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Gene–environment interactions in asthma

¹ Centre for Research in Environmental Epidemiology, Municipal Institute of Medical Research (IMIM), Barcelona, Spain
² Inserm, U780 Epidemiology and Biostatistics, Villejuif, France, and Université Paris Sud, Faculté de Médecine, IFR69, Villejuif, France
³ Genes and Disease Program, Centre for Genomic Regulation and Universitat Pompeu Fabra, Barcelona, Spain
⁴ Centre for Research in Environmental Epidemiology, Municipal Institute of Medical Research (IMIM), Barcelona, Spain and Medical School, University of Crete, Heraklion, Greece

Correspondence to:
Correspondence to:
Dr M Kogevinas
Centre for Research in Environmental Epidemiology, Municipal Institute of Medical Reseach (IMIM), 80 Dr Aiguader Rd, Barcelona 08003, Spain; kogevinas@imim.es

Keywords: asthma; genes; environment; occupational; interaction

The first 150 words of the full text of this article appear below.

Asthma is a complex disease with a diverse genetic and environmental component.¹ Asthma shows a high level of phenotypic heterogeneity characterised by obstruction of the airways of the lung and is related with atopy, bronchial hyperresponsiveness (BHR), and increased IgE levels. Over the last decades asthma has become a major cause of morbidity in children from developed countries with an estimated prevalence of 5–10%.^2–5 It has been estimated that about 300 million persons worldwide have asthma (http://www.ginasthma.com/).

Studies in twins and family studies indicate that the genetic component of asthma is likely to be high,^6–9 although the individual genes identified have only modest effects and an unknown pattern of inheritance. The most common chromosomal linkage regions observed in genome-wide linkage studies are 2q14–q32, 5q31–q33, 6p21.3, 7q31, 11q13, 12q14.3–q24.31, 13q14, 14q11.2–q13, 16p21, 17q11.2, and 20p13.^1,4 Several asthma and atopy genes have been identified by positional cloning including the genes . . . [Full text of this article]

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