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Phosphine Quickview (CASRN 7803-51-2)

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.

Disclaimer: This QuickView represents a snapshot of key information. We suggest that you read the IRIS Summary to put this information into complete context.

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Status of Data for Phosphine

File First On-Line: 01/31/1987; Last Significant Revision: 07/01/1995

Category (section)
Status
Last Revised
Oral RfD Assessment On-line 12/01/1993
Inhalation RfC Assessment On-line 07/01/1995
Carcinogenicity Assessment On-line 12/01/1996
Synonyms
  • 7803-51-2
  • Celphos
  • Delicia
  • Detia
  • Detia Gas Ex-B
  • Fosforowodor
  • Hydrogen phosphide
  • Phosphine
  • Phosphorus trihydride
  • Phosphorwasserstoff
  • RCRA Waste Number P096
  • UN 2199
Phosphine Source Documents
Chronic Health Hazard Assessments for Noncarcinogenic Effects

Reference Dose for Chronic Oral Exposure (RfD)

Critical Effect
Point of Departure*
UF RfD
Body weight and clinical parameters NOEL : 2.6 x10-2 mg/kg-day 100 3 x10-4 mg/kg-day

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

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Reference Concentration for Chronic Inhalation Exposure (RfC)

Critical Effect
Point of Departure*
UF RfC
Decreased body weight NOAEL (HEC): 2.5 x10-1 mg/m3 1000 3x10-4 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
    • D (Not classifiable as to human carcinogenicity)
  • Weight-of-Evidence Narrative:
    • Based on inadequate data in animals and no tumor data in humans. While phospine has not been associated with cancer in humans, there is some evidence of chromosomal damage (transient chromatid deletions, gaps and breaks, persistent chromosomal translocations). A relationship between these genetic effects and the development of cancer in humans is sometimes postulated.
    • This may be a synopsis of the full weight-of-evidence narrative. See IRIS Summary.

Quantitative Estimate of Carcinogenic Risk from Oral Exposure

  • Not Assessed under the IRIS Program.

Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure

  • Not Assessed under the IRIS Program.

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