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The aim of this study was to elucidate further whether occupational exposure to non-sensitising air pollution at workplaces increases the risk of adult onset asthma. One hundred and twenty persons with asthma diagnosed by general practitioners, aged 20–65 years, were compared with 446 referents matched for age and gender and living in the same community as the cases. Information about occupation, exposure to specific allergens, smoking habits, dwellings and atopy was obtained from a postal questionnaire. The subjects' occupations were categorised as clean or polluted, based on the judgement of the referents on their respective occupations. Three years or more of work in air-polluted workplaces resulted in an odds ratio of 1.7 (95% confidence interval 1.0–2.7). Stratification of the material on smoking habits, gender or atopy did not alter the results, nor did exclusion of subjects exposed to specific allergens of statistical significance in this material, e.g. flour dust. Smoking per se did not bring any risk of asthma. Working in buildings affected by dampness and mould brought a fourfold significant risk. In this study occupational exposure to unspecific air pollution at workplaces was associated with an increased risk of adult-onset asthma.

Exposure to organic solvents is still common in industrial and other work environments, and increases the risk of chronic toxic encephalopathy (CTE). Genetic variation in metabolic enzymes for solvents and other xenobiotics may modify the risk of developing toxic effects. Therefore, we investigated the presence of null genotypes for glutathione S-transferases M1 and T1 (GSTM1, GSTT1) and two genetic polymorphisms of microsomal epoxide hydrolase (mEPHX) in relation to the risk for chronic toxic encephalopathy (CTE) when exposed to solvents and smoking. We genotyped 115 patients who were classified into three categories: CTE (n3/4-56), incipient CTE (n3/4-27) and non-CTE (n3/4-32) patients. DNA was isolated from leucocytes and the GSTM1 and GSTT1 null genotypes were determined by multiplex-polymerase chain reaction. The two polymorphisms of mEPHX were analysed by PCR-RFLP (restriction fragment length polymorphism) based assays. All analyses were performed blindly with regard to both exposure and disease status. An increased binomial regression risk ratio3/4-2.5, 95% confidence interval (CI) 1.5-4.2, of the GSTM1 null genotype for CTE was found in smokers and for the GSTT1 null genotype (binomial regression risk ratio 1.5, 95% CI 1.0-2.0). In nonsmokers, the GSTM1 null genotype did not confer any risk for CTE. None of the studied mEPHX polymorphisms were associated with an increased risk for CTE. We suggest that the GSTM1 null genotype in smokers is a possible risk for solvent-induced CTE.

Purpose: This case-control study was undertaken to elucidate the controversy concerning whether low-level, long-term exposure to non-sensitising air pollution at workplaces may cause asthma. Methods: A case-control study of 192 adult-onset asthma cases aged 20-65 years and 323 controls was conducted in the southeast of Sweden. Cases were identified from computerised registers from the region, diagnosed 2000-2004 and diagnoses were confirmed via medical files. Referents were randomised from the population register of the region. Exposure was monitored by a 16-page questionnaire. Special attention was devoted to identifying and in the final analyses excluding subjects exposed to sensitising agents. Results: Three years or more of occupational exposure to air pollution from dust, smoke, fumes or vapours before the year of diagnosis by analyses adjusting for age yielded an increased risk for asthma (OR = 2.3, 95% CI 1.2-4.2) in men, while in women, no risk was seen. In a multiple logistic regression analysis in men without allergy in childhood, a significant risk was seen (OR = 2.8, 95% CI 1.07-7.4), when subjects exposed to identified allergens were excluded. In women, no excess risk was observed from occupational air pollution. Conclusion: The results of this study support an association between occupational exposure to low level non-sensitising air pollution and adult-onset asthma in men. Funding Agencies|Swedish Cancer and Allergy Foundation||Forss (Medical Research Council of Southeast Sweden)|2002-413

Objectives: The aim was to investigate different occupational and leisure time exposures as determinants for cryptogenic polyneuropathy. Methods: A case-referent study was conducted in Sweden including 232 cases of cryptogenic polyneuropathy 40–79 years of age at diagnosis who were enrolled from the out-patient neurology departments of 3 hospitals. From the population register 853 referents were randomly selected. Information on occupational and leisure time exposure was obtained from a postal questionnaire. The response rate was 71% for cases and for referents. Crude odds ratios (CORs) and logistic regression odds ratios (LORs) were calculated for exposures with 5 or more exposed cases and referents taken together. The reference category was defined as individuals unexposed to any of the occupational or leisure time risk factors in the questionnaire. Results: As expected, male sex and increasing age were significant determinants for cryptogenic polyneuropathy. Occupational exposures in men to Stoddard solvent, petrol exhausts, herbicides or hand and foot vibrations generated significantly increased CORs. LORs >3.50 were found in men for occupational exposure to sulphur dioxide, xylene, methyl ethyl ketone, herbicides and in women for occupational exposure to lead, nitrous oxide and insecticides. Only solvent exposure in leisure time remained significant in the regression analysis indicating that not only occupational exposures were of importance. Interactions between occupational and leisure time exposure were seen for several agents. Conclusions: Several known determinants for polyneuropathy, from animal studies and case reports, were confirmed. New determinants were also indicated, i.e. sulphur dioxide, xylene and methyl ethyl ketone.

As a result of the Chernobyl accident in 1986, exposure to radioactive cesium is still a concern in the contaminated regions of Belarus. We tested the hypothesis that long-term radiation exposure from the Chernobyl accident might increase the urinary excretion of the oxidative stress marker, 8-hydroxydeoxyguanosine (8-OHdG), in Belarussian children. Urinary 8-OHdG was determined in two groups of children (-n = 31 and n = 46) -living in contaminated and uncontaminated areas of Belarus, respectively (the majority of the unexposed children lived in the capital Minsk). The children from the contaminated areas had a significantly higher annual summary effective dose but significantly lower urinary 8-OHdG levels than the children from the uncontaminated areas. Unexpectedly, children living in uncontaminated urban areas had significantly higher urinary 8-OHdG levels than children living in uncontaminated rural areas. There was no statistically significant effect of sex or body mass index on urinary 8-OHdG, but there was a weak significant inverse correlation to age as well as to the annual summary effective dose. These findings suggest that radiation from the Chernobyl accident is now a less important contributor to oxidative stress in Belarussian children than urban living.

Objectives This case-referent study was performed to investigate the possibility of nonspecific air pollution at workplaces increasing the risk of bronchial asthma for formerly healthy adults. Methods Seventy-nine cases of asthma, diagnosed at a lung clinic, among persons aged 20--65 years were compared with 304 referents drawn randomly from the population of the catchment area. Questionnaire information was obtained regarding occupation, exposure to suspect allergens, place of residence, smoking habits, and atopy. The subjects' occupations were categorized into four air pollution classes based on how the referents reported air pollution in their respective occupations. Results Three years or more of work in air-polluted occupations resulted in an odds ratio of 3.0 (OR) (95% confidence interval 1.5--6.1) in a comparison with work in occupations with slight or no air pollution. Stratification of the material for smoking habits or atopy did not alter the results. Nor did the exclusion of specific exposures to asthmatogenic agents such as isocyanates, stainless steel welding, or aluminum salts change the effects of the nonspecific air pollution at workplaces. Smoking per se was associated with an almost doubled risk for asthma (OR 1.9, 95% confidence interval 1.1--3.4). Conclusion The results of this study support an association between occupational exposure to nonspecific air pollution and the development of bronchial asthma.