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Vinyl-chloride monomer (VCM) is classified as a known carcinogen of the liver; for lung cancer, some results suggest a potential association with polyvinyl chloride (PVC) dust. We evaluated the relationship between lung cancer mortality and exposure as PVC baggers in a cohort of workers involved in VCM production and polymerization in Porto Marghera (Venice, Italy) considering both employment status and smoking habits. The workers were studied between 1973 and 2017. A subset of them (848 over 1658) was interviewed in the 2000s to collect information about smoking habits and alcohol consumption. Missing values were imputed by the Multivariate Imputation by Chained Equations (MICE) algorithm. We calculated standardized mortality ratios (SMR) and 95% confidence intervals (95% CIs) using regional reference rates by task (never, ever, and exclusively baggers) and by smoking habits. Mortality rate ratios (MRR), adjusted for age, calendar time, time since first exposure, and smoking habits, were obtained via Poisson regression using Rubin's rule to combine results from imputed datasets calculating the fraction of information due to non-response. Lung cancer mortality was lower than the regional reference in the whole cohort (lung cancer SMR = 0.92; 95% CI 0.75-1.11). PVC baggers showed a 50% increase in lung cancer mortality compared to regional rates (SMR = 1.48; 95% CI 0.82-2.68). In the cohort analyses, a doubled risk of lung cancer mortality among PVC baggers was confirmed after adjustment for smoking and time-dependent covariates (MRR = 1.99, 95% CI 1.04-3.81). Exposure to PVC dust resulting from activity as bagger in a polymerization PVC plant was associated with an increase in lung cancer mortality risk after adjustment for smoking habits.

To ascertain whether the current risk of lung cancer in former asbestos workers was higher than in the general population, 1,557 past asbestos workers were recruited during statutory health examinations (from 2000 onward) and followed up for mortality. Standardized mortality ratios (SMRs) were calculated. Poisson regression was used to adjust the rate ratios (RRs) for confounders. SMR was about 1.00 in workers with or without pleural plaques and 4.62 (95% confidence interval: 0.61-18.1) in those with asbestosis. Adjusted RRs for lung cancer were 4.70 (0.99-22.5) for asbestosis, 4.35 (0.97-19.5) for former smokers, 6.82 (1.38-34.4) for current smokers. Currently, lung cancer mortality in past asbestos workers is similar to the general population, probably because workers more exposed /more susceptible could have died from lung cancer before the beginning of follow-up.

Background: In a mesothelioma lawsuit, the Public Prosecutor commissioned an expert evidence on the legal accountability for the disease, because the patient experienced multiple exposures to asbestos in both occupational and environmental settings., Objectives: To collect information on asbestos exposure from all available sources and to quantify the contribution of each source of exposure as a percentage of the total risk., Methods: We retrieved information on jobs done and asbestos exposure from a work colleague and a database maintained by the National Institute for Insurance of Occupational Accidents/Diseases, respectively. Information on environmental exposure was searched through the scientific literature. The contribution of each source of exposure was quantified with a method of risk apportionment, taking into account time elapsed since first and last exposure, intensity and frequency of exposure and carcinogenic potency of asbestos fiber mix., Results: The subject worked in the maintenance of railway electrification system. The mechanical compression stress induced on the ballast during passage of trains released chrysotile (from fragmented stones) and crocidolite (through abrasive action of crushed gravel on the underbody of rolling stocks insulated with friable crocidolite). Despite the low cumulative exposure (about 2 ff×years/cc), 99% of the mesothelioma risk was attributable to the work done because of the high content of crocidolite of inhaled asbestos., Conclusions: The report of an uncommon source of occupational asbestos exposure and a scientifically based method to allocate mesothelioma risk among multiple exposure could help to recognize mesothelioma as occupational disease in the workers employed in maintenance of the railway electrification system under the Italian National Railways.

Cytochrome P4501A2 (CYP1A2) is a key enzyme for lung carcinogen activation and lung inflammation. We studied the interactions of the CYP1A2 functional variants -3860G/A(rs2069514),-2467T/delT(rs3569413),-163C/A(rs762551)] with occupational/environmental carcinogenic exposures in the development of lung cancer in a case-control study nested in the Danish prospective cohort "Diet, Cancer and Health." At enrollment (1993-1997), blood samples for genotype analyses and information on lifestyle were collected 5 (mean value) years before the onset of the disease. The study population included 425 lung cancer cases and 786 subcohort members, who were gender- and age-matched. We found that -163A carriers were at increased risk of lung cancer (P=0.035) in a multivariate COX regression model, which was adjusted for personal habits (i.e., cumulative smoking, passive smoke at home, alcohol intake, and fruit intake) and occupational exposure. Additionally, the interaction between -2467delT and smoking increases lung cancer risk in males, especially light smokers (<21.5 pack-years, P=0.004). The increased lung cancer risk found in -163C carriers, independent of smoking status, and in -2467delT male smokers, suggests that these variants could influence lung cancer development through different mechanisms (i.e. lung carcinogen activation and lung inflammation)., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Low-dose computed tomography (CT) has been found to detect more Stage IA lung cancer than chest x-ray., Aims: To investigate whether lung cancer screening with CT was effective and acceptable in former asbestos workers., Methods: CT scanning was carried out following the protocol previously described in the literature. A questionnaire was used to assess cumulative asbestos exposure. An economic analysis was also performed. Informed consent was obtained from all patients., Results: A total of 1119 male asbestos workers (58% of invited) were examined, of whom 65% were smokers or ex-smokers. Mean age was 57.1 years with mean cumulative exposure to asbestos of 123 fibres/ml x years. Pleural plaques were found in 375 workers (32%), while 338 workers (29%) were included in the radiological follow-up, which led to 25 biopsies (13 of lung, 9 of pleura, 3 of both) and five screen-detected lung cancers (0.4%), one in Stage I. Incidence rate was 149 per 10(5), equal to that in the male general population of similar age. The expenses for diagnosis were 1014 and 244962 Euro per screened subject and screen-detected lung cancer case, respectively., Conclusions: Screening adherence and frequency of detection were low, while costs and radiation dose were high. In spite of a high cumulative asbestos exposure, lung cancer risk was not increased relative to the general population. The screening programme was not felt to be cost-effective from the perspective of the government as a third-party funding agency.

This study aimed to identify new genetic characteristics contributing to individual susceptibility to smoke-induced lung cancer. Despite functional evidence of a possible role of cytochrome P450 1A2 (CYP1A2) in lung cancer susceptibility, no studies have evaluated the influence of CYP1A2 genotypes on lung cancer risk. We investigated the interaction between CYP1A2-T2467delT (allele*1D) polymorphism and smoking in Tunisian lung cancer cases (n=101 male smokers) separately for the histological types squamous cell carcinoma (SCC) (n=60) and adenocarcinoma (n=41), and in controls (n=98 male smokers) using a case-only study design. A significant interaction between CYP1A2-T/delT or delT/delT genotypes and tobacco consumption (pack-years) adjusted for age was evident (OR (95% CI) 7.78 (1.52-42.8)) in the SCC cases who smoked relatively less (< or =33 pack-years, I quartile value), but not in adenocarcinoma and controls. Our results suggest that CYP1A2-T2467delT polymorphism has an important role in lung carcinogenesis, especially SCC, among smokers.

The aim of this study was to confirm the exposure-dependent reduction in lung cancer risk reported for dairy farmers exposed to endotoxin and to evaluate the consequence of leaving dairy farming and taking employment in industry or services, where exposure to microbial agents is lower. Standardized mortality ratios, with 95% confidence intervals, for 2,561 self-employed dairy farmers were estimated, considering the general population of Veneto, Italy, from 1970 to 1998 as the reference. Sixty-two lung cancer cases, whose information was checked against clinical records, were compared with 333 controls in a cohort-nested case-control study. Odds ratios with 95% confidence intervals were estimated by logistic regression analysis. A downward trend of standardized mortality ratios for lung cancer across tertiles of number of dairy cattle on the farm was significant (p < 0.05) from 1970 to 1984 but not from 1985 to 1998, when most subjects were no longer dairy farmers. Age- and smoking-adjusted odds ratios for lung cancer significantly decreased with increasing number of dairy cattle (p for trend = 0.001) for workers for whom < or =15 but not >15 years had elapsed from the end of work to the end of follow-up. In conclusion, increased levels of endotoxin (or other associated environmental factors) might be protective against lung cancer; protection diminishes over time after that exposure is removed.

Previous studies have suggested that those in occupations exposed to endotoxin have a reduced rate of lung/respiratory cancer. An initial investigation found a significantly reduced risk of all sites malignant neoplasms in white male crop and livestock farmers, and black male and female crop farmers. This study provides data on lung/respiratory cancers in the same workers. Data were obtained from occupation and industry-coded US death certificates collected from 26 states for the period 1984-1993. Cause, sex, and race specific proportionate mortality ratios (PMRs) were calculated using a National Institute of Occupational Safety and Health computer program. A pooled relative risk (PRR) was obtained by summing up separately and then dividing the sex-race specific observed and expected cases, separately in crop and livestock farmers. Deaths from respiratory cancer were 12,482 and 2,290, and deaths from lung cancer were 12,091 and 2,201. In each sex and race group respiratory and lung cancer PMRs are generally lower than unity. Lung cancer PRR was 0.80 (0.78-0.81) in crop farmers and 0.70 (0.67-0.73) in livestock farmers, a significant difference (p < 0.0001). Comparison of our findings with those by Nieuwenhuijsen et al. [1999] reporting personal exposure measurements in groups of Californian farmers (endotoxin averaging 132.5 EU/m(3) during livestock farming against 19.9 EU/m(3) during field crop and fruit farming), suggests a decreasing lung cancer risk with increasing endotoxin exposure, and supports a possible dose-response relationship between the two.

A meta-analysis of epidemiologic studies for textile industry workers was undertaken in an attempt to evaluate whether the cancer risk varies within the textile industry in relation to the job held or the textile fiber used. We combined studies published up until 1990, when an ad hoc IARC Monograph was issued, and those published after 1990 with the aim of appreciating evidence of reversing trends in cancer risk. Observed and expected cases reported in the original studies were summed up and the totals were divided to obtain a pooled relative risk (PRR) with a 95% confidence interval (CI) estimated with a fixed-effect model. We calculated a chi-square test (chi2) of heterogeneity among studies. When PRR and chi2 were both significant, PRR and CI were calculated with a random-effect model and the source of heterogeneity was investigated. Lung cancer risk was around 0.4 in the first study on cotton workers published in 1936, around 0.7 in subsequent studies, mostly published in the 1970s and 1980s, and around 1.0 in the last studies published in the 1990s. Papers published in the 1970s and 1980s produced consistent risk estimates for lung cancer risk, which was significantly lower than 1.0 in workers exposed to cotton (PRR = 0.77; CI = 0.69-0.86) and wool dust (0.71; 0.50-0.92), as well as in carders and fiber preparers (0.73; 0.54-0.91), weavers (0.71; 0.56-0.85), and spinners and weavers (0.78; 0.66-0.91). Lung cancer PRRs did not significantly deviate from 1.0 in textile workers using synthetic fibers or silk, and in dyers. Increased PRRs were found for sinonasal cancer in workers exposed to cotton dust, and in workers involved in spinning or weaving (4.14; 1.80-6.49). PRR was 1.46 (1.10-1.82) for cancer of the digestive system in textile workers using synthetic fibers or silk, and 1.34 (1.10-1.59) for colorectal cancer in spinners and weavers. The increased bladder cancer PRR in dyers (1.39; 1.07-1.71) is generally attributed to textile dye exposure. In studies published after 1990, there is a general tendency to move toward unity for all the cancer risk estimates, leading to an increasing heterogeneity among studies. Since adjustment for smoking made little difference to the findings, the latter could be attributed to the exposure to textile dusts. The recent findings could be due to a lowering of dust concentration in the workplaces. The reduction of cases of upper respiratory tract cancer parallels with a corresponding increase of lung cancer cases. So, preventive measures have paradoxically increased the lung cancer burden to the textile workers.