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Polychlorinated biphenyls (PCBs) Quickview (CASRN 1336-36-3)

Health assessment information on a chemical substance is included in IRIS only after a comprehensive review of toxicity data by U.S. EPA health scientists from several Program Offices, Regional Offices, and the Office of Research and Development.

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Status of Data for Polychlorinated biphenyls (PCBs)

File First On-Line: 05/01/1989; Last Significant Revision: 10/01/1996

Category (section)
Last Revised
Oral RfD Assessment Message 06/01/1994
Inhalation RfC Assessment No
Carcinogenicity Assessment Yes 10/01/1996
Under Re-Assessment
  • 1336-36-3
  • Aroclor
  • Aroclor 1221
  • Aroclor 1232
  • Aroclor 1242
  • Aroclor 1248
  • Aroclor 1254
  • Aroclor 1260
  • Aroclor 1262
  • Aroclor 1268
  • Aroclor 2565
  • more...
Revision History
Date Section Description
06/01/1997 II.C.3. Units corrected in Upper-bound Unit Risk
Chronic Health Hazard Assessments for Noncarcinogenic Effects

Reference Dose for Chronic Oral Exposure (RfD)

Information reviewed but value not estimated. See IRIS Summary.

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Reference Concentration for Chronic Inhalation Exposure (RfC)

Not Assessed under the IRIS Program.

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Carcinogenicity Assessment for Lifetime Exposure
  • Weight-of-Evidence Characterization
    • B2 (Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals)
  • Weight-of-Evidence Narrative:
    • A 1996 study found liver tumors in female rats exposed to Aroclors 1260, 1254, 1242, and 1016, and in male rats exposed to 1260. These mixtures contain overlapping groups of congeners that, together, span the range of congeners most often found in environmental mixtures. Earlier studies found high, statistically significant incidences of liver tumors in rats ingesting Aroclor 1260 or Clophen A 60 (Kimbrough et al., 1975; Norback and Weltman, 1985; Schaeffer et al., 1984). Mechanistic studies are beginning to identify several congeners that have dioxin-like activity and may promote tumors by different modes of action. PCBs are absorbed through ingestion, inhalation, and dermal exposure, after which they are transported similarly through the circulation. This provides a reasonable basis for expecting similar internal effects from different routes of environmental exposure. Information on relative absorption rates suggests that differences in toxicity across exposure routes are small. The human studies are being updated; currently available evidence is inadequate, but suggestive.
    • This may be a synopsis of the full weight-of-evidence narrative. See IRIS Summary.

Quantitative Estimate of Carcinogenic Risk from Oral Exposure

Oral Slope Factor(s)
Extrapolation Method
2 per mg/kg-day Linear extrapolation below LED10s
Drinking Water Unit Risks
  • Dose-Response Data (Carcinogenicity, Oral Exposure)
    • Tumor Type: Liver hepatocellular adenomas, carcinomas, cholangiomas, or cholangiocarcinomas
    • Test Species: Female Sprague-Dawley rats
    • Route: Oral, Diet
    • Reference: Brunner et al., 1996 Norback and Weltman, 1985

Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure

Inhalation Unit Risk(s)
Extrapolation Method
1 x10-4 per µg/m3
(Low risk and persistence; upper-bound unit risk)
Linear extrapolation below LED10s

Inhalation Concentrations at Specified Risk Levels

Risk Level
E-4 (1 in 10,000) 1 µg/m3(Low risk and persistence; upper-bound unit risk)
E-5 (1 in 100,000) 1x10-1 µg/m3(Low risk and persistence; upper-bound unit risk)
E-6 (1 in 1,000,000) 1x10-2 µg/m3(Low risk and persistence; upper-bound unit risk)

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