section 6 toxicity assessment

SECTION 6TOXICITY ASSESSMENT

6.1 OBJECTIVES AND GENERAL APPROACH

The purpose of the toxicity assessment is to identify the toxicity values that are used, inconjunction with the exposure doses calculated in the exposure assessment (Volume I,Section 5), to evaluate potential human carcinogenic risks and noncancer health effects inthe risk characterization (Volume I; Section 7). Chemicals that have evidence ofcarcinogenicity are referred to as carcinogens. Excessive exposure to all chemicals potentiallycan produce adverse noncancer health effects, while the potential for causing cancer islimited to carcinogens; therefore, noncancer toxicity values can be developed for allchemicals, while cancer toxicity values can. be developed only for carcinogens. Thenoncancer toxicity values are termed reference doses (RfDs), and the cancer toxicity valuesare termed cancer slope factors (CSFs). The derivation of these values is discussed in detailin Subsections 6.2.2 (Cancer Slope Factors) and 6.3.1 (Reference Doses).

Most published toxicity values are based on data from studies on laboratory animals.Although human toxicity data are preferred, only a limited number of chemicals have been

. studied in humans, and the data from most human studies (e.g., epidemiological studies) arecomplicated by confounding factors. For example, individuals may have been exposed toother potentially harmful chemicals in addition to the one in question. Because animalstudies are better controlled, they serve as the basis for most toxicity values. The toxicresponse of humans and test animals to the same chemical may differ, however. Thesepotential differences are taken into account when deriving toxicity values by usingapproaches that are highly conservative. These protective approaches are discussed inSubsections 6.2 and 6.3.

The toxicity values used in the risk assessment were obtained or developed in the followingorder of preference:

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• Obtained from EPA's Integrated Risk Information System (IRIS) database.

• Obtained from EPA's Health Effects Assessment Summary Tables (HEAST).

• Obtained from the EPA Region HI Risk-Based Concentration Table (valuesdeveloped by EPA's National Center for Environmental Assessment only).

• Derived using published EPA guidance.

• Derived using other approaches where EPA guidance was not available.

EPA databases and documents were the preferred source of toxicity values. Of the EPAsources, values entered into the Integrated Risk Information System (IRIS, 1996) werepreferentially used, because these values have undergone extensive EPA review, and havebeen verified by either EPA's Carcinogen Risk Assessment Verification Endeavor (CRAVE)Work Group or EPA's Reference Dose/Reference Concentration (RfD/RfC) Work Group.If a toxicity value was not present on IRIS, EPA's Health Effects Assessment Summary Tables(HEAST) (EPA, 1995a) was consulted for an appropriate value. The toxicity values listedin HEAST have undergone a less intensive review than those in IRIS. They are consideredby EPA to be provisional values, but are approved by EPA for use in conducting riskassessments for both Superfund and RCRA sites. Several toxicity values that were used inthe risk assessment were developed by EPA's National Center for EnvironmentalAssessment (NCEA). These values, which were obtained from the EPA Region III Risk-Based Concentration Table (EPA, 1996a), also are developed as provisional values, andhave undergone a lesser degree of scientific review.

The toxic response to a chemical may vary with the route of exposure (i.e., oral [ingestion],inhalation, or dermal [skin]). The specific tissues or organs that are affected by a chemical,and the nature and extent of damage to a given tissue or organ also may differ betweenexposure routes; therefore, where possible, different toxicity values are developed for eachchemical for each potential exposure route. To date, EPA has developed toxicity values forthe oral and inhalation routes only. Although dermal toxicity values have not been derivedby EPA, EPA provides guidance for deriving dermal values. The approach to derivingdermal values is presented in Subsections 6.2.4 and 6.3.3. Cancer slope factors for polycyclic J K

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aromatic hydrocarbons also were developed using EPA guidance. This approach is discussedin Subsection 6.2.6.

Several approaches were developed to derive additional provisional toxicity values in caseswhere EPA toxicity values or specific guidance for deriving values were not available. Oneapproach was the use of route-to-route extrapolation, the use of a toxicity value for oneexposure route to derive a toxicity value for another exposure route. This approach isdiscussed in Subsections 6.2.3 and 6.3.2. An approach also was developed to derive toxicityvalues to evaluate the potential health risks posed by the short-term inhalation exposuresthat could occur following process upset conditions. The chronic and subchronic toxicityvalues developed by EPA, or by using EPA guidance, are not appropriate for evaluating thehealth hazards posed by brief exposures to chemicals. The approach used to develop short-. term toxicity values is discussed in Subsection 6.4. Other approaches that were used toderive additional provisional toxicity values are discussed in Subsection 6.3.4.

The use and development of provisional toxicity values for chemicals that have not beenreviewed extensively by EPA results in a risk assessment that is more conservative than moscEPA risk assessments, which use toxicity values from IRIS and HEAST. The inclusion ofprovisional toxicity values allows more chemicals to be taken into account when evaluatingpotential carcinogenic risks and noncancer health effects.

If a toxicity value could not be obtained or derived for a chemical by the proceduresdescribed previously, the potential carcinogenic risks or noncancer health effects posed bythat chemical through the applicable exposure routes were not evaluated quantitatively.There were five carcinogenic chemicals for which neither an oral nor an inhalation cancerslope factor was available or could be derived, and three carcinogenic chemicals for whichonly one cancer slope factor was available or could be derived. There were 72 chemicals forwhich neither an oral nor an inhalation reference dose was available, and 4 chemicals forwhich only an oral or inhalation reference dose was available or could be derived. Theeffect of the lack of toxicity values for these chemicals on the evaluation of risk is addressedin Subsection 6.5.

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Subsections 6.2 and 6.3 discuss in detail the derivation of the cancer slope factors andreference dos'es used in the risk assessment. Subsection 6.4 discusses the derivation of theshort-term toxicity values that were used to evaluate potential process upset conditions.

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62 CARCINOGENIC EFFECTS

62.1 Weight-of-Evidence Categorization

The potential carcinogenicity of chemicals is evaluated by EPA's Carcinogen RiskAssessment Verification Endeavor (CRAVE) Work Group. CRAVE first determines theweight-of-evidence for a chemical to cause cancer, and then cancer slope factors aredeveloped if sufficient carcinogenicity data are available.

CRAVE assigns a weight-of-evidence classification to each evaluated chemical as follows:Group A (human carcinogen), Group B (probable human carcinogen), Group C (possiblehuman carcinogen), Group D (not classifiable), or Group E (no evidence of carcinogenicity).An explanation of the EPA carcinogenicity classification system is presented in Volume II,Appendix 6A, Table 6A-2. The chemicals that were evaluated for potential cancer risk inthis risk assessment include those that EPA has categorized in Group A, B, or C based ontheir evidence of carcinogenicity in animals and humans, and those that currently have nocarcinogenicity classification by EPA (i.e., the categorization is under review), but for whiclia cancer slope factor was available (i.e., beta-naphthylamine and the dioxin congeners otherthan 2,3,7,8-TCDD). Beta-naphthylamine has been classified .as a known human carcinogenby two other groups that evaluate the evidence of carcinogenicity for chemicals in theenvironment. Those organizations are the International Agency for Research on Cancer(IARC, 1987), and the National Toxicology Program (NTP, 1994). Available datademonstrate that beta-naphthylamine has caused bladder tumors hi dye-manufacturingworkers.

The chemicals that were considered as carcinogens and their EPA carcinogenicityclassifications are presented in Volume II, Appendix 6A, Table 6A-1.

622 Derivation of Cancer Slope Factors

The toxicity values used to evaluate cancer risk are termed cancer slope factors. Generally,the slope factor is a plausible upper-bound estimate of the probability of a response per unit

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intake of a chemical over a lifetime. As the cancer slope factor increases in value, the morepotent the chemical is as a carcinogen.

When developing cancer slope factors, it is assumed that the risk of cancer is related todose. The slope factors are usually developed from studies in laboratory animals andsometimes from human epidemiological studies, in which the subjects are exposed torelatively high doses of the chemical. The approach assumes that the results of studies usinghigh doses can be extrapolated to low dose exposures, with some risk of cancer remaininguntil the dose reaches zero. This is a no-threshold approach that assumes that even a smallnumber of molecules (possibly even a single molecule) of a carcinogen causes changes ina cell that could eventually lead to cancer. Figure 6.2-1 illustrates a hypothetical dose-response curve for a carcinogenic, no-threshold effect. EPA usually derives slope factors byusing a linearized, multistage model, and the slope factors reflect the 95,% upper-boundconfidence limit of the cancer potency of the chemical. The linearized multistage model isbelieved to be highly protective (i.e., it is likely to over-predict the true cancer potency ofa chemical).

The oral, inhalation, and dermal cancer slope factors used in this risk assessment areexpressed as an inverse dose, in units of milligrams per kilogram per day (mg/kg-day)"1.When EPA develops inhalation toxicity values to express carcinogenic potency through theinhalation exposure route, the values are usually developed as an inhalation unit risk factor.The unit risk factor is expressed as an inverse concentration in air in units of microgramsper cubic meter (jig/m3)"1. Because exposure through all exposure routes is calculated in thisrisk assessment as a dose in units of mg/kg-day, the inhalation unit risks were converted toslope factors, in accordance with EPA guidance (EPA, 1995a), using the following equation.The conversion assumes an adult body weight of 70 kilograms, and an inhalation rate of 20cubic meters of air per day (m3/day).

Cancer slop Factor = Inhalation Unit Risk (ug/m3)-1 x 70 kg x 1,000 ug/mg(mg/kg-day)-1 20 m3/day


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6.2.3 Route-to-Route Extrapolation

EPA has derived oral and/or inhalation cancer slope factors for many carcinogens. For fiveof the carcinogens, however, neither an oral nor an inhalation slope factor was available(see Subsection 6.2.7). For a number of carcinogens, only one slope factor (i.e., oral orinhalation) was available. In some cases where only one slope factor was available, theavailable slope factor was used as a provisional value to evaluate the other (oral orinhalation) exposure route. The use of the toxicity value developed for one exposure routeto evaluate toxicity from another exposure route is an example of route-to-routeextrapolation. The approach assumes that if a chemical acts as a carcinogen by one exposureroute, it is also carcinogenic by other exposure routes. EPA has used route-to-routeextrapolation to develop cancer slope factors for a number of chemicals. Route-to-routeextrapolation was used by EPA to develop inhalation cancer slope factors for- a number ofthe chemicals at the Drake Chemical site, including aldrin, bromoform, carbon tetrachloride,chlordane, chloroform, 1,2-dichloroethane, hexachlorobenzene, and 1,1,2-trichloroethane.

In deriving additional provisional slope factors for this risk assessment, route-to-routeextrapolation was used for chemicals that are known to cause tumors by a systemicmechanism (i.e., tumors at a site other than the site of administration) by either the oral orthe inhalation route, and for chemicals that have evidence of causing localized tumorsthrough both ingestion and inhalation (i.e., the carcinogenic polycyclic aromatichydrocarbons [PAHs]). There are many examples of chemicals that have been shown tocause tumors of a systemic nature by both the ingestion and inhalation routes, including anumber of the Drake Chemical site chemicals (e.g., acrylonitrile and carbon tetrachloride[Perera et al., 1989]). Some chemicals, such as several of the polycyclic aromatichydrocarbons (e.g., benzo(a)pyrene, dibenzo(a,h)anthracene), have been shown to causelocalized tumors in both the respiratory and gastrointestinal tracts (Perera et al., 1989). Theonly polycyclic aromatic hydrocarbon, however, for which EPA has developed a cancer slopefactor is benzo(a)pyrene, which has an oral slope factor.


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In deriving slope factors for this risk assessment, all of the route-to-route extrapolation wasfrom the oral to the inhalation route and was applied only to the organic compounds.Several of the inorganic chemicals (i.e., cadmium, chromium VI, and nickel) had only aninhalation slope factor; however, the evidence of carcinogenicity for these chemicals isprimarily for localized respiratory tract tumors in inhalation studies. Evidence forcarcinogenicity in oral studies is lacking for these chemicals (IRIS, 1996); therefore, route-to-route extrapolation was not applied to metals and metal compounds. Route-to-routeextrapolation was used to derive cancer slope factors for 20 chemicals.

In this risk assessment, no adjustments were made to the cancer slope factors when usingroute-to-route extrapolation (i.e., the same cancer slope factor was used for both routes).Although chemicals may cause cancer through more than one exposure route, the cancerpotency of the chemical may vary with the route of entry, being dependent on the relativerate of absorption, metabolism near the site of entry, and the potential target tissues. Thesefactors were not taken into account when deriving additional provisional slope factors forthis risk assessment, adding uncertainty to the derived provisional values.

62.4 Dermal Slope Factorsi

Although EPA "has developed oral and/or inhalation slope factors for a number ofcarcinogens, dermal slope factors have not been derived for any chemicals. EPA haspublished guidance, however, for calculating dermal slope factors for chemicals for whichan oral slope factor is available. In accordance with EPA guidance (EPA, 1989b), a dermalslope factor was derived for each applicable chemical by dividing its oral slope factor by anappropriate gastrointestinal absorption factor. This results in the conversion of the oral slopefactor, which represents the carcinogenic potency of the administered dose, to a dermalslope factor, which represents the carcinogenic potency of the absorbed dose. Theconversion is necessary to be able to calculate risk through the dermal pathway. The dermalslope factors must be consistent with the dermal doses, which are calculated in the exposureassessment as absorbed doses. The oral and inhalation doses, by contrast, are calculated asadministered doses, and are evaluated using cancer slope factors based on the administered


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dose. The following approach was used to estimate gastrointestinal absorption factors, and

was used in the derivation of both dermal cancer slope factors and dermal reference doses(see Subsection 6.3.3).

Ideally, each oral slope factor should be adjusted by a gastrointestinal absorption factor thatis derived from data from the critical study on which the oral slope factor was based.Because information regarding percent gastrointestinal absorption in the critical studies wasusually not available, assumptions were made regarding the gastrointestinal absorption ofeach chemical. The percent absorption assumed for each chemical was based on the methodby which the test animals or human subjects were dosed (i.e.> the route of administration)in the applicable oral study. The routes of administration used in the critical studies arepresented in Volume n, Appendix 6A, Table 6A-1. A gastrointestinal absorption factor of0.90 (90%) was assumed if the chemical was administered by gavage, inhalation, pill,capsule, or in the drinking water. A factor of 0.50 (50%) was assumed if the chemical wasadministered in the diet. Chemicals usually are administered to test animals in a readilybioavailable form. Absorption of chemicals that are dissolved in water or that areadministered in gavage vehicles (e.g., corn oil), by inhalation, or as a pill or capsule, usuallyis highly efficient; therefore, percent absorption through these vehicles was assumed to behigh (i.e., 90%). The absorption of chemicals that are administered in the diet, however,potentially may be hindered by the sorption of the chemicals to unabsorbed components ofthe feed; therefore, the percent absorption from feed was assumed to be moderate (i.e.,50%).

Information regarding the route of administration was not available for all oral toxicityvalues. A gastrointestinal absorption factor of 0.9 was assumed for the volatile organicchemicals lacking route of administration information. Because of their tendency tovaporize, volatile compounds usually are not administered in the diet, since accuratedeterminations of dose to the animal are not possible; therefore, it was assumed that thesechemicals were administered by one of the methods with a predicted higher absorptionefficiency. For all other chemicals lacking route of administration information, agastrointestinal absorption factor of 0.5 was assumed. The use of a lower absorption

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efficiency assumes that a smaller quantity of the chemical caused the observed toxic effects;the use of a lower absorption factor results in a more health-protective toxicity value (i.e.,higher cancer slope factor or lower reference dose).

Dermal slope factors were derived for 63 of the chemicals evaluated for the Drake Chemicalsite. The dermal slope factors are listed in Volume II, Appendix 6A, Table 6A-1.

62.5 Toxicity Equivalence Factors for Dioxin and Dioxm-Like Compounds

For the polychlorinated dibenzodioxins and dibenzofurans (i.e., dioxins), EPA has developedtoxicity equivalence factors (TEFs). The toxicity equivalence factors relate the carcinogenicpotency of the chemicals in these groups that are structurally and lexicologically related (i.e.,congeners), to the carcinogenic potency of a reference chemical for which a cancer slopefactor has been derived. The reference compound is 2,3,7,8-tetrachlorodibenzo-p-dioxin(2,3,7,8-TCDD).

In this risk assessment, the exposure doses for each dioxin congener of concern wereadjusted in the exposure assessment by a toxicity equivalence factor, thereby expressing thedoses as 2,3,7,8-TCDD toxic equivalents (TEQs). The conversion of the doses to 2,3,7,8-TCDD toxic equivalents was discussed in Volume I, Section 5, Subsection 5.6.3. Because thedoses for each dioxin congener are expressed as 2,3,7,8-TCDD equivalents, the cancer slopefactor for 2,3,7,8-TCDD was used to calculate the risk posed by each congener.

Chlorinated dibenzo-p-dioxins (CDDs) and chlorinated dibenzofurans (CDFs) constitute afamily of 210 structurally-related chemicals (EPA, 1989a, 1994b). The most widely studiedof these compounds is 2,3,7,8-TCDD (synonyms: TCDD or dioxin), which is considered themost toxic chemical of the family. TCDD is carcinogenic in rodents (e.g., rats, mice, andhamsters) and is classified as a B2 carcinogen in the EPA weight-of-evidence classificationsystem.


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Dioxins can have from one to eight chlorine substitutions. TCDD has four chlorines ("tetra")substituted on the parent molecule (i.e., the molecular structure common to the dioxins orfurans). Only a very small subset of dioxins with four to eight chlorine substitutions isconsidered to have TCDD-like toxicological activity. Four of the chlorine.substitutions mustbe in the 2,3,7,8 positions on the parent molecule. There are 17 congeners, including TCDD,that are considered to have TCDD-like toxicity. Monochlorinated, dichlorinated, andtrichlorinated dioxins do not exhibit any TCDD-like activity.

The fraction of TCDD-like activity shared by these compounds is expressed as a toxicityequivalence factor. The toxicity equivalence factor is the ratio of the activity of the specificcongener to that of TCDD in short-term animal toxicity assays. TCDD, being the mostpotent of the dioxins, has a toxicity equivalence factor of 1. All other dioxin-like compoundswith TCDD-like activity have toxicity equivalence factors that are a fraction of 1 (0.001 to0.5). For example, 1,2,3,7,8-PCDD (1,2,3,7,8-pentachlorodibenzo-p-dioxin) has a toxicityequivalence factor of 0.5 and, therefore, is considered one-half as toxic as TCDD whenidentical doses of the two compounds are administered. Of the several scientificorganizations that have developed toxicity equivalence factor systems, the EPA-recommended approach (EPA, 1989a) is used in this risk assessment, consistent withbaseline risk assessments conducted by the Superfund program. Table 6.2-1 lists the toxicityequivalence factors for 17 dioxins with TCDD-like activity according to EPA.

The relative toxicities of the dioxin and furan congeners of concern, expressed as toxicityequivalence factors, were determined from the ability of the dioxin-like compounds tostimulate the activity of a liver enzyme in animals called aryl hydrocarbon hydroxylase(AHH). Stimulation of the intracellular aryl hydrocarbon receptor (the Ah receptor) in theliver also is thought to correlate very highly with the biological activity of the dioxin-likecompounds and to be predictive of the ability of TCDD and dioxin-like compounds to causecancer. The biochemistry is complex and not completely understood, but it appears thatbinding of TCDD to the Ah receptor results in molecular biological changes that leadeventually to cancer. The evidence to date implies that binding to the Ah receptor is anecessary step for all biological effects of TCDD (EPA, 1994b).


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In this risk assessment, toxicity equivalence factors were multiplied by the predictedexposure concentrations of the 17 dioxin congeners to obtain the toxic equivalent dose (seeSubsection 5.6.3). Doses of toxic equivalents for each exposure pathway were summed toobtain an overall dioxin toxic equivalent dose. TCDD has a cancer slope factor of 1.5E+05(mg/kg-day)'1 for both the oral and inhalation routes (EPA, 1995a); therefore, this cancerslope factor was multiplied by the toxic equivalent doses for the oral and inhalationpathways to obtain total cancer risks for carcinogenic dioxins.

6.2.6 Relative Potency Factors for Polycyclic Aromatic Hydrocarbons (PAHs)

A number of polycyclic aromatic hydrocarbons (PAHs), including benzo(a)anthracene,benzo(a)pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, chrysene, dibenzo(a,h)-anthracene, and indeno(l,2,3-cd)pyrene, are considered by EPA to be carcinogenic. EPAhas derived an oral slope factor of 7.3 (mg/kg-day)"1 for benzo(a)pyrene (IRIS, 1996);however, the remaining six polycyclic aromatic hydrocarbons listed above have not beenassigned cancer slope factors because of the limitations of the cancer studies performed onthese chemicals. Currently, there is no inhalation unit risk factor for benzo(a)pyrene thatEPA has found acceptable (EPA, 1993a). Furthermore, there is no basis for judgment thatbenzo(a)pyrene or other polycyclic aromatic hydrocarbons will be equipotent by oral andinhalation routes (EPA, 1993a).

Until chemical-specific oral cancer slope factors are developed for each of the other sixcarcinogenic polycyclic aromatic hydrocarbons, EPA (1993a) recommends an interim relativepotency approach to evaluating oral carcinogenic potential. The approach, which is basedon the results of a group of carcinogenicity studies in animals, evaluates the carcinogenicpotential of each of the six carcinogenic polycyclic aromatic hydrocarbons relative to thecarcinogenic potential of benzo(a)pyrene. Benzo(a)pyrene has been assigned a relativepotency of 1.0, which is equivalent to an oral slope factor of 7.3 (mg/kg-day)"1 and the othercarcinogenic polycyclic aromatic hydrocarbons have been assigned relative potenciesbetween 0 and 1.0, as shown in Table 6.2-2. Because of the lack of sufficient data to quantify

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carcinogenicity by the inhalation route, a relative potency approach has not yet been

developed.

Each of the seven polycyclic aromatic hydrocarbons considered in this assessment isevaluated separately with regard to estimating stack emissions, modeling fate and transportin the environment, and quantifying human doses. The relative potency factors are appliedin the toxicity assessment to calculate provisional cancer slope factors for each of theevaluated carcinogenic polycyclic aromatic hydrocarbons. Provisional slope factors werederived for each of these chemicals by multiplying the cancer slope factor forbenzo(a)pyrene by the relative potency factor developed for the chemical.

62.7 Summary of Cancer Slope Factors

The oral, inhalation, and dermal cancer slope factors that were used to calculate potentialcancer risks are summarized in Volume II, Appendix 6A, Table 6A-1. The table alsopresents the source or basis of each slope factor.

Neither a verified nor a provisional oral or inhalation cancer slope factor was available for5 of the 71 carcinogenic chemicals (less than 1%). Of these five carcinogens, four (butylbenzyl phthalate, 2-methylphenol, 4-methylphenol, and methyl mercury), are categorized byEPA as Group C carcinogens (i.e., possible human carcinogen). EPA currently is notdeveloping cancer slope factors for Group C carcinogens. None of these four chemicals havebeen classified as to their carcinogenicity by either the International Agency for Researchon Cancer (IARC, 1987) or the National Toxicology Program (NTP, 1994).

The fifth carcinogen, lead, is classified by EPA in Group B2 (probable human carcinogen).EPA has recommended, however, that the carcinogenicity of lead not be quantitated for thepurpose of rislc assessment because of the uncertainty of its carcinogenic potency (IRIS,1996). EPA has stated further that lead does not appear to be a potent carcinogen and that,at low doses, "the noncancer effects of lead are of greatest concern for regulatory purposes"(EPA, 1988). The International Agency for Research on Cancer has classified inorganic lead

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as a Group 2B carcinogen (possible human carcinogen) (IARC, 1987); the National

Toxicology Program considers two lead compounds, lead acetate and lead phosphate, as"reasonably anticipated to be carcinogens" (NTP, 1994).

Three of the inorganic chemicals (cadmium, chromium VI, and nickel) have an inhalationcancer slope factor only. The inhalation slope factors for these chemicals are based onlocalized (i.e., respiratory tract) tumors. EPA has not evaluated these chemicals forcarcinogenicity through oral exposure; data supporting their potential carcinogenicitythrough ingestion are lacking or limited (IRIS, 1996).

In cases where a cancer slope factor was not available for a carcinogen, the potential cancerrisk posed by that carcinogen through the relevant exposure routes was not evaluated. Thepotential effect of the lack of cancer slope factors on the estimation of total cancer risk isaddressed in Subsection 6.5, Summary of Uncertainties.

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Table 62-1

Toxicity Equivalence Factors (TEFs) for Dioxins and Furans*

'EPA, 1989a, 1994a.

Compound TEF

Chlorodibenzo-p-dioxins (CDDs)2,3,7,8-TCDD1,2,3,7,8-PeCDD1,2,3,4,7,8-HxCDD1,2,3,6,7,8-HxCDD1,2,3,7,8,9-HxCDD1,2,3,4,6,7,8-HpCDD

OCDD

10.50.1

0.010.001

Chlorodibenzofurans (CDFs)2,3,7,8-TCDF

1,2,3,7,8-PeCDF2,3,4,7,8-PeCDF1,2,3,4,7,8-HxCDF1,2,3,6,7,8-HxCDF1,2,3,7,8,9-HxCDF2,3,4,6,7,8-HxCDF1,2,3,4,6,7,8-HpCDF1,2,3,4,7,8,9-HpCDFOCDF

0.10.050.50.1

0.01

0.001

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Table 62-2

Relative Potency Factors for CarcinogenicPolycyclic Aromatic Hydrocarbons (PAHs)

Drake Chemical SiteLock Haven, PA

PAH

Benzo(a)pyreneBenzo(a)anthraceneBenzo(b)fluorantheneBenzo(k)fluorantheneChryseneDibenzo(a,h)anthraceneIndeno( l,2,3-cd)pyrene

Relative Potency Factor*

1.00.10.10.010.0011.00.1

*EPA, 1993.

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FREQUENCY OF OCCURRENCE OF CANCER

(LOGARITHMIC SCALE)

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NOTE:

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VV -5 -4 -3 -2 -110 10 10 10 10

DOSE, ARBITRARY UNITS(LOGARITHMIC SCALE)

Drake Chemical Siteu _, Lock Haven, Pennsylvaniacy of occurence based on

tared dose range FIGURE 6.2-1cy of occurence based on HYPOTHETICAL DOSE-RESPONSE CURVE FORated dose range A NQ THRESHOLD CARCINOGENIC EFFECT

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6.3 NONCANCER HEALTH EFFECTS6.3.1 Derivation of Reference Doses (RfDs)

The toxicity values used in this risk assessment to estimate the potential for adversenoncancer health effects are termed reference doses. The term reference dose (RfD) refersto the daily intake of a chemical to which an individual can be exposed without anyexpectation of noncancer health effects (e.g., organ damage, biochemical alterations)occurring during a given exposure duration (EPA, 1989b). As the reference dose decreasesin value, the more toxic is the chemical in producing noncancer health effects.

Unlike the approach used in deriving cancer slope factors, it is assumed when derivingreference doses that a threshold dose exists below which there is no potential for toxicity(EPA, 1989b). Figure 6.3-1 illustrates the concept of a toxicity threshold as it applies to adose-response curve for a noncancer effect.

A reference dose is derived from either a no-observed-adverse-effect level (NOAEL) orlowest-observed-adverse-effect level (LOAEL) obtained from human or animal studies. ANOAEL is the highest dose of a chemical at which no toxic effects were observed in any ofthe test animals or subjects. The NOAEL is derived from the experimental study thatevaluates the "most sensitive toxic endpoint (critical effect) for the chemical. This endpointis significant when comparing the potential for noncancer health effects among differentchemicals with differing organ toxicities (see Volume I, Subsection 7.3). A LOAEL is thelowest dose at which a toxic effect was observed. A LOAEL is used to derive a referencedose in the absence of a suitable' NOAEL.

A reference dose is derived from a NOAEL or LOAEL by applying an uncertainty factorof 10 for each of the following: use of data from an animal study, use of a LOAEL ratherthan a NOAEL, and variation in human sensitivity. An uncertainty factor of 10 also isapplied if data from a subchronic study are used to derive a chronic reference dose (seefollowing discussion). A modifying factor of up to 10 also may be applied to account foradditional uncertainties in the database. The application of uncertainty and modifying

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factors results hi the derivation of reference doses that are likely to be highly protective (i.e.,they are likely to over-estimate the potential for noncancer health effects).

EPA has derived reference doses for two different exposure periods. Subchronic referencedoses have been developed to evaluate exposure periods in humans of from 2 weeks to 7years. Chronic reference doses have been developed to evaluate human exposures of greaterthan 7 years. In this risk assessment, chronic reference doses were used to evaluatenoncancer health effects for all oral exposure routes, and for the inhalation of volatileorganics through household water use because, exposure through the related pathways isassumed to occur over a period of 30 or 40 years. Subchronic reference doses were used toevaluate the inhalation of chemicals from the ambient air (i.e., direct inhalation of dispersedstack emissions) because exposure to chemicals through the inhalation of ambient air isassumed to occur only during the 60-day trial burn period. If a subchronic inhalationreference dose was not available for a particular chemical, but a chronic inhalationreference dose had been developed, the chronic inhalation reference dose was used. Chronicreference doses also were used to evaluate the child and infant scenarios (excluding theambient air inhalation pathway), although exposure periods of 6 years and 1 year wereassumed for the child and infant, respectively. The use of a chronic reference dose toevaluate subchronic exposure is an approach that tends to over-estimate the potential fornoncancer health effects. The chronic reference dose often is less (i.e., more health-protective) than, but never greater than, the subchronic reference dose, because anindividual generally can be exposed to higher chemical concentrations over a shorter periodof time with no evidence of adverse toxic effects.

Reference doses are expressed as a dose in units of milligrams per kilogram per day(mg/kg-day). When deriving noncancer toxicity values for the inhalation exposure route,EPA often expresses the value as a reference concentration (RfC) in units of milligrams percubic meter of air (mg/m3). Because exposure doses for all pathways, including theinhalation pathway, are calculated in units of milligrams per kilogram per day (mg/kg-day),the reference concentrations were converted to inhalation reference doses, in accordancewith EPA guidance (EPA, 1995a), using the following equation. The conversion assumes an

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adult body weight of 70 kilograms and an inhalation rate of 20 cubic meters of air per day(m3/day).

Reference1 Etose = Reference Concentration (mg/m3) x 20 m3/day(mg/kg-day) 70 kS

6.3.2 Route-to-Route Extrapolation

Route-to-route extrapolation also was used to develop reference doses for chemicals forwhich only one reference dose, either oral or inhalation, was available. Extrapolation wasapplied only if the toxicity endpoint (i.e., the most sensitive toxic effect on which thereference dose was based) was a systemic effect (i.e., it did not occur at the site ofadministration). This approach assumes that if a chemical causes systemic toxic effects byeither the inhalation or oral route, it will cause systemic toxic effects by both routes. Thetoxicity endpoints for the EPA-derived reference doses are presented in Volume II,Appendix 6A, Tables 6A-4 and 6A-5. If no information was available from EPA concerningthe toxicity endpoint of the reference dose (EPA, 1995a, 1996a, 1996b; IRIS, 1996), route-to-route extrapolation was not performed.

Only chronic toxicity values were used in the risk assessment to evaluate noncancer healtheffects resulting from oral exposures; therefore, in deriving oral reference doses throughroute-to-route extrapolation, extrapolation was from the chronic inhalation reference doseto the chronic oral reference dose only. When evaluating the noncancer .health effectsresulting from inhalation exposures, however, either a chronic or subchronic inhalationreference dose was used, depending on the exposure route. Chronic inhalation referencedoses were used to evaluate the inhalation of volatile organic compounds vaporized fromsurface water through household water use. Subchronic inhalation reference doses were usedpreferentially to evaluate the inhalation of ambient air because of the anticipated short, 60-day trial bum period.

In deriving a chronic inhalation reference dose through route-to-route extrapolation,extrapolation was from the chronic oral reference dose to the chronic inhalation reference

06/19/96MK01\RPT:11098213.003\d»kevl.s6 6.3-3 , ll:32am

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dose only. In deriving subchronic inhalation reference doses through route-to-routeextrapolation, either a subchronic or a chronic oral reference dose was used.

Although subchronic inhalation reference doses were the preferred values used in the riskassessment to evaluate the ambient air inhalation pathway, chronic inhalation referencedoses also were used, by default, when a subchronic reference dose was unavailable. Route-to-route extrapolation was used to derive a subchronic inhalation reference dose if neithera subchronic nor a chronic inhalation reference dose was available. When using route-to-route extrapolation to derive a subchronic inhalation reference dose, the subchronic oralreference dose was used preferentially; in the absence of a subchronic oral reference dose,the chronic oral reference dose was used.

In this risk assessment, no adjustments were made to the reference doses when using route-to-route extrapolation (i.e., the same reference dose was used for both routes). The one-to-one extrapolation adds uncertainty to the derived provisional values by not accounting forroute-specific differences in chemical absorption, metabolism, and potential target tissues.Route-to-route extrapolation was used to derive reference doses for 66 of the chemicals atthe Drake Chemical site.

6.3.3 Dermal Reference Doses

EPA has not derived dermal reference doses for any chemicals, but has provided guidancefor deriving these values for chemicals for which an oral reference dose is available. Inaccordance with EPA guidance (EPA, 1989b), dermal reference doses were derived bymultiplying each oral reference dose by an appropriate gastrointestinal absorption factor.The gastrointestinal absorption factor for each chemical was selected based on the route ofadministration used in the study on which the oral reference dose was based. The route ofadministration for each oral reference dose is presented hi Volume II, Appendix 6A, Table6A-4.

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&R309I38

The approach to selecting the gastrointestinal absorption factor was the same as theapproach used in the derivation of dermal cancer slope factors, and is explained inSubsection 6.2.4. The derived dermal reference doses estimate the toxicity of the absorbeddose. They are used in the risk characterization in conjunction with the calculated dermaldoses, which also are expressed as absorbed doses, to evaluate the potential for noncancerhealth effects through the dermal pathway.

Dermal reference doses were derived for 91 of the chemicals evaluated for the DrakeChemical site. The dermal reference doses are listed in Volume II, Appendix 6A, Table6A-4.

6.3.4 Other Derivation Approaches

Other approaches were used to develop reference doses for specific chemicals. Theseincluded the development of an updated oral reference dose for manganese, a provisionalinhalation reference dose for manganese, and a provisional oral reference dose for fenac.

EPA has recently updated its file on manganese, based on a re-evaluation of existingmanganese data. This file, which has been verified, is not yet available on IRIS. Because therevised file is scheduled to appear on IRIS within the next few months, it was used todevelop an updated oral reference dose for manganese (EPA, 1996b). Using the informationand guidance presented hi the revised file, an oral reference dose of 2.4E-02 mg/kg-day wasderived for manganese to evaluate exposures resulting from soil and drinking wateringestion. It was derived by subtracting the manganese content of the average United Statesdiet (i.e., 5 mg/day) from a critical dose of 10 mg/day. The difference, 5 mg/day, wasdivided by a modifying factor of 3 and a body weight of 70 kilograms. The critical dose isdefined as a NOAEL based on chronic human consumption of manganese in the diet.Manganese is an essential trace nutrient for animals and plants, which means that aminimum level is required in the diet to maintain proper functioning of the organism.Health effects resulting from manganese deficiency have been observed hi many mammalianspecies.

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A subchronic inhalation reference dose of 1.4E-04 mg/kg-day was derived for manganesefrom the chronic inhalation reference concentration (EPA, 1996b; IRIS, 1996). The chronicreference concentration for manganese is based on data from a subchronic study, andincludes an uncertainty factor of 10 to extrapolate from a subchronic to a chronic exposure(IRIS, 1996). The subchronic inhalation reference dose for manganese was derived bymultiplying the chronic reference concentration by a factor of 10 to extrapolate back to asubchronic exposure, and then converting the reference concentration to a reference doseas described in Subsection 6.3.1.

The provisional oral reference dose for fenac for this assessment was derived from an LD.,0(i.e., dose at which 50% of the test animals died) from an oral study in rats (EPA, 1996b).The LD50 was modified by an uncertainty factor of 10,000 to derive an oral reference doseof 7.0E-02 mg/kg-day.

6.3.5 Summary of Reference Doses

The oral, inhalation, and dermal reference doses that were used in the risk characterizationto evaluate the potential for adverse noncancer health effects are summarized in Volumen, Appendix 6A, Tables 6A-4 and 6A-5. The tables also present, for each reference dose,the toxicity endpoint of the critical study from which the reference dose was derived, thebasis of the value (i.e., chronic oral, subchronic oral, chronic inhalation, or subchronicinhalation reference dose), and a reference (i.e., source) for the value. For the oralreference doses, the route of administration that was used in the critical study also isindicated.

Neither a verified nor a provisional oral or inhalation reference dose was available for 72of the 163 chemicals evaluated for the Drake Chemical site (approximately 44%). Of these72 chemicals, 39 (over 50%), including the 17 dioxin congeners, are considered carcinogensand were evaluated for potential cancer risk. EPA generally does not derive reference dosesfor Group A and B carcinogens because, for most carcinogens, the potential risk of cancerusually outweighs the concern for potential adverse noncancer health effects. A possible

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exception is the dioxins. The potential for adverse noncancer health effects resulting fromexposure to dioxins is discussed in Subsection 6.3.6.

Three chemicals lacked an inhalation reference dose, and one chemical lacked an oralreference dose. None of these chemicals are classified as carcinogens and, therefore, werenot evaluated for cancer risk.

In cases where a reference dose was not available for a chemical, the potential fornoncancer health effects resulting from exposure to that chemical through the affectedexposure routes was not evaluated. The potential effect of the lack of reference doses onthe evaluation of risk is addressed in Subsection 6.5, Summary of Uncertainties.

6.3.6 Potential Noncancer Health Effects of Lead

Toxicity studies have not demonstrated a dose level for lead exposure below which no toxiceffects are observed. Thus, EPA considers the noncancer toxic effects of lead not to havea threshold level and has not established a reference dose (IRIS, 1996). In the absence ofa reference dose or cancer slope factor for lead (see Subsection 6.2.7), lead was evaluatedin this risk assessment by comparing predicted lead concentrations in air, soil, and surfacewater with federal regulatory guidelines for these media (see Subsection 7.3.7).

6.3.7 Potential Noncancer Health Effects of Dioxins

EPA has concluded that adequate evidence exists to suggest that exposure to 2,3,7,8-TCDDand related congeners results in a broad spectrum of noncancer effects in animals, some ofwhich may occur in humans (EPA, 1994, 1995c). The effects range from adaptive changesat or. near background levels of exposure to adverse effects that increase in severity asexposure levels increase above background levels. Enzyme induction, alterations in hormonelevels, and indicators of altered cellular function are examples of effects of currentlyunknown significance that may or may not be early indicators of a toxic response. Clearly


W309IUI

adverse effects possibly including the induction of cancer may not be detectable untilexposures exceed background levels by 10 to 100 times.

The conclusion that humans could respond to exposures to 2,3,7,8-TCDD and dioxin-likecompounds with adverse noncancer health effects is based on the fact that these compoundsaffect cellular regulation at a molecular level in diverse animal species that have been shownto respond with adverse effects. In addition, similar effects on cellular regulation have beendemonstrated in human cells in experimental cell cultures.

It is well known that individual animal species vary in their sensitivity to different effectsresulting from exposure to 2,3,7,8-TCDD. The available evidence indicates that humans aremost likely in the middle of the range of sensitivity rather than at either extreme. Thus,humans do not appear to be either extremely sensitive or extremely insensitive to theindividual effects of 2,3,7,8-TCDD and dioxin-like compounds.

In general, biochemical, cellular, and organ-level effects have been observed in experimentsin which only 2,3,7,8-TCDD was studied. Specific data on the effects of other dioxin-likecompounds like pentachlorinated and hexachlorinated dioxins and furans generally are notavailable. As mentioned in Subsection 6.2.5.1, dioxin-like compounds exhibit the commonproperty of binding to the intracellular aryl hydrocarbon (Ah) receptor. Based on differencesin receptor binding capacity, toxicity equivalence factors (TEFs) have been developed forthe dioxin congeners with chlorines in the 2,3,7,8 ring positions.

A conclusion of the draft dioxin reassessment issued by EPA in 1994 is that it isinappropriate to develop a reference dose for dioxins because dioxins are persistentcompounds in the environment and because background exposures to dioxins are not lowcompared with incremental environmental exposures (EPA, 1994b). For most compoundsfor which reference doses are applied, the compounds are not persistent, and backgroundexposures generally are low and are not taken into account. Because existing backgroundlevels of dioxins are higher than a reference dose that could be developed, the draft dioxinreassessment has concluded that it is not appropriate to use the reference dose approach


&R3Q9IU2

in evaluating exposures to dioxins. This conclusion does not mean, however, that anyincremental exposure to dioxins would cause an increase in potential noncancer healtheffects.

Based on the findings of the draft dioxin reassessment, EPA has recommended using, on aprovisional basis, a "margin-of-exposure" approach for evaluating potential noncancer healtheffects arising from incremental exposures to dioxins. Using this approach, the ratio of theestimated daily adult dose of dioxins from a particular source (in this case, the DrakeChemical site incinerator trial burn emissions) to the average daily intake of dioxins in thegeneral population, is determined. Similarly, the ratio of the estimated daily dose of dioxinsto breast-feeding infants, from the trial burn emissions to the average daily intake of dioxinsby the overall population of breast-feeding infants, is calculated. This approach will be usedto estimate the noncancer effects of dioxins emitted by the Drake Chemical site incinerator.

6.3.8 Endocrine Disrupters

An environmental endocrine disrupter is defined as an exogenous agent that interferes withthe synthesis, secretion, transport, binding, action, or elimination of natural hormones in thebody. These hormones are responsible for the maintenance of homeostasis, reproduction,development, and/or behavior.

The term endocrine disrupter applies to any member of a broad class of compounds withthe ability to perturb. the finely-tuned endocrine system that is fundamental to normalfunction in cells, tissues, and organisms at a variety of levels of biological organization.Examples of chemicals suspected of being environmental endocrine disrupters are thepesticides atrazine, DDT, endosulfan, chlordane, heptachlor, 2,4,5-T, and 2,4-D. Otherchemicals suspected of being endocrine disrupters are polychlorinated biphenyls, and dioxinsand furans. The potential noncancer health effects of dioxins were addressed in Subsection6.3.6.


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The current concern about endocrine disrupters stems from a body of diverse historicalinformation, augmented by new findings, which has been integrated into a workinghypothesis that the combination of exposure to both exogenous and endogenous hormone-mimetic compounds (i.e., compounds that mimic hormone function) can impact normalhormone function and potentially lead to adverse effects, particularly on reproductivefunction.

This hypothesis, however, lacks the scientific detail and precision necessary for it to beevaluated in a risk assessment such as this. Examples of its limitations include the following:

Few empirical data to support the designation of specific chemicals as"endocrine disrupters."

Lack of a clear structure-activity basis among the diverse group of chemicalsconsidered to be "endocrine disrupters."

Multiple modes of action currently considered to be "endocrine disruption."

Given the current limited state-of-the-science, it is premature to attempt to evaluate thepotential risks of complex mixtures of chemicals with respect to endocrine disruption.


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DOSE*, ARBITRARY UNITS(LOGARITHMIC SCALE)

NOAEL = No-observed-adverse-effect level for critical target organ

LOAEL = Lowest-observed-adverse-effect level for critical target organ(it is assumed that no toxicity data are available for doses betweenthe NOAEL and LOAEL)

TD = Dose at which toxic response is maximum

*DOSE = Usually expressed in mg chemical per kg body weight

Drake Chemical SiteLock Haven, Pennsylvania

FIGURE 6.3-1HYPOTHETICAL DOSE-RESPONSE CURVE FORA THRESHOLD NONCARCINOGENIC EFFECT

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6.4 ACUTE INHALATION TOXICITY VALUES

In addition to assessing the potential for risk posed by subchronic or chronic exposure to thechemicals from the Drake Chemical site, the risk assessment addresses the potentialnoncancer health effects posed by a short-term inhalation exposure resulting from a processupset. The acute .upset condition was defined as a single opening of the thermal relief valve(TRY) for a short period of tune (approximately 25 minutes), resulting hi the short-termrelease of chemicals into the ambient air (see Volume I, Section 2, Subsection 2.4). Thepurpose of the upset condition analysis was to predict if serious irreversible health effectsare possible following this single upset.

Short-term exposure to chemical concentrations is referred to as acute exposure, and thetoxic effects resulting from such exposures are described as acute health effects (or acutetoxicity). The acute toxic effects of a chemical may differ from the subchronic or chronictoxic effects observed after longer exposures at lower levels, and can range from relativelymild effects, such as eye or nose irritation, to serious organ damage or death.

Although EPA has not developed verifed acute inhalation toxicity values, the agency hasbegun to develop guidelines that can be used as a framework for the development ofprovisional acute inhalation values (EPA, 1993b, 1995b). These provisional values have beenbased on the results of acute inhalation assessments published by several organizations, andinclude the following:

• Emergency Response Planning Guidelines (ERPGs; AIHA, 1994).

• Levels of Concern (LOCs; EPA, 1995b).

• Immediately Dangerous to Life and Health (IDLH) values (NIOSH, 1994).

• • Threshold Limit Value—Short-Term Exposure Limits (TLV-STELs) andThreshold Limit Value-Ceilings (TLV-Cs) (ACGIH, 1995).


W309U6

The hierarchy and definitions of the guidelines used to derive Estimated Acute-ReferenceConcentrations (EA-RfCs) for the protection of human health are discussed in the followingparagraphs.

An Emergency Response Planning Guideline-2 (ERPG-2) was usedpreferentially where such values were available. The ERPG-2 is defined as"the maximum airborne concentration below which it is believed nearly allindividuals could be exposed for up to 1 hour without experiencing ordeveloping irreversible or other serious health effects or symptoms that couldimpair abilities to take protective action" (AIHA, 1994).

A Level of Concern (LOG) value (EPA, 1995b) was used if no EmergencyResponse Planning Guideline (ERPG-2) value was available. A Level ofConcern value is applicable to members of the general population and isusually derived by EPA by dividing the Immediately Dangerous to Life andHealth (IDLH) value by an uncertainty factor of 10 (EPA, 1995b).

If an ERPG-2 or Level of Concern was not available, then the lowest of the following values(adjusted with appropriate uncertainty factors) was selected as the Estimated Acute-Reference Concentration (EPA, 1993b). This approach is more protective of human healththan the guidance prepared by the Federal Emergency Management Agency (FEMA) forEPA (EPA, 1993b):

• Immediately Dangerous to Life and Health (IDLH) values are established bythe National Institute for Occupational Safety and Health (NIOSH) andrepresent the maximum airborne chemical concentration from which anindividual could escape within 30 minutes without any escape-impairingsymptoms or any irreversible health effects (NIOSH, 1994; EPA, 1993b).Immediately Dangerous to Life and Health values were divided by anuncertainty factor of 10 to ensure that the values would protect the generalpublic. This approach is consistent with EPA's general approach of dividingthe Immediately Dangerous to Life and Health value by a factor of 10 toobtain the Level of Concern.

• A Threshold Limit Value—Short-Term Exposure Limit (TLV-STEL) is a 15-minute time-weighted average concentration that should not be exceeded byworkers during a workday. Exposures to this concentration should not belonger than 15 minutes and should not occur more than four separate timesper day (ACGIH, 1995).


AR309U7

A Threshold Limit Value—Ceiling (TLV-C) is a concentration that should notbe exceeded by workers during any time period during the working day(ACGIH, 1995). The Threshold Limit Value—Ceiling was divided by anuncertainty factor of 10 to ensure that the values were protective of humanhealth.

Each EA-RfC was expressed in units of micrograms per cubic meter (jig/m3) of air. TheEA-RfC represents the inhalation exposure limit that should not pose harmful effects asdefined previously in a resident during a 1-hour exposure period. The referenceconcentrations are used in the risk characterization for comparison with modeled 1-houraverage ambient air concentrations based on process upset conditions. The 1-hour ambientair concentrations were calculated using the maximum acute emission rates and the unityair concentrations estimated for the location where maximum inhalation exposure by anymember of the population potentially could occur (see Volume I, Section 3).

The calculated acute inhalation toxicity values, and the values that were selected as the EA-RfCs, are summarized in Volume II, Appendix 6B, Table 6B-1. An EA-RfC was derived forapproximately 70 of the 162 chemicals evaluated for the Drake Chemical site through theinhalation pathway. In cases where an EA-RfC could not be derived, the potential for acutehealth effects resulting from short-term inhalation exposure due to process upset conditionswas not evaluated.


A1309IU8

6.5 SUMMARY OF UNCERTAINTIES

There are a number of uncertainties associated with the approaches used to develop toxicityvalues used in this risk assessment. The main approaches and the basis for each approachare summarized in Table 6.5-1. The table indicates a qualitative estimate (low, medium, orhigh) of the potential magnitude of effect of the uncertainty associated with each approachon the calculation of potential cancer risk and/or noncancer hazard indices (see Volume I,Section 7). The probable direction of the effect on the calculated cancer risks and/or hazardindices (over-estimate, under-estimate, or unknown) also is indicated.


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SECTION 7RISK CHARACTERIZATION

7.1 INTRODUCTION

Chemicals emitted from the Drake Chemical site incinerator during the trial burn willdisperse into the atmosphere as well as deposit on soils and surface water in the vicinity ofthe facility. Exposure to these substances by individuals living and working in the areasurrounding the incinerator potentially can occur through several pathways. These pathwayswere identified in Volume I, Section 5 (see Figure 5.5-1). The risk characterization sectionexplains how potential risks were estimated and summarizes the results of this risk analysis.

The objective of the risk characterization section is to evaluate the likelihood ofcarcinogenic risks and noncancer health effects (i.e., hazard indices) from all chemicalsbased on a combination of the daily doses calculated in the exposure assessment for eachscenario (Volume I, Section 5) and the toxicity values determined in the toxicity assessment(Volume I, Section 6). In accordance with standard EPA risk assessment guidance (EPA,1989), the potential for human carcinogenic risks and noncancer health effects of chemicalsare evaluated separately because these effects are believed to occur by different toxicologicalprocesses with different types of dose-response relationships. Carcinogenic risks arecalculated for those chemicals with weight-of-evidence classifications as A, B, or Ccarcinogens. Noncancer health effects were evaluated for all chemicals (i.e., includingcarcinogens) for which toxicity criteria were available.

The general approaches used to calculate carcinogenic risks and noncancer health effectsare summarized in Subsection 7.2. The results of the risk evaluation are summarized inSubsection 7.3. Uncertainties associated with the risk characterization are discussed inSubsection 7.4. Subsection 7.5 presents the summary and conclusions of the riskcharacterization.

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.1-1 9:55am

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72 APPROACHES TO EVALUATING CHEMICAL RISKS

7.2.1 Lifetime Carcinogenic Risks

In accordance with EPA policy (EPA, 1989), carcinogenic risk is expressed as the probabilitythat an individual will develop cancer during a lifetime as the result of exposure to emissionsfrom the incinerator trial burn. This predicted risk is expressed as the risk in excess of thebackground probability of developing cancer, which currently is believed to be about 1 in4 nationally, or 250,000 in 1 million (Travis, et al., 1988); therefore, the carcinogenic riskin this report is most accurately expressed as the lifetime excess risk. As an example, alifetime excess risk of 2E-06 means that the risk of developing cancer during ah individual'slifetime due to emissions from the incinerator trial bum is 2 chances in 1 million, in additionto the background probability.

The method for calculating the oral, inhalation, or dermal carcinogenic risk of a chemicalfor an individual is:

Lifetime Excess Carcinogenic Risk = EDI x CSF

where:

EDI = Estimated daily intake of a carcinogen averaged over a 70-year lifetime(mg/kg-day).

CSF = Chemical and route-specific cancer slope factor (mg/kg-day)"1.

An individual (e.g., subsistence farmer) may be exposed to more than one carcinogenicchemical in a medium (i.e., air, soil, or water), and may be exposed additionally to severalcarcinogens by more than one pathway. Thus, the total lifetime excess cancer risk for anindividual exposed to all chemicals is estimated by summing the cancer risks calculated foreach chemical in each medium for each exposure pathway. This approach is in accordancewith the EPA guidelines on chemical mixtures, in which risks associated with carcinogensare considered additive (EPA, 1986, 1989).

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.2-1 3:01pm

In general, lifetime excess risks that are less than IE-06 (1 in 1 million) are considered tobe so small that they are negligible, especially when compared with other risks. EPA hasused an excess cancer risk of IE-04 (1 chance in 10,000) for reasonable maximum exposuresas a level above which remedial action generally is warranted at Superfund sites (EPA,1991a).

7.2.2 Noncancer Health Effects7.2.2.1 General

The potential for noncancer toxicity to occur in an individual by a given exposure pathwayis evaluated by comparing the estimated daily intake of a chemical received during aspecified exposure period with a reference dose (RfD) derived for a similar exposure period.This ratio is the hazard quotient (HQ):

HQ = EDI/RfD

where:

HQ = Hazard quotient.

EDI = Estimated daily intake for a chemical averaged over the exposureperiod (mg/kg-day).

RfD = Chemical- and route-specific reference dose (mg/kg-day) derived fora similar exposure period.

Because individuals may be exposed to more than one chemical and by more than onepathway, it is customary to perform an analysis of total noncancer health effects by summingthe hazard quotients for all chemicals and all pathways for each population age group (e.g.,child, adult) in each scenario. This sum is called the hazard index (HI). If the hazard indexis less than or equal to one, it is believed that there is no significant potential for noncancerhealth effects in that age group, even in the most susceptible members of the population.If the hazard index exceeds one, there may be a risk of noncancer health effects. However,a value greater than one does not mean an adverse effect will definitely occur. The

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.2-2 3-Olpm

AR309I55

assumptions used to derive reference doses are highly protective of human health, so thatdaily exposure doses somewhat greater than the reference dose may not actually causeadverse effects.

The summation of hazard quotients of different chemicals assumes that the noncancereffects of all chemicals are additive. However, many chemicals exert their toxicities byacting on different organs by different toxicological mechanisms. In addition, referencedoses generally are developed based on the most sensitive endpoint, or critical toxicityeffect, experimentally measured for the chemical (i.e., that organ showing toxicity at thelowest dose of the chemical). For example, the oral reference dose for cadmium is basedon adverse effects in the kidneys, whereas the oral reference dose for methyl mercury isbased on adverse effects in the central nervous system. Consequently, these effects are hotadditive. Thus, the calculated hazard index for a chemical mixture is usually an over-estimation of the potential for noncancer health effects to occur in a single individual.

7.2.2.2 Dioxins

As discussed earlier in Volume I, Section 6, EPA has concluded that a quantitativeevaluation of the noncancer health effects of dioxins using a reference dose approach is notappropriate (EPA, 1994a). Therefore, the potential for noncancer health effects of dioxinsreleased from the incinerator was assessed by determining the margin of exposure betweendoses received from incinerator emissions as compared to estimated background doses. Thiswas done by determining the ratio of the average daily dose rate resulting from exposureto the incinerator to the background exposure doses estimated for dioxins in adults (EPA,1994a). The background dioxin dose is the total dose of 2,3,7,8-TCDD equivalents from allpathways of exposure for the general United States population based on past and currentactivities. A similar comparison was made between the dose received by the infant over 1year to the estimated daily background exposures for infants (EPA, 1994a).


AR3091 56

7.2.2.3 Lead

EPA does not believe it is appropriate to evaluate the potential health risks of lead usingthe reference dose approach (IRIS, 1996). Lead was evaluated in this risk assessment byperforming a screening analysis, which compared the predicted incremental increases in leadconcentrations in air, soil, and water resulting from incinerator releases to availableregulatory guidelines for acceptable lead levels in those environmental media. Predicted airlead concentrations were compared with the National Ambient Air Quality Standard(NAAQS) for lead (EPA, 1995a). Predicted soil lead concentrations were compared withthe RCRA risk-based soil lead concentration (EPA, 1994b), and surface-water (reservoir)concentrations were compared with the EPA drinking water action levels for lead (EPA,1995b).

7.2.3 Acute Noncancer Health Effects During a Process Upset

A temporary process upset leading to an opening of the thermal relief valve (TRV) mightresult in a short-term release of chemicals to air that could have potential acute healtheffects. In order to simulate a worst-case scenario, maximum emission rates of chemicalswere used in the analysis. Additionally, the acute inhalation toxicity criteria were derivedto be protective of human health during a 1-hour exposure. The predicted maximum off-site1-hour ambient air concentration of each chemical as a result of this upset was comparedto the respective Estimated Acute-Reference Concentrations (EA-RfCs) (see Volume I,Section 6, Subsection 6.4, and Volume II, Appendix 6B). This ratio is the hazard quotientfor acute exposure:

HQacute = AIC/EA-RfC

where:

= Hazard quotient for acute inhalation exposure for a chemical.

AIC = Chemical-specific acute inhalation concentration in air resultingfrom releases associated with a process upset (jig/m3).

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EA-RfC = Chemical-specific estimated Acute-Reference Concentration

The total risk from acute inhalation exposures is estimated by summing the hazard quotientvalues for all chemicals in air.

7.2.4 Impact of Process Upsets on Inhalation Carcinogenic Risks

The incremental increase in potential carcinogenic risks by inhalation associated withperiodic process upsets during the entire duration of the trial burn was evaluated for each

chemical. The approach was to average the total air concentration of each chemical thatwould occur as a result of three 25-minute upsets and one 1-minute upset over the 2-monthtrial burn period with the respective 30-day average used to represent normal operations.Averaging the acute upset concentrations will result in an incremental increase in the 30-dayaverage compared to normal conditions. Since air concentrations are directly related to theinhalation carcinogenic risk, the expected increased carcinogenic risks due to the upsets canbe determined by calculating the ratio of the 30-day averages with and without upsets.


AB3Q9I58

7.3 RESULTS7.3.1 Lifetime Carcinogenic Risks for the Subsistence Farmer and Resident

Table 7.3-1 presents a complete summary of the predicted total lifetime excess carcinogenicrisks (i.e., for all chemicals) through all exposure pathways evaluated for the subsistencefarmer (adult, child, and nursing infant) and the resident (adult, child, and nursing infant).The detailed risks presented by chemical are shown in the tables in Volume II, Appendix7A. As expected, the total calculated risks for the subsistence farmer scenario were slightlyhigher than those for the resident scenario based on ingestion of beef and milk originatingon the farm. The total carcinogenic risk for the adult subsistence farmer was 8.6E-07. Thechild of the subsistence farmer showed a risk of 5.6E-06, and the nursing infant of thesubsistence farmer showed a risk of 2E-06. Total carcinogenic risks for the resident scenariowere less with the adult resident having a risk of 1. IE-07, the child showing a risk of2.5E-07, and the infant of the resident showing a risk of 3.IE-07.

Table 7.3-2 summarizes those chemicals and exposure pathways exceeding a carcinogenicrisk of IE-06, and indicates their percentage contribution to the carcinogenic risk in thesepopulations. Only risks to the infant and child of the subsistence farmer exceeded IE-06.The total risks primarily were due to exposures through the dairy milk and the mother'smilk ingestion pathways. Two polycyclic aromatic hydrocarbons (indeno[l,2,3-cd]pyrene anddibenzo[a,h]anthracene) were the greatest contributors to risk from dairy milk ingestion bythe child of the subsistence farmer. About 70% of the total risk for the infant of thesubsistence farmer was due to 4,4'-DDE through the ingestion of mother's milk. All otherchemicals contributed excess cancer risks less than IE-06. Volume II, Appendix 7A presentsall of the risk calculations.

7.3.2 Noncancer Health Effects for the Subsistence Farmer and Resident

Table 7.3-3 presents the noncancer hazard indices .for all chemicals for the subsistencefarmer (adult, child, and nursing infant) and resident (adult, child, and nursing infant).Total pathway hazard indices are presented for all indirect pathways. Inhalation hazard


1R3Q9I59

indices are presented separately (in the last column) because it is inappropriate to addsubchronic (2-month) exposures with chronic exposures (EPA, 1989). No scenario exceededa hazard index of one. The highest hazard indices were 5E-02 for the indirect pathways forthe child of the subsistence farmer, and 3.8E-01 for inhalation for the child of the resident.Even if the subchronic inhalation hazard index for each scenario and age group were to beadded to the respective total hazard index for the indirect pathways, the hazard indiceswould-still be less than one. Since all hazard indices were less than one, it was notnecessary to determine hazard quotients by toxicity endpoints. Additionally, it is importantto note that the noncancer hazard indices are over-estimated for the inhalation pathwaybecause the calculated subchronic exposure doses were compared to chronic reference dosesfor most chemicals. Collectively, these results indicate that chemicals released by the facilityduring the trial burn are not expected to produce any noncancer health effects.

7.3.3 Carcinogenic Risks and Noncancer Health Effects for the RecreationalFisherman

Ingestion of recreationally caught fish from Bald Eagle Creek resulted in predictedcarcinogenic risks and noncancer health effects well below levels of regulatory concern.Total carcinogenic risks to the adult and child were 5.5E-08 and 1.8E-08, respectively (Table7.3-4). These risks are 22 and 67 times lower, respectively, than the IE-06 benchmark(EPA, 1991a). Noncancer hazard indices for the adult and child were 5.3E-03 and 6.8E-03,respectively, which are over two orders of magnitude (a factor of 100) lower than the hazardindex-benchmark of one (EPA, 199 la).

7.3.4 Noncancer Health Effects of Dioxins

The determination of the margin-of-exposure between average daily dioxin doses receivedfrom exposure to the incinerator and background doses is summarized in Table 7.3-5. Boththe calculated exposure doses and the background doses are expressed in 2,3,7,8-TCDDtoxicity equivalents (TEQs) as discussed in Volume I, Section 6. The average daily dose ofdioxins that an adult will receive through all direct and indirect pathways ranges from less

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.3-2 S:14pm

AR309I60

than 0.01% (resident) to less than 0.03% (subsistence farmer) of the background dose

(Table 7.3-5). Stated differently, the adult subsistence farmer dose is approximately 3,330times lower than what is expected from background exposure, and the adult resident doseis approximately 10,000 times lower than the expected background dose.

Infants who breast feed potentially will receive approximately 0.001% (resident) to 0.005%(subsistence farmer) of the infant background dose. Again, stated differently, the resultsindicate that the dioxin doses received by the nursing infant of the resident and subsistencefarmer are 100,000 and 20,000 times lower, respectively, than what is expected frombackground exposures.

The incinerator, therefore, contributes a negligible amount of dioxins to the existingbackground levels (EPA, 1994a). These results indicate that any dioxins formed duringincineration will not be expected to cause a significant increase in potential noncancerhealth effects of dioxins from background exposure.

7.3.5 Potential Inhalation Health Effects from Releases During Process Upsets

7.3.5.1 Acute Noncancer Health Effects

Acute hazard quotients for the inhalation of chemicals at the location of maximum impactreleased to air during a single opening of the thermal relief valve were determined. Thesum of all hazard quotients (hazard index) is 2.2E-02. The detailed results are presentedin Volume II, Appendix 7C. Since the hazard index is less than one, these results indicatethat there is no likelihood of significant adverse health effects associated with acuteinhalation exposure to airborne releases that might occur during a process upset (i.e.,opening of the thermal relief valve).


AR3Q9I6I

7.3.5.2 Incremental Inhalation Carcinogenic Risks Associated with Process Upsets

The increase in carcinogenic risk associated with process upsets was calculated only for theresident scenario because this scenario would have the greatest potential impact due to theproximity to the incinerator. The impact on the farmer would be much lower. The increasein inhalation carcinogenic risk for the resident due to process upsets during the 2-month trialburn was 15 times for the child and approximately 2 times for the adult (see Table 7.3-6).However, the total inhalation risks for both the child and adult resident were still belowIE-06 at 8.5E-07 and 2.4E-08, respectively. These results indicate that process upsets arenot expected to significantly increase the inhalation cancer risks associated with the 2-monthtrial burn. The detailed calculations are shown in Volume II, Appendix 7D.

7.3.6 Evaluation of Lead Emissions

The predicted lead concentrations in soil, air, and water due to incinerator releases duringthe 2-month trial burn were compared to published regulatory guidelines for lead (Table7.3-7). Predicted soil concentrations of lead in both the resident (0.0076 milligrams perkilogram [mg/kg]) and the subsistence farmer (0.0022 mg/kg) scenarios are approximately50,000 to 200,000 times lower than the RCRA soil cleanup level for lead (400 mg/kg) (EPA,1994b). The predicted soil concentrations were based on the shallow (i.e., 0.4-inch) mixingdepth. Using this mixing depth results in a high predicted soil lead concentration, whichlikely will not be exceeded.

For the principal drinking water source (Keller Reservoir), the predicted lead concentration(0.015 micrograms per liter [ng/L]) was 1,000 times lower than the drinking water actionlevel (15 jig/L) (EPA, 1995b). The maximum predicted lead impact to surface water in theCastanea Reservoir (0.058 jig/L) was approximately 260 times lower than the 15 u.g/Ldrinking water action level.

The maximum predicted air concentration for the resident during the 2-month trial burn(0.0011 micrograms per cubic meter [u.g/m3]) was 1,400 times lower than the health-based


AR309I62

NAAQS (1.5 u.g/m3) (EPA, 1995a, 1991b). For the subsistence farmer, the predicted airlead concentration (0.00034 ng/m3) was 4,400 times lower than the guideline.

These results indicate that lead releases from the incinerator will only negligibly increaseenvironmental lead levels in soil, water, or air, and that these increases will not cause anysignificant impact to human health.

7.3.7 Comparison of Predicted Air Concentrations for Criteria Pollutants with NationalAmbient Air Quality Standards

Predicted ambient air concentrations of carbon monoxide, nitrogen dioxide, sulfur dioxide,and particulate matter (PM10) for both the subsistence farmer and resident scenarios werecompared to NAAQS (EPA, 1995a, 1991b). Table 7.3-8 shows the results of thesecomparisons. Predicted air concentrations of carbon monoxide, sulfur dioxide, andrespirable particulate matter (PM10) were all less than 1% of their respective air standardsfor both the subsistence farmer and the resident. Predicted nitrogen dioxide air levels wereapproximately 4.9% of the NAAQS at the resident location, and 1.5% of the NAAQS at thesubsistence farmer location.; These results indicate that the incinerator will have nosignificant health impacts, on current air quality standards for the criteria air pollutants.

7.3.8 Analyses of Seven Additional Products of Incomplete Combustion

As described in Volume I, Section 2, Subsection 2.3.2.2, seven additional products ofincomplete combustion (PICs) were evaluated. This included an assessment of lifetimecarcinogenic risks and noncancer health effects for all of the exposure scenarios previouslyevaluated, and an acute inhalation noncancer evaluation based on a potential thermal reliefvalve opening (process upset condition) for chemicals with existing toxicity criteria.

Based on the same assumptions used in the risk assessment for the primary list ofapproximately 180 chemicals, carcinogenic risks and noncancer hazard indices werepredicted. In each scenario (infant, child, and adult subsistence farmer; infant, child, and

„„ ^ 06/19/96MK01\RPT:11098213.003\drakevl.s7 7.3-5 5:14pm

AR309I63

adult resident; child and adult recreational fisherman), the carcinogenic risks were all1.7E-12 or less (see Table 7.3-9). The noncancer hazard indices for the scenarios and agegroups just listed were all 2.4E-04 or less (see Table 7.3-10). Therefore, predicted healthimpacts of these additional products of incomplete combustion cause negligible increasesin total carcinogenic risk (see Subsection 7.3.1) and noncancer hazard indices (seeSubsection 7.3.2).

Evaluation of process upset conditions (opening of the thermal relief valve) for the sevenadditional products of incomplete combustion showed that the total acute hazard index is1*.8E-05 (see Table 7.3-11) for the resident scenario. This was the only scenario evaluatedbecause it would result in the highest potential risk from process upsets due to its proximityto the incinerator. The subsistence farmer acute hazard index would be much lower. Theadditional impacts of these seven products of incomplete combustion will have a negligibleeffect on the total acute inhalation hazard quotient of 2.2E-02 (see Subsection 7.3.5.1).Therefore, no acute health effects are anticipated from these compounds in the event of athermal relief valve opening.

Emissions and lexicological data on these additional products of incomplete combustion areincluded in Volume II, Appendix 7E.


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Table 7.3-2

Chemicals and Pathways Exceeding a Carcinogenic Risk of IE-06Drake Chemical SiteLock Haven, PA

Chemical

Indeno(l,2,3-cd)pyreneDibenzo(a,h)anthracene4,4'-DDE

ExposurePathway

Dairy milk8Daiiy milk*

Mother's milkb

CarcinogenicRisk

• 2.7E-06, 1.5E-061.4E-06

Percent of TotalRisk

48C27°70d

a Child of the subsistence farmer.b Infant of the subsistence farmer.c Total risks for indeno(l,2,3-cd)pyrene and dibenzo(a,h)anthracene includes all exposurepathways listed in Table 7.3-1.

d Total risk for 4,4'-DDE represents that from mother's milk ingestion only.

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Table 7.3-4

Carcinogenic Risk and Noncancer Hazard Indices for theRecreational Fisherman*Drake Chemical SiteLock Haven, PA

Total Carcinogenic Risk

AdultChild

5.5E-081.8E-08

Noncancer Hazard IndexAdultChild

5.3E-036.8E-03

"Based on fish ingestion from Bald Eagle Creek.


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Table 7.3-6

Effects of Episodic" Upsets of the Thermal Relief Valve onInhalation Carcinogenic Risks to the Resident from the Trial Burn


Scenario

Resident

Age Group

Child

Adult

Inhalation Carcinogenic Risk

Under NonupsetConditions1"

5.4E-08

1.5E-08

Under UpsetConditions'

8.5E-07

2.4E-08

* Several upsets of the thermal relief valve were assumed to occur during the 2-month trial burn (seeSubsection 7.3.5.2).

b Denotes the inhalation carcinogenic risks based on the maximum 30-day average air concentrationsunder normal operating conditions.

c The total air concentrations of each chemical averaged during the process upsets were summed withthe 30-day average air concentrations. The ratios of the upset emission air concentrations to thenonupset emission air concentrations for organic and inorganic chemicals were multiplied with theoriginal chemical-specific risks (organic ratio average, 1.8; inorganic ratio average, 2.6). Organic andinorganic risks then were summed to obtain the inhalation carcinogenic risk under upset conditions (seeSubsection 735.2, and Volume II, Appendix 7D).

MK01\RPT:11098213.003\drakevl.s7 7.3-12 9-55am

AB309I70

Table 7.3-7

Comparison of Exposure Concentrations of Lead with Health Guideline ValuesDrake Chemical SiteLock Haven, PA

Scenario

Resident

Subsistence Fanner

Resident/SubsistenceFarmer

Resident

Subsistence Farmer

Medium

Soils3

Soils8

Keller ReservoirCastanea Reservoir

Air

Air

ExposureConcentration

7.6E-03 mg/kg

2.2E-03 mg/kg

1.5E-02 u-g/Lc5.8E-02 u-g/L0

1.1E-03 ug/m3

3.4E-04 tig/m3

Guideline Value

400 nig/kg"

400 rag/kg"

15 ng/L"15 u-g/Ld

1.5 u.g/m3e

1.5 tig/m*

Percent of GuidelineValue

0.002

0.0005

0.10.4

0.07

0.02

a Predicted lead concentrations in soil based on particulate deposition modeling using a 0.4-inch (1-centimeter) mixing depth (see VolumeII, Appendix SB).

b EPA, 1994d.

c Predicted surface-water lead concentration based on deposition to surface water body and on contribution from soil runoff in thewatersheds.

d EPA, 1995b.

' The NAAQS for lead is based on a 3-month average (EPA, 1991b).

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.3-13 . 9:55am

W309I7I

Table 7.3-8

Comparison of Predicted Air Concentrations of Carbon Monoxide (CO),Nitrogen Dioxide (NO2), Sulfur Dioxide (SO2), and Particulate Matter (PM10)

to Primary National Ambient Air Quality Standards (NAAQS)Drake Chemical SiteLock Haven, PA

Chemical

CO

NO2

1 houravgc

8 houravgc

SO2

PM10

Predicted'Air Concentration

(Hg/m3)

SubsistenceFarmer

18.9

10.5

1.5

0.20

0.06

Resident

18.9

10.5

4.9

0.65

0.20

NAAQS"(Hg/m3)

40,000

10,000

100

80

50

Percent of NAAQS

SubsistenceFarmer

0.05

0.10

1.50

0.25

0.10

Resident

0.05

0.10

4.90

0.80

0.40

* The predicted air concentrations for NOj, SO2, and PMlo are the maximum 30-day average ground-levelambient air concentrations based on the dispersion modeling for residential and agricultural uses (per VolumeI, Section 5 and Volume II, Appendix 5A).

b NO2, SO2 and PM10 guidelines are based on annual average air concentrations (EPA, 1991b, 1995a).

c The predicted air concentrations for CO represent maximum off-site 1-hour and 8-hour average concentrationsand, therefore, these concentrations were used to represent both the subsistence farmer and resident locations.

CO = Carbon monoxide.

NO2 = Nitrogen dioxide (includes nitrogen oxide and nitric acid).

SO2 = Sulfur dioxide (includes sulfur oxide).

PM10 = Particulate matter (respirable fraction of particulate matter with particle diameters lessthan 10 microns).


W309I72

Table 7.3-9

Lifetime Carcinogenic Risks Through Direct and Indirect Pathwaysfor Additional Products of Incomplete Combustion


Scenario

SubsistenceFarmerb

Residentb

RecreationalFishermand

Age GroupAdultChildInfant0

AdultChildInfanf

Adult

Child

Lifetime Excess Carcinogenic Risk3

3.4E-13l.OE-121.6E-14

5.4E-131.7E-122.5E-14

1.1E-15

1.4E-15

a Represents the excess carcinogenic risk totaled for all direct and indirect exposurepathways for the seven additional products of incomplete combustion (see VolumeI, Section 2, Subsection 2.3.2.2).

b Does not include the addition of fish ingestion risks.c Only mother's milk ingestion was evaluated.d Only fish ingestion risks were evaluated in this pathway.


&8309I73

Table 7.3-10

Hazard Indices Through Direct and Indirect Pathwaysfor Additional Products of Incomplete Combustion


Scenario

SubsistenceFarmerb

Resident"

RecreationalFisherman*1

Age Group

Adult

Child

Infant0

Adult

Child

Infant0

Adult

Child

Hazard Indices3

Indirect Pathway

7.8E-05

2.2E-04

1.1E-07

8.2E-05

2.4E-04

1.7E-07

6.5E-07

. 8.5E-07

Inhalation

2.4E-06

8.9E-06

-

7.8E-06

2.7E-05

-

-

-

a Represents the hazard indices totaled for all indirect exposure pathways and for directinhalation for the seven additional products of incomplete combustion (see Volume I,Section 2, Subsection 2.3.2.2).

b Does not include the addition of fish ingestion risks.0 Only mother's milk ingestion was evaluated.d Only fish ingestion risks were evaluated in this pathway.

06/19/96MK01\RPT:11098213.003\drakevl.s7 7.3-16 3-14pm

AR309I7U

Table 7.3-11

Inhalation Hazard Quotients for the Resident for AdditionalProducts of Incomplete Combustion Under Upset Conditions


Scenario

Resident13

Acute Inhalation Hazard Index3

1.8E-05

Represents the sum of all acute hazard quotients for the seven additional products ofincomplete combustion (see Volume I, Section 2, Subsection 2.3.2.2) by the inhalationpathway during an upset of the thermal relief valve.

One-hour acute upset emissions were modeled to the point of maximum impact.


&E309175

7.4 UNCERTAINTY

The principal uncertainties in the risk assessment process have been presented separatelyin each section. There are, however, several important uncertainties associated with the riskcharacterization process, as identified in Table 7.4-1. A more detailed discussion of theoverall .impacts of the uncertainties is included in Volume I, Section 8.

There are several limitations with the addition of carcinogenic risks. First, unit cancer risksfor each chemical are derived as the 95% upper-bound confidence limit of cancer potency,and therefore, the total carcinogenic risk that is calculated can become artificially moreconservative (i.e., over-estimated) as risks are added. Moreover, risks are added equally forall carcinogens, regardless of the weight-of-evidence class to which a carcinogen has beenassigned (see Volume I, Section 6). Therefore, the addition of carcinogenic risks acrosschemicals and pathways may over-estimate total risk.

For noncancer health effects, the hazard index (HI) approach assumes that multipleexposures to all chemicals should be added. This methodology is appropriate for chemicalsthat induce toxic effects on the same target organ, but over-estimates risk when it combinesexposures that adversely affect different organs.

Additivity of carcinogenic risk estimates and hazard quotients assumes that the chemicalsdo not act either antagonistically or synergistically. Antagonism refers to the process bywhich the toxicity of one chemical is reduced or eliminated by the presence of anotherchemical. Synergism refers to the process by which the total toxicity of a mixture ofchemicals is greater than the sum of their individual toxicities. Although there is scientificliterature to support the premise that these processes can occur, information on chemicalmixtures currently is not sufficient to quantify these types of interactions (EPA, 1995a).Moreover, the assumption of additivity of cancer risks and noncancer health effects, asstated above, is considered to be highly protective of human health.

06/19/96MK01\RPT:llQ98213.003\drakevl.s7 . 7.4-1 . . 9:55am

Fish consumption risk was not included in the subsistence farmer and resident scenarios, butwas evaluated separately as the recreational fisherman scenario (see Tables 7.3-1,7.3-3, and7.3-4). This results in a potential under-estimation of total carcinogenic risks in thesubsistence farmer and resident, if one assumes that the fisherman also could be thehypothetical subsistence farmer or resident evaluated in the risk assessment. Totalcarcinogenic risks through direct and indirect pathways of exposure for the child and adultsubsistence farmers and residents (Table 7.3-1) were added to the carcinogenic risksassociated with fish consumption in the child (1.8E-08) and adult (5.5E-08) recreationalfisherman. The following total carcinogenic risks were calculated:

Carcinogenic Risks• Adult subsistence farmer 9.2E-07• Child subsistence fanner 5.6E-06• Adult resident 1.7E-07• Child resident 2.7E-07

There was no significant change to the child of the subsistence farmer risk (5.6E-06). Allother risks increased slightly, but were still within the acceptable range.

Using this same approach for indirect noncancer health effects also results in a slightincrease in total hazard indices through indirect pathways of exposure for the child and adultsubsistence farmers and residents. The hazard indices for the child and adult through fishconsumption are 6.8E-03 and 5.3E-03, respectively. The following are the total hazardindices through indirect exposure with the addition of noncancer hazard indices through fishconsumption:

Noncancer Hazard Indices• Adult subsistence fanner 1.2E-02• Child subsistence farmer 6.0E-02• Adult resident 7.0E-03• Child resident l.OE-02


AH309I77

Again, these slight increases do not alter the conclusion that indirect noncancer healtheffects are below regulatory levels of concern (i.e., hazard index is less than one).Therefore, any degree of under-estimation of total risks by exclusion of fish consumptioncarcinogenic and noncancer health effects is low.


AE309I78

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7-4'4 AR309I79

7.5 SUMMARY AND CONCLUSIONS

Total lifetime excess carcinogenic risk for the subsistence farmer is less than IE-05. The•majority of the risk for the subsistence farmer is associated with only a few chemicals of theapproximately 180 organics and inorganics evaluated, and these risks are predominantlyassociated with ingestion of dairy milk or mother's milk. For the resident, total lifetimecarcinogenic risk (for all pathways) is less than IE-06.

The noncancer hazard indices for both the subsistence farmer and resident are less thanone, indicating that noncancer health effects are not a concern. Risk from ingestion ofcontaminated fish by the recreational fisherman is low both for carcinogenic and noncancerhealth risks. Assuming the fisherman is a subsistence fanner or resident, the addition ofthese health risks results only in a small increase in total risk that is still within acceptableregulatory limits. Predicted average daily dioxin exposure doses are significantly less thanbackground doses for both the infant and adult in all scenarios, as determined by themargin-of-exposure approach, and, therefore, are expected to cause only a negligibleincrease in the potential noncancer health effects of dioxins.

Short-term acute inhalation health effects resulting from an opening of the thermal reliefvalve are not -of concern based on the observation that the acute hazard index is less thanone. Incremental impacts of multiple acute upsets on long-term emission rates undernormal (nonupset) conditions likewise does not appreciably increase inhalation carcinogenicrisk during the 60-day trial burn.

Predicted lead concentrations in air, water, and soil are significantly less than healthguidelines, indicating that adverse health impacts of lead are negligible. Predicted airconcentrations of criteria pollutants (i.e., NOX, SO2, CO, and PMJO) are all significantly lessthan health-based NAAQS. Risks associated with the inclusion of seven additional productsof incomplete combustion are negligible.


A1309I80

SECTION 8UNCERTAINTY AND SENSITIVITY ANALYSES

8.1 INTRODUCTION

The results presented in Volume I, Section 7, are estimates of potential risks that are basedon many assumptions about predicted exposure and toxicity. To ensure that the trial burnis protective of human health, conservative judgments of exposure potential or lexicologicaleffects are made. As a result, many of the assumptions made in a typical risk assessmentlead to an over-estimation of actual risk. This is true for this trial burn risk assessment,which is intermediate between a screening-level risk assessment that uses a number ofsimplifying assumptions and an in-depth site-specific risk assessment. It is important thatall interested parties understand that these risk estimates need to be evaluated inconjunction with the exposure and toxicity information used to develop these risk estimates.

In the preceding technical sections, evaluations of the uncertainty associated with eachtechnical component were developed and incorporated in summary tables that categorizethe degree and direction of the uncertainty, i.e., whether the uncertainty tends to under-estimate or over-estimate the risk. In this risk assessment, the degree of the uncertainty wasconsidered to be high, and the overall direction or result of the exposure and toxicityassumptions was to over-estimate risks.

This section of the risk assessment has two purposes. First, specific factors that havecontributed to the uncertainty in each of the technical sections are summarized, inSubsection 8.2, with a focus on the major contributors to estimated risk. Second, two keyapproaches that impact exposure and risk estimates are evaluated in a sensitivity analysisto determine the impacts of alternative assumptions or decisions. The sensitivity analysesare presented in Subsection 8.3.


AE309I8!

8.2 UNCERTAINTY ANALYSIS SUMMARY

As noted previously, detailed discussions of uncertainty were presented in each technicalsection of the risk assessment. In an intermediate-level pre-trial-bum risk analysis in whichincinerator emissions can only be estimated, it is difficult to quantitatively determine themagnitude of the effect of a particular uncertainty on risk. Nevertheless, professionaljudgment was used to assign a low, medium, or high qualifier to the effect of eachuncertainty on the risk estimates.

Table 8.2-1 presents those uncertainties that were assigned a "high" potential effect on therisk estimates. As seen in Table 8.2-1, most of the uncertainties result in a significant over-estimation of risk. For comparison purposes, Table 8.2-2 presents those uncertainties thatmay potentially under-estimate risks. As seen from this table, the majority of under-estimates are expected to have a "low" potential effect on the risk estimates.

In summary, there are many more potential over-estimates of risk than under-estimates.Thus, the cancer risks and noncancer hazard indices calculated in this analysis are likely tobe a significant over-estimate of actual risk.


A1309I82

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AR309I89

8.3 SENSITIVITY ANALYSES\

The purpose of this subsection is to investigate three alternative technical approaches thatwould affect exposure and risk estimates, and determine their potential impacts on theoverall risk estimates. These approaches are:

• The use of an alternative dispersion model to the Industrial Source ComplexVersion 3 model (ISC3) used in the base case. This alternative model is theCALPUFF model.

• The use of an alternative dispersion model to the INPUFF model used for thethermal relief valve release to evaluate the impact of calm wind conditions onthe predicted concentrations. This alternative model is the CALPUFF model.

• The use of an alternative trivalent:hexavalent chromium ratio in incineratoremissions.

This sensitivity analysis investigates these alternative approaches in order to determine theirimpacts on predicted risks. .To accomplish this for the alternative dispersion model, thetotal risk results from exposure to the chemicals of concern in the base case (see VolumeI, Section 7) are presented in a side-by-side comparison with the risk from the alternativeapproach. For the chromium ratio issue, the risks for this chemical for the three approachesare compared directly.

8.3.1 Selection of Models

The ISC3 air dispersion model was used to estimate off-site ambient air concentrations anddeposition rates in the risk assessment. This is an EPA-approved air quality dispersionmodel that has been widely used for applications such as health risk assessments. Severalmore sophisticated air quality dispersion models have been developed that utilize time- andspace-varying meteorological conditions. One of these models, developed by EarthTech,Inc., is the CALMET/CALPUFF dispersion model, and it differs from the ISC3 model inthe following ways:

06/20/96MK01\RPT:1109S213.003\drakevl.s8 8.3-1 4:44pm

AE309I90

• The CALMET/CALPUFF model is a state-of-the-science, multilayered,multispecies, non-steady-state puff dispersion model that can simulate theeffects of time- and space-varying meteorological conditions on pollutanttransport, transformation, and removal.

• The CALPUFF model can use the three-dimensional meteorological fieldsdeveloped by the CALMET model, or simple single station winds in a formatconsistent with the meteorological files to support the ISC3 dispersion model.

• The CALPUFF model used the three-dimensional meteorological field tosimulate the wind conditions and terrain effects in the Lock Haven, PA area.

• The CALMET/CALPUFF model can perform dispersion calculations duringcalm wind and inversion/stagnation conditions.

Because of some of the inherent differences in the way the CALMET/CALPUFF modelevaluates local meteorological data, land use, and topography, the predicted maximumconcentration and deposition locations for the resident and subsistence farmer scenarios arenot the same as in the ISC3 model. The maximum concentration and deposition amountsalsd differ. To determine the magnitude of these differences, the maximum ambientconcentrations and deposition rates within the same 4-month period (July through October)were predicted by CALPUFF and compared to the ISC3 results. All of the sameassumptions were used in the risk assessment under this approach.

The results of this comparison are shown in Table 8.3-1. While the resident and subsistencefarmer locations changed, along with changes in the predicted ambient concentration anddeposition amounts, the resultant changes to the calculated risks were very small. Allnoncancer hazard indices remained below one, and cancer risks are below IE-05.

The INPUFF model was used to estimate off-site ambient concentrations due to thermalrelief valve releases. The INPUFF model was selected because it can handle the varyingemission rates, short-term durations, and varying exit velocities associated with a thermalrelief valve release. The CALPUFF model results for the thermal relief valve release werea factor of four higher than those determined from INPUFF. Since the predicted


HB309I9I

concentrations based on INPUFF were orders of magnitude below acute and chronic healthvalues, a factor of four increase due to calm wind conditions is considered negligible.

8.3.2 Chromium Ratio

This analysis relates to the assumed 85:15 ratio of trivalent chromium emissions tohexavalent chromium emissions, as described in Volume I, Section 5, Subsection 5.5.4.2.Carcinogenic inhalation risks and indirect (oral) noncancer health effects from chromiumVI emissions were small (less than 3.9E-09 carcinogenic risk and less than 5. IE-05 hazardindex for all scenarios) using this assumption. If a worst case assumption of 100% hexavalentchromium emissions is assumed, the greatest carcinogenic risk (child resident scenario)would increase approximately sevenfold from 3.9E-09 to 2.7E-08, still well below a level ofconcern. All other scenarios would result in even smaller levels of carcinogenic risk.

For noncancer health effects, the same approximate sevenfold increase would apply if totalchromium emissions were in the hexavalent form. This would result in a maximum hazardindex of 3.6E-04 for the child farmer scenario. Therefore, it can be concluded that even ifthe worst-case ratio (i.e., all chromium emissions are in the hexavalent form) was assumedfor chromium emissions, there would be no significant impact on the estimated risks.


HR309I92

Table 8.3-1

Comparison of Risks Using the Industrial Source Complex Model (ISC3)and the CALMET/CALPUFF Model


Receptor Base Case - ISC3 Model1

Total Carcbogenic

CALMET/CALPUFF Model

Risk"Subsistence farmerAdultChildInfant

8.6E-075.6E-062.0E-06

9.4E-076.2E-062.2E-06

ResidentAdultChildInfant

LIE-072.5E-073.1E-07

1.2E-072.6E-073.2E-07

Recreational fisherman0AdultChild

5.5E-081.8E-08

5.1E-081.6E-08

Hazard IndicesTotal

IndirectPathways .

Subsistence farmerAdultChildInfant

6.4E-035.0E-021.7E-02

ResidentAdultChildInfant

1.3E-033.0E-034.0E-03

Recreational fisherman0AdultChild

InhalationTotal IndirectPathways

3.3E-021.2E-01

—

8.3E-036.6E-021.9E-02

1.1E-013.8E-01~

1.9E-034.3E-033.6E-03

5.3E-036.8E-03

Inhalation

3.6E-021.3E-01

—

7.9E-022.8E-01

—

6.4E-038.4E-03

•See Tables 73-1, 7.3-3, and 7.3-5.""Includes total indirect pathways and inhalation.Trom ingestion of fish only.


8.4 SUMMARY

There is uncertainty in most risk assessments. To address this uncertainty, assumptions aremade that often result in an over-estimation of exposure and risks. In this assessment,estimates of risks for each of the receptor populations potentially exposed to incineratoremissions for the base-case conditions are below levels of concern defined by EPA forSuperfund remedies (i.e., carcinogenic risk below IE-04, and a noncancer hazard index lessthan one), even with a high degree of over-estimation of risk.

In addition, two key assumptions used in the risk assessment were evaluated to determineif different decisions or choices would have a significant impact on the risk estimates. These"sensitivity analyses" showed that, while the different assumptions changed the total risks,the changes were insignificant.

It can be concluded with a high level of confidence, therefore, that the trial burn of theincinerator at the Drake Chemical site will not result in significant risks to the localcommunity.

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W309I9I*

SECTION 9REFERENCES

References for Section 1

EPA (U.S. Environmental Protection Agency). 1995. Health Effects Assessment SummaryTables (HEAST). FY 1995 Annual. Office of Solid Waste and Emergency Response,Washington, DC. 9200.6-303 (95-1). EPA/540/R-95/036. PB95-921199. May 1996.

EPA (U.S. Environmental Protection Agency). 1994a. Health Assessment Document for2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Volume III of III.Review Draft. Office of Research and Development, Washington, DC. EPA/600/BP-92/001C. August 1994.

EPA (U.S. Environmental Protection Agency). 1994b. Exposure Assessment Guidance forRCRA Hazardous Waste Combustion Facilities. Draft. April 1994.

EPA (U.S. Environmental Protection Agency). 1994c. Guidance for Performing ScreeningLevel Risk Analyses at Combustion Facilities Burning Hazardous Wastes. Draft. Office ofEmergency and Remedial Response, Office of Solid Waste. April, October, and December1994.

EPA (U.S. Environmental Protection Agency). 1994d. National Oil and HazardousSubstances Pollution Contingency Plan. 40 CFR Part 300. 59 FR 47384.

EPA (U.S. Environmental Protection Agency). 1993. Addendum to the Methodology forAssessing Health Risks Associated with Indirect Exposure to Combustor Emissions. ReviewDraft. Office of Research and Development, Washington, DC. EPA/600/AP-93/003.November 1993.

EPA (U.S. Environmental Protection Agency). 1992. Guidance for Data Useability in RiskAssessment (Part A). Final. Office of Emergency and Remedial Response, Office of SolidWaste, Washington, DC. 9285.7-09A. PB92-963356. April 1992.

EPA (U.S. Environmental Protection Agency). 1990. Methodology for Assessing Health RisksAssociated with Indirect Exposure to Combustor Emissions. Interim Final. Office of Healthand Environmental Assessment, Washington, DC. EPA/600/6-90/003. January 1990.

EPA (U.S. Environmental Protection Agency). 1989. Risk Assessment Guidance forSuperfund: Human Health Evaluation Manual, Part A. Interim Final. Office of Solid Wasteand Emergency Response. OSWER Directive 9285.701A.

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EPA (U.S. Environmental Protection Agency). 1988a. Record of Decision, Drake ChemicalSite, Lock Haven, PA. Stanley Laskowski, Acting Regional.Administrator. 29 September1988.

EPA (U.S. Environmental Protection Agency). 1988b. Phase HI Remedial Investigation,Volume I - Narrative, Drake Chemical Site, Lock Haven, Pennsylvania. Prepared by NUSCorporation. March 1986. pp. 302016-302193.

EPA (U.S. Environmental Protection Agency). 1986. Feasibility Study of RemedialAlternatives (Phase II), Buildings and Contaminated Structures, Drake Chemical Site, LockHaven, Pennsylvania. Prepared by NUS Corporation. March 1986. pp. 301321-301446.

EPA (U.S. Environmental Protection Agency). 1984. Remedial Investigation Report (PhaseI), Leachate Stream Area, Drake Chemical Site, Lock Haven, Clinton County, Pennsylvania,Prepared by NUS Corporation. March 1984. pp. 300338-300550.

IRIS (Integrated Risk Information System). 1996. Computerized Database of ToxicologicalInformation for Hazardous Chemicals. Maintained by EPA. Accessed May 1996.

MRI (Midwest Research Institute). 1994. Trial Bum Plan for the Drake Chemical SuperfundSite's Mobile Hazardous Waste Incinerator. Volume I, Trial Bum Plan. Prepared for RUSTInternational, Inc., Palos Heights, IL. Submitted by MRI, Kansas City, MO. MRI ProjectNo. 3620-01. 24 October 1994.

RTI (Research Triangle Institute). 1995. Screening Level Risk Assessment for Proposed TrialBum at Drake Chemical Superfund Site. Methodology and Preliminary Draft Risk Results.Prepared for U.S. Army Corps of Engineers, Lock Haven, PA. Submitted by RTI, ResearchTriangle Park, NC. 22 December 1995.

WESTON (Roy F. Weston, Inc.). 1995. Draft, Drake Chemical Incinerator Risk Assessment.Prepared for U.S. Environmental Protection Agency, Region III, Philadelphia, PA.Submitted by Roy F. Weston, Inc., West Chester, PA, under SATA Contract No. 68S5-3002.5 December 1995.


CFR (Code of Federal Regulations). 1996. Title 40, Part 264, Subpart O.

Dellinger, B. 1996. "Estimate of Organic Mass Emission Rates from the Drake RemedialAction Incinerator." University of Dayton Research Institute.

EPA (U.S. Environmental Protection Agency). 1994. Exposure Assessment Guidance forRCRA Hazardous Waste Combustion Facilities. Office of Solid Waste and EmergencyResponse. EPA 530-R-94-021. April 1994.

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EPA (U.S. Environmental Protection Agency). 1992a. Guidance for Data Useability in RiskAssessment (Part A). Final. Office of Emergency and Remedial Response, Office of SolidWaste, Washington, DC. 9285.7-09A. PB92-963356. April 1992.

EPA (U.S. Environmental Protection Agency). 1992b. Supplemental Guidance to RAGS:Calculating the Concentration Term. Office of Solid Waste and Emergency Response.Publication 9285.7-081. May 1992.

EPA (U.S. Environmental Protection Agency). 1992c. Screening Procedures for Estimatingthe Air Impacts of Incineration at Superfund Sites. Office of Air Quality Planning andStandards. EPA ASF-23. February 1992.

EPA (U.S. Environmental Protection Agency). 1988. Final Phase III Remedial Investigation,Volume I — Narrative and Volume IV —Appendices H-l through H-4, Drake Chemical Site,Lock Haven, Clinton County, Pennsylvania. August 1988.

EPA (U.S. Environmental Protection Agency). 1985. Remedial Investigation Report (PhaseII), Drake Chemical Site, Lock Haven, Clinton County, Pennsylvania. January 1985.

Mitre (U.S. Mitre Corporation). 1983. Hazardous Waste Stream Trace Metal Concentrationsand Emissions. Prepared for U.S. Environmental Protection Agency, Office of Solid Waste.November 1983.

Montgomery Watson. 1994. Test Pit Excavation Report, Drake Chemical Superfund Site.Prepared for U.S. Army Corps of Engineers. October 1994.

PADEP (Pennsylvania Department of Environmental Protection). 1995. Air QualityEquivalency Document for Drake Superfund Site. 8 December 1995.

USAGE (U.S. Army Corps of Engineers). 1993. Specifications (for Fixed-Price ServicesContract), Drake Chemical Superfund Site, On-Site Incineration. Volume 3 of 3. AttachmentsI through VIII. Prepared by U.S. Army Corps of Engineers, Omaha District. April 1993.


EPA (U.S. Environmental Protection Agency). 1995. Draft User's Guide for the IndustrialSource Complex (ISC3) Dispersion Models (Revised). Volumes I and II.


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EPA (U.S. Environmental Protection Agency). 1986a. INPUFF 2.0 - A Multiple SourceGaussian PUFF Dispersion Algorithm, User's Guide. Research Triangle Park, NC. EPA-6-0018-86/024.

EPA (U.S. Environmental Protection Agency). 1986b. Guidelines on Air Quality Models.Supplements A, B, and C. Research Triangle Park, NC. EPA 450/2r78-027R.

Schwerde, D. and J. Palmier. 1996. Sensitivity of the ISC3 to Impact Parameters. Preprintto the 9th Joint Conference on the Applications of Air Pollution Meteorology, AmericanMeteorological Society, and Air and Waste Management Association, Atlanta, GA. January1996.

Scire, J. et al. 1995a. A User's Guide for the CALMET Meteorological Model. EarthTech,Concord, MA

Scire, J. 1995b. A User's Guide for the CALPUFF Dispersion Model. EarthTech, Concord,MA,

USAGE (U.S. Army Corps of Engineers). 1996. Personal Communication, D. Modricker.


IfcEPA (U.S. Environmental Protection Agency). 1995a. Mercury Study Report to Congress. ™1FVolume 2. Preliminary Draft. Office of Research and Development. EPA/600/P-94/002A6.

EPA (U.S. Environmental Protection Agency). 1995b. Risk Assessment for the WasteTechnologies Industries (WTI) Hazardous Waste Incinerator Facility (East Liverpool, OH).Volume V, Human Health Risk Assessment (HHRA): Evaluation of Potential Risks fromMultipathway Exposure to Emissions. Preliminary Draft. U.S. EPA Region V, Waste,Pesticides, and Toxics Division, Chicago, IL. November 1995.

EPA (U.S. Environmental Protection Agency). 1994a. Exposure Assessment Guidance forRCRA Hazardous Waste Combustion Facilities. Office. of Solid Waste and EmergencyResponse. EPA 530-R-94-021. April 1994.

EPA (U.S. Environmental Protection Agency). 1994b. Guidance for Performing ScreeningLevel Risk Analyses at Combustion Facilities Burning Hazardous Wastes. Draft. Office ofEmergency and Remedial Response, Office of Solid Waste. April, October, and December1994.

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EPA (U.S. Environmental Protection Agency). 1993. Addendum to the Methodology.forAssessing Health Risks Associated with Indirect Exposure to Combustor Emissions. ReviewDraft. Office of Research and Development, Washington, DC. EPA/600/AP-93/003.November 1993.

EPA (U.S. Environmental Protection Agency). 1990. Methodology for Assessing Health RisksAssociated with Indirect Exposure to Combustor Emissions. Interim Final. Office of Healthand Environmental Assessment, Washington, DC. EPA/600/6-90/003. January 1990.

EPA (U.S. Environmental Protection Agency). 1989. Development of Risk AssessmentMethodology for Land Application and Distribution and Marketing of Municipal Sludge.

Haan, C.T. and B.J. Barfield. 1978. Hydrolqgy and Sedimentology of Surf ace Mined Lands.

Marcinkevage, R. City Engineer, City of Lock Haven Engineering Department, PersonalCommunication, 18 April and 29 April 1996.

PADEP (Pennsylvania Department of Environmental Protection). Bureau of Dams,Waterways, and Wetlands. Database for existing dams and water supply sources in Centre,Clinton, and Lycoming Counties, Pennsylvania.

USDA (U.S. Department of Agriculture). 1966. Soil Survey, Clinton County, Pennsylvania.

USGS (U.S. Geological Survey). Stream flow data for USGS stations 01551500 and01547950; physical characteristics data for USGS stations 01548000,01547950,01545800, and01551500. USGS Lemoyne, PA District Office.


ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profile forPolycyclic Aromatic Hydrocarbons. U.S. Department of Health and Human Services, PublicHealth Sendee. October 1993.

EPA (U.S. Environmental Protection Agency). 1995a. EPA Region III Risk-BasedConcentration Table. Roy L. Smith, Ph.D., Toxicologist, U.S. EPA Region III, Philadelphia,PA. 20 October 1995.

EPA (U.S. Environmental Protection Agency). 1995b. Assessing Dermal Exposure from Soil.EPA 'Region III Technical Guidance Manual, Risk Assessment. U.S. EPA Region III,Philadelphia, PA, Office of Superfund Programs. EPA/903-K-95-003. December 1995.

EPA (U.S. Environmental Protection Agency). 1995c. Drinking Water Regulations andHealth Advisories. Office of Water, Washington, DC. May 1995.


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EPA (U.S. Environmental Protection Agency). 1995d. Risk Assessment for the WasteTechnologies Industries (WTI) Hazardous Waste Incinerator Facility (East Liverpool, OH).Volume V, Human Health Risk Assessment (HHRA): Evaluation of Potential Risks fromMultipathway Exposure to Emissions. Preliminary Draft. U.S. EPA Region V, Waste,Pesticides, and Toxics Division, Chicago, IL. November 1995.

EPA (U.S. Environmental Protection Agency). 1995e. Mercury Study Report to Congress.Volumes I and n. Office of Research and Development, Washington, DC.EPA/600/P-94/002Ab. January 1995.

EPA (U.S. Environmental Protection Agency). 1994a. Exposure Assessment Guidance forRCRA Hazardous Waste Combustion Facilities. Draft. April 1994.

EPA (U.S. Environmental Protection Agency). 1994b. Guidance for Performing ScreeningLevel Risk Analyses at Combustion Facilities Burning Hazardous Wastes. Draft. Office ofEmergency and Remedial Response, Office of Solid Waste. April, October, and December1994.

EPA (U.S. Environmental Protection Agency), 1994c. Estimating Exposure to Dioxin-LikeCompounds. Volume II, Properties, Sources, Occurrence, and Background Exposures. ReviewDraft. Office of Research and Development, Washington, DC. EPA/600/6-88/005Cb.

EPA (U.S. Environmental Protection Agency), 1994d. Health Assessment Document for2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Volume III of III.Review Draft. Office of Research and Development, Washington, DC. EPA/600/BP-92/001C. August 1994.


EPA (U.S. Environmental Protection Agency). 1992. Dermal Exposure Assessment:Principles and Applications. Interim Report. Office of Research and Development,Washington, DC. EPA/600/8-91/011B. January 1992.

EPA (U.S. Environmental Protection Agency). 199la. Human Health Evaluation Manual,Supplemental Guidance: "Standard Default Exposure Factors." Office of Solid Waste andEmergency Response. OSWER Directive 9285.6-03. 25 March 1991.

EPA (U.S. Environmental Protection Agency), 199 Ib. Human Health Evaluation Manual,Part B: "Development of Risk-Based Preliminary Remediation Goals." OSWER Directive9285.7-01B. 13 December 1991.

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EPA (U.S. Environmental Protection Agency). 1990a. Methodology for Assessing HealthRisks Associated with Indirect Exposure to Combustor Emissions. Interim Final. Office ofHealth and Environmental Assessment. Washington, DC. EPA/600/6-90/003. January1990.

EPA (U.S. Environmental Protection Agency). 1990b. Risk Assessment Guidance forSuperfund. Volume I, Human Health Evaluation Manual, Supplemental Guidance: "StandardExposure Factors." Final Draft. Office of Solid Waste and Emergency Response. OSWERDirective 9285.6-03. 4 December 1990.

EPA (U.S. Environmental Protection Agency). 1990c. Standards for Owners and Operatorsof Hazardous Waste Incinerators and Burning of Hazardous Wastes in Boilers and IndustrialFurnaces. Federal Register 55:17862-17921.

EPA (U.S. Environmental Protection Agency). 1990d. Operations and Research at the U.S.EPA Incineration Research Facility. Annual report for FY89. Risk Reduction EngineeringLaboratory, Office of Research and Development, Cincinnati, Ohio. EPA/600/9-90/012.

EPA (U.S. Environmental Protection Agency). 1989a. Risk Assessment Guidance forSuperfund. Volume I, Human Health Evaluation Manual, Part A. Interim Final.EPA/540/1-89/002. December 1989.

EPA (U.S. Environmental Protection Agency). 1989b. Exposure Factors Handbook. Officeof Health and Environmental Assessment. EPA/600/8-89/043.

Hallenbeck, W.H., S.P. Breen, and G.R. Brenniman. 1993. "Cancer Risk Assessment for theInhalation of Metals from Municipal Solid Waste Incinerators Impacting Chicago." Bull.Environ, Contam. Toxicol 51:165-170.

HSDB.(Hazardous Substances Data Bank), 1996. Peer-Reviewed Computer Database ofEnvironmental Fate, Toxicity and Hazardous Property Data for Hazardous Chemicals..Maintained by the National Library of Medicine. Washington, DC.

IRIS (Integrated Risk Information System. 1996. Computerized Database of ToxicologicalInformation for Hazardous Chemicals. Maintained by EPA. Accessed May 1996.

Lyman, W.J., W.F. Reehl, and D.H. Rosenblatt, 1982. Handbook of Chemical PropertyEstimation Methods. Environmental Behavior of Organic Compounds. McGraw-Hill BookCompany. NY.

McLachlan, M.S. 1996. "Bioaccumulation of Hydrophobic Chemicals in Agricultural FoodChains." Environ, ScL Technol. 30:252-259.

Pao, E.M., K.H. Fleming, P.M. Guenther, and S.J. Mickle. 1982. Foods Commonly Eatenby Individuals: Amounts Per Day and Per Eating Occasion. Consumer Nutrition Center,Human Nutrition Information Service. U.S. Department of Agriculture. Hyattsville, MD.


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Smith, A.H. 1987. "Infant Exposure Assessment for Mother's Milk Dioxins and Furans,Derived from Waste Incinerator Emissions." Risk Analysis 7:347.

USAGE (U.S. Army Corps of Engineers). 1996. Letter from Mr. David Modricker(USAGE, Allegheny Mountain Resident Office) to Mr. Roy Schrock (U.S. EPA Region III,Philadelphia, PA). April 1996.

USDA (U.S. Department of Agriculture). 1983. Food Intakes: Individuals in 48 States, Year1977-78. Nationwide Food Consumption Survey. 1977-78, Report No.1-1.


ACGIH (American Conference of Governmental Industrial Hygienists). 1995. 1995-1996Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents and BiologicalExposure Indices (BEIs). Cincinnati OH.

AIHA (American Industrial Hygiene Association). 1994. Emergency Response PlanningGuidelines. February 1994.

EPA (U.S. Environmental Protection Agency). 1996a. EPA Region III Risk-BasedConcentration Table. U.S. EPA Region HI, Philadelphia PA. 30 April 1996.

.»

EPA (U.S. Environmental Protection Agency). 1996b. Personal Communication (telephone)between Roy Smith, Toxicologist and Nancy Jafolla, Toxicologist, EPA Region III,Philadelphia, PA, and Robert Warwick, Toxicologist, Roy F. Weston, Inc., West Chester,PA. Subject: Derivation of provisional reference doses. 10 May 1996.

EPA (U.S. Environmental Protection Agency). 1995a. Health Effects Assessment SummaryTables (HEAST). FY 1995 Annual Office of Solid Waste and Emergency Response,Washington, DC. 9200.6-303 (95-1). EPA/540/R-95/036. PB95-921199. May 1996.

EPA (U.S. Environmental Protection Agency). 1995b. Most Current IDLHs for the WTIAccident Analysis. Memorandum from C. Bogard, EPA Region V, RCRA PermittingBranch, to C. Matthiessen, CEPPO.

EPA (U.S. Environmental Protection Agency). 1995c. Risk Assessment for the WasteTechnologies Industries (WTI) Hazardous Waste Incinerator Facility (East Liverpool, OH).Volume V, Human Health Risk Assessment (HHRA): Evaluation of Potential Risks fromMultipathway Exposure to Emissions. U.S. EPA Region V, Waste, Pesticides, and ToxicsDivision, Chicago, IL. November 1995.

EPA (U.S. Environmental Protection Agency). 1994a. Estimating Exposure to Dioxin-LikeCompounds. Volume II, Properties, Sources, Occurrence, and Background Exposures. ReviewDraft. Office of Research and Development, Washington, DC. EPA/600/6-88-005Cb.


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EPA (U.S. Environmental Protection Agency). 1994b. Health Assessment Document for2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related. Compounds. Volume III of III.Review Draft. Office of Research and Development, Washington, DC. EPA/600/BP-92/001C.

EPA (U.S. Environmental Protection Agency). 1993a. Provisional Guidance for QuantitativeRisk Assessment of Polycyclic Aromatic Hydrocarbons. Office of Research and Development,Washington, DC. EPA/600/R-93/089.

EPA (U.S. Environmental Protection Agency). 1993b. Handbook of Chemical HazardAnalysis Procedures. U.S. Federal Emergency Management Agency, Washington, DC. NTISPB93-158756.

EPA (U.S. Environmental Protection Agency). 1989a. Risk Assessment Guidance forSuperfund, Volume I: Human Health Evaluation Manual (Part A). Interim Final. Office ofSolid Waste and Emergency Response, Washington, DC. EPA/540/1-89/002.

EPA (U.S. Environmental Protection Agency). 1989b. Interim Procedures for EstimatingRisks Associated with Exposures to Mixtures of Chlorinated Dibenzo-p-Dioxins and-Dibenzofurans (CDDs and CDFs) and 1989 Update. Risk Assessment Forum. EPA/625/3-89/016.

EPA (U.S. Environmental Protection Agency). 1988. "Drinking Water Regulations:Maximum Contaminant Level Goals and National Primary Drinking Water Regulations forLead and Copper." 40 CFR Parts 141 and 142. Federal Register 53(160):31516.

IARC (International Agency for Research on Cancer). 1987. IARC Monographs on theEvaluation of Carcinogenic Risks to Humans. Supplement 7. Lyon, France.

IRIS (Integrated Risk Information System). 1996. Computerized Database of ToxicologicalInformation for Hazardous Chemicals. Accessed May 1996.

NIOSH (National Institute of Occupational Safety and Health). 1994. Pocket Guide toChemical Hazards. U.S. Department of Health and Human Services. Cincinnati, OH.

NTP (National Toxicology Program). 1994. Seventh Annual Report on Carcinogens, Summary.U.S. Department of Health and Human Services. Research Triangle Park, NC.

Perera, F., T. Brennan, and J.R. Fouts. 1989. "Comment on the Significance of PositiveCarcinogenicity Studies Using Gavage as the Route of Exposure." Environ. Health Persp.79:315-321.


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ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profilefor Polycyclic Aromatic Hydrocarbons. U.S. Department of Health and Human Services,Public Health Service.

EPA (U.S. Environmental Protection Agency). 1995a. Health Effects Assessment SummaryTables (HEAST). FY 1995 Annual. Office of Solid Waste and Emergency Response,Washington, DC. 9200.6-303 (95-1). EPA/540/R-95/036. PB95-921199. May 1995.

EPA (U.S. Environmental Protection Agency). 1995b. Drinking Water Regulations andHealth Advisories. Office of Water, Washington, DC. May 1995.

EPA (U.S. Environmental Protection Agency). 1994a. Health Assessment Document for2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. Volume III of III.Review Draft. Office of Research and Development, Washington, DC. EPA/600/BP-92/001C. August 1994.

EPA (U.S. Environmental Protection Agency). 1994b. Revised Interim Soil Lead Guidancefor CERCLA Sites and RCRA Corrective Action Facilities. OSWER Directive 9355.4-12.1994.

EPA (U.S. Environmental Protection Agency). 1991a. Role of the Baseline Risk Assessmentin Superfund Remedy Selection Decisions. Memorandum from Don R. Clay, AssistantAdministrator.

EPA (U.S. Environmental Protection Agency). 199Ib. Subchapter C - Air Programs. Part50 - National Primary and Secondary Ambient Air Quality Standards. Code of FederalRegulations. 50:693-697. Revised 1 July 1991.

EPA (U.S. Environmental Protection Agency). 1989. Risk Assessment Guidance forSuperfund. Volume I, Human Health Evaluation Manual, Part A. Interim Final.EPA/540/1-89/002. December 1989.

EPA (U.S. Environmental Protection Agency). 1986. Guidelines for the Health RiskAssessment of Chemical Mixtures. 51 FR 34014. 24 September 1986.

IRIS (Integrated Risk Information System). 1996. Computerized Database of ToxicologicalInformation for Hazardous Chemicals. Maintained by EPA. Accessed May 1996.

Travis, C.C. and H.A. Hattemer-Frey. 1988. "Determining an Acceptable Level of Risk."Environmental Science and Technology. Volume 22, No. 8, pp. 873-876.


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ATSDR (Agency for Toxic Substances and Disease Registry). 1993. Toxicological Profilefor Polycyclic Aromatic Hydrocarbons. U.S. Department of Health and Human Services,Public Health Service.

ATSDR (Agency for Toxic Substances and Disease Registry). 1992. Toxicological Profilefor Manganese and Compounds.

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section 6 toxicity assessment

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