ESTIMATES OF THE PUBLIC HEALTH BENEFITS
AND RISKS ATTRIBUTABLE TO EQUIPPING LIGHT
DUTY MOTOR VEHICLES WITH OXIDATION CATALYSTS
J.F. Finklea, W.C. Nelson, J.B. Moran,
G.G. Akland, R.I. Larsen, D.I. Hammer,
and J.H. Knelson
National Environmental Research Center
Office of Research and Development
Environmental Protection Agency
Research Triangle Park, North Carolina
February 1, 1975
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Introduction
National standards limiting emissions of carbon monoxide, hydrocarbons,
and oxides of nitrogen from light duty motor vehicles were established
primarily to protect public health. Since implementation of the first stand-
ards in the late 60's, the Federal Government has required further reductions
in permissible emission levels with final statutory standards being established
in the 1970 Clean Air Act Amendments and targeted for achievement in the nrid-70's
While the amendments, in effect, established the final emission levels of the
pollutants, they did not permit EPA to establish the techniques by which such
levels would be achieved. In meeting the standards for carbon monoxide and
hydrocarbons,domestic automobile manufacturers chose to employ the oxidation
catalys.t for most engine families. While there is current debate over the
statutory oxides of nitrogen standard, it is likely that reduction catalysts
will be utilized to achieve the required emissions reduction of that pollutant
should the statutory standard remain at the planned level.
The required reductions in the emissions of carbon monoxide, hydro-
carbons, and oxides of nitrogen were based upon the need to protect
public health from adverse effects attributable to carbon monoxide,
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nitrogen dioxide,and to oxidants.for which the key precursors are the
hydrocarbons. The application of oxidation catalysts will make it
possible to reduce substantially emission levels of carbon monoxide and
hydrocarbons. EPA has long been aware that the three regulated pollutants
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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 com-
pounds, and oxygenates. Emission control approaches employed to achieve
the various emissions standards through the 1974 model year generally only
altered the relative concentrations of species already present in the
exhaust. The use of oxidation catalysts, on the other hand, alters emis-
sion products far more dramatically. Certain non-regulated emission
products of public health concern are dramatically decreased, while others
are created or dramatically increased.
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 in-
formation 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 pre-
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ferences 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. The relationship between exposure and disease
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may be obscured because the latency period between exposure and effects
may be quite long. Furthermore, a single environmental agent may con-
tribute 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 mutually 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, transpor-
tation, power generation and other problems involving energy and our environ-
ment. Under optimum circumstances assembling the needed scientific informa-
tion will require several years. In the meantime scientists must provide at
least "rough assessments for decision makers who face tight, legally required
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action schedules and deal with shifting political and social realities.
This paper attempts to put into perspective the benefit/risk aspect
of equipping light duty motor vehicles with oxidation catalysts by examining
the public health impact of changing emissions and changing air quality on
the urban population of our nation. Major benefits should follow the
expected reduction in exposures to carbon monoxide and photochemical oxidants.
However, major risks are likely to accompany the increases in exposures
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to acid-sul fate-aerosols which can be attributed to the use of oxidation
catalysts. It is also well to recall that changes in exposures to a
number of other pollutants whose effects are not yet well quantified could
well have measurable public health impacts and that the temporal and
geographic patterns of change can become an important consideration for
decision makers.
METHODS AND ASSUMPTIONS
Comparison of public health benefits and risks requires a complex
assessment with five major steps; First, emissions factors for a changing
vehicle population are calculated. Second. the impact of emissions changes
on ambient air quality are projected. Third, probable changes in human
exposures to the pollutants of major interest are -estimated.- Fourth, dose-..
response functions for the adverse effects of greatest interest are constructed
using the best-judgment assessments of available healthtIntelligence. Fifth.
public health benefits and risks are then estimated.
Calculation of Changes in Emissions; Projected changes in carbon monoxide
and hydrocarbon emissions were made assuming that 1975 interim Federal Standards
_for the .forty-nine states will be followed by statutory standards'for 1976 and
\ .
subsequent model years. These calculations were based on the 1975 Federal Test
Procedures and they assume an age distribution for the automobile population
like that seen in 1973, a miles-driven distribution like that seen in 1973, and
emissions controls that function in individual vehicles .at the standard
specified for the model year/ ' Appropriate calculations were likewise made
for a number of unregulated pollutants emitted by vehicles not equipped with
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oxidation catalysts.- Sucfypollutants include polynuclear aromatic hydrocar-
bons, phenols, aldehydes, participate nitrogen, and lead. When considering
lead, it was assumed that the 1975 models and subsequent model years would
require lead-free fuel and that the EPA promulgated lead phase-down regulations
would apply. When considering unregulated pollutants emitted from catalyst-
equipped vehicles, the authors applied the previously-mentioned assumptions
regarding the age and miles-driven distributions for future vehicle populations.
Emissions factors for particulate sulfates and suIfuric acid, aluminum and
its compounds, platinum and its compounds, and particulate nitrogen were based
upon measurements made with prototype 1975 model year vehicles equipped with
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various types of oxidation catalysts. »*»"
Impact of Emissions Changes on Ambient Air Quality: Since past air
monitoring data for automotive emissions and for photochemical oxidants are
limited, it was necessary to choose air quality distributions for carbon
monoxide and for photochemical oxidants which provide an upper boundary for
calculation of benefits associated with the use of catalytic converters.
For carbon monoxide''(Table 1) the average carboxyhemoglobin level in non-smokers
was chosen as the most appropriate indicator of recent average exposures to
carbon .monoxide emitted primarily from mobile sources. When meteorological
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conditions are adverse, such exposures are likely to increase by a factor of
about four and carboxyhemoglobin levels will increase by a factor of about three.
It is thought that the carboxyhemoglobin distribution utilized reflects an
estimate of baseline exposures for calculation of benefits attributable to
carbon monoxide control. In the case of photochemical oxidants, the South
Coast Air Basin of California was considered one part of the problem and other
United States cities with populations over 100,000 were considered separately.
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The maximum hourly oxidant concentrations for each day during a pre-catalyst
year are assumed to average approximately 140 vg/m* (.07 ppm) in Los Angeles and
60 yg"/m3 (.03 ppm). elsewhere (see Table 1). In fact, oxidant estimates may
somewhat overstate the severity of the oxidant problem in our major cities
during 1973-1974. Unfortunately, air monitoring stations for oxidants
outside California were few in number until state implementation plans
recently required more extensive monitoring. Thus, it will be a year or
more before the more adequate oxidant data are available to establish..lower
boundary and best judgment estimates for public health benefits associated
with the use of oxidation catalysts.
For unregulated emissions, two different types of air quality assumptions
were applied. In the case of lead, phenols and polynuclear aromatics, one
assigned air quality levels to homes, arterial throughways, the workplace
and commercial establishments and time-weighted averages based on activity
256
levels were applied. ' ' In the case of particulate sulfates and sulfuric
acid, urban sulfate distributions for each region were estimated using water
soluble sulfate measurements from National Air Sampling Network Stations.
Baseline air quality levels for aluminum and its compounds, particulate
nitrogen and noble metals were also obtained from National Air Sampling
\
Network reports.
Exposure Assessments Were Made; For carbon monoxide it was assumed that
equipping the entire vehicle population with oxidation catalysts/would eliminate
exogenous carbon monoxide exposure for non-smokers. Their carboxyhemoglobin
values were so adjusted. This, of course, overstates the exposure reduction
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that is, in fact, achievable and it may seem to provide an upper boundary
for calculating benefits. However, this is not necessarily the case as the
dose-response function employed for carbon monoxide may actually under-
estimate the number of premature cardiac deaths resulting by several fold.
For photochemical oxidants the report also assumed that catalytic converters
would reduce urban levels so that only natural background levels, which are
not now relatable to adverse health effects, would be encountered. For both
photochemical oxidants and carbon monoxide, a simple proportionate rollback
model was applied when assessing the benefits of interim years before the
entire vehicle population is equipped with oxidation catalysts, thus, benefits
are somewhat underestimated for the first few years and overestimated in the
later years.
For particulate sulfate and sulfuric acid, incremental increases in ex-
posures associated with the use of oxidation catalysts were estimated using
the carboxyhemoglobin surrogate detailed in reference 2. The low COHb
surrogate estimate was employed, which is likely to provide a low particulate
sulfate and sulfuric acid exposure estimate for major urban centers and
Southern California (see Table 2). The COHb surrogate provides a means of
>»
estimating Durban population exposures to catalyst incremental particulate
sulfate and sulfuric acid which is independent of any assumed human activity
pattern and suggests incremental exposure estimates which are lower than
those projected using the physical exposure models also discussed in reference
2.
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An approximation of how regulated and unregulated mobile source
emissions are likely to change is shown in Table 2. It is clear that
substantial reductions in exposures to carbon monoxide, photochemical
oxidants, phenols, polynuclear aromatic hydrocarbons, and lead parti-
culate will occur. Exposures to oxides of nitrogen will not be measurably
altered by oxidation catalysts. On the other hand, increased exposures
to particulate sulfate and sulfuric acid, and possibly aluminum and its
compounds, and platinum and its compounds will follow the introduction
of vehicles equipped with oxidation catalysts.
Construction of Dose-Response Functions for Adverse Effects of
Greatest Interest: For carbon monoxide, a dose-response function link-
ing elevated levels of carboxyhemoglobin to excess death following mycardial
infarction was established utilizing data from laboratory animals and
9 10
from human volunteer studies of less severe cardiac.effects. ' While
adverse effects might occur with very low carboxyhemoglobin levels, it was
assumed for this report that no adverse effect could be demonstrated below
a carboxyhemoglobin level of two percent. A linear increase in adverse effei
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was assumed up to a carboxyhemoglobin level of 10 percent (See Table 3). Un-
fortunately, it is not now possible to assess some of the most important poten-
tial adverse effects of oxidant exposures like co-carcinogenesis, acceleration
of aging, and mutagenesis. However, one can estimate benefits associated with
the likely improvement of health in certain groups exposed to oxidants: less
aggravation of asthma and chronic heart and lung disorders, and a reduced
frequency of irritation symptoms in healthy persons.** It was assumed that
oxidant levels which produced respiratory tract irritation in healthy young
adults would likewise aggravate asthma or heart and lung disorders in susceptible
population segments (See Table 3). For particulate sulfate and sulfuric acid,
dose-response functions were constructed for increased daily mortality ,
aggravation of heart and lung disorders in the elderly, aggravation of asthma,
increased frequency of acute lower respiratory illness, and increased frequency
of chronic respiratory disease symptoms in adults (See Table 3).
Estimating Public Health Benefits and Risks; Three steps are required
to estimate how changes in air quality will influence public health. First,
the population at risk must be specified. Second, air quality distributions
must be linked with dose-response functions to calculate adverse health effects
attributable to any specific pollutant exposure. Third, adverse health effects
V,
attributable to baseline pollutant exposures must be compared with effects from
future projected air quality distributions. The choice of populations at risk
and the assignment of baseline risks are summarized in Table 4. Procedures
are detailed elsewhere for defining baseline risks and populations at risk
including asthmatics, elderly persons with cardio-respiratory disorders, healthy
adults, children, and those susceptible to a premature cardiac death. 7»'°>1'
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For each population segment, it was assumed that both the benefits and
risks associated with the use of catalytic converters would be limited
to urban regions of 100,000 or larger.
RESULTS
General: Our best efforts allow only a rough approximation of the benefits
and public health risks attributable to equipping light duty motor vehicles
with oxidation catalysts. Two major problems are persistently encountered:
First, best judgment estimates are framed in considerable uncertainty, and,
second, we simply lack the ability to quantify a number of probably signi-
ficant benefits. However, it is unlikely that major national decisions
affecting public health, energy and transportation can wait until our ability
to make benefit-risk analyses of motor vehicle emissions is significantly
improved.
It is very important to remember that it is much easier to calculate
the economic costs of emissions controls than to develop the health damage
functions and calculate health costs. With our present limited health
intelligence base and with the present methodological difficulties in assign-
ing health costs, there would be a tendency to underestimate the true health
costs. A cost-benefit approach will require rather precise dose response
functions for each adverse effect related 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
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investments for five to ten years. In our opinion, precipitous movement
to a cost-benefit philosophy in the 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.
.Mortality; One expects that reducing carbon monoxide exposures will^
reduce premature deaths from myocardial infarctions and that increasing
particulate sulfate-sulfuric acid will increase the risk of premature death
in elderly persons already afflicted with chronic heart and lung disorders.
A benefit-risk comparison of the projected effects on mortality shows that
oxidation catalysts should after ten model years prevent modest numbers of
premature deaths (Table 5 and Appendix A). It is difficult to generalize,
but one might hypothesize that deaths attributable to carbon monoxide exposure
are more likely to occur in somewhat younger persons.
There are a number of other important aspects of the comparison; First,
even our high estimates of benefits may prove too low by a factor of three or
more if carbon monoxide exposures are higher than now estimated or if such
exposures play a significant role in producing or accelerating atherosclerosis.
-v.
Our estimates of carbon monoxide exposure are only approximate because human
activity patterns have not been well described in the areas where large amounts
of carbon monoxide are emitted at or near ground level. The time spent in a
shopping center, in an urban street canyon, on a busy arterial throughway or
adjacent to these sources is likely to be a more important determinant of
exposure than general ambient levels away from such sources. Second, not all
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regions equally share risks and benefits. Initially, benefits can be
expected in large cities of both the eastern and western United States.
Later, one can maintain net benefits in large western cities but a net
public health risk for excess mortality will be created in the east.
Third, most of the benefits attributable to catalyst use will occur in
the first four to six model years when vehicles with more stringent
controls are replacing uncontrolled or poorly controlled vehicles. The
risk attributable to catalyst-equipped vehicles will rise almost linearly
over time. There is little doubt that most of the mortality reduction
attributable to use of oxidation catalysts during the first four model years
would have likewise resulted over a somewhat longer period from the continued
sales of new cars meeting the 1973-1974 national emissions standards for
light duty motor vehicles. Unlike catalyst-equipped vehicles, 1973-1974 model
year cars did not increase mortality risk because they did not emit appre-
ciable amounts of particulate sulfates and sulfuric acid.
Other Effects of Carbon Monoxide; There are a number of other as yet
poorly quantified benef1ts_j)f_c_arbon monoxide^ control^ including possible
improvements in mental performance among drivers and in the workplace. These
benefits would, of course, also be achievedrff~carbon monoxide exposures
^
were reduced by means other than the use of oxidation catalysts. In summary
it can be concluded that effective control of "carbon monoxide emissions is
necessary to protect public health even though all public health benefits
cannot now be precisely quantified.
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Aggravation of Asthma; Elevated ambient levels of photochemical oxidants
and participate sulfate-sulfuric acid can aggravate asthma. In other words,
known asthmatics are more likely to experience one or more asthma attacks
on more polluted days. However, it has proved very difficult to relate
pollutant levels to the severity of any single asthmatic attack or to the
number of attacks experienced by any individual patient on any given day.
The present benefit-risk analysis (Table 6 and Appendix B) indicates that
any reductions in asthma attributed to reductions in photochemical oxidants
will be overwhelmed in all geographic areas by an increased risk attributable
to emissions of particulate sulfate-sulfuric acid. Statistically, one expects
increased risks for asthma to begin rather promptly with measurable adverse
effects seen in most cities around the fourth model year. The dose-response
function utilized for asthma probably overestimates the public health risk
because one has assumed warmer temperatures than exist during much of the
winter. In summary.there is every indication that the use of oxidation
catalysts will be accompanied by a net aggravation of asthma throughout the
nation. '
Aggravation of Heart and Lung Disease; Elevated ambient levels of photo-
N.
chemical oxidants and particulate sulfate-sulfuric acid are thought to aggravate
symptoms experienced by elderly persons with chronic heart and lung disorders.
In other words, elderly persons are more likely to report that they feel their
own symptoms have worsened on more polluted days. At the present time we
cannot reliably quantify what such aggravation means in terms of medical care.
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We do, however, believe that these persons not only report a worsening of
symptoms but that also more of them prematurely die on such days. Our
present benefit-risk approximation (Table 7 and Appendix C) shows that a net
increase in aggravation of heart and lung disorders can be expected to
occur when the entire vehicle population is equipped with oxidation catalysts.
^Other observations may be equally important. First,' geographically.
one can expect most of the benefits in the far west and most of the increased
risks in the eastern United States. Second, net benefits in Southern California
can be expected for four to six model years whereas net benefits are not
projected elsewhere at any time. Third, additional dose-response data might
well substantially increase the benefits allocated to Southern California.
One can, of course, retain the benefits in Southern California and not experienc
the risks by desulfurizing gasoline.
Acute Lower Respiratory Disease in Children; Laboratory studies in animals
indicate that exposure to elevated levels of photochemical oxidants are
likely to increase the risk for excess acute respiratory disease in man.
Existing epidemiologic studies have not yet been able to disentangle oxidant
effects from the other major determinants of such illnesses. Nevertheless,
s.
it is the test judgment of the authors that measurable health benefits in the
form of reduced acute respiratory morbidity would follow the reduction of
peak oxidant exposures now experienced in Southern California. Against this
benefit one must weigh the risks that are projected to.occur nationally
as vehicles are equipped with oxidation catalysts (Table 8 and Appendix D).
Interestingly enough, the present analysis projects little or no catalyst
associated risk.among children living in Southern California but substantial
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risks for children in the eastern United States. In summary, the use of
catalysts In Southern California might well lead to a reduction in acute
respiratory morbidity and thus represent a substantial-net benefit not
quantified by the present analysis.
Chronic Respiratory Disease Symptoms; Chronic respiratory disease symp-
toms of interest include persistent cough, production of sputum, shortness of
breath and at times more severe symptoms accompanied by marked functional
impairment. A variety of underlying pathologic conditions affecting the
lower airways and alveoli are associated with these symptoms. In any case,
an increased frequency of persistant cough accompanied by sputum among
general population is considered to represent an adverse health effect. At
present there is net a substantial body of laboratory or epidemiologic
evidence indicating that either photochemical oxidants or carbon monoxide
constitutes a risk factor for chronic respiratory disease. However,
responsible scientists will not be surprised if future studies reveal a
contributing role for photochemical oxidants in these disease processes.
The present benefit-risk analysis (Table 9 and Appendix E) shows that
the use..of oxidation catalysts will result in a substantial increased risk
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for chronic respiratory disease. Again, one is struck by geographical and
temporal factors. Almost all of the projected risks occur in the eastern
United States while most of the hypothesized benefits are likely to occur
1n the most impacted areas of the west. Substantial risks will begin
occurring only after the expected exposures projected for two to four model
years are maintained for several additional years. In other words, public
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health risks are likely to increase rapidly after the fourth to sixth model
year. If one were to equip Southern California vehicles with oxidation
catalysts and desulfurize fuel supplies in that area, one could avoid
any public health risk and maximize any reductions in chronic respiratory
illness that might be achievable through the reduction of exposures to
photochemical oxidants.
Prevalence of Irritation Symptoms Among Otherwise Healthy Adults: " Physician;
but not the general public, may at times be inclined to overlook the importance
of rather subtle increases in eye irritation, transient cough, ill defined
chest discomfort and the common headache. Increases in the frequency of such
symptoms after laboratory or ambient exposures to elevated levels of
photochemical oxidants, especially peroxyacylnitrate (PAN), are well documented.
Increases in irritation symptoms, especially transient cough, can also be
hypothesized to follow exposures to elevated levels of particulate sulfate-
sulfuric acid but no dose-response function is available. Consequently, the
present benefit-risk analysis projects that irritation symptoms will be clearly
reduced especially i n Southern Californi a by the use of oxidation catalyst
(Table 10 and Appendix F). Somewhat unexpectedly, the greatest projected
lessening -of "excess symptom days" occurs for the common headache. This
projection is the least defensible of.the group as causative mechanisms for
aggravation of the complex symptom are not yet defined.
Qther Significant Public Health Problems Where Benefits are Poorly Defined:-
Photochemical oxidants represent a complex group of pollutants indexed by ozone a
including a number of the most biologically worrisome gaseous air pollutants
"currently encountered; There 1s reason to believe that photochemical oxidants
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cause not only respiratory effects but a variety of systemic changes that
constitute adverse health effects. Scientists are legitimately concerned
that photochemical oxidants may act as carcinogens or co-carcinogens, that
they can accelerate aging and that they may contribute to mutations. It
is also known that catalysts will further reduce general population exposures
to polynuclear aromatic and phenolic compounds and that this grouping contains
a number of suspected carcinogens and co-carcinogens. ' There is also reason
to believe that photochemical oxidants and carbon monoxide may aggravate other
clinical conditions that are less common than those previously discussed.
For example, either of these pollutants might exacerbate the symptoms of
certain hemolytic anemias or decrease the functional reserves of other pre-
sumably susceptible population segments, like newborn infants, children
with congenital heart disease, cystic fibrosis patients, and apparently well
but elderly persons. In any case, there is every reason to believe that the
present analysis does not consider substantial benefits associated with the
control of carbon monoxide and hydrocarbon emissions. Likewise, it is
probably that increased exposures to particulate sulfate and sulfuric acid
will also result in other health risks which are not well-defined in this
analysis. In balance though ^Uj's^ thejapini ori^ of the authors that the net
s.
effect of these poorly-defjjiedjnsks^ would be ir^ the^ direction _of favoring
stringent control of_automoti ye pollutants .
Health Problems Associated with Lead, Aluminum Compounds and Noble Metals
It is not within the. scope of the present report to discuss in detail the
health effects of airborne lead. Suffice it to say that the use of leaded
gas is not considered compatible with oxidation catalysts and that the use
of such devices will preclude the use of lead as a fuel additive in catalyst-
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fequipped vehicles, except under emergency conditions. If the lead content
of fuel is not reduced for public health reasons, there still is every
reason to believe that public health benefits relatable to decreased lead
exposures can occur as catalyst-equipped vehicles come tb-o^tiTl^ife^he -'r "'
. ',--. . . - . - ;>' ..*,.' . ^
vehicle population and thus lead to a reduction in the emissions of lead.
In urban areas it is likely that blood lead levels and lead burdens would
be significantly reduced among those not overly exposed to other sources
of environmental lead. There is a growing suspicion that one should consider
not only classical lead poisoning but also other chronic effects of lead
exposure. For example, there is legitimate concern about the behavioral
implications of elevated lead levels and a conjectured increase in the risk
for respiratory cancer associated with simultaneous exposure to lead and
polynuclear aromatic compounds. Health.scientists in the Environmental
Protection Agency strongly advocate reducing lead emissions from motor vehicles.
In the case of aluminum, aluminum compounds and noble metals, it is now
thought unlikely that equipping light duty motor vehicles with oxidation
/
catalysts will result in any direct inhalation hazard for the next few years.
However, our information is not complete enough to assure that these substances
will pose up hazard to public health or to the environment. More information
on fabrication, use, disposal, exposures and effects will be required. It is
known that both aluminum and noble metal compounds can, under some circumstances,
be rather potent pulmonary irritants. Very little is known about the effects
of chronic exposure to noble metals and their compounds. .Hopefully, oxidation
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catalysts will prove durable enough in the hands of the consumer so that
exposures to these substances will continue to be minimal.
Discussion
When considering the net effect of all of the benefit-risk assessments
individually discussed (Table 11), it does not appear that the use of oxida-
tion catalysts for ten or more model years represents a consistent major
net public health benefit. However, closer examination of geographic difference
and probable temporal trends is necessary before reaching any final conclusions.
Clearly, a large portion of the quantified benefits will accrue from the use
of oxidation catalysts in Southern California while most health risks will be
in the eastern United States. Likewise, the use of oxidation catalysts can be
continued somewhat longer without the full range of major adverse effects in Cali-
fornia than in other parts of the nation. Even so, somewhere between the fourth and
tenth model year the use of oxidation catalysts appears to become a public
health liability in every locale unless steps are taken to reduce emissions
of particulate sulfates and sulfuric acid. One assumption of the present
analysis is that only cities 100,000 or larger will be affected. This is
-v,
probably not the case. An alternate analysis for all' urban regions is
included among the appendices but the conclusions reached by either route
are the same. A persistent vexing aspect of the analysis is the realization
that a number of probable health benefits are not presently quantified.
Nevertheless, it is quite apparent that the continued use of oxidation catalysts
to control carbon monoxide and hydrocarbon emissions from light-duty motor
vehicles is at best an uncertain, mixed blessing.
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The reader should recall the major directions of bias in the assumptions
for this report and the reasons for these assumptions. When considering
carbon monoxide, study assumptions undoubtedly1 overestimated the degree
of control that is possible. In fact, all carbon monoxide exposure to persons
who do not smoke tobacco will not be eliminated by the use of catalyst con-
verters. This bias would tend to set an upper bound on benefits. It is thought
that the assumed ambient exposures for carbon monoxide and human activity
patterns are more or less reasonable approximations for the exposures and
activity patterns of populations living in larger urban areas. In the case
of photochemical oxidants, study assumptions are thought to overestimate
existing exposures outside of California and to bound exposures within the
Southern California. Furthermore, the analysis assumes control of mobile sources
of hydrocarbons can in fact, reduce oxidant exposures to natural background
levels which are well below the known thresholds for adverse health effects.
The net result is to assign an upper boundary for the quantifiable benefits
of catalyst use. The analysis did not specifically consider the benefits of
reducing photochemical oxidant exposures for less than or more than the peak
hour experienced in a given day. When considering particulate sulfate and
sulfuric aqid, best judgment exposure estimates for each city size in each
region were applied instead of applying upper boundary estimates of exposure.
Furthermore, adverse effects attributable to short-term exposures lasting
up to two or three hours could easily aggravate respiratory disorders and
these are not considered. Thus, the net direction of bias is probably to
underestimate the risks attributable to the use of oxidation catalysts. On
the other hand, one does not have to consider as large a set of unquantifiable
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major adverse health effects when considering exposures to participate sulfates
and snlfuric acid as was the case with photochemical oxidants.
The present analysis assumes that oxidation catalysts will be required
on all new vehicles after the 1975 model year to achieve statutory emissions
standards for hydrocarbons and carbon monoxide. A wide number of alternate
emissions scenarios can be similarly evaluated. However, it should be pointed
out that the present analysis is probably not sufficiently precise to quantify
the public health impact of minor changes in emissions factors. It should be
recalled that for the next five or six model years one anticipates replacing
"blde^vehicles having little or no emissions control with vehicles that have
much more .stringent controls. The real impact of modest changes in the
relative -effectiveness of alternate emissions standards will be seen in how
well the control devices utilized function in the hands of the consumer and in
other characteristics of the vehicle population such as number of cold starts.
vehicle miles driven, growth in vehicle population, transportation controls,
and impact of urban mass transit systems. :
Characteristics of the vehicle population will also significantly affect
several-dimensions of the particulate sulfate-sulfuric acid exposure problem.
The present analysis assumes no further growth in the vehicle population.
* t «
Projections are that the present static vehicle population will continue to
grow in the next few years, but the rate of future growth and the place of
growth is not now clear. Failure to include some growth factor probably leads
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also assumed fuel economy, vehicle model weight distributions, vehicle age
distribution, and constant miles-driven distribution based on the 1973
vehicle populations. The authors expect that lighter vehicles with better
fuel economy will be introduced during the period covered by this analysis.
There is, however, as yet no reason to assume that the miles-driven or
vehicle age distributions will significantly change. The net effect of
such changes might lessen somewhat the public health risks that are pro-
jected to occur as vehicles equipped with catalysts comprise an even greater
portion of the total population, although the use of the low carboxyhemoglobin
exposure estimator in this analysis may tend to mitigate such inaccuracies,
particularly in major urban centers. Another relevant consideration is that
of catalyst durability in the hands of the consumer. A realistic concern is
that the consumer may use leaded fuel should gasoline shortages recur or
operating problems be encountered with low-octane unleaded fuel. In this
case, the benefits and risks associated with oxidation catalysts will both
be reduced as the catalyst loses effectiveness.
Other important sets of considerations not addressed in the present
analysis are effects of controls on other air pollutants, welfare effects,
and regional differences in sulfur content of gasoline, vehicle density, and
\
vehicle model weight distributions. For example, reductions in hydrocarbons
might alter the rate for atmospheric transformation of sulfur dioxide into sul-
furic acid, '.control of oxidants should reduce plant damage, and increased
urban levels of sulfuric acid could be expected to damage materials. It is
not clear whether visibility would change. Because of high fuel sulfur, one
would expect higher emissions of particulate sulfate and sulfuric acid in
Southern California than was projected in this analysis.
-------
-23-
How might mobile source emissions of particulate sulfate and sulfuric
acid interact with changes in emissions of sulfur dioxide from stationary
sources? The present analysis assumes that 1970 levels of particulate
sulfate would remain unchanged as vehicles equipped with oxidation catalysts
became predominant in the vehicle population. A comparison of catalyst
associated exposures with 1970 baseline exposures shows that exposures
attributable to oxidation catalysts become a significant part of the total
exposure problem in all larger urban areas after two to four model years (Table
?). Actually, the .lower exposure estimator mentioned in Table ?. was used in
1 ' * ~~
the present analysis1. The sulfate problem would loom even larger if the higher
exposure estimator thought more appropriate for the largest cities, and certainly
Southern California, had been utilized for these cities. If o«?,e assures that state
implementation plans were able to reduce sulfur dioxide emissions and urban
particulate sulfate levels by 50 to 60%, then the use of catalytic converters
eould completely negate any benefits from such control. This would also mean
that the public health risks projected in this report would be greatly reduced
if not entirely eliminated. More worrisome is the possibility that planned
sulfur dioxide emissions limitations for stationary sources will be dramatically
relaxed arid unrestrained energy demands may accelerate growth in emissions of
sulfur oxides. In that case, it is likely that the public health risks
i"associated with catalytic converters would be substantially higher than these
projected by the present analysis. Of course, 1f ambient sulfate levels are
not greatly changed during the next few years, the estimates of risk projected
In this analysis are less likely to be in error.
-------
-24-
There are a number of regulatory options which can maximize the public
health benefits attributable to emissions controls and minimize any health
risks. One option is the desulfurization of gasoline,'an option which
might prove quite practical for an area like Southern California where the
benefits of stringent emission controls are quite large. Another option
is the application of a particulate emission standard which could effectively
regulate mobile source emissions of lead, other metals, sulfates, and
sulfuric.acid. Such a standard, applied to new vehicles, has many desirable
health aspects.
Major Caveats
Throughout this report, major caveats affecting benefit-risk assessments
have been clearly stated but it is well to repeat the more important ones:
First, it is difficult to define precisely how the characteristics of
vehicle population, and consequent emission factors and emissions will change.
However, this factor does not seem as important as other major uncertainties.
Second, better estimates of the links between emissions, air quality,
and human exposure are needed before benefit-risk models can precisely
evaluate different emissions control scenarios.
Third, major uncertainties exist in existing dose-response functions for
adverse health effects. Indeed, dose-response relationships simply are not
well documented for a number of effects of greatest concern.
Fourth, existing air monitoring data do not allow more than boundary
estimates of benefits associated with the use of oxidation catalysts.
-------
-25-
. Fifth, the Impact of national decisions on the control of sulfur
oxide emissions from stationary sources can drastically alter the
projections of this report.
Conclusions
The introduction and continued sales of light-duty motor vehicles
equipped with oxidation catalysts will probably result in a net public
health risk unless the sulfur content of gasoline is reduced or particu-
!.1at^m.issio.ns. are controlled by other means. Geographically, a larae
portion of the projected health benefits can be expected in Southern
California while the health risks will be concentrated but not limited to
the eastern United States. Temporally, benefits attributable to the first
few model years might be greater than benefits '.occurring as later models
are introducedPbecause catalyst-equipped cars initially replace largely
uncontrolled vehicles. In any case, it is likely that after four model years,
public health risks will exceed benefits in all areas of the country unless
other regulatory steps are taken. The use of oxidation catalysts clearly
represents a complex issue involving public health, established and proposed
\
regulatory^mandates, energy considerations, and the national economy.
-------
-26-
REFERENCES
1. Moran J. B. Lead in Gasoline: Impact of Removal on Current and
Future Automotive Emissions. APCA. Denver. June 1974.
2. Estimated Changes in Human Exposure to Suspended Sulfate Attributable
to Equipping Light-Duty Motor Vehicles with Oxidation Catalysts/
Effects of Particulate Sulfates on Human Health/Automotive Sulfate
Emissions. EPA. Jan. 11, 1974.
3. Finklea, J. F. et al. The Role of Environmental Health Assessment in
the Control of Air Pollution. EPA intramural report. Aug. 27, 1974.
4. EPA Memo Finklea, J. F. to H. Miller, November 21, 1973, entitled,
Comments on Draft of HEW Response on the Potential Health Hazards
from the Use of Catalytic Converters.
5. Moran, J. B. et al. Projected Changes in Pclynuclear Aromatic Hydro-
carbon Exposures from Exhaust and Tire Wear Debris of Light-Duty
Motor Vehicles. EPA intramural report. May 1974.
6. Bridbord, K. et al. 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 intra-
mural report. May 1974.
-,
7. Health-Effects of Increasing Sulfur Oxides Emissions. EPA intramural
report. NERC-RTP. Aug. 18, 1974.
8. Hammer, D. I. et al. Los Angeles Student Nurse Study. Archives of
Environ. Health. Vol. 28. May 1974.
9. Anderson, E. W. et al. Effect of Low-Level Carbon Monoxide Exposure
on Onset and Duration of Angina Pectoris. Annals of Int. Medicine.
Vol. 79, No. 1. July 1973.
-------
-27-
10. EPA Memo Knelson to Finklea, Dec. 26, 1974, entitled "Excess Cardiac
Deaths Related to CO Exposure: Extrapolation from Animal Dose-
Response Data."
11. EPA Memo Nelson to Finklea, December 26, 1974, entitled "Documenting
CO and Oxidant Populations at Risk."
-------
Table 1
BASELINE AIR QUALITY DISTRIBUTIONS
ASSUMED FOR BENEFIT-RISK CALCULATION
Pollutant
Carbon
Monoxide . :
Photochemical
Oxidant : :
.
Geographic Area
Major U.S.
Cities
Major Urban
Centers :
S. California
(Best judgment)
S. California
(Worst Case)
Data
Reference
Los Angeles
Survey by
Stewart
CAMP :
(Colorimetric)
CHESS :
( Chemi 1 umi nescence)
CARB ;
(Colorimetric)
Geometric Mean
1.8 percent*
Car boxy hemo-
globin
60 yg/m3**
140 pg/m3**
240 'Vg/m **
^1*a nHavd ftovia+'inn
of Geometric Mean
1.50
2.22
2.22
2.22
*Equivalent to an average 8-hour carbon monoxide exposure of 13 to 16 mgm/m , depending on
activity level. Peak 8-hour exposures during the year associated with this distribution
range from 48 to 62 mgm/iri3 depending on the activity level.
**Maximum Hourly Values
-------
TABLE ?.
PREDICTED CHANGES IN 24-HOUR KXPOSURES TO POLLUTANTS
EMITTED BY LIGHT DUTY MOTOR VEHICLES
(For Persons Living Near and Traversing Major ArterSal Throughways and Working 1n Urban Centers)
Pollutant
Carbon Monoxide*
Oxidants**
Phenols
Polynuclear Aromatic*
Hydrocarbons
Lead Participate
Particulate Nitrogen**
Participate Sul fates**
and Sulfurlc Acid
Aluminum and Its
Compounds
Platinum and Its
Compounds
Oxides of Nitrogen**
Direction of
Predicted Change
Decreased
Decreased
Decreased
Decreased
Decreased
Little or
No Change
Increased
Increased
New
Pollutant
No Change
Predicted Changes from Existing Urban Levels
After Two Model Years
Are Catalyst Equipped
Moderate (20%) Decrease
Moderate (30%) Decrease 1n
Hydrocarbon Emissions Leads
' to Modest (14%) Decrease in
Oxidants***
Significant (27%) Decrease
Moderate ( 23%) Decrease
Slgnlf leant C 25%) Decrease
Less Than One Per
. Moderate (10 to 25%) Increase
Small (2 to 6%) Increase
o
Minute (up to .05 nanograms/M )
Levels Not Measureable
After Four Model Years
Are Catalyst Equipped
Significant! (40%) Decrease
Significant (48%) Decrease 1n
Hydrocarbon Emissions Leads to
Moderate (22%) Decrease in
Oxidants
Significant (49%) Decrease
Significant (45%) Decrease
Significant (70%) Decrease
After Ten Model Years
Are Catalyst Equipped
Significant (84%) Decrease
Significant (86%) Decrease 1n
Hydrocarbon Emissions Leads to
Further(39%) Decrease in
Oxidants
Signif1cant(89S) Decrease
Significant (82%) Decrease
Significant (up to 95%)0ecrease
Cent of Present Urban Nitrate Levels
Significant (25 to 60%)
Increase
Modest (4 to 12%) Increase
Minute (up to .10 nanograms/M '
Levels Not Measurable
Significant (75 to 200%)
Increase
Modest (10 to 30%) Increase
Exposures First Become
Measurable
/
Oxidation Catalyst Should Have Little or No Effect on Oxides of Nitrogen
*Appl1es to persons who do not smoke tobacco and are not occupationally exposed to these pollutants.
**In these cases one 1s dealing with changes In exposures Involving large areas., <
***This refers to mobile sources only. In 1970 mobile sources contributed about 451 of anthropogenic hydrocarbon emissions, but the
proportion varied greatly from city to city.
-------
Table 3
DOSE RESPONSE FUNCTIONS LINKING POLLUTANT
EXPOSURES TO SELECTED ADVERSE HEALTH EFFECTS
(Best Judgment) . .
Pollutant
Carbon
Monoxide
Photochemical
Oxidants
\
i .
Adverse Health Effect*
i
Excess Cardiac
Deaths
Aggravation of Heart and
Lung Disease in Elderly
Patients
Agravation of Asthma
Eye Discomfort
Cough
Chest Discomfort
Headache
Threshold Concentration
of Pollutant and Expo-
sure Duration '*o)
Two percent carboxy-
hemoglobin
3
540 yg/m for one hour
or longer
540 yg/m for one hour
or longer
300 vg/m3 for one hour
or more
3
540 vg/m for one hour
or more
3
600 vg/m for one hour or
more 3
100 yg/m for one hour
or more
Characteristic of Dose Response Function
SI ope
0:05 3
- 0.00017
0.00017
0.00032
0.00017
0.00010
0.00003
- .
Intercept
(Y0)
-0.1
' 0.2
- 0.02
Q.09
1
0.125
, 0.03
0.105
Acceptable Upper
Limit of Pre-
diction**
Ten percent
carboxyhemoglobin
3
v/1400 yg/m
-M400 yg/m
r '"
^1400 yg/m3
M400 yg/m
M400 yg/m
-------
TABLE 3 (continued)
Pollutant
Adverse Health Effect*
Threshold Concentration
of Pollutant and Expo-
sure Duration
Characteristic of Dose Response Function
Slope
Intercept
Acceptable Upper
Limit of Pre-
diction**
Particulate
Sulfate-
Sulfuric Acid
Increase Daily Mortality
Aggravation of Heart and
Lung Disease in Elderly
Patients
Agravation of Asthma
Excess Acute Lower
Respiratory Disease in
Children
Excess Risk for Chronic
Bronchitis
Non-smokers
Cigarette Smokers
25 yg/m for 24 hours or
longer
9 yg/m for 24 hours or
longer
6-10 yg/m for 24 hours
or longer
3
13 yg/m for several
years
3
10 yg/m-for up to 10 years
15 yg/m for up to 10 years
0.00252
0.0141
0.0335
0.0769
-0.0631
-0.127
-0.201
-1.000
^60 yg/m"
yg/mw
yg/nT
0.1340
0.0738
-1.42
-1.14
^30 yg/m:;
<30 yg/m
*Plotted as percent excess over base rate for each study in every effects category for CO and sulfates.
For oxidants plotted as a "hockey stick" function of the general form
Y = YQ for XLXQ. Y = YQ + b (X-XQ) for/ X > XQ where XQ,b, and YQ
are the threshold concentration, slope, and intercept respectively as shown above.
**Extrapolations above these limits are less reliable.
-------
Table 4
BRIEF SUMMARY OF POPULATIOH-AT-RISK AND BASELINE
ESTIMATES FOR ADVERSE HEALTH EFFECTS COIISinrRfn IN
lllb ULNtFll-RlSK ANALYSIS OF CATALYTIC CONVERTERS
Adverse Health
Effect
Increased
Mortality
Aggravation of
Heart and Lung
Disease In Elderly
Patients
Aggravation of
Asthma
Excess Acute
Lower Respira-
tory Disease In
Children
Chronic Bron-
chitis Symptoms
'
Eye Discomfort
Cough
Chest Discomfort
Headache
Pollutant
Partlculate
Sulfate-Sulfurlc
Acid
Carbon Monoxide
Photochemical :
Oxldants
Partlculate
Sulfate-Sulfurlc'
Acid
Photochemical
0x1 dan ts
Partlculate
Sulfate-Sulfur1c;
Add
Partlculate : .
Sulfate-sulfuric
Acid
Partlculate \
Sulfate-Sulfurlc;
Acid ;
Photochemical :
Oxldants
Photochemical :
Oxldants '
Photochemical
Oxldants
Photochemical
Oxldants
Assumed Baseline
Frequency of the
Disorder
2137 Deaths per Day
Prevalence of One out
of 200 Persons per Year
One out of Five Persons
with the Disorder Com-
plains of Symptom
Aggravation on Any Given
Day
Same
One out of 50 Persons
Experiences an Attack
Each Day or Seven
Attacks Each Year for
Each Person
Same
Six out of 100 Children
Experience This Illness
Each Year
Prevalence of Two
Persons per 100 for
Non-smokers
Prevalence of Ten
Persons per 100 for
Cigarette Smokers
Prevalence of Five
Persons per 100 per
Day
Prevalence of Ten
Persons per 100 per
Day
Prevalence of Two
Persons per 100 per
Day
Prevalence of Ten
Persons per 100 per
Day .
Djflnltion of Populatlon-at-Rlsk
Total 1970 Census population residing
In urban areas of 100,000 or larger
One-sixth of persons suffering myocardlal
Infarctions or sudden coronory death
The prevalence of chronic heart, and lung
disease (.27) among those age 65 or older
living In urban areas of 100,000 or larger
Same
The prevalence of asthma 1n the general
population (.03) living In urban areas
of 100,000 or larger
Same
Children from birth through age 13
living 1n urban areas of 100,000 or
larger
Sixty-two percent of the population
age 21 or older living 1n urban areas
of 100,000 or larger
Thirty-eight percent of the population
age 21 or older living in urban areas
of 130,000 or larger
Otherwise healthy population living in
urbai areas of 100,000 or larger. This
excludes persons with asthma or heart
and lung disease
Same
Same
Same
Estimated Number
at Risk
83.4 X 106
7 X 104
8.3 X 106
Same
2.5 X 106
Same
22.0 X 106
31.2 X 106
19.2 X 106
72.6 X 106
Same
/
, Same
Same
Reference
1
10
7
7
7
7
7
7
7
8,11
8,11
8.11
8.11
For the benefit-risk analysis these populations were separately Identified t'or each electric reliability
region (7) before national estimate* Mere made.
-------
Table 5
BENEFIT-RISK COMPARISON OF OXIDATION CATALYSTS:
MORTALITY ESTIMATES*
Number of Model
Years Equipped**
2
4
10
Geographic
Area
Total
Total
'f
Eaiiffc
i '-i ~\£ i *JtL £ j.' '
W@a fc» ?£fl
Total V
Mortality Estimates***
Reduction (Benefit)
Associated with
Decreased Carbon
Monoxide Exposures
Low
b 462
-------
Table 6
BENEFIT-RISK COMPARISON OF OXIDATION CATALYSTS:
AGGRAVATION OF ASTHMA*
Number of Model
Years Equipped**
2
4
10
Geographic
Area
Total
Total
East
West
Total
"est****
(worst case
oxidants)
Estimates of Changes in Frequency in Asthma Attacks***
Reduction (Benefit)
Associated with
Decreased Photo-
chemical Oxidants
Low
less than
24
less than
24
1
5
6
23
High
less than
41
less than
41
. 5
12
17
36
Increment (Risk) Associated
with Sulfate-Sulfuric Acid
Exposures Attributable to
Use of Oxidation Catalysts
Low
904
1875
2944
977
3921
977
High*****
904
1875
2944
977
3921
977
.thousands)
Net Benefit or (Risk)
Attributable to Use
of Oxidatipn Catalysts
Low
more than :
(880) :
more than
(1851)
(2943)
(972)
(3915)
(954)
High
more than
(863)
more than
(1834)
(2939)
(965)
(3904)
(941)
*Assumes 1970 particulate sulfate-sulfuric acid exposures not altered by ..air pollution controls or growth.
**Vehicular assumptions detailed in reference (2)
***Best judgment estimates
****Assumes worst case oxidant exposures in Southern California
*****Because of the shape of the dose-response function, it does not matter . . ._/ ,
whether incremental sulfate-sulfuric acid exposures are in phase or reversed / i
-------
Table 7
BENEFIT-RISK COMPARISON OF OXIDATION CATALYSTS:
AGGRAVATION OF HEART AND LUNG DISORDERS*
Number of Model
Years Equipped**
2
4
10
Geographic
Area
Total :
Total
East
West
Total
West****
(Worst Case'
Days of Aggravation of Heart and Lung Disorders (thousands)***
Reduction (Benefit)
Associated with
Decreased Photo- :
chemical Oxidants :
Low
less than
672
less than
672
70
187
257
602
High
less than
1211
less than
1211
212
392 ""
604
999
Increment (Risk) Associated
with Sulfate-Sulfuric Acid :
Exposures Attributable to :
Use. of Oxidation Catalysts
Low
2322
5146
10,617
1,892
12,509
1,892
Hiqh :
2916
6112
10,749
2,408
13,157
2,408
Net Benefit or (Risk)
Attributable to Use
of Oxidation Catalysts
Low
more than :
(1650)
more than :
(4474) :
(10,547) :
(1,705)
(12,252)
(1,290)
High
more than
(1705)
more than
(4901 )
(10,537)
(2,016)
(12,553)
(1,409)
*Assumes 1970 particulate sulfate-surfuric acid exposures not altered by air pollution controls or growth
**Vehicular assumptions detailed in reference (2)
***Best judgment estimates
****Assumes worst case oxidant exposures in Southern California
-------
Table 8
BENEFIT-RISK COMPARISON OF OXIDATION CATALYSTS
EXCESS ACUTE LOWER RESPIRATOR" DISEASE IN CHILDREN*
Number of Model
Years Equipped**
2
4
10
Geographic
Area
Total
Total
East
West
Total
Estimates of Change in Frequency of Acute Lower Respiratory Disease (thousands)***
Reduction (Benefit)
Associated with
Decreased Photo-
chemical Oxidants
Low
Benefits
not
quanti
fied
High
Benefits
not
quanti-
fied
Increment (H/isk) Associated ; .
with Sulfate-Sulfuric Acid :
Exposures Attributable to
Use of Oxidation Catalysts :
Low
88
184
407
7
414
High****
88 :
184
407 :
7
414 '.
Net Benefit or (Risk)
Attributable to Use
of Oxidation Catalysts
Low
(88) :
(184) :
(407)
(7)
(414)
Hiqn****
(88)
084)
(407)
(7)
(414)
*Assumes 1970 particulate sulfate-sulfuric acid exposures not altered by air pollution controls or growth
**Vehicular assumptions detailed in reference (2)
***Best judgment estimates
****Becasue of the dose-response function shape, it does not matter whether
incremental sulfate exposures are in phase or reversed.
-------
Table 9
Benefit-Risk Comparison of Oxidation Catalysts:
Chronic Respiratory Disease Symptoms*
t
Number
of Model
Years
Equipped
2
4 -
10
Geographic
Area
Total
Total
East
West
Total
Change in Prevalence of Chronic Respiratory Disease
Symptoms (in thousands)***
Reduction (Benefit)
Associated with
Decreased Photochemical
Ox id ants
M^M^V^B«M»^^»»^^^B»^>'^^
Low
Benefit
Not
Quantified
-i ^^~~-^^mf^-^*~-^-^
High
Benefit
Not
Quantified
Increment (Risk)
Associated with
Sulfate-Sulfuric
Acid Exposures
Attributable to Use
of Oxidation
Catalysts
v^^^v^^^^^^^^^**^^^r
Low
205
424
883
51
934
v#__V«W«_ta.V b^^^B-««Pl
High****
205
424
883
51
934
Net Benefit
or (Risk)
Attributable
to Use of
Oxidation
Catalysts
Low
(205)
(424)
(883)
(51)
(934)
^^^^^^^^^^^v**^^
High****
(205)
(424)
(883)
(51)
(934)
* Assumes 1970 particulate sulfate-sulfuric acid exposures not altered by air
pollution controls or growth.
** Vehicular assumptions detailed in reference (2).
*** Best judgment estimates.
**** Because of dose-response function shape, it does not matter whether incremental
sulfate exposures are in-phase or reversed.
-------
Table 10
BENEFIT-RISK COMPARISON OF OXIDATION CATALYSTS:
IRRITATION SYMPTOMS
Irritation
Symptom
Eye
Discomfort
Transient *
Cough
Chest
Discomfort
Headache
Number of Model
Years Equipped**
.10
10
10
10
Geographic
Area
East
West
Total
West (worst
case)****
East
West
Total
West (worst
case)****
East
West
Total
West (worst
.case')****
East
West
Total
West (worst
case)****
Estimates of change in Irritation Symptom Frequency (thousands)***
Reduction (Benefit)
Associated with
Decreased Photo-
chemical Oxidants
Low
53
83
136
216
21
52
73
182
0
2
2
10
No
Estimate
High
79
107
186
471
58
107
165
304
4
5
9
18
1520
889
2409
1066
Increment (Risk) Associated
with Sulfate-Sulfuric Acid
Exposures Attributable to
Use of Oxidation Catalysts
Low
RRITATION SYMPTOM INCREASE
i i
o- . '
CO
LU
E
CO
to
cC
to
» 1
CO
> . .
_1
-------
Table 11
SUMMARY OF NET BENEFITS OR (RISKS)
ATTRIBUTABLE TO USE OF OXIDATION CATALYSTS
Adverse Health
Effect
Excess
Premature
Deaths
Aggravation
of Asthma
Aggravation of
Heart and Lung -
Disorders
Excess Acute
Lo^r Respira-
t^7 Disease in
Children
Chronic
Respiratory
Disease
Symptoms
Irritation
Symptoms in
Healthy
Individuals
Other than
Headache
Headache
Unit
Thousands
of.
Deaths
Thousands
of Days
with an
Attack
Thousands
of Days :
Symptoms
Worsened
Thousands
of
Illnesses
Thousands
of Individ-
uals Affected
Thousands
of Excess
Symptom
Days
\
Thousands
of Excess
Headaches
Geographic
Area
East
West
Total
East
West
Total
East
..West
Total
East
West
Total
East
West
Total
East
West
Total
East
West
Total
Net Benefit o
Attributable
All Light Out
with Oxidatio
Low
(0.135)
0.395
0 260
(2943)
(972)
(3915)
(10,547)
(1705)
(12,252)
(407)
(7)
(414)
(883)
(51)
(934)
74
137
211
Not
Estimated
r (Risk
to Equipping
y Motor Vehicles
n Catalysts
High
(0.761)
1.030
0 269
(2939)
(965)
(3904)
(10,537)
(2016)
(12,553)
(407)
(7)
(414)
(883)
(51)
(934)
141
219
360
1520
889
2409
Increased Risk of ;
Cancer, Mutations,
Accelerated Aging
and Other Adverse
Effects
Beneficial But Benefits Cannot
Yet Be Quantified
-------
TABLE \2
SUSPENDED WATER SOLUBLE 'JREAri SULFATE LEVELS
BY ENERGY REGION AfJD POPULATION CLASS:
IMPACT OF CATALYST SULFA7E EMISSIONS
ON 24-HOUR MEDIAN OWCEKTRATIONS*.**
Urban Peculation Class: >2 Million''
Electric Power Region?
Northeast and Mid Atlantic
(f.'PCC - KAAC)
East Central (ECAR)
Mid-Amarica (MAIN)
Southeastern (SERC)
Mid-Continental (MARCA)
Southwest Including Texas
(SKPP - ERCOT)
Western (WSCC)
Median Sulfate Levels
(ugm/M3)(Base)
17.2
14.1
17.0
14.0
4.8
4.9
Incremental Percentage
Increase in Sulfate Levels
Attributable to Use of
Oxidation Catalysts After:
2 years 4 years 10 years
15 30 75
18
15
19
36
31
37
92
76
93
54
53
108
106
270
265
Urban Population Class: 100,000 to 2 Million3
Northeast and Mid Atlantic
(NPCC - KAAC)
East Central (ECAR)
Mid-America (MAIN)
Southeastern (SERC)
Mid-Continental (MARCA) :
Southwest Including Texas
(SKPP - ERCOT) " x
'.-.'astern (WSCC)
13.3
10.4
7.3
8.2
5.8
5.2
4.3
12
24
60
15
22
19
28
31
31
44
39
55
61
77
no
97
138
154
37
74
186
* Assumes no coversion of power plants to coal.
'* Assumes median urban sulfate concentrations (24-hour) will not change from 1970 base
levels.
1 Assurr.es hijgh estimate, catalyst sulfate exposure model (carboxyhemoglobin surrogate)
for urban centers,,
2 See figure. A.I for geographic boundaries of these regions
J Assumes lew estimate catalyst sulfate exposure model (carboxyhemoglobin surrogate) for
suburban dre
-------
Appendix A
Mortality Estimates
-------
FIGURE A.I.'REGIONAL ELECTRIC RELIABILITY COUNCILS
iiiiwsccj
ERGOT
-------
Table A.I. Baseline Estimates of Premature
Mortality Attributable to Particulate
Sulfate-Sulfuric Acid Exposures Dis-
tributed by Electric Power Reliability
Regions
Electric Power
Reliability Region
Northeast Power Coordinating
Council (NPCC) and Mid
Atlantic Area Coordinating
Group (MAAC)
East Central Area Reliability
Coordination Agreement (ECAR)
Mid America Interpool
Network (MAIN)
Southeastern Electric
Reliability Council (SERC)
Kid Continent Area Reliability
Coordination Agreement (MARCA).
Southwest Power Pool (SWPP) :
and Electric Reliability
Council of Texas (ERCOT)
Western Systems Coordinating
Council (WSCC)
East**
N.
West** ^
Total
Baseline Mortality Attributed to
Particulate Sulfate-Sulfuric Acid in 1970*
Under Best Judgment
Estimate* :
1195
217 :
434
134 :
23
17 :
L;
2 .
1980
42
2022
Under Least
Square Estimates
7540
1801
2245
1527
174
341
76
13,113
591
13,704
*Best judgment functions are used in the formal benefit risk analysis
**East equals NPCC + MAAC + ECAR + MAIN + SERC
West equals SWPP + ERCOT + MARCA + WSCC
-------
Table A.2.Estimated Mortality Increase Attributable
to Carbon Monoxide Emitted from Motor
Vehicles by Electric Power Region and Urban
Population Exposure Category.
Electric
Power
Region
- -
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Premature Deaths Following Myocardial Infarction (MIJ*
Immediately After MI
Urban >
100,000
^^^^*^^*..^^^^m^^^ff^^^^^v~~^~~* I II 1
150
69
69
39
72
9
102
360
150
510
All
. Urban
^ ^^^^^^^^^^^^^^^^^^^^^
246
120
138
90
102
30
180
606
300
906
During Recuperative Period
Urban >
100,000
^^^^-^^^^i < ^.^^^^^^^^^^^^i^^^-
250
115
115
65
120
15
170
600
250
- 850
All
Urban
410
200
230
150
170
50
300
1010
500
1510
*These are lowar best judgment estimates. Upper best judsment estimates are at
least threefotd higher and the upper boundary estimates might be an order of
magnitude higher.
-------
Table A.3, Projected'Mortality Increase from Sulfate
Aerosols Emitted fro:n Motor Vehicles by Electric
Power Region, Motor Vehicle Model Years, and
Urban Population Exposure Category.*
Electric
Power
Region
NPCC-KAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MRCA
WSCC
East
West
Total
Urban > 100,000
2
117
19
14
0
46
0
1
196
1
197
Model Years
4
258
42
31
0
102
1
. 1
433
2
435
10
*663
104
79
1
249 .
2
2
1095
5
1100
All Urban (towns > 2,500)
Model Years
2
147
26
17
2
47
1
1
237
4
241
4
323
57
38
4
104
4
1
522
9
531
10
820
141
96
12
253
9
2
1310
23
1333
* Assures_incremental and base exposure distributions are reversed and
.best judgment dose-response function.
-------
Tcbla A.4^roj5cted_Mortality Increase from Sulfate
*Aorcsols knitted from Motor Vehicles by Electric
Power Region, Motor Vehicle .'-'ode! Years, and
Urban.Population Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
UP. or A
f'U~lf \wf~t
wscc
East
West
Total
Urban > 100,000
Z
376
81
67
3
147
4
6
671
13
684
Model Years
4
831
189
159
10
321
10
20
1500
40
1540
10
1963
493
431
50
754
30
90
3641
170
3311
All Urban (towns > 2,500)
2
513
126
97
22
155
15
6
891
43
934
Model. Years
4
1144
298
239
61
343
37
22 '
2024
120
2144
10
2754
. 797
. 695
. 213
833
108
114
5079
440
5519
*Assurnes incremental and base exposure distributions are in phase and
best judgment dose-response function.
-------
Tcble A.5. Dejected "ortality Increase from Sulfate
Airosols Emitted from Motor Vehicles by Electric
Pc-.ver Region, "otor Vehicle Model Years, and
Urban Population Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
2
952
224
194
10
.324
8
14
1,694
32
l',726
Model Years
4
2,200
546
475
24
762
18
32
3,983
74
4,057
10
4,920
1 ,599
1 ,451..
'l60
1,859
,79
189
9,829
428
10,257
All Urban (towns > 2,500)
Model Years
2
1,270
343
298
76
354
25
15.
2,265
116
2,381
4
2,963
834
733
188
836.
58
36
5,366
282
5,648
10
7,294
2,707
2,681
942
2,241
226
278
14,923
1,446
16,369
* Assumes incremental and base exposure distributions are reversed and
least Squares dose-response function.
\
-------
Table A.6'.:'roject£d .'ii/rtai ity Increase fro.Ti Sulfate
.' Aerosols Emitted from Motor Vehicles by Electric
Power Reg-ion, rotor Vehicle; "c-Jel Years, and
Urban Population Exposure Cetagory.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
2
1 ,202
383
354
60
-458
23
96
2,397
184
2,581
Model Years
4
2,450
816
766
167
947
65
261
4,979
493
5,472
10
5,039
1,793
1,728
523
1,998
167
856
10,558
1,546
12,104
All Urban (towns > 2,500)
Model Years
2
1,783
652
643
244
548
92
123
3,626
459
4,085
4
3,675
1,403
1 ,422
584
1,156
213
361
7,656
1,158
8,814
10
7,695
3,129
3,308
1,527
2,514
545
1,328
" 16,646
3,400
20,046
*Assu;Ties incremental and base exposure distributions are in phase and
least squares dose-resDonse-.fimr.tion.
-------
Appendix B
Excess Asthma Attack Estimates
-------
Table B.I. Baseline Estimates of Excess Asthmatic
Attributable to Participate Sulfate-
Sulfuric Acid Exposures Distributed by
Electric Power Reliability Region
Electric Power :
Reliability Region
Northeast Power Coordinating :
Council (NPCC) and Mid : :
Atlantic Area Coordinating ; :
Group (MAAC) : ;
East Central Area Reliability; :
Coordination Agreement (ECAR); :
Mid America Interpool
Network (MAIN) ! :
Southeastern Electric ;
Reliability Council (SERC) !;
Mid Continent Area Reliability:
Coordination Agreement (MARCA; :
Southwest Power Pool (SWPP) ; ;
and Electric Reliability ; ;
Council of Texas (ERCOT) ; :
Western Systems Coordinating :
East** " - x
West** :
\
Total '. ::::: V/Y/YVY.-V-.'YVVVVYV-.'V
Baseline Excess Asthmatic Attacks
(thousands) Attributed to Particulate
Sulfate-Sulfuric Acid in 1970
Under Best Judgment : :
Estimate . :
3421 : ;
ins i ;
1073 !
1209 ;
125 \-\
377 i
136 :
6821 :
638 ;
7459
Under Least Squares
Estimate
3073
1233
1028
.1469
188
587
432
6803
1207
8010
*Best judgment estimates used in formal risk-benefit analysis
**East equals NPCC + MAAC + ECAR + MAIN + SERC
West equals SWPP + ERCOT + MARCA + WSCC
-------
Table B.2. Estimated Excess Asthmatic Attacks
Attributable to Oxidants Emitted from
Motor Vehicles by Electric Power Region
and Urban Population Exposure Category.
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT J
MAIN ;
MARCA
WSCC-SC
East
West-SC
i
Total -SC
SC (.07)**
SC (.12)**
Excess Asthma Attacks (thousands)
.27 Threshold*
Urban >
100,000
.1 ;
o : ;
o ! ;
0 ; :
0 ': :
0 \ :
0 ; :
i ;
0 :
1
5
23
All
Urban
1
0
1
0
0
0
0
2
0
2
6
26
.20 Threshold*
Urban>>
100,000
2 ;
1
i ;
i ;
1 ;
0 :
1
5
2
7
10
36
All
Urban
3
2
2
1
1
0
2
8
3
11
12
41
*.27 is low benefit estimate and .20.is high -benefit estimates
** Best judgment - Southern California
*** Worst case - Southern California
-------
Tabla B.3^.?i"oj^ctc"i rit'-r.i Increase in Thousands
*from Sulfate Asrosois Emitted from Motor
Vehicles by Electric Power Region, Motor
Vehicle Model Years, and Urban Population
Exposure Category.
>, Electric
Power
Region
NPCC-MAAC
.
^II^F '
SWPP- ERGOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
2
311
136
137
62
139
16
103
723
181
'904
4
624
276
280
138
280
34
243
1,460
415
1,875
10
1,249
. 557
573
313
565
74
590
2,944
977
3,921
All Urban (towns > 2,500)
.
Model Years
2
499
245. .
278
156
187
51
165
1,209
372
1,581
4
1,003
498
568
331
378
110
406
2,447
847
3,294
10
2,015
1,009
1,164
710
767
243
1,023
4,955
1,976
6,931
-------
Table B.4. ?reject=;' ».3th;::a Increase in Thousands
frc;r, Sulf:t; /\-!-:;ols E;.,Ut3J fro;n "otor
Vehicles by Electric Pov/er Region, Motor
Vehicle Model Years, and Urban Population
Exposure Category.*
Electric
Power
Region .
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
2
192
87
91
58
88
'13
122
458
193
£51
Model Years
4
383
174
182
115
176
26
244
915
385
i
1,300
10
766
348
364
230
350
52
489
1,828
771
2,599
All Urban (towns > 2,500)
Model Years
2
311
158
185
121
121
44
218
775
383
1,158
4
621
317
371
242
241 .
88
436
1,550
766
2,316
10
1,243
634
741
483
480
176
8/4
3,098
1,533
4,631
*Assumes incremental and base exposure distributions are in phase and
least squares dose-response function. Due to the shape of the dose-
response function, there is no change in estimates when incremental
exposures are distributed in a reverse fashion,-that is opposite to
the baseline sulfate distribution.
-------
Appendix C
Estimates of Heart and Lung
Disease Symptom Aggravation
-------
Table C.I. Baseline Estimates of Aggravation of
Heart and Lung Disorders Attributable
to Particulate Sulfate - Sulfuric Acid
Exposures bistributed by Electric Power
Reliability Region (in thousands)
Electric Rover
Reliability
Region :
Northeast Power Coordinating :
Council (NPCC) and Mid
Atlantic Area Coordinating :
Group (MAAC) : :
East Central Area Reliability:
Coordination Agreement (ECAR):
Mid America Interpool : :
Network (MAIN) ; :
Southeastern Electric : :
Reliability Council (SERC) !:
Mid Continent Area Reliability
Coordination Agreement (MARCA)
Southwest Power Pool (SWPP) :
and Electric Reliability :
Council of Texas (ERCOT) :
Western Systems Coordinating :
Council (WSCC
East** ^
West**
Total
Baseline Symptom Aggravation Attributed
to Particulate Sulfate-sulfuric Acid in 1970
Under Best Judgment
Estimate
10,121
2,553
3,118 J
2,509 ^
321 :
695
179
18,301
1,195
19,496.
Under Least Squares
Estimate
16,064
5,259
5,187
6,263
848
2,290
1,107
32,773
4,245
37,018
*Best judgment estimates used in formal risk-benefit analysis
**East equals NPCC + MAAC + ECAR + MAIN + SERC
West equals SMPP + ERCOT + MARCA + WSCC
-------
Table C.3. Projected Increase for Aggravation of Heart and
Lung Disease in Thousands from Sulfate Aerosols
Emitted from Motor Vehicles by Electric Power
Region, Motor Vehicle Model Years, and Urban
Population Exposure Category.*
Electrfc
Power
Region
NPCC-r!AAC
ECAR
SERC
SWPP-ER30T
MAIN
MARCA
wscc
East
West
Total
Urban > 100,000
Model Years
,
2
1,215
420
414
124
512
'48
1S3
2,561
355
2,916
4
2,446
870
869
30S
1,042
107
470
5,227
835
6,112
10
4,930
1,820
1,857
815
2,142
253
1,340
10,749
2,408
13,157
All Urban (towns > 2,500)
Model Years
2
1,884
739
806
392
653
154
260
4,082
8C5
4,888
4
3,822
1,540
1,710
883
1,348
345
716
8,420
1,944
10,364
10
7,787
3,249
3,702
2,076
2,823
823
e.,t-i3
17,561
5,109
22,670
*Ass'j~£:5 incremental and base exposure distributions are in phase and
best judgment dose-resoonse function.
-------
Table c.4. Projected Increase in Aggravation of Heart
and Lung Disease in Thousands from Sulfate
Aerosols EniUici frcrn liotor V^-icles by
Electric Power Region, Motor Vehicle Model
Years, and Urban Population Exposure
Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
wscc
East
West
Total
Urban > 100,000
Model Years
2
1,159
326
299
34
444 ?
19
41
2,228
94
2,322
4
2,411
780
723
101
972
51
108
4,886
260
5,146
10
4,917
1,786
1 ,800
691
2,114
224
977
10,617
1 ,892
12,509
>
All Urban (towns > 2,500)
Model Years
2
1,666
534
526
189
520
59
50
3,246
298
3,544
4
3,653
1,338
1,383
553
1,198
151
136
7,572
840
8,412
10
7,720
3,171
3,577
1,905
2,765
702
1,555
17,233
4,162
21,395
* Assumes incremental and base exposure distributions are reversed and
best judgment dose-response function.
-------
Table C.5.Projected Increase for Aggravation of Heart and
Lung Disease in Thousands from Sulfate Aerosols
Emitted fron !!otor Vehicles by Electric Fewer
Region, Motor Vehicle Model Years, and Urban
Population Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
2
1,164
467
497
300
529
82
530
2,657
912
3,569
Model Years
4
2,329
934
996
616
1,060
166
1,127
5,319
1,909
7,228
10
4,657
1,868
1,996
1,259
2,121
337
2,382
10,642
3,978
14,620
All Urban (towns > 2,500)
Model Years
2
1,888
849
1,013
652
725
270
933
4,475
1,855
6,330
4
3,777
1,699
2,029
1,322
1 ,452
553
2,000
8,957
3,875
12,832
10
7,555
3,401
4,066
2,674
2,907
1,133
4,245
17,929
8,052
25,981
*Assumes incremental and base exposure distributions are in phase and
Least squares dose-response function, i
-------
Table C.6. Projected Increase in Aggravation of Heart
and Lung Disease in Thousands from Sulfate
Aerosols Emitted from Motor Vehicles by
Electric Power Region, Motor Vehicle Model
Years, and Urban Population Exposure
Category.*
Electric
Power
.Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
2
1,164
466
496
288
329
79
473
2,655
840
3,495
Model Years
4
2,328
933
995
611
1,060
165
1,109
5,316
1,885
7,201
10
4,657
1,868
1,996
1,259
2,121
337
2,382
10,642
3,978
14,620
All Urban (towns > 2,500)
Model Years
2
1,887
847
1,010
640
724
255
835
4,468
1,730
6,198
4
3,776
1,698
2,028
1,317
1 ,452
547
1,971
8,954
3,835
12,789
10
7,555
3,401
4,066
2,674
2,907
1,132
4,244
17,929
8,050
25,979
*Assumes incremental and base exposure distributions are reversed and
least squares dose-response function.
-------
Appendix D
Estimates of Excess Acute Lower Respiratory Disease
-------
Table D.I
Baseline Estimates of Acute Lower Respiratory Disease in Children
Attributable to Particulate Sulfate-Sulfuric Acid Exposures
Distributed by Electric Power Reliability Region
Electric Power
Reliability
Region
Northeast Power Coordinating
Council (NPCC) and Mid-
Atlantic Area Coordinating
Group (MAAC)
East Central Area Reliability
Coordination Agreement (ECAR)
Mid-America Interpool
Network (MAIN)
Southeastern Electric
Reliability Council (SERC)
Mid-Continent Area Reliability
Coordination Agreement (MARCA)
Southwest Power Pool (SWPP)
and Electric Reliability
Council of Texas (ERCOT)
Western Systems Coordinating
Council (WSCC)
\
East**
West**
Total
Baseline Cases of Acute Lower Respiratory
Disease Attributed to Parti cul ate Sulfate-
Sulfuric Acid in 1970
(in thousands)
Under Best Judgment
Estimate*
187
25
69
23
0
0
0
303-
0
303
Under Least Squares
Estimate
214
58
68
36
0
3
0
376
3
379
* Best Judgment Estimates used in formal risk-benefit analysis
** East equals NPCC+MAAC+ECAR+MAIN+SERC
West equals SWPP+ERCOT+MARCA+WSCC
-------
Table D.2
Projected Acute Lower Respiratory Disease Increase
in Thousa.-.cs from Sulfate Aerosols Emitted from
Motor Vehicles by Electric Power Region, Motor
Vehicle Xcdel Years, and Urban Population
Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCGT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
2
46
14
10
0
18
0
0
88
0
88
4
92
36
19
0
37
0
0
184
0
184 -
10
184
82
62
0
79
3
4
407 :
7 ;
414".
All Urban (towns > 2,500)
Model Years
2
75
21
10
0
18
0
0
124
0
124
4
149
61
26
0
37
0
0
273
0
273
10
299
144
117
33
95
7
4
655
44
699
*Assur.es incremental and base exposure distributions are in phase and
best judgment dose-response function.
-------
Table D.3
Projected Acute Lower Respiratory Disease Increase
In YnouSG.-iuJ r>:;.; Sulfate Aerosols Emitted from
Motor Vehicles by Electric Power Region, Motor
Vehicle Model Years, and Urban Population
Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
2
28
14
14
0
13
0
0
69
0
69
4
54
27
28
0
26
2
6
135
8
143
10
109
54
55
18
52
6
37
270
61
331
All Urban (towns > 2,500)
Model Years
2
45
25
28
10
18
0
0
116
10
126
4
88
49
56
19
36
6
6
229
31
260
10
177
98
111
57
72
20
47
458
124
582
*Assumes incremental and base exposure distributions are in phase and
least squares dose-response function.
-------
Appendix E
Estimates of Excess Chronic Respiratory Disease
-------
Table E.I
Baseline Estimates of Chronic Respiratory Disease (CRD) Symptoms
Attributable to Participate Sulfate-Sulfuric Acid Exposures
Distributed by Electric Power Reliability Region
Electric Power
Reliability
Regi on
Northeast Power Coordinating
Council (NPCC) and Mid-
Atlantic Area Coordinating
Group (MAAC)
East Central Area Reliability
Coordination Agreement (ECAR)
Mid-America Interpool
Network (MAIN)
Southeastern Electric
Reliability Council (SERC)
Mid-Continent Area Reliability
Coordination Agreement (MARCA)
Southwest Power Pool (SWPP)
and Electric Reliability
Council of Texas (ERCOT)
Western Systems Coordinating
Council (WSCC)
East**
West**
Total
. Baseline Estimates of CRD
Attributed to Parti cul ate
Sulfate-Sulfuric Acid in 1970
Under Best Judgment
Estimate*
Non-
Smoke rs
265
51
79
31
0
0
0
426
0
426
Cigarette
Smokers
149
7
56
11
0
0
0
223
0
223
Under Least Squares
Estimate
Non-
Smoke rs
339
79
98
49
0
2
0
565
2
. 567
Cigarette
Smokers
150
5
57
10
0
0
0
222
0
222
* Best Judgment Estimates used in formal risk-benefit analysis
** East equals NPCC+MAAC+ECAR+MAIN+SERC
West equals SWPP+ERCOT+MARCA+WSCC
-------
Table E.2
Projected Chronic Respiratory Disease
-'ja in Tiv:js-a::c5 for i.'cns.r.o-'.e-rs from
.
Sulfate Aerosols Emitted from Motor Vehicles
by Electric Power Region, 'Motor Vehicle
Model Years, and Urban Population Exposure
Category.*
*
Electric
Power
Region
'
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
2
41
17
11
0
15
0
0
84
0
84'
4
81
35
29
0
33
1
0
178
1
179
10
i
163
70
65
14
69
6
31
367
51
418
All Urban (towns > 2,500)
Model Years
2
66
31
27
6
18
0
0
142
6
148
4
132
64
64
19
43
1
0
303
20
323
10
264
128
139
59
93
19
31
624
109
733
*Assu?nss incremental and base exposure distributions are in phase and'
: best judgment dose-response function.
\
-------
Table E.3
.Projected Chronic Respiratory Disease
'Increase in Thousands for Honsmokers from
Sulfate Aerosols Emitted from Motor Vehicles
by Electric Pov/er Region, Motor Vehicle
Model Years, and Urban Population Exposure
Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
2
45
19
19
0
19
0
0
102
0
102
4
90
39
40
0
38
3
6
207
9
216
10
180
78
81
24
78
9
52
417
85
502
All Urban (towns > 2,500)
Model Years
2
73
35
40
. 14
26
0
0
174
14
188
4
146
71
83
28
53
8
6
353
42
395
10
292
142
166
80
108
28
63
708
171
879
*Assumes incremental and base exposure distributions are in phase and
least squares dose-response function.
-------
Table E.4
s*
Projected Chronic Rfrsoiratory Disease Increase
In Thou'^-.cs for Sr.okers frcn Sulfete Aerosols
Emitted frcr, .".o:or Vefiicles by Electric Power
Region, Motor Vehicle Model Years, and Urban
Population Exposure Category."
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
i
2
66
17
13
0
25
0
0
121
0
121
4
134
33
27
0
51
0
0
245
0
245
10
111
87
57
0
102
0
0
516
0
516
All Urban (towns > 2,500)
Model Years
2
73
17
13
0
25
0
0
128
0
128
4
184
33
27
0
51 .
0
0
295
0
295
10
407
132
83
10
107
:o
:o
729
10
739
*Assumes incremental and base exposure distributions are in phase and
best judgment dose-response function.
N.
-------
Table E.5
'Projected Chronic Respiratory Disease Increase
In Thousands for Smokers from Sulfate Aerosols
Emitted from Motor Vehicles by Electric Pov/er
Region, Motor Vehicle Model Years, and Urban
Population Exposure Category.*
Electric
Power
Region
NPCC-MAAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC
East
West
Total
Urban > 100,000
Model Years
,
2
69
18
14
0
27
0
0
128
0
128;
4
142
35
28
0
54
0
0
259
0
259
10
288
91
58
0
108
0
0
545 .
0
545
All Urban (towns > 2,500)
Model Years
2
70
18
14
0
27
0
0
129
0
129
4
189
35
28
0
54
0
0
306
0
306
10
426
136
81
8
112
0
0
755
8
763
*Assumes incremental and base exposure distributions are in phase and
l^ast squares dose-response function.
-------
Appendix F
Estimates of Irritation Symptom
Frequency
-------
Table F.I
Estimated Adverse Health Effects (000)
Attributable to Oxidants Emitted from
Motor Vehicles by Electric Power Region
and Urban Population Exposure Category.
Electric
Power
Region
:;PCC-;;AAC
ECAR
SERC
SWPP-ERCOT
MAIN
MARCA
WSCC-SC
East
West-SC
Total -SC .
SC (.07}***
SC (.12)****
Eye Discomfort
.15 Threshold*
Urban >
100,000
23
10
10
6
10
2
6
53
14
67
--. 69
- "202.
All
Urban
37
18
21
13
14
6
15
90
34
124
79
231
.13 Threshold**
Urban >
100,000
34
15
15
9
15
2
9
79
20
99
87
235
All
Urban
55
27
31
19
20
7
22
133
48 .
181
100
269
Cough
.27 Threshold*
Urban >
100,000
8
4
4
2
5
1
2
21
5
26
. 47
177
All
Urban
13
7
8
4
6
2
5
' . 34 .
11
45
.54
203
.20 Threshold
Urban >
100,000
25
11
11
7
11
2
6
58
. 15
73
92
289
All
Urbe
40
20
22
14
' 15
6
16
97
36
133
106
331
* low benefit estimate
** high benefit estimate
*** best judgment - Southern California
**** worst use - Southern California
------- |