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Rationale: Racial residential segregation has been associated with worse health outcomes, but the link with chronic obstructive pulmonary disease (COPD) morbidity has not been established.Objective...

Retinopathy is a microvascular complication of diabetes mellitus (DM); however, it is also increasingly recognized in persons without DM. The microvascular diseases may play a prominent role in coronary heart disease (CHD) development in individuals with DM. We performed the study to evaluate the relation between non-DM retinopathy and CHD and also the association between baseline retinopathy and incidence and progression of CHD in individuals with and without DM. We included 5709 subjects with and without DM from the Multi-Ethnic Study of Atherosclerosis, who had retinal photos and coronary artery calcium score (CACS) available. We studied the association between baseline retinopathy and incidence and progression of coronary artery calcification (CAC) in subjects with and without DM. In DM group, the presence of retinopathy was significantly associated with an increased rate of CAC (RR 1.3 (95% CI [1.02, 1.66]) after adjusting for age, sex, race, follow-up time, and CHD risk factors. In non-DM group, the presence of retinopathy was not significantly associated with increased risk of CAC, however, the interaction between presence of retinopathy and DM status was not statistically significant. Within the DM group with CAC present at baseline, the presence of retinopathy was significantly associated with greater CAC progression (113 Agatson units (AU) greater, (95% CI [51-174]). In the non-DM group with present CAC at baseline; the presence of retinopathy was associated with 24 (95% CI [-0.69, 48.76]) AU higher CAC progression. All findings were adjusted for CHD risk factors. In conclusion, after adjustment for major CHD risk factors, retinopathy was associated with progression of CAC in both DM and non-DM individuals. However, the association was stronger in those with DM.

BACKGROUND: Evidence links fine particulate matter (PM(2.5)) to Alzheimer’s Disease (AD), but no community-based prospective cohort studies in older adults have evaluated the association between long-term exposure to PM(2.5) and markers of AD neuropathology at autopsy. OBJECTIVE: Using a well-established autopsy cohort and new spatiotemporal predictions of air pollution, we evaluated associations of 10-year PM(2.5) exposure prior to death with Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC score). METHODS: We used autopsy specimens (N=832) from the Adult Changes in Thought (ACT) study, with enrollment ongoing since 1994. We assigned long-term exposure at residential address based on two-week average concentrations from a newly developed spatiotemporal model. To account for potential selection bias, we conducted inverse probability weighting (IPW). Adjusting for covariates with tiered models, we performed ordinal regression for Braak and CERAD and logistic regression for dichotomized ABC score. RESULTS: 10-year average (SD) PM(2.5) from death across the autopsy cohort was 8.2 (1.9) μg/m(3). Average (SD) age at death was 89 (7) years. Each 1 μg/m(3) increase in 10-year average PM(2.5) prior to death was associated with a suggestive increase in the odds of worse neuropathology as indicated by CERAD score (OR: 1.35 (0.90, 1.90)) but a suggestive decreased odds of neuropathology as defined by the ABC score (OR: 0.79 (0.49, 1.19)). There was no association with Braak stage (OR: 0.99 (0.64, 1.47)). CONCLUSIONS: We report inconclusive associations between PM(2.5) and AD neuropathology at autopsy among a cohort where 94% of individuals experienced 10-year exposures below the current EPA standard. Prior studies of AD risk factors and AD neuropathology are similarly inconclusive, suggesting alternative mechanistic pathways for disease or residual confounding.

Increased outdoor concentrations of fine particulate matter (PM2.5 ) and oxides of nitrogen (NO2 , NOx ) are associated with respiratory and cardiovascular morbidity in adults and children. However, people spend most of their time indoors and this is particularly true for individuals with chronic obstructive pulmonary disease (COPD). Both outdoor and indoor air pollution may accelerate lung function loss in individuals with COPD, but it is not feasible to measure indoor pollutant concentrations in all participants in large cohort studies. We aimed to understand indoor exposures in a cohort of adults (SPIROMICS Air, the SubPopulations and Intermediate Outcome Measures in COPD Study of Air pollution). We developed models for the entire cohort based on monitoring in a subset of homes, to predict mean 2-week-measured concentrations of PM2.5 , NO2 , NOx , and nicotine, using home and behavioral questionnaire responses available in the full cohort. Models incorporating socioeconomic, meteorological, behavioral, and residential information together explained about 60% of the variation in indoor concentration of each pollutant. Cross-validated R2 for best indoor prediction models ranged from 0.43 (NOx ) to 0.51 (NO2 ). Models based on questionnaire responses and estimated outdoor concentrations successfully explained most variation in indoor PM2.5 , NO2 , NOx , and nicotine concentrations.

ObjectiveTo examine whether long-chain omega-3 polyunsaturated fatty acid (LCn3PUFA) levels modify the potential neurotoxic effects of particle matter with diameters 2.5) exposure on normal-appearing brain volumes among dementia-free elderly women.MethodsA total of 1,315 women (age 65–80 years) free of dementia were enrolled in an observational study between 1996 and 1999 and underwent structural brain MRI in 2005 to 2006. According to prospectively collected and geocoded participant addresses, we used a spatiotemporal model to estimate the 3-year average PM2.5 exposure before the MRI. We examined the joint associations of baseline LCn3PUFAs in red blood cells (RBCs) and PM2.5 exposure with brain volumes in generalized linear models.ResultsAfter adjustment for potential confounders, participants with higher levels of RBC LCn3PUFA had significantly greater volumes of white matter and hippocampus. For each interquartile increment (2.02%) in omega-3 index, the average volume was 5.03 cm3 (p < 0.01) greater in the white matter and 0.08 cm3 (p = 0.03) greater in the hippocampus. The associations with RBC docosahexaenoic acid and eicosapentaenoic acid levels were similar. Higher LCn3PUFA attenuated the inverse associations between PM2.5 exposure and white matter volumes in the total brain and multimodal association areas (frontal, parietal, and temporal; all p for interaction ConclusionsFindings from this prospective cohort study among elderly women suggest that the benefits of LCn3PUFAs on brain aging may include the protection against potential adverse effects of air pollution on white matter volumes.

Author(s): Galiatsatos, Panagis; Woo, Han; Paulin, Laura M; Kind, Amy; Putcha, Nirupama; Gassett, Amanda J; Cooper, Christopher B; Dransfield, Mark T; Parekh, Trisha M; Oates, Gabriela R; Barr, R Graham; Comellas, Alejandro P; Han, Meilan K; Peters, Stephen P; Krishnan, Jerry A; Labaki, Wassim W; McCormack, Meredith C; Kaufman, Joel D; Hansel, Nadia N | Abstract: RationaleIndividual socioeconomic status has been shown to influence the outcomes of patients with chronic obstructive pulmonary disease (COPD). However, contextual factors may also play a role. The objective of this study is to evaluate the association between neighborhood socioeconomic disadvantage measured by the area deprivation index (ADI) and COPD-related outcomes.MethodsResidential addresses of SubPopulations and InteRmediate Outcome Measures in COPD Study (SPIROMICS) subjects with COPD (FEV1/FVC l0.70) at baseline were geocoded and linked to their respective ADI national ranking score at the census block group level. The associations between the ADI and COPD-related outcomes were evaluated by examining the contrast between participants living in the most-disadvantaged (top quintile) to the least-disadvantaged (bottom quintile) neighborhood. Regression models included adjustment for individual-level demographics, socioeconomic variables (personal income, education), exposures (smoking status, packs per year, occupational exposures), clinical characteristics (FEV1% predicted, body mass index) and neighborhood rural status.ResultsA total of 1800 participants were included in the analysis. Participants residing in the most-disadvantaged neighborhoods had 56% higher rate of COPD exacerbation (Pl0.001), 98% higher rate of severe COPD exacerbation (P=0.001), a 1.6 point higher CAT score (Pl0.001), 3.1 points higher SGRQ (Pl0.001), and 24.6 meters less six-minute walk distance (P=0.008) compared with participants who resided in the least disadvantaged neighborhoods.ConclusionParticipants with COPD who reside in more-disadvantaged neighborhoods had worse COPD outcomes compared to those residing in less-disadvantaged neighborhoods. Neighborhood effects were independent of individual-level socioeconomic factors, suggesting that contextual factors could be used to inform intervention strategies targeting high-risk persons with COPD.

Background: Atrial fibrillation (AF) is associated with substantial morbidity and mortality. Short-term exposures to air pollution have been associated with AF triggering; less is known regarding associations between long-term air pollution exposures and AF incidence. Objectives: Our objective was to assess the association between long-term exposures to air pollution and distance to road on incidence of AF in a cohort of U.S. women. Methods: We assessed the association of high resolution spatiotemporal model predictions of long-term exposures to particulate matter (PM10 and PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and distance to major roads with incidence of AF diagnosis, identified through Medicare linkage, among 83,117 women in the prospective Women’s Health Initiative cohort, followed from enrollment in Medicare through December 2012, incidence of AF, or death. Using time-varying Cox proportional hazards models adjusted for age, race/ethnicity, study component, body mass index, physical activity, menopausal hormone therapy, smoking, diet quality, alcohol consumption, educational attainment, and neighborhood socioeconomic status, we estimated the relative risk of incident AF in association with each pollutant. Results: A total of 16,348 incident AF cases were observed over 660,236 person-years of follow-up. Most exposure–response associations were nonlinear. NO2 was associated with risk of AF in multivariable adjusted models [Hazard Ratio (HR)=1.18; 95% confidence interval (CI): 1.13, 1.24, comparing the top to bottom quartile, p-for-trend=

BACKGROUND AND AIM: Age-related cognitive decline is a growing public health issue as increases in life expectancy and the aging of the population are expected to raise the prevalence of cognitive ...

BACKGROUND AND AIM: While long term exposure to fine particulate matter (PM₂.₅) has been linked to all-cause dementia, less is known about potential modification of these effects by greenspace expo...

Background: Air pollution may be associated with elevated dementia risk. Prior research has limitations that may affect reliability, and no studies have evaluated this question in a population-based cohort of men and women in the United States. Objectives: We evaluated the association between time-varying, 10-y average fine particulate matter (PM2.5) exposure and hazard of all-cause dementia. An additional goal was to understand how to adequately control for age and calendar-time-related confounding through choice of the time axis and covariate adjustment. Methods: Using the Adult Changes in Thought (ACT) population-based prospective cohort study in Seattle, we linked spatiotemporal model-based PM2.5 exposures to participant addresses from 1978 to 2018. Dementia diagnoses were made using high-quality, standardized, consensus-based protocols at biennial follow-ups. We conducted multivariable Cox proportional hazards regression to evaluate the association between time-varying, 10-y average PM2.5 exposure and time to event in a model with age as the time axis, stratified by apolipoprotein E (APOE) genotype, and adjusted for sex, education, race, neighborhood median household income, and calendar time. Alternative models used calendar time as the time axis. Results: We report 1,136 cases of incident dementia among 4,166 individuals with nonmissing APOE status. Mean [mean ± standard deviation (SD)] 10-y average PM2.5 was 10.1 (±2.9) μg/m3. Each 1-μg/m3 increase in the moving average of 10-y PM2.5 was associated with a 16% greater hazard of all-cause dementia [1.16 (95% confidence interval: 1.03, 1.31)]. Results using calendar time as the time axis were similar. Discussion: In this prospective cohort study with extensive exposure data and consensus-based outcome ascertainment, elevated long-term exposure to PM2.5 was associated with increased hazard of all-cause dementia. We found that optimal control of age and time confounding could be achieved through use of either age or calendar time as the time axis in our study. Our results strengthen evidence on the neurodegenerative effects of PM2.5. https://doi.org/10.1289/EHP9018

Few studies have examined associations between neighborhood built environments (BE) and longitudinally measured cognition. We examined whether four BE characteristics were associated with six-year change in global cognition and processing speed. We obtained data on 1816 participants without dementia from the Multi-Ethnic Study of Atherosclerosis. BE measures included social destination density, walking destination density, proportion of land dedicated to retail, and network ratio (street connectivity). Global cognition was measured with the Cognitive Abilities Screening Instrument (CASI) and processing speed with the Digit Symbol Coding test (DSC). Multivariable random intercept logistic models tested associations between neighborhood BE at 2010–2012 and maintained/improved cognition (versus decline) from 2010–2018, and mediation by minutes of physical activity (PA)/week. The sample was an average of 67 years old (standard deviation = 8.2) (first cognitive measurement) and racially/ethnically diverse (29% African American, 11% Chinese, 17% Hispanic, 44% White). Compared to individuals with no walking destinations in the 1-mile surrounding their residence, those with 716 walking destinations (maximum observed) were 1.24 times more likely to have maintain/improved DSC score (Odds ratio: 1.24, 95% confidence interval: 1.03–1.45). No other associations were observed between BE and cognition, and PA minutes/week did not mediate the association between walking destination density and DSC change. This study provides limited evidence for an association between greater neighborhood walking destinations and maintained/improved processing speed in older age and no evidence for associations between the other BE characteristics and cognition. Future studies with finer grained BE and cognitive measures and longer-term follow up may be required.

Background: Air pollution contributes to cardiovascular morbidity, including heart failure. Exposure to pollutants has been associated with hypertension and inflammation, which contribute to cardiac remodeling. Few studies have investigated long-term air pollution concentrations and measures of cardiac structure, and no large longitudinal analyses have investigated this association. Hypothesis: Long-term air pollution concentrations are associated with magnetic resonance imaging-derived measures of left ventricular structure and function. Methods: In the Multi-Ethnic Study of Atherosclerosis (MESA), we investigated cross-sectional and longitudinal associations between modeled fine particulate matter (PM2.5), oxides of nitrogen (NOX) and ozone (O3) concentrations and left ventricular mass index (LVMI), mass to volume ratio, ejection fraction, and circumferential strain by cardiac magnetic resonance imaging (CMR) at two time points roughly 10 years apart. Multivariable linear regression was used to estimate the association between pollutants and both cross-sectional and longitudinal CMR measures. Results: At MESA Exam 1 (2000-2002), 4,825 participants in our cross-sectional analysis sample had a mean age of 61 years (standard deviation: 10), 53% were women, 40% were white, 13% were Chinese-American, 25% were African-American, and 21% were Hispanic. At Exam 1, Higher concentrations of PM2.5 and NOX in the year prior to Exam 1 were associated with higher LVMI at Exam 1 (1.6% per 5ug/m3 higher PM2.5, 95% CI: 0.3, 2.9; 1.8% per 40 parts per billion [ppb] NOX, 95% CI: 0.3, 3.3) and higher O3 was associated with lower LVMI (-3.5% per 10ppb, 95% CI: -6.0, -1.0). In longitudinal analyses, higher NOX was associated with a worsening of LV circumferential strain (-0.87% per 40ppb, 95% CI: -1.69, -0.05). Conclusions: Our study offers mixed evidence of a cross-sectional association between higher PM2.5 and NOx concentrations and greater LVMI. We also found associations between greater O3 concentration and lower cross-sectional LVMI, though this association may be confounded by other pollutants. These findings suggest a role for NOX, PM2.5, and O3 in cardiac remodeling. Additional work is needed to clarify that role and better understand the biological underpinnings of these associations.

Background Millions of Americans are living in food deserts in the United States, however the role of the local food environment on COPD has not been studied. The aim of this study is to determine the association between food deserts and COPD-related outcomes. Method In this cross-sectional analysis we linked data collected from SPIROMICS (SubPopulations and InteRmediate Outcome Measures in COPD Study) between 2010 and 2015 and food desert data, defined as an underserved area that lacks access to affordable healthy foods, from the Food Access Research Atlas. COPD outcomes include percentage of predicted forced expiratory volume in one second (FEV1%), St. George’s Respiratory Questionnaire (SGRQ), COPD Assessment Test (CAT), 6-min walk distance test (6MWD), exacerbations, and air trapping. We used generalized linear mixed models to evaluate the association between living in food deserts and respiratory outcomes, adjusting for age, gender, race, education, income, marital status, BMI, smoking status, pack years, and urban status Results Among 2713 participants, 22% lived in food deserts. Participants living in food deserts were less likely to be white and more likely to have a lower income than those who did not live in food deserts. In the adjusted model controlling for demographics and individual income, living in food deserts was associated lower FEV1% (β = – 2.51, P = 0.046), higher air trapping (β = 2.47, P = 0.008), worse SGRQ (β = 3.48, P = 0.001) and CAT (β = 1.20, P = 0.003) scores, and 56% greater odds of severe exacerbations (P = 0.004). Results were consistent when looking at food access alone, regardless of whether participants lived in low income areas. Conclusions Findings suggest an independent association between food desert and food access alone with COPD outcomes. Health program planning may benefit from addressing disparities in access to food.

Rationale: Black adults have worse health outcomes compared with white adults in certain chronic diseases, including chronic obstructive pulmonary disease (COPD).Objectives: To determine to what degree disadvantage by individual and neighborhood socioeconomic status (SES) may contribute to racial disparities in COPD outcomes.Methods: Individual and neighborhood-scale sociodemographic characteristics were determined in 2,649 current or former adult smokers with and without COPD at recruitment into SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). We assessed whether racial differences in symptom, functional, and imaging outcomes (St. George's Respiratory Questionnaire, COPD Assessment Test score, modified Medical Research Council dyspnea scale, 6-minute-walk test distance, and computed tomography [CT] scan metrics) and severe exacerbation risk were explained by individual or neighborhood SES. Using generalized linear mixed model regression, we compared respiratory outcomes by race, adjusting for confounders and individual-level and neighborhood-level descriptors of SES both separately and sequentially.Measurements and Main Results: After adjusting for COPD risk factors, Black participants had significantly worse respiratory symptoms and quality of life (modified Medical Research Council scale, COPD Assessment Test, and St. George's Respiratory Questionnaire), higher risk of severe exacerbations and higher percentage of emphysema, thicker airways (internal perimeter of 10 mm), and more air trapping on CT metrics compared with white participants. In addition, the association between Black race and respiratory outcomes was attenuated but remained statistically significant after adjusting for individual-level SES, which explained up to 12-35% of racial disparities. Further adjustment showed that neighborhood-level SES explained another 26-54% of the racial disparities in respiratory outcomes. Even after accounting for both individual and neighborhood SES factors, Black individuals continued to have increased severe exacerbation risk and persistently worse CT outcomes (emphysema, air trapping, and airway wall thickness).Conclusions: Disadvantages by individual- and neighborhood-level SES each partly explain disparities in respiratory outcomes between Black individuals and white individuals. Strategies to narrow the gap in SES disadvantages may help to reduce race-related health disparities in COPD; however, further work is needed to identify additional risk factors contributing to persistent disparities.

BackgroundAir pollution may affect the risk of respiratory infection, though research has focused on uncommon infections or infections in children. Whether ambient air pollutants increase the risk of common acute respiratory infections among adults is uncertain, yet this may help understand whether pollutants influence spread of pandemic respiratory infections like COVID-19.ObjectiveTo estimate the association between ambient air pollutant exposures and respiratory infections in adults.MethodsDuring five study examinations over 12 years, 6536 participants in the multiethnic study of atherosclerosis (MESA) reported upper respiratory tract infections, bronchitis, pneumonia or febrile illness in the preceding 2 weeks. Using a validated spatiotemporal model, we estimated residential concentrations of ambient PM2.5, NOx and NO2 for the 2–6 weeks (short-term) and year (long-term) prior to each examination.ResultsIn this population aged 44–84 years at baseline, 10%–32% of participants reported a recent respiratory infection, depending on month of examination and study region. PM2.5, NOx and NO2 concentrations over the prior 2–6 weeks were associated with increased reporting of recent respiratory infection, with risk ratios (95% CIs) of 1.04 (1.00 to 1.09), 1.15 (1.10 to 1.20) and 1.21 (1.10 to 1.33), respectively, per increase from 25th to 75th percentile in residential pollutant concentration.ConclusionHigher short-term exposure to PM2.5 and traffic-related pollutants are associated with increased risk of symptomatic acute respiratory infections among adults. These findings may provide an insight into the epidemiology of COVID-19.

Supplemental Digital Content is available in the text., Background: Emerging evidence from animal and human studies indicates that exposure to traffic-related air pollution may adversely affect fertility. Methods: Among 7,342 female pregnancy planners from the United States and 1,448 from Canada, we examined the association between residential proximity to major roads and fecundability, the per-cycle probability of conception. From 2013 to 2019, women 21–45 years old who were trying to conceive without fertility treatment completed an online baseline questionnaire and follow-up questionnaires every 8 weeks for up to 12 months or until pregnancy. We geocoded residential addresses reported at baseline and during follow-up, and calculated distance to nearest major roads and length of major roads within buffers of 50, 100, 300, and 400 meters around the residence as proxies for traffic-related air pollution. We used proportional probabilities regression models to estimate fecundability ratios (FRs) and 95% confidence intervals (CIs), adjusting for individual- and neighborhood-level characteristics. Results: In the United States, the FR comparing women who lived

Introduction: Air pollution is associated with reduced cognitive performance and accelerated cognitive decline in older adults. Less is known regarding air pollution’s contribution to all-cause dem...

Introduction Exposure to noise might influence risk of Alzheimer's disease (AD) dementia. Methods Participants of the Chicago Health and Aging Project (≥65 years) underwent triennial cognitive assessments. For the 5 years preceding each assessment, we estimated 5227 participants' residential level of noise from the community using a spatial prediction model, and estimated associations of noise level with prevalent mild cognitive impairment (MCI) and AD, cognitive performance, and rate of cognitive decline. Results Among these participants, an increment of 10 A-weighted decibels (dBA) in noise corresponded to 36% and 29% higher odds of prevalent MCI (odds ratio [OR] = 1.36; 95% confidence interval [CI], 1.15 to 1.62) and AD (OR = 1.29, 95% CI, 1.08 to 1.55). Noise level was associated with worse global cognitive performance, principally in perceptual speed (-0.09 standard deviation per 10 dBA, 95% CI: -0.16 to -0.03), but not consistently associated with cognitive decline. Discussion These results join emerging evidence suggesting that noise may influence late-life cognition and risk of dementia.

Background: Exposure to household air pollution (HAP) from cooking with biomass fuel affects billions of people. We hypothesized that HAP from woodsmoke, compared to other household fuels, was associated with adverse cardiovascular outcomes, of which there have been few studies. Methods: A cross-sectional study was completed in 299 females aged 40–70 years in Kaski District, Nepal, during 2017–18. All participants underwent a standard 12-lead ECG, ankle and brachial systolic blood pressure measurement, and 2D color and Doppler echocardiography. Current stove type was confirmed by inspection. Blood pressure, height, and weight were measured using a standardized protocol. Hypertension was defined as ≥140/90 mmHg or prior diagnosis. Hemoglobin A1c (HbA1c) was obtained, with diabetes mellitus defined as a prior diagnosis or HbA1C ≥ 6.5%. We used adjusted linear and logistic multivariable regressions to examine the relationship of stove type with cardiac structure and function. Results: The majority of women primarily used liquified petroleum gas (LPG) stoves (65%), while 12% used biogas, and 23% used wood-burning cook-stoves. Prevalence of major cardiovascular risk factors was 35% with hypertension, 19% with diabetes mellitus, and 15% current smokers. After adjustment, compared to LPG, wood stove use was associated with increased indexed left atrial volume (β = 3.15, 95% CI 1.22 to 5.09) and increased indexed left ventricular end diastolic volume (β = 7.97, 95% CI 3.11 to 12.83). There was no association between stove type and systemic hypertension, left ventricular mass, systolic dysfunction, diastolic dysfunction, pulmonary hypertension, abnormal ankle-brachial index, or clinically significant ECG abnormalities. Conclusion: Biomass fuel use was associated with increased indexed left atrial volume and increased indexed left ventricular diastolic volume in Nepali women, suggesting subclinical adverse cardiac remodeling from HAP in this cross-sectional study. We did not find evidence of an association with hypertension or typical cardiac sequelae of hypertension. Future studies to confirm these results are needed.

Background: There is mounting evidence that long-term exposure to air pollution is related to accelerated cognitive decline in aging populations. Factors that influence individual susceptibility remain largely unknown, but may involve the apolipoprotein E genotype E4 (APOE-ε4) allele. Objectives: We assessed whether the association between long-term exposure to ambient air pollution and cognitive decline differed by APOE-ε4 status and cognitive risk factors. Methods: The Washington Heights Inwood Community Aging Project (WHICAP) is a prospective study of aging and dementia. Neuropsychological testing and medical examinations occur every 18–24 months. We used mixed-effects models to evaluate whether the association between markers of ambient air pollution (nitrogen dioxide [NO2]), fine [PM2.5], and coarse [PM10] particulate matter) and the rate of decline in global and domain-specific cognition differed across strata defined by APOE-ε4 genotypes and cognitive risk factors, adjusting for sociodemographic factors and temporal trends. Results: Among 4821 participants with an average of 6 years follow-up, higher concentrations of ambient air pollution were associated with more rapid cognitive decline. This association was more pronounced among APOE-ε4 carriers (p

Background: Air pollution may be associated with elevated dementia risk, but prior research has limitations that may affect reliability, and no prior studies have evaluated this question in a community-based cohort of men and women in the United States. Methods: We evaluated the association of long-term fine particulate matter (PM2.5) exposure with all-cause dementia during the period 1978-2018 in the Adult Changes in Thought (ACT) study based in Seattle, Washington, USA. PM2.5 exposures linked to participant addresses were obtained from a spatiotemporal model spanning 40 years. Research quality dementia diagnoses were made using standardized diagnosis protocols at biennial follow-ups. We conducted multivariate Cox proportional hazards regression to evaluate the association between time-varying, 10-year average PM2.5 exposure and time to event in a model based on age, stratified by apolipoprotein E (APOE) genotype, and adjusted for sex, education, race, neighborhood median household income, and calendar time. Findings: Mean (standard deviation) 10-year average PM2.5 was 10.0 (2.9) µg/m3, which is below the current national air quality standard. Each 1 µg/m3 increase in the moving average of 10-year PM2.5 was associated with a 16% greater hazard of all-cause dementia (1.16 (1.03, 1.31). Interpretation: In this community-based prospective cohort study with uniquely extensive exposure data and research quality outcome ascertainment, elevated long-term exposure to PM2.5 was associated with an increased hazard of all-cause dementia. These results add to growing evidence on the neurodegenerative effects of air pollution and suggest that reducing exposures across the population could contribute to reducing the burden of dementia. Funding: NIEHS F31ES030972-02, NIEHS T32ES015459, NIA T32AG052354, NIEHS and NIA R01ES026187, U01 AG006781, NIEHS ES026187, NIA AG05136, R01 AG056711 and U01 NS091272, the University of Washington Retirement Association Aging Fellowship, and the Seattle Chapter of the Achievement Rewards for College Scientists (ARCS) Foundation. Declaration of Interests: The authors have no conflicts of interest to disclose. Ethics Approval Statement: ACT participants signed forms indicating their informed consent to enroll in the study. Study procedures were approved by the University of Washington and Kaiser Permanente Institutional Review Boards.

Importance Few studies have investigated the association of long-term ambient ozone exposures with respiratory morbidity among individuals with a heavy smoking history. Objective To investigate the association of historical ozone exposure with risk of chronic obstructive pulmonary disease (COPD), computed tomography (CT) scan measures of respiratory disease, patient-reported outcomes, disease severity, and exacerbations in smokers with or at risk for COPD. Design, Setting, and Participants This multicenter cross-sectional study, conducted from November 1, 2010, to July 31, 2018, obtained data from the Air Pollution Study, an ancillary study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study). Data analyzed were from participants enrolled at 7 (New York City, New York; Baltimore, Maryland; Los Angeles, California; Ann Arbor, Michigan; San Francisco, California; Salt Lake City, Utah; and Winston-Salem, North Carolina) of the 12 SPIROMICS clinical sites. Included participants had historical ozone exposure data (n = 1874), were either current or former smokers (≥20 pack-years), were with or without COPD, and were aged 40 to 80 years at baseline. Healthy persons with a smoking history of 1 or more pack-years were excluded from the present analysis. Exposures The 10-year mean historical ambient ozone concentration at participants’ residences estimated by cohort-specific spatiotemporal modeling. Main Outcomes and Measures Spirometry-confirmed COPD, chronic bronchitis diagnosis, CT scan measures (emphysema, air trapping, and airway wall thickness), 6-minute walk test, modified Medical Research Council (mMRC) Dyspnea Scale, COPD Assessment Test (CAT), St. George’s Respiratory Questionnaire (SGRQ), postbronchodilator forced expiratory volume in the first second of expiration (FEV1) % predicted, and self-report of exacerbations in the 12 months before SPIROMICS enrollment, adjusted for demographics, smoking, and job exposure. Results A total of 1874 SPIROMICS participants were analyzed (mean [SD] age, 64.5 [8.8] years; 1479 [78.9%] white; and 1013 [54.1%] male). In adjusted analysis, a 5-ppb (parts per billion) increase in ozone concentration was associated with a greater percentage of emphysema (β = 0.94; 95% CI, 0.25-1.64;P = .007) and percentage of air trapping (β = 1.60; 95% CI, 0.16-3.04;P = .03); worse scores for the mMRC Dyspnea Scale (β = 0.10; 95% CI, 0.03-0.17;P = .008), CAT (β = 0.65; 95% CI, 0.05-1.26;P = .04), and SGRQ (β = 1.47; 95% CI, 0.01-2.93;P = .048); lower FEV1% predicted value (β = −2.50; 95% CI, −4.42 to −0.59;P = .01); and higher odds of any exacerbation (odds ratio [OR], 1.37; 95% CI, 1.12-1.66;P = .002) and severe exacerbation (OR, 1.37; 95% CI, 1.07-1.76;P = .01). No association was found between historical ozone exposure and chronic bronchitis, COPD, airway wall thickness, or 6-minute walk test result. Conclusions and Relevance This study found that long-term historical ozone exposure was associated with reduced lung function, greater emphysema and air trapping on CT scan, worse patient-reported outcomes, and increased respiratory exacerbations for individuals with a history of heavy smoking. The association between ozone exposure and adverse respiratory outcomes suggests the need for continued reevaluation of ambient pollution standards that are designed to protect the most vulnerable members of the US population.

Rationale: Rural residence is associated with poor outcomes in several chronic diseases. The association between rural residence and chronic obstructive pulmonary disease (COPD) exacerbations remains unclear.Objectives: In this work, we sought to determine the independent association between rural residence and COPD-related outcomes, including COPD exacerbations, airflow obstruction, and symptom burden.Methods: A total of 1,684 SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study) participants with forced expiratory volume in 1 second/forced vital capacity < 0.70 had geocoding-defined rural-urban residence status determined (N = 204 rural and N = 1,480 urban). Univariate and multivariate logistic and negative binomial regressions were performed to assess the independent association between rurality and COPD outcomes, including exacerbations, lung function, and symptom burden. The primary exposure of interest was rural residence, determined by geocoding of the home address to the block level at the time of study enrollment. Additional covariates of interest included demographic and clinical characteristics, occupation, and occupational exposures. The primary outcome measures were exacerbations determined over a 1-year course after enrollment by quarterly telephone calls and at an annual research clinic visit. The odds ratio (OR) and incidence rate ratio (IRR) of exacerbations that required treatment with medications, including steroids or antibiotics (total exacerbations), and exacerbations leading to hospitalization (severe exacerbations) were determined after adjusting for relevant covariates.Results: Rural residence was independently associated with a 70% increase in the odds of total exacerbations (OR, 1.70 [95% confidence interval (CI), 1.13-2.56]; P = 0.012) and a 46% higher incidence rate of total exacerbations (IRR 1.46 [95% CI, 1.02-2.10]; P = 0.039). There was no association between rural residence and severe exacerbations. Agricultural occupation was independently associated with increased odds and incidence of total and severe exacerbations. Inclusion of agricultural occupation in the analysis attenuated the association between rural residence and the odds and incidence rate of total exacerbations (OR, 1.52 [95% CI, 1.00-2.32]; P = 0.05 and IRR 1.39 [95% CI, 0.97-1.99]; P = 0.07). There was no difference in symptoms or airflow obstruction between rural and urban participants.Conclusions: Rural residence is independently associated with increased odds and incidence of total, but not severe, COPD exacerbations. These associations are not fully explained by agriculture-related exposures, highlighting the need for future research into potential mechanisms of the increased risk of COPD exacerbations in the rural population.

Background: Particulate matter (PM) is a complex mixture. Geographic variations in PM may explain the lack of consistent associations with breast cancer. Objective: We aimed to evaluate the relationship between air pollution, PM components, and breast cancer risk in a United States-wide prospective cohort. Methods: We estimated annual average ambient residential levels of particulate matter

Background: Ambient air pollution is classified as a human carcinogen by the International Agency for Research on Cancer (IARC). However, epidemiologic studies supporting this classification have focused on lung cancer mortality rather than incidence, and spatial and temporal resolutions of exposure estimates have varied considerably across studies. Methods: We evaluated the association of outdoor air pollution and lung cancer incidence among never-smoking participants of the Women’s Health Initiative (WHI) study, a large, US-based cohort of postmenopausal women (N = 65,419; 265 cases). We used geospatial models to estimate exposures to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) based on residential addresses at baseline and throughout follow-up. We also characterized exposures to traffic-related air pollution by proximity to major roadways. We estimated hazard ratios (HRs) for the risk of lung cancer in association with these exposure metrics using Cox proportional hazards regression models. Results: No compelling associations of PM2.5 and NO2 exposures with lung cancer risk were observed. An increased risk of lung cancer was observed when comparing those individuals with residences

The receptor for advanced glycation end products (RAGE) is underexpressed in idiopathic pulmonary fibrosis (IPF) lung, but the role of RAGE in human lung fibrosis remains uncertain.To examine (1) the association between IPF risk and variation at rs2070600, a functional missense variant in AGER (the gene that codes for RAGE), and (2) the associations between plasma-soluble RAGE (sRAGE) levels with disease severity and time to death or lung transplant in IPF.We genotyped the rs2070600 single-nucleotide polymorphism in 108 adults with IPF and 324 race-/ethnicity-matched control subjects. We measured plasma sRAGE by ELISA in 103 adults with IPF. We used generalized linear and additive models as well as Cox models to control for potential confounders. We repeated our analyses in 168 (genetic analyses) and 177 (sRAGE analyses) adults with other forms of interstitial lung disease (ILD).There was no association between rs2070600 variation among adults with IPF (P = 0.31). Plasma sRAGE levels were lower among adults with IPF and other forms of ILD than in control subjects (P 0.001). The rs2070600 allele A was associated with a 49% lower sRAGE level (95% confidence interval [CI], 11 to 71%; P = 0.02) among adults with IPF. In adjusted analyses, lower sRAGE levels were associated with greater disease severity (14% sRAGE decrement per 10% FVC decrement; 95% CI, 5 to 22%) and a higher rate of death or lung transplant at 1 year (adjusted hazard ratio, 1.9 per logarithmic unit of sRAGE decrement; 95% CI, 1.2-3.3) in IPF. Similar findings were observed in a heterogeneous group of adults with other forms of ILD.Lower plasma sRAGE levels may be a biological measure of disease severity in IPF. Variation at the rs2070600 single-nucleotide polymorphism was not associated with IPF risk.

Key Points Question Are long-term exposure to ambient air pollution and proximity to traffic associated with subclinical atherosclerosis? Findings In this population-based cross-sectional study of 8867 Chinese participants, long-term exposure to ambient nitrogen dioxide and fine particulate matter with aerodynamic diameter less than 2.5 μm was independently associated with a higher coronary artery calcium score, a key atherosclerotic marker. Associations with ozone and proximity to traffic were less consistent. Meaning Long-term exposure to ambient air pollution may be an important risk factor for coronary atherosclerosis., This population-based cross-sectional study of 8867 Chinese participants examines the association of long-term exposure to air pollution and proximity to traffic with the coronary artery calcium score, a marker for coronary atherosclerosis., Importance Epidemiologic evidence of the mechanisms of the association between long-term exposure to air pollution and coronary heart disease (CHD) is limited and relies heavily on studies performed in Europe and the United States, where air pollution levels are relatively low. In particular, the association between air pollution and CHD in patients with underlying risks for CHD is understudied. Objective To determine whether air pollution and proximity to traffic are associated with the coronary artery calcium (CAC) score, a key atherosclerotic marker. Design, Setting, and Participants In this prospective, population-based cross-sectional study in a large-scale setting in China, 8867 consecutive patients aged 25 to 92 years with suspected CHD were recruited between November 17, 2015, and September 13, 2017. Participants were excluded if they had previous myocardial infarction, stenting, or coronary artery bypass grafting or incomplete risk factors and exposure data. Each participant underwent assessment of CAC and CHD risk factors at baseline. Data were analyzed from December 2017 to November 2018. Exposures Annual means of fine particulate matter with aerodynamic diameter less than 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) were estimated at the participants’ residences using a validated geostatistical prediction model. Exposure to a nearby roadway was also estimated. Main Outcomes and Measures Computed tomography measurement of CAC score. Results The mean (SD) age of the 8867 participants was 56.9 (10.4) years; 4378 (53.6%) were men. Annual mean (SD) PM2.5, NO2, and O3 measurements were 70.1 (20.0), 41.4 (14.7), and 93.9 (10.5) μg/m3, respectively. The mean (SD) CAC score was 91.4 (322.2) Agatston units. Exposure to PM2.5 and NO2, adjusting for CHD risk factors and multiple pollutants, were independently associated with increases in CAC scores of 27.2% (95% CI, 10.8% to 46.1%) per 30 μg/m3 PM2.5 and 24.5% (95% CI, 3.6% to 49.7%) per 20 μg/m3 NO2. For PM2.5, odds of both detectable CAC (Agatston score >0; odds ratio, 1.28; 95% CI, 1.13 to 1.45) and severe CAC (Agatston score >400; odds ratio, 1.59; 95% CI, 1.20 to 2.12) were increased. Associations of CAC with PM2.5 and NO2 were greater among male participants (PM2.5: 42.2%; 95% CI, 24.3% to 62.7%; NO2: 45.7%; 95% CI, 25.3% to 69.5%) and elderly participants (PM2.5: 50.1%; 95% CI, 28.8% to 75.0%; NO2: 55.5%; 95% CI, 31.8% to 83.6%) and those with diabetes (PM2.5: 62.2%; 95% CI, 30.9% to 101.0%; NO2: 31.2%; 95% CI, 13.9% to 51.0%). Independent association with CAC score was 9.0% (95% CI, −1.4% to 20.4%) for O3 per 15 μg/m3 and 2.4% (95% CI, −0.6% to 5.4%) for distance near roadway per 50% decrease. Conclusions and Relevance In this large Chinese study, long-term exposures to PM2.5 and NO2 were independently associated with severity of CAC. This finding may provide support for the pathophysiological role of coronary atherosclerosis through which air pollution exposure may be associated with CHD.

BACKGROUND: Limited research suggests ambient air pollution impairs fecundity but groups most susceptible have not been identified. We studied whether long-term ambient air pollution exposure prior to an in vitro fertilization (IVF) cycle was associated with successful livebirth, and whether associations were modified by underlying infertility diagnosis. METHODS: Data on women initiating their 1(st) autologous IVF cycle in 2012-13 were obtained from four U.S. clinics. Outcomes included pregnancy, pregnancy loss, and livebirth. Annual average exposure to fine particulate matter (PM(2.5)), PM(10), and nitrogen dioxide (NO(2)) prior to IVF start were estimated at residential address using a validated national spatial model incorporating land-use regression and universal kriging. We also assessed residential distance to major roadway. We calculated risk ratios (RR) using modified Poisson regression and evaluated effect modification (EM) by infertility diagnosis on additive and multiplicative scales. RESULTS: Among 7,463 eligible participants, 36% had a livebirth. There was a non-significant indication of an association between PM(2.5) or NO(2) and decreased livebirth and increased pregnancy loss. Near roadway residence was associated with decreased livebirth (RR: 0.96, 95% CI: 0.82, 0.99. There was evidence for EM between high exposure to air pollutants and a diagnosis of diminished ovarian reserve (DOR) or male infertility and decreased livebirth. CONCLUSIONS: Despite suggestive but uncertain findings for the overall effect of air pollution on fecundity, we found a suggestive indication that there may be synergistic effects of air pollution and DOR or male infertility diagnosis on livebirth. This suggests two possible targets for future research and intervention.

Novel technology permits quantification of common carotid artery (CCA) displacement, which is traditionally ignored. We evaluated associations with CCA displacement and cardiovascular disease (CVD) risk and events in a large, multi-ethnic cohort. Right CCA longitudinal displacement (LD), transverse displacement (TD), and grayscale median (GSM) were evaluated using ultrasound speckle-tracking and texture analysis software in 2050 participants. Regression analyses were used to define relationships between CCA LD, TD, GSM, and CVD risk factors. Cox proportional hazards models were used to assess relationships between LD, TD, and incident CVD events. Participants were mean (SD) 64 (10) years old. There were 791 cases with a CVD event over a 12-year median follow-up. The mean LD was 0.29 (0.20) mm. In multivariable models including age, sex, race/ethnicity, heart rate, and CVD risk factors, LD was associated positively with active smoking (β = 0.08, p < 0.001) and inversely with black (β = −0.08, p < 0.001), Chinese (β = −0.05, p < 0.001), and Hispanic (β = −0.04, p < 0.05) race/ethnicities relative to white individuals, heart rate (β = −0.03/10 beats/min, p < 0.001), and diastolic blood pressure (β = −0.01/5 mmHg, p < 0.05). In fully adjusted models, LD and TD were associated with GSM ( p < 0.01), but neither predicted incident CVD events (LD: hazard ratio (HR) 0.77 [0.48 to 1.24], p = 0.3; TD: HR 1.12 [0.8 to 1.57], p = 0.5). CCA LD and TD are associated with race/ethnicity and CVD risk factors but not incident CVD events. LD and TD are not measures of arterial stiffness but their association with GSM suggests that lower LD and TD may be related to structural changes within the carotid arterial wall.

Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene–smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene–smoking interaction analysis and 38 were newly identified (P

Objective— Lp(a) [lipoprotein(a)] is a well-described risk factor for atherosclerosis, but Lp(a)-associated risk may vary by race/ethnicity. We aimed to determine whether race/ethnicity modifies Lp(a)-related risk of carotid atherosclerotic plaque outcomes among black, white, Chinese, and Hispanic individuals. Approach and Results— Carotid plaque presence and score were assessed by ultrasonography at baseline (n=5155) and following a median 9.4 year period (n=3380) in MESA (Multi-Ethnic Study of Atherosclerosis) participants. Lp(a) concentrations were measured by immunoassay and examined as a continuous and categorical variable using clinically-based cutoffs, 30 and 50 mg/dL. Lp(a) was related to greater risk of prevalent carotid plaque at baseline in whites alone (all P P P =0.04). In prospective analyses, whites with Lp(a) ≥50 mg/dL were found to have greater risk of plaque progression (relative risk, 1.12; P =0.03) and higher plaque scores (all P Conclusions— Race was found to be a modifying variable in Lp(a)-related risk of carotid plaque, and Lp(a) levels may have greater influence on plaque burden in whites than in black individuals. Borderline results in Hispanics suggest that elevated Lp(a) may increase the risk of carotid plaque, but follow-up studies are needed.

Rationale: Air pollution may influence sleep through airway inflammation or autonomic nervous system pathway alterations. Epidemiological studies may provide evidence of relationships between chronic air pollution exposure and sleep apnea. Objectives: To determine whether ambient-derived pollution exposure is associated with obstructive sleep apnea and objective sleep disruption. Methods: We analyzed data from a sample of participants in MESA (Multi-Ethnic Study of Atherosclerosis) who participated in both the Sleep and Air studies. Mean annual and 5-year exposure levels to nitrogen dioxide (NO(2)) and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM(2.5)) were estimated at participants’ homes using spatiotemporal models based on cohort-specific monitoring. Participants completed in-home full polysomnography and 7 days of wrist actigraphy. We used multivariate models, adjusted for demographics, comorbidities, socioeconomic factors, and site, to assess whether air pollution was associated with sleep apnea (apnea–hypopnea index ≥ 15) and actigraphy-measured sleep efficiency. Results: The participants (n = 1,974) were an average age of 68 (±9) years, 46% male, 36% white, 24% Hispanic, 28% black, and 12% Asian; 48% had sleep apnea and 25% had a sleep efficiency of ≤88%. A 10 ppb annual increase in NO(2) exposure was associated with 39% greater adjusted odds of sleep apnea (95% confidence interval [CI], 1.03–1.87). A 5 μg/m(3) greater annual PM(2.5) exposure was also associated with 60% greater odds of sleep apnea (95% CI, 0.98–2.62). Sleep efficiency was not associated with air pollution levels in fully adjusted models. Conclusions: Individuals with higher annual NO(2) and PM(2.5) exposure levels had a greater odds of sleep apnea. These data suggest that in addition to individual risk factors, environmental factors also contribute to the variation of sleep disorders across groups, possibly contributing to health disparities.

Emphysema on CT is associated with accelerated lung function decline in heavy smokers and patients with COPD; however, in the general population, it is not known whether greater emphysema-like lung on CT is associated with incident COPD. We used data from 2045 adult participants without initial prebronchodilator airflow limitation, classified by FEV1/FVC>upper limit of normal, was associated with increased odds of incident airflow limitation at 5-year follow-up on both prebronchodilator (adjusted OR 2.62, 95% CI 1.47 to 4.67) and postbronchodilator (adjusted OR 4.38, 95% CI 1.63 to 11.74) spirometry, independent of smoking history. These results support investigation into whether emphysema-like lung could be informative for COPD risk stratification.

The prenatal period is a critical exposure window when the developing respiratory and immune systems are susceptible to damaging impacts of environmental toxicants. Several reviews have suggested adverse effects of prenatal exposure to nitrogen dioxide (NO2) and particulate matter less than 10 μm in diameter (PM10) on child airway health, though notable limitations, including suboptimal exposure assessment, were identified.1,2 More recent studies found an increased risk of childhood asthma with elevated prenatal fine particulate matter (PM2.5) exposure.3–5 The mechanisms through which air pollution may contribute to the development of asthma include increased maternal systemic inflammation, endothelial changes, and oxidative stress; reduced placental growth and nutrient transport; epigenetic changes; and direct effects of particles crossing the placental barrier.2 Factors that may amplify risk have been identified, including male fetal sex, maternal history of asthma, and high prepregnancy body mass index (BMI).3,4,6,7 To date, studies have largely assessed exposures as averages within trimesters or across the whole pregnancy period. Maturational phases with distinct morphological lung development are well recognized: terminal bronchioles are formed during the pseudoglandular phase; the canalicular phase includes distal airway formation, differentiation of epithelial cells, angiogenesis, and vascular development; formation of terminal sacs, thinning of the alveolar walls, and maturation of the pulmonary surfactant system occur during the saccular phase; and alveolarization and microvasculature maturation occur during the prenatal alveolar phase.8 However, such developmentally relevant windows of vulnerability have not been explicitly examined in previous studies of PM2.5 and pediatric lung health. We utilized finely spatiotemporally resolved exposures to examine associations between exposure to PM2.5 during established morphogenic phases of prenatal lung development and child asthma in 2 pregnancy cohorts.

Evidence suggests that lung injury, inflammation and extracellular matrix remodelling precede lung fibrosis in interstitial lung disease (ILD). We examined whether a quantitative measure of increased lung attenuation on computed tomography (CT) detects lung injury, inflammation and extracellular matrix remodelling in community-dwelling adults sampled without regard to respiratory symptoms or smoking.We measured high attenuation areas (HAA; percentage of lung voxels between −600 and −250 Hounsfield Units) on cardiac CT scans of adults enrolled in the Multi-Ethnic Study of Atherosclerosis.HAA was associated with higher serum matrix metalloproteinase-7 (mean adjusted difference 6.3% per HAA doubling, 95% CI 1.3–11.5), higher interleukin-6 (mean adjusted difference 8.8%, 95% CI 4.8–13.0), lower forced vital capacity (FVC) (mean adjusted difference −82 mL, 95% CI −119–−44), lower 6-min walk distance (mean adjusted difference −40 m, 95% CI −1–−80), higher odds of interstitial lung abnormalities at 9.5 years (adjusted OR 1.95, 95% CI 1.43–2.65), and higher all cause-mortality rate over 12.2 years (HR 1.58, 95% CI 1.39–1.79).High attenuation areas are associated with biomarkers of inflammation and extracellular matrix remodelling, reduced lung function, interstitial lung abnormalities, and a higher risk of death among community-dwelling adults.

Objective: To determine the value of neurologist ambulatory care in chronic neurologic diseases in a large administrative claims dataset detailing costs, adverse events, and health care utilization. Methods: The Optum proprietary claims dataset (2010–2012) was examined to describe direct health care costs, as well as specific outcome metrics for a large population of persons with chronic neurologic illnesses. In phase I of the study, we detail neurologist involvement and differences in annualized allowed third--party payments within episode treatment groups (ETGs) for 10 neurologic illnesses. For phase II, we examined health care utilization for ETGs of epilepsy, Parkinson disease (PD), stroke, and multiple sclerosis (MS) with and without neurologist involvement. Reported outcomes were unadjusted differences and odds ratios between treatment groups. Results: For phase I, a total of 1,913,605 ETGs for 10 neurologic conditions were identified, 30.1% meeting criteria for neurologist involvement. All conditions had higher direct costs when neurologists were involved with care, ranging from a 25% increase for Alzheimer dementia to 100% more for MS care. In phase II, fractures, infections, emergent care, and inpatient admission were less with neurologist ambulatory care, while neurologist care was associated with greater utilization of disease-specific treatments (immunotherapies in MS anticoagulation in atrial fibrillation–associated stroke, deep brain stimulation and dopaminergic therapies in PD). Conclusion: Neurologist involvement with care is associated with greater unadjusted allowed payments, but fewer adverse events and less acute care utilization.

Background and Purpose— Long-term exposure to ambient air pollution is associated with higher risk of cardiovascular disease and stroke. We hypothesized that long-term exposure to air pollution would be associated with magnetic resonance imaging markers of subclinical cerebrovascular disease. Methods— Participants were 1075 stroke-free individuals aged ≥50 years drawn from the magnetic resonance imaging subcohort of the Northern Manhattan Study who had lived at the same residence for at least 2 years before magnetic resonance imaging. Cross-sectional associations between ambient air pollution and subclinical cerebrovascular disease were analyzed. Results— We found an association between distance to roadway, a proxy for residential exposure to traffic pollution, and white matter hyperintensity volume; however, after adjusting for risk factors, this relationship was no longer present. All other associations between pollutant measures and white matter hyperintensity volume were null. There was no clear association between exposure to air pollutants and subclinical brain infarcts or total cerebral brain volume. Conclusions— We found no evidence that long-term exposure to ambient air pollution is independently associated with subclinical cerebrovascular disease in an urban population-based cohort.