Prenatal susceptibility to carcinogenesis by xenobiotic substances including vinyl chloride.

Rice, Jerry M.

doi:10.1289/ehp.8141179

Cited by 13 publications

(2 citation statements)

References 16 publications

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“…A genetic polymorphism in glutathione transferase that renders this nitroso defense mechanism less active appears to increase prenatal vulnerability to this source of dietary carcinogen (Neilsen et al 2011). Thus, human evidence is consistent with findings in animals of brain tumors from TP or PN nitroso exposure (Naito, Naito, and Ito 1981;Rice 1981;Zeller, Ivankovic, and Zeller 1978).…”

Section: Introductionsupporting

confidence: 85%

Comparison of carcinogenic potency across life stages: implications for the assessment of transplacental cancer risk

Dzubow

Fields

Ginsberg

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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Cancer development from in utero exposure has been documented for a variety of agents with the most commonly studied compounds exhibiting mutagenic and genotoxic carcinogen properties. Age-dependent adjustment factors (ADAFs) are applied by the US Environmental Protection Agency to many such carcinogens when assessing cancer risk from early postnatal (PN) exposures; however, this approach has not been widely considered for transplacental (TP) exposure. To explore this question and further evaluate prenatal susceptibility a database of early life animal studies developed by California Office of Environmental Health Hazard Assessment (OEHHA) enhanced with additional literature searching was evaluated. Nine genotoxic carcinogens and one mixture (cigarette smoke) have data available via TP only, PN only and adultonly protocols. Potency comparisons across these lifestages displayed similarly greater potency in male liver and brain compared to adult-only exposure. Both TP and PN exposures were not markedly different than adult-only for other targets such as female liver and blood-borne tumors. Similarity in TP and PN targets and potency for carcinogen action suggests that a 10-fold ADAF may be applied for TP exposure as is currently applied to PN exposure. A similar conclusion was reached by OEHHA. The implications of this heightened TP vulnerability are greatest for lessthan-lifetime exposure and this approach might be used to assess the level of cancer risk from exposures during pregnancy. A case example employing a mutagenic flame retardant was used to exemplify application of a TP ADAF for evaluating risks during pregnancy.

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Section: Introductionsupporting

confidence: 85%

Comparison of carcinogenic potency across life stages: implications for the assessment of transplacental cancer risk

Dzubow

Fields

Ginsberg

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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“…'' Alternative diagnosis of these tumors as undifferentiated nasal cavity carcinomas has been suggested (53). mors of the nervous system.…”

Section: Vinyl Chloridementioning

confidence: 99%

Tumors of the Nervous System in Carcinogenic Hazard Identification

Rice

Wilbourn

2000

Toxicol Pathol

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In the absence of adequate data on humans, it is biologically plausible and prudent to regard agents and mixtures for which there is sufficient evidence of carcinogenicity in experimental animals, usually rats and mice, as if they presented a carcinogenic risk to humans. Prediction of cancer sites in humans from bioassay data in rodents is much less certain, however, regardless of organ or tissue. For tumors of the nervous system, there is practically no basis for judging the validity of such predictions, as only ionizing radiation is known to cause tumors of the central nervous system (CNS) in humans. Brain tumors are relatively uncommon findings in bioassays and are rare in untreated rodents, even in rats, which appear to be the most susceptible species. However, CNS tumors have been readily induced in rodents by systemic exposures to some chemicals, notably N-nitrosoalkylureas and other alkylating agents and certain alkyl hydrazine derivatives. CNS tumors in rodents have played a significant role in carcinogenic hazard evaluations of several other chemicals, including acrylonitrile, ethylene oxide, and acrylamide, and have been implicated as part of the tumor spectrum induced by vinyl chloride and certain inorganic lead compounds. In some of these evaluations, it is not certain that all tumors diagnosed as primary brain tumors were correctly identified. Diagnostic difficulties have been presented by undifferentiated small-cell tumors that may invade the brain, including carcinomas of the nasal cavity and undifferentiated schwannomas arising in cranial nerve ganglia, and by the difficulty of reliably distinguishing between focal reactive gliosis and early glial neoplasms. The most striking experimental finding regarding the induction by chemicals of tumors of the nervous system is the dramatically greater susceptibility of the fetal and neonatal nervous system to some carcinogens, as compared with the susceptibility of the nervous system in adults of the same species.

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Reproductive Toxicology

Henck¹

2015

Hamilton &Amp; Hardy's Industrial Toxicology

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Prenatal susceptibility to carcinogenesis by xenobiotic substances including vinyl chloride.

Cited by 13 publications

References 16 publications

Comparison of carcinogenic potency across life stages: implications for the assessment of transplacental cancer risk

Comparison of carcinogenic potency across life stages: implications for the assessment of transplacental cancer risk

Tumors of the Nervous System in Carcinogenic Hazard Identification

Reproductive Toxicology

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