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HEALTH CONSEQUENCES OF SULFUR OXIDES:.
SUMMARY AND CONCLUSIONS
BASED UPON CHESS STUDIES OF 1970-1971
John F. Finklea, M.D., Carl M. Shy, M.D., G.J. Love, Sc-.D.,
Carl G. Hayes, Ph.D., William C. Nelson, Ph.D.,
Robert S. Chapman, M.D. and Dennis E. House, M.S.
Human Studies Laboratory
National Environmental Research Center
Environmental Protection Agency
Research Triangle Park, North Carolina
August 15, 1973
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NOTICE
This document Is a preliminary draft. It
has not been formally released by EPA
and should not at this stajre be construed
to represent Agency policy. It is beinjr
circulated for comment on its technical
accuracy and policy implications.
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INTRODUCTION
In this final paper of the CHESS monograph, we will summarize results
r i
from the different CHESS areas, make comparisons of data obtained for each
health indicator, and attempt to draw conclusions concerning the level of
pollutant exposure associated with undesirable health effects. Epidemiologic
studies grouped into the CHESS program provided dose-response information
relating short-term and long-term sulfur oxide exposures to adverse health
effects. The individual research reports presented in the monograph often
suggested pollutant-disease associations but left a number of problems
unanswered. These problems include (1) the relative contribution of various
air pollutants, especially sulfur dioxide, total suspended particulates and
suspended sulfates to observed disease frequencies; (2) the importance of
intervening influences, or covariates, such as occupational exposures, socio-
economic status, residential mobility, cigarette smoking; (3) the association
s
between chronic disease prevalence and current vs. past pollutant exposures;
(4) the precise pollutant threshold for excess "disease in exposed communities.
Obviously, epidemiologic .studies alone cannot resolve all, or any one,
of the above problems. The findings of this monograph must be substantiated
by replicated observations in different years and under different circumstances,
Well controlled human and animal studies are required to isolate several of
the important intervening variables which are inherent to studies of free
i
living populations, and to elucidate the precise nature of the pollutant-
. j
disease relationship. Hence, the conclusions put forth in this overview
cannot be definitive, but are offered ia the sense of developing more refined
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quantitative and scientific hypotheses concerning pollutant-health effect
associations in a rea.l-life environment. In the CHESS program itself, we are
repeating our observations, using essentially the same health indicators in
the same (and more) communities. These results wvlT provide one form of
data verification required for scientifically defensible air quality standards.
In relating observed health effects to possible pollutant thresholds,
wherever practical and possible, three threshold estimates were provided:
a "worst case estimate," which attributes an observed adverse health effect
to the lowest pollution exposure suggested by the epidemiologic studies
after considering only the strongest and most established covariates; a
"least case estimate," which attributes an observed adverse health effect
to the highest pollution exposure level suggested by the epidemiologic studies
after considering effects of all covariates and a "best judgment estimate"
based upon a synthesis of several studies. The best judgment estimate duly
considers interactions between pollutants and is at times based upon special
analyses that were necessary when individual studies raised questions regarding
interactions involving pollutants or intervening variables.
A. Responses to Long-Term Pollutant Exposures
1. Summary of Chronic Respiratory Disease Studies
Chronic bronchitis prevalence rates observed in four CHESS areas are
2-5
given in Table 1. In each of the four studies," a very consistent pattern
of excess chronic bronchitis (as defined in this monograph) was found among
residents of more polluted communities. In each case, these differences
i
were statistically significant. Mean respiratory symptom scores, which
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take into account less severe as well as more classical chronic respiratory
symptoms, are tabulated for each-CHESS area,in Table 2. Symptom scores
substantiate the consistent pattern of excess respiratory symptoms among
participants from more polluted neighborhoods.
52 3
In the New York, Utah, and Idaho-Montana surveys where parents of
school children were studied, several consistent.findings,were observed.
For both smokers and nonsmokers there was a male excess of chronic respiratory
disease, whether defined in terms of bronchitis prevalence or of symptom
scores. Chronic bronchitis rates and symptom scores were higher among
male and female smokers. Finally, male and female nonsmokers, exsmokers
and current smokers had higher chronic bronchitis rates and symptom scores
in the high as opposed to the low exposure areas.
Despite considerable variation in the population characteristics and
pollutant exposures of the above three CHESS areas, the relative contribution
of cigarette smoking alone was greater than the effect of the air pollution
gradient (Tables 3 and 4), with the exception of males in New York.
'Among males in the Salt Lake and Rocky Mountain CHESS areas, and among all
females, air pollution alone was associated with an excess bronchitis rate
(when compared with nonsmokers of low exposure neighborhoods) ranging from
1.5 to 3.8 percent. Among New York City males, this excess was 11.3
percent - an unusually high figure requiring verification in subsequent
study years. Cigarette smoking alone accounted for an excess bronchitis
rate of 9.3 to 16.6 percent in the three CHESS areas. Thus, the relative
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contribution of air pollution alone ranged from one-third to one-seventh
as strong as that of cigarette smoking as a'determinant of chronic
bronchitis prevalence in communities (with the exception of males in
New York, where air pollution appeared to make a slightly larger contribution
than smoking - a finding difficult to accept in the light of other evidence).
The range of observed differences in the relative contributions of smoking
/ ,
and pollution is not surprising, in view of the quantitative and qualitative
differences in pollution profiles of the communities studied, as well as the
community differences in smoking patterns. The sum of the evidence suggests
that, while personal cigarette smoking is the largest determinant of
bronchitis prevalence among parents of school children, air pollution
itself is a significant and consistent contributing factor, leading to
increased bronchitis rates in nonsmokers as well as smokers from polluted
communities.
4
Among young white military recruits studied in the Chicago area,
s
air pollution was associated with a considerably smaller excess in bronchitis
-rates (Table 3) than was found in the other CHESS areas, and the contribution
of air pollution was relatively much less than that of cigarette smoking.
However, there was evidence that even among these young (18-24 year old)
inductees,'respiratory symptoms were more prevalent among persons from
more polluted communities. Black and white inductees showed similar
effects of pollution on bronchitis rates (Tables 1 and 3). In the case
of blacks, these effects were superimposed on higher base rates among
persons residing in relatively clean outstate areas. Whether these high
rates are attributable to sources of indoor pollution or other environmental
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factors, whether these baseline rates are indeed verifiable remains to be
studied. Strangely, cigarette sraokipg alone was associated with no excess
bronchitis in blacks, while cigarette smoking and air pollution combined
accounted for more bronchitis than the additive effect,pf both pollution
and smoking. Among whites, air pollution and cigarette smoking were generally
additive in their effect on bronchitis rates among smokers within polluted
communities of each of the four CHESS areas.
Attempts were made to assess the length of residence in polluted areas
2-4
required for development of excess bronchitis rates. These findings
should be accepted in a very preliminary vein because relatively small
sample sizes were available for analysis after populations were finely
subdivided into smoking and residence-duration specific groups. The
overall evidence suggests that immigrants into polluted areas reported
excess chronic bronchitis after two to seven years of exposure. Further
5
evidence from the New York study indicated that movement from polluted
s
to clean communities could effect a substantial decline in bronchitis rates,
.while migration into a polluted community seems to result in high bronchitis
rates like those of the long-time residents of high exposure neighborhoods.
These conclusions should be taken'as hypotheses for further testing, but
they justify some optimism about current efforts to improve air quality.
An important feature of the CHESS program is the plan to re-survey residents
of the high exposure neighborhoods during and after achievement of desirable
air quality. These studies can provide considerably more firmness to the
conclusions stated in this monograph.
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Other covariates such as age, race, sex, socioeconomic status and
occupational exposure were controlled, insofar as possible, by the
selection of study areas and by appropriate adjustments.in statistical
r i
analyses. Covariates other than occupational exposure played a relatively
minor role as determinants of bronchitis prevalence. Participants with
known occupational exposure were analyzed separately, and- in none of the
above quantitative assessments concerning air pollution and cigarette
smoking was the occupationally exposed group included. Occupational exposure to
irritating dusts, fumes and aerosols added to the effects of ambient air pollution
and cigarette smoking in producing a higher prevalence of chronic bronchitis
93
among exposed workers."' In general, occupational exposures made a quantitative
contribution somewhat larger than that of air pollution and one-half as large
as cigarette smoking.
Table 5 lists current (i.e. during the year of the survey) and past
exposures ~ (within 10 years) estimated for those communities in which excess
s
bronchitis was observed in the four CHESS studies. The precise exposure
or dose which should be associated with excess respiratory symptoms could
not be determined because accurate measures of past exposures were not made
and the duration of exposure required to produce excess respiratory disease
is not known. Current exposures may be taken as. a worst case estimate for
the chronic bronchitis effect, and past exposures as a least case estimate.
In the best judgment of the investigators, excess chronic bronchitis in the
Salt Lake Basin could be reasonably attributed to sulfur dioxide levels of
^
3 3
92 to 95 yg/m and/or suspended sulfate levels of 15 yg/m . This was the
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only CHESS area in which low concentrations of total suspended participates
occurred in the face of elevated sulfur oxide pollution. Pollutant concentrations
measured in 1971 were unlikely determinants of the excess bronchitis rates
in the high exposure Salt Lake Basin community. In the other CHESS areas,
combinations of particulate matter and sulfur oxide exposures occurred, and
the investigators judged that the lowest pollutant .concentrations which could
reasonably be associated with excess chronic bronchitis were past exposures
3 3
.to 100-177 yg/m sulfur dioxide, 80-118 yg/m total suspended particulates
3
and 9-14 yg/m suspended sulfates. The individual contribution of each pollutant
could not be identified.
From these data, it appeared that excess bronchitis may be reasonably
associated with community exposures to sulfur oxides alone, in the form of
annual levels of 92 to 95 yg/m S0? and 15 yg/m suspended sulfates. When
higher levels of particulate matter are present, annual exposures to 100
33 3
yg/m S0?, 120 yg/m total suspended particulate and 14 yg/m suspended
sulfate are reasonably associated with excess bronchitis. None of the
'CHESS areas experienced elevated exposures to total suspended particulates
without concomitant increases in sulfur oxide levels. Overall, these data
support the existing primary national standards" of 80 yg/m annual mean (arithmetic
for SOp and 75 yg/m annual mean (geometric) for total suspended particulates.
A national standard for suspended sulfates has not been established.
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2. Summary of Lower Respiratory Disease Studies of Children
In the lower respiratory disease (LRD) studies conducted in the
Salt Lake Basin and Rocky Mountain CHESS areas, ' three findings were
consistently observed. First, for all combinations of disease and numbers
of illness episodes, no significant association between total LRD and pollution
was found for children whose parents had been residents of their communities
for less than three years. Second, for single and repeated episodes of
croup and repeated episodes of any LRD, families of children who had lived
three or more years in the high exposure communities reported more illness
across all ages of children from 0 to 12 years than did their counterparts
in the less polluted communities. Third, for single and repeated illness
episodes and for residence duration, there was no association of pollution
exposure with pneumonia or number of hospitalizations for total LRD. The
only inconsistencies noted were that for children who had lived three or
more years in their community both single and repeated episodes of bronchitis
and single episodes of any LRQ were significantly associated with pollution
exposure in the Utah study, whereas these associations were not found in
the Rocky Mountain study.
The effects of the age and socioeconomic covariates were very consistent
in the two LRD studies. In almost every instance, significantly higher
illness rates occurred at younger ages, while there were very few significant
associations with socioeconomic levels of the household. In Utah, no
significant differences in illness rates of males and females were
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observed. In the Rocky Mountain study, male ana female crnldren who nad
lived in their communities for less than three years had similar illness
rates with the exception of single episodes'of croup. But, in every
instance, male children who had been residents of their community for three
or more years had higher illness rates than females. ' The reason for this
inconsistent sex effect is unknown.
The increase in the rates of single or repeated/episodes of LRD, croup,
and bronchitis attributable to high air pollution exposure can be determined
from the data in Table 6. This table gives the illness rates over a three
year reporting period for children who had been residents of their communities
for three or more years. During the three year periods covered by the two
studies, the mean annual S09 concentrations in the high exposure communities
3 3
were 92 yg/m in the Salt Lake Basin study and as high as 177 yg/m in the
Rocky Mountain study. Hence, a "worst case" estimate of the annual S0?
concentration associated with increased LRD is 92 yg/m while the "least
3
case" estimate is 177 yg/m . (The national primary standard for S0? is 80
3
ng/m annual arithmetic mean). During the same periods, mean annual suspended
s
' 3
sulfate concentrations in the high exposure communities were 15 ymg/m in
.the Salt Lake Basin study and as low as 7.2 yg/m "in the Rocky Mountain study.
For suspended sulfates, a "worst case" estimate of the annual concentration
3
associated with increased LRD is 7.'2 yg/m while-the "least case" estimate
3
is 15 yg/m . (A national standard for this pollutant does not exist.) Total
suspended particulate levels in the Rocky Mountain communities ranged from
3
65 to 102 yg/m , representing the worst case and least case estimates respectively
for this pollutant. (The national primary standard for total suspended particu-
3
lates is 75 yg/m annual geometric mean.)
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It is interesting to note that larger increases in total LRD and two
of its components were observed in the high pollution community of the Salt
Lake Basin study than in the corresponding communities in the Rocky Mountain
study. Also, the mean annual suspended sulfate concentration was higher
in the high pollution community in the Salt Lake Basin study than in the
Rocky Mountain study. The opposite was true for SCL. This suggests that
' " / , t
increases in LRO frequency are probably associated with suspended sulfates
rather than S0_.
Several cautions should be remembered when interpreting the results of
the LRD studies. First, the data were collected by asking the childrens'
parents about illness frequency over a three year period. Hence, the recall
ability of the parents could affect the validity of the data as could the
degree of cooperation of the parents. However, it does not seem likely that
this source of error affected the communities differently and thereby affected
ป,
the community comparisons. Second, there could be differences in diagnostic
criteria among the communities in a study. In both LRD studies, a sample
of physicians were asked to diagnose six respiratory syndromes so that a
determination of differences in diagnostic criteria could be made. No differences
were found in either study. Third, the communities observed in the studies
were mainly white and middle class. Therefore, the results of these studies
may not apply to other ethnic or socioeconomic groups. Fourth, a majority
of the pollution exposure data in both studies was'estimated from emissions
data. The degree to which these give reasonable estimates of individual
exposures may be questionable.
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On the basis of the two LRD studies in the monograph, and in the best
judgment of the investigators, it seems reasonable to conclude that there
is a positive association between lower respiratory disease frequency in
children and pollution exposure, and that excess respiratory disease may
reasonably be associated with community exposures to approximately 95 yg/m
SCL and 15 yg/m suspended sulfates. From these studies, there is no evidence
c. . ~ , , ,
that elevated levels of total particulate matter are required to produce
the adverse effect.
3. Summary of Acute Respiratory Disease Studies of Families
Table 7 summarizes findings for total acute respiratory disease
(combined upper and lower tract disease) among family members in the
12 13
Chicago and New York studies. With the exception of fathers, who
often have greater occupational exposures and daily changes of exposure
due to place of work, a consistent excess acute respiratory disease
rate was reported among family members living in more polluted
**
neighborhoods. The relative excess in acute respiratory illness rates
within more polluted neighborhoods varied from 3 to 40 percent. A range
estimate of 5 to 20 percent relative excess includes all but the most
extreme values. Unfortunately, the low exposure community for the Chicago
study also had elevated pollutant concentrations of sulfur oxides and
particulates; this community does not therefore afford a satisfactory
baseline illness rate. In New York, the "High I" (or "Intermediate I")
community consistently reported considerably higher illness rates in all
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family segments than in the "High II" community, even though measured pollutant
concentrations were somewhat lower in the "High I" neighborhood. Other environ-
mental factors, including the proximity of a large international airport;
may have influenced the illness reporting of residents in the "High I" New
York community. For these reasons it was difficult to determine the magnitude
of excess illness associated with specific pollutant levels in these two
studies. A conservative estimate (i.e. closer to-the least case than the
3
worst case estimate) would be that exposures (see Table 8) to 210 yg/m
3 3
.S02, with 104 yg/m total suspended particulates and approximately 16 yg/m
suspended sulfates was associated with a 5 to 20 percent excess of acute
respiratory illness in various family members. This estimate largely discounts
the high illness experience of the "High I" New York community and the relatively
low current S0? levels in New York and Chicago. Further observations of
acute respiratory illness in these and other CHESS areas are being made and
should considerably refine the quantitative estimates given above.
12
The Chicago study also provided evidence of increased susceptibility
s
to epidemic A /Hong Kong influenza among otherwise healthy families exposed
3
during the previous three years to atmospheric levels of 106 to 119 yg/m
3 3
-SO-, 151 to 159 yg/m total suspended particulates, and 14 yg/m suspended
sulfates.
The effects of other factors on the incidence of ARD were most
interesting (Table 9). In both Chicago and in the'New York City areas,
socioeconomic status was a significant factor in the incidence of upper
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respiratory disease; more illness was reported by respondents of the
* ' *
upper-middle socioeconomic level. No effect of socioeconomic level on
reporting of lower respiratory disease was observed.
Personal cigarette smoking apparently had little effect on the initial
contracting of respiratory infections but was a significant determinant
" ' / f
in the development of lower tract illness as a result of the initial
infection.
Parental smoking also was a significant factor in the development of
lower tract illness among nonsmoking young members of their households.
This latter is a most significant association and provides additional
evidence that smoking is more than a means of self pollution and affects
other individuals in the immediate environment as well.
Data collected during studies of ARD are difficult to interpret
because in addition to the effects of all other environmental factors, the
incidence of illness depends first of all on exposure to infectious agents.
The fact that many of these agents are more virulent than others in itself
may affect the ease with which infections are recognized and reported.
Also a mild attenuated agent may protect against infection with a more
virulent one, thus tlie recognizable illness rate may depend upon the
sequence in which successive exposures to infectious agents occur. These
difficulties must be recognized, but controlling for them is impossible
without a prohibitively large and expensive laboratory activity.
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Consequently, the credibility of the results depends not only on the careful
* f ..
collection and analysis of data, but also on the reproducibility of associations
between increased illness and higher pollution exposure. This latter factor
f *'
provides the greatest strength to the data reported in this monograph. The
consistency with which increased illness rates were observed to be associated
with higher pollution exposure levels in different' parts'of the country and
in the various segments of the population add greatly to the credibility of
the results.
Differences observed between metropolitan areas, e.g. between New York and
Chicago, were anticipated to be greater than those that would be found between
neighborhoods within a single area. These differences can be accounted for
by the fact that data were collected in each metropolitan area by different
survey groups; thus techniques were consistent within the same area but may
have varied somewhat from area to area as a result of differences in execution
of the same study protocol. Furthermore, a more conservative definition of
lower respiratory symptoms was employed in the. Chicago than in the New York
surveys. As a result lower respiratory diseases were reported at lower
frequencies in Chicago than in Mew York. These definitions have since
been standardized for all CHESS areas.
4. Summary of Pulmonary Function Studies
, Ventilatory function of elementary school children, measured by the
three-quarter second forced expiratory volume (FEV.. -,_), was diminished in
I U. / o
areas of elevated exposure to sulfur oxides. In all cases, observed
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14
decrements were subtle. In the New York study, only the older children
(age nine to 13 years) who had been exposed' to substantially elevated
pollutant concentrations for the first five to ten years of life suffered
reduced ventilatory function. The best available estimates of these remote
3
annual average exposures were as follows: sulfur dioxide, 131-435 yg/m ;
3
total suspended particulates, 75-200 yg/m ; suspended sulfates, 18-28
yg/m .
From the New York study, the authors could not determine the relative
importance of specific pollutants in reducing ventilatory function. From
the Cincinnati study, however, suspended sulfates emerged as a pollutant
of particular concern. In all Cincinnati neighborhoods, sulfur dioxide
3
concentrations were at or below the moderate level of 57 yg/m during the
time of testing, permitting suspended sulfates to be assessed in the
relative absence of sulfur dioxide. Ventilatory function in white children
3
exposed to suspended sulfate concentrations of about 9.5 yg/m was lower
3
than that of white children exposed to concentrations of about 8.3 yg/m .
Black children in Cincinnati were all exposed to-suspended sulfate concentra-
tions of about 8.9 yg/m , and these children demonstrated no differences in
ventilatory function.
From the study results, the authors developed "worst case," "least
case," and best judgment estimates of pollution exposures required to
reduce ventilatory function (Table 10). From the Cincinnati study, it
3
was conceivable that one year's exposure to 9 yg/m of suspended sulfates,
in the presence of moderate levels of sulfur dioxide and total suspended
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3 3
participates C57 yg/m and 96 yg/m , respectively) might alone account for
reduced ventilatory function. The New York,study strongly indicated a more
moderate interpretation, however. It was the authors' best judgment that
eight to nine years of exposure to about 10 to 13 yg/m of suspended sulfates
might reduce ventilatory function. If these suspended sulfate exposures
were accompanied by exposures to about 200-250 yg/m of sulfur dioxide and
3 -/..
about 100-150 ug/m of total suspended particulates, further reductions in
FE\L ,.. might be expected.
u. /o
Clearly, these best judgments are based on suggestive, not conclusive,
evidence. In Cincinnati, for example, the socioeconomic-racial patterns of
exposure to suspended nitrates were very similar to suspended sulfate
exposure patterns. Though absolute levels of suspended nitrates were much
lower than suspended sulfates, possible effects of suspended nitrates could
not be ruled out. Also, the ventilatory performance of black children in
Cincinnati remains somewhat confusing. At present, it is impossible to
disentangle the effects of objective environmental factors from these
childrens1 possible subjective responses to the all-white testing teams.
The contribution of other covariates to pulmonary function results in
school children is summarized in Table 11. Height, age, sex and race are
well recognized in the literature as significant determinants of pulmonary
function in children, and these variables were taken into account in
analyzing the CHESS data. Table 12 summarizes the CHESS pulmonary function
findings to date. These studies have been repeated in New York and other
CHESS areas for two successive years and will be reported in subsequent
papers.;
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B. Responses to Short-Term Pollutant Exposures
1, Summary of Studies on Panels' of Asthmatics and Cardiopulmonary
Subjects
In contrast to the health indicators previously summarized in this
r i
paper, studies on panels of subjects gave the investigators the opportunity
to relate daily changes in symptom status to daily changes in pollutant
- / , i
levels. One pattern immediately emerged from the asthma studies conducted
in the Salt Lake Basin and New York. As shown in Table 13, daily
asthma attack rates in the Salt Lake Basin were more consistently
correlated with colder outdoor temperature than with any measured
pollutant. Therefore, an analysis of asthma attack rates against daily
pollutant concentrations was carried out within two temperature ranges:
30 to 50ฐ F and greater than 50ฐ F. These dara are summarized, for SOp,
total suspended particulates (TSP) and suspended sulfates (SS) in Figures
1 and 2 for Salt Lake and in Figures 3 and 4 for New York. Inspection of
these figures reveals one quite consistent finding: asthma attack rates were
most closely related to stepwise increases in the levels of suspended sulfates.
'Virtually no relationship between S0? and attack rates appeared. Total
suspended particulates (with the exception of Figure 4) and suspended
sulfates (with the exception of Figure 1) were positively and stepwise
correlated with daily asthma attack rates. In the Salt Lake Basin, where
the effects of total particulates and suspended sulfates were partitioned,
a higher, frequency of asthma attacks was observed at the same daily TSP
concentration when a high sulfate fraction was present in the atmosphere
(Figure 5). Thus, it appeared that sulfate levels were a stronger determi-
nant than TSP of asthma attack rates in the Salt Lake Basin. However,
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in the cold dry climate of the Basin, the effect of cold temperatures
was considerably stronger than that of sulfates (Figure 6), and the
pollutant threshold for the asthma response was much higher in colder
than in more moderate temperatures.
In New York, asthma attack rates were more consistently associated
with daily suspended sulfate levels than with either SO- or TSP (Figures
3 and 4). As in Utah, the pollutant threshold for the asthma response
was higher in colder than in more moderate temperatures (Figure 7), but
unlike Utah, attack rates were generally higher on days with more
moderate than with colder temperatures.
Thus, the effect of temperature was somewhat inconsistent between the
two study areas; colder temperatures were associated with higher attack
rates in the Salt Lake Basin but not in New York. It is difficult to compare
the temperature effect in the two studies because they extended over different
seasons of the year. In each case, the sulfate threshold was higher on
colder days; and, in each case, elevated daily sulfate levels were quite
'consistently associated with increased asthma attack rates.
The pattern of daily aggravation of symptoms in cardiopulmonary
subjects in New York was very similar to that of asthma with respect to
temperature and pollutants. In each of the three New York neighborhoods,
cold temperatures were directly related to increased symptom rates in
subjects with combined heart and lung-disease (Table 14). Elevated suspended
sulfates were the only pollutant consistently associated with symptom
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aggravation, as shown in Table 14 and Figures 8 and 9. Daily S0?
and TSP could not be associated with- symptom aggravation in the heart
and lung panel, which was the most sensitive to variations in daily
pollutant concentrations.
The pollutant thresholds for S0?, TSP and suspended sulfates among
the several cardiopulmonary and asthmatic panels at different temperature
ranges are summarized in Table 15. Although this table presents pollutant
thresholds for SCL and TSP, the above discussion should make it clear that
suspended sulfate levels demonstrated the only consistent relationship with
daily aggravation of symptoms in these diseased panelists. Thus, while adverse
effects were occurring at daily concentrations below the short-term (24-hour)
primary standard for S0? and TSP, the investigators would attribute these
effects to suspended sulfate concentrations on those days rather than to
S0? or TSP. It was the best judgment of the investigators that significant
aggravation of cardiopulmonary symptoms could be attributed to 24-hour
- 3
suspended sulfate levels as low as 8-10 yg/m on cooler days (20-40ฐF)
or warmer days (41+ฐF). The investigators intuitively felt that the chemical
composition and particle size involved in sulfate exposures were critical
determinants of the threshold for'the adverse response. Since these sulfate-
symptom relationships were manifested even in the low exposure communities
of the Salt Lake and New York CHESS areas, there was evidence that suspended
sulfates emanating from point or urban sources penetrated well beyond the
suburban ring and adversely affected persons living in more distant
i
communities. Such penetration might involve smaller respirable particles,
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acid mist or other atmospheric transformation products of sulfur oxide
' ' * i
emissions. The magnitude of such remote exposures and their overall
health importance cannot yet be quantified.
C. Conclusions
In this CHESS monograph, we have brought together an'driginal series
of studies describing a variety of pollutant relationships with several
tiealth indicators. The pollutants of main concern were sulfur dioxide,
total suspended particulates and suspended sulfates. We have examined the
impact of community differences in exposure to these pollutants on chronic
respiratory disease in adults, acute lower respiratory disease in children,
acute respiratory illness in families, aggravation of symptoms in subjects
with pre-existing asthma and cardiopulmonary disease, and lung function of
school children. These health indicators were selected because past studies
by many investigators indicated that the frequency of these responses in a
community was affected by sulfur oxides and particulates. Our studies more
than substantiate these findings.
Our results can be divided into two groups: (1) health indicators
responsive to cumulative, long-term pollutant exposures and (2) health
indicators sensitive to daily or shorter-term variations in pollutant
exposure. Least case, worst case, and best judgment estimates concerning
the pollutant thresholds for long-term exposures are given in Table 16.
Best judgment estimates are recapitulated for long-term exposures in Table
j*
17. Our findings support the existing national primary standard for long-
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term, or annual average, exposures, insofar as we have measured the
desirability of these standards in te,rms of chronic respiratory disease
in adults, acute lower respiratory disease in children, acute respiratory
disease in families, and lung function of children. With regard to short-
r i
term exposures, least case, worst case, and best judgment estimates were
given in Table 15, and best judgment estimates are recapitulated in Table
' / .
18. Our data indicate that adverse effects on elderly subjects with heart
and lung disease, and on panels of asthmatics, are being experienced even
on days below the national primary standard for 24-hour levels of S0_ and
total suspended particulates. However, as is evident from the presentation
given above, these adverse health effects should be attributed to suspended
sulfate levels rather than to the observed concentrations of S02 and TSP.
The consistency of the relationship between symptom aggravation and sulfate
levels, and the lack of consistency for this relationship with other
pollutants, leads us to this conclusion.
Having identified atmospheric suspended sulfates as an environmental
pollutant of present concern to health, we by no means have acquired
sufficient intelligence to establish a national standard for this pollutant.
We know little about the environmental determinants of atmospheric suspended
sulfates, and less about the means to control sulfate levels or to bring
about significant reductions in sulfate concentrations in urban, suburban
and rural areas (particularly of the northeastern .U.S.). In identifying
the need for control of sulfates, we have raised a series of unstated
questions and issues. Are all sulfates equally biologically reactive?
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Are sulfates reactive because of the chemical properties associated with
'' ' 0 j-
specific chemical compounds, or because of physical properties such as
particle size or pH? Are sulfates equally reactive in humid and dry air,
r i '
at warm and cold temperatures? These biological issues must be addressed
and satisfactorily resolved, because our strategies to control sulfate
levels may be critically dependent on the nature of the sulfate-biologic
response relationship. If acid mist is the problem, we may be able to
neutralize the sulfur oxides emitted at the source, without more stringent
reductions in sulfur oxide emissions than are presently required to achieve
primary national standards. On the other hand, if atmospheric transformation
products of SOp are implicated, we may be forced to restrict even more
severely .the sulfur content of fossil fuels. Until more definition of
these issues is achieved, however, our findings strongly argue against
any measures that would allow more sulfur loading of the atmosphere.
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REFERENCES
1. C. M. Shy, W. B. Riggan, J. G. French, W. C. Nelson, R. C. Dickerson
F. B. Benson, J. F. Finklea, A. V. Colucci, D,. I. Hammer and V. A.
Newill. An Overview of CHESS. In: Health Consequences of Sulfur
Oxides: A Report from CHESS, 1972, pp.
2. D. E. House, J. F. Finklea, C. M. Shy, D. C. Calafiore, W. B. Riggan,
J. W. Southwick and L. J. Olsen. Prevalence of Chronic Respiratory
Disease-Symptoms in Adults: 1970 Survey of'Salt take Basin Communities.
In: Health Consequences of Sulfur Oxides: A Report from CHESS, 1972,
pp. '
3. C. G. Hayes, D. I. Hammer, C. M. Shy, V. Hasselblad, C. R. Sharp,
J. P. Creason and Kathryn E. McClain. Prevalence of Chronic
Respiratory Disease Symptoms in Adults: 1970 Survey of Five Rocky
Mountain Communities. In: Health Consequences of Sulfur Oxides:
A Report from CHESS, 1972, pp.
4. J. F. Finklea, J. Goldberg, V. Hasselblad, C. M. Shy, C. G. Hayes.
Prevalence of Chronic Respiratory Disease Symptoms in Military
Recruits, 1969-1970. In: Health Consequences of Sulfur Oxides:
A Report from CHESS, 1972, pp.
5. H. E. Goldberg, J. F. Finklea, C. J. Nelson, Walter Steen,
R. S. Chapman, D. H. Swanson and A. A. Cohen. Prevalence of
Chronic Respiratory Disease Symptoms in Adults: 1970 Survey of
New York Communities. In: Health Consequences of Sulfur Oxides:
A Report from CHESS, 1972, pp.
6. M. B. Hertz, L. A. Truppi, T. D. English, G. W. Sovocool, R.M. Burton,
L. Thomas Heiderscheife, and D. 0. Hinton. Human Exposure to Air
Pollutants in Salt Lake Basin Communities: 1940-1971. In: Health
Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
7. T. D. English, D. I. Hammer, Jose M. Sune, L. A. Truppi, W. E. Culver,
R. C. Dickerson, and W. B. Riggan. Human Exposure to Air Pollutants
in Five Rocky Mountain Communities: 1940-1970. In: Health Consequences
of Sulfur Oxides: A Report from CHESS,-1972, pp.
8. D. 0. Hinton, T. D. English, B. F. Parr, V. Hasselblad, R. C. Dickerson,
and J. G. French. Human Exposure to Air Pollutants in the Chicago-
Northwest Indiana Metropolitan Region: 1950-1971. In: Health Consequences
of Sulfur "Oxides: A Report from CHESS, 1972, pp.
9. T. D. English, W. B. Steen, R. G. Ireson, P. B. Ramsey, R. M. Burton,
and L. T. Heiderscheit. Human Exposure to Air Pollution in Selected
New York-Mew Jersey Metropolitan Communities: 1944-1971. In: Health
Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
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10. W. C. Nelson, J. F. Finklea, D. E. House, D. C. Calafiore, M. B.
Hertz, and D. H. Swanson. Frequency of Acute Lower Respiratory
Disease in Children: Retrospective Survey of Salt Lake Basin in
Communities, 1967-1970. In: Health Consequences of Sulfur Oxides:
A Report from CHESS, 1972, pp.
11. J. F. Finklea, D. I. Hammer, D. E. House, C. R., S,harp, W. C. Nelson
and 6. R. Lowrimore, Frequency of Acute Lower Respiratory Disease
in Children: Retrospective Survey of Five Rocky Mountain Communities,
1967-1970. In: Health Consequences of Sulfur Oxides: A Report from
CHESS, 1972, pp.
12. J. F. Finklea, J. G. French, G. R. Lowrimore, J. Goldberg, C. M. Shy
and W.-C. Nelson. Prospective Surveys of Acute Respiratory Disease
in Volunteer Families 1969-1970 Chicago Nursery School Study. In:
Health Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
13. G. J. Love, A. A. Cohen, J. F. Finklea, J. G. French, G. R. Lowrimore,
W. C. Nelson, P. B. Ramsey, Prospective Surveys of Acute Respiratory
Disease in Volunteer Families 1970-1971 New York Studies. In: Health
Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
14. C. M. Shy, V. Hasselblad, J. F. Finklea, R. M. Burton, M. Pravda,
R. S. Chapman, and A. A. Cohen. Ventilatory Function in School
Children: T970-1971 Testing in New York Communities. In: Health
Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
15. C. M. Shy, C. J. Nelson, Ferris Benson, W. B. Riggan, V. A. Newill
and R. S. Chapman. Ventilatory Function in School Children:
1967-1968 Testing in Cincinnati Neighborhoods. In: Health
Consequences of Sulfur Oxides: A Report from CHESS, 1972, pp.
16. J. F. Finklea, D. C. Calafiore, C. J. Nelson, W. B. Riggan, C. G. Hayes,
Aggravation of Asthma by Air Pollutants: 1971 Salt Lake Basin Studies.
In: Health Consequences of Sulfur Oxides: A Report from CHESS, 1972,
PP.
17. J. F. Finklea, J. H. Farmer, A. A. Cohen, G. J. Love, D. C. Calafiore
and G. W. Sovocool. Aggravation of Asthma by Air Pollutants: 1970-
1971 New York Studies. In: Health Consequences of Sulfur Oxides:
A Report from CHESS, 1972, pp.
18. H. E. Goldberg, A. A. Cohen, J. F. Finklea, J. H. Farmer, F. B. Benson,
and G. J. Love. Frequency and Severity of Cardiopulmonary Symptoms in
Adult Panels: 1970-1971 New York Studies. In: Health Consequences
of Sulfur Oxides: A Report from'CHESS, 1972, pp.
19. - A. A. Cohen, S. Bromberg, R. W. Buechley, L. T. Heiderscheit, and
C. M. Shy. Asthma and Air Pollution from a Coal-Fueled Power
Plant. To be published in Am. J. Public Health, August 1972.
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TABLE 1
SMOKING AND SEX SPECIFIC CHRONIC BRONCHITIS PREVALENCE RATES (PERCENT) BY
COMMUNITY EXPOSURE IN FOUR CHESS AREAS
CHESS Area
Pollutant Exposure*
Salt Lake Basin
- Low '
Intermediate I-
Intermediate II
High
Pocky Mountain
Pooled Low
Pooled High
Chicano
Black
Low
Intermediate
High
White
Low
Intermediate
High
New York
Low
High "I
High II
Percent Chronic Bronchitis
Nonsmoker
'Male
3.0
3.6
2.3
6.8
1.25
3.47
8.8
7.8
9.3
4.2
5.4
5.4
4.6
18.0
14.2
Female
2.3
2.0
4.7
5.2
1.08
2.54
2.0
7.5
4.9
Exsmoker
'Male
2.6
3.4
5.4
6.0
1.45
4.82
13.9
18.0
18.7
' / * ป
Female
5.3
4.0
7.0
7.1
3.12
2.80
3.8
9.0
4.5
Smoker
Male
19.9
18.6
20.1
26.8
17.05
18.63
8.8
12.7
13.0
17.6
18.8
17.8
13.9
21.3
22.1
Female
17.8
14.7
15.3
22.2
11.78
12.38
13.9
19.8
16.6
*Refer to previous reports in this monograph (References 2-5) for numerical
data on current and past exposures. The pollutant gradients presented in
this column do not represent equal class intervals.
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TABLE 2
MEAN RESPIRATORY SYMPTOM SCORES FOR ALL STAGES OF CHRONIC RESPIRATORY
SYMPTOMS IN FOUR CHESS AREAS
CHESS Area
Pollutant Exposure*
Salt Lake Basin
Low
- Intermediate I
Intermediate II
High
Rocky Mountain
Pooled Low
Pooled High
Chicane
Black
Low
Intermediate
High
White '
Low
Intermediate
High
New York
Low
Hia'i'i I
High. 1 1
Mean Symptom Score
Nonsmoker
Male
T.54
1.56
1.48
1..94
1.33
1.38
2.10
2.24
2.34
1.76
1.82
1.84
1.81
2.41
2.35
Female
1.36
1.37
1.55
1.73
1.23
1.29
1.29
1.76
1,61
Exsrnoker
Male
1.48
1.54
1.82
1.87
1.41
1.58
2.05
2.56
2.51
Female
1.65
1.79
1.83
2.02
1.30
1.45
1.37
2.00
1.72
Smoker
Male
2.73
2.88
2.99
3.32
2.65
2.72
2.47
2.61
2.71
2.90
2.93
2.91
2.48
2.76
2.76
Feiiiale
2.57
2.53
2.44
2.98
2.20
2.34
2.30
2.68
2.53-
*Refer to previpus reports in this monograph (References 2-5) for numerical
data on current and past exposures. The pollutant gradients presented in
this column do not represent equal class intervals.
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TABLE 3
MALES: EXCESS CHRONIC BRONCHITIS ATTRIBUTABLE TO AIR POLLUTION AND
SMOKING, AND RELATIVE CONTRIBUTION OF EACH FACTOR
Factor
Air Pollution Alone
Smoking Alone
Air Pollution + Smoking
Air Pollution Alone
Smoking Alone
Excess Chronic Bronchitis Prevalence (Percent)*
new
York
11.3
9.3
17.1
1
0.32
Salt
Lake
3.8
16.6
23.3
1
4.4
Rocky
Mountain
2.2
15.8
17.4
1
7.2
Chicane
l.'hi-tes
1.2 .
13.4
13.6
1
11.2
Blacks
0.7
0.0
4.2
NA
*Excess prevalence:absolute excess above rate experienced by nonsmokers in the low
exposure community of the same CHESS area.
NA: not ascertainable
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TABLE 4
FEMALES: EXCESS CHRONIC BRONCHITIS ATTRIBUTABLE TO AIR POLLUTION AND
SMOKING, AND RELATIVE CONTRIBUTION OF EACH FACTOR
Factor
Air Pollution Alone
Smoking Alone
Air Pollution + Smoking
Air Pollution A.I one
Smoking Alone
i
Excess Chronic Bronchitis Prevalence (Percent)*
New York
4.0
11.9
16 = 1
1
3.0
Salt Lake
2.2
12.8
19.2
1
5.8
Rocky Mountain
1.5
10.7
11.8
1
7.1
* Excess prevalence absolute excess above rate experienced by nonsmokers in the low
exposure community of the same CHESS area.
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TABLE 5
RANGE OF POLLUTANT EXPOSURES ASSOCIATED WITH
EXCESS CHRONIC BRONCHITIS
CHESS
Area
Salt Lake
Rocky Mountain
Chicago
New York
National Primary
Air Quality
Standard
Current Exposures
(annual average)
s%
yg/m
62
177-374
96-217
50-144
80
TSP
yg/m
66
65-102
103-155
63-104
75
so4
yg/m
12.4
7.2-11.3
14.5
13.2-16
-
' / ,
Exposures Within Past 10
Years* (annual average)
so2
yg/m
92-95
177-374
100-282
144-404
80
TSP
yg/m
53-70
62-179
118-177
80-203
75
so4
/ 3
yg/m
15.0
6.9-19.9
14.1-17.3
9-26
-
*Estimated from emissions data and pollutant trends.
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TABLE 6
AGE-SEX-SOCIOECONOMIC STATUS ADJUSTED THREE YEAR LRD ATTACK RATES
PER 100 CHILDREN BY POLLUTION EXPOSURE, NUMBER OF EPISODES,
AND STUDY AREA
Disease
Category
1 CD
Li\U
CROUP
DDnMTUTTTC
DKUINUnl 1 Ib
Pollution
Exposure *
Low
High
Low
High
Low
High
Low
High
Low
High
Low
High
Mi imKo v
of
Episodes
>_ 1
>_2
>_ 1
>_ 2
L 1
^2
Study
* / * ป
Rocky
Mountain
H'32 (NS)***
ฃ* (p<.001)
^2 (p<.001)
I'.l (P*'05)
14'9 (NS)
15.8 l'Nb;
1'} (NS)
Area
Salt Lake
Basin**
H'l (P<.ooi)
ll:l (p*-001)
is:? (p^001^
i3:l (p<-001)
I*'* (p<.001)
lois (D<-001^
*Consult references 10 and 11 for numerical data on air pollution exposures.
**Rates given for low pollution exposure are weighted averages of the age-sex-
sbcioeconomic status adjusted rates for the Low, Intermediate I, and Intermediate
II communities.
***Probability that the difference between the two rates is as large or larger than
that observed.under the hypothesis of no difference. NS denotes p > .05.
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TABLE 7
RELATIVE RISK OF TOTAL ACUTE RESPIRATORY ILLNESS IN FAMILIES LIVING
IN NEW YORK AND CHICAGO CHESS AREAS
Family
Segment
Preschool
Children
School
Children
Mothers
Fathers
Community Air
Pollution Exposure*
Low
High I**
High II***
Low
High I
High II
Low
High I
High II
Low
High I
High II
Relative Risk of Total
Acute Respiratory Illness
Chica'go
1.00 (9.37)
1.06
1.09
1.00 (4.56)
1.39
1.06
1.00 (5.00)
1.19
1.19
1.00 (3.09)
0.95
1.19
New York
1.00 (7.88)
1.40
1.03
1.00 (6.22)
1.20
1.03
1.00 (4.45)
1.14
1.05
1.00 (3.44)
1.17
0.88
*Consult references 12 and 13 for numerical data on air pollution
exposures.
**High I: In Chicago, equivalent to "High" neighborhood
In New York, equivalent to "Intermediate I" neighborhood
***High II: In Chicago, equivalent to "Highest" neighborhood
In New York, equivalent to "Intermediate II" neighborhood
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TABLE 8
RANGE OF POLLUTANT EXPOSURES IN NEW YORK AND CHICAGO NEIGHBORHOODS
HAVING EXCESS ACUTE RESPIRATORY DISEASE RATES IN FAMILIES
CHESS
Areas
Chicago
High I
High II
New York
High I
High II
National Primary
Air Quality
Standard
Current Exposures
(annual average)
SY
yg/m
51
106
50-63
50-58
80
TSP
yg/m
126
151
63-84
87-104
75
SO-4
yg/m
(14.5)*
(14.5)
13.2
14.3
-
Previous 2 Years
(annual average)
i
Sฐ2
yg/m
83
119
144
210
80
' TSP
yg/m
135
159
80
104
75
Sฐ<3
yg/m
(14.1)*
(14.1)
13.4
16.2
r
*Estimate from Chicago Stations of the National Air Surveillance Network.
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TABLE 9
EFFECTS OF SELECTED FACTORS
ON ACUTE RESPIRATORY DISEASE
FACTOR
AIR POLLUTION
SOCIOECONOMIC
STATUS
PERSONAL CIGARETTE
SMOKING
PARENTAL SMOKING
EFFECT ON CHILDREN
STATISTICAL SIGNIFICANCE OF FACTOR
UPPER TRACT
DISEASE
CHICAGO
< 0.05
< 0.001
NS
<0.10
N.Y.
NS
< 0.005
NS
NS
LOWER TRACT
DISEASE
CHICAGO
<0.05
NS
<0.10
< 0.001
N.Y.
< 0.005
NS
< 0.005
< 0.001
o
CD
m
ฃ2
-~i
m
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TABLE 10
O
uu
LEAST CASE, WORST CASE, AND BEST JUDGMENT ESTIMATES OF AIR POLLUTION EXPOSURE
SUFFICIENT TO PROMOTE IMPAIRMENT OF CHILDHOOD VENTILATORY FUNCTION
1-
c
ซ
c
c
rJype of Estimate
:> -
^
Worst Case
Least Case
Best judgment
Duration of Exposure
(years)
1
9
8-9
National Primary Air Quality Standard
0
Pollutant (Annual Average in yg/m
Sulfur Dioxide
57
435
200-250
80
Total Suspended Parti culates
96
200 .
100-150
75
Suspended Sul fates
9
28
10-13
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UJ
CC
O
TABLE 11
Summary of Effects of Covariates Observed in
CHESS Pulmonary Function Studies
~Covariate
Effect
ca. Height
oln all'studies, height was the most significant .determinant of FEVn 7r, being somewhat
less important in children aged 5 through 8 years (0.045 liters per'inch) than in
children aged 9 through 13 years (0.063 liters per inch).
2. Age
In New York, children aged 9 through 13 years demonstrated area differences in FEV
while children aged 5 through 8 years did not.
0.75
In all children tested age was a significant determinant of FEVn 7t-, being somewhat
more important in children aged 5 through 8 years (0.045 liters per year) than in -
children aged 9 through 13 years (0.019 liters per year).
3. Sex
In New York, area differences in FEVn 7r were statistically significant for boys aged
9 through 13 years, but not for girls'of the same age.
The FEVft 7K of boys was consistently higher than that of girls of the same age and
height.0>/t)
4. Race
In Cincinnati the FEVn 7C- of black children was consistently lower than that of white
children. u>/s
In Cincinnati, white children demonstrated area differences in FEVn 7C, while black
children did not.
0.
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UJ
TABLE 12
t
or
Summary of Findings in CHESS Pulmonary Function Studies
Location
Cincinnati
CD
O
O
Time
1967-68
Age Group Tested
Second Grade
Findings
White children exposed to average suspended
sulfate levels of 9.5 yg/m had lower FEV
than white children exposed to average
suspended sulfate levels of 8.3 yg/m
0.75
The FEVg 75 of black children did not vary with
air polTuUon. exposure
The FEVQ 75 of black and white children was
lowest Vrt winter.
ซThe FEVQ 75 of black children was consistently
lower tnan that of whites.
New York
1970-71
All Elementary Grades
The FEVn 75 of white children aged 9 through 13
years, who had been exposed to high levels of
sulfur oxides and particulates during the first
decade of life, was lower than that of children
who had not been so exposed.
This finding was statistically significant
in males, but not in females.
The FEVQ 75 of children aged.5 through.8 years
did not vary consistently-with pollution exposure,
The FEV
in wint
FEVn 7(- of children in all grades was
inter.
lowest
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CO
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o
UJ
^fe
TABLE 13
o
z:
O
O
SIMPLE CORRELATION OF ASTHMA ATTACKS
WITH ENVIRONMENTAL FACTORS
ENVIRONMENTAL
FACTORS
MIN. TEMP.
TSP
S0ฃ
SUSP. S04
N02
CORRELATION IN CHESS AREAS
SALT LAKE BASIN
LOW
-SS
N
N
-S
N
MID
-SS
N
N
N
_c
d
HIGH
-SS
+SS
N
+SS
N
NEW YORK
LOW
N
N
N
+S
-f-SS
MID. 1
N
N
N
N
N
MID. II
+S
N
-SS
N
N
S - p<0.05 SS = p<0.01 N - NOT SIGNIFICANT
- = INVERSE CORRELATION += POSITIVE CORRELATION
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UJ
en
o
TABLE 14
NEW YORK HEART AND LUNG PANELS:
;ORRELATION OF DAILY EXPOSURES WITH SYMPTOM AGGRAVATION
COH1UNITY
EXPOSURE
LOW
INTERMEDIATE-!
INTERMEDIATE-II,
EXPOSURE TO
S02
0.23*
-0.09
0.08
TSP
O.lg*
-0.05
0.09
SS
i
0.28**
0.26**
0.18*
N02
0.15*
-0.04
-0.06
MAX. TEMP.
-0.33**
-0.15*
-0.19**
p < 0.05
p<0.01
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TABLE 1 5
Summary of CHESS Studies Relating Pollutant Thresholds for Adverse Health Effects to Short-Term Air Quality Standards
for Sulfur Dioxide, Total Susnended Partlculates and Suspended Sulfates
Adverse Effect
on Human Health
Aggravation of Chronic
Heart and Lung Disease
Symptoms in the "Well"11
Aggravation of Cardio-
Respiratory Symptoms' in
Elderly Patients With
Heart Disease11
Aggravation of Chronic Lung
Disease Symptoms In Elderly
Patients with Chronic Lung
Disease11
Aggravation of Cardio-
Respiratory Symptoms 1n
Elderly Patients With
Combined Heart and Lung
Disease11
Aggravation of Asthma
Manifest by Higher Attack
Rates9ปio
Type of
Estimate
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
%
Worst Ca'se
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment '
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
(pa/m3)
24-Hour Pollutant Threshold Levels for Adverse Health Effects
Minimum
24-Hour
Temperature
ฐF
20-40ฐ
>40ฐ
>40ฐ
20-40ฐ
>40ฐ
20-40ฐ
>40ฐ
30-50ฐ
>50ฐ
National Standard Sulfur Dioxide
Primary Air ,,c
Quality Standard ' 365
Significant Harm Level 2620a
Between 81 and 365
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
Between 81 and 365
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
No Effect Below Primary Standard
No Effect Below Primary Standard
Mo Proven Effect Below Primary
Standard
No Effect Below Primary Standard
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
.No Effect Below Primary Standard
No Effect Below Primary Standard
No Proven Effect Below Primary " '
Standard
181
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
No Effect Below Primary Standard
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
No Effect Below Primary Standard
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
23
No Effect Below Primary Standard
180-250D
Total Suspended Parti culates
260
1000a
No Effect Below Primary Standard
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
68
No Effect Below Primary Standard
80-100
Between 76 and 260
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
Between 76 and 260
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
Between 76 and 260
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
47
No Effect Below Primary Standard
80-100
76
No Effect Below Primary Standard
No Proven Effect Below Primary
Standard
Between 61 and 75
No Effect Below Primary Standard
107
Between 61 and 75
No Effect Below Primary Standard
71
suspended Sulfates
No Standard
No Standard
0
No Effect
8-10
2
10
8-10
10
10-20
10
6
No Effect
10
11
12
12 .
9
10
10
6
17
10
\
8
No Effect
9-10
.._!-
10
>8
a/ Significant Harm Levels also consider the probable Interaction between sulfur dioxide and suspended particulates by setting as" a 24-hour significant harm
level the following value: Concentration of Sulfur Dioxide (jjci/m3) x Concentration of Total Suspended Partlculates (ug/mj) x A Constant (490 x 10J).
b'/'This judgmaot estimate based on the presently reported studies and on the CHESS study of asthma in New Cumberland, W. Virginia which was previously
reported. 17 .
-------
LU
TABLE 16
o
SUMMARY OF CHESS STUDIES RELATING LONG-TERM POLLUTANT EXPOSURES INVOLVING SULFUR DIOXIDE, TOTAL
SUSPENDED PARTICULATES AND SUSPENDED SULFATES TO ADVERSE EFFECTS ON HUMAN HEALTH
-J
y
ป
D
ฃ Mverse Effect
D on Human Health
3
Increase in Prevalence of
Chronic Bronchitis in Adults
Increases in Acute Lower
Respiratory Tract
Infections in Children
Increase in Frequency or
Severity of Acute
Respiratory Illness in
Otherwise Healthy Families
Subtle Decreases in Childhood
Ventilatory Function
Type of
Estimate
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Worst Case
Least Case
Best Judgment
Duration
8f
sure
(Years)
3
10
6
3
3
3
1
3
3
1
9
8-9
Annual Average Levels Linked to Adverse
Health Effects (yg/m3)
Sulfur
Dioxide
(80)*
62
374
95
92
177
95
50
210
106
57
435
200
Total
Suspended
Parti culates
(75)*
65
179
100
65
102
102
104
159
151
96
200
100
Suspended
, Sul fates
(No Standard)
12
20
15
7.2
15
15
14
16
15
9
28
13
*National primary ambient air quality standard in parentheses.
.the equivalent arithmetic mean would be about 85 yg/m.
The particulate standard is a geometric mean and
-------
DRAFT
DO NOT QUOTE OR CITE
TABLE 17
LONG-TERM EXPOSURE: POLLUTANT THRESHOLDS FOR ADVERSE EFFECTS
(BEST JUDGMENT)
Effect
Increased Prevalence of Chronic
Bronchitis
.Increased Acute Lower Respiratory
Disease in Children
Increased Frequency of Acute
Respiratory Disease in Families
Decreased Lung Function of
Children
Present Standard
*
3
Threshold f -Annual yg/m
so2
95
95
106
200
80 .
TSP
100
102
151
100
75
(Geometric)
SS
15
15
15
13
-
-------
TABLE 18
O
UJ
POLLUTANT THRESHOLDS
(BEST JUDi
EFFECT
AGGRAVATION OF
SYMPTOMS IN ELDERLY
AGGRAVATION OF
ASTHUiA
PRESENT STANDARD
THRESHOLD, 24-hoisr jjg/m3
"
SO?
'
>365
180-250
365
TSP
80-100
70
260
SS
8-10
8-1D
o
o
-------
Figure 1
O
LU
81
S02
<60 61-75 >76
TSP
1.0
JL .85 -89
<6 6.1-8.08.1-10.0 >10.1
SS
-------
CD
CD
QJ
ซcS
CD
21
CD
Q
Figure 2
SALT LAKE BASIN: ASTHMA
(MINIMUM TEMPERATURES 51 ฐF)
1.5
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ATTACK
i n
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SS
-------
LU
Figure 3
ce
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8.1-10.0 >10.1
6.1-8.0
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Figure 4
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-------
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ctr
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Figure 5
SALT LAKE
CD
O
O
ASTHMA
ATTACK
RATE
PER
100
25
20
15
10
5
0
0
: ASTHMA ATTACKS RATES
TEMPERATURE >51ฐF)
I
I
I
WITH HIGH SULFATES
WITHOUT HIGH
SULFATES
(26)
(71)
100
150
200
-------
Figure 6
ce
O
SALT LAKE BASIN: ASTHMA ATTACK RATES
20
O
O
ASTHMA
ATTACK
RATE 15
PER
100
10
0
0
48 12 16 20 ,24
SUSPENDED SULFATES, |ig/m3
28
-------
FIGURE 7
o
or
o
NEW YORK: ASTHMA ATTACK RATES
ASTHMA
ATTACK
PER
1J
0
0
SUSPENDED SUIFATES, |Jg/m3
-------
o
oc
o
uu
10.1
SS
-------
UJ
O
ex.
O
Figure 9
NEW YORK HEART
RELATIVE SYMPTOM RISK ON HIGH AND LOW EXPOSURE DAYS
(MINIMUM TEMPERATURE >
O
O
1.
RISK . ftft
OF LUU
SYMPTOMS 0.
0.92
0
0.
.1 8.1-1
6.1-8.0 10.M2.0
v r
SS
------- |