relationship from 

the experts' responses: 

2.5 (2

(COHb >-2 ) for COHb >3, 

PV 1 0 for COHb <3. (6-12) 

Finally, we consider the increase in premature births related to CO 

exposure. If we let PpR denote the increase (in terms of a percentage of 

all babies born) in premature births and measure the COHb level in percent, 

the expected dose-response curve is 

53 
P.57 

ln(-

PB 

100-P 

-) = -6.9167 + 1.135(COHb), 

or, equivalently, 

PB 

PPB = i0° 

0.00019e 

1.135(COHb) 

1.135(COHb) (6-13) 

l+0.00019e 

As in the previous case, the dependent variable is expressed in log-odds 

form. 

54 
P.58 

Chapter 7. ESTIMATES OF RISK 

The purpose of this chapter is to provide quantitative estimates of 

risk to human health if different alternative standards are adopted (and 

just met). For each standard the exposure data discussed in Chapter 4 

provides an estimate of the number of people exposed to various levels of 

COHb. The dose-response relationships developed in Chapter 6 indicate the 

magnitudes of different health effects for each level of COHb. Here, the 

exposure data and dose-response relationships are combined to estimate the 

number of people experiencing the health effects of interest, with probabilities as well as point estimates for the major health effects. Results 

are reported for each of four cities (Los Angeles, Philadelphia, St. Louis, 

and Chicago), the U.S. urban population, and groups particularly sensitive 

to CO. 

7.1 Combination of Exposure Data and Dose-Response Relationships 

The procedure used to determine risk estimates for the health effects 

involves the combination of exposure data and dose-response relationships. 

For the major health effects discussed in Section 6.1 and the other health 

effects discussed in Section 6.2, the procedure can be carried out in five 

steps: 

Step 1: For each COHb level, determine the number of people exposed 

from the exposure data of Chapter 4, 

Step 2: For each COHb level, determine the number of these 

individuals exposed who are in a particularly sensitive 

group (e.g., angina patients), 

55 
P.59_ 

Step 3: For each COHb level, determine the likelihood of the 

particular health effect of concern, 

Step 4: For each COHb level, multiply the number of individuals in 

the relevant sensitive group (from Step 2) times the likelihood of the particular health effect given that COHb level 

(from Step 3) to determine the number of cases of the health 

effect resulting from the given COHb level, 

Step 5: Sum up the results of Step 4 over all possible COHb levels 

to estimate the total number of cases of the health effect 

induced by CO. 

It is important to keep the following in mind when interpreting the 

number of CO-induced health effects. These numbers represent an estimate 

of the additional cases of the health effect relative to the number of 

cases expected with background CO levels (i.e., pristine air quality). 

Thus, even a "strict" CO standard will result in additional cases of a 

health effect. However, this may be less than the number of additional 

cases with the status quo circumstances regarding CO air quality. 

Angina Attacks 

The number of CO-induced angina attacks is computed for both "peopledays" and "people-hours" exposure information. The underlying assumption 

in using people-days for exposure is that a person is likely to have only 

one CO-induced angina attack per day, but the same person could have 

several (a maximum of 365) CO-induced angina attacks over the course of a 

year. The use of people-hours implies that a person may have attacks 

56 
P.60 

several times in a day if his or her COHb level reaches high enough levels 

on several occasions during the same day. 

It is reasonable to expect that risk estimates based on people-hours 

provide an upper bound on the number of CO-induced angina attacks per year. 

The reasoning is as follows. If a person has had an attack, the COHb level 

is likely high and he or she will likely rest or reduce activity.' The 

resulting COHb level for this individual will be lower than what otherwise 

would have been the case, which tends to reduce the chance of additional 

attacks during the same day. The same argument might apply to people-days 

data but with less force as higher COHb levels may often not occur on 

consecutive days and restricted activity an hour after an angina attack may 

be more likely than a day afterwards. We did not use people-years for 

angina attacks since clearly it provides an unrealistically low lower bound 

- a person is very unlikely to have only one angina attack per year. 

For the initial analysis below, it is assumed that the distribution of 

angina patients at different levels of COHb is the same as the distribution 

of exposure for the overall population. In Section 7.3, we provide risk 

estimates under the assumption that the exposure of angina patients follows 

the exposure pattern of a special group. To obtain CO induced angina 

attacks the steps outlined above are conducted as follows: 

Step 1: For each level of COHb, the exposure data provides the 

number N. of people-days (or people-hours) exposed to this 

COHb level i during a year. 

57 
P.61 

Step 2: Based on available data, we estimate tha.t 4 percent (U.S. 

Environmental Protection Agency [1981]) of the adult 

population has angina and that adults comprise 68.9 percent 

of the population. Thus, the number A. of angina 

patient-days (or patient-hours) in a year at COHb level i is 

given by 

A = (0.04)(0.689)N . (7-1) 

Step 3: For a given COHb level, the median dose-response curve given 

in (6-2) is used to derive P (i), percentage of angina 

A 

patients suffering additional attacks due to the COHb level 

i. The likelihood that a patient would suffer that effect 

is then P (i)/100. 

A 

Step 4: Now the number of CO induced angina attacks for a given COHb 

level is given by the product of A. and P (i)/100. 

1 A 

Step 5: The results in Sept 4 are aggregated over the possible COHb 

levels to provide the estimated total number N of angina 

A 

attacks per year based both on people-days and people-hours 

exposure information. Thus, 

NA = Z V P A(i)/100) - (7"2) 

i 

The results can also be represented as a percentage of total 

angina person-days or total angina person-hours by dividing 

by EA. which yields 

i 

N. EA (P (i)/100) 

_ = i X A . (7-3) 

EA. EA. 

. 1 . 1 

l l 

58 
P.62 

The computed figures indicate the median number of CO-induced angina 

attacks per year based on people-days and people-hours of exposure. 

Because of uncertainty about the does-response relationship, the analysis 

is also conducted for the lower and upper dose-response curves (representing the 0.025 and 0.975 fractiles of P ) discussed in Section 6.1. 

A 

Heart Attacks 

The computation of the number N of CO-induced heart attacks is based 

on the people-year exposure information. Thus, we are assuming that a 

person will have at most one CO-induced heart attack per year. The 

percentage increase in heart attacks is also reported. The steps of the 

computation are similar to these described for angina attacks: 

Step 1: Use people-year exposure information to obtain N.. 

Step 2: Five percent of adults have coronary heart disease (U.S. 

Environmental Protection Agency [1981]). Since 68.9 percent 

of the population are adults, the number (HA), of coronary 

patients exposed to COHb level i is 

(HA). = (0.05)(0.689)N.. (7-4) 

Step 3: The dose-response curve (6-3) provides the percentage P (i) 

HA 

increase of heart patients for COHb level i. 

Step 4: The number of CO-induced heart attacks as sociated with COHb 

level i is the product of (HA), and P (i)/100. 

Step 5: The results in Step 4 are aggregated over the various COHb 

levels to provide the estimated number N of CO-induced 

heart attacks per year for each standard: 

N ^ = E(HA)i(PRA(i)/100). (7-5) 

i 

59 
P.63 

The procedure is repeated for the lower and upper doseresponse curves given by (6-4) and (6-5), respectively. 

There were 1.25 million heart attacks (see Duval [1972]) in 1972, when 

the total population of the U.S. was estimated by the U.S. Bureau of the 

Census to be 203.302 million. Thus*, we assume the number of heart attacks 

per year represents 0.61 percent of the population, a base from which 

percentage increases in heart attacks due to CO exposure can be calculated. 

Deaths among cardiovascular patients 

High COHb levels result in a higher incidence of heart attacks. 

Furthermore, those patients who are having a heart attack (whether 

CO-induced or not) have a higher probability of death if exposed to a high 

COHb level at the time of the attack. These two effects are combined to 

derive additional deaths due to CO exposure as follows: 

Step 1: Use people-years exposure information to obtain N.. 

Step 2: The sensitive individuals exposed to heart attacks at COHb 

level i are the number of coronary heart disease patients 

(HA). given by (7-4) and those who will have heart attacks 

not induced by CO which number (0.61/100)Ni. 

Step 3: The probability Pn(i) of a heart attack being fatal within a 

year at COHb level i is given by (6-6). It is furthermore 

estimated that 60 percent of heart attack victims die 

immediately or within a year. This estimate, provided by 

Dr. Aronow, is higher than published estimates which range 

from 27 percent for acute myocardial infarction to 55 

60 
P.64 

percent for coronary heart disease (U.S. Department of 

Health and Human Services [1977]). Thus, as a conservative 

estimate, the probability P that a heart attack 

is fatal at background CO levels is taken as 0.6. 

Step 4: Additional deaths associated with COHb level i for heart 

attacks that would have occurred anyway are given by 

D.. = (0.61/100)N.P_(i). (7-7) 

il l D 

Also, high COHb levels lead to additional heart attacks for 

individuals with COHb level i. As indicated in the previous 

Step 4 for heart attacks, the number of these cases is (HA). 

(Pu.(i)/100). The additional deaths for these extra heart HA 

attacks is given by 

Di2 = (HA)i(p

HA(

i)/100) V-i)- (7"8) 

The estimated total number of CO-induced deaths D. for a 

l 

given COHb level i is obtained from 

D. - D±1 + D.2. (7-9) 

Step 5: The results in Step 4 are aggregated over the different COHb 

levels to provide the estimated number of CO-induced heart 

attack deaths per year. This is also expressed as a 

percentage increase in deaths, and the analysis is repeated 

for the lower and upper dose-response curves. 

Aggravation of Angina 

CO exposures results in a reduced time to onset of pain among 

exercising angina patients. We say that an angina patient is aggravated if 

61 
P.65 

activity is limited due to earlier onset of an angina attack. The 

calculations for the estimated number of aggravated cases of angina per 

year are similar to that for additional angina attacks with the following 

modifications: 

Step 1: Use people-days for exposure data N.. 

Step 2: The number of angina patient-days exposed at COHb level i is 

given by (7-1). 

Step 3: The percentage P (i) of angina patients with an aggravated 

AA 

condition at COHb level i is given by (6-8). 

Step 4: The number of aggravated cases of angina at COHb level i is 

Ai(PM(i)/100). 

Step 5: The results in Step 4 are aggregated to provide the estimated total number of aggravated cases of angina per year. 

Aggravation of COPD 

Patients with chronic obstructive pulmonary disease will experience 

reduced time to hypoxia at higher levels of CO exposure. The steps for the 

calculation of the estimated total number of aggravated COPD patients due 

to CO exposure are similar to that for aggravation of angina: 

Step 1: Use people-days for exposure data N.. 

Step 2: The population of patients with COPD is estimated to be 

6.9 percent of the total population (U.S. Environmental 

Protection Agency [1981]). Thus, the number of COPD 

patient-days exposed is 

(COPD). = 0.069N.. (7-10) 

62 
P.66 

Step 3: The percentage P (i) of COPD patients with an aggravated 

condition at COHb level i is given by (6-10). 

Step 4: The estimated number of aggravated cases of COPD patients at 

COHb level i is (COPD) (P(i)/100) . 

Step 5: The results in Step 4 are aggregated over COHb levels to 

provide the estimated total number of aggravated cases of 

COPD per year. 

Aggravation of Peripheral Vascular Disease 

Exposure to CO causes a reduced time to onset of vascular pain in much 

the same way as it reduces the time to onset of pain for angina patients. 

The calculations for the total number of aggravated cases of peripheral 

vascular patients are similar to those for aggravation of angina. In this 

case, however, in Step 2 the number of patient days exposed is calculated 

by multiplying N. by 0.3/100 since the percentage of peripheral vascular 

patients in the population is 0.3 percent (U.S. Environmental Protection 

Agency [1981]). 

Vigilance Effects 

An exposure to CO reduces the vigilance of even the healthy members of 

society. Thus, this effect relates to the total population rather than to 

a particular segment such as cardiovascular patients: 

Step 1: Use people-days for exposure data N.. 

Step 2: The number of people exposed is simply N.. 

63 
P.67 

Step 3: The percentage Pv(i) of individuals experiencing impairment 

of vigilance at COHb level i is given by (6-12). 

Step 4: The number of people with vigilance effects at COHb level i 

is given by N.(P (i)/IOO). 

Step 5: The results in Step 4 are aggregated to derive the estimated 

number of people with vigilance effects per year. 

Incidences of Prematurity 

It is believed that a sustained CO exposure during pregnancy causes an 

increase in the rate of premature babies. The exposure data provide an 

estimate of maximum daily or maximum yearly COHb levels experienced by a 

person. It is not clear whether a person is exposed to these higher COHb 

levels on a sustained basis (e.g., over the entire day). Our calculations 

therefore provide an upper bound on the number of premature babies for each 

standard: 

Step 1: Use people-years for exposure data. 

Step 2: The number of babies born per year is approximately 1.5 

percent of the total population. Thus the total number of 

exposures at COHb level i is (PB). = 0.015N.. 

Step 3: From (6-13), we obtain the percentage increase P (i) in 

Pu 

premature births as a function of COHb level i. 

Step 4: The additional number of premature babies associated with 

COHb level i is given by (PB) . (P_o(i)/100). 

l PB 

Step 5: The results in Step 4 are aggregated to provide the 

estimated upper bound for the number of CO-induced premature 

64 
P.68 

babies per year for each standard. The percentages reflect 

the number of additional prematurity cases as a percentage 

of the total number of births. 

7.2 Risk Estimates for Four Cities 

The procedure described in Section 7.1 was applied for the eight CO 

standards listed in Table 1.1. The analysis was conducted for each of four 

cities - Los Angeles, Chicago, Philadelphia, and St. Louis. The risk 

estimates for these four cities are presented in Tables 7.1 - 7.4. 

In the risk estimate tables, the columns "ANALY 1" through "ANALY 8" 

represent the eight standards in the same order as they are presented in 

Table 1.1. The rows refer to different health effects, with results given 

in terms of both total number of CO-induced cases relative to the number of 

cases expected at background CO levels and a percentage figure described 

below for the separate health effects. 

Angina Days 

This health effect estimates the total number of additional CO-induced 

angina attacks per year assuming that at most one attack will occur on any 

given day. The LO, ME, and HI estimates correspond to the lower, median, 

and upper dose-response curves (i.e., the 0.025, 0.50, and 0.975 

fractiles). For example, if standard 2, corresponding to ANALY 2 in Table 

7.1, is adopted and is just met, then we estimate that then there is a 

0.025 chance that the number of CO-induced angina attacks in a year in Los 

Angeles is less than 1.16 million, a 0.50 chance that the number of such 

65 
P.69 

attacks is less than 2.92 million, and a 0.975 chance that the number is 

less than 6.85 million. These figures (1.16 million, 2.92 million, and 

6.85 million) represent, respectively, 1.49 percent, 3.76 percent, and 8.82 

percent of available person-days for angina patients in a one-year period 

in Los Angeles. 

Angina Hours 

Using angina hours, the possibility that a person could have more than 

one CO-induced angina attack in a day is allowed. Once again, the LO, ME, 

and HI figures correspond to the .025, .50, and .975 fractiles of the 

distribution. The percentages are percentages of the available 

person-hours for angina patients in each city. 

Heart Attacks 

The number of additional heart attacks per year is represented by this 

estimate. For example, with standard 2 indicated by Analysis 2, the median 

number of additional heart attacks in Los Angeles is 2100, the 0.025 

fractile is 1050 heart attacks, and the 0.975 fractile is 4200 heart 

attacks. The percentages are percentage increases in heart attacks; e.g., 

the median estimate of 2100 corresponds to a 4.46 percent increase in heart 

attacks in Los Angeles. 

66 
P.70 

Heart Fatalities 

In estimating the total number of additional CO-induced deaths 

associated with heart attacks, both additional deaths for heart attacks 

that are not considered as CO-induced and deaths for the additional 

CO-induced attacks are included. With Analysis 4 in Los Angeles, for 

example, the median estimate is 927 deaths, which represents a 3.28 percent 

increase in deaths. The lower and upper estimates are 426 and 1870 deaths. 

Angina Aggravation 

This estimate involves the estimated number of additional incidences 

of aggravation among angina patients per year, in terms of person-days. 

That is, a patient is assumed to have at most one incidence of aggravation 

per day. With Analysis 6 in Los Angeles, we expect 6.22 million 

incidences, and this amounts to 8.01 percent of the available person-days 

for angina patients. 

COPD Aggravation 

This estimate is identical in nature to the estimate of angina 

aggravation, but it pertains to COPD patients instead of angina patients. 

PVD Aggravation 

This estimate is also identical in nature to the estimate of angina 

aggravation, but it pertains to peripheral vascular disease patients 

instead of angina patients. 

67 
P.71 

Vigilance Aggravation 

This risk estimate describes the estimated number of incidences of 

vigilance impairment per year. It is calculated by assuming that an 

individual cannot have more than one such incidence per day. 

Premature Birth Incidence 

This estimate indicates the expected number of additional premature 

babies born per year. For example, with Analysis 8, an upper bound for the 

expected number of additional premature babies in a year in Los Angeles is 

2170. 

7.3 Analysis for Sensitive Groups 

For each standard and each major health effect, we have given low, 

median, and high estimates of the additional number (in absolute terms and 

in percentage terms) expected to experience the health effect. These three 

estimates are the 0.025, 0.50, and 0.975 fractiles of the distribution of 

the number expected to experience the health effect. The populations in 

question are in fact the sensitive groups - angina patients for angina and 

coronary heart disease patients for heart attacks. 

To provide more information about the percentage of a sensitive group 

that might suffer CO-induced adverse health effects in a year, we fit probability distributions to the number of such health effects. Using the 

0.025, 0.5, and 0.975 fractile estimates, we found that lognormal distri68 
P.72 

butions provided very close approximations to the data. This is partially 

due to the fact that we expect the distributions to be unimodal and skewed 

to the right. The resulting probability distribution is illustrated in 

Figure 7.1 for additional heart attacks in Los Angeles given standard 8. 

To fit this curve, we used the information in Table 7.1 indicating that 

0.025 fractile for additional heart attacks in Los Angeles in 1650, the 0.5 

fractile in 3290, and the 0.975 fractile is 6590. 

From such distributions, we can find the probability that at least x 

percent (for any x) of the sensitive group will suffer a CO-induced health 

effect in a given year. In order to find these probabilities, we first 

determine how many people constitute x percent of the sensitive group. The 

right-hand cumulative probabilities for these values are the desired probabilities. Alternatively, we can work directly with percentages by fitting 

lognormal distributions for percentages. 

We tabulated the probabilities that at least 1, 5, and 10 percent of 

the sensitive group will experience CO-induced health effects for angina 

attacks, heart attacks, and fatalities associated for heart attacks. The 

results for Los Angeles, Chicago, Philadelphia, and St. Louis are given in 

Tables 7.5 - 7.8. For example, in Los Angeles with Analysis 8, among 

coronary patients, 

P(At least 1 percent suffer CO-related heart attacks during a year) = 

0.731, 

P(At least 5 percent suffer CO-related heart attacks during a year) = 

0.00, 

69 
P.73 

and P(At least 10 percent suffer CO-related heart attacks during a year) = 

0.00. 

The probability that at least 1 percent suffer heart attacks is illustrated 

in Figure 7.1. The EPA exposure analysis takes the population of Los 

Angeles as 7.72 million. Five percent of the adults, which are 68.9 

percent of the population, are coronary patients. Thus there are 0.226 

million coronary patients in Los Angeles, so one percent represents 2660. 

On Figure 7.1, the probability of 2660 or more additional heart attacks is 

0.731. As indicated, there is essentially no chance that as many as 5 

percent will be affected. 

7.4 Analysis for Special Exposure Group 

In the analyses presented in Sections 7.2 and 7.3, it is assumed 

because of the exposure data used that individuals in the sensitive groups 

had distributions of exposure similar to the rest of the population. 

However, the distributions may differ since sensitive individuals are those 

suffering from some health problems such as angina, cardiovascular disease, 

or chronic obstructive pulmonary disease. People with these health 

problems might tend to have different activity patterns and hence different 

distributions of exposure. 

Given the information available about the cohort groups used in the 

EPA exposure analysis, it is possible to select a few cohort groups with 

physiological parameters (e.g., ventilation rate) that seem roughly 

characteristic of the sensitive groups. These cohorts were chosen to 

constitute a special exposure group. Analyses corresponding to those in 

70 
P.74 

Sections 7.2 and 7.3 were run using exposure data for the special exposure 

group instead of for the entire population. Risks estimates for this 

alternative analysis are given in Tables 7.9 - 7.12, and probabilities for 

1 percent, 5 percent, and 10 percent of the sensitive groups are presented 

in Tables 7.13 - 7.16. As expected, a comparison of Tables 7.9 - 7.16 with 

Tables 7.1 - 7.8 indicates that an individual with the exposure pattern of 

the special exposure group would be less likely to suffer adverse health 

effects and would be expected to suffer fewer such effects than an 

individual with the exposure pattern of the general population. 

7.5 Risk Estimates for the U.S. Urban Population 

We have presented results for four cities (Los Angeles, Chicago, 

Philadelphia, and St. Louis), since output from the exposure model was 

available only for those cities. Without exposure data from other cities, 

it is difficult to provide reasonable risk estimates for the entire U.S. 

urban population. To provide a very rough estimate of risks for the U.S. 

urban population, we have taken a weighted average of the results for the 

four cities, with the weights reflecting population size. The EPA exposure 

analysis took the populations (in millions) of these cities to be 7.72 for 

Los Angeles, 2.36 for Chicago, 2.94 for Philadelphia, and 1.21 for St. 

Louis. Much of the urban population lives in areas less densely populated 

than the four cities analyzed. To the extent that CO pollution levels are 

expected to correlate positively with population densities, the estimates 

for the urban population might be considered as an upper bound. 

71 
P.75 

The estimates of the number of people suffering each health effect of 

interest are given in Table 7.17 for the entire urban population using 

general exposure data. The probabilities that 1, 5, and 10 percent of the 

sensitive groups suffer the health effects are provided in Table 7.18. A 

similar analysis using exposure data for the special exposure group 

described in Section 7.4 is presented in Tables 7.19 and 7.20. 

7.6 Sensitivity Analysis 

The analyses reported in this chapter provide a good indication of the 

sensitivity of our results to changes in the inputs. First, the analyses 

for upper and lower dose-response curves indicate the sensitivity of the 

results to changes in these functions. The number of people expected to be 

affected by CO increases as we move from the lower dose-response curve to 

the median curve and finally to the upper curve for a given standard and 

.city. However, in terms of comparisons of standards, the results are 

similar for the three dose-response curves. For example, the standard 

associated with Analysis 4 tends to provide low risk estimates relative to 

other standards for all situations, and the standards associated with 

Analysis 3 and Analysis 8 tend to provide high risk estimates relative to 

other standards. In this sense, the results of the risk assessment appear 

to be quite robust. 

Second, the consideration of the special exposure group provides 

information about the sensitivity of the results to variations in exposure 

patterns. Once again, the results change in absolute terms, with the data 

from the special exposure group yielding lower risk estimates than the 

72 
P.76 

exposure data from the general population. However, the relative 

comparison of standards does not change much, if at all. In relative 

terms, the results are once again quite robust. 

Finally, the effect of varying some model parameters can be quite 

straightforward. For example, it has been estimated that 60 percent of all 

heart attack victims die within a year, and this figure was used in the 

calculation of risk estimates concerning deaths associated with heart 

attacks. If the 60 percent figure is too high and should be reduced by 

some factor, this simply reduces the risk estimates for heart-attack deaths 

by the same factor. Thus, the effect of varying this figure can be 

determined in a straightforward manner. Specific comments on desired 

sensitivity analyses are discussed in Sections 8.2 and 8.3. 

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Chapter 8. SUMMARY AND DISCUSSION 

As stated in Chapter 1, the purpose of this report is to demonstrate 

the development and presentation of an analysis of possible ambient air 

quality standards for one major pollutant, carbon monoxide. The primary 

objective of the analysis is to relate, via a risk assessment model, 

adverse health effects to alternative carbon monoxide standards. In this 

chapter we briefly summarize the analysis, and discuss ways in which the 

analysis could be further refined. 

8.1 Summary of the Analysis 

Given the objective of relating adverse health effects to CO standards, a key issue is the development of an overall structure for the risk 

assessment model. Two other major issues involve the choice of health 

effects and the modeling of dose-response relationships. Finally, exposure 

data and dose-response models must be combined to arrive at the final quantitative risk estimates. The manner in which the analysis addresses these 

concerns is summarized below. 

Structure of the Model. An important aspect of the modeling process is the 

decomposition of the problem into manageable components. These components 

can then be separately analyzed and logically integrated to provide results 

concerning the primary objective of the risk assessment (i.e., risk estimates for CO-induced health effects associated with different CO standards) . The decomposition of the problem, of course, is dictated to a large 

extent by the types of information that are both useful and obtainable. 

74 
P.78 

The component models of our decomposition are 

1. the relationship between a CO standard and the actual ambient air 

quality in terms of ambient CO levels, 

2. the relationship between ambient CO levels and the degree of 

exposure of people to different CO levels, 

3. the physiological responses of people to their exposure to CO, 

4. the adverse health effects related to physiological responses, 

and 

5. the relationship between individual adverse health effects and 

specific risk output estimates. 

The structure of the risk assessment shown in Figure 3.2, involving these 

component models, was judged to be the most appropriate structure given the 

information available and given the constraints on cost and time associated 

with this study. 

Exposure to Carbon Monoxide. The National Ambient Air Quality Standard 

Exposure Model (NEM) was used to generate exposure estimates associated 

with the various CO standards under consideration. This model adjusts 

actual data regarding measurements of CO levels at a number of sites to 

estimate the air quality that would be expected under alternative standards 

(assuming each standard is just met). The next step translates air quality 

data into exposure data, using extensive empirical results regarding 

activity patterns of the members of the population in the four cities for 

which risk estimates are generated. Since CO-induced health effects occur 

because exposure to CO leads to increased COHb levels in the blood, the 

last step of the exposure analysis involves the conversion of data regarding CO exposure to information concerning COHb levels. This is accomp75 
P.79 

lished via the Coburn model. The output of the exposure analysis is a set 

of distributions of COHb exposure in terms of person-hours, person-days 

(i.e., the maximum COHb exposure during a day), and person-years (i.e., the 

maximum COHb exposure during a year). 

Health Effects. Previous empirical and epidemiological findings indicate 

several adverse health effects related to CO exposure. The groups that 

appear to be quite sensitive to the increased COHb levels that result from 

CO exposure include coronary heart disease patients, chronic obstructive 

pulmonary disease patients, and pregnant women with their fetuses. Unfortunately, it has not been judged feasible to gather data concerning the 

health effects of CO exposure in the real world (as opposed to the laboratory) . Laboratory studies provide useful information but do not address 

directly the questions of primary interest in our risk assessment. 

However, the professional judgments of medical experts about CO-induced 

health effects constitute valuable information. Thus, we interviewed 

several health experts to assess their estimates (in quantitative terms as 

well as in qualitative terms) of health risks from low-level CO exposure. 

After evaluating the previous empirical and epidemiological findings and 

the information from experts, we decided to concentrate on three major 

CO-induced health effects: additional angina attacks, additional heart 

attacks, and additional deaths from heart attacks. In addition to these 

major health effects, we also analyze five other effects: aggravation of 

angina, aggravation of chronic obstructive pulmonary disease, aggravation 

of peripheral vascular disease, impairment of vigilance, and incidence of 

prematurity. 

76 
P.80 

Dose-Response Relationships. To analyze quantitatively CO-induced health 

effects, it is necessary to relate COHb levels to these health effects. 

Information used to select the health effects included in the analysis was 

also used to estimate dose-response relationships, with the COHb level 

representing the dose and the percentages of additional CO-induced cases of 

the health effects (additional as compared with what would be expected 

given COHb levels associated with background-level CO occurring naturally) 

representing the responses. The development of dose-response relationships 

involved some model building in the sense of curve fitting, and this was 

done for all of the health effects being considered. For the three major 

health effects, uncertainty concerning the dose-response curve was modeled 

probabilistically, with distributions of the final risk output estimates 

conditional upon COHb levels. For the other health effects, only expected 

dose-response relationships were estimated. 

Risk Estimates. The final step in the risk assessment is the combination 

of exposure data and dose-response models to arrive at the quantitative 

risk estimates presented in Chapter 7. This was done for the eight 

standards listed in Table 1.1 for each of four cities - Los Angeles, 

Chicago, Philadelphia, and St. Louis. The following estimates were 

generated for the major health effects: 

1. distributions of the final risk output estimates (e.g., the 

number of additional heart attacks), summarized by medians, 0.025 

fractiles, and 0.975 fractiles, 

2. probabilities that at least 1, 5, or 10 percent of the sensitive 

groups will suffer adverse health effects. 

77 
P.81 

For the other health effects, only point estimates of the final risk output 

estimates (e.g., the annual expected number of cases of aggravation of 

chronic obstructive pulmonary disease) were found. 

In the main analysis, we assumed that individuals in the sensitive 

groups (e.g., angina patients) have distributions of exposure similar* to 

the rest of the population. Because of their health problems, these 

individuals may tend to have different activity patterns and hence 

different distributions of exposure. A supplementary analysis was 

conducted with a special exposure group consisting of individuals with 

physiological parameters more characteristic of the sensitive groups. 

The main results pertain to the four cities for which exposure 

information was available. To provide a rough estimates of risks for the 

entire U.S. urban population, we found a weighted average of the results 

for the four cities, with the weights reflecting population size. 

8.2 Discussion of the Results 

The results of the analysis are presented in twenty tables in Chapter 

7, and it is difficult to provide a brief summary of all of these figures. 

The results present an overall picture of the health risks associated with 

each standard that was analyzed. Perhaps the most striking point is the 

insensitivity of the relative results for the eight standards. The magnitudes of the risk estimates vary from city to city, from high estimates to 

low estimates, and from the general population exposure to the special 

exposure group. But the relative values across standards do not vary 

78 
P.82 

greatly. Standard 4 (9 ppm, 8-hour average, 1 allowable exceedance) 

consistently tends to lead to the lowest risk estimates, and standards 6 (9 

ppm, 8-hour average, 5 allowable exceedances) and 5 (12 ppm, 8-hour 

average, 5 allowable exceedances) are low relative to the others. At the 

other extreme, standards 3 (35 ppm, 1-hour average, 1 allowable exceedance) 

and 8 (25 ppm, 1-hour average, 5 allowable exceedances) tend to provide the 

highest (i.e., the worst) risk estimates. The relative ordering of 

standards in terms of risk estimates appears to be consistent with what 

might have been anticipated a priori. 

The special exposure group led to lower risk estimates than the population exposure group. This is not surprising, since individuals with 

health problems reflected by the physiological parameters of the special 

exposure group would be expected to have somewhat reduced activity levels 

and hence reduced levels of COHb exposure. 

To evaluate the numerical risk estimates in any detail shades into 

risk evaluation. The objective of this study was to develop a risk 

assessment, not a risk evaluation. Next, we will provide some indication 

as to how the risk assessment itself might be refined further. 

8.3 Potential Refinements of the Analysis 

The analysis conducted and reported here is by no means the final word 

on the subject. The assessment of health risks associated with alternative 

standards is a very complex problem, and the information available is cer79 
P.83 

tainly less than perfect. Given the current state of knowledge concerning 

ambient air quality, exposure, physiological responses, and ultimate health 

effects and given the constraints on time and cost imposed in this study, 

we feel that the analysis provides a reasonable overall picture of the 

health risks associated with various CO standards. Relaxation of the 

constraints and/or further advances in the state of knowledge would permit 

further refinement of the analysis. Ultimately, of course, decisions 

regarding the degree of refinement of a risk assessment hinge upon 

tradeoffs between the anticipated gains from and the additional costs of 

various refinements. Without making such value judgments, we will attempt 

to list some potential refinements. 

Major changes in the overall structure of the model do not seem 

necessary or desirable. We feel that the structure is sound and that much 

more is to be gained by refining the individual components of the model. 

First, we consider the exposure data. The NEM model represents a significant attack on an extremely complex problem. There are, however, many 

possible improvements to the model. In terms of data collection regarding 

ambient air quality, it would be desirable to increase the number of sites 

in order to reduce the impact of purely local effects at individual sites. 

Site-to-site variability is surely sufficient to make large samples valuable. Also, the rollback model used to relate current air quality to the 

air quality expected given that a standard is imposed and just met deserves 

further attention. As for activity levels, it would be helpful to have 

data regarding activity patterns for the specific sensitive groups identified in our analysis. In addition, the activity pattern in times of par80 
P.84 

ticularly poor air quality (e.g., a smog alert) may not be the same as at 

other times for which activity data are available and utilized as in the 

existing exposure model. 

The study of health effects and the development of dose-response relationships might be improved. If it would be possible to conduct laboratory 

experiments to collect data bearing directly on the relationship between 

COHb levels and the major health effects identified in our analysis, the 

resulting data would help to refine the dose-response estimates. Further 

information concerning health effects (e.g., potential long-term effects of 

an increased number of angina attacks) would also be useful. In the 

absence of "hard data" on these issues, more extensive assessment of 

experts' judgments would be desirable. In particular, feedback regarding 

estimated dose-response curves could be given to experts and additional 

assessments could be made. This process could be iterated several times. 

In this regard, it would-appear to be quite valuable to bring a group of 

experts together to interact with each other in a structured group meeting. 

The purpose of the meeting would be to provide a state-of-current-knowledge 

representation of the probabilistic dose-response functions. 

One refinement to the analysis is to more carefully define the 

sensitive groups. The current analysis assumed that the same dose-response 

curves pertained to all individuals within a sensitive group. It may be 

that these groups can be appropriately divided (i.e., coronary patients who 

have had heart attacks and coronary patients who have not had heart 

attacks). Different dose-response curves may apply to the subgroups. This 
P.85 

might be particularly useful with respect to improving parameter estimates 

such as the probability that a heart attack victim dies within a year. 

The extrapolation of the risk estimates for the four cities to 

estimate health effects to the entire U.S. urban population is very shaky. 

More information is needed about how representative (or unrepresentative) 

these four cities are of urban environments and urban populations. For 

example, how does the air quality in smaller urban areas compare with that 

in large areas such as the four cities used in the study? 

The analysis conducted de facto assumes that members of sensitive 

groups are non-smokers, since the exposure model includes this assumption. 

The scope of this study was to include this assumption. However, if an 

adequate way to include the characteristic that members of the population 

do smoke is found, the resulting analysis would be useful. It is known 

that regular smokers generally have a much higher COHb level than 

non-smokers. Thus, it may be the case that the ambient CO level may have a 

much smaller effect on CO-related health effects for smokers than 

non-smokers. If this were the case, the estimates provided in Tables 7.1 -

7.20 would be higher than corresponding estimates which included the 

effects of smoking. 

82 
APPENDIX A. Representative interviews with experts. 

The information about health effects in Section 5.4 was gathered in 

individual interviews with medical experts. This Appendix illustrates the 

general nature of those interviews (not all of the specific details of the 

interviews) by presenting two representative examples. The information 

here is based on the notes at the time of the interviews and the 

recollections of the interviewer. It represents a condensed summary of the 

interaction between the interviewer and the experts, not the verbatim 

questions and responses. The first case involves two interviews with Dr. 

Wilbert S. Aronow, Chief, Cardiovascular Section, Veterans Administration 

Hospital, Long Beach, California. 

The First Interview with Dr. Aronow 

Interviewer: What are the health effects of low-level Carbon Monoxide 

(CO) exposures in healthy people? 

Expert: Very minimal. At 2 percent COHb, healthy people experience a 

reduction in maximal exercise time. This could be relevant for 

athletes. At higher levels, of course, such as for nonsmoking foundry 

workers, the effects have been demonstrated to be serious. 

Interviewer: Do low levels of CO exposure cause cardiovascular damage in 

normal people? 

Expert: I cannot say - we know that the condition is aggravated if a 

person already is a cornonary heart patient. 

Interviewer: At what level of COHb might aggravation of angina occur? 

Expert: It has been demonstrated at 2 percent. 

83 
P.87 

Interviewer: If we take a sample of 1000 angina patients, would you say 

that all experience aggravation of the condition at 2 percent COHb? 

Expert: Maybe not all 1000 patients, but I guess that 90 percent or more 

will experience aggravation of the condition. 

Interviewer: At 1 percent COHb, what percentage of angina patients might 

experience aggravation? 

Expert: I do not know. 

Interviewer: Will you guess less than 1 percent will experience 

aggravation? 

Expert: No! More than that. I would guess 5 percent. 

Interviewer: At 1.5 percent COHb, how many people will experience 

aggravation? 

Expert: More than 10 percent. Let me say 20 percent. 

Interviewer: Do you agree with the following: 

COHb(percent) Percent of patients experience aggravation 

1.0 5 

1.5 20 

2.0 >90 

Expert: Yes! But, I could be wrong if an experiment is conducted. 

Interviewer: Will you be willing to make a policy based on these numbers? 

Expert: Yes! If no other study data is available. 

Interviewer: What is the relationship of angina with cardiovascular 

damage and ultimately death? 

Expert: Of people with angina, 20 percent have 1 vessel disease, 40 

percent have 2 vessel disease, and 40 percent have 3 vessel disease. 

Further, of the patients who have 1 vessel disease, 90 percent will be 

alive by the end of 5 years; of the patients who have 2 vessel 

84 
disease, 65 percent will be alive by the end of 5 years; and of the 

patients who have 3 vessel disease, 45 percent will be alive by the 

end of 5 years. 

Interviewer: So the average annual mortality for coronary heart patients 

will be approximately 8 percent. 

Expert: Yes, 60 percent will be alive at the end of 5 years. Also, if we 

look at the people who have heart attacks, 60 percent will die: 50 

percent die before reaching the hospital (sudden death); and another 

10 percent die during hospitalization. 

Interviewer: How many people who have peripheral vascular disease will 

have reduced time to onset of pain at 2 percent COHb? 

Expert: I would say 90 percent. 

Interviewer: At 1.5 percent COHb? 

Expert: Twenty percent. 

Interviewer: At 1 percent COHb? 

Expert: Five percent. 

Interviewer: But, your experiment showed aggravation of this condition at 

higher levels of COHb as compared with angina. 

Expert: That is because the experiment was conducted at somehwat higher 

levels. I would expect these patients to be no better off than the 

angina patients with CO exposures. 

Interviewer: Could a coronary heart patient get myocardial infarction on 

an acute basis if exposed to CO? 

Expert: It depends on the severity of his disease. People with unstable 

angina or in distress could be tipped over to myocardial infarction by 

an exposure to CO. There are at least 10 percent of angina patients 

with unstable angina pectoris—actually much more than 10 percent. 

85 
Interviewer: At 3 percent COHb how many coronary heart patients could get 

a heart attack? 

Expert: I would guess greater than 10 percent. 

Interviewer: At a 1.5-2 percent COHb level? 

Expert: I would guess 5 percent. 

Interviewer: If a person is having a heart attack", could higher levels of 

COHb due to CO exposure cause death? 

Expert: At 1.5-2 percent COHb, I would guess 1-5 percent of people may 

die and at 2-3 percent COHb, 10 percent of people may die because of 

CO exposure. 

Interviewer: Could people die of angina? 

Expert: No, but these patients develop other conditions and eventually a 

majority of them die of heart related causes. 

Interviewer: Do patients with chronic obstructive pulmonary disease 

(COPD) also suffer aggravation of their conditions at low levels of CO 

exposure? 

Expert: Most certainly. 

Interviewer: How would you rank the following groups in terms of 

sensitivity? 

Expert: Asthmatics - most sensitive 

Emphysema - next most sensitive 

Chronic bronchitis - sensitive 

Interviewer: At 3 percent COHb, what percent of people with COPD suffer 

aggravation of their condition (a significant reduction in time to 

onset of marked dyspnea during exercise)? 

Expert: I would guess greater than 90 percent. 

Interviewer: How about at 1.5 percent COHb? 

86 
P.90 

Expert: About 5 percent. Actually, I would guess that these people have 

the same or may even have a little worse effects as the angina 

patients. So we could go by: 

COHb(percent) Percent of Patients with Aggravation 

1.0 5 

1.5 20 

2.0 >90 

Interviewer: Are there other groups who are affected by low-level CO 

exposure? 

Expert: Yes, anemia patients and fetuses, but you should talk to experts 

in these areas to get better information. 

The Second Interview with Dr. Aronow 

Results of the second interview with Dr. Aronow are summarized by the 

following tables and comments. 

Angina patients who may experience reduced time to onset of pain 

COHb(percent) Patients (percent) 

1.0 5 

1.5 20 

2.0 >90 

2.5 99 

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P.91 

Angina Patients who may experience additional angina attacks 

Patients with stable Patients with unstable 

COHb(percent) angina (percent) angina (percent) 

1.0 0-5 (2% median) 

1.5 5-20 (10% median) 

2.0 10-40 (25% median)' 50-99 

2.5 40 (median) 

4.0 60 

5.0 80 

The range indicates the 5th and 95th percentile. Four to five million 

people have angina and more than 10 percent have unstable angina. The 

cause of pain is a discrepancy between oxygen demand and supply to the 

heart muscle which causes angina attack. For unstable angina the 

discrepancy is worse. 

Peripheral vascular disease patients who may experience reduced time to 

onset of pain 

COHb(percent) Patients (percent) 

1.0 5 

1.5 20 

2.0 >90 

2.5 99 

88 
P.92 

PVD patients who experience additional attacks 

COHb(percent) Patients (percent) 

1.0 2 

1.5 10 

2.0 20 

2.5 40 

Additional cases of heart attacks among those who already have heart 

disease 

COHb(percent) Increase in heart attacks (percent) 

1.5 1 

2.0 5 

3.0 10 

4.0 15 

5.0 20 

Additional deaths among those who are having a heart attack 

COHb(percent) Increase (percent) 

1.5 1 

2.0 5 

3.0 10 

4.0 15 

5.0 20 

Low levels of CO do not cause atherosclerosis but they may precipitate 

anginal pains, myocardial infarction and even death. In the presence of 

higher COHb levels due to expsoure to CO, the progress of anginal attacks 

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P.93 

and movement to unstable angina and then to myocardial infarction and 

utlimately to death is faster. Approximately five and one-half million 

people have angina, and approximately 1,250,000 people have myocardial 

infarction each year. Of individuals with stable angina, 5 percent die 

within a year. With unstable angina, 15 percent die within a year. Given 

a myocardial infarction (i.e., heart attack), 65 percent die within a year 

(50 percent die before getting to a hospital, 10 percent die in the 

hospital, 5 percent die within a year after hospital discharge). In each 

of the above three categories, the chance of dying increases with frequent 

exposures to CO leading to 2 percent COHb. For instance, with stable 

angina, the following increases in the probability of dying might result 

from frequent CO exposure. 

By end 

1 

5 

10 

of the year 

Percent 

of dyin 

chs 

% wi 

background 

5 

25 

50 

ince 

th 

COHb <1% 

Percent chance of dying wh< 

exposed to CO resulting in 

2% COHb 

6 

30 

60 

5-6% COHb 

15-20 

COPD patients 

COHb(percent) 

1.0 

1.5 

2.0 

3.0 

Patients with aggravation (percent) 

5 

20 

90 

99 

90 
Aggravation of COPD is defined as a significant reduction in time to onset 

of marked dyspnea during exercise. The patients with chronic obstructive 

lung disease also have a higher chance of dying if exposed to 2 percent 

COHb levels. 

Authors Comment. Dr. Aronow requested that we mention in the report that 

he provided his estimates based on his clinical judgment. His willingness 

to share these professional judgments is greatly appreciated. 

The following summarizes an interview with Dr. Thomas L. Kurt, 

Clinical Associate Professor of Internal Medicine at the University of 

Texas Health Science Center at Dallas on October 15, 1981. 

Normal People 

Immediate Health Effects 

At 2-3 percent COHb, no immediate health effects. Vigilance effects 

occur at about 4 percent COHb and have not been verified at lower levels. 

Long Term Health Effects 

There is an overwhelming evidence that low levels of CO exposure (2-3 

percent COHb) cause atherosclerosis in nonsmoking normal people in long 

run. Dr. Kurt mentioned that he maintains this view in spite of the recent 

Astrup study. 

91 
P.95 

A question was asked about two hypothetical cities with 100,000 

population each where all other things except the levels of CO are the 

same. The level of CO in city B is high enough to cause 2-3 percent COHb 

levels in its residents as compared with city A which has extremely low 

levels of CO (less than 1 percent COHb levels in the residents). What will 

the difference be in the health effects experienced by the residents of the 

two cities? 

Dr. Kurt replied that at the end of 5-10 years you will see more 

atherogenesis if examined under microscope. You will not see clinical 

manifestation of the disease. 

Will you see more anginal cases? No! Not in 5-10 years but in 15-20 

years you will observe clinical manifestation of the disease, such as 

people having chest pain leading to heart attacks and sudden deaths. 

Prevalence of coronary heart disease will increase by 20 percent. 

Will there be an increase in respiratory disease? 

No! Exposure to CO on a chronic basis does not increase the 

prevalence of respiratory disease but it does increase incidences of 

aggravation of the preexisting condition. 

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P.96 

Patients with Cardiovascular Disease 

Angina Patients 

COHb(percent) 

1.5 

2.0 

2.5 

Additional daily angina cases (percent) 

Some effect but statistically undetectable 

20 

30 

Heart Attacks 

COHb (percent) 

2 

Additional cases of heart attacks(percent) 

20 

Deaths 

More deaths will occur because CO will precipitate more heart attacks. 

But, -the percentage of deaths among those who have heart attacks will 

remain about the same. 

Patients with Respiratory Disease 

Bronchitis and Emphysema 

A 2 percent COHb level will precipitate dyspnea but will not cause 

chronic bronchitis. 

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P.97 

Asthma 

A 2 percent COHb level will not precipitate an asthma attack, but will 

aggravate it if an attack is already taking place. For example, an otherwise mild attack could cause worsening of the symptom to medium and a 

medium attack could become a serious attack in the presence of CO. 

Other Effects 

Lower weight of the babies at birth and therefore a higher likelihood 

of premature babies. Since there is a higher death rate among premature 

babies, indirectly CO may cause higher death rates among new born babies. 

Levels at which the Health Effects Begin 

At 1.5 percent COHb, some health effects begin. The threshold is 

about 1.7-1.8 percent COHb. There will be an increase in the incidence as 

well as seriousness of the health effects as we go from 1.8 to 3 percent 

COHb. (Note: This question was asked since Dr. Kurt's study showed the 

presence of threshold but no increase in the incidences above the 

threshold). 

Other Issues 

1. Based on Standardized Mortality Rates, the number of heart 

attacks/year/100,000 population vary from 350 in Denver to 800 in 

a coastal city such as Boston. 

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P.98 

2. Of patients with heart attacks who go to a hospital, 15-30 

percent die. 

3. COHb has a half-life of four hours. That is, a 10 percent CQHb 

level will decrease to 5 percent in four hours if a person is in 

CO free environment. 

4. Interaction effects with other pollutants should be taken into 

account in the study of health effects of a pollutant. 

5. Health effects vary depending on how physically active the person 

is. For example, resting individuals will not experience some 

health effects as compared to those who are moderately 

exercising. 

6. Besides COHb, if a person is taking certain drugs or is working 

under circumstances that reduce oxygen supply, the health effects 

will be more severe. 

7. There are other mechanisms of CO toxicity such as combining with 

myoglobin, combining with cytochrome oxidase, and interference 

with the electron transfer in NAD system. 

8. Aronow work needs to be confirmed by other researchers, even 

though I (Dr. Kurt) believe the results since they are 

corroborated by some other human and animal studies. 

9. Most studies are done on normal people - studies should also be 

done on general population. Studies on special groups such as 

fire fighters, coke oven workers, and foundry workers could be 

useful in the construction of a dose-response curve since they 

experience higher levels of CO exposures. 

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P.99 

REFERENCES 

Anderson, E. W., R. J. Andelman, J. M. Strauch, N. J. Fortuin, and 

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100 
P.4 

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101 
P.5 

List of FIGURES: 

Figure 2-1 COHb level and time until exercise-induced angina. 

Figure 2-2 Perinatal mortality rates and maternal smoking level. 

Figure 2-3 Risk of congenital abnormality according to age and smoking 

habit. (Himmelberger, 1978. Figure taken from Surgeon 

General's 1980 report on "The Health Consequences of Smoking 

for Women.") 

Figure 2-4 Mean percentages of signals correctly identified by the 

nonsmokers in the alerted test and as a function of time in 

the vigil. (O'Hanlon, 1972.) 

Figure 2-5 Relationship between COHb and decrement in maximum aerobic 

power. (U.S. EPA, 1979.) 

Figure 3-1 Overview of the risk assessment model. 

Figure 3-2 The structure of the risk assessment model. 

Figure 4-1 Sample people-occurrences for COHb levels from exposure 

model. 

Figure 4-2 Sample people exposed for COHb levels from exposure model. 

Figure 6-1 Dose-response data and curve for the percentage of 

additional angina attacks to angina patients. 

Figure 6-2 Dose-response data and curve for the percentage of 

additional heart attacks to heart attack patients. 

Figure 6-3 Dose-response data and expected dose-response curve on 

relating COHb levels and the percentage of angina patients 

with aggravated condition. 

Figure 7-1 Probability distribution for annual CO-induced heart attacks 

in Los Angeles under Standard 8. 

List of TABLES: 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

1 

2 

2 

2 

2 

4 

4 

4 

4 

4 

4 

5 

6 

6 

6 

7 

7 

7 

7 

1 

1 

2 

3 

4 

1 

2 

3 

4 

5 

6 

1 

1 

2 

3 

1 

2 

3 

4 

ANALYZED AMBIENT CARBON MONOXIDE STANDARDS 

COHb LEVEL AND REDUCED TIME TO ONSET OF ANGINA 

MATERNAL SMOKING LEVEL AND CHILDREN'S MEDICAL TREATMENT 

COHb LEVEL AND DECREMENTS IN VIGILANCE 

CARBOXYHEMOGLOBIN LEVELS AFTER VARIOUS EXPOSURES 

SAMPLE POLLUTANT ENCOUNTER DATA FROM EXPOSURE MODEL 

SAMPLE PEOPLE EXPOSED DATA FROM EXPOSURE MODEL 

SAMPLE PEOPLE AT PEAK EXPOSURE DATA FROM EXPOSURE MODEL 

PEOPLE-OCCURRENCES FOR COHb LEVELS FROM EXPOSURE MODEL 

PEOPLE EXPOSED FOR COHb LEVELS FROM EXPOSURE MODEL 

PEOPLE AT PEAK EXPOSURE FOR COHb LEVELS FROM EXPOSURE MODEL 

INTERVIEWED HEALTH EXPERTS 

DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE OF ANGINA PATIENTS SUFFERING ADDITIONAL ATTACKS (P ) 

DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE INCREASE IN HEART ATTACKS (P ) 

DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE OF ANGINA PATIENTS WITH AGGRAVATED CONDITION (PAA) 

RISK ESTIMATES FOR LOS ANGELES 

RISK ESTIMATES FOR CHICAGO 

RISK ESTIMATES FOR PHILADELPHIA 

RISK ESTIMATES FOR ST. LOUIS 

102 
P.6 

Table 7.5 PROBABILITY THAT 1, 5, or 1.0 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR LOS ANGELES 

Table 7.6 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR CHICAGO 

Table 7.7 PROBABILITY THAT 1, 5, or 10 PERCENT QF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR PHILADELPHIA 

Table 7.8 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR ST. LOUIS 

Table 7.9 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR LOS ANGELES 

Table 7.10 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR CHICAGO 

Table 7.11 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR PHILADELPHIA 

Table 7.12 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR ST. LOUIS 

Table 7.13 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR LOS ANGELES 

Table 7.14 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR CHICAGO 

Table 7.15 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR PHILADELPHIA 

Table 7.16 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR ST. LOUIS 

Table 7.17 RISK ESTIMATES FOR U.S. URBAN POPULATION 

Table 7.18 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR U.S. URBAN POPULATION 

Table 7.19 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR U.S. URBAN 

POPULATION 

Table 7.20 PROBABILITY THAT 1, 5, OR 10 PERCENT CF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR U.S. URBAN POPULATION 

103 
P.7 

10.0 

5 o 

O- LU 

^° 

fc O 

cr 

UJ 

a. 

.a 

I 

O 

u 

7.5-

5.0-

2.5-

0.0 

•20 

PDEC = 2.56+4.63 COHb 

• • 

l ^ 

60 80 

PDEC: PERCENT DECREASE IN TIME UNTIL 

EXERCISE-INDUCED ANGINA 

Figure 2-1. COHb level and time until exercise—induced angina. 
P.8 

5 -

£ 4 

< 

cc 

>-

l3 -

< 

l-

< 

* 2 

cc 

LU 

a. 

S 

/ 

y s 

/ 

/ 

/ / 

/ 

/ ^ Meyer etal. (1975) 

/ -Blacks 

/ 

Meyer etal. (1975)-Whites 

Meyer etal. (1976) 

1 -

• Data points 

I 

0 

Nonsmoker's 

I I 

1-9 1-

mean 

3.9 

-10 

I 

1-20 

(i.e. less 

than 1 

pack) 

I I 

10+ 11 + 

mean 

12.2 

20"* 

NUMBERS OF CIGARETTES PER DAY 

Figure 2-2. Perinatal mortality rates and maternal smoking level. 
P.9 

0.1 

< 

<3 > 

Z h-

° Zl 

•*••- s 

> o 

t- z 

< 

m O 

tr 

a. 

0.05 -

0.0 

• • . 

• • Heavy Smoker: 

"*•*•'• ^ Moderate Smoker: 

*^"«^. ^ 1-19 Cigarettes/d 

^Nonsmoker 

20 

^ l I 

30 40 

MATERNAL AGE 

I 

50 

Figure 2-3. Risk of congenital abnormality according to age and 

smoking habit. (Himmelberger, 1978. Figure taken 

from Surgeon General's 1980 report on "The Health 

Consequences of Smoking for Women.") 
P.10 

CO 

Z 

g 

< 

iz 

111 

Q 

< 

Z 

(J 

u 

UJ c 

tr 

O 

o 

90 

80* 

7 0 -

6 0 -

5 0 -

Alerted Test 

VIGIL (minutes) 

Figure 2-4. Mean percentages of signals correctly identified by the 

nonsmokers in the alerted test and as a function of time 

in the vigil. (O'Hanlon, 1972) 
P.11 

X 

< 

O 

> 

z 

CO 

< 

LU 

cc 

o 

LU 

Q 

Figure 2-5. Relationship between COHb and decrement in maximum 

aerobic power. (U.S. EPA, 1979) 
P.12 

Basic Input: Alternative Ambient CO Standard 

Risk Assessment Model 

Output Measures: Estimates of CO Induced 

Health Effects 

Figure 3-1. Overview of the risk assessment model. 
P.13 

c Basic Input: Alternative 

Ambient CO Standard D 

Component Model 1: Relates 

CO Standard and Ambient 

CO Levels 

c Ambient CO Quality 

I 3 

Component Model 2: Relates 

Ambient CO Levels and Human 

Exposure to Different Levels 

c Human Exposure to CO 3 

Component Model 3: Relates 

CO Exposure and Resulting 

COHb Levels 

Physiological Responses 

I J 

Component Model 4: Relates 

COHb Levels and Different 

Health Effects 

c Adverse Health Effects J 

Component Model 5: Relates 

Health Effects to Risk 

Output Measures 

(

Output 

Induce*. 

Measures: Estimates of CO 

ed Health Effects 

) 

Figure 3-2. The structure of the risk assessment model. 
P.14 

Figure 4-1 SAMPLE PEOPLE - OCCURRENCES FOR COHb LEVELS 

FROM EXPOSURE MODEL 

Los Angeles Best Estimate with No Additives 

0 2 4 6 8 

COHb Concentration (Percent) 

15 Oct 1981 
P.15 

Figure 4-2 SAMPLE PEOPLE EXPOSED FOR COHb LEVELS FROM EXPOSURE MODEL 

Los Angeles Best Estimate with No Additives 

10 

B 

O 

U 

a; 

CG 

o 

w 

* & . 

S 10 

10

 6 r 

10

 5

 -

10 

4 _ 

0 2 46 8 

COHb Concentration (Percent) 

15 Oct 1981 
P.16 

tn 

•>-* 9 ~Z 01 ^ 

'—CO C o O 

••* ** CD CO 

c — — ca 

5 -2 

"o **5 

» "2 

& • * 

JS o> 

c = 

k_ ** -

a 2 

o5 

100 -

8 0 -

6 0 -

4 0 -

2 0 -

0 

L 

• Aggregated Oata from Table 6-1 

1 Ranges from Dr. Aronow 

J_ in Table 6-1 

0.975 Fractile Curves*' 

I I 

Median 

Curve 

• ^^ ^ 

H).025 Fractile Curve 

I I I * 

COHb LEVEL (%) 

Figure 6-1. Dose-response data and curve for the percentage of 

additional angina attacks to angina patients. 
P.17 

4 0 -

c 

a 

s

 3 ° -

03 

2 0 -

CO 

c 

O '— 

°*5 

*a 

2 10-

< 

I 

a. 

• Data from Table 6-2 

• Another Point Estimated 

I Ranges of Other Estimates 

2 3 4 

COHbLEVEL (%) 

Figure 6-2. Dose-response data and curve for the percentage of 

additional heart attacks to heart attack patients. 
P.18 

COHb (%) 

Figure 6-3. Dose-response data and expected dose-response 

curve on relating COHb levels and the percentage 

of angina patients with aggravated condition. 
P.19 

CO 

Z 

0.025 / 

Fractile / 

Estimate^^r 

1 i 

0.5 Fractile 

^^^*V,Estimate 

73 1 % fc 

of Area 

1 1 

Fit Lognormal 

Distribution 

1 

0.975 

Fractile 

Estimate 

i i "•' 

2000 2660 4000 

ADDITIONAL HEART ATTACKS 

6000 8000 

Figure 7-1. Probability distribution for annual CO-induced 

heart attacks in Los Angeles under Standard 8. 
P.20 

Table 1.1 ANALYZED AMBIENT CARBON MONOXIDE STANDARDS 

Allowable 

Averageing Exceedances 

Alternative CO Standard Time (Daily Maximum) 

Standard Level (ppm) (hours) (expected number 

per year) 

1 Status quo (1981) 

2 25 1 1 

3 35 1 1 

4 9 8 1 

5 12 8 1 

6 9 8 5 

7 12 8 5 

8 25 1 5 
Table 2.1 COHb LEVEL AND 

Investigator 

Aronow [1978J 

Aronow [1981] 

Aronow [1978] 

Aronow [1980] 

Anderson and Isbell [1973] 

Anderson et al. [1973] 

Anderson et al. [1973] 

Aronow, et al. [1972] 

REDUCED 

Pe 

TIME TO ONSET OF ANGINA 

rcent 

Ca rboxyhemoglobi n 

Initial 

Mean 

1.25 

1.09 

1.30 

1.73 

1.03 

1.40 

1.6 

1.12 

a Added pollutants in freeway air 

Final 

Mean 

1.77 

2.02 

2.28 

5.37 

2.68 

2.90 

4.5 

5.08 

or tobacco 

Measure 

of 

Blood 

Venous 

Venous 

Venous 

Venous 

Venous 

Venous 

Venous 

Arterial 

smoke may have 

• 

Ambient CO 

Exposure 

& Location 

2 hrs., ventilated room, 

with tobacco smoke 

50 ppm, 1 hr. lab 

2 hrs., unventilated room, 

with tobacco smoke 

100 ppm, in lab, until COHb 

at desired level 

50 ppm, 2 hrs. lab 

50 ppm, 4 hrs. lab 

100 ppm, 4 hrs. lab 

53 ppm, freeway 

increased these figures. 

Mean Percentage 

Reduction 

in Time 

Until 

ExerciseInduced • 

Angina Pain 

22a 

10 

38a 

35 

16 

16 

17 

33a 

-

Type 

of 

Exercise 

Bicycle 

Bicycle 

Bicycle 

Bicycle 

Bicycle 

Treadmill 

Treadmill 

Bicycle 

j 
P.22 

Table 2.2 MATERNAL SMOKING LEVEL AND CHILDREN'S MEDICAL TREATMENT 

MATERNAL 

SMOKING 

LEVEL 

(Cigs./day) 

INCREASED 

DOCTOR 

VISITS 

PER CHILD 

(Percent relative to 

nonsmoking mothers) 

INCREASED 

HOSPITALIZATIONS PER CHILD 

(Percent relative to 

nonsmoking mothers) 

UNDER 

AGE 1 AGE 1-5 

0 

1-10 

10+ 

0.0 

8.4 

36 

0.0 

21.4 

275.0 

0.0 

47.7 

47.1 

Source: Rantakallio [1969] 
Table 2.3 COHb LEVEL AND DECREMENTS IN VIGILANCE 

Reference COHb (percent) 

Measure of 

Vigilance Performance Results 

Fodor and 

Winneke [1972] 

Estimated 

2.3, 3.1, 4.3 

Auditory Vigilance decrement in vigilance at first, 

then it increased 

Groll-Knapp 

et al. [1972] 

Estimated 

3.0 - 7.6 

Auditory Vigilanc e dose-relate d decrement in 

vigilanc e 

Beard and 

Grandstaff [1975] 

Mean Values 

1.8, 5.2 , 7.5 

Visua l Vigilanc e bigge r decrements i n vigilanc e 

a t 1.8% and 5.2% COHb, than 

a t 7.5% 

Horvath e t al . 

[1971] 

At end of test 

2.3, 6.6 

Visual Vigilance decrement in vigilance for the 

group with 6.6% as final mean COHb 

Winneke [1974] 5.1, 10.0 Auditory Vigilance no effect 

Benignus et al. 

[1977] 

4.61-12.62 Visual Numeric 

Monitoring Task 

no effect 
P.24 

Table 2.4 CARBOXYHEMOGLOBIN LEVELS AFTER VARIOUS EXPOSURES 

(Source: CO and Human Vigilance - Horvath et al. [1971]) 

COHb Saturation Level (percent) After Exposure 

Carbon Monoxide 

Inhaled(ppm) 0 Minutes 60 to 65 Minutes 135 to 140 Minutes 

0 

26 

111 

0.8+0.35(0.4-1.6 ) 

0.8+0.57(0.4-1.2 ) 

0.9+0.46(0.5-1.8 ) 

0.8±0.23(0.5-1.3 ) 

1.6±0.60(1.1-1.9) 

4.2+1.15(3.3-6.7 ) 

0.8+0.21(0.6-1.2 ) 

2.3±0.55(1.9-2.4 ) 

6.6+1.27(5.7-9.8 ) 

Figures in parentheses represent ranges. 

~\ 
Table 4.1 SAMPLE POLLUTANT ENCOUNTER DATA FROM EXPOSURE MODEL 

CO /BE ANALYSIS 1 (A? XS ) FOP LOS ANGELES 

BEST eSTIf4TE CARBON MONOXIOE LOS ANGELES 

PL..LUTANT ENCOUNTERS FOR 9 HOUR AVERAGING TIME 

P.25 

CONCENTRATION 1 

EXCEEDED 1 

(PPM ) 1 

30.0 1 

65.0 1 

40.0 1 

33.0 1 

30.0 1 

25.0 1 

20.0 1 

15.0 1 

10.0 1 

5.0 1 

0.0 1 

MAX. CONCENTRATION 1 

PEOPLE AT MAXIMUM 1 

LOU EXERCISE 1 

132.000 1 

1,670.000 1 

6,060.000 1 

53.600,000 1 

754.000.000 1 

10.700.000,000 1 

62.500,000.000 1 

32.1 1 

16.500 1 

MEDIUM EXERCISE 

165.000 

15.700,000 

606.000,000 

4,260.000.000 

17.6 

9.200 

HIGH EXERCISE 

592.000 

94,700.000 

943,000,000 

10.3 

592,000 

ANY EXERCISE 

132.000 

1.970,000 

9.060.000 

53.900,000 

770.000.000 

11.400,000.000 

67.600.000,000 

32.1 

16.300 

•*- .. . . 

. - - + • ..... -•- .... 

'POLLUTANT ENCOUNTERS' IS THE SAME AS PERSON HOUPS OF EXPOSURE FOR 1 HOUR AVERAGINO TIME. 

'ANY EXERCISE* MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
Table 4.2 SAMPLE PEOPLE EXPOSED DATA FROM EXPOSURE MODEL 

O /BE ANALYSIS 1 (AS IS) FOR LOS ANGELES 

BEST ESTIMATE CARBON MONOXIDE LOS ANGELES 

PEOPLE EXPOSEO FOR 0 HOUR AVERAGING TIME 

CONCENTRATION 

EXCEEDED 

( PPM ) 

50.0 

i 45.0 

1 40.0 

1 35.0 

1 >0.0 

1 25.0 

1 20.0 

1 15.0 

1 10.0 

1 5.0 

1 0.0 

1 MAX. CONCENTHATIO'. 

1 PEOPLE AT MAXIMUM 

LOW EXERCISE 1 

33.200 1 

152,000 1 

-.76,000 1 

2.440.000 | 

7.120,000 1 

7,720.000 1 

7,•'10,000 1 

32.1 1 

16,300 1 

MEDIUM EXERCISE 1 

61.600 1 

3.590.000 1 

6.940.000 1 

7,200.000 1 

17.6 1 

9,200 1 

HIGH EXERCISE 1 

592,000 1 

2.700,000 1 

2.910.000 1 

10.3 1 

592.000 1 

ANY EXERCISE 

33,200 

152.000 

179,000 

2,990,000 

7,120.000 

7,720,000 

7,720,000 

32.1 

16,500 

'ANY EXERCISE' MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
P.27 

Table 4.3 SAMPLE PEOPLE AT PEAK EXPOSURE DATA FROM EXPOSURE MODEL 

CO /BE ANALYSIS 1 (AS IS) FOR LOS ANGELES 

BEST ESTIMATE CARBON MONOXIDE LOS ANGELES 

PEOPLE AT PEAK EXPOSURE FOR 9 HOUR AVERAGING TIME 

1 CONCENTRATION 1 

1 RANGE 1 

I (PPM) 1 

1 50.0 < 

1 45.0 < 

1 40.0 < 

1 33.0 < 

1 30.0 < 

1 25.0 < 

1 20.0 < 

1 15.0 < 

1 10.0 < 

1 5.0 < 

1 0. 0 < 

C < = 

c < = 

C <s 

C < = 

C < = 

c < = 

c < = 

c < = 

C <s 

c < = 

c < = 

100.0 1 

50.0 1 

45.0 1 

40.0 1 

35.0 1 

30.0 1 

25.0 1 

20.0 1 

15.0 1 

10.0 1 

5.0 1 

1 MAX. CONCENTRATION 1 

1 PEOPLE AT MAXIMUM 1 

LOW 

2 

4 

EXERCISE 1 

33.200 1 

119,000 1 

25,900 1 

,720.000 1 

,230.000 1 

597,000 1 

32.1 1 

16.300 1 

MEDIUM EXERCISE 1 

61,600 1 

3,530,000 1 

3.350.000 1 

260,000 1 

17.6 1 

0.200 1 

HIGH EXERCISE 1 

502.000 1 

2.110.000 1 

114,000 1 

10.3 1 

592,000 1 

ANY EXERCISE 

33,200 

119,000 

25,000 

2,720,000 

4,230,000 

597,000 

32.1 

16,300 

..m..........*..m.m.-. . .^. ..... . ...... . + ....... . ... + . 

ANY EXERCISE' MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
Table 4.4 PEOPLE-OCCURRENCES FOR COHb LEVELS FROM EXPOSURE MODEL 

CO /BE ANALYSIS 1 (AS IS) FOR LOS ANGELES 

BEST ESTIMATE CARBON MONOXIDE LOS ANGELES 

PEOPLE • OCCURRENCES OF EXPOSURE FOR CARBOXY HEMOGLOBIN 

1 CONCENTRATION 

1 EXCEEDED 

1 (PERCENT) 

1 5.00 

1 4.50 

1 4.00 

1 3.50 

1 3.00 

1 2.50 

1 2.00 

1 1.50 

1 1.00 

1 0.50 

1 0.00 

1 MAX. CONCENTRATION 

1 PEOPLE AT MAXIMUM 

1 

1 

1 LOW EXERCISE 1 

354.000 1 

1.700.000 1 

9,950.000 1 

77,900.000 1 

693.000.000 1 

5,210.000,000 1 

15.500.000.000 1 

57,600.000.000 1 

62.500.000.000 1 

4.50 1 

16.300 1 

MEDIUM EXERCISE 1 

1.960.000 1 

36.600,000 1 

335.000.000 1 

1.010,000,000 1 

3.930,000,000 1 

4.200.000,000 1 

2.97 1 

221.000 1 

HIGH EXERCISE 

210.000 

16,600,000 

176,000.000 

746.000.000 

944,000,000 

2.10 

210.000 

ANY EXERCISE 

354,000 

1,700,000 

9,950.000 

79,900.000 

730.000.000 

5,570,000,000 

16,700.000.000 

62.200,000.000 

67,600,000,000 

4.50 

16.300 

.+..................+.... 

'ANY EXERCISE' MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
Table 4.5 PEOPLE EXPOSED FOR COHb LEVELS FROM EXPOSURE MODEL 

CO /BE ANALYSIS 1 (AS IS) FOR LOS ANGELES 

BEST ESTIMATE CARBON MONOXIDE LOS ANGELES 

PEOPLE EXPOSED FOB CARBOXY HEMOGLOBIN 

P.29 

1 CONCENTRATION 1 

1 EXCEEOED 1 

1 (PERCENT) 1 

1 5.00 1 

1 4.50 1 

1 4.00 1 

1 3.50 1 

1 3.00 1 

1 2.50 1 

1 2.00 1 

1 1.50 1 

1 1.00 1 

1 0.50 1 

i o.oo ; 

1 MAX. CONCENTRATION 1 

1 PEOPLE AT MAXIMUM 1 

LOU EXERCISE 1 

152.000 1 

152.000 1 

691.OCO 1 

1.60O.OCO 1 

6.620,OCO 1 

7.640,000 1 

7,720,000 1 

7,7?0.000 1 

7.720.000 1 

4.50 1 

16,300 1 

MEDIUM EXERCISE 1 

600.000 1 

1.070.000 1 

4.600,000 1 

6,940,000 1 

7,200.000 1 

7.200,000 1 

2.97 1 

221.000 1 

HIGH EXERCISE 1 

210.000 1 

1.560,000 1 

2,630,000 1 

2.610,000 1 

2.010.000 1 

2.10 1 

210.000 1 

ANY EXERCISE 

152.000 

152.000 

691,000 

1.660,000 

6.620.000 

7,660.000 

7.720,000 

7,720,000 

7.720,OOO 

4.50 

16,500 

. . ..........4.... . + ..... . ..«, . . . • .. . 

'ANY EXERCISE' MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
P.30 

Table 4.6 PEOPLE AT PEAK EXPOSURE FOR COHb LEVELS FROM EXPOSURE MODEL 

CO /BE ANALYSIS 1 (AS IS) FOR LOS ANGELES 

BEST ESTIMATE CARBON MONOXIDE LOS ANGELES 

PEOPLE AT PEAK EXPOSURE FOR CARBOXY HEMOGLOBIN 

CONCENTRATION 1 

RANGE 1 

(PERCENT) 1 

5.00 < 

4.50 < 

4.00 < 

3.50 < 

3.00 < 

2.50 < 

2.00 < 

1.50 < 

1.00 < 

0.50 < 

0.00 < 

C 

c 

c 

c 

c 

c 

c 

c 

c 

c 

c 

< = 

< : 

<s 

<5 

<: 

< = 

< 2 

< z 

< : 

< *s 

< s 

10.00 1 

5.00 1 

4.50 1 

4.00 1 

3.50 1 

3.00 1 

2.50 1 

2.00 1 

1.50 1 

1.00 1 

0.50 1 

MAX. CONCENTRATION 1 

PEOPLE AT MAXIMUM 1 

LOU EXERCISE i 

152.000 1 

539,000 1 

993,000 1 

4,950,000 1 

1.020.000 1 

79,700 1 

4.50 1 

16.300 1 

MEDIUM EXERCISE 1 

600.000 1 

1,270.000 1 

2.930.000 1 

2.140.000 1 

260.000 1 

2.97 1 

221.000 1 

HIGH EXERCISE 1 

I • 

210.000 1 

1.350.000 1 

1.070.000 1 

179.000 1 

2.10 1 

210,000 1 

ANY EXERCISE 

152,000 

539.000 

995,000 

4.950.000 

1,030.000 

63.500 

4.50 

16.300 

................ 

•+---••--•- • .•..................+........ — —..+........ . ....- + 

'ANY EXERCISE' MEASURES EXPOSURE INDEPENDENT OF EXERCISE LEVEL. 
P.31 

Table 5.1 INTERVIEWED HEALTH EXPERTS 

1. Dr. Wilbert S. Aronow 

2. Dr. Steven Ayres 

3. Dr. Rodney Beard 

4. Dr. Vernon Benignus 

5. Dr. Clarance Collier 

6. Dr. Ann Coulson 

7. Dr. Edward Crandall 

8. Dr. Sheldon Friedlander 

9. Dr. Steven Horvath 

10. Dr. Thomas L. Kurt 

11. Dr. Laurence Longo 

12. Dr. Mohammed Mustafa 

13. Dr. Stanley Rokaw 

14. Dr. Don Tashkin 
P.32 

Table 6.1 DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE OF 

ANGINA PATIENTS SUFFERING ADDITIONAL ATTACKS (P ) 

Aggregated Data Assessed Expert Data P 

COHb(percent) 

1.0 

1.5 

2.0 

2.5 

4.0 

5.0 

P (percent) 

2 

10 

20 

35 

60 

80 

Aronow 

0-5(2 median) 

5-20(10 median) 

10-40(25 median) 

40 

60 

Kurt 

20 

30 

Mustafa 

10-20 
P.33 

Table 6.2 DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE 

INCREASE IN HEART ATTACKS (P ) 

CIA 

COHb(percent) P (percent) 

HA 

1.5 1 

2.0 5 

3.0 10 

4.0 15 

5.0 20 
P.34 

Table 6.3 DOSE-RESPONSE RELATIONSHIP BETWEEN COHb LEVELS AND PERCENTAGE OF 

ANGINA PATIENTS WITH AGGRAVATED CONDITION (P ) 

Ax\. 

COHb(percent) P (percent) 

1.0 5 

1.5 20 

2.0 90 

2.5 99 

3.0 100 
P.35 

Table 7.1 RISK ESTIMATES FOR LOS ANGELES 

(Using general exposure data) 

IMPACT 

ANGINA 

HAYS(LO) 

LA 

ANALY 1 

0.154E+07 

( 1.98%) 

ANALY 2 ANALY 3 ANALY 4 

0.116E+07 

( 1.49%) 

0.180E+07 

( 2.31%) 

0.697E+06 

< 0.90%) 

ANALY S 

0.843E+06 

< 1.09%) 

ANALY 6 

0.796E+06 

( 1.02%) 

ANALY 7 ANALY 8 

0.106E+07 

( 1.362) 

0.168E+07 

( 2.16%) 

ANGINA 

DAYS(ME) 

0.381E+07 

( 4.91%) 

0.292E+07 

< 3.76%) 

0.439E+07 

( 5.66%) 

0.180E+07 

( 2.32%) 

0.217E+07 

< 2.79%) 

0.205E+07 

( 2.64%) 

0.269E+07 

( 3.47%) 

0.413E+07 

< 5.32%) 

ANGINA 

DAYS(HI) 

0.863E+07 

(11.11%) 

0.685E+07 

( 8.82%) 

0.975E+07 

(12.56%) 

0.439E+07 

( 5.65%) 

0.522E+07 

( 6.73%) 

0.496E+07 

( 6.39%) 

0.637E+07 

( 8.20%) 

0.925E+07 

(11.92%) 

ANGINA 

HRS (LO) 

0.199E+08 

( 1.07%) 

0.164E+08 

( 0.88%) 

0.223E+08 

( 1.19%) 

0.119E+08 

( 0.64%) 

0.134E+08 

( 0.72%) 

0.129E+08 

< 0.69%) 

0.154E+08 

( 0.83%) 

0.212E+08 

( 1.14%) 

ANGINA 

HRS (ME) 

0.509E+08 

( 2.73%) 

0.423E+08 

( 2.27%) 

0.565E+08 

( 3.03%) 

0.310E+08 

( 1.66%) 

0.348E+08 

( 1.87%) 

0.335E+08 

( 1.80%) 

0.399E+08 

( 2.14%) 

0.539E+08 

( 2.90%) 

ANGINA 

HRS (HI) 

0.121E+09 

( 6.52%) 

0.103E+09 

( 5.52%) 

0.133E+09 

( 7.15%) 

0.774E+08 

( 4.15%) 

0.860E+08 

( 4.62%) 

0.831E+08 

( 4.46%) 

0.975E+08 

( 5.23%) 

0.128E+09 

( 6.87%) 

HEART 

ATTA(LO) 

0.159E+04 

( 3.37%) 

0.105E+04 

( 2.23%) 

0.172E+04 

( 3.66%) 

0.383E+03 

( 0.81%) 

0.705E+03' 

( 1.50%) 

0.500E+03 

( 1.06%) 

0.997E+03 

( 2.12%) 

0.165E+04 

( 3.50%) 

HEART 

ATTA(ME) 

0.317E+04 

( 6.74%) 

0.210E+04 

( 4.46%) 

0.345E+04 

( 7.32%) 

0.766E+03 

( 1.63%) 

0.141E+04 

( 3.00%) 

0.100E+04 

( 2.13%) 

0.199E+04 

( 4.23%) 

0.329E+04 

( 6.99%) 

HEART 

ATTA(HI) 

0.635E+04 

(13.48%) 

0.420E+04 

( 8.92%) 

0.689E+04 

(14.64%) 

0.153E+04 

( 3.25%) 

0.282E+04 

( 5.99%) 

0.200E+04 

( 4.25%) 

0.399E+04 

( 8.47%) 

0.659E+04 

(13.99%) 

HEART 

FATA(LO) 

0.194E+04 

( 6.85%) 

0.127E+04 

( 4.51%) 

0.211E+04 

( 7.45%) 

0.462E+03 

( 1.63%) 

0.853E+03 

( 3.02%) 

0.604E+03 

( 2.14%) 

0.121E+04 

( 4.28%) 

0.201E+04 

( 7.12%) 

HEART 

FATA(ME) 

0.394E+04 

(13.93%) 

0.258E+04 

< 9.12%) 

0.429E+04 

(15.18%) 

0.927E+03 

( 3.28%) 

0.172E+04 

( 6.08%) 

0.121E+04 

( 4.30%) 

0.244E+04 

( 8.64%) 

0.409E+04 

(14.48%) 

HEART 

FATA(HT) 

0.813E+04 

(28.78%) 

0.527E+04 

(18.64%) 

0.888E+04 

(31.42%) 

0.187E+04 

( 6.61%) 

0.349E+04 

(12.34%) 

0.245E+04 

( 8.68%) 

0.499E+04 

(17.65%) 

0.846E+04 

(29.94%) 

ANGINA 

AGGRAVA 

0.131E+08 

(16.82%) 

0.967E+07 

(12.45%) 

0.153E+08 

(19.72%) 

0.542E+07 

( 6.98%) 

0.665E+07 

( 8.56%) 

0.622E+07 

( 8.01%) 

0.876E+07 

(11.27%) 

0.143E+08 

(18.40%) 

COPD 

AGGRAVA 

0.327E+08 

(16.82%) 

0.242E+08 

(12.45%) 

0.383E+08 

(19.72%) 

0.136E+08 

( 6.98%) 

0.166E+08 

( 8.56%) 

0.156E+08 

( 8.01%) 

0.219E+08 

(11.27%) 

0.358E+08 

(18.40%) 

PUD 

AGGKAUA 

0.142E+07 

(16.82%) 

0.105E+07 

(12.45%) 

0.167E+07 

(19.72%) 

0.590E+06 

( 6.98%) 

0.724E+06 

( 8.56%) 

0.678E+06 

( 8.01%) 

0.953E+06 

(11.27%) 

0.156E+07 

(18.40%) 

VICTl. 

AGGRAVA 

0.241Et*06 

( 0.01%) 

0.434E+05 

( 0.00%) 

0.499E+06 

( 0.02%) 

0.0 

( 0.0 %) 

0.0 

( 0.0 %) 

0.0 

( 0.0 %) 

0.170E+05 

( 0.00%) 

0.3A9E+06 

( 0.01%) 

PREMAr 

INCI DEN 

0.193Kf04 

( 1.67%) 

0.11AE+04 

( 1.00%) 

0.233E+04 

( 2.01%) 

0.550E+03 

( 0.47%) 

0.765E+03 

( 0.66%) 

0.639E+03 

( 0.55%) 

0.106E+04 

( 0.91%) 

0.217E+04 

( 1.87%) 
Table 7.2 RISK ESTIMATES FOR CHICAGO 

(Using general exposure data) 

P.36 

CHICAGO 

IMPACT ANALY 1 ANALY 2 

ANGINA 0.319E+06 0.320E+06 

DAYS(LO) ( 1.34%) ( 1.35%) 

ANGINA 0.807E+06 0.810E+06 

DAYS(ME) ( 3.39%) ( 3.40%) 

ANGINA 0.189E+07 0.190E+07 

DAYS(HI) ( 7.96%) ( 7.98%) 

ANGINA 0.309E+07 0.310E+07 

HRS (LO) ( 0.54%) ( 0.54%) 

ANGINA 0.807E+07 0.811E+07 

HRS (ME) ( 1.41%) ( 1.42%) 

ANGINA 0.202E+08 0.203E+08 

HRS (HI) ( 3.54%) ( 3.56%) 

HEART 

FATA(LO) 

HEART 

FATA(HI) 

ANALY 3 ANALY 4 

0.565E+06 

( 2.38%) 

0.135E+07 

( 5.66%) 

0.289E+07 

(12.16%) 

0.478E+07 

( 0.84%) 

0.121E+08 

( 2.12%) 

0.287E+08 

( 5.03%) 

0.160E+06 

( 0.67%) 

0.422E+06 

( 1.77%) 

0.107E+07 

( 4.49%) 

0.128E+06 

( 0.02%) 

0.342E+06 

( 0.06%) 

0.866E+06 

( 0.15%) 

ANALY 5 

0.220E+06 

( 0.93%) 

0.572E+06 

( 2.40%) 

0.141E+07 

( 5.92%) 

0.233E+07 

( 0.41%) 

0.618E+07 

( 1.08%) 

0.159E+08 

( 2.78%) 

ANALY 6 

0.195E+06 

( 0.82%) 

0.509E+06 

( 2.14%) 

0.127E+07 

( 5.34%) 

0.212E+07 

( 0.37%) 

0.563E+07 

( 0.99%) 

0.145E+08 

( 5%) 

ANALY 7 

0.286E+06 

( 1.20%) 

0.730E+06 

( 3.07%) 

0.174E+07 

( 7.31%) 

0.284E+07 

( 0.50%) 

0.746E+07 

( 1.31%) 

0.188E+08 

( 3.30%) 

ANALY 8 

0.430E+06 

( 1.81%) 

0.106E+07 

( 4.44%) 

0.237E+07 

( 9.98%) 

0.390E+07 

( 0.68%) 

0.100E+08 

( 1.76%) 

0.245E+08 

( 4.29%) 

HEART 0.311E+03 0.314E+03 0.563E+03 0.125E+03 0.222E+03 0.179E+03 0.2B9E+03 0.453E+03 

ATTA(LO) ( 2.16%) ( 2.18%) ( 3.91%) < 0.87%) ( 1.54%) ( 1.25%) ( 2.01%) ( 3.15%) 

HEART 0.623E+03 0.629E+03 0.113E+04 0.250E+03 0.444E+03 0.359E+03 0.577E+03 0.906E+03 

ATTA(ME) ( 4.33%) ( 4.37%) ( 7.82%) ( 1.74%) ( 3.08%) ( 2.49%) ( 4.01%) ( 6.29%) 

HEART 0.125E+04 0.126E+04 0.225E+04 0.500E+03 0.888E+03 0.718E+03 0.115E+04 0.181E+04 

ATTA(HI) ( 8.65%) ( 8.74%) (15.64%) ( 3.48%) ( 6.17%) ( 4.99%) ( 8.02%) (12.58%) 

0.378E+03 0.381E+03 

< 4.37%) ( 4.42%) 

0.688E+03 

( 7.97%) 

0.151E+03 

( 1.75%) 

0.268E+03 

( 3.11%) 

0.217E+03 

( 2.51%) 

0.350E+03 

( 4.05%) 

0.552E+03 

( 6.39%) 

HEART 0.764E+03 0.771E+03 0.140E+04 0.303E+03 0.541E+03 0.436E+03 0.707E+03 0.112E+04 

FATA(ME) ( 8.84%) ( 8.93%) (16.25%) ( 3.51%) < 6.26%) ( 5.05%) ( 8.18%) (12.98%) 

0.156E+04 0.158E+04 

(18.06%) (18.23%) 

0.291E+04 

(33.72%) 

0.611E+03 

( 7.07%) 

0.110E+04 

(12.72%) 

0.883E+03 

(10.22%) 

0.144E+04 

(16.69%) 

0.231E+04 

(26.75%) 

ANGINA 0.258E+07 0.259E+07 0.457E+07 0.917E+06 0.152E+07 0.126E+07 0.224E+07 0.358E+07 

AGGRAVA (10.83%) (10.87%) (19.21%) ( 3.85%) ( 6.41%) ( 5.30%) ( 9.41%) (15.03%) 

COPD 0.645E+07 0.647E+07 0.114E+08 0.230E+07 0.382E+07 0.316E+07 0.560E+07 0.895Ef07 

AGGRAVA (10.83%) (10.87%) (19.21%) ( 3.85%) ( 6.41%) ( 5.30%) ( 9.41%) (15.03%) 

PUD 0.281E+06 0.281E+06 0.497E+0A 0.998E+05 0.166E+06 0.137E+06 0.244E+06 0.389E+06 

AGGRAVA (10.83%) (10.87%) (19.21%) ( 3.85%) ( 6.41%) ( 5.30%) ( 9.41%) (15.03%) 

VIGIL 0.331E+05 0.382E+0S 0.446E+06 0.0 0.0 0.0 0.250E+05 0.120E+06 

AGGRAVA ( 0.00%) ( 0,00%) ( 0.05%) (0.0% ) (0.0% ) (0.0% ) ( 0.00%) ( 0.01%) 

PREMAI 0.372E+03 0.375E+03 0.941E+03 0.169E+03 0.241E+03 0.211E+03 0.325E+03 0.612E+03 

INC I DEN ( l.-05%) ( 1.06%) ( 2.667.) < 0,4H%) ( 0.68%) < 0.60%) ( 0.92%) ( 1.73%) 
Table 7.3 RISK ESTIMATES FOR PHILADELPHIA 

(Using general exposure data) 

IMPACT 

PHILA 

ANALY 1 ANALY 2 ANALY 3 ANALY 4 ANALY 5 ANALY 6 ANALY 7 ANALY 8 

ANGINA 

DAYS(LO) 

0.230E+06 

( 0.78%) 

0.305E+06 

( 1.03%) 

0.493E+06 

( 1.67%) 

0.164E+06 

( 0.56%) 

0.197E+06 

( 0.67%) 

0.209E+06 

( 0.71%) 

0.283E+06 

( 0.96%) 

0.495E+06 

( 1.68%) 

ANGINA 

DAYS(ME) 

0.584E+06 

( 1.98%) 

0.758E+06 

( 2.57%) 

0.117E+07 

< 3.96%) 

0.428E+06 

( 1.45%) 

0.508E+06 

( 1.72%) 

0.536E+06 

< 1.82%) 

0.709E+06 

( 2.40%) 

0.117E+07 

( 3.98%) 

ANGINA 

DAYS(HI) 

0.140E+07 

( 4.75%) 

0.177E+07 

( 5.99%) 

0.258E+07 

( 8.73%) 

0.107E+07 

( 3.61%) 

0.124E+O7 

< 4.21%) 

0.130E+07 

( 4.41%) 

0.167E+07 

( 5.65%) 

0.259E+07 

( 8.76%) 

ANGINA 

HRS (LO) 

0.283E+07 

( 0.40%) 

0.349E+07 

( 0.49%) 

0.499E+07 

( 0.70%) 

0.214E+07 

( 0.30%) 

0.157E+07 

( 0.22%) 

0.266E+07 

( 0.38%) 

0.331E+07 

( 0.47%) 

0.500E+07 

( 0.71%) 

ANGINA 

HRS (ME) 

0.737E+07 

( 1.04%) 

0.895E+07 

( 1.26%) 

0.124E+08 

< 1.75%) 

0.5A4E+07 

( 0.80%) 

0.412E+07 

( 0.58%) 

0.695E+07 

( 0.98%) 

0.853E+07 

( 1.20%) 

0.125E+08 

( 1.76%) 

ANGINA 

HRS (HI) 

0.183E+08 

( 2.58%) 

0.218E+0B 

( 3.07%) 

0.291E+08 

< 4.11%) 

0.143E+08 

( 2.02%) 

0.105E+08 

( 1.48%) 

0.173E+08 

( 2.45%) 

0.209E+08 

( 2.95%) 

0.291E+08 

( 4.11%) 

HEART 

ATTA(LO) 

0.424E+03 

< 2.36%) 

0.655E+03 

( 3.65%) 

0.965E+03 

( 5.38%) 

0.216E+03 

( 1.21%) 

0.331E+03 

( 1.85%) 

0.365E+03 

( 2.04%) 

0.613E+03 

( 3.42%) 

0.967E+03 

( 5.39%) 

HEART 

ATTA(ME) 

0.847E+03 

( 4.72%) 

0.131E+04 

( 7.31%) 

0.193E+04 

(10.76%) 

0.433E+03 

( 2.41%) 

0.663E+03 

( 3.70%) 

0.730E+03 

( 4.07%) 

0.123E+04 

( 6.83%) 

0.193E+04 

(10.79%) 

HEART 

ATTA(HI) 

0.169E+04 

( 9.45%) 

0.262E+04 

(14.61%) 

0.38AE+04 

(21.52%) 

0.866E+03 

( 4.83%) 

0.133E+04 

( 7.39%) 

0.146E+04 

( 8.14%) 

0.245E+04 

.(13.67%) 

0.387E+04 

(21.58%) 

HEART 

FATA(LO) 

0.514E+03 

( 4.78%) 

0.801E+03 

( 7.44%) 

0.119E+O4 

(11.05%) 

0.261E+03 

< 2.43%) 

0.401E+03 

( 3.73%) 

0.442E+03 

( 4.11%) 

0.748E+03 

( 6.95%) 

0.119E+04 

(11.08%) 

HEART 

FATA(ME) 

0.104E+04 

( 9.67%) 

0.163E+04 

(15.1-5%) 

0.244E+04 

(22.68%) 

0.526E+03 

( 4.89%) 

0.810E+03 

( 7.53%) 

0.894E+03 

( 8.31%) 

0.152E+04 

(14.13%) 

0.245E+04 

(22.74%) 

HEART 

FATA(HI) 

0.213E+04 

(19.79%) 

0.338E+04 

(31.37%) 

0.513E+04 

(47.67%) 

0.106E+04 

( 9.89%) 

0.165E+04 

(15.33%) 

0.182E+04 

(16.94%) 

0.314E+04 

(29.20%) 

0.514E+04 

(47.81%) 

ANGINA 

AGGRAVA 

0.157E+07 

( 5.31%) 

0.216E+07 

( 7.32%) 

0.360E+07 

(12.20%) 

0.107E+07 

( 3.62%) 

0.134E+07 

( 4.53%) 

0.142E+07 

( 4.82%) 

0.199E+07 

( 6.75%) 

0.362E+07 

(12.27%) 

COPD 

AGGRAVA 

0.393E+07 

( 5.31%) 

0.541E+07 

( 7.32%) 

0.901E+07 

(12.20%) 

0.267E+07 

( 3.62%) 

0.334E+07 

( 4.53%) 

0.356E+07 

( 4.82%) 

0.-499E+07 

( 6.75%) 

0.907E+07 

(12.27%) 

PVIi 

AGGRAVA 

0.171E+06 

( 5.3 1%) 

0.235E+06 

( 7.32%) 

0.392F+06 

(12.20%) 

0.116E+06 

( 3.62%) 

0.145E+06 

( 4.53%) 

0.155E+06 

( 4.82%) 

0.217E+06 

( 6.75%) 

0.394E+06 

(.12.27%) 

V I G.[ I... 

AGGRAVA 

0.512Et*05 

( 0.00%) 

0.188E+06 

( 0.02%) 

0.743E+06 

( 0.07%) 

0.350E+04 

( 0.00%) 

0.161E+05 

( 0.00%) 

0.286E+05 

( 0.00%) 

0.137E+06 

( 0.01%) 

0.748E+06 

( 0.07%) 

PREMA I' 

INCIDEN 

0.629L*: + 03 

( 1.43%) 

0.134E+04 

( :s.o:r/.) 

0.327E+04 

( 7.427.) 

0.2A9E+03 

( 0.61%) 

0.434E+03 

( 0.98%) 

0.518E+03 

( 1.17%) 

0.113E+04 

( 2.35%) 

0.328E+04 

( 7.44%) 
Table 7.4 RISK ESTIMATES FOR ST. LOUIS 

(Using general exposure data) 

IMPACT 

ANGINA 

DAYS(LO) 

ANGINA 

DAYS(ME) 

ST LOUIS 

ANALY 1 ANALY 2 

0.135E+06 0.116E+06 

( 1.11%) ( 0.95%) 

0.345E+06 0.299E+06 

< 2.85%) ( 2.46%) 

ANALY 3 

0.146E+06 

( 1.20%) 

0.371E+06 

( 3.05%) 

ANALY 4 

0.115E+06 

( 0.95%) 

0.298E+06 

( 2.46%) 

ANALY 5 ANALY 6 

0.203E+06 

( 1.67%) 

0.499E+06 

( 4.11%) 

0.148E+06 

< 1.22%) 

0.377E+06 

( 3.10%) 

ANALY 7 

0.989E+05 

( 0.81%) 

0.256E+06 

( 2.11%) 

ANALY 8 

0.223E+06 

( 1.83%) 

0.541E+06 

( 4.46%) 

ANGINA 

DAYS(HI) 

0.828E+06 0.726E+06 

( 6.82%) < 5.99%) 

0.881E+06 

( 7.26%) 

0.725E+06 

( 5.97%) 

0.113E+07 

( 9.34%) 

0.893E+06 

( 7.36%) 

0.630E+06 

( 5.19%) 

0.121E+07 

( 9.99%) 

ANGINA 

HRS (LO) 

0.175E+07 0.183E+07 

( 0.60%) ( 0.63%) 

0.226E+07 

( 0.77%) 

0.151E+07 

( 0.52%) 

0.161E+07 

( 0.55%) 

0.161E+07 

( 0.55%) 

0.185E+07 

( 0.63%) 

0.242E+07 

( 0.83%) 

ANGINA 

HRS (ME) 

0.457E+07 0.476E+07 

( 1.56%) < 1.63%) 

0.580E+07 

( 1.98%) 

0.397E+07 

( 1.36%) 

0.422E+07 

( 1.45%) 

0.422E+07 

( 1.44%) 

0.480E+07 

( 1.64%) 

0.615E+07 

( 2.11%) 

ANGINA 

HRS (HI) 

0.114E+08 0.118E+08 

< 3.89%) ( 4.03%) 

0.140E+08 

( 4.80%) 

0.100E+08 

( 3.42%) 

0.106E+08 

( 3.62%) 

0.106E+08 

( 3.62%) 

0.119E+08 

( 4.07%) 

0.148E+08 

( 5.05%) 

HEART 0.182E+03 0.210E+03 0.323E+03 0.818E+02 0.136E+03 0.132E+03 0.214E+03 0.348E+03 

ATTA(LO) ( 2.46%) ( 2.85%) ( 4.37%) ( 1.11%) ( 1.84%) ( 1.79%) ( 2.89%) ( 4.72%) 

HEART 

ATTA(ME) 

0.363E+03 0.421E+03 

< 4.92%) ( 5.70%) 

0.646E+03 

( 8.75%) 

0.164E+03 

( 2.22%) 

0.272E+03 

( 3.69%) 

0.264E+03 

( 3.58%) 

0.427E+03 

( 5.79%) 

0.696E+03 

( 9.44%) 

HEART 0.726E+03 0.842E+03 0.129E+04 0.327E+03 0.544E+03 0.528E+03 0.854E+03 0.139E+04 

ATTA(HI) ( 9.84%) (11.40%) (17.50%) ( 4.43%) ( 7.37%) < 7.15%) (11.57%) (18.87%) 

HEART 0.221E+03 0.256E+03 0.396E+03 0.987E+02 0.165E+03 0.160E+03 0.260E+03 0.428E+03 

FATA(LO) ( 4.98%) ( 5.78%) ( 8.94%) < 2.23%) ( 3.72%) ( 3.61%) ( 5.87%) ( 9.66%) 

HEART 0.446E+03 0.519E+03 0.809E+03 0.199E+03 0.333E+03 0.322E+03 0.527E+03 0.875E+03 

FATA(ME) (10.08%) (11.73%) (18.26%) ( 4.48%) ( 7.51%) ( 7.28%) (11.91%) (19.76%) 

HEART 0.914E+03 0.107E+04 0.169E+04 0.401E+03 0.677E+03 0.656E+03 0.108E+04 0.183E+04 

FATA(HI) (20.64%) (24.11%) (38.05%) ( 9.06%) (15.29%) (14.81%) (24.49%) (41.30%) 

ANGINA 

AGGRAVA 

0.105E+07 0.884E+06 

( 8.64%) ( 7.29%) 

0.114E+07 

( 9.37%) 

0.881E+06 

( 7.26%) 

0.159E+07 

(13.09%) 

0.116E+07 

( 9.53%) 

0.735E+06 

( 6.05%) 

0.174E+07 

(14.37%) 

COPD 

AGGRAVA 

0.262E+07 0.221E+07 

( 8.64%) ( 7.29%) 

0.285E+07 

( 9.37%) 

0.221E+07 

( 7.26%) 

0.398E+07 

(13.09%) 

0.290E+07 

( 9.53%) 

0.184E+07 

( 6.05%) 

0.437E+07 

(14.37%) 

PVD 

AGGRAVA 

0.114E+06 0.963E+05 

( 8.64%) ( 7.29%) 

0.124E+06 

( 9.37%) 

0.959E+05 

( 7.26%) 

0.173E+06 

(13.09%) 

0.126E+06 

( 9.53%) 

0.800E+05 

( 6.05%) 

0.190E+06 

(14.37%) 

VIG.II. 0.773E + 04 0.232EI-04 0.207E t-05 0.232E+04 0.118E+06 0.219E+05 0.0 0.158E + 06 

AGGRAVA ( 0.00%) ( 0.00%) ( 0.00%) ( 0.00%) ( 0.03%) ( 0.00%) ( 0.0 %) ( 0.04%) 

PREMAT 0.235E+03 0.306EfO3 0 . 779E + 03 0.993E + 02 0.154E+03 0.150E+03 0.310E + 03 0.905E+03 

INCIDEN ( 1.29%) ( l.o8%) ( 4.29%) ( 0.55%) ( 0.85%) ( 0.82%) ( 1.71%) ( 4.99%) 

12.56.1: 
P.39 

Table 7.5 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR LOS ANGELES 

(Using general exposure data) 

PROP CALCULAT LA 

IMPACT 

ANG(.1%) 

ANG<5%> 

ANG(10%) 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ANALY 1 

99.99% 

45.59% 

4.26% 

69.46% 

0.00% 

0.0 % 

99.43% 

2.53% 

0.01% 

ANALY 2 

99.83% 

24.36% 

1.21% 

24.79% 

0.0 % 

0.0 7. 

91.32% 

0.08% 

0.00% 

ANALY 3 

100.00% 

58.59% 

7.72% 

77.25% 

0.00% 

0.0 7. 

99.71% 

4.36% 

0.01% 

ANALY 4 

96.30% 

4.36% 

0.06% 

0.02% 

0.0 % 

0.0 % 

6.04% 

0.0 7. 

0.0 7. 

ANALY 5 

98.6 2% 

9.25% 

. 0.22% 

3.36% 

0.0 7. 

0.0 7. 

58.56% 

0.00% 

0.0 % 

ANALY 6 

98.11% 

7.49% 

0.16% 

0.24% 

0.0 % 

0.0 •/. 

21.87% 

0.0 % 

0.0 % 

ANALY 7 

99.67% 

19.2 4% 

0.78% 

20.24% 

0.0 % 

0.0 % 

88.69% 

0.04% 

0.00% 

ANALY 8 

99.99% 

52.96% 

6.02% 

73.11% 

0.00% 

0.0 % 

99.58% 

3.25% 

0.01% 

Table 7.6 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR CHICAGO 

(Using general exposure data) 

PROB CALCULAT CHICAGO 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(.L0%) 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ANALY 1 

99.64% 

17.71% 

0.65% 

22.08% 

0.0 % 

0.0 % 

89.85% 

0.05% 

0.00% 

ANALY 2 

99.65% 

17.89% 

0.66% 

22.89% 

0.0 % 

0.0 % 

90.32% 

0.06% 

0.00% 

ANALY 3 

100.00% 

58.69% 

6.94% 

82.57% 

0.01% 

0.0 % 

99.84% 

6.47% 

0.03% 

ANALY 4 

88.15% 

1.35% 

0.01% 

0.03% 

0.0 % 

0.0 % 

a. 69% 

0.0 7. 

0.0 % 

ANALY 5 

96.80% 

5.29% 

0.09% 

4.03% 

0.0 % 

0.0 7. 

61.77% 

0.00% 

0.0 % 

ANALY 6 

94.41% 

3.27% 

0.04% 

0.91% 

0.0 % 

0.0 % 

37.66% 

0 . 00% 

0.0 % 

ANALY 7 

99.25% 

12.87% 

0.38% 

16.15% 

0.0 % 

0.0 % 

85.45% 

0.02% 

0.0 % 

ANALY 8 

99.97% 

36.44% 

2.43% 

62.19% 

0.00% 

0.0 % 

99.03% 

1 . 55% 

0 . 0 0 7. 
P.40 

Table 7.7 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR PHILADELPHIA 

(Using general exposure data) 

PROB CALCULAT PHILA 

IMPACT 

ANG(1%> 

ANG(5%) 

ANGU0%> 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ANALY 1 

92.88% 

1.83% 

0.01% 

30.30% 

0.00% 

0.0 % 

93.63% 

0.13% 

0.00% 

ANALY 2 

98.21% 

5.91% 

0.08% 

77.11% 

0.00% 

0.0 % 

99.71% 

4.31% 

0.01% 

ANALY 3 

99.95% 

26.70% 

1.07% 

96.35% 

0.27% 

0.00% 

99.99% 

28.17% 

0.66% 

ANALY 4 

77.64% 

0.37% 

0.00% 

0.71% 

0.0 % 

0.0 % 

34.15% 

0.00% 

0.0 % 

ANALY 5 

87.26% 

* 0.93% 

0.01% 

11.03% 

0.0 7. 

0.0 % 

79.41% 

0.01% 

0.0 % 

ANALY 6 

89.66% 

1.22% 

0.01% 

17.21% 

0.0 % 

0.0 % 

86.39% 

0.03% 

0.0 %' 

ANALY 7 

97.31% 

4.45% 

0.05% 

70.84% 

0.00% 

0.0 % 

99.49% 

2 . 78% 

0.01% 

ANALY 8 

99.95% 

27.00% 

1 . 10% 

96.90% 

0.28% 

0.00% 

99.99% 

28.43% 

0.68% 

Table 7.8 PROBABILITY THAT 1, 5, or 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR ST. LOUIS 

(Using general exposure data) 

PROB CALCULAT 

IMPACT 

ANG( 17.) 

ANG(5%) 

ANG(10%) 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ST LOUIS 

ANALY 1 

98.81% 

9.85% 

0.24% 

34.47% 

0.00% 

0.0 7. 

94.94% 

0 . 20% 

0.00% 

ANALY 2 

97.26% 

5.64% 

0.10% 

51.07% 

0.00% 

0.0 % 

98.03% 

0.72% 

0.00% 

ANALY 3 

99.25% 

12.61% 

0.36% 

89.64% 

0.04% 

0.0 % 

99.94% 

11.79% 

0. 10% 

ANALY 4 

97.21% 

5.57% 

•0.10% 

0.35% 

0.0 % 

0.0 % 

25.64% 

0.00% 

0.0 % 

ANALY 5 

99.94% 

30.25% 

1 .667. 

10.90% 

0.0 % 

0.0 % 

79.20% 

0.01% 

0.0 % 

ANALY 6 

99.33% 

13.30% 

0.39% 

9.34% 

0.0 % 

0.0 % 

76.60% 

0.01% 

0.0 7. 

ANALY 7 

94.26% 

2.88% 

0.03% 

52.77% 

0.00% 

0.0 % 

98.22% 

0.81% 

0 . 00% 

ANALY 8 

99.97% 

36.95% 

2.44% 

93.06% 

0.08% 

0 . 00% 

99.97% 

16.78% 

0 .20% 
P.41 

Table 7.9 RISK ESTIMATES FOR SPECIAL E-XPOSURE GROUP FOR LOS ANGELES 

SPEC ESTIMATE LA 

IMPACT ANALY 1 ANALY 2 ANALY 3 ANALY 4 ANALY 5 ANALY 6 ANALY 7 ANALY 8 

ANGINA 0.755E+06 0.565E+O6 0.893E+06 0.327E+06 0.376E+06 0.360E+06 0.490E+06 0.821E+06 

DAYS(LO) ( 0.97%) ( 0.73%) ( 1.15%) ( 0.42%) ( 0.48%) ( 0.46%) ( 0.63%) < 1.06%) 

ANGINA 0.196E+07 0.149E+07 0.229E+07 0.877E+06 0.101E+07 0.963E+06 0.130E+07 0.212E+07 

DAYS(ME) ' ( 2.52%) ( 1.91%) ( 2.95%) ( 1.13%) ( 1.30%) (' 1.24%) ( 1.67%) ( 2.73%) 

ANGINA 0.480E+07 0.375E+07 0.552E+07 0.233E+07 0.264E+07 0.254E+07 0.331E+07 0.514E+07 

DAYS(HI) ( 6.18%) ( 4.83%) ( 7.11%) ( 3.00%) ( 3.41%) ( 3.27%) ( 4.27%) ( 6.62%) 

ANGINA 0.917E+07 0.731E+07 0.105E+08 0.533E+07 0.583E+07 0.567E+07 0.680E+07 0.988E+07 

HRS <L0) ( 0.49%) < 0.39%) ( 0.56%) (.0.29%) ( 0.31%) < 0.30%) ( 0.36%) ( 0.53%) 

ANGINA 0.243E+08 0.195E+08 0.277E+08 0.144E+08 0.157E+08 0.153E+08 0.182E+08 0.260E+08 

HRS (ME) ( 1.30%) ( 1.05%) ( 1.48%) ( 0.77%) ( 0.84%) ( 0.82%) < 0.98%) < 1.40%) 

ANGINA 0.622E+08 0.510E+08 0.699E+08 0.384E+08 0.418E+08 0.407E+08 0.478E+08 0.663E+08 

HRS (HI) ( 3.34%) ( 2.74%) ( 3.75%) ( 2.06%) ( 2.24%) ( 2.18%) ( 2.57%) ( 3.56%) 

HEART 0.11SE+04 0.589E+03 0.118E+04 0.147E+03 0.294E+03 0.294E+03 0.589E+03 0.118E+04 

ATTA(LG) ( 2.50%) ( 1.25%) ( 2.50%) ( 0.31%) ( 0.62%) ( 0.62%) ( 1.25%) ( 2.50%) 

HEART 0.235E+04 0.118E+04 0.235E+04 0.294E+03 0.589E+03 0.589E+03 0.118E+04 Q.235E+04 

ATTA(ME) ( 5.00%) ( 2.50%) ( 5.00%) ( 0.62%) ( 1.25%) ( 1.25%) ( 2.50%) ( 5.00%) 

HEART 0.471E+04 0.235E+04 0.471E+04 0.589E+03 0.118E+04 0.118E+04 0.235E+04 0.471E+04 

ATTA(HI) (10.00%) ( 5.00%) (10.00%) ( 1.25%) ( 2.50%) ( 2.50%) ( 5.00%) (10.00%) 

HEART 0.143E+04 0.711E+03 0.143E+04 0.177E+03 0.354E+03 0.354E+03 0.711E+03 0.143E+04 

FAIA(LO) ( 5.06%) ( 2.52%) ( 5.06%) ( 0.63%) ( 1.25%) ( 1.25%) ( 2.52%) ( 5.06%) 

HEART 0.290E+04 0.143E+04 0.290E+04 0.354E+03 0.711E+03 0.711E+03 0.143E+04 0.290E+04 

I-ATA(ME) (10.25%) ( 5.06%) (10.25%) ( 1.25%) ( 2.52%) ( 2.52%) ( 5.06%) (10.25%) 

HEART 0.593E+04 0.290E+04 0.593E+04 0.711E+03 0.143E+04 0.143E+04 0.290E+04 0.593E+04 

FATA(HI) (21.00%) (10.25%) (21.00%) ( 2.52%) ( 5.06%) ( 5.06%) (10.25%) (21.00%) 

ANGINA 0.509E+07 0.335E+07 0.639E+07 0.993E+06 0.135E+07 0.123E+07 0.255E+07 0.570E+07 

AGGRAVA ( 6.56%) ( 4.32%) ( 8.22%) ( 1.28%) ( 1.74%) ( 1.58%) ( 3.29%) ( 7.34%) 

COPD 0.127E+08 0.840E+07 0.160E+08 0.249E+07 0.338E+07 0.308E+07 0.640E+07 0.143E+08 

AGGRAVA ( 6.56%) ( 4.32%) ( 3.22%) ( 1.28%) ( 1.74%) ( 1.58%) ( 3.29%) ( 7.34%) 

PVD 0.554E+06 0.365E+06 0.695E+06 0.108E+06 0.147E+06 0.134E+06 0.278E+06 0.621E+06 

AGGRAVA ( 6.56%) ( 4.32%) ( 3.22%) ( 1.28%) ( 1.74%) ( 1.58%) ( 3.29%) ( 7.34%) 

VIGIL 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 

AGGRAVA ( 0.0 7.) ( 0.0 %) ( 0.0 7.) ( 0.0 7.) ( 0.0 7.) ( 0.0 %) ( 0.0 %) ( 0.0 %) 

PREhAT 0.I1SE+04 0.654E+03 0.115E+04 0.371E+03 0.475E+03 0.475E+03 0.654E+03 0.115E+04 

INC I DEN ( 0.99%) ( 0.56%) ( 0.99%) ( 0.32%) ( 0.41%) ( 0.41%) ( 0.56%) ( 0.99%) 
Table 7.10 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR CHICAGO 

P.42 

SPEC ESTIMATE CHICAGO 

IMPACT ANALY 1 ANALY 2 

ANGINA 0.101E+06 0.101E+06 

DAYS(LO) ( 0.42%) ( 0.42%) 

ANGINA 0.270E+06 0.270E+06 

•DAYS(ME) ( 1.14%) ( 1.14%) 

ANALY 3 

0.134E+06 

( 0.56%) 

0.354E+06 

( 1.49%) 

ANALY 4 

0.817E+05 

( 0.34%) 

0.220E+06 

( 0.92%) 

ANALY 5 

0.886E+05 

( 0.37%) 

0.238E+06 

( 1.00%) 

ANALY 6 ANALY 7 ANALY 8 

0.839E+05 

( 0.35%) 

0.226E+06 

< 0.95%) 

0.978E+05 

( 0.41%) 

0.262E+06 

( 1.10%) 

0.114E+06 

( 0.48%) 

0.302E+06 

( 1.27%) 

ANGINA 

DAYS(HI) 

0.711E+06 0.711E+06 

< 2.99%) ( 2.99%) 

0.905E+06 

( 3.80%) 

0.S88E+06 

( 2.47%) 

0.632E+06 

( 2.66%) 

0.603E+06 

( 2.54%) 

0.691E+06 

( 2.90%) 

0.786E+06 

( 3.30%) 

ANGINA 

HRS (LO) 

0.111E+07 0.112E+07 

( 0.20%) ( 0.20%) 

0.144E+07 

( 0.25%) 

0.469E+06 

( 0.08%) 

0.904E+06 

( 0.16%) 

0.831E+06 

( 0.15%) 

0.105E+07 

( 0.18%) 

0.128E+07 

( 0.22%) 

ANGINA 

HRS (ME) 

0.300E+07 0.301E+07 

( 0.53%) < 0.53%) 

0.386E+07 

( 0.68%) 

0.128E+07 

( 0.22%) 

0.244E+07 

( 0.43%) 

0.225E+07 

< 0.39%) 

0.283E+07 

( 0.50%) 

0.344E+07 

( 0.60%) 

ANGINA 

HRS (HI) 

0.800E+07 0.802E+07 

( 1.40%) ( 1.41%) 

0.101E+08 

( 1.78%) 

0.346E+07 

( 0.61%) 

0.6S6E+07 

( 1.15%) 

0.605E+07 

( 1.06%) 

0.757E+07 

( 1.33%) 

0.912E+07 

( 1.60%) 

HEART 0.180E+03 0.180E+03 0.360E+03 0.450E+02 0.900E+02 

ATTA(LO) ( 1.25%) ( 1.25%) ( 2.50%) ( 0.31%) ( 0.62%) 

HEART 0.360E+03 0.360E+03 0.720E+03 0.900E+02 0.180E+03 

ATTA(ME) < 2.50%) ( 2.50%) < 5.00%) < 0.62%) ( 1.25%) 

0.900E+02 

( 0.62%) 

0.180E+03 

( 1.25%) 

0.180E+03 

( 1.25%) 

0.360E+03 

( 2.50%) 

0.360E+03 

( 2.50%) 

0.720E+03 

( 5.00%) 

HEART 

ATTA(HI) 

0.720E+03 0.720E+03 

( 5.00%) ( 5.00%) 

0.144E+04 

(10.00%) 

0.180E+03 

( 1.25%) 

0.360E+03 

< 2.50%) 

0.360E+03 

( 2.50%) 

0.720E+03 

( 5.00%) 

0.144E+04 

(10.00%) 

HEART 

FATA(LO) 

0.217E+03 0.217E+03 

( 2.52%) ( 2.52%) 

0.437E+03 

( 5.06%) 

0.541E+02 

( 0.63%) 

0.108E+03 

( 1.25%) 

0.108E+03 

( 1.25%) 

0.217E+03 

( 2.52%) 

0.437E+03 

( 5.06%) 

HEART 

FATA(ME) 

0.437E+03 0.437E+03 

( 5.06%) ( 5.06%) 

0.885E+03 

(10.25%) 

0.108E+03 

( 1.25%) 

0.217E+03 

< 2.52%) 

0.217E+03 

( 2.52%) 

0.437E+03 

( 5.06%) 

0.885E+03 

( 10.25%) 

HEART 

FATA(HI) 

0.885E+03 0.885E+03 

(10.25%) (10.25%) 

0.181E+04 

(21.00%) 

0.217E+03 

( 2.52%) 

0.437E+03 

( 5.06%) 

0.437E+03 

( 5.06%) 

0.885E+03 

(10.25%) 

0.181E+04 

(21.00%) 

ANGINA 

AGGRAVA 

0.353E+06 0.353E+06 

( 1.48%) ( 1.48%) 

0.652E+06 

( 2.74%) 

0.214E+06 

( 0.90%) 

0.263E+06 

( 1.10%) 

0.222E+06 

( 0.93%) 

0.334E+06 

( 1.40%) 

0.459E+06 

( 1.93%) 

COPD 

AGGRAVA 

0.884E+06 0.884E+06 

( 1.48%) ( 1.48%) 

0.163E+07 

( 2.74%) 

0.536E+06 

( 0.90%) 

0.658E+06 

( 1.10%) 

0.556E+06 

( 0.93%) 

0.835E+06 

( 1.40%) 

0.115E+07 

( 1.93%) 

PVD 

AGGRAVA 

0.384E+05 0.384E+05 

( 1.48%) ( 1.48%) 

0.709E+05 

( 2.74%) 

0.233E+05 

( 0.90%) 

0.286E+05 

( 1.10%) 

0.242E+05 

( 0.93%) 

0.363E+05 

( 1.40%) 

0.499E+05 

( 1.93%) 

VIGIL 

AGGRAVA 

0.0 0.0 

( 0.0 %) ( 0.0 7.) 

0.0 

( 0.0 7.) 

0.0 

( 0.0 %) 

0.0 

( 0.0 %) 

0.0 

( 0.0 7.) 

0.0 

( 0.0 %) 

0.0 

( 0.0 %) 

PREMAT 

INCIDEN 

0.200E+03 0.200E+03 

( 0.56%) ( 0.56%) 

0.350E+03 

( 0.99%) 

0.113E+03 

( 0.32%) 

0.145E+03 

( 0.41%) 

0.145E + 03' 

( 0.41%> 

0.2OOE+03 

( 0.56%) 

0.350E+03 

( 0.99%) 
Table 7.11 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR PHILADELPHIA 

SPEC ESTIMATE PHILA 

IMPACT 

ANGINA 

DAYS(LO) 

ANGINA 

DAYS(ME) 

ANGINA 

DAYS(HI) 

ANGINA 

HRS (LO) 

ANGINA 

HRS (ME) 

ANGINA 

HRS (HI) 

HEART * 

ATTA(LO) 

HEART 

ATTA(ME) 

HEART 

ATTA(HI) 

HEART 

FATA(LO) 

HEART 

FATA(ME) 

HEART 

FATA(HI) 

ANGINA 

AGGRAVA 

COPD 

AGGRAVA 

PVD 

AGGRAVA 

VIGIL 

AGGRAVA 

PREMAT 

INC I DEN 

ANALY 1 

0.160E+06 

( 0.54%) 

0.407E+06 

( 1.38%) 

0.997E+06 

( 3.38%) 

0.170E+07 

( 0.24%) 

0.451E+07 

( 0.64%) 

0.117E+08 

( 1.65%) 

0.560E+03 

( 3.12%) 

0.112E+04 

( 6.25%) 

0.224E+04 

(12.50%) 

0.683E+03 

( 6.35%) 

0.139E+04 

(12.89%) 

0.286E+04 

(26.56%) 

0.766E+06 

( 2.60%) 

0.192E+07 

( 2.60%) 

0.834E+05 

( 2.60%) 

0.885E+05 

( 0.01%) 

0.931E+03 

( 2.11%) 

ANALY 2 

0.265E+06 

( 0.90%) 

0.641E+06 

( 2.17%) 

0.148E+07 

( 5.03%) 

0.728E+07 

( 1.03%) 

0.184E+08 

( 2.60%) 

0.430E+08 

( 6.07%) 

0.897E+03 

( 5.00%) 

0.179E+04 

(10.00%) 

0.359E+04 

(20.00%) 

0.110E+04 

(10.25%) 

0.226E+04 

(21.00%) 

0.473E+04 

(44.OOX) 

0.148E+07 

( 5.02%) 

0.371E+07 

( 5.02%) 

0.161E+06 

( 5.02%) 

0.390E+06 

( 0.04%) 

0.258E+04 

( 5.85%) 

ANALY 3 

0.479E+06 

( 1.62%) 

0.110E+07 

( 3.73%) 

0.241E+07 

( 8.18%) 

0.415E+07 

( 0.59%) 

0.102E+08 

( 1.44%) 

0.242E+08 

( 3.41%) 

0.123E+04 

( 6.87%) 

0.247E+04 

(13.75%) 

0.493E+04 

(27.50%) 

0.153E+04 

(14.22%) 

0.316E+04 

(29.39%) 

0.673E+04 

(62.56%) 

0.311E+07 

(10.53%) 

0.778E+07 

(10.53%) 

0.338E+06 

(10.53%) 

0.127E+07 

( 0.12%) 

0.639E+04 

(14.49%) 

ANALY 4 

0.946E+05 

( 0.32%) 

0.251E+06 

( 0.85%) 

0.656E+06 

( 2.22%) 

0.108E+07 

( 0.15%) 

0.291E+07 

( 0.41%) 

0.777E+07 

( 1.10%) 

0.280E+03 

( 1.56%) 

0.560E+03 

( 3.13%) 

0.112E+04 

( 6.25%) 

0.339E+03 

( 3.15%) 

0.683E+03 

( 6.35%) 

0.139E+04 

(12.89%) 

0.359E+06 

( 1.22%) 

0.898E+06 

( 1.22%) 

0.390E+05 

( 1.22%) 

0.0 

( 0.0 %) 

0.329E+03 

( 0.74%) 

ANALY 5 

0.130E+06 

< 0.44%) 

0.338E+06 

( 1.15%) 

0.848E+06 

( 2.87%) 

0.144E+07 

( 0.20%) 

0.383E+07 

( 0.54%) 

0.101E+08 

< 1.42%) 

0.448E+03 

( 2.50%) 

0.897E+03 

( 5.00%) 

0.179E+04 

(10.00%) 

0.545E+03 

( 5.06%) 

0.U0E + 04 

(10.25%) 

0.226E+04 

(21.00%) 

0.607E+06 

( 2.05%) 

0.152E+07 

( 2.05%) 

0.660E+05 

( 2.05%) 

0.0 

( 0.0 %) 

0.576E+03 

( 1.30%) 

ANALY 6 

0.149E+06 

( 0,51%) 

0.379E+06 

( 1.28%) 

0.928E+06 

( 3.14%) 

0.155E+07 

( 0.22%) 

0.412E+07 

( 0.58%) 

0.108E+08 

( 1.52%) 

0.448E+03 

( 2.50%) 

0.897E+03 

( 5.00%) 

0.179E+04 

(10.00%) 

0.545E+03 

( 5.06%) 

0.110E+04 

(10.25%) 

0.226E+04 

(21.00%) 

0.699E+06 

< 2.37%) 

0.175E+07 

( 2.37%) 

0.761E+05 

( 2.37%) 

0.885E+05 

( 0.01%) 

0.576E+03 

( 1.30%) 

ANALY 7 

0.234E+06 

( 0.79%) 

0.574E+06 

< 1.94%) 

0.134E+07 

( 4.55%) 

0.220E+07 

( 0.31%) 

0.571E+07 

( 0.81%) 

0.144E+08 

( 2.03%) 

0.785E+03 

( 4.37%) 

0.157E+04 

( 3.75%) 

0.314E+04 

(17.50%) 

0.962E+03 

( 8.94%) 

0.197E+04 

(18.27%) 

0.410E+04 

(38.06%) 

0.124E+07 

( 4.21%) 

0.311E+07 

( 4.21%) 

0.135E+06 

( 4.21%) 

0.302E+06 

( 0.03%) 

0.160E+04 

( 3.62%) 

ANALY 8 

0.488E+06 

( 1.65%) 

0.111E+07 

( 3.76%) 

0.243E+07 

( 8.22%) 

0.416E+07 

( 0.59%) 

0.103E+08 

( 1.45%) 

0.243E+08 

( 3.43%) 

0.123E+04 

( 6.87%) 

0.247E+04 

(13.75%) 

0.493E+04 

(27.50%) 

0.153E+04 

(14.22%) 

0.316E+04 

(29.39%) 

0.673E+04 

(62.56%) 

0.312E+07 

(10.56%) 

0.781E+07 

(10.56%) 

0.339E+06 

(10.56%) 

0.139E+07 

( 0.13%) 

0.639E+04 

(14.49%) 
Table 7.12 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR ST. LOUIS 

SPEC ESTIMATE ST LOUIS 

IMPACT ANALY 1 ANALY 2 ANALY 3 ANALY 4 ANALY 5 ANALY 6 ANALY 7 ANALY 8 

ANGINA 

DAYS(LO) 

ANGINA 

DAYS(ME) 

ANGINA 

DAYS(HI) 

ANGINA 

HRS (LO) 

ANGINA 

HRS (ME) 

ANGINA 

HRS (HI) 

HEART 

ATTA(LO) 

HEART 

ATTA(ME) 

HEART 

ATTA(HI) 

HEART 

FATA(LO) 

HEART 

FATA(ME) 

HEART 

FATA(HI) 

ANGINA 

AGGRAVA 

COPD 

AGGRAVA 

PVD 

AGGRAVA 

VIGIL 

AGGRAVA 

PREMAT 

INCI DEN 

0.648E+05 

( 0.53%) 

0.171E+06 

( 1.41%) 

0.436E+06 

( 3.59%) 

0.798E+06 

( 0.27%) 

0.213E+07 

< 0.73%) 

0.562E+07 

( 1.92%) 

0.185E+03 

( 2.50%) 

0.369E+03 

( 5.00%) 

0.738E+03 

(10.00%) 

0.224E+03 

( 5.06%) 

0.454E+03 

(10.25%) 

0.930E+03 

(21.00%) 

0.294E+06 

( 2.42%) 

0.736E+06 

( 2.42%) 

0.320E+05 

( 2.42%) 

0.0 

( 0.0 %> 

0.237E+03 

( 1.30%) 

0.552E+05 

( 0.45%) 

0.147E+06 

( 1.21%) 

0.382E+06 

( 3.15%) 

0.839E+06 

( 0.29%) 

0.224E+07 

( 0.77%) 

0.586E+07 

( 2.01%) 

0.185E+03 

( 2.50%) 

0.369E+03 

( 5.00%) 

0.738E+03 

(10.00%) 

0.224E+03 

( 5.06%) 

0.454E+03 

(10.25%) 

0.930E+03 

(21.00%) 

0.212E+06 

( 1.75%) 

0.532E+06 

( 1.75%) 

0.231E+05 

( 1.75%) 

0.0 

( 0.0 %) 

0.237E+03 

( 1.30%) 

0.740E+05 

( 0.61%) 

0.192E+06 

( 1.58%) 

0.483E+06 

< 3.98%) 

0.108E+07 

( 0.37%) 

0.283E+07 

( 0.97%) 

0.718E+07 

( 2.46%) 

0.277E+03 

( 3.75%) 

0.554E+03 

( 7.50%) 

0.111E+04 

(15.00%) 

0.338E+03 

( 7.64%) 

0.689E+03 

(15.56%) 

0.143E+04 

(32.25%) 

0.349E+06 

( 2.87%) 

0.873E+06 

( 2.87%) 

0.379E+05 

( 2.87%) 

0.0 

( 0.0 %) 

0.630E+03 

( 3.47%) 

0.549E+05 

( 0.45%) 

0.146E+06 

( 1.20%) 

0.381E+06 

( 3.14%) 

0.693E+06 

( 0.24%) 

0.187E+07 

( 0.64%) 

0.500E+07 

( 1.71%) 

0.692E+02 

( 0.94%) 

0.138E+03 

( 1.88%) 

0.277E+03 

( 3.75%) 

0.834E+02 

( 1.88%) 

0.168E+03 

( 3.79%) 

0.338E+03 

( 7.64%) 

0.211E+06 

( 1.73%) 

0.527E+06 

( 1.73%) 

0.229E+05 

( 1.73%) 

0.0 

< 0.0 %) 

0.862E+02 

( 0.47%) 

0. 105E+06 

( 0.86%) 

0.262E+06 

( 2.16%) 

0.627E+06 

( 5.17%) 

0.731E+06 

( 0.25%) 

0.197E+07 

< 0.67%) 

0.524E+07 

< 1.79%) 

0.115E+03 

( 1.56%) 

0.231E+03 

( 3.13%) 

0.461E+03 

( 6.25%) 

0.139E+03 

( 3.15%) 

0.281E+03 

( 6.35%) 

0.571E+03 

(12.89%) 

0.540E+06 

( 4.45%) 

0.135E+07 

( 4.45%) 

0.588E+05 

( 4.45%) 

0.878E+05 

( 0.02%) 

0.13SE+03 

( 0.74%) 

0.759E+05 

( 0.63%) 

0.197E+06 

( 1.62%) 

0.493E+06 

( 4.06%) 

0.731E+06 

( 0.25%) 

0.197E+07 

( 0.67%) 

0.523E+07 

( 1.79%) 

0.115E+03 

( 1.56%) 

0.231E+03 

( 3.13%) 

0.461E+03 

( 6.25%) 

0.139E+03 

( 3.15%) 

0.281E+03 

( 6.35%) 

0.571E+03 

(12.89%) 

0.361E+06 

( 2.98%) 

0.904E+06 

( 2.98%) 

0.393E+05 

( 2.98%) 

0.0 

( 0.0 %> 

0.135E+03 

( 0.74%) 

0.478E+05 

( 0.39%) 

0.128E+06 

( 1.06%) 

0.340E+06 

( 2.81%) 

0.850E+06 

( 0.29%) 

0.226E+07 

( 0.78%) 

0.592E+07 

( 2.03%) 

0.185E+03 

( 2.50%) 

0.369E+03 

( 5.00%) 

0.738E+03 

(10.00%) 

0.224E+03 

( 5.06%) 

0.454E+03 

(10.25%) 

0.930E+03 

(21.00%) 

0.145E+06 

( 1.20%) 

0.364E+06 

( 1.20%) 

0.158E+05 

( 1.20%) 

0.0 

( 0.0 %) 

0.237E+03 

( 1.30%) 

0.118E+06 

( 0.97%) 

0.287E+06 

( 2.36%) 

0.673E+06 

( 5.55%) 

0.118E+07 

( 0.40%) 

0.305E+07 

( 1.04%) 

0.764E+07 

( 2.61%) 

0.277E+03 

( 3.75%) 

0.554E+03 

( 7.50%) 

0.111E+04 

(15.00%) 

0.338E+03 

< 7.64%) 

0.689E+03 

(15.56%) 

0.143E+04 

(32.25%) 

0.599E+06 

< 4.94%) 

0.150E+07 

< 4.94%) 

0.652E+05 

( 4.94%) 

0.161E+06 

( 0.04%) 

0.630E+03 

( 3.47%) 
P.45 

Table 7.13 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR LOS ANGELES 

(Using special exposure group data) 

PROB CALCULAT LA 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(10%) 

HEA(1%) 

HEA(5%) 

HEA(10%> 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ANALY 1 

97.50% 

6.42% 

0.13% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 2 

91.02% 

1.99% 

0.02% 

0.93% 

0.0 % 

0.0 % 

37.95% 

0.00% 

0.0 % 

ANALY 3 

99.01% 

11.45% 

0.32% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 4 

59.47% 

0.12% 

0.00% 

0.0 % 

0.0 % 

0.0 % 

0.00% 

0.0 % 

0.0 % 

ANALY 5 

69.83% 

0.27% 

0.00% 

0.00% 

0.0 7. 

0.0 % 

1.03% 

0.0 % 

0.0 % 

ANALY 6 

66.64% 

0.21% 

0.00% 

0.00% 

0.0 % 

0.0 % 

1.03% 

0.0 % 

0.0 % 

ANALY 7 

85.26% 

1.02% 

0.01% 

0.93% 

0.0 % 

0.0 % 

37.95% 

0.00% 

0.0 % 

ANALY 8 

98.40% 

8.62% 

0.20% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

Table 7.14 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR CHICAGO 

(Using special exposure group data) 

PROB CALCULAT CHICAGO 

IMPACT 

ANG(IX) 

ANG(5%) 

ANG(10%) 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT (5%) 

FAT(10%) 

ANALY 1 

59.84% 

0.12% 

0.00% 

0.93% 

0.0 % 

0.0 % 

37.95% 

0.00% 

0.0 % 

ANALY 2 

59.84% 

0.12% 

0.00% 

0.93% 

0.0 % 

0.0 % 

37.95% 

0.00% 

0.0 % 

ANALY 3 

79.18% 

0.52% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 4 

43.47% 

0.03% 

0.00% 

0.0 % 

0.0 % 

0.0 % 

0.00% 

0.0 % 

0.0 % 

ANALY 5 

49.73% 

0.05% 

0.00% 

0.00% 

0.0 % 

0.0 % 

1.03% 

0.0 % 

0.0 % 

ANALY 6 

45.62% 

0.04% 

0.00% 

0.00% 

0.0 % 

0.0 % 

1.03% 

0.0 % 

0.0 % 

ANALY 7 

• 57.42% 

0.10% 

0.00% 

0.93% 

0.0 % 

0.0 % 

37.95% 

0.00% 

0.0 % 

ANALY 8 

68.49% 

0.22% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 
Table 7.15 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR PHILADELPHIA 

(Using special exposure group data) 

PROB CALCULAT PHILA 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(10%) 

HEA(1%) 

HEA(5%) 

H£A(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ANALY 1 

74.95% 

0.23% 

0.00% 

61.46% 

0.00% 

0.0 % 

98.98% 

1.47% 

0.00% 

ANALY 2 

96.16% 

2.44% 

0.02% 

95.03% 

0.14% 

0.00% 

99.99% 

21.41% 

0.35% 

ANALY 3 

99.94% 

22.31% 

0.66% 

99.49% 

1.89% 

0.00% 

100.00% 

55.36% 

4.10% 

ANALY 4 

36.53% 

0.01% 

0.00% 

4.38% 

0.0 % 

0.0 % 

63.22% 

0.00% 

0.0 % 

ANALY 5 

60.52% 

0.08% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 6 

69.85% 

0.14% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 7 

93.12% 

1.41% 

0.01% 

89.66% 

0.04% 

0.0 % 

99.94% 

11.81% 

0.10% 

ANALY 8 

99.95% 

22.90% 

0.67% 

99.49% 

1.89% 

0.00% 

100.00% 

55.36% 

4.10% 

Table 7.16 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL SUFFER 

ADVERSE HEALTH EFFECTS FOR ST. LOUIS 

(Using special exposure group data) 

PROB CALCULAT 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(10%> 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

ST LOUIS 

ANALY 1 

75.60% 

0.37% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 2 

64.74% 

0.16% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY 3 

83.07% 

0.67% 

0.00% 

79.32% 

0.01% 

0.0 % 

99.77% 

5.06% 

0.02% 

ANALY 4 

64.40% 

0.16% 

0.00% 

0.07% 

0.0 % 

0.0 % 

12.72% 

0.0 % 

0.0 % 

ANALY 5 

95.44% 

2.82% 

0.03% 

4.38% 

0.0 % 

0.0 % 

63.22% 

0.00% 

0.0 % 

ANALY 6 

84.35% 

0.75% 

0.00% 

4.38% 

0.0 % 

0.0 % 

63.22% 

0.00% 

0.0 % 

ANALY 7 

54.21% 

0.08% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.41% 

0.23% 

0.00% 

ANALY U 

97.40% 

4.04% 

0.04% 

79.32% 

0.01% 

0.0 % 

99.77% 

5.06% 

0.02% 
Table 7.17 RISK ESTIMATES FOR U.S. URBAN POPULATION 

(Using general exposure data) 

IMPACT ANALY 1 ANALY 2 ANALY 3 ANALY 4 ANALY 5 ANALY 6 ANALY 7 ANALY 8 

ANGINA 0.217E+08 0.200E+08 0.314E+08 0.123E+08 0.131E+08 0.157E+08 0.180E+08 0.311E+08 

DAYS(LO) ( 1.30%) ( 1.21%) ( 1.89%) ( 0.77%) ( 1.09%) ( 0.94%) ( 1.09%) ( 1.87%) 

ANGINA 0.545E+08 0.507E+08 0.761E+08 0.332E+08 0.4S3E+08 0.403E+08 0.459E+08 0.756E+08 

DAYS(ME) ( 3.28%) ( 3.05%) ( 4.58%) ( 2.00%) ( 2.76%) ( 2.43%) ( 2.76%) ( 4.55%) 

ANGI'NA 0.127E+09 0.120E+09 0.169E+09 0.820E+08 0.109E+09 0.976E+08 0.109E+09 0.169E+09 

DAYS(HI) ( 7.66%) ( 7.20%) (10.18%) ( 4.93%) ( 6.55%) ( 5.38%) ( 6.59%) (10.16%) 

ANGINA 0.260E+09 0.253E+09 0.350E+09 0.147E+09 0.189E+09 0.198E+09 0.242E+09 0.334E+09 

HRS (LO) ( 0.65%) ( 0.64%) ( 0.88%) ( 0.37%) '( 0.48%) ( 0.50%) ( 0.61%) ( 0.84%) 

ANGI'NA 0.673E+09 0.656E+09 0.886E+09 0.387E+09 0.496E+09 0.520E+09 0.628E+09 0.849E+09 

HRS (ME) ( 1.69%) ( 1.65%) ( 2.22%) ( 0.97%) ( 1.24%) ( 1.30%) ( 1.57%) ( 2.13%) 

ANGINA 0.165E+10 0.161E+10 0.210E+10 0.972E+09 0.125E+10 0.130E+10 0.155E+10 0.203E+10 

HRS (HI) ( 4.13%) ( 4.05%) ( 5.27%) ( 2.44%) ( 3.12%) ( 3.27%) ( 3.39%) ( 5.08%) 

HEART 0.261E+05 0.275E+05 0.436E+05 0.101E+05 0.170E+05 0.154E+05 0.263E+05 0.422E+05 

ATTA(LO) ( 2.59%) ( 2.73%) ( 4.33%) ( 1.00%) ( 1.68%) ( 1.53%) ( 2.61%) ( 4.19%) 

HEART 0.522E+05 0.550E+05 0.873E+05 0.201E+05 0.339E+05 0.309E+05 0.526E+05 0.844E+05 

ATTA(ME) ( 5.18%) ( 5.46%) ( 8.66%) ( 2.00%) ( 3.37%) ( 3.07%) ( 5.22%) ( 8.38%) 

HEART 0.104E+06 0.110E+06 0.175E+06 0.403E+05 0.678E+05 0.618E+05 0.105E+06 0.169E+06 

ATTA(HI) (10.36%) (10.92%) (17.32%) ( 4.00%) ( 6.73%) ( 6.13%) (10.43%) (16.76%) 

HEART 0.317E+05 0.335E+05 0.535E+05 0.12*E+05 0.205E+05 0.187E+05 0.320E+05 0.518E+05 

FATA(LO) ( 5.25%) ( 5.54%) ( 8.85%) ( 2.01%) ( 3.39%) ( 3.09%) ( 5.29%) ( 8.56%) 

HEART 0.643E+05 0.679E+05 0.109E+06 0.244E+05 0.414E+05 0.377E+05 0.648E+05 0.106E+06 

FATA(ME) (10.63%) (11.23%) (18.09%) ( 4.04%) ( 6.85%) ( 6.23%) (10.72%) (17.49%) 

HEART 0.132E+06 0.140E+06 0.22SE+06 0.493E+05 0.842E+05 0.766E+05 0.133E+06 0.220E+06 

FATA(HI) (21.82%) (23.09%) (37.72%) ( 8.16%) (13.92%) (12.67%) (22.01%) (36.45%) 

ANGINA 0.362E+09 0.383E+09 0.625E+09 0.135E+09 0.231E+09 0.210E+09 0.365E+09 0.604E+09 

AGGRAVA (10.40%) ( 9.48%) (15.12%) ( 5.43%) ( 8.15%) ( 6.92%) ( 8.37%) (15.02%) 

COPD 0.433E+09 0.394E+09 0.629E+09 0.226E+09 0.339E+09 0.288E+09 0.348E+09 0.625E+09 

AGGRAVA (10.40%) ( 9.48%) (15.12%) < 5.43%) ( 8.15%) ( 6.92%) ( 8.37%) (15.02%) 

PVD 0.395E+08 0.418E+08 0.682E+08 0.148E+08 0.252E+08 0.229E+08 0.398E+08 0.659E+08 

AGGRAVA (10.40%) ( 9.48%) (15.12%) ( 5.43%) ( 8.15%) ( 6.92%) ( 8.37%) (15.02%) 

VIGIL 0.285E+07 0.363E+07 0.216E+08 0.129E+06 0.426E+07 0.115E+07 0.246E+07 0.200E+08 

AGGRAVA < 0.00%) ( 0.01%) ( 0.04%) ( 0.00%) ( 0.01%) ( 0.00%) ( 0.00%) ( 0.03%) 

PREMAT 0.123E+08 0.153E+08 0.370E+08 0.477E+07 0.717E+07 0.711E+07 0.138E+08 0.362E+08 

INC I DEN ( 1.36%) ( 1.69%) ( 4.10%) ( 0.53%) ( 0.79%) ( 0.79%) ( 1.52%) ( 4.01%) 
Table 7.18 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR U.S. URBAN POPULATION 

(Using general exposure data) 

PROB CALCULAT 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(10%) 

HEA( 17.) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FAT(5%) 

FAT(10%) 

TOTAL 

ANALY 1 

99.57% 

15.70% 

0.50% 

40.06% 

0.00% 

0.0 % 

96.30% 

0.32% 

0.00% 

ANALY 2 

99.27% 

12.34% 

0.34% 

46.07% 

0.00% 

0.0 % 

97.37% 

0.51% 

0.00% 

ANALY 3 

99.98% 

39.14% 

2.7.1% 

89.12% 

0.03% 

0.0 % 

99.94% 

11.31% 

0.09% 

ANALY 4 

92.72% 

z*» ^*"~*% 

0.02% 

0.14% 

0.0 % 

0.0 % 

17.02% 

0.0 % 

0.0 % 

ANALY 5 

98.64% 

8.46% 

0.18% 

6.75% 

0.0 % 

0.0 % 

70.94% 

0.00% 

0.0 % 

ANALY 6 

97.09% 

5.21% 

0.08% 

3.89% 

0.0 % 

0.0 % 

61.25% 

0.00% 

0.0 % 

ANALY 7 

98.63% 

8.63% 

0.19% 

40.89% 

0.00% 

0.0 % 

96.47% 

0.34% 

0.00% 

ANALY 8 

99.98% 

38.62% 

2.68% 

37.22% 

0.02% 

0.0 % 

99.91% 

9.61% 

0.06% 
Table 7.19 RISK ESTIMATES FOR SPECIAL EXPOSURE GROUP FOR 

U.S. URBAN POPULATION 

SPEC ESTTMATE 

IMPACT ANALY 1 ANALY 2 ANALY 3 ANALY 4 ANALY 5 ANALY 6 ANALY 7 ANALY 8 

ANGINA 0.103E+08 0.104E+08 0.164E+08 0.638E+07 0.878E+07 0.809E+07 0.926E+07 0.173E+08 

DAYS(LO) ( 0.62%) ( 0.63%) ( 0.99%) ( 0.38%) ( 0.54%) ( 0.49%) ( 0.56%) ( 1.04%) 

ANGINA 0.268E+08 0.267E+08 0.405E+08 0.171E+08 0.233E+08 0.212E+08 0.240E+08 0.421E+08 

DAYS(ME) ( 1.61%) ( 1.61%) ( 2.44%) ( 1.03%) ( 1.40%) ( 1.27%) ( 1.44%) ( 2.53%) 

ANGINA 0.671E+08 0.665E+08 0.958E+08 0.450E+08 0.586E+0S 0.540E+08 0.604E+08 0.9S4E+08 

DAYS(HI) ( 4.04%) ( 4.00%) ( 5.77%) ( 2.71%) < 3.53%) ( 3.25%) ( 3.63%) ( 5.92%) 

ANGINA 0.120E+0 9 0.190E + 09 0.177E+0 9 0.756E + 08 0.922E + 08 0.917E + 08 0.U5 E + 09 0..174E+09 

HRS (LO) ( 0.30%) ( 0.48%) ( 0.44%) ( 0.19%) ( 0.23%) ( 0.23%) ( 0.29%) ( 0.44%) 

ANGINA 0.319E+09 0.492E+09 0.456E+09 0.204E+09 0.248E+09 0.246E+09 0.305E+09 0.448E+09 

HRS (ME) ( 0.80%) ( 1.23%) ( 1.14%) ( 0.51%) ( 0.62%) ( 0.62%) ( 0.76%) ( 1.12%) 

ANGINA 0.829E+09 0.122E+10 0.114E+10 0.546E+09 0.658E+09 0.654E+09 0.793E+09 0.112E+10 

HRS (HI) ( 2.08%) ( 3.06%) ( 2.85%) ( 1.37%) ( 1.65%) ( 1.64%) ( 1.99%) ( 2.80%) 

HEART 0.236E+05 0.252E+05 0.394E+05 0.787E+04 0.134E+05 0.134E+05 0.236E+05 0.394E+05 

ATTA(LO) ( 2.34%) ( 2.50%) ( 3.91%) ( 0.78%) ( 1.33%) ( 1.33%) ( 2.34%) ( 3.91%) 

HEART 0.472E+05 0.504E+05 0.787E+05 0.157E+05 0.268E+05 0.268E+05 0.472E+05 0.787E+05 

ATTA(ME) ( 4.69%) ( 5.00%) ( 7.81%) ( 1.56%) ( 2.66%) ( 2.667.) ( 4.69%) ( 7.81%) 

HEART 0.945E+05 0.101E+06 0.157E+06 0.315E+05 0.535E+05 0.535E+05 0.945E+05 0.157E+06 

ATTA(HI) ( 9.37%) (10.00%) (15.62%) ( 3.12%) ( 5.31%) ( 3.31%) ( 9,37%) (15.62%) 

HEART 0.287E+05 0.307E+05 0.483E+05 0.950E+04 0.162E+05 0.162E+05 0.288E+05 0.483E+05 

FAIAd-O) ( 4.75%) ( 5.09%) ( 8.00%) ( 1.57%) ( 2.68%) ( 2.68%) ( 4.76%) ( fl.00%) 

HEART 0.581E+05 0.625E+05 0.989E+05 0.191E+05 0.327E+05 0.327E+05 0.584E+05 0.989E+05 

FATA(ME) ( 9.61%) (10.34%) (16.36%) ( 3.16%) ( 5.41%) ( 5.41%) ( 9.66%) (.16.36%) 

HEART 0.119E+06 0.129E+06 0.207E+06 0.386E+05 0.665E+05 0.665E+05 0.L20E+06 0.207E+06 

FATA(HI) (19.70%) (21.37%) (34.20%) ( 6.39%) (1.1.00%) (1.1.00%) (19.89%) (34.20%) 

ANGINA 0.327E+09 0.354E+09 0.567E+09 0.106E+09 0.182E+09 0.182E+09 0.330E+09 0.567E+09 

AGGRAVA ( 3.27%) ( 3.14%) ( 6.09%) ( 1.28%) ( 2.34%) ( 1.97%) ( 2.52%) ( 6.19%) 

COPD 0.136E+09 0.131E+09 0.253E+09 0.533E+08 0.972E+00 0.8.18E+08 0.105E+09 0.258E+09 

AGGRAVA ( 3.27%) ( 3.14%) ( 6.09%) ( 1.28%) ( 2.34%) ( 1.97%) ( 2.52%) ( 6.19%) 

PVD 0.356E+08 0.387E+08 0.619E+08 0.116E+08 0.199E+08 0.199E+08 0.3A0E+08 0.619E+08 

AGGRAVA ( 3.27%) ( 3.14%) ( 6.09%) ( 1,28%) ( 2.34%) ( 1.97%) ( 2.52%) < 6.1.9%) 

VIGIL 0.125E+07 0.S50E+07 0.178E+08 0.0 0.301E+07 0.125E+07 0.425E+07 0.251E+08 

AGGRAVA ( 0.00%) ( 0.01%) ( 0.03%) ( 0.0 %) ( 0.00%) ( 0.00%) ( 0.01%) ( 0.04%) 

PREMAT 0.112E + 08 0.137E+08 0.451E + 08 0.421E + 07 0.649E + 07 0.649E + 07 0.137E + 08 0.45.I.E + 08 

INC.! DEN ( 1.24%) ( 2.07%) ( 4.99%) ( 0.46%) ( 0.72%) ( 0.72%) ( 1.51%) ( 4.99%) 
Table 7.20 PROBABILITY THAT 1, 5, OR 10 PERCENT OF SENSITIVE GROUP WILL 

SUFFER ADVERSE HEALTH EFFECTS FOR U.S. URBAN POPULATION 

(Using special exposure group data) 

PROB CALCULAT TOTAL 

IMPACT 

ANG(1%) 

ANG(5%) 

ANG(10%) 

HEA(1%) 

HEA(5%) 

HEA(10%) 

FAT(1%) 

FA 1(5%) 

FAT(10%) 

••ALY 1 

83.84% 

0.73% 

0.00% 

29,51% 

0.00% 

0.0 % 

93.39% 

0.13% 

0.00% 

ANALY 2 

84.18% 

0.68% 

0.00% 

36.22% 

0.00% 

0.0 % 

95.54% 

0.27% 

0.00% 

ANALY 3 

97.65% 

4.86% 

0.06% 

82.52% 

0.01% 

0.0 % 

99.84% 

6.91% 

0.03% 

ANALY 4 

51.80% 

0.06% 

0.00% 

0.01% 

0.0 % 

0.0 % 

4.93% 

0.0 7. 

0.0 % 

ANALY 5 

75.75% 

0.31% 

0.00% 

1 .47% 

0.0 % 

0.0 % 

45.38% 

0.00% 

0.0 % 

ANALY* 6 

68.88% 

0.19% 

0 .00% 

1 .4 7% 

0.0 % 

0.0 % 

45.38% 

0.00% 

0.0 % 

ANALY 7 

77.69% 

0.38% 

0.00% 

29.51% 

0.00% 

0.0 % 

93.49% 

0.14% 

0.00% 

ANALY 8 

98.23% 

5.54% 

0.07% 

82.52% 

0.01% 

0.0 % 

99.84% 

6.91% 

0.03%