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0445

Pyrene; CASRN 129-00-0

Human health assessment information on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data, as outlined in the IRIS assessment development process. Sections I (Health Hazard Assessments for Noncarcinogenic Effects) and II (Carcinogenicity Assessment for Lifetime Exposure) present the conclusions that were reached during the assessment development process. Supporting information and explanations of the methods used to derive the values given in IRIS are provided in the guidance documents located on the IRIS website.

STATUS OF DATA FOR Pyrene

File First On-Line 09/01/1990

Category (section)
Status
Last Revised
Oral RfD Assessment (I.A.) on-line 07/01/1993
Inhalation RfC Assessment (I.B.) no data 09/01/1994
Carcinogenicity Assessment (II.) on-line 01/01/1991

_I.  Chronic Health Hazard Assessments for Noncarcinogenic Effects

_I.A. Reference Dose for Chronic Oral Exposure (RfD)

Substance Name — Pyrene
CASRN — 129-00-0
Last Revised — 07/01/1993

The oral Reference Dose (RfD) is based on the assumption that thresholds exist for certain toxic effects such as cellular necrosis. It is expressed in units of mg/kg-day. In general, the RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. Please refer to the Background Document for an elaboration of these concepts. RfDs can also be derived for the noncarcinogenic health effects of substances that are also carcinogens. Therefore, it is essential to refer to other sources of information concerning the carcinogenicity of this substance. If the U.S. EPA has evaluated this substance for potential human carcinogenicity, a summary of that evaluation will be contained in Section II of this file.

__I.A.1. Oral RfD Summary

Critical Effect
Experimental Doses*
UF
MF
RfD

Kidney effects (renal
tubular pathology,
decreased kidney
weights)

Mouse Subchronic
Oral Bioassay

U.S. EPA, 1989

NOAEL: 75 mg/kg/day

LOAEL: 125 mg/kg/day

 
3000
1
3E-2 mg/kg/day  

*Conversion Factors: None

__I.A.2. Principal and Supporting Studies (Oral RfD)

U.S. EPA. 1989. Mouse Oral Subchronic Toxicity of Pyrene. Study conducted by Toxicity Research Laboratories, Muskegon, MI for the Office of Solid Waste, Washington, DC.

Male and female CD-1 mice (20/sex/group) were gavaged with 0, 75, 125, or 250 mg/kg/day pyrene in corn oil for 13 weeks. The toxicological parameters examined in this study included body weight changes, food consumption, mortality, clinical pathological evaluations of major organs and tissues, and hematology and serum chemistry. Nephropathy, characterized by the presence of multiple foci of renal tubular regeneration, often accompanied by interstitial lymphocytic infiltrates and/or foci of interstitial fibrosis, was present in 4, 1, 1, and 9 male mice in the control, low-, medium-, and high-dose groups, respectively. Similar lesions were seen in 2, 3, 7, and 10 female mice in the 0, 75, 125, and 250 mg/kg treatment groups. The kidney lesions were described as minimal or mild in all dose groups. Relative and absolute kidney weights were reduced in the two higher dosage groups. Based on the results of this study, the low dose (75 mg/kg/day) was considered the NOAEL and 125 mg/kg/day the LOAEL for nephropathy and decreased kidney weights.

__I.A.3. Uncertainty and Modifying Factors (Oral RfD)

UF — An uncertainty factor of 3000 reflects 10 each for intra- and interspecies variability, 10 for the use of a subchronic study for chronic RfD derivation, and an additional 3 to account for the lack of both toxicity studies in a second species and developmental/reproductive studies.

MF — None

__I.A.4. Additional Studies/Comments (Oral RfD)

White and White (1939) fed six male rats (unspecified strain) a diet containing 2000 mg pyrene/kg for 40 days. The average reported food intake for two animals was 6.1 g/day, and the average body weight for these two animals was 94.3 g. A decrease in body weight gain was observed in two animals. The authors stated that this body weight gain was representative of the whole group; although there was no change in food intake. White and White (1939) also observed enlarged livers and increased hepatic lipid content in animals treated with pyrene, benzpyrene or methylcholanthrene in the diet; however, incidence data were not reported and it is unclear whether this effect occurred in the pyrene treated rats. Interpretation of this study is further complicated by the lack of experimental controls and statistical analysis, small sample size, and incomplete reporting of histopathology results.

__I.A.5. Confidence in the Oral RfD

Study — Medium
Database — Low
RfD — Low

Confidence in the principal study is medium, as it was a well-designed experiment that examined a variety of toxicological endpoints and identified both a NOAEL and LOAEL for the critical effect. Confidence in the database is low, due to the lack of supporting subchronic, chronic, and developmental/reproductive studies. Accordingly, confidence in the RfD is low.

__I.A.6. EPA Documentation and Review of the Oral RfD

Source Document — This assessment is not presented in any existing U.S. EPA document.

Other EPA Documentation — U.S. EPA, 1989

Agency Work Group Review — 11/15/1989

Verification Date — 11/15/1989

__I.A.7. EPA Contacts (Oral RfD)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC)

Substance Name — Pyrene
CASRN — 129-00-0

Not available at this time.

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_II.  Carcinogenicity Assessment for Lifetime Exposure

Substance Name — Pyrene
CASRN — 129-00-0
Last Revised — 01/01/1991

Section II provides information on three aspects of the carcinogenic assessment for the substance in question; the weight-of-evidence judgment of the likelihood that the substance is a human carcinogen, and quantitative estimates of risk from oral exposure and from inhalation exposure. The quantitative risk estimates are presented in three ways. The slope factor is the result of application of a low-dose extrapolation procedure and is presented as the risk per (mg/kg)/day. The unit risk is the quantitative estimate in terms of either risk per ug/L drinking water or risk per ug/cu.m air breathed. The third form in which risk is presented is a drinking water or air concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1 in 1,000,000. The rationale and methods used to develop the carcinogenicity information in IRIS are described in The Risk Assessment Guidelines of 1986 (EPA/600/8-87/045) and in the IRIS Background Document. IRIS summaries developed since the publication of EPA's more recent Proposed Guidelines for Carcinogen Risk Assessment also utilize those Guidelines where indicated (Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to Section I of this IRIS file for information on long-term toxic effects other than carcinogenicity.

_II.A. Evidence for Human Carcinogenicity

__II.A.1. Weight-of-Evidence Characterization

Classification — D, not classifiable as to human carcinogenicity

Basis — Based on no human data and inadequate data from animal bioassays.

__II.A.2. Human Carcinogenicity Data

None.

__II.A.3. Animal Carcinogenicity Data

Inadequate. Groups of 14-29 newborn male and 18-49 newborn female CD-1 mice on 1, 8, and 15 days of age received intraperitoneal injections of pyrene (purity unknown) in dimethyl sulfoxide (DMSO) (total dose = 40, 141 or 466 ug/mouse), or DMSO alone (Wislocki et al., 1986). Tumors were evaluated in animals that died spontaneously after weaning and in all remaining animals at 1 year after exposure. The mid-dose group was initiated 10 weeks after the other groups and had a separate vehicle control. The survival rate in the high-dose groups (male and female) was 25 to 35%; most of the mice died between the last injection and weaning. This high mortality was not observed in the control, low- or mid-dose groups (the survival rates were not stated). A statistically significant increase in the incidence of liver carcinomas occurred in the mid-dose males (3/25) relative to their vehicle control group (0/45), but not in the high-dose males (1/14) or low-dose males (0/29) or in female mice, when compared with their respective controls. The incidences of total liver tumors (adenomas and carcinomas), lung tumors or malignant lymphomas were not statistically significantly elevated in treated animals. The results of this 1-year experiment were not considered to be positive because of the overall lack of tumorigenic response in the short-term.

Mouse skin-painting assays of pyrene as a complete skin carcinogen or as an initiator of carcinogenicity were either not positive or inconclusive (Badger et al., 1940; Horton and Christian, 1974; Van Duuren and Goldschmidt, 1976; Salaman and Roe, 1956; Scribner, 1973).

A subcutaneous pyrene injection did not produce tumors in Jackson A mice; the mice were observed for 18 months after injection (Shear and Leiter, 1941).

__II.A.4. Supporting Data for Carcinogenicity

In DNA damage assays in Escherichia coli and Bacillus subtilis pyrene was not mutagenic (Ashby and Kilbey, 1981). In bacterial gene mutation tests both positive (Kinae et al., 1981; Bridges et al., 1981; Matijasevic and Zeiger, 1985; Sakai et al., 1985; Kaden et al., 1979; Bos et al., 1988) and negative (McCann et al., 1975; LaVoie et al., 1979; Ho et al., 1981; Bos et al., 1988) results have been reported. The consensus conclusion on the international collaborative study (which involved 20 bacterial test sets) was that protocol or evaluation criteria were critical factors in individual test verdicts. Pyrene induced increased incidence of mitotic gene conversion but not other genetic endpoints in yeast (de Serres and Hoffman, 1981). Pyrene did not induce an increase in sex-linked recessive lethals in Drosophila (Valencia and Houtchens, 1981).

Mixed results have also been observed in mammalian assays in vitro, again with protocol and evaluation criteria being a factor in at least some of the cases. In the collaborative study Evans and Mitchell (1981) concluded pyrene was positive for SCE induction in CHO cells when all concentrations were different from controls, but no apparent increase when the concentration was increased 10-fold. In the same volume, two other laboratories reported pyrene negative both for SCE and for chromosome aberrations in CHO cells (Brookes and Preston, 1981). Tong et al. (1981) also reported that pyrene did not induce SCE in a rat liver epithelial cell system. Jotz and Mitchell (1981) reported pyrene was positive in the L5178Y mouse lymphoma gene mutation assay.

Pyrene did not induce chromosome aberrations (as detected by micronuclei) or SCE in bone marrow of several mouse strains receiving i.p. injections of pyrene (Purchase and Ray, 1981). Results of mammalian cell transformation assays in a variety of cell types have not been positive (DiPaolo et al., 1969; Pienta et al., 1977; Casto, 1979; Chen and Heidelberger, 1969; DiPaolo et al., 1972; Kakunaga, 1973; Evans and DiPaolo, 1975).

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_II.B. Quantitative Estimate of Carcinogenic Risk from Oral Exposure

None.

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_II.C. Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure

None.

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_II.D. EPA Documentation, Review, and Contacts (Carcinogenicity Assessment)

__II.D.1. EPA Documentation

Source Document — U.S. EPA, 1990

The 1990 Drinking Water Criteria Document for Polycyclic Aromatic Hydrocarbons has undergone Agency and external review.

__II.D.2. EPA Review (Carcinogenicity Assessment)

Agency Work Group Review — 02/07/1990

Verification Date — 02/07/1990

__II.D.3. EPA Contacts (Carcinogenicity Assessment)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address).

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_III.  [reserved]
_IV.  [reserved]
_V.  [reserved]


_VI.  Bibliography

Substance Name — Pyrene
CASRN — 129-00-0
Last Revised — 08/01/1991

_VI.A. Oral RfD References

U.S. EPA. 1989. 13-Week Mouse Oral Subchronic Toxicity with Pyrene. TRL Study #042-012. Study conducted by Toxicity Research Laboratories, Muskegon, MI for the Office of Solid Waste, Washington, DC.

White, J. and A. White. 1939. Inhibition of growth of the rat by oral administration of methylcholanthrene, benzpyrene, or pyrene and the effects of various dietary supplements. J. Biol. Chem. 131: 149-161.

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_VI.B. Inhalation RfC References

None

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_VI.C. Carcinogenicity Assessment References

Ashby, J. and B. Kilbey. 1981. Summary report on the performance of bacterial repair, phase induction, degranulation, and nuclear enlargement assays. In: Evaluation of Short-Term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Elsevier, North Holland, New York. p. 33-48.

Badger, G.M., J.W. Cook, C.L. Hewett, et al. 1940. The production of cancer by pure hydrocarbons. V. Proc. R. Soc. London Ser. B. 129: 439-467.

Bos, R.P., J.L.G. Theuws, F.J. Jongeneelen and P.Th. Henderson. 1988. Mutagenicity of bi-, tri- and tetra-cyclic aromatic hydrocarbons in the "taped-plate assay" and in the conventional Salmonella mutagenicity assay. Mutat. Res. 204: 203-206.

Bridges, B.A., D.B. McGregor and E. Zeiger, et al. 1981. Summary report on the performance of bacterial mutation assays. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 49-67.

Brookes, P. and R.J. Preston. 1981. Summary report on the performance of in vitro mammalian assays. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 77-85.

Casto, B.C. 1979. Polycyclic hydrocarbons and Syrian hamster embryo cells: Cell transformation, enhancement of viral transformation and analysis of DNA damage. In: Polynuclear Aromatic Hydrocarbons, P.W. Jones and P. Leber, Ed. Ann Arbor Science Publ., Ann Arbor, MI. p. 51-66.

Chen, T.T. and C. Heidelberger. 1969. Quantitative studies on the malignant transformation of mouse prostate cells by carcinogenic hydrocarbons in vitro. Int. J. Cancer. 4: 166-178.

Dean, B.J. 1981. Activity of 27 coded compounds in the RL1 chromosome assay. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 570- 579.

de Serres, F.J., G.R. Hoffman, J. Von Borstel, et al. 1981. Summary report on the performance of yeast assays. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 68-76.

DiPaolo, J.A., P. Donovan and R. Nelson. 1969. Quantitative studies of in vitro transformation by chemical carcinogens. J. Natl. Cancer Inst. 42(5): 867-874.

DiPaolo, J.A., K. Takano and N.C. Popescu. 1972. Quantitation of chemically induced neoplastic transformation of BALB/3T3 cloned cell lines. Cancer Res. 32: 2686-2695.

Evans, C.H. and J.A. DiPaolo. 1975. Neoplastic transformation of guinea pig fetal cells in culture induced by chemical carcinogens. Cancer Res. 35: 1035-1044.

Evans, E.L. and A.D. Mitchell. 1981. Effect of 20 coded chemicals on sister chromatid exchange frequencies in cultured Chinese hamster cells. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 538-550.

Ho, C-H., B.R. Clark, M.R. Guerin, B.D. Barkenhus, T.K. Rao and J.L. Epler. 1981. Analytical and biological analyses of test materials from the synthetic fuel technologies. IV. Studies of chemical structure-mutagenic activity relationships of aromatic nitrogen compounds relevant to synfuels. Mutat. Res. 85: 335-345.

Horton, A.W. and G.M. Christian. 1974. Carcinogenic versus incomplete carcinogenic activity among aromatic hydrocarbons: Contrast between chrysenes and benzo[b]triphenylene. J. Natl. Cancer Inst. 53(4): 1017-1020.

Jotz, M.M. and A.D. Mitchell. 1981. Effects of 20 coded chemicals on the forward mutation frequency at the thymidine kinase locus in L5178Y mouse lymphoma cells. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 580-593.

Kaden, D.A., R.A. Hites and W.G. Thilly. 1979. Mutagenicity of soot and associated polycyclic aromatic hydrocarbons to Salmonella typhimurium. Cancer Res. 39: 4152-4159.

Kakunaga, T. 1973. A quantitative system for assay of malignant transformation by chemical carcinogens using a clone derived from BALB/3T3. Int. J. Cancer. 12: 463-473.

Kinae, N., T. Hashizume, T. Makita, I. Tomita, I. Kimura and H. Kanamori. 1981. Studies on the toxicity of pulp and paper mill effluents - 1. Mutagenicity of the sediment samples derived from Kraft paper mills. Water Res. 15: 17-24.

Lake, R.S., M.L. Kropko, M.R. Pezzutti, R.H. Shoemaker and H.J. Igel. 1978. Chemical induction of unscheduled DNA synthesis in human skin epithelial cell cultures. Cancer Res. 38: 2091-2098.

LaVoie, E.J., E.V. Bedenko, N. Hirota, S.S. Hecht and D. Hoffmann. 1979. A comparison of the mutagenicity, tumor-initiating activity and complete carcinogenicity of polynuclear aromatic hydrocarbons. In: Polynuclear Aromatic Hydrocarbons, P.W. Jones and P. Leber, Ed. Ann Arbor Science Publishers, Ann Arbor, MI. p. 705-721.

Martin, C.N., A.C. McDermid and R.C. Garner. 1978. Testing of known carcinogens and noncarcinogens for their ability to induce unscheduled DNA synthesis in HeLa cells. Cancer Res. 38: 2621-2627.

Matijasevic, Z. and E. Zeiger. 1985. Mutagenicity of pyrene in Salmonella. Mutat. Res. 142: 149-152.

McCann, J.E., E. Choi, E. Yamasaki and B.N. Ames. 1975. Detection of carcinogens as mutagens in the Salmonella/microsome test: Assay of 300 chemicals. Natl. Acad. Sci. 72(12): 5135-5139.

Perry, P.E. and E.J. Thompson. 1981. Evaluation of the sister chromatid exchange method in mammalian cells as a screening system for carcinogens. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, F.J. de Serres and J. Ashby, Ed. Elsevier/North Holland, NY. p. 560-569.

Pienta, R.J., J.A. Poiley and W.B. Libherz, III. 1977. Morphological transformation of early passage golden Syrian hamster embryo cells derived from cryopreserved primary cultures as a reliable in vitro bioassay for identifying diverse carcinogens. Int. J. Cancer. 19: 642-655.

Popescu, N.C., D. Turnbull and J.A. DiPaolo. 1977. Sister chromatid exchange and chromosome aberration analysis with the use of several carcinogens and noncarcinogens: Brief communication. J. Natl. Cancer Inst. 59(1): 289-293.

Probst, G.S., R.E. McMahon, L.E. Hill, C.Z. Thompson, J.K. Epp and S.B. Neal. 1981. Chemically-induced unscheduled DNA synthesis in primary rat hepatocyte cultures: A comparison with bacterial mutagenicity using 218 compounds. Environ. Mutagen. 3: 11-32.

Purchase, I.F.H. and V. Ray. 1981. Summary report on the performance of in vivo assays. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 86-95.

Rice, J.E., T.J. Hosted, Jr. and E.J. LaVoie. 1984. Fluoranthene and pyrene enhance benzo[a]pyrene -- DNA adduct formation in vivo in mouse skin. Cancer Lett. 24: 327-333.

Robinson, D.E. and A.D. Mitchell. 1981. Unscheduled DNA synthesis response of human fibroblasts, WI-38 cells, to 20 coded chemicals. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland. p. 517-527.

Sakai, M., D. Yoshida and S. Mizusdki. 1985. Mutagenicity of polycyclic aromatic hydrocarbons and quinones on Salmonella typhimurium TA97. Mutat. Res. 156: 61-67.

Salaman, M.H. and F.J.C. Roe. 1956. Further tests for tumor-initiating activity: N,N-di-(2-chloroethyl)-p-aminophenylbutyric acid (CB1348) as an initiator of skin tumor formation in the mouse. Br. J. Cancer. 10: 363-378.

Scribner, J.D. 1973. Brief Communication: Tumor initiation by apparently noncarcinogenic polycyclic aromatic hydrocarbons. J. Natl. Cancer Inst. 50: 1717-1719.

Shear, M.J. and J. Leiter. 1941. Studies in carcinogenesis. XVI. Production of subcutaneous tumors in mice by miscellaneous polycyclic compounds. J. Natl. Cancer Inst. 2: 241-258.

Tong, C., S.V. Brat and G.M. Williams. 1981. Sister-chromatid exchange induction by polycyclic aromatic hydrocarbons in an intact cell system of adult rat-liver epithelial cells. Mutat. Res. 91: 467-473.

U.S. EPA. 1990. Drinking Water Criteria Document for Polycyclic Aromatic Hydrocarbons (PAHs). Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Cincinnati, OH for the Office of Drinking Water, Washington, DC. ECAO-CIN-D010, September, 1990. (Final Draft)

Valencia, R. and K. Houtchens. 1981. Mutagenic activity of 10 coded compounds in the Drosophila sex-linked recessive lethal test. In: Evaluation of Short-term Tests for Carcinogens. Report of the International Collaborative Program. Progress in Mutation Research, Vol. 1, F.J. de Serres and J. Ashby, Ed. Amsterdam, Elsevier, North Holland, NY. p. 651-659.

Van Duuren, B.L. and B.M. Goldschmidt. 1976. Cocarcinogenic and tumor-promoting agents in tobacco carcinogenesis. J. Natl. Cancer Inst. 51(6): 1237-1242.

Wislocki, P.G., E.S. Bagan, A.Y.H. Lu et al. 1986. Tumorigenicity of nitrated derivatives of pyrene, benz[a]anthracene, chrysene and benzo[a]pyrene in the newborn mouse assay. Carcinogenesis. 7(8): 1317-1322.

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_VII.  Revision History

Substance Name — Pyrene
CASRN — 129-00-0

Date
Section
Description
09/01/1990 I.A. Oral RfD summary on-line
09/01/1990 VI. Bibliography on-line
01/01/1991 VI.C. Carcinogen assessment references added
07/01/1991 I.A.7. Primary and secondary contacts changed
08/01/1991 VI.A. U.S. EPA, 1989 citation clarified
01/01/1992 IV. Regulatory Action section on-line
07/01/1993 I.A.6. Other EPA Documentation added
09/01/1994 I.B. Inhalation RfC now under review
08/01/1995 I.B. EPA's RfD/RfC and CRAVE workgroups were discontinued in May, 1995. Chemical substance reviews that were not completed by September 1995 were taken out of IRIS review. The IRIS Pilot Program replaced the workgroup functions beginning in September, 1995.
04/01/1997 III., IV., V. Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary Data were removed from IRIS on or before April 1997. IRIS users were directed to the appropriate EPA Program Offices for this information.

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_VIII.  Synonyms

Substance Name — Pyrene
CASRN — 129-00-0
Last Revised — 09/01/1990

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