Occupational exposure to combustion products rich in polycyclic aromatic hydrocarbons and particles is associated with an increased risk of lung cancer. This study aimed to evaluate whether the risk depended on the age at which the individuals were exposed.
Data from 1042 lung cancer cases and 2364 frequency-matched population controls selected from all men aged 40-75 years residing in Stockholm County, Sweden, at any time between 1985 and 1990, included detailed questionnaire information on occupational, residential, and smoking history. Occupational exposures were assessed by an occupational hygienist, and exposure to air pollution from road traffic was estimated based on dispersion models.
We found that individuals exposed to combustion products in their twenties were at higher risk than those never exposed (adjusted OR = 1.46; 95% CI 1.02, 2.10). The association was still evident after adjusting for a number of potential confounders, including lifetime cumulative exposure and latency. No clear association was found in those exposed at older ages.
Exposure to combustion products at a young age was associated with elevated risk of lung cancer. Exposure-reduction programs should be aware of the susceptibility of the younger employees.
BACKGROUND: Air pollution is suspected to cause lung cancer. The purpose was to investigate whether the concentration of nitrogen oxides (NOx) at the residence, used as an indicator of air pollution from traffic, is associated with risk for lung cancer. METHODS: We identified 679 lung cancer cases in the Danish Cancer Registry from the members of three prospective cohorts and selected a comparison group of 3,481 persons from the same cohorts in a case-cohort design. Residential addresses from January 1, 1971, were traced in the Central Population Registry. The NOx concentration at each address was calculated by dispersion models, and the time-weighted average concentration for all addresses was calculated for each person. We used Cox models to estimate incidence rate ratios after adjustment for smoking (status, duration, and intensity), educational level, body mass index, and alcohol consumption. RESULTS: The incidence rate ratios for lung cancer were 1.30 [95% confidence interval (95% CI), 1.07-1.57] and 1.45 (95% CI, 1.12-1.88) for NOx concentrations of 30 to 72 and >72 microg/m3, respectively, when compared with
A case-control study using logistic regression included 500 employees of the nuclear works (162 patients with lung carcinoma and 338 healthy controls). After examination of radiation and nonradiation causative factors 5 proved statistically significant. For them the following chance proportions were obtained: smoking 6.6, plutonium pneumosclerosis 4.6, plutonium incorporation 3.1, chronic nonspecific pulmonary diseases 2.1, external gamma-radiation 1.6. Attributive risk for the total of the radiation factors makes up 25% at the most while of the nonradiation factors at least 70%.
A case-control study of male-female differences in cigarette smoking and lung cancer was conducted during 1981-1985 in Toronto, St. Catharine's, and Niagara Falls, Ontario, Canada. In total, 442 female and 403 male histologically verified cancer cases were individually matched by age and area of residence to each other and to 410 female and 362 male randomly selected population controls. Subjects were interviewed concerning their exposures to various life-style factors, and in particular, they received detailed questioning regarding their lifelong histories of usage of tobacco products. It was found that, for both sexes, a greatly elevated risk of developing lung cancer was associated with cigarette consumption, increasing with pack-years of cigarettes smoked and declining with duration of time since quitting smoking. Furthermore, the association was significantly (p = 0.010) and appreciably stronger for females than for males. At a history of 40 pack-years relative to lifelong nonsmoking, the odds ratio for women was 27.9 (95% confidence interval (CI) 14.9-52.0) and that for men was 9.60 (95% CI 5.64-16.3). Higher odds ratios for females were also seen within each of the major histologic groupings. Thus, the higher elevated risk of lung cancer currently observed in other studies for female ever smokers compared with male ever smokers, while possibly attributable in part to greater smoking cessation among males, may be due to higher susceptibility among females.
It has been suggested that the well known associations between smoking and cancer may in part reflect inadequately controlled confounding due to occupational exposures. The purpose of the present analysis is to describe the association between cigarette smoking and both lung and bladder cancers, taking into account the potential confounding effects of over 300 covariates, most of which represent occupational exposures. A population-based case-control study was undertaken in Montreal to investigate the associations between a large variety of environmental and occupational exposures, on the one hand, and several types of cancer, on the other. Interviews were carried out with male incident cases of several sites of cancer, including 857 lung cancers and 484 bladder cancers. A group of non-smoking-related cancers, comprising 1,707 interviewed subjects, was used as one control group. Additionally, 533 population controls were interviewed and constituted a second control group. Interview information included detailed lifetime smoking histories, job histories, and other potential confounders. Each job history was reviewed by a team of experts who translated it into a history of occupational exposures. These occupational exposures, as well as nonoccupational covariates, were treated as potential confounders in the analysis of cigarette smoking effects. Regardless of whether population controls or cancer controls were used, the odds ratio (OR) between smoking and lung cancer (ranging from 12 to 16 for ever vs never smokers) was not materially affected by adjustment for occupational exposures. The odds ratios for bladder cancer (ranging from 2 to 3) were also unaffected by confounding due to occupational exposures.(ABSTRACT TRUNCATED AT 250 WORDS)
The authors report the association between exposure to pulsed electromagnetic fields (PEMFs) and cancer in a nested case-control study of electric utility workers in Quebec, Canada (follow-up, 1970-1988), and France (follow-up, 1978-1989), among whom 2,679 cases of cancer were identified. Exposures were assessed through a job-exposure matrix based on about 1,000 person-weeks of measurements from exposure meters worn by workers. Exposures were considerably higher in Quebec than in France. No association was found between PEMFs and cancers previously suspected of association with magnetic fields (leukemia, other hematopoietic cancers, brain cancer, or melanoma). However, there was a clear association between cumulative exposure to PEMFs and lung cancer, with odds ratios rising to 3.11 (95% confidence interval (CI) 1.60-6.04) in the highest exposure group (84 cases). This association with largely confined to Quebec, where there was a monotonic exposure-response relation with an odds ratio of 6.67 (95% CI 2.68-16.57) in the highest exposure group (32 cases). The association is substantial and was not explained by smoking or other occupational exposures. However, several factors limit the strength of the evidence for a causal relation: lack of precision in what the meters measured; little previous evidence for this association; and no elevated risk for lung cancer in the utility workers overall in comparison with the general population.
Comment In: Am J Epidemiol. 1996 Apr 15;143(8):8418610695
To study the possible work related reasons for the increased incidence of many cancers among seafarers.
A case-control study, nested in a cohort of all male seafarers (n = 30 940) who, according to the files of the Seamen's Pension Fund, had worked on board Finnish ships for any time during the period 1960-80. Cases of cancer of the lung, nervous system, kidney, and pancreas, leukaemia, lymphoma, and all cases histologically defined as mesotheliomas were identified from the Finnish Cancer Registry in 1967-92. The preceding numbers of years at sea in various occupational categories were collected according to the type of ship (dry cargo ship, tanker, passenger vessel, icebreaker, other vessel).
The incidence for lung cancer among engine crew increased with the increase in employment time, the odds ratio (OR) after three years being 1.68 (95% CI 1.17 to 2.41). The OR of lung cancer for deck officers was 0.42 (95% CI 0.29 to 0.61). Deck personnel on icebreakers had a significantly increased risk of lung cancer > or =20 years after first employment (OR 3.41, 95% CI 1.23 to 9.49). The OR for mesothelioma among engine crew with a latency of 20 years was 9.75 (95% CI 1.88 to 50.6). The OR for renal cancer among deck officers after three years employment was 2.15 (95% CI 1.14 to 4.08), but there was no increase by employment time or by latency. A rise of OR for lymphoma was detected among deck personnel on tankers, if the employment had lasted over three years (OR 2.78, 95% CI 0.98 to 7.92). The risk pattern for leukaemia was similar to that of lymphoma, the OR among deck personnel on tankers varying from 2.26 (95% CI 1.01 to 5.06) to 6.86 (95% CI 1.62 to 28.8) depending on the length of employment.
Results indicate that occupational exposures of deck crews on tankers add to their risk of renal cancer, leukaemia, and possibly lymphoma. Engine crews have an asbestos related risk of mesothelioma, and the engine room conditions also seem to increase risk of lung cancer.
Cites: Ann Occup Hyg. 1987;31(3):345-553426034
Cites: Tidsskr Nor Laegeforen. 1983 Dec 10;103(34-36):2312-66665778
Cites: Am J Ind Med. 1988;14(6):657-93232685
Cites: Am J Ind Med. 1990;17(6):711-252343876
Cites: Br J Ind Med. 1990 May;47(5):292-72357448
Cites: Am J Ind Med. 1991;19(5):673-62053581
Cites: Ann N Y Acad Sci. 1991 Dec 31;643:321-321809146
Cites: Tidsskr Nor Laegeforen. 1983 Dec 10;103(34-36):2317-206665779
Cites: J Occup Med. 1985 Dec;27(12):881-44087053
Cites: Br J Cancer. 1992 Sep;66(3):568-781520596
Cites: Occup Environ Med. 1994 Dec;51(12):804-117849863
Cites: Am J Ind Med. 1995 Apr;27(4):555-647793425
Cites: Ann Occup Hyg. 1995 Jun;39(3):347-617793753
Cites: Bull Inst Marit Trop Med Gdynia. 1993-1994;44-45(1-4):65-737580353
Cites: Cancer Causes Control. 1996 Mar;7(2):231-98740736
Cites: J Occup Environ Med. 1998 Aug;40(8):675-99729749
BACKGROUND: Exposures in nickel refineries represent complex chemical mixtures, but only the effect of nickel has been evaluated quantitatively in epidemiologic studies of nickel workers. METHODS: For a Norwegian refinery, time- and department-specific exposure estimates were developed for arsenic, sulfuric acid mists, and cobalt in air on the basis of personal measurements and chemical data on raw materials and process intermediates. Exposure to asbestos, as well as employment in high-risk occupations outside the refinery, were assessed. We conducted a case-control study nested in a cohort of refinery workers, with 213 cases (diagnosed 1952-1995) and 525 age-matched controls. We analyzed lung cancer risk, adjusted for smoking, by cumulative exposure and duration of work. RESULTS: There was a substantial association between cumulative exposure to water-soluble nickel and lung cancer risk. Weaker effects were suggested for exposure to arsenic at the refinery and for occupational exposures outside the refinery for 15 years or more. No detectable excess risk was found for refinery exposure to asbestos or sulfuric acid mists, and no dose-related increase in risk was seen from cobalt. CONCLUSIONS: Exposure to water-soluble nickel remained the most likely explanation for the excess lung cancer risk in the cohort. Other occupational exposures did not confound the strong dose-related effect of nickel to any appreciable degree.
Although it has been hypothesized that carbon black exposure may carry an excess risk of lung cancer, evidence to date is insufficient to assess the hypothesis properly. The relationship between workplace exposure to carbon black and lung cancer risk was examined in a population-based case-control study carried out in Montreal, Canada. Detailed job histories were elicited from 857 incident cases with histologically confirmed lung cancer as well as from 1,360 cancer controls and 533 population controls. Job histories were evaluated by a team of hygienists and chemists for evidence of exposure to a host of occupational substances, including carbon black. Logistic regression analyses adjusting for smoking and other nonoccupational and occupational potential confounders suggested no significant increase in risk with relatively low exposure to carbon black. Some increase in risk for all lung cancers was apparent with relatively high exposure using cancer controls (OR = 2.17; 95% CI = 0.95-4.91) and population controls (OR = 1.52; 95% CI = 0.58-3.97). Individuals with relatively high exposure had a significantly greater risk of oat-cell carcinoma using either control series (OR = 5.05; 95% CI = 1.72-14.87 using cancer controls and OR = 4.82; 95% CI = 1.36-17.02 using population controls). These results provide some evidence for an association between exposure to carbon black and lung cancer.
Lung tissue, both normal and cancerous, has been found to express estrogen receptors and patterns of expression have differed between men and women, suggesting a possible role for hormone-related factors in lung carcinogenesis in women. Few epidemiological studies have examined hormone-related variables and lung cancer risk and the findings have not been consistent. We investigated the association between characteristics of menstruation and pregnancy in relation to lung cancer risk in a population-based case-control study carried out in Montreal, Canada, including 422 women with lung cancer and 577 controls. For each variable, odds ratios (OR) and 95% confidence intervals (CI) were estimated using unconditional logistic regression modeling. Associations were also examined according to level of smoking and by lung cancer histology. All statistical tests were two-sided. Most characteristics of menstruation and pregnancy were not associated with lung cancer risk. However, an increased risk was observed for women who had had a non-natural menopause, which predominantly included women who had had a bilateral oophorectomy, compared with women who had had a natural menopause (OR = 1.92, 95% CI: 1.22-3.01). An inverse association with age at menopause was suggested. These results did not vary by level of smoking and they were similar for adenocarcinomas compared with other histological types. Our results suggest that hormonal factors, related to early menopause and/or ovary removal, may play a role in the risk of lung cancer. Further studies are needed to confirm these findings, and to assess the possible contribution of hormone replacement therapy.