Fine particulate matter measured by satellites predicts the risk of age-related macular degeneration in a longitudinal cohort study.

Although studies have revealed that ambient particulate matter (PM) has detrimental effects on the ocular surface, there have been limited reports detailing the effect of ambient PM on the posterior segment of the eye. A large-scale longitudinal cohort study evaluating the association between fine PM, especially PM2.5, and the retina could elucidate the risk of ambient pollutants for retinal diseases. We investigated the association between PM2.5 and the development of age-related macular degeneration (AMD). We conducted a population-based cohort study of 4,284,128 participants in Taiwan between 2001 and 2011. PM2.5 was continuously measured by satellites and subsequently assigned to each geographic district along with its postcode. A time-dependent Cox proportional-hazard model was used to assess the overall effects of average PM2.5. We used distributed lag non-linear models to evaluate the dose-response relationship between PM2.5 and AMD development. The annual mean of PM2.5 exposure was 34.23 ± 7.17 µg/m3. The PM2.5 concentrations were highest in spring, followed by those in winter, autumn, and summer. Twelve thousand ninety-five new AMD cases were reported during the study period. After adjusting for covariates, the AMD risk increased by 19% (95% confidence interval 1.13-1.25) for a 10 µg/m3 PM2.5 increase. The present study demonstrated that chronic exposure to PM2.5 increases the risk of AMD. Almost half of the Taiwanese live in a polluted area where the PM2.5 levels are higher than the World Health Organization recommended air quality guideline of 10 µg/m3 had a 1.4-fold risk, which significantly increases concern about their visual health and social burden.

Effect of exposure to fine particulate matter during pregnancy and infancy on paediatric allergic rhinitis.

BACKGROUND: The effect of prenatal and postnatal exposure to fine particulate matter (PM2.5) on the development of allergic rhinitis (AR) is poorly understood. We further identified the vulnerable period for AR development to determine methods to decrease adverse effects. METHODS: We used a large population-based birth cohort of 140 911 singleton live infants in Taichung, Taiwan with a highly temporal-resolution satellite-based hybrid model to evaluate the effects of prenatal and early postnatal exposure on the onset of AR. RESULTS: Among 140 911 children, 47 276 (33.55%) were cases of incident AR. The mean age of the children with AR at initial diagnosis was 2.97±1.78 years. We identified a significant association of AR with an interquartile range (IQR 17.98 µg/m3) increase in PM2.5 from 30 gestational weeks to 52 weeks after birth. The exposure-response relationship revealed that AR had a significant positive association between PM2.5 of 26-76 µg/m3 (adjusted hazard ratios ranged from 1.00 to 1.05). CONCLUSION: Our study provides evidence that both prenatal and postnatal exposures to PM2.5 are associated with later development of AR. The vulnerable time window may be within late gestation and the first year of life. Further study is required to confirm the vulnerable time period of PM2.5 on AR.

Particulate Air Pollution and Progression to Kidney Failure With Replacement Therapy: An Advanced CKD Registry-Based Cohort Study in Taiwan.

RATIONALE & OBJECTIVE: Limited evidence concerns fine particulate matter (with aerodynamic diameter ≤ 2.5µm [PM2.5]) exposure and the risk for kidney failure with replacement therapy (KFRT). This study assessed whether PM2.5 exposure was associated with progression of chronic kidney disease (CKD) to KFRT. STUDY DESIGN: Prospective cohort study. SETTING & PARTICIPANTS: 6,628 adult patients with CKD were recruited from the Advanced CKD Program in Taiwan between 2003 and 2015. EXPOSURE: Satellite-based spatiotemporal models were used to calculate each individual's 1-year PM2.5 exposure before the date of enrollment into the Advanced CKD Program. OUTCOMES: Time to KFRT (defined as initiation of maintenance hemodialysis, peritoneal dialysis, or kidney transplantation) and time to all-cause mortality. ANALYTICAL APPROACH: Multivariable proportional hazard regression analyses were used to estimate the association of PM2.5 with KFRT and all-cause mortality. Restricted cubic splines were used to explore dose-response relationships. RESULTS: The study population included 6,628 adult patients with CKD who were aged 20 to 90 years. 941 KFRT events and 1,653 deaths occurred during follow-up. The adjusted HR for progression to KFRT was 1.19 (95% CI, 1.08-1.31) per 7.8µg/m3 greater PM2.5, an amount spanning the interquartile range. There was evidence of a dose-response relationship (adjusted HRs of 1.16 [95% CI, 0.90-1.51], 1.19 [95% CI, 0.94-1.52], and 1.42 [95% CI, 1.12-1.80] for low, medium, and high PM2.5 levels). There was no significant association between PM2.5 and all-cause mortality (adjusted HR, 1.01 [95% CI, 0.95-1.08]). LIMITATIONS: Misclassification of PM2.5 exposure assessment and the potential for residual confounding. CONCLUSIONS: Our findings suggest that long-term exposure to PM2.5 is associated with increased risk for progression to KFRT in patients with CKD.

Exposure to fine particulate matter (PM2.5) and pediatric rheumatic diseases.

Few studies have assessed the association between fine particulate matter (PM2.5) exposure during pregnancy and infancy and pediatric rheumatic diseases (PRDs). The goal of this study was to investigate the association of PM2.5 with PRDs, and to explore sensitive windows of exposure. Therefore, we conducted a cohort-based case-control study to investigate the association between weekly exposure to PM2.5 and PRDs in Taiwan. Our birth cohort consisted of infants born in 2004-2014 (n = 1,991,592) who were followed from conception to the end of 2015. There were 2363 cases of incident PRDs in children, and 23,630 children served as controls using density matching (1:10) based on date of birth, gender, and gestational week. We used a linear mixed effect (LME) model to incorporate the aerosol optical depth (AOD), meteorological variables, and land-use data to predict daily PM2.5 concentrations. We also performed conditional logistic regression with distributed lag non-linear models (DLNMs) to assess the effects of weekly average PM2.5 on PRDs, as well as dose-response relationships. In DLNMs, exposure to PM2.5 during pregnancy (11-40 weeks) or infancy (1-14 weeks after birth) was associated with incident PRDs adjusting for potential confounding factors, and for carbon monoxide and sulfur dioxide. In the dose-response association, the odds ratios of PRDs were significantly increased for PM2.5 exposures between 26 and 54 µg/m3. In addition, exposure to PM2.5 above 81 µg/m3 dramatically increased the risk of PRDs. In conclusions, our study provides new data to suggest that PM2.5 exposure from 11-40 gestational weeks to 1-14 weeks after birth can increase the risk for PRDs in a non-linear dose-response fashion.

The effects of exposure to air pollution on the development of uterine fibroids.

BACKGROUND: Air pollution may cause specific genetic or epigenetic abnormalities and lead to the development of uterine fibroids (UFs). However, there have been limited studies evaluating the relationship between air pollutant exposure and the development of UFs. METHODS: We conducted a 10-year cohort-based case-control study in Taiwan from 2001 to 2010 using National Health Institute Research Database (NHIRD) to assess the association between air pollution and the UFs development among Taiwanese women. The case group consisted of 11,028 women newly diagnosed with UFs during the study period and the control group was 44,112 women aged 25-45 years using density sampling with a 1:4 matching on the date of birth from 224,675 women in 2001-2010. The average age of onset was 36 ±â€¯4.37 years old. Daily concentrations of PM2.5 were estimated by linear mixed-effects model integrating aerosol optical depth (AOD) and meteorological variables; daily concentrations of O3, CO, NO2 and SO2 were calculated by the Inverse Distance Weighting (IDW). The annual cumulative exposure to air pollutants during the study period was calculated corresponding to residential zip codes. RESULTS: In the conditional logistic regression adjusting for confounders, the adjusted odds ratio (aOR) for UFs per 10 µg/m3 increase in PM2.5 was 1.105 (95% confidence interval: 1.069, 1.141), per 10 ppb increase in O3 was 1.075 (95% confidence interval: 1.039, 1.113), respectively. CONCLUSIONS: Our study suggests that exposure to PM2.5 and O3 may increase the risk of developing UFs. Further studies are needed to confirm this novel finding.

Association of Air Pollution Exposure and Interleukin-13 Haplotype with the Risk of Aggregate Bronchitic Symptoms in Children.

Interleukin-13(IL-13) might play an important role in driving aggregate bronchitic symptoms pathogenesis. However, none of the studies assessed the interaction between air pollutants exposure and IL-13 gene on the risk of aggregate bronchitic symptoms in non-asthma children. To assess the independent and joint effects of the exposure to air pollution and IL-13 haplotypes on the risk of aggregate bronchitic symptoms, we conducted a cross-sectional study and focused on non-asthma children. The study population consisted of 2944 children. The effect of each air pollutant on the risk of aggregate bronchitic symptoms was estimated as odds ratios per interquartile range (IQR) change. In the multiple logistic regressions, adjusted for confounding factors, the risk of chronic phlegm was associated with PM2.5 exposure (aOR, 1.59; 95% CI, 1.07-2.37 per 12.51µg/m3 change), O3 exposure (aOR, 1.54 95% CI, 1.05-2.27 per 8.28ppb change) and SO2 exposure (aOR, 1.19; 95% CI, 1.02-1.39 per 0.98ppb change). Our study further provides the evidence that gene-environment interactions between IL-13 haplotype and O3 exposure on chronic phlegm (95% CI for interaction, 1.01-1.38). Identifying children who are more sensitive to air pollution helps us to provide them an efficient prevention to avoid aggregate bronchitic symptoms.