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1,3-Butadiene Quickview (CASRN 106-99-0)

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 1,3-Butadiene

File First On-Line: 03/31/1987; Last Significant Revision: 11/05/2002

Category (section)
Last Revised
Oral RfD Assessment Discussion 11/05/2002
Inhalation RfC Assessment Yes 11/05/2002
Carcinogenicity Assessment Yes 11/05/2002
  • 106-99-0
  • Biethylene
  • Bivinyl
  • Butadieen
  • Buta-1,3-dieen
  • Butadien
  • Buta-1,3-dien
  • Butadiene
  • 1,3-Butadiene
  • Butadiene, 1,3-
  • alpha,gamma-Butadiene
  • more...
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)

Critical Effect
Point of Departure*
Ovarian atrophy BMCL10 (HEC): 1.98 mg/m3 1000 2x10-3 mg/m3

* The Point of Departure listed serves as a basis from which the Inhalation RfC was derived. See Discussion of Conversion Factors and Assumptions for more details.

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Carcinogenicity Assessment for Lifetime Exposure
  • Weight-of-Evidence Characterization
    • Carcinogenic to humans
  • Weight-of-Evidence Narrative:
    • Under EPA's 1999 Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1999), 1,3-butadiene is characterized as carcinogenic to humans by inhalation. This characterization is supported by the total weight of evidence provided by the following: (1) sufficient evidence from epidemiologic studies of the majority of U.S. workers occupationally exposed to 1,3-butadiene, either to the monomer or to the polymer by inhalation, showing increased lymphohematopoietic cancers and a dose-response relationship for leukemias in polymer workers (see Section II.A.2), (2) sufficient evidence in laboratory animal studies showing that 1,3-butadiene causes tumors at multiple sites in mice and rats by inhalation (see Section II.A.3), and (3) numerous studies consistently demonstrating that 1,3-butadiene is metabolized into genotoxic metabolites by experimental animals and humans (see Section II.A.4). The specific mechanisms of 1,3-butadiene-induced carcinogenesis are unknown however, the scientific evidence strongly suggests that the carcinogenic effects are mediated by genotoxic metabolites of 1,3-butadiene, i.e., the monoepoxide, the diepoxide, and the epoxydiol.
    • This may be a synopsis of the full weight-of-evidence narrative. See IRIS Summary.

Quantitative Estimate of Carcinogenic Risk from Oral Exposure

  • Information reviewed but value not estimated. See IRIS Summary.

Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure

Inhalation Unit Risk(s)
Extrapolation Method
3 x10-5 per µg/m3 Linear extrapolation from LEC01 (0.254 ppm); LEC01 derived from linear relative rate model (RR = 1 + (B)(x)) using lifetable analysis with leukemia incidence data; an adjustment factor of 2 was applied.

Inhalation Concentrations at Specified Risk Levels

Risk Level
E-4 (1 in 10,000) 3 µg/m3
E-5 (1 in 100,000) 3x10-1 µg/m3
E-6 (1 in 1,000,000) 3x10-2 µg/m3

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