Domestic airborne pollutants and asthma and respiratory symptoms in middle age.

BACKGROUND AND OBJECTIVE: The role of indoor air pollution as a risk factor for asthma and respiratory symptoms in middle age is unclear. We investigated associations between indoor air pollution sources and (i) asthma phenotypes and (ii) asthma-related respiratory symptoms in middle-aged adults. METHODS: Subjects (n = 5729) who participated in the 2004 survey of the Tasmanian Longitudinal Health Study completed respiratory and home environment questionnaires. Associations between indoor air pollution sources, and asthma phenotypes and asthma-related respiratory symptoms were estimated. RESULTS: Recent mould in the home was associated with current asthma (odds ratio (OR) 1.26; 95% confidence interval 1.06-1.50), wheeze (OR 1.34; 1.17-1.54) and nocturnal chest tightness (OR 1.30; 1.12-1.51). Stratified by atopy and gender, recent mould was associated with current non-atopic asthma only in males (OR 3.73; 1.29-10.80). More rooms affected by mould were associated with significant trends for current asthma, wheeze and nocturnal chest tightness. Home environmental tobacco smoke was associated with doctor-diagnosed asthma (OR 1.25; 1.02-1.53), wheeze (OR 1.69; 1.41-2.03), nocturnal chest tightness (OR 1.54; 1.26-1.88), with current asthma only in non-smokers (OR 2.09; 95%: 1.30-3.35) and with current asthma only in males (OR 1.74; 95%: 1.25-2.42). Among heating appliances, reverse cycle air conditioning was negatively associated with doctor-diagnosed asthma (OR 0.84; 0.70-1.00). Neither electric nor gas stove use was associated with either asthma phenotype or with asthma-related respiratory symptoms. CONCLUSIONS: In middle age, reducing home exposure to mould and environmental tobacco smoke might reduce asthma and asthma-related respiratory symptoms.

Childhood eczema and rhinitis predict atopic but not nonatopic adult asthma: a prospective cohort study over 4 decades.

BACKGROUND: The evidence on whether the atopic march observed in childhood (ie, the progression from eczema to allergic rhinitis and asthma) extends to adulthood is sparse, and there is no evidence on whether the progression leads to a specific phenotype of asthma. OBJECTIVE: We sought to assess whether childhood eczema and rhinitis are risk factors for specific phenotypes of adult asthma. METHODS: Participants of the Tasmanian Longitudinal Health Study recruited in 1968 (age range, 6.0-7.0 years) were followed up at age 44 years. The risk of current atopic or nonatopic asthma in middle age characterized by sensitization to aeroallergens given childhood eczema, rhinitis, or both was calculated by using multinomial logistic regression. RESULTS: No association was found between childhood eczema or rhinitis and nonatopic adult asthma. In contrast, childhood eczema and rhinitis in combination predicted both new-onset atopic asthma by middle age (adjusted multinomial odds ratio [aMOR], 6.3; 95% CI, 1.7-23.2) and the persistence of childhood asthma to adult atopic asthma (aMOR, 11.7; 95% CI, 3.6-37.9). Participants with childhood eczema alone were at increased risk of new-onset atopic asthma (aMOR, 4.1; 95% CI, 1.9-8.8), whereas rhinitis alone predicted the persistence of childhood asthma to atopic asthma (aMOR, 2.7; 95% CI, 1.3-5.6). Of all asthma, 29.7% of persistent atopic asthma and 18.1% of new-onset atopic asthma could be attributed to having childhood eczema and rhinitis. CONCLUSION: Childhood eczema and rhinitis are strongly associated with the incidence and persistence of adult atopic asthma.