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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

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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

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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

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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.

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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.

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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

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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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176 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.