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OCR for page 152
9
Estimating Health Risks at
Hazardous Waste Sites:
Decisions and Choices
Despite Uncertainty
ROBERT G. TARDIFF AND MICHAEL GOUGH
The purpose of this paper is to discuss the approaches cur-
rently being used to estimate the risks posed by hazardous waste
sites. We present some of the complex characteristics of waste
sites, a synopsis of risk assessment methodology, and a summary
of several examples of comprehensive quantitative risk estima-
tions. Finally, we discuss some of the inherent uncertainties in risk
assessments and somes means of dealing with them to reach
conclusions usable in risk management.
BAC:KGROU~D
By definition, hazardous waste sites contain a myriac] of sum
stances, the composition of which is known to varying extents
at each site. Because most sites offer incomplete containment,
the substances escape at differing rates into surface and ground
water and into air. (This situation is particularly true for those
facilities constructed without the benefit of state-othe-art con-
tainment technology, as is the case for virtually all sites identified
by EPA for remediation under the Comprehensive Environmental
Response, Compensations and Liability Act.) Such dynamic pro-
cesses can expose humans in a number of ways. For example, at a
single site, workers might for several months of their lives inhale
highly volatile compounds and experience skin contact with sub-
stances bound to dust; by contrast, nearby residents might ingest
152
OCR for page 153
ESTIMATING HEALTH RISKS
153
for many decades contaminants that had migrated from the site
to the water in their wells.
Waste substances are absorbed into the body at different ef-
ficiencies through the skin, gastrointestinal tract, and respiratory
system. They vary greatly in their toxic properties for exam-
ple, some can cause cancer, others birth defects, injury to neural
functions, and a panoply of damage throughout the body. Their
toxic potencies also vary considerably under Mitering and iden-
tical conditions of exposure. Often other characteristics, such as
flammability and explosivity, also contribute to the complexity of
the chemical makeup and the evaluation of risks to humans.
ASSESSMENT 0] RISES TO CAN EEAITH
Regardless of the details of the situation at any site, the four
steps of risk assessment (as described originally by a committee of
the National Research Council, 1983) provide an orderly means for
analyzing scientific information, identifying critical data, elucidat-
ing uncertainties, and comparing estimates of risk and safety (i.e.,
acceptable risk). Briefly, the four steps are hazard identification,
dose-response assessment, exposure assessment, and risk charac-
terization, the definitions of which are provided in the National
Research Council report and further elaborated in a publication
by the ENVIRON corporation (1986~.
In practice, risk assessments are usefully divided into those
done for substances that cause cancer and mutations and those
done for all other toxic ejects. The underlying premise for such
a ctistinction is that the essential molecular step in mutation and
at least some forms of cancer is an irreversible change in the DNA
that is passed on to subsequent generations of cells. A single
interaction, therefore, is sufficient to cause a mutation or to ini-
tiate cancer. For other forms of toxicity a critical concentration
or "threshold" of a toxicant is needed, occasionally for a substan-
tial period, before functional damage occurs, and such damage is
generally repaired on cessation of exposure.
A consequence of this distinction is that any exposure, no
matter how small, to carcinogens (at least, to "initiators") and
mutagens is associated with a probability of injury. By contrast,
for other toxicants, there are definable levels of exposure above
which injury (whether mild or severe will depend on the magnitude
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154
HAZARDOUS WASTE SITE MANAGEMENT
of the dose) can occur and below which no harm is expected; these
are called reference doses (Rim) or acceptable daily intakes (ADI).
Historically, risk assessments have been applied largely to
single substances, but the need for comprehensive evaluations of
complex exposure from operations such as manufacturing facili-
ties and waste sites has spurred the development of methods for
assessing risks from mixtures. The assessment of mixtures is usu-
ally complicated by data on constituents that vary enormously in
quality and magnitude.
In practice, assessing the risks of exposures to mixtures has
been approached in one of three ways: (1) relative potency, (2)
toxicity/carcinogenicity equivalency, and (3) comparative toxic-
ity. For carcinogens, unit cancer risk (UCR) values are derived
by considering the data generated from standard tests and ap-
plying standardized extrapolation techniques (U.S. EPA, 1985~.
The results permit consistent comparisons (i.e., relative potency)
between individual carcinogens to help in deciding on the allo-
cation of resources for controls. They are particularly useful in
providing convincing evidence for setting priorities to maximize
public health benefits through intervention. To deal with mix-
tures of carcinogens, EPA (1986) proposed guidelines by which
to amalgamate cancer risks. Prunarily, the guidelines call for the
use of an additivity model, and they make provisions for dealing
with synergism should data indicate its existence among groups of
carcinogens at waste sites.
Gold et al. (1984) reviewed the world literature on animal
testing of carcinogens and for each of 770 chemicals calculated the
dose necessary to cause cancer in half of a group of exposed ani-
mals. The potency of those carcinogens varied by approximately
eight orders of magnitude. Figure ~1 scales the animal carcinoma
yens from the most potent (2,3,7,8-tetrachIorodibenz~p-dioxin, or
TODD) to the least potent (FD&C Green No. 1~.
Because of the enormity of the expense in obtaining cancer
bioassay data, only a small fraction of the compounds in commerce
has been subjected to such experimental scrutiny. Consequently,
the toxicologic data base for numerous substances at waste sites
is grossly deficient for risk estimation purposes. To remedy that
deficiency, toxicity/carcinogenicity equivalence schemes have been
devised for substances that cause (or are presumed to cause) the
same type of toxic injury (e.g., cancer, liver damage, central ner-
vous system disability). The schemes are based largely on the
OCR for page 155
ESTIMATING HEALTH RISKS
a' 100ng
o
0 0
u' ~
> 0
0
_
_
.~ hi, 100,ug
._ ~
3 ~
-
o
Y
_
u' ~10 mg
-
In
o
-
c,
10,ug
1 me
In
o
~100 me
_
.. .~ a,
0
\_
0 ._
10 9
TODD
Actinomycin D
Aflatoxin B1
Bis-(chloromethyl) ether
Sterl~matocystin
DBCP
Diethylstilbestrol
Procarbazine HCI
EDB
2-AAF
Auramine-O
Aniline HCI
DOT
2,4,6-Trichlorophenol
Metronidazole
FD & C Red No.1
FD & C Green No. 1
FIGURE 9-1 Range of carcinogenic potency in male rats.
155
proposition that chemicals of like structure cause similar types of
injury but have different potencies. Such analytic judgments are
more commonly referred to as structure-activity relationships. An
example is an EPA scheme to compute the carcinogenic potency
(i.e., the toxicity equivalence factors) of 75 chlorinated dioxins and
135 chlorinated furans in the absence of cancer test data for most
of the congeners (Berlin and Barnes, 1986~. A similar scheme is
currently under development for the class of polynuclear aromatic
hydrocarbons (PAHs or PNAs). Such schemes afford the oppor-
tunity to achieve a collective estimate of cancer risks without
ignoring biologic reality about differences in potency.
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156
HAZARDOUS WASTE SITE M,4NAGEM:ENT
TABLE 9-1 Chronic Toxicity Scoring
ADIs for Non
Unit Cancer Risk carcinogens Chronic
(mg/kg/day)~1 (mg/kg/day) 1 Score
> 1o2 < 10 7 9
1o~7_lo~6 8
1o~6_lo~5 7
10-5-10-4 6
10 4-10 3 5
~ 10~2_1o~3 > 10 3-10 2 4
10 2_1o 1 3
< 10 4-10-5 10~1 1 2
1 1
aExposure at the acceptable daily intake (ADI) level is assumed
to be associated with a 10-5 risk of a toxic effect; ADIs for
carcinogens are doses associated with a 10-5 risk of cancer.
For noncancer toxicity the potencies of substances damaging
the same target organ are combined for the same degree of injury,
and a determination of the appropriate margin of safety is then
made for the group. The final step is to amalgamate the conclu-
sions about the risks from noncarcinogens with those for carcino-
gens. A procedure to convert ADIs and UC~ to a comparable
scale has been developed for this purpose. ADIs are calculated
to cause no risk, and UCRs assume that there is some risk at all
doses. To make a common scale, ADIs are "signed a finite risk
(lo-5 is suggested). As shown in Table 9-1, the AD] and UCR
of a substance can be compared to select a single chronic toxicity
score.
EXPOSURE CONS~ERATIONS
Hazardous substances can escape from waste sites as vapors
or fumes, dissolved in water, or attached to dust particles and
carried by wind and water. Vapors, fumes, and particulates can
be inhaled; some chemicals carried by dirt can be absorbed through
OCR for page 157
ESTIMATING HEALTH RISKS
157
the skin; particulates can be ingested; and contaminants can elute
into drinking water.
An additional route of exposure results from chemicals en-
tering the food chain. Examples of this exposure route include
incorporation into plants eaten directly by humans and those
consumed by food-producing animals such as fish. Fish are a
particularly serious concern because they bioconcentrate highly
lipid-soluble substances present in their aqueous environment.
Water in the vicinity of waste sites is another grave concern.
The United States has many ground water reservoirs that are
ideally situated to receive liquid wastes deposited in unlined cav-
ities. In the worst of situations, such wastes are actually buried
beneath the water table, where solubilization and distribution are
greatly enhanced. Once distributed in ground water, pollutants
often biodegrade extremely slowly, if at all, because of anaerobic
conditions; and they may remain in the aquifer for geologic time
because of the extreme difficulty of their removal. Such wastes are
also known to migrate to surface waters where they are subject to
the same natural forces as other industrial substances present in
streams.
Human exposure to water-borne wastes can occur by ingestion
(direct and during food preparation), inhalation (e.g., while show-
ering), and dermal contact (e.g., while bathing). For water that
is extracted directly for human use without benefit of treatment,
exposure is to the wastes themselves or their degradation prod-
ucts (e.g., viny! chloride is at times a product of trichIoroethylene
metabolism by soil microorganisms). Where water is drawn by
a community utility for treatment and distribution, exposure is
more difficult to determine or estimate because of competing in-
fluences. First, the filtration system is likely to remove, to varying
degrees of effectiveness, substances absorbed to particulate mat-
ter, thereby reducing exposure to waste substances. Second, the
oxidizing processes (e.g., chlorination for disinfection) will proba-
bly change the chemical character of the pollutants, in some cases
to more toxic halogenated products.
The assessment of human exposure to the diverse substances
likely to emanate from a hazardous waste site is a highly complex
and sometimes speculative enterprise. All too often the character-
ization of risks is more dependent on exposure assessment than on
knowledge of the type and quality of the hazard data.
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158
NAZARDOUSWASTESITEA4NAGEMENT
U1UST1lATIONS OF 1tISE ASSESSMENTS
AT HAZA1lDOUS WASTE SITES
ENVIRON has been involved in assessing risks and providing
information from those assessments to decisionmakers concerned
with many different types of waste sites. Five of those sites, de-
picting widely Mitering circumstances, are described briefly in the
paragraphs that follow. These illustrations indicate site complex-
ity as well as the diversity of bases for public health concern. At
some sites, for example, inhalation and dermal contact are the
most important routes of exposure; at others, fish and water are
much more significant.
Manufactured Gas Sites
Before the widespread availability of natural gas after World
War IT, public utilities manufactured "town gas" from coal or
of! by a process known as gasification. During their decades of
operations, gasification sites produced many PAHs, phenols, and
aliphatic compounds as by-products; several inorganic chemicals
from the coal or of] were also deposited in the soil around the
plants.
For its risk analysis, ENVIRON sifted through lists of all the
chemicals found at gasifies sites on the bases of toxicity, likelihood
of exposure, and regulatory status. Substances such as cyanide,
which is lethal at low concentrations, and carcinogens were ranked
high on the basis of toxicity. Substances that are present in high
concentrations and that axe likely to migrate from the site were
scored high on the basis of likelihood of exposure. The third fac-
tor reflected governmental concerns about hazardous substances
and the need for risk assessors to devote some attention to those
chemicals singled out for public concern. The sifting produced a
list of 30 chemicals. Thirty is a manageable number; the complete
list of chemicals was too large.
Along with the identification of the 30 substances, we made
a detailed examination of nine former gasifies sites. Information
was collected about the presence of ground and surface water,
about whether the site was paved or bare soil, and about nearby
activities. (A nearby school or residential area is of more concern
than a sparsely populated industrial area.) In addition, the types
of wastes were characterized as liquid (tar), buried wastes, and
surface wastes.
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ESTIMATING HEALTH RISKS
159
Models of air, water, and dust transport of the wastes were
used to make estimates of exposure. In general, inhalation and skin
absorption appeared to be the most important exposure routes
at the sites.: Combined with information about toxicity, those
exposure estimates were used to calculate various health risks
(Table 9-23.
As benchmarks, the levels of exposure to the 16 PAHs and 14
other chemicals from the sites will be compared to "background"
levels of exposure to the same chemicals from all other sources.
Because the 30 chemicals are ubiquitous, these comparisons will
provide information about how much additional risk may be asso-
ciated with the former gasifies plants. The intensity of remediation
efforts will probably depend, in part, on whether exposure from
the gasifies sites constitutes a large or small fraction of background
exposures.
The Hyde Park Landfill
Love Canal is probably the most notorious waste site in the
world. It is, in fact, only one of four large sites formerly used for
the disposal of industrial chemical wastes in the Niagara Falls, New
York, area. Another of the four, the Hyde Park landfill, contains
between 0.5 and 1.5 tons of TODD, more than at any other site
in the world. In addition, the Hyde Park landfill contains tons
of chlorinated organic compounds, pesticides, and pesticide by-
products.
The levels of possible exposures of nearby residents were es-
timated under two different circumstances: (1) improving con-
tainment and collecting and destroying leach ate from the site and
(2) excavation and removal of the contents of the landfill. Our
analysis showed that risks from vapors and dusts during an exca-
vation would far outweigh risks from improved containment. EPA
and New York State accepted the analysis and its conclusions and
selected containment as the better management choice.
Another significant route of exposure is through the migration
of leachate to surrounding waters and the bioconcentration of
chemicals in fish. In the case of the landfill, this route is made more
important because fish consumption around Niagara Falls is higher
than the national average and because the concentration of TODD
in fish is 5,000-fold the concentration of the chemical in water. Yet
little is known directly about the chemical's concentration near
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160
HAZARDOUS WASTE SITE ~NAGE~NT
TABLE 9-2 Cancer Potencies and Acceptable Daily Intakes
(ADIs) for Gasifier Wastes
Cancer Potency ADI
(mg/kg/day) 1 (mg/kg/day) 1
Chemical Inhalation Ingestion
Noncarcinogenic PAHe
Acenaphthene
Acenaphthylene
Anthracene
Fluoranthene
Fluorene
Naphthalene
Phenanthrene
Pyrene
Carcinogenic PAHs
Benzota) anthracene
Benzota~pyrene
Benzotb~fluoranthene
Benzo (k~fluoranthene
Benzo(E~)perylene
Chrysene
D ibenzo ~ a,h) anthracene
Indeno(1,2,3-cd~pyrene
6.10 11.5
0.10
0.02
0.0006
0.02
NAa
0.005
0.007
0.06
Volatile Inorganics
Benzene 0.026 0.0445
1,2-Cresol 0.11
1,4-Cresol 0.11
Ethylbensene 0.10
n-Hexane 0.29
Phenol 0.01
Toluene 0.42
Xylenes 1.00
Inorganics
Arsenic 50.0 15.0
Cadmium 7.8
Chromium 41.0 0.003b
Cyanide 0.15C
Lead 0.02
bNo suitable data available.
ADI for total inorganic Cr. adjusted to account for other routes of
exposure.
Adjusted to account for other routes of exposure.
NOTE: PAH = polynuclear aromatic hydrocarbon.
OCR for page 161
ESTIMATING HEALTH RISKS
161
the landfill. These uncertainties have led the company responsible
for the landfill, along with EPA and New York State, to fund a
study about the amount of dioxin in local fish. Table ~3 presents
illustrative risk estimates for several routes of exposure, including
fish consumption.
In summary, at this site, TODD was present in large amounts,
and consideration of its toxicity and the potential exposures to
it drove the risk assessment. Yet risks from other compounds
are also being considered, despite the predominance of concern
about dioxin; a monitoring program will analyze air and water
from the Hyde Park landfill to detect possible contamination from
other chemicals. This detection effort should be easier, given that
the other contaminants are more mobile and are present in larger
amounts.
Widespread Ground Water Contamination
This example involves a chemical company that manufactures
several hundred different products: dyes, epoxy resins, specialty
chemicals, plastics, and others. At various times in the past,
wastes were disposed onsite in a sludge disposal area, an unlined
landfill, in various lagoons and basins, and in the process areas of
the plant. A plume of volatile organic chemicals and base/neutral
extractable compounds that is about 380 acres in area is now
present in the ground water near the plant.
The flow of the plume was analyzed, and it was found that
it endangers no currently used drinking water wells. The plant
owner offered to seal irrigation wells that contained chern~cals in
excess of drinking water standards; now only a single well, which
is used for lawn irrigation, is active. Those findings and actions
eliminated most of the concerns about ingestion but not all of
them: some ground water seeps into recreational marshlands and
into a recreational river. In both those cases the expected chemical
contamination was analyzed, and it was determined that, although
contamination was widespread, it was at low levels. No chemical
on EPA's list of priority pollutants was present above the detection
litany. ENVIRON analyzed possible exposures through ingestion
of and skin contact with contaminated water and soil, as well as
through inhalation of volatile organic chemicals. The estimated
upper bound to risks for cancer following lifetime exposure in the
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162
HAZARDOUS WASTE SITE MANAGEMENT
TABLE 9-3 Examples of Riak Eatimates Derived for Select Exposure Scenarioe
Related to the Hyde Park Landfill
Fish Ingestion Fish Ingestion Inhalation (High)
Carcinogen Noncarcinogen Carcinogen
Compound (mg/kg) (mg/kg) (mg/m~)
RISK* MDD/ADI RISK*
1. Acenaphthene NA NA NA
2. Acenaphthylene NA NA NA
3. Aldrin NA NA NA
4. Anisole (methyl phenyl ether) NA 3.17E-07 NA
5. Anthracene NA NA NA
6. benzo(a)-Anthracene NA NA NA
7. dibenzo(~,~)-Anthracene NA NA NA
8. Arsenic NA NA 1.17E-18
9. Benzene 7.34E-13 NA 9.81E-10
10. Benzidine 9.36E-11 NA 1.55E-06
11. Benzochlorodifluoride NA NA NA
12. 2,3-Benzofuran NA NA NA
13. Benzoic acid NA 1.12E-07 NA
14. Bromobenzene NA NA NA
15. Bromodichloromethane NA NA NA
16. p-Bromofluorobenzene NA NA NA
17. Bromoform NA NA NA
18. Bromomethane NA NA NA
19. 4-Bromophenyl phenyl ether NA NA NA
20. n-Butylbenzene NA NA NA
21. sec-Butylbenzene NA NA NA
22. tert-Butylbenzene NA NA NA
23. Butyl benzoate NA 1 34E-07 NA
24. Butyl benzyl phthalate NA NA NA
25. di-n-butyl phthalate NA 7.59E-O9 NA
26. Carbon tetrachloride 5.46E-14 NA 4.21E-11
27. Chlorendic acid 3.44E-09 3.19E-04 2.72E-17
28. Chlorobenzene NA 1.06E-06 NA
29. m-Chlorobenzoic acid NA 3.42E-07 NA
30. o-Chlorobenzoic acid NA NA NA
31. p-Chlorobenzoic acid NA NA NA
32. m-Chlorobensotrifluoride NA NA NA
33. o-Chlorobenzotrifluoride NA NA NA
34. p-Chlorobensotrifluoride NA 2.07E-07 NA
35. 1-Chlorocyclohexene NA NA NA
36. Chloroethane NA 1.17E-11 NA
37. bis(2-Chloroethoxy) methane NA NA NA
38. bis(2-Chloroethyl) ether NA NA NA
39. 2-Chloroethylvinyl ether NA NA NA
40. Chlaroform 1.13E-12 NA 3.25E-O9
41. Chloromethane NA 1.16E-11 NA
42. 4-Chloro-3-methyl phenol NA NA NA
43. 2-Chloronaphthalene NA NA NA
44. 2-Chlorophenol NA 2.91E-08 NA
45. m-Chlorotoluene NA 2.90E-10 NA
46. o-Chlorotoluene NA 7.71E-08 NA
47. p-Chlorotoluene NA 3.97E-08 NA
48. o/P-Chlorotoluene NA NA NA
49. Chryeene NA NA NA
50. Cumene NA NA NA
51. Cyclopropylbenzene NA NA NA
52. p-Cymene NA NA NA
53. p p-DDD NA NA NA
54. ~-DDE NA NA NA
55. oo-DDT NA NA NA
56. Dibromochloromethane NA NA NA
57. m-Dichlorobensene NA 1.66E-08 NA
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166
HAZARDOUS WASTE SITE MANAGEMENT
TABLE 9-3 Continued
Fish Ingestion Fish Ingestion Inhalation (High)
Carcinogen Noncarcinogen Carcinogen
Compound (mg/kg) (mg/kg) (mg/m 3 )
RISK* MDD/ADI RISK*
114. Octachlorocyclopentene NA NA NA
115. PCB, 1016/1242 NA NA NA
116. PCB, 1221 NA NA NA
117. PCB (Aroclor 1248) 6.34E-09 1.60E-04 1.52E-09
118. PCB, 1254 NA NA NA
119. PCB, 1260 NA NA NA
120. Pentachlorobenzene NA 4.51E-08 NA
121. Pentachloroethane S.28E-15 NA 8.50E-13
122. Pentachlorophenol NA NA NA
123. benzo(g~)-Perylene NA NA NA
124. Phenathrene NA NA NA
125. Phenol NA 2.62E-07 NA
126. Phenyl benzoate NA 6.37E-09 NA
127. n-Propylbenzene NA NA NA
128. Pyrene NA NA NA
129. benzo(a)-Pyrene NA NA NA
130. ideno(1,2,3-~)-Pyrene NA NA NA
131. Styrene NA NA NA
132. 2,3,7,8-TCDD 3.42E-08 7.20E-03 1.91E-09
133. 1,2,3,4-Tetrachlorobenzene NA 7.71E-07 NA
134. 1,2,4,5-Tetrachlorobenzene NA 6.09E-06 NA
135. 1,1,2,2-Tetrachloroethane S.05E-14 NA 6.48E-11
136. Tetrachloroethylene 2.64E-12 NA 1.04E-09
137. Tetrachlorotoluenes NA NA NA
138. Toluene NA 9.SOE-09 NA
139. 1,2,3-Trichlorobenzene NA 4.26E-08 NA
140. 1,2,4-Trichlorobenzene NA 1.90E-06 NA
141. 1,3,5-Trichlorobenzene NA 2.36E-09 NA
142. 1,1,1-Trichloroethane NA 1.97E-10 NA
143. 1,1,2-Trichloroethane 6.13E-15 NA 1.86E-11
144. Trichloroethylene 6.64E-13 NA 6.76E-10
145. Trichlorofluoromethane NA 2.93E-11 NA
146. 2,4,5-Trichlorophenol NA 3.46E-07 NA
147. 2,4,6-Trichlorophenol 5.79E-14 NA 2.06E-12
148. Trichlorotoluenes NA 2.99E-08 NA
149. 1,2,4-Trimethylbenzene NA NA NA
150. 1,3,5-Trimethylbenzene NA NA NA
151. Vinyl chloride NA NA NA
152. m-Xylene NA 2.97E-07 NA
153. o-Xylene NA 1.43E-06 NA
154. E-Xylene NA 9.62E-07 NA
*Upper bound lifetime cancer risk.
NOTE: ADI = acceptable daily intake, MDD = maximum daily dose, and
NA = not applicable.
OCR for page 167
ESTIMATING HEALTH RISKS
167
Inhalation (Lower) Inhalation (Lower) Der:T~a1 (Water) De,,.,al (Water)
Carcinogen Noncarcinogen Carcinogen Noncarc~nogen
(mg/m3 ) (mg/m 3 ) (mg/kg) tmg/kg)
Inhalation (High)
Noncarcinogen
(mGlm 3 )
MDD/ADI RISK*MDD/ADI RISK* MDD/ADI
114. NA NA NA NA NA
115. NA NA NA NA NA
116 NA NA ~ NA NA NA
117 3.41E-06 1.73E-11 1.34E-07 4.04E-11 1.89E-06
118. NA NA NA NA NA
120 8.35E-O9 NNAA 3.29E-10 NNAA 9.35E-11
121. NA 9.64E-15 NA 4.56E-16 NA
122. NA NA NA NA NA
123. NA NA NA NA NA
124. NA NA NA NA NA
125 1.47E-05 NA 5.78E-07 NA 4.51E-06
126 1.19E-07 NA 4.71E-10 NA 1.34E-O9
128 NA NNAA NNAA NA NA
129. NA NA NA NA NA
130. NA NA NA NA NA
131. NA NA NA NA NA
132. 3.58E-05 2.17E-11 1.41E-06 2.37E-10 9.26E-05
133. 1.42E-07 NA 5.58E-O9 NA 1.54E-O9
134. 1.42E-06 NA 5.58E-08 NA 1.54E-08
135. NA 7.35E-13 NA 3.55E-14 NA
136. NA 1.18E-11 NA 5.58E-13 NA
137. NA NA NA NA NA
138. 9.15E-07 NA 3.61E-08 NA 1.02E-08
139. 3.56E-08 NA 1.40E-O9 NA 3.86E-10
140. 1.83E-06 NA 7.23E-08 NA 2.05E-08
141. 1.21E-O9 NA 4.76E-11 NA 1.35E-11
142. 3.31E-08 NA 1.30E-O9 NA 3.78E-10
143. NA 2.11E-13 NA 1.02E-14 NA
144. NA 7.69E-12 NA 3.63E-13 NA
145. 2.76E-O9 NA 1.09E-10 NA 3.15E-11
146. 1.84E-07 NA 7.23E-O9 NA 3.13E-O9
147. NA 2.34E-14 NA 3.36E-15 NA
148. 1.50E-08 NA 5.89E-10 NA 1.29E-10
149. NA NA NA NA NA
150. NA NA NA NA NA
151. NA NA NA 3.11E-15 NA
152. 1.91E-05 NA 7.54E-07 NA 2.13E-07
153. 3.51E-05 NA 1.38E-06 NA 3.91E-07
154. 2.18E-05 NA 8.60E-07 NA 2.44E-07
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168
HAZARDOUS WASTE SITE MANAGEMENT
marsh or river ranges from 10-7 to 10-~2, which is less than that
generally found to be significant by public health officials.
Single-Compound Disposal
For more than 15 years, a facility manufacturing metal compo-
nents depended on one solvent, trichIoroethylene (TCE), to carry
out its fabrication process. A few other chemicals were used but
in much smaller quantities. Whereas the disposal of all chemi-
cals presumably was carefully controlled, the company was unable
to account for all of the TCE (in contrast to near complete ac-
countability for other substances); however, the missing TCE was
explained as resulting from the chemical's high volatility and its
consequent loss to the atmosphere.
Although large losses to the atmosphere certainly had oc-
curred, it became clear that the underground holding tank for the
solvent had also ruptured and leaked considerable quantities of
TCE into the ground. Furthermore, records indicated that on sev-
eral occasions drums of the solvent had been ruptured accidentally
by the improper use of forklifts, also discharging large volumes of
the solvent to the ground. By this time, a plume of the solvent
had begun to migrate offsite in the direction of a city's potable
water well field, more than 2 miles away.
A risk assessment was performed to determine the nature and
magnitude of the possible health threat to the local community.
In the meantime, the use of all privately operated wells for human
consumption wan halted, and replacement water was provided from
another source known not to contain TCE. The risk assessment
conclucled that if the plume were allowed to migrate unchanged,
the unwanted substance would contaminate the water supply of
the entire community of some 80,000 residents in 2 to 5 years. The
anticipated risk was conservatively estimated to be on the order of
1 per 100,000, a value in excess of EPA's guideline for concern of
1 per 1,000,000. On this basis, corporate management decided to
excavate the contaminated soil that was feeding the plume and to
construct monitoring wells to determine if the contamination was
being abated. In addition, a community information program, in
which the state health agency was a participant, was instituted to
ensure the dissemination of all relevant information to potentially
affected residents.
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ESTIMATING HEALTH RISKS
169
Future Risk to a Major Aquifer
In the southeast United States, local officials learned acciden-
tally of an illicit ("midnight" ~ waste dumping activity immediately
adjacent to a well field that supplied more than half of the potable
water to a population in excess of 600,000. Indirect evidence sug-
gested that some of the wastes were in liquid form, that the volume
was probably quite large (hundreds, perhaps thousands, of tons),
and that the wastes were buried over several acres. Limited sam-
pling of the site revealed the presence of large numbers of metal
drums and a handful of toxic compounds, all present below the
water table. Most important, a hydrogeologic investigation re-
veaTed that the ground was porous (no clay lens was present to
act as a barrier against migration); that the materials had been
deposited in a sinkhole that acted as a funnel into the underground
aquifer; that the rock formation underlying one part of the area
was greatly fractured, providing direct pathways to the well field;
and that the direction of the flow of ground water was from the
waste site to the well field.
On the strength of such evidence the authorities obtained
judicial authorization to excavate the site before the well water,
whose quality up to that time had been exceptionally high, became
irreparably damaged. During the excavation, additional, albeit
limited, sampling indicated that the volume of wastes was indeed
large and that the number of compounds necessarily of commercial
origin was greater than 100.
After the excavation the water authority sued the owners of
the waste site to recover remedial costs. The court required the
authority to demonstrate, postremediation, that there had been
sufficient danger to the well field and to the health of those served
by it to warrant reimbursement for its remedial initiative.
A risk assessment was undertaken to estimate the danger the
waste site had posed and might have posed in the future, had the
source of chemicals not been removed. In addition to data about
the landfill contents the results of water analyses from monitoring
wells demonstrated that the more mobile pollutants were intruding
into the well field.
The risk assessment focused on 100 compounds (Table 9-4~;
examined their chronic toxicity (including the ability to cause can-
cer) particularly in relation to the older members of a population
(because the community was composed largely of senior citizens);
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170
HAZARDOUS WASTE SITE MANAGEMENT
TABLE 9-d Future Rial: to a Major Aquifer
Chemical UCR (mg/kg/day) 1 ADI (mg/kg/day)
1.1 x 101
Acenaphthene
Acenaphthylene
Acetone
Anthracene
Areenic
Bensene
Benzidine
Benzo~ajanthracene
B enso (k ~ fluoranthene
Benzo(0perylene
Beryllium
B romodichloromethane
Bromophenyl phenyl ether, d
Butyl benzyl phthalate
Cadmium
Carbon tetrachloride
Chlordane
Chlorobensene
Chloroethane
B is (2 -chloroethoxy) methane
Bis(2-chloroethyl~ether 1.1 -2
Chloroform 8.1 x 10
Bis(2-chloroisopropyl~ether
Chloro-~-methyl phenol, d
Chlorophenol, 2
Chloro-m-cresol, ]2
Chromium
Cyanide
DDD
DDE
DDT
Diazinon
D ibromochloromethane
Dichlorobensene, 1,2
Dichlorobensene, 1,3
Dichlorobensene, 1,`
Dichlorobensidine, 8,3
Dichloroethane, 1,1
Dichloroethane, 1,2
Dichloroethylene, 1,1
Dichloroethylene, c~-1,2
Dichloroethylene, trane-1,2
Dichloromethane
Dichlorophenol, 2,4
Dichloropropane, 1,2
Dichloropropylene, c~e and
bane-1 S
~ ,
Diethyl phthalate
Dimethyl phthalate
Dir~ethylphenol, 2,4
10 Dinitrophenol, 2,4
1.5 x 1012
2.9 x 1O2
2.S x 10
1.1 x 10
1.1 x 10
6.1 x 10
1.6
S.d x 10 1
1.7
9.1 x 10 2
1.2
1.d x 10 2
6.1 xlO 2
S.7x 10
2.9
7.0 xlO 4
l.3xlO
s.0 x 10
B.0 x 10
2.d x 10 `,
7.0 x 10_E;
5.0 x 10
S.0 x 10 2
6.d x 10
1.0 x 10
1.0 x 10
B.3xlO
d.d x 10
6.S x 10
1.0 2
2.0 x 10
5.0 xlO
2.0xlO ~
9.0 x 10 2
6.9 x 10
-1
1.1 x 10
1.2 xlO 1
1.0 x 10_2
l.l x lO_2
l.l x lO_2
6.0 x 10
3.OxlO
1.0 x 10
1.0 x 10
l.lx
2.0 x 10
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ESTIMATING HEALTH RISKS
TABLE 9-d Continued
Chemical UCR (mg/kg/day) 1 ADI (mg/kg/day)
S.lxlO 1
Dinitrotoluene, 2,4
Di-n-butyl phthalate
Di-n-octyl phthalate
Ethyl bensene
Bist2-ethylhexyl~phthalate 8.5 x 10 3
Fluoranthene
Fluorene
Heptachlor epoxide
Hexachlorobensene
Hexachlorobut adiene
Hexachlorocyclohexane
Hexachlorocyclohexane, ,B
Hexachlorocyclohexane, ~
Hexachloroethane
Hydrogen sulfide
Isophorone
Kelthane (Dicofol)
Lead
Malathion
Mercury
Methyl chloride
Methyl-4,5-Dinitrophenol, 2
Methyl-d,6-Dinitrophenol, 2
Methyl ethyl ketone
Methyl isobutyl ketone
Naphthalene
Nickel
Nitrobensene
Nitrophenol, 2
Nitrophenol, 4
Nitrosodimethylamine, N- 2.ff x 10
Nitrosodi-n-propylamine, N
Parathion
Pentachlorophenol
Phenanthrene
Phenol
Pyrene
Selenium
Sil`,er
Tet rachloroethylene
Tetrahydrofurane
Toluene
Trichlorobensene, 1,2,4
Trichloroethane, 1,1,1
Trichloroethane, 1,1,2
Trichloroethylene
Trichlorofluoromethane
Trichlorophenol, 2,4,ff
Trimethylbensene (mixed isomer)
Xylenes
1 7 -2
7.8 x 10
1.S
1.S 2
1.d x 10
1.2
5.1x10 2
5.7 x 10 2
2.0x10 2
1.S
1.0 1
1.3x10 1
i.0 x 10 2
2.0 x 10
S.0xl0 5
2.0x10 5
S.OxlO
3.5 x 10 2
2.0 x 10
2.0 x 10
2.0x10 2
2.0x10
1.0
S.0 x 10 2
l.O x lO_
1.S x 10
1.S x 10
S.OxlO ~
S.0%10 2
S.OxlO
1.0 x 10
l.OxlO 1
1.0x10 1
S.0 x 10
2.0 x 10
S.0 x 10_2
2.0x10 2
2.9 x 10
2.0x10 1
S.OxlO 1
2.S
NOTE: ADI = acceptable daily intake, UCR = unit cancer risk.
171
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172
HAZARDOUS WASTE SITE MANAGEMENT
and evaluated their potency in relation to what would likely be
safe levels of exposure. The compounds were scrutinized for their
ability to move offsite and contaminate water in the municipal
well field and for the degree of difficulty in removing them from
potable water.
The data base was adequate to perform all steps of the eval-
uation save one: it was not possible to estimate the maximum
concentrations of contaminants in the well field. Despite that lim-
itation, it was successfully argued that the future hazards would
probably be sufficient to cause imminent danger to public health
(by exceeding consistently the likely public health standards). The
authorities met their burden of proof and received a favorable judg-
ment to obtain full reimbursement for the costs of remediation.
DIS CUSSION
Data Problems
Quantitative conclusions about the health risks associated
with a site often appear precise and accurate. That appearance
is not always correct, however. Estimates often do not explicitly
represent the large variations in the quality of the underlying data.
Some of the more glaring problems glossed over in numerical esti-
mates include (1) extrapolation from brief durations of exposure
to much longer exposure periods, even a lifetime; (2) reliance on
studies of limited pathological observations and of narrow designs;
and (3) sometimes, recourse to unverified information. Ordinarily,
compensation can be made for poor-quality studies and major de-
viations between test data and environmental conditions through
the judicious (and at times arbitrary) application of "safety" fac-
tors (perhaps as small as 10 or at times as great as 100,000) to
define lower levels of acceptable exposure. Some degree of comfort
may be generated by such practices, and major public injuries are
not known to have occurred as a result of them. Nevertheless,
the extent of safety inherent in the procedures remains indefinable
without the undertaking of targeted research.
Additional Uncertainties
Other components of the analysis necessarily incorporate un-
certainties for which control ~ often beyond the grasp of con-
ventional and ethical research and testing. Some of the major
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ESTIMATING HEALTH RISKS
173
unknowns include the need to apply information from labora-
tory animals to humans. Although both test and target species
are mammals, they differ in substantive ways that may produce
errors in either direction-in the application of toxicity data to
humans. Even if one species is capable of closely reproducing
a pathological lesion caused by a chemical in another species,
the injury may appear at a totally different organ in the second
species. That phenomenon, particularly prevalent in carcinogen-
esis, may be related to differences either in metabolic pathways
or in the distribution of binding sites. Quantitative differences in
toxic potency also occur among species, which are related largely
to quantitative differences in kinetics of absorption, distribution,
biotransformation, and excretion of toxicants and to differences in
the rate of repair of molecular and cellular lesions.
Many of these issues considered to be of concern for single
substances are thought to be of even greater concern for complex
mixtures. Activation and detoxication rates might be altered in
the presence of other substances at toxic doses; reserve capacities
or organs might be depleted significantly by toxic doses; and,
finally, repair rates in pathologically affected organs might be
changed as the result ot multiple Insults.
~71 1 ~1 ~ ~ ~. ~-
. .
wnen sucn underlying DlOlOglC understanding exists, it serves
as the basis for considering differences between the dose-response
characteristics of test animals and humans. In turn, that basis
provides the foundation for solidly based environmental standards
of exposures to the waste products.
CONCLUSIONS AND CATIONS
Quantitative risk assessment is the only method currently
available to estimate risks from waste sites. Both the underlying
data about toxicity and methods for extrapolation have greater
or lesser amounts of uncertainty. On a more positive note the de-
mands of risk assessment are forcing the development of standard-
ized data bases for health effects; they are also contributing to the
development of extrapolation methods. Nevertheless, uncertain-
ties must always be considered and conveyed to the decisionmaker
so that the strengths and limitations of the risk estimates are am
propriately considered in selecting risk management approaches.
The most pressing need is for more biologic information to
guide extrapolation methods. In part, that information will come
OCR for page 174
174
HAZARDOUS WASTE SITE MANAGEMENT
from standard toxicologic tests of substances present in waste
sites, but more fundamental research is probably the real key
to improvement. Research on biologic mechanisms, shared and
unshared between test animals and humans, needs considerable
emphasis.
Along with such data and information will come increasing
opportunities for interactions among biologists, statisticians, risk
assessors, and decisionmakers. The fostering of those interactions
is important to the proper use of vital information and to direct
research in obtaining that information.
:RE}?E1lENCES
Bellin, J. S., and D. G. Barnes. 1986. Interim procedures for estimating risks
associated with exposures to mixtures of chlorinated dibenzo-p-dioxins
and -dibenzofurans (CDDs and CDFs). U.S. Environmental Protection
Agency, Washington, D.C.
ENVIRON Corporation. 1986. Elements of Toxicology and Chemical Risk
Assessment. Washington, D.C.
Gold, L. S., C. B. Sawyer, R. Magaw, and nine others. 1984. A carcinogenic
potency database of the standardization results of animal bioassays.
Environmental Health Perspectives 58:9-31.
National Research Council. 1983. Risk Assessment in the Federal Govern-
ment. Washington, D.C.: National Academy Press.
U.S. EPA. 1986. Guidelines for the health risk assessment of chemical
mixtures. Federal Register 51:34014-34025. September 24.
U.S. EPA, Carcinogen Assessment Group. 1985. Relative Carcinogenic Po-
tencies Among 55 Chemicals Evaluated by the Carcinogen Assessment
Group as Suspect Human Carcinogens. From Mutagenicity and Carcino-
geneity Assessment of 1,3-Butadiene. EPA 600/8-85-004F. Washington,
D.C. August.
PROVOCATEUR'S COMMENTS
William Cibulas
~ found Dr. Tardiff's paper very interesting in that it touched
upon several important issues that all of us involved in quantita-
tive risk assessment of hazardous waste sites are concerned with.
However, like many papers written in this field, it leaves us with
many unanswered questions concerning the future of quantitative
risk assessment. ~ hope this is not an overstatement, but in my
opinion, the tone of the paper appears to be very pro quantitative
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ESTIAf4TING HEALTH RISKS
175
risk assessment and numbers oriented. Scientists must be very
careful and understand the limitations of risk assessment when
making public health decisions.
One of the major questions that we at the Agency for Toxic
Substances and Disease Registry (ATSDR) are continually faced
with deals with the issue of inhalation exposures from volatile
organic compounds in contaminated ground water. Often, this
issue arises after an affected household has already been placed on
an alternative water supply for consumption. The question then
is, can my baby bathe in this water? Is it still okay to shower
with this water? Based on some recent work by Julian Andelman
at the University of Pittsburgh and some of our own estimates
of risk, ATSDR often concludes that if water is unacceptable for
drinking for any length of time, it may be unacceptable for all other
indoor uses for this same period, including showering, bathing,
and washing clothes and dishes. ~ have questions concerning the
relative risk assumed from drinking 2 liters of water contaminated
with volatile organic compounds compared to the risks that one
assumes from exposure to all other indoor uses of this water.
My second question deals with those compounds that act by
secondary mechanisms. Dr. Tardiff touched on this subject when
he discussed TODD and current scientific thought that it is acting
as a promoter and not a direct-acting carcinogen. As you know,
there is currently no practical method to derive any distinction of
carcinogens based on any principles of carcinogenic action. All car-
cinogens, whether they are proven human carcinogens or suspected
animal carcinogens, are treated the same way. My question would
be, after hearing Dr. Tardiff's comment, are compounds that are
proving to be promoters and not direct-acting carcinogens better
treated as threshold compounds? ~ do not think we have done this
yet.
The third issue deals with high-dose/Iow-dose effects. As
many of you are aware, there is growing concern over the selection
of the maximum tolerated dose, or the MTD, for use in the chronic
bioassay. For those of you who will be attending the Society of
Toxicology meeting next week, there will be a whole symposium
devoted to the use of the MTD in the chronic bioassay. Although
there are only 20 to 30 known or proven carcinogens, approxi-
mately one-half of the chemicals tested in chronic bioassays have
been shown to produce some excess of tumors in at least one of the
animal species tested. Frequently, the only statistically significant
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HAZARDOUS WASTE SITE MANAGEMENT
increase in tumors is in those animals that were treated at the
MID, or at a concentration at which we might expect some toxi-
city in those animals. Thus, this discussion becomes particularly
relevant as we are now beginning to find that certain essential ele-
ments, such as estrogens, selenium, and tocopherols, are proving to
be carcinogens at high doses. ~ wonder about the use of the MTD
in the chronic bioassay and what appears to be a growing trend of
treating high-dose carcinogens as noncarcinogens, or compounds
that have thresholds, when we are looking at them in low-level
concentrations.
The final question deals with one of the specific critiques, the
Hyde Park landfill, for which you quantify both the carcinogenic
and noncarcinogenic risks from dermal exposure to contaminated
water. My guess is you would reference Dr. Brown's paper on der-
mal exposures from VO~contaminated water in the quantitation
step. ~ was wondering if there are any recent studies that deal
with a dermal exposure that perhaps would be more relevant at
low-level concentrations.
Representative terms from entire chapter:
waste site
