title: Parental and neonatal risk factors for atopy, airway hyper-responsiveness, and asthma.
abstract: BACKGROUND
  Previous studies have not resolved the importance of several potential risk factors for the development of childhood atopy, airway hyperresponsiveness, and wheezing, which would allow the rational selection of interventions to reduce morbidity from asthma. Risk factors for these disorders were examined in a birth cohort of 1037 New Zealand children.
  
  
  METHODS
  Responses to questions on respiratory symptoms and measurements of lung function and airway responsiveness were obtained every two to three years throughout childhood and adolescence, with over 85% cohort retention at age 18 years. Atopy was determined by skin prick tests at age 13 years. Relations between parental and neonatal factors, the development of atopy, and features of asthma were determined by comparison of proportions and logistic regression.
  
  
  RESULTS
  Male sex was a significant independent predictor for atopy, airway hyper-responsiveness, hay fever, and asthma. A positive family history, especially maternal, of asthma strongly predicted childhood atopy, airway hyperresponsiveness, asthma, and hay fever. Maternal smoking in the last trimester was correlated with the onset of childhood asthma by the age of 1 year. Birth in the winter season increased the risk of sensitisation to cats. Among those with a parental history of asthma or hay fever, birth in autumn and winter also increased the risk of sensitisation to house dust mites. The number of siblings, position in the family, socioeconomic status, and birth weight were not consistently predictive of any characteristic of asthma.
  
  
  CONCLUSIONS
  Male sex, parental atopy, and maternal smoking during pregnancy are risk factors for asthma in young children. Children born in winter exhibit a greater prevalence of sensitisation to cats and house dust mites. These data suggest possible areas for intervention in children at risk because of parental atopy.
authors.affiliation: Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: M R
authors.initials: MR
authors.lastname: Sears
authors.forename: M D
authors.initials: MD
authors.lastname: Holdaway
authors.forename: E M
authors.initials: EM
authors.lastname: Flannery
authors.forename: G P
authors.initials: GP
authors.lastname: Herbison
authors.forename: P A
authors.initials: PA
authors.lastname: Silva
mesh_terms: D001249:Asthma / Q000209:etiology* / Q000235:genetics; D001722:Birth Order; D001724:Birth Weight; D016535:Bronchial Hyperreactivity / Q000209:etiology* / Q000235:genetics; D002675:Child, Preschool; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000209:etiology* / Q000235:genetics; D008297:Male; D015999:Multivariate Analysis; D006255:Rhinitis, Allergic, Seasonal / Q000209:etiology / Q000235:genetics; D012307:Risk Factors; D012621:Seasons; D012737:Sex Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
chemical_list: D014028:Tobacco Smoke Pollution