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Sökning: WFRF:(Kogevinas M) > (2005-2009)

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1.
  • Castro-Giner, F., et al. (författare)
  • Joint effect of obesity and TNFA variability on asthma : two international cohort studies
  • 2009
  • Ingår i: European Respiratory Journal. - 0903-1936 .- 1399-3003. ; 33:5, s. 1003-1009
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is a risk factor for asthma. Adipose tissue expresses pro-inflammatory molecules including tumour necrosis factor (TNF), and levels of TNF are also related to polymorphisms in the TNF-alpha (TNFA) gene. The current authors examined the joint effect of obesity and TNFA variability on asthma in adults by combining two population-based studies. The European Community Respiratory Health Survey and the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-alpha (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7-3.2; OR for TNFA -308 polymorphism 1.3, 95% CI 1.1-1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5-14.4; OR for G/G genotype 1.7, 95% CI 0.8-3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma.
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  • Castro-Giner, F, et al. (författare)
  • TNFA -308G>A in two international population-based cohorts and risk of asthma
  • 2008
  • Ingår i: European Respiratory Journal. - Sheffield : European respiratory society journals. - 0903-1936 .- 1399-3003. ; 32:2, s. 350-361
  • Tidskriftsartikel (refereegranskat)abstract
    • Genetic association studies have related the tumour necrosis factor-alpha gene (TNFA) guanine to adenine substitution of nucleotide -308 (-308G>A) polymorphism to increased risk of asthma, but results are inconsistent. The aim of the present study was to test whether two single-nucleotide polymorphisms, of TNFA and of the lymphotoxin-alpha gene (LTA), are associated with asthma, bronchial hyperresponsiveness and atopy in adults, by combining the results of two large population-based multicentric studies and conducting a meta-analysis of previously published studies. The European Community Respiratory Health Survey (ECRHS) and Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) used comparable protocols, including questionnaires for respiratory symptoms and measures of lung function and atopy. DNA samples from 11,136 participants were genotyped at TNFA -308 and LTA 252. Logistic regression employing fixed and random effects models and nonparametric techniques were used. The prevalence of asthma was 6%. The TNFA -308G>A polymorphism was associated with increased asthma prevalence and with bronchial hyperresponsiveness. No consistent association was found for atopy. The LTA 252A>G polymorphism was not associated with any of the outcomes. A meta-analysis of 17 studies showed an increased asthma risk for the TNFA -308 adenine allele. The tumour necrosis factor-alpha gene nucleotide -308 polymorphism is associated with a moderately increased risk of asthma and bronchial hyperresponsiveness, but not with atopy. These results are supported by a meta-analysis of previously published studies.
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  • Sunyer, Jordi, et al. (författare)
  • Lung function decline, chronic bronchitis, and occupational exposures in young adults
  • 2005
  • Ingår i: Am J Respir Crit Care Med. ; 172:9, s. 1139-45.
  • Tidskriftsartikel (refereegranskat)abstract
    • Rationale: Occupational exposures to vapors, gas, dust, or fumes have been shown to be a risk factor of airway obstruction in cross-sectional studies in the general population.Objectives: Our aim was to study the relationships between specific occupations and occupational exposures during a 9-yr follow-up period and changes in lung function and symptoms of chronic bronchitis.Methods: Subjects from the general population aged 20 to 45 yr were randomly selected in 1991-1993 within the European Community Respiratory Health Survey. Follow-up took place from 1998 to 2002 among 4,079 males and 4,461 females in 27 study centers. A total of 3,202 men and 3,279 women twice completed lung function measurements. Job history during follow-up was linked to a job exposure matrix and consequently translated into cumulative exposure estimates.Main Results: Individuals exposed to dusts, gases, and fumes during the period of follow-up did not have a steeper decline of FEV(1) than did individuals with consistently white-collar occupations without occupational exposures (relative change among men and women, + 1.4 and -3.1 ml/yr, respectively; p > 0.2), nor an increase of prevalence or incidence of airway obstruction defined as an FEV(1)/FVC ratio of less than 0.7. The incidence of chronic phlegm increased in men exposed to mineral dust (relative risk, 1.94 [1.29-2.91]) and gases and fumes (relative risk, 1.53 [0.99-2.36]), which was not modified by smoking.Conclusion: Occupational exposures to dusts, gases, and fumes occurring during the 1990s are associated with incidence of chronic bronchitis, although these did not impair lung function in a population of relatively young age.
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  • Ellison-Loschmann, L., et al. (författare)
  • Socioeconomic status, asthma and chronic bronchitis in a large community-based study
  • 2007
  • Ingår i: European Respiratory Journal. - 0903-1936 .- 1399-3003. ; 29:5, s. 897-905
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study investigated the relationship between socioeconomic status, using measures of occupational class and education level, and the prevalence and incidence of asthma (with and without atopy) and chronic bronchitis using data from the European Community Respiratory Health Survey (ECRHS). Asthma and chronic bronchitis were studied prospectively within the ECRHS (n=9,023). Incidence analyses comprised subjects with no history of asthma or bronchitis at baseline. Asthma symptoms were also assessed as a continuous score. Bronchitis risk was associated with low educational level (prevalence odds ratio (POR) 1.9; 95% confidence interval (CI) 1.4-2.8) and occupatsional class (1.8; 1.2-2.7). Incident bronchitis also increased with low educational level (risk ratio (RR) 2.8; 95%CI 1.5-5.4). Prevalent and incident asthma with no atopy were associated with low educational level. Subjects in the low occupational class (incident risk ratio (IRR) 1.4; 95%CI 1.2-1.7) and education group (IRR 1.3; 95% CI 1.1-1.6) had higher mean asthma scores than those in higher socioeconomic groups. Lower educational level was associated with increased risk of prevalent and incident chronic bronchitis and asthma with no atopy. Lower socioeconomic groups tended to have a higher prevalence and incidence of asthma, particularly higher mean asthma scores. Adjustment for variables associated with asthma and bronchitis explained little of the observed health differences by socioeconomic status.
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  • McLean, D., et al. (författare)
  • Cancer mortality in workers exposed to organochlorine compounds in the pulp and paper industry : An international collaborative study
  • 2006
  • Ingår i: Journal of Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 114:7, s. 1007-1012
  • Tidskriftsartikel (refereegranskat)abstract
    • The objective of this study was to evaluate cancer mortality in pulp and paper industry workers exposed to chlorinated organic compounds. We assembled a multinational cohort of workers employed between 1920 and 1996 in 11 countries. Exposure to both volatile and nonvolatile organochlorine compounds was estimated at the department level using an exposure matrix. We conducted a standardized mortality ratio (SMR) analysis based on age and calendar-period-specific national mortality rates and a Poisson regression analysis. The study population consisted of 60,468 workers. Workers exposed to volatile organochlorines experienced a deficit of all-cause [SMR = 0.91, 95% confidence interval (CI), 0.89-0.93] and all-cancer (SMR = 0.93, 95% CI, 0.89-0.97) mortality, with no evidence of increased risks for any cancer of a priori interest. There was a weak, but statistically significant, trend of increasing risk of all-cancer mortality with increasing weighted cumulative exposure. A similar deficit in all-cause (SMR = 0.94, 95% CI, 0.91-0.96) and all-cancer (SMR = 0.94, 95% CI, 0.89-1.00) mortality was observed in those exposed to nonvolatile organochlorines. No excess risk was observed in cancers of a priori interest, although mortality from Hodgkin disease was elevated (SMR = 1.76, 95% CI, 1.02-2.82). In this study we found little evidence that exposure to organochlorines at the levels experienced in the pulp and paper industry is associated with an increased risk of cancer, apart from a weak but significant association between all-cancer mortality and weighted cumulative volatile organochlorine exposure.
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9.
  • Murta-Nascimento, C., et al. (författare)
  • Epidemiology of urinary bladder cancer: from tumor development to patient's death
  • 2007
  • Ingår i: World J Urol. - 0724-4983. ; 25:3, s. 285-295
  • Tidskriftsartikel (refereegranskat)abstract
    • Urinary bladder cancer (UBC) ranks ninth in worldwide cancer incidence. It is more frequent in men than in women. We review the main established/proposed factors, both environmental and genetic, associated with bladder cancer etiology and prognosis. Data were extracted from previous reviews and original articles identified from PubMed searches, reference lists, and book chapters dealing with the reviewed topics. Evaluation and consensus of both the contribution of each factor in bladder cancer burden and the appropriateness of the available evidences was done during an ad hoc meeting held during the 18th Congress of the European Society for Urological Research. Cigarette smoking and specific occupational exposures are the main known causes of UBC. Phenacetin, chlornaphazine and cyclophosphamide also increase the risk of bladder cancer. Chronic infection by Schistosoma haematobium is a cause of squamous cell carcinoma of the bladder. NAT2 slow acetylator and GSTM1 null genotypes are associated with an increased risk of this cancer. Vegetables and fresh fruits protect against this tumor. Regarding prognosis, there is little knowledge on the predictive role of environmental exposures and genetic polymorphisms on tumor recurrence and progression and patient's death. Although active tobacco smoking is the most commonly studied factor, no definitive conclusion can be drawn from the literature. More research is needed regarding the effect of complex etiological factors in bladder carcinogenesis. Subgroup analysis according to stage, grade, and molecular features may help in identifying specific etiological and prognostic factors involved in different bladder cancer progression pathways.
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10.
  • Torén, Kjell, 1952, et al. (författare)
  • An international prospective general population-based study of respiratory work disability.
  • 2009
  • Ingår i: Thorax. - 1468-3296. ; 64:4, s. 339-44
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Previous cross-sectional studies have shown that job change due to breathing problems at the workplace (respiratory work disability) is common among adults of working age. That research indicated that occupational exposure to gases, dust and fumes was associated with job change due to breathing problems, although causal inferences have been tempered by the cross-sectional nature of previously available data. There is a need for general population-based prospective studies to assess the incidence of respiratory work disability and to delineate better the roles of potential predictors of respiratory work disability. METHODS: A prospective general population cohort study was performed in 25 centres in 11 European countries and one centre in the USA. A longitudinal analysis was undertaken of the European Community Respiratory Health Survey including all participants employed at any point since the baseline survey, 6659 subjects randomly sampled and 779 subjects comprising all subjects reporting physician-diagnosed asthma. The main outcome measure was new-onset respiratory work disability, defined as a reported job change during follow-up attributed to breathing problems. Exposure to dusts (biological or mineral), gases or fumes during follow-up was recorded using a job-exposure matrix. Cox proportional hazard regression modelling was used to analyse such exposure as a predictor of time until job change due to breathing problems. RESULTS: The incidence rate of respiratory work disability was 1.2/1000 person-years of observation in the random sample (95% CI 1.0 to 1.5) and 5.7/1000 person-years in the asthma cohort (95% CI 4.1 to 7.8). In the random population sample, as well as in the asthma cohort, high occupational exposure to biological dust, mineral dust or gases or fumes predicted increased risk of respiratory work disability. In the random sample, sex was not associated with increased risk of work disability while, in the asthma cohort, female sex was associated with an increased disability risk (hazard ratio 2.8, 95% CI 1.3 to 5.9). CONCLUSIONS: Respiratory work disability is common overall. It is associated with workplace exposures that could be controlled through preventive measures.
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