title: Passive smoking and lung function in alpha(1)-antitrypsin heterozygote schoolchildren.
abstract: BACKGROUND
  A study was performed to determine whether Pi heterozygotes exposed to smoking have a higher risk of reduced lung function than Pi M homozygotes.
  
  
  METHODS
  The effect of passive smoking on lung function was investigated in a cross sectional study of 997 primary and secondary schoolchildren aged 11-13 years categorised by Pi phenotype as either PiM homozygotes or Pi heterozygotes. Data on respiratory health and risk factors were collected by questionnaire, lung function was measured by spirometric tests, bronchial hyperresponsiveness was evaluated by methacholine test, atopic status was evaluated by skin prick testing, and a blood sample was collected to determine Pi phenotype. Urinary cotinine and creatinine concentrations were determined and assessment of exposure was made from questionnaire data and urinary cotinine concentrations. The results were analysed by multiple regression analysis.
  
  
  RESULTS
  Sixty one subjects (6.1%) were found to be Pi heterozygotes. Lung function did not differ between homozygotes and heterozygotes. There was a reduction in lung function in subjects exposed to parental smoking in the overall sample: FEV(1)/FVC ratio (-0.78%), FEF(25-75) (-0.11 litres), and FEF(75) (-0.13 litres). Interaction terms between parental smoking and Pi status were significant with regard to FEV(1)/FVC ratio (p=0.035) and FEF(50) (p=0.023). In subjects exposed to parental smoking the decrement in lung function in Pi heterozygotes tended to be greater (FEV(1)/FVC ratio = -2.57, FEF(25-75) = -0.30, FEF(50) = -0.43, and FEF(75) = -0.29) than in PiM homozygotes. These results did not change significantly when the urinary cotinine concentration was used as an exposure variable.
  
  
  CONCLUSIONS
  The detrimental effect of environmental tobacco smoke on lung function in schoolchildren is confirmed. This harmful effect is greater in Pi heterozygotes than in PiM homozygotes.
authors.affiliation: Respiratory Physiology Department, Catholic University, Largo F. Vito, 100168 Rome, Italy. gmcorbo@yahoo.com
authors.forename: G M
authors.initials: GM
authors.lastname: Corbo
authors.forename: F
authors.initials: F
authors.lastname: Forastiere
authors.forename: N
authors.initials: N
authors.lastname: Agabiti
authors.forename: V
authors.initials: V
authors.lastname: Dell'Orco
authors.forename: R
authors.initials: R
authors.lastname: Pistelli
authors.forename: G
authors.initials: G
authors.lastname: Massi
authors.forename: C A
authors.initials: CA
authors.lastname: Perucci
authors.forename: S
authors.initials: S
authors.lastname: Valente
mesh_terms: D000293:Adolescent; D016085:Bronchoconstrictor Agents; D002648:Child; D003367:Cotinine / Q000652:urine; D005260:Female; D005540:Forced Expiratory Flow Rates / Q000235:genetics; D005541:Forced Expiratory Volume / Q000235:genetics; D006579:Heterozygote; D006720:Homozygote; D006801:Humans; D008171:Lung Diseases / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D016210:Methacholine Chloride; D010641:Phenotype; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*; D014797:Vital Capacity / Q000235:genetics; D000515:alpha 1-Antitrypsin / Q000235:genetics*
chemical_list: D016085:Bronchoconstrictor Agents; D014028:Tobacco Smoke Pollution; D000515:alpha 1-Antitrypsin; D016210:Methacholine Chloride; D003367:Cotinine