title: Interleukin gene polymorphisms in pneumoconiosis.
abstract: Inhaled asbestos fibres are known to cause inflammation processes with the result of lung or pleural fibrosis and malignancies. Interleukins (IL), such as IL-1β, IL-6 and IL-10, have various functions in the regulation of the inflammatory response and in proliferative processes after inhalation of silica dust and can, therefore, influence the pathogenesis of asbestos-induced fibrosis and carcinogenesis. Polymorphisms within these genes may be associated with susceptibility to silica and asbestos-induced lung diseases. Thus, IL-1β, IL-6 and IL-10 polymorphisms were examined to determine an association with asbestos or silica-induced fibrosis or malignancies. Association studies were performed in 1180 individuals, using control subjects (n=177), fibrosis patients (n=605), lung cancer (LC) patients (n=364) and malignant mesothelioma (MM) patients (n=34). IL-1β (C-511T; C+3954T), IL-6 (G-174C) as well as IL-10 (G-1082A) polymorphisms were investigated. Compared to a healthy (control) group, a higher risk was seen for malignant mesothelioma patients in all investigated polymorphisms. The IL-6 -174C allele showed a tendency towards a higher risk for fibrosis or asbestos-induced lung cancer (ORasbestosis, 1.338; 95% CI, 0.71-2.53; ORsilicosis, 1.226; 95% CI, 0.54-2.81; ORfibrosis other aetiology, 1.313; 95% CI, 0.58-2.98 and ORLC asbestos, 2.112; 95% CI, 0.75-5.92). The IL-10 -1082A carrier seemed to be at higher risk for silicosis (ORsilicosis, 2.064; 95% CI, 0.78-5.49) but not for asbestosis. In summary, this study did not reveal sufficient evidence for a significant association of the investigated interleukin polymorphisms with asbestos or silica-induced diseases in the population studied.
authors.affiliation: Institute and Polyclinic for Occupational and Social Medicine, Justus-Liebig University, D-35392 Giessen, Germany. simone.helming@arbmed.med.uni-giessend.de
authors.forename: Simone
authors.initials: S
authors.lastname: Helmig
authors.forename: Martin
authors.initials: M
authors.lastname: Grossmann
authors.forename: Jelena
authors.initials: J
authors.lastname: Wübbeling
authors.forename: Joachim
authors.initials: J
authors.lastname: Schneider
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D016022:Case-Control Studies; D005838:Genotype; D005858:Germany; D006801:Humans; D018836:Inflammation Mediators; D007378:Interleukins / Q000235:genetics*; D008171:Lung Diseases / Q000150:complications / Q000235:genetics; D008875:Middle Aged; D011009:Pneumoconiosis / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D011110:Polymorphism, Genetic; D055815:Young Adult
chemical_list: D018836:Inflammation Mediators; D007378:Interleukins