Several studies with animal research associate air pollution in Alzheimer's disease (AD) neuropathology, but the actual impact of air pollution on the risk of AD is unknown. Here, this study investigates the association between long-term exposure to ozone (O3) and particulate matter (PM) with an aerodynamic diameter equal to or less than 2.5 μm (PM2.5), and newly diagnosed AD in Taiwan. We conducted a cohort study of 95,690 individuals' age ≥ 65 during 2001-2010. We obtained PM10 and O3 data from Taiwan Environmental Protection Agency during 2000-2010. Since PM2.5 data is only accessible entirely after 2006, we used the mean ratio between PM2.5 and PM10 during 2006-2010 (0.57) to estimate the PM2.5 concentrations from 2000 to 2005. A Cox proportional hazards model was used to evaluate the associations between O3 and PM2.5 at baseline and changes of O3 and PM2.5 during the follow-up period and AD. The adjusted HR for AD was weakly associated with a raised concentration in O3 at baseline per increase of 9.63 ppb (adjusted HR 1.06, 95% confidence interval (CI) 1.00-1.12). Further, we estimated a 211% risk of increase of AD per increase of 10.91 ppb in O3 over the follow-up period (95% CI 2.92-3.33). We found a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM2.5 over the follow-up period (95% CI 2.21-2.56). These findings suggest long-term exposure to O3 and PM2.5 above the current US EPA standards are associated with increased the risk of AD.

There is limited evidence that long-term exposure to ambient air pollution increases the risk of childhood autism spectrum disorder (ASD). The objective of the study was to investigate the associations between long-term exposure to air pollution and newly diagnostic ASD in Taiwan. We conducted a population-based cohort of 49,073 children age less than 3 years in 2000 that were retrieved from Taiwan National Insurance Research Database and followed up from 2000 through 2010. Inverse distance weighting method was used to form exposure parameter for ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particles with aerodynamic diameter less than 10 µm (PM10). Time-dependent Cox proportional hazards (PH) model was performed to evaluate the relationship between yearly average exposure air pollutants of preceding years and newly diagnostic ASD. The risk of newly diagnostic ASD increased according to increasing O3, CO, NO2, and SO2 levels. The effect estimate indicating an approximately 59% risk increase per 10 ppb increase in O3 level (95% CI 1.42–1.79), 37% risk increase per 10 ppb in CO (95% CI 1.31–1.44), 340% risk increase per 10 ppb increase in NO2 level (95% CI 3.31–5.85), and 17% risk increase per 1 ppb in SO2 level (95% CI 1.09–1.27) was stable with different combinations of air pollutants in the multi-pollutant models. Our results provide evident that children exposure to O3, CO, NO2, and SO2 in the preceding 1 year to 4 years may increase the risk of ASD diagnosis.

Background: Lung development is a multistage process from conception to the postnatal period, disruption of which by air pollutants can trigger later respiratory morbidity. Objective: We sought to evaluate the effects of weekly average fine particulate matter (particulate matter with an aerodynamic diameter less than 2.5 mm [PM 2.5 ]) exposure during pregnancy and infancy on asthma and identify vulnerable times to help elucidate possible mechanisms of the effects of PM 2.5 on asthma symptoms. Methods: A birth cohort study including 184,604 children born during 2004-2011 in Taichung City was retrieved from the Taiwan Maternal and Child Health Database and followed until 2014. A daily satellite-based hybrid model was applied to estimate PM 2.5 exposure for each subject. A Cox proportional hazard model combined with a distributed lag nonlinear model was used to evaluate the associations of asthma with PM 2.5 exposure during pregnancy and infancy. Results: The birth cohort contained 34,336 asthmatic patients, and the mean age of children given a diagnosis of asthma was 3.39 6 1.78 years. Increased exposure to PM 2.5 during gestational weeks 6 to 22 and 9 to 46 weeks after birth were significantly associated with an increased incidence of asthma. The exposure-response relationship indicated that the hazard ratio (HR) of asthma increased steeply at PM 2.5 exposure of greater than 93 mg/m 3 during pregnancy. Additionally, the HRs remained significant with postnatal exposure to PM 2.5 between 26 and 72 mg/m 3 (range, 1.01-1.07 mg/m 3), followed by a sharp increase in HRs at PM 2.5 exposure of greater than 73 mg/m 3. Conclusion: Both prenatal and postnatal exposures to PM 2.5 were associated with later development of asthma. The vulnerable time windows might be within early gestation and midgestation and infancy.

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