TECHNICAL REPORT DATA (fuut rt»d Instntcttora on the rtvmt before completing) REPORT NO. EPA/600/8-88/011 3. RECIPIENT'S ACCESSION HO. PB88-17951Q . TITLE AND SUBTITLE Health Effects Assessment for Acenaphthylene B. REPORT DATE B. PERFORMING ORGANIZATION CODE . AUTHOR(S) B. PERFORMING ORGANIZATION REPORT NO ft. PERFORMING ORGANIZATION NAME AND ADDRESS 10. PROGRAM ELEMENT NO. 11. CONTRACT/GRANT NO. TZ. SPONSORING AGENCY NAME AND ADDRESS 13. TYPE OF REPORT AND PERIOD COVERED 'Environmental Criteria and Assessment Office Office of Research and Development li.S. Environmental Protection Agency Cincinnati. OH 45268 __ 14. SPONSORING AGENCY CODE EPA/600/22 SUPPLEMENTARY NOTES This report summarizes and evaluates information relevant to a preliminary interim assessment of adverse health effects associated with specific chemicals or compounds. The Office of Emergency and Remedial Response (Superfund) uses these documents in preparing cost-benefit analyses under Executive Order 32991 for decision-making under CERCLA. All estimates of acceptable intakes and carcinogenic potency presented in this document should be considered as preliminary and reflect limited resources allocated to this project. The intent in these assessments is to suggest acceptable exposure levels whenever sufficient data are available. The interim values presented reflect the relative degree of hazard associated with exposure or risk to the chemical(s) addressed. Whenever possible, two categories of values have been estimated for systemic toxicants (toxicants for which cancer is not the endpoint of concern). The first, RfD$ or subchronic reference dose, is an estimate of an exposure level that would not be expected to cause adverse effects when exposure occurs during a limited time interval. The RfD is an estimate of an exposure level that would not be expected to cause adverse effects when exposure occurs for a significant portion of the lifespan. For compounds for which there is sufficient evidence of careinbgenicity, qi*s have been computed, if appropriate, based on oral and inhalation data if available. 17. KEY WORDS AND DOCUMENT ANALYSIS DESCRIPTORS b.IDENTIFIERS/OPEN ENDED TERMS c. COSATi Field/Group U.S. BivlroTiineirtal Protection Agency E-^Ti--n 5, Library (5PL-]6) £vO S. Dearborn ?t:-oot, lioois 1670 CMcago, IL 60604 1BL DISTRIBUTION STATEMENT 19. SECURITY CLASS (This Rtport) 21. NO. OF PAGES Public 20. SECURITY CLASS Unclassified 22. PRICE EPA ?«• 222CM (R««. 4-77) PREVIOUS BOITIOM i» OMOLCTK ------- ------- EPA/600/8-88/011 May, 1987 HEALTH EFFECTS ASSESSMENT FOR ACENAPHTHYLENE ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT OFFICE OF RESEARCH AND DEVELOPMENT U.S. ENVIRONMENTAL PROTECTION AGENCY CINCINNATI. OH 45268 U.S. Environmental Protection Ar Region 5, Library "' 2'30 S. Dearborn ------- DISCLAIMER This document has been reviewed In accordance with the U S Environmental Protection Agency's peer and administrative review policies and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. 1V ------- PREFACE 4 This report summarizes and evaluates Information relevant to a prelimi- nary Interim assessment of adverse health effects associated with acenaph- thylene. All estimates of acceptable Intakes and carcinogenic potency presented In this document should be considered as preliminary and reflect limited resources allocated to this project. Pertinent toxlcologlc and environmental data were located through on-line literature searches of the TOXLINE, CANCERLINE and the CHEMFATE/DATALOG data bases. The basic literature searched supporting this document Is current up to Hay, 1986. Secondary sources of Information have also been relied upon In the prepara- tion of this report and represent large-scale health assessment efforts that entail extensive peer and Agency review. The following Office of Health and Environmental Assessment (OHEA) sources have been extensively utilized: U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Polynuclear Aromatic Hydrocarbons. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Water Regula- tions and Standards, Washington, DC. EPA 440/5-80-069. NTIS PB 81-117806. U.S. EPA. 1980b. Hazard Profile for Acenaphthylene. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Waste, Washington, DC. U.S. EPA. 1983. Reportable Quantity Document for Acenaphthylene. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington, DC. The Intent 1n these assessments 1s to suggest acceptable exposure levels whenever sufficient data were available. Values were not derived or larger uncertainty factors were employed when the variable data were limited 1n scope tending to generate conservative (I.e., protective) estimates. Nevertheless, the Interim values presented reflect the relative degree of hazard associated with exposure or risk to the chemlcal(s) addressed. Whenever possible, two categories of values have been estimated for systemic toxicants (toxicants for which cancer Is not the endpolnt of concern). The first, RfD$ (formerly AIS) or subchronlc reference dose. Is an estimate of an exposure level that would not be expected to cause adverse effects when exposure occurs during a limited time Interval (I.e., for an Interval that does not constitute a significant portion of the Hfespan). This type of exposure estimate has not been extensively used, or rigorously defined, as previous risk assessment efforts have been primarily directed towards exposures from toxicants 1n ambient air or water where lifetime exposure 1s assumed. Animal data used for RFD§ estimates generally Include exposures with durations of 30-90 days. Subchronlc human data are rarely available. Reported exposures are usually from chronic occupational exposure situations or from reports of acute accidental exposure. These values are developed for both Inhalation (RfD§j) and oral (RfD$o) exposures. 111 ------- t The RfD (formerly AIC) Is similar 1n concept and addresses chronic exposure. It 1s an estimate of an exposure level that would not be expected to cause adverse effects when exposure occurs for a significant portion of the Ufespan [see U.S. EPA (1980a) for a discussion of this concept]. The RfD 1s route-specific and estimates acceptable exposure for either oral (RfOg) or Inhalation (RfDj) with the Implicit assumption that exposure by other routes Is Insignificant. Composite scores (CSs) for noncardnogens have also been calculated where data permitted. These values are used for ranking reportable quan- tities and the methodology for their development Is explained 1n U.S. EPA (1983). For compounds for which there Is sufficient evidence of carclnogenldty RfD$ and RfO values are not derived. For a discussion of risk assessment methodology for carcinogens refer to U.S. EPA (1980a). Since cancer 1s a process that Is not characterized by a threshold, any exposure contributes an Increment of risk. For carcinogens, q-|*s have been computed, 1f appro- priate, based on oral and Inhalation data 1f available. 1v ------- ABSTRACT Data sufficient for risk assessment were not available for acenaph- thylene; therefore, no risk assessment values were derived. A Russian Inhalation study where rats were exposed to acenaphthylene dust suggests a carcinogenic role for this compound (Rotenberg and Mashblts, 1965). The lungs appear to be a target organ for acenaphthylene by either Inhalation (Rotenberg and Mashblts, 1965; Reshetluk et al., 1970) or oral (Rotenberg and Mashblts, 1965) exposure. Continued mutagenlclty testing and short-term animal cardnogenlclty assays to clarify the carcinogenic role of acenaph- thylene are recommended as a first step In the testing of acenaphthylene. ------- ACKNOWLEDGEMENTS The Initial draft of this report was prepared by Syracuse Research Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria and Assessment Office, Cincinnati, OH. Or. Christopher DeRosa and Karen Blackburn were the Technical Project Monitors and John Helms (Office of Toxic Substances) was the Project Officer. The final documents In this series were prepared for the Office of Emergency and Remedial Response, Washington, DC. Scientists from the following U.S. EPA offices provided review comments for this document series: Environmental Criteria and Assessment Office, Cincinnati, OH Carcinogen Assessment Group Office of A1r Quality Planning and Standards Office of Solid Waste Office of Toxic Substances Office of Drinking Water Editorial review for the document series was provided by the following: Judith Olsen and Erma Durden Environmental Criteria and Assessment Office Cincinnati, OH Technical support services for the document series was provided by the following: Bette Zwayer, Jacky Bohanon and Kim Davidson Environmental Criteria and Assessment Office Cincinnati, OH vl ------- TABLE OF CONTENTS Page 1. 2. 3. ENVIRONMENTAL CHEMISTRY AND FATE ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . . . TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 3.1. SUBCHRONIC 3.1.1. Oral 3.1.2. Inhalation 3.2. CHRONIC 3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS 3.4. TOXICANT INTERACTIONS . . 1 , , 4 . . 5 . . 5 . . 5 5 . . 6 . . 7 . . 7 5 ft 7. 4.1. HUMAN DATA , 4.2. BIOASSAYS , 4.2.1. Oral , 4.2.2. Inhalation , 4.3. OTHER RELEVANT DATA 4.4. WEIGHT OF EVIDENCE REGULATORY STANDARDS AND CRITERIA RECOMMENDATIONS REFERENCES 8 8 8 8 8 8 10 11 12 V11 ------- LIST OF ABBREVIATIONS CAS Chemical Abstract Service CS Composite score Kow Octanol/water partition coefficient LD5Q Dose lethal to 50X of recipients MED Minimum effective dose NOEL No-observed-effect level PAH Polycycllc aromatic hydrocarbon ppm Parts per million RV,j Dose-rating value RVe Effect-rating value ------- 1. ENVIRONMENTAL CHEMISTRY AND FATE Selected physical and chemical properties and environmental fate of acenaphthylene are presented In Table 1-1. Acenaphthylene Is widely distributed 1n the environment. In air. acenaphthylene will be present partly In the vapor phase and partly In the sorbed state onto aerosol particles. Acenaphthylene adsorbed to partlcu- lates could potentially travel great distances before ultimately being removed by rainfall or dry deposition (NRC, 1983; Pankow et a"!., 1984). Acenaphthylene In the vapor phase Is expected to undergo direct photolysis or oxidation by reaction with hydroxyl radicals or ozone (estimated oxida- tion half-life -1 hour) (HSDB, 1986; NRC, 1983; U.S. EPA, 1986a). In water, acenaphthylene will be present partly 1n solution and partly as sorbed onto suspended particles and sediments. The dissolved portion may undergo rapid hydrolysis and significant blodegradatlon (Callahan et al., 1979). The adsorbed portion may persist for years In sediments (Bjoerseth et al., 1979). Based on the relatively high log K value, acenaphthylene 1s expected to strongly adsorb to soil, thus persisting In the upper few centimeters. In soil. It may undergo blodegradatlon. Human exposure data specific for acenaphthylene could not be located 1n the available literature. U.S. EPA (1980a), however, reviewed monitoring studies In which total PAH content of groundwater varied from 0.003-0.04 jig/l and total PAH content of surface water ranged from 0.24-2.5 vg/i. In finished drinking water from 15 U.S. cities, total PAH content ranged from 0.3-138.5 ng/l. with samples from only two cities >10 ng/t (Basu and Saxena, 1977; 1978). The other major sources of oral exposure of humans to PAH Is through food. Borneff (1977) estimated this contribution 0082H -1- 12/03/86 ------- TABLE 1-1 Selected Physical and Chemical Properties and Environmental Fate of Acenaphthylene CAS number: Chemical class: Molecular weight: Vapor pressure: Mater solubility: Log octanol/water partition coefficient: Bloconcentratlon factor: Half-lives In Air: Hater: Soil: 208-96-8 polycycllc aromatic hydrocarbon 152.20 10~8 to 10~2 mm Hg at 20°C (estimated) 3.93 mg/i at 25°C (estimated) 4.07 (estimated) 18.0 green mussels (Perna verldls) NA NA NA Callahan et al., 1979 Callahan et al., 1979 Callahan et al., 1979 Hungspreugs et al., 1984 NA = Not available 0082h -2- 12/03/86 ------- at ~3-4 mg total PAH/year. These data do not Indicate what proportion of total PAH content of water and food 1s acenaphthylene, so 1t 1s not possible to estimate human Intakes of acenaphthylene alone. The data reviewed and presented by U.S. EPA (1980a) Imply that acenaphthylene may be a small pro- portion of the total PAH content of water and food, since this compound 1s not listed by name In tables that present levels of the more abundant PAHs. Overall, human exposure to acenaphthylene may be expected to occur by both oral and Inhalation routes and H Is Impossible to predict which route may be the more Important. 0082h -3- 09/03/86 ------- 2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS Pertinent data regarding the absorption of acenaphthylene following oral or Inhalation exposure could not be located In the available literature. 0082h -4- 09/03/86 ------- 3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 3.1. SUBCHRONIC 3.1.1. Oral. In a Polish study reported 1n an abstract, Knobloch et al. (1969) administered acenaphthylene orally to rats at a dose of 0.6 g/kg for 40 days. Treatment-related effects observed were considerable body weight loss, changes In renal function, changes In the peripheral blood pattern and Increased serum amlnotransferase activities. In a Russian study (Rotenberg and Mashblts, 1965), acenaphthylene In oil was administered orally to white mice at a dose 1/10 the LD5Q [LOrQ = 1760 (range of 2800 to 1100) mg/kg] every other day for 2 months. Treated mice showed a significant lag In weight gain as compared with controls. Hlstopathologlcal examination of organs showed signs of stasis 1n the paren- chymatous organs and albuminoid degeneration of the liver. The most severe changes were observed In the lungs, which showed hemorrhage with destruction of the Interalveolar septa and focal bronchial pneumonia. Purulent foci were observed In Isolated cases, and bronchogenlc lung cancer was diagnosed 1n one mouse. Further details of this study were not provided. 3.1.2. Inhalation. In a Russian study (Rotenberg and Hashblts, 1965), acenaphthylene was administered to white rats Intratracheally In a sunflower oil solution or by blowing acenaphthylene powder Into the trachea. The dosing regimen used was not provided. The pulmonary tracts of animals sacrificed 1 month after the experiment began showed signs of tracheobron- chH1s and hyperemla, edema and necrosis of the epithelium In the trachea and bronchi with the formation of ulcers. No further details of this study were available. 0082h -5- 09/03/86 ------- In an additional study reported by Rotenberg and Mashblts (1965). white rats were exposed to acenaphthylene dust at 0.5-1.25 mg/rn3 for 4 hours/day for 4 months. After 3 weeks of exposure, a delay In weight gain and a tendency toward decreased blood pressure were observed. Hlstopathologlcal examination revealed various degrees of malignancy In the lungs of almost all treated rats. Focal bronchitis and perlbronchUls with bronchlollzatlon of the alveolar and metaplasia of the bronchial epithelium were observed 1n the mildest cases. Advanced cases showed desquamatlon of the bronchial and alveolar epithelium, paplllar growths In the epithelium and. In three rats. Isolated regions of carcinoma 1n the form of strands of epithelial cells. Further details of this study were not provided. In a Russian study by Reshetluk et al. (1970), -100 white male rats were exposed to vapors of acenaphthylene at a concentration of 18±2.5 mg/m3, 4 hours/day, 6 exposures/week for 5 months. In exposed rats, reflexes of the upper airways were altered and an Increase 1n the concentration of nucleic acids In the liver was observed. Hlstopathologlcal examination of the lungs revealed aspeclflc pneumonia as the major pathology of Inhalation exposure to acenaphthylene. Changes observed In the lungs Included desquamatlon of the cells 1n the alveolar epithelium and focal bronchitis accompanied by hyperplasla and metaplasia of the bronchial epithelium. No signs of malig- nant growth were observed In this study. No further details of this study were available. 3.2. CHRONIC Pertinent data regarding the toxic effects of acenaphthylene following chronic oral or Inhalation exposure could not be located In the available literature. 0082H -6- 12/03/86 ------- " 313. TERATOGEHICITY AND OTHER REPRODUCTIVE EFFECTS Pertinent data regarding teratogenlc and other reproductive effects following oral or Inhalation exposure could not be located In the available literature. 3.4. TOXICANT INTERACTIONS Without providing details, Reshetluk et al. (1970) stated that Inhala- tion of naphthalene caused an Increase In the sensitivity of rats to a single Inhalation exposure of acenaphthylene at 7 mg/m3. Observations recorded Include an Increase In oxygen "composition" (as written by translator — probably should read "consumption") (60%), an Increase In body (0.6*0.2°) and skin temperature (0.4+0.2°), an Increase In blood peroxldase activity (38%), and decreases 1n blood sugar concentration (10%) and ascorbic acid In the lungs (33%). 0082H -7- 12/03/86 ------- 4. CARCINOGENIC1TY 4.1. HUMAN DATA Pertinent data regarding the carcinogenic potential of acenaphthylene In humans following oral or Inhalation exposure could not be located In the available literature. 4.2. BIOASSAYS 4.2.1. Oral. Pertinent data regarding the oncogenlcHy of acenaphthylene In orally exposed animals could not be located 1n the available literature. 4.2.2. Inhalation. Rotenberg and Mashblts (1965) reported "various degrees of malignancy11 In the lungs of almost all of an unspecified number of rats exposed to acenaphthylene dust at 0.5-1.25 mg/m3 for 4 hours/day for 4 months. Further details were not provided. In another Russian study with male white rats, hlstopathologlcal lesions Including hyperplasla and metaplasia of the bronchial epithelium, but no signs of malignancy, were reported following Inhalation of acenaphthylene vapors at 18 mg/m3, 4 hours/day, 6 days/week for 5 months (Reshetluk et a!., 1970). 4.3. OTHER RELEVANT DATA Acenaphthylene has tested negative for reverse mutations In Salmonella typhlmuMum strains TA1537 and TA1538 with S-9 metabolic activation (Gatehouse, 1980) and 1n strains TA98 and TA100 with and without S-9 from 3-methylcholantrene Induced rats (Florin et al., 1980). Acenaphthylene was mutagenlc In S. typhlmurlum strain TM677 with S-9 metabolic activation (Kaden et al.. 1979). 4.4. WEIGHT OF EVIDENCE Acenaphthylene has not been evaluated for Mr> carclnogenlclty In humans and has not been adequately studied for Us carcinogenic activity 1n 0082H -8- 01/20/87 ------- animals; therefore, H can be placed In IARC Group 3 and In EPA Group 0, not classified, according to the CAG classification scheme (U.S. EPA, 1986b). Given Us structural realtlonshlp to known carcinogenic PAHs, however, prudent public health policy would dictate minimizing exposure until more Is known about the health hazards. 0082h -9- 01/20/87 ------- 5. REGULATORY STANDARDS AND CRITERIA No standards or criteria are available for acenaphthylene alone. The U.S. EPA (1980a) derived ambient water quality criteria for PAH based upon the excess cancer risk associated with benzo(a)pyrene, a known animal carcinogen. For excess cancer risks of 10-s, 10-« and 10-7, these criteria are 28.0, 2.8 and 0.28 ng/i, respectively, for consumption of 6.5 g of aquatic organism and 2 I of water/day. Based on consumption of aquatic organisms alone, these criteria are 311.0, 31.1 and 3.11 ng/i, respectively. 0082h -10- 01/20/87 ------- 6. RECOMMENDATIONS Because of the lack of data for the carclnogenlcHy and threshold tox1c1ty of acenaphthylene, risk assessment values cannot be derived. Acenaphthylene Is a PAH, a class of chemicals that Includes known carcinogens. In a Russian study, malignancies 1n the lungs of rats were associated with Inhalation exposure to acenaphthylene dusts (Rotenberg and MashbHs, 1965). CarclnogenlcHy testing of acenaphthylene should be a priority. MutagenlcHy studies of acenaphthylene have been negative In S. typhlmurlum strains TA1537, TA1538, TA98 and TA100 (Gatehouse, 1980; Florin et al., 1980), but positive In strain TM677 (Kaden et al., 1978). If adequate testing Indicates that acenaphthylene Is not carcinogenic, effort should be made to determine thresholds for noncardnogenlc toxldty. Exposure data specifically for acenaphthylene could not be located, but assuming exposure similar to other PAHs, both oral and Inhalation routes of exposure may be of concern. From the Russian studies (Rohenberg and MashbHs, 1965; Reshetluk et al., 1970), the lungs appear to be the target organ; additional studies may define this further. Continued mutagenldty testing, particularly In eukaryotlc systems, and short-term animal assays may be useful to qualitatively estimate the oncogenldty of this compound. 0082h -11- 01/20/87 ------- £8/02/10 -21- M2800 '•8CSIV1 '9CI-12L :(2)8Z. ' iESLVl ;suip6p sauau.;i|dpua3p pasn^-6utJ g't jo •$ "0861 'Q 'asnoqajpg sauip aq; 6u^sn /^;pius6e;nuj JQJ siuan^nsuoo a^oois oooeqo; 6uvuaaj3$ '0861 'Itazuj '^'3 pue LLPAJOQ -^ *6jaq;ny n '*i ' Vd3 'II ' '6/.6L * I •00 ' 621 i 4Vd3 'S'H (P0861 4Vd3 *S' jo 39Vd QNV 3WniOA *C 'jjaujog Xq APMJON *M ' jo 'UOJIAU3 tPjoj. -ps '^Mdej6o;euiojij3 sp6 A"jpi[idpD ssp|.6 UIQJJ stassnuj pup s;uaiuvpas ui suoqjpoojpXq T PUP uaz;nu>| -^ 4-v ' -saDjnos suoqjr.oojpKy (P0861 'Vd3 *S'fl uv pup ja;e« Bu^uijp *s°n 'QLBl 'Puaxps *C PUP 'X'a 'nspg (P086L 'Vd3 *S*n ui pauD) 'HO ' PUP tf-6662-i-V3 'ON *Q'd Vd3 pup APJ jo '1M3H *Vd3 "S'n '8-St22-8-VD LLBl 'Puaxe$ •[• pup ~ycQ 'nspg 'L ------- HSOB (Hazardous Substance Data Bank). 1986. No. 2661. On-Llne. Hungspreugs, M., S. SUplpat, C. Tonapong, R.F. Lee, H.L. Wlndom and K.R. Tenore. 1984. Heavy metals and polycycllc hydrocarbon compounds In benthlc • I* ------- U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Polynuclear Aromatic Hydrocarbons. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Water Regulations and Standards, Washington, DC. EPA ------- HSDB (Hazardous Substance Data Bank). 1986. No. 2661. On-Une. Hungspreugs, M., S. Sllplpat, C. Tonapong, R.F. Lee, H.L. Wlndom and K.R. Tenore. 1984. Heavy metals and polycycllc hydrocarbon compounds In benthlc organisms of the upper gulf of Thailand. Marine Poll. Bull. 15(6): 213-218. Kaden, O.A., R.A. HHes and W.G. ThUly. 1979. HutagenlcHy of soot and associated polycycllc aromatic hydrocarbons to Salmonella typhlmurlum. Cancer Res. 39(10): 4152-1459. Knobloch, K., et al. 1969. Acute and subacute toxldty of acenaphthene and acenaphthylene. Med. Pracy. 20: 210. (Cited In U.S. EPA, 1983) NRC (National Research Council). 1983. Polycycllc aromatic hydrocarbons. Evaluation of sources and effects. Natl. Acad. Press, Washington, DC. p. 3-7. Pankow, J.F., L.H. Isabella and W.E. Asher. 1984. Trace organic compounds 1n rain. I. Sampler design and analysis by adsorption/thermal desorptlon (ATD). Environ. Sc1. Techno!. 18: 310-318. Reshetluk, A.L., E.I. Talaklna and P.A. En'lakova. 1970. Toxlcologlc assessment of cenaphthene and acenaphthylene. Gig. Tr. Prof. Zabol. 14(6): 46-47. Rotenberg, lu.S. and P.O. MashbHs. 1965. Toxlcologlc aspects of acenaph- thylene. G1g. Tr. Prof. Zabol. 9(9): 53-54. 0082h -13- 01/20/87 V ? feviromental ------- U.S. EPA. 1980a. Ambient Water Quality Criteria Document for Polynuclear Aromatic Hydrocarbons. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Water Regulations and Standards, Washington, DC. EPA 440/5-80-069. NTIS PB 81-117806. U.S. EPA. 1980b. Hazard Profile for Acenaphthylene. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Solid Haste, Washington, DC. U.S. EPA. 1983. Reportable Quantity Document for Acenaphthylene. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Emergency and Remedial Response, Washington, DC. U.S. EPA. 1986a. Graphical Estimations Modeling System (GEMS). Fate of Atmospheric Pollutants (PAP) Data Base. U.S. EPA, Office of Toxic Sub- stances. Washington, DC. On-Hne. U.S. EPA. 1986b. Guidelines for Carcinogenic Risk Assessment. Federal Register. 51(185): 33992-34003. 0082h -14- 02/09/87 ------- |