Abstract:
Historically, the primary belief has been that asthma is an atopic disease with the strongest risk factor for developing asthma being exposure to an allergen. However, researchers have begun to question that long held belief and are beginning to study other postnatal environmental factors such as stress. Research delving into maternal postnatal distress and the subsequent effects seen upon the developing neonatal immune system as it pertains to asthma has gained momentum.
With that in mind, the focus of this research was 1) to determine if skin infections are more likely to be seen in young children who have been exposed to maternal distress, 2) to determine if skin infections in children from infancy to age 2 are associated with asthma, independent of atopic dermatitis, and 3) to determine if the association between early life skin infection and asthma was independent of recent stress biomarkers such as cortisol and dehydroepiandrostrone (DHEA). To meet the objectives listed above, the 1995 SAGE (Study of Asthma, Genes and the Environment) Manitoba birth cohort of 13980 children was used. Maternal postnatal distress, skin infection and atopic dermatitis in the infant, asthma at age 11 and other risk factors for asthma were derived from Manitoba’s health care databases. For objective 3, data on stress biomarkers (Cortisol/DHEA ratio) were obtained from the SAGE nested case-control study.
Multivariable logistic regression analysis confirmed the first objective that skin infections (adj. OR 1.25, 95% CI 1.13-1.39) and or atopic dermatitis (adj. OR 1.46, 95% CI 1.26-1.70) seen in children from birth to age 2 could be used as indirect markers of stress. The second objective determined that children who exhibited an early skin infection, from birth to age two, were at an increased risk for developing asthma by age 11 independent of atopic dermatitis. However, this finding was dependent upon frequency of health care use. Those children that exhibited an early skin infection and had less than 24 health care visits over 7 years were 1.33 times (95% CI 1.01-1.75) more likely to acquire asthma by age 11 than those who did not have an early skin infection. Children with fewer health care visits were 1.44 times more likely to have asthma. The third objective was not met because the association between early skin infection and asthma was not independent of the Cortisol/DHEA ratio. However, the univariate results for skin infection in the nested case-control study were not significant. The findings of this thesis may be used by family physicians or paediatricians when looking for tangible markers that may indicate infants at risk for developing asthma by school age.
