title: Genetic and environmental influence on lung function impairment in Swedish twins.
abstract: BACKGROUND
  The understanding of the influence of smoking and sex on lung function and symptoms is important for understanding diseases such as COPD. The influence of both genes and environment on lung function, smoking behaviour and the presence of respiratory symptoms has previously been demonstrated for each of these separately. Hence, smoking can influence lung function by co-varying not only as an environmental factor, but also by shared genetic pathways. Therefore, the objective was to evaluate heritability for different aspects of lung function, and to investigate how the estimates are affected by adjustments for smoking and respiratory symptoms.
  
  
  METHODS
  The current study is based on a selected sample of adult twins from the Swedish Twin Registry. Pairs were selected based on background data on smoking and respiratory symptoms collected by telephone interview. Lung function was measured as FEV1, VC and DLco. Pack years were quantified, and quantitative genetic analysis was performed on lung function data adjusting stepwise for sex, pack years and respiratory symptoms.
  
  
  RESULTS
  Fully adjusted heritability for VC was 59% and did not differ by sex, with smoking and symptoms explaining only a small part of the total variance. Heritabilities for FEV1 and DLco were sex specific. Fully adjusted estimates were 10 and 15% in men and 46% and 39% in women, respectively. Adjustment for smoking and respiratory symptoms altered the estimates differently in men and women. For FEV1 and DLco, the variance explained by smoking and symptoms was larger in men. Further, smoking and symptoms explained genetic variance in women, but was primarily associated with shared environmental effects in men.
  
  
  CONCLUSIONS
  Differences between men and women were found in how smoking and symptoms influence the variation in lung function. Pulmonary gas transfer variation related to the menstrual cycle has been shown before, and the findings regarding DLco in the present study indicates gender specific environmental susceptibility not shown before. As a consequence the results suggest that patients with lung diseases such as COPD could benefit from interventions that are sex specific.
authors.affiliation: Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Jenny
authors.initials: J
authors.lastname: Hallberg
authors.forename: Anastasia
authors.initials: A
authors.lastname: Iliadou
authors.forename: Martin
authors.initials: M
authors.lastname: Anderson
authors.forename: Maria Gerhardsson
authors.initials: MG
authors.lastname: de Verdier
authors.forename: Ulf
authors.initials: U
authors.lastname: Nihlén
authors.forename: Magnus
authors.initials: M
authors.lastname: Dahlbäck
authors.forename: Nancy L
authors.initials: NL
authors.lastname: Pedersen
authors.forename: Tim
authors.initials: T
authors.lastname: Higenbottam
authors.forename: Magnus
authors.initials: M
authors.lastname: Svartengren
mesh_terms: D000368:Aged; D002245:Carbon Dioxide / Q000378:metabolism; D003430:Cross-Sectional Studies; D005260:Female; D005541:Forced Expiratory Volume; D020022:Genetic Predisposition to Disease; D040941:Heredity; D006801:Humans; D016014:Linear Models; D008168:Lung / Q000378:metabolism / Q000503:physiopathology*; D008171:Lung Diseases / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D010991:Plethysmography; D011653:Pulmonary Diffusing Capacity; D012042:Registries; D018570:Risk Assessment; D012307:Risk Factors; D012737:Sex Factors; D012907:Smoking / Q000009:adverse effects*; D013548:Sweden; D013997:Time Factors; D014427:Twins / Q000235:genetics*; D014797:Vital Capacity
chemical_list: D002245:Carbon Dioxide