title: Genome screen for asthma and bronchial hyperresponsiveness: interactions with passive smoke exposure.
abstract: BACKGROUND
  Asthma is a common respiratory disease caused by the interaction of genetic susceptibility and exposure to various environmental factors. Passive smoke exposure, characterized by parental smoking, has been shown to be a risk factor for the development of atopy and asthma.
  
  
  OBJECTIVE
  We sought to perform a genome-wide linkage screen for asthma and bronchial hyperresponsiveness (BHR) and to determine the influence of passive tobacco smoke exposure during childhood on the results of genetic linkage studies to investigate gene-environment interactions.
  
  
  METHODS
  A genome-wide linkage screen for asthma and BHR was performed in 200 families ascertained through a parent with asthma. Analyses were performed separately for the entire sample and for the smoking-exposed and nonexposed families.
  
  
  RESULTS
  For asthma and BHR, the strongest evidence for linkage was observed for chromosomes 3p and 5q. The families in which the children were exposed to passive smoking accounted for the evidence for linkage of BHR to 5q ( P < .001), but evidence for linkage to 3p was found in both sets of families. Similar results were observed for asthma. However, there was no observed difference in the frequency of asthma or BHR in the offspring from the smoke-exposed compared with the nonexposed families.
  
  
  CONCLUSIONS
  The results from this study demonstrate that the influence of susceptibility genes for a common disease such as asthma might not be apparent unless there is the appropriate exposure to environmental stimuli, such as passive exposure to cigarette smoke. This approach should be useful for identification of asthma susceptibility genes.
authors.affiliation: Center for Human Genomics, Department of Pediatrics, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA. dmeyers@wfubmc.edu
authors.forename: Deborah A
authors.initials: DA
authors.lastname: Meyers
authors.forename: Dirkje S
authors.initials: DS
authors.lastname: Postma
authors.forename: O Colin
authors.initials: OC
authors.lastname: Stine
authors.forename: Gerard H
authors.initials: GH
authors.lastname: Koppelman
authors.forename: Elizabeth J
authors.initials: EJ
authors.lastname: Ampleford
authors.forename: Hajo
authors.initials: H
authors.lastname: Jongepier
authors.forename: Timothy D
authors.initials: TD
authors.lastname: Howard
authors.forename: Eugene R
authors.initials: ER
authors.lastname: Bleecker
mesh_terms: D000328:Adult; D001249:Asthma / Q000209:etiology* / Q000235:genetics; D016535:Bronchial Hyperreactivity / Q000209:etiology* / Q000235:genetics; D002893:Chromosomes, Human, Pair 3; D002895:Chromosomes, Human, Pair 5; D005190:Family; D005260:Female; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008126:Lod Score; D008297:Male; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D014028:Tobacco Smoke Pollution