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Issues in Risk Assessment (1993) / Chapter Skim
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RELATIONSHIP BETWEEN TOXICITY AND CARCINOGENICITY OBSERVED AT MTD
Pages 33-42

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From page 33...
... Please use the print version of this publication as the authoritative version for attribution. between toxicity (as quantified by the MTD)
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From page 34...
... Please use the print version of this publication as the authoritative version for attribution. phenomenon, but might be a secondary response to the induction of chronic toxicity.
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From page 35...
... Please use the print version of this publication as the authoritative version for attribution. urothelium by a factor of 2-10.
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From page 36...
... Some chemicals induced tumors at sites where toxicity was not in evidence, and some induced toxicity in some organs without inducing carcinogenesis. However, the majority of both mutagenic and nonmutagenic carcinogens induced tumors that were associated with chronic toxicity, although many of the same chemicals caused chronic toxicity at other sites that was not associated with carcinogenesis.
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From page 37...
... Please use the print version of this publication as the authoritative version for attribution. TABLE 2-2 Chemicals That Induced Both Subchronic and Chronic Toxicity but Not Carcinogenicity at Same Sitesa Rats Mice Chemical Site Lesion Site Lesion OF TOXICITY Noncarcinogens 2,4-Dichlorophenol None -- Liver Syncytial alteration Dimethoxane Forestomach Hyperplasia Forestomach Hyperplasia Hydrochlorothiazide Kidney Nephropathy, mineralization None -à -Methyldopa sesquihydrate None -- Kidney Nephropathy, karyomegaly Carcinogens p-Chloroaniline HCl Bone marrow, liver Hyperplasia, hemosiderin Kidney Hemosiderin Nitrofurantion Testes Degeneration Testes Degeneration Tribromoethane Liver Inflammation, vacuolization Liver Inflammation, vacuolization Malonaldehyde, Na salt Glandular stomach; bone marrow Ulcer, inflammation; hyperplasia Pancreas Atrophy Furosemide None -- Kidney Nephropathy aFrom Tennant et al.
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From page 38...
... Please use the print version of this publication as the authoritative version for attribution. TABLE 2-3 Chemicals That Induced Toxicity and Carcinogenicity at Same Sitea Chemical Mutagen Rats Mice Site Lesion Site Lesion OF TOXICITY Glycidol + Forestomach Dysplasia, carcinoma Forestomach Hyperplasia, carcinoma p-Chloroaniline HCl + Spleen; Fibrosis, metaplasia, sarcoma; Liver Hemosiderosis, adrenal hyperplasia, hepatocellular tumors pheochromocytoma N,N-Dimethylaniline + Spleen Fibrosis, metaplasia, sarcoma Forestomach Hyperplasia, squamous cell tumors Nitrofurantoin + Kidney Nephropathy, tubular cell Ovary Atrophy, ovarian tumors adenoma and carcinoma 4-Vinyl-1-cyclohexene + Skin Hyperplasia, basal and Skin, ovary Hyperplasia, basal and diepoxide squamous cell carcinoma squamous cell tumors; atrophy, ovarian tumor N-Methylolacrylamide - None -- Ovary Atrophy, granulosa cell tumors Benzofuran - Kidney Nephropathy, tubular cell Liver; forestomach; Syncytial changes, liver adenocarcinoma lung tumors; hyperplasia, carcinoma; hyperplasia, CORRELATIONS BETWEEN CARCINOGENIC POTENCY AND OTHER MEASURES 38
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From page 39...
... Please use the print version of this publication as the authoritative version for attribution. Chemical Mutagen Rats Mice Site Lesion Site Lesion Ochratoxin A - Kidney Degeneration, hyperplasia, tubular cell Not determined OF TOXICITY tumors Hexachloroethane - Kidney Nephropathy, hyperplasia, tubular cell Not determined - adenocarcinoma d-Limonene - Kidney Mineralization, nephropathy, hyperplasia, None - tubular cell adenocarcinoma Hydroquinone - Kidney Nephropathy, tubular cell adenoma Liver Syncitial cell alteration, liver tumors Phenylbutazone - Kidney Papillary necrosis, nephropathy, Liver Degeneration, hypertrophy, necrosis, transitional-cell carcinoma liver tumors aFrom Tennant et al.
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From page 40...
... Please use the print version of this publication as the authoritative version for attribution. toxic condition's effect on carcinogenesis might not be detected with data from chronic or even subchronic bioassays; for example, it is possible that a chemical very early in the course of a bioassay induces toxicity that enhances its carcinogenic response, but that, because of an adaptive cellular response, no chronic proliferative lesions other than tumors develop.
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From page 41...
... Please use the print version of this publication as the authoritative version for attribution. also induce toxicity and nonneoplastic proliferative lesions at doses that also are associated with neoplasia.
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From page 42...
... Please use the print version of this publication as the authoritative version for attribution.OF TOXICITY CORRELATIONS BETWEEN CARCINOGENIC POTENCY AND OTHER MEASURES 42
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Key Terms

  • carcinogenic potency
  • tubular cell
  • chronic toxicity
  • proliferative lesions
  • induced toxicity

  • lower doses
  • cell tumors
  • squamous cell
  • liver tumors
  • induced tumors

  • chronic administration
  • caused chronic
  • subchronic bioassays
  • nonneoplastic proliferative
  • risk associated

  • target cells
  • toxic effects
  • mutagen rats
  • tumor promotion
  • afrom tennant

  • bone marrow
  • increased rates
  • cell carcinoma
  • cell adenoma
  • cause cell

  • syncitial cell
  • cell hyperplasia
  • resulting cell
  • cell adenocarcinoma
  • granulosa cell


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