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Occupational exposures and fluorescent oxidation products in 723 adults of the EGEA study

2015; European Respiratory Society; Volume: 46; Issue: 1 Linguagem: Inglês

10.1183/09031936.00177614

1399-3003

Orianne Dumas, Régis Matran, Farid Zerimech, Brigitte Decoster, Hélène Huyvaert, Ismaïl Ahmed, Nicole Le Moual, Rachel Nadif,

Contact Dermatitis and Allergies

Occupational asthma can be induced by a variety of agents, including high and low molecular weight sensitisers, and respiratory irritants [1]. The role of exposure to cleaning products and disinfectants in work-related asthma is increasingly recognised, although the specific substances that increase asthma risk are not well identified [2]. Some of the numerous agents contained in these products are chemical sensitisers, but most are hypothesised to act as respiratory irritants [2]. While high molecular weight sensitisers are known to cause occupational asthma through a typical allergic response, the pathophysiological mechanisms involved in occupational asthma induced by low molecular weight (LMW) chemicals, and in irritant-induced asthma, remain poorly understood [1, 3, 4]. Associations between occupational exposures to asthmogenic chemicals and irritants and oxidative stress were found The authors thank all those who participated in the study and in the various aspects of the examinations and all those who supervised the study centres. The authors are grateful to the three CIC-Inserm units at Necker, Grenoble and Marseille (France), which supported the study and where subjects were examined. They are also grateful to the three biobanks in Lille (CIC Inserm), Evry (Centre National de Genotypage) and Annemasse (Etablissement Français du Sang; France) where biological samples are stored. The authors thank Sylwester Karpiel (INSERM U1018, Centre for research in Epidemiology and Population Health (CESP), Respiratory and Environmental Epidemiology Team, Villejuif, France) for his contribution to this work. They are indebted to all the individuals who participated, without whom the study would not have been possible. The EGEA cooperative group are as follows. Coordination: V. Siroux (epidemiology, PI since 2013); F. Demenais (genetics); I. Pin (clinical aspects); R. Nadif (biology); F. Kauffmann (PI 1992–2012). Respiratory epidemiology: Inserm U 700, Paris: M. Korobaeff (Egea1) and F. Neukirch (Egea1); Inserm U 707, Paris: I. Annesi-Maesano (Egea1–2); Inserm CESP/U 1018, Villejuif: F. Kauffmann, N. Le Moual, R. Nadif, MP. Oryszczyn (Egea1–2) and R. Varraso; Inserm U 823, Grenoble: V. Siroux. Genetics: Inserm U 393, Paris: J. Feingold; Inserm U 946, Paris: E. Bouzigon, F. Demenais and M.H. Dizier; CNG, Evry: I. Gut (now CNAG, Barcelona, Spain) and M. Lathrop (now McGill University, Montreal, Canada). Clinical centres: Grenoble: I. Pin and C. Pison; Lyon: D. Ecochard (Egea1), F. Gormand and Y. Pacheco; Marseille: D. Charpin (Egea1) and D. Vervloet (Egea1–2); Montpellier: J. Bousquet; Paris Cochin: A. Lockhart (Egea1) and R. Matran (now in Lille); Paris Necker: E. Paty (Egea1–2) and P. Scheinmann (Egea1–2); Paris-Trousseau: A. Grimfeld (Egea1–2) and J. Just. Data and quality management: Inserm ex-U155 (Egea1): J. Hochez; Inserm CESP/U 1018, Villejuif: N. Le Moual; Inserm ex-U780: C. Ravault (Egea1–2); Inserm ex- U794: N. Chateigner (Egea1–2); Grenoble: J. Quentin-Ferran (Egea1–2).