Observations of the site-specific carcinogenicity of vinyl chloride to humans.

Infante, Peter F.

doi:10.1289/ehp.814189

Cited by 17 publications

(4 citation statements)

References 10 publications

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“…Although Infante17 suggested that the lung should be considered a target organ for the carcinogenic effects of exposure to vinyl chloride, Doll18 argued that any risk of lung cancer was small and associated with the oldest cohorts who were possibly exposed to higher concentrations of vinyl chloride. Two recent studies conducted in Italy have again suggested increased risks of lung cancer among vinyl chloride workers 19…”

Section: Discussionmentioning

confidence: 99%

Historical cohort study of 10 109 men in the North American vinyl chloride industry, 1942–72: update of cancer mortality to 31 December 1995

Mundt

Dell²,

Austin³

et al. 2000

Occup Environ Med

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Objectives-To update and assess mortality from neoplasms to 31 December 1995 among 10 109 men employed in a job exposed to vinyl chloride for at least 1 year between 1942 and 1972 at any of 37 North American factories. Previous analyses indicated associations between employment in vinyl production and increased mortality risk from cancers of the liver and biliary tract, due to increased mortality from angiosarcoma of the liver, and brain cancer. Methods-Standardised mortality ratio (SMR) analyses, overall and stratified by several work related variables, were conducted with United States and state reference rates. Cox's proportional hazards models and stratified log rank tests were used to further assess occupational factors. Results-895 of 3191 deaths (28%) were from malignant neoplasms, 505 since the previous update to the end of 1982. Mortality from all causes showed a deficit (SMR 83, 95% confidence interval (95% CI) 80 to 86), whereas mortality from all cancers combined was similar to state referent rates. Mortality from cancers of the liver and biliary tract was clearly increased (SMR 359, 95% CI 284 to 446). Modest excesses of brain cancer (SMR 142, 95% CI 100 to 197) and cancer of connective and soft tissue (SMR 270, 95% CI 139 to 472) were found. Stratified SMR and Cox's proportional hazard analyses supported associations with age at first exposure, duration of exposure, and year of first exposure for cancers of the liver and soft tissues, but not the brain. Conclusions-Excess mortality risk from cancer of the liver and biliary tract, largely due to angiosarcoma, continues. Risk of mortality from brain cancer has attenuated, but its relation with exposure to vinyl chloride remains unclear. A potentially work related excess of deaths from cancer of connective and soft tissue was found for the first time, but was based on few cancers of assorted histology. (Occup Environ Med 2000;57:774-781)

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Section: Discussionmentioning

confidence: 99%

Historical cohort study of 10 109 men in the North American vinyl chloride industry, 1942–72: update of cancer mortality to 31 December 1995

Mundt

Dell²,

Austin³

et al. 2000

Occup Environ Med

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“…Both models were designed to model only VC’s effects on the liver, despite scientific consensus that it is a multisite carcinogen in humans and experimental animals (Byren et al 1976; Cooper 1981; Drew et al 1983; Feron et al 1979; Hagmar et al 1990; IARC 1979, 1987; Infante 1981; Maltoni and Lefemine 1975; Maltoni et al 1981; Monson et al 1974; Mundt et al 2000; Smulevich et al 1988; Tabershaw and Gaffey 1974; Wagoner et al 1980; Waxweiler et al 1976, 1981; Weber et al 1981; Wong and Whorton 1993; Wong et al 1991; Wu et al 1989). …”

Section: Us Epa Standard Based On Overall Risk Of Liver Cancer Notmentioning

confidence: 99%

Vinyl Chloride: A Case Study of Data Suppression and Misrepresentation

Sass

Castleman

Wallinga

2005

Environ Health Perspect

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When the U.S. Environmental Protection Agency (EPA) finalized its 2000 update of the toxicological effects of vinyl chloride (VC), it was concerned with two issues: the classification of VC as a carcinogen and the numerical estimate of its potency. In this commentary we describe how the U.S. EPA review of VC toxicology, which was drafted with substantial input from the chemical industry, weakened safeguards on both points. First, the assessment downplays risks from all cancer sites other than the liver. Second, the estimate of cancer potency was reduced 10-fold from values previously used for environmental decision making, a finding that reduces the cost and extent of pollution reduction and cleanup measures. We suggest that this assessment reflects discredited scientific practices and recommend that the U.S. EPA reverse its trend toward ever-increasing collaborations with the regulated industries when generating scientific reviews and risk assessments.

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“…Vinyl chloride, I, a well-established carcinogen [17][18][19], is activated metabolically to its ultimate carcinogenic form, chlorooxirane, I1 [ 17,20,21]…”

Section: Introductionmentioning

confidence: 99%

A computational study of some isomerization equilibria and their possible relation to vinyl chloride carcinogenicity

Murray¹,

Politzer²

1987

Int J of Quantum Chemistry

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AbstrertThere is considerable evidence indicating that the primary in vivo DNA alkylation product of vinyl'chloride, believed to be r#ponsible for its carcinogenicity, is the 7-N-(2-oxoethyl) derivative of guanine. Using a rqxesentative keto-enol system, we have studied computationally two possible equilibria involving this adduct. The t h t is between the t-oxoethyl derivatives of the keto and enol forms of the representative system, whereas the second is between the 2-oxoethyl derivative of the keto form and the corresponding hemiacetal. In the case of the analogous guanine derivatives, such equilibria could lead to disruption of the hydrogen bonding between guanine and cytosine in DNA and could cause miscoding and replicational and transcriptional errors. An ab initio self-consistent field molecular orbital study has been carried out using the GAUSSIAN 82 system of programs. Optimized structures and energies have been calculated at the 3-21G level for the representative keto-enol system and its 2-oxoethyl and hemiacetal forms. The formation of the 2-oxoethyl adduct was found to have no significant effect upon this keto-enol equilibrium, which strongly favors the keto form. Our calculations further show hemiacetal formation to be an unlikely possibility for this system. On the basis of these results and recent data on guanine tautomers, we speculate about the d o g o u s equilibria involving the guanine derivatives.

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Observations of the site-specific carcinogenicity of vinyl chloride to humans.

Cited by 17 publications

References 10 publications

Historical cohort study of 10 109 men in the North American vinyl chloride industry, 1942–72: update of cancer mortality to 31 December 1995

Historical cohort study of 10 109 men in the North American vinyl chloride industry, 1942–72: update of cancer mortality to 31 December 1995

Vinyl Chloride: A Case Study of Data Suppression and Misrepresentation

A computational study of some isomerization equilibria and their possible relation to vinyl chloride carcinogenicity

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