Indoor environment and tobacco smoke exposure in relation to allergic disease and lung function

Abstract

Asthma and other allergy related diseases are the most common chronic diseases in childhood, and have become a major public health concern. The rapid increase in the occurrence of these diseases, especially in high-income countries, has led to the study of the role ofvarious environmental and lifestyle factors. The overall aim of this thesis was to evaluate the association between indoor environmental factors and the development of allergic diseases in childhood and adolescence, and more specifically, to study the association between tobacco smoke exposure during pre- or postnatal life as well as exposure to indoor mold or dampness and allergic diseases from birth to age 16 years. We used data from the Swedish prospective birth cohort BAMSE (N = 4089) and in study III data from BAMSE combined with four other European birth cohorts (N = 10860).

We found that exposure to maternal smoking during pregnancy was associated with asthma up to adolescence, especially early-transient asthma. Additionally, exposure to high doses of maternal smoking during pregnancy (≥10 cigarettes/day) was associated with persistent asthma as well as persistent rhinoconjunctivitis up to age 16 years. Based on spirometry, exposure to maternal smoking during pregnancy was also associated with lower FEV1/FVC ratios at age 16 years. Additionally, indices from impulse oscillometry indicated increased peripheral airway resistance at age 16 years among subjects exposed to maternal smoking during pregnancy.

Exposure to secondhand smoke (SHS) during infancy was associated with overall increased risks of asthma, rhinitis, and eczema up to adolescence. However, we found suggestive evidence that the association between SHS during infancy and asthma was likely driven by exposure in utero. Our findings indicate that exposure to SHS during infancy, without prior exposure to maternal smoking during pregnancy, was associated with food allergen sensitization up to age 16 years. Furthermore, exposure to SHS during infancy was associated with increased risks ofrhinitis without concomitant sensitization and eczema with concomitant sensitization. SHS exposure during other periods of childhood was not associated with the onset of asthma or rhinoconjunctivitis in adolescence.

Compared with non-smokers, participants who smoked daily or occasionally tended to have reduced FEV1/FVC ratios at age 16 years, even after controlling for maternal smoking during pregnancy. Using indices from impulse oscillometry (IOS) we found increased peripheral airway resistance among adolescent smokers. These findings were corroborated when we used saliva cotinine concentrations to discriminate smokers from non-smokers. Exposure to indicators of mold or dampness during infancy were associated with increased risk of asthma up to age 16 years, as well as an increased risk of persistent asthma. We also found suggestive evidence of an association between reported mold odor or visible mold during infancy and rhinitis up to age 16 years. No association between exposure to indicators of mold or dampness and IgE sensitization was observed.

In conclusion, findings from the studies included in this thesis suggest that exposure to maternal smoking during pregnancy is associated with asthma and measures of airway obstruction, such as reduced FEV1/FVC ratios, up to adolescence. Exposure to SHS during infancy seems to be associated with food allergen sensitization and rhinitis up to age 16 years. Adolescent smoking is associated with reduced FEV1/FVC ratios and increased peripheral airway resistance at age 16 years. Exposure to indicators of mold or dampness during infancy may be associated with an increased risk of asthma, and more specifically with persistent asthma up to age 16 years. The results from this thesis can be used to help inform public health policy as well as clinicians to motivate their patients to abstain from smoking. Indoor mold and dampness is a modifiable risk factor related to the onset and persistence of asthma in children and adolescence, and further research should focus on identifying the causal agents.