National Toxicology Program

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. ¹

Names (NTP)

• Dibenzofuran
• (1,1'-BIPHENYL)-2,2'-DIYL OXIDE
• 2,2-BIPHENYLENE OXIDE
• DIPHENYLENE OXIDE

Human Toxicity Excerpts

• None found

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Non-Human Toxicity Excerpts

• GENOTOXICITY: Dibenzofuran did not induce mutagenicity in Salmonella strains TA98, TA100, TA1535, or TA1537 in the absence and presence of S-9. [Mortelmans K et al; Toxicol Appl Pharmacol 75: 137-46 (1984) ]**PEER REVIEWED**
  
• GENOTOXICITY: Dibenzofuran did not induce genotoxicity with or without metabolic activation in Salmonella TA98 at concentrations from 0.025-1.6 mol/plate and TA100 at concentrations from 0.05- 4.0 mmol/plate. [Matsumoto M et al; Toxicol Lett 40 (1): 21-8 (1988) ]**PEER REVIEWED**
  
• GENOTOXICITY: Dibenzofuran is not mutagenic with or without metabolic activation in several strains of Salmonella typhimurium assay. [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Dibenzofuran (132-64-9). Available from: http://www.epa.gov/iris/index.html on the Substance File List as of September 18, 2003. ]**PEER REVIEWED**
  
• ALTERNATIVE IN VITRO TESTS: A series of derivatives of dibenzofuran and dibenzosuberol block rhinovirus replication in vitro as judged by their ability to hinder the cytopathic effect in cells infected with HRV14 or HRV16. ... 2-hydroxy-3-dibenzofuran carboxylic acid was equally effective against HRV16 and HRV14, with IC50 values of 25 microM in cytopathy assays. Dibenzosuberenone showed minor differences in selectivity, with IC50 values of 10 and 30 microM for HRV16 and HRV14 cytopathy, respectively. Likewise, dibenzosuberenone effectively prevented the production of HRV16 proteins, viral RNA, and infectious virus particles when present at concentrations above 30 microM. [Murray MA, Babe LM; Antiviral Res 44(2): 123-31 (1999) ]**PEER REVIEWED**
  
• OTHER TOXICITY INFORMATION: Previous studies on the immunotoxicity of a complex mixture of polynuclear aromatic hydrocarbon (PAH) by-products from a manufactured gas plant indicated possible synergistic interactions which were investigated by determining the immunosuppressive effects of a reconstituted PAH mixture in female B6C3F1 mice challenged with TNP-haptenated sheep red blood cells (SRBCs) (T-cell-dependent) or trinitrophenyl-lipopolysaccharide (TNP-LPS) (T-cell-independent) antigens. The reconstituted PAH mixture contained ... 17 congeners: 2-rings (indan, naphthalene, 1- and 2-methylnaphthalene), 3-rings (acenaphthylene, acenaphthene, dibenzofuran, fluorene, phenanthrene and anthracene), and > or = 4-rings (pyrene, fluoranthene, benz[a]anthracene, chrysene, benzo[b]fluoranthene, benzo[k]fluoranthene and benzo[a]pyrene), and resembled mixtures identified as by-products from manufactured gas plants. The reconstituted mixture and the 2-, 3- and > or = 4-ring PAH fractions all caused a dose-dependent decrease in the splenic plaque-forming cell (PFC) response to SRBCs or TNP-LPS, and their ED50 values for the four treatment groups were 86, 354, 145, and 23 or 163, 439, 637 and 31 mg/kg, respectively. The corresponding ED50 values for decreased serum anti-TNP IgM levels for these same mixtures were (TNP-haptenated SRBCs, T-cell-dependent) 144, 231, 42 and 27 units, respectively, and (TNP-LPS, T-cell-independent) 161, 406, 312 and 69 units, respectively. The suppression of anti-TNP IgM titers was similar to the suppression of the PFC response and shows that antigen-specific immunoglobulin titer can be used as a biomarker of PAH exposure. A direct comparison of the immunotoxic responses of the reconstituted PAH mixture and the corresponding dose of the > or = 4-ring PAHs indicated that the latter fraction was primarily responsible for the activity of the reconstituted mixture. [Harper N et al; Toxicology 109 (1): 31-8 (1996) ]**PEER REVIEWED**
  
• OTHER TOXICITY INFORMATION: The potential non-additive interactions of polynuclear aromatic hydrocarbon (PAH) mixtures as inducers of Cyp1a-1 and Cyp1a-2 gene expression were investigated in B6C3F1 mice using a reconstituted PAH mixture ... of ... 2-, 3- and > or = 4-ring PAH fractions ... . The > or = 4-ring PAH fraction and reconstituted mixture induced hepatic microsomal ethoxyresorufin O-deethylase (EROD) activity and Cyp1a-1 mRNA levels, whereas the 2- and 3-ring PAHs were only weakly active. Direct comparison of the potencies of the reconstituted mixture and > or = 4-ring PAHs showed that the Cyp1a-1 induction activity of the reconstituted mixture was due to the > or = 4-ring PAHs. The reconstituted PAH mixture and > or = 4-ring PAHs also induced Cyp1a-2 hepatic mRNA levels and microsomal methoxyresorufin O-deethylase (MROD) activity; however, their dose-response curves indicated that the reconstituted PAH mixture was more potent as a Cyp1a-2 inducer than the > or = 4 ring PAHs. The differences in potency were due to 3-ring PAHs which were found to be strong inducers of hepatic Cyp1a-2 mRNA levels and microsomal MROD activity at the lowest dose administered (37 mg/kg). The 3-ring mixture caused a maximal 29-fold increase in hepatic MROD activity at a dose of 292 mg/kg, but only 28% of maximal induction of EROD activity. Northern analysis of liver mRNA from mice treated with 3-ring PAHs showed that there was minimal induction of Cyp1a-1 mRNA levels. The 3-ring PAHs did not competitively bind to the mouse hepatic cytosolic aryl hydrocarbon (Ah) receptor suggesting that 3-ring PAHs are a new class of Cyp1a-2 inducers which do not act through the Ah receptor. [Chaloupka K. et al; Chem-Biol Interactions 96 (3): 207-21 (1995) ]**PEER REVIEWED**
  
• OTHER TOXICITY INFORMATION: Treatment of B6C3F1 mice with ... /tricyclic hydrocarbons including/ dibenzofuran resulted in induction of hepatic microsomal methoxyresorufin O-deethylase (MROD) activity. ... Results of competitive binding studies indicated that the tricyclic hydrocarbons did not competitively displace [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin or [3H]benzo[a]pyrene from the mouse hepatic cytosolic aryl hydrocarbon (Ah) receptor or 4S carcinogen binding protein respectively. The data indicate that ... /these/ tricyclic hydrocarbons induce Cyp1a2 gene expression in B6C3F1 mice via an Ah receptor-independent pathway. Thus, tricyclic hydrocarbons induce Cyp1a2 without the co-induction of Cyp1a1 and therefore these relatively non-toxic compounds can be used to further probe the role of Cyp1a2 in the metabolism and metabolic activation of diverse chemical carcinogens. [Goldstein LS et al; Environ Health Perspect 106 (Suppl 6): 1325-30 (1998) ]**PEER REVIEWED**
  

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Human Toxicity Values

• None found

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Non-Human Toxicity Values

• LD50 Guinea pig (Hartley, male, 3-4 wk old) oral 5-10 ug/kg bw/30 days /2,3,7,8-tetrabromodibenzofuran/ [WHO; Environ Health Criteria 88: Polychlorinated Dibenzo-para-dioxins and Dibenzofurans p.277 (1989) ]**PEER REVIEWED**
  

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Absorption, Distribution and Excretion

• None found

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Metabolism/Metabolites

• None found

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TSCA Test Submissions

• None found

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Footnotes

¹ Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.