Background: Inhalation of fine particulate matter (PM) can cause systematic inflammation and oxidative stress, which may further aggravate the development and progression of asthma. Although nutritional intake of fatty acids and antioxidants may attenuate some effects of fine PM, the role of the inflammatory potential of diet has not been addressed. Therefore, we aimed to investigate possible modulatory effects of dietary inflammatory potential on the association between indoor air pollution and childhood asthma-related outcomes.Methods: In a sample of 501 children (48.1% females, aged 7-12 years) from 20 public schools located in Porto, Portugal, we evaluated airway reversibility, exhaled nitric oxide levels, atopy, and current respiratory symptoms. Dietary inflammatory index was calculated based on information collected through a reported 24-hour recall questionnaire, and participants were categorized as having an anti-inflammatory or pro-inflammatory diet. Concentrations of indoor PM2.5 and PM10 were measured to assess indoor air quality. Generalized linear mixed models were used to investigate the proportion of effects explained by the exposure to PM2.5 and PM10.Results: After adjustment, the exposure effect of PM2.5 and PM10 levels on children with asthma was higher for those having a pro-inflammatory diet (OR = 1.44, 95% CI:1.01-2.21; and OR = 1.29, 95% CI: 1.03-1.68, respectively) compared to those having an anti-inflammatory diet.
Conclusion:These findings suggest that the quality of diet might affect the association between indoor pollution and asthma in children, highlighting the relevance | 291 de CASTRO MeNdeS eT Al. de CASTRO MeNdeS eT Al.effect was estimated by odds ratio (OR) and 95% confidence interval (95% CI). Additionally, β and 95% CI were estimated for continuous variables. Lung function parameters, exhaled NO, and all subjective and objective measures of asthma were included as outcomes, considering "medical diagnosis" and "under asthma treatment" as primary outcomes and "positive bronchodilation" and "asthma symptoms" as secondary outcomes. The values of DII were grouped into one of the two categories according to the inflammatory potential of the diet: anti-inflammatory, when the values were below zero; and pro-inflammatory, when the values were higher. Shivappa et al's review pointed out 45 food parameters, and they were scored with +1, −1, or 0 according to their inflammatory effects: pro, anti, or null, respectively. Accordingly, we aggregated children based on their proor anti-inflammatory individual DII score. 17 No children obtained an individual score equal to 0. The estimates were assessed in several models: a model for main effects (Model 1); a model considering an interaction between PM2.5 or PM10 and dietary inflammatory index (Model 2); and a model adjusted for age, sex, exposure to tobacco at home, maternal smoking during pregnancy, atopy, body mass categories, and school (Model 3). Model 3 considered the interaction only if it was significant in Model 2. A 0.05 level of signi...