Ambient Air Pollution Exposures and Risk of Parkinson Disease.
ABSTRACT: Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.
Project description:Short-term exposures to outdoor air pollutants have been associated with lower lung function, but the results are inconsistence. The effects of different pollutant levels on lung function changes are still unclear. We quantified the effects of outdoor air pollution exposure (NO2, PM10, O3, and PM2.5) on lung function among 1,694 female non-smokers from the Wuhan-Zhuhai Cohort in China by using linear mixed model. We further investigated the associations in the two cities with different air quality levels separately to quantify the effects of different pollutant level exposure on lung function. We found the moving averages of NO2, PM10, and PM2.5 concentrations were significantly associated with reduced FVC. In city at high pollutant level, the moving average of NO2, PM10, O3, and PM2.5 exposures were significantly associated with both FVC and FEV1 reductions. In the low-level air pollution city, PM10 (Lag03-Lag05) and O3 concentrations (Lag01-Lag03) were significantly associated with reduced FVC, while PM10 (Lag03-Lag05), O3 (Lag0-Lag03), and PM2.5 (Lag04-Lag06) exposure were significantly associated with reduced FEV1. Our results suggest that outdoor air pollution is associated with short-term adverse effects on lung function among female non-smokers. The adverse effects may persist for longer durations within 7 days at higher air pollutant levels.
Project description:A body of literature has suggested an elevated risk of lung cancer associated with particulate matter and traffic-related pollutants.We examined the relation of lung cancer incidence with long-term residential exposures to ambient particulate matter and residential distance to roadway, as a proxy for traffic-related exposures.For participants in the Nurses' Health Study, a nationwide prospective cohort of women, we estimated 72-month average exposures to PM2.5, PM2.5-10, and PM10 and residential distance to road. Follow-up for incident cases of lung cancer occurred from 1994 through 2010. Cox proportional hazards models were adjusted for potential confounders. Effect modification by smoking status was examined.During 1,510,027 person-years, 2,155 incident cases of lung cancer were observed among 103,650 participants. In fully adjusted models, a 10-?g/m3 increase in 72-month average PM10 [hazard ratio (HR) = 1.04; 95% CI: 0.95, 1.14], PM2.5 (HR = 1.06; 95% CI: 0.91, 1.25), or PM2.5-10 (HR = 1.05; 95% CI: 0.92, 1.20) was positively associated with lung cancer. When the cohort was restricted to never-smokers and to former smokers who had quit at least 10 years before, the associations appeared to increase and were strongest for PM2.5 (PM10: HR = 1.15; 95% CI: 1.00, 1.32; PM2.5: HR = 1.37; 95% CI: 1.06, 1.77; PM2.5-10: HR = 1.11; 95% CI: 0.90, 1.37). RESULTS were most elevated when restricted to the most prevalent subtype, adenocarcinomas. Risks with roadway proximity were less consistent.Our findings support those from other studies indicating increased risk of incident lung cancer associated with ambient PM exposures, especially among never- and long-term former smokers.
Project description:Despite the importance of understanding the connection between air pollution exposure and diabetes, studies investigating links between air pollution and glucose metabolism in nondiabetic adults are limited.We aimed to estimate the association of medium-term air pollution exposures with blood glucose and glycated hemoglobin A1c (HbA1c) among nondiabetics.This study included observations from nondiabetic participants (nobs=7,108) of the population-based Heinz Nixdorf Recall study at baseline (2000–2003) and follow-up examination (2006–2008). Daily fine particulate matter (aerodynamic?diameter?2.5??m,?PM2.5; aerodynamic?diameter?10??m,?PM10), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) exposures were estimated at participants’ residences using the spatiotemporal European Air Pollution Dispersion (EURAD) chemistry transport model. We evaluated the associations between medium-term air pollution exposures (28- and 91-d means) and glucose metabolism measures using mixed linear regression and adjusting for season, meteorology, and personal characteristics. A range of other exposure windows (1-, 2-, 3-, 7-, 14-, 45-, 60-, 75-, 105-, 120-, and 182-d means) were also evaluated to identify potentially relevant biological windows.We observed positive associations between PM2.5 and PNAM exposures and blood glucose levels [e.g., 28-d PM2.5: 0.91 mg/dL (95% CI: 0.38, 1.44) per 5.7??g/m3]. PM2.5, PM10, and PNAM exposures were positively associated with HbA1c [e.g., 91-d PM2.5: 0.07 p.p. (95% CI: 0.04, 0.10) per 4.0??g/m3]. Mean exposures during longer exposure windows (75- to 105-d) were most strongly associated with HbA1c, whereas 7- to 45-d exposures were most strongly associated with blood glucose. NO2 exposure was not associated with blood glucose or with HbA1c.Medium-term PM and PNAM exposures were positively associated with glucose measures in nondiabetic adults. These findings indicate that reducing ambient air pollution levels may decrease the risk of diabetes. https://doi.org/10.1289/EHP2561.
Project description:The associations between ambient air pollutants and tuberculosis seasonality are unclear. We assessed the temporal cross-correlations between ambient air pollutants and tuberculosis seasonality. Monthly tuberculosis incidence data and ambient air pollutants (PM2.5, PM10, carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2)) and air quality index (AQI) from 2013 to 2017 in Shanghai were included. A cross-correlogram and generalized additive model were used. A 4-month delayed effect of PM2.5 (0.55), PM10 (0.52), SO2 (0.47), NO2 (0.40), CO (0.39), and AQI (0.45), and a 6-month delayed effect of O3 (-0.38) on the incidence of tuberculosis were found. The number of tuberculosis cases increased by 8%, 4%, 18%, and 14% for a 10 μg/m3 increment in PM2.5, PM10, SO2, and NO2; 4% for a 10 unit increment in AQI; 8% for a 0.1 mg/m3 increment in CO; and decreased by 4% for a 10 μg/m3 increment in O3. PM2.5 concentrations above 50 μg/m3, 70 μg/m3 for PM10, 16 μg/m3 for SO2, 47 μg/m3 for NO2, 0.85 mg/m3 for CO, and 85 for AQI, and O3 concentrations lower than 95 μg/m3 were positively associated with the incidence of tuberculosis. Ambient air pollutants were correlated with tuberculosis seasonality. However, this sort of study cannot prove causality.
Project description:Maternal ambient air pollution exposure is associated with reduced birthweight. Few studies have examined the effect on growth in utero and none have examined the effect of exposure to particulates less than 2.5µm (PM2.5) and possible effect modification by smoking status.Examine the effect of maternal exposure to ambient concentrations of PM10, PM2.5 and nitrogen dioxide (NO2) for in utero fetal growth, size at birth and effect modification by smoking status.Administratively acquired second and third trimester fetal measurements (bi-parietal diameter, femur length and abdominal circumference), birth outcomes (weight, crown heel length and occipito-frontal circumference) and maternal details were obtained from routine fetal ultrasound scans and maternity records (period 1994-2009). These were modelled against residential annual pollution concentrations (calendar year mean) adjusting for covariates and stratifying by smoking status.In the whole sample (n=13,775 pregnancies), exposure to PM10, PM2.5 and NO2 was associated with reductions in measurements at birth and biparietal diameter from late second trimester onwards. Among mothers who did not smoke at all during pregnancy (n=11,075), associations between biparietal diameter and pollution exposure remained significant but were insignificant among those who did smoke (n=2700). Femur length and abdominal circumference were not significantly associated with pollution exposure.Fetal growth is strongly associated with particulates exposure from later in second trimester onwards but the effect appears to be subsumed by smoking. Typical ambient exposures in this study were relatively low compared to other studies and given these results, it may be necessary to consider reducing recommended "safe" ambient air exposures.
Project description:BACKGROUND:Ambient air pollution may increase the risk of overweight and obesity in children. However, available evidence is still scarce and has mainly focused on ambient air pollution exposure occurring at home without considering the school environment. The aim of this study is to assess whether exposure to ambient air pollution at home and school is associated with overweight and obesity in primary school children. METHODS:We studied 2660 children aged 7-10?years during 2012 in Barcelona. Child weight and height were measured and age- and sex-specific z-scores for body mass index (zBMI) were calculated using the WHO growth reference 2007. Overweight and obesity were defined using the same reference. Land use regression models were used to estimate levels of nitrogen dioxide (NO2), particulate matter <2.5??m (PM2.5), <10??m (PM10) and coarse (PMcoarse) at home. Outdoor levels of NO2, PM2.5, elemental carbon (EC), and ultrafine particles (UFP) were measured in the schoolyard. Multilevel mixed linear and ordered logistic models were used to assess the association between ambient air pollution (continuous per interquartile range (IQR) increase and categorical with tertile cutoffs) and zBMI (continuous and ordinal: normal, overweight, obese), after adjusting for socio-demographic characteristics. RESULTS:An IQR increase in PM10-home (5.6??g/m3) was associated with a 10% increase in the odds of being overweight or obese (odds ratio (OR)?=?1.10; 95% CI?=?1.00, 1.22). Children exposed to the highest tertile of UFP-school (>27,346 particles/cm3) had a 30% higher odds of being overweight or obese (OR?=?1.30; 95%CI?=?1.03, 1.64) compared to the lowest tertile of UFP exposure. We also observed that exposure to NO2, PM2.5 or EC at schools was associated with higher odds of overweight or obese at medium compared to low levels of exposure. Home and school exposures did not show any significant associations with zBMI (except PM2.5-school comparing tertile 2 vs tertile 1) but were similar in direction. CONCLUSIONS:This study suggests that exposure to ambient air pollution, especially at school, is associated with childhood risk for overweight and obesity. A cautious interpretation is warranted because associations were not always linear and because school and home air pollution measurements were not directly comparable.
Project description:The association between air pollution and childhood respiratory disease is inconsistent. In the present study, we investigated a short-term effect of ambient air pollutants and daily childhood lower respiratory diseases (CLRD). Daily air pollutants, weather data, and CLRD data were collected from January 2014 to April 2015 (452 days) in Nanjing, China. Time-series regression and generalized additive models were used to assess the effects of air pollutants (PM10, PM2.5, NO2, SO2, O3, and CO) on CLRD. We observed that an interquartile range (IQR) increase in concentrations of PM10, NO2, and SO2 significantly increased the daily CLRD with 6 days cumulative effects (difference of estimates: 2.8%, 95% CI: 0.6-5.0%; 4.1%, 1.2-7.0%; 5.6%, 2.6-8.6%, respectively). However, no significant association was found in IQR concentrations of PM2.5, O3, and CO. Specifically, elevated PM10, PM2.5, NO2, and SO2 significantly increased the numbers of CLRD in cool season (3.6%, 1.5-5.7%; 2.4%, 0.3-4.5%; 4.9%, 2.9-7.0%; 6.3%, 3.7-9.0%, respectively). Additionally, the effect estimates of PM10, NO2, and SO2 in female and age >27 months were more pronounced than in male and age ?27 months. This study suggested that short-term exposure to ambient PM10, NO2, and SO2 were associated with the increased CLRD numbers.
Project description:Exposure to ambient air pollution has been associated with reduced size of newborns; however, the modifying effect of maternal ethnicity remains little explored among South Asians.We investigated ethnic differences in the association between ambient air pollution and newborn's size.Pregnant women were recruited between 2007 and 2010 for the Born in Bradford cohort study, in England. Exposures to particulate matter (? 10 ?m, PM10; ? 2.5 ?m, PM2.5), PM2.5 absorbance, and nitrogen oxides (NOx, NO2) were estimated using land-use regressions models. Using multivariate linear regression models, we evaluated effect modification by maternal ethnicity ("white British" or "Pakistani origin," self-reported) on the associations of air pollution and birth weight, head circumference, and triceps and subscapular skinfold thickness.A 5-?g/m3 increase in mean third trimester PM2.5 was associated with significantly lower birth weight and smaller head circumference in children of white British mothers (-43 g; 95% CI: -76, -10 and -0.28 cm; 95% CI: -0.39, -0.17, respectively), but not in children of Pakistani origin (9 g; 95% CI: -17, 35 and -0.08 cm; 95% CI: -0.17, 0.01, respectively) (p(int) = 0.03 and < 0.001). In contrast, PM2.5 was associated with significantly larger triceps and subscapular skinfold thicknesses in children of Pakistani origin (0.17 mm; 95% CI: 0.08, 0.25 and 0.21 mm; 95% CI: 0.12, 0.29, respectively), but not in white British children (-0.02 mm; 95% CI: -0.14, 0.01 and 0.06 mm; 95% CI: -0.06, 0.18, respectively) (p(int) = 0.06 and 0.11). Patterns of associations for PM10 and PM2.5 absorbance according to ethnicity were similar to those for PM2.5, but associations of the outcomes with NO2 and NOx were mostly nonsignificant in both ethnic groups.Our results suggest that associations of ambient PM exposures with newborn size and adiposity differ between white British and Pakistani origin infants.Schembari A, de Hoogh K, Pedersen M, Dadvand P, Martinez D, Hoek G, Petherick ES, Wright J, Nieuwenhuijsen MJ. 2015. Ambient air pollution and newborn size and adiposity at birth: differences by maternal ethnicity (the Born in Bradford study cohort). Environ Health Perspect 123:1208-1215; http://dx.doi.org/10.1289/ehp.1408675.
Project description:BACKGROUND:Poor sleep quality is associated with poor quality of life and may even lead to mental illnesses. Several studies have indicated the association between exposure to air pollution and sleep quality. However, the evidence is very limited in China, especially in rural areas. METHODS:Participants in this study were obtained from the Henan Rural Cohort established during 2015-2017. Sleep quality was evaluated using the Pittsburgh Sleep Quality Index (PSQI) in the baseline survey. Poor sleep quality was defined by the global score of PSQI?>?5. Participants' exposures to PM2.5, PM10 (particulate matter with aerodynamic diameters ?2.5??m and 10??m, respectively) and NO2 (nitrogen dioxide) during the three years before the baseline survey were estimated using a satellite-based prediction. The associations between long-term exposure to air pollutants and sleep quality were examined using both the linear regression and logistic regression models. RESULTS:The IQRs (interquartile range) of mean levels of participants' exposures to PM2.5, PM10 and NO2 were 3.3?µg/m3, 8.8?µg/m3, and 4.8?µg/m3, respectively. After adjusted for potential confounders, the global score of PSQI (and 95%CI, 95% confidence intervals) increased by 0.16 (0.04, 0.27), 0.09 (-0.01, 0.19) and 0.14 (0.03, 0.24), associated with per IQR increase in PM2.5, PM10 and NO2, respectively. The odds ratios (and 95%CI) of poor sleep quality associated with per IQR increase in PM2.5, PM10 and NO2 were 1.15 (1.03, 1.29), 1.11 (1.02, 1.21) and 1.14 (1.03, 1.25), respectively. CONCLUSIONS:Long-term exposures to PM2.5, PM10 and NO2 were associated with poor sleep quality in rural China. Improvement of air quality may help to improve sleep quality among rural population of China.
Project description:Limited evidence links air pollution exposure to chronic cough and sputum production. Few reports have investigated the association between long-term exposure to air pollution and classically defined chronic bronchitis.Our objective was to estimate the association between long-term exposure to particulate matter (diameter <10??m, PM10; <2.5?m, PM2.5), nitrogen dioxide (NO2), and both incident and prevalent chronic bronchitis.We estimated annual average PM2.5, PM10, and NO2 concentrations using a national land-use regression model with spatial smoothing at home addresses of participants in a prospective nationwide U.S. cohort study of sisters of women with breast cancer. Incident chronic bronchitis and prevalent chronic bronchitis, cough and phlegm, were assessed by questionnaires.Among 47,357 individuals with complete data, 1,383 had prevalent chronic bronchitis at baseline, and 647 incident cases occurred over 5.7-y average follow-up. No associations with incident chronic bronchitis were observed. Prevalent chronic bronchitis was associated with PM10 [adjusted odds ratio (aOR) per interquartile range (IQR) difference (5.8??g/m3)=1.07; 95% confidence interval (CI): 1.01, 1.13]. In never-smokers, PM2.5 was associated with prevalent chronic bronchitis (aOR=1.18 per IQR difference; 95% CI: 1.04, 1.34), and NO2 was associated with prevalent chronic bronchitis (aOR=1.10; 95%?CI=1.01,?1.20), cough (aOR=1.10; 95% CI: 1.05, 1.16), and phlegm (aOR=1.07; 95% CI: 1.01, 1.14); interaction p-values (nonsmokers vs. smokers) <0.05.PM10 exposure was related to chronic bronchitis prevalence. Among never-smokers, PM2.5 and NO2 exposure was associated with chronic bronchitis and component symptoms. Results may have policy ramifications for PM10 regulation by providing evidence for respiratory health effects related to long-term PM10 exposure. https://doi.org/10.1289/EHP2199.