Genetic/environmental determinants of adult chronic obstructive pulmonary disease and possible links with childhood wheezing.

Abstract

Epidemiological evidence and similarities in underlying inflammatory mechanisms suggest that childhood respiratory conditions and adult onset chronic obstructive pulmonary disease (COPD) may have a common aetiology. The prevalence of COPD in the UK has been estimated to be 10% in males and 11% in females, and like asthma, is thought to have a polygenic contribution with a complex interplay between genetic and environmental factors. The only proven genetic factor so far identified in its pathogenesis is alpha1-antitrypsin deficiency, although this accounts for less than 1% of individuals with disease. Environmental exposures are significant but the observation that only 15% of smokers develop COPD and only some young children exposed in utero develop recurrent wheezing points to as yet undefined contributory genetic factors. The similarity in response to medication also suggests some features in common and a central question must be whether those adults who develop COPD had transient viral-associated wheeze (VAW) or non-specific bronchial hyperresponsiveness (BHR) in childhood? Similarities between some of the childhood wheezing syndromes and adult onset COPD invites a re-examination of possible links between the two conditions.