Influence of early life exposures on incidence and remission of asthma throughout life

Abstract

Background Knowledge of the effects of early environmental and congenital factors on the natural history of asthma may provide important clues to the pathogenesis of asthma. Objective We assessed associations between potential, early determinants and the incidence and remission of asthma throughout life, and tested whether the strength and direction of these associations varied in childhood, adolescence, and adulthood. Methods The data pertaining to the individual asthma history of 18,156 subjects, age 0 to 44 years, who attended the clinical stage of the European Community Respiratory Health Survey were analyzed retrospectively by life-event methods. Onset of asthma was defined as age at the first attack, and asthmatic patients were considered to be in remission if they had not been under treatment or had an attack of asthma in the past 24 months. Onset and remission were evaluated in 3 time windows: <10, 10 to 20, and ≥20 years of age. The associations of asthma with early determinants were estimated by hazard ratios (HRs). Results A family history of asthma or allergy was associated with a higher risk of developing asthma (HR, 1.89; 95% CI, 1.67-2.13) and a lower chance of remission (HR, 0.79; 95% CI, 0.64-0.99) throughout life. No matter what one's genetic predisposition was, early, acute respiratory infections were associated with an increased lifelong risk of asthma onset (pooled HR, 3.19; 95% CI, 2.75-3.69), whereas early contact with older children, which is a marker of prolonged, intermittent exposure to infectious agents, conferred permanent protection against asthma (HR, 0.84; 95% CI, 0.74-0.96) and increased the chance of remission in childhood asthma (HR, 1.50; 95% CI, 1.10-2.04). Pet ownership had a protective effect only in childhood (HR, 0.78; 95% CI, 0.74-0.96), whereas maternal smoking did not show a significant association with asthma. Female sex was negatively associated with the onset of asthma in childhood (HR, 0.62; 95% CI, 0.52-0.75) and positively in adulthood (HR, 2.01; 95% CI, 1.61-2.51). The pattern of associations was similar in sensitized (positive assay to specific IgE) and nonsensitized asthmatic patients. Conclusion Genetic predisposition and exposure to infectious agents are major early determinants that influence a subsequent history of asthma. The length and type of exposure to infectious agents seem able either to promote or to suppress an anti-inflammatory process, unrelated to IgE, which can partially interfere with an acquired predisposition for asthma.