Mortality from liver angiosarcoma, hepatocellular carcinoma, and cirrhosis among vinyl chloride workers.

BACKGROUND: Occupational exposure to vinyl chloride monomer (VCM) has been established as a cause of hepatocellular carcinoma (HCC) and liver angiosarcoma (ASL). However, some controversy remains due to conflicting results on liver cirrhosis, and to evidence on HCC based on few confirmed cases. The aim of the study is to clarify the association between VCM exposure and mortality from liver diseases. METHODS: In a cohort of 1658 workers involved in VCM production and polymerization, Poisson regression was adopted to estimate rate ratios (RR) across categories of VCM exposure for mortality due to ASL (n = 9), HCC (n = 31) confirmed by histological/clinical records, and the combination of deaths from liver cirrhosis and from liver cancer with clinical/histological evidence of cirrhosis (n = 63). RESULTS: Cumulative VCM exposure was associated with study outcomes; RRs in the highest compared to the lowest exposure category were: ASL 91.1 (95%Confidence Interval 16.8-497), HCC 5.52 (2.03-15.0), liver cirrhosis 2.60 (1.19-5.67). CONCLUSIONS: The risk of death from liver cirrhosis, as well as from HCC in the largest available series of confirmed cases, increased with VCM exposure.

Osteopontin, asbestos exposure and pleural plaques: a cross-sectional study.

BACKGROUND: Osteopontin (OPN) is a plasma protein/cytokine produced in excess in several malignancies. In a recent study OPN was reported as being related to the duration of asbestos exposure and presence of benign asbestos-related diseases; however, it was unclear whether this protein was an indicator of exposure or effect. METHODS: In 193 workers, 50 with pleural plaques (PP), in whom different indicators of past asbestos exposure were estimated, OPN plasma levels were assessed using commercial quantitative sandwich enzyme immunoassays according to the manufacturer's instructions. RESULTS: Osteopontin increased with increasing age and several aspects of asbestos exposure, without differences related to the presence of pleural plaques. At multivariable regression analysis, the explanatory variables with a significant independent influence on OPN were length of exposure (positive correlation) and time elapsed since last exposure (positive correlation). CONCLUSIONS: Since asbestos in lung tissue tends to wane over time, OPN should decrease (rather than increase) with time since last exposure. Therefore, OPN cannot be a reliable biomarker of exposure nor effect (presence of pleural plaques).

Asbestos exposure and benign asbestos diseases in 772 formerly exposed workers: dose-response relationships.

BACKGROUND: Since previous studies have provided conflicting results, we investigated the relationship between the risk of benign asbestos-related diseases and different aspects of asbestos exposure in previous asbestos workers who underwent low-dose computed tomography (CT). METHODS: CT scans were carried out in 772 subjects. A questionnaire was employed to collect data on smoking habits and duration, peak and cumulative exposure, and time since first exposure to asbestos. Multiple logistic regression models with stepwise selection of variables were used to evaluate the associations. RESULTS: Fourteen (1.8%) cases of asbestosis, 187 (24.2%) of pleural plaques (PP), and 50 (6.5%) of diffuse pleural thickening (DPT) were found. The significant risk factors were: cumulative exposure for asbestosis (P for trend = 0.004); time since first exposure (P for trend <0.001), and peak exposure (P for trend <0.001) for PP; and time since first exposure for DPT (P for trend = 0.024). CONCLUSIONS: Parenchymal asbestosis and PP are associated with different aspects of asbestos exposure. DPT appears to be less specific for asbestos exposure.