The relationship among IL-13, GSTP1, and CYP1A1 polymorphisms and environmental tobacco smoke in a population of children with asthma in Northern Mexico

Exposure to environmental tobacco smoke (ETS) during early childhood increases the risk of developing asthma. The intention of this study was to genotype a population of children from Coahuila state in Northern Mexico and to determine whether polymorphisms of the CYP1A1, GSTP1, and IL13 genes are associated with exposure to ETS and subsequently a higher risk for asthma. IL13 plays an important role in the development of allergic response, particularly those related with airway inflammation. CYP1A1 and GSTP1 are xenobiotic-metabolizing enzymes induced by repeated exposure to toxicants. Polymorphisms of these genes have been related with ETS exposure and increased risk for asthma. To assess the effect of IL13 (−1112 C > T and Arg110Gln), GSTP1 (Ile105Val), and CYP1A1 (Ile462Val) on asthma risk and ETS exposure, we recruited 201 unrelated children and classified them into four groups: (1) control without ETS exposure; (2) control with ETS exposure; (3) with asthma and with ETS exposure and (4) with asthma and without ETS exposure. No association among ETS exposure, asthma, and the studied polymorphisms was denoted by multivariate analysis of this population.

► We genotyped a population of asthmatic and non-asthmatic children from Northern Mexico.
► Three genes were analyzed: IL13 (−1112 C > T and Arg110Gln), GSTP1 (Ile105Val) and CYP1A1 (Ile462Val) and exposure to environmental tobacco smoke was assessed, as well.
► Polymorphisms studied here were not useful markers for predicting bronchial asthma.
► Further studies including larger samples, clinical assessments, and individuals from different regions are required.