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Objectives: To examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters., Methods: We assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes., Results: The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013-2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m 3 increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01)., Conclusion: This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans., (© 2024. The Author(s).)

Background: Ambient air pollution, including traffic-related air pollution (TRAP), increases cardiovascular disease risk, possibly through vascular alterations. Limited information exists about in-vehicle TRAP exposure and vascular changes., Objective: To determine via particle filtration the effect of on-roadway TRAP exposure on blood pressure and retinal vasculature., Design: Randomized crossover trial. (ClinicalTrials.gov: NCT05454930)., Setting: In-vehicle scripted commutes driven through traffic in Seattle, Washington, during 2014 to 2016., Participants: Normotensive persons aged 22 to 45 years ( n = 16)., Intervention: On 2 days, on-road air was entrained into the vehicle. On another day, the vehicle was equipped with high-efficiency particulate air (HEPA) filtration. Participants were blinded to the exposure and were randomly assigned to the sequence., Measurements: Fourteen 3-minute periods of blood pressure were recorded before, during, and up to 24 hours after a drive. Image-based central retinal arteriolar equivalents (CRAEs) were measured before and after. Brachial artery diameter and gene expression were also measured and will be reported separately., Results: Mean age was 29.7 years, predrive systolic blood pressure was 122.7 mm Hg, predrive diastolic blood pressure was 70.8 mm Hg, and drive duration was 122.3 minutes (IQR, 4 minutes). Filtration reduced particle count by 86%. Among persons with complete data ( n = 13), at 1 hour, mean diastolic blood pressure, adjusted for predrive levels, order, and carryover, was 4.7 mm Hg higher (95% CI, 0.9 to 8.4 mm Hg) for unfiltered drives compared with filtered drives, and mean adjusted systolic blood pressure was 4.5 mm Hg higher (CI, -1.2 to 10.2 mm Hg). At 24 hours, adjusted mean diastolic blood pressure (unfiltered) was 3.8 mm Hg higher (CI, 0.02 to 7.5 mm Hg) and adjusted mean systolic blood pressure was 1.1 mm Hg higher (CI, -4.6 to 6.8 mm Hg). Adjusted mean CRAE (unfiltered) was 2.7 μm wider (CI, -1.5 to 6.8 μm)., Limitations: Imprecise estimates due to small sample size; seasonal imbalance by exposure order., Conclusion: Filtration of TRAP may mitigate its adverse effects on blood pressure rapidly and at 24 hours. Validation is required in larger samples and different settings., Primary Funding Source: U.S. Environmental Protection Agency and National Institutes of Health., Competing Interests: Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M23-1309.

Background: Based on human and animal experimental studies, exposure to ambient carbon monoxide (CO) may be associated with cardiovascular disease outcomes, but epidemiological evidence of this link is limited. The number and distribution of ground-level regulatory agency monitors are insufficient to characterize fine-scale variations in CO concentrations., Objectives: To develop a daily, high-resolution ambient CO exposure prediction model at the city scale., Methods: We developed a CO prediction model in Baltimore, Maryland, based on a spatiotemporal statistical algorithm with regulatory agency monitoring data and measurements from calibrated low-cost gas monitors. We also evaluated the contribution of three novel parameters to model performance: high-resolution meteorological data, satellite remote sensing data, and copollutant ( PM 2.5 , NO 2 , and NO x ) concentrations., Results: The CO model had spatial cross-validation (CV) R 2 and root-mean-square error (RMSE) of 0.70  and  0.02  parts per million (ppm), respectively; the model had temporal CV R 2 and RMSE of 0.61 and 0.04  ppm , respectively. The predictions revealed spatially resolved CO hot spots associated with population, traffic, and other nonroad emission sources (e.g., railroads and airport), as well as sharp concentration decreases within short distances from primary roads., Discussion: The three novel parameters did not substantially improve model performance, suggesting that, on its own, our spatiotemporal modeling framework based on geographic features was reliable and robust. As low-cost air monitors become increasingly available, this approach to CO concentration modeling can be generalized to resource-restricted environments to facilitate comprehensive epidemiological research. https://doi.org/10.1289/EHP10889.

Background: Population studies support the adverse associations of air pollution exposures with child behavioral functioning and cognitive performance, but few studies have used spatiotemporally resolved pollutant assessments., Objectives: We investigated these associations using more refined exposure assessments in 1,967 mother-child dyads from three U.S. pregnancy cohorts in six cities in the ECHO-PATHWAYS Consortium., Methods: Pre- and postnatal nitrogen dioxide ( NO 2 ) and particulate matter (PM) ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 ) exposures were derived from an advanced spatiotemporal model. Child behavior was reported as Total Problems raw score using the Child Behavior Checklist at age 4-6 y. Child cognition was assessed using cohort-specific cognitive performance scales and quantified as the Full-Scale Intelligence Quotient (IQ). We fitted multivariate linear regression models that were adjusted for sociodemographic, behavioral, and psychological factors to estimate associations per 2-unit increase in pollutant in each exposure window and examined modification by child sex. Identified critical windows were further verified by distributed lag models (DLMs)., Results: Mean NO 2 and PM 2.5 ranged from 8.4  to  9.0  ppb and 8.4  to  9.1   μ g / m 3 , respectively, across pre- and postnatal windows. Average child Total Problems score and IQ were 22.7 [standard deviation (SD): 18.5] and 102.6 (SD: 15.3), respectively. Children with higher prenatal NO 2 exposures were likely to have more behavioral problems [ β : 1.24; 95% confidence interval (CI): 0.39, 2.08; per 2  ppb NO 2 ], particularly NO 2 in the first and second trimester. Each 2 - μ g / m 3 increase in PM 2.5 at age 2-4 y was associated with a 3.59 unit (95% CI: 0.35, 6.84) higher Total Problems score and a 2.63 point (95% CI: - 5.08 , - 0.17 ) lower IQ. The associations between PM 2.5 and Total Problems score were generally stronger in girls. Most predefined windows identified were not confirmed by DLMs., Discussion: Our study extends earlier findings that have raised concerns about impaired behavioral functioning and cognitive performance in children exposed to NO 2 and PM 2.5 in utero and in early life. https://doi.org/10.1289/EHP10248.

Purpose of Review: Epidemiological studies of short- and long-term health impacts of ambient air pollutants require accurate exposure estimates. We describe the evolution in exposure assessment and assignment in air pollution epidemiology, with a focus on spatiotemporal techniques first developed to meet the needs of the Multi-ethnic Study of Atherosclerosis and Air Pollution (MESA Air). Initially designed to capture the substantial variation in pollutant levels and potential health impacts that can occur over small spatial and temporal scales in metropolitan areas, these methods have now matured to permit fine-scale exposure characterization across the contiguous USA and can be used for understanding long- and short-term health effects of exposure across the lifespan. For context, we highlight how the MESA Air models compare to other available exposure models., Recent Findings: Newer model-based exposure assessment techniques provide predictions of pollutant concentrations with fine spatial and temporal resolution. These validated models can predict concentrations of several pollutants, including particulate matter less than 2.5 μm in diameter (PM 2.5 ), oxides of nitrogen, and ozone, at specific locations (such as at residential addresses) over short time intervals (such as 2 weeks) across the contiguous USA between 1980 and the present. Advances in statistical methods, incorporation of supplemental pollutant monitoring campaigns, improved geographic information systems, and integration of more complete satellite and chemical transport model outputs have contributed to the increasing validity and refined spatiotemporal spans of available models. Modern models for predicting levels of outdoor concentrations of air pollutants can explain a substantial amount of the spatiotemporal variation in observations and are being used to provide critical insights into effects of air pollutants on the prevalence, incidence, progression, and prognosis of diseases across the lifespan. Additional enhancements in model inputs and model design, such as incorporation of better traffic data, novel monitoring platforms, and deployment of machine learning techniques, will allow even further improvements in the performance of pollutant prediction models.

Background: Limited data suggest air pollution exposures may contribute to pediatric high blood pressure (HBP), a known predictor of adult cardiovascular diseases., Methods: We investigated this association in the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) study, a sociodemographically diverse pregnancy cohort in the southern United States with participants enrolled from 2006 to 2011. We included 822 mother-child dyads with available address histories and a valid child blood pressure measurement at 4-6 y. Systolic (SBP) and diastolic blood pressures (DBP) were converted to age-, sex-, and height-specific percentiles for normal-weight U.S. children. HBP was classified based on SBP or DBP ≥ 90 th percentile. Nitrogen dioxide ( NO 2 ) and particulate matter ≤ 2.5 μ m in aerodynamic diameter ( PM 2.5 ) estimates in both pre- and postnatal windows were obtained from annual national models and spatiotemporal models, respectively. We fit multivariate Linear and Poisson regressions and explored multiplicative joint effects with maternal nutrition, child sex, and maternal race using interaction terms., Results: Mean PM 2.5 and NO 2 in the prenatal period were 10.8 [standard deviation (SD): 0.9] μ g / m 3 and 10.0 (SD: 2.4) ppb, respectively, and 9.9 (SD: 0.6) μ g / m 3 and 8.8 (SD: 1.9) ppb from birth to the 4-y-old birthday. On average, SBP percentile increased by 14.6 (95% CI: 4.6, 24.6), and DBP percentile increased by 8.7 (95% CI: 1.4, 15.9) with each 2 - μ g / m 3 increase in second-trimester PM 2.5 . PM 2.5 averaged over the prenatal period was only significantly associated with higher DBP percentiles [ β = 11.6 (95% CI: 2.9, 20.2)]. Positive associations of second-trimester PM 2.5 with SBP and DBP percentiles were stronger in children with maternal folate concentrations in the lowest quartile ( p interaction = 0.05 and 0.07, respectively) and associations with DBP percentiles were stronger in female children ( p interaction = 0.05). We did not detect significant association of NO 2 , road proximity, and postnatal PM 2.5 with any outcomes., Conclusions: The findings suggest that higher prenatal PM 2.5 exposure, particularly in the second trimester, is associated with elevated early childhood blood pressure. This adverse association could be modified by pregnancy folate concentrations. https://doi.org/10.1289/EHP7486.

Background: 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., Objectives: Our objective was to estimate the association between long-term exposure to particulate matter (diameter <10 μm, PM 10 ; <2.5μm, PM 2.5 ), nitrogen dioxide (NO 2 ), and both incident and prevalent chronic bronchitis., Methods: We estimated annual average PM 2.5 , PM 10 , and NO 2 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., Results: 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 PM 10 [adjusted odds ratio (aOR) per interquartile range (IQR) difference (5.8   μg/m 3 )=1.07; 95% confidence interval (CI): 1.01, 1.13]. In never-smokers, PM 2.5 was associated with prevalent chronic bronchitis (aOR=1.18 per IQR difference; 95% CI: 1.04, 1.34), and NO 2 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., Conclusions: PM 10 exposure was related to chronic bronchitis prevalence. Among never-smokers, PM 2.5 and NO 2 exposure was associated with chronic bronchitis and component symptoms. Results may have policy ramifications for PM 10 regulation by providing evidence for respiratory health effects related to long-term PM 10 exposure. https://doi.org/10.1289/EHP2199.

Background: Some but not all past studies reported associations between components of air pollution and breast cancer, namely fine particulate matter ≤2.5 μm (PM2.5) and nitrogen dioxide (NO2). It is yet unclear whether risks differ according to estrogen receptor (ER) and progesterone receptor (PR) status., Methods: This analysis includes 47,591 women from the Sister Study cohort enrolled from August 2003 to July 2009, in whom 1,749 invasive breast cancer cases arose from enrollment to January 2013. Using Cox proportional hazards and polytomous logistic regression, we estimated breast cancer risk associated with residential exposure to NO2, PM2.5, and PM10., Results: Although breast cancer risk overall was not associated with PM2.5 [HR = 1.03; 95% confidence intervals (CI), 0.96-1.11], PM10 (HR = 0.99; 95% CI, 0.98-1.00), or NO2 (HR = 1.02; 95% CI, 0.97-1.07), the association with NO2 differed according to ER/PR subtype (P = 0.04). For an interquartile range (IQR) difference of 5.8 parts per billion (ppb) in NO2, the relative risk (RR) of ER(+)/PR(+) breast cancer was 1.10 (95% CI, 1.02-1.19), while there was no evidence of association with ER(-)/PR(-) (RR = 0.92; 95% CI, 0.77-1.09; Pinteraction = 0.04)., Conclusions: Within the Sister Study cohort, we found no significant associations between air pollution and breast cancer risk overall. But we observed an increased risk of ER(+)/PR(+) breast cancer associated with NO2., Impact: Though these results suggest there is no substantial increased risk for breast cancer overall in relation to air pollution, NO2, a marker of traffic-related air pollution, may differentially affect ER(+)/PR(+) breast cancer., (©2015 American Association for Cancer Research.)

Rationale: Limited prior data suggest an association between traffic-related air pollution and incident asthma in adults. No published studies assess the effect of long-term exposures to particulate matter less than 2.5 μm in diameter (PM2.5) on adult incident asthma., Objectives: To estimate the association between ambient air pollution exposures (PM2.5 and nitrogen dioxide, NO2) and development of asthma and incident respiratory symptoms., Methods: The Sister Study is a U.S. cohort study of risk factors for breast cancer and other health outcomes (n = 50,884) in sisters of women with breast cancer (enrollment, 2003-2009). Annual average (2006) ambient PM2.5 and NO2 concentrations were estimated at participants' addresses, using a national land-use/kriging model incorporating roadway information. Outcomes at follow-up (2008-2012) included incident self-reported wheeze, chronic cough, and doctor-diagnosed asthma in women without baseline symptoms., Measurements and Main Results: Adjusted analyses included 254 incident cases of asthma, 1,023 of wheeze, and 1,559 of chronic cough. For an interquartile range (IQR) difference (3.6 μg/m(3)) in estimated PM2.5 exposure, the adjusted odds ratio (aOR) was 1.20 (95% confidence interval [CI] = 0.99-1.46, P = 0.063) for incident asthma and 1.14 (95% CI = 1.04-1.26, P = 0.008) for incident wheeze. For NO2, there was evidence for an association with incident wheeze (aOR = 1.08, 95% CI = 1.00-1.17, P = 0.048 per IQR of 5.8 ppb). Neither pollutant was significantly associated with incident cough (PM2.5: aOR = 0.95, 95% CI = 0.88-1.03, P = 0.194; NO2: aOR = 1.00, 95% CI = 0.93-1.07, P = 0.939)., Conclusions: Results suggest that PM2.5 exposure increases the risk of developing asthma and that PM2.5 and NO2 increase the risk of developing wheeze, the cardinal symptom of asthma, in adult women.

Objectives: To examine whether long-term air pollution exposure is associated with central hemodynamic and brachial artery stiffness parameters. Methods: We assessed central hemodynamic parameters including central blood pressure, cardiac parameters, systemic vascular compliance and resistance, and brachial artery stiffness measures [including brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR)] using waveform analysis of the arterial pressure signals obtained from a standard cuff sphygmomanometer (DynaPulse2000A, San Diego, CA). The long-term exposures to particles with an aerodynamic diameter < 2.5 μm (PM2.5) and nitrogen dioxide (NO2) for the 3-year periods prior to enrollment were estimated at residential addresses using fine-scale intra-urban spatiotemporal models. Linear mixed models adjusted for potential confounders were used to examine associations between air pollution exposures and health outcomes. Results: The cross-sectional study included 2,387 Chicago residents (76% African Americans) enrolled in the ChicagO Multiethnic Prevention And Surveillance Study (COMPASS) during 2013–2018 with validated address information, PM2.5 or NO2, key covariates, and hemodynamics measurements. We observed long-term concentrations of PM2.5 and NO2 to be positively associated with central systolic, pulse pressure and BAR, and negatively associated with BAD, and BAC after adjusting for relevant covariates. A 1-µg/m3 increment in preceding 3-year exposures to PM2.5 was associated with 1.8 mmHg higher central systolic (95% CI: 0.98, 4.16), 1.0 mmHg higher central pulse pressure (95% CI: 0.42, 2.87), a 0.56%mmHg lower BAD (95% CI: -0.81, -0.30), and a 0.009 mL/mmHg lower BAC (95% CI: -0.01, -0.01). Conclusion: This population-based study provides evidence that long-term exposures to PM2.5 and NO2 is related to central BP and arterial stiffness parameters, especially among African Americans. [ABSTRACT FROM AUTHOR]

BACKGROUND: Population studies support the adverse associations of air pollution exposures with child behavioral functioning and cognitive performance, but few studies have used spatiotemporally resolved pollutant assessments. OBJECTIVES: We investigated these associations using more refined exposure assessments in 1,967 mother–child dyads from three U.S. pregnancy cohorts in six cities in the ECHO-PATHWAYS Consortium. METHODS: Pre- and postnatal nitrogen dioxide (NO2) and particulate matter (PM) ≤2.5 µm in aerodynamic diameter (PM2.5) exposures were derived from an advanced spatiotemporal model. Child behavior was reported as Total Problems raw score using the Child Behavior Checklist at age 4–6 y. Child cognition was assessed using cohort-specific cognitive performance scales and quantified as the Full-Scale Intelligence Quotient (IQ). We fitted multivariate linear regression models that were adjusted for sociodemographic, behavioral, and psychological factors to estimate associations per 2- unit increase in pollutant in each exposure window and examined modification by child sex. Identified critical windows were further verified by distributed lag models (DLMs). RESULTS: Mean NO2 and PM2.5 ranged from 8.4 to 9.0 ppb and 8.4 to 9.1 µg/m³, respectively, across pre- and postnatal windows. Average child Total Problems score and IQ were 22.7 [standard deviation (SD): 18.5] and 102.6 (SD: 15.3), respectively. Children with higher prenatal NO2 exposures were likely to have more behavioral problems [b: 1.24; 95% confidence interval (CI): 0.39, 2.08; per 2 ppb NO2], particularly NO2 in the first and second trimester. Each 2-µg/m³ increase in PM2.5 at age 2–4 y was associated with a 3.59 unit (95% CI: 0.35, 6.84) higher Total Problems score and a 2.63 point (95% CI: -5.08, -0.17) lower IQ. The associations between PM2.5 and Total Problems score were generally stronger in girls. Most predefined windows identified were not confirmed by DLMs. DISCUSSION: Our study extends earlier findings that have raised concerns about impaired behavioral functioning and cognitive performance in children exposed to NO2 and PM2.5 in utero and in early life. [ABSTRACT FROM AUTHOR]

BACKGROUND: Limited data suggest air pollution exposures may contribute to pediatric high blood pressure (HBP), a known predictor of adult cardiovascular diseases. METHODS: We investigated this association in the Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) study, a sociodemographically diverse pregnancy cohort in the southern United States with participants enrolled from 2006 to 2011. We included 822 mother–child dyads with available address histories and a valid child blood pressure measurement at 4–6 y. Systolic (SBP) and diastolic blood pressures (DBP) were converted to age-, sex-, and height-specific percentiles for normal-weight U.S. children. HBP was classified based on SBP or DBP =90th percentile. Nitrogen dioxide (NO2) and particulate matter =2.5 μm in aerodynamic diameter (PM2.5) estimates in both pre- and postnatal windows were obtained from annual national models and spatiotemporal models, respectively. We fit multivariate Linear and Poisson regressions and explored multiplicative joint effects with maternal nutrition, child sex, and maternal race using interaction terms. RESULTS: Mean PM2.5 and NO2 in the prenatal period were 10.8 [standard deviation (SD): 0.9] μm/m³ and 10.0 (SD: 2.4) ppb, respectively, and 9.9 (SD: 0.6) μmg/m³ and 8.8 (SD: 1.9) ppb from birth to the 4-y-old birthday. On average, SBP percentile increased by 14.6 (95% CI: 4.6, 24.6), and DBP percentile increased by 8.7 (95% CI: 1.4, 15.9) with each 2-μmg/m³ increase in second-trimester PM2.5. PM2.5 averaged over the prenatal period was only significantly associated with higher DBP percentiles [Β= 11.6 (95% CI: 2.9, 20.2)]. Positive associations of second-trimester PM2.5 with SBP and DBP percentiles were stronger in children with maternal folate concentrations in the lowest quartile (푝interaction = 0.05 and 0.07, respectively) and associations with DBP percentiles were stronger in female children (푝interaction = 0.05). We did not detect significant association of NO2, road proximity, and postnatal PM2.5 with any outcomes. CONCLUSIONS: The findings suggest that higher prenatal PM2.5 exposure, particularly in the second trimester, is associated with elevated early childhood blood pressure. This adverse association could be modified by pregnancy folate concentrations. [ABSTRACT FROM AUTHOR]

BACKGROUND: Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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 [ABSTRACT FROM AUTHOR]