Effect of TNF and LTA polymorphisms on biological markers of response to oxidative stimuli in coal miners: a model of gene-environment interaction

Nadif, Rachel; Jedlicka, Anne; Mintz, Margaret; Bertrand, Jean-Pierre; Kleeberger, Steven R.; Kauffmann, F.

doi:10.1136/jmg.40.2.96

Cited by 48 publications

(23 citation statements)

References 49 publications

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“…The study design has been described elsewhere [14]. Briefly, unrelated coal miners (aged 34-50 yrs) were recruited in 1990 to be contrasted according to exposure and chest radiography.…”

Section: Study Samplementioning

confidence: 99%

“…Briefly, the lungs were divided into six areas: the upper zones above the carina, the middle zones between the level of the carina and the lower pulmonary veins, and the lower zones below the level of the lower pulmonary veins. Micronodules were defined as opacities ,7 mm in diameter and nodules were defined as opacities [7][8][9][10][11][12][13][14][15][16][17][18][19][20] At each survey (1990, 1994 and 1999), chest radiographs taken in the yearly medical examination were interpreted by two independent and experienced physicians, according to the International Labour Office (ILO) standardised classification of radiographs of pneumoconiosis [18]. The films were presented in random order, without any information about the occupational and medical history of the subjects.…”

Section: Radiographic Examinationmentioning

confidence: 99%

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IL18andIL18R1polymorphisms, lung CT and fibrosis: a longitudinal study in coal miners

et al. 2006

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It has been suggested that interleukin (IL)-18 plays a role in the development of inflammatory and fibrosing lung diseases.Associations of polymorphisms in the genes coding for IL-18 (IL18 /G-656T, C-607A, G-137C, T113G, C127T) and its receptor (IL18R1 /C-69T) with coal workers' pneumoconiosis (CWP) were studied in 200 miners who were examined in 1990, 1994 and 1999. Coal-dust exposure was assessed according to job history and ambient measures. The main health outcome was lung computed tomography (CT) score in 1990. Internal coherence was assessed by studying CT score in 1994, 4-yr change in CT score and CWP incidence and prevalence.CT score in 1990 was a good predictor of radiographic grade in 1999 and, therefore, an appropriate subclinical quantitative trait. The IL18 -137C allele was associated with lower CT score in 1990 and 1994 (1.24 versus 1.69 and 1.57 versus 2.46, respectively), slower progression of CT score between 1990 and 1994 and lower pneumoconiosis prevalence in 1999 relative to the G allele (0.33 versus 0.77 and 8.2 versus 19.6%, respectively). Smoking-or dust-adjustment, and stratification on IL18R1 genotype and adjustment for haplotype effects did not change the conclusions.In conclusion, the results of the present study suggest a role for IL18 in reducing the development of this fibrosing lung disease.

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“…The study design has been described elsewhere [14]. Briefly, unrelated coal miners (aged 34-50 yrs) were recruited in 1990 to be contrasted according to exposure and chest radiography.…”

Section: Study Samplementioning

confidence: 99%

Section: Radiographic Examinationmentioning

confidence: 99%

IL18andIL18R1polymorphisms, lung CT and fibrosis: a longitudinal study in coal miners

et al. 2006

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“…Interactions of PI and smoking [56], CD14 and toll-like receptors in the context of the hygiene hypothesis [57,58] may be found. Interactions with oxidant exposure, such as smoking [59], air pollution [60] or occupational exposure [61], and with aspirin [62] have been evidenced as well as gene-by-gene interactions [63]. In conclusion, it has become essential to consider all the genes in a pathway, and due to the number of potential candidate genes already identified, there is a need for well-founded gene-byenvironment hypotheses and their subsequent testing (table 2).…”

Section: Gene-environment Interactionmentioning

confidence: 99%

Post-genome respiratory epidemiology: a multidisciplinary challenge

Kauffmann

2004

Eur Respir J

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Post-genome respiratory epidemiology: a multidisciplinary challenge. F. Kauffmann and the Post Genome Respiratory Epidemiology group. #ERS Journals Ltd 2004. ABSTRACT: The introduction of genetic approaches in respiratory epidemiology is novel for most epidemiologists, and the post-genome phase poses new challenges. After describing specific questions pertinent to the field of asthma and chronic obstructive pulmonary disease, two main methodological aspects regarding technological and scientific advances are presented in this review. The first one concerns biological aspects in the genome and post-genome phases, i.e. how to study the genome, the transcriptome and the proteome. The second area concerns genetic epidemiology, considering design (case control and family based) and statistical analytical issues. Key aspects are large sample size, good phenotyping and the consideration of environment-by-gene interaction according to windows of opportunity.Needs that have been identified include the following. 1) Networking for setting standards in the field and access to sufficiently large samples. 2) Multidisciplinarity; the collaboration of epidemiologists, clinicians, geneticists and specialists in bioinformatics, in addition to specialists in disciplines less familiar to epidemiologists, to be prepared for new phenotypic characterisations based on transcriptome and proteome. 3) Training in genetic analytical techniques for some respiratory epidemiologists, as well as in respiratory epidemiology for some genetic epidemiologists.Implications for research, considering ethical aspects, public health aspects and organisational aspects in the field of genetic and environmental respiratory epidemiology also need to be addressed.

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“…Regarding pneumoconiosis, such changes are associated with chronic inflammatory processes linked to the formation of reactive oxygen species (ROS) in the lower respiratory tract [9,12]. Elevated and continuous ROS production or inadequate ROS removal may overcome the antioxidant defense system and cause oxidative stress, which is an imbalance between antioxidants and oxidants in favor of the latter, leading to cell damage [2,13,14]. Aerobic organisms have antioxidant defense systems that deal with ROS produced as a result of aerobic respiration and substrate oxidation, or generated in response to internal and external stimuli [13,15].…”

mentioning

confidence: 99%

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

Amaral¹,

Joca²,

Carvalho³

et al. 2016

Biomonitoring

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group and individuals without asbestosis, respectively. Linear regression analysis showed that 28,4% and 50,5% of comet assay results were increased by exposure to asbestos and developed asbestosis. The results of CAT and GST were not difference between the groups. These results supports the association of genotoxic damage and the onset of asbestosis by chrysotile asbestos exposure in workers of this study.Keywords: asbestos, occupational exposure, genotoxicity. IntroductionAsbestosis is a form of pneumoconiosis caused by inhaling asbestos, a generic commercial designation for a group of naturally-occurring mineral silicate fibres of the serpentine (chrysotile asbestos) and amphibole series (actinolite, amosite, anthophyllite, crocidolite and tremolite) [1]. Inhaling any kind of asbestos fibers causes the development of intense interstitial pulmonary fibrosis, which involves an inflammatory reaction, production of collagen and the formation of granuloma [2][3][4][5].Asbestosis and other diseases related to asbestos are increasing worldwide [6,7] and several studies have shown that exposure to asbestos has contributed to occupationally-related cancer. Each year, approximately 125 million people around the world are occupationally exposed to asbestos and at least 100,000 people die because of diseases related to this exposure (for example asbestos-related lung cancer, mesothelioma, or asbestosis [1]) despite the fact that "chrysotile manufacturers, governments of asbestos-producing nations, and some asbestos miners' unions contend either that their products do not cause disease or that there is insufficient evidence to reach a reliable conclusion", as stated by Pezerat (2009) [8]. Abstract: Genotoxic effects of occupational workers exposed to asbestos can be evaluated using different biomarkers as oxidative stress enzymes in conjuction with comet assay. This study assessed changes to oxidative stress enzymatic parameters and genotoxic damage in workers occupationally exposed and non-exposed to chrysotile asbestos, who attended the outpatient Clinic of the Center for Worker Health Studies and Human Ecology (CESTEH/ENSP/FIOCRUZ) in Brazil. Chest radiography and spirometry were performed to assess clinical progression of symptoms. The traditional visual score comet assay in peripheral whole blood cells was used to assess DNA damage, and oxidative stress was evaluated by measuring catalase (CAT) and glutathione S-transferase (GST) activities. Respiratory alterations were observed in 53% of workers exposed, as determined by pulmonary function and bronchodilation, and 6 workers were diagnosed with asbestosis. The comet assay was statistically significantly higher in the exposed group and individuals with asbestosis compared to the non-exposed

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Effect of TNF and LTA polymorphisms on biological markers of response to oxidative stimuli in coal miners: a model of gene-environment interaction

Cited by 48 publications

References 49 publications

IL18andIL18R1polymorphisms, lung CT and fibrosis: a longitudinal study in coal miners

IL18andIL18R1polymorphisms, lung CT and fibrosis: a longitudinal study in coal miners

Post-genome respiratory epidemiology: a multidisciplinary challenge

Evaluation of Genotoxic Effects of Asbestos on Occupationally Exposed Workers in Brazil

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