United States Office of Policy Analysis
Environmental Protection Office of Policy, Planning
Agency and Evaluation
February, 1987
Unfinished Business:
A Comparative Assessment
of Environmental Problems
Appendix I
Report of the Cancer Risk
Work Group
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COMPARATIVE RISK PROJECT
REPORT OP THE CANCER WORK GROUP
FEBRUARY 198?
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Table of Contents
Introduction 1
The Ranking Process .1
Relative Ranking of Environmental Problems 3
General Difficulties With the Ranking Process 11
Difficulties in Ranking Problem Areas 12
Observations 15
Recommendations 17
APPENDIX A; General Process for Estimating Carcinogenic Risk
APPENDIX B: Risk Calculations for Specific Environmental Problems
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COMPARATIVE RISK PROJECT
REPORT OF THE CANCER WORK GROUP
INTRODUCTION
The Cancer Work Group was directed to evaluate the cancer
risk associated with 31 environmental problem areas under EPA's
jurisdiction, and then to rank them according to the relative
magnitude of their cancer risk. The work group was composed
of senior managers and technical staff representing all Agency
program offices (Air and Radiation, Pesticides and Toxic Sub-
stances, Solid Waste and Emergency Response, and Water).
Individuals were chosen largely on the basis of their famili-
arity with cancer risk assessment methods, particularly with
respect to such analyses undertaken within their programs.
In addition to the program offices, the Office of Research and
Development, Office of Policy, Planning and Evaluation, and
the Regional Offices were represented on the work group.
This report discusses the process we used for ranking the
environmental problems, identifies the difficulties we had in
evaluating cancer risks, and presents the relative rankings.
It also highlights several issues that affected the ranking of
specific environmental problems. The final section of the re-
port provides some observations on the difficulty of evaluating
and ranking cancer risk. Appendix A presents further detail
on the methods used to estimate cancer risks, and Appendix B
presents quantitative estimates of cancer incidence and indi-
vidual risks for each environmental problem for which such
estimates exist.
The ranking should not be regarded as a list establishing
priorities for regulation. Our assessment was limited to only
one dimension -- that of cancer risk. We did not evaluate a
host of factors important in regulatory decision making, such
as how extensively risks can be reduced through regulation,
the cost of reducing cancer risk, EPA's statutory authority,
and the extent of ecological, welfare, and non-cancer health
effects. In addition, because available data were often limited
and did not allow for comparison between problems, we relied
heavily on our professional Judgment, rather than on quantita-
tive methods. Nonetheless, the information we developed will
be useful in setting EPA's priorities.
THE RANKING PROCESS
We did not conduct new research as a part of this effort.
Instead, we extracted information from risk assessment work
performed in support of other regulatory activities.
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During the first phase of this project, we compiled infor-
mation on the cancer risks of each environmental problem. In
general, this information was based on EPA risk assessments
performed in support of specific regulatory activities. We
presented the information on the cancer risks of each environ-
mental problem in the form of "data sheets," which indicated
the substances examined and the extent of exposure. In most
cases, these assessments used cancer potency estimates developed
by EPA's Carcinogen Assessment Group (GAG), adhering to the
methods outlined in EPA's Guidelines for Carcinogen Risk Assess-
ment (51 PR 33992). Exposure data were generated either by
using exposure models or by extrapolating from monitored data.
(Appendix A of this report discusses these methods in detail.)
After a detailed review of the data sheets, we met to
discuss the information on cancer risks, to review the methods
program offices used to estimate the cancer risks, and to rank
the environmental problems as to the relative magnitude of
their risks. We first placed the 31 environmental problem
areas into five categories. In addition, the work group chose
not to rank two environmental problems to avoid counting the
same risks twice. After reaching a consensus on this grouping
of the problems, we ranked each problem ordinally by comparing
the environmental problems within each category.
As a starting point for our rankings, we relied on the
information presented in the data sheets. It soon became clear
that we could not base our rankings solely on this information.
For example, for some problem areas, only a few chemical assess-
ments were compiled, while for others, many were compiled.
This led to large differences in how well the problem areas
were quantified. At best, for some problems, most of the
toxicologically well-characterized chemicals were covered.
Thus, the best coverage still could not consider the large
number of substances that have insufficient toxicity data.
For other problems, only one or two chemical assessments were
compiled — more as examples of the potential extent of the
risk from the problem area than as attempts at quantification.
In addition, the methods and assumptions used to estimate
exposure and risk were not consistent across environmental
problem areas. This introduced a potential bias in comparing
risks. The degree of uncertainty about estimates of cancer
incidence varied considerably among environmental problems.
Finally, the methods we used to develop national estimates of
cancer incidence from available data were not always compar-
able, nor was it possible to make them so. As a result, we
considered these qualitative factors in our deliberations on
the final ranking.
After this meeting, the ranking results were circulated
for the work group to review and to reach a consensus on. In
addition, work group members prepared summaries of the data
sheets for each environmental problem, and then circulated
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them to the other members for review. These appear in Appen-
dix B of this report.
As a final step, we reevaluated our rankings and discussed
the observations that appear in this report.
RELATIVE RANKING OP ENVIRONMENTAL PROBLEMS
Table 1 displays the results of the relative ranking of
environmental problem areas on the basis of cancer risk. Prob-
lem areas have been placed into five categories of decreasing
magnitude, with the fifth category containing problem areas
for which no risk was identified. In addition, problem areas
were ranked numerically within each category. The second
column indicates the substances or sources of exposure that
are considered in the quantitative analyses for each environ-
mental problem, as presented in Appendix B. The third column
summarizes the rationale for the individual rankings and other
comments not directly related to the ranking itself (such as
the presence of particularly high individual risks).
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TABLE 1
RANK
CATEGORY 1
PROBLEM AREA
Consensus Ranking of Environmental Problem Areas
On the Basis of Population Cancer Risk*
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
1 Vforker
(tied) Exposure to
Chemicals
1 Indoor Radon
(tied)
3 Pesticide
Residues on Foods
4 Indoor
(tied) Air Pollutants
Other than Radon
Formaldehyde
Tetrachloroethylene
Asbestos
Methylene chloride
Radon and its decay products
1 Herbicide
3 Fungicides
1 Insecticide
1 Growth regulator
Tobacco smoke
Benzene
p-Dichlorobenzene
Chloroform
Carbon tetrachloride
Tetrachloroethylene
Trichloroethylene
Ranked highest of any single environmental problem,
along with Indoor Radon — based on work group con-
sensus. About 250 cancer cases were estimated
annually from four substances, but workers face
potential exposures to over 20,000 substances.
Individual risk can be very high.
Also ranked the highest. Current estimates are 5,000
to 20,000 lung cancers annually from exposures within
homes. Some of these are a consequence of the joint
action of radon and tobacco smoke. Individual risks
can be very high.
Cancer incidence estimate of about 6,000 annually,
based on exposure to 200 potential oncogens (one-third
of total pesticides in use) — extrapolated from seven
known oncogens. Assessment does not account for so-
called inert materials in pesticides.
Quantitative assessment estimates 3,500-6,500
cancers annually. Environmental tobacco smoke is
responsible for the majority. Risks from organics
estimated on the basis of monitoring 600 U.S. homes.
Individual risks can be very high. Potential for some
double counting with Consumer Exposure to Chemicals
and with Drinking fcfetter.
The five categories represent decreasing magnitude of cancer risk, with Category 1 representing problem areas with
the highest relative risk, and Category 5 representing problem areas for which no cancer risk has been identified.
Problems are also ranked numerically within each category.
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RANK
PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
4
(tied)
Consumer
Exposure to
Chemicals
Hazardous/
Toxic Air
Pollutants
Formaldehyde
Methylene chloride
p-Dichlorobenzene
Asbestos
20 substances, classes
of substances, or
waste streams
The risk from these four chemicals is about 100-135
cancers annually. There are an estimated 10,000 chem-
icals in consumer products. Even though exposures are
generally intermittent, risks are believed to be high,
given the concentrations to which individuals are
exposed. Consumers are exposed through such products
as cleaning fluids, pesticides, particleboard and
other building materials, and numerous asbestos-
containing products. Considerable double counting
with Indoor Air and Other Pesticide Risks.
A quantitative assessment of 20 substances estimates
approximately 2,000 cancer cases annually. This is a
subset of the large total number of pollutants to
which people are exposed in ambient air. Individual
risks can be very high. Potential for some double
counting with Active Hazardous Waste Sites Municipal
Hazardous Waste Sites, and Contaminated Sludge.
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01
I
|Category 2|
Depletion of
Stratospheric
Ozone
Hazardous Waste
Sites -
Inactive
Increased UV radiation
(Chlorofluorocarbons,
Halon 1301,
Chlorocarbons)
Trichloroethylene
Vinyl chloride
Arsenic
Tetrachloroethylene
Benzene
1,2-Dichloroethane
Current nonmelanoma and melanoma skin cancer deaths
at 10,000 annually. Ozone depletion projected to
result in steadily increasing risks, with an additional
10,000 annual deaths projected for the year 2100.
This problem is ranked in Category 2 because of the
considerable uncertainties concerning estimates of
future risk. If estimates are correct, would rank
higher. Needs further research.
Nationwide cancer incidence from six chemicals esti-
mated at just over 1,000 annually. Considerable uncer-
tainty, since nationwide risk estimates are based on
extrapolating from 35 sites to about 25,000 sites
nationwide. Individual risks can be very high. Po-
tential for some double counting with Drinking Water.
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RANK PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
Drinking
Water
10 Application
of Pesticides
11 Radiation
Other than
Indoor Radon
Ingestion and/or
inhalation of 23
substances
1 Herbicide
3 Fungicides
1 Insecticide
1 Growth regulator
Occupational exposures
Consumer products
Industrial emissions
Quantitative assessment estimates about 400-1,000
cancer cases annually, based on home surveys of public
water systems. Most cases are from radon and trihalo-
methanes. Potential for some double counting with
Indoor Radon, Indoor Air Pollution, and several cate-
gories related to contaminated ground water.
Approximately 100 cancers annually estimated by a
method analogous to that used for Pesticide Residues
on Food. Small population exposed, but uniformly
high individual risks.
Risks associated with medical exposures and natural
background levels excluded; would rank higher if
these were included. Two-thirds of assessed risk
of 360 annual cancers results from building materials.
Individual risks can be very high. Nonionizing
radiation not considered due to lack of data.
12 Other
Pesticide Risks
13 Hazardous
Waste Sites -
Active
Consumer use
Professional exterminator use
Several carcinogens from
each of the following:
Hazardous waste storage tanks
Hazardous waste in boilers/
furnaces
Hazardous waste incineration
Waste oil
Few quantitative estimates available. Consensus
estimate of 150 cancers annually, based loosely on
discussion of termiticide risks. Less data here
than for other pesticide areas.
No nationwide risk estimates are available, but proba-
bly fewer than 100 cases annually. Risk estimates are
sensitive to assumptions regarding the proximity of
future wells to waste sites. Solid waste management
units were excluded from analysis. Individual risks
can be very high. Possible double counting with
Drinking Water and Hazardous/Toxic Air Pollutants.
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RANK
PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
14 Nonhazardous
Waste Sites -
Industrial
Arsenic
1,1,2,2-Tetrachloroethane
Chloroform
Benzene
No analysis of cancer incidence. Instead, based on the
consensus of the work group. Judged less severe than
hazardous waste, worse than municipal. Potential for
some double counting with Drinking Water.
15
New Toxic
Chemicals
None
Very difficult to assess future uses of new chemicals
and the risks of using chemicals never manufactured.
Consensus was that this problem poses moderate risks.
[Category 3|
16 Nonhazardous
Waste Sites -
Municipal
17 Contaminated
Sludge
Several pollutants/waste streams
from the following:
Municipal landfills
Municipal sludge incineration
Municipal waste incineration
Up to 22 carcinogens from the
following:
Land application
Distribution and marketing
Landfilling
Incineration
Ocean disposal
Quantitative estimate of about 40 cancers annually.
This estimate does not include risks from municipal
surface impoundments. Potential for some double
counting with Hazardous/Toxic Air Pollutants,
Contaminated Sludge, and Drinking Water.
Analyses and regulatory development are ongoing.
Preliminary results estimate approximately 40 cancers
annually. Most of this risk comes from incineration
and landfilling. Potential for some double counting
with Hazardous/Toxic Air Pollutants, Nonpoint Source
Discharges to Surface Water, and Nonhazardous Waste
Sites - Municipal.
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RANK
PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
18
Mining Waste
Arsenic
Cadmium
19
20
21
Releases from
Storage Tanks
Nonpoint
Source Discharges
to Surface Ifeter
Other
Ground-Water
Contamination
Benzene
None
Methylene chloride from
septic systems
22
Criteria
Air Pollutants
Lead
Ozone
Particulate matter
Nitrogen oxides
Sulfur oxides
Carbon monoxide
Estimate of 10-20 cancer cases annually largely due to
arsenic. Severity of problem is relatively low because
remote locations expose a relatively small population.
This assessment excludes oil and gas operations.
Individual risks can be very high. Potential for
double counting with Drinking Water.
Preliminary analysis suggests relatively low cancer
incidence « 1 annually), but exposure modeling not as
conservative as several other solid waste problems
(behavior that limits exposure is assumed). Potential
for double counting with Drinking Water.
Judged to be more serious than other surface water
categories, but no quantitative analysis is available.
Generally, risks from other ground-water contamination
are not estimated due to a lack of information with
respect to sources, their locations, and concentration
levels. Individual risks generally less than 10~6,
with rough estimate of population risk well under 1
case per year. However, this is an estimate of a
small portion of total risk, as we examined one chemi-
cal at just one of many sources (septic systems).
Potential for some double counting with Drinking Vfeter.
This assessment excludes carcinogenic particles and
VOCs (controlled to reduce ambient ozone), which are
considered under Hazardous/Toxic Air Pollutants.
Ranked relatively low because none of the criteria pol-
lutants has been adequately shown to cause cancer. If
any are shown to be carcinogenic (e.g., lead), or if
VOCs and carcinogenic particles are included in the
definition of Criteria Air Pollutants, this problem
would move to a higher category.
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oo
I
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I Category 4|
RANK PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
23 Direct Point
Source Discharges
to Surface Water
None
No quantitative assessment is available. Only
ingestion of contaminated seafood was considered,
since the impact of drinking water was covered
elsewhere.
24 Indirect,
Point Source
Discharges to
Surface Water
None
Same as above.
25 Accidental
Releases -
Toxics
None
Because of the short duration of personal exposure to
accidental releases, cancer risk judged to be very
small. Long-term effects on ground-water exposures
were not considered here. Non-cancer health effects
are of much greater concern. Nature of substances
and exposures ranks this problem above oil spills.
I
ID
I
26
Accidental
Releases -
Oil Spills
None
See above. Oil spills will be of greater concern for
welfare and ecological effects.
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I Category 5| (Listed Alphabetically)
PROBLEM AREA
SUBSTANCES/
EXPOSURES INVESTIGATED
COMMENTS
Biotechnology
None
Dilemma of ranking this problem is similar to that for
new chemicals, but even less information is available.
No known instances of carcinogenic bioengineered
substances.
C02 and Global
Warming
None
Cancer is not considered a significant aspect of this
environmental problem. No assessment was undertaken.
Other Air
Pollutants
None
By definition, carcinogenic pollutants in the outdoor
air are considered under Hazardous/Toxic Air Pollutants.
Therefore, no cancer risk was assessed here.
[Not Ranked)
Discharges None
to Estuaries,
Cosatal Waters and
Oceans
Discharges None
to Wetlands
This category represents a conglomeration of other
categories. The work group chose not to rank it to
to minimize double counting.
See Discharges to Estuaries, Coastal Waters, and Oceans,
above.
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GENERAL DIFFICULTIES WITH THE RANKING PROCESS
Generating a relative ranking of environmental problem
areas would have been a simple quantitative exercise if we
could have obtained consistent methods and complete informa-
tion for all of the problem areas. And even though the 1986
Guidelines for Carcinogen Risk Assessment were helpful in
establishing a consistent set of ground rules, the quality,
consistency, and completeness of information on the different
environmental problems was highly variable. The risk assess-
ment guidelines warn that estimates of cancer risk generated
from those methods are not indicative of true risk. Estimates
of true risk are currently not possible, given our limited
knowledge of carcinogenesis.
Quantitative Estimates Were Based on Existing Analyses
The quantitative risk estimates we compiled for this
project were adapted from analyses previously undertaken by
EPA program offices. In most cases, we developed these esti-
mates only to consider the relative merits of different regu-
latory options. While uncertainties in such an analysis are
often great in the context of a well-defined regulatory objec-
tive, they become much greater when comparisons are made between
the outcomes of diverse analyses.
Ranking Reflects Population Risk Rather Than Individual Risk
Another area of judgment involved the consideration of
population versus individual risks. In general, regulation of
environmental problems may be warranted in either of two situa-
tions. On one hand, exposure of large numbers of individuals
to a relatively small cancer risk may result in an unacceptable
number of "expected" cancers associated with an environmental
problem (high population risks). On the other hand, very high
excess cancer risk to a few individuals (high individual risks)
may also prove unacceptable, even if the expected number of
cases is small.
For the purposes of this report, the rankings of environ-
mental problems were based primarily on population risk. How-
ever, where problems pose particularly high risks to indivi-
duals, we highlighted this fact. Unfortunately, estimating the
size of the population exposed to these high risks was beyond
the scope of this project.
Ordinal Ranking May Confer False Accuracy
Several work group members were very uneasy about ranking
each of the environmental problems ordinally. They believe
that this approach would confer a false degree of accuracy on
the ranking when, in fact, the differences between two or three
adjacently ranked problems might be impossible to discern.
Alternatively, other work group members saw the ordinal ranking
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as desirable, so long as the high degree of uncertainty in the
process was clearly stated. The work group agreed to present
an ordinal ranking, with problem areas organized into five
general categories according to the magnitude of population
risk.
Comparative Ranking Is Based on Work Group Judgment
Because of the many uncertainties associated with develop-
ing a quantitative risk assessment for each of the 31 environ-
mental problems, it was impossible to conduct a highly quanti-
tative analysis with a great deal of confidence. We relied
extensively on our collective professional judgment to rank the
problem areas and used the quantitative results presented by
each program office to supplement this judgment. Therefore,
the ranking relies primarily on the opinion of well-informed
EPA professionals. Indeed, while we believe that the ranking
would not change dramatically, a work group composed of differ-
ent members may well have arrived at somewhat different conclu-
sions. Thus, this ranking should be interpreted cautiously,
taking into consideration the constraints the data base imposes
on this project.
DIFFICULTIES IN RANKING PROBLEM AREAS
For various reasons, ranking the problem areas was very
difficult. For example, data were lacking in many areas, risks
were not identifiable for some areas, and variations in coverage,
analytical methods, and levels of confidence complicated the
ranking.
Ranking May Reflect Inadequate Data
The information compiled for this project has been taken
from cancer risk assessments previously conducted by EPA.
Thus, we do not present quantitative information for several
problems that are of primary interest to EPA because of fac-
tors other than cancer. The consensus of the work group was
that these environmental problems pose relatively low cancer
risks. However, this assessment may be biased by a lack of
quantitative information.
For Some Problems, Risks Were Unidentifiable
We could not identify cancer risk for three environmental
problems: Other Air Pollutants, C02 and Global Warming, and
Biotechnology. We have not considered Other Air Pollutants in
this analysis because we assumed that the risk associated with
carcinogenic air pollutants, by definition, would be captured
under Hazardous/Toxic Air Pollutants. And, though C02 and
Global Warming may have large ecological and welfare effects,
no mechanism by which this problem may increase cancer incidences
is known. Finally, there are no data to indicate that cancer
risks are associated with biotechnology.
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Variations in Coverage Complicated Ranking
The extent to which the available quantitative information
estimated total cancer risk varied widely among environmental
problems. In general, incomplete coverage complicated the
ranking in two situations:
1. Not all carcinogens in a problem area were covered.
The assessments for a few environmental problems, such as
Indoor Radon, theoretically considered all the cancer-causing
substances associated with those problems. In other cases,
such as Pesticide Residues on Poods, we extrapolated from a
few suspected carcinogens to the universe of potential carcino-
gens within the problem area. For most problem areas, the
quantitative analysis addressed only a subset of the total
number of pollutants. An extreme example of this is Worker
Exposure to Chemicals, where only four substances were examined,
when workers may be exposed to as many as 20,000 substances.
2. Not all routes of exposure were covered. Because of
intermedia transfer of carcinogenic substances (e.g., air and
water pollution from hazardous waste sites), a given problem
may pose cancer risks through several routes of exposure.
However, in trying to address the most important routes of
exposure, quantitative assessments were rarely based on more
than a single exposure pathway. As a result, risks in problem
areas in which intermedia transfers can take place may be
understated relative to others.
Definitions and Boundaries of Problems Influenced Ranking
The boundary assigned to the definition of each problem
area strongly influenced its ranking. For example, two clas-
ses of air pollutants -- volatile organic compounds and parti-
culate matter -- have some carcinogenic components. Both
classes are controlled by EPA regulations developed to reduce
criteria air pollutants. However, we chose to examine these
carcinogenic pollutants in the context of Hazardous/Toxic Air
Pollutants. Thus, if we had defined this problem differently,
Criteria Air Pollutants would rise considerably in the ranking.
We recognized at an early stage that there is considerable
overlap in risks included in some problem areas. As a result,
we did not consider Wetlands and Estuaries to avoid double
counting of risk. The cancer risks that could be attributed
to these environmental problems, which result largely through
the consumption of contaminated seafood, are included in the
other problem areas dealing with discharges into surface and
ground waters. The "comments" section of Table 1 identifies
problem areas where such double counting of cancer risk was a
factor.
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Using a Variety of Analytical Methods Complicated Ranking
The carcinogenic potencies of substances were estimated
from two types of data. For the majority of substances suspec-
ted to cause cancer, potency estimates were based on the results
of animal bioassays. Human epidemiologic data are available
for only a few substances. This difference in the type of
data used to assess risk probably introduces a bias between
problem areas, particularly with respect to problem areas that
rely entirely on human data (e.g., Indoor Radon).
Various methods of assessing exposure may also have biased
comparisons of different problem areas. Not all analyses made
exposure assumptions with the same degree of conservatism.
Although we attempted to rank problem areas under a consistent
set of assumptions, we could not always do so, given the wide
variety of exposure situations. An example of this relates to
the issue of mitigating behavior. For some environmental prob-
lems, people may take actions to reduce their exposure once
they know they are at risk, even if there is no regulatory
program to protect them. For example, people may stop drinking
water that tastes bad or is known to be polluted. However,
with the exception of the evaluation of risks from Underground
Storage Tanks, no mitigating behavior is assumed to occur when
we estimated cancer risks from the problem areas.
A similar situation exists in the evaluation of Drinking
Water. Given that the majority of risks attributed to Inactive
Hazardous Waste Sites result from drinking contaminated ground
water, it initially may appear somewhat contradictory that
Drinking Water ranks below this problem area. However, the
Drinking Water calculations were based on contaminants actually
detected in public water systems, while calculations for Inactive
Hazardous Waste Sites were based on extrapolation from a small
number of investigated sites to the total population of sites.
(On the other hand, Inactive Hazardous Waste Sites did not
account for inhalation or dermal exposures.) Clearly, if the
cancer risks associated with all sources of ground-water con-
tamination were considered under Drinking Water, the risks
associated with this problem area would increase.
Different Levels of Confidence Complicated Ranking
Finally, the quality of information for the various envi-
ronmental problems varied considerably. While there remains a
high degree of uncertainty for any cancer risk assessment, we
felt much more comfortable with our understanding of a problem
area such as Radiation than we did for Stratospheric Ozone
Depletion. It is unclear how this uncertainty may have biased
our rankings, but it is likely to have had an effect.
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OBSERVATIONS
The final ranking of the 31 environmental problems Is
heavily influenced by judgment. As such, it cannot be defen-
ded purely on scientific grounds. Rather, this final ranking
represents the consensus of a work group composed- of the senior
technical staff and managers at EPA who are best qualified to
make such judgments.
In this section we present several observations on the
ranking itself, and on the ranking process.
EPA's Role Is Limited
Four of the six problem areas that ranked in the highest
category are areas for which EPA has limited regulatory pro-
grams. For two of these, Worker and Consumer Product Exposures,
EPA shares jurisdiction with other federal agencies which
have primary jurisdiction in most cases. And, though EPA is
the lead agency on the other two, Indoor Radon and Indoor Air
Pollution, neither program lends itself to a conventional
regulatory approach.
Inhalation Is The Major Exposure Route for High-Risk Problems
With the exception of Pesticide Residues on Food, the
major route of exposure for all problem areas in the highest
risk category is inhalation.
High Population Risk Often Means High Individual Risk
Although the problem areas were ranked on the basis of
population risk, four of the six that ranked in the highest
category also pose high individual risks. The two that do not
are Dietary Exposures to Pesticide Residues on Food and Consumer
Product Exposures.
Risks from Acute and Indirect Exposure Rank Low
Two types of problems ranked in Category 4 (the lowest
category for which there is evidence of cancer risk): those
related to accidental releases and discharges from point sources
to surface waters. The problems related to accidental releases
were ranked relatively low because exposure to carcinogens is
acute, rather than chronic (that is, exposure is of short,
rather than long, duration). It is possible that these problems
would rank in a higher category if potentially chronic exposures
related to ground-water contamination were considered. The
two problem areas related to discharges to surface waters were
ranked low mainly because people are only indirectly exposed
to them, primarily through the relatively minor pathway of
contaminated seafood.
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Ordinal Rankings Are Not Precise
Ranking environmental problems was complicated by a lack
of information, uncertainties in estimating exposures, the
diversity of methods used to assess different problems and to
project national cancer incidence from smaller-scale studies,
and differences in the degree of coverage of potential carcin-
ogens. The ranking is thus best described as a consensus
judgment. Therefore, we do not believe the ordinal rankings
have great precision. Rather, they generally indicate the
relative cancer effects for each environmental problem. For
this reason, the work group warns against placing too great a
reliance on the ordinal ranking, particularly when similarly
ranked problems are compared.
Dividing Lines Between Risk Categories Are Fuzzy
We believe that the risks associated with environmental
problems grouped in one category are different from those
grouped in another category. However, the precise location of
the dividing lines between the categories was somewhat arbitrary,
Often, the risk associated with a problem ranked at the bottom
of one category was similar to the risk of a problem at the
top of the next category.
Quality of Exposure Data Is Highly Variable
In general, the quality of human exposure data for the 31
environmental problem areas varies greatly, making comparisons
difficult. Though in all cases exposure estimates are less
than ideal, they are particularly lacking for problem areas
relating to surface waters, ground water, solid waste, and new
chemicals.
Relatively Few Substances Have Been Tested for Carcinogeniclty
In general, the number of substances for which we have
reasonably good cancer data (e.g., animal bioassay or human
epidemiology) is a small subset of the number of chemicals to
which the public is exposed. Because so little is known about
the vast majority of chemicals, it is difficult to compare
problem areas with only a few substances (e.g., Indoor Radon)
with those represented by many substances (e.g., Worker Expo-
sure to Chemicals).
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RECOMMENDATIONS
Because this ranking is based only on cancer risk, we
have not made recommendations regarding policy or resource
allocation. We believe such recommendations should appear
only in the Overview Report, which will contain the results of
the four separate work groups for this project. However, we
do have the following recommendations based on the experience
of working on this project.
Data Base Needs Expansion
Significant improvements in the precision of the ranking
will be possible only if a greatly expanded data base is avail-
able. In general, developing new data on carcinogenic substances
and human exposures to carcinogens in the environment takes a
considerable amount of time. Thus, it is not likely that
there will be enough new information to warrant a new attempt
to rank these problems for several years.
Next Step Should Consider Addressability
An important step in evaluating how to use the information
presented here will be to analyze each environmental problem
to ensure that suitable action can be taken, that taking such
action is within EPA's mandate, and that the prospective imp-
rovements in health and/or welfare warrant the expenditure
of resources. As a follow-up to this project, we recommend
that EPA more comprehensively evaluate the environmental
problem areas examined here.
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APPEDNIX A
GENERAL PROCESS FOR ESTIMATING CARCINOGENIC RISK
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Appendix A
General Process for Estimating Carcinogenic Risk
This appendix describes the way EPA generally assesses cancer risk. The
first section outlines the methods EPA uses to estimate cancer potency for
suspected or known human carcinogens. Included in this section is a list of
the carcinogens we considered in making quantitative estimates of cancer
risk, as well as the potencies that have been computed for each of these.
Following this is a general discussion of how exposures are estimated in EPA
analyses. Exposure assessments for individual problems areas are outlined
in Appendix B.
We evaluated both chemical and physical (i.e., radon and other radiation
sources) carcinogen hazards in this comparative ranking. The risks from
radiation-induced cancer are addressed in Appendix B in the section on Radia-
tion (page B-49). The risk estimates for chemical carcinogens were prepared
by EPA's scientists according to procedures described in EPA's Guidelines
for Carcinogen Risk Assessment (51 FR 33992, September 24, 1986).
ASSESSING CARCINOGENS
Selecting Data
In selecting experimental data to use to estimate potential cancer risks
to humans, the quality of the data, its relevance to human modes of exposure
and other technical details must be examined. Wiere possible, estimates were
based upon human epidemiologic data (see Table A-l). In the absence of human
data, data from animal species were used. Often, several studies were avail-
able for a given agent that involved different animal species, strains, and
sexes, at several doses and different routes of exposure. Wien this was the
case, tumor incidence data were separated according to organ site and tumor
type and all biologically and statistically acceptable data sets were ex-
amined. The range of the risk estimates were calculated, giving due regard
to biological relevance (particularly in the case of animal studies) and
the appropriateness of the route of exposure. It was assumed that human
sensitivity is as high as the most sensitive responding animal species
unless there was evidence to the contrary. Therefore, the greatest evidence
is generally given to the biologically acceptable data set from long-term
animal studies showing the greatest sensitivity, again with due regard to
biological and statistical considerations.
Wiere a single study revealed two or more significantly elevated tumor
sites or types, extrapolations were conducted on sites or types selected on
biological grounds. To obtain a total estimate of carcinogenic risk, data
from animals with one or more significantly elevated tumor site or type were
pooled and used for extrapolation. If the tumor sites or types actually
occur independently, this procedure is the same as summing the risks from
the several kinds of statistically significant tumors. The pooled estimates
generally were used in preference to risk estimates based on single sites or
types.
Benign tumors were usually combined with malignant tumors for risk esti-
A-l
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mates unless the benign tumors were not considered to have the potential to
progress to the associated malignancies of the same morphologic type, as in
the case of tumors associated with exposure to formaldehyde.
Choosing a Mathematical Extrapolation Model
Because risks to low exposure levels cannot be measured directly by
either animal experiments or epidemiologic studies, several mathematical
models have been developed to extrapolate from high to low dose. However,
while different extrapolation models may fit the observed data reasonably
well, they may lead to considerable differences in the projected risk at low
doses. No single mathematical procedure is yet recognized by the scientific
community as the most appropriate for low-dose extrapolation in carcinogenesis.
To adequately protect human health, EPA has adopted a procedure whereby
it strives to define an upper bound of the risk, rather than estimating the
true risk — a task that EPA believes is normally undefinable. Although
mechanisms of carcinogenesis remain are largely unknown, at least some ele-
ments of the process have been elucidated — e.g, linearity of tumor initia-
tion. Thus, a linear multistage model has been adopted to define the plausi-
ble upper bound for risk. In further support of a linear model, it has been
shown that if a carcinogenic agent acts by accelerating the same stages of
the carcinogenic process that lead to the background occurrence of cancer,
the added effect of the carcinogen at low dose is virtually linear. Thus, a
model that is linear at low dose is plausible.
Therefore, the linearized multistage model low-dose extrapolation proce-
dure was used in the risk estimates compared for this project. Vfe emphasize
,that the linearized multistage model leads to a plausible upper limit to the
risk, which is consistent with some likely mechanisms of carcinogenesis.
Such an estimate, however, does not necessarily give a realistic prediction
of the risk.
In certain cases, the linearized multistage model cannot be used success-
fully with the observed data. For example, it is unsuitable when the data
are not monotonic or flatten out at high doses. In these cases it may be
necessary to adjust the procedure to achieve low-dose linearity. In addition,
a different low-dose extrapolation model might be conidered more appropriate
when pharmacokinetic or metabolism data are available, or when other substan-
tial evidence on the mechanistic aspects of the carcinogenesis process exists.
Extrapolating Animal Exposures to Humans
Low-dose risk estimates derived from laboratory animal data extrapolated
to humans are complicated by a variety of factors that differ among species
and potentially affect the response to carcinogens. Included among these
factors are differences between humans and experimental test animals with
respect to life span, body size, genetic variability, population homogeneity,
existence of concurrent disease, such pharmacokinetic effects as metabolism
and excretion patterns, and the exposure regimen. For many suspected or
known carcinogens, it is not currently possible to account for these factors.
The approach for making interspecies comparisons was to use standarized
scaling factors, such as mg per kg body weight per day and per lifetime, ppm
A-2
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in the diet or water, and mg per t&2 body surface area per day. In the
absence of comparative toxicological, physiological, metabolic, and pharmaco-
kinetic data for a given suspect carcinogen, the extrapolation of body weight
weight to the 0.67 power (approximating surface area) was considered to be
appropriate.
Ultimately, the risk extrapolations were made and were presented in any
of several forms, called a potency or unit risk estimate. Under an assumption
of low-dose linearity, the unit cancer risk is expressed as the excess life-
time risk due to a continuous lifetime exposure of one unit of carcinogen
concentration. Several types of units used for analyses are shown in Table
A-l and A-2. Risks from airborne carcinogens are typically defined in terras
of lifetime exposes of ug/m3 or ppm. Drinking water risks are expressed
as either lifetime risks of exposure to a ug/1 or mg/kg body weight/day.
Other ingestion risks also use this type of expression. Typically, these
estimates are characterized as being upper-limit values in that the risks
are not likely to be higher than these values and may be significantly lower.
The listing of potency values derived from the same methodologic approach
are comparable only to a certain point, which at best may be characterized as
suitable only for prioritization purposes. This limited confidence in com-
paring potency estimates stems from the inherent requirement for judgment and
differing qualities of individual data sets which were ultimately combined to
produce a specific risk estimation.
Potency Estimates Used For This Report
Tables A-l and A-2 present the potency estimates used in the regulatory
risk assessments summarized in Appendix B. In addition to the potency esti-
mate (expressed in the units cited in the original assessment), information
is presented on the route of exposure, whether the estimate is based on
human (epidemiologic) data, and which environmental problem area(s) relied
on a given potency.
In general, differing potency estimates for the same chemical result
merely from differing units used in analyses. Occasionally, potencies for a
given substance will vary with the route of exposure (e.g., vinyl chloride).
In at least one case, that of chloroform at Municipal Nonhazardous Waste
Sites, an outdated potency estimate is cited, because we could not easily
incorporate the most recent estimate into the analysis.
A-3
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Table A-l
Cancer Potency Estimates Used To Generate Quantitative
Risk Estimates: Nonradiation-Based Estmiates
Substance
Acenapthene
Acrylamide
Acrylonitrile
Alachlor
Potency Estimate
11.5 mg/kg/day
3.7 mg/kg/day
2.4 x 10"1 mg/kg/day
1.0 x 1CT1 mg/kg/day
Alar (Daminozide) 2.3 x 10~2 mg/kg/day
Arsenic
15 mg/kg/day
Route Of Exposure
Ingestion
Ingestion
Ingestion
Ingestion
Ingestion
Ingestion
4.3 x 10~3 ug/m3/lifetime Inhalation
Asbestos
Benzene
7.6 x 1CT3 ug/m3/lifetime
Not reported
8.3 x 10~6 ug/m3/lifetime
2.9 x 10~2 rag/kg/day
Inhalation
Inhalation
Ingestion
Beryllium
8.4 mg/kg/day
Ingestion
Inhalation
Human
Problem Areas Data?
Hazardous Waste - Active No
Drinking Water No
Hazardous Waste - Active No
Drinking Water No
Pesticide Residues No
Pesticide Application No
Pesticide Residues No
Pesticide Application No
Mining Waste Yes
Nonhaz. Waste — Industrial Yes
Hazardous Waste — Inactive Yes
Hazardous Waste — Active Yes
Drinking Water Yes
Contaminated Sludge Yes
Haz./Toxic Air Pollutants Yes
Nonhaz. Waste — Municipal Yes
Haz./Toxic Air Pollutants Yes
Worker Exposures Yes
Haz./Toxic Air Pollutants Yes
Hazardous Waste - Inactive Yes
Storage Tanks Yes
Nonhaz. Waste — Industrial Yes
Hazardous Waste — Active Yes
Drinking Water Yes
Indoor Air
Drinking Water Yes
Contaminated Sludge Yes
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I
Ul
Substance
1,3-Butadiene
Cadmium
Carbon
Tetrachloride
Chlordane
Chlordimeform
Potency Estimate Route of Exposure
2.8 x 10-4 ug/m3/lifetime Inhalation
1.8 x 10-3 ug/m3/lifetime Inhalation
6.10 mg/kg/day Ingestion
Inhalation
1.5 x 10-5 ug/m3/lifetime Inhalation
1.3 x 10"! mg/kg/day Ingestion
1.6 mg/kg/day Ingestion
1.28 mg/kg/day Ingestion
9.4 x 10"! mg/kg/day Ingestion
Chloroform 2.3 x 10"5 ug/m3/lifetime Inhalation
Chromium
(hexavalent only)
Coke Oven
Emissions
Dibromo-
chloropropane
para-Dichlorodi-
benzene
1,2-Dichloroethane
8.1 x 10~2 mg/kg/day
7.0 x 10~2 mg/kg/day
41 mg/kg/day
1.2 x 10-2 ug/m3/lifetime
6.2 x 10"3 mg/kg/day
1.4 mg/kg/day
6.0 x 10-3 mg/kg/day
2.6 x 10-5 ug/m3/lifetime
9.1 x 10-2 mg/kg/day
Ingestion
Ingestion
Both
Both
Both
Inhalation
Inhalation
Ingestion
Inhalation
Inhalation
Ingestion
Human
Problem Areas Data?
Haz./Toxic Air Pollutants No
Haz./Toxic Air Pollutants Yes
Hazardous Waste — Active Yes
Nonhaz. Waste — Municipal Yes
Contaminated Sludge Yes
Haz./Toxic Air Pollutants No
Indoor Air No
Drinking Water No
Drinking Water No
Contaminated Sludge No
Pesticide Residues No
Pesticide Application No
Haz./Toxic Air Pollutants No
Indoor Air No
Hazardous Waste — Active No
Nonhaz. Waste — Industrial No
Hazardous Waste — Active Yes
Nonhaz. Waste — Municipal Yes
Contaminated Sludge Yes
Haz./Toxic Air Pollutants Yes
Haz./Toxic Air Pollutants Yes
Drinking Water No
Consumer Products No
Indoor Air No
Haz./Toxic Air Pollutants No
Hazardous Waste — Inactive No
Drinking Water No
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Substance
Potency Estimate
2,4-Dinitrotoluene 3.1 x 10"1 mg/kg/day
Dioxin (2378-TCDD) 1.6 x 10~5 rag/kg/day
Eplchlorhydrin 9.9 x 10"3 mg/kg/day
Route Of Exposure
Ingestion
Ingestion
Ingestion
Problem Areas
Hazardous Waste — Active
Drinking Water
Drinking Water
Human
Data?
No
No
No
>
I
Ethylene Dibromide 2.0 x 10"~3 ug/1/lifetime Ingestion
Ethylene Oxide 1.0 x 10~4 ug/m3/lifetime Inhalation
Ethylene Thiourea 6.3 x 10~1 mg/kg/day Ingestion
Foplet
Formaldehyde
3.5 x 10~3 mg/kg/day Ingestion
1.3 x 10~5 ug/m3/lifetime Inhalation
Gasoline Vapors 3.1 x 10~3 ppm/lifetime Inhalation
Methylene Chloride 4.1 x 10~6 ug/m3/lifetime Inhalation
7.5 x 10~3 rag/kg/day Ingestion
1.4 x 10~2 mg/kg/day Both
Polycyclic Organic 3.6 x 10~^ ug/1/lifetime Ingestion
Hydrocarbons
Polychlorinated 4.3 mg/kg/day Ingestion
Biphenyls
Products of
Incomplete
Combustion
4.3 x 10"1 ug/m3/lifetime Inhalation
Drinking Water
Haz./Toxic Air Pollutants
Pesticide Residues
Pesticide Application
Pesticide Residues
Pesticide Application
Haz./Toxic Air Pollutants
Consumer Products
Worker Exposures
Haz./Toxic Air Pollutants
Haz./Toxic Air Pollutants
Drinking Water
Worker Exposures
Consumer Products
Hazardous Waste — Active
Drinking Water
Drinking Water
Contaminated Sludge
Haz./Toxic Air Pollutants
No
No
No
No
No
No
No
No
No
No
No
No
No
No
No
No
No
No
No
-------
>
Substance
Telone II
1,1,2,2 - Tetra-
chloroethane
Tetrachloro-
ethylene
Tobacco Smoke
Toluene Dlamine
Toxaphene
Potency Estimate
1.7 x 10-5 mg/kg/day
2.0 x 10-1 mg/kg/day
5.8 x 1(T7 ug/m3/lifetime
5.0 x 10~2 mg/kg/day
2.0 x 10~2 mg daily tar/
40 years
2.9 x lO"1 mg/kg/day
1.1 mg/kg/day
Trichloroethylene 1.3 x 10~6 ug/m3/lifetime
1.1 x ID'2 mg/kg/day
Route of Exposure
Ingestion
Ingestion
Inhalation
Both
Inhalation
Ingestion
Ingestion
Inhalation
Ingestion
TSDF Emissions
Vinyl Chloride
1.5 x 10~5 ug/m3/lifetime Inhalation
4.1 x 10~6 ug/m3/lifetime Inhalation
2.3 mg/kg/day Ingestion
1.8 x 10~2 mg/kg/day Ingestion
Human
Problem Areas Data?
Pesticide Residues No
Pesticide Application No
Nonhaz. Waste — Municipal No
Haz./Toxic Air Pollutants No
Indoor Air No
Worker Exposures No
Hazardous Waste — Inactive No
Hazardous Waste — Active No
Indoor Air Yes
Hazardous Waste — Active No
Drinking Water No
Contaminated Sludge No
Haz./Toxic Air Pollutants No
Indoor Air No
Hazardous Waste — Inactive No
Drinking Water No
Haz./Toxic Air Pollutants No
Haz./Toxic Air Pollutants Yes
Hazardous Waste — Inactive No
Drinking Water No
Nonhaz. Waste — Municipal No
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Table A-2
CO
Cancer Potency Estimates Used to Generate Quantitative
Substance
Radiation (Total Pop.)
Radiation (Adults)
Radium 226
Radium 228
Radon
Risk Estimates: Radiation-Baded Estimates
Potency Estimate
) 3.0 x 10~4 fatal cancers/person-rem
2.0 x 10~4 fatal cancers/person-rem
1.0 x 10-5 pCi/1/lifetime
5.0 x 10~6 pCi/1/lifetime
1.2 x 10~3 cancers/person- WLM
1.0 x 10~7 pCi/1/lifetime
1.5 x 10~5 person/yr/WLM
Problem Areas
Radiation
Radiation
Drinking Water
Drinking Water
Radiation
Indoor Radon
Drinking Water
Mining Waste
Human
Data?
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Uranium
1.4 x 10-6 pCi/1/lifetime
Drinking Water
Yes
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ASSESSING EXPOSURE
The main objective of any exposure assessment is to provide reliable
data and/or estimates of exposure for use in a risk assessment. Exposure
assessment may be defined as the determination or estimation (qualitative or
quantitative) of the magnitude, frequency, duration, and route of exposure.
Exposure assessments may consider past, present, and future exposures with
different techniques used for each phase — e.g., biological accumulation for
past exposures, measurement of existing exposure, and modeling of future
exposures.
The exposure asessments we used in this ranking process varied consider-
ably. This was largely due to the availability of data for each particular
environmental issue. Thus, Appendix B describes the information used to
assess each of the environmental problems. Below, we describe the relevant
sections of EPA's Guidelines for Exposure Assessment (51 FR 34042, September
24, 1986). In some cases, these guidelines were not taken into account
because many of analysis were undertaken before the guidelines were developed.
Further, the broad nature of the assessments used for this project make
much of the detail outlined in the guidelines overly ambitious. Therefore,
caution should be exercised in evaluating the exposure estimates.
The guidelines emphasize that risk assessments will be conducted on a
case-by-case basis, giving full consideration to all relevant scientific
information. The guidelines also stress that this information will be fully
presented in EPA risk assessment documents, and that EPA scientists will
identify the strengths and weaknesses of each assessment by describing uncer-
tainties, assumptions, and limitations, as well as the scientific basis
and rationale for each assessment. Finally, the guidelines are formulated
in part to bridge gaps in risk assessment methodology and data. By identify-
ing these gaps and the importance of the missing information to the risk
assessment process, EPA wishes to encourage research and analysis that will
lead to new methods of assessing risk.
The scope of exposure assessments may vary. It depends on a variety of
factors, including available data, regulatory concern, resources available,
degree of exposure, perceived toxicity. Assessments used in this project
generally extrapolated to a national level, facilitating the use of a great
many assumptions with considerable uncertainty.
Five major aspects of exposure should be addressed in any exposure
assessment: the sources of the pollutant of concern; the exposure pathways
and environmental fate; measured or estimated concentrations; exposed popula-
tions; and integrated exposure analysis. These five features are appropriate
for exposure assessments in general, whether the assessments are of a global,
national, regional, local, site-specific, work-place-related, or other scope.
The topics are appropriate for exposure assessments on new or existing chemi-
cals and radiation sources, as well as single-media and multimedia assessments.
Since exposure assessments are performed at different levels of detail, the
extent to which any assessment addresses these aspects will vary.
Sources
The points at which a substance is believed to enter the environment
A-9
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(indoor or outdoor) should be described, along with any known rates of entry.
The assessment should describe hte human activities related to the substance
and the environmental releases resulting from those activities. Seasonal
variations in environmental releases, if applicable, should also be examined.
The environmental releases can be described in terms of geographic and tempo-
ral distribution, as well as the receiving environmental media.
Exposure Pathways and Environmental Fate
The exposure pathways section should address how a pollutant moves from
the source to the exposed population or subject. For a less detailed assess-
ment, broad generalizations on environmental pathways and fate may be made.
In the absence of data — e.g., for new substances — fate estimates may have
to be predicted by analogy with data from other substances. Fate estimates
may also be made by using measurements and/or models and laboratory-derived
process rate coefficients. At any level of detail, certain pathways may be
judged insignificant and not pursued further.
Measured or Estimated Concentrations
Measurements are used to identify releases and to quantitatively estimate
both release rates and environmental concentrations. Some examples of uses
of measurements are: sampling of stacks or discharge pipes for emissions to
the environment, testing of products for chemical or radionuclide content,
testing of products for chemical or radioactive releases, sampling of appro-
priate points within a manufacturing plant to determine releases from indus-
trial processes or practices, sampling of potentially exposed populations
using personal dosimeters, and sampling of solid waste leachate for chemical
content. These data should be characterized as to accuracy, precision, and
representativeness. If actual environmental measurements are unavailable,
concentrations can be estimated by various means, including the use of fate
models (see previous section) or by analogy with existing chemicals.
Concentrations of pollutants should be estimated for all environmental
media (air, surface water, etc.) that may contribute to significant exposures.
Generally, the environmental concentrations are estimated from measurements,
mathematical models, or a combination of the two. If environmental measure-
ments are not limited by sample size or inaccuracies, then exposure assess-
ments based on measurements have precedence over estimates based on models.
The concentrations must be estimated and presented in a format consis-
tent with available dose-response information. For carcinogens, an estimate
of long-term average concentration will usually be sufficient. Future envi-
ronmental concentrations resulting from current or past releases may also
be projected. Moreover, if the agent has natural sources, the contribution
of these to environmental concentrations may be relevant.
When the estimates of the environmental concentrations are based on
mathematical models, the model results should be compared to available mea-
surements, and any significant discrepancies should be discussed. Reliable,
analytically determined values must be given precedence over estimated values
whenever significant discrepancies are found.
A-10
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Exposed Populations
Populations may be selected before an analysis is undertaken, but fre-
quently the populations will be identified as a result of the sources and
fate studies. An analysis of the distribution of the pollutant will reveal
which populations will be subject to potentially high exposure rates. This
population will then form the focus of the exposure assessment. Census and
other survey data may be used to identify and describe the population exposed
to various contaminated environmental media. Site-specific assessments then
had to be extrapolated to a national level. The methods for this step were
chosen on a case-by-case basis.
Integrated Exposure Analysis
The integrated exposure analysis combines the estimation of environmental
concentration (sources and fate information) with the description of the ex-
posed population to yield exposure estimates. Data should be provided on the
size of the exposed populations; duration, frequency, and intensity of expo-
sure; and routes of exposure. To the extent possible, behavioral and biologi-
cal characteristics of the exposed populations should be considered. In addi-
tion, an estimate of the uncertainty associated with them should be provided.
Depending on the scope of the exposure assessment, the total exposure
may be fractionated into one or more "exposure scenarios" to facilitate
quantification. For example, seven very broad scanarios are recognized:
occupational, consumer, transportation, disposal, food, drinking water, and
ambient exposures. Investigation of only one scenario may be necessary for
the scope of some assessments, as was the case for most of the environmental
issues we compared in this document. Ideally, however, all relevant exposure
scenarios should be considered.
ASSESSING RISK
Risk estimates may be in three forms: (1) the dose corresponding to a
given individual risk level; (2) excess individual lifetime risks; or (3)
the number of cancers (or cancer deaths) produced per year in the exposed
population — e.g., population risk. In this project, we have focused our
main attention on estimates of population risk, which we made by combining
potency estimates (or unit risks) with human exposure data. Irrespective of
the form we chose, however, the degree of precision and accuracy in the
numerical risk estimates usually does not allow us to use more than one
significant figure. In characterizing the risk due to concurrent exposure
to several carcinogens, the risks can be considered to be additive, unless
there is specific information to the contrary.
In every quantitative risk estimation the results are highly uncertain.
For this reason, we are usually estimating the the upper limit of risk as
opposed to an estimate of the true risk. In addition, the uncertainties due
to experimental and epidemiologic variability as well as uncertainty in the
exposure assessment can be important. There are major uncertainties in
extrapolating both from animals to humans and from high to low doses. There
are important differences in the way species and strains take in, metabolize,
and distribute carcinogens among their organs, as well as their differences
A-ll
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in target site susceptibility. Similarly, human populations are highly variable
with respect to genetic constitution, diet, occupational, and home environment,
activity patterns, and other cultural factors. The hazard assessment should
always be presented along with the risk estimates to ensure that there is an
appreciation of the weight of evidence for carcinogenicity that underlies the
quantitative risk estimates. These and other factors need to be examined when
considering the results of quantitative cancer risk assessment.
A-12
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APPENDIX B
RISK CALCULATIONS FOR SPECIFIC ENVIRONMENTAL PROBLEMS
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Appendix B
Risk Calculations for Specific Environmental Problems
This appendix presents summaries of the cancer risk information compiled
for all of the environmental problems investigated. Each of these summaries
begins with a short definition of the nature of the environmental problem,
describing its boundaries and giving examples of the problem to the extent
possible. This is followed by a discussion of the contaminants assessed, as
well as other information relevant to examining the extent of the total
problem assessed for this project.
Each summary discusses the methods used for estimating quantitative
risks. Where an approach differed from the approach taken by EPA's Carcino-
gen Assessment Group (GAG), these cancer potencies are presented, along with
an explanation of why a different approach was taken. The methods used to
estimate exposure will also be explained in this section, including the
extrapolation from specific exposures to nationwide estimates, whether contam-
inant concentration estimates are based on measured or modelled data, and
whether nonstandard assumptions are made with respect to human intake of air,
food, or water.
The final section of each summary presents the results of the risk
assessment for both population and maximum individual risk, where possible.
Some summaries also comment on the extent to which risk estimates are likely
to improve in the near future.
Throughout the summaries, uncertainties and caveats specific to each
environmental problem are addressed as they arise in the discussion. Where
particular uncertainties or caveats do not easily fit into the structure of
the summary, they are addressed at the end of the summary.
The descriptions of the individual environmental problems are arranged
in the order in which they were ranked.
B-l
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CATEGORY 1
# 1: Marker Exposure to Chemicals (tied with Indoor Radon)
PROBLEM DEFINITION
Vforkers are exposed to chemical substances in a wide range of occupa-
tional settings. These include chemical manufacturing and processing, and
the use of chemicals in industry and the trades.
According to 1977 figures, over 20,000 chemical substances are in com-
merce at greater than 10,000 kg in any one year. In addition, manufacturing
and processing operations generate a significant number of by-product
streams that are an additional source of potential exposure to workers.
Because of the diverse nature of processes and equipment and the great
range their of physical and chemical properties, occupational exposure
varies greatly in different settings. However, unlike most other environ-
mental problems, exposure to chemicals in the work place is not mediated
by environmental pathways and often occurs in confined indoor environments.
Further, significant exposures can take palce to the workers even where
relatively small amounts of the substance are involved.
Exposure to workers handling pesticides is discussed under Application
of Pesticides. Exposure to workers involved in transporting and disposing
of chemicals and wastes, as well as exposures to miners, are also not con-
sidered in this analysis.
EPA'S RESPONSIBILITIES IN PROTECTING WDRKERS
The primary federal responsibility for occupational safety and health
resides in the Occupational Safety and Health Administration. However, the
Toxic Substances Control Act (TSCA) requires EPA, in evaluating chemical
risks, to consider the full "life cycle" of chemical substances — i.e.,
manufacturing, processing, using, and disposing of chemicals. Under Section
4 of TSCA, EPA must identify which chemicals should be tested for potential
toxicity (including carcinogenicity) and require industry to test them. In
doing so, EPA must take into account the full range of potential exposures,
including exposure in the work place.
Under Section 5 of TSCA, EPA has evaluated potential occupational and
other areas of risk from over 7,000 "new chemicals." EPA has taken action
on at least 200 of these chemicals to protect workers from potential risks.
A number of regulatory actions taken under Section 4(f) and referrals of
identified problems to other agencies under Section 9 of TSCA have been
driven by concern for occupational risks. Finally, under the new Superfund
Amendments and Reauthorization Act and the recently passed asbestos abate-
ment legislation (AHERA) , EPA is given major responsibilities in protecting
publicsector employees from certain occupational chemical hazards.
B-2
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POLLUTANTS ADDRESSED IN THIS SUMMARY
Criteria for Selection of Occupational Hazards
Only limited data exist wiith respect to that portion of current cancer
incidence that may be attributed to chemical exposure in the work place.
Estimates of the contribution of occupational factors to national cancer
death rates vary from a few percent to 20 percent. To provide some perspec-
tive on the comparative risks presented by occupational exposures to chemi-
cals, as opposed to other exposures to chemicals, the cancer work group chose
substances for which estimates of both cancer potency and exposure are avail-
able. These include formaldehyde, tetrachloroethylene, methylene chloride,
and asbestos.
Evidence of the carcinogenicity of the first three of these substances
is relatively recent. As such, exposures to these substances may be higher
than exposure to substances for which evidence of carcinogenicity has been
available for some time (e.g., benzene, vinyl chloride, asbestos).
Extent to Which Risks of Selected Chemicals Represent
Total tybrk Place Cancer Risks to tibrkers
The exposure of workers to chemical substances is relatively high when
compared with the exposure of other populations. Because most occupational
settings are often indoors significant levels of airborne contamination can
result. Unless steps are taken to specifically mitigate exposure, the close
proximity of workers to the substances and processing equipment increases
the likelihood and magnitude of exposure.
The greatest number of chemical substances are likely to be found in the
occupational setting. This results from the fact that is because all commer-
cial substances must be manufactured, and a majority are used, in commercial
settings. Wiile the fraction of commercial chemical substances that are
carcinogenic is not known, it is highly likely that the risks associated
with the four substances assessed for this project represent a very small
fraction of the overall risks of cancer from chemicals in the work place.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
Cancer potencies (unit risks) used to derive estimates of individual
risk and expected annual incidence of cancers are consistent with those
developed by the Carcinogen Assessment Group. However, for tetrachloro-
ethylene and for methylene chloride, unit risk estimates are derived from
the risk assessment conducted by the Office of Toxic Substances. These assess-
ments are currently being reevaluated by an other EPA work group. For methylene
chloride, this effort includes reviewing additional data developed by industry.
Exposure Assessment
The exposure-related information used to evaluate occupational risks in
eludes estimates of both the number of workers exposed and the magnitude of
the individual exposure. The magnitude of exposure involves estimates of air
B-3
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concentration (the degree of contact in the case of dermal exposure) and the
duration of exposure. Unless otherwise indicated, individual workers are
assumed to be exposed 8 hours daily, 5 days a week, over a 40-year working
lifetime.
To evaluate worker exposure, the work group has relied on the predictive
methodologies developed by the Office of Toxic Substances. It has also
used available work-place monitoring data, typically developed by industry
to monitor compliance with existing standards.
The exposure estimates used to for this project have a number of limita-
tions. For example, estimates of the total number of workers exposed to a
chemical agent are often based on the total number of workers known to be in-
volved in a particular industry sector. The fraction of these workers actual-
ly exposed to the agent may not be well characterized. The actual magnitude
of exposure will typically have a broad distribution, based on the range of
equipment and practices in the user industry. In addition, it is often not
known to what extent monitoring data are "representative" of exposures ex-
perienced by the majority of workers.
For these reasons, exposures are sometimes expressed as a range of
values. In these cases, a single value — which represents the average or
mean of the actual exposures anticipated — is used to estimate total occupa-
tional risks.
ESTIMATED RISK
The estimates of occupational risks are based on the exposure estimates
and unit-risk estimates described above. The anticipated incidence of cancer
based on 40 year exposure period for these four substances is shown below.
Estimated Occupational
Substance Annual Cancer Incidence
Formaldehyde 100
Methylene Chloride 90
Tetrachloroethylene 10
Asbestos 55
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CATEGORY 1
#1; Indoor Radon (tied with Worker Exposure to Chemicals)
PROBLEM DEFINITION
Radon is a radioactive noble gas produced by the decay of radium, which
occurs naturally in almost all soil and rock. Because radon is chemically
inert, it is not retained by most body tissues and poses very little direct
health risk. However, inhaled radioactive decay products of radon, known as
radon daughters, deposit in the air passages of the lung, and emit alpha par-
ticles that irradiate bronchial epithelium, possibly leading to lung cancer.
Concentrations of radon daughters are ordinarily given in units of working
levels (WL), which were first derived in occupational studies. Exposure
(concentration x time) is usually expressed in working-level months (WLM).
The greatest health risks from radon occur when it moves through the
soil into houses where it is trapped, producing a build-up of the radon
daughters. Radon can also emanate from a house's building materials or
enter a house through drinking water (see Drinking Water) or natural gas
that is piped in.
RISK ASSESSMENT METHODOLOGY
That inhaled radon daughters can cause lung cancer is well documented
for both laboratory animals and humans. Risk estimates are based on epidemi-
ological studies of exposed cohorts of miners, primarily uranium miners. It
is assumed that the risk is proportional to past WLM exposure (adjusted for
a 10-year minimum latency period between exposure and cancer onset), with no
threshold.
Laboratory experiments at the cellular level, as well as on whole ani-
mals, suggest that the risk from alpha particle irradiation is likely to be
proportional to dose. However, at relatively high doses the risk per unit
dose falls off because of cell killing. Human epidemiclogical evidence is
consistent with this view.
National exposure estimates are derived from monitoring data collected
in homes across the U.S. and extrapolated to the entire country.
In calculating risk, EPA uses a relative risk model. This model assumes
that the risk of lung cancer is proportional to the baseline incidence rate
of the disease in the population. Effectively, this means that as baseline
lung cancer rates vary according to population characteristics (primarily
age, sex, and smoking histories), estimates of risks of radon-induced lung
cancer vary in parallel. The evidence in favor of a relative risk model is
not conclusive, but studies of U.S. uranium miners strongly indicate that
smoking and radon are more than additive and quite possibly multiplicative
in their effects on lung cancer risk.
Based on an examination of the epidemic logical evidence on miners exposed
to various levels of radon, EPA has adopted a range of relative risk factors:
l%-4% pe~r WLM (EPA, 1986). In other words, the chance of developing lung
B-6
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cancer increases by between 1% and 4% for every WLM of exposure*. In evalu-
ating the risk to the general public, EPA adjusts the estimated exposure for
reduced average breathing rates in the general population, as compared to
miners, and for differences in the lung morphology of children (EPA, 1986).
Consequently, EPA's risk estimates for the general public correspond to a
range of about 0.6% to 2.4% per WLM, when expressed in standard units of
exposure.
ESTIMATE OF RISK
The number of lung cancers induced by radon each year has been estimated
to lie in the range of 5,000 to 20,000. The number of predicted cancers is
approximately proportional to the average level of radon daughters in homes.
This average level is still uncertain, but estimates have recently been rising
as more homes are measured for radon. Moreover, if lung cancer estimates are
calculated using a relative risk model, they will vary with changes in the
baseline incidence of lung cancer. Because lung cancer rates have been in-
creasing in recent years, the 5,000 - 20,000 estimate may have to be revised
upward.
Some may question these estimates on the ground that when the fraction
of excess lung cancers attributed to radon is added to the fraction attributed
to smoking (about 85% according to the Surgeon General), the total may exceed
100%. There is actually no inconsistency, because both radon and smoking
may be causal factors for a single lung cancer. Indeed, according to the
relative risk model, for the great majority of radon induced lung cancers,
smoking is also causal.
REFERENCE
U.S. EPA. Final Rule for Radon-222 Emissions from Licensed Uranium Mill
Tailings; Background Information Document. EPA 520/1-86-009. August 1986.
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CATEGORY 1
#3: Pesticide Residues on Foods
PROBLEM DEFINITION
EPA currently registers pesticide products for agricultural use that
contain at least 600 active ingredients. These include chemicals used as
insecticides, fungicides, herbicides, and rodenticides. Due to the wide use
of these agents on food crops and their potential to induce deleterious tox-
ic effects, including cancer, all require thorough assessment of their po-
tential hazard to humans. EPA also registers several hundred other nonagri-
cultural pesticide products. Although these may not result in significant
dietary exposure to humans, they nevertheless require similar hazard assess-
ment because of other modes of human exposure.
The spectrum of toxic effects capable of being induced by pesticides is
great. It includes specific organ toxicity, reproductive/teratogenic effects,
mutagenic effects, and cancer. Many of these changes are often produced by
single pesticide chemicals in the controlled laboratory environment, but
actually may result from additive and/or synergistic effects of exposure to
multiple pesticides in concert under normal agricultural, as well as nonagri-
cultural, use conditions. Thus, the scope of this environmental problem is
wide, resulting from the use of avast number of pesticides in the greater
human environment.
As is the case for innumerable other chemicals to which humans are ex-
posed, an area of great concern with respect to the use of pesticides is the
induction of cancer. The actual number of pesticides that have the potential
to induce a carcinogenic response is not known with certainty. The Office of
Pesticide Programs is currently surveying its inventory of pesticide chemicals
to determine which have had a sufficient number of valid rodent oncogenicity
studies performed on them (usually two oncogenicity studies per chemical) to
estimate the magnitude of this problem. To date, it is estimated that about
200 of the total of 600 agricultural use chemicals subject to EPA registra-
tion have been adequately tested for oncogenicity in animals. Of these 200
chemicals, about 60 have been identified as being potential oncogens. By
extrapolation, therefore, the Office of Pesticide Programs considers it
reasonable to assume that from the total of 600 agricultural-use pesticide
active ingredients, as many as one-third, or 200, could be oncogenic.
RISK ASSESSMENT METHODOLOGY
Data Sources
EPA's two main sources for toxicologic data on pesticide chemicals are
the regulated industry and the National Toxicology Program (NTP). The primary
source of data is agricultural chemical companies in support of the field
testing and registration of pesticides on crops within the United States.
These companies have data on both new and existing pesticides. The Office
of Pesticide Programs has already reviewed an extensive number of toxicity
studies on such chemicals, but its inventory is far from complete, particular-
ly in the case of older pesticides that were used domestically before the
B-8
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initiation of more comprehensive testing for oncogenicity. To obtain this
additional information, EPA has established a "data-call-in" procedure, where-
by pesticide manufacturers must provide EPA all the data available on pesti-
cides subject to EPA registration.
Through its Toxicology Research and Testing Program, the NTP has complet-
ed short- and long-term animal toxicology and mutagenicity tests on several
pesticides. In addition, several other pesticides are being tested or are
scheduled for testing. The NTP studies, which primarily involve older pesti-
cide chemicals, are published as technical reports that are available to the
general public and/or in the open scientific literature. The Office of
Pesticide Programs is in close communication with the NTP on a routine basis
and regularly receives newly generated data for evaluation and incorporation
into its regulating activities.
Data Assessment
All toxicologic data received by the Office of Pesticide Programs in sup-
port of a pesticide application are independently reviewed by professional
staff scientists employed in the Toxicology Branch. All toxicologic studies
submitted by industry are evaluated in-house because of their critical nature
in hazard identification. Similarly, all toxicologic studies obtained from
the NTP or other public sources are reevaluated within the Branch as a matter
of internal procedure.
For the following reasons, the data assessment or review process is
extensive, complex, and time-consuming:
o The Office of Pesticide Programs is evaluating 600-1,000 active
ingredients in pesticides for registration.
o Each of the active ingredients has been the subject of many complex
biological studies that have been performed to characterize its toxi-
cological profile. These studies commonly include several acute
toxicity tests, mutagenicity studies, reproduction and teratology
tests, pharmacokinetic assessments, subchronic and chronic tests, and
one or more oncogenicity studies.
o Each study requires a thorough, detailed review by a staff scientist
to assess its scientific validity and content. This review may require
from 8 hours for a single acute toxicity test to 240 hours for a
single oncogenicity study. Very often, 1,000 hours (0.5 person-year)
are spent reviewing all of the studies submitted in support of the
registration of a single pesticide ingredient.
o If oncogenic effects are apparent in the data base, additional work
in reviewing the data base and in assisting regulatory activity is
required, often involving 0.25 person-year/chemical.
Exposure Estimates
National exposure to pesticide residues is estimated either by using
tolerances or by determining actual pesticide residues on food as it is
consumed. The Office of Pesticide Programs uses tolerances to regulate the
use of agricultural chemicals. They represent the legal maximum of pesticide
B-9
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residues that are allowed to remain on raw agricultural commodities.
To estimate human exposure to pesticide residues on food crops, we added
these tolerances, the average daily per capita food consumption figures for
the crops, and the exposure figures for each crop. This addition provides
the total maximum residue contribution (TMRC) for each particular pesticide
chemical. The TMRC represents an upper-limit estimate of average human expo-
sure to pesticide residues because it includes tolerances for all raw agricul-
tural commodities on which the pesticide is used.
The estimation of pesticide-related human cancer risks within the Office
of Pesticide Programs requires a determination of the actual residue levels
on foods as they are consumed, and the effect of food processing on the resi-
dues that are contained in the foods. To obtain this information, the Office
of Pesticide Programs has recently developed a food consumption matrix, known
as the Tolerance Assessment System (TAS). This system provides data (1) on
the primary foods consumed by particular segments of the U.S. population —
such as children, the aged, and ethnic or regional groups; (2) on the range
of variation of consumption within any group; (3) on whether the food is
consumed raw, cooked, or processed; and (4) on seasonal variations in food
consumption.
In summary, TMRCs, based on levels of residue tolerances, provide a guide-
post for dietary exposure assessments in relation to raw agricultural commodi-
ties. The TAS, however, facilitates the translation of residues on raw agri-
cultural commodities into human exposure estimates by generating much more
extensive and accurate residue data that can be matched to food items as they
are consumed. The result is an estimate of actual residue consumption that
can be used to address specific issues, such as human cancer risks related
to dietary exposure of the U.S. population to pesticides.
The Office of Pesticide Programs has already used the TAS in regard to
several oncogenic pesticide chemicals. It has found that, on the average,
the actual exposure of humans to the pesticides in question is approximately
50 times less than described using tolerance methods.
Risk Calculation
The quantification of human cancer risk from pesticide residues is based
on animal toxicologic data. The oncogenic dose-response data in an animal
study, are extrapolated into regions of progressively lower exposure. Using
mathematical models accepted by EPA yeilds a sliding scale linking risk
probabilities to exposure. Potency estimates (expressed as risks per unit
exposure in mg/kg/day) for humans are calculated for low doses. These methods
are consistent with EPA's Guidelines for Carcinogenic Risk Assessment.
ESTIMATED RISKS
In the present survey, a sample of the human population risk from pesti-
cide residues was obtained by evaluating exposure information, using TMRC or
tolerance methods for seven oncogenic chemicals.
The average population risk for these seven chemicals from dietary expo-
sure was estimated to be 100,000 people per lifetime for each chemical. Cal-
B-10
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culations using TMRCs are known to represent an upper limit of Che population
risk, and calculations using TAS average exposure may be as much as 50-fold
lower than those based on TMRCs. Thus, the value of 100,000 people/lifetime/
chemical was divided by 50 to yield a more representative risk estimate of
2,000 people/lifetime/chemical. Further mathematical manipulation of the
figure to reach a risk estimate for each chemical on a yearly basis (i.e.,
dividing 2,000 people/lifetime/chemical by 70 years, the average lifespan)
yields a value of approximately 30 people/year/ chemical as the expected
risk. Since the Office of Pesticide Programs has estimated that as many as
200 pesticide chemicals may be oncogenic, the total annual population risk
from dietary exposure to these chemicals is about 6,000 people/year (i.e.,
30 people/year/chemical x 200 oncogenic chemicals)"^
UNCERTAINTIES
Several uncertainties are associated with human risk assessments resul-
ting from exposure to pesticide residues. The prominent uncertainties include
the following examples.
First, the actual amount of pesticide residues consumed by humans is
not known with certainty. Estimations of consumption are usually made for
residues contained on individual crops, and these are often added together
to obtain "representative" values. However, the entire national crop is
often not treated at the same time with a particular pesticide. In addition,
food crops are not equally consumed by all Americans. There are usually
significant differences in consumption for ethnic, age, sex, socioeconomic,
and regional groups, and food processing may alter the levels of residues on
foods. Finally, there may in fact be residues of multiple pesticides on
crops. Factors such as these make determinations of actual residues consumed
difficult to obtain. However, the TAS in use in the Office of Pesticide
Programs takes most of these factors into account. It is assumed to be a
good predictor of the types and amounts of pesticide residues consumed by
humans.
Second, there is uncertainty in extrapolating observed toxicological
effects in animals to expected effects in humans. For example, different
species respond differently to toxic chemicals, experimental animals are
usually exposed to pesticides on a continuing basis at high dosage levels in
order to deliberately evoke and thus define toxic responses for chemicals,
and some toxic effects occur in animals but are rarely seen in the human
population (e.g., liver tumors in mice). To the extent that is possible,
the Office of Pesticide Programs attempts to minimize these problems by
thoroughly evaluating all available animal toxicity data on individual pesti-
cides before extrapolating possible hazards to humans. It does this through
the Toxicology Branch Peer Review Committee, which conducts "weight-of-the-
evidence" meetings on pesticides and determines, using the EPA Guidelines
for Carcinogen Risk Assessment, whether they are likely to be human oncogens.
Third, the mathematical low-dose extrapolation procedures used in animal
studies to quantify human risks for pesticide residues are uncertain. This
uncertainty stems largely from the fact that the mechanisms of action respon-
sible for inducing oncogenic responses for pesticides are unknown. This
situation, however, pertains to all chemicals reported to be oncogens.
B-ll
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CATEGORY 1
#4; Indoor Air Pollution (tied with Consumer Products Exposure)
PROBLEM DEFINITION
On average, people spend nearly 90 percent of their time indoors. More-
over, for many pollutants, indoor levels are considerably higher than outdoor
levels. Therefore, for most persons, indoor exposures to air pollution
predominate over outdoor exposures.
Indoor air pollution is an accumulation of contaminants in building air.
The sources of these contaminants are primarily within the building, although
outdoor sources also contribute. Building design, construction, and operation
also affect the accumulation and dispersion of indoor air pollutants. The
primary means of limiting this accumulation of indoor pollutants is air ex-
change between indoor and outdoor microenvironments. In general, concentra-
tions of indoor pollutants are directly proportional to the number of sources
per unit volume and inversely proportional to the the rate at which more pol-
luted indoor air is exchanged with less polluted outdoor air. National trends
toward energy conservation, increased use of synthetic chemicals, and ignorance
of good ventilation and housekeeping practices have all led to a rise in
indoor air pollution.
Indoor Air Pollution in Residential Buildings
There are about 100 million housing units in the U.S., with roughly two
million new housing units built each year. The Department of Energy has
estimated that air exchange rates in new construction are, on average, 50
percent lower than the national average. Given this trend in air exchange
rates, the concentration of indoor pollutants will double if emission rates
stay the same.
Carcinogenic indoor pollutants may be generated by a variety of sources.
Some of these are outlined below.
o New types of insulation: Urea-formaldehyde foam insulation came into
widespread use in retrofitting older, uninsulated homes in the late
1970's. The indoor air pollution potential of this material , which
emits free formaldehyde, was not well understood. As a result, many
homeowners have been exposed to considerable indoor concentrations
of fo rmaldehyde.
o Pesticides; An estimated 84% of U.S. households use pesticides in
the home. Recently, EPA's Office of Pesticide Programs has begun
regulatory action to address the carcinogenic potential of some pesti-
cide products. In some cases, termiticides have been misapplied in
homes by commercial applicators, whereby chlordane has been accidental-
ly introduced into subslab heating ducts, contaminating the home.
o Environmental Tobacco Smoke (ETS): The 1986 Surgeon General's Report
has identified ETS as a cause of disease, including lung cancer, in
nonsmokers. A 1986 report of the National Academy of Sciences has
estimated that ETS in the home causes about a 30% increase in lung
B-12
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cancer risk in nonsmoking spouses. Estimates of lung cancer mortality
range from about 500 to 7,000 deaths per year.
o Ventilation; Furnaces, hot water heaters, woodstoves, and fireplaces
in overtight houses may require more combustion air than is available,
resulting in negative pressures creating backdrafting of chimneys.
Carcinogenic termiticides have accidentally been introduced into
forced-air heating systems. Overtight homes may have high levels of
humidity leading to overgrowth of molds and fungi, producing carcin-
ogenic mycotoxins. Electrostatic precipitator air cleaners and filters
that are not cleaned may yield carcinogenic volatile organic compounds
(VOCs) from trapped tobacco smoke.
o Asbestos; Friable asbestos on furnaces and pipes in older homes and
misused asbestos shingles may increase cancer risks.
o Organics: Emissions of volatile organic compounds from (1) oven
cleaners and hairsprays, (2) arts and crafts materials and home work-
shops, (3) solvents from cleaning and waxing agents, and (4) paints
and refinishing compounds may increase exposure to a variety of air
toxics. EPA°s Total Exposure Assessment Methodology (TEAM) study has
found such carcinogens as benzene, ethylbenzene, trichloroethane,
trichloroethylene, tetrachloroethylene, carbon tetrachloride, chloro-
form, and meta- and para-dichlorobenzenes to be commonly present in
indoor air. Wood preservatives have caused toxic levels of pentachloro-
phenol to accumulate in log dwellings wrongly built with treated logs.
Emissions of VOCs from drinking water may increase exposure to carcino-
genic air toxics. Emissions of benzene and other carcinogenic hydro-
carbons may occur from gasoline tanks of automobiles in parking garages
in residences and commercial buildings and become entrained in the
building air by diffusion. Some limited attempts at assessing carcino-
genic risks of indoor VOCs in residential structures have been made
and are summarized on page B-15.
Indoor Air Pollution in Nonresidential Buildings
This discussion will be confined to nonindustrial nonresidential buil-
dings. The carcinogenic risks of pollutants in such buildings generally
have not been quantified, except for tobacco smoke. Indoor air pollution in
industrial buildings is considered under Worker Exposure to Chemicals.
In new and remodeled buildings, paints, solvents, glues, caulking, new
carpeting, emissions from particle board, and other sources, outgas, causing
high initial levels of volatile organic compounds which generally diminish as
the building ages. Buildings usually are not outgassed at high temperatures
before occupancy, and may even be occupied before completion of construction
or during remodeling. Further, ductwork may not be protected from entry of
dusts, including roofing tar or asbestos generated during construction.
Ventilation systems designed primarily for thermal load control may
leave the building unventilated for long periods of time, allowing pollutant
loadings to build up. Ventilation rates designed for acceptable indoor air
quality may not be required by local building codes, nor enforced if they are.
B-13
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RISK ASSESSMENT METHODOLOGY
Since extensive measurements do not exist for the wide range of poten-
tial indoor carcinogens in buildings, modeling on the basis of limited mea-
surements is at present the only method to for assessing the cancer risk of
selected pollutants. A simple indoor air pollution transport model based on
the mass-balance equation has been developed to relate the concentration
A(t) of a pollutant at time t to the generation rate G, removal rate R, and
the building volume V:
A(t) = [G/(VR)J x [1 - e-Rt] .
For pollutants that are emitted more or less continuously, the time-depen-
dent part of this equation becomes unity, and the equilibrium concentration
of the pollutant Aeq (e.g., in units of micrograms per cubic meter or ppm)
is determined by the ratio of the source emission density (G/V) (e.g., in
units of micrograms per hour per cubic meter) to the removal rate R (e.g.,
in units of air changes per hour; one air change per hour is 1.44 times the
halflife for pollutant removal). The amount of pollutant inhaled, I, in
units of mass inhaled per unit time is given by the equation:
I = A B T,
where A is the average concentration of the pollutant in the building during
time T, B is the average breathing rate of the individual over time T, and T
is the duration of time spent in the building. The lifetime risk, X, of
exposure to a given pollutant is then estimated from the equation:
X = I D L,
where D is the dose-response function for the pollutant (e.g., cancer cases
or deaths per 100,000 person-years per unit mass of pollutant inhaled per
unit time), and L is the exposure lifetime in years. Using analogous methods,
Wallace (1986), Tancrede et al. (1986), and Repace and Lowrey (1985) have
published preliminary risk assessments on a limited number of indoor pollu-
tants.
A summary of the quantitative information compiled for this report
follows.
Environmental Tobacco Smoke (ETS)
There is a considerable amount of epidemiologic data on smokers, with
smoking associated with cancers of the lung, larynx, oral cavity, esophagus,
bladder, pancreas, and kidney. With respect to passive smoking, epidemiologic
studies have definitely established a link between exposure to environmental
tobacco smoke and lung cancer, with some reports suggesting increases in
brain tumors and hematopoeitic cancers.
A potency estimate has been calculated by Repace and Lowrey (1985),
using a phenomenological model. This model predicts five lung cancer deaths
per 100,000 person-years per milligram of tobacco tar inhaled per day or,
alternatively, 2 x 10~3 for of 40 years exposure (Repace and Lowrey, 1986).
Using a potency estimate derived from a 1-hit or multistage model (extrap-
olating from risks in smokers) yields a potency estimate that is one-tenth
B-14
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as large. However, these results are inconsistent with epidemic logic obser-
vations in nonsmokers. Repace and Lowrey (1986) have postulated that these
underestimates result from the large doses received by smokers; the slope of
the exposure-response relationship for somewhat lower exposures experienced
by nonsmokers is steeper than predicted by extrapolations from smokers.
There have been several attempts to quantify the cancer risks from ETS
exposure. According to the National Acadamy of Science (NAS, 1986), domestic
exposure is expected to increase risk of lung cancer by 30%. The aforemen-
tioned phenomenological model of Repace and Lowrey estimates very similar
results, on the order of 26%. Total estimated mortality from domestic expo-
sure is 2,400 lung cancer deaths/year (NAS, 1986); total estimated mortality
from domestic plus work place exposure is 5,000 lung cancer deaths/year
(Repace and Lowrey, 1985). Based on Repace-Lowrey phencmenological model,
estimated lifetime risk to most-exposed individual is 3% (3 x 10~2).
Volatile Organic Indoor Pollutants
With respect to the nationwide U.S. population risks, the best estimate
available has been developed by Wallace (1986). On the basis of monitoring
results from 600 homes in four states (New Jersey, North Carolina, North Da-
kota, and California), Wallace estimates 1,240 deaths per year across the na-
tion from six organic pollutants (benzene, para-dichlorobenzene, chloroform,
carbon tetrachloride, tetrachloroethylene , trichloroethylene). These risks
are based on potency estimates developed by EPA's Carcinogen Assessment
Group (CAG).
Tancrede et al. (1986) calculated average lifetime risks of 2xlO~3 on
the basis of monitoring of four homes in the Netherlands. Risks at the 98th
percentile from 45 selected indoor pollutants are on the order of 10~2. This
study used risk estimates based on "human, animal data, and analogy"; it is
difficult to assess how these potencies compare to CAG estimates.
B-15
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REFERENCES
IARC Monograph 38 (1986).
National Research Council, Committee on Passive Smoking, Board on Environmental
Studies and Toxicology (1986) Environmental Tobacco Smoke: Measuring Exposures
and Assessing Health Effects. National Academy Press, Washington, B.C.
Repace, J.L., and A.H. Lowrey (1985). Environment International 11; 3-23.
Repace J.L. and A.H. Lowrey (1986). Environmental Carcinogenisis Reviews (in
press).
Tancrede, M. , R. Wilson, L. Zeise, and E.A.D. Crouch. The Carcinogenic Risk
Of Organic Vapors Indoors: A Survey. Energy & Environmental Policy Discussion
paper, JFK School of Govt. , Harvard Univ. , June 1986.
U.S. Surgeon General (1986). The Health Consequences of Involuntary Smoking.
Wallace, L.A. (1986). "Estimating Risk from Measured Exposures to 6 Suspect
Carcinogens in Personal Air & Drinking Water in 600 U.S. Residences." Air
Pollution Control Association paper 86-66.4.
Weiss, S. (1986) Am. Rev. Resp. Pis. 133: 1-3.
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CATEGORY 1
#4; Consumer Product Exposure (tied with Indoor Air Pollution)
RROBLEM DEFINITION
This problem area includes risks that are incurred as a result of the
direct exposure of users to chemical substances in consumer products. There
are over 10,000 chemical substances in consumer products. These substances
are present in two categories of products: (1) in formulations and mixtures
of various types (paints, solvents, glues, detergents, polishes, deoderizers,
etc.), and in (2) manufactured articles (clothing, housewares, batteries,
etc). Wiile exposure to the chemicals in manufactured articles is usually
limited, experience has shown that potential risks can sometimes be signifi-
cant — e.g«, TRIS used on pajamas, friable asbestos in electrical products,
DEHP in plastic articles mouthed by young children, and formaldehyde emissions
from pressed-wood products.
This envirormental problem area does not include the exposure of the
general public that results from substances released from the product into
the environment and transported beyond the immediate vicinity of the user—
e.g., contamination of drinking water or nonpoint source air pollution.
Wiere consumer products, used indoors, contaminate the indoor air, any re-
sulting risks are likely to be double counted as a consumer product risk and
as an indoor air problem.
EPA'S RESPONSIBILITY TOWARD PROTECTING CONSUMERS
The Consumer Product Safety Commission has the major federal responsi-
bility for ensuring that chemicals used in consumer products do not present
health risks. However, EPA has been given several responsibilities related
to identifying and reducing risks in consumer products. The Toxic Substances
Control Act (TSCA) requires EPA to consider the full exposure to chemicals
in regulating under the Act. Under Section 4 of TSCA EPA must identify which
chemicals should be tested for potential toxicity (including carcinogenicity)
and require industry to test them. A number of Test Rules published by EPA
have been based, in whole or in part, on the concern for consumer risks.
EPA's proposed ban of certain asbestos products and phase-down of the
manufacture and import of asbestos was based on concern for the life cycle
exposure (including consumer exposure) to asbestos. EPA's priority review
of methylene chloride under 4(f) of TSCA was based in large part on the
potential carcinogenic risks presented to users of paint strippers containing
this substance.
POLLUTANTS ADDRESSED IN THIS SUMMARY
Criteria for Selection of Consumer Hazards
Because of market pressures, carcinogenic substances in consumer products
are often replaced by substitutes. However, the carcinogenic potential of
these substitutes is often not well characterized.
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To illustrate the risks consumer products can present, three substances
were chosen for which information on their potential carcinogenicity is
relatively recent: methylene chloride, para-dichlorobenzene, and formaldehyde.
Asbestos was also included as there is a considerable amount of information
available on consumer exposure to this carcinogen.
Extent to Which Risks of Selected Chemicals
Represent Total Cancer Risks to Consumers
The potential exposure of consumers to chemical substances in consumer
products is relatively high in comparison to typical environmental exposures.
Numerous household products contain a great number of chemical substances.
For example, hundreds of chemical constituents may be present in paints,
solvents, thinners, and other related products. These products are typically
used indoors, and are assumed to be safe by their users. Little effort is
typically made to avoid or mitigate exposure to them.
While relatively few chemicals with established carcinogenic potential
are found in these products, many of their consituents are in similar chemi-
cal/structural classes, but have not been tested in long-term animal bioassays.
Because of the number of users of such products and the magnitude of exposures,
the risks of the few selected substances presented here are probably only a
fraction of those that are likely to be identified as a result of future
testing.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
Cancer potencies (unit risks) used to derive estimates of individual
risk and expected annual incidence of cancers are consistent with those
developed by the Carcinogen Assessment Group. For methylene chloride, the
unit risk estimate was derived from the risk assessment conducted by the
Office of Toxic Substances. The assessment is currently being reevaluated
by EPA in order to review additional data and a number of issues raised by
industry.
Exposure Assessment
The exposure-related information used to evaluate consumer risks includes
estimates of both the number of individuals exposed to the substance and the
magnitude of the individual exposure. The magnitude of exposure involves
estimates of concentrations of the chemicals in the air and statistics on
both the frequency of use and the duration of exposure anticipated for each
use. Estimates of air concentration are based on both monitoring data and
an indoor air model.
The consumer exposure estimates used in these analyses reflect a number
of uncertainties, stemming largely from lack of current data on product com-
position and use patterns. The models used to predict concentrations typi-
cally rely on assumptions on the details of the indoor environment.
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ESTIMATED RISK
The estimates of risks to consvuners from the four substances are based
on the exposure estimates and unit risk estimates contained in agency risk
assessment documents. These are presented below.
Estimated Annual
Substance Cancer Incidence
Formaldehyde 50
Methylene Chloride 30
Asbestos 5
para-Dichlorobenzene 9-50
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CATEGORY 1
#6: Hazardous/Toxic Air Pollutants
PROBLEM DEFINITION
Approximately 60,000 to 70,000 known chemicals are in commerce today in
the United States. An additional large number of chemicals are formed in
chemical processes and by atmospheric reaction processes. A substantial
portion of these substances can become airborne and, when inhaled by humans
in sufficient concentrations, can be harmful to their health.
Toxic air pollutants are emitted from a wide variety of stationary and
mobile sources. Obvious sources are large industrial facilities, combustion
sources of various types and sizes, and motor vehicles. Some less traditional
but equally important sources include commercial facilities that use solvents
and facilities that treat, store, and dispose of hazardous wastes. While
higher concentrations of toxic air pollutants are generally found in large
urban or industrialized areas, the limited available ambient monitoring
data indicate large variations within and between urbanized areas.
This report merges the terms "hazardous air pollutant" and "toxic air
pollutant" to comprise a general category of particulate and gaseous pollutants
in the ambient air. Strictly speaking, the hazardous air pollutants are pol-
lutants that meet the statutory requirements of section 112 of the Clean Air
Act. This section requires the EPA Administrator to establish emission stan-
dards for pollutants that "...cause, or contribute to, air pollution which
may reasonably be anticipated to result in serious irreversible, or incapaci-
tating reversible, illness...." "Toxic air pollutant" is a more general
term for any airborne chemical substance that may pose a human health threat.
This problem area considers only routine, continuous emissions of pol-
lutants. Further, it assumes that exposure to toxic air pollutants occurs
only outdoors on a continuous basis for a lifetime (70 years). This assess-
ment also does not consider the potential role of toxic air pollutants, such
as carbon tetrachloride or chlorofluorocarbons in the depletion of stratos-
pheric ozone. Both Indoor Air and Depletion of Stratospheric Ozone are
considered under their own environmental problem areas.
POLLUTANTS ADDRESSED IN THIS SUMMARY
Criteria for Selection of Hazardous/Toxic Air Pollutants
Table 1 shows the toxic air pollutants selected for assessment. The
initial procedures that the Office of Air Quality Planning and Standards
(OAQPS) followed for setting priorities identified many hundreds of poten-
tially toxic air pollutants. After reviewing available health literature
and source information, OAQPS selected approximately 50 chemicals, many of
which were potent carcinogens with the potential for significant human expo-
sures. OAQPS then conducted more detailed analyses and developed estimates
of cancer risk. Only those pollutants with an estimated cancer incidence in
excess of one per year were retained for this analysis. As a result, this
analysis estimates the cancer risk from 20 substances, or categories of
substances.
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Legislatively excluded from section 112 and this problem area are the
six so-called criteria air pollutants (particulate matter, ozone, carbon
monoxide, sulfur oxides, nitrogen dioxide, and lead). These pollutants are
regulated under sections 108-110 of the Clean Air Act and are treated under
the Criteria Air Pollutant environmental problem. Although toxic air pol-
lutants and the criteria pollutants are classified separately, certain toxic
air pollutants are constituents of particulate matter, and some are volatile
organic compounds that may contribute to the formation of ozone.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
Most of the carcinogenic potency estimates for the pollutants listed
in Table 1 were developed by EPA's Carcinogen Assessment Group (CAG). The
potency estimates for some of the toxic air pollutants warrant special comment.
o The inhalation unit risk estimate for asbestos was derived by
OAQPS staff, based on potency estimates developed by the
Office of Health and Environmental Assessment (U.S. EPA,
1985a).
o The potency of the mixture of polychlorinated dibenzo-p-dioxins
and polychlorinated dibenzofurans was based on the CAG unit
risk estimate for 2 ,3 ,7 ,8-tetrachlorodibenzo-p-dioxin (TCDD).
The mixture was converted to TCDD equivalents, based on the
relative potency of compounds in the mixture compared to the
potency of TCDD (U.S. EPA, I986a).
o The potency estimate for formaldehyde was based on the unit
risk estimate for malignant tumor formation, rather than on
total tumors (U.S. EPA, 1986b).
o The unit risk estimate for products of incomplete combustion
(PIC) was derived from dose-response data that use benzo[a]pyrene
(BaP) levels as a surrogate for this large category of BaP-
related pollutants (U.S. EPA, 1985b).
o The potency of emissions from hazardous waste treatment, storage,
and disposal facilities (TSDFs) was based on the unit risk
estimate for carbon tetrachloride. It was assumed that the
potency of the carcinogenic fraction of TSDF emissions may be
as low as that of methylene chloride or as high as carbon
tetrachloride. The unit risk estimate for carbon tetrachloride
was used to estimate the upper end of a range of preliminary
risk estimates (U.S. EPA, 1985c).
Exposure Assessment
Exposure assessments estimate concentrations of a pollutant and the
numbers of people exposed to these concentrations. Two approaches for deter-
mining ambient air concentrations in the vicinity of emission sources are
the use of monitoring data, which are direct measurements of pollutant concen-
trations in the ambient air, and the use of emission estimates coupled with
dispersion modeling to predict concentrations to which humans are exposed.
B-21
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Use of Monitoring Data
Monitoring data were used to estimate at least a portion of the risk
associated with exposure to carbon tetrachloride, formaldehyde, products of
incomplete combustion, and vinyl chloride. Using direct measurements of
ambient concentrations to estimate risk 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,
as well as the errors associated with dispersion modeling. There is, however,
significant potential for error in using monitoring data to estimate risk.
For example, monitoring data are usually available for a relatively
small number of areas for each pollutant, so certain assumptions must be
made in extending these data to the rest of the nation. Further, monitors
are often located away from major sources, and the air quality data are
subject to errors in sampling and analytical methods. Finally, ambient con-
centrations measured over a period of at least a year should be used in the
estimation of the long-term exposure concentrations that are associated with
the development of cancer, but ambient data are rarely collected for an
entire year.
Use of Emission Estimates
To predict human exposure to a pollutant using dispersion modeling
techniques, one must first estimate the emissions from a source. Emission
estimates for point sources are located at a specific site, whereas estimates
for area and mobile sources are apportioned over the entire area being con-
sidered. Sources of information for emission estimates include data gathered
from industry under the authority of the Clean Air Act (section 114) or
other regulatory authorities, material balance calculations, published infor-
mation on emission factors, and actual measurements of emission rates.
Given the diverse nature of the sources of information, the quality of the
estimates may vary considerably.
Emission estimates for benzene, 1,3-butadiene, and formaldehyde in auto-
mobile exhaust were determined using the Mobile Sources Emissions Model
(Mobile3) developed by the Office of Mobile Sources (US EPA, 1984). Mobile3
is a computer program that calculates emission factors for hydrocarbons
(HC), carbon monoxide (CO), and oxides of nitrogen (NOx) from highway motor
vehicles. Mobile3 calculates emission factors for eight individual vehicle
types in two regions of the country. Emission estimates generated by MobileS
depend on a variety of conditions, such as ambient temperature, speed, and
mileage accrual rates.
Use of Dispersion/Exposure Modelling
Developed by OAQPS, the Human Exposure Model (HEM) was used to estimate
human exposure for most of the pollutants in Table 1 (US EPA, 1986c). The
HEM estimates the population exposed to various concentrations of air pol-
lutants emitted from point and area sources and the carcinogenic risk asso-
ciated with this exposure. The HEM consists of (1) an atmospheric dispersion
model, (2) population distribution information based on 1980 Bureau of the
Census data, and (3) a procedure for estimating risks due to the predicted
exposure. The inputs needed to operate this model are such source data as
emission rate, plant location, height of the emission release point, and the
temperature of the off gases.
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The model estimates the magnitude and distribution of ambient air concen-
trations of the pollutant at distances of 0.2 km to 50 km from the source.
These concentration estimates are coupled with the population to estimate
public exposure to the pollutant. The HEM then predicts population and
individual lifetime risks if a unit risk number determined from health data
is used as input for the pollutant.
The model relies on information provided in a data base developed by
the U.S. Census Bureau. The HEM contains several simplifying assumptions
and uncertainties, some of which may contribute to either an over- or under-
estimation of the health risk. The model assumes that most exposure occurs
at populationweighted centers (centroids) of block group or enumeration dis-
tricts (the locations of actual residences are not known), that people re-
side at these centroids for their entire lifetimes (assumed to be 70 years
for calculating cancer risk), that no net population migration or growth
occurs, that indoor concentrations of pollutants emitted from the sources
being studied are assumed to be the same as outdoor concentrations, that
plants emit pollutants at an average emission rate for 70 years, that the
only source of exposure is the direct inhalation of ambient air (resuspension
of pollutants via dust is not considered), and that all terrain is flat.
There are several areas of uncertainty associated with the input required
for running the HEM. The meteorological data set selected for each facility
may not be representative of the actual conditions at that site. There is
often considerable uncertainty associated with the emission estimates and
the plant parameters used to characterize the emission source. Finally, if
the plant is not correctly located in the model calculation, there will be a
problem matching population census data with concentrations.
Estimation of Risk
To estimate the annual cancer incidence associated with exposure to the
toxic air pollutants in Table 1, the following equation was used:
n
JT_(Ci x PC ) x U.K.
i i
Ia =
70
where la = annual incidence;
C = ambient air concentration at a specific location
(modeled annual concentration or monitoring data);
PC = population exposed to a specific concentration (c);
and
U. R. = cancer unit risk estimate for lifetime exposure (70
year s).
A second measure of risk — maximum individual lifetime risk — was cal-
culated to estimate the highest probability that an individual will develop
cancer from ambient exposure to a pollutant over a 70-year period. This
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was done by multiplying the unit risk estimate by the highest average annual
ambient air concentration of a pollutant (usually nearest to a source) for
all sources modeled.
ESTIMATED RISKS
The estimated number of people subject to the maximum individual risks
for each pollutant in Table 1 varies considerably. This estimate of risk is
best used along with the annual incidence estimate as a relative indicator
of the risk that may be associated with exposure to a pollutant, rather
than as an absolute measure of maximum risk.
As shown in Table 1, the estimated annual population risk or incidence
of cancer for the toxic air pollutants in this analysis totaled 2,054. The
maximum individual lifetime risks ranged from 2.4 out of 10 (2.4 x 10~1) to
8.1 out of 100,000 (8.1 x 10~5), with many maximum risks estimated to be
in the 10~2 and 10~3 ranges. As an example for translating these figures,
the maximum individual lifetime risk estimate of 1.1 x 10~2 for chloroform
implies that one out of 100 people near a particular point source, breathing
a given concentration of chloroform for 70 years, will develop cancer as a
result of that exposure.
The exposure and risk assessments for most of these pollutants are con-
tinually being reviewed and updated. As such, the risk estimates presented
in Table 1, although subject to change, reflect the most current estimates.
UNCERTAINTIES AND CAVEATS
Following are some of the important caveats surrounding this analysis:
o Only routine releases are considered in this section. Accidental
releases are discussed under a separate environmental problem
area.
o Quantitative risk estimates were generated for only 20 substances
or categories of substances. Major factors preventing analysis
of more pollutants were the limitations of exposure data and
the lack of quantitative estimates of cancer potencies. As
such, the risks outlined in Table 1 represent less than 100
percent of the total risk.
o No consideration is given to the possible synergistic or anta-
gonistic effects of exposure to mixtures of chemicals. Urban
air is characterized by the presence of hundreds of pollutants,
and little is known about how these substances may interact
once they enter the human body.
o Estimates of cancer risk for each pollutant in this analysis
may change as more detailed analyses are conducted and as the
risk assessment methodologies are refined.
o Atmospheric transformation of toxic air pollutants was not
explicitly considered.
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The potency and exposure estimates used to estimate both annual
population and individual lifetime risk assume a 70-year exposure
to the compound in question. Obviously, people spend a substan-
tial portion of their lives indoors in environments where
exposures to toxic pollutants can be higher, lower, or similar
to those that occur outdoors.
Exposure estimation techniques employ several simplifying assump-
tions that may over- or underestimate exposure.
Ambient air quality data, rather than modeled levels estimated
by dispersion modeling, were used to estimate exposure concentra-
tions for several compounds.
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TABLE 1
ESTIMATED NATIONWIDE RISKS FROM
HAZARDOUS/TOXIC AIR POLLUTANTS
Pollutant
Arsenic (inorganic)
Asbestos
Benzene
1 ,3-butadiene
Cadmium
Carbon tetrachloride
Chloroform
Chromium (VI)
Coke oven emissions
1, 2-Dichloroethane (EDC)
Dioxins /dibenzof urans
Ethylene oxide
Formaldehyde
Gasoline vapors (marketing)
Methylene chloride
Products of incomplete
combustion (PIC)
Tetrachloroethylene
Trichloroethylene
Vinyl chloride
TSDFc emissions
Estimated
Annual
Incidence
2
82
90a
223a
7
69
10
75
7
4
10
58
435a
77
35
610a,b
5
4
11
240
Maximum
Individual
Lifetime Risk
1.9 x 10-3
2.3 x 10~3
1.5 x 10-3
2.4 x 10-1
2.8 x 10-3
5.7 x 10-3
1.1 x 10-2
8.7 x 10-3
3.4 x 10-2
1.2 x 10~2
1.4 x 10~3
1.9 x 10"3
1.6 x 10~4
5.7 x ID'3
2.8 x ID"3
-
1.3 x 10- 4
8.1 x 10-5
3.5 x ID"3
-
Total
2054
NOTE: Annual incidence and maximum individual risk should
be regarded as rough estimates due to uncertainties in the
unit risk values and exposure assessments. These estimates
are subject to change. Annual incidence is rounded to the
nearest whole number.
a Includes contribution from mobile sources. The Office of
Mobile Sources is currently revising its component of
the risk estimates for some of these pollutants.
b Potency estimate and annual incidence for PIC taken from
US EPA, 1985a. These estimates were based on the use of
benzo[a]pyrene as a surrogate for PIC.
c TSDF = hazardous waste treatment, storage, and disposal
facilities.
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REFERENCES
1. US EPA 1984. User's Guide to Mobile3. Office of Mobile Sources, EPA
460/3-84-002.
2. US EPA 1985a. "Airborne Asbestos Health Assessment Update." Office of
Health and Environmental Assessment. EPA 600/8-84-003F.
3. US EPA 1985b. The Air Toxics Problem in the United States; An Analysis
of Cancer Risks for Selected Pollutants. Office of Air and Radiation;
Office of Policy, Planning and Evaluation. EPA 450/1-85-001.
4. US EPA 1985c. Preliminary Source Assessment for Hazardous Vfaste Air
Emissions from Treatment, Storage and Disposal Facilities (TSDFs).
Final Report, prepared by GCA Corporation for the Office of Air Quality
Planning and Standards.
5. US EPA 1986a. "Interim Procedures for Estimating Risks Associated with
Mixtures of Chlorinated Dibenzo-p-dioxins and Dibenzofurans (CDDs and
CDFs)." Draft Report. Prepared for EPA's Risk Assessment Forum.
6. US EPA 1986b. "Assessment of Health Risks to Garment Vforkers and Certain
Home Residents from Exposure to Formaldehyde." Preliminary Draft Report,
Office of Toxic Substances.
7. US EPA 1986c. User's Manual for the Human Exposure Model (HEM). Office
of Air Quality Planning and Standards. EPA 450/5-86-001.
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CATEGORY 2
#7: Stratospheric Ozone Depletion
PROBLEM DEFINITION
By preventing most potentially harmful ultraviolet radiation (UV-B)
from penetrating to the earth's surface, the ozone layer acts as an important
shield protecting human health, welfare, and the environment. The possibil-
ity that the production, use, and release of chlorofluorocarbons (CFCs) could
deplete stratospheric ozone was first theorized in a 1974 article in Nature
by Molina and Rowland.
The major consequence of ozone depletion would be an increase in harmful
UV-B radiation, particularly that in the more damaging region of the UV spec-
trum. Under current atmospheric conditions, the latitudinal exposure to
UV-B varies greatly, with more UV-B received by those closer to the equator.
This variability in exposure takes place largely because of changes in the
solar angle and a natural latitudinal gradient in ozone thickness.
On the basis of both epidemiological studies that relate the natural
variation in UV-B exposure to skin cancer incidence and laboratory studies
in which tumors have been induced and promoted by UV-B, researchers have con-
clusively demonstrated that both basal and squamous skin cancers are associ-
ated with cumulative exposure to UV-B (NAS, 1984). Wiile infrequently fatal
(somewhat less than 1 percent of cases currently result in fatalities), these
are the two most common types of skin cancer, with approximately 500,000
cases per year (Scotto, 1986). A relatively good understanding exists of
these cancers, with a 1 percent ozone depletion projected to increase basal
skin cancer by 1 to 3 percent and squamous skin cancer by 2 to 5 percent
(U.S. EPA, 1986, based on data in Scotto, 1986).
Melanoma is a less common but far more deadly type of skin cancer. In
1985, there were about 25,000 cases and 5,000 fatalities in the U.S. (Scotto,
1986). Recent studies of melanoma have tended to reinforce the hypothesis
that UV-B is one of the causes of melanoma, although the relationship appears
much more complex, and is perhaps related to peak and possibly youthful
exposure (EPA, 1986). Recent efforts to quantify this relationship have
produced the following dose-response relationship: a 1 percent ozone deple-
tion is projected to increase melanoma incidence by 1 to 2 percent and melanoma
fatalities by 0.8 to 1.5 percent (EPA, 1986, based on data in Scotto, 1986).
POLLUTANTS ADDRESSED IN THIS SUMMARY
The likelihood of ozone depletion will be influenced by the future con-
centrations of many trace gases. Aside from trace gases that have de minimis
effects, potential ozone depleters include chlorofluorocarbons (CFC 11,12,113,
22, and Halon 1211); Halon 1301 (not a chlorofluorocarbon); and chlorocarbons
(CC14 and 0130013). Trace gases that may buffer ozone depletion include C02>
CH4, and, in some cases, N20.
Part B of the Clean Air Act charges EPA to consider "any substance" that
may affect the ozone layer." EPA's Integrated Assessment Model was therefore
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developed to assess the atmospheric effects of all trace gases likely to
affect the stratosphere. The model incorporates each of the trace gases
listed above.
RISK ASSESSMENT METHODOLOGY
EPA's Science Advisory Board is currently completing its review of the
methodologies and results presented in this summary. Both the approaches
and results are subject to revision.
Dose-Response Relationships
A strong consensus exists on the role of UV-B in the induction and pro-
motion of non-melanoma skin cancer (basal and squamous). Dose-response rela-
tionships for basal and squamous skin cancer incidence are based on the re-
sults of epidemiological investigations undertaken by the National Cancer
Institute (NCI) (Scotto , Fears, and Fraumeni, 1981). The relationships cur-
rently included in the model are power functions that express the change in
incidence as a percentage change that can be multiplied by the baseline in-
cidence to compute the increased age-specific incidence. An advantage of
this formulation is that the change in exposure can be expressed as a change
relative to baseline, thereby avoiding potential difficulties in specifying
the absolute levels of changes in exposure to UV. The coefficients used in
the models were derived from the regression coefficients presented in Scotto,
Fears, and Fraumeni (1981). Results presented in the draft risk assessment
are based on a measure of UV where wavebands are weighted by a DNA action
spectrum.
A separate dose-response relationship for mortality from non-melanoma
skin cancer has not been estimated. For purposes of modeling, the current
relationship between mortality and non-melanoma incidence are assumed to
apply.
The role of UV-B in melanoma skin cancer is more uncertain. The metho-
dologies used to relate UV-B to melanoma were developed for use in the Inte-
grated Analysis Model based on an extensive review of the literature and
data analysis. The review was conducted with the cooperation and participa-
tion of other EPA offices (Carcinogen Assessment Group and Office of Standards
and Regulations), government agencies (NCI and NASA), and academics (from
Johns Hopkins University, University of South Carolina, and University of
Cincinnati). The work is currently under review by EPA's Science Advisory
Board.
The dose-response models for melanoma incidence are of the same form as
for non-melanoma. The coefficients were derived from data presented in Scotto
and Fears (in press) and are are assumed to be applicable for the DNA action
spectrum.
A separate analysis of melanoma mortality has been performed by Pitcher
(in press). The coefficients estimated as the result of that investigation
are used to model the potential increase in mortality due to melanoma skin
cancer. The coefficients are estimated using peak UV values, weighted by the
DNA action spectrum.
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Exposure Assessment
Projections of future emissions of potential ozone-depleting compounds
were developed based on a range of long-term estimates prepared for EPA/
United Nations Environment Programme workshops on future demand. In the
short term, the scenarios incorporate market-based analysis. For the long
term, they are based on the application of historical relationships between
production and economic and population growth. Estimates for compounds that
may buffer depletion were based on a review of independent projections.
The effects of trace gas emissions on the stratospheric ozone layer are
modeled based on a parameterized version of a state of the art, one-dimen-
sional model (Connell, 1986). Consequent changes in UV are modeled based on
a model of ozone and UV radiation developed in conjunction with NASA and
National Oceanic and Atmospheric Administration.
Because the risks of skin cancer vary with race, age, and sex, the popu-
lation at risk was characterized by these variables using Census Bureau data.
To reflect differences in current UV exposure, the assessment split the popu-
lation into three geographic regions. For each region, the current and ex-
pected size and age distribution were projected to the year 2000, based on
estimates of migration and birth/death rates. After 2000, these distributions
were held constant. Aggregate increases in population were based on estimates
prepared by Keyfritz and used in previous EPA studies (Seidel and Keyes, 1983),
Estimation of Risk
Using the risk assessment methodology discussed above, estimates of UV-B
effects on basal, squamous, and melanoma skin cancer were presented in the
draft risk assessment, An Assessment of the Risks of Stratospheric Modifica-
tion. For the central case scenario of ozone depletion, changes in non-mela-
noma and melanoma skin cancer for three cohorts of individulals alive today
or born by the year 2074 are shown in Table 1. On the basis of this table,
approximately 10,000 additional cancer cases annually will be attributable
to ozone depletion by the year 2100. The sensitivity of these estimates to
trace gas emission scenarios is shown in Table 2. The sensitivity to dose-
response coefficients is shown in Table 3.
OVERALL ASSESSMENT OF UNCERTAINTY
A strong consensus exists that UV-B radiation induces and promotes basal
and squamous skin cancer. The model and coefficients used in this analysis
are within the range of reported results.
The effect of UV-B on melanoma is much more uncertain. The theories,
methodologies, and data used in this analysis have been preliminarily reviewed
by the Science Advisory Board.
For projections of future ozone depletion, the largest quantitative
uncertainties involve assumptions concerning future emissions of CFCs and
other trace gases. With respect to modeling the atmospheric consequences of
trace gas growth, there exists the possibility that some overlooked or mis-
sing factor or oversimplified process has lead to over- or underpredictions
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of changes in ozone. Because of these and other uncertainties complicating
the evaluation of this problem area, we ranked it lower than the analytical
results would indicate.
TABLE i
Human Health Effects: Central Case
Additional Cumulative Cases and Deaths by Population Cohort
HEALTH EFFECTS
POPULATION
ALIVE TODAYS
NUMBERS NUMBERS
BORN 1985-2029t> BORN 2030-2074^
Non-Melanoma Skin Tumors
Additional Basal Cases
Additional Squmaous
Additional Deaths
630,600
386,900
16,500
5,012,900
3,185,800
135,000
17,630,500
12,122,400
509,300
Melanoma Skin Tumors
Additional Cases
Additional Deaths
12,300 109,800 430,500
3,900 32,200 115,100
a/ Analysis period for health effects: 1985-2074.
b_/ Analysis period for health effects: 1985-2118.
c/_ Analysis period for health effects: 2030-2164.
SOURCE: U.S. EPA (1986), An Assessment of the Risks of Stratospheric Modification,
draft report. Washington, D.C.
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TABLE 2
Human Health Effects: Emission Scenarios
Additional Cumulative Cases and Deaths Over Lifetimes of People in the U.S
Alive Today and Born in the Next 88 Years
EMISSIONS SCENARIOS EXTREME CASES
HEALTH EFFECTS Low Central High Lowest Highest
Non-Melanoma Skin Tumors
Additional Basal Cases 1,599,500 23,274,000 83,755,700 -1,616,100 135,317,800
Additional Squamous Cases 823,400 15,695,100 71,808,100 -856,600 117,809,809
Additional Deaths 35,700 660,800 2,952,400 -36,700 4,837,400
Melanoma Skin Tumors
Additional Cases 47,300 552,600 1,897,400 -40,500 3,079,500
Additional Deaths 12,100 151,200 502,800 -11,200 809,700
SOURCE: U.S. EPA (1986), An Assessment of the Risks of Stratospheric Modification,
draft report. Washington, D.C.
B-32
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TABLE 3
Human Health Effects: Sensitivity to Dose-Response Relationship
Additional Cumulative Cases and Deaths Over Lifetimes of People
in U.S. Alive Today and Born in Next 88 Years
HEALTH EFFECTS
SENSITIVITY OF EFFECT TO UV DOSE
Low Central High
Non-Melanoma Skin Tumors
Additional Basal Cases
Additional Squamous Cases
Additional Deaths
14,046,400
9,242,000
109,200
23,274,000
15,695,100
660,800
34,130,500
24,385,300
10,203,000
Melanoma Skin Tumors
Additional Cases
Additional Deaths
384,300
134,300
552,600
151,200
732,100
168,500
SOURCE: U.S. EPA (1986), An Assessment of the Risks of Stratospheric Modification,
draft report. Washington, D.C.
B-33
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REFERENCES
Connell, P.S. (1986). A Parameterized Numerical Fit to Total Ozone Column
Changes Calculated by the LLNL 1-D Model of the Troposphere and Stratosphere.
Lawrence Livermore National Laboratory, Livermore, CA.
Molina, M.J., and F.S. Rowland (1974). "Stratospheric Sink for Chlorofluoro-
methanes: Chlorine Atom-Catalyzed Destruction of Ozone." Nature, 249,
810-812.
National Academy of Sciences (1984). Causes and Effects of Changes in
Stratospheric Ozone. National Academy Press, Washington, B.C.
Pitcher, H. (in press). "Melanoma Death Rates and Ultraviolet Radiation in
the United States, 1950-1979."
Scotto, J. (1986). "Nonmelanoma Skin Cancer ~ UVB Effects." In UNEP/EPA,
Effects of Changes in Stratospheric Ozone and Global Climate, Volume II.
U.S. EPA, Washington, D.C.
Scotto, J., and T.R. Fears (in press). "The Association of Slar Utraviolet
Radiation and Skin Melanoma Among Caucasians in the United States." Cancer
Investigations.
Scotto, J. , T.R. Fears, and J.F. Fraumeni (1981). Incidence of Nonmelanoma
Skin Cancer in the United States. Publication Number (NIH) 82-2433, National
Cancer Institute, Washington, D.C.
Seidel, S. and D. Keyes (1983). Can We Delay a Greenhouse Warming? U.S EPA,
Washington, D.C.
U.S. EPA (1986). An Assessment of the Risks of Stratospheric Modification.
draft report, U.S. EPA, Washington, D.C.
B-34
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CATEGORY 2
#8: Hazardous Waste Sites - Inactive
PROBLEM DEFINITION
Although a wide variety of sites are covered under this subject, all
are characterized by the presence of hazardous waste at the site and the
absence of any current manufacturing, treatment, storage, or disposal activity
at the site. This category includes inactive hazardous waste sites covered
under the Comprehensive Environmental Response, Compensation, and Liability
Act of 1980 (CERCLA, known as Superfund) and the National Oil and Hazardous
Substances Pollution Contingency Plan (NCP), which provides procedures for
addressing the problem of inactive hazardous waste sites under CERCLA.
The NCP establishes a system for ranking the degree of hazard at sites
identified by the Comprehensive Environmental Response, Compensation, and
Liability Inventory System (CERCLIS), the master list of inactive hazardous
waste sites that have been reported to EPA. These sites are found throughout
the country and vary from mine tailings to pesticide spills to abandoned man-
ufacturing facilities. The sites are investigated and ranked, and the ones
presenting the most significant hazards are placed on the National Priorities
List (NPL) and become eligible for money from the Superfund for remedial
action to reduce the hazards.
Some sites do not meet the criteria for inclusion on the NPL, but may
pose some hazard nonetheless. The cancer work group has included non-NPL
sites in its extrapolation to the universe of potential inactive hazardous
waste sites.
A wide variety of exposures are possible from hazardous waste sites.
These include exposure to volatilized contaminants in air, inhalation of
wind-entrained dust, inadvertent soil ingestion, dermal absorption from soil,
contact and ingestion of surface water contaminated by leaching or running
off from sites, and contaminants leaching into ground water. Exposure to
surface or ground water can include dermal contact and inhalation of volatile
organics, as well as ingestion of drinking water. Out of the wide array of
possible exposure pathways, ingestion of contaminated ground water poses the
overall highest individual and population risks for the sites included in
this analysis.
Because consideration of cumulative risks due to all exposure routes
would be very difficult, and because much less information is available for
the other routes, only risks due to ground-water ingestion were considered
for this problem area. This simplification, however, did not significantly
distort estimated population risk because ingestion of ground water probably
captures the majority of population cancer risk at the sites. This is not
necessarily the case for individual risks.
B-35
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POLLUTANTS ADDRESSED IN THIS SUMMARY
Initially, information on ground-water concentrations and carcinogenic
risk was abstracted for all chemicals assessed at any of the 35 Superfund
sites investigated in either public health evaluation or feasibility studies.
From this list, six chemicals were taken as representative: arsenic, vinyl
chloride, tetrachloroethylene, trichloroethylene, 1,2-dichloroethane, and
benzene. Generally, these chemicals were associated with the highest concen-
trations, the highest individual risk, and high frequency of occurrence.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
The cancer potencies used in this section were all derived by the Car-
cinogen Assessment Group. They are subject to the interpretations and caveats
to which all such values are subject.
Exposure Assessment
Approach and Data Sources
The basic analytical approach consisted of four steps: (1) estimate the
mean individual cancer risk for each chemical, based on available risk assess-
ment documents; (2) estimate the number of people exposed per site; (3) esti-
mate the total number of sites; and (4) multiply individual risk times popu-
lation times number of sites.
Baseline public health evaluations or endangerment assessments performed
as part of the Remedial Investigation/Feasibility Study process for Superfund
sites were the source of data used for estimation of individual cancer risk
at uncontrolled hazardous waste sites. These assessments usually evaluate
the site under an assumption of no remedial action. Thirty-five risk assess-
ment or feasibility study documents for Superfund sites in several EPA regions
were reviewed. Of these, 20 contained quantitative estimates of cancer risk
via ground-water ingestion, and individual risk data were extracted from
them. Ground-water exposure pathways were the focal point for analysis
because most data were available for them.
Risk estimates were abstracted for a maximum of five carcinogens at each
site (usually fewer than five carcinogens were evaluated in the assessments
reviewed). Both maximum risk and average risk estimates were generally pre-
sented and abstracted in the assessments. The following six frequently oc-
curring high-risk potential carcinogens were identified: arsenic, vinyl
chloride, tetrachloroethylene, trichloroethylene, 1,2-dichloroethane, and
benzene. The reported chemical-specific cancer risks were averaged across
the sites at which that chemical was reported. This was combined with fre-
quency of detection in samples from sites analyzed by the Contract Lab Program
(CLP) to extrapolate to expected national cancer risks from inactive hazardous
waste sites.
B-36
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Extrapolation to Human Population
Population estimates were determined by estimating the number of inactive
hazardous waste sites, and then multiplying it times the average number of
people exposed at each site. The total number of sites was determined by
combining the total expected number of NPL sites (1,800) with non-NPL inactive
hazardous waste sites. (U.S. EPA, 1984) This non-NPL number was estimated
from the projected CERCLIS site inventory of 25,000, minus the 1,800 NPL
sites, and assuming that site investigations will find that two-thirds show
no risk, which has been program experience. (U.S. EPA, 1984)
The exposed population at sites was based on statistics in the Hazard
Ranking System data base. The mean number of ground-water users within three
miles of NPL sites is 11,773. We assume that 10 percent are potentially
affected by site contamination, because many ground-water users within three
miles may be upgradient, too far away, or not hydraulically connected to
site contamination. We further assume that the population exposed at non-NPL
sites is half that at NPL sites, because of the population bias in getting
listed on the NPL. Consequently, the total affected population (via ground
water) from all inactive hazardous waste sites is estimated to be 6.8 million.
This number was combined with chemical-specific individual cancer risks to
estimate excess cancer risks on a per chemical basis.
Estimates of the concentrations of carcinogens to which individuals are
exposed were based on a distribution of wells within three miles of the sites.
Actual concentrations at these wells were used, rather than on-site concentra-
tions.
Estimated Risks
Tables 1 through 3 summarize data from the public health evaluations and
feasibility studies. Table 1 presents all chemicals reported in more than
one of the public health evaluations or feasibility studies that were inves-
tigated for this analysis, with maximum and best-guess concentration data
and risk predictions averaged for all sites having that chemical. Frequency
of appearance in Public Health Evaluations (PHEs) refers to the number of
times the chemical was found in the PHEs of the 35 sites investigated. These
values were used as the basis for selecting the the six chemicals of concern.
Percent frequency at sites from CLP samples refers to the percentage of
sites whose samples have been analyzed by the CLP as part of the remedial
investigation for the Superfund program at which a chemical was found.
These values were used to estimate the number of sites at which a chemical
may be of concern. The highest average individual risk was for vinyl chloride,
with a maximum excess individual cancer risk of 0.2, and a best-guess cancer
risk of 0.1.
Table 2 presents annual excess cancer cases estimated for the top six
chemicals from Table 1. These estimates assume an exposed population of
1,173 at each site, as determined by the methodology above. These estimates
refer only to the 35 sites investigated for the analysis, and not to the
universe of all inactive hazardous waste sites. Vinyl chloride was associated
with the highest number of excess cancer cases, with 30 and 15 excess cases
for maximum and best-guess risks, respectively.
B-37
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Table 3 presents annualized excess cancer cases for the top six chemi-
cals, extrapolated to the entire potential universe of inactive hazardous
waste sites. These values represent the estimated number of excess cancer
cases among the estimated exposed population of 6.8 million, as determined
by the methodology above. Maximum excess cancer cases per year for all
sites range from 1,300 for vinyl chloride to 9 for benzene. Best-guess
values range from 650 for vinyl chloride to 0.9 for benzene.
UNCERTAINTIES AND CAVEATS
This analysis attempts to capture the most significant risks from Super-
fund sites. Because this analysis is limited to only six of the literally
hundreds of chemicals found at inactive hazardous waste sites, it may under-
estimate actual total risk from these sites. However, field experience at
sites indicates that the majority of risks at most sites is due to a few
chemicals.
In addition, only one of many possible exposure pathways has been analyzed,
And, while it may be the most significant pathway, several sites used in this
analysis did not have any reported exposure to ground water. On the other
hand, the estimates of affected sites and exposed population may overestimate
the actual number of cancer cases in the population.
Many assumptions are built into the numbers used from other sources and
are inherent in these extrapolation methods. Taken as a whole, these assump-
tions place severe limitations on the accuracy of the projections. Major
assumptions include the following:
o Site-specific risk assessment reports are both comprehensive
and accurate. In some cases these were small-budget assess-
ments based on very limited site data. Therefore, the
uncertainty in the individual risk numbers is high. In
general, these numbers are probably conservative because of
conservative assumptions in the exposure and toxicity assess-
ments (e.g., use of future-use scenarios, full lifetime
exposure, upper-bound potency estimates) on which the risk
analyses are based.
o Individual risk distributions and mean risks derived from
the 35 sample sites adequately represent the overall popu-
lation of thousands of uncontrolled waste sites. This is
a very small sample size, and it is highly unlikely to be
representative, given the great variability in uncontrolled
waste site conditions and the sample site selection approach.
(The only criterion for inclusion was ready availability of
a risk assessment report.) This assumption also implies
that non-NPL sites have comparable risk levels to NPL sites
because all sample sites examined were NPL sites.
o There will be no interventions to eliminate or reduce risk at
these sites.
B-38
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TABLE i
Potential Carcinogens That Are Found in Ground Water and
That Appear in
More Than One Superfund
Public Health Evaluation/Feasibility Study
Chemicals
Trichloroethylene
Vinyl Chloride
Benzene
Tetrachloroethylene
Arsenic
1,2-Dichloroethane
Chloroform
PCBs
1 , 1-Dichloroethene
Methylene Chloride
Frequency
of Appear-
ance in
PHEs I/
10
9
9
6
4
4
3
3
3
2
1,1,2-Trichloroethane 2
N-nitrosodiphenylamine 2
Percent
Frequency
at Sites
(from CLP)
27.9
6.8
30.4
22.6
40.8
9.4
27.8
8.1
12.9
76.7
4.4
8.9
Mean
Maximum
Concen-
tration 2/
(ug/1)
40,000
5,500
1,622
1 2 , 000
95
9,000
2,800
27
72
1.2 x 106
1,500
90
Mean
Maximum
Individual
Risk 3/
2 x 10-2
2 x 10-1
3 x 10-4
2 x 10~2
2 x 10-2
2 x 10-2
7 x 10-3
3 x 10-3
2 x lO-^
4 x 10-2
3 x 10-3
9 x 10-7
Mean
Best-Guess
Concentra-
tion 4/
ug/1
20,000
1,400
280
1,050
9.8
81
98
4
5.6
53,000
23
— •—
Mean
Best-Guess
Individual
Risk _5/
1 x 10-2
1 x 10-1
3 x 10-5
1 x 10~3
4 x 10~3
2 x ID"3
2 x ID"4
1 x ID'3
2 x ID"5
8 x 10-4
3 x ID"4
8 x 10-7
_!/ Out of a total of 35 sites.
2J Data from 20 NPL sites. Averages are calculated with data from sites
having that chemical reported in public health evaluations only.
_3/ Data from 17 NPL sites. Averages are calculated with data from sites
having that chemical reported in public health evaluations only.
kj Data from 7 NPL sites. Averages are calculated with data from sites
having that chemical reported in public health evaluations only.
5/ Data from 15 NPL sites. Averages are calculated with data from sites
having that chemical reported in public health evaluations only.
B-39
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TABLE 2
Projected Annual Excess Cancer Cases for Selected
Chemicals at
35 Sites Having Public Health
Evaluations!./
Chemicals
Trichloroethylene
Vinyl Chloride
Benzene
Tetrachloroethylene
Ars enic
1 , 2-Dichloroethane
Maximum Excess
Cancer Cases
4
30
0.45
2
1.3
1.3
Best-Guess Excess
Cancer Cases
2
15
0.045
0.1
0.3
0.13
I/ Assuming an average of 1,173 people exposed to ground water at each site.
~ See text for method. Annual number of cases represents the lifetime number
of projected cases divided by an average 70-year lifetime.
B-40
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TABLE 3
Projected Annual Excess Cancer Cases for Selected
Chemicals at the Entire Universe
of Inactive Hazardous Waste Sites 1
Maximum Excess Best-Guess Excess
Cancer Cases Cancer Cases
Trichloroethylene 540 270
Vinyl Chloride 1,300 650
Benzene 9 0.9
Tetrachloroethylene 440 21
Arsenic 775 154
1,2-Dichloroethane 180 18
_!_/ Total population potentially exposed to inactive hazardous waste sites is
estimated to be 6.8 million. See text for method. Annual number of cases
represents the lifetime number of projected cases divided by an average 70
year lifetime.
B-41
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o The number of actual uncontrolled sites will not increase signi-
ficantly over that projected by EPA (i.e. , almost all existing
sites have already been discovered) (U.S. EPA, 1984).
o The mean exposed population via ground water contaminated by
sites can be derived from the estimated number of ground-water
users within three miles. On the basis of our past experience,
we would not expect these numbers to correlate very well.
o The entire exposed population either is equally susceptible ,(i.e.,
no sensitivity variation), or the distribution of susceptibility
is symmetric around the potency value used.
o There are no interactive effects (e.g., synergism) resulting from
concurrent exposure to chemicals from sources other than uncon-
trolled waste sites, as well as several chemicals from one site.
o The distributions of individual risk and exposed population are
independent (i.e., there is no association between population
size and risk level). If these distributions are skewed (likely)
and not independent (possible), the population risk estimates
could be significantly in error.
Clearly, the number and nature of assumptions required to estimate population
risks cast great doubt on the reliability of the numbers presented.
REFERENCE
U.S. EPA, Office of Solid Waste and Emergency Response. Extent of the Hazar-
dous Release Problem and Future Funding Needs, CERCLA Section 301(a)(l)(C)
Study. Final report. December 1984.
B-42
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CATEGORY 2
#9: Drinking Water As It Arrives as the Tap
PROBLEM DEFINITION
Since 1975, EPA's Of ice of Drinking Water has conducted several national
surveys. The 1975 National Organics Reconnaissance Survey and the 1975
National Organics Monitoring Survey primarily examined the presence of tri-
halomethanes in U.S. drinking water supplies. The 1977-81 National Screening
Program and the 1978 Community tetter Supply Survey have demonstrated the
presence in surface waters of organic contaminants in drinking water, generally
at levels lower than 10 micrograms per liter (ug/1).
The 1982 Ground tetter Supply Survey (GfoSS) examined approximately 1,000
drinking water supplies that used ground water as a source. Five hundred
supplies were selected at random, and 500 were selected by states as having
high potential for contamination by organic chemicals. Approximately 21 per-
cent of the randomly selected systems had one or more volatile organic chemi-
cals (VOCs) at detectable levels (primarily in the low ug/1 range). Approxi-
mately 16 percent of the smaller systems (<10,000 people) in the random sample
sample contained some concentrations of the VOCs at levels measurable at less
than 1 ug/1, while approximately 28 percent of the large supplies (>10,000
people) contained these levels of VOCs. In the state-selected portion of
the survey, higher frequencies of occurrence were found at all levels.
In addition, synthetic organic chemicals of industrial origin (including
pesticides) have been detected with increasing frequency, especially in
ground-water sources. Some surface waters are being contaminated with indus-
trial and municipal wastes, although in many cases, application of pollution
controls has apparently improved surface water quality in recent years. Con-
tamination of surface water by other pesticides during runoff can be a signi-
ficant problem in certain areas, such as in Ohio, where treated drinking
water levels of locally used agricultural pesticides have been shown to
parallel seasonal use.
POLLUTANTS ADDRESSED IN THIS SUMMARY
The Comparative Risk Project examined the pollutants that are the subject
of regulation (see table). These pollutants are determined by the results
of monitoring surveys, as well as by explicit direction given in the 1986
amendments to the Safe Drinking tetter Act. They consist of a wide variety
of volatile and synthetic organic contaminants, including pesticides; several
organic chemicals falling under a group known as trihalomethanes; and several
natural and man-made radionuclides, including radon. The regulations that
will be proposed will eliminate most of the known risk of exposure to contam-
inated drinking water.
RISK ASSESSMENT METHODOLOGY
Evaluating the toxicology of potentially carcinogenic substances is a two-
phase process. In the first phase, the toxicological data base for noncarcino-
B-43
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genie toxic effects was evaluated in the same manner as that for noncarcino-
gens. This involves determining acceptable daily intakes, which are exposure
levels that are estimated not to pose significant risk to humans when re-
ceived daily over a lifetime.
In the second phase, an assessment is made of both the evidence of the
carcinogenic potential of a substance (e.g., long-term bioassays in rodents
and human epidemiology) and the information that provides indirect evidence
(e.g., mutagenicity and other short-term test results). The objectives of
this assessment are (1) to determine the strength of evidence that the sub-
stance is an animal or human carcinogen, and (2) to provide an upper-bound
estimate of the possible risks of human exposure to the substances in drinking
water.
One issue considered in assessing carcinogenicity is the data on inhala-
tion and ingestion. If the data show the chemical to be carcinogenic through
ingestion, then the chemical will be considered a potential carcinogen and
evaluated based upon the carcinogenicity data. If the chemical has been
shown to be carcinogenic through inhalation and not ingestion, it will not be
be considered a potential carcinogen via drinking water. A third case consists
of chemicals that are shown to be carcinogenic through inhalation, but the
data on their carcinogenicity through ingestion are either not available or
equivocal. In these situations, carcinogenicity will be determined on a
case-by-case basis by examining the applicablity of the inhalation data to
drinking water exposure.
Exposure Assessment
Drinking water exposures are estimated for three classes of substances.
Volatile Organic Chemicals. The results of six federal surveys were
combined into estimates of national exposure using a multinomial distribution.
This method estimates the proportion of the total exposures for a given range
of concentrations on the basis of the observed relative frequency of that
range in the surveys.
Synthetic Organic Chemicals (Pesticides). Data on the occurrence of
SOCs in drinking water are quite limited. Estimates are based upon data on
use of ground water and vulnerability of ground water to SOC contamination,
and limited surface water data.
Radionuclides. Exposure is based upon various surveys and sources, in-
cluding, to a limited extent, monitoring data for compliance with the Interim
Regulations for Radionuclides. For example,
o for radium 226, exposure is based on a 1980-81 survey of 2,500
public ground-water supplies in 27 states by EPA's Office of
Radiation Programs (ORP), as well as studies conducted in New
England and in the Coastal Plain and Piedmont regions;
o for radon exposure is based on data from the above-
mentioned New England and ORP studies; and
B-44
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for natural uranium. Exposure is based on data from the
U.S.G.S. Natural Uranium Resource Evaluation Program,
in which more than 55,000 ground-water samples and
34,000 surface-water samples were analyzed during the
late 1970s.
ESTIMATED RISKS
The following table shows the cancer risks from different pollutants in
drinking water.
Contaminant
Vinyl Chloride
Trichloroethylene
Carbon Tetrachloride
1,2 Dichloroethane
Benzene
para-Dichlorobenzene
Toxaphene
Chlordane
Alachlor
Epichlorohydrin
Dioxin
PAHs
PCBs
Phthalates
Acrylanide
DBCP
EDB
Trlhalomethanes
Heptachlor Epoxide & Heptachlor
Radium - 226
Radium - 228
Natural Uranium
Radon - 222
Concentration
Resulting in
10~6 Risk
(ug/1)
0.015
2.6
0.27
0.38
1.3
2.0a
0.03
0.0218
0.15
3.54
2.2 x 10-7
2.8
0.008
b
0.01
0.025
5 x 10-4
b
.00065
0.1 pCi/ld
0.2 pCi/1
0.7 pCi/1
Population
Exposed
(Millions)
0.9
1.3
0.5
0.023
0.033
0
0.9
4.5
10.0 pCi/1
2.4
2.4
>45
7.0
1
>1
>100
>100
Cases Per
Year
40
<1
12
<1
<1
0
0.2
3.4
2.4
8
322C
42
3-60
3-60
1-10
30-600
a/ Draft potency estimate.
_b/ Under review by the Carcinogen Assessment Group (GAG).
c/ Current estimate for systems serving 10,000 or more people, having a
concentration of 100 ug/1 or more. May be different if CAG risk estimate
for chloroform, currently under review, changes.
d/ Picocuries per liter.
B-45
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CATEGORY 2
#10: Application of Pesticides
PROBLEM DEFINITION
The summary for Pesticide Residues on Foods (ranked third by the cancer
work group) notes that about 200 pesticide chemicals are potentially oncogenic.
These chemicals are professionally applied by workers to protect agricultural
crops.
RISK ASSESSMENT METHODOLOGY
Data Sources and Assessment
The sources and assessment of data are the same as described under the
summary for Pesticides Residues on Food. That is, data are usually generated
by the pesticide companies and augmented by the NTP testing program. As
indicated, data assessment is extensive, both because risk assessment of
pesticides involves a very large number of chemicals, and the amount of data
for each chemical often requires over 1,000 hours of basic review time.
Exposure Estimates
The exposure estimates for pesticide application pose the most complex
issue in assessing risks from actual use. Generally, a matrix of exposure
scenarios must be developed, depending on some of the following factors:
o the assignment of the worker in the crew, e.g., mixer/loader, pilot,
tractor driver, flagman;
o the application protocol — e.g., single or multiple applications,
Ib/acre needed for control;
o the formulation to be used — e.g., liquid, dust, granular; and
o the protective equipment and clothing to be used — e.g. , closed
systems, respirators, gloves, enclosed tractor cabs.
For the most frequently encountered exposure scenarios, actual data on
the deposit of some chemicals on workers are available. This information is
often used for modelling the exposure of other similarly applied chemicals,
taking into account the different application rates between chemicals.
Exposure in the agricultural setting is usually limited to several days
or weeks during the year and varies from chemical to chemical, even among
uses of the same chemical. These determinations are generally linked to the
use directions on the pesticide product — e.g., apply to dormant fruit trees,
apply at fruit set, or apply as needed when infestation of pest reaches a
certain level.
It is obvious that the exposure scenarios can cover a multitude of com-
binations and permutations of the factors described. Usually the exposure
B-46
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assessment is limited to several major scenarios, but for widely used chemi-
cals there can be as many as 50 different exposure scenarios estimated.
Addressing all the variables, the exposure is calculated on both a
daily basis and an annual basis — i.e., daily exposure times expected use-
days per year, and expressed as mg/kg body weight/year.
The major route of exposure of agricultural workers is through the skin.
Especially for oncogenic risk assessment, it is desirable to know what pro-
portion of the chemical deposited on the skin is expected to penetrate.
Animal studies designed to answer this question can be carried out but often
the results are not very satisfactory in a scientific sense and provide only
a crude or partial answer for extrapolation to the human experience.
The estimate of the exposed population — i.e., the number of individual
workers involved with a particular pesticide application — is in most in-
stances not very accurate, and data on the number of workers are generally
not readily available. The production volume of a chemical is sometimes
used to predict the number of individuals exposed.
In a qualitative sense, the exposure of agricultural workers to pesti-
cides is a reality. The quantitative estimate is difficult because of the
diversified agricultural practices, application equipment, and protective
equipment. A large number of farm workers may not be fully cognizant of the
proper handling of pesticides. Thus, certification of pesticide applicators
may provide a more uniform and careful use of pesticides.
The problem of determining the number of workers applying a certain
pesticide is further compounded by the fact that work crews may use several
chemicals in succession. However, a composite risk assessment is not per-
formed, thus potentially underestimating the individual risk.
Similarly, a pesticide may be labeled for use once a year (e.g., herbi-
cides). However, an application crew may treat a larger growing area for
several days according to changing growing seasons and practices. Thus, the
individual worker may experience a larger exposure than deducted from use
directions.
Although the uncertainties are substantial for estimating risks to pesti-
cide applicators, there is a growing concern over a higher than expected
cancer rate among farm workers. Wiile these findings cannot necessarily be
solely attributed to pesticide use, it would seem prudent to keep farm worker
risk at a minimum from all sources of potential oncogenic risks.
Risk Calculation
The extrapolation of long-term animal data to obtain a potency estimate
in human equivalents is performed as described under the summary on exposure
to Pesticides Residues on Foods. Since the animal data for determining
oncogenic effects are usually based on a lifetime daily oral exposure, the
exposure of agricultural workers is amortized as follows:
1. The yearly exposure is used for risk calculation, and the average
daily exposure is calculated by dividing the yearly exposure by 365.
B-47
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2. It is assumed that a worker is exposed for 40 years out of a lifetime
of 70 years.
3. The difference between dermal and inhalation absorption versus oral
absorption, if known, is factored in.
ESTIMATED RISKS
In the experience of the Office of Pesticides Programs, the individual
lifetime risk for an applicator is usually much higher than the individual
lifetime risk for the general population consuming pesticide residues on
food. The difference in individual lifetime risk can be three to four orders
of magnitude. Often the individual risk is calculated to be as high as one
in ten. However, since the population of agricultural workers is very small
as compared with the general population, the population risk becomes smaller
for the pesticide applicator.
After analyzing several representative agricultural pesticides, it was
determined that the average lifetime population risk is about 35 persons/
lifetime/chemical. Thus the yearly risk/chemical would be 0.5 person/year/
chemical (i.e., 35/70 with 70 years being the average lifetime). The total
yearly risk from all pesticide chemicals estimated to be oncogens (200)
would be 0.5 x 200 = 100 persons/year.
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CATEGORY 2
#11: Radiation Other Than Indoor Radon
PROBLEM DEFINITION
Ionizing radiation was among the first environmental causes of cancer
to be identified. Cancer may develop at any of several sites, largely deter-
mined by the type and location of exposure. From a collective dose stand-
point, the largest sources of radiation, by far, are natural background
radiation and medical treatments. Excluding doses due to radon, the average
person in the United States receives about 100 mrem per year from natural
radiation, plus a similar amount from medical procedures.
EXPOSURES ADDRESSED IN THIS SUMMARY
This section deals with exposures to ionizing radiation via occupational,
consumer product, and industrial emissions. Exposure to indoor radon is
mostly covered under the problem areas Indoor Radon and Drinking Water.
Radon exposures included under this problem area are occupational exposures,
and that small fraction of radon exposure resulting from industrial emissions.
Exposures to other types of electromagnetic radiation are not discussed
here. The potential carcinogenic impact of enhanced exposure to ultraviolet
light is treated under Depletion of Stratospheric Ozone. Although there are
conflicting data from both animal and epidemiological studies suggesting that
environmental exposures to microwaves and lower-frequency fields may cause
cancer, this possibility is neither verified nor quantifiable as yet. Finally,
because medical treatments are clearly outside EPA's purview and because
natural background radiation is largely unavoidable, these exposures are not
included in this section.
RISK ASSESSMENT METHODOLOGY
For the purpose of risk assessment, EPA's Office of Radiation Programs
uses a risk factor of 2.8 x 10~4 fatal cancers per rad of whole-body low
linear energy transfer (low-LET) ionizing radiation to the general population
(EPA, 1984). In other words, exposure to one rad of low-LET radiation is
estimated to increase one's chances of contracting a fatal cancer by appoxi-
mately one in 3,500. This estimate is primarily derived from epidemiological
studies on the Japanese A-bomb survivors. It represents a linear extrapola-
tion from doses above 50 rads and is an average of "absolute" and "relative"
risk model projections (i.e., projections that assume that the excess absolute
or relative risk per unit dose is constant over time).
The risk to adults is lower than for children. Consequently, for occu-
pational exposures, a lower risk factor is used here: 2xlO~4 (two out of
10,000) fatal cancers per rad. When the radiation is non-uniformly distribu-
ted over the body, the dose and associated risk for each organ must be calcu-
lated separately, as described in the reference cited above (EPA, 1984).
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The methodology for assessing risk from exposure to radon daughters is
discussed under Indoor Radon. For internal alpha emitters other than inhaled
radon daughters, the risk per rad-absorbed dose to any organ is assumed to
be eight times that for low-LET radiation.
All these risk factors reflect estimates of fatal cancers. Given cur-
rent cancer survival statistics, roughly an equal number of nonfatal cancers
should also be projected if the radiation dose is uniformly delivered to the
whole body. Otherwise, the situation must be examined on an organ-by-organ
basis. In particular, lung cancer is about 90% fatal. Hence, estimates of
fatal cancers resulting from radon exposure can be used to approximate total
cancers as well.
ESTIMATED RISKS
Following are estimations of the risk of dying from cancer from being
exposed to occupational, consumer product, and industrial sources of radiation.
Occupational Exposures
EPA has published a review of occupational exposures to ionizing radia-
tion in the United States (Kumazawa et al., 1984). The review treats four
classes of occupational exposures. One of those classes, the enhanced expo-
sure to cosmic radiation received by flight crews and attendants, is not
considered here because it is outside EPA's purview.
The largest class of people occupationally exposed to radiation encom-
passes several major categories of workers, including those employed in indus-
try, medicine, research, and defense. On the basis of monitoring data, about
1.7 million workers were potentially exposed to radiation in 1985, and about
850,000 received detectable doses of ionizing radiation. The collective dose
estimated from the monitoring data was 175,000 person-rem. Assuming two out
of 10,000 (2xlO~^) fatal cancers per person-rem, about 35 fatal cancers
would be expected from this exposure. Most of the dose would be low-LET
radiation delivered fairly uniformly to the whole body. Hence, in addition
to the fatal cancers, a comparable number of nonfatal cancers would be pro-
jected. We estimate the maximum lifetime occupational dose to be about 100
rem, implying a maximum estimated lifetime risk of about 2%.
A second class of exposed people consists of students and visitors at
Department of Energy facilities. In 1980, 41,500 people in this category re-
ceived measurable doses. The collective dose was approximately 3,900 person-
rem, implying about 0.8 (1.6) projected fatal (total) cancers.
The final class reflects radon exposures to miners. In 1980, 17,700
miners were exposed to radon in uranium mines (13,500) and nonuranium mines
(4,200). About 60% of these miners received a measurable exposure of 0.7 WLM
or more, and the collective exposure for all miners was about 7,500 person-
WLM, based on monitoring data. (Concentrations of radon daughters are ordinari-
ly given in units of working levels (WL). Exposure (concentration x time) is
usually expressed in working level months (WLM).) If we assume that the base-
line mortality from lung cancer among miners is about 7% (which is reasonable
for an essentially all-male population), about 10 fatal lung cancers annually
would be calculated on the basis of a 2% relative risk per WLM. The maximum
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lifetime exposure may be about 60 WLM, corresponding to an estimated lifetime
risk of about 9%.
The estimates relating to occupational exposures are summarized in
Table 1. As shown in the table, for one year's occupational exposure, 46
fatal cancers and 82 total cancers are projected.
Exposures from Consumer Products
The largest source of collective dose in this category is from decay of
naturally occurring radionuclides in building materials — e.g., bricks used
in construction of homes. Many people would regard this exposure as part of
natural background. Obviously, it would be impractical to control much of
this exposure in any way, particularly where construction is already complete.
Some fraction of the exposure due to new construction might be limited (e.g.,
by restricting the use of phosphate mine tailings in wallboard or some types
of slag in cinder block) , but we have not tried to estimate the magnitude of
this fraction. The remaining dose from consumer products is contributed by
a variety of small sources, including television sets, radium dial watches
and clocks, and smoke detectors.
As shown in Table 2, about 300 fatal cancers per year are attributed to
radiation doses received from consumer products. If doses from building
materials are excluded, only about 68 fatal cancers would be calculated.
Roughly an equal number of nonfatal cancers would be projected in addition
to the fatal cancers.
Exposures to Industrial Emissions
As background for standard setting, the Office of Radiation Programs has
estimated the number of fatal cancers resulting annually from exposures to
radionuclides emitted by various industrial sources (EPA, 1982; EPA, 1983;
EPA, 1984). Since these documents were published, EPA has slightly revised
its risk estimates for radon. However, those previous estimates of radon-
induced lung cancers would be consistent with current central estimates
derived on the basis of a 2% per WLM relative risk coefficient (EPA, 1986).
Therefore, we have used the previously published estimates of fatal cancers
induced by industrial emissions, without change, for radon emissions, as well
as for emissions of other radionuclides.
The projected fatal cancers from the most significant classes of sources
is summarized in Table 3. Not included is the impact of emissions from nu-
clear power plants, which is very small. The Nuclear Regulatory Commission
has estimated the collective dose to the public from such emissions in 1982
to be about 130 person-rem (Baker and Peloquin, 1986) . Based on a risk
factor of 2.8 x 10~Vrem, this would correspond to about 0.04 fatal cancers
induced annually from this source. As shown in the table, about 10 fatal
cancers are estimated to be induced annually in the general population by
industrial emissions of radionuclides. Most of the projected cancers from
these sources are lung cancers, so nonfatal cancers can be neglected.
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SUMMARY
Based on the restricted classes of sources treated here, ionizing radia-
tion may cause about 360 fatal cancers a year. Almost two-thirds of these,
however, are from radiation emitted by building materials. In addition to
these fatal cancers, a comparable number of nonfatal cancers would be projec-
ted. For perspective, employing the same risk assessment methodology, one
would project roughly 10,000 fatal cancers induced by radiation each year
from medical exposures and natural background (apart from radon).
Table 1
Annual Impact of
Occupational Exposures5
Occupational Dose Exposure Fatal Total Max. Individual
Class (Person-rem) (WLM) Cancersb Cancers Lifetime Risk
Major categories
other than miners 175,000 35 70C 2%
Students and
visitors
Miners
Total
3900
178,900
7500
7500
0.8
10
46
1.6C
lid
82c,d
—
9%
9%
a/Source of exposure data: Kumazawa et al., 1984.
b/Assumes a risk factor of 2xlO~^ fatal cancers/person-rem for whole-body
exposures to low-LET radiation and .02 x baseline lung cancer fatality
rate/WLM for radon exposures.
c/Assumes approximately 1 nonfatal cancer for every fatal cancer induced by
whole-body irradiation.
d/Assumes about 90% of all radon-induced lung cancers are fatal.
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Table 2
Consumer Product Exposures
Source
Building
materials
Televisions
Other
Total
to
Average Dosea
(mrem/yr)
3-4
0.5
0.5
4-5
Ionizing Radiation
Collective Dose
(Person-rem/yr)
700,000 - 1,000,000
120,000
120,000
approx. 1,000,000
Fatal Cancers^
(per year)
196-280
34
34
approx. 300
a./References: National Academy of Sciences, 1980.
b/Based on a risk factor of 2.8x10"^ fatal cancers/person-rem.
Table 3
Fatal Cancers from Exposures to Radionuclides
Source of Emissions
Fatal Cancers/yr
Coal plants
Phosphate industry
Uranium mines
Uranium mills
1.3*
0.1*
3*
6**
VU.S. EPA, 1984.
**/U.S. EPA, 1982, 1983.
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REFERENCES
Baker, D.A., and Peloquin, R.A. Population Dose Commitments Due to Radioac-
tive Releases from Nuclear Power Plant Sites in 1982. NUREG/CR-2850, PNL-
4221, Vol. 4, June 1986.
Kumazawa, S., Nelson, D.R., and Richardson, A.C.B. Occupational Exposure to
Ionizing Radiation in the United States. EPA 152011-84-005, 1984.
National Academy of Sciences. The Effects on Populations of Exposure to Low
Levels of Ionizing Radiation: 1980. National Academy Press, 1980.
U.S. EPA. Final Environmental Impact Statement for Remedial Action Standards
for Inactive Uranium Processing Sites (40 CFR 192), Vol. I. EPA 520/4-82-013-1,
1982.
U.S. EPA. Final Enviornmental Impact Statement for Standards for the Control
of By-Product Materials from Uranium Ore Processing (40CFR 192), Vol. I.
EPA 520/1-83-008-1, 1983.
U.S. EPA. Background Information Document: Final Rules for Radionuclides,
Vol. II. EPA 520/1-84-022-2, 1984.
U.S. EPA. Final Rule for Radon-222 Emissions from Licensed Uranium Mill
Tailings; Background Information Document. EPA 520/1-86-009, August 1986.
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CATEGORY 2
#12: Other Pesticide Risks
PROBLEM DEFINITION
Two other sections on pesticides describe the problems associated with
pesticide residues on food and exposure of agricultural workers to pesticides.
Other uses of pesticides are generally designated as domestic, household, and
industrial uses and includes hospital and household disinfectants, fumigants,
termiticides, and wood presentatives. For most of these chemicals, testing
for oncogenic effects is not available. Termiticides and some wood preserva-
tives, however, have been implicated as posing an oncogenic risk.
The following considerations are mainly directed at these uses. However,
the many chemicals of unknown oncogenic potential may significantly alter the
comparative risk standing of "other pesticides."
RISK ASSESSMENT METHODOLOGY
Data Sources and Assessment
The data source for these consumer/household pesticides are the same as
for the other pesticides — i.e., registrant-generated data, National Toxicology
Program data, and, to a small degree, data from the scientific literature
data. For chemicals where no oncogenicity data are available, data call-in
letters will be issued in the next few months. Thus, several years may pass
until new studies will be completed.
For those chemical where oncogenicity data are already available, scien-
tific evaluations similar to those performed on agricultural pesticides will
be necessary. For chemicals not yet tested, a tiered testing regimen is
proposed, which includes an assessment of oncogenicity based on exposure
estimates, and an assumed value of cancer potency (Q^*).
Exposure Estimation
For most consumer pesticides modeled, exposure estimates are not avail-
able. By their very nature, the uses are not strictly controlled by labelling.
For example, hospital disinfectants are certainly used every working day but
the of mg/person/day has never been estimated.
On the other hand, for termiticides, air mentoring in treated houses has
demonstrated that exposure is rather significant, both with respect to magni-
tude and duration. We also have determined that the use of home or farm
wood perservatives results in significant exposure, even though these products
are not used on a daily basis.
In summary, exposure estimation for these "other pesticide" uses is very
complex and includes a large number of scenarios and contains many uncertainties.
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RISK ESTIMATION
If better data existed, the basic risk calculations would be similar to
those described elsewhere for pesticides. But since neither the exposed popu-
lation nor the daily exposure is well defined, it is extemerly difficult to
develop reliable figures. However, the cancer work group agreed that a yearly
nationwide annual incidence of 150 cancer cases may be a reasonable assumption.
This opinion was arrived at by a one-on-one comparison with other environmental
problem areas, using professional judgment to determine which one of each set
of two is expected to be worse.
UNCERTAINTIES
The following uncertainties are associated with estimating the risks of
cancer from exposure to "other pesticides."
o The number of chemicals involved is large.
o Only a few consumer chemicals have adequate oncogenicity
data.
o The exposed population is unknown, but is likely to be large
for some chemicals.
o Daily and lifetime exposures are not known and are difficult
to determine. For example, label directions are less likely
followed by the general public than by agricultural workers.
o Exposure is by dermal contact or inhalation, and correlating
these exposures to ingestion data on pesticides is difficult.
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CATEGORY 2
#13: Hazardous Waste Sites — Active
PROBLEM DEFINITION
This category includes the risks posed by a number of sources, including
RCRA landfills and surface impoundments (both open and closed), hazardous
waste storage tanks, hazardous wastes burned in boilers and furnaces, hazar-
dous waste incinerators, waste oil, and solid waste management units (SMUs).
The primary routes of exposure are ground water for landfills, surface im-
poundments, storage tanks, and SMUs and air for boilers and furnaces, in-
cinerators, and waste oil.
POLLUTANTS ADDRESSED IN THIS SUMMARY
The pollutants evaluated for each source are as follows:
RCRA Landfills and Surface Impoundments
Pollutants were selected based on analyses of wastes disposed at 55
RCRA facilities that plan to continue operating. Constituents in wastes and
concentrations are based on data from the waste, environment, and technology
(WET) model. Constituents of major concern include 2,4-dinitrotoluene,
arsenic, acenapthene, toluene diamine, benzene, and acrylonitrile. (An
alternative modelling exercise examined the entire range of wastes and con-
stituents included in the WET data base.)
Hazardous Waste Storage Tanks
One study (ICF/Pope-Reid, 1986) used methylene chloride and 1,1,1-tri-
chloroethane as representative of the types and toxicities of wastes stored
in tanks. Another examined 32 waste streams and 36 toxic chemicals.
Hazardous Wastes Burned in Boilers and Furnaces
The carcinogens evaluated include metals (chromium, cadmium, and arsenic),
products of incomplete combustion (PICs: chloroform, tetrachloroethylene,
benzene, and carbon tetrachloride), and polycyclic organic hydrocarbons (a
weighted average of POHCs in high-heat-value liquid wastes).
Hazardous Waste Incinerators
Two waste streams were used as representative of the range of wastes
incinerated. One consisted of 50 percent polychlorinated biphenyls (PCBs)
(presumed to be 1254 substituted) and the other 50 percent ethylene dichloride.
Both streams were assumed to contain four carcinogenic metals: arsenic, cad-
mium, chromium (VI), and nickel. PIC concentrations used were based on
available test data.
Waste Oil
The four carcinogens in waste oil that were assessed are arsenic, cad-
mium, chromium (VI), and PCB-1254.
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Solid Waste Management Units (SMUs)
No information is available on representative constituents,
The waste streams used in the various analyses summarized in this sum-
mary are representative of the range of wastes that are either disposed of
or are burned. Consequently, any estimate of risk is unlikely to be under-
estimated. Conservative assumptions often were made regarding the concentra-
tions of carcinogens in waste streams.
RISK ASSESSMENT METHODOLOGY, ESTIMATED RISKS, AND UNCERTAINTIES
Estimates of the risk posed by each source were developed as follows.
RCRA Landfills and Surface Impoundments
The liner location model was used to project ground-water contamination
around 55 facilities with 67 units that plan to continue operating. The
modelling extrapolated over a 400-year period. Risks were estimated assuming:
(1) current well distributions, (2) people continue to drink contaminated
water, (3) no degradation of contaminants, and (4) unlined facilities.
Under these assumptions only two facilities appear to cause health risks (45
facilities had no drinking water wells within two miles).
Extrapolating these results to the 1,500 open and closed RCRA facilities
yields an estimate of 0.3 cancers per year. An upper-bound estimate of 384
cancers per year was developed by assuming 1,000 people were drinking water
from wells located at the facility boundary. (Since most of this risk was
from arsenic, the estimate would drop by an order of magnitude if an updated
GAG potency for ingested arsenic were used.)
The lower estimate may underestimate cancer incidence because facilities
that plan to continue operating may have significantly less contamination
problems than those that close. Further, the current distribution of wells
may change considerably over time, possibly increasing the potential for
future exposure. Other modelling work that was conducted to analyze the
effects of the land disposal ban conservatively places cancer incidence
around 30 to 40 cases per year.
Significant uncertainty exists regarding the distribution of future
wells, actual migration of contaminants from RCRA facilities, the synergistic
effects of multiple contaminants, and the potential for chemical reactions
among and transformation of chemical constituents.
Hazardous Waste Storage Tanks
There are about 15,000 hazardous waste storage tanks and about 11,400
small-quantity-generator facilities with tanks. Health risks may arise if a
tank fails and the subsequent leak contaminates ground-water drinking sources.
To define alternative scenarios, existing analyses of risks from leaking
tanks assume a deterministic tank failure rate (e.g., failure in 20 years
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with a specified release rate) or a probabalistic failure rate, and use
various hydrogeologic settings and waste streams. Individual risks are
estimated to be in the range of one cancer for every 100,000 exposed (10~5).
No estimates of annual cancer incidence are available.
Hazardous Wastes Burned in Boilers and Furnaces
Concentrations of metals, POHCs, and PICs were estimated within a 50-km
radius for a representative sample of boilers and furnaces using the indus-
trial source complex air dispersion model. Risk estimates were based on the
assumption of 70 years of continuous exposure.
Aggregate cancer incidence was estimated to be about 0.3 cases per year.
Individual risks occasionally are as high a 10~5 and, most often, lower than
10~6.
Uncertainties in the analysis arise from lack of information on waste
composition, destruction performance of boilers and furnaces, and potential
clustering of devices, which would affect risks to most exposed individuals.
Hazardous Waste Incinerators
Air dispersion models were used to estimate concentrations of metals,
POHCs, and PICs in a 50-km radius around four large commercial incinerators.
Two waste streams were used to represent the range of wastes that are cur-
rently incinerated.
Cancer incidence was averaged for the four incinerators and was extrapo-
lated to the 235 on-site and commerical incinerators across the country.
Risk was adjusted downward by a factor of five to account for the large amount
of waste assumed in the initial analysis and by a factor of eight to reduce
metal concentrations and adjust for average toxicity of POHCs. Annual cancer
incidence from incinerator emissions is estimated to be about five cases.
Uncertainties in the analysis are mostly with regard to metal concentra-
tions in hazardous wastes, the efficiency of air pollution control devices
in removing metals from off-gas streams, and the amount and type of PICs.
Waste Oil
Releases of contaminants to air, surface water, and ground water were
modelled for model facilities representing nine major oil disposal and reuse
methods. Exposures from airborne contaminants resulting from waste oil
burning, estimated in an earlier analysis as responsible for approximately 40
percent of total waste oil risks, were examined within a radius of 50 km for
the model facilities. Nationwide annual cancer incidence is estimated to be
about two cases from this exposure route, after adjusting for overly conser-
vative assumptions in the initial analysis.
Solid Waste Management Units
There are about 9,000 SMUs. They are ill-defined, and the contami-
nation associated with them is undetermined. A unit may consist of buried
asphalt, old spills of material, or an industrial landfill contaminated
with hazardous materials.
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The extent of the human health problem posed by these sites is unknown.
Many could be located fairly close to drinking water supplies.
REFERENCES
ICF and Pope-Reid Associates, Inc. "Hazardous Waste Tanks Risk Analysis."
Draft report. March 1986.
IEC and ICF, Inc. Regulatory Analysis of Proposed Restrictions on Land
Disposal of Hazardous Waste. Prepared for U.S. EPA, Office of Solid Waste,
Economic Analysis Branch, December 1985.
Sobotka & Co., Inc. "Comparative Risk Analysis of Sources of Groundwater
Contamination." Phase 3 draft report. Prepared for U.S. EPA, Office of
Policy Analysis, Sepember 25, 1986.
Temple, Barker and Sloane, Inc. "Background Document: Regulatory Impact
Analysis of Proposed Standards for Management of Used Oil." Prepared for
U.S. EPA, Office of Solid Waste, November 1985.
U.S. EPA, Office of Solid Waste, Economic Analysis Branch. "Cross-Program
Analysis of Land Disposal Regulations."
U.S. EPA. Assessment of Incineration As a Treatment Method for Liquid Organic
Hazardous Wastes, "Background Report IV: Comparisons of Risks from Land-Based
and Ocean-Based Incineration." March 1985.
U.S. EPA. "Regulatory Analysis for Waste-as-Fuel Technical Standards, Proposed
Rule." Draft report. October 1986.
U.S. EPA. "Comparison of Risks from Land-Based and Ocean-Based Incineration
of Hazardous Wastes." Supplemental analysis. October 1986.
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CATEGORY 2
#14: Non-Hazardous Waste Sites — Industrial
PROBLEM DEFINITION
This category includes risks posed by the 3,400 industrial landfills
and 15,000 industrial surface impoundments throughout the country. The
primary route of exposure is through ground water.
POLLUTANTS ADDRESSED IN THIS SUMMARY
Pollutants included for analysis are arsenic, chloroform, benzene, and
1,1,2,2-tetrachloroethane. These are the major carcinogens for the three
industries analyzed for this summary (iron and steel, pulp and paper, and
organic chemicals).
RISK ASSESSMENT METHODOLOGY
The liner location model was used to simulate individual health risks
from unlined surface impoundments containing raw waste from five industries:
iron and steel, fabricated metals, pulp and paper, inorganic chemicals, and
organic chemicals. For each industry, a prototype surface impoundment con-
taining raw waste was modeled in 64 environmental settings. Ground-water
concentrations were simulated over a 400-year time horizon (200 years of
release plus 200 years of transport) at wells 60m, 600m, and 1500m hydrau-
lically downgradient from the source. Only individual risks were estimated
in this analysis. The model calculates running 70-year (lifetime) average
exposures beginning with each year of the 400-year simulation, and estimates
risks based on these 70-year average exposures. Average risks are reported
by summing the risks for each of the 400 years, and dividing by 400.
Surface impoundments for the fabricated metals and inorganic chemicals
industries did not have carcinogenic consitutents of concern. Therefore,
the cancer risks from these two industries were not modeled.
The table below shows the range of individual risk associated with each
carcinogen for each of the other three industrial sources.
Industries Arsenic Chloroform Benzene
Iron and Steel 3x10~5 - 6x1O"1
Pulp and Paper — 2xlO~4 - IxlO"8
Organic Chemicals — lxlO~6 - lx!0~5 1x10"^ - 1x10~3
The highest individual risk across sources was for arsenic (6 x 10~1).
However, this would drop by about an order of magnitude if a more recent
potency estimate were used. Chloroform and benzene also had significant
individual risk in some of the environmental settings. The chemical 1,1,2,2-
tetrachloroethane was also modeled for pulp and paper, but showed no risk.
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When risks were modeled under the assumption that people would stop
drinking water as soon as one of the contaminant concentrations exceeded the
taste and order threshold, risks for organic chemicals from surface impound-
ments were considerably lower. Risks from the other two categories were not
affected under this assumption.
No attempt has been made to estimate population cancer risk from this
problem area.
REFERENCE
Sobotka & Co., Inc. "Comparative Risk Analysis of Sources of Groundwater
Contamination." Phase 3 draft report. Prepared for U.S. EPA, Office of
Policy Analysis, September 25, 1986.
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CATEGORY 2
#15: New Chemicals
PROBLEM DEFINITION
New chemicals are defined as those not listed on the TSCA Inventory of
Existing Chemical Substances. New substances typically enter the market as
substitutes for existing chemicals. Therefore, risks considered in this envi-
ronmental problem category cover the range of exposure scenarios presented
by existing chemicals.
Approximately 1,800 Premanufacture Notifications of intent to manufac-
ture new chemical substances are submitted to EPA each year. Of these,
approximately half are actually manufactured and used commercially.
The term "new" chemicals as used in this summary refers to industrial
chemicals. New pesticides are considered elsewhere, and new food additives
and drugs are not considered in the overall Comparative Risk Project.
EPA'S RESPONSIBILITY IN THIS AREA
The Toxic Substances Control Act (TSCA) requires that industry notify
EPA at least 90 days before manufacturing or importing a new chemical sub-
stance. The notification must include exposure-related data and available
information on the health effects (including potential carcinogenicity) of
the new substance. EPA reviews these data to evaluate the potential risks
posed by the new substance. Where concerns are identified, EPA takes action
to control exposure to it, pending the development of additional data.
POLLUTANTS ADDRESSED IN THIS SUMMARY
In the great majority of cases, the chemical identity and use of new
chemicals are claimed confidential by the submitter. Therefore this analysis
does not identify the risks presented by specific new chemicals.
RISK ASSESSMENT METHODOLOGY
EPA's assessment of risk focuses on the third year after market intro-
duction. Therefore, it does not reflect the risks that may be realized in
the longer term when use and production increase.
ESTIMATED RISKS
Most new chemicals are manufactured for relatively few customers in re-
sponse to a limited commercial demand. Although specific data are not avail-
able, it is generally believed that most new chemicals only have a limited
commercial life and do not significantly penetrate existing markets. In
spite of this fact, slowly but inevitably, the current spectrum of existing
chemicals will be substantially replaced by new chemical substances that have
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been "screened" by EPA review. To the extent that this review identifies
potential carcinogens and prohibits their marketing, overall carcinogenic
risks of chemicals in commerce will decrease. In this regard, the program
has in the past six years taken action to limit exposure or prevent the
marketing of over 100 potentially carcinogenic substances. However, given
the nature of this environmental problem, it is not possible to present a
more quantitative estimate of risk.
In addition, the heightened industry awareness that results from the
requirement to undergo independent review of potential risk before marketing
has probably resulted in industry's decision to not submit for EPA review
chemicals likely to be considered potential carcinogenics.
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CATEGORY 3
#16: Non-Hazardous Waste Sites — Municipal
PROBLEM DEFINITION
This category includes the risk posed by both open and closed municipal
landfills, municipal sludge and refuse incinerators, and municipal surface
impoundments. The primary route of exposure is ground water for municipal
landfills and surface impoundments and air for sludge and refuse incinerators,
POLLUTANTS ADDRESSED IN THIS SUMMARY
The pollutants addressed for each source are as follows.
Municipal Landfills
Carcinogenic constituents included for analysis are considered typical
of constituents in leachate generated from the codisposal of municipal solid
waste, nonhazardous waste, household waste, and hazardous wastes from small-
quantity generators. (It would not be typical of landfills that received
substantial quantities of hazardous waste.) The constituents modelled are
vinyl chloride, arsenic, 1,1,2,2-tetrachloroethane, dichloromethane, and
carbon tetrachloride.
Municipal Sludge Incinerators
The constituents modelled include the following metals: arsenic, beryl-
lium, cadmium, chromium, mercury, and nickel; and the following organics:
aldrin, benzo(a)pryrene (BAP), chlordane, DEHP, PCBs, toxaphene, and vinyl
chloride.
Municipal Refuse Incinerators
The major constitutents included in the analysis were dioxins, BAP, cad-
mium, chromium, arsenic, and beryllium. The analysis did not assess formalde-
hyde and other organics and trace metals.
Municipal Surface Impoundments
No pollutants were analyzed for these sites.
RISK ASSESSMENT METHODOLOGY AND ESTIMATED RISKS
Estimates of risk posed by each source were developed as follows.
Municipal Landfills
Concentrations of contaminants in ground water were modelled at 60m,
600m, and 1,500m for 14 different environmental settings and 11 different
hydrogeologic settings using the liner-location ground-water model. The
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10-4 -
10-5 -
10-6 -
10-7 -
10-8 -
10-9 -
10-5
10-6
10-7
10-8
10-9
10-10
same leachate, representative of codisposed wastes, was used for each com-
bination of settings. Modelling analyzed a 300-year period, and the risks
at each well distance were calculated as the mean average lifetime risk over
300 years. The modelling results were then weighted to account for the
relative frequencies of environmental settings, hydrogeological settings,
landfill sizes, and well distances observed in the actual populations of
subtitle D (nonhazardous waste) facilities.
This resulted in the following distribution of average individual cancer
risk at municipal landfills.
Range of Individual Risk Frequency of Occurence
12%
28%
27.5%
13%
3.5%
2%
14%
Annual cancer incidence is estimated by: (1) multiplying the weighted
average risk from the above distribution (8 x 10"6) by (2) an estimate of
the average population living within one mile of such sites (about 600) by
(3) the number of open and closed landfills (9,100 + 30,000 = 39,100), and
(4) dividing by 70 (average lifetime). This procedure yields an estimate of
about three cancer cases per year resulting from exposure to wastes from
municipal landfills.
The major uncertainties in the analysis are the simulated release rates,
constituents present in leachate, particularly for closed landfills, and
future population exposure.
Municipal Sludge Incinerators
Approximately 309 sludge incinerators operate at 195 facilities. About
80 percent are multiple hearth, 11 percent are fluidized-bed, and the remainder
are electric infra-red, co-combustion with refuse, or other.
Three air dispersion models were used to estimate concentrations in a
50-km radius around the model facilities: the ISCLT model for flat terrain,
LONG Z for rural settings, and COMPLEX I for urban settings. Model facilities
were selected to be representative of the capacity, stack height, stack gas
exit velocity, population distribution, terrain, and meteorology of actual
incinerators. Actual plants were assigned to each model facility, based on
similarity in characteristics. Emissions were then adjusted to account for
the actual amount of sludge burned and whether the sludge was a light indus-
trial or heavy industrial sludge.
The resulting estimate of cancer incidence is about 23 cases per year,
most of which are caused by emissions of metals. The maximum individual
risk was estimated to be as high as one in 1,000 (10"-*).
Uncertainties in the analysis arise from uncertainty about metal concen-
tration in sludge and the form of chromium emitted (hexavalent was assumed).
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Municipal Refuse Incinerators
Based on very preliminary modelling and national extrapolation, excess
cancer incidence is estimated at 3-14 cases per year, and maximum individual
risk at about 10~3. Most of the modelled risk is from dioxins. However,
the analysis is based on very limited data, and the estimates are speculative.
Municipal Surface Impoundments
There are about 20,000 municipal surface impoundments in the United
States. No analysis has yet been performed on the extent to which these
sites contaminate ground water.
REFERENCES
U.S. EPA, Office of Solid Waste, Economic Analysis Branch. "Preliminary and
Ongoing Municipal D Analysis."
U.S. EPA, Office of Policy Analysis. "Crossmedia Impacts of Utilization and
Disposal of Municipal Sludges." May 1986.
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CATEGORY 3
#17: Contaminated Sludge
PROBLEM DEFINITION
In 1983-84, in preparing technical regulations for the use/disposal of
sewage sludge from publicly owned treatment works (POTWs), EPA considered
the following use/disposal options: land application to human food-chain
and non-food-chain crops, distribution and marketing of sludge or sludge-
derived products for use as soil conditioners and nutrients, landfilling,
incineration, and ocean disposal.
It is difficult to determine if sludge is a factor in causing cancer
and, if so, the extent of that problem. The initial regulation is being de-
signed to forestall as many of the environmental consequences of sludge
disposal as possible.
POLLUTANTS ADDRESSED IN THIS SUMMARY
Forty-one chemicals were selected for the initial regulation based on a
survey of sludge from 40 POTWs representative of national sludge quality. Of
these, 24 are known or suspected carcinogens according to either EPA's Office
of Pesticide Programs or the Carcinogen Assessment Group. A list of these
chemicals and the disposal options being considered appears at the end of
this summary.
RISK ASSESSMENT METHODOLOGY AND RISK ESTIMATES
The methodologies developed are comprised of environmental models that
consist of mathematical expressions or algorithms. The models predict the
movement of pollutants from sludge placed on or into the land, emissions from
sludge that is incinerated, or dispersion from sludge dumped into the ocean
through several environmental compartments or media to reach a receptor or
target organism at a calculated concentration. This concentration of pol-
lutant is then compared with either an environmental impact or a human health
criterion. This criterion is a concentration of a pollutant, that, when
exceeded, will harm the environment or human health.
Several quantitative risk estimates from a previous analysis are presen-
ted in the following paragraphs. These estimates were derived in a report
developed by EPA's Office of Policy Analysis using methods that have not
been formally adopted by EPA (U.S. EPA, 1986). Therefore, in all cases these
estimates are preliminary; more detailed analyses are currently under way.
Land Application
Sludge may be applied to land as a soil conditioner and provider of sup-
plemental nutrients. The broad term "land application" includes many specific
end uses, such as applying sludge for growing row crops, pasture lands, com-
mercial forests, highway landscape, turf farms, and nurseries. In addition,
land application includes "dedicated" land disposal — the application of
sludge to POTW land as an alternative to other methods of disposal.
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The risks from three types of land application have been estimated.
Application of sludge to pasture land has been associated with appoximately
0.6 cancers annually, while crop land application results in about 0.5 cases
a year. Most of these are risks are linked to PCBs, which tend to accumulate
in plants. Dedicated use yields an estimate of 0.3 cancers annually, resul-
ting from surface water runoff. Other exposure routes were not considered
significant.
Distribution and Marketing
With this is type of land application, the primary exposure route is
ingestion of food crops treated with (and contaminanted by) sludge. Distribu-
tion and marketing products are expected to be transported and used at far
greater distances from the POTWs where the sludge originated than the usual
land application practices. In addition, less experienced users (e.g., home-
owners' application to home gardens or lawns) are involved. Therefore, dis-
tribution and marketing practices pose a potentially greater hazard than
land application practices.
Distribution and marketing of sludge has been modeled to currently ac-
count for just under two cancer cases annually. Just over half of these pro-
jected cases result from toxaphene exposure.
Landfilling
Landfills are a widely used and well-documented sludge disposal option.
About 45 percent of all sludge generated ends up in a landfill. The two
major routes of sludge landfill disposal are monofill (sludge only) and co-
disposal with municipal refuse, with the latter predominating.
For the purposes of this analysis, we assumed that vapor loss does not
constitute a real cancer hazard. While benzene, trichloroethylene, and other
organics are quite volatile, the concentrations generated are generally very
low. We also assumed that suspension of contaminant particles from the work
face is insignificant, given that the necessary wind velocities rarely occur.
In addition, because of the general practice of covering the work face with
fresh soil and digging drainage ditches, surface runoff does not pose serious
cancer risks. We therefore assumed that ground-water contamination presents
the greatest threat to human health.
Approximately 13 cancer cases per year have been estimated to result
from ground water contaminated by landfilled sludge. However, this figure
would decrease by about an order of magnitude if this analysis were redone
using a revised potency esi:nate for ingested arsenic.
Incineration
Incineration is a major disposal practice for sludge in the United States.
While this risk analysis is continuing, preliminary results are available on
the basis of an extrapolation from eight model plants to the entire 309
operating sludge incinerators in the nation. This extrapolation yields an
estimate of 23 cases annually from the inhalation of carcinogens emitted by
sludge incinerators. However, over 90 percent of this estimate result from
exposure to chromium, which was assumed to be in the hexavalent form. If
the any of the chromium actually emitted is in the trivalent form, these
risks may be overstated.
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Ocean Disposal
With ocean disposal, sewage sludge is barged for dispersion at a federally
approved dumpsite. In general, state authorities and EPA issue a dumping
permit to either one large POTW or several small ones.
Using several conservative assumptions, risks were estimated from the
consumption of seafood contaminated by sludge from 27 POTWs that dispose of
the sludge off the coast of New Jersey. Based on this analysis, over two
cases a year were estimated; no national assessment is available.
OVERALL RISK ESTIMATE
The combination of the results of these preliminary analyses results in
a total estimate of approximately 40 cases annually. However, there are
considerable uncertainties and assumptions implicit in this estimate. We
hope that future analyses will improve the reliability of these estimates.
Known or Suspected Carcinogens Being Evaluated
Under Section 405(d) of the Clean Water Act
Pollutant Disopsal Options
Aldrin LA, I, OD
Arsenic LA, LF, I
Benzene LF, I
Benzidene OD
Benzo(a)pyrene LA, LF, I, OD
Beryllium LA, I
Bis(2-ethylhexyl)phthalate LA, LF, I, OD
Cadmium LA, LF, I, OD
Carbon Tetrachloride I
Chlordane LA, LF, I, OD
Chloroform I
Chromium LA, LF, I
DDT/DDE/DDD LA, LF, OD
Dieldrin LA, I, OD
Dimethyl Nitrosamine LF
Heptachlor LA, OD
Hexachlorobenzene LA
Methylene Chloride LA, I
PCBs LA, LF, I, OD
Pentachlorophenol LA
Tetrachloroethylene I
Toxaphene LA, LF, I, OD
Trichloroethylene LA, LF
Vinyl Chloride I
LA = Land Application and Distribution and Marketing
LF = Landfilling
I = Incineration
OD = Ocean Dumping
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REFERENCE
U.S. EPA, Office of Policy Analysis, Regulatory Integration Division. "Cross-
media Impacts of Utilization and Disposal of Municipal Sludges." May, 1986.
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CATEGORY 3
#18; Mining Waste
PROBLEM DEFINITION
This category includes risks posed by mining operations, smelting and
refining wastes, and oil and gas operations. The primary route of exposure
is ground water.
POLLUTANTS ADDRESSED IN THIS SUMMARY
A formal risk analysis was only conducted for smelting and refining
wastes. The carcinogens addressed were arsenic, cadmium, and nickel.
RISK ASSESSMENT METHODOLOGY AND ESTIMATED RISKS
The risks posed by each source are as follows.
Mining Operations
A risk assessment has not been completed for the mining industry.
General information on mining operations suggests that population cancer
risks are low. To a large extent, this is because the average population
within five km of the 300 or so active mines is about 5 percent of that
surrounding RCRA Subtitle C (hazardous waste) facilities. Only 22 percent
of mines have public drinking water wells within five km, and about 68 per-
cent of these wells serve fewer than 1,000 people.
Smelting and Refining Waste
The liner location model was used to model risk from 29 landfills and
surface impoundments receiving wastes from 29 actual smelting and refining
facilities in four categories: aluminum, copper, lead, and zinc. The fa-
cilities modeled were selected as a representative sample of the entire popu-
lation of smelting and refining facilities in the United States. Site-specific
information on waste type and volume, environmental setting, and exposed
populations was used as input to the model. The individual and population
cancer risks from arsenic, cadmium, and nickel were estimated over 100 years.
Arsenic was responsible for almost all of the cancer risk. Of the 29
units modeled, 16 had cancer risk, all due to arsenic. Average individual
cancer risk ranged from two cases for every million people exposed (2 x 10""°)
to four for every ten people exposed (4 x 10~*). Extrapolating the results
nationally on the basis of population surrounding smelting and refining
sites yields an estimate of about 112 cancer cases per year. However, this
would be reduced by about an order of magnitude if a more recent potency
factor were used for ingested arsenic.
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Oil and Gas Operations
Carcinogenic compounds have been observed in ground water and surface
water around oil and gas operations, but no concentration data are available.
REFERENCES
Buc and Associates, Inc. "Location of Mines and Factors Affecting Exposure."
Draft report. Prepared for U.S. EPA, Office of Solid tvaste. June 30, 1986.
ICF, Inc. "Analysis of Human Health Risks Associated with the Management of
Hazardous Waste from the Primary Smelting and Refining Industries." Feb-
ruary 1985.
U.S. EPA, Office of Solid Waste. Report to Congress, Wastes from the Extrac-
tion and Benefication of Metallic Ores, Phosphate Rock, Asbestos, Overburden
from Uranium Mining, and Oil Shale. December 1985.
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CATEGORY 3
#19: Releases from Storage Tanks
PROBLEM DEFINITION
This category includes risk posed by releases from storage tanks,
primarily underground storage tanks containing gasoline. The primary
route of exposure is ingestion of ground water.
POLLUTANTS ADDRESSED IN THIS SUMMARY
The risk analysis evaluates the risk posed only by benzene. Risks from
toluene and ethylene dibromide (an additive in leaded gasoline) have been
generally assessed and are small relative to risks posed by benzene.
RISK ASSESSMENT METHODOLOGY
The underground storage tank model (a Monte Carlo simulation model) was
used to predict the number of leaks and the distribution of plume sizes for
a range of scenarios. The scenarios were defined by different combinations
of tank design, vadose zones, and ground-water velocities. The results were
weighted according to the actual distribution of such factors. Wells were
assumed to draw from the uppermost saturated zone, rather than from lower
aquifers. No degradation of benzene was assumed to occur, but exposure
was assumed to stop after a leak was detected. The number of people exposed
was based on the national average density per acre of people using private
or public wells times the modelled area of the plume of contaminated ground
water.
ESTIMATED RISK
Yearly national cancer incidence was estimated to be less than one,
both case where people were assumed to stop drinking contaminated water when
the taste and odor threshold was exceeded and where they were assumed to
continue drinking contaminated water.
UNCERTAINTIES
Major uncertainties in the analysis involve the rate of tank failures,
the actual migration of and extent of contaminated ground water, and the
effects of mitigating behavior on exposure. In addition, this analysis are
preliminary and ongoing.
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CATEGORY 4
#20; Nonpoint Source Discharges to Surface Water
PROBLEM DEFINITION
Chemicals can reach the aquatic environment not only from delineated
point sources, such as industrial facilities, but also in the runoff of
pesticides and stormwater from the land, infiltration from ground water, and
air pollutants settling in water. Currently, because of the legislative
framework, nonpoint-source pollution is dealt with through the ambient water
quality criteria and standards program.
POLLUTANTS ADDRESSED IN THIS SUMMARY
A great number of environmental pollutants are of potential concern
under this environmental problem. With respect to carcinogens, perhaps
the greatest risk relates to the runoff of agricultural chemicals into
surface water, primarily due to the large volume of substances entering
surface waters in this way.
No specific pollutants are adressed in this summary, as cancer risk
assessments have not been performed beyond that of the water quality criteria.
RISK ASSESSMENT METHODOLOGY
Cancer potencies developed by the Carcinogen Assessment Group or Office
of Pesticide Programs are used when necessary. However, no quantitative
cancer risk analysis is available for assessing the riks from this problem.
RISK ESTIMATES
There is no quantitative estimate of cancer risk for this problem. The
work group ranked it relatively low due to limited human exposure, but the
consensus view was that this was the most serious of the surface water
problems.
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CATEGORY 3
#21: Other Ground-Water Contamination
PROBLEM DEFINITION
Ground water can be polluted by an abundance of different sources, most
of which are listed in a 1984 report prepared by the Office of Technology
Assessment (see table). The majority of the listed sources that may release
carcinogenic contaminants are conceptually addressed in discussions of other
environmental problems in this document, such as hazardous waste sites, under-
ground storage tanks, wastewater, sludge, agricultural praccticea, and
landfills.
Table {/—Source* of Groundwator Contamination
ipools)
Category I—Sources designed to discharge »
Subsurface percolation (eg, septic tanks and
Injection wells
Hazardous waste
Non-hazardous waste (ag, brine disposal and drainage)
Norvwaste (ag, enhanced recovery, artificial recharge,
solution mining, and in-situ mining)
Land application
Wastewater (ag, spray irrigation)
Wastewater byproducts (ag, sludge)
Hazardous waste
Non-hazardous waste
Category Il-Sources designed to store, treat, and/or
dispose of substances; discharge through unplanned
Open burning and detonation sites
Radioactive disposal sites
Category Ill-Sources designed te
Landfills
Industrial hazardous waste
Industrial non-hazardous waste
Municipal sanitary
Open dumps, including illegal dumping (waste)
Residential (or local) disposal (waste)
Surface impoundments
Hazardous waste
Non-hazardous waste
Waste tailings
Waste piles
Hazardous waste
Non-hazardous waste
Materials stockpiles (non-waste)
Graveyards
Animal burial
Aboveground storage tanks
Hazardous waste
Non-hazardous waste
Non-waste
Underground storage tanks
Hazardous waste
Non-hazardous waste
Non-waste
Containers
Hazardous waste
Non-hazardous waste
Non-waste
Pipelines
Hazardous waste
Non-hazardous waste
Non-waste
Materials transport and transfer operations
Hazardous waste
Non-hazardous waste
Norvwaste
Category IV—Sources dtethergliig susalaneea as
Irrigation practices (ag, return flow)
Pesticide applications
Fertilizer applications
Animal feeding operations
De-icing salts applications
Urban runoff
Percolation of atmospheric pollutants
Mining and mine drainage
Surface mine-related
Underground mine-related
Category V—Sources provMktg conduit or Inducing
discharge through altered Hew patterns
Production wells
Oil (and gas) wells
Geothermal and heat recovery wells
Water supply wells
Other wells (norvwaste)
Monitoring wells
Exploration wells
Construction excavation
Category VI—Naturally occurring
Is creeled andfor exacerbated by human activity
Groundwater—surface water interactions
Natural leaching
Salt-water intrusion/brackish water upconing (or intrusion of
other poor-quality natural water)
SOURCE. Offlc* of ftcfrKHogf Aimmunt, 1984
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For the purposes of this document, "other ground-water pollutants" are
defined here as sources of carcinogenic contaminants that are unaddressed
elsewhere in the document. Such sources may include residential waste disposal
sites (e.g., septic tanks, dumps), stockpiles of materials, graveyards,
railroad yards, and naturally occurring carcinogenic substances (e.g., arsenic
and selenium), as well as unidentified sources of ground-water contamination.
Under the right hydrogeologic conditions, any substance released on the
land surface or subsurface can contaminate ground water. The major problem
in estimating cancer risks from ground-water contamination is a lack of
information on what the sources are, where they are located, where they are
actually contaminating the ground water, how significant the contamination
is, and how many people it is affecting. Comprehensive information to
answer these necessary questions is not available. Consequently, the extent
of ground-water supplies contaminated by carcinogenic substances is unknown.
POLLUTANTS ADDRESSED IN THIS SUMMARY
The criteria for selecting sources were first to determine the sources
of ground-water contamination, and then to select the sources that were most
likely to contain carcinogens. Carcinogenic sources discussed in other
sections were eliminated. For the remaining sources, the only cancer risk
estimates available were for methylene chloride, which is used as a septic
tank degreaser.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
Methylene chloride is the only potential carcinogen studied by EPA's
Office of Policy, Planning and Evaluation (OPPE) for septic tank activity.
Many carcinogens enter septic tanks from normal household use of chemicals
(e.g., paint).
Exposure Assessment
Domestic septic tanks are cleaned usually every five years. This analysis
assumed the worst case, which was that they are cleaned yearly.
A septic system includes septic tanks, cesspools, and the leachfields.
Three categories of density of septic tank systems were analyzed: low density
is septic tanks of less than ten units within one square mile, medium density
is 0-40 units per square mile, and high density is greater than 40 units per
square mile.
The relative distribution of the systems by location was derived from
the 1980 Bureau of the Census Report and the 1970 Census of Housing Reports.
Heath (1984) combined the map from the latter publication with a map of
ground-water regions to arrive at density calculations.
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Estimation of Risk
In the past, general procedures for estimating risks from ground-water
contaminants have followed the flow chart in the attached figure.
The Liner Location model and the Prickett Random Walk Particle Tracking
model produced ground-water concentrations of methylene chloride for over 400
years. These concentrations were then translated into doses. The risk
estimate equation multiplies the dose by a dose-response factor:
R = 1 - exp[-H x (D-t)k]
r = risk
H = potency of constituent
D = dose
K = factor describing shape of dose-response
curve = 1 for carcinogens, = 1
t = response threshold, = 0(mg/kg/day)
Potential concentrations of carcinogens reaching ground water were
calculated based on 64 hydrogeologic settings over 400 years. In all of
the settings that were modeled, individual lifetime cancer risks did not
exceed one in 10,000 (10~5 )(based on the potency of methylene chloride).
However, the risk fell between one in a million (10~6) and one in 10 million
(10~7) in approximately half of the settings. Based on this, the OPPE
study concluded that the risk presented by methylene chloride in septic
systems is "not significant." Populations risks were not estimated in this
report (U.S. EPA, 1986).
UNCERTAINTIES AND CAVEATS
The OPPE study is the first of its kind in defining carcinogenic and non-
carcinogenic ground-water risks. It thus provides a basis from which to
expand and improve ground-water risk analyses. However, the study has severe
limitations for estimating cancer risk.
For example, the study calculates individual risk only and does not
estimate population risk, which may be significant. However, a rough estimate
of the population risk associated with this problem indicates a cancer incidence
of less than one case every six years.
In addition, the following assumptions were made to reduce the time
involved and simplify the complexity of this ground-water problem to make
analysis feasible. The greater the number of assumptions, the less accurate
the results are likely to be.
1. The models do not represent multiple sources or multiple
chemical constituents. Septic tanks can release several
carcinogens into ground water. Interactions between chemicals
may greatly influence risks.
2. An average rate of release of the chemical was assumed.
Because actual rates of release are not constant, failure
and release rates are not characterized well.
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MLT.;'JDS AND ANALYSIS FLOW CHART
SOURCE SELECTION
- Potential Risk
- Analytical Feasibility
- Data Availability
- Usefulness of Results
SOURCE CHARACTERIZATION
- Size
- Constituents
- Failure/Release
- Geographic Distribution
MODEL ENVIRONMENT CONSTRUCTION
- Depth to Ground water
- Net Hydrologic Recharge
- Aquifer Configuration
- Groundwater Velocity
CONTAMINANT TRANSPORT MODELING
- Contaminant Release
- Unsaturated Zone Algorithm
- Saturated Zone Model
- Distance to Receptors
HEALTH RISK ESTIMATION
- Dose Estimation
- Nature of Effect
- Dose-Response Function
- Risk Algorithm
RISK ANALYSIS
- Source Impact on
Human Health Risks
- Environmental
Vulnerability
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3. Important soil and hydrogeologic parameters remained constant
across all environments. Actual hydrogeologic environments
fluctuate significantly, and are not isotopic and homogeneous,
as assumed in both models.
4. With respect to the hydrogeologic settings used for studying
risk, calculations are probably underestimated. Once again,
this is because septic tanks are placed in the best-drained
areas locally, and these areas are the most vulnerable
hydrogeologic settings.
5. Drinking water wells were assumed to be located 600 meters
(1,800 feet) directly downgradient from the septic tanks. In
actual residential settings, rural septic tanks and water
well systems are most often less than 600 meters apart.
REFERENCES
Carcinogen Assessment Group (GAG). "Relative Carcinogenic Potencies Among
54 Chemicals Evaluated by the Carcinogen Assessment Group as Suspected
Human Carcinogens." Washington, B.C. Revised May 1985.
Heath, K. "Groundwater Regions of the United States." U.S. Geologic Survey
Water Supply Paper 2242. U.S. Geologic Survey. Reston, VA., 1984.
U.S. Office of Technology Assessment. Protecting the Nations Ground Water
from Contamination. OTA-0-233. Washington, D.C., 1984.
U.S. Department of Commerce, Bureau of the Census. "Detailed Housing Charac-
teristics, U.S. Summary." 1970 Census of Housing. Washington, D.C., 1970.
U.S. Department of Commerce, Bureau of the Census. "Number of Inhabitants,
U.S. Summary." 1980 Census of Population. PC80-1-A1. Washington, D.C.,
1980.
U.S. Environmental Protection Agency, Office of Policy, Planning, and Evalua-
tion. "Comparative Impact Analysis of Sources of Ground-Water Contamination,
Phase II." Draft report. Washington, D.C., 1986.
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CATEGORY 3
#22: Criteria Air Pollutants
PROBLEM DEFINITION
Sections 108 and 109 of the Clean Air Act provide for the establish-
ment of national ambient air quality standards (NAAQS) for air pollutants
from "numerous or diverse mobile or stationary sources." Termed "criteria
pollutants," the six pollutants listed under section 108 are lead, particu-
late matter, nitrogen dioxide, ozone, sulfur oxides, and carbon monoxide.
ASSESSMENT OF RISK
Several of the criteria air pollutants and their metabolic or atmos-
pheric by-products have been identified as possible human carcinogens or
co-carcinogens. The human cancer risks associated with exposure to these
pollutants have not been quantified due to inadequate toxicological, phar-
macokinetic and epidemiological data. Therefore, estimating the cancer
risks of the criteria pollutants is impossible at this time.
For the purposes of this project, the potential cancer risk associated
with exposure to criteria pollutants should be considered to be low. How-
ever, to some extent this low ranking is an artifact of the way the work
group defined this problem area.
To control ambient ozone concentrations, EPA has focused on preventing
the emissions of diverse organic compounds, some of which are carcinogenic.
In addition, carcinogenic particles, such as chromium and asbestos, make
up a portion of what is controlled to meet standards for particulate
matter. Indeed, it is likely that the criteria pollutants program has
thus far been more successful in the control of airborne carcinogens than
any other activity administered by EPA. However, the work group has elected
to consider the risks associated with organics and carcinogenic particles
under Hazardous/Toxic Air Pollutants.
A brief discussion of the carcinogenic potential of each criteria
pollutant follows.
Lead
At relatively high concentrations, lead displays some evidence of
carcinogenicity in experimental animals, such as the rat. Lead may act as
either an initiator or a promoter of carcinogenicity. The role that lead
may play in the induction of human neoplasia has not been established.
Epidemiological studies of workers exposed to lead provide no defini-
tive findings. However, statistically significant elevations in respiratory
tract and digestive system cancer in workers exposed to lead and other
agents warrant concern. Also, since lead acetate can produce renal tumors
in some experimental animals, it may be prudent to assume that lead compounds
may be carcinogenic in humans (U.S. EPA, 1986a).
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In light of the recent preliminary determination by the Carcinogen
Assessment Group to classify lead as a probable human carcinogen (Class
B2), consideration should be given to performing a quantitative cancer
risk assessment for lead.
Particulate Matter
Particulate matter represents a broad class of chemically and physically
diverse substances that exist as discrete particles (liquid droplets or
solids) . Levels of polycyclic organics and some inorganic carcinogens
associated with particulate matter may have contributed to elevated cancer
rates in urban areas during the high particulate pollution of the 1940-60s.
Since then levels of some particulate carcinogens have declined, as has,
presumably, their carcinogenic risk.
Studies of current U.S. air suggest that the mutagenicity of particle
extracts is dominated by organic particle fractions that may not have been
of significance in the past. The available evidence does not show that
current particle exposures contribute to cancer, nor does it disprove any
effect. The presence of mutagens in organic particulate fractions from
unidentified sources and the potential interaction between these or other
particles and carcinogens from cigarettes or occupational exposures suggest
some need for caution and further study (U.S. EPA, 1982a).
Nitrogen Oxides
A few epidemiological studies have attempted to link environmental
nitrates, nitrites, and nitroso compounds (derived from various oxides of
nitrogen in the atmosphere) with human cancer. The criteria document for
nitrogen oxides states that atmospheric nitrogenous compounds have not been
shown to contribute significantly to the in vivo formation of nitrosamines
in humans or that ambient air levels of nitrosamines represent a significant
health hazard. There is no direct evidence that nitrogen oxides contribute
to human cancer (U.S. EPA, 1982b).
Ozone
Except for the data on ozone-induced genotoxicity in peripheral blood
lymphocytes, the potential genotoxic effects of ozone in humans is unknown.
Epidemiological data on the contribution of ozone and other photochemical
oxidants to human cancer are inconclusive. Recent studies have suggested
that exposure of laboratory animals to ozone may increase the incidence of
lung tumors. Due to the limited and equivocal nature of the available data,
no conclusive statement can be made at this time regarding the potential
carcinogenicity of ozone (Hassett et al., 1985; Last et al., 1986; U.S. EPA,
1986b).
Sulfur Oxides
Sulfur dioxide and bisulfite have been reported to be mutagenic in
microbial test systems at acidic pH. Negative results have been reported for
mammalian cells and insects. Inconclusive evidence suggests that S02 may be
a carcinogen or co-carcinogen with benzo[a]pyrene. Available epidemiological
studies neither prove nor negate the possibility that S02, acting alone or
with particulate carcinogens, may contribute to cancer. Because of the
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positive results of mutagenicity studies and the results of the cancer studies,
the criteria document concludes that "SC>2 must remain suspect*as a carcinogen
or co-carcinogen" (U.S. EPA, 1982c).
Carbon Monoxide
There is no evidence to suggest that exposure to carbon monoxide poses
a cancer risk.
REFERENCES
Hassett et al. JNCI, 7_5, 1985
Last et al. JNCI, in press.
U.S. EPA, 1982a. Review of the National Ambient Air Quality Standards for
Particulate Matter; Assessment of Scientific and Technical Information,
OAQPS Staff Paper. EPA-450/5-82-001, January 1982.
U.S. EPA, 1982b. Air Quality Criteria for Oxides of Nitrogen. EPA-600/
8-82-026, September 1982.
U.S. EPA, 1982c. Review of the National Ambient Air Quality Standards for
Sulfur Oxides: Assessment of Scientific and Technical Information,
OAQPS Staff Paper. EPA-450/5-82-007, November 1982.
U.S. EPA, 1986a. Air Quality Criteria for Lead, Vol. IV. EPA-600/8-831
028dF, June 1986.
U.S. EPA, 1986b. Air Quality Criteria for Ozone and Other Photochemical
Oxidants. EPA-600/8-84-020eF. August 1986.
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CATEGORY 4
#23: Direct Point Source Discharges to Surface Water
#24: Indirect Point Source Discharges to Surface Water
PROBLEM DEFINITION
The Criteria and Standards Division handles these problems together by
addressing them in terms of ambient water quality criteria. Because of this
approach, the Division is concerned with the universe of chemicals that reach
surface water (both fresh- and saltwater) from industrial outfalls and treat-
ment plant effluents. The approach also indirectly addresses contaminants
from man-made and natural nonpoint sources by establishing maximum safe
limits in water, regardless of the source.
POLLUTANTS ADDEESSED IN THIS SUMMARY
The chemicals in surface water originally addressed by EPA were mandated
by consent decree: the so-called priority pollutants. Since 1980, little
has been done in terms of human health.
Using lists prepared from EPA monitoring data, state information, and
lists compiled by a number of offices within EPA, the Office of Water Regula-
tions and Standards (OWRS) has compiled a list of 1,500 chemicals of concern.
Of these, we ranked 150 chemicals based on human and aquatic toxicity, poten-
tial carcinogenicity, and exposure. This ranking yielded 45 chemicals that
will be addressed during fiscal year 1987. Unfortunately, risk estimates
are not yet available.
While this approach will eventually address about 10% of the chemicals
on our current lists, we expect that it covers a much greater portion of the
total problem. Since the chemicals on the list dictated by Section 307(a)
of the Clean Water Act have already been looked at, at least half of the
total problem will be addressed after we finish assessing the 150 chemicals
we are now working on.
RISK ASSESSMENT METHODOLOGY
Cancer Potencies
OWRS generally uses potency estimates developed by the Carcinogen Assess-
ment Group for'all chemicals it is concerned with.
Exposure Assessment
The objective of the health assessment portions of the Ambient Water
Quality Criteria Documents is to estimate ambient water concentrations of
contaminants, which in the case of suspect or proven carcinogens, represent
various levels of incremental cancer risk. These health assessments typically
discuss four elements: exposure, pharmacokinetics, toxic effects, and cri-
terion formulation. These are described below.
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The exposure section summarizes information on exposure routes. Most
criteria are based solely on exposure from consumption of water containing
a specified concentration of a pollutant and from consumption of seafood that
is assumed to have bioconcentrated pollutants from the surrounding water.
The relative contribution of a pollutant to cancer risk varies with its
propensity to bioconcentrate.
The pharmacokinetics section reviews data on absorbtion, distribution,
metabolism, and excretion to assess the biochemical fate of the compounds in
mammalian systems.
The toxic effects section reviews information on acute, subacute, and
chronic toxicity, as well as specific information on mutagenicity, tetrato-
genicity, and carcinogenicity of the substance.
The criterion formulation section reviews highlights of the text and
specifies a rationale for development and a mathematical derivation of the
"criterion number."
Carcinogenic risks are estimated by extrapolation from animal toxicity
or human epdemiology studies using the following basic exposure assumptions:
o 70-kg male person as the exposed individual;
o average consumption of fresh- and saltwater shellfish and other sea-
food products equal to 6.5 grams per day; and
o average ingestion of 2 liters of water per day.
The criteria based on these assumptions should protect an adult male
experiencing average exposure conditions. The assessments, as indicated
above, do not account for special segments of the population, or the possi-
bility of exposures from other media.
RISK ESTIMATES
At present, risk estimates are not available for these problem areas.
The cancer work group ranked them on the basis of their professional judgment,
with no backing quantitative analysis.
UNCERTAINTIES AND CAVEATS
Much of the uncertainty associated with the program focuses on deter-
mining what pollutants may be present in the aquatic environment. Monitoring
efforts have historically been directed toward the priority pollutants, so a
fair body of data exists for them. Other substances have not been analyzed,
so little information on exposure can be found. It follows that even less
is known about their potential carcinogenicity.
There is also concern about the extent of the problem as related to
sediments. They can act as a temporary sink for pollutants, which can be
released over time to the water column.
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In general, given the lack of cancer risk analysis, there is considerable
uncertainty abount the magnitdue of these problems. The relatively low
probability for large population exposure moved these problems to their low
ranking.
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Category 4
#25: Accidental Releases - Toxics
No information is available on which to base estimates of potential can-
cer effects. While such effects probably are minor due to the acute nature
of exposure, they are likely to be higher than the effects from oil spills
because of the toxic nature of these substances. Acute health effects and
ecological effects would be of greater concern.
The cancer work group did not explicitly consider potential chronic
exposures related to the ingestion of ground water contaminated by accdental
releases.
#26; Accidental Releases - Oil Spills
The likely cancer effects from oil spills are negligible, primarily
because exposure is likely to be acute. Of greater concern are welfare and
ecological effects.
The cancer work group did not explicitly consider potential chronic
exposures related to the ingestion of ground water contaminated by accdental
releases.
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CATEGORY 5 (no risk identified)
Biotechnology
EPA has little or no information that indicates that biotechnology may
lead to increased risk of cancer. As research and analysis increase in this
area, the magnitude of the potential environmental risks biotechnology poses
will become better understood. However, cancer risks are not expected to be
a major concern. For these reasons, the cancer work group could not identify
any effect of biotechnology on the cancer incidence in the United States.
CO? and Global Warming
The long-term effects associated with a global warming as a result of
anthrogenic emissions of carbon dioxide and other "greenhouse" gases are
likely to be extremely wide-ranging. As a result, this environmental problem
may indirectly affect cancer incidences in the United States. However, the
cancer work group could not identify cancer risks associated with this envi-
ronmental problem. Given the obvious major ecological and welfare effects
of C02 and global warming, relatively little effort is planned in the near
future to further assess the cancer impacts of this issue.
Other Air Pollutants
Under the set of definitions adopted by the cancer work group, outdoor
air pollutants (other than criteria pollutants) that affect cancer incidence
are being considered under Hazardous/Toxic Air Pollutants. For this reason,
no cancer risk is attributed to this problem area.
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NOT RANKED
To Estuaries, Coastal feters, and Oceans from All Sources
To Wetlands from All Sources
These environmental problems focus on the receptors of pollutants, while
other environmental problems are related to sources of pollutants. Wa chose
not to rank them because the risks associated with them are discussed else-
where under such source-related problems as Direct Point, Indirect Point,
and Nonpoint Discharges to Surface feters. While it was impossible to com-
pletely avoid accounting for the same risk under different problem areas, we
generally tried to minimize double counting.
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