MedWire News: Variations in the so-called asthma gene, ADAM33, interact with exposure to cigarette smoke in utero to influence lung function in childhood, a study has found.

The research, if confirmed, underlines the importance of maternal cigarette smoking as an environmental risk factor for reduced lung function, acting in concert with genetic factors such as ADAM33.

The finding is reported in the journal Allergy by Dutch researchers, who analyzed data from a birth cohort study, the Prevention and Incidence of Mite Allergy. The study, which began in 1996, included 4146 children, 1327 of whom were considered at high risk based on a positive maternal history of atopy.

Dirkje Postma (University of Groningen) and fellow authors first sought to verify the previously reported association between ADAM33 genotype and asthma risk.

As expected, children carrying the rs511898 A allele, the rs528557 C allele, or the rs2280090 A allele were more likely to have developed asthma with or without bronchial hyperresponsiveness (BHR) by the age of 8 years compared with children with the GG genotypes.

Further analysis revealed that, among children whose mothers smoked during pregnancy, the rs528557 C allele was associated with impaired lung function at age 8 years compared with the GG genotype. Conversely, among children whose mothers did not smoke during pregnancy, the rs528557 C allele was associated with increased lung function.

Similar interactions between ADAM33 genotype and in utero cigarette smoke exposure were present for both Rint (a measure of airway resistance) and BHR at age 8 years. No significant interactions were found between ADAM33 genotypes and smoke exposure in the first year of life, however.

Postma et al say their results support a gene–environment interaction between ADAM33 genotype and in utero cigarette smoke exposure on indices of lung function at the age of 8 years.

“Our study highlights that it is important to investigate cigarette smoking during pregnancy as a risk factor for early-life lung function and BHR development, in interaction with genetic factors like ADAM33,” they conclude.

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