Risk Of Lung Cancer In Workers Research Articles

Lung cancer risk in workers occupationally exposed to polycyclic aromatic hydrocarbons with emphasis on the role of DNA repair gene

ObjectiveWorkers in secondary aluminum production plants are occupationally exposed to polycyclic aromatic hydrocarbons (PAHs). We aimed to monitor the concentrations of PAHs in air and in serum of workers at two secondary aluminum production plants. We also investigated the potential risk of lung cancer development among PAHs exposed workers with emphasis on the role of A1AT mutation and APEX1 gene polymorphisms.MethodsThis study included 177 workers from administrative departments and production lines. Blood samples were obtained for estimation of benzo(a)pyrene diol epoxide albumin adduct (BPDE-Alb adduct), anti-Cyclin-B1 marker (CCNB1) and squamous cell carcinoma antigen (SCCAg). Genes’ polymorphism for human apurinic/apyrimidinic endonuclease (APEX1) and alpha-1-anti-trypsin (A1AT) gene mutation were detected.ResultsThere was a significant increase in the level of BPDE-Alb adduct among exposed workers in comparison to non-exposed group. Moreover, 41.67% of exposed workers in El Tebbin had BPDE-Alb adduct level ≥ 15 ng/ml versus 29.6% of workers in Helwan factory. There was a significant increase in tumor markers (SCCAg and CCNB1) among workers whose BPDE-Alb adduct ≥ 15 ng/ml. There was a significant increase in the level of BPDE-Alb adducts in exposed workers carrying homozygous APEX1 genotype Glu/Glu. Furthermore, exposed workers with the Glu/Glu genotype had high tumor markers levels. There was a significant increase in levels of BPDE-Alb adducts in workers carrying A1AT mutant allele. Moreover, workers with mutant A1AT genotype had significantly high tumor markers (SCCAg and CCNB1) levels.ConclusionTherefore, we conclude that aluminum workers may be at a potential risk of lung cancer development due to PAHs exposure. Although PAHs concentrations in air were within the permissible limits, yet evidence of DNA damage was present as expressed by high BPDE-albumin adduct level in exposed workers. Also, elevation of tumor markers (SCCAg and CCNB1) in exposed workers points to the importance of periodic biological monitoring of such workers to protect them from cancer risk.

Respiratory cancer mortality and incidence in an updated cohort of Canadian nickel production workers

ABSTRACTRespiratory cancer mortality and incidence were examined in an updated cohort of >56,000 Canadian nickel mining and refining workers. There was little evidence to suggest increased lung cancer risk in workers who had no experience in high-risk sintering operations that were closed by 1972, apart from that which would be expected from probable increased smoking prevalence relative to the comparison population. There was no substantive evidence of increased laryngeal cancer risk in the cohort, nor was there evidence of increased pharyngeal cancer risk in nonsinter workers. Nasal cancer incidence was elevated in nonsinter workers, but excess risks appeared to be confined to those hired prior to 1960. These findings lead us to tentatively conclude that occupationally-related respiratory risks in workers hired over the past 45 years are either very low or nonexistent.

Increased lung cancer mortality among chrysotile asbestos textile workers is more strongly associated with exposure to long thin fibres

BackgroundAnimal data and physical models suggest that the carcinogenicity of asbestos fibres is related to their size and shape.ObjectivesTo investigate the influence of fibre length and diameter on lung cancer...

Lung Cancer Risk in Workers in the Meat and Poultry Industries – A Review

Laboratory and in vivo studies in primates, and serological evidence in humans, indicate that food animal oncogenic viruses show potential for causing cancer in humans. However, until fairly recently, supporting analytic epidemiologic studies have been lacking and have concentrated on lung cancer. We conducted an extensive Medline search and reviewed 60 studies investigating lung cancer risk in highly exposed workers in the meat and poultry industries. The overwhelming majority of studies of different designs (including all the cohort mortality and cancer incidence studies) indicate at least a 30% excess risk of lung cancer in meat and poultry plant workers, even after controlling for smoking. Evidence points to food animal oncogenic microorganisms as one of the main causes. This has important public health implications because the general population is also widely exposed. Studies carried out thus far have not had sufficient statistical power to investigate other potentially carcinogenic exposures within the industries. Thus, large studies that can adequately control for occupational and non-occupational confounding factors are needed, so that the possible role of food animal oncogenic viruses in the occurrence of human lung cancer can be clearly defined.

Lung Cancer Risk in Workers with Silicosis in the Czech Republic

Lung Cancer Risk in Workers with Silicosis in the Czech Republic

Lung cancer risk in workers exposed to poly(vinyl chloride) dust: a nested case-referent study

Background: There have been few investigations of an association between poly(vinyl chloride) (PVC) dust exposure and an increase in lung cancer incidence, and their conclusions have been inconsistent. Aims: To...

Lung cancer risk of workers in shoe manufacture and repair.

The occupational lung cancer risk in manufacturing and repair of shoes was studied by pooling of two major case-control studies from Germany. Some 4184 incident hospital-based cases of primary lung cancer and 4253 population controls, matched for sex, age, and region of residence were intensively interviewed with respect to their occupational and smoking history. Based on the occupational coding and a free text search, all individuals who had ever worked in shoe manufacturing or repair for at least half a year were identified. Shoemaker-years were calculated as the cumulated duration of working in shoe manufacturing or repair. Odds ratios (OR) and 95% confidence intervals (CI) were calculated via conditional logistic regression. Additional adjustment for smoking and occupational asbestos exposure was used. Seventy-six cases and 42 controls who had ever worked in shoe manufacture or repair (OR = 1.89, 95% CI: 1.29-2.78). After adjustment for smoking, this risk was lowered to 1.69 (95% CI: 1.09-2.62). Further adjustment for asbestos exposure only slightly changed the risk estimates upwards. The smoking adjusted OR in males was 1.50 (95% CI: 0.93-2.41) and 2.91 (95% CI: 0.90-9.44) in females. Logistic regression modeling showed a positive dose-effect relationship between duration of exposure in shoe manufacture and repair and lung cancer risk. The odds ratio for 30 years of exposure varied between 1.98 and 2.24 depending on the model specified. The study demonstrates an increased lung cancer risk for shoemakers and workers in shoe manufacturing. The risk seems to double after being 30 years in these occupations.

Adjustment for the confounding effect of cigarette smoking in an historical cohort mortality study of workers in a fiberglass manufacturing facility.

In 1986 a statistically significant lung cancer SMR based on U.S. white male national mortality rates was reported for male fibrous glass workers for follow-up through 1982 of a cohort of U.S. man-made mineral fiber workers. The Newark, Ohio, plant of Owens-Corning, which comprised 38% of the fibrous glass workers in that cohort, also exhibited a statistically significant lung cancer standardized mortality ratio based on U.S. white male mortality rates. A case-control study of the Newark workers demonstrated that a history of cigarette smoking and not exposure to respirable glass is the most important factor in lung cancer risk for workers at the Newark plant. We provide an estimate of the extent of confounding by cigarette smoking for the Newark plant nationally based lung cancer standardized mortality ratio with data not previously available and which suggests that adjusting for the confounding effect of cigarette smoking could reduce the lung cancer standardized mortality ratio to a non-statistically significant level.