Acute Inhalation Toxicity of Vinyl Chloride to Laboratory Animals

Mastromatteo, Ernest; Fisher, A. M.; Christie, Helen; H, Danziger

doi:10.1080/00028896009344092

Cited by 40 publications

(5 citation statements)

References 2 publications

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“…Studies in animals. A state of unconsciousness was produced in animals acutely exposed via inhalation to vinyl chloride concentrations of approximately 100,000 ppm (Mastromatteo et al, 1960;Jaeger et al, 1974 ) . Chronic inhalation exposure of animals to high levels of vinyl chloride caused nerve damage and cerebellar degeneration (Viola, 1970;Viola et al, 1971 ).…”

Section: _20 Yearsmentioning

confidence: 99%

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

et al. 1999

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In support of Superfund re-authorization legislation, the Division of Toxicology of the Agency for Toxic Substances and Disease Registry (ATSDR) prepared a chemical-specific consultation document for Congress that identified those chemicals with carcinogenic, neurological, or developmental adverse effects having a latency period longer than 6 years. The review was limited to the top 50 substances listed on ATSDR's 1997 Priority List of Hazardous Substances (Priority List). Among the top 50 chemicals, a review of the technical literature indicated that 38 (76%) were classified as "reasonably anticipated," "possibly," or "probably" capable of causing cancer in humans, based either on human and animal data. Eight chemicals (16%) had well-established cancer latency periods in humans of 6 years or more following exposure. Three substances (6%)--arsenic, creosote, and benzidine--had data indicating latency periods longer than 6 years. The technical literature review likewise confirmed the potential for neurological and developmental effects with a latency of 6 years. Twenty-seven (54%) of the top 50 substances caused acute and/or chronic neurotoxic effects; a number of these also caused neurological effects that persisted beyond 6 years (or the equivalent in animal studies) such as: behavioral problems, neurological deficiencies, reduced psychomotor development, cognitive deficiencies, and reduced IQ. Twenty-eight substances (56%) caused adverse developmental effects in offspring of exposed individuals or animals including increased fetal and infant mortality, decreased birth weights and litter sizes, and growth delays. Latency periods for related chemicals are expected to be similar due to structural and toxicological similarities.

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Section: _20 Yearsmentioning

confidence: 99%

Agency for Toxic Substances and Disease Registry's 1997 priority list of hazardous substances. Latent effects—carcinogenesis, neurotoxicology, and developmental deficits in humans and animals

et al. 1999

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“…Acute liver injury after vinyl chloride (VCM) has been noted briefly in earlier reports (1,2). Mastromatteo et al (1) reported the appearance of fatty infiltration but could not demonstrate fat on frozen sections in guinea pigs exposed to 30% VCM for 30 min.…”

Section: Introductionmentioning

confidence: 99%

Acute liver injury by vinyl chloride: involvement of endoplasmic reticulum in phenobarbital-pretreated rats.

Reynolds¹,

Jaeger²,

Murphy³

1975

Environ Health Perspect

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A single 6-hr exposure to vinyl chloride monomer (5%) produces extensive vacuolization of centrolobular liver parenchyma and focal midzonal necrosis in the hepatic lobuole in phenobarbital-pretreated rats. Ultrastructurally, vacuolization consists of dilation of cysternae of rough endoplasmic reticulum and in the same cells smooth endoplasmic reticulum coalesces into discreet aggregates resembling denatured membranes. The findings support the hypothesis that vinyl chloride is hepatotoxic because it is converted into a toxic metabolite by components of the mixed function oxidase system of liver endoplasmic reticulum.ImagesFIGURE 1. AFIGURE 1. BFIGURE 1. CFIGURE 2.FIGURE 3.FIGURE 4.FIGURE 5.

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“…rhythmias (2), and sensitization of the myocardium (3). Relatively high concentrations of VC (1040o in air) for 30 min produced narcosis and/or death in mice, rats, and guinea pigs (4). The guinea pigs were found to be more resistant.…”

Section: Introductionmentioning

confidence: 92%