Vinyl chloride: still a cause for concern.

Abstract

Vinyl chloride (VC) is both a known carcinogen and a regulated chemical, and its production capacity has almost doubled over the last 20 years, currently 27 million tons/year worldwide. According to recent reports it is still a cause for concern. VC has been found as a degradation product of chloroethylene solvents (perchloroethylene and trichloroethylene) and in landfill gas and groundwater at concentrations up to 200 mg/m(3) and 10 mg/L, respectively. Worldwide occupational exposure to VC still seems to be high in some countries (e.g., averages of approximately 1,300 mg/m(3) until 1987 in one factory), and exposure may also be high in others where VC is not regulated. By combining the most relevant epidemiologic studies from several countries, we observed a 5-fold excess of liver cancer, primarily because of a 45-fold excess risk from angiosarcoma of the liver (ASL). The number of ASL cases reported up to the end of 1998 was 197 worldwide. The average latency for ASL is 22 years. Some studies show a small excess risk for hepatocellular carcinoma, and others suggest a possible risk of brain tumors among highly exposed workers. Lung cancer, lymphomas, or leukemia do not seem to be related to VC exposure according to recent results. The mutation spectra observed in rat and human liver tumors (ASL and/or hepatocellular carcinoma) that are associated with exposure to VC are clearly distinct from those observed in sporadic liver tumors or hepatic tumors that are associated with other exposures. In rats, the substitution mutations found at A:T base pairs in the ras and p53 genes are consistent with the promutagenic properties of the DNA adduct 1,N(6)-ethenoadenine formed from VC metabolites. Risk assessments derived from animal studies seem to overestimate the actual risk of cancer when comparing estimated and reported cases of ASL.ImagesFigure 1Figure 2

Health risks posed by use of Di-2-ethylhexyl phthalate (DEHP) in PVC medical devices: A critical review

“…Since the early 1970s VCM has been recognized as an occupational carcinogen, causally related to angiosarcoma of the liver. More recent research has identi®ed associations between workplace vinyl chloride exposure and hepatocellular carcinoma and brain cancer [Kielhorn et al, 2000]. While strict occupational exposure limits for VCM were instituted throughout the world in the mid-1970s, exposures may remain high in some countries [Kielhorn et al, 2000].…”

“…More recent research has identi®ed associations between workplace vinyl chloride exposure and hepatocellular carcinoma and brain cancer [Kielhorn et al, 2000]. While strict occupational exposure limits for VCM were instituted throughout the world in the mid-1970s, exposures may remain high in some countries [Kielhorn et al, 2000]. Community exposures also continue to occur through air emissions from production facilities.…”

Novel Aerobic Perchloroethylene Degradation by the White-Rot Fungus Trametes versicolor

“…Most of the halorespirers, which are able to gain energy from the dehalogenation reaction, and facultative anaerobes catalyze further conversion of PCE to less chlorinated compounds. To date, only Dehalococcoides ethenogenes strain 195 has been known to degrade PCE to the nontoxic compound ethene (11), while most other natural biotic and abiotic processes degrade PCE to result in toxic products (such as cis-dichloroethylene) and carcinogenic intermediates (such as vinyl chloride) (12)(13)(14)(15)(16).…”

Mortality among chemical workers at Texas City plant: 1940–2001

“…However, these associations are much weaker than between vinyl chloride and angiosarcoma of the liver with the presence of other risk factors such as hepatitis B virus. (Wong et al 1986;Kielhorn et al 2000;London and McGlynn 2006) Since only one person died of liver cancer among workers hired between 1970 and 2001 (SMR = 61), the risk factor(s) may have been eliminated or controlled in recent years. Indeed, in employees Table 4 Standardized mortality ratio (SMR) for deaths due to Cancer of central nervous system, benign brain tumors, and all brain tumors combined, in cohort subsets * Statistically signiWcant at P < 0.05…”