Diego Lopez Peralta

and 15 more

Background: There is limited information on risk factors for eczema in adults. Recent evidence suggests that air pollution may be associated with increased incidence of eczema in adults. We aimed to assess this possible association. Methods: Ambient air pollution exposures (distance from a major road, nitrogen dioxide [NO2], fine particulate matter with an aerodynamic diameter ≤2.5 µm [PM2.5]) were assessed for the residential address of Tasmanian Longitudinal Health Study participants at ages 43 and 53 years. Eczema incidence (onset after age 43 years), prevalence (at 53 years) and persistence were assessed from surveys, while sensitisation was assessed using skin prick tests. The presence or absence of eczema and sensitisation was classified into four groups: no atopy or eczema, atopy alone, non-atopic eczema, and atopic eczema. Adjusted logistic and multinomial regression models were fitted to estimate associations between ambient air pollution and eczema, and interaction by sex was assessed. Results: Of 3153 participants in both follow ups, 2369 had valid skin prick tests. For males, a 2.3 ppb increase in baseline NO2 was associated with increased risk of prevalent eczema (OR=1.15 [95%CI 0.98-1.36]), both non-atopic (OR=1.39 [1.02-1.90]) and atopic eczema (OR=1.26 [1.00-1.59]). These associations were not seen in females (P for interaction=0.08, <0.01). For both sexes, a 1.6 µg/m3 increase in PM2.5 exposure at follow-up was associated with increased odds of aeroallergen sensitisation (OR=1.15 [1.03-1.30]). Conclusion: Increased exposure to residential ambient air pollutants was associated with an increased risk of eczema, only in males, and aeroallergen sensitisation in both genders.

Hong Yao Yu

and 11 more

Background: While a parental history of asthma has been widely reported as a risk factor for childhood asthma, less is known about the impact of multigenerational family history of asthma on the occurrence of asthma in children. Methods: From 2012 to 2013, a cross-sectional study was carried out in seven Chinese cities. Participants were randomly selected from 94 middle schools, elementary schools and kindergartens. Questionnaires, from which information on asthma, environmental exposure and family members (parents, paternal grandparents and maternal grandparents) affected by asthma were obtained, were completed by the children’s parents or guardians. Two-level logistic regressions were used to assess hereditary patterns of asthma, adjusted for potential confounding factors. Mediation analysis was performed to estimate the potential mediation effect of parents on the association between grandparental asthma and offspring asthma. Results: A paternal grandfather (OR: 2.59, 95%CI: 2.14-3.13), paternal grandmother (OR: 2.40, 95%CI: 1.93-2.99), maternal grandfather (OR: 2.08, 95%CI: 1.71-2.53) and maternal grandmother (OR: 2.08, 95%CI: 1.67-2.59) with asthma were associated with childhood asthma, independent of parental asthma. Of the children who had two family members with asthma, the risk of childhood asthma was highest when both parents had asthma (OR: 15.92, 95%CI: 4.66-54.45) or when both father and paternal grandfather had asthma (OR: 11.11, 95%CI: 5.77-21.38). Parents had a small proportion of mediation effect on the association between grandparental asthma and childhood asthma. Conclusions: A family history of grandparental asthma was associated with childhood asthma and parents only partially mediate the association.