THE ROLE OF ENVIRONMENTAL HEALTH
ASSESSMENT IN THE CONTROL OF AIR POLLUTION
John F. Finklea, M.D., Carl M. Shy/M.D., John B. Moran,
William C. Nelson, Ph.D., Ralph I. Larsen and Gerald G. Akland
National Environmental Research Center
Office of Research and Development
Environmental Protection Agency
Research Triangle Park, North Carolina
August 27, 1974
"This report has been approved for publication. Approval does not
signify that the contents necessarily reflect the views and policies of
the Environmental Protection Agency, nor does mention of trade names or
commerical products constitute endorsement or recommendation for use."
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1.1 INTRODUCTION
The Clean Air Act, which is the legislative basis for air pollution
control in the United States, has as its primary, as yet uncompromised,
goal the protection of public health. Clearly then environmental health
assessments should play a key role in decisions made to implement this
legislation, which is basically a public health law. In this report the
authors will define an environmental health assessment, briefly review
the public health provisions of the Clean Air Act, and illustrate the
vexing problems encountered by sketching three examples of environmental
health assessments. The three illustrative assessments chosen relate first
to the health basis for the health-related or primary ambient air quality
standards; second, to a stationary source problem, the emission of sulfur
oxides from steam electric power plants; and third, to a mobile source problem,
the probable health impact of equipping light duty motor vehicles with
oxidation catalysts. To illustrate the health research programs required
to meet the legal mandate of the Clean Air Act will concentrate on health
evaluation of the primary air quality standards.
1.2 ENVIRONMENTAL HEALTH ASSESSMENTS
Elucidating the health consequences of changes in environmental quality
is one of the.most challenging scientific tasks facing mankind today. Four
major types of difficulties are customarily encountered when one attempts
to develop the dose-response relationships linking environmental agents to
adverse effects on human health. First, there is usually insufficient
information regarding the magnitude and frequency of exposure to environmental
agents because health-related environmental monitoring has been an under-
developed activity and because the wide variations observed in human preferences
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and activity patterns make the translation of environmental monitoring
into, human exposure models a complex endeavor. Second, the links
between exposure and disease are complex. For example, the effects of
infrequent short-term peak exposures may well differ markedly from the
effects of long-term exposures or frequent short-term exposures repeated
over an extended time frame. One must also realize that the relationship
between exposure and disease may be obscured because the latency period between
exposure and effects may be quite long. Furthermore, a single environmental
agent may contribute to a number of different disorders and a single disorder
may result from a combination of circumstances and not result from one
or more environmental agents acting alone. Third, health effects studies are
limited by the shortcomings of vital records and the imperfections in
morbidity assessment. Fourth, one usually lacks a biologically coherent
research data base with clearly interlocking and muturally supporting clinical,
occupational, epidemiologic and toxicologic studies. Progress in each of
these areas has been made during recent months and years. However, the
residual scientific uncertainties clearly demonstrate that our technical ..
information base must be rapidly augmented if we are to assure a reasonable
foundation for sound policy decisions affecting economic growth, transportation,
power generation and other problems involving energy and our environment.
Under optimum circumstances assembling the needed scientific information
will require years. In the meantime scientists must provide at least
rough assessments for decision makers who must face tight, legally required
action schedules and deal with shifting political and social realities.
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1.3 PUBLIC HEALTH AND THE CLEAN AIR ACT
The Clean Air Act, as amended in 1971, provides a number of mechanisms
that can be used to protect public health. The most important legal
provision involves the establishment and attainment of health related
ambient air quality standards for ubiquitous air pollutants arising from
multiple sources. These primary air quality standards are to be achieved
through state implementation plans and Federal emissions standards for
stationary mobile and complex sources of air pollutants. Health related air
quality standards are established for six pollutants; particulate matter,
sulfur oxides, nitrogen dioxide, carbon monoxides, hydrocarbons and
photochemical oxidants. The Clean Air Act specifically requires that
primary air quality standards be set to fully protect public health and
that the standards contain an adequate margin of safety. Thus the law
assumes that there exists a "no effects" threshold for each pollutant and
for every adverse health effect. As will be seen in a subsequent case
report, the health assessments required by this provision are extremely
difficult and contain many unresolved scientific uncertainties.
Another public health provision of the Clean Air Act requires that
national emissions standards for stationary sources of hazardous air
pollutants be established. A pollutant may be labelled hazardous if
exposures result in irreversible illness or serious but reversible
health disorders. Pollutant emissions currently controlled under this
provision include mercury, asbestos and beryllium. In general such
pollutant exposures are in the vicinity of a limited number of industrial
facilities and more restricted giographically than exposures to pollutants
for which health-related ambient air quality standards are established.
For pollutants controlled under either of the preceding mechanisms,
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significant harm levels, that is, short-term exposures which are not to
be exceeded, must also be established. Significant harm levels are
generally substantially higher than levels allowed by the air quality
standards. In a legal sense when significant harm levels are exceeded,
exposures causing imminent and substantial endangerment to health may
follow. In practice, significant harm levels are intended to trigger
the control actions necessary to prevent episodic accumulations of
pollutants and the resulting adverse health effects previously recorded
in a number of European and American cities.
Two other public health provisions of the Clean Air Act are less
widely understood. Fuels and fuel additives that adversely effect
either public health or the performance of air pollution control devices
.may be prohibited. In addition the section on mobile sources grants
authority to regulate emissions which may adversely affect public
health but which are not explicitly targeted for reductions in the law.
The only specific pollutant problem thus far addressed under these
latter two provisions is the phase down of the lead content of gasoline.
The Clean Air act also provides mechanisms for the control of emissions
from stationary sources that involve pollutants about which there are
health concerns but which for one reason or another are not immediately
controllable by one of the other mechanisms already described. For
example, emission of acid mists from sulfuric acid plants are being
controlled under this provision.
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1.4 CASE STUDY: ASSESSMENT OF HEALTH-RELATED AMBIENT AIR QUALITY STANDARDS.* . -
Primary ambient air quality standards have been established to protect
human health from adverse effects attributable to ubiquitous air pollutants
arising from multiple sources. Health assessment of these standards involves
answering the following questions:
0 What is our risk philosophy?
0 What is an adverse health effect?
0 Who must be protected?
0 What population segments are susceptible?
0 What kinds of information are needed to control an air pollutant?
0 What should a minimally adequate health intelligence base assess?
0 What is our present health information base?
0 How uncertain are our present "best judgments" for effects thresholds?
0 What safety margins are contained in the present primary ambient air
quality standards?
0 Can we compare health risks attributable to air pollution with more
familiar risks?
0 What are the consequences of the present scientific uncertainties?
1.4.1 What Is Our Risk Philosophy?
As stated earlier, the Clean Air Act requires that primary air quality standar
be set to protect fully the public health and that these standards
contain an adequate margin of safety. Thus, the law assumes that there
exists a "no-effects" threshold for each pollutant and for every adverse
* This assessment was first prepared for the October 1973 Conference on
Health Effects of Air Pollution sponsored by the National Academy of Sciences ^
National Research Council
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health effect. This risk philosophy may not prove tenable in the long
run. It may well prove true that susceptible segments of the population
exhibit subtle adverse health effects when exposed to natural background
levels of air pollutants. The stringent air pollution controls necessary
to reduce pollutants to natural background levels would be difficult to
develop and probably prohibitively costly to apply.
Several alternative philosophies might be considered. One could
retain the present no threshold risk philosophy for healthy members of
the general population to guard against an increased risk of developing
certain acute and chronic diseases. However, one might choose to allow
some subtle aggravation of pre-existing disorders. Another change in
philosophy would be to adopt the cost-benefit approach. Here one would
balance control costs against health benefits. This approach is superficially
attractive but in fact it is very difficult to apply. Basically, it is
much easier to calculate the control costs than to develop the health
damage functions. With our present limited health intelligence base and
with the present methodological difficulties in assigning Health costs, . .
there would be a tendancy to underestimate the true health costs. It is
also not clear that our society is at present willing to consider seriously
this sort of trade-off. A cost-benefit approach will require rather
precise dose response functions for each adverse effect real ted to the
primary ambient air quality pollutants taken individually or in combination.
Generating these functions would be a major scientific endeavor requiring
substantial increments in public investments for five to ten years. In
my opinion, precipitous movement to a cost-benefit'.p.hi.lospj^^i'i.fi^'He
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absence of greatly improved health damage functions would tend to slow
drastically the air pollution control effort and leave a rather large
but poorly defined residual of continuing ill health.
1.4.2 What Is An Adverse Health Effect?
Adverse effects include both the aggravation of pre-existing diseases
and an increased frequency of health disorders. In addition, good
preventive medicine would dictate that evidence for an increased risk of
future disease is an adverse health effect. Discussion of what constitutes
an adverse effect may become quite vigorous at times. This is certainly
expected when one considers the spectrum of biological response to
pollutant exposures. (Figure 1.1) Most reasonable persons would agree
that mortality (death) and morbidity (illness) constitute adverse effects.
With few exceptions unique disorders do not follow exposure to the
pollutants for which we have established primary ambient air quality
standards. There is even more room for honest disagreement when one
tries to ascertain which changes in body function indicate a risk for
clinical disease and which are either simply adaptive or of uncertain
significance. A similar problem hinders evaluation of tissue residues.
The occurrence of tissue residues of pollutant exposures, that is,
pollutant burdens, is well established for a number of pollutants covered
by the primary ambient air quality standards. Tissue "residues" of
particulate air pollution, carbon monoxide and perhaps for other gases
are recognized. One can safely say that every member of our urban
society carries some sort of pollutant burden. Relating these burdens
quantitatively to environmental exposures and to adverse health effects poses .
a series of difficult, only partially resolved, problems. .. . .
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•1.4.3 Who Must Be Protected?
The Clean Air Act requires that primary ambient air quality standards
be set to protect fully both specifically susceptible subgroups and healthy
members of the population. The Act excludes persons who require an artificial
environment, that is, those who are not free living. In theory at least,
accelerated mortality of hospitalized or institutionalized patients with severe
pre-existing illnesses might not be an appropriate adverse effect upon which
to base an ambient air quality standard. In practice, the implications of
this restriction have not been emphasized and mortality studies have been
duly considered. On the other hand, possible adverse effects on a
large number of relatively small susceptible segments of the population
have not been specifically and separately considered in setting standards.
It is assumed that the protection provided to larger susceptible population
segments and the margins of safety included in the standards will protect
these smaller segments for which we have little or no quantitative exposure-
response information.
1.4.4 What Population Segments Are Susceptible?
Especially susceptible population segments include persons with
pre-existing diseases which may be aggravated by exposures to elevated
levels of pollutants in the ambient air. Some quantitative information
is available on the aggravating effects of air pollutants on asthma,
chronic obstructive lung disease and chronic heart disease. Asthmatics
constitute two to five percent of the general population; three to five
percent of the adult population report persistent chronic respiratory
disease symptoms; and seven percent of the general population report
heart disease severe enough to limit their activity. The distribution of these
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conditions by age, sex, ethnic group, social status and place of residence
must be quantified in any cost-benefit assessment. One could be legitimately
concerned about the aggravating effect of air pollutants on a number of
other susceptible population segments: persons with hemolytic anemias,
patients with cerebrovascular disease, persons with malignant neoplasms,
premature infants and patients with multiple handicaps. Little quantitative
information exists about the aggravating effect of pollutants on these
disorders.
Air pollutants may also increase the risk in the general population
for the development of certain disorders. Many if not all of the general
population may experience irritation symptoms involving the eyes or
respiratory tract during episodic air pollution exposures. Similarly,
even healthy members of the general population may experience impaired
mental activity or decreased physical performance after sufficiently
high pollution exposures. The general population, especially families
with young children, is almost universally susceptible to common acute
respiratory illnesses including colds, sore throats, bronchitis and
pneumonia. Air pollutants can increase either the frequency of severity
of these disorders-. Personal air pollution with cigarette smoke, occupational
exposures to irritating dusts and fumes and possibly familial factors
increase the risk of developing chronic obstructive lung disease and
respiratory cancers in large segments of our population. Air pollutants
can also contribute to the development of these disorders. A few animal
studies indicate that air pollutants may also accelerate atherosclerosis
and coronary artery disease. These conditions affect most of our adult
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population even though they may be clinically silent. There is legitimate
concern but few reliable studies to indicate that air pollutants may
cause embryotoxicity, fetotoxicity, teratogenesis and mutagenesis. It
is difficult to define what segment of the unborn population might be
most at risk. In fact these events are poorly recorded and the relevant
existing data are not readily accessible.
1.4.5 What Kinds of Information Are Needed.to Control an Air Pollutant?
Ambient air quality standards rest upon a broad interlocking
scientific information base. Weaknesses in one or more of these knowledge
areas may severely constrain efforts to establish a health-related air
quality standard or to reduce the levels of ambient air pollution. Realistic
assessment of our current information base shows that major gaps exist for
each of the pollutants covered by the primary ambient air quality standards.
Knowledge areas of interest involve measurement methods, emissions
sources, pollutant transport and transformation, air monitoring data,
health effects, welfare effects, predictive models linking emissions to
air quality, control technology and an understanding of the impacts of contro.l
strategies.
1.4.6 What Should a'Minimally Adequate Health Intelligence Base Assess?
A minimally adequate health intelligence base should ascertain the
effects of long-term low level exposures and the effects of single or
repeated short-term exposures. It should be remembered that acute adverse
effects may be attributable to the cumulative effect of long-term lower
level exposures as well as to the effect of short-term peak exposures.
Chronic effects may follow short-term peak exposures as well as
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long-term low-level exposures. In general it is easiest to ascertain what
acute effects follow short-term fluctuations in air quality. Less complete
information is available on the acute and chronic effects which
follow long-term low level exposures. Very little is known about the
chronic effects of peak exposures. The present primary air quality standards
usually consider only an annual average or a single short-term averaging
time. It is assumed that the necessary air quality controls will also
protect against repeated short-term exposures that are less than the
standards. This is an untested assumption and further refinement of the
standards may prove necessary.
All reasonably expected adverse health effects should be considered
when setting a standard. In fact adverse effects which are postulated but
not proven have not always been carefully considered. Failure to consider
what is reasonably expected but not yet elucidated ignores a large
important area of uncertainty. The effects of air pollutants on respiratory
cancers, on the unborn infant and on aging represent three areas of
great uncertainty.
Most adverse health effects are best evaluated by blending complementary
research approaches. Epidemiology, clinical research and animal toxicology
each have their advantages and limitations. Epidemiologic studies are
set in the real world and thus allow consideration of the effect of complex
long and short-term pollutant exposures on susceptible segments of the
population. However, community studies utilize rather crude health measurements
They must cope with a host of strong covariates and are restricted to a
limited range of exposures. Clinical studies utilize .more sophisticated
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health measurements and carefully controlled exposures of human volunteers.
Susceptible segments of the population may be studied and many of the
bothersome covariates found in community studies may be avoided. However,
long-term exposures cannot be easily evaluated. Toxicology studies provide
the opportunity to control strong covariates carefully, to utilize a wide
range of pollutant exposures and to examine body tissues. Unfortunately,
differences between species and lack of appropriate laboratory
models for all susceptible segments of the population limit the usefulness
of animal studies. Thus, it is apparent that all three research approaches
may be necessary and that the design of these studies should provide
biological bridges between them in terms of exposure levels considered and
health indicators utilized. It is rare that this blend of information
can be found and thus not at all unexpected that reputable scientists
will disagree on-whether or not an adverse effect can be attributed to
a given pollutant expsoure. One could hardly expect otherwise since most
of the scientists have their roots if not their total experience in a
single research approach.
In community studies, the association between a pollutant exposure .
and an adverse effect must be considered in terms of its biological
plausibility, its coherence, its consistency and the observed exposure-
response relationship. An assocation is most likely to be causal if it
fits in with our overall biological knowledge, if it is demonstrated by
more than one research approach, if it is consistently observed by different
investigators at different times or in different places and if increased
levels of exposure are accompanied by increased frequency of the disorder
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or if decreases in exposure are accompanied by decreases in the frequency
of the disorder. Using these rules of thumb, there is ample reason
to be concerned about the adverse health effects of industrial and urban
air pollution and there is an obvious urgency to improve our health effects
information base.
We do not have good exposure response functions for each adverse
effect. In fact, we must candidly admit significant uncertainties in
our estimates of the effects thresholds for each adverse effect associated
with each currently regulated ambient air pollutant. In general, the
best we can do at present is to define "lower boundary," "upper boundary,"
and "best judgment" estimates for each."no effect" threshold estimate.
Hopefully, these two boundary assumptions would provide limits for the arena
in which reasonable men might disagree. That is, there should be general
agreement that pollution levels higher than the upper boundary assumption
result in a particular adverse health effect.
Under the upper boundary or a least case assumption, only residual
effects remaining after the consideration of all covariates are attributed
to pollutant exposures. When considering a single study, only the highest
current and past pollutant exposures are associated with an adverse effect
and when considering a group of studies, an adverse effect is attributed
only to exposure levels repeatedly associated with excess disease. For
example, in the frequently encountered situation where high exposure and
low socioeconomic status geographically concur, the effect of low economic
level on illness frequency would be identified first. Any excess illness
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which could not be accounted for by economic level would be quantified
as a residual effect. After all covariates were considered the final
residual excess would be called an air pollution related health effect.
Upper boundary estimates attribute the smallest possible effect to
pollutant exposures, do not allow for interaction between covariates and
exposure, and give a maximum quantitative estimate of human exposures
associated with .adverse responses.
Lower boundary or worst case assumptions attribute adverse health effects
first to covariates which are known to be strong determinants of
disease frequency, such as c'igarette smoking in the case of chronic
bronchitis. But covariates which are not well founded as determinants of
illness frequency are eliminated from final analyses, and air pollution
exposure is assumed to have contributed to the relatively larger residual
in excess illness frequency. When considering any single study, an adverse
health effect is attributed to the lowest exposure level associated with the
effect. Likewise, if information on past exposure is of low quality or
unavailable, current exposures are assumed to represent past experience. Worst
case assumptions, therefore, give minimum estimates of exposures associated
with adverse health responses, and tend to maximize the proportion of disease
frequency attributable to pollutant exposure.
The truth may lie at either end of the quantitative range which can
be derived from least case and worse case assumptions. When health
intelligence cannot give precise quantitative information, the decision
maker should be provided with least and worst case range estimates. At
that point, the degree of control becomes a function of other policy
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considerations, including control costs, alternate control strategies
(and the health effects of these), the severity or magnitude of the effect,
the population at risk, etc. Failure to present range estimates leaves
less room for control options and forces decisions based on one set of
numbers derived from arbitrary interpretations of study results.
A minimally adequate health intelligence base should carefully
consider the health effects of pollutant interactions. To some extent,
standards based upon community studies consider interactions. There are,
however, only a limited number of clinical of toxicology studies that
have evaluated interactions between ambient air pollutants. This is a
clearly defined research need.
1.4.7 What Is Our Present Health Information Data Base for the Primary
Ambient Air Quality Standards?
For each of the pollutants covered by the primary ambient air quality
standards, the authors have attempted to summarize the following
information:
0 What adverse effects might be reasonably suspected? . .
0 What research studies with dose-response information are available?
0 What are the lower boundary (worst case), upper boundary
(least case) and best judgment estimates for effects threshold?
0 What safety margins are contained in the primary standards?
Where appropriate short-term exposures are considered before long-term
exposures.
Sulfur dioxide particulate sulfates j_a_ useful proxy for acid sulfate
aerosols) and total suspended particulates are considered together because
the assessment of their effects is largely based upon community studies
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in which it is difficult if not impossible to disentangle the effects
attributable to one pollutant from those attributable to another pollutant
or to a mixture of the pollutants. Studies which were initially thought
to have considered isolated exposures to urban particulates really
involved exposures containing substantial amounts of acid sulfate aerosols.
An overview of the available research studies that contained good exposure
overview of the available research studies that contained good exposure
date is presented in Table 1.1. Two cautionary thoughts are appropriate:
additional studies are becoming available and the format chosen does not
accurately reflect the number of general toxicology studies that have been
completed. In other words, we would expect that others might construct a slightly
different matrix. Nevertheless, the table demonstrates that with few
exceptions there is an obvious imbalance between the research approaches
and that we have little quantitative data about several effects of major
concern.
Our best judgment estimates for 24 hour exposures which produce adverse
effects are summarized and compared to the relevant existing standards in
Table 1.2. Aggravation of pre-existing cardiorespiratory symptoms in
the elderly, aggravation of asthma and irritation of the respiratory
tract seem to occur a level lower than those permitted by the relevant
primary ambient air quality standards. The effects noted at sulfur dioxide
and suspended particulate levels lower than the standard are in our opinion
most likely due to elevated levels of finely divided acid sulfate aerosols
which arise from reactions involving sulfur dioxide, particulates and
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aerosols in the atmosphere. The lower boundary, upper boundary and best
judgment threshold estimates for each adverse effect associated with short-term
exposures and their associated safety margins were also reviewed. Four points
are worth emphasizing: first, the estimates are based on community studies;
second, the range between the lower and upper boundary estimates is quite
large for both sulfur dioxide and total suspended particulates; third, the
estimated effects thresholds for particulate sulfates are an order of
magnitude lower than those for sulfur dioxide or total suspended particulates;
and fourth, the safety margins present in the standards are quite modest
being in all cases equal to or less than the standard itself.
The same procedure was then repeated for long-term (annual average)
exposures involving sulfur dioxide, total suspended particulate and particulate
sulfates. A word of caution should be interjected: annual average estimates
do not always adequately consider the effects of repeated short-term peak
exposures. For example the lowest best judgment estiamte for an effects
threshold for increased prevalence of chronic respiratory disease symptoms
is based upon annual average estimates in a smelter community where repeated
short-term peak exposures occurred. The lowest annual average exposures
involving less marked fluctuations in short-term levels were considerably
higher. The annual average standards do seem to protect public health
against adverse effects associated with long term exposures to sulfur
dioxide and total suspended particulates (Table 1.3). However, one cannot
be assured that finely divided particulates or acid aerosol exposures sufficiently
high to cause some adverse health effects will not occur even after
existing standards are met. When a more detailed tabular summary of
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upper and lower boundary estimates was examined, one again encountered a
rather wide range between boundary estimates indicating a substantial
uncertainty in the threshold estimate. The duration of exposure necessary
to produce an adverse effect is noted to be quite long, three to ten
years. Alternatively this period might be considered a combination of
the exposure necessary to produce an adverse effect plus the necessary
latent periods for the onset of the effect. .The safety margins contained
in the annual average standards seem a little more adequate than was the
case with the short-term standards.
Nitrogen oxide exposures are now controlled on the basis of an
ambient air quality standard for nitrogen dioxide. Investigators have
expressed concern that exposures to aerosols containing nitrogen compounds
have not been adequately considered. An overview of the expected adverse
effects and the applicable health research studies (Table 1.4) shows that
relatively few health studies are available. Those which are available
do provide a biologically coherent picture, however, even though there
is too little information to construct a dose response function. The
uncertainties in this data base are very large because little or not
data is available on several major effects of public health concern.
There is no short-term Federal standard for nitrogen dioxide. Air
quality distribution models for cities with continuous air monitoring stations
show that the present annual average standard for nitrogen dioxide is
roughly equivalent to a one hour level of 1400 pg/m . Even this extreme
value is substantially below the best judgment estimates for an adverse
effects (excluding odor) following short-term exposures (Table 1.5).
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Best judgment and boundary estimates for long-term nitrogen dioxide
exposures (Table 1.6) are complicated by the need to consider a variety
of averaging times. The situation is further clouded by the pivotal
nature of community studies conducted in Chattanooga in neighborhoods
near the Volunteer Army Arsenal Plant which emitted acid aerosols as well
as nitrogen dioxide. Within the uncertainties posed by the available
health studies, the. existing standard seems adequate with a margin of
safety greater than those previously described for sulfur oxides and
suspended particulates. Clearly, the large uncertainties in the existing
information base warrant a greatly augmented research effort.
Adverse health effects attributable to carbon monoxide (Table 1.7)
differ markedly from those associated with the other ambient air quality
pollutants. Decreased oxygen transport and interferences with tissue
respiratory mechanisms result in a different array of worrisome effects.
Clinical studies of carbon monoxide effects predominate. A limited number
of experimental animal studies and population studies involving certain
of the adverse effects associated with cigarette smoking may also be .relevant.
Best judgment estimates for exposure thresholds for adverse effects
following one hour exposures at sea level assuming various levels of alveolar
ventilation were computed in terms of carboxyhemoglobin levels (Table 1.8)
and ambient exposures (Table 1.9). The procedure was then repeated for 3
hour exposures (Tables 1.10 and 1.11). Rest was defined as an alveolar
ventilation rate of five liters per minute, light activity as an alveolar
ventilation rate of ten liters per minute and exercise as an alveolar
ventilation rate of fifteen liters per minute. Because the relationship
between ambient carbon monoxide and carboxyhemoglobin is non-linear, the
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two methods of approach yield slightly different safety margins with the
ambient approach giving the larger safety margin. The boundary estimates
for each short-term effect did not show as much variation as was seen
with the previously discussed pollutants and thus the thresholds and
safety margins are more certain. No best judgment estimates are possible
for postulfated adverse effects following long-term exposures.
Adverse health effects associated with photochemical oxident exposures
involve a different set of considerations (Table 1.12). Photochemical
oxidants include compounds other than ozone which are quite irritating to
the eyes. Ozone itself is thought to be radiomimetic thus focusing
concern on accelerating aging, increased risk for malignancies, mutagenesis,
embryotoxicity and teratogenesis. Information on suceptibility to acute
respiratory disease, risk for mutations and impaired fetal survival is
limited to animal studies. Photochemical oxidants are of interest for
another reason, namely mnay of the studies were conducted some years ago
before research and pollutant measurement methodologies were refined.
These pioneer studies may not have adequately addressed the problem.
The best judgment exposure thresholds for adverse effects may be
compared to the one hour standard for photochemical oxidants measured as
ozone (Table 1.13). Adverse effects are consistently observed when peak
o
hourly exposures to ozone alone exceed 400 pg/mj with several thresholds
being substantially lower. Boundary estimates for effects thresholds revealed
a variable range and thus a variable degree of uncertainty. There is little
uncertainty regarding irritation phenomenon and a great deal of uncertainty
when considering other adverse effects. No estimates are possible for two
of the more severe health effects - accelerated aging and malignancies.
It is also worth emphasizing that assessment of potentially grave health
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effects depends on a small number of largely unconfirmed studies. Safety
margins seemed quite variable and the effects of pollutant interactions are
not considered.
1.4.8 How Uncertain Are Our Present Best Judgments for Effects Thresholds?
The smallest degrees of uncertainty are associated with adverse effects
attributable to carbon monoxide and with irritation symptoms following
photochemical oxidant exposures. -Larger degrees of uncertainty exist
for almost every other adverse effect. In most cases this uncertainty is
larger than the safety margins contained in the standard. Uncertainties
in the threshold effects estimate tend to escalate scientific disagreements
and foster delays in arriving at a consensus view of the most appropriate
air pollution controls. Uncertainty may be very expensive because control
costs are generally exponential functions.
1.4.9 What Safety Margins Are Contained in the Primary Ambient Air Quality
Standards?
The safety margins contained in each of the primary ambient air
quality standards may be compared by calculating and comparing the safety
margin that is associated with the lowest best judgment estimate for an
effects threshold. A range of safety margins for each pollutant can also
be calculated from the array of safety margins associated with the various
adverse effects attributed to each pollutant (Table 1.14). Several factors
must be kept in mind when considering these calculations. First, safety
margins are not as precise as the percentage estimates would at first seem
to indicate because of the underlying uncertainties in measurement methods
and in estimates of effects thresholds. Second, consistency in safety
margins was not a major consideration in setting primary ambient air quality
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standards. Third, the apparent margins of safety have decreased as more
complete health studies on susceptible populations have'become available.
Fourth, the safety margins contained in the primary ambient air quality
standards are much smaller than those maintained for the control of
ionizing radiation and most environmental chemicals. In no case does
the safety margin for a pollutant clearly exceed the standards for that
pollutant. Even the most extreme best judgment safety margin is less than
ten times the relevant standard. Finally, there is little or no safety
margin associated with the sulfur dioxide-suspended particulate-fine
particul ate sulfate combinatijon.
1.4.10 Can We Compare Health Risks Associated with Air Pollution to
more Familiar Risks?
Much more work needs to be done in this area but several useful
observations can be made with reference to aggravation of asthma, 'aggravation
of cardiorespiratory symptoms, frequency of chronic respiratory disease
symptoms and frequency of common respiratory illnesses.
Subfreezing temperatures seem to obliterate any effect of ambient
air polluants upon asthma. Asthmatics may either stay indoors or may be
maximally stressed by low temperatures and unable to respond to pollutants.
The effect of a sudden change in termperature is roughly comparable to the
effects seen by the range of day to day variability in the level of air
t
pollutants in the urban United States. The same observation is approximately
correct when one considers worsening or the onset of cardiorespiratory
symptoms in the elderly population.
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Personal pollution among cigarette smokers is a stronger determinant
than ambient air pollution in contributing to the development of chronic
respiratory disease symptoms. The 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. 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 various communities 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, air
pollution itself is a significant and consistent contributing factor,
increasing bronchitis rates both in non-smokers as well as smokers from
•polluted communities.
Families living in more polluted urban areas report excesses in
common respiratory illnesses which were roughly comparable to the excesses
in acute respiratory illness observed nationally during years of epidemic
influenza like 1965-1966 and 1968-1969.
The preceding comparisons are admittedly quite general and are intended
only to provide the best immediate perspective possible.
1.4.11 What Are the Consequences of Our Present Uncertain Scientific
Information Base?
As previously noted, control costs are generally exponential functions.
Therefore uncertainties about a standard which itself requires the
stringent control of emissions will inevitably result in major uncertainties
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in the justification of control costs. The uncertainties inherent in
the present standards are without a doubt billion dollar uncertainties.
For example, the proposed control strategies for sulfur oxides and
mobile sources may not achieve the needed reductions in acid aerosols
and fine particulate sulfates and nitrates even though their gaseous
precursors sulfur dioxide and nitrogen oxides are reduced to acceptable
levels. Clearly, it is wise to resolve major uncertainties as rapidly
as possible to avoid wasteful expenditures and to assure the development
of needed new control technology.
1.5 CASE STUDY: ASSESSMENT OF HEALTH EFFECTS OF INCREASING EMISSIONS OF SULFUR**
OXIDES FROM STEAM ELECTRIC POWER PLANTS
Health-related air quality standards for sulfur oxides and particulates,
the most important pollutants emitted by steam electric power plants, are
scheduled to be met before the end of this decade. Meeting emission and air
quality standards will prove a difficult challenge for an electric utility
industry already facing other major obstacles in its efforts to meet the growing
power demands of our nation. The most difficult standard to attain relate the
need to reduce sulfur oxides emissions. The effect of not meeting standards
and allowing sulfur Oxides emissions to grow can be better understood after
assessing the best available answers to the following questions:
0 Why control sulfur oxides?
0 How are sulfur oxides emissions changing?
0 What are the relationships linking sulfur dioxide to ambient levels
of acid sulfate aerosols?
*This assessment, with explanatory appendices is available as an intramural
Environmental Protection Agency report entitled, Health Effects of Increasing
Sulfur Oxides Emissions.
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0 What adverse health effects are attributable to elevated ambient levels
of sulfur oxides?
0 How will growth in emissions from steam electric power plants alter
human exposures to acid-sulfate aerosols?
0 What is the magnitude of the public health problem likely to follow a
growth in emissions?
0 What important caveats must be kept in mind?
1.5.1 Why Control Sulfur Oxides?
For at least another decade industrial nations will combust increasing
quantities of fossil fuels that contain organic and inorganic sulfur compounds.
Unless specifically controlled, the sulfur compounds in fossil fuels utilized
by steam electric power plants will be emitted into the air as sulfur dioxide
.and, to a lesser extent as sulfur trioxide. These sulfur oxides are transformed
in power plant pTumes and later in the atmosphere into acid-sulfate aerosols
(strong acids and sulfate salts). Acid-sulfate aerosols are fine particulates
which have a long atmospheric residence and which are capable of penetrating
deeply into the human respiratory tract where they may become entrapped.
Acid-sulfate aerosols can adversely affect human health, vegetation, fish,
materials, and visibility.
1.5.2 How Are Sulfur Oxides Emissions Changing?
Two important concurrent changes in sulfur oxides emissions have taken
place in recent years:
0 Urban emissions from area sources, industrial sources and power plants
have decreased.
0 Suburban and rural emissions from steam electric power plants have
increased.
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Urban emissions of sulfur oxides from home heating and industrial sources
began to decrease just after World War II and air pollution control efforts
during the late 1960's only reinforced a trend that was already well established.
Concern about urban air pollution did however cause a number of utilities to
seek low sulfur fuels which have since become scarce and increasingly expensive.
Precise estimates are not available but it is likely that sulfur oxide emissions
in our major cities were decreased by about 50% between 1960 and 1970. Further
reductions are envisioned under the state implementation plans required by the
Clean Air Act amendments.
On the other hand, suburban and rural emissions of sulfur oxides rapidly
increased between 1960 and 1970. This is in large part attributable to a con-
tinued growth in sulfur oxides emissions from steam electric power plants which
can be appreciated by study of the regional and national trends shown in Table 1.15.
Were.it not for steam-electric power plants, nationwide emissions of sulfur
oxides between 1950 and 1969 would have decreased by 15% instead of increasing
by 36"4. If emission standards and existing air quality standards are met,
sulfur dioxide emissions from steam electric power plants must be substantially
reduced. The emission picture will be further complicated by the need to im-
port increasing quantities of high sulfur petroleum and utilize more high sulfur
domestic coal.
1.5.3 What Are the Relationships' Linking Sulfur Dioxide to Ambient Levels of
Acid-Sulfate Aerosols?
Sulfur dioxide is transformed in the atmosphere to sulfur trioxide and
sulfuric acid by a number of different complex mechanisms whose effective trans-
formation rates vary from 1 to 20% per hour. The predominant mechanism can be
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expected to vary from place to place and over time. Sulfuric acid aerosols and
the salts that form with ammonia or metallic cations may be transported for
long distances. Urban acid-sulfate aerosols contain at least three components:
first, a component intruding from rural sources and distant urban plumes; second,
a component arising from sulfur oxide emissions in the urban area; and third, a
component of natural origin. Acid-sulfate aerosols are removed by rainout and
washout. Sulfur trioxide in smaller amounts is also emitted directly from com-
bustion sources and is rapidly transformed into sulfuric acid aerosol, thus
associating worrisome levels of sulfuric acid with power plant plumes. Power
plants in the eastern half of the United States are spatially arranged (Figure
1.2) so that moving air parcels replenish their sulfur loading more rapidly
than acid-sulfate aerosols can be removed by natural processes. The increased
acid-sulfate aerosol loading is associated with increases in atmos-
pheric turbidity; rainfall acidity and ambient air levels of suspended particulate
sulfates in urban and rural areas. Water soluble suspended particulate sulfates
collected on a high volume air sampler are a useful but imperfect proxy for
acid-sulfate aerosols. Increased acid-sulfate aerosol loadings mean that ambient
air entering downwind metropolitan regions may contain bothersome levels of pollu-
tants before emissions from the local air quality control region contribute a
further increment.
Where urban emissions of sulfur dioxide predominate and where arriving air
parcels are not already polluted, there is a good (.5-.7) correlation between
24 hour ambient levels of sulfur dioxide and ambient levels of suspended sulfates.
Measurements around industrial facilities during full operation and during shut-
downs demonstrate a clear relationship between local ambient levels of sulfur
dioxide and suspended sulfates. There is not always a good correlation between
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29
ambient levels of sulfur dioxide and suspended sulfates. Poor correlations are
expected when photochemical smog is present, when local industrial emissions
introduce catalytic metals or reactive hydrocarbons. Poor correlations are also
distant emissions and thus intruding acid-sulfate aerosols are allowed to increase.
Thus, it is important to consider regional emission patterns when projecting
changes in acid-sulfate levels. Though our data base is far from satisfactory,
there is evidence that acid-sulfate aerosols, as measured by their suspended sul-
fate proxy, did decrease substantially in urban areas where sulfur dioxides were
stringently controlled during the late 19GO's. However, regional emissions in-
creased because of locating steam electric power plants in rural areas and because
urban areas varied in the timing and the stringency of emissions controls. The
rate of regional increase over the short period covered by the suspended sulfate
data base, which begins in the early 1960's and ends in 1970, was probably
initially more than balanced by local control measures, but this decrease would
not be expected to persist very long. Thus, regional levels of suspended sulfates
may well increase substantially during the present decade. Based on our present
understanding, one can assume an increase in acid-sulfate aerosols which is
proportional to regional increases in sulfur dioxide emissions. This assumption
will of course have to be validated and perhaps altered by research now underway
and projected for the future.
1.5.4 What Adverse Health Effects Are Attributable to Elevated Ambient Levels
of_ Sulfur Oxides?
Short term exposures to elevated levels of sulfur oxides, especially
acid-sulfate aerosols, are thought to aggravate asthma and pre-
existing heart and lung disorders. Elevated short term exposures
to acid-sulfate aerosols are also likely to have been largely responsible for
perceptible increases in daily mortality observed during air
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30
pollution episodes. Repeated short term peak exposures or more even
elevations in annual average exposures to acid-sulfate aerosols lasting
several years are likely to result in excess acute lower respiratory
disease in children excess risk for chronic respiratory disease symptoms
in adults and decreased ventilatory function in children.
These effects were observed in community studies (see references)
where levels of sulfur dioxide, acid-sulfate aerosols and suspended
particulate matter were usually but not always simultaneously elevated.
Unfortunately, it is only now becoming possible to develop laboratory
animal models and clinical protocols that allow one to mount complementary
studies on the effects of finely divided acid-sulfate aerosols on susceptible
population segments. Early toxicology studies exposing healthy young
adult animals for short periods to sulfur dioxide alone or to sulfur
dioxide and particulate have shown equivocal results. Construction of
dose response functions for acid sulfate aerosols utilized in the present report is
hampered by four problems: first, suspended sulfates must be employed
as a proxy for acid-sulfate aerosols; second, for some studies one had
to recapitulate sulfate exposure from prediction equations that utilized
existing air monitoring data for sulfur dioxide and suspended particulates
(Table 1.16); third, it was necessary to measure excess risk of illness
rather than direct illness rates because studies differed in their
locale and their methods of ascertainment of illness; fourth, it should
be emphasized that the derived dose-response functions are best judgment
threshold functions not precise mathematical fits. Best judgment estimates
were utilized because the data points available for the assessment of a
single adverse effect were not independent. In the assessment of a
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31
single adverse effect each constituent study yielded very few data
points and the control or "no effects" level assumed for each constituent
study could differ from the "no effects" levels assumed for other studies
used in the assessment of a single adverse effect. Moreover, a single
adverse health effect might be differently defined or ascertained in any
set of studies. Thus the authors deliberately chose to emphasize the
roughness of their assessment by a best judgment approach, in general,
these best judgment functions (Table 1.17) are more conservative in that
they predict less excess illness than would be the corresponding mathematical
fits (Table 1.18). For asthma, the estimates may be high as only warm
days were considered by the dose-response function. Despite these
handicaps, the functions should roughly quantify the expected adverse
effects associated with various exposures to sulfur oxides. Major
research efforts are necessary to improve these functions. Collecting
such information will, however, require several years and decision-
makers require rough information before the refined functions will be
available. , .
1.5.5 How Mill Growth in Emissions from Steam Electric Power Plants Alter
Human Exposures tp_ Acid Sulfate Aerosols?
Emissions from steam-electric power plants contribute to two different types
of human exposure: infrequent short-term elevations which are a hazard for.
especially susceptible subgroups and long-term exposures resulting from changes
in overall urban and regional levels of acid-sulfate aerosols.
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The impact of short-term fumigations depends upon fuel consumed, plant
location, stack height, topography, meteorology, population susceptibility and
population density in the impact area. As yet, national estimates for the
adverse effects of infrequent short-term exposures are not available. Estimates
of such exposure increments have been made for a number of locales. Sulfur
dioxide exposure increments of greater than 900 yg/m for 24 hours have been
predicted and observed in areas impacted by emissions from steam-electric power
plants combusting high sulfur coal. Over an area of one square kilometer most
impacted around urban power plants incremental sulfur dioxide exposures of
greater than 120 to 190 y/gnr and incremental acid-sulfate aerosol exposures
•3
up to 6 yg/m could be expected for about 20 days each year if these plants
utilized coal or oil containing typical quantities of sulfur (2-3%). Estimates
of the associated increments in daily mortality, aggravation of asthma and
symptoms of heart and lung disease in the elderly show only modest increments
in symptom aggravation.
More progress has been made in roughly quantifying the expected increases
in acid-sulfate aerosol exposures and the associated adverse health effects
that are expected to accompany increasing sulfur oxides emissions over a power
region or over several metropolitan areas. Briefly the steps employed are as
fol1ows:
0 First, populations of each power region were placed into one of four
strata (based on the 1970 census): rural (including places of less
than 2500); urban places of less than 100,000; urban areas larger than
100,000 but less than 2,000,000; and urban areas larger than 2,000,000.
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0 Next, a cumulative frequency distribution for the expected 24 hour
suspended sulfate exposures and summary statistics (arithmetic and
geometric means and their standard deviations) were estimated based
upon the sulfate distributions monitored at all National Air Sampling
Network sites within each population class in each power region Table
1.19). The most current year, usually 1970 but sometimes 1969, available
from each site was utilized.
0 Next, it was assumed the regional increases in sulfur dioxide emissions
would be accompanied by proportionate increases in suspended sulfates
in power regions east of the Mississippi River: NPCC-MAAC, ECAR, MAIN,
SERC. No increases in sulfate levels for other regions were postulated
even though currently non-predictable increases are likely to occur on
a limited scale. Stated another way, regional transport of acid-sulfate
aerosols was assumed only for power regions generally east of the
Mississippi. Thus any adverse health effects occurring west of the
Mississippi are left out of the present estimate.
With these assumptions in mind, changes in acid-sulfate aerosol exposure.
were estimated using the suspended sulfate proxy. Two cases were considered:
first, meeting .power demands while attaining emission and air quality standards;
and second, meeting national electric power needs without meeting clear air
requirements. In the latter case expected exposures in 1975, 1977 and 1980 were
calculated for each population strata in power regions generally east of the
Mississippi.
1.5.6 What Is The Magnitude Of The Public Health Problem Likely To Follow A
Growth In Emissions?
To answer this question one must use dose-response functions to calculate
the expected adverse effects assuming that exposures are reduced as standards
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are met and compare these effects with adverse effects calculated from the
previously ascertained dose-response functions and the expected acid-sulfate
aerosol exposures assuming that standards are not met. Differences of interest
can then be calculated by subtraction. This step, however, was preceded
by defining the specific segments of population at risk and the expected base-
line frequencies of the adverse effects of interestutilizing data from the
National Health Survey and the Statistical Abstract of the U.S. for 1972.
The adverse health effects attributable to not meeting clean air standards
will be considerable (Table 1.20). Using our best judgment estimates the
number of excess or premature deaths may reach over 6,000 per year by 1980 and
the total excess between 1975 and 1980 could exceed 25,000. Each year an
average elderly person will experience an unnecessary 5 to 10 days when their
chronic heart and lung disorder will be perceptibly aggravated. If standards
are not met, the.excess number of aggravation days for our senior citizens
would be 20 to 30 million days each year and total over 160 million days during
the years 1975 to 1980. Each year a typical asthmatic might expect one to two
unnecessary asthma attacks. If standards are not met, the excess number of
asthma attacks would be 6 to 10 million each year and could total over 50 million
during the years 1975 through 1980. Each year otherwise healthy children would
experience 400 to 900 thousand more common but severe acute respiratory dis-
orders like croup, acute bronchitis and pneumonia. Between 1975 and 1980
children would be burdened more frequently with persistent chronic respiratory
disease symptoms. In 1975 an excess of over 900,000 adults would be involved
and by 1980 an excess of over 1,500,000 adults might be expected to report
persistent chronic respiratory disease symptoms. If a least squares fit esti-
mate is utilized (Table 1.21), the picture is not substantially changed. One
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35
is still faced with thousands of premature deaths and millions of excess
illnesses.
In summary, present rough estimates conclude that substantial excess
adverse health effects can be expected each year if clean air requirements are
not met: thousands of premature deaths, millions of days of illness among
susceptible segments of the population, hundreds of thousands of needless acute
lower respiratory illnesses in otherwise healthy children and hundreds of
thousands of chronic respiratory disorders among adults. If the health impact
of short-term fumigations prove greater than expected or if regional effects
occur in the western power regions, the calculations of excess adverse effects
given here may prove overly conservative.
It is important to remember that the present ambient sulfur dioxide stand-
ards would be about what is necessary to protect public health if dispersion
conditions were good and if acid-aerosols did not intrude from up wind sources.
One should also recall that the sulfur oxides criteria document recognized the
problem of acid aerosols but that the knowledge at that time led one to believe
that long range transport of aerosols was not a major constraint for air quality
standards. Newer information has shown that long range transport is a signifi-
cant constraint.
We have seen that meeting clean air act requirements for reducing sulfur
oxide emissions from power plants should prove beneficial in protecting public
health and that any residual adverse health effects would be quite modest under
our best judgment estimates. Residual effects would be somewhat more signifi-
cant under the least squares fit estimates. In either case one would still be
faced with the problem of adverse effects among asthmatics and the elderly who
are especially susceptible population segments. In. other words, meeting Clean
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36
Air Act requirements should greatly benefit, but not completely protect public
health from adverse effects attributable to acid sulfate aerosol exposures.
1.5.7 What Important Caveats Must Be Kept In Mind?
0 The answers to the preceding questions are current best judgments but
they are clouded by significant scientific uncertainties involving many key
aspects of the sulfur oxides problem. These have been dealt with in some detail
in previous technical reviews and briefing documents that are public information.
0 Interpretations of historical trends in emissions and air quality are
hampered by a very limited data base. Indeed, our current monitoring systems
for sulfur dioxide, suspended sulfates, strong acids, precipitation chemistry,
trace metals, ammonia, and hydrocarbons are not adequate enough to answer perti-
nent questions about the origin, transformation and removal of sulfur oxide air
pollutants. Simultaneous monitoring in urban, suburban and rural settings is
required.
0 Current measurements of suspended sulfates serve as a useful proxy for
acid-sulfate aerosols but measurements that delineate particle size and chemical
composition are required for sulfur compounds and other aerosol components.
Aerosols of natural and man-made origins must be characterized and differentiated.
0 The mechanisms and rates for the transformation of sulfur dioxide to
acid-sulfate aerosols in plumes and in the atmosphere are not well understood.
Plumes from controlled and uncontrolled industrial and power plant combustion
sources should be studied.
0 Predictive models which will give needed precision to estimates of long
range transport and the influence of emission height must be developed.
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0 More soundly based dose-response functions for the adverse effects on
public health and welfare must be developed. Interlocking clinical, epidemio-
logical and laboratory animal studies are required to reduce scientific uncer-
tainties about adverse health effects. Carefully designed studies of plant
damage, material degradation, visibility impairment and climatic changes are
required to develop reasonable damage functions for adverse effects on the public
welfare.
0 Sound societal judgments can be based only on a sound scientific informa-
tion base. Failure to acquire the needed information will lead to needless
discord and likely to one or more national economic or public health tragedies.
1.6 CASE STUDY: HEALTH IMPACT OF EQUIPPING LIGHT-DUTY MOTOR VEHICLES WITH
OXIDATION CATALYSTS
One of the most difficult challenges posed by the Clean Air Act is the
regulation of pollutants emitted from motor vehicles. Statutory national
standards were established to reduce emissions of carbon monoxide, hydrocarbon
and oxides of nitrogen from light duty motor vehicles. Additional, controversial
transportation control measures have been proposed to reduce automotive emissions
even further in a number of metropolitan areas so that health-related ambient
air quality standards can be met as quickly as possible.
1.6.1 Background
While the Clean Air Act as amended, in effect, established the final
emission levels of the pollutants, it did not permit the Federal Government to
establish the techniques by which such levels would be achieved. The domestic
automobile manufacturers have chosen the oxidation catalyst as the technology
of choice for most engine families in achieving the 1975 interim standards and
the statutory carbon monoxide and hydrocarbon standards. While there is current
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38
debate over the statutory emission standard for oxides, of nitrogen,
it is certainly possible that reduction catalysts may be utilized to
achieve the required emissions reduction of that pollutant should the
statutory standard remain unchanged. The required reductions in the
emissions of carbon monoxide, hydrocarbons, and oxides of nitrogen are
based upon the need to protect public health from adverse effects attributable
to exposures involving carbon monoxide, nitrogen dioxide, and oxidants
for which the key precursors are the hydrocarbons. The use of oxidation
catalysts will make it possible to achieve substantially reduced emission
levels of carbon monoxide and hydrocarbons. Scientists have for sometime
been aware that these three regulated pollutants do not solely comprise
the products emitted from light .duty motor vehicles. Non-regulated
emission products of both past and current concern include total particulates,
particulate lead, polynuclear aromatic hydrocarbons, phenols, sulfur
compounds, particulate metals, aldehydes, nitrogen compounds, and oxygenates.
Limited research in Federal and industrial laboratories over the past
several years has examined the effect of fuel and fuel additive composition on
both regulated and non-regulated emission products. With the exception of
metal-containing additives, fuel composition and fuel additives have been found,
in general, to cause an alteration of the relative concentrations of species
already present in exhaust; rather than cause the emissions of new pollutants.
Use of metal-containing additives however causes the emission of exhaust
particulates which contains that metal.
In general emission control approaches which were initially employed
to achieve the various emissions reductions required through the 1974
model year only altered the relative concentrations- of pollutant species
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39
already present in the exhuast. The use of oxidation catalysts, on the
other hand, alters emissions products far more dramatically. Certain
non-regulated emissions products of public health concern are dramatically
decreased, while others are created or dramatically increased.
This case study will attempt to lend perspective to what has proved
to be an extremely complex risk benefit problem by examining the impact
of catalyst-specific emission products on persons living near major
arterial throughways, traversing these throughways, and working in major
urban centers. Where possible these exposure changes are compared to
present ambient urban air pollutant levels. An attempt is then made to
project future impacts as the percentage of catalyst-equipped vehicles
Increases.
1.6.2 How Are Mob.ile Source Emissions Changing?
Federal mobile source emissions standards for light duty vehicles
were first established for 1968 model year vehicles. Future reductions
in carbon monoxide and hydrocarbons were achieved by 1970 standards.
The 1970 Clean Air Act Amendments mandated that a 90% reduction in •
carbon monoxide and hydrocarbons from 1970 standards be achieved by 1975
and that 90% reduction in oxides of nitrogen emissions from 1971 vehicles
be achieved by 1976. As a result of energy related legislation, achievement
of these statutory emissions standards can be extended up to two years.
The Federal Environmental Protection Agency has published regulations
requiring that a fuel of very low lead and phosphorus content (Federal
Register, January 10, 1973) be available by July 1, 1974, for use in
1975 model year catalyst-equipped vehicles. These regulations are based
upon the adverse effects of lead and phosphorus on catalyst performance.
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Additionally, regulations have been published (Federal Register, December
6, 1973) requiring a step-wise reduction in maximum gasoline lead levels.
These regulations are based upon public health considerations. These two regula-
tions will have the combined effect of reducing lead emitted from light
duty motor vehicles by 60-65% by 1979.
The use of oxidation catalyst technology to achieve emissions
standards for carbon monoxide and hydrocarbons will also affect emission
levels of certain non-regulated emissions of public health concern.
Attainment of the statutory standards for carbon monoxide and hydrocarbons
will also result in a 95+% reduction in the emissions of polynuclear
aromatic hydrocarbons and phenols and 80-90% reduction in the emission
of aldehydes except possibly for aromatic aldehydes formed from organic
sulfur in fuel. The use of oxidation catalyst technology, however, will
result in new emissions of platinum and palladium and increased emissions
of materials such as particulate sulfates and sulfuric acid, aluminum
and its compounds, partiuclate nitrogen, and, perhaps, hydrogen sulfide,
phosphene, and unusual organic species.
1.6.3 How Will Human Exposures Tp_ Automotive Pollutants Be Changed?
Predicted changes in 24-hour exposures to a number of pollutants
emitted from light duty motor vehicles are shown in Table 1.22. Three cases
are studied: first, after 2 model years of vehicles are equipped with
oxidation catalysts; second, after four model years and, third, after
10 model years of vehicles are so equipped. Median day and worst day
pollutant exposure levels are presented. The predicted incremental
exposures are attained by using a carbon monoxide dispersion - suspended
lead surrogate model developed to predict the daily (24-hour) incremental
exposure of these pollutants to a person living near a major arterial highway.
(See references for the technical details of this model).
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1.6.3.1 Benefits associated with the use of catalyst technology. It is
apparent from Table 1.22 that substantial reductions in exposures to carbon
monoxide, lead particulate, polynuclear aromatic hydrocarbons, and phenols will
occur as a result of the attainment of stringent emissions standards through the
utilization of oxidation catalysts. Oxidant exposures will also be reduced be-
cause emissions of hydrocarbons, a key oxidant precursor, are controlled by oxi-
dation catalysts.
1.6.3.2 Problems associated-with the use of catalyst technology. It is
also evident from Table 1.22 that exposures to certain pollutants will increase
as catalysts are introduced into the Nation's vehicle population. Increased or
new exposures to aluminum and its compounds, noble, metals, and acid-sulfate
aerosols. Aluminum and its compounds, while perhaps not detrimental in themselves,
might be expected to potentiate the ability of sulfates and sulfuric .
acid aerosols to act as respiratory irritants. Emission of aluminum •
compounds results from deterioration of the catalyst support material,
alumina. Platinum, palladium, and their compounds are pollutants new to
the urban environment. The incremental levels of these noble metals
should be significantly lower than first estimates of exposure due to
substantially lower emission levels from later prototype 1975 vehicles.
In fact, many of the vehicles now being tested do not emit detectable
levels of these metals. Therefore, the authors currently believe that
the exposure estimates presented in Table 1.22 reflect the maximum
exposures which might occur. The Federal Government has initiated
appropriate research to assess the potential for adverse public health
effects due to the introduction of noble metals and their compounds into
the ecosystem where methylation could produce compounds with considerable
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toxic potential.
Acid-sulfate aerosols composed of participate sulfates and sulfuric
acid comprise the major problem associated with the use of oxidation
catalysts. All current gasoline contains sulfur, the national average being
around 300 ppm. Currently, non-catalyst vehicles emit this sulfur as
sulfur dioxide gas. This sulfur dioxide is dispersed in the atmosphere
and slowly reacts to form particulate sulfate. On a national inventory
basis, sulfur dioxide from mobile sources constitutes about 1% of the
total sulfur dioxide emissions. Oxidation catalytic techniques have
been used since the late 1800's to produce sulfuric acid from sulfur
dioxide. It, therefore, was not entirely unexpected to find that the
oxidation catalyst systems envisioned for light duty motor vehicles
oxidized some of the exhaust sulfur dioxide to sulfur trioxide which, in
the presence of water vapor, reacts almost instantaneously to form
sulfuric acid aerosol.
1.6.4 Can One Quantify Health Impact of Changes In Acid-Sulfate Aerosol Exposures?
If one does not wish to assume a particular human activity pattern,
one can still estimate changes in acid sulfate aerosol exposures likely
to involve urban residents by using exposure models derived from carboxyhemoglobin
levels measured in blood donors who claimed to be non-smokers (see
references for the methodology involved). Carboxyhemoglobin levels in
non-smokers vary from city to city and from neighborhood to neighborhood
with higher carboxyhemoglobin levels being observed in central cities
and around complex area sources of carbon monoxide like airports and
shopping centers.
Since exposure to carbon monoxide may arise from sources other than
motor vehicles, projections of sulfate aerosol exposures utilizing the
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43
carboxyhemoglobin surrogate model may tend to overestimate somewhat the
incremental acid sulfate aerosol exposures attributable to the use of
oxidation catalysts.
The estimated percentage increases in the median 1 daily urban sulfate ex-
posures after 2, 4, and 10 model years are catalyst-equipped and are calculated
in Table 1.23. In each electric power region, urban population centers exceeding
2 million, and urban centers with populations between 100,000 and 2 million are
considered separately since larger cities generally have higher sulfate levels.
It is apparent that the acid-sulfate aerosol exposures associated with oxidation
catalysts are likely to increase significantly the median daily sulfate levels to
which urban populations are exposed. The actual incremental exposure will of
course depend upon vehicular density and other factors. However, the proportionate
increase depends not only on vehicular density but also the level of suspended
particulate sulfate already found in urban air. In any case, increments of public
health concern are likely in most cities after four model years and are equipped
with oxidation catalysts.
If one were to accept the dose response functions for acid-sulfate aerosols
previously described in the preceding case study, it seems methodologically
simple to construct rough quantitative estimates of the adverse health effects
expected. However, that is not necessarily the case because one cannot be
assured that incremental acid-sulfate aerosol exposures attributable to oxidation
catalysts will be distributed in the same fashion as base sulfate exposures.
In other words the worst or highest exposure day attributable to oxidation
catalysts may or may not coincide with the worst day for sulfate exposures at-
tributable to other sources. This exposure problem can be appreciated by exami-
ning projections for a major eastern city, New York (Table 1.24). Here, the
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44
percentage increase in median daily sulfate exposures due to oxidation .catalysts
was examined after 2 and 4 years of vehicles are catalyst-equipped. In addition,
the percentage increase in the 90th percentile day was projected under two
boundary conditions: first, assuming that the incremental catalyst-related sul-
fate exposure frequency distribution is the same as the urban sulfate distribution,*
i.e. high incremental sulfate exposures occur on the same day as high ambient
air exposures occur; and second, that the high incremental catalyst exposures
on the low ambient level day. Table 1.25 translates these percentage increases
in sulfate level exposures due to catalysts into the increased number of days
per year during which exposures would exceed the current threshold estimates
for aggravation of cardiorespiratory disease and for perceptible increases in
daily mortality counts (10 and 25 ygn/M3 respectively). After two model years
are equipped with catalysts, least case - worst case projections indicate that
the threshold for illness aggravation might be exceeded 4 to 15 days each year
and the threshold for excess mortality 6 to 25 days each year. After four model
years almost every day would exceed the threshold for illness aggravation and
20 to 76 additional days would exceed the threshold for excess mortality.
1.6.5 What Other Health Impacts Can Be Projected?
The reductions in emissions of carbon monoxide, hydrocarbons, and oxides of
nitrogen as required by past, current, and the future statutory light duty motor
vehicle emissions standards will result in decreased exposures of the public, to
these pollutants and to photochemical oxidants. Catalyst technology application
to achievement of the 1975 and thereafter standards.will also benefit the public
through reduced exposures to polynuclear aromatic hydrocarbons, lead particulates,
and phenols. As yet the health benefits of these reductions can not be even
"T""
-------
45
roughly quantified in terms of illness prevention or reduction.
The potential public health risk associated with increased exposures to
platinum and palladium, aluminum, and particulate nitrogen compounds is felt to
be minor but no rough quantitative estimates are possible.
1.6.6 Add4t4onal Complications
The long distance transport of pollutants discussed in an accompanying
case study is not limited to acid-aerosol sulfate aerosols. In the 1960's
elevated oxidant visibility reduction and plant damage due to photochemical
air pollution were identified in urban areas in the U. S. outside California,
the first site of photochemical air pollution characterization and identification.
Such photochemical oxidation pollution occurs in varying degrees due to the
emission of hydrocarbons and oxides of nitrogen from mobile sources. As in the
case of sulfates, it was believed that local control of these pollutants would
result in substantial decreases in oxidant levels independent of other communi-
ties.
Recently, experimental evidence has been accumulating, both from more
extensive monitoring, as well as specific field research projects. Qualita-
tively, we now have evidence of longer distant transport of air masses containing
oxidant precursors with continued oxidant formation. Such preliminary results
suggest the movement of ozone and ozone precursors (volatile hydrocarbons and
oxides of nitrogen) for hundreds of miles over land and water. While central
city oxidant levels have been reduced principally as a result of 1968-1974 mobile
source emission standards, long distant transport of ozone and its precursors
may be occuring to such an extent as to significantly reduce the effectiveness
of local strategies including transportation controls in the reduction of oxi-
dants. It is evident from the data presented that increased reductions in hy-
drocarbons are essential to assure reduced oxidant levels on a regional as well
-------
46
as local basis. The environmental and public health consequences of the oxidant
problem are, however, less well understood than the acid sulfate aerosol and no
rough quantitative estimates are possible.
The acid sulfate aerosol problem must also be viewed within the context of
complex pollutant interactions. For example, without oxidation catalysts
unrestricted emissions of certain hydrocarbons may alter atmospheric processes
sufficiently to aggravate the existing acid-sulfate aerosol problem. Certainly,
a national strategy which results in continued increases in ambient acid-sulfate
aerosol levels in our urban areas cannot be viewed as a benefit to the public
health. Thus, some combination of mobile and stationary source controls will be
required. These are complex issues where the benefits are potentially large,
the potential dis-benefits also large, and the control costs substantial.
1.7 SUMMARY AND CONCLUSIONS
Existing legislation requires that air pollution be controlled to protect
public health. The health assessments required to evaluate air quality standards
and to support decisions on the control of mobile and stationary source emis-
sions present a series of complex scientific challenges. ... .
. *
Assessment of the health-related air quality standards reveals no
reason for abruptly changing these air quality goals. However, vexing
uncertainties in the scientific information base remain. Thus there are
often rather large differences between upper and lower boundary estimates •
of a threshold for adverse health effects. In addition, there is a sub-
stantial body of evidence indicating that fine particulate aerosols like
the acid-sulfate aerosols are injurious, but the broad scientific informa-
tion base necessary to establish aerosol standards is lacking.
-------
47
Assessment of the health effects of increasing sulfur oxide emissions
is likewise difficult because of the uncertainties involved in our scien-
tific information base. However, present rough estimates conclude that
substantial excess adverse health effects can be expected each year if
clean air requirements are not met: thousands of premature deaths,
millions of days of illness among susceptible segments of the population,
hundreds of thousands of needless acute lower respiratory illnesses in
otherwise healthy children and hundreds of thousands of chronic respiratory
disorders among adults. If the health impact of short-term fumigations
prove greater than expected or if regional effects occur in the western
power regions, the calculations of excess adverse effects given here may
prove overly conservative. It is important to remember that the present
ambient sulfur dioxide standards would be about what is necessary to
protect public health from effects attributable to acid sulfate aerosols
if dispersion conditions were good and if acid-aerosols did not intrude from
up wind sources. One should also recall that the sulfur oxides criteria
document recognized the problem of acid aerosols but that the knowledge
at that time led one to believe that long range transport of aerosols was
not a major constraint for air quality.
Assessment of the health impact.of equipping light duty motor vehicles
with oxidation catalysts demonstrates that these emission control devices
are at best a mixed blessing. Emissions of a number of pollutants capable
of adversely effecting public health including carbon monoxide, phenols,
aldehydes and polynuclear aromatics are dramatically reduced by these
devices. Likewise, catalytic converters will reduce other hydrocarbon
emissions which are not known to affect health adversely but which are an
-------
48
important precursor of photochemical oxidants that do adversely affect
health. Unfortunately, oxidation catalysts will also alter emissions pat-
terns so that sulfafesieafrid sulfufcic acid emissions will be greatly increased
and worsen a public 'health problem whose dimensions are not completely under-
stood. The degree of public controversy engendered by the health
assessments just deiisaibed is a function of the scientific uncertainties
contained in each pM^isiaifer*"assessment. Another major determinant of
the amount of controversy involved is whether or not the decision affects
a vested industrial, environmental or governmental interest that is
politically and economically potent. Since control costs usually rise
exponentially as one approaches an emission or ambient standard, uncertainties
about exposure response relationships can result in violent controversy
and cause major economi£..,pr.ob,l.ems. In general, the amount of scientific
information demanded seems directly related to the degree of public
controversy. Despite attempts-to augment the scientific information
base for air pollution control, it is unlikely that scientific uncertainties
will be sufficiently resolved to prevent disruptive disputes among
reasonable persons for another decade.
-------
49
FIGURE 1.1
OFJBIOLOGICAL RESPONSE
fO POLLUTANT EXPOSURE"
. PATHOPHYSIOLOGIC
_. CHANGES _ _.
PHYSIOLOGIC CHANGES OF
UNCERTAIN SIGNIFICANCE
ADVERSE
HEALTH
ICTS
POLLUTANT BURDENS
PROPORTION OF POPULATION AFFECTED
-------
ELECTRIC POWER REGIONS
SHADED AREA INDICATES TVA POWER SYSTEM
Figure 1 ,'i
-------
52
Table 1.2
BEST JUDGMENT
."EXPOSURE 'THRESHOLDS FOR ADVERSE EFFECTS
.{SHORT TERM)
• EFFECTS
Mortality Harvest
Aggravation of
symptoms in elderly
Aggravation of
asthma
Acute irritation
symptoms •
Present Standard
24-HOUR
Sulfur
Dioxide-
300 to 400
365
»
100 to 250 .
340
365
THRESHOLD (ug/m3)_
Total Suspended Particulfl-2
Parti dilates Sulfatcr
250 to 300 No Data
80 to 100 8 to 10
100 8 to 10
170 No Data
•>rr\ No
"u Standard
-------
53
Table 1.3 \
DGST JUDGMENT
EXPOSURE THRESHOLDS FOR ADVERSE EFFECTS
(LONG TERM)
EFFECT
' Annual _THRES!_ [OLO_( u cj/m)
Sulfur total Suspcn.-Jccf'l'articulatC'
Dioxide- ('articulate Sulfato
Decreased lung
function of children
Increased acute
lower respiratory
disease in fami1ies
Increased prevalence
of chronic bronchitis
200
90 to 100
95
100
80 to 100
100
11
Present Standard
80
75 Mo
(Geometric) Standard
-------
54 .
Table \A
ADVLRSF. ITfTCTS WHICH MIGHT BE
AI'imiHITLtJ III
.NITROGEN DIOXIDE EXPOSURES
EXPECTED EFFECT
RESEARCH APPROACH
EPIDEMIOLOGY
CLINICAL
TOXICOLOGY
AT LOW EXPOSURE LF.VCLS
(
-------
55
Table 1.5 .
BEST JUUGKCHT
EXPOSURE THRESHOLDS FOR AI)VL:liSE EFFECTS
DUE TO NITROGEN DIOXIDE
(SHORT TERM)
EFFECT
Diminished exercise tolerance
Susceptibility to acute ...
respiratory infection
Ditiii iii shed lung function
Present Standard
THRESHOLD >
-------
56
Table 1.6 '
BEST JUDGKCHT
EXPOSURE THRESHOLDS FOR ADVERSE EFFECTS'
• i
DUE TO NITROGEN DIOXIDE
(LONG TERM)
EFFECT
Increased susceptibility to acute
respiratory infection
.Increased severity of acute
respiratory disease
«
Increased risk of chronic respiratory
disease
Decreased lung fuhction
Present Standard
THRESHOLD (jug/m3)*
188
111
170**
188
100 ug/ni3 annual average
'•Annual average equivalent
**-Dcj$cd solely on animal studies
-------
57
: ""Table 1.7
ADVERSE nrr.ar, wniai MIGHT BE
LUGICAI.I.Y i:xi'i:ni:i) TO I-OI.LOU
CARBON .'wrioxiuE LXPOSUKE •
EXPECTED r:rrccT
DiMKMSili.D tXEKCISE
TOLEKAKCE
DECREASED MENTAL
ACTIVITY
' AGGRAVATION OF' HEART
DISEASE
INCREASED RISK OF
HEART DISEASE
IMPAIRED FETAL'
UEVELOhifJlT
SOURCE OF IIITELLIGEIICE
HUMAN STUDIES • \
EPIDEMIOLOGY
' KO. DATA
NO DATA
THREE- STUDIES
STUDIES OF
SHOKli-JG
STUDIES OF
SMOKING
CLINICAL
STUDIES
Tl!!- EC STUDIES
MULTIPLE
STUDIES
MULTIPLE
STUDIES
HO DATA
KO DAT/V
TOXICOLOGY
NO DATA
LIMITED STUDIES
NO DATA
LIMITED STUDIES
LIMITED STUDIES
-------
58
Table 1.8
BUST JUDGMENT CXPOSUIIE THRESHOLDS TOR ADVERSE EITCC7S
f)UE-TO CAUIlONKONQXini:
'(Short Term, 1 hour) .
Effect
Diminished Exorcise Tolerance
in Heart Disease Patients
Decreased Physical Performance
in Normal Adults
Interference with Mental . .
Activity
/ *3 \
Present Standard { /j° r'^{m for)
\ i HP. /
Threshold 2 Carboxyhcnnylobin
Rest
3
7
5
. 1.4
Light Activity
3
7
5
t.5
Exercise
3
7.
5
' 1.8
-------
59
Table. 1.9. '
•BEST JUDGMENT CXPOSURC TIIKKSIIOI.nS FOR ADVERSE EFFECTS
.DUG TO CMIJOII KOu'DXJUi:
(Short Term, One Hour)
I
EFFECT
Diminished Exercise
Tolerance in Heart '
Disease Patients
Decreased Physical
Per forma nee in
Normal Adults
Interference with
Mental Activity
Present Standard (One Hour)
Rest.
143
355
*
2-19 . '
Threshold mg/in^
Light Activity
90
223 '
IliG
Moderate Cxcrcise
73
**
179
125
10 mg/n)3
-------
60
Table 1.10
nnsr t)i)m;Ki:nT i:xi'o:.imi; Tnijrsimi.ir, rnn AI)VI:U:;U r.nicTS
UUL* TO (;AI:I:O;I KOIUXIUI;
(Short Term, {} hours)
i
Effect
Diminished Cxcrcisc Tolerance
In Heart Disease Patients
Decreased Physical
in (Normal Adults
Interference vn'.th
Acti vi ty
Present Standard '
Performance
Mental
«
/10mg/in3 for)
V, 8 hrs. /
'. Threshold'/. Corl>oxyhcr.ioglobin
Rest
3 '
7
5
1.4
l.icjht Activity
3
7
5
1.4
txcrcise
3
7
5
1.5
-------
61
Table 1.11
DL:ST ouDGndT cxi'or.up.F. TW'.i:snoi.DS rop. ADVERSE EFFECTS
DUE TO CAkriO;,'
' (Short Term, c Hours)
Effect
Oir.nnir.hcd Exercise Tolercnce-
in Heart Disease Patients
Decreased Physical Performance
"in Koran 1 Adults
Interference v/ith Mental
Activity
Present Standard (8 hour)
» 4
Threshold ing/in3
Host
-29.
71
50
•
Light Activity
24
59
41 •
. t
Exercise
23 .
55 -
39
"lomg/m3
-------
62
iir.ALiii HIT.CTS wiucii I'.
Table a. 12
i;r. ATTiuuurr.i) 10 i'iioinr.i;rwr.Ai. OXIUAUT rxpo:;ir,:r:,
Cxpcctcd L'ffcct
• *"•**-
• " ' • J1?*
Aggravation of asthma
*
Aggravation of chronic
obstructive lung disease.^
Aggravation of heart "•'-""
disease
Aggravation of hc-matopoietic
disorders
Accelerated aging
• Irritation of eyes
and respiratory tract in
healthy subjects
Decreased cardiopulr.ionary :
reserve.- in healthy subjects
Increased susceptibility
acute respiratory disease "...
Increased risk of chronic
lung disease
Respiratory maligancies
l-'.utagcnesis, crribryotoxic.ity ...
and tertogcnesis ..
• •" *
Tr^c.i.looy
Single. Study
Three early
studies
Three early
studies
No Data
No Data
Multiple
studies
Two studies
Single
study
Single
study
Single study
No Data
He search Apju
Clinical
Studies
Mo Data
Tv/o early
studies.
Mo Data
Single
study
No Data.
Multiple
studies
Tv.'o studies
No Data
Single
study
No Data
No Data
oncli-
Toxicology
No Data
No Data
No Data
No Data
No Data
Multiple
studies
No Data
Multiple
studies
Tv.'o
studies
Single study
Tv/o Studies
-------
63
Table.1..13.
IJHST Junc'iniT
EXPOSURE Tiii'.rsnoi.ir. FOR AIJVFRSF. EFFECTS
DUE TO I'jIOTOC.'OJCAL OXJDAilTS
(SHOUT TERM)
EFFECT
AGGRAVATION OF ASTI!!',A
AGGRAVATION OF CHRONIC LUUG DISEASE
AGGRAVATION OF CERTAIN ANEMIAS
IRRITATION OF EYES
IRRITATION OF RESPIRATORY TRACT IN
OTHERWISE HEALTHY ADULTS- .
DECREASED CARDIOPULMONARY RESERVE
IN HEALTHY ADULTS
INCREASED SUSCEPTIBILITY TO ACUTE *
RESPIRATORY DISEASE
RISK OF MUTATIONS*
IMPAIRED, FETAL SURVIVAL*
DECREASED VISUAL ACUITY.*
PRESENT STANDARD (one hour)
» .-- ... _.....,.., .,_.,„.,,. ...... „ ... . — .. .,
TIIKI. SI 101.1
yUCJ/I.H
500 -
1 <500
400 to 500
200 to 300 .
500 to GOO
•• •
240 to 740
160 **
400 to GOO **
200 to 400 **
400 to 1000
160 iicj/m3
ITM
.25
<1.25
.20 to .25
.10 to .15
}25 to .30
.12 to !si '
.03**
.20 to .30**
.10 to .20**
.20 to .5C
.00
* INVOLVE EXPOSURES .OF THREE TO SEVEN HOURS DAILY FOR UP TO THREE WEEKS
** BASED SOLELY ON ANIMAL STUDIES •
-------
Table.1,1.4
SAFETY FACTORS CONTAINED IN PRIMARY AMBIENT AIR QUALITY STANDARDS
POLLUTANT
SULFUR
DIOXIDE
t
ACID
AEROSOLS
TOTAL
SUSPENDED
PARTICULATES
NITROGEN
DIOXIDE
CARBON
MONOXIDE
PHOTOCHEMICAL
OXIDANTS
LOWEST BEST JUDGMENT
ESTIMATE FOR AN
EFFECTS THRESHOLD
300 TO 400 wg/m3
(SHORT-TERM)
91 ug/m3 (LONG-TERM)
8 ng/m3 (SHORT-TERM)
15 ug/m3 (LONG-TERM)
70 TO 250 ug/m3
(SHORT-TERM)
, 100 ug/m3 (LONG-TERM)
141 jjg/m3 (LONG-TERM)
23 (8 HOUR) mg/m3
73 (1 HOUR) mg/m3
200 (SHORT-TERM)
ADVERSE EFFECT
MORTALITY HARVEST
INCREASED FREQUENCY
OF ACUTE RESPIRA- '
TORY DISEASE
INCREASED ASTHMATIC
ATTACK
INCREASED INFECTIONS
IN CHILDREN
AGGRAVATION OF
RESPIRATORY DISEASES
INCREASED PREVALENCE
IN CHRONIC BRONCHITIS
INCREASED SEVERITY
OF ACUTE RESPIRATORY
ILLNESS
DIMINISHED EXERCISE
TOLERANCE IN HEART
PATIENTS
INCREASED SUSCEPTI-
BILITY TO INFECTION
STANDARD
365 ug/m3
(24 hour)
80jjg/m3
(yearly)
NONE
t
: NONE
260 ug/m3
(24 hour)
75 ug/m3
(yearly)
100 yg/m3
(yearly)
10 mg/m3 (8 ho
40 mg/m
(1 hour)
160
(1 hour)
SAFETY MARGIN FOR
LOWEST BEST JUDGMENT
ESTIMATE, V '
NONE
14
NONE
NONE
NONE
33
41
jr) 130
82
25
to
'SAFETY MARGIN-EFFECTS THRESHOLD MINUS STANDARD DIVIDED BY STANDARD x 100.
-------
65
Table 1.15
Thirty Year Trend in Sulfur Oxides Emissions
from Steam Electric Power Plants
Electric Power Region
Northeast Power Coordinating
Council (NPCC) and Mid
Atlantic Area Coordinating
Group (MAAC)
Bast Central Area Reliability
/Coordination Agreement (ECAR)
Mid America Interpool
Network (MAIN)
Southeastern Electric
Reliability Council (SERC)
Mid Continent Area Reliability
Coordination Agreement (iMARCA)
Southwest Power Pool (SVIPP)
and Electric Reliability
Council of Texas (ERCOT)
Western Systems Coordinating
Council (WSCC)
Yearly Sulfur Dioxide Emissions (Millions of Tons)
1950 1960 1969 1980 Estimates
Standards Standards
Not Met Met
.9
2.0
1.0
0.4
1.3
3.6
1.6
1.8
0.26 0.3
3.1
2.7
3.6
0.6
0.05 0.16 0.4
0.04 0.09 0.2
3.4
6.2 10.0
3.7
6.5
1.2
2.2
1.1
1.0
2.3
1.0
2.2
0.4
0.4
0.5
United States**
4.6
8.9
16.7
28.1
7.8
Nationwide Sulfur Oxides***
Emissions
23.8
23.3
32.4
Not available
*Assumes growth in power generation to 3.2 trillion KWH by 1980. "Standards not met"
•assumes continued use of"oil imports but no further effort to meet Clean Air Act
requirerrients restricting sulfur dioxide emissions.
**1974 estimate 20.8 million tons.
***1940 emissions 21.5.
-------
66
Table 1.16
Recapitulating 24-hour Levels o'f Suspended Sulfates from
Measured Levels of Sulfur Dioxide**
Y = 9 + ,03x 1959 - 1960 Nashville*
sulfate in sulfur dioxide Study (n=.8)
yg/m in yg/m
Y = 9 + .05x '1966-1967 NASN data***
sulfate in sulfur dioxide from 8 inland cities
yg/m3 in yg/nr (f = .5)
Recapitulating Annual Average Suspended Sulfate Levels from
Measured Levels of Sulfur Dioxide
Y = 9 + .04x • Pooled NASN data from
sulfatg in sulfur dioxide NY City, Chicago and New
in yg/m3 Jersey - 1962 - 1967
(o= .6)
*Similar recapitualtion equations are available which link particulates and
suspended sulfates
**used for English and Japanese studies where like Nashville intruding sulfates
were not a problem
***used for U.S. studies
-------
Adverse Health Effect*
Increase Daily Mortality
(4 studies)
Aggravation of Heart and
Lung Disease in Elderly
Patients (2 studies)
Aggravation of Asthma
;(4 studies)
Excess Acute Lower
Respiratory Disease in
Children (4 studies)
Excess Risk for Chronic
Bronchitis (6 studies)
Non Smokers
Cigarette Smokers
Table 1.17
Dose Response Functions Linking Acid-Sulfate Aerosol
Exposures to Selected Adverse Health Effects
(Best Judgment)
Threshold Concentration of
Suspended Sulfates and
Exposure Duration
25 yg/m3for 24 hours or
longer
9 yg/m3 for 24 hours or
longer
Characteristic of Dose Response Function
Slope Intercept • Upper Limit of
Prediction Base
0.00252
0.0141
10 yg/m3 for up to 10 years 0.1340
15 yg/m3 for up to 10 years 0.0738
-0.0631
-0.127
6-10 yg/m3for 24 hours or 0.0335 -0.201
longer
13 yg/ma for several years 0.0769 -1.000
-1.42
-1.14
for Suspended.
Sul fates (yg/nr)**
^60
^60
-^35
^30
*Plotted as percent excess over base rate for each study in every effects category.
**Extrapolations above these limits are less reliable. In later analyses such extrapolations were
unusual occuring rarely with mortality and asthma.
-------
Table 1.18
Adverse Health Effect*
Increase Daily Mortality
(4 studies)
Aggravation of Heart and
Lung Disease in Elderly
Patients (2 studies)
Aggravation of Asthma
(4 studies)
Excess Acute Lower
Respiratory Disease in
Children (4 studies)
Excess Risk for Chronic
Bronchitis (6 studies)
Non smokers
Cigarette smokers
Dose Response Functions Linking Acid-Sulfate Aerosol
Exposures to Selected Adverse Health Effects
(Leasgt Squares Fit)
Threshold Concentration of
Suspended Sulfates and
Exposure Duration
12 yg/m for 24 hours or
longer
3
4 yg/m for 24 hours or .
longer
3 yg/tri for 24 hours or
longer
0
10 yg/nu for up to 10 yrs
15 yg/m for up to 10 yrs
Characteristic of Dose Response Function
Slope Intercept Upper Limit of
Prediction Base
for Suspended
0.00319
0.0131
0.0205
9 yg/m3 for several years 0.0457
0.1481
0.0785
-0.0394
-0.044
-0.029
-0.425
-1.42
-1.23
Sulfates
^60
^60
**
-------
.TAble 1.19 .
Sulfate Cumulative Frequency Distribution By
Energy Region and Population Class,r-yg/m3
A. Population Class > 2 Million
Frequency Distribution, % _Arith. _Geo.
Energy Power Region Min 10 20 30 40 50 60 70 80 90 Max. x, sD x,. • sD
1. NPCC-MAAC 6.8 9.6 11.2 13.3 14.6 17.2 18.5 20.8 23.9 33.9 55.4 19.3 9.3 17.3 1.55
No. of cities = 4 .
3. ECAR 3.4 8.3 10.2 11.7 12.5 14.1 16.9 19.1 22.1 24.0 28.0 16.1 7.1 14.6 1.61
. ' No. of cities =2
3. MAIN 4.5 7.6 11.0 13.7 15.4 17.0 21.1 22.4 24.4 28.3 49.6 19.0 9.0 16.5 1.66
No of cities = 2
4. SERC 6.2 8.4 9.8 12.0 13.1 14.0 14.4 18.1 20.5 26.1 84.7 16.310.5 14.7 1.57
No. of cities - Z o%
UD
5. MA.RCA • No cities .
6. SUPP-ERCOT 3.6 3.6 3.8 4.2 4.4 4.8 6.6 7.9 8.7 10.8 13.4 6.4 2.9 6.0 1.53
No. of cities « 1
7.. WSCC 1.0 1.9 2.6 3.9 4.7 4.9 5.6 6.0 6.7 7.7 10.4 6.9 3.5 4.3 1.88
No. of cities = 2
-------
Table 1.19 (continued)
Sulfate Cumulative Frequency Distribution by
Energy Region and Population Class, pg/m3
B. Population Class — 100,000 to 2,000,000
Frequency Distribution, % Arith. _ Geo.
Energy Power Region Min 10 20 30 40 50 60 70 80 90• . Max. x, sD x, - sD
1. NPCC-MAAC 2,7 7.5 8.9 10.3 11.5 13.3 14.8 14.9 18.8 23.2 45.3 14.7 6.4 13.0 1.6
.No. of cities = 14 •
2. ECAR 2.0 5.6 6.7 7.8 8.9 10.4 11.8 12.9 16.2 19.1 37.1 11.6 5.3 8.8 1.64
No. of cities =15
3. MAIN 2.0 3.9 4.6 5.5 6.3 7.3 8.4 9.2-11.2 15.6 45.9 8.9 6.0 7.5 1.7
No. of cities =6
4. SERC 0.2 4.3 5.5 6.5 7.3 8.2 9.3 10.3 12.0 14.3 55.2 9.4 4.9 8.0 1.7
'Ao. of cities = 24
5. MARCA 1.1 3.1 3.7 4.4 5.1 5.8 7.3 8.6 10.9 13.6 44.3 7.9 5.6 6.4 1.9
No. of cities =7
6. SHPP-ERCOT '0.0 2.4 3.0 3.7 4.3 5.2 5.9 7.1 8.4 9.5 44.0 6.1 3.8 4.9 1.8
No. of cities - 18
7. WSCC 0.0 1.8 2.6 3.3 3.8 4.3 4.8 5.5 6.3 7.7 37.7 '4.9 3.1 3.5 1.95
No. of cities =11 • •
-------
Table 1.10 (continued)
Sulfate Cumulative Frequency Distribution by
Energy Region and Population Class, yg/m3
C. Population Class 2,500 to 100,000
Frequency Distribution,^ _Arith. Geo..
Energy Power Region M1n. 10 20 30 40 50 60 70 80 90 Max. x, sD x, sO
1. NPCC-MAAC . 1.7 6.0 8.2 9.3 10.3 12.4 14.4 15.8 18.8 24.1 39.9 14.1 7.5 12.1 1.73
Mo. of sites =22
2. ECAR 2.9 5.1 6.1 7.1 3.2 9.6 11.5 12.6 15.0 19.2 X 12.0 9.6 10.0 1.71
No. of sites =8
3. MAIN 2.7 4.4 5.3 6.2 7.2 8.2 8.8 10.1 12.1 16.7 32.0 9.8 5.5 8.3 1.64
Ho. of sites = 6
4. SERC 1.1 4.7 5.8 7.1 7.6 8.7 9.7 11.1 12.8 16.5 34.9 10.3 6.5 8.8 1.64
Ho of sites = 7
5. MARCA 0.2 2.4 3.9 5.2 6.2 6.9 7.4 8.1 9.3 11.7 15.2 7.5 6.4 5.7 2.10
No of sites * 3 •
6. SUPP-ERCOT 2.7 4.9 5.5 6.2 7.8 9.0 9.5 10.6 12.5 16.2 32.5 9.8 5.3 8.8 1.64
No. of sites = 2
7. WSCC 0.0 1.9 2.4 2.9 3.1 3.5 3.9 4.4 5,0 6.9 26.0 4.0 2.5 3.5 1.68
No of sites = 6
-------
Table 1.20 '
Best Judgment Estimates of Adverse Health Effects Attributable to
Sulfur Oxides Exposures in the Eastern United States*
Adverse Health Effects
Population
at Risk
(Millions)
Premature Deaths from 137.4
Increased Daily Mortality
Days of Aggravated Heart 3.7
and Lung Disease (Millions)
Increased Number of 4.1
Asthmatic Attacks (Millions)
Lower Respiratory Disease
in Children (Thousands)
35.2
Chronic Respiratory **(83.5)
Diease Symptoms (Thousands)
Non-Smokers
Cagarette Smokers
51.8
31.7
Estimates of Illness Attributable to Acid Sulfate Aerosols
Standards Met Standards Not Met Excess Adverse Effects
1975 1977 1970 1975 1977 1980 1975 1977 1980
& 1980
308
5.3
2.5
48
(85)
1.2
0.8
1963 3225 4200 6057 2918 4193 6050
18.3 24.4 28.0 33.8 19.2 26.8 32.7
6.8 8.8 9.8 11.5 6.2 9.0 10.7
303 486 623
438 623
(0) (649) (1034) (1294) (1785) (949) (1294) (1785)
73 0 426 645 779 992 572 779 992
12 0 223 389 515 793 377 515 793
ro
*Effects following short-term fumigations are not included.
**This is a point prevalence count others are yearly incidence talleys.
-------
Table
Least Squares Estimates of Adverse Health Effects Attributable to
Sulfur Oxides Exposures in the Eastern United States*
Adverse Health Effects
Premature Deaths from
Increased Daily Mortality
Days of Aggravated Heart
and Lung Disease (Millions)
Increased Number of
Asthmatic Attacks (Millions)
Lower Respiratory Disease
in Children (Thousands)
Chronic Respiratory
Disease Symptoms (Thousands)
Non-Smokers
Cigarette 'Smokers
Population
at Risk
(Millions)
137.4
3.7
4.1
35.2
**(83.5)
51.8
31.7
-Estimates of Illness Attributable
Standards Met Standards Not Met
1975 1977 & 80 1970 1975 1977
3002 432 12997 18338 21600
26.7
3.7
67
(106)
97
9
.17.8 44.7
2.2 6.8
3 376
• (4) (787)
4 565
. 0 222
51.9
8.1
565
(1241)
844
397
55.6
8.8
664
(1522)
. 996
526
to Acid Sulfate Aerosols
Excess Adverse Effects
1980 1975 1977 1980
27234 1533.6 21168 26802
61.5
9.8
838
(2066) ;(
1252
814
25.2 37.8
4.4 6.6
498 661
:i!45) . (1518)
747 992
398 526
43.7
7.6
835
(2062
1248
814
*Effects following short-term fumigations are not included.
**This is a point prevalence count others are yearly incidence talleys.
-------
Table 1.22
PREDICTED CHANGES IN 24-HOUR EXPOSURES TO ROLLUTANTS
EMITTED BY LIGHT DUTY MOTOR VEHICLES
(Dispersion Model Estimates)
(For Persons Living Near and Traversing Major Arterial Throughways and Working in Urban Centers'-- See Attachment 1)
Pollutant
Carbon Monoxide*
Lead Particulate
Polynuclear Aromatic*
Hydrocarbons
Phenols-
Particulate Sulfates**
•and Sulfuric Acid
j- Aluminum and Its
"-Compounds
Platinum and Its
Compounds
Particulate Nitrogen**
Oxidants**
Oxides of Hi trogcn**
Direction of
Predicted Change
Decreased
Decreased
Decreased
Decreased
Increased
Increased
New
Pollutant
Little or No
Change
Decreased
No Change
Predicted Changes from Existing Urban Levels
After Two Model Years
Are Catalyst Equipped
Moderate (20%) Decrease
Significant (25%) Decrease.
Moderate (23%) Decrease
Significant (27%) Decrease
Moderate (10 to 25%) Increase
Small (2 to 6%) Increase
Minute (up to .05 nanograms/M^)
Levels Not Measureable
After Four Model Years Are
Catalyst Equipped
Significant (40%) Decrease
Significant (70%) Decrease
Significant (45%) Decrease
Significant (49%) Decrease
Significant (25 to 50%) Increase
Modest (4 to 12%) Increase •
Minute (up to .10 nanograms/M^)
Levels Not Measureable
After Ten Model Years
Are Catalyst Equipped
Significant (84%) Decrease
Si.jrn'ficant (up to 95*) Decrease
Significant (82%). Decrease
Significant (89?i) Decrease
Significant (75 to 200%) Increase
Modest (10 to 30%) Increase
Exposures First Become
Measureable
Less Than One Per Cent of Present Urban Nitrate Levels
Moderate (30%) Decrease in Hydro-'
carbon Emissions Leads to Modest
Decrease in Oxidants***
Significant (48%) Decrease in
Hydrocarbon Emissions Leads to
Moderate Decrease in Oxidants
•Significant (86%) Decrease in
Hydrocarbon Emissions Leads to
Further Decrease in Oxidants
Oxidation Catalyst Should Have Little or No tffect on Oxides of Nitrogen
*Applies to persons who do not smoke tobacco and are not occupationally exposed to these pollutants.
**In these cases one is dealing with changes in exposures involving large areas.
***This refers to mobile sources only. In 1970 mobile sources contributed about 45% of anthropogenic hydrocarbon emissions, but the
proportion varied greatly from dty to city.
-------
TABLE 1.23
SUSPENDED WATER SOLUBLE URBAN SULFATE LEVELS
BY ENERGY REGION AND POPULATION CLASS:
IMPACT OF CATALYST SULFATE EMISSIONS
ON 24-HOUR MEDIAN CONCENTRATIONS*'
**
Urban Population Class: >2 Million^
Electric Power Region?
Northeast and Mid Atlantic
(NPCC. - MAAC)
East Central (ECAR)
Mid-America (MAIN)
Southeastern (SERC)
Mid-Continental (MARCA)
Southwest Including Texas
(SWPP - ERCOT)
Western (WSCC)
Median Sulfate Levels
(Mgm/M3)(Base)
Incremental Percentage
Increase in Sulfate Levels
Attributable to Use of
Oxidation Catalysts After:
2 years 4 years 10 years
75
92
76
93
270
265
Northeast and Mid Atlantic
(NPCC - MAAC)
East Central (ECAR)
.Mid-America (MAIN)
Southeastern (SERC)
Mid-Continental (MARCA)
Southwest Including Texas
(SWPP - ERCOT)
Western (WSCC)
tic
as
Urban
tic
as
17.2
14.1
17.0
14.0
'4.8
4.9
Population Class :
13.3
10.4
7.3
8.2
5.8
5.2
15
18
15
19
54
53
100,000 to 2 Mi
12
15
22
19
28
31
30
36
31
37
108
106
Ilion3
24
31
44
39
' 55
61
4.3
37
.74
60
77
no
97
138
154
186
* Assumes no coversion of power plants to coal.
t
** Assumes median urban sulfate concentrations (24-hour) will not change from 1970 base
levels.
1 Assumes high estimate catalyst sulfate exposure model (carboxyhemoglobin surrogate)
for urban centers.
2 See figure 1.2 for geographic boundaries of these regions
3 Assumes low estimate catalyst sulfate exposure model (carboxyhemoglobin surrogate) for
suburban areas.
-------
76
Table I. 2*
SUSPENDED '.vATER SOLUBLE S'JLFATE LEVELS FOR A MAJOR
METROPOLITAN EASIER,'! CITY: IMPACT-OF CATALYST
SULFATE EMISSION'S OF 24-HOUR MEDIAN AND
90th PERCENTILE CONCENTRATIONS*
Base Case
New York City - 1970
24-Hour Sulfate Concen-
trations (vgni/i-l3)
Median Day
90th Percent!le
Day
NEW YORK CITY
Dov.'ntcvm
Catalyst Increment
Percentace Increase in Sulfate Levels Due to
Catalyst Increment'After 2 and 4 Years
2 Years 4 Years
•'edian Day 90th Percen- Median Day 90th Percan-
• tile Day1 tile Day1
20.2
37.3
12.8
4.3 - 11.5
25.6
8.6 - 23
*Assuni2S base year (1970) sulfate levels do not change. Assumes no conversion
of pov/er plants to coal.
Percentage increases reflect tv.'o cases:
(A) frequency distribution of catalyst incremental sulfates is the same
'as that for the NYC ambient sulfates (high percentage)
(B) frequency distribution is the opposite (lov; percentage)
-------
77
TABLE 1.25
NUMBER OF DAYS DOWNTOWN NEW YORK CITY EXCEEDS SPECIFIED
AMBIENT 24-HOUR SULFATE LEVELS: IMPACT OF
CATALYST-EQUIPPED VEHICLES AFTER 2 and 4 YEARS*
Number of Days Sulfate Levels Exceed:**
New York City (1970) 10 ygm/M3(l) 25 ygm/M3(2)
Base Case . 332 110
After 2 years catalyst- 347 . 135
equipped vehicles
After 4 years catalyst- 352 . 186
equipped vehicles '
* Assumes base case (1970) sulfate levels do not change and no power plants
are converted to coal.
** Assumes catalyst incremental sulfate frequency distribution is the same as
NYC ambient sulfate fr.eqij£,ncy distribution.
(1) Judgment estimate of threshold for illness aggravation.
t
(2) Judgment estimate for "-"threshold for perceptible increase in daily mortality.
-------
/8
I. REFERENCES FOR ASSESSMENT OF AIR QUALITY STANDARDS
A. Total Suspended Particulates
1. Martin, A. E. and Bradley, W. "Mortality, Fog and Atmospheric
Pollution^-'-Ttonthl-y:Bull. Ministry Health 19/.56-59, (1969).
2. Lawther, P. J. "Compliance with the Clean Air Act: Medical
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and Can'ad£s.$s.BTv.ttve pollution of the Atmosphere in the Detroit
River Area." International Joint Commission (United States and
Canada). p.'HS,- (1969).
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Pollution and Morbidity in New York City." J. Amer. Med. Assoc.,
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Braverman, M.M. "Report on an Air Pollution Incident in New York
City, November 1953." Public Health Reports. 77:7-16, (1962).
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-------
79
9. Holland, W.W., Reid, D.D., Seltser, R., and Stone, R.W. "Respiratory
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(1973).
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80
B. Sulfur Oxides
1. Federal Register, Vol. 36_, No. 84, Part II, pp. 8186-G190, April
30, 1971.
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3. Joosting, P. E. "Air Pollution Permissibility Standards Approached
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Symptoms, and Antismoking Propaganda: An Experiment." Lancet, Vol. 1,
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5. Lunn, J. E., Knowelden, J., and Handyside, A.J. "Patterns of Respiratory
Illness in Sheffield Infant School Children." Brit. J. Prev. Soc.
Med., Vol. 2]_, pp. 7-16, (1967).
6. Wicken, A. J. and Buck, S. F. "Report on a Study of Environmental
Factors Associated with Lung Cancer and Bronchitis Mortality
in Areas of North East England." Tobacco Research Council, London,
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7. Carnow, B. W., Senior, R. M., Karsh, R., Wesler, S. andAvioli, L.V.,
"The Role of Air Pollution in Chronic Obstructive Pulmonary Disease."
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S02 Levels and Perturbations in Mortality. A Study in the New York-
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81
9. H. E. Goldberg, Cohen, A.A., Finklea, J.F., Fanner, J.H, Benson, F.B.
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Truppi, L. and VanBruggen, J. Family Surveys of Irritation Symptoms
During Acute Air Pollution episodes: 1970 Summer and 1971 Spring
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Chapman, R.S. and House, D.E. Health Consequences of Sulfur
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and Swanson, D.H. Frequency of Acute Lower Respiratory Disease in
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and Nelson, W.C. Prospective Surveys of Acute Respiratory Disease in
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82
15. 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
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DHEW, Submitted by Dr. David P. Rail, NIEHS, October 1973.
C. Nitrogen Oxides
1. C.M. Shy, et. al. The Chattanooga School Children Study: Effects of
Community Exposure to Nitrogen Dioxide. II. Incidence of Acute Respiratory
Illness. J. Air Pol. Control Assoc. 20(9):582-588, (1970).
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Community Exposure to Nitrogen Dioxide. I. Methods, Description of
Pollutant Expsoure, and Results of Ventilatory Function Testing. J. Air
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47(2):391-398.'(1971).
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5. P.K. Mueller and M. Hitchcock. Air Quality Criteria - Toxicological
Appraisal for Oxidants, Nitrogen Oxides and Hydrocarbons. J. Air Pol.
Control Assoc. l_9:670-676, (1969).
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Dioxide: II. Effects on Histopathology of Lung Tissue. Arch. Environ.
Health 18:186-192, (1969).
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83
7. H. V. Thomas, P. K. Mueller and G. Wright. Response of Rat Lunq
Mast Cells to Nitroaen Dioxide Inhalation. J.. Air Pol. Control.
Assoc. 19:670-076. (1969).
0. H.V. Thomas. P.K. Mueller and R.L. Lvman. Lipooeroxidation of Lunq
Lim'ds in Rats Exoosed to Nitroaen Dioxide. Science lu9:532-534. (1963V.
9. G. Freeman and G.B. Havdon. Emphysema after Low-Level Exposure to
N02. Arch. Environ. Health 3:125-123, (1964).
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Factors in Emphysema and a Model System with NO,,. Yale J. Biol. Med.
40:566-575. 1968.
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Changes in the Bronchial Alveolar System of Mice Following Low
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Fluid of Guinea Pigs Exposed to 0.4 ppm Nitrogen Dioxide. Disc-Gel
Electrophoresis for Amount and Types. Arch. Environ. Health 27:90-.93,
(1973).
14. G. D. von Nieding, H. Krekeler, R. Fuchs, H.M. Wagner and K. Koppenhagen.
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Diffusion, Perfusion and Ventilation in the Lungs. Int. Arch. Arbeitsmed.
31:61-72, (1973).
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Absorption of N02 in Low Concentrations in the Respiratory Tract and
Its Acute Effects on Lung Function and Circulation. Presented at the
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84
16. F.E. Speizer and B.G. Ferris, Jr. Expsoure to Automobile Exhaust.
I. Prevalence of Respiratory Symptoms and Disease. Arch. Environ.
Health 2^:313-313, June 1973.
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Pulmonary Function Measurements. Arch. Environ. Health 26_:319-324, June 1973.
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Automobile Exhaust. III. An Environmental Assessment. Arch.
Environ. Health 26_: 325-329, June 1973.
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relationships. Contract No. 63-01-0471, Submitted to the Environmental
Protection Agency, Washington, D.C., September 1973.
D. Carbon Monoxide
1. Aronow, Harris, Isbell, Rohaw and Imperato: Effect of Freeway Travel
on Angina Pectoris. Ann Intern Med. _77_:669-676, (1972).
2. Anderson, Andelman, Strauch, Fortuin and Knelson: Effect of Low-Level
Carbon Monoxide Exposure on Onset and Duration of Angina Pectoris.
A Study of Ten Patients with Ischemic Heart Disease. Ann Intern Med
713:46-50, (1973).
3. Chevalier, et al: Reaction of nonsmokers to Carbon Monoxide Inhalation:
Cardiopulmonary Responses at Rest and During Exercise. JAMA 198(10):
1961-1064, (1966).
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Disease and Carboxyhemoglobin Levels in Tobacco Smokers. Brit Med J 1_:
761-765, (1973).
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33-39, (1972).
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85
6. Astrup, et. al, Effect of Moderate CO Exposure on Fetal Development.
Lancet 2: 1220-1222, (1972).
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Arch Environ Health 21_: 154-164, (1970).
0. J. H. Schulte, Effects of Mild Carbon Monoxide Intoxication. .
Arch Environ Health £1:524-530, (1963).
9. Aronow and Isbell, Carbon Monoxide Effect on Exercise-Induced Angina
Pectoris. Ann Intern Med 79_: 392-395, (1973).
10. Anderson, Strauch, Knelson, and Fortuin, Effects of CO on Exercise
Electrocardiograms and Systolic Time Intervals. Circulation 44_:135, (1971)
11. McFarland, et al, The Effects of Carbon Monoxide and Altitude on
Visual Thresholds. Aviation Medicine, 15(6):3Gl-399, December 1944.
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with Small Doses of Carbon Monoxide. Am J Public Health, 57^:2002-2011,
(1967).
13. Ayres, et al, Systemic and Myocardial Hemodynamic Responses to
Relatively Small Concentrations of Carboxyhemoglobin. Arch Environ
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E. Photochemical Oxidants
1. D. Bates, Hydrocarbons and Oxidants: Clinical Studies paper presented
at Conference on Health Effects of Air Pollutants, National Academy of
Sciences, Washington, D. C. Oct. 4, 1973.
2. D.V. Bates, et. al. Short-term Effects of Ozone on the Lung. J. Appl.
Physiol 32(2), Feb. 1972.
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Aerospace Med. 33:969-973, Aug. 19£2.
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86
4. R. Brinkman, H.B. Lamberts and T.S. Veings. Radiomimetic Toxicity of
Ozonized Air. Lancet 1(7325):133-136, January 1954.
5. D. I. Coffin, Et al, Effect of Air Pollution on Alternation of
Susceptibility to Pulmonary Infection. Presented at the 3rd Annual
Conference on Atmospheric Contamination in Confined Spaces. Dayton (19G7).
6. D. I. Coffin, et al, Influence of Ozone on Pulmonary Cells, Arch
Env. Health 16:633-636, May 1963.
7. D. E. Gardner, Environmental Influences on Living Alveolar Macrpphages,
Thesis, University of Cincinnati, 1971.
8. J. A. Goldsmith and J. A. Nadel. Experimental Exposure of Human Subjects
to Ozone. JAPCA 19:329, (1969).
9. D. I. Hammer, et al. Los Angeles Pollution and Respiratory Symptoms.
Relationship During a Selected 23-day Period. Arch. Env. Health 10:
475-480, March 1965.
10. D. I. Hammer, et al, Photochemical Oxidants and Symptom Reporting
Among Student Nurses in Los Angeles. In-house Technical Reprot,
Human Studies Laboratory, U.S. Environmental Protection Agency, -•
Research Triangle Park, N.C. Feb. 1973.
11. V. Hasselblad, et al. Regression Using "Hockey Stick" Function.
In-house Technical Report, Division of Health Effects Research,
U.S. Environmental Protection Agency, Research Triangle Park, N. C.
12. M. Hazucha, F. Silverman, C. Parent, S. Fields and D. V. Bates.
Pulmonary Function in Man After Short-term Exposure to Ozone. Arch.
Env. Health 27:133-133, September 1973.
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87
13. M. Kleinfeld, C. Giel and I. R. Tabershaw. Health Hazards Associated
with Inert Gas-Shield Metal Arc Welding. Arch. Ind. Health 15:27-31, (1957)
14. D. Kerr, University of Maryland Medical Center, Personal Communication
to John Knelson, EPA, NERC, Research Triangle Park, N. C.
15. S. Miller and R. Ehrlich. Susceptibility to Respiratory Infections in
Animals Exposed to Ozone: Susceptibility to Klebsiella Pneumoniae.
J. Infec. Dis. 103(2):145-149, Sept.-Oct., 1958.
16. H. L. Motley, R. H. Smart and C. I. Leftwich. Effect of Polluted
Los Angeles Air (Smog) on Lung Volume Measurements. J. Amer. Med.
Assoc. 171_: 1469-1477, Nov. 1959.
17. J. W. Lagerwerff, Prolonged Ozone Inhalation and Its Effects on
Visual Parameters. Aerospace Medicine 34:479-436, June 1973.
18. M. R. Purvis, S. Miller and R. Ehrligh. Effect of Atmospheric
Pollutants on Susceptibility to Respiratory Infection: 1. Effect
of Ozone. J. Infec. Dis. 109(@);233-242, Nov.-Dec., 1961.
19. J. E. Remmers, and 0. J. Balchum. Effects of Los Angeles Urban Air
Pollution Upon Respiratory Function of Emphysematous Patients: The .
Effects of the Naiero Environment on Patients with .Chronic Respiratory
Disease. Presented at Air Pollution Control Assoc. Meeting,
Toronto, June 1965.
20. N. A. Richardson and W. C. Middleton. Evaluation of Filters for
Removing Irritants from Polluted Air. Heating, Piping, Air
Conditioning 30:147-154, Nov. 1953.
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21. N. A. Richardson and W. C. Middleton. Evaluation of Filters for
Removing Irritants from Polluted Air. Univ. of Calif., Dept. of
Engineering, Los Angeles, June 1957.
22. N. A. Renzetti and V. Gobran. Studies of Eye Irritation Due to
Los Angeles Smog 1954-1956. Air Pollution Foundation, San Marino,
California, Junly 1957.
23. C. E. Schoettlin and E. Landau. Air Pollution and Asthmatic Attacks
in the Los Angeles Area. Public Health Repts. 7(5:545-548, 1961.
24. W. S. Wayne, P. F. Wehrle and R. E. Carroll. Oxidant Air Pollution
and Athletic Performance. J. Amer. Med. Assoc. 199(12):901-904,
March 20, 1967.
25. W. A. Young, D. B. Shaw and D. V. Bates. Effects of Low Concentrations
of Ozone on Pulmonary Function in Man. J. Appl. Physiol. 19:765-708,
July 1964.
26. R. E. Zelac, et al, Inhaled Ozone as a Mutagen: I. Chromosome
Aberrations Induced in Chinese Hamster Lymphocytes. Environ. Research
4:262-232, 1971. •
27. R. E. Zelac, et al. Inhaled Ozone as a Mutagen. II. Effect on
the Frequency of Chromosome Aberrations Observed in Irradiated
Chinese Hamsters. Environ. Research 4:325-343, 1971.
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II. References Upon Which Dose-Response Estimates Used in Assessment
of Increasing Sulfur Oxides Were Based
A. Mortality
1. Lindebsrg, W. Air Pollution in Norway. III. Correlations Between
Air Pollutant Concentrations and Death Rates in Oslo. Published by
the Smoke Damage Council, Oslo, Norway. 1968.
2. Martin, A.E. and W. Bradley. . Mortality, Fog and Atmospheric
Pollution. Hon. Bull. Min. Health (London). J9_: 56-59, 1960.
3. Lawther, P. J. Compliance with the Clean Air Act: Medical Aspects.
J. Inst. Fuels (London). 36_: 341-344, 1963.
4. Glasser, M., and L. Greenburg. Air Pollution Mortality and Weather.
New York City 19GO-1S64. (Presented at the Epidemiology Section of
the Annual Meeting of the American Public Health Association,
Philadelphia, November 11, 1969.
5. Brasser, L. J., P. E. Joosting, and 0. von Zuilen. Sulfur Dioxide--
To What Level is it Acceptable? Research Institute for Public.
Health Engineering. Delft, Netherlands. Report G-300. July 1967.
(Originally published in Dutch, September 1966).
6. Watanabe, H. and F. Kaneko. Excess Death Study of Air Pollution
In: Preceedings of the Second International Clean Air Congress.
(Englund, H.M. and W. T. Beery (eds.) New York, Academic Press,
1971. p. 199-200. •
7. Nose, Yoshikatsu and Yoshimitsu Nose. Air Pollution and Respira-
tory Diseases. Part IV. Relationship Between Properties of Air
Pollution and Obstructive Pulmonary Diseases in Several Cities in
Yamaguchi Prefective. J. Jap. Soc. Air Pollut. 5_(1): 130, 1970.
Proceedings of the Japan Society of Air Pollution, llth. Annual
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Meeting, 1970). .
8. Buechley, R. W., Riggan, W.B., V. Hasselblad, and 0. B. Van Bruggen.
S02, Levels and Perturbations in Mortality. Arch. Environ. Hlth.,
27(3): 134, 1973.
B. Aggravation of Heart and Lung Disease in the Elderly
1. Carnow, B. W., R. M. Senior, R. Karsh, S. Wesler, and L. V. Avioli.
The Role of Air Pollution in Chronic.Obstructive Pulmonary Disease.
Amer. Med. Assoc. 21_4_(5): 894-899. November 2, 1970.
2. Goldberg, H.E., J.F. Finklea, J.H. Farmer, A.A. Cohen, F.B. Benson and
G.J. Love. Frequency and Severity of Cardiopulinonary Symptoms in Adult
Panels: 1970-1971 New York Studies. To be published in Health
Consequences of Air Pollution: A Report from the CHESS Program. 1970-
1971'. EPA #650/1-74-004. pp. 5-85. June 1974.
C. Aggravation of Asthma .
1. French, J.G. Internal Memorandum on 1971-1972 CHESS Studies of
Aggravation of Asthma.
2. Sugita, 0., M. Shishido, E. Mi no, S. Kenji, M. Kobayashi, C. Suzuki,
N. Sukegawa, K. Saruta, and M. Watanabe. The Correlation Between
Respiratory Disease Symptoms in Children and Air Pollution. Report No.
1 - A questionnaire Health Survey. Taiki Osen Kenkyu 5_(1):134, 1970.
3. Finklea, J. F., J. H. Farmer, G. J. Love, D. C. Calafiore and G. W.
Sovocool. Aggravation of Asthma by Air Pollutants: 1970-1971 New
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York Studies. To be Published in Health Consequences of Air Pollution
A Report from the CHESS Program, 1970 - 1971. EPA #650/1-74-004,
page 5-71, June 1974.
4. Finklea, J. F., D. C. Calafiore, C. J. Nelson, w. B. Riggan and
C. B. Hayes. Aggravation of Asthma by Air Pollutants: 1971
Salt Lake Basin Studies. To be published in Health, Consequences
of Air Pollution: A Report from the CHESS Program, 1970-1971.
EPA # 650/1-74-004, page 2-75, June 1974.
D. Excess Acute Lower Respiratory Disease in Children
. 1. Nelson, W. C., J. F. Finklea, D. E. House, D. C. Calafiore, M. B.
Hertz and D. H. Swans'on. Frequency of Acute Lower Respiratory
Disease in Children: Retrospective Survey of Salt Lake Basin
Communities: 1967-1970. To be published in Health Consequences
of Air Pollution: A Report from the CHESS Program, 1970-1971. .
EPA #650/1-74-004, page 2-55, June 1974.
2. Finklea,'J.' F., D. I. Hammer, D. E. House, C. R. Sharp, W. C. Nelson
and G. R. Lowrimore. Frequency of Acute Lower Respiratory Disease
in Children: Retrospective Survey of Five Rocky Mountain Communities.
To be published in Health Consequences of Air Pollution: A Report
from the CHESS Program, 1970-1971. EPA 1650/1-74-004, page 3-35,
June 1974.
3. Douglas, J.W.B. and R. E. Waller. Air Pollution and Respiratory
Infection in Children. Brit. J. Prev. Soc. Hed. 20:1-8, 1966.
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4. Lunn, J. E., J. Knowelden, and A. J. Handyside. Patterns of
Respiratory Illness in Sheffield Infant School Children. Brit. J.
Prev. Soc. Med. 21.: 7-16, 1967.
5. Love, G. J., A. A. Cohen, J. F. Finklea, J. G. French, G. R. Lowrimore,
W. C. Nelson and P. B. Ramsey. Prospective Surveys of Acute Respiratory
Disease in Volunteer Families: 1970-1971 New York Studies. To be
published in Health Consequences of Air Pollution: A Report from the
CHESS Program, 1970-1971. EPA 1650/1-74-004, page 5-49, June 1974.
6. Hammer, D. I. Frequency of Acute Lower Respiratory Disease in Two
Southeastern Communities, 1968-1971. EPA intramural report, March 1974.
E. Excess Chronic Respiratory Disease
1. Burn, J. L. and J. Pemberton. Air Pollution, Bronchitis, and Lung
Cancer in Salford. Int. J. Air Water Pollut. 7:15, 1963.
2. Goldberg, H...J. F. Finklea, C. J. Nelson, W. B. Stern, R. S. Chapman,
D. H. Swanson, and A. A. Cohen. Prevalence of Chronic Respiratory
Symptoms in Adults: 1970 Survey of New York Communities. To be
published in Health Consequences of Air Pollution: A Report from
the CHESS Program, 1970-1971. EPA #650/1-74-004, June 1974.
3. House, D. E.,J. F. .Finklea, C. M. Shy, D. C. Calafiroe, W.. B. Riggan,
J. W. Southwick and L. J. Olsen. Prevalence of Chronic Respiratory
Disease Symptoms in Adults: 1970 Survey of Salt Lake Basin
Communities. To be published in Health Consequences of Air Pollution:
A Report from the CHESS Program, 1970-1971. EPA £650/1-74-004, June 1974.
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4. Hayes, C. G., D. I. Hammer, C. M. Shy, V. Hasseiblad, C. R. Sharp,
J. P. Creason and K. E. McClain. Prevalance of Chronic Respiratory
Disease Symptoms in Adults: 1970 Survey of Rocky Mountain Communities.
To be published in Health Consequences of Air Pollution: A Report
from the Ch'ESS Program, 1970-1971. EPA =650/1-74-004, June 1974.
5. Yashizo, T. Air Pollution and Chronic Bronchitis. Osaka Univ. Med. J.
20;10-12, December 1968:
6. House, D. E. Preliminary Report on Prevalence of Chronic Respiratory
Disease Symptoms in Adults: 1971 Survey of Four New Jersey
Communities. EPA intramural report, May-1973.
7. Galke, W. and House, D. E. Prevalence of Chronic Respiratory
Disease Symptoms in Adults: 1971-1972 Survey of Two Southeastern
United States Communities. EPA intramural report, February'1974.
8. Galke, W. and House, D. E. Prevalence of Chronic Respiratory Disease
Symptoms in New York Adults -.1972. EPA intramural report, February 1974
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94
III. References for Assessment of Health Impact of Equipping Light Duty
Motor Vehicles with Oxidation Catalysts
1. Finklea, J. F.,'Moran, J. B., Knelson, J. H., Turner, D..BX and"
Niemeyer, L. E. Estimated Changes in Human Exposure to Suspended
Sulfate Attributable to Equipping Light Duty Motor Vehicles with
Oxidation Catalysts. .EPA intramural report, January. 1974".
2. Finklea, J. F. Comments on the Potential Health Hazards from
the Use of Catalytic Converters. Internal EPA memorandum of
November 21, 1973.
3. Moran, J. B., Colucci, A. and Finklea, J. F. Projected Changes
in Polynuclear Aromatic Hydrocarbon Exposures.from Exhaust and
Tire Wear Debris of Light Duty Motor Vehicles. EPA intramural
report, May 1974.
4. Bridbord, K., Moran, J. B., Knelson, J. H. and Finklea, J. F.
Projected Reductions in Lead Exposures and Blood Lead Levels
Attributable to the Use of Catalyst Equipped Vehicles and
Phase-Down Regulations for Lead in Gasoline. EPA intramural
report, May 1974.
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