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THE MAGNITUDE AND MATURE
PROBLEM
STATES
OF THE AIR TOXICS
IN THE UNITED
U.S. Environmental Protection Agency
Office cf Air and Radiation
Office of Policy, Planning and Evaluation
September 1984
Elaine Haemi segger
Alan Jones
Bern Steigerwald
Vivian Th oms on
This document is a preliminary draft. It has not been
formally released by the U.S. Environmental Protection Agency and
snould not at this stage be construed to represent pee~-reviewed
Ager.cy policy. It is currently undergoing external review for
tecnni cal meri t.
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September 14, 1984
MEMORANDUM
SUBJECT: Goals and Context of the Attached Draft Report
FROM: Elaine Haemisegger
Alan Jones
Bern Steigerwald
Vivian Thomson
TO: Readers of the Report
Attached is a draft of an EPA staff report entitled, "The Magnitude
and Nature of the Air Toxics Problem in the United States." The attached
copy has been reviewed internally, but is currently undergoing external
peer review, and thus represents work in progress.
We feel that you should fully understand the context and goals of the
study and that certain caveats be made explicit to ensure that the study
and its conclusions are interpreted correctly. The analysis was undertaken
to orient EPA to the problem of air toxics, to stimulate policy discussion,
and to guide further studies. Despite the fact that quantitative estimates
of risk are presented in this report, the study will not be used to support
specific regulatory initiatives. Rather, its goal was to obtain quickly
some estimate of the magnitude and nature of the air toxics problem nationally,
and as such should be regarded as a "scoping" study only. Consideration of
the limited scope of the study, as well as the caveats and assumptions that
are discussed in the text of the report, is an important responsibility of
those reading and using this report. Some of the important caveats to keep
in mind are:
- Every attempt was made to use the best available data. However,
existing data on air toxics potencies, emissions, and ambient
levels are extremely limited, in terms of adequacy and quality.
- Most of the potency estimates used in the study are plausible
upper-bound estimates: that is, the actual unit risks are not
likely to be higher than those used in the study, but could be
considerably lower. In many cases the potency estimates are
preliminary.
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- The weight of evidence of carcinogenicity for the compounds
listed varies greatly, from very limited to very substantial.
Further, the extent of evaluation and health review performed
varies considerably among compounds. However, for this
report, a conservative scenario (i.e., that all compounds
examined are human carcinogens) has been assumed.
- Risk estimates for many air pollutants could not be calculated
due to data limitations. This also held true for many source
types examined in the study.
- Many assumptions and extrapolations are necessary to transform
ambient or modeled levels of air pollutants into exposure
estimates. Whether such assumptions introduce a high or low bias
into the results is difficult to assess. However, it is clear
that the use of such assumptions injects a considerable degree of
uncertainty into the analyses.
In summary, because of data limitations, the risk estimates presented
in this report should be regarded as only rough approximations of total
incidence and individual risks. Estimates presented for individual
compounds are highly uncertain and should be used with extreme caution. As
more data become available, the risk estimates will undoubtedly change. As
such, the portrait of the air toxics problem depicted in this study should
be regarded as a snapshot, the form and substance of which will certainly
change as new data become available.
A final point concerns the actions EPA is currently taking on some of
the sources and pollutants discussed in this report. Some of those actions
are as follows:
- An Air Toxics Group has been established to: review the results of
the study, assess source controllability, disseminate the results
to a wide range of interest groups for discussion and input, and
develop strategy options.
- The Administrator has committed to reviewing 20 to 25 air pollutants
over the next two years for potential listing and regulation as
hazardous air pollutants.
- Standard-setting activities under Section 112 of the Clean Air Act
are underway for asbestos, arsenic, benzene, coke oven emissions,
and radionuclides.
- Grant and technical support to State and local agencies for air
toxics activities has been increased.
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- Task Forces on dioxin, wood smoke, and gasoline marketing have
been established.
- Research on air toxics monitoring, health effects (e.g., the
effects of various nickel and chromium species), and emissions
has been increased.
Thus, while this report stops short of recommending options for
dealing with the sources and pollutants discussed, it represents a first
step in the development of a comprehensive air toxics strategy.
Attachment
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ACKNOWLEDGMENTS
Many individuals and organizations within EPA participated in
this study. The report is based primarily on a series of detailed
analyses and reviews done specifically for the study, often in
cooperation with private companies under contract to EPA. These
are listed below. We thank the authors for their efforts and for
contributing so much to this analysis.
Joe Bufalini, Bruce Gay, Basil Dimitriades. "Production of
Hazardous Pollutants through Atmospheric Transformations."
June 1984.
Elaine Haemisegger. "Hazardous Air Pollutants: An Exposure and
Risk Assessment for 35 Counties." September 1984. (Contractor:
Versar; American Management Systems, Inc.)
Jim Hardin. "Issue Paper — National Air Toxics Problem:
Radionuclides," August 1984
Bill Hunt, Bob Faoro, Tom Curran, Jena Muntz. "Estimated
Cancer Incidence Rates for Selected Toxic Air Pollutants
Using Ambient Air Pollution Data". July 1984. (Contractor:
PEDCo).
Tom Lahre. "Characterization of Available Nationwide Air Toxics
Emissions Data." June 1984. (Contractor: Radian Corp.)
Nancy Pate. "Review of the Clement Associates Report on Evidence
for Cancer Associated with Air Pollution." June 1984.
Bob Schell. "Estimation of the Public Health Risks Associated
with Exposure to Ambient Concentration of 87 Substances."
July 1984. (Contractor: Radian Corp.)
Bob Schell. "Definition of the Air Toxics Problem at the State/Local
Level." June 1984. (Contractor: Radian Corp.)
Vivian Thomson. "Indoor Air Pollution: Ramifications for Assessing
the Magnitude and Nature of the Air Toxics Problem in the United
States." July 1984.
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ACKNOWLEDGMENTS (Continued)
Donn Viviani, Doreen Sterling, Robert Kayser. "Acceptable
Risk Levels and Federal Regulations: A Comparison of National
Emission Standards for Hazardous Air Pollutants (NESHAP) with
Other Federal Standards Based on Quantitative Risk Asessment
(QRA)." May 1984.
Others wi»thin EPA provided assistance during the study.
We especially wish to recognize the following:
Carol Cox
Alan Ehrlich
Greg Glahn
Sue Perli n
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TABLE OF CONTENTS
Page
Executive Summary i
I. Introduction 1
II. Risk Assessment Methods 6
A. Estimates of Potency or Unit Risk 6
1. Why Cancer? 6
2. Why Not Assess Other Health Effects? 6
3. Estimating Potency 8
B. Estimates of Exposure 10
1. Monitori ng Data 11
2. Emission Estimates and Dispersion 13
Modeli ng
III. Magnitude of the Ambient Air Toxics Problem 16
A. Introduction 16
B. Summaries of Individual Analyses 18
1. Survey of State and Local Agencies, 18
Canada, and Europe
2. Evaluation of Cancer Associated with 21
Air Pollution Using Epidemiological
Studi es
3. NESHAPS Study 27
4. 35 County Study 32
5. Ambient Air Quality Study 39
6. Other Pollutants, Sources and Pathways 46
C. Summary of the Magnitude of the Air Toxics 67
Problem
D. Perspective and Context: Other Cancer Risks 71
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TABLE OF CONTENTS
conti nued
Page
IV. Nature of the Air Toxics Problem 75
A. Pollutants 75
B. Sou rces 76
C. Geographic Variability 79
D. Indirect Control of Air Toxics 83
V. Adequacy of Data Bases 85
VI. Conclusions 90
Attachment A - Pollutants Examined, Upper-Bound
Risk Values, Preliminary Approximations of
Incidence and Maximum Lifetime Risk
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LIST OF TABLES
Number Page
1 NESHAPS Study: Preliminary Approximation 29
of Annual Incidence and Maximum Lifetime Risk
2 35 County Study: Preliminary Approximation 34
of Annual Incidence
3 Ambient Air Quality Study: Preliminary 42
Approximation of Annual Incidence
4 Ambient Air Quality Study: Preliminary 44
Approximation of Individual Lifetime Risks
5 Ambient Air Quality Study: Preliminary 45
Approximation of Additive Lifetime Risks
6 Estimates of Incidence and Individual Risk 49
Due to Radionuclides Emitted to Air
Preliminary Estimates of Incidence and 61
Individual Risks Associated with Air Releases
from One Treatment, Storage and Disposal
Faci1ity
Summary Table: Preliminary Approximation of 69
Annual Incidence Estimates per Million Popula-
tion from the NESHAPS Study, the Ambient Air
Quality Study and the 35 County Study
Perspective and Context: Statistics on Cancer 72
Risks
10 Sources of Selected Compounds Examined in 77
This Study
11 Percent of Incidence Associated With Point and 80
Area Sources Based on 35-County Study
12 Comparison of Measured Air Quality for Selected 81
Cities and Pollutants; ngm/m^
13 Comparison of Sources of Risk in Several Counties 82
Selected from 35-County Study
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Executive Summary DO NOT QUOTE OR CITE
This report summarizes the results of a project which was
designed to define the dimensions of the ambient air toxics
problem in the United States. The analyses that make up this
study examined four basic questions concerning the magnitude
and nature of the air toxics problem:
(1) What is the approximate magnitude of the air toxics
problem, as represented by numerical estimates of
cancer incidence associated with air pollution?
(2) What is the nature of the air toxics problem in terms
of major, pollutants and major sources, and what is
their relative importance?
(3) Does the air toxics problem vary geographically, and
if so, in what ways?
(4) Are current air toxics data bases adequate, and what
are the significant data gaps?
We limited the study to cancers that may be associated with
direct inhalation, since other health effects and pathways
could not be quantified. Cancer unit risk values were obtained
from EPA's Carcinogen Assessment Group (CA6) and Clement Associates.
Four major analyses formed the quantitative core of the study.
The Ambient Air Quality Study used air toxics ambient data for
five metals, 11 organic compounds, and benzo(a)pyrene (B(a)P) to
estimate excess cancer incidence and individual lifetime risks.
Ambient data were available for approximately 170 sites for the
metals and for about 50 sites for BaP, whereas fewer data were
available for volatile organic compounds.
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A second analysis reviewed epidemiological studies that evaluated
the association between air pollution and lung cancer using health
statistics. In this analysis, ambient and occupational B(a)P data
were used as an indicator for pollutants associated with incomplete
combustion (PIC). A dose-response coefficient relating lung cancer
and B(a)P concentrations was generated from these studies. Cancer
incidence associated with exposure to PIC was estimated by applying
this dose-response coefficient to current ambient B(a)P concentrations
and BaP emission estimates.
The other two core analyses (the "NESHAPS Study" and the "35
County Study") used exposure models to estimate incidence and maximum
individual risks. Exposure modeling combines emissions estimates,
meteorological dispersion models, population distribution data, and
i
cancer potency (unit risk values) to estimate excess annual cancer
incidence and maximum lifetime individual risks. The NESHAPS Study
provides national estimates for about 40 compounds. The 35-County
Study was limited to 22 compounds and 35 counties, but was designed
to allow city-to-city comparisons and more detailed assessment of
source contributions.
Other attempts were made to supplement the information derived
from the four quantitative studies. All 50 state air pollution
agencies and 33 local agencies were contacted to determine whether
they had any quantitative risk information on air toxics. Canada
and the Commission of European Communities were also contacted.
This poll revealed that virtually no other studies are available
that quantify excess cancer incidence from air toxics.
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Four additional reports were prepared to assist in interpreting
the results of the study. A comprehensive review summarized emission
data for over 90 compounds by source type, geographic distribution,
growth trends, and data quality. Other papers were prepared on
atmospheric transformation of air pollutants; indoor/outdoor relation-
ships for air toxics; and the risk estimates used by other program
offices within EPA in regulating toxics. Quantitative risk assessments
available from other EPA activities for asbestos, radionuclides,
and gasoline marketing were incorporated into the report. Also, a
short section is provided to allow the results of this study to be
put into perspective with the estimated 440,000 annual cancer
deaths from all causes in the U.S. and other available estimates of
risk associated with diet, smoking, and all environmental pollution.
Finally, the study examined several source categories with insufficient
data for quantitative risk estimates at this time, such as hazardous
and municipal waste disposal and Superfund sites, and summarized
all available information on air releases.
The goal of this study was to examine the magnitude and nature
of the air toxics problem using existing data and standard EPA
quantitative risk assessment techniques. Therefore, no attempt was
made to examine the various controversies surrounding risk assessment
techniques. Methods commonly used within EPA for risk assessment were
used for this study. For example, we relied on upper-bound potency
estimates generated by EPA's Carcinogen Assessment Group (CA6) and
by Clement Associates; exposure modeling techniques used incorporate
such traditional approaches as assuming 70 years of continuous exposure
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to a given pollutant concentration. The study's objective was not
to evaluate existing risk assessment tools, but rather to apply
those tools in as comprehensive a fashion as possible. However,
where appropriate, we have attempted to point out the possible
effects of considering non-traditional approaches (e.g., considering
the effect of indoor exposures).
We readily acknowledge that risk analysis for carcinogens
is uncertain, that all of the analyses were limited by data gaps,
and that wide-ranging assumptions were necessary. As more data
become available, these risk estimates will undoubtedly change.
As such, the portrait of the air toxics problem depicted in this
study should be regarded as a snapshot, the form and substance of
which will certainly change as new data become available.
In order to be most useful the studies have been presented
in a very quantitative fashion. Careful interpretation is needed
and we caution against misuse of the estimates contained in this
report. The analysis was undertaken in order to orient EPA to the
problem of air toxics, to stimulate policy discussion, and to
guide further study. It is not intended to lead directly to
decisions on whether a specific compound is a carcinogen or whether
source control is needed. It is likely that further studies will
show that some of the pollutants included in the current study are
not carcinogens; also that many other compounds, sources and effects
not now able to be evaluated for lack of information will be
determined to be a problem. Consideration of caveats, disclaimers,
and assumptions is an important responsibility of those using this
report.
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Given the scope, omissions, methods, and assumptions discussed
in this report, the Study Team believes that the following conclusions
can be drawn from this study:
(1) The four analyses that attempted to quantify
risks du.e to 15 to 45 toxic air pollutants resulted
in estimates of annual cancer incidence that ranged
from 6 to 9 cases per million people annually*
Those same analyses resulted in estimates of total
national cancer incidence due to 15 to 45 toxic air
pollutants that ranged from 1,600 to 2,000 per year.
(2) Maximum lifetime individual risks of 10-4 ^ 1n iQ
or greater in the vicinity of point sources were estimated
for 25 pollutants. Maximum lifetime individual risks
of 10~3 or greater were estimated for 12 pollutants.
(3) Additive lifetime individual risks in urban areas due
to simultaneous exposure to 10 to 15 pollutants ranged
from 10~3 to 10-4. These risks, which were calculated
from monitoring data, did not appear to be related to
specific point sources, but rather represented a portion
of the total risks associated with the complex mixtures
typical of urban ambient air.
(4) While there is considerable uncertainty associated with
the estimates for some substances, the study as a whole
indicated that the following pollutants may be important
contributors to aggregate incidence from air toxics:
metals, especially chromium, arsenic, and nickel; asbestos;
products of incomplete combustion; formaldehyde; benzene;
ethylene oxide; gasoline vapors; and chlorinated organic
compounds, especially chloroform, carbon tetrachl ori de,
perch! oroethyl ene, and t ri chl oroethyl ene.
(5) Both point and area sources appear to contribute signifi-
cantly to the air toxics problem. Large point sources
are associated with many high individual risks; area
sources appear to be responsible for the majority of
aggregate incidence.
(6) A wide variety of source types contributes to individual
risk and aggregate incidence from air toxics. These
include: mobile sources; combustion of wood, coal and
oil; solvent usage; metallurgical industries; chemical
production and manufacturing; gasoline marketing; and
waste oil disposal.
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(7) Some low-production organic chemicals appear to contribute
little to aggregate risk. For example, 21 organic
chemicals were estimated to account for a total of
less than 1.0 excess cancer cases per year nationwide.
However, some organic chemical plants involved with these
compounds appear to cause high individual risks for
those living nearby. For example, the maximum
lifetime individual risk for 4,4-methylene dianiline
was estimated at 1.5xlO~3.
(8) While the study indicated that non-traditional sources
such as Publicly Owned Treatment Works (POTW's) and
Treatment, Storage and Disposal Facilities (TSDF's)
may not be dominant contributors to nationwide air toxics
incidence, it appears that such sources may pose risks in
some locations. For example, a municipal sewage treatment
plant in a major metropolitan area was estimated to
account for 18 percent of the area's total aggregate
incidence, and individual lifetime risks for a single
compound at one TSDF were estimated as high as 10-5.
(9) Criteria pollutant control programs appear to have
done more to reduce air toxics risks than have programs
for specific toxic compounds. This seems reasonable
considering the sources of air toxics, the multi-pollutant
nature of the problem, and the relative intensity of
these programs.
(10) For those cities with sufficient data for analysis,
large city-to-city and neighborhood-to-neighborhood
variation in pollutant levels and sources was found.
However, our current data base is inadequate to accu-
rately characterize most local air toxics problems.
(11) Even after many regulations under Section 112 of the
Clean Air Act are in place, it appears that arsenic and
benzene may still be significant contributors to aggregate
risk. This seems to demonstrate that to be fully effective
the base for air toxics programs needs to be broadened to
include emissions from small area sources, such as combustion,
road vehicles, and solvent usage.
Factors which may have caused the risk estimates discussed
above to understate total air toxics risks are as follows:
(1) Risk estimates for many substances which have been found
in the ambient air could not be calculated, due to data
limitations. Urban ambient air is characterized by the
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presence of dozens, perhaps hundreds, of separate
substances. These include many organic compounds; fine
particulate matter, including metals and polycylic
aromatic hydrocarbons; and criteria pollutants.
(2) Indoor concentrations of certain pollutants (e.g., radon,
tobacco smoke, formaldehyde, and other volatile organic
compounds) are commonly several times higher than outdoor
concentrations. While risk assessment could not be
performed for all these pollutants, the estimated cancer
incidence associated with passive smoking (3,000 to 14,000
annually) and radon (1,000 to 20,000 annually) clearly
show that indoor sources are a major contributor to air
toxics risks.
(3) Risks due to compounds formed by reactions in the atmos-
phere could not be quantified in the exposure models, but
there are indications that those risks may be significant.
For example, formaldehyde is formed in the atmosphere by
the breakdown of other organic compounds, and some compounds
(e.g., toluene) may be converted into toxic substances
through photochemical reactions.
Factors which may have caused the risk estimates discussed
above to be overstated are as follows:
(1) EPA unit risk estimates generally are regarded as
plausible, upper-bound estimates. That is, the unit
risks are not likely to be higher, but could be consid-
erably lower.
(2) The degree to which outdoor-source related emissions of
many pollutants (e.g., trace metals) penetrate inside
is largely unknown. Should emissions from outdoor
sources not penetrate completely indoors, then we will
have over-stated risks, since we have assumed constant
exposures to levels equalling those of outdoor air.
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Progress has been slow in making regulatory decisions on
hazardous air pollutants under Section 112 of the Clean Air Act, and
many observers, including States, Congress, environmentalists, and
EPA management, have expressed concern about EPA's inaction. The
most recent and formal criticism of EPA's implementation of Section
112 came from the General Accounting Office (6AO) in response to a
request from Congressman John Dingell. On August 26, 1983, GAO
released a report entitled, "Delays in EPA's Regulation of Hazardous
Air Pollutants". The Administrator testified at hearings called by
Chairman Dingell on November 7, 1983, responding to the GAO report
and commenting on issues associated with Section 112.
During internal discussions before the hearings, it became clear
that EPA did not have a good understanding of the dimensions of the
national air toxics problem, either in terms of size or causes. A
cursory analysis suggested that a group of pollutants that were being
considered for regulation under 112 might account for no more than an
estimated few hundred cancer cases each year. This led to some
fundamental questions concerning the magnitude and nature of risks
caused by air toxics.
o Do air toxics present a significant health problem, or does
current concern stem from the fear caused by the specter
of environmentally caused cancers?
o If air toxics do pose a significant health problem, what sources
and pollutants are responsible?
o Is there an important part of the national air toxics problem
that cannot be effectively addressed using Section 112?
o Will a comprehensive program demand the active, coordinated
participation of State and local air pollution agencies?
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The Deputy Administrator decided that a broad scoping study
of the air toxics problem was needed before management could begin
to outline a comprehensive national program. An ad hoc study,
called the "Six Month Study" because of its original intended duration,
was started in November 1983. Many offices and individuals within
EPA contributed to this effort, but the study was primarily a
cooperative effort between the Office of Air and Radiation (OAR)
and the Office of Policy, Planning and Evaluation (OPPE). This
report summarizes the results of that study.
In order to prepare the most useful report possible, decisions
were made in the early days of the study to emphasize four general
issues that would be most useful to policymakers as they attempt
to define the scope and direction of a national air toxics program.
1. The magnitude of the air toxics problem
We have attempted to characterize the size of the problem by
presenting quantitative estimates of cancer risk. More precisely,
we have presented estimates of the annual incidence of cancer that
may be linked to air pollution, and estimates of lifetime individual
risks.
2. The nature of the air toxics problem
What pollutants and source categories contribute to the public
health threat from air toxics? What is their relative significance?
3. Geographic variabi1ity
EPA's strategy for regulating air toxics may be influenced by
the city-specific nature of the problem. Some sources of air toxics
may be relatively widespread and found in most areas of the nation.
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Other sources may vary a great deal from city to city and
controlling them may require considerable flexibility, both in
terms of the pollutants and sources controlled, as well as the most
effective regulatory approach. An urban area will probably have
different priorities than a national program, and may still have
significant problems after federal regulations are in place.
4. Adequacy of data bases
This study is the most comprehensive attempt to date to assemble
and analyze all available data on air toxics. Therefore, it is a
useful vehicle for evaluating existing data bases, and identifying
knowledge gaps. This summary should help programs set priorities and
plan for future data gathering efforts, while providing policymakers
with some insight into the relationship between the national problem
and current EPA information collection and management efforts.
The resources and time available required that the study be
limited, in most cases, to gathering, organizing, and evaluating
exi sti ng information. This, in turn, suggested that the results
would be less than definitive, would include major data gaps and
assumptions, and would require a great deal of judgment to interpret
properly. The final report supports these expectations. Risk
analysis for carcinogens is very uncertain, and assessing air toxics
is complicated by the poor quality of available data. For several
potentially significant issues, the lack of information prevents any
analysis, and even in those areas with relatively good information,
we had to make important assumptions.
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Consideration of caveats, disclaimers, and assumptions is an
important responsibility of those using this report. Some of the
major assumptions used in this risk analysis are presented in the
following section. Specific limitations associated with individual
analyses are presented in the summaries of each of those studies.
Because of the long list of uncertainties associated with
such a study, we chose a wide variety of analytical approaches
in attempting to assess the national air toxics problem. A brief
summary of each individual analysis follows.
1. Survey of State and Local Agencies, Canada and Europe
We surveyed 50 State agencies and 33 local agencies, Canada,
and several European nations to determine if they had completed
quantitative assessments of air toxics exposures within their
boundari es.
2. Epidemiological Evidence
We evaluated existing reports that reviewed epidemiological
evidence on lung cancer and its relationship to air pollution.
3. Ambient Air Quality Data
Ambient air quality data were gathered, and then matched to
population data to estimate cancer risks.
4. Emissions of Air Toxics
Available information on air emissions of toxic substances was
gathered, organized, and analyzed.
5. NESHAPS Study
Finally, two other studies used exposure models to estimate
total expected incidence, the relative importance of pollutants and
sources, and city-to-city variability. Both of these studies use
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emission estimates, meteorological dispersion models, population
distribution data, and cancer potency numbers to derive their risk
estimates. The first of these is a national study that concen-
trates on approximately 40 pollutants being considered for listing
under Section 112 and that are candidates for National Emission
Standards for Hazardous Air Pollutants (NESHAPS).
6. 35 County Study
The second study based on emission estimates and dispersion
modeling analyzes in more detail the risks caused by 22 pollutants
in 35 counties. This study also attempts to assess sources that
are not typically considered major sources of air pollution.
The results of these disparate analyses are discussed separately,
followed by a discussion of sources and pollutants not covered by
the six studies, and then brought together in a summary section on
the magnitude of the problem.
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II. RISK ASSESSMENT METHODS
A. Estimates of Potency or Unit Risk
1. Why cancer?
In our attempt to determine the magnitude of the air toxics
problem and the relative significance of pollutants and sources, we
relied solely on cancer risk estimates. There were several reasons
for this deci si on.
o Cancer is a significant cause of death in the U.S.: approximately
20% (440,000 per year) of all U.S. deaths are caused by cancer.
o A link has been established between urban areas and higher lung
cancer rates.
o Several identified air pollutants are known to be human carcino-
gens (e.g., benzene, arsenic, and vinyl chloride).
o The public is concerned about cancer, and about the link between
environmental pollution and cancer incidence.
o The only accepted basis for extrapolation to low levels of
exposure for estimating risk is with cancer.
o Ambient air concentrations are likely to be lower than the thre-
hold for most chronic and sub-chronic health effects, whereas
there is a considerable degree of scientific support for using
the non-threshold assumption in assessing carcinogens.
2. Why not assess other health effects?
Except for the criteria pollutants, ambient air concentrations
of most compounds usually appear to be too low to be linked easily
to health effects other than cancer, with the possible exception of
impacts on very sensitive individuals. Most acute health effects are
caused by concentrations in the several parts per million range,
while ambient concentrations of most compounds tend to be in the
parts per billion range.
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Mutagenicity and teratogenicity are receiving more emphasis,
however. For example, although ethylene dibromide and ethylene
oxide are of concern primarily because of carcinogenicity, these
compounds have be.e.n shown to be mutagenic in test systems, and
2,3,7,8-TCDD has been shown to be a developmental toxin in animals.
Although examples like these exist, the data for most compounds are
too limited to qualitatively determine whether the substances are
potentially mutagenic or teratogenic. For those few substances
with enough data to pass the qualitative weight of evidence test,
there is rarely enough information to develop any reliable dose-response
estimates. While it is generally accepted that there are thresholds
for some teratogenic effects in test animals, data are seldom
available that will allow the calculation of threshold levels.
The uncertainty is compounded when animal data are used to
predict human teratogenic effects. For teratogens, there tend to
be multiple end points and the timing of exposure often is crucial;
these may not be the same for animals and humans. In contrast,
however, there is underlying biological support for a non-threshold
mechanism for carcinogenesis in both animals and humans. Furthermore,
it is generally accepted that if a chemical is carcinogenic in test
animals, it is likely to be carcinogenic in humans. Since only
animal data are available for most compounds, quantitative risk
estimates can be established routinely only for cancer.
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3. Estimating Potency
Assessing the risk of cancer caused by exposure to toxic
substances in the environment is a complex, controversial, and
uncertain business. The risk per unit dose estimates for most of
the pollutants covered by this analysis were developed by the
Carcinogen Assessment Group (CAG) in EPA's Office of Health and
/
Environmental Assessment (OHEA) in the Office of Research and
Development. To calculate such estimates, OHEA makes several
significant assumptions, each of which adds a measure of
uncertainty to the numerical estimates. The major assumptions used
by CAG in assessing carcinogenic potency* are described as follows:
o Experimental data showing that a substance is carcinogenic
in animals are used as evidence that the substance may be
carcinogenic in humans as well.
o In the absence of human data, the results of such animal
bioassays are used to estimate the probability of carcinogenic
effects in humans, and such extrapolations assume humans to be
as sensitive as the most sensitive animal species tested.
o CAG uses a nonthreshold, multistage model that is linear
at low doses to extrapolate from high dose response data
(either occupational studies or animal bioassays) to the low
doses typically caused by exposure to ambient air. In other
words, carcinogenic substances are assumed to cause some risk
at any exposure level. These unit risk values represent
plausible upper bounds, that is, they are unlikely to be higher
but could be substantially lower.
Quantitative estimates of carcinogenic potency (the unit risk
value) are expressed as the excess chance of contracting cancer
from a 70 year lifetime exposure to a concentration of 1 ug/rn-^ of
a given substance. Generally the unit risk value represents
cancer cases, not deaths. However, since the epidemiological studies
that generated the potency number for PIC (products of imcomplete
combustion) are based on lung cancer mortality, the PIC estimates
used in this report imply lung cancer deaths.
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o CAG assumes that exposed individuals are represented by a
reference man having a standard weight, breathing rate, etc.
No reference is made to health, race, nutritional state,
etc.
Some have charged that some of the Agency's methods may lead
to overestimates of risk. However, there are other factors that
may tend to offset conservatism in the techniques. These include:
o People are exposed to complex mixtures of chemicals. Data
are not available to demonstrate or deny the existence of
either synergistic or antagonistic health effects at low
exposu res.
o Virtually all animal and human data are based on exposure to
adults. There may be enhanced risk associated with fetal,
child, and/or young adult exposures to some agents.
o There may be high susceptibility for some population groups
because of metabolic differences or inherent differences in
their response to effects of carcinogens.
The Administration recently took a position on some of the more
controversial assumptions above. On May 22, 1984, the White House
Office of Science and Technology Policy (OSTP) released their final
report, Review on the Mechanisms of Effect and Detection of Chemical
Carci nogens. The report's statement of principles concludes that
available information "does not allow one to define the existence
or location of a threshold" for carcinogenicity. Furthermore, the
principles state that "a model which incorporates low-dose linearity
is preferred when data and information are limited as is the usual
case and when much uncertainty exists regarding the mechanisms of
carcinogenic action."
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In summary, this study is based on methods for assessing cancer
potency now in use throughout EPA. No judgments were made regarding
the appropriateness of these methods, nor did we attempt to use
alternative techniques. We felt that a comprehensive analysis
of risk assessment techniques was beyond the scope of this study,
and that alternative methods would make risk comparison with other
programs more difficult.
B. Estimates of Exposure
Risk assessment for cancer usually requires three basic kinds of
information: an estimate of the potency of the compound or group
of compounds being considered (the unit risk value), information on
the sources and emissions of that substance, and the concentrations
that different numbers of people breathe. Whereas the preceding
discussion focused on the methods and uncertainties associated with
estimating potency, this section discusses the methods, assumptions
and uncertainties associated with estimates of exposure.
For most of the analyses summarized in this report, two measures
of risk were calculated. The first, lifetime individual risk, is a
measure of the probability of an individual developing cancer as a
result of exposure to an ambient concentration of an air pollutant
or group of air pollutants.2 Often, the maximum lifetime individual
risk is also presented, which usually applies to individuals living
nearest the source. In an attempt to gauge the significance of
additive risks, we also calculated multi-pollutant individual risks
2 A maximum individual lifetime risk estimate of 3.0x10-4, for
example, near a point source implies that if 10,000 people breathe a
given concentration for 70 years then at the upper bound three of
the 10,000 will develop cancer as the result of the exposure to
that pollutant from the source.
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caused by several pollutants measured in the same area. These
multi-pollutant risks were not associated with a specific point
sou rce.
Aggregate or population risk estimates, on the other hand, are
estimates of the annual incidence of excess cancers for the entire
affected population. These estimates are calculated by multiplying
the estimated concentrations of the pollutant by the unit risk value
and by the number of people exposed to different concentrations.
This calculation yields an estimate of the total number of excess
cancers that may occur over a 70 year period; the total must then
be divided by 70 (because of the assumed duration of exposure) to
estimate annual incidence.
1. Monitorlng Data
Two major techniques were used to estimate ambient concentra-
tions for this study, and each has its own set of uncertainties.
The first was to use ambient air quality measurements. Intuitively,
estimates based on ambient data appear more reliable. The estimates
are based on direct measurements of ambient concentrations instead
of a modeled estimate of the concentrations resulting from environ-
mental releases. Monitoring avoids the problems of incomplete
emission inventories, incomplete knowledge on current control
status, a lack of knowledge concerning pollutants formed or destroyed
in the atmosphere and the list of errors associated with dispersion
modeli ng.
However, there is significant potential for error in using
monitoring data to estimate aggregate risk. The most important is
the classic problem of extrapolating measurements at a single site
to a much larger geographic area in order to estimate population
exposure. To estimate concentrations in a city, we were forced to
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average measured values and assume that these values applied to the
entire area. The number of monitoring sites in a metropolitan area
ranges from one or two to a maximum of ten in Baltimore and
Philadelphia. Because of this limited coverage and because monitors
are often intentionally located away from major sources, using
monitoring data probably is especially unsuitable for estimating
maximum individual risk.
Second, estimating annual incidence forced us to extrapolate
the available data for a relatively small number of areas to the
rest of the nation. For trace metals and organic particulates, the
National Air Monitoring System and State and Local Air Monitoring
Systems (NAMS/SLAMS) contain data for counties representing a total
of 25 million to 75 million people. Data on volatile organics are
available for areas with a total population of only 2 million to 25
mi 11i on people.
Third, because cancer risk assessment assumes long term
exposures, the most useful data are long term average concentrations,
preferably annual averages. Very few studies have collected ambient
samples for toxics continuously for an entire year. For purposes
of this study, monitoring data for 20 days a year was labeled as
being sufficient for calculating an annual average. This was
available for most of the trace metals. For organics, annual
averages were calculated if monitoring data were available for 10
separate days spread over at least two quarters.
Finally, all air quality data are subject to errors in sampling
and analytical methods. These problems are greater for air toxics
than for criteria pollutants, but are generally considered less
significant than the other potential sources of error.
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2. Emission Estimates and Dispersion Modeling
Several of the analyses presented in this report relied on
emission estimates and dispersion modeling to estimate ambient
concentrations. A major advantage of this method over ambient data
is the ability to characterize the contribution of various sources.
Also, emission modeling provides continuous geographical coverage
and, therefore, is more comprehensive than monitoring at identifying
"hot spots" that are of concern because of high individual risk.
Finally, modeling generally allows a larger number of pollutants to
be considered, and it avoids the problem of geographic extrapol a.ti on.
Emission estimates and dispersion modeling were used in
three analyses that are summarized in this report: the 35 County
Study, the NESHAPS Study, and work completed by the Office of
Radiation Programs on radionuclides. Conceptually, the models
all operate the same way. Emission estimates for area and mobile
sources are apportioned uniformly over the entire area being
considered, while point sources are located at a specific site.
Emission estimates for point sources are developed using available
sources of information, which may vary widely in quality. The emission
estimates are loaded into the computer dispersion model along with
information on stack height and diameter, emission velocity and
temperature. Meteorological data (wind speed, direction, and
stability) from the nearest of over 300 National Climate Center
sites is entered into the model along with population distribution
information from 1980 census data. Running the models results in
estimates of ambient concentrations at different distances from
the source. The dispersion models were run for 50 km in the 35
County study, 20-50 km in the NESHAPS analysis depending on the
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pollutant, and 80 km for the radionuclides analysis. The appropriate
choice for the outer boundary when estimating pollutant dispersion is
a matter of considerable debate.
Some of the major issues surrounding the use of both monitoring
and dispersion modeling techniques in estimating exposure are as
•
f o 11 ow s:
o The dispersion models assume flat terrain and average
meteorological conditions. Rough terrain in the area
surrounding a source, such as a valley, would probably cause
higher concentrations near point sources and lower
concentrations further away from the source.
o Although exposure estimates apply to a certain point in time,
our risk assessments assume that the people that live in an
area are exposed to the estimated ambient concentrations for
70 years. In other words, we assume that the plant operates for
70 years, that no one moves in or out of an area, and that no
one moves around within the area. Few plants operate for 70
years, and most people change homes several times during their
life; however, an individual may still be exposed to emissions
of the same or different toxic compounds after moving from an
area.
o A related issue is the assumption that people are continually
exposed to outdoor ambient concentrations. In fact, most
Americans spend 80 to 90% of their time indoors. Thus, a
significant part of total exposure to air toxics occurs indoors.
Unfortunately, we were unable to quantify the risks due to
indoor exposures to the substances examined in this study.
However, there are strong indications that indoor levels of
many volatile organic compounds are higher than outdoor levels,
since there are many indoor sources of organic compounds.
No indoor/outdoor comparisons were found for the metals examined
in this study, but the limited data available for other trace
metals show that indoor air levels are sometimes higher and
sometimes lower than outdoor levels.
o Dispersion modeling is often extended to only 20 km from the
source, a technique which can lead to understatement of risk
if extending dispersion increases significantly the number of
people exposed. To see what difference a 50 km boundary would
make, five organic substances were modeled to that distance, and
the change increased annual cancer incidence by a factor of
1.35.
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Dispersion estimates are rarely based on site-specific
meteorology. Often, data from hundreds of kilometers away
must be used.
In running the dispersion models, we do not consider increases
in concentrations that could result from reentrainment of
toxic particles from streets, rooftops, etc. With the exception
of radionuclides, we also do not consider background concentra-
tions and emissions from other sources not explicitly included
in the analyses, including toxics formed in the atmosphere.
Emission estimates are generated using data and assumptions
that could be in error. For example, although the 35 County
Study incorporates plant-specific emission estimates whenever
possible, the pollutant releases for the remaining sources
were developed by applying speciating factors against the VOC
and TSP data in the National Emission Data System (NEDS).
Unfortunately, some of the information in NEDS is of
questionable consistency and quality for the purposes of
quantitative risk assessment.
For other analyses, estimates are based on plant capacity and
emission factors. These studies assume that plants continuously
operate at an assumed percentage of capacity and that no changes
in emission rates occur. Malfunctions are not considered.
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III. MAGNITUDE OF THE AMBIENT AIR TOXICS PROBLEM
A. Introducti on
One of the major goals of this study was to improve our under-
standing of the size of the overall public health problem caused by
air toxics, a task that has been colorfully characterized in the
trade press as determining whether the air toxics problem is "an
elephant or a mouse." Although the study is the most comprehensive
effort to date to define the aggregate risk from air toxics, the
results are not totally satisfying. First, the pollutant coverage
is spotty. Constrained by available data on emissions and risk,
the various analyses were able to include only 15-45 of the hundreds
of potential carcinogens in the atmosphere. Second, from the
standpoint of exposure and risk estimation, only the inhalation
pathway and cancer are assessed. Ingestion of air pollutants, and
skin cancer that could be caused by the effect of air pollution on
the stratospheric ozone layer were not considered. Third, the
range of error for individual estimates is«great, requiring judgment
in order to interpret properly. Finally, no quantitative estimates
are available for many potentially important source categories,
e.g., Superfund sites, hazardous waste disposal and pollutants
formed in the atmosphere.
At the onset of the study, we identified several analytic
techniques for assessing the nature and magnitude of the air toxics
problem. Each methodology offered different advantages, as well as
varying degrees of resolution and uncertainty. Rather than select
one approach for the analysis of such a complex issue, we chose to
complete several studies:
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o An assessment of the hazardous air pollutant problem based on
state and local experience;
o An evaluation of epidemiological evidence on cancer and
its relationship to air pollution;
o An estimate of national exposure and risk from about 40
pollutants being considered for listing under Section 112
of the Clean Air Act;
o A more detailed estimate and analysis of exposure and risk
in 35 counties for about 20 pollutants, including consideration
of sources that were not considered sources of air emissions
in the past, such as municipal sewage treatment plants (POTWs)
and waste oil combustion;
o An analysis of existing ambient air quality data for metals
and volatile organic compounds;
o A discussion of pollutants and sources either not covered
by the analyses above, e.g., radionuclides, asbestos and
gasoline marketing, or not easily quantified, e.g., dioxin
and combustion of hazardous waste in boilers.
In this chapter, we will first describe each of these studies
in more detail and summarize their findings on the magnitude of the
ambient air toxics problem. We have expressed the magnitude of the
problem in three ways: annual national cancer incidence; annual
incidence per million people; and lifetime individual risk. We
then summarize and compare the results from each effort, and develop
general conclusions.
Again, we must caution against misuse of the results of this
scoping study. The analysis was not undertaken to lead directly
to decisions on carcinogenicity nor source regulation. Use of the
results should be limited to: 1) identifying the potential signifi-
cance of the risk caused by air toxics from a national and regional
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perspective; 2) assisting the Agency in setting research and
regulatory priorities; 3) identifing those pollutants and sources
for which only scant data exist and should therefore be explored in
more detail; and 4) assisting in developing long-term goals and
gen.eral strategi e.s. f or air toxics.
B. Summaries of Individual Analyses
1. Survey of State and Local Agencies, Canada, and Europe
The responsibility of dealing with air toxics is not unique to
EPA or this nation. Several State and local agencies have active
air toxics programs, and have a great deal of experience in dealing
with these problems. Also, other industrialized nations have the
same public concern over environmental cancers as the United States.
We reasoned that they may have the same need as EPA to define the
risks from air toxics in order to justify programs and to set
priorities. Therefore, a portion of the study involved communication
with Canada, the European Community, all States, and 33 major local
air agencies^,^,5 on their risk assessment activities.
3 Memorandum from B.J. Steigerwald to Alan Jones et al.,
"Air Toxics Program in Canada," EPA, April 16, T9~8TT~
4 Memorandum from Delores Gregory, OIA, to B.J. Steigerwald, EPA,
OAR, "E.G. Regulation of Hazardous Air Pollutants," May 3, 1984.
5 Radian Corporation, "Definition of the Air Toxics Problem at the
State/Local Level," EPA Contract 68-02-3513, Work Assignment 45.
June 1984.
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Of these, only California has attempted to quantify public
health risks from air toxics. Officials in Canada believe that
risk assessment will be increasingly important in their toxics
programs, but they have not yet developed methods and do not apply
risk assessment in any systematic way. They will evaluate in
•
detail the results of this study. Cables were sent to the Commission
of the European Communities through EPA's Office of International
Activities and discussions were held with individuals involved in
toxics programs in Europe. There is much information available
from the international community on the potential toxicity of
various compounds, but nothing seems to be available on cancer
incidence or on individual risks from exposure to ambient air.
The California estimate was an isolated analysis published in
1982 to support proposed legislation on air toxics.6 It used air
quality data for nine specific compounds to calculate excess
lifetime cancer rates per million population in the Los Angeles
basin. Potency for each compound was determined in a unique way
using an air equivalent of EPA's Water Quality Criteria rather
than the unit risk value used in EPA's risk assessment procedures.
Therefore, the results are not directly comparable to our results
obtained using air quality data for Los Angeles. For the nine
compounds selected, the California analysis estimates about 1000
excess lifetime cancers per million people or about 14 annual cases
per million. The study was used by the California Air Resources Board
6 Batchelder, J. et al.. Proposed Amendments to Chapter 1, Part III
of Title 17, CaTTfornia Administrative Code, Regarding the Emission
of Toxic Air Contaminants." California Air Resources Board;
September 1982.
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for orientation purposes only and to show that the problem deserved
additional attention. They do not recommend the study be given
weight beyond its original purpose.
Since most State and local agencies included in the poll
expressed concern over air toxics but could not quantify their
concern directly,, we explored other more subtle indicators of the
problem. Counting air "episodes," "incidents," or "complaints"
involving health scares produced no usable statistics. An evaluation
of source permits indicated that, at least for States with fenceline
ambient standards, air toxics programs could require substantial
resources and often require controls beyond those needed for criteria
pollutants.
For example, about 1000 new source permits a year are issued
in Michigan for emissions of toxic pollutants. New York reviews
36,000 operating permits every 1 to 5 years under their air toxics
regulation; this number increased by 6000 emission points in the
past 2 years. Illinois reviews 5000-6000 permits each year that
involve emissions of air toxics. In a recent detailed study of 42
permits for source categories likely to emit toxics, Illinois found
that 20 of the sources were required to control beyond that needed
for criteria pollutants.
In summary, essentially no other agency has attempted to
quantitatively define risks from air toxics. However, general
concern about the problem is universal, and an increasing number of
States have begun to issue air toxics permits to large numbers of
new and existing sources. These permits are generally based on
diffusion modelling and compliance with fenceline ambient standards
that are derived from occupational guidelines.
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2. Evaluation of Cancer Associated with Air Pollution
Using Epidemiological Studies
Background
The traditional way to demonstrate the effect of environmental
pollution on public health has been to perform an epidemiological
study. A variety of such studies has been attempted for air
pollution. Our primary source of data on these was a report prepared
by Clement Associates for EPA which described and critically evaluated
the evidence for cancer associated with air pollution.7,8
The Clement report assembled 3 main types of evidence linking
cancer incidence to air pollution: epidemiological studies, laboratory
studies on mutagenicity of airborn materials, and ambient air
monitoring data for pollutants known to be carcinogens. Data from
the mutagenicity and monitoring studies confirmed other reports
that extracts of airborne material from polluted air and emissions
from motor vehicles and stationary sources are mutagenic or carcinogenic
•
in experimental bioassy systems.
7 Clement Associates, Inc., "Review and Evaluation of Evidence for
Cancer Associated with Air Pollution." (EPA-450/5-83-006) Review
Draft. November 9, 1983.
8 Pate, Nancy, "Review of the Document 'Review and Evaluation of
the Evidence for Cancer Associated with Air Pollution1 and
Assessment of this Approach for Better Defining the Extent and
Magnitude of the Air Toxics Issue." June 1984.
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The report also reviewed epidemiological studies linking
air pollution and lung cancer by using levels of benzo(a)pyrene
(BaP), a known potent carcinogen, as an indicator of air pollution.9
Using selected of these studies, the Clement report presented
calculations of the number of lung cancer deaths which could be
associated with a given level of air pollution as characterized by
BaP concentrations, By combining lung cancer mortality from
the 1960's with estimated levels of BaP in the 1930's and 1940's.
Clement estimated that roughly 10,000 cases of lung cancer per
year (11%) during the 1960's were attributable to air pollution.
Unfortunately, because of the long lag time between exposure and
onset of cancer, these findings are not directly relevant to the
hazard posed by current air pollution, particularly since BaP
concentrations have generally declined by a factor of 10 since the
1960's.10
9 BaP is a ubiquitous pollutant generally found in emissions from
incomplete combustion, especially of wood and coal in small
combustion units and in motor vehicle exhaust (soot and smoke).
BaP is one of the literally hundreds of organic particulates known
as polynuclear organic compounds; many polynuclear organics are
carcinogenic, many are not.
10 Pate, Nancy. 0_p_. cit.
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Despite this limitation in the direct use of the results of
epidemiological studies, we felt we could not ignore the polynuclear
organics represented by BaP in this analysis. Even though overall
BaP emissions have decreased significantly since the 1930's and
1940's, BaP-related compounds are still present in the ambient air
and may still represent an important part of the air toxics problem.
For example, a recent study completed in New Jersey examined ambient
BaP concentrations and mutagenicity of organics extracted from
inhalable particulate matter samples. BaP levels increased by
tenfold during the.winter relative to the summer, and mutagenicity
tests found winter particulate matter samples to be 1-1/2 to 3
times as mutagenic as summer samples.H
Thus, we decided to use the dose/response coefficient derived
from data cited in the Clement report and to combine it with current
air quality data and emissions of BaP to estimate cancer incidence
associated with the large category of BaP-related pollutants which
we will refer to in this study as Products of Incomplete Combustion
(PIC). The Clement report presented 14 estimates obtained from 12
separate reports of the dose/response relationship between air
pollution levels as indexed by BaP concentrations and lung cancer
rates. Of these 14 estimates, 6 were derived from occupational
epidemiological studies, while 8 were derived from general population
studies that related cancer deaths in the period 1959-1975 to BaP
levels from 1958-1969.
11 Lioy, Paul J., and Daisey, Joan M. "The New Jersey Project on
Airborne Toxic Elements and Organic Substances (ATEOS): A Summary
of 1981 Summer and 1982 Winter Studies", Journal of the Air
Pollution Control Association, Volume 33, Number 7, July 1983.
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Clement Associates adjusted the dose/response coefficients
in these general population studies downward to account for the
decline in ambient BaP levels during the lag periods between
exposure and death from lung cancer. In accordance with recom-
mendations by research groups within EPA, certain of the occupa-
tional dose/response estimates presented in the Clement report were
revised (for example, the Carcinogen Assessment Group's latest
estimate f.or coke oven emissions was substituted for that appearing
in the Clement report). The final potency estimates (as expressed
by lung cancer deaths per year per ng/m^ BaP) for the occuptational
studies varied from 0.46 to 0.88 x 10 ~ 5, whereas those for the
general population studies varied from 0.3 to 1.4 x 10"5. When the
potencies for each of the two categories of studies were averaged,
estimates of 0.69 x 10~5 (general population) and 0.71 x 10~5
(occupational) were obtained. A value of 0.7 x 10~5 was selected
and combined with estimates of population exposure to BaP; based on
air quality data, an estimate of 821 incidences of lung cancer per
year attributable to PIC was estimated, whereas 148 deaths per year
were estimated using BaP emissions data and the more limited population
studied in the 35-County Study.
The reader should be alerted to several key limitations of
using BaP levels as a surrogate for exposure to a complex mixture
of compounds, as we have done in this analysis. A major weakness
of using the potency estimates derived from the occupational studies
is that the mix of PIC in the exposures studied (coke oven
emissions, roofing tar fumes, and gas fumes) almost certainly
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differs from that of the ambient air. A limitation of general
population studies is that BaP in these studies is used as a
surrogate for all air pollution, not just PIC, and BaP ambient
levels in the 1930's and 1940's had to be estimated. In addition,
the proportion of -carcinogenic activity attributable to BaP in
PIC mixtures is known to vary between source categories and
sometimes within a source category (e.g., different automobiles).
The impact of this varying ratio of BaP to other compounds is
further complicated since synergistic and antagonistic effects
between BaP and other PIC compounds are known to occur, but at
present are virtually unquantifiable. All of these factors indi-
cate strongly that BaP is almost certainly not a stable index of
the carcinogenicity of polluted air.
In spite of the limitations of the BaP-surrogate method, it
appeared that there was no better alternative for estimating risk
due to PIC. Simply citing risk estimates for mixtures from specific
sources of PIC was not an option, since quantitative risk estimates
are available for only one mixture--coke oven emissions--which
comprises only a small fraction of total estimated PIC emissions.
Also, sufficient data on potency and emissions do not exist to
characterize PIC risks on a compound by compound basis.
It should be noted that there are precedents for using BaP
as a surrogate in just this way. The National Academy of Sciences
(NAS) recently used BaP as a proxy to estimate the cancer risk
from polycyclic aromatic hydrocarbons (a chemically defined
analogue of our more loosely defined "PIC"). In a 1983 report
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entitled, "Polycycllc Aromatic Hydrocarbons: Evaluation of
Sources and Effects," the NAS estimated cancer risks as follows:
This appendix...assumes that benzo(a )pyrene (BaP) can be
used as a proxy for PAH's and that human exposure to BaP
in the ambient air at an average concentration of 1 ng/m^
over an entire lifetime has the effect of increasing by
0.02-0.06% the risk of dying prematurely (at or before
the age of 70) because of lung cancer. Although the
appropriateness of BaP as a surrogate for PAH's in general
has been questioned, it has been so used extensively in the
past, and much of the available information refers to it as
an indicator for exposure to PAH's. (p. D-l)
By way of comparison with the potency estimate used in our analysis
(0.7 x 10-5), the NAS lifetime potency estimates translate into 0.3 to
0.9 x 1Q-5 lung cancer deaths per year per ng/m^ BaP.
Parenthetically, we might add that the same NAS report
presented estimates of cumulative lung-cancer incidence due to
lifelong exposure to diesel exhaust from various types of vehicles.
These estimates varied from a low of 20 per 100,000 to a high of
787 per 100,000 for two different makes of automobiles, compared
to that of 43 per 100,000 for coke oven emissions.
Thus, we acknowledge that there are real analytical problems
associated with estimating risk due to PIC and that there is vari-
ation in the BaP-surrogate potency estimates. However, since this
report was intended to focus policy and planning activities and was
not meant to serve as the basis for regulatory acton, we decided
to include the incidence estimate for PIC as a preliminary estimate
of the magnitude of the PIC problem.
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3. NESHAPS Study
Background
The NESHAPS study was one of two analyses that employed dispersion
modeling to assess exposure and risk due to air toxics.12 EPA's
Human Exposure Model (HEM) was employed to convert point source
emission estimates into estimated ambient levels. The study
was designed to examine in more detail the growing belief that
sources covered in the past under NESHAPS, i.e., industrial producers
and users of the chemicals of concern, may be responsible for only
a small part of the air toxics problem. The risk estimates in this
study are national in scope, and consider emissions obtained from
traditional air pollution inventories. The sources covered include
mobile and area sources, but the emphasis was on point sources.
Consideration of some potentially important pollutants, such as
radionuclides, gasoline vapors and products of incomplete combustion
(PIC), and nontraditional sources, such as POTWs and hazardous
waste disposal were not included in this analysis.
The original intent of this effort was to estimate exposure
and risk for 87 pollutants: the original 37 candidates for listing
under Section 112 and 50 additional substances identified by EPA's
Office of Air Quality Planning and Standards (OAQPS). OAQPS identified
12 Schell, R.M. "Estimation of the Public Health Risks Associated
with Exposure to Ambient Concentrations of 87 Substances;"
OAQPS, USEPA, July 1984.
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th is latter grouping of pollutants using the Hazardous Air Pollutant
Prioritization System (HAPPS) developed by Argonne National Labora-
tories. They also considered ambient air monitoring data for
organics and production data. Unfortunately, after a great deal of
effort to gather all available dose-response data on these pollutants,
we were only able to quantitatively analyze 42 compounds (see Table
1). The qualitative judgment regarding the carcinogenicity of some
of these compounds is still an open question, and they are included
here for analytical purposes only- All of the unit risk values
used in this report are presented in Attachment A.
Emission estimates for 27 of the 42 compounds were developed
using OAQPS staff analyses and other OAQPS contract documents.
For the remaining 15 compounds, little information was available.
Surrogate estimates of exposure were made for these using a
"best-fit" approach with known compounds based on physical
properties, uses, and production volumes.
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TABLE 1
PRELIMINARY APPROXIMATION OF ANNUAL
AND MAXIMUM LIFETIME RISK
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INCIDENCE
Pollutants Havi ng
Some Evidence of
Carci nogeni city*
Preliminary Approx-
imation of
Maximum Individual
Lifetime Risk**
Preliminary Approx-
imation of
Incidence**
Aery 1 ami de
Acryl oni tri le
Al lyl chlori de
Arseni c
Benzene
Benzyl chlori de
Beryllium
1,3 Butadi ene
Cadmi urn
Carbon Tetrachl ori de
Chloroform
Ch romi urn"1"
Coke Oven Emissions
Di ethanol ami ne
Dimethyl nit rosami ne
Dioctyl phthalate
Epi chl orohydri n
Ethyl acrylate
Ethyl ene
Ethylene dibromide
7.4x10-5
3.8x10-3
1.3x10-6
6.5x10-3
8.0x10-3
3.0x10-5
1.0x10-4
9.7x10-6
7.5x10-4
5.8x10-4
3.0x10-3
1.6x10-1
2.0x10-2
2.0x10-7
5.4x10-5
9.8x10-6
1.9x10-6
4.7x10-5
4.9x10-4
1.6x10-4
0.01
0.42
<0.01
4.70
32.30
<0.01
1.20
0.01
16.30
14.00
0.27
330.0
8.60
<0.01
0.05
<0.01
<0.01
<0.01
<0.01
26.70
* The weight of evidence of carcinogenicity for the compounds
listed varies greatly, from very limited to very substantial.
Further, the extent of evaluation and health review performed
varies considerably among compounds. However, for the purposes
of this report, a conservative scenario (i.e., that all
compounds examined could be human carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these
estimates, they should be regarded as rough approximations of
total incidence and maximum lifetime individual risk. Estimates
of incidence for individual compounds are much less certain.
These incidence and maximum risk estimates have been performed
to provide a rough idea of the possible total magnitude of the
air toxics problem, and will be used only for priority-setting
and to provide policy guidance.
* Risk estimates assume that all species of chromium and nickel
are carcinogenic, although only certain species have evidence
of carcinogenicity. Current data do not allow differentiation
among species.
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TABLE 1 (cont.)
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NESHAPS STUDY:
PRELIMINARY APPROXIMATION OF ANNUAL INCIDENCE
AND MAXIMUM LIFETIME RISK
Pollutants Having
Some Evidence of
Careinogenicity*
Preliminary Approx-
imation of
Maximum Individual
Lifetime Risk**
Preliminary Approx-
imation of
Incidence**
Ethylene dichloride
Ethylene oxide
Formal dehyde
4,4 Isopropyl i denedi phenol
Mel ami ne
Methyl Chloride
Methylene chloride
4,4 Methylene dianiline
Nickel t
Ni trobenzene
Nitrosomorphol i ne
Pentachl orophenol
Perchloroethy lene
PCBs
Propylene dichloride
Propylene oxide
Sty rene
Terephthal i c aci d
Titanium dioxide
Tri chloroethyl ene
Vinyl chloride
Vi ny 1 i dene chl ori de
2.9x10-4
6.8x10-3
6.1x10-4
1.1x10-6
1.5x10-6
1.2x10-5
9.0x10-6
1.5x10-3
1.6x10-3
1.2x10-6
6.0x10-9
1.7x10-5
4.6x10-4
3.0x10-4
2.1x10-6
3.0x10-2
3.3x10-5
1.5x10-6
3.2x10-7
1.0x10-4
3.8x10-3
4.2x10-3
44.00
47.80
1.60
0.03
<0.01
<0.01
1.0
0.02
80.00
<0.01
<0.01
0.12
2.90
0.21
<0.01
0.97
<0.01
<0.01
0.01
9.70
11.70
0.04
Total
634.7
* The weight of evidence of carci nogeni ci ty for the compounds
listed varies greatly, from very limited to very substantial.
Further, the extent of evaluation and health review performed
varies considerably among compounds. However, for the purposes
of this report, a conservative scenario (i.e., that all
compounds examined could be human carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these
estimates, they should be regarded as rough approximations of
total incidence and maximum lifetime individual risk. Estimates
of incidence for individual compounds are much less certain.
These incidence and maximum risk estimates have been performed
to provide a rough idea of the possible total magnitude of the
air toxics problem, and will be used only for priority-setting
and to provide policy guidance.
Risk estimates assume that all species of chromium and nickel
are carcinogenic, although only certain species have evidence
of carcinogenicity
among species.
Current data do not allow differentiation
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-30-
Fi ndi ngs
For the 42 compounds included in the NESHAPS analysis, a total
nationwide annual cancer incidence of 635 was calculated (see
Table 1). Roughly 93 percent of these can be attributed to eight
compounds. These compounds, ranked in descending order, are as
follows: chromium; nickel; ethylene oxide; ethylene dichloride;
benzene; ethylene dibromide; cadmium; and carbon tetrach1oride. 13
Maximum individual risks 10~3 or greater were estimated for 12
compounds: acrylonitrile; arsenic; benzene; chloroform; chromium;
coke oven emissions; ethylene oxide; 4-4 methylene dianiline;
nickel; propylene oxide; vinylidene chloride; and vinyl chloride.
In addition to the usual uncertainties, there are further
complications with the risk estimates for several compounds, including
chromium, nickel, carbon tetrachloride, and formaldehyde. These
considerations demonstrate the need for caution in interpreting such
studies.
In the case of chromium, only the hexavalent form has been
proven to be carcinogenic with a unit risk value of 1.2xlO~2 compared
The individual percentage contributions of each compound are:
chromium (52%); nickel (13%); ethylene oxide (8%); ethylene
dichloride (7%); benzene (5%); ethylene dibromide (4%);
cadmium (3%); and carbon tetrachloride (2%).
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to arsenic at 4.29x10-3. There is now insufficient evidence to
determine that the trivalent form is also carcinogenic. The
NESHAPS analysis, however, assumes that total chromium releases are
carcinogenic and that trivalent chromium is as potent as hexavalent.
There is no information now available on the ratio of trivalent to
hexavalent for emissions or ambient concentrations, but some occupa-
tional exposure studies suggest that the trivalent form may dominate.
On the other hand, several important source categories are known to
emit at least some hexavalent chromium and there is some evidence
that changes in the valence state can occur in the atmosphere. The
problem of speciation adds one more layer of uncertainty to the
risk estimates for chromium.
The situation for nickel is similar. Only two rare nickel
subspecies (nickel subsulfide and nickel carbonyl) are considered
carcinogenic; however, the unit risk factor for these forms is
applied to total nickel emissions. Although research is underway,
there is little information available at present on ambient concen-
trations of the different nickel forms.
Carbon tetrachloride is a very stable organic compound that has
a half-life of about 35 years compared to a half-life of hours or
days for most other common volatile organic compounds. As a result,
carbon tetrachloride is accumulating in the atmosphere. Therefore,
current emissions are associated with cancer risks now, and in the
future, by increasing background concentrations. The NESHAPS
analysis only covers risk from current emissions and known sources,
and estimates incidence at 14 per year. If current background
levels are considered, the incidence estimate increases to about 85
per year. Carbon tetrachloride also has the potential to deplete
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stratospheric ozone and thereby indirectly increase the incidence
of skin cancer. For example, it is estimated that by the year
2020 U.S. emissions of carbon tetrach1oride could be responsible
for between 500 and 22,000 excess cases of skin cancer annually
in the U.S., resulting in 3-220 excess deaths per year-
Formaldehyde can be formed in large quantities in the atmosphere,
and the risks posed by the resulting ambient concentrations are not
able to be considered in exposure analyses based on emission estimates
alone. Assessments based on ambient monitoring data should provide
a more complete accounting of actual risk due to formaldehyde,
because they cover concentrations resulting from both emissions and
atmospheric formation.
3. 35 County Study
Background
In contrast to the national scope of the NESHAPS study, the 35
County Study was designed to address the air toxics problem from a
more local perspective.^ Building on the work of EPA's Integrated
Environmental Management Division (IEMD) in its geographic demonstra-
tion projects in Philadelphia, Baltimore and Santa Clara Valley, this
analysis explored the following:
0 the incidence of cancer resulting from exposure to
several pollutants and sources in specific localities;
0 the pollutants and sources that are the most significant
contributors to the problem; and
0 the geographic variability of pollutants, sources, and exposures.
Versar; American Management Systems, Inc. "Hazardous Air Pollutants:
An Exposure and Risk Assessment for 35 Counties." September 1984.
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The analysis focused on traditional sources, i.e.,
large point sources such as power plant and industrial facilities,
and area sources, such as motor vehicles, space heating, gasoline
marketing, and solvent usage. However, it also included "nontradi-
tional" sources, such as woodstoves, waste oil combustion, and
sewage treatment plants. Data limitations did not permit emission
estimates or any extensive exposure modeling for TSDFs (hazardous
waste treatment, storage and disposal facilities), Superfund sites,
hazardous waste in boilers, municipal waste incinerators, municipal
landfills, and sewage sludge incinerators. The Agency has initiated
various studies to explore emissions and risks for most of these
sources in more detail. Information on these efforts, as well as
any preliminary findings, is provided in the Other Sources, Pollutants
and Pathways section at the end of this chapter.
The analysis characterized exposure and risk associated with
22 compounds (see Table 2). Most of these compounds were screened
using one or more of the following criteria:
0 Sufficient evidence of carcinogenicity;
0 Significant release rates; and
0 Readily available emissions information.
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TABLE 2
D"1. .. <~T
i\*r I
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35 COUNTY STUDY:
PRELIMINARY APPROXIMATION OF ANNUAL
INCIDENCE
Pollutants Having Some
Evidence of Carcinogenicity *
Preliminary Approximation
Inci dence**
(20% of U.S. Population)
of
PIC***
Benzene
Ch romi urn"!"
Formaldehyde
Vinyl chloride
Trichloroethy1ene
Gasoline Vapors
Perch!oroethylene
Acrylonitri1e
Coke oven emissions
Ethylene dichloride
Arsenic
Cadmium
Benzo(a)pyrene
Ethylene dibromide
148.0
18.5
13.4
10.0
8.2
6.8
6.8
6.7
4.2
2.4
1.5
1.1
1.1
1.1
1.0
**
The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purposes of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of total incidence.
Estimates for individual compounds are much less certain. These incidence
estimates have been performed to provide a rough idea of the possible
total magnitude of the air toxics problem, and will be used only for
priority-setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number
compounds, probably consisting primarily of polynuclear organics.
of
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air pollution. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
Risk estimates assume that all species of chromium and nickel are
carcinogenic, although only certain species have evidence of carcino-
genicity. Current data do not allow differentiation among species.
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TABLE 2 (Cont. )
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35 COUNTY STUDY:
PRELIMINARY APPROXIMATION OF ANNUAL
INCIDENCE
Pollutants Having Some
Evidence of Carcinogenicity*
Preliminary Approximation of
Inci dence**
(20% of U.S. Population)
NickelT
Carbon tetrachloride
Chioroform
Styrene
B e ry 11 i u m
1,3-Butadi ene
Pentachlorophenol
Total
0.7
0.2
0.1
0.02
0.01
0.01
< 0.01
231.84
**
***
The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purposes of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of total incidence.
Estimates for individual compounds are much less certain. These incidence
estimates have been performed to provide a rough idea of the possible
total magnitude of the air toxics problem, and will be used only for
priority-setting and to provide policy guidance.
"Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air pollution. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
Risk estimates assume that all species of chromium and nickel are
carcinogenic, although only certain species have evidence of carcino-
genicity- Current data do not allow differentiation among species.
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-35-
Emissions estimates were developed using several techniques.
Whenever possible, the analysis relied on plant-specific data and
EPA documents on emissions from specific source categories. Where
this information was unavailable, surrogate loadings were developed
•
using the information in the National Emissions Data System (NEDS),
and apportioning factors that speciate the VOC and PM data into
individual toxic constituents. The NEDS data vary a great deal
in quality, and some of it is very poor. However, an extensive
effort was made to screen the NEDS information for the 35 counties
to correct for any obvious inaccuracies in release rates, source
locations and stack specifications.
For the "non-traditional" sources (POTWs, waste oil combustion,
woodsmoke, and gasoline marketing), we developed special algorithms.
To calculate volatile releases for eight compounds (ethylene
dichloride, vinyl chloride, perchloroethylene, trichloroethylene,
benzene, chloroform, carbon tetrachloride and aery 1onitrile) from
sewage treatment plants, we modeled thirteen prototype sewage treat-
ment plants (POTWs) using information provided by EPA's Industrial
Facilities Discharge (IFD) file, the NEEDS Survey, and a study
conducted by the effluent guidelines program to determine the fate
of priority pollutants in 50 POTWS.15,16 Tne sewage treatment
15 Fate of Priority Pollutants in Publicly Owned Treatment Works,
Vol. I. (EPA 440/1-82-303). September 1982.
16 For further explanation on the methodology for estimating POTW
volatilization, see: Versar; American Management Systems, Inc.
"Hazardous Air Pollutants: An Exposure and Risk Assessment for
35 Counties." Appendix D. September 1984.
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plants in each of the 35 counties were assigned to one of the model
plants based on the following factors: the percent of inflow to
the POTW attributable to industrial dischargers; the types of
industries that discharge to the POTW; and the level of treatment
at .the POTW. The .modeled sewage treatment plant emissions were
treated as point sources in the exposure assessment.
Toxic emissions from waste oil combustion were characterized
using data from Office of Solid Waste (OSW) documents on: the
typical contaminant concentrations found in used oil; the estimated
amount of waste oil burned in each State; the destruction efficien-
cies for metals and organic compounds burned in industrial and
residential, institutional and commercial (RIC) boilers; and the
percentage of total waste oil burned in each type of boiler.1?
The study of waste oil focused on the following hazardous air
pollutants: chromium; nickel; cadmium; beryllium; arsenic; benzene;
benzo(a )pyrene; perchloroethylene; and trichloroethylene. Waste
oil emissions were modeled as area sources.
Air toxics releases from woodsmoke were estimated for two
sources--fireplaces and wood stoves.18 Using available information,
we developed factors for six compounds (benzo(a )pyrene, formalde-
For further explanation on the methodology for estimating
toxics emissions from waste oil combustion, see: Versar;
American Management Systems, Inc. "Hazardous Air Pollutants:
An Exposure and Risk Assessment for 35 Counties." Appendix C.
September 1984.
For further explanation on the methodology for estimating
woodsmoke emissions, see: Versar; American Management Systems,
Inc. "Hazardous Air Pollutants: An Exposure and Risk Assessment
for 35 Counties." Appendix B. September 1984.
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hyde. beryllium, nickel, cadmium, and arsenic) that relate pollutant
emissions to the quantity of wood burned in each county. Data on
wood consumption in each county were obtained from NEDS. The break-
down on the amount- of wood burned in wood stoves vs. fireplaces in
each area was provided by an industry association. Wood smoke was
modeled as an area source.
Finally, air toxics emissions from gasoline marketing were
calculated using the VOC data in NEDS and apportioning factors
developed from varied sources.19 The pollutants considered are:
gasoline vapors; benzene; ethylene dibromide; and ethylene dichloride.
On the choice of geographic sites, we decided to concentrate
on counties, as data are rarely disaggregated below this level, and
chose 35 counties to explore in detail. The counties selected fall
into one of three categories:
0 Densely populated, highly industrialized;
0 Densely populated, low industrial activity; or
•
0 Low population density, highly industrialized.
These counties also contain a wide range of industrial bases and
geographic locations. Although only about one percent of the
counties in the U.S., the 35 counties account for roughly 20% of
19
Op. cit.
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U.S. population (1980 Census Data), 20% of total national VOC
emissions, and 10% of total PM emissions.
As with the NESHAPS analysis and other Agency studies on
exposure, the 35 County Study employs dispersion modeling to
calculate dose and- exposure. EPA's Office of Toxic Substances'
fate and transport model, GAMS, was used in this effort. To
facilitate running the model more quickly and efficiently, we used
an approach that only allowed us to calculate annual aggregate
incidence for the 35 counties.
Fi ndi ngs
Multiplying the results from the exposure modeling by the
appropriate unit risk values resulted in the incidence estimates
presented in Table 2. The estimated aggregate incidence of cancer
for the 22 pollutants and 35 counties is 231 per year. As shown,
eight substances account for roughly 95% of the total risk. These
pollutants, ranked in descending order, are as follows: PIC (products
of incomplete combustion); benzene; chromium; formaldehyde; vinyl
chloride; trichloroethylene; gasoline vapors; and perchloroethylene.
PIC alone contributes almost 64% to total incidence.
Many of the basic problems discussed in the NESHAPS analyses
are applicable to the 35 County Study. For example, it was not
possible to speciate emission estimates for chromium and nickel
in our analyses. Also, the 35 County Study only considers emissions
of carbon tetrachloride from a limited number of sources. Background
concentrations due to the long half-life of carbon tet were not
modeled, although they may significantly contribute to cancer risks.
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-39-
5. Ambient Air Quality Study
Background
As part of the overall study, we used ambient air quality data
to estimate cancer incidence and individual risks.20 Two basic
groupings of compounds were used in this analysis: those for which
fairly extensive data were available (five metals and B(a)P); and
those for which less extensive data could be found (nine organic
compounds). The metals and B(a)P data were drawn from the National
Air Data Bank's Storage and Retrieval of Aerometric Data (SAROAD)
system, whereas the data for organic compounds came from a variety
of sources. For the most part, the data on organics were obtained
from studies which used different sampling and analytical methods
and a variety of sampling periods.
Every attempt was made to gather all available data on air
toxics. For example, for organic compounds the data base incorporated
air toxics data compiled from a variety of sources by Dr- Hanwant
Singh of SRI International, and from more recent monitoring studies
20 Hunt, Bill et al., "Estimated Cancer Incidence Rates from Selected
Toxic Air Pollutants Using Ambient Air Data." OAQPS, OAR, EPA.
July 1984.
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performed in the cities of Baltimore, Los Angeles, Houston,
Philadelphia, and in northern New Jersey. As far as we know, this
effort represents the most comprehensive attempt yet to compile
nationwide air data for toxic substances and to perform risk
assessments based on those data.
•
It is appealing to use ambient air quality data—as opposed
to modeled estimates—to estimate risks because these data represent
the actual ambient concentrations to which people are exposed.
However, the reader is reminded of three cautions which were presented
in the previous section on Estimates of Exposure. First, we must
assume that data collected at a limited number of sites can be
extrapolated to represent city-wide and county-wide levels, and
that these data in turn can be extrapolated to the national level.
Second, we must often use data that were collected over a short
time period, e.g., 24 hours, and assume that in the aggregate
they are representative of concentrations for much longer periods,
e.g., annual averages. Third, we assume that people are continuously
exposed to outdoor ambient levels.
National estimates of cancer incidence were calculated for
metals (see Table 3) by estimating county averages based on 1979 to
1982 data for the approximately 170 counties that had data, using
these averages to extrapolate to those counties that lacked data,
and then applying unit risk values. A national incidence number
for PIC was estimated by dividing the country into eleven regions
and using urban/rural B(a)P concentrations in combination with
urban/rural population figures for each region.
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-41-
Estimating incidence for the volatile organic compounds was
somewhat more difficult, given that ambient data on these compounds
are scarce and often derived from short-term studies. In order to
provide at least minimal seasonal balance when computing annual
averages, we established a data completeness criterion^! for
organic compounds in urban areas which greatly reduced the amount
of data that could be used. Only data from studies performed in
Baltimore, Philadelphia, Los Angeles, Houston, and northern New
Jersey met the criterion. For these cities, an average level was
calculated for each organic compound, and these averages were then
combined with population figures to calculate incidence. Next,
these estimates were extrapolated to the national level by using
urban population data. Non-urban risks were calculated by using
non-urban pollutant levels and population data, and these were
added to urban risks to obtain national estimates.
As Table 3 shows, seven compounds are associated with greater
than 50 cancers per year. These seven pollutants are as follows:
arsenic, PIC, benzene, carbon tetrachloride, chloroform, chromium,
and formaldehyde. The national incidence estimate based on ambient
data for the compounds shown in Table 3 is approximately 1870 per
year. The estimated incidence per million population for those
pollutants is about 8.1 per year.
21 More than 2 sites per county, and at least 10 samples over
2 quarters in a single calender year.
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TABLE 3
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AMBIENT AIR QUALITY STUDY: PRELIMINARY APPROXIMATION OF
ANNUAL INCIDENCE
Pollutants Having
Some Evidence of
Carci nogeni city*
Preiimi nary
Approximation of
Incidence**
Incidence per
Million Population**
Arseni c
Berrzo(a)py rene
PIC***
Benzene
B e ry 1 1 i u m
Cadmi urn
Carbon tet rachl oride
Chi orof orm
60.0
5.4
820.9
248.6
0.1
14.6
84.7
106.7
0.26
0.023
3.57
1.08
0.0004
0.06
0.37
0.46
**
The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purpose of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of total incidence.
Estimates for individual compounds are much less certain. These
incidence estimates have been performed to provide a rough idea of the
possible total magnitude of the air toxics problem, and will be used
only for priority-setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air polluton. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
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TABLE 3 (Cont.)
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AMBIENT AIR QUALITY STUDY: PRELIMINARY APPROXIMATION OF
ANNUAL INCIDENCE
Pollutants Havi ng
Some Evidence of
Carcinogenicity*
Prelimi nary
Approximation of
Inci dence**
Incidence per
Mi llion Population**
Ch romi urn"1"
Formal dehyde
Methyl chloride
Methyl chloroform
Methylene chloride
Nickel1"
Perchloroethyl ene
Tri chl oroethylene
Vi nyl i dene chl ori de
Total
242.0
191.3
0.9
0.1
7.4
15.0
25.4
25.4
20.4
1868.9
1.05
0.83
0.004
0.0004
0.03
0.07
0.11
0.11
0.09
8.12
* The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purpose of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of total incidence.
Estimates for individual compounds are much less certain. These
incidence estimates have been performed to provide a rough idea of the
possible total magnitude of the air toxics problem, and will be used
only for priority-setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air polluton. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
t Risk estimates assume that all species of chromium and nickel are car-
cinogenic, although only certain species have evidence of carcinogeni-
city. Current data do not allow differentiation among species.
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Individual lifetime risks were also estimated for metals,
PIC, and organics (Table 4). Individual risks ranged up to 10~3
for some of the trace metals and PIC, whereas individual risks for
the organics tended to be in the range of 10-* anc| lower. It should
be noted that the sites where these data were collected are generally
not located near points of expected maximum concentrations.
Therefore, the individual risk estimates for single pollutants
based on air quality data tended to be lower than those based on
exposure modeling of emissions from point sources.
However, in order to provide better understanding of risks in
urban areas, individual risks were estimated not only on an
individual pollutant basis, but also for many pollutants measured
at the same site. The results of this analysis are presented in
Table 5 for several urban areas that have attempted a more compre-
hensive definition of their problem through air quality monitoring.
These multi-pollutant individual risks represent the summed individual
risks at each site using monitoring data that were available for 10
to 15 organics, metals, and PIC. Table 5 shows that these multi-
pollutant individual risks range around lxlO~3 for all of the areas
with sufficient data for analyses. Lifetime individual risks for
single pollutants at these sites varied from 10~3 to 10~9j pollutants
causing risks in the 10~3 to 10"* range included chromium, PIC,
carbon tetrachloride, benzene, and chloroform. To our knowledge,
none of the monitoring sites were near major point sources of the
relevant compounds, although all sites were centrally located in
major urban areas.
It is important to note that the uncertainties associated with
extrapolating data collected at a few monitoring sites to an entire
urban area do not apply to these estimates of multi-pollutant
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TABLE 4
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AMBIENT AIR QUALITY STUDY: PRELIMINARY APPROXIMATION OF
INDIVIDUAL LIFETIME RISKS
Pollutants Having Some
Evidence of
Carci nogeni city*
Preli mi nary Approximation
of Maximum Lifetime
Individual Risk**
Arseni c
B(a)P
PIC***
Benzene
Beryl 1 ium
Cadmi urn
Carbon tetrachloride
Ch loroform
3.99xlO-3
2.47xlO-5
3.75xlO-3
1.54xlO-4
2.40x10-7
1.47x10-3
1.54x10-4
7.70xlO-5
**
The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purpose of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of maximum lifetime
individual risk. Estimates for individual compounds are very uncertain,
These risk estimates have been performed to provide a rough idea of
the possible total magnitude of the air toxics problem, and will be
used only for priority-setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air polluton. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
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TABLE 4 (Cont. )
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AMBIENT AIR QUALITY STUDY: PRELIMINARY APPROXIMATION OF
INDIVIDUAL LIFETIME RISKS
Pollutants Having Some
Evidence of
Carci nogenici ty*
Preliminary Approximation
of Maximum Li fetime
Individual Risk**
Chromi urn"1"
Fo rma1dehyde
Methyl chloride
Methyl chloroform
Methylene chloride
Nickel"!"
Perchloroethylene
Tri chloroethylene
Vi ny1i dene chlori de
1.44x10-3
•
4.91x10-5
4.60x10-7
2.25x10-8
8.28x10-7
2.84x10-5
1.88x10-5
2.59xlO-5
6.72x10-6
* The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purpose of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of maximum lifetime
individual risk. Estimates for individual compounds are very uncertain.
These risk estimates have been performed to provide a rough idea of the
possible total magnitude of the air toxics problem, and will be used
only for priority-setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air polluton. There are many
limitations of using the B(a)P surrogate method to estimate PIC
all PIC estimates presented in this report must be regarded as
uncertain. Refer to pp
the PIC unit risk value
. 21-26 for a
was derived.
more detailed explanation
risks:
hi ghly
of how
Risk estimates assume that all species of chromium and nickel are car-
cinogenic, although only certain species have evidence of carcinogeni-
city. Current data do not allow differentiation among species.
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TABLE 5
AMBIENT AIR QUALITY STUDY: PRELIMINARY APPROXIMATION OF
ADDITIVE LIFETIME RISKS*
Urban Area A Monitoring Site 1 2.6xlO~3
Monitoring Site 2 2.6xlQ-3
Urban Area B Monitoring Site 1 0.7xlO~3
Monitoring Site 2 0.7xlQ-3
Urban Area C Monitoring Site 1 l
Monitoring Site 2 1 .2xlQ-3
Urban Area D Monitoring Site 1 0.9xlQ-3
Monitoring Site 2 l.OxlO-3
* These estimates are based on a sum of estimated lifetime
individual risks for PIC (products of incomplete combustion),
2 to 3 metals and 6 to 10 organic compounds for each monitoring
site. Because of the uncertainties in the data used to make
these estimates, they should be regarded as rough approximations
of individual risk. Estimates for individual compounds are much
less certain. These incidence estimates have been performed to
provide a rough idea of the possible total magnitude of the air
toxics problem, and will be used only for priority-setting and
to provide policy guidance.
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individual risk. All that is involved is summing individual risks
from a pollutant mixture at a given urban location. Thus, with the
assumption that risks are additive, we can say that, even in neighbor-
hoods not located near major point sources, urban dwellers may
experience individual risks of 10~3 to 10~4 due to mul ti -pol lutant air
exposures.
6. Other Pollutants, Sources and Pathways
One of the principal findings of this study of air toxics is
that there are important gaps in our knowledge of this problem. This
study estimates cancer risks caused by 15-45 substances, when there
may be many more potential carcinogens in the ambient air. The
International Association for Research on Cancer (IARC), the National
Toxicology Program, and EPA's Carcinogen Assessment Group have each
identified over 100 compounds as carcinogenic. Many of these
compounds are probably not air pollutants, but it is clear that this
study does not quantitatively address a large number of pollutants
that exist in significant quantities in the ambient air. This
study attempted also to address all known or suspected sources of
air toxics, as well as known pollutants. Unfortunately, we were
unable to quantify the risks caused by several source categories,
including several nontraditi onal sources. In addition, each of the
individual analyses missed some sources or pollutants.
However, some of the sources and pollutants not included in
the major analyses have been subjects of quantitative analysis by
others. The following section summarizes available information on
the pollutants and sources that (1) were not covered by the individual
analyses; or (2) could not be quantitatively assessed because of
data limitations.
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POLLUTANTS
Dioxin
Only isolated estimates are provided for individual risks from
emissions of dioxin and these are limited to municipal incinerators.
The exposure pattern for dioxin appears to be complex and available
data are inconsistent; however, this is true for many compounds
that we have included in the study. Dioxin is unique because
exposure and risk are being studied in great detail by EPA's Dioxin
Task Force. The study team believed that there was little value at
this time in attempting an estimate of the aggregate risk from air
exposure for a pollutant that is currently being analyzed elsewhere
in such detai 1.
Asbestos
Asbestos is now receiving a great deal of attention as a
contaminant of indoor air from past use of asbestos-containing
building materials. Asbestos is also commonly found in the ambient
air, although at much lower levels than indoors, and selected sources
are already covered by federal emission standards under Section 112
of the Clean Air Act. Sampling and analysis for asbestos in the
atmosphere presents significant problems and concentrations vary by
several orders of magnitude. The available data suggest an average
of three nanograms/m3 and 30 fibers per nanogram.22 Coupling this
22 "Guidance for Controlling Friable Asbestos-Containing Materials
in Buildings." EPA Office of Pesticides and Toxic Substances,
EPA 560/5-83-002, March 1983.
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-48-
with an average risk factor for lung cancer and mesothelioma,23
gives a national estimate of over 100 excess cancers per year, or
about 0.5 per million population per year. This estimate covers
outdoor exposures only.
Radionuclides
EPA's Office of Radiation Programs (ORP) is currently proceeding
to regulate radionuclides as a hazardous pollutant based on the
widespread human exposure to these compounds in the ambient air,
and the numerous studies that document the incidence of cancer
resulting from exposure to ionizing radiation in many species of
animals and human populations.
ORP has recently summarized their exposure and risk assessment
for radionuclides.24 As shown in Table 6, the total national
estimated incidence for radionuclides is 17.5 per year; maximum
lifetime individual risks range from 4 x 10~2 to 5 x 10~7. The
major sources of radionuclides include nuclear power plants, national
defense weapons facilities, industrial plants, coal-fired boilers
and natural sources. The incidence calculation does not consider
exposure to indoor concentrations of radon.
23 Schneiderman, Nisbet, and Brett: "Assessment of Risks Posed by
Exposure to Low Levels of Asbestos in the General Environment",
Berichte. Bundes-Gesundheits-AMT, pp. 3-1 to 3-28, April 1981.
24 Hardin, J. "Issue Paper. National Air Toxics Problem: Radio-
nuclides." EPA, Office of Radiation Programs, August 1984.
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TABLE 6
ESTIMATES OF INCIDENCE AND INDIVIDUAL RISK DUE TO
RADIONUCLIDES EMITTED TO AIR*
Source An
Dept. of Energy
Faci lities
Nuclear Regulatory
Maximum Individual
nual Cancer Incidence Lifetime Risk
0.08
0.01
2 x 10-4
2 x 10-5
Commission (NRC)
Li censed Facilities
Federal Facilities 0.01 5 x 1Q-?
Uranium Fuel Cycle 5 1 x 10~4
Faci1ities
Uranium Mill Tailings 7 4 x 10~2
Piles
Uranium Mines 2.2 N/A
Phosphorus Plants 0.05 1 x 10~3
Coal-Fired Boilers 3 4 x 10~5
Sources of Natural Radio- 0.1 2 x 10"3
nucli des to Ai r
TOTAL 17.45
* Because of uncertainties in underlying data, the values presented
in this table should be regarded as estimates of incidence and
maximum lifetime risk. This table was provided by EPA's Office
of Radiation Programs. Please refer to footnote 24 for a more
detailed explanation of the methodology.
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Recent studies have indicated that indoor air concentrations
of various pollutants can greatly exceed ambient conditions. As
a result, risk assessments based on ambient levels may be an
understatement of the actual situation. In the case of radionuclides,
recent estimates place the annual incidence of cancer due to indoor
radon exposure at between 1,000 and 20,000. A more detailed discussion
of the ramifications of indoor air on the hazardous air pollutant
problem is provided in the section of this report on Perspective
and Context.
Other Pollutants
It is apparent that urban ambient air is characterized by the
presence of hundreds of organic compounds; fine particulate matter,
including metals and organic particulates; and significant concentra-
tions of the other criteria pollutants, including sulfur and nitrogen
oxides, and carbon monoxide. There are relatively few data available
on how all of these substances may interact once they enter the
human body.
An example of the complexity of urban air is shown in Figure I,
a gas chromatogram from lEMD's monitoring program in Baltimore. It
represents the concentrations and number of gaseous organics in the
ambient air as detected by gas chromatography/mass spectroscopy.
Each peak represents a separate organic compound. The peaks corre-
sponding to some compounds are labeled. Tentatively identified
compounds added up to the following totals:
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RIC
63/12/84
14:56:68
DATA:
CALI:
1518 ttl
1518 #2
SCAMS
1 TO 1400
100.0-1
SAMPLE: SITEft2 P«27 UME466A 36.9L TAGttS482A
COHDS.: FSCC 30H DB-5 0 FOR 6 TO 120 GIB
RANGE: G 1,1400 LABEL: H 0, 4.0 QUAH: A 8* 1.8 J 0 BASE: U 29, 3
229
O >-i
I- U.
RIC
565248,
n>
1236
o
O
400
5:00
7:30
8@0
10:00
1000
12:30
1200
15:00
1460 SCAM
17:30 TIME
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-52-
Alkanes 39.1 ug/m3
Aromatics 34.8 ug/m3
Halogenated compounds 9.8 ug/m3
Oxygenated compounds 7.5 ug/m3
Alkenes 3.4 ug/m3
SOURCES
Atmospheric Transformation
Most population exposure models begin with estimates of emis-
sions and they inherently cannot handle toxic compounds that may be
formed or rapidly destroyed in the atmosphere. The exposure models
used in the NESHAPS and 35 County studies assume that all exposures
occur within several hours of emission (within 20 to 50 km of the
source) and no corrections are made for transformation of pollutants
in the atmosphere.
As part of the study, EPA's Office of Research and Development
was asked to review the possibility that chemical reactions in the
atmosphere could form toxic compounds or increase the potency of
emitted pollutants.25 Ozone is the prime example of this phenomenon
for criteria pollutants. Although work in this area has not been
extensive, the study identified several potentially significant
examples of atmospheric transformation.
25 Bufalini, Gay and Dimitriades. "Production of Hazardous
Pollutants Through Atmospheric Transformation." ESRL, ORD,
USEPA, June 1984.
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Formaldehyde and acrolein are formed readily in a variety of
photochemical reactions involving emissions from many types of
natural and man-made hydrocarbon emissions. For formaldehyde, an
important contributor to total risk in this study, atmospheric
formation may produce several times the amount directly emitted
from all sources. This may explain some of the major differences
between the risks estimates obtained by using exposure models vs.
measured data.
Experimental evidence is also available that photooxidation
of compounds with little evidence of carcinogenicity, such as toluene
and propylene, produce substances with significant mutagenicity.
The compounds responsible have not been fully identified. In
other experiments, phosgene has been produced photochemically from
chlorinated hydrocarbons such as solvents. The studies suggest
that a hundred times more phosgene may be formed in the atmosphere
than is emitted directly. As a final example, studies of the
mutagenic activity of polycyclic organic particulates show large
increases in activity when the material is subjected to mixtures of
ozone and nitrogen oxides. Organic particulates are a ubiquitous
group of pollutants generally associated with incomplete combustion
(mobile sources, small units burning wood, coal, and oil). They are
represented by PIC in this report and may be a major contributor to
risks from air toxics in many communities.
Gasoline Marketing
Gasoline marketing includes a series of emission points ranging
from major bulk terminals to filling of individual vehicles at self-
service stations. These sources are receiving special attention within
EPA because of the significance of their emissions, the potential
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economic impact of control on thousands of service stations, the
alternative of onboard controls, litigation on benzene under Section
112, and the importance of gasoline marketing for ozone attainment
strategies. EPA's Gasoline Marketing Task Force has developed detailed
estimates of the risk from these facilities that cover benzene,
i
ethylene dibromide, ethylene dichloride, and gasoline vapors. The
Task Force estimated an aggregate incidence of 43 excess cancers
per year from all gasoline marketing sources, and this estimate
was used in portions of this study.
Woodstoves
As indicated in the Ambient Air Quality and 35 County studies,
products of incomplete combustion may be a significant hazardous
air pollutant problem. At present, there is great interest n
woodstoves based on recent studies that suggest that residential
wood combustion contributes about 40% of total national emissions
of polycyclic organic matter (POM). POM compounds found in wood
smoke include BaP and polycyclic organic ketones. In addition, one
EPA study suggests that the emissions rate of mutagenic and carcino-
genic substances from woodstoves is at least several orders of
magnitude greater than from other combustion sources used to heat
homes. Findings from the 35 County Study also support this concern,
i.e., roughly 80% of the annual estimated cancer incidence for BaP
from heating in the 35 counties is attributable to wood combustion.
There are currently no effects data on the human health risks
attributable specifically to wood smoke. As a result, the 35 County
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-55-
Study assessed the potential human health hazard posed by wood
combustion considering the health effects associated with only a
few individual compounds (BaP, formaldehyde, nickel, cadmium,
beryllium, and arsenic). The estimated annual cancer incidence
in the 35 counties resulting from exposure to these compounds is
32, including the use of BaP exposure as a surrogate for PIC.
EPA recognizes the need to explore woodstoves in more
detail and has established a committee that soon will recommend
research and regulatory initiatives to the Agency. These recom-
mendations will include: a comprehensive research program on
health effects, emission testing procedures, and control techniques;
establishment of a variety of technical assistance programs on wood
smoke; and consideration of a new source performance standard for
woodstoves. The Integrated Cancer Assessment Project (IACP), which
is scheduled to begin this fall, also plans to assess the contribu-
tion of woodstove emissions to the total organics, POM, and mutagenic
activity in the airsheds to be studied.
Sewage Treatment Plants
Sewage Treatment Plants have become a source of interest for
air releases based primarily on work undertaken by EPA's Integrated
Environmental Management Division (IEMD) in some of their geographic
demonstration projects. Preliminary findings suggest that many POTWs
located in urban areas with industrial indirect dischargers may emit
volatile organic compounds in excess of 100 kkg/year. Using a POTW
algorithm developed for the 35 County Study, we estimated an annual
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-56-
cancer incidence in the 35 counties of 2.3 for the nine pollutants
that were able to be considered.
Given the paucity of data on air releases from sewage treat-
ment plants, there is a need to explore this topic in more detail.
The IEMD will continue to monitor and model POTWs as part of its
activities in future work on geographic sites; EPA's Pretreatment
Task Force may also explore potential air emissions from sewage
treatment plants.
Hazardous Waste Combustion in Boilers
Although insufficient data were available to quantify the
problem of disposal of hazardous waste in boilers, the Office of
Solid Waste (OSW) has attempted to assess the risk resulting from
the burning of hazardous waste using a model boiler approach. OSW
has also just completed the Survey of Handlers and Burners of Used
or Waste Oil and Waste-Derived Fuel Material (Track 2) which should
provide useful information for future studies on risk.
The OSW model boiler approach considers three boiler sizes and
•
estimates exposure and risk for three metropolitan areas: New York;
Cleveland; and Los Angeles. These cities were chosen because they
represent a wide variety of exposure characteristics for densely
populated, highly industrialized areas. As information on quantity,
distribution and toxic content of the hazardous material burned was
limited at the time OSW initiated this analysis, this study tends
to depict a worst-case scenario. The study findings suggest that:
0 Risks to the most exposed individuals (MEI) are much
greater than to the average exposed individual (AEI).
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-57-
Lifetime individual risks for the MEI in these three
regions range from 5xlO~6 to 1.4x10-5, depending on the
boiler type.26
Risks to the AEI in these three regions ranged from 1.2x10-7
to 6x10"', depending on the boiler type.
0 Estimated annual cancer incidence in these three regions
range from .01 to .2, depending on the boiler type.
0 The risk associated with metals is potentially much higher
than that for organics. Using metal concentrations found
in virgin fuel, the analysis shows that metals contribute
roughly 52% to the total estimated incidence. The burning
of hazardous material with metal concentrations higher than
these could increase the problem.
OSW has just received the survey results and although the
analysis has just begun, some preliminary findings on the burning
of waste-derived fuel material (WDFM)27 are as follows:
0 924 million gallons of WDFM are burned each year; and
0 About 200 million gallons of this material are estimated to
be hazardous, as defined by the Resource Conservation and
Recovery Act (RCRA); and
0 Chemical manufacturing, pulp and paper, lumber, primary metals,
and petroleum refining industries burn about 90% of total WDFM.
26 "Draft Preliminary Risk Assessment for Burning Hazardous Waste in
Boilers." Office of Solid Waste, EPA. February 16, 1984, p.2.
27 "Status of the Data Collection Effort for the U.S. EPA:
Survey of Handlers and Burners of Used or Waste Oil and Waste-
Derived Fuel Material: Track II." December 1983, pp. 3-4. It
should be noted that WDFM is a broader category than hazardous
waste. For the purposes of the survey, WDFM was defined as "any
material that is a constituent of a fuel, or is destined to be
burned as a fuel, that is not a conventional fuel material."
Examples of conventional fuel are: distillate fuel oil; residual
fuel oil; natural gas; coal; liquified petroleum gas; and refuse-
derived fuels.
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OSW is initiating analyses to identify boiler operating practices;
characterize the specific wastes being burned; and determine the
quantity and geographic distribution of these hazardous wastes. This
information will be used to complete an exposure and risk assessment
that will support the Regulatory Impact Analysis for the regulation
of burning hazardous waste and used oil fuels. The tentative schedule
for completing this analysis is the end of FY 85.
Waste Oil Combustion
The Office of Solid Waste (OSW) estimates that 500 to 550
million gallons of used oil are recycled as fuels each year-28
Most of these fuels are burned in boilers, but may also be burned
in kilns, space heaters, and diesel engines. Because of contamina-
tion during use and because of mixing, used oils typically contain
elevated levels of toxic metals, such as arsenic and chromium, and
organics, such as BaP and PCBs. Burning used oils may result in
elevated ambient concentrations of some of these contaminants,
particularly when the combustion sources are clustered.^9 The
potential emissions of metals--lead, arsenic, cadmium, and chromium--
appear to be the most significant. The 35 County Study also found
these substances to be important. We estimated a total annual
28 U.S.EPA, "Composition and Management of Used Oil Generated in
the U.S." December 1983.
29 U.S.EPA, "A Risk Assessment of Waste Oil Burning in Boilers
and Space Heaters." Draft, January 1984.
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-59-
cancer incidence of 6.7 from waste oil combustion in the 35 counties.
Chromium accounted for most of the incidence (90%), followed by
arsenic (9.5%) and cadmium (0.5%).
OSW is currently developing emission standards for waste oil
combustion and will evaluate these risks more closely, for inhalation
and other exposure pathways.
Hazardous Waste. Faci Titles
Over the past several years, there has been an increasing
concern that treatment, storage and disposal facilities (TSDFs)
may be an important source of air emissions. There have been many
efforts to quantify releases of volatile organic compounds from
TSDFs. In general, these analyses have either focused on individual
facilities, using ambient monitoring to estimate atmospheric pollutant
concentrations, or on national estimates, employing emission models
to assess air releases. In addition, Westat, Inc. recently completed
an extensive survey of TSDFs for the Office of Solid Waste (OSW) that
provides a great deal of background information on the quantity,
constituency and distribution of hazardous waste generated and managed
by TSDFs throughout the country.
The recently completed survey estimates that a total of
71.3xl09 gallons (264xl06 metric tons) of waste is managed by
hazardous waste facilities and that over 50% of this quantity is
treated, stored and/or disposed of in impoundments and landfills.
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In addition, the survey indicates that over 70% of the total
hazardous waste is generated by the chemicals industry. If we
make the assumption that a substantial amount of the chemical
industry's waste consists of volatile organic compounds, there is
a clear potential for significant volatile releases from TSDFs.
Although the survey information yields some interesting
findings on the types and quantity of hazardous waste managed
at TSDFs, it is nonetheless one step removed from actual emission
estimates. There have been several recent attempts to estimate
releases from TSDFs at the national level using emission modeling.
Unfortunately, these studies have come under severe criticism.
It is apparent that estimating volatilization from TSDFs is still
in its infancy and these models generally require further refinement
and validation.
The monitoring data on ambient concentrations around specific
TSDFs is probably more persuasive in making the case that TSDFs
are potentially significant sources of air toxics. We used air
toxics concentration data from a study of one TSDF, the BKK land-
fill in California,30 to explore the potential hazard from the
volatilization of organic compounds. This was the only data set
found that attempted to capture actual ambient concentrations to
which individuals living around the TSDF would most likely be
exposed. The results are presented in Table 7. It is important
30 "Ambient Air Monitoring and Health Risk Assessment for Suspect
Human Carcinogens around the BKK Landfill in West Covina."
California Department of Health Services, California Air
Resources Board and South Coast Air Quality Management District.
1983.
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-61-
TABLE 7
PRELIMINARY ESTIMATES OF INCIDENCE AND INDIVIDUAL RISKS ASSOCIATED WITH
AIR RELEASES FROM ONE TREATMENT, STORAGE AND DISPOSAL FACILITY
Pollutants Havi ng
Some Evidence of Concentration**(ug/m3)
Carcinogeni city* Max M i n
Preliminary Approximati on
of Individual Lifetime Risk***
Max Min
Benzene
Chloroform
Vinyl Chloride
Perch loro-
ethy lene
Trichl oro-
ethy lene
Et hy 1 ene
di chlori de
Total Additive
3.8
1.0
12.1
6.8
5.4
6.3
Li fetime Ri sk
0.0
0.0
0.0
0.0
2.1
0.8
2.6x10-5
l.OxlO-6
3.2x10-5
1.2x10-5
2.2x10-5
4.4x10-5
1.4x10-4
0.0
0.0
0.0
0.0
8.6x10-
5.6x10-
1.4x10-5
6
6
* The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purposes of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Concentration data source: California Department of Health
Services, California Air Resources Board and South Coast
Air Quality Management District. "Ambient Air Monitoring and
Health Risk Assessment for suspect Human Carcinogens around
the BKK Landfill in West Covina." 1983.
*** Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of lifetime individual
risk. These estimates are drawn from measurements made at one TSDF,
and should not be considered representative of usual TSDF emissions,
but rather illustrative of potential TSDF emissions.
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-62-
that these numerical estimates be interpreted as an isolated
example, providing only a rough indicator of risk. The numbers
exhibited in this table suggest that risks around this landfill
are similar to those near major point sources. The lifetime
individual risks for the highest observed values range from
10~5 to 10~6; tne maximum additive lifetime individual risk for the
six compounds is 1.4 x 10*4.
Superfund Sites
As with hazardous waste facilities, there is evidence suggesting
that uncontrolled or abandoned hazardous waste facilities, i.e.,
Superfund sites, may be significant sources of air toxic releases.
Information provided by the Hazard Ranking System (MRS) [40 CFR Part
300: Appendix AJ, is one indication of this potential.
For an abandoned hazardous waste site to be listed as a Superfund
site and placed on the National Priorities List (NPL), the site must
receive a specified score using the HRS. In the HRS, air releases
must be significantly above background concentrations and "observed"
in order to receive a score. In contrast, only a "potential" for
release to surface or ground water is required in the HRS. The
requirement for an observed release for air resulted from a lack of
any better method for considering the air route; no good, consistent
correlation was found between physical/chemical properities of
wastes and their potential for air migration. To date, the HRS has
placed 109 sites on the NPL due to high air scores. Of these, 43
were listed for particulate, heavy metal or radium releases. The
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remaining 67 sites are those with volatile organic compounds.
These 109 facilities represent a total of 16% of all currently
listed NPL sites.
Municipal waste disposal: incinerators and landfills
Few attempts have been made to assess the risks that may be
attributable to air toxics emissions from municipal incinerators and
municipal landfills. Our search for risk assessments on municipal
waste treatment led to only one study designed specifically for
the purposes of assessing risks. In this study, dioxin emissions
from several municipal incinerators were measured, and maximum
individual risks estimated at levels varying from 10-5 to 10-6.31
The investigators concluded that the levels of dioxin from the six
incinerators monitored did not present a public health hazard for
the residents living in the immediate vicinity.
In another EPA-sponsored analysis, very preliminary estimates
were made of emissions of several metals and organic compounds from
municipal incinerators. These estimates indicated that maximum
individual risks from poorly-run facilities may in certain cases
exceed those measured in the dioxin risk assessment described above;
well-run facilities appear to pose risks approximately 10 to 100
times less than those of poorly-run facilities.32 These latter
estimates could be performed only by using a variety of assumptions,
31 TCDD Emissions from Municipal Waste Combustors. Memorandum from
Michael Cook to Regional Dioxin Coordinators. U.S. EPA, Office
of Solid Waste and Emergency Response. Dec. 16, 1983.
32 David Sussman, U.S. EPA Office of Solid Waste. Pers. comm.
June 1984.
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since no systematic program has been undertaken to monitor stack
emissions from municipal incinerators for the purposes of risk analysis.
No broad-based studies characterizing risks due to air toxics
emissions from municipal landfills were identified. However, there
is speculation that emissions may in some cases be high due to
decomposing plastics, discarded solvents, and mobilization of volatile
organics to the atmosphere by methane gas. Two ad hoc studies
performed at municipal landfills on Long Island and in the Los
Angeles area provide preliminary confirmation of such speculation.
At the Long Island landfill, vinyl chloride was detected in the
landfill gases at 90 ppm; at the Los Angeles landfill, landfill gas
concentrations of vinyl chloride reached 20 to 30 ppm, and ambient
levels near the landfill exceeded those found away from the land-
fill. 33»34 in addition, stack emissions of vinyl chloride from a gas
collection facility at this same Los Angeles landfill exceeded the
vinyl chloride NESHAP emission limit (10 ppm) established for other
source categories; Since their initial detection, these emissions
have been abated. The Los Angeles air pollution control authorities
are currently conducting a monitoring program near selected Los
Angeles landfills to evaluate the need for air emissions controls.
Drinking Water Treatment Facilities
The Office of Drinking Water and the Office of Policy Analysis
are conducting a study of air emissions from aeration facilities
at drinking water treatment plants. Aeration is used to remove
volatile organics from surface water before it is pumped to
33 Marcus Kantz, EPA Region 3. Personal communication. May 1984.
34 Edward Camarena, South Coast Air Quality Management District,
Personal Communication. June 1984.
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-65-
residential communities for use. A second issue regarding these
facilities concerns potential air emissions of chloroform from
chlorination of drinking water supplies. In lEMD's monitoring
program in Philadelphia, the highest ambient concentrations of
chloroform were measured at the monitoring site on the grounds
of the drinking water treatment plant. These findings are still
preliminary and must be examined in greater detail.
Sewage Sludge Incineration
EPA's Office of Water Regulations and Standards and the Office
of Policy Analysis are examining the issue of air emissions from
sewage sludge incineration. The Water Office is specifically
interested in whether the New Source Performance Standard (NSPS)
for sewage sludge incinerators promulgated under the Clean Air Act
is adequate. The NSPS regulates emissions of particulate matter, but
does not consider the potential health effects of the toxic constituents
of those emissions.
PATHWAYS
Ingesti on
This study considers inhalation effects only. The quantitative
risks due to human ingestion of air pollutants are not covered,
although several such pathways are possible and anecdotal examples are
available. In Tacoma, Washington, researchers discovered that
children living near the ASARCO copper smelter have elevated levels
of arsenic in their urine; one possible exposure route is via
ingestion of contaminated soil. Fish in Lake Superior contain
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-66-
toxaphene that was deposited in the lake after being carried by the
wind from areas where toxaphene was used as a pesticide. In Maryland,
some analyses suggest that as much as 30% of some metals loadings
to the Baltimore Harbor may be due to air deposition, either direct
deposition or urban runoff. Half of the 1000+ chemicals inventoried
in the Great Lakes appear to result at least in part from air
deposition.
Stratospheric Ozone Depletion and Skin Cancer
The analysis did not consider the possible health effects
caused by a reduction in the stratospheric ozone layer. Carbon
tetrachloride, and other chlorinated organics with long atmospheric
lifetimes, have the potential to affect the ozone layer, and could
indirectly increase the incidence of skin cancer. For example, it
is estimated that by the year 2020 U.S. emissions of carbon tetra-
chloride could be responsible for between 500 and 22,000 excess
cases of skin cancer annually in the U.S., resulting in 3-220
excess deaths per year-
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C. Summary of the Magnitude of the Air Toxics Problem
Estimated risks from air toxics have been presented for each
major analytical study: the NESHAP Study, the 35 County Study, and
the Ambient Air Quality Study. The results differ among the three
studies because of differences in technical approaches, pollutants
and sources covered, and emissions estimates, making interpretation
and integration of the disparate results difficult. The most useful
statistic for summarizing the results of all three studies seems to
be annual incidence per million population. Table 8 summarizes this
statistic for the 17 pollutants/pollutant groups for which sizeable
risks were estimated in any of the three analyses. It should be
noted that these national estimates were derived differently in each
of the studies: those from ambient air data weighted urban and rural
population and concentrations to arrive at a national average; the
national aggregate values calculated for the NESHAPS Study and for
asbestos, radionuclides, and gasoline marketing were spread over the
total national population of 230 million; and the population living
in the 35 counties was used to calculate incidence per million for
the 35 County Study.
The estimated annual incidence per million people for the
pollutants included in this report were 7.1 for the NESHAPS analysis,
8.9 for the Ambient Air Quality Study, and 5.5 based on the 35 County
Study. These totals are surprisingly close. However, this closeness
is somewhat coincidental and disguises large inconsistencies in the
pollutant-by-pollutant estimates. For instance, chromium accounts
for only 0.29 cases per million in the 35 County study and 1.43 in the
Ambient Air Data Analysis. Volatile organic compounds contribute a
total of 3.1 per million based on the ambient measurements and only
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0.8 for the NESHAPS data. A major contributor to these estimates is
the pollutant category we have labeled products of incomplete combustion
(PIC). It is unique among the pollutants examined and deserves
special mention. PIC is used in this study to represent a large
number of air pollutants associated with lung cancer in epidemiological
studies of people exposed in the 1940's and 1950's. We assumed that
*
these exposures were dominated by products of incomplete combustion.
The unit risk factor was derived by using B(a)P as a surrogate for
PIC, and is based on these epidemiological studies. This method of
quantifying risk is unusual and the fact that major risks are calculated
for PIC makes the calculation controversial. The alternative is to
exclude PIC and to ignore the implications of the epidemiological
studies and the contribution of these compounds, some of which are
proven carcinogens. More detail on the deviation of the unit risk
value for PIC is provided on pages 21 to 26.
Although incidence per million population is an important
statistic, aggregate national totals also provide perspective and
allow comparison with other cancer statistics. The annual inci-
dence estimates derived from the incidence rate for the major analyses
(Table 8) are:
NESHAPS - 1,633 (national estimate)
Ambient Air - 2,047 (national estimate)
35 County - 231 (for 35 counties only)
Individual lifetime risk is another way of expressing risk
and was included in most of our studies. Individual lifetime risk
estimates describe the risk to a specific individual at a specific
location (usually the worst-case site), whereas aggregate incidence
applies to an entire population. Partially because of methodology,
maximum individual risks almost always occur within 0.1 and 0.3 km from
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TABLE 8
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SUMMARY TABLE: PRELIMINARY APPROXIMATION OF ANNUAL INCIDENCE
ESTIMATES PER MILLION POPULATION FROM THE NESHAPS STUDY, THE
AMBIENT AIR QUALITY STUDY AND THE 35 COUNTY STUDY**
Po 1 lutants Ha vi ng
Some Evidence of
Carcinogeni city*
NESHAPS
Ambient Ai r
Data
35 County
Study
Six Month Study Risk Estimates
Formaldehyde 0.01
Benzene 0.14
Ch romi urn"1" 1.43
Cadmi urn 0.07
Nickel1" 0.35
Arsenic 0.02
Trichloro-
ethylene 0.04
Perch 1oro-
ethylene 0.01
Ethylene di-
chloride 0.19
Ethylene oxide 0.21
Carbon tetra-
chloride 0.06
0,
1,
1.
0.
0,
83
08
05
06
07
0.26
0.1 1
0.11
N/A
N/A
0.37
0.21
0.39
0.29
0.02
0.02
0.02
0.15
0.14
0.03
N/A
0.004
* The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purposes of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of incidence. Estimates
for individual compounds are much less certain. These incidence esti-
mates have been performed to provide a rough idea of the possible total
magnitude of the air toxics problem, and will be used only for priority-
setting and to provide policy guidance.
Risk estimates assume that all species of chromium and nickel are
carcinogenic, although only certain species have evidence of carcino-
genicity. Current data do not allow differentiation among species.
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TABLE 8 (Cont.)
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SUMMARY TABLE: PRELIMINARY APPROXIMATION OF ANNUAL INCIDENCE
ESTIMATES PER MILLION POPULATION FROM THE NESHAPS STUDY, THE
AMBIENT AIR QUALITY STUDY AND THE 35 COUNTY STUDY**
Pol lutants Ha vi n
Some E vi dence of
Carcinogeni city*
Ethylene di-
bromi de
Chi orof orm
Gasoline vapors
All other
Risk Estimates f
Radi onucl i des
Asbestos
PIC***
Gasol i ne Market
TOTAL
9
AMBIENT AIR
NESHAPS DATA
0.12
< 0.01
N/A
0.10
rom Other EPA Efforts
0.08
0.50
3.57
ing 0.20
7.1
N/A
0.46
N/A
0.14
0.08
0.50
3.57
0.20
8.9
35 COUNTY
STUDY
0.02
0.002
0.15
0.34
0.08
0.50
3.10
5.5
* The weight of evidence of carcinogenicity for the compounds listed
varies greatly, from very limited to very substantial. Further, the
extent of evaluation and health review performed varies considerably
among compounds. However, for the purposes of this report, a conser-
vative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates,
they should be regarded as rough approximations of incidence. Estimates
for individual compounds are much less certain. These incidence esti-
mates have been performed to provide a rough idea of the possible total
magnitude of the air toxics problem, and will be used only for priority-
setting and to provide policy guidance.
*** "Products of Incomplete Combustion" (PIC) refers to a large number of
compounds, probably consisting primarily of polynuclear organics. The
PIC unit risk value was derived from dose-response data which use B(a)P
levels as a surrogate for PIC or total air pollution. There are many
limitations of using the B(a)P surrogate method to estimate PIC risks:
all PIC estimates presented in this report must be regarded as highly
uncertain. Refer to pp. 21-26 for a more detailed explanation of how
the PIC unit risk value was derived.
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the fenceline of major sources. The values are very susceptible to
errors in modeling assumptions, population location, and emission
estimates, and it is difficult to interpret the results of national
studies. In our analysis, maximum risks near point sources frequently
reached one in a thousand (10~3) or greater and were routinely
greater than 10~4. For example, in the NESHAPS study, 12 pollutants
presented a risk of lxlO~3 or greater in at least one location, and
25 pollutants (nearly half of those studied in the NESHAPS analysis)
presented risks greater than 1x10"^.
The ambient air data were used to calculate an aggregate
individual risk for multi-pollutant exposures. Since these
aggregate individual risks were based on measured data for a
specific sampling site, they were subject to less uncertainty than
most of the risk estimates in this report and may be used as an
important indicator of the general magnitude of the urban air
toxics problem. However, the amount of data available fall short
of that needed for a comprehensive analysis of any of the urban
areas and the results should not be used for city-to-city comparison.
Since reasonably complete monitoring data were needed to
estimate these aggregate risks, only a few urban areas with the best
data bases could be included. Generally, these were large cities
with medium to heavy industrialization. The additive risks ranged
from 0.7x10-3 to 2.6x10-3 based on measurements of two to three metals,
BaP as an indicator for PIC's, and six to ten volatile organics
monitored at the same or very proximate locations (Table 5). These
locations generally were in center city and were not associated
with specific point sources.
It is not possible to estimate the number of people exposed
to such multi-pollutant risks. However, it is interesting to
compare them to the estimates of annual incidence per million
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reported earlier. A lifetime risk of 2.6x10-3 equates to 2,600
excess cancer cases per million population for a 70-year period,
or 37 per million per year; a lifetime risk of 0.7x10-3 equates
to about 10 per million per year. These estimates are compatible
with the average incidence numbers presented in Table 8.
D. Perspective and Context: Other Cancer Risks
One way to evaluate the importance of the air toxics risks
presented above is to compare them to those linked to other factors.
For example, Doll and Peto estimate that about 65% (286,000) of annual
cancer deaths appear to be related to smoking (30%) or diet (35%), and
that about 2% of total cancer deaths (8800) are associated with
environmental pollution.35
The magnitude of the air toxics problem presented in this study
is given for PIC in terms of cancer deaths, and as cancer cases for
other pollutants. Therefore, they should be compared both to statistics
regarding total cancer cases and cancer deaths. Table 9 presents
estimates of 1983 cancer mortality and morbidity made by the American
Cancer Society-36 This table shows that about 850,000 cancer cases and
440,000 cancer deaths were projected for 1983. The ACS reports also
that 135,000 lung cancer cases and 117,000 lung cancer deaths are
projected for 1983.
If indoor air exposures are considered, this analysis may
not accurately estimate the potential number of cancers associated
with air toxics exposures. Historically, indoor, non-occupational
air quality has been virtually ignored by EPA and other Federal
35 Doll, Richard, and Richard Peto. "The Causes of Cancer:
Quantitative Estimates of Avoidable Risks of Cancer in the United
States Today." Journal of the National Cancer Institute. June, 1981
36 American Cancer Society, 1982. Cancer facts and figures, 1983.
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TABLE 9
PERSPECTIVE AND CONTEXT:
STATISTICS ON CANCER RISKS*
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TOTAL ESTIMATED CANCER CASES (1983)*
850,000 (3700/mi 1 lion)
TOTAL ESTIMATED CANCER DEATHS (1983)*
440,000 (1900/million)
Diet**
Smoki ng**
Environmental pollution**
154,000 (670/million)
132,000 (570/mi1 lion)
8,800 (38/million)
CANCER CASES ASSOCIATED WITH INDOOR AIR EXPOSURES
***
Radon 1,000 to 20,000
Passive smoking 3,000 to 14,000
Formaldehyde (conventional homes) 160
(4 to 91/mil. )
(13 to 61/mil. )
(0.7/million)
Other organics (PCE, TCE,
benzene)
No risk estimates available;
however, indoor levels
exceed outdoor levels by
several times.
**
Source: American Cancer Society, 1982. Cancer Facts and
Figures, 1983.
These estimates are presented for illustrative purposes only,
since many consider that such attribution of cancer cases to
a particular exposure oversimplifies the multi-causal nature of
cancer. The estimates were derived by combining the estimated
percent of cancer deaths attributed to diet, smoking, and pollu'
tion presented in Doll and Peto (see reference 35) with the
American Cancer Society estimates of total 1983 cancer deaths
(reference 36).
*** Source: see reference 37.
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agencies despite the fact that the average American spends about
80% to 90% of his or her time indoors. Recent data show that
indoor radon exposures may cause from 1,000 to 20,000 lung cancer
cases annually, and EPA estimates show that 3,000 to 14,000 cancer
cases may be caused by passive smoking.37 in addition, indoor levels
of formaldehyde routinely exceed outdoor levels by an order of
magnitude, while indoor levels of other organics such as benzene,
trichloroethylene, and tetrachloroethy1ene may exceed outdoor
levels by 2 to 5 times for the median-exposed individual and up to
50 times for the most-exposed individual.38 Combined with the
large amount of time that Americans spend indoors, these data
indicate that our estimates of the magnitude of the air toxics
probl em--based only on outdoor ambient levels—may underestimate
the extent of the toxics inhalation problem as far as certain
organic compounds are concerned, since these compounds can be
be emitted indoors.
It is also possible that our analysis has somewhat overstated
risks due to the metals examined in the study- No indoor/outdoor
data could be found for the specific metals examined in this study;
however, there are limited data indicating that other trace
metals (e.g., vanadium, manganese) show indoor/outdoor ratios
somewhat less than 1.0.37
37 Thomson, Vivian. "Indoor Air Pollution: Ramifications for
Assessing the Magnitude and Nature of the Air Toxics Problem
in the United States." U.S. EPA, Office of Policy Analysis.
July 1984.
38 Wallace, Lance et a 1. "Total Exposure Assessment Methodology
(TEAM) Study: FT rst Season - Northern New Jersey." Interim
Report. U.S. EPA, Office of Research and Development.
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Few data are available characterizing the cancer risks due
to ambient environmental exposures other than air pollution. As
part of this study, EPA's Chemical Coordination Staff (CCS) attempted
to compare regulatory risk levels across several of EPA's program
offices. CCS concluded that such comparisons are difficult to
make, since EPA has in fact made few regulatory decisions for car-
cinogens based on quantitative risk assessment. However, a few
examples of risk-assessment based decisions were found. For instance,
the EPA recently banned most uses of the pesticide ethylene dibromide
after estimating that EDB exposures might cause as many as 13,000
cancer cases per year. EPA has also banned most uses of chlordane/
heptachlor, based on estimates of 500 cancer cases caused annually,
and the asbestos school inspection program was started after risks
were estimated at approximately 60 cancer cases annually.39
As previously discussed, the maximum individual risks estimated
in this study ranged widely, from 1Q-1 to less than 10~6. Risks of
10~3 ancj greater were commonly estimated for major point sources, and
the combined lifetime individual risks based on ambient data were
•
in the 10"3 range. CCS's analysis shows that, on average, EPA has
taken regulatory action based on maximum individual risks in the
10~3 t0 iQ-4 range, although there may be differences among program
offi ces:
Although the data is somewhat limited, OAR (the Office of Air
and Radiation) generally appears to use a marginally higher
level of individual risk (both before and after regulation)
than other offices. However, when viewed from an aggregate
risk perspective, risks to the total population are not much
different from those of other offices."
39 Viviani, Donn et a!. " Acceptable Risk Levels and Federal Regula-
tions: A CompaTTson of National Emission Standards for Hazardous
Air Pollutants (NESHAP) with Other Federal Standards Based on
Quantitative Risk Assessment." U.S.EPA, OPTS. May 1984.
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IV. NATURE OF THE AIR TOXICS PROBLEM
Whereas previous sections of this report focused on the
magnitude of the national air toxics problem, the following section
will discuss the causes of air toxics exposures and risks. Four
questions will be addressed, using the results of the studies and
analyses previously discussed:
- Pol lutants
What pollutants appear to cause most of the air toxics problem
as we understand it now?
- Sources
What sources appear to be major contributors to air toxics
risks?
ic variability
Do air toxics problems vary geographically?
- Indirect control
Can we estimate the degree to which indirect control of
air toxics is effected through the criteria pollutant programs?
A. Pollutants
Table 8 summarizes the annual incidence per million population
estimated by the NESHAP Study, the Ambient Air Quality Data analysis,
and the 35-County Study for the pollutants/pollutant groups showing
the highest risks. Table 8 shows that approximately 17 pollutants/
pollutant groups account for most of the risks: PIC, chromium,
nickel, benzene, arsenic, cadmium, carbon tetrachl ori de, chloroform,
ethylene dibromide, ethylene dichloride, ethylene oxide, formaldehyde,
gasoline vapors, perch loroethyl ene, tri chl oroethyl ene, asbestos, and
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radionuclides. Thus, it appears that the pollutants responsible for
most of the cancer cases associated with air toxics consist of a
mixture of metals, volatile organic compounds, and products of incomplete
combustion. Many of these same pollutants (for example, chromium,
benzene, and arsenic) also show maximum individual risks in the 10-1
to 10-3 range.
An interesting feature of the analysis is the relatively low
aggregate risk estimated for many of the synthetic organic chemicals:
national incidence totalled less than 1.0 cancer cases per year for
21 such compounds. This fact is noteworthy since it has been speculated
that such "exotic" chemicals may be major sources of air toxics
risks. The reader should bear in mind, however, that the low incidence
estimates are based on exposure modeling, and have not been verified
by ambient data. In addition, maximum individual risks associated
with some of these chemicals ranged up to 10~3.
B. Sources
An examination of emissions associated with the pollutants listed
above shows, not surprisingly, a diverse and complex group of sources.
Table 10 gives a source breakdown for several of the more important
pollutants examined in the study. For example, chromium is emitted
from major point sources such as steel and refractory manufacturing,
as well as from fuel combustion. Formaldehyde is emitted from mobile
sources, chemical plants, fuel combustion, indoor sources (such as
particleboard), and is formed photochemically in the atmosphere.
Carbon tetrachloride is set apart from the rest of the major risk
pollutants in that it has an unusually long half-life estimated to
exceed 35 years. Thus, although the short-term risks from direct
emissions of carbon tetrach1oride may be low (as indicated by the
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TABLE 10
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SOURCES OF SELECTED COMPOUNDS EXAMINED IN THIS STUDY
Pollutant
Sources
Arsenic
Benzene
Ch1oroform
Ch romi urn
Ethylene Oxide
Formaldehyde
Nickel
Perchloroethylene
PIC
Combustion sources such as waste oil
burning, utility boilers (coal-fired),
wood smoke, smelters, glass manufacturing
Road vehicles, gasoline marketing,
petroleum refining
Solvent usage, water treatment
Waste oil burning, steel manufacturing,
refractory manufacturing, metals
manufacturing, combustion sources
Chemical industry, sterilant
Road vehicles, formaldehyde manufacturing,
petroleum refining, oil and gas combustion
Combustion sources
Solvent usage, dry cleaning facilities
BaP sources include use of wood and coal
in small combustion units, coke operations,
internal combustion engines
Trichloroethy lene
Solvent usage
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NESHAP and 35-County Study), ambient levels will continue to increase:
half of 1984 emissions will still be in the atmosphere in 2019.
The complexity and diversity of air toxics sources are under-
scored by the following observations concerning emissions of the
most significant pollutants listed in Table 8.40
- SOCMI sources are responsible for greater than 20% of total
emissions for only 3 of the major pollutants.
- Mobile sources account for greater than 20% of emissions for
only 3 of the major pollutants.
- Solvent usage is responsible for greater than 20% of emissions
for only 3 major pollutants.
- Fuel combustion in stationary sources accounts for greater than
20% of emissions for only 4 of the major pollutants.
Another orientation to which source types appear to be important
contributors to the air toxics problem can be had by using the
individual risk or incidence estimates from the NESHAP and the 35
County Studies. For pollutants that were evaluated directly, area
and point sources each accounted for about half of the aggregate
incidence (45 percent for area sources, 55 percent for point sources
for the NESHAP study; 53 percent area, 47 percent point in the 35
County Study). When PIC is included (using BaP as a surrogate) area
sources become more dominant, accounting for 85 percent of the incidence
in the 35 County Study and 75 percent of total incidence estimated
based on the NEHSAP study. This result is consistent with the fact
that PIC is estimated to account for a large portion of aggregate
Lahre, Tom. "Characterization of Available Nationwide Air Toxics
Emissions Data." June 13, 1984.
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incidence and that nearly all BaP emissions appear to come from area
sources (principally motor vehicles, and combustion of wood, coal and
oil in small heating units). The contribution of the most significant
source types based on cancer incidence as determined by the 35 County
Study are shown in Table 11.
The second measure of risk used in this study is maximum individual
risk. The NESHAP study indicates that the highest individual risk is
generally associated with large point sources.
C. Geographic Variability
A final method of characterizing the nature of the air toxics
problem is to examine geographic variability in ambient air quality
and in air toxics risks. Mean ambient concentrations for selected
metals and organic compounds are shown for several cities in Table 12.
These data may be for different years and are not for matched sites;
therefore, detailed comparison is not warranted. However, they do
indicate that ambient levels of air toxics can vary widely from city
to city, with ratios commonly ranging from 5/1 to 10/1.
The 35 County Study also allowed us to examine the ways in which
risks vary from one county to the next. The results are shown in
Table 13 (PIC was excluded from this data set because the uncertainty
in the emission estimates for BaP make detailed city-specific compari-
sons especially unreliable). For example, the percent of risk from point
sources varies from 52 percent in in County 4 to 25 percent in County
2. Similarly, petroleum refining accounts for 22% of total risk in
County 2, but Q% in Counties 3 and 4. There are, however, source
categories (road vehicles and waste oil burning) that account for
approximately the same percent of risks across counties, primarily
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TABLE 11
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PERCENT OF INCIDENCE ASSOCIATED WITH POINT AND AREA
SOURCES BASED ON THE 35 COUNTY STUDY*
Point Sources
Chemicals Production
Metals Manufacturing
Petroleum Ref i ni ng
Rubber Production
Utilities
POTWs
All Other
% Total
Inci dence
(w/o PIC)
1 1
8
5
5
4
3
11
% Total
Inci dence
(w/PIC)
4
3
2
2
1
1
4
TOTAL POINT
47
15
Area Sources
Road Vehicles
Solvent Usage
Gasol i ne Marketi ng
Waste Oi 1 Burni ng
Heati ng
Wood smoke (stoves/fireplaces)
All other
TOTAL AREA
23
1 1
9
9
0.5
1.5
53
60
4
3
3
12
3
85
* Because of the uncertainties in the incidence estimates used to
derive these estimates, they should be regarded as rough indicators
only. These computations have been performed to provide a rough
idea of the nature of the air toxics problem, and will be used only
for priority-setting and to provide policy guidance.
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TABLE 12
COMPARISON OF MEASURED AIR QUALITY FOR SELECTED CITIES
AND POLLUTANTS; ngm/m3
City
Pollutant ABC
Arsenic* 7.4 3.7 3.2
Benzo(a)pyrene 1.7 0.5 0.2
Chromium* 93.5 9.3 25.3
Nickel* 18.6 3.0 24.8
Benzene** 11.0
Carbon tetra-
chloride** 4.2
Chloroform** 9.9
Methyl chloro-
form** 17.1
Trichloro-
ethylene** 1.4
D E F G
33.5 7.0 6.0
0.3 0.2 0.4
13.4 17.0 60.0
8.6 18.0 23.0
14.8 15.7 9.5
0.3 2.4 2.6
0.4 1.5 7.9
6.3 2.2 25.1
2.0 0.4 2.8
* Concentrations expressed in nanograms/m3.
** Concentrations expressed in micrograms/m3.
-------
TABLE 13
COMPARISON OF SOURCES OF RISK IN SEVERAL COUNTIES SELECTED FROM 35 COUNTY STUDY
* **
All 35
County 1 County 2 County 3 County 4 County 5 Counties Combined
Percent of risk from area sources, point sources, and POTW's
Area
Point
POTW's
61
38
1
66
25
9
Percent of risk from given source categpries
48
50
2
41
52
7
67
32
1
51
46
3
Road vehicles 31
Petroleum refining 13
Chemical production 5
Solvent usage 8
Waste oil burning 8
26
1
3
18
11
23
22
21
5
9
14
0
24
10
12
31
0
2
17
10
23
5
10
10
8
00
Percent of risk from given pollutants
Formaldehyde
Chromium
Benzene
Vinyl chloride
Perchloroethylene
18
9
30
2
10
7
14
24
0
10
29
8
24
2
3
5
10
20
25
6
30
12
25
0
11
12
17
23
11
8
* For pollutants evaluated directly; excludes PIC.
**
Because of the uncertainties in the incidence estimates used to derive these estimates, they should
be regarded as rough indicators only. These computations have been performed to provide a rough
idea of the nature of the air toxics problem, and will be used only for priority-setting and to
provide policy guidance.
o
o
o
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because these risks are strongly linked to population. Thus, two
main types of sources appear to emerge from the analysis: sources
accounting for approximately equal portions of risk from one area to
the next, and those sources peculiar to a particular area. While the
data bases used in these analyses are at present inadequate'to accurately
define most areas' air toxics problems, the data do support the
intuitive prediction that reducing air toxics risks will necessitate
dealing with certain types of problems at the local level.
If we consider air toxics emissions data, we also find regional
variation. For example, of the 86 compounds covered in the emissions
study^l, a large concentration of organic substances were found
to be produced in an area stretching from Corpus Christi, Texas to
New Orleans, Louisiana. Eighteen organic compounds are produced
entirely in Texas and Louisiana and almost 50% of the remaining 88
organic compounds examined in the emissions study are manufactured
in those two states. As noted earlier in the report, emissions of
many of the synthetic organics are associated with only very low
annual i nci dence.
D. Indirect Control of Air Toxics
Toxic compounds are emitted into the atmosphere from many
sources that are regulated for criteria pollutants. Metals and
*
polynuclear compounds usually are emitted as particulate matter and
most of the volatile organic compounds are ozone precursors. As
such, they are regulated under SIP's, NSPS, and Title II on motor
Lahre, Tom. Op. cit.
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vehicles. Also, reduction in emissions for some of the compounds--
especially solvents--are accomplished for economic reasons to
recover lost product or energy.
We attempted to evaluate available analyses on the effects of
such indirect control of toxic air compounds.42 TWO studies were
found. One focused on nine potential air toxics, including benzene,
chloroform, and chromium, and evaluated the impact of existing
regulations on major point sources. Control of metals from point
sources was generally high, ranging from 80 to 98%. Much more
variation and less control was apparent for organics, with the
percentage control ranging from 30 to 90%.
A second study was less quantitative but provided estimates
for 37 compounds and included area sources and motor vehicles. Air
quality trends, rather than control regulations, were evaluated to
estimate the indirect control of toxic particulates. Generally,
reductions of 30 to 70% have been observed since the 1950's. In
addition, SIP's and NSPS are credited with reducing emissions of
15 chemicals from the chemical industry by 10 to 80% and 8 solvents
by 30% nationwide. Motor vehicle controls remove up to 90% of
several potentially toxic compounds from exhaust gases.
It is apparent, even from these cursory analyses, that indirect
control can be very significant for toxic compounds. At this time,
it appears that control under criteria pollutant provisions of the
Clean Air Act far exceeds the impact of Section 112 regulations.
Since sources are already controlled by criteria pollutant programs,
the remaining risks will probably be more difficult to control.
42 Lahre, Tom. Op. cit.
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V. ADEQUACY OF DATA BASES
There are two principal informational problems in the
quantitative assessment of air toxics risks. The first involves
basic health factors such as evidence of carcinogenicity, potency,
the presence or absence of thresholds, and synergism. These are
well-known knowledge gaps basic to cancer, and strategic discussions
on air toxics will not influence their resolution. No attempt was
made in this study to use new assumptions or procedures; we relied
on techniques and methods in use across EPA.
In the short term, the more relevant problem to understanding
the air toxics issue is the lack of data on emissions and air
quality that makes difficult solid problem definition for many
situations and impedes policy discussions on risk assessment. The
problem is widely recognized and universally frustrating. In the
poll of State/local agencies, ten were interviewed in depth on
their air toxics problems. All perceived a need for better emissions
data. The contractor who conducted the interviews concluded that •
"The agencies do not seem to have adequate data that would enable
them to perform risk assessments for the toxic pollutants emitted."43
With the exception of radonuclides, the study consistently
found major weaknesses in the data base for air toxics, both in the
43 Radian Corp. "Definition of the Air Toxics Problem at the
State/Local Level." EPA Contract No. 68-02-3513; Work
Assignment 45, June 1984.
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coverage and in the quality of information available. If more
than one source of data existed, inconsistencies were the norm.
Most of the air quality data could not be used for population
exposure and were clearly not obtained for risk assessment purposes.
Many potentially large source categories could not even be included
in the study due to a lack of data. These sources included
incineration, hazardous waste disposal, atmospheric formation,
and Superfund sites.
Today, air quality data are generally collected to determine
trends for criteria pollutants; very few data are available for
developing population exposure estimates for toxics. Despite
significant efforts to assemble monitoring data for all sources,
this analysis could only cover about eighteen pollutants.
!
0 More air quality data were found for metals than for B(a)P
or volatile organics. However, while 170 counties with a
total population of about 60 million had monitoring data,
only 30 counties had data for more than one site and essentially
no measurements were optimal for exposure assessment.
0 Data for BaP were found for about 50 counties. However,
most of the measurements were taken 3-5 years ago and only
one county had data for more than one site.
° For volatile organic compounds, OAQPS evaluated over 250
references with thousands of entries for over 40 pollutants.
However, even with the most relaxed criteria for data
completeness, only five cities had data that allowed estimates
of annual averages for more than one site, and two of those five
had data only because of the monitoring programs conducted as
part of lEMD's multimedia studies in Baltimore and Philadelphia.
EPA does not routinely measure ambient levels of potentially
toxic VOCs, and only a few states, e.g., California, routinely
gather such data. Of the available reports examined for this
analysis, most involve spot measurements for 24 hours or less
as part of a narrow study. Only 45 areas in the nation had
one valid calendar quarter worth of data for any toxic VOCs
(total of five days of data in the quarter) and only 12 areas
had two valid quarters of five days each.
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Emission inventories for toxic compounds also have major
problems. About 250 references were evaluated in this Study.
Based on this analysis, the most significant concerns were:^4
0 inconsistent coverage of sources;
0 highly variable emission estimates;
0 poorly defined source categories;
0 obvious anomalies and gaps;
0 form of metals not shown (speciation );
0 poor coverage of dispersive end uses, e.g., solvents; and
0 changing data base with time.
In an effort to quantify the quality of the information
available, emissions data for each of the 93 pollutants reported
were given a "Confidence Score" by the reviewers. This is commonly
used in evaluating emission inventories and is a subjective rating
of the adequacy of the data for a specific pollutant. The results
are summarized below.
0 5 pollutants scored "A" (consistent among
information sources; recent detailed study);
0 22 scored "B" (reasonable agreement among several
information sources);
0 59 scored "C" (sketchy data or significant variability
in the estimates);
0 7 scored "D" (virtually no information found).
The detailed report on emissions also discusses some examples
of inconsistencies found in the data. For example, five references
Lahre, T. "Characterization of Available Nationwide Air Toxics
Emissions Data." EPA Contract No. 68-02-3513, Task No. 46,
June 1984.
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were found for chloroform with emissions ranging from 3999 kkg/year
to 11,800 kkg/year (kkg = 1,000 kilograms). For chloroform, the
subcategory of solvent use accounted for percentages of total
emissions ranging from 6.2% to 92% in the various studies and
production emissions varied from 1.7% to 11.7%. Water chlorination
•
was mentioned as a source of chloroform emissions in only one study.
Not only are emissions data scarce and often inconsistent, but
systems and institutions are not in place to collect, store, or
retrieve data that may become available. There is an almost complete
lack of standardization, definition, and data systems. If data are
collected, they are collected for a single, short-term purpose.
For monitoring programs, there are no standard methods or
guidance available on network design, siting of monitors, and
averaging times. The Aerometric Information Retrieval System (AIRS)
is being developed by EPA, but until it becomes available in 1987,
there is no central repository for air toxics monitoring data.
A comparison with criteria pollutants helps explain why the
data base for toxics is relatively inadequate. There are eight
pollutants tracked or regulated under SIPs, while toxic compounds
of interest number from 50-100. About $30 million per year of EPA
grants to state and local agencies are used for data gathering on
criteria pollutants, while only about $1 million is used for air
toxics. In addition, ambient concentrations of toxics are almost
always 100 times less than criteria pollutants. Metals, such as
chromium and cadmium, are rarely seen at 0.01 ug/m3, whereas TSP
is measured in tens of ug/m3. The TSP primary annual ambient
standard is set at 75 ug/m3. Regulation of criteria pollutants is
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DRAFT
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based simply on attainment of a uniform ambient level everywhere-
However, toxics regulation often is driven by risk analysis
which requires population exposure estimates and, therefore, a more
comprehensive data base. Institutional support has been developed
for criteria pollutants over a period of two decades. This infra-
structure includes data systems (SAROAD, NEDS), regulations requiring
monitoring networks, and comprehensive emission inventories (SIPs),
standard methods of sampling and analysis, and formal quality
assurance programs. None of these are yet available for air toxics.
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VI. CONCLUSIONS
Given that this analysis was a scoping effort undertaken for
purposes of orientation and not to directly support regulation, and
considering the omissions and uncertainties discussed in this
report, the Study Team believes that the following conclusions
can be drawn from this study:
(1) The four analyses that attempted to quantify
risks due to 15 to 45 toxic air pollutants resulted
in estimates of annual cancer incidence that ranged
from 6 to 9 cases per million people annually.
Those same analyses resulted in estimates of total
national cancer incidence due to 15 to 45 toxic air
pollutants that ranged from 1,600 to 2,000 per year.
(2) Maximum lifetime individual risks of 10"^ or greater
in the vicinity of point sources were estimated for 25
pollutants. Maximum lifetime individual risks of
10-3 or greater were estimated for 12 pollutants.
(3) Additive lifetime individual risks in urban areas due
to simultaneous exposure to 10 to 15 pollutants ranged
from 10-3 to 10-4. These risks, which were calculated
from monitoring data, did not appear to be related to
specific point sources, but rather represented a portion
of the total risks associated with the complex mixtures
typical of urban ambient air.
•
(4) While there is considerable uncertainty associated with
the estimates for some substances, the study as a whole
indicated that the following pollutants are important
contributors to aggregate incidence from air toxics:
metals, especially chromium, arsenic, cadmium, and nickel;
asbestos products of incomplete combustion; formaldehyde;
benzene; ethylene oxide; gasoline vapors; and chlorinated
organic compounds, especially chloroform, carbon tetra-
chloride, perchloroethylene, and trichloroethylene.
(5) Both point and area sources appear to contribute signifi-
cantly to the air toxics problem. Large point sources
are associated with many high individual risks; area
sources appear to be responsible for the majority of
aggregate incidence.
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(6) A wide variety of source types contribute to individual
risk and aggregate incidence from air toxics. These
include: mobile sources; combustion of wood, coal and
oil; solvent usage; metallurgical industries; chemical
production and manufacturing; gasoline marketing; and
waste oil disposal.
(7) Some low-production organic chemicals appear to contribute
little to aggregate risk. For example, 21 synthetic
organic chemicals were estimated to account in total for
less than 1.0 excess cancer cases per year nationwide.
However, some organic chemical plants involved with these
compounds appear to cause high individual risks for those
living nearby. For example, the maximum lifetime individual
risk for 4,4-methylene dianiline was estimated at 1.5xlO~3.
(8) While the study indicated that non-traditional sources
such as Publicly Owned Treatment Works (POTW's) and
Treatment, Storage and Disposal Facilities (TSDF's)
may not be dominant contributors to nationwide air toxics
incidence, it appears that such sources may pose risks in
some locations. For example, a municipal sewage treatment
plant in a major metropolitan area was estimated to
account for 18 percent of the area's total aggregate
incidence, and individual lifetime risks for a single
compound at one TSDF were estimated as high as 10~5.
(9) Criteria pollutant control programs appear to have
done more to reduce air toxics risks than have programs
for specific toxic compounds. This seems reasonable,
considering the sources of air toxics, the multi-pollutant
nature of the problem and the relative intensity of these
programs .
(10) For those cities with sufficient data for analysis,
there appear to be significant differences across cities
and neighborhoods in risk levels, and the pollutants and
sources that cause risk. However, our current data base
is inadequate to accurately characterize most local air
toxics problems.
(11) Even after many regulations under Section 112 of the Clean
Air Act are in place, it appears that arsenic and benzene
will still be significant contributors to aggregate risk.
This seems to demonstrate that to be fully effective an
air toxics program needs to broaden its base, including
emissions from small area sources, such as combustion,
road vehicles, and solvent usage.
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92 DRAFT
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Factors which may have caused the risk estimates discussed
above to understate total air toxics risks are as follows:
(1) Risk estimates for many substances which have been found
in the ambient air could not be calculated, due to data
limitations. Urban ambient air is characterized by the
presence of dozens, perhaps hundreds, of separate
substances. These include many organic compounds; fine
particulate matter, including metals and polycylic
aromatic hydrocarbons; and criteria pollutants.
(2) Indoor concentrations of certain pollutants (e.g., radon,
tobacco smoke, formaldeyde, and other volatile organic
compounds) are commonly several times higher than outdoor
concentrations. While risk assessment could not be
performed for all these pollutants, the estimated cancer
incidence associated with passive smoking (3,000 to 14,000
annually) and radon (1,000 to 20,000 annually) clearly
show that indoor sources are a major contributor to air
toxics risks.
(3) Risks due to compounds formed by chemical reactions in
the atmosphere could not be quantified in the exposure
models, but there are indications that those risks may be
significant. For example, formaldehyde is formed in the
atmosphere by the breakdown of other organic compounds,
and some compounds (e.g., toluene) may be converted into
toxic substances through photochemical reactions.
Factors which may have caused the risk estimates discussed
above to be overstated are as follows:
(1) EPA potency estimates generally are regarded as plausible,
upper-bound estimates. That is, the unit risks are not
likely to be higher, but could be considerably lower.
(2) The degree to which outdoor-source related emissions of
many pollutants (e.g., trace metals) penetrate inside
is largely unknown. Should emissions from outdoor
sources not penetrate completely indoors, then we will
have over-stated risks, since we have assumed constant
exposures to levels equalling those of outdoor air.
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DRAFT
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ATTACHMENT A
SUMMARY TABLE
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES, PRELIMINARY
APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK
-------
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES, PRELIMINARY APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK
Pollutants Having Some
Evidence of
Carcinogenicity*
Ac ryl amide
Acrylonitrile
Allyl Chloride
Arsenic
Asbestos
Benzene
Benzo-a-Pyrene
Benzyl Chloride
Beryllium
1,3 Butadiene
Cadmium
I/
Unit Risk
Value
1.7x10-5
6.8x10-5
5.5x10-8
4.3x10-3
I/
6.9x10-6
3.3x10-3
1.2x10-5
4.0xlO-4
4.6x10-7
2.3x10-3
Source
CLEM
CAG
CAG
CAG
CLEM
CAG
CAG
CLEM
CAG
CLEM
CAG
Preliminary Approximation
of Annual Incidence**
NESHAPS
0.01
0.42
<0.01
4.7
32.3
<0.01
1.2
0.01
16.3
35 2/
County
4.2
1.1
18.5
1.1
0.01
0.01
1.1
Air
Quality
60
248.6
5.4
0.1
14.6
Other
Preliminary Approxima-
tion of Incidence Per
106 Population**
35
County
0.02
0.5
0.39
0.02
<0.001
<0.001
0.02
Air
Quality
0.26
0.5
1.08
0.02
<0.001
0.06
NESHAPS
<0.01
.002
<0.01
.02
0.5
0.14
<0.01
0.01
<0.01
.07
Preliminary Approx-
imation of Maximum
Lifetime Individual
Risk** (xlQ4)
NESHAPS
0.74
38
0.01
65
80
0.3
1.0
0.1
7.5
Air
Quality
40
1.5
0.25
0.002
14.7
o
o
o
X
o
* The weight of evidence of carcinogenicity for the compounds listed varies greatly, from very limited to very substan-
tial. Further, the extent of evaluation and health review performed varies considerably among compounds. However,
for the purposes of this report, a conservative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates, they should be regarded as rough approxima-
tions of total incidence and maximum lifetime individual risk. Estimates for individual compounds are very uncertain.
These incidence and maximum risk estimates have been performed to provide a rough idea of the possible total magnitude
of the air toxics problem, and will be used only for priority-setting and to provide policy guidance.
-------
-2-
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES, PRELIMINARY APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK
Pollutants Having Some
Evidence of
Carcinogenicity*
Carbon Tetrachloride
Chloroform
Chromium''"
Coke Oven Emissions
Diethanolamine
Dimethyl nitrosami ne
Dioctyl Phthalate
Epichlorohydrin
Ethyl Acrylate
Unit Risk"
Value
1.5x10-5
1.0x10-5
1.2x10-2
6.2x10-4
1.1x10-7
5.4x10-3
1.3x10-7
2.2x10-7
5.0x10-7
Source
CAG
CAG
CAG
CAG
CLEM
CAG
CLEM
CAG
CLEM
Preliminary Approximation
of Annual Incidence**
NESHAPS
14
0.27
330.0
•
8.6
<0.01
0.05
<0.01
<0.01
<0.01
35 2/
County
0.2
0.1
13.4
2.4
Air
Quality
84.7
106.7
242
Other
Preliminary Approxima-
tion of Incidence Per
106 Population**
3S
County
0.004
0.003
0.29
0.05
Air
Quality
0.37
0.46
1.05
NESHAPS
.06
<0.01
.11
.04
<0.01
<0.01
<0.01
<0.01
<0.01
Preliminary Approx-
imation of Maximum
Lifetime Individual
Risk** (xlO^)
NESHAPS
5.8
30
1600
200
<0.01
0.54
0.1
0.02
0.47
Air
Quality
1.54
0.77
14.4
o
o
o
zo
O
* The weight of evidence of carcinogenicity for the compounds listed varies greatly, from very limited to very substan-
tial. Further, the extent of evaluation and health review performed varies considerably among compounds. However,
for the purposes of this report, a conservative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates, they should be regarded as rough approxima-
tions of total incidence and maximum lifetime individual risk. Estimates for individual compounds are very uncertain.
These incidence and maximum risk estimates have been performed to provide a rough idea of the possible total magnitude
of the air toxics problem, and will be used only for priority-setting and to provide policy guidance.
t Risk estimates assume that all species of chromium and nickel are carcinogenic, although only certain species have
evidence of carcinogenicity. Current data do not allow differentiation among species.
-------
—3—
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES, PRELIMINARY APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK
Pollutants Having Some
Evidence of
Carcinogenicity*
Ethylene
Ethylene Di bromide
Ethylene Di chloride
Ethylene Oxide
Formaldehyde
Gasoline Vapors
Gasoline Marketing
4,4 150 Propylidene
Di phenol
Mel ami ne
Methyl Chloride
I/
Unit Risk
Value
2.7x10-6
5.1x10-4
7.0x10-6
3.6x10-4
6.1x10-6
7.5x10-7
7.5x10-7
1.4x10-6
4.1x10-7
1.4x10-7
Source
CLEM
CAG
CAG
CAG
CAG
CAG
CAG
CLEM
CLEM
CLEM
Preliminary Approximation
of Annual Incidence**
NESHAPS
<0.01
26.7
44
47.8
1.6
0.03
<0.01
<0.01
35 Z/
County
1.0
1.5
10.0
6.8
Air
Quality
191.3
0.9
Other
43
Preliminary Approxima-
tion of Incidence Per
106 Population**
35
County
0.02
0.04
0.21
0.15
Air
Quality
0.83
<0.01
NESHAPS
<0.01
0.12
0.19
0.21
0.01
<0.01
<0.01
<0.01
Preliminary Approx-
imation of Maximum
Lifetime Individual
Risk** (xlO4)
NESHAPS
4.9
1.6
2.9
68
6.1
<0.01
<0.01
0.12
Air
Quality
0.73
0.49 a
o
z
c
c:
— i
m
O
3O
0
m
<0.01
* The weight of evidence of Carcinogenicity for the compounds listed varies greatly, from very limited to very substan-
tial. Further, the extent of evaluation and health review performed varies considerably among compounds. However,
for the purposes of this report, a conservative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates, they should be regarded as rough approxima-
tions of total incidence and maximum lifetime individual risk. Estimates for individual compounds are very uncertain.
These incidence and maximum risk estimates have been performed to provide a rough idea of the possible total magnitude
of the air toxics problem, and will be used only for priority-setting and to provide policy guidance.
-------
-4-
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES, PRELIMINARY APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK.
Pollutants Having Some
Evidence of
Carcinogenicity*
Methyl Chloroform
Methylene Chloride
4,4 Methylene Di aniline
Nickel*
Nitrobenzene
Nitrosomorpholine
Pentachlorphenol
Perchloroethylene
Products Incomplete Comb
PCBs
I/
Unit Risk
Value
2.6x10-9
1.8x10-7
2.1x10-5
3.3x10-4
1.2x10-7
2.5x10-5
3.9x10-7
1.7x10-6
5x10-1
1.2x10-3
Source
CAG
CA6
CLEM
CAG
CLEM
CLEM
CLEM
CAG
£/
CLEM
Preliminary Approximation
of Annual Incidence**
NESHAPS
1.0
0.02
80
<0.01
<0.01
0.12
2.9
0.21
35 2/
County
0.7
<0.01
6.7
148
Air
Quality
0.1
7.4
15.0
25.4
820.9
Other
Preliminary Approxima-
tion of Incidence Per
106 Population**
35
County
' 0.02
0.14
3.1
Air
Quality
<0.01
0.03
0.07
0.11
3.57
NESHAPS
.004
<0.01
.35
<0.01
<0.01
.001
.01
3.57
.001
Preliminary Approx-
imation of Maximum
Lifetime Individual
Risk** (xlO4)
NESHAPS
0.1
15.0
16
<0.01
<0.01
0.17
4.6
3.0
Air
Quality
<0.01
<0.01
0.28
c
(
<
<
c
(
0.19 '
c
37.5 c
r
* The weight of evidence of carcinogenicity for the compounds listed varies greatly, from very limited to very substan-
tial. Further, the extent of evaluation and health review performed varies considerably among compounds. However,
for the purposes of this report, a conservative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates, they should be regarded as rough approxima-
tions of total incidence and maximum lifetime individual risk. Estimates for individual compounds are very uncertain.
These incidence and maximum risk estimates have been performed to provide a rough idea of the possible total magnitude
of the air toxics problem, and will be used only for priority-setting and to provide policy guidance.
t Risk estimates assume that all species of chromium and nickel are carcinogenic, although only certain species have
evidence of carcinogenicity. Current data do not allow differentiation among species.
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-5-
POLLUTANTS EXAMINED, UPPER-BOUND RISK VALUES,.PRELIMINARY APPROXIMATIONS OF INCIDENCE AND MAXIMUM LIFETIME RISK
Pollutants Having Some
Evidence of
Carcinogenicity*
Propylene Di chloride
Propylene Oxide
Radionuclides
Styrene
Terephthalic Acid
Titanium Dioxide
Trichloroethylene
Vinyl Chloride
Vinylidene Chloride
I/
Unit Risk
Value
7.2x10-7
1.2x10-4
varies
2.9x10-7
1.8x10-8
5.6x10-7
4.1xlO-6
2.6xlO-6
4.2x10-5
Source
CLEM
CLEM
5/
CLEM
CLEM
CLEM
CAG
CAG
CAG
Preliminary Approximation
of Annual Incidence**
NESHAPS
<0.01
0.97
<0.01
<0.01
0.01
9.7
11.7
0.04
35 Z/
County
0.02
6.8
8.2
Air
Quality
25.4
20.4
Other
17.5
Preliminary Approxima-
tion of Incidence Per
106 Population**
35
County
<0.01
0.15
0.2
Air
Quality
0.11
0.09
NESHAPS
<0.01
.004
<0.01
<0.01
<0.01
.04
.05
<0.01
Preliminary Approx-
imation of Maximum
Lifetime Individual
Risk** (xlO4)
Air
NESHAPS Quality
0.02
300
0.33
<0.01
<0.01
1.0
38
42
0.07
S
o
.0
0.26 3
o
•so
o
0.07 m
* The weight of evidence of carcinogenicity for the compounds listed varies greatly, from very limited to very substan-
tial. Further, the extent of evaluation and health review performed varies considerably among compounds. However,
for the purposes of this report, a conservative scenario (i.e., that all compounds examined could be human
carcinogens) has been assumed.
** Because of the uncertainties in the data used to make these estimates, they should be regarded as rough approxima-
tions of total incidence and maximum lifetime individual risk. Estimates for individual compounds are very uncertain.
These incidence and maximum risk estimates have been performed to provide a rough idea of the possible total magnitude
of the air toxics problem, and will be used only for priority-setting and to provide policy guidance.
-------
FOOTNOTES - ATTACHMENT A, SUMMARY TABLE
"Pollutants Examined, Upper-Bound Risk Values, Preliminary
Approximations of Incidence and Maximum Lifetime Risk"
_!_/ The unit risk value is the estimated probability of contracting cancer as the
result of a constant exposure over 70 years to an ambient concentration of
one microgram per cubic meter (ug/m^). "CAG" denotes risk values obtained
from EPA's Carcinogen Assessment Group; "CLEM" denotes risk values obtained
from Clement Associates.
2_l The population of the counties covered in the 35 County Study (about 47.3 million)
represents approximately 20% of the national population.
_3_/ The unit risk value used for asbestos was that a lifetime risk of 10-6 for lung cancer
would result from an exposure to 10 fibers/cc and that a lifetime risk of 10-6 for
mesothelioma would result from an exposure to 5 fibers/cc; 30 fibers per nanogram
were assumed.
£/ "Products of Incomplete Combustion" (PIC) refers to a large number of compounds,
probably consisting primarily of polynuclear organics. The PIC unit risk value was
derived from dose-response data which use Benzo(a)Py rene (BaP) levels as a surrogate
for PIC or total air pollution. There are many limitations of using the B(a)P
surrogate method to estimate PIC risks: all PIC estimates presented in this report
must be regarded as highly uncertain. Refer to pp. 21-26 for a more detailed explana-
tion of how the PIC unit risk value was derived.
5y Estimates of cancer and genetic risks are based on those found in the 1980 National o
Academy of Science Report, "Effects on Population of Exposures to Low Levels of z
Ionizing Radiation" (BEIR - 3 reports). 3
o
SO
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