Lack of association between -251 T>A polymorphism of IL8 and lung cancer risk.
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Female↗
Biomedical subjects
Paolo Boffetta
Publications and source records attributed to Paolo Boffetta.
Dietary patterns and risk of cancer of the oral cavity and pharynx in Uruguay.
From 1995 to 2002, a case-control study on food groups and risk of cancer of the oral cavity and pharynx was conducted in Montevideo, Uruguay. Two hundred thirty cases were frequency-matched to 460 controls on age, residence, and urban/rural status. The study was restricted to men. The relationship between foods and risk of oral and pharyngeal squamous cell carcinoma was examined through: 1) individual food group analysis, 2) factor analysis, and 3) determination of empirical scores. The results were similar. Factor analysis generated 2 patterns, which were labeled as "stew" and "vegetables and fruits." The stew pattern loaded positively on boiled meat, cooked vegetables, potato, and sweet potato. This pattern was directly associated with risk of oral and pharyngeal cancer [odds ratio (OR), 3.75; 95% confidence interval (CI), 1.99-7.06; P value for trend=0.0002]. The vegetables and fruits factor loaded positively on raw vegetables, citrus fruits, other fruits, liver, fish, and desserts. This pattern was inversely associated with risk of oropharyngeal carcinoma (OR, 0.34; 95% CI, 0.18-0.64; P value for trend=0.0008). Joint effects of high intake of risk foods and low intake of protective foods were associated with a risk of 12.0 (95% CI, 4.1-34.6). Our study confirms the important role of dietary factors in oral and pharyngeal cancer risk and suggests that the analysis of dietary patterns is a powerful tool to investigate the links between nutrition and cancer.
Adult↗
Chromosomal aberrations in lymphocytes of healthy subjects and risk of cancer.
There is evidence that increased frequency of chromosomal aberration (CA) in peripheral blood lymphocytes is a predictor of cancer, but further data are needed to better characterize CA as marker of cancer risk. From the archives of 15 laboratories we gathered cytogenetic records of 11,834 subjects who were free of cancer at the moment of blood drawing and who underwent cytogenetic examination for preventive purposes in the Czech Republic during 1975-2000. We linked these records to the national cancer registry, revealing a total of 485 cancer cases. Subjects were classified according to the percentiles of CA distribution within each laboratory as low (0-33rd percentile), medium (34-66th percentile), and high (66-100th percentile). Subjects were further classified by occupational exposure and by subclass of CA. We found a significant association between the overall cancer incidence and the presence of chromosome-type aberrations [relative risk (RR) for high vs. low CA level = 1.24; 95% confidence interval (CI), 1.03-1.50] but not chromatid-type aberrations. Stomach cancer showed a strong association with frequency of total CA (RR = 7.79; 95% CI, 1.01-60.0). The predictivity of CA observed in subjects exposed to various classes of carcinogens did not significantly differ from the group of nonexposed subjects. This study contributes to validation of CA as a predictive marker of cancer risk, in particular, of stomach cancer; the association between CA frequency and cancer risk might be limited to chromosome-type aberrations.
Adult↗
Cancer in the Norwegian printing industry.
OBJECTIVES: The aim of this study was to investigate cancer risk among Norwegian workers in the printing industry, particularly lung and bladder cancer. METHODS: Cancer incidence was investigated from 1953 through 1998 in a cohort of 10 549 male members of a trade union in the printing industry in Oslo and nearby areas. Rates from the region, were used to calculate standardized incidence ratios (SIR) separately for the skilled and unskilled workers. Smoking data from a sample of the cohort were utilized for evaluating the risk estimates of smoking-related cancers. Specific exposure data were not available. RESULTS: Among the skilled workers, significantly elevated risks of cancer of the urinary bladder [standardized incidence ratio (SIR) 1.47, 95% confidence interval (95% CI) 1.19-1.79], liver (SIR 1.92, 95% CI 1.15-2.99), pancreas (SIR 1.46, 95% CI 1.07-1.94) and colon (SIR 1.27, 95% CI 1.05-1.55) were observed, whereas an increased risk of lung cancer in this group was confined to those born before 1910. Among the unskilled workers, there were significantly increased risks of cancer of the mouth, esophagus, stomach, larynx, lung, and all sites. CONCLUSIONS: The study showed that workers in the printing industry were at increased risk of several types of cancer. In particular the increased risk of bladder cancer among the skilled workers is suggestive of an occupational cause. However, no specific agent could be identified as an occupational carcinogen. The results did not support the hypothesis of a generally increased risk of lung cancer. The risk pattern for unskilled workers may reflect confounding by nonoccupational factors.
Aged↗
Supraglottic and glottic carcinomas: epidemiologically distinct entities?
In the time period 1988-2000, a case-control study on laryngeal cancer was conducted in Montevideo, Uruguay. Four-hundred eighty-one (481) cases newly diagnosed and microscopically confirmed as squamous cell carcinomas were included. These cases were frequency matched with 481 nonneoplastic controls, admitted to the same hospitals as the cases. The purpose of our study was to compare odds ratios (ORs) by laryngeal subsite (supraglottis and glottis). ORs of supraglottic cancers displayed much higher risks than glottic carcinomas for most tobacco variables and for red wine intake. The differences between subsites were statistically significant, displaying heterogeneity between both subsites. Moreover, whereas black tobacco smokers displayed a significant increased risk of 1.7 (95% confidence interval [CI] 1.2-2.5) compared to smokers of blond (flue-cured) tobacco among supraglottic tumors, no effect of this type of tobacco was observed in glottic lesions. It could be suggested that concerning tobacco and alcohol effects, supraglottic and glottic squamous cell cancers are probably distinct epidemiologic entities.
Adult↗
Amount of DNA in plasma and cancer risk: a prospective study.
Levels of plasma DNA concentrations in cancer patients have been shown to be higher than the plasma DNA concentrations found in healthy subjects. The value of plasma DNA levels for development of neoplastic or pulmonary disease was evaluated in a large prospective study. Plasma samples (n = 1,184) were analyzed from 776 controls, 359 cases of cancer (lung, bladder, oral cavity, pharynx, larynx, leukemia) and 49 deaths from chronic obstructive pulmonary disease (COPD), including never smokers and ex-smokers, from 9 countries across Europe. The amount of plasma DNA was variable across the European Prospective Investigation into Cancer and Nutrition (EPIC) centers. High DNA concentrations in some centers might be due to the type of population recruited and/or the treatment of the samples. An elevated and statistically significant odds ratio (OR) was found for COPD deaths (OR = 2.53; 95% CI = 1.06-6.02), while nonsignificant increased ORs were present for oral cancers, cancers of the pharynx and larynx and leukemia. When the analyses were stratified by time since recruitment (below or above 36 months), the increased ORs were limited to the more recent period of recruitment, i.e., a time elapsed between blood drawing and disease onset lower than 36 months. This was particularly true for COPD deaths (OR = 12.7; 95% CI = 1.57-103) and leukemia (OR = 2.37; 95% CI = 1.20-4.67).
Adult↗
Epidemiology of environmental and occupational cancer.
Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, while results for lung cancer are less consistent. Several good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air, with a relative risk in the order of 1.06 for exposure at 100 Bq/m3. In several Asian populations, an increased risk of lung cancer results among women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A total of 29 occupational agents are established human carcinogens, and another 30 agents are suspected carcinogens. In addition, at least 12 exposure circumstances entail exposure to carcinogens. Exposure is still widespread for many important occupational carcinogens, such as asbestos, coal tar, arsenic and silica, in particular in developing countries. Although estimates of the global burden of occupational and environmental cancer result in figures in the order of 2% and less than 1%, respectively, these cancers concentrate in subgroups of the population; furthermore, exposure is involuntary and can, to a large extent, be avoided.
Air Pollution, Indoor↗
GST, NAT, SULT1A1, CYP1B1 genetic polymorphisms, interactions with environmental exposures and bladder cancer risk in a high-risk population.
Tobacco smoking and occupation are major risk factors of bladder cancer via exposure to polycyclic aromatic hydrocarbons (PAHs) and aromatic amines. Glutathione S-transferase (GST) M1, T1 and P1 are involved in the detoxification of PAH reactive metabolites. Two N-acetyltransferase isozymes, NAT2 and NAT1, have major roles in catalyzing the N-acetylation and O-acetylation of aromatic amines. Cytochrome p450 1B1 (CYP1B1) and sulfotransferase 1A1 (SULT1A1) are also involved in the metabolism of PAHs and aromatic amines. It is hypothesized that the genetic polymorphisms of these metabolic enzymes have an effect on the individual susceptibility to bladder cancer in particular by interacting with relevant environmental exposures. A hospital-based case-control study among men in Brescia, Northern Italy recruited 201 incidence cases and 214 controls from 1997-2000. Occupational exposures were blindly coded by occupational physicians. Genotyping of polymorphisms were carried out with PCR-RFLP method. Unconditional multivariate logistic regression was applied to model the association between genetic polymorphisms and bladder cancer risk. Effect modifications by age of onset, smoking and occupational exposures to PAHs and aromatic amines were evaluated. We also conducted an analysis of interaction between genetic factors. GSTM1 and GSTT1 null genotype were associated with an increased risk of bladder cancer with an odds ratio (OR) of 1.69 (95% confidence interval [CI] = 1.11-2.56) and 1.74 (95% CI = 1.02-2.95), respectively. The effect of GSTM1 null was seen particularly in heavy smokers, and there was a combined effect with occupational exposure of aromatic amines (OR = 2.77, 95% CI = 1.08-7.10). We observed a trend (p-value < 0.01) of increasing cancer risk comparing subjects with normal GSTM1 and T1 activity to subjects with one (OR = 1.82, 95% CI = 1.16-2.85) or both null genotypes (OR = 2.58, 95% CI = 1.27-5.23). NAT2 slow acetylator was associated with marginally increased risk of bladder cancer (OR = 1.50, 95% CI = 0.99-2.27), and the OR for the joint effect with occupational exposure of aromatic amines was 3.26 (95% CI = 1.06-9.95). SULT1A1 Arg213His polymorphism showed a marginal protective effect. These findings suggest that individual susceptibility to bladder cancer may be modulated by GSTM1, GSTT1 and NAT2 polymorphisms.
Adult↗
Association of metabolic gene polymorphisms with tobacco consumption in healthy controls.
Polymorphisms in genes that encode for metabolic enzymes have been associated with variations in enzyme activity between individuals. Such variations could be associated with differences in individual exposure to carcinogens that are metabolized by these genes. In this study, we examine the association between polymorphisms in several metabolic genes and the consumption of tobacco in a large sample of healthy individuals. The database of the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens was used. All the individuals who were controls from the case-control studies included in the data set with information on smoking habits and on genetic polymorphisms were selected (n = 20938). Sufficient information was available on the following genes that are involved in the metabolism of tobacco smoke constituents: CYP1A1, GSTM1, GSTT1, NAT2 and GSTP1. None of the tested genes was clearly associated with smoking behavior. Information on smoking dose, available for a subset of subjects, showed no effect of metabolic gene polymorphisms on the amount of smoking. No association between polymorphisms in the genes studied and tobacco consumption was observed; therefore, no effect of these genes on smoking behavior should be expected.
Arylamine N-Acetyltransferase↗
Genetic polymorphisms of MPO, COMT, MnSOD, NQO1, interactions with environmental exposures and bladder cancer risk.
Tobacco smoking and occupational exposure are major risk factors of bladder cancer via exposure to polycyclic aromatic hydrocarbons (PAHs) and aromatic amines, which lead to oxidative stress and DNA damage. Several enzymes, which play key roles in oxidative stress are polymorphic in humans. Myeloperoxidase (MPO) produces a strong oxidant for microbicidal activity, and activates carcinogens in tobacco smoke. Catechol-O-methyltransferase (COMT) catalyzes the methylation of endo- and xenobiotics and prevents redox cycling. NAD(P)H:quinone oxidoreductase (NQO1) catalyzes the two-electron reduction of quinoid compounds, which also protects cells from redox cycling. Manganese superoxide dismutase (MnSOD) protects cells from free radical injury. To test the hypothesis that the risk of bladder cancer can be influenced by polymorphisms in the genes that modulate oxidative stress, in particular by interacting with environmental carcinogens, we conducted a hospital-based case-control study among men in Brescia, Northern Italy. We recruited and interviewed 201 incident cases and 214 controls from 1997 to 2000. Occupational exposures to PAHs and aromatic amines were coded blindly by occupational physicians. Unconditional multivariate logistic regression was applied to model the association between genetic polymorphisms and bladder cancer risk and the effect of modifications of smoking and occupational exposures were evaluated. MPO G-463A homozygous variant was associated with a reduced risk of bladder cancer with an OR of 0.31 (95% CI = 0.12-0.80). MnSOD Val/Val genotype increased the risk of bladder cancer with OR of 1.91 (95% CI = 1.20-3.04), and there was a combined effect with smoking (OR = 7.20, 95% CI = 3.23-16.1) and PAH (OR = 3.02, 95% CI = 1.35-6.74). We did not observe an effect of COMT Val108Met polymorphism. These findings suggest that individual susceptibility of bladder cancer may be modulated by MPO and MnSOD polymorphisms, and that the combination of genetic factors involved in oxidative stress response with environmental carcinogens may play an important role in bladder carcinogenesis.
Adult↗
Pooled analysis of alcohol dehydrogenase genotypes and head and neck cancer: a HuGE review.
Possession of the fast metabolizing alleles for alcohol dehydrogenase (ADH), ADH1B*2 and ADH1C*1, and the null allele for aldehyde dehydrogenase (ALDH), ALDH2*2, results in increased acetylaldehyde levels and is hypothesized to increase the risk of head and neck cancer. To examine this association, the authors undertook a Human Genome Epidemiology review on these three genes and a pooled analysis of published studies on ADH1C. The majority of Asians had the fast ADH1B*2 and ADH1C*1 alleles, while the majority of Caucasians had the slow ADH1B*1/1 and ADH1C*1/2 genotypes. The ALDH2*2 null allele was frequently observed among Asians, though it was rarely observed in other populations. In a pooled analysis of data from seven case-control studies with a total of 1,325 cases and 1,760 controls, an increased risk of head and neck cancer was not observed for the ADH1C*1/2 genotype (odds ratio = 1.00, 95% confidence interval: 0.81, 1.23) or the ADH1C*1/1 genotype (odds ratio = 1.14, 95% confidence interval: 0.92, 1.41). Increased relative risks of head and neck cancer were reported for the ADH1B*1/1 and ALDH2*1/2 genotypes in several studies. Recommendations for future studies include larger sample sizes and incorporation of relevant ADH and ALDH genes simultaneously, as well as other genes. These considerations suggest the potential for the organization of a consortium of investigators conducting studies in this field.
Alcohol Dehydrogenase↗
Secondhand smoke exposure in adulthood and risk of lung cancer among never smokers: a pooled analysis of two large studies.
The interpretation of the evidence linking exposure to secondhand smoke with lung cancer is constrained by the imprecision of risk estimates. The objective of the study was to obtain precise and valid estimates of the risk of lung cancer in never smokers following exposure to secondhand smoke, including adjustment for potential confounders and exposure misclassification. Pooled analysis of data from 2 previously reported large case-control studies was used. Subjects included 1263 never smoking lung cancer patients and 2740 population and hospital controls recruited during 1985-1994 from 5 metropolitan areas in the United States, 11 areas in Germany, Italy, Sweden, United Kingdom, France, Spain and Portugal. Odds ratios (ORs) of lung cancer were calculated for ever exposure and duration of exposure to secondhand smoke from spouse, workplace and social sources. The OR for ever exposure to spousal smoking was 1.18 (95% CI = 1.01-1.37) and for long-term exposure was 1.23 (95% CI = 1.01-1.51). After exclusion of proxy interviews, the OR for ever exposure from the workplace was 1.16 (95% CI = 0.99-1.36) and for long-term exposure was 1.27 (95% CI = 1.03-1.57). Similar results were obtained for exposure from social settings and for exposure from combined sources. A dose-response relationship was present with increasing duration of exposure to secondhand smoke for all 3 sources, with an OR of 1.32 (95% CI = 1.10-1.79) for the long-term exposure from all sources. There was no evidence of confounding by employment in high-risk occupations, education or low vegetable intake. Sensitivity analysis for the effects of misclassification (both positive and negative) indicated that the observed risks are likely to underestimate the true risk. Clear dose-response relationships consistent with a causal association were observed between exposure to secondhand smoke from spousal, workplace and social sources and the development of lung cancer among never smokers.
Aged↗
Dietary patterns and risk of gastric cancer: a case-control study in Uruguay.
BACKGROUND: Gastric cancer is a frequent malignancy in the Uruguayan population. In northern counties, incidence rates reach high figures (age-standardized rates [ASR], 37.3 per 100,000 men and 18.3 per 100,000 women). Diet is a major determinant in gastric carcinogenesis. Because foods or food groups have the advantage over nutrients in being most directly related to dietary recommendations, we decided to conduct a case-control study on the relationships between food groups and risk of gastric cancer. For this purpose, we included 240 cases and 960 controls. METHODS: In the present study we employed three analytical approaches: (1) individual food group analysis, (2) factor analysis, and (3) analysis of empirical scores of risk. Individual analysis of food groups was performed by multiple unconditional logistic regression, with food groups being the explanatory variables. Nineteen food groups were created and categorized in tertiles according to the control distribution. Factor analysis aggregated intercorrelated foods in broader eating patterns. In this study we were able to identify three factors or patterns, arbitrarily labeled "starchy," "healthy," and "mixed." Finally, empirical scores of risk were created after examining the risk of each individual food and summing each significant item. This resulted in a risk enhancing score and a protective score. Both scores were categorized in tertiles according to the control distribution. RESULTS: The individual analysis of food groups showed increased risks of gastric cancer for rice, salted meat, stewed meat, white bread, potatoes, and tubers. On the other hand, raw vegetables, total fruits, legumes, and black tea were inversely associated with risk of gastric cancer. All three dietary patterns, generated by factor analysis, were significantly associated with gastric carcinoma risk. Whereas the starchy factor was directly associated with gastric cancer, the healthy and mixed patterns were strongly protective. Finally, the risk enhancing empirical score displayed an increased risk of gastric cancer (odds ratio [OR], 4.1, 95% confidence interval [CI], 2.6-6.6), whereas the protective score showed an important reduction in risk, of 0.38. CONCLUSION: This study displayed consistent results from three different approaches. Concerning different food groups, stewed and processed meat are rich in salt; rice, tubers, and winter squash are sources of starch; and vegetables and fruits are rich in ascorbic acid and carotenoids. All these substances have been strongly related to gastric carcinogenesis. Furthermore, this study suggests that diets rich in vegetables and fruits and with low amounts of salty and starchy foods are recommendable for the prevention of gastric cancer.
Adult↗
Cigarette smoking and risk of large cell carcinoma of the lung: a case-control study in Uruguay.
In the time period 1988-2000, a case-control study on large cell carcinoma of the lung was conducted in Montevideo, Uruguay. The study included 149 cases (139 men and 10 women) and 596 controls (556 men and 40 women) afflicted with diseases not related with tobacco smoking. Cases and controls were frequency matched on age, sex, residence and urban/rural status. According to our results, large cell carcinoma was strongly related with cigarette smoking (OR for heavy smokers 155.2, 95% CI: 30.6-786.1). Furthermore, all cases displayed higher risks for intensity compared with smoking duration. Smokers of black tobacco showed odds ratios (ORs) significantly higher than those presented by smokers of blond tobacco and smoking cessation displayed a reduction in risk of 95%, close to the risk of never smokers. Finally, filter use was not associated with any reduction in risk. It could be concluded that undifferentiated large cell carcinoma of the lung could be included among those lung tumors classified as Kreyberg I cancers.
Adult↗
Smoking-adjusted incidence of lung cancer by occupation among Norwegian men.
OBJECTIVE: To use aggregated data on smoking habits and lung cancer incidence in occupations assumed to carry no lung cancer risk to control for confounding in other occupational groups. METHODS: Lung cancer incidence was observed from 1971 to 1991 for 53 occupational groups and a group of economically inactive men in a national cohort study. Data on occupation and smoking habits were collected from national surveys during 1965-1980. The relationship between smoking habits and lung cancer incidence was estimated on aggregated level using data from 12 occupational groups that were initially assumed not to be exposed to occupational lung carcinogens. The estimated relationship was used to control confounding from smoking in the other groups. The results were presented as smoking-adjusted incidence ratios. RESULTS: A significant excess risk was found for 26 groups. It was estimated that about 20% of all lung cancer among men could be related to occupation after adjusting for the effect of smoking. CONCLUSIONS: Our method provided a clearer picture of the occupational risk and could be useful in other situations where individual information on smoking habits is lacking.
Adult↗
Occupational risk factors for lung cancer in men and women: a population-based case-control study in Italy.
OBJECTIVE: We investigated the role of occupation in lung cancerogenesis in two Northern Italian areas. METHODS: During 1990-1992, occupational histories were obtained for 1171 incident lung cancer cases (956 men, 176 women) and 1553 population controls (1253 men, 300 women) and were evaluated for having been employed in jobs entailing exposure to known or suspected lung carcinogens. A further exploratory analysis on other job titles and branches of industry was conducted. RESULTS: Among men, we found a smoking-adjusted odds ratio (OR) of 2.1 (95% confidence interval: 1.6-2.8) for exposure to known carcinogens, corresponding to a population attributable risk of 9.5% (6.0-13.0). Non-ferrous metal workers and painters had a significantly increased risk. No association was found for exposure to suspected carcinogens. In the exploratory analysis, the OR was increased for cleaners (OR: 2.7; 1.0-7.4), bakers (5.7; 1.4-24), tailors (6.9; 1.2-39), plumbers and pipe fitters (2.6; 1.0-6.4), welders and flame-cutters (5.6; 2.1-15), dockers and freight handlers (1.7; 1.0-2.7) and construction workers (1.4; 1.1-1.9). Female glass workers, laundry/dry cleaners and workers in rubber industry had an increased risk. CONCLUSIONS: The study indicates that a sizable proportion of lung cancers among men may be due to occupational exposures and suggests that exposure to lung carcinogens occurs in different jobs in women compared to men.
Aged↗
Mortality among workers employed in the titanium dioxide production industry in Europe.
OBJECTIVES: To assess the risk of lung cancer mortality related to occupational exposure to titanium dioxide (TiO2). METHODS: A mortality follow-up study of 15,017 workers (14,331 men) employed in 11 factories producing TiO2 in Europe. Exposure to TiO2 dust was reconstructed for each occupational title; exposure estimates were linked with the occupational history. Observed mortality was compared with national rates, and internal comparisons were based on multivariate Cox regression analysis. RESULTS: The cohort contributed 371,067 person-years of observation (3.3% were lost to follow-up and 0.7% emigrated). 2652 cohort members died during the follow-up, yielding standardized mortality ratios (SMRs) of 0.87 (95% confidence interval [CI] 0.83-0.90) among men and 0.58 (95% CI 0.40-0.82) among women. Among men, the SMR of lung cancer was significantly increased (1.23, 95% CI 1.10-1.38); however, mortality from lung cancer did not increase with duration of employment or estimated cumulative exposure to TiO2 dust. Data on smoking were available for over one third of cohort members. In three countries, the prevalence of smokers was higher among cohort members compared to the national populations. CONCLUSIONS: The results of the study do not suggest a carcinogenic effect of TiO2 dust on the human lung.
Adolescent↗
Occupational exposure to vinyl chloride, acrylonitrile and styrene and lung cancer risk (europe).
Several industry-based cohort studies have addressed the risk of lung cancer following exposure to vinyl chloride, acrylonitrile and styrene, with inconsistent results and usually without smoking adjustment. These exposures are addressed here in a large case-control study with full adjustment for smoking. Almost 6000 subjects were included in a case-control study conducted in seven European countries. For each job they held, local experts assessed the exposure to a number of occupational agents, including vinyl chloride, acrylonitrile and styrene, on the basis of detailed occupational questionnaires. Information on tobacco consumption and other risk factors was also collected. The odds ratio (OR) for ever exposure to vinyl chloride was 1.05 (95% confidence interval, CI: 0.68-1.62) and a modest, non-significant increase in the risk of lung cancer was found in the highest exposed subgroup. The OR for ever exposure to acrylonitrile was 2.20 (95% CI: 1.11-4.36) with a positive dose-response relationship between estimated cumulative exposure and lung cancer risk. No association between exposure to styrene and lung cancer risk was found. In conclusion, we cannot exclude a weak association between occupational exposure to vinyl chloride and lung cancer risk. Exposure to acrylonitrile was associated in our study with risk of lung cancer. Exposure to styrene does not seem to increase lung cancer risk.
Acrylonitrile↗