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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.

SUBMITTER: Liu R

PROVIDER: S-EPMC5089873 | biostudies-other | 2016 Nov

REPOSITORIES: biostudies-other

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Ambient Air Pollution Exposures and Risk of Parkinson Disease.

Liu Rui R Young Michael T MT Chen Jiu-Chiuan JC Kaufman Joel D JD Chen Honglei H

Environmental health perspectives 20160610 11

<h4>Background</h4>Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).<h4>Objective</h4>We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 μm in diameter (PM10) and < 2.5 μm in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.<h4>Methods</h4>Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 20 ...[more]

PMID: 27285422

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Project description:ImportanceThe development of Parkinson disease (PD) may be promoted by exposure to air pollution.ObjectiveTo investigate the potential association between exposure to particulate matters (PM2.5 and PM10), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and carbon monoxide (CO) and the risk of incident PD.Design, setting, and participantsThis retrospective cohort study used data from the Korean National Health Insurance Service. Among the 1 021 208 Korean individuals in the database, those who had lived in Seoul from January 2002 to December 2006 (n = 176 875) were screened for eligibility. A total of 78 830 adults older than 40 years without PD and who lived in Seoul between January 2002 and December 2006 were included in this study. Individuals diagnosed with PD before 2006 (n = 159) and individuals 40 years or younger (n = 97 886) were excluded. Each participant was followed up with annually from January 2007 to December 2015, thereby adding up to 757 704 total person-years of follow-up. Data were analyzed from January to September 2020.ExposuresIndividual exposure levels to PM2.5, PM10, NO2, O3, SO2, and CO were estimated based on the participants' residential address at the district level. To evaluate long-term exposure to air pollution, time-varying 5-year mean air pollutant exposure was calculated for each participant.Main outcomes and measuresThe outcome measure was the association between air pollution and the risk of incident PD measured as hazard ratios after adjusting for demographic factors, socioeconomic factors, and medical comorbidities.ResultsAt baseline, the mean (SD) age of the 78 830 participants was 54.4 (10.7) years, and 41 070 (52.1%) were female. A total of 338 individuals with newly diagnosed PD were identified during the study period. Exposure to NO2 was associated with an increase in risk of PD (hazard ratio for highest vs lowest quartile, 1.41; 95% CI, 1.02-1.95; P for trend = .045). No statistically significant associations between exposure to PM2.5, PM10, O3, SO2, or CO and PD incidence were found.Conclusions and relevanceIn this large cohort study, a statistically significant association between NO2 exposure and PD risk was identified. This finding suggests the role of air pollutants in PD development, advocating for the need to implement a targeted public health policy.

Project description:BACKGROUND:Residential proximity to major roadways, and prenatal exposures to particulate matter <2.5??m (PM2.5) and ozone (O3) are linked to poor fetal outcomes but their relationship with childhood development is unclear. OBJECTIVES:We investigated whether proximity to major roadways, or prenatal and early-life exposures to PM2.5 and O3 increase the risk of early developmental delays. STUDY DESIGN:Prospective cohort. SETTINGS:New York State excluding New York City. PARTICIPANTS:4089 singletons and 1016 twins born between 2008 and 2010. EXPOSURES:Proximity to major roadway was calculated using road network data from the NY Department of Transportation. Concentrations of PM2.5 and O3 estimated by the Environmental Protection Agency Downscaler models were spatiotemporally linked to each child's prenatal and early-life addresses incorporating residential history, and locations of maternal work and day-care. OUTCOMES:Parents reported their children's development at ages 8, 12, 18, 24, 30 and 36 months in five domains using the Ages and Stages Questionnaire. Generalized mixed models estimated the relative risk (RR) and 95% CI for failing any developmental domain per 10 units increase in PM2.5 and O3, and for those living <1000?m away from a major roadway compared to those living further. Models adjusted for potential confounders. RESULTS:Compared to those >1000?m away from a major roadway, those resided 50-100?m [RR: 2.12 (1.00-4.52)] and 100-500?m [RR: 2.07 (1.02-4.22)] away had twice the risk of failing the communication domain. Prenatal exposures to both PM2.5 and ozone during various pregnancy windows had weak but significant associations with failing any developmental domain with effects ranging from 1.6% to 2.7% for a 10??g/m3 increase in PM2.5 and 0.7%-1.7% for a 10?ppb increase in ozone. Average daily postnatal ozone exposure was positively associated with failing the overall screening by 8 months [3.3% (1.1%-5.5%)], 12 months [17.7% (10.4%-25.5%)], and 30 months [7.6%, (1.3%-14.3%)]. Findings were mixed for postnatal PM2.5 exposures. CONCLUSIONS:In this prospective cohort study, proximity to major roadway and prenatal/early-life exposures to PM2.5 and O3 were associated with developmental delays. While awaiting larger studies with personal air pollution assessment, efforts to minimize air pollution exposures during critical developmental windows may be warranted.

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Ambient Air Pollution Exposures and Risk of Parkinson Disease.

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Ambient Air Pollution Exposures and Risk of Parkinson Disease.

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