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BACKGROUND: Evidence suggests that long-term exposure to air pollution may increase the risk of dementia and related cognitive outcomes. A major source of air pollution is automotive traffic, which is modifiable by technological and regulatory interventions. OBJECTIVES: We examined associations of four traffic-related air pollutants with rates of cognitive decline in a cohort of older adults. METHODS: We analyzed data from the Chicago Health and Aging Project (CHAP), a longitudinal (1993-2012) community-based cohort study of older adults that included repeated assessments of participants' cognitive performance. Leveraging previously developed air pollution models, we predicted participant-level exposures to the tailpipe pollutants oxides of nitrogen ([NO.sub.X]) and nitrogen dioxide (N[O.sub.2]), plus the nontailpipe pollutants copper and zinc found in coarse particulate matter [PM with aerodynamic diameter 2.5 [micro]m to 10 [micro]m ([PM.sub.2.5-10,Cu]) and [PM.sub.2.5-10,Zn], respectively], over the 3 y prior to each participant's baseline assessment. Using generalized estimating equations, we estimated covariate-adjusted associations of each pollutant with rates of cognitive decline. We probed the robustness of our results via several sensitivity analyses, including alterations to the length of the exposure assessment window and exploring the influence of pre- and post-baseline selection bias. RESULTS: Using data from 6,061 participants, estimated associations of these pollutant exposures with cognitive decline were largely inconsistent with large adverse effects. For example, a standard deviation (5.8 ppb) increment in [NO.sub.X] corresponded to a slightly slower rate of cognitive decline [e.g., mean difference in change in global score, 0.010 standard unit/5 y, 95% confidence interval (CI): -0.016, 0.036]. The results of most of our sensitivity analyses were in generally similar to those of our main analyses, but our prebaseline selection bias results suggest that our analytic results may have been influenced by differential survivorship into our study sample. DISCUSSION: In this large prospective cohort study, we did not observe compelling evidence that long-term TRAP exposure is associated with cognitive decline. https://doi.org/10.1289/EHP14585, Introduction The hypothesis that long-term exposureto air pollution increases the riskofdementia and dementia-related outcomes continuestoreceive support from epidemiological evidence. (1-22) If air pollution elevates these risks, interventions could be implemented [...]

Introduction Neuropathological studies indicate that abnormal tau may first appear in the locus coeruleus (LC) starting early in life, (1,2) with substantial accumulation occurring during the course of Alzheimer's disease [...], BACKGROUND: Increased exposure to ambient air pollution, especially fine particulate matter [less than or equal to]2.5 [micro]m ([PM.sub.2.5]) is associated with poorer brain health and increased risk for Alzheimer's disease (AD) and related dementias. The locus coeruleus (LC), located in the brainstem, is one of the earliest regions affected by tau pathology seen in AD. Its diffuse projections throughout the brain include afferents to olfactory areas that are hypothesized conduits of cerebral particle deposition. Additionally, extensive contact of the LC with the cerebrovascular system may present an additional route of exposure to environmental toxicants. OBJECTIVE: Our aim was to investigate if exposure to [PM.sub.2.5] was associated with LC integrity in a nationwide sample of men in early old age, potentially representing one pathway through which air pollution can contribute to increased risk for AD dementia. METHODS: We examined the relationship between [PM.sub.2.5] and in vivo magnetic resonance imaging (MRI) estimates of LC structural integrity indexed by contrast to noise ratio ([LC.sub.CNR]) in 381 men [mean age = 67.3; standard deviation (SD) = 2.6] from the Vietnam Era Twin Study of Aging (VETSA). Exposure to [PM.sub.2.5] was taken as a 3-year average over the most recent period for which data were available (average of 5.6 years prior to the MRI scan). We focused on [LC.sub.CNR] in the rostral-middle portion of LC due to its stronger associations with aging and AD than the caudal LC. Associations between [PM.sub.2.5] exposures and LC integrity were tested using linear mixed effects models adjusted for age, scanner, education, household income, and interval between exposure and MRI. A co-twin control analysis was also performed to investigate whether associations remained after controlling for genetic confounding and rearing environment. RESULTS: Multiple linear regressions revealed a significant association between [PM.sub.2.5] and rostral-middle [LC.sub.CNR] (b = -0.16; p = 0.02), whereby higher exposure to [PM.sub.2.5] was associated with lower [LC.sub.CNR]. A co-twin control analysis found that, within monozygotic pairs, individuals with higher [PM.sub.2.5] exposure showed lower [LC.sub.CNR] (b = - 0.11; p = 0.02), indicating associations were not driven by genetic or shared environmental confounds. There were no associations between [PM.sub.2.5] and caudal [LC.sub.CNR] or hippocampal volume, suggesting a degree of specificity to the rostral-middle portion of the LC. DISCUSSION: Given previous findings that loss of LC integrity is associated with increased accumulation of AD-related amyloid and tau pathology, impacts on LC integrity may represent a potential pathway through which exposure to air pollution increases AD risk. https://doi.org/10.1289/EHP14344

Introduction Outdoor air pollution is classified as a Group 1 carcinogen based primarily on evidence of associations with lung cancer. (1) It has increasingly been associated with a higher incidence [...]

Introduction Growing evidence links air pollution to late-life cognitive health. Currently, the strongest evidence supports an effect of particulate matter (PM) air pollution. (1) In comparison with PM, fewer studies [...], BACKGROUND: Evidence linking gaseous air pollution to late-life brain health is mixed. OBJECTIVE: We explored associations between exposure to gaseous pollutants and brain magnetic resonance imaging (MRI) markers among Atherosclerosis Risk in Communities (ARIC) Study participants, with attention to the influence of exposure estimation method and confounding by site. METHODS: We considered data from 1,665 eligible ARIC participants recruited from four US sites in the period 1987-1989 with valid brain MRI data from Visit 5 (2011-2013). We estimated 10-y (2001-2010) mean carbon monoxide (CO), nitrogen dioxide (N[O.sub.2]), nitrogen oxides (N[O.sub.x]), and 8-and 24-h ozone ([O.sub.3]) concentrations at participant addresses, using multiple exposure estimation methods. We estimated site-specific associations between pollutant exposures and brain MRI outcomes (total and regional volumes; presence of microhemorrhages, infarcts, lacunes, and severe white matter hyperintensities), using adjusted linear and logistic regression models. We compared meta-analytically combined site-specific associations to analyses that did not account for site. RESULTS: Within-site exposure distributions varied across exposure estimation methods. Meta-analytic associations were generally not statistically significant regardless of exposure, outcome, or exposure estimation method; point estimates often suggested associations between higher N[O.sub.2] and N[O.sub.x] and smaller temporal lobe, deep gray, hippocampal, frontal lobe, and Alzheimer disease signature region of interest volumes and between higher CO and smaller temporal and frontal lobe volumes. Analyses that did not account for study site more often yielded significant associations and sometimes different direction of associations. DISCUSSION: Patterns of local variation in estimated air pollution concentrations differ by estimation method. Although we did not find strong evidence supporting impact of gaseous pollutants on brain changes detectable by MRI, point estimates suggested associations between higher exposure to CO, N[O.sub.x], and N[O.sub.2] and smaller regional brain volumes. Analyses of air pollution and dementia-related outcomes that do not adjust for location likely underestimate uncertainty and may be susceptible to confounding bias. https://doi.org/10.1289/EHP13906

Introduction Fine particulate matter (P[M.sub.2.5], aerodynamic diameter Inflammation and coagulation are important biological mechanisms for the observed associations between these health effects and particulate matter (PM) of all sizes. However, [...], Background: In contrast to fine particles, less is known of the inflammatory and coagulation impacts of coarse particulate matter (P[M.sub.10-2.5], particulate matter with aerodynamic diameter [less than or equal to]10 [micro]m and >2.5 [micro]m). Toxicological research suggests that these pathways might be important processes by which P[M.sub.10-2.5] impacts health, but there are relatively few epidemiological studies due to a lack of a national P[M.sub.10-2.5] monitoring network. Objectives: We used new spatiotemporal exposure models to examine associations of both 1-y and 1-month average P[M.sub.10-2.5] concentrations with markers of inflammation and coagulation. Methods: We leveraged data from 7,071 Multi-Ethnic Study of Atherosclerosis and ancillary study participants 45-84 y of age who had repeated plasma measures of inflammatory and coagulation biomarkers. We estimated P[M.sub.10-2.5] at participant addresses 1 y and 1 month before each of up to four exams (2000-2012) using spatiotemporal models that incorporated satellite, regulatory monitoring, and local geographic data and accounted for spatial correlation. We used random effects models to estimate associations with interleukin-6 (IL-6), C- reactive protein (CRP), fibrinogen, and D-dimer, controlling for potential confounders. Results: Increases in P[M.sub.10-2.5] were not associated with greater levels of inflammation or coagulation. A 10-[micro]g/[m.sup.3] increase in annual average P[M.sub.10-2.5] was associated with a 2.5% decrease in CRP [95% confidence interval (CI): -5.5, 0.6]. We saw no association between annual average P[M.sub.10-2.5] and the other markers (IL-6: -0.7%, 95% CI: -2.6, 1.2; fibrinogen: -0.3%, 95% CI: -0.9, 0.3; D- dimer: -0.2%, 95% CI: -2.6, 2.4). Associations consistently showed that a 10-[micro]g/[m.sup.3] increase in 1- month average P[M.sub.10-2.5] was associated with reduced inflammation and coagulation, though none were distinguishable from no association (IL-6: -1.2%, 95% CI: -3.0, 0.5; CRP: -2.5%, 95% CI: -5.3, 0.4; fibrinogen: -0.4%, 95% CI: -1.0, 0.1; D-dimer: -2.0%, 95% CI: -4.3, 0.3). Discussion: We found no evidence that P[M.sub.10-2.5] is associated with higher inflammation or coagulation levels. More research is needed to determine whether the inflammation and coagulation pathways are as important in explaining observed P[M.sub.10-2.5] health impacts in humans as they have been shown to be in toxicology studies or whether P[M.sub.10-2.5] might impact human health through alternative biological mechanisms. https://doi.org/10.1289/EHP12972

Introduction Idiopathic Parkinson's disease (PD) is the second-most prevalent neurodegenerative disease in the US, primarily affecting adults 65 years of age or older. (1) Despite an increasing disease burden due [...], Background: Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent. Objectives: This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter [less than or equal to]2.5 [micro]m (P[M.sub.2.5]) and nitrogen dioxide (N[O.sub.2]). Methods: We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003-2009 (35-80 years of age) and followed through 2018. Exposures of interest included address-level ambient P[M.sub.2.5] and N[O.sub.2] in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 (n = 163). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: N[O.sub.2] exposure in 2009 was associated with PD risk in a dose- response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in N[O.sub.2], adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8 ppb increment in N[O.sub.2] was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of N[O.sub.2] with PD risk was limited to women in urban, rural, and small town areas and women with [greater than or equal to]50th percentile ADI but not among women from suburban areas or areas with Discussion: In this nationwide cohort of US women, higher level exposure to ambient N[O.sub.2] is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. https://doi.org/10.1289/EHP13009

In April 1972, the recently established National Institute of Environmental Health Sciences (NIEHS), under the leadership of David Rall, made a bold decision to launch a journal called Environmental Health [...]

Introduction Decline in episodic memory (e.g., the ability to remember details from daily experience, as well as the spatial and temporal context of events) is commonly associated with normal cognitive [...], BACKGROUND: Episodic memory decline varies by age and underlying neuropathology. Whether ambient air pollution contributes to the heterogeneity of episodic memory decline in older populations remains unclear. OBJECTIVES: We estimated associations between air pollution exposures and episodic memory decline according to pollutant, exposure time window, age, and latent class subgroups defined by episodic memory trajectories. METHODS: Participants were from the Women's Health Initiative Memory Study-Epidemiology of Cognitive Health Outcomes. Older women (n = 2,056; 74-92 years of age) completed annual (2008-2018) episodic memory assessments using the telephone-based California Verbal Learning Test (CVLT). We estimated 3-y average fine particulate matter [PM with an aerodynamic diameter of [less than or equal to]2.5 [micro]m (P[M.sub.2.5])] and nitrogen dioxide (N[O.sub.2]) exposures at baseline and 10 y earlier (recent and remote exposures, respectively), using regionalized national universal kriging. Separate latent class mixed models were used to estimate associations between interquartile range increases in exposures and CVLT trajectories in women [less than or equal to]80 and > 80 years of age, adjusting for covariates. RESULTS: Two latent classes were identified for women 80-y-old cognitively resilient class [-0.10/y (95% CI: -0.24, 0.03)] and steady-decliner class [-0.11/y (95% CI: -0.27, 0.05)]. Associations with recent N[O.sub.2] exposure in women >80years of age were stronger and statistically significant when 267 women with incident probable dementia were excluded [e.g., -0.12/y (95% CI: -0.22, -0.02) for the cognitively resilient class]. In contrast with changes in CVLT over time, there were no associations between exposures and CVLT scores during follow-up in any subgroup. DISCUSSION: In a community-dwelling U.S. population of older women, associations between late-life exposure to ambient air pollution and episodic memory decline varied by age-related cognitive trajectories, exposure time windows, and pollutants. https://doi.org/10.1289/EHP7668

Introduction Neurodegenerative diseases, including Alzheimer's disease (AD) and related dementias (ADRD), pose a growing burden on our rapidly aging society (Livingston et al. 2020). In 2016, dementia was the fifth [...], 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 ([PM.sub.2.5]) 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 [PM.sub.2.5] 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 [PM.sub.2.5] 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 [+ or -] standard deviation (SD)] 10-y average [PM.sub.2.5] was 10.1 ([+ or -]2.9) [micro]g/[m.sup.3]. Each 1-[micro]g/[m.sup.3] increase in the moving average of 10-y [PM.sub.2.5] 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 [PM.sub.2.5] 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 [PM.sub.2.5]. https://doi.org/10.1289/EHP9018

Racism systematically constructs inequities by conferring advantages upon one racial/ethnic group at the expense of others. Power and privilege are distributed unevenly across space and time--as are the characteristics of [...]

BACKGROUND: Air pollutants may contribute to the development of Parkinson's disease (PD), but empirical evidence is limited and inconsistent. OBJECTIVES: This study aimed to prospectively investigate the associations of PD with ambient exposures to fine particulate matter with aerodynamic diameter = 2.5μm (PM2.5) and nitrogen dioxide (NO2). METHODS: We analyzed data from 47,108 US women from the Sister Study, enrolled from 2003–2009 (35–80 years of age) and followed through 2018. Exposures of interest included address-level ambient PM2.5 and NO2 in 2009 and their cumulative averages from 2009 to PD diagnosis with varying lag-years. The primary outcome was PD diagnosis between 2009 and 2018 (푛 = 163). We used multivariable Cox proportional hazards and time-varying Cox models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: NO2 exposure in 2009 was associated with PD risk in a dose-response manner. The HR and 95% CI were 1.22 (95% CI: 1.03, 1.46) for one interquartile [4.8 parts per billion (ppb)] increment in NO2, adjusting for age, race and ethnicity, education, smoking status, alcohol drinking, caffeine intake, body mass index, physical activity, census region, residential area type, area deprivation index (ADI), and self-reported health status. The association was confirmed in secondary analyses with time-varying averaged cumulative exposures. For example, the multivariable adjusted HR for PD per 4.8 ppb increment in NO2 was 1.25 (95% CI: 1.05, 1.50) in the 2-year lag analysis using cumulative average exposure. Post hoc subgroup analyses overall confirmed the association. However, statistical interaction analyses found that the positive association of NO2 with PD risk was limited to women in urban, rural, and small town areas and women with = 50th percentile ADI but not among women from suburban areas or areas with < 50th percentile ADI. In contrast, PM2.5 exposure was not associated with PD risk with the possible exception for women from the Midwest region of the US (HRinterquartile-range = 2.49, 95% CI: 1.20, 5.14) but not in other census regions. DISCUSSION: In this nationwide cohort of US women, higher level exposure to ambient NO2 is associated with a greater risk of PD. This finding needs to be independently confirmed and the underlying mechanisms warrant further investigation. [ABSTRACT FROM AUTHOR]

I am excited to have been handed the editorial pen for Environmental Health Perspectives (EHP), and it is with enthusiasm that I take on the role as the journal's new [...]

Introduction Air pollution is classified by the International Agency for Research on Cancer (IARC) as a Group 1 carcinogen (Loomis et al. 2013), consistent with the epidemiologic evidence for the [...], Background: Particulate matter (PM) is a complex mixture. Geographic variations in PM may explain the lack of consistent associations with breast 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 Results: During follow-up (mean = 8.4y), 2,225 invasive and 623 ductal carcinoma in situ (DCIS) cases were identified. [PM.sub.2.5] and N[O.sub.2] were associated with breast cancer overall [HR= 1.05 (95% CI:0.99, 1.11) and 1.06 (95% CI:1.02, 1.11), respectively] and with DCIS but not with invasive cancer. Invasive breast cancer was associated with [PM.sub.2.5] only in the Western United States [HR =1.14 (95% CI:1.02, 1.27)] and N[O.sub.2] only in the Southern United States [HR= 1.16 (95% CI:1.01, 1.33)]. [PM.sub.2.5] was associated with a higher risk of invasive breast cancer among two of seven identified compositionbased clusters. A higher risk was observed [HR = 1.25 (95% CI: 0.97, 1.60)] in a California-based cluster characterized by low S and high Na and nitrate (N[O.sup.-.sub.3]) fractions and for another Western United States cluster [HR = 1.60 (95% CI: 0.90,2.85)], characterized by high fractions of Si, Ca, K, and Al. Conclusion: Air pollution measures were related to both invasive breast cancer and DCIS within certain geographic regions and PM component clusters. https://doi.org/10.1289/EHP5131

Introduction Ground-level ozone ([O.sub.3]) is a powerful oxidizing agent and is one of the most harmful air pollutants currently addressed by air quality standards in the European Union and United [...], Background: Long-term ozone ([O.sub.3]) exposure is associated with cardiovascular mortality, but little is known about the associations between [O.sub.3] and subclinical arterial disease. Objectives: We studied the longitudinal association of exposure to [O.sub.3] and progression of key subclinical arterial markers in adults: intima-media thickness of common carotid artery ([IMT.sub.CCA]), carotid plaque (CP) burden, and coronary artery calcification (CAC). Methods: CAC was measured one to four times at baseline and at follow-up exams (1999-2012) by computed tomography (CT) in 6,619 healthy adults, recruited at age 45-84 y without cardiovascular disease (CVD), over a mean of 6.5 y (standard deviation: 3.5 y). [IMT.sub.CCA] and CP burden were quantified in 3,392 participants using carotid artery ultrasound imaging acquired over a mean of 9 y (1.7 y). Over 91% and 89% participants had at least one follow-up [IMT.sub.CCA] and CAC measurement, respectively. Residence-specific [O.sub.3] concentrations were estimated by a validated spatiotemporal model spanning from 1999 to 2012. This model relied on comprehensive monitoring data and geographical variables to predict individualized long-term average concentrations since baseline. Linear mixed models and logistic regression model were used to evaluate relationships of long-term average exposure to [O.sub.3] with longitudinal change in [IMT.sub.CCA], CAC, and CP formation, respectively. Results: Mean progression rates of [IMT.sub.CCA] and CAC were 12 [+ or -] 0.5 [micro]m and 25 [+ or -] 1.4 Agatston units per year. CP formation was identified in 55% of the subjects. A 3-ppb increase in long-term average [O.sub.3] exposure was associated with a 5.6-pm [95% confidence interval (CI): 1.4, 9.7] greater increase in [IMT.sub.CCA] over 10 y. A 3-ppb increase in [O.sub.3] was also associated with new CP formation [odds ratio (OR): 1.2 (95% CI: 1.1, 1.4)] but not CAC progression [-8 Agatston units (95% CI: -18, 2)]. Associations were robust in the analysis with extended covariate adjustment, including copollutants, i.e., nitrogen oxides (N[O.sub.x]) and particulate matter with diameter Conclusion: Over almost a decade of follow-up, outdoor [O.sub.3] concentrations were associated with increased rate of carotid wall thickness progression and risk of new plaque formation, suggesting arterial injury in this cohort.

Introduction Catecholamines act as both neurotransmitters and hormones produced by the sympathetic branch of the autonomic nervous system (ANS). Among other things, catecholamines play an important role in regulating heart [...], Background: Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines. Objectives: To examine the association of long-term air pollutants with three urinary catecholamines: dopamine (DA), epinephrine (EPI), and norepinephrine (NE). As a secondary aim, we also examined the association between short-term (or acute) exposure to fine particulate matter [particulate matter with aerodynamic diameter [less than or equal to] 2.5[micro]m ([PM.sub.2.5])] and those catecholamines. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) and two of its ancillary studies, the MESA Air Pollution Study and the MESA Stress Study, to provide exposure and outcome data. DA, EPI, and NE from urine samples were collected from 2004 to 2006 from 1,002 participants in the New York, New York, and Los Angeles, California, study sites. Spatiotemporal models incorporated cohort-specific monitoring and estimated annual average pollutant concentrations ([PM.sub.2.5], N[O.sub.2], N[O.sub.x] and black carbon) at participants&apos; homes the year prior to urine collection. Secondarily, short-term [PM.sub.2.5] was evaluated (day of, day prior, and 2- to 5-d lags prior to urine collection). Several covariates were considered confounders (age, race, sex, site, socioeconomic status, cardiovascular disease risk factors, psychosocial stressors, and medication use) in linear regression models. Results: A 17 ppb higher annual N[O.sub.x] concentration was associated with 6.3% higher mean EPI level [95% confidence interval (CI): 0.3%, 12.6%]. A 2-[micro]g/[m.sup.3] higher annual ambient [PM.sub.2.5] concentration was associated with 9.1% higher mean EPI (95% CI: 3.2%, 15.3%) and 4.4% higher DA level (95% CI: 1%, 7.9%). N[O.sub.2], black carbon, and short-term [PM.sub.2.5] exposures were not significantly associated with any of the catecholamines. Conclusions: We found an association between EPI and long-term concentrations of [PM.sub.2.5] and N[O.sub.x] and an association between DA and long-term ambient [PM.sub.2.5]. These novel findings provide modest support for the hypothesis that air pollutant exposures are related to sympathetic nervous system activation.

Introduction The notion of translational research is usually described through the bench-to-bedside application of basic research discovery to clinical treatment. This framework typically describes the 'translation' of a scientific discovery [...], Background: Environmental health scientists may find it challenging to fit the structure of the questions addressed in their discipline into the prevailing paradigm for translational research. Objective: We aim to frame the translational science paradigm to address the stages of scientific discovery, knowledge acquisition, policy development, and evaluation in a manner relevant to the environmental health sciences. Our intention is to characterize differences between environmental health sciences and clinical medicine, and to orient this effort towards public health goals. Discussion: Translational research is usually understood to have evolved from the bench-to-bedside framework by which basic science transitions to clinical treatment. Although many health-related fields have incorporated the terminology and context of translational science, environmental health research has not always found a clear fit into this paradigm. We describe a translational research framework applicable to environmental health sciences that retains the basic structure that underlies the original bench-to-bedside paradigm. We propose that scientific discovery (T1) in environmental health research frequently occurs through epidemiological or clinical observations. This discovery often involves understanding the potential for human health effects of exposure to a given environmental chemical or chemicals. The practical applications of this discovery evolve through an understanding of exposure-response relationships (T2) and identification of potential interventions to reduce exposure and improve health (T3). These stages of translation require an interdisciplinary partnership between exposure sciences, exposure biology, toxicology, epidemiology, biostatistics, risk assessment, and clinical sciences. Implementation science then plays a crucial role in the development of environmental and public health practice and policy interventions (T4). Outcome evaluation (T5) often takes the form of accountability research, as environmental health scientists work to quantify the costs and benefits of these interventions. Conclusion: We propose an easily visualized framework for translation of environmental health science knowledge-from discovery to public health practice-that reflects the crucial interactions between multiple disciplines in our field. https://doi.org/10.1289/EHP4067

BACKGROUND: Poor olfaction is common in older adults and may have profound adverse implications on their health. However, little is known about the potential environmental contributors to poor olfaction. OBJECTIVE: We investigated ambient fine particulate matter [PM ≤ 2.5 μm in aerodynamic diameter (PM2.5)] and nitrogen dioxide (NO2) in relation to poor olfaction in middle-aged to older women. METHODS: The Sister Study is a nationwide cohort of 50,884 women in the United States with annual average air pollutant exposures estimated based on participants' residences from enrollment (2003-2009) through 2017. This analysis was limited to 3,345 women, 50-79 years of age as of January 2018, who completed the Brief Smell Identification Test (B-SIT) in 2018-2019. Poor olfaction was defined as a B-SIT score of ≤ 9 in the primary analysis. We conducted multivariable logistic regressions, accounting for covariates and study sampling design. RESULTS: Overall, we found little evidence for associations of air pollutants with poor olfaction. The odds ratio (OR) and 95% confidence interval (CI) of poor olfaction for each interquartile range (IQR) increment of air pollutants in 2006 were 1.03 (95% CI: 0.91, 1.17) for PM2.5 (per 3.3 μg/m³) and 1.08 (95% CI: 0.96, 1.22) for NO2 (per 5.7 ppb). Results were similar in the analyses using the most recent (2017) or the cumulative average (2006-2017) air pollutant exposure data. Secondary analyses suggested potential association in certain subgroups. The OR per IQR was 1.35 (95% CI: 1.11, 1.65) for PM2.5 among younger participants (< 54.2 years of age) and 1.87 (95% CI: 1.29, 2.71) for NO2 among current smokers. DISCUSSION: This study did not find convincing evidence that air pollutants have lasting detrimental effects on the sense of smell of women 50-79 years of age. The subgroup analyses are exploratory, and the findings need independent confirmation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Epidemiologic studies of fine particulate matter [aerodynamic diameter [less than or equal to] 2.5 [micro]m ([PM.sub.2.5])] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in [...]

Introduction Air pollution is a well-established risk factor for adverse respiratory outcomes, including chronic lung diseases (Andersen et al. 2011; Karakatsani et al. 2003; Lindgren et al. 2009; Schikowski et [...], Background: Coarse particulate matter ([PM.sub.10-2.5]) is primarily mechanically generated and includes crustal material, brake and tire wear, and biological particles. [PM.sub.10-2.5] is associated with pulmonary disease, which can lead to right ventricular (RV) dysfunction. Although RV characteristics have been associated with combustion-related pollutants, relationships with [PM.sub.10-2.5] remain unknown. Objectives: To quantify cross-sectional associations between RV dysfunction and [PM.sub.10-2.5] mass and components among older adults and susceptible populations. Methods: We used baseline cardiac magnetic resonance images from 1,490 participants (45-84 y old) from the Multi-Ethnic Study of Atherosclerosis and assigned 5-y residential concentrations of [PM.sub.10-2.5] mass, copper, zinc, phosphorus, silicon, and endotoxin, using land-use regression models. We quantified associations with RV mass, end-diastolic volume, and ejection fraction after control for risk factors and copollutants using linear regression. We further examined personal susceptibility. Results: We found positive associations of RV mass and, to a lesser extent, end diastolic volume with [PM.sub.10-2.5] mass among susceptible populations including smokers and persons with emphysema. After adjustment for copollutants, an interquartile range increase in [PM.sub.10-2.5] mass (2.2 [micro]g/[m.sup.3]) was associated with 0.5 g (95% CI: 0.0, 1.0), 0.9 g (95% CI: 0.1, 1.7), and 1.4 g (95% CI: 0.4, 2.5) larger RV mass among former smokers, current smokers, and persons with emphysema, respectively. No associations were found with healthy individuals or with ejection fraction. Conclusions: Alterations to RV structure may represent a mechanism by which long-term [PM.sub.10-2.5] exposure increases risks for adverse respiratory and cardiovascular outcomes, especially among certain susceptible populations. https://doi.org/10.1289/EHP658

Environmental Health Perspectives (EHP) took a major step in extending its international presence when we began translating selected journal content into Chinese in 2001. Today, after 85 issues and more [...]

Introduction Many cohort studies of the long-term effects of fine particulate matter ([PM.sub.2.5]) air pollution on health have used exposure prediction models to estimate individual level long-term concentrations at cohort [...], INTRODUCTION: Recent cohort studies have used exposure prediction models to estimate the association between long-term residential concentrations of fine particulate matter ([PM.sub.2.5]) and health. Because these prediction models rely on [PM.sub.2.5] monitoring data, predictions for times before extensive spatial monitoring present a challenge to understanding long-term exposure effects. The U.S. Environmental Protection Agency (EPA) Federal Reference Method (FRM) network for [PM.sub.2.5] was established in 1999. OBJECTIVES: We evaluated a novel statistical approach to produce high-quality exposure predictions from 1980 through 2010 in the continental United States for epidemiological applications. METHODS: We developed spatio-temporal prediction models using geographic predictors and annual average [PM.sub.2.5] data from 1999 through 2010 from the FRM and the Interagency Monitoring of Protected Visual Environments (IMPROVE) networks. Temporal trends before 1999 were estimated by using a) extrapolation based on [PM.sub.2.5] data in FRM/IMPROVE, b) [PM.sub.2.5] sulfate data in the Clean Air Status and Trends Network, and c) visibility data across the Weather Bureau Army Navy network. We validated the models using [PM.sub.2.5] data collected before 1999 from IMPROVE, California Air Resources Board dichotomous sampler monitoring (CARB dichot), the Children's Health Study (CHS), and the Inhalable Particulate Network (IPN). RESULTS: In our validation using pre-1999 data, the prediction model performed well across three trend estimation approaches when validated using IMPROVE and CHS data ([R.sup.2] = 0.84-0.91) with lower [R.sup.2] values in early years. Model performance using CARB dichot and IPN data was worse ([R.sup.2] = 0.00-0.85) most likely because of fewer monitoring sites and inconsistent sampling methods. CONCLUSIONS: Our prediction modeling approach will allow health effects estimation associated with long-term exposures to [PM.sub.2.5] over extended time periods ≤ 30 years. http://dx.doi.org/10.1289/EHP131

We thank Ahmed et al. for their interest in our article. The correspondents comment on the generalizability of study results to a broader population and emphasize the need to consider [...]

Introduction Large population studies have routinely demonstrated that exposure to air pollution is associated with increased risk of cardiovascular morbidity and mortality (Brook et al. 2010). Low-socioeconomic status (SES) has [...], BACKGROUND: Long-term fine particulate matter ([PM.sub.2.5]) exposure is linked with cardiovascular disease, and disadvantaged status may increase susceptibility to air pollution-related health effects. In addition, there are concerns that this association may be partially explained by confounding by socioeconomic status (SES). OBJECTIVES: We examined the roles that individual- and neighborhood-level SES (NSES) play in the association between [PM.sub.2.5] exposure and cardiovascular disease. METHODS: The study population comprised 51,754 postmenopausal women from the Women's Health Initiative Observational Study. [PM.sub.2.5] concentrations were predicted at participant residences using fine-scale regionalized universal kriging models. We assessed individual-level SES and NSES (Census-tract level) across several SES domains including education, occupation, and income/wealth, as well as through an NSES score, which captures several important dimensions of SES. Cox proportional-hazards regression adjusted for SES factors and other covariates to determine the risk of a first cardiovascular event. RESULTS: A 5 µg/[m.sup.3] higher exposure to [PM.sub.2.5] was associated with a 13% increased risk of cardiovascular event [hazard ratio (HR) 1.13; 95% confidence interval (CI): 1.02, 1.26]. Adjustment for SES factors did not meaningfully affect the risk estimate. Higher risk estimates were observed among participants living in low-SES neighborhoods. The most and least disadvantaged quartiles of the NSES score had HRs of 1.39 (95% CI: 1.21, 1.61) and 0.90 (95% CI: 0.72, 1.07), respectively. CONCLUSIONS: Women with lower NSES may be more susceptible to air pollution-related health effects. The association between air pollution and cardiovascular disease was not explained by confounding from individual-level SES or NSES. Environ Health Perspect 124:1840-1847; http://dx.doi.org/10.1289/EHP199

Introduction Air pollution is a complex and dynamic mixture consisting of particulate matter (PM), gases, organic components, and metals (Block et al. 2012). Numerous studies have consistently shown deleterious effects [...], BACKGROUND: Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD). OBJECTIVE: We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 [micro]m in diameter ([PM.sub.10]) and < 2.5 [micro]m in diameter ([PM.sub.2.5]) and nitrogen dioxide (N[O.sub.2]) 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 [PM.sub.10], [PM.sub.2.5], and N[O.sub.2] 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 N[O.sub.2] exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to [PM.sub.10] (O[R.sub.Q5 vs. Q1] = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to [PM.sub.2.5] (O[R.sub.Q5 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 [PM.sub.2.5] (O[R.sub.Q5 vs. Q1] = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and [PM.sub.10] (O[R.sub.Q5 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 [PM.sub.10], [PM.sub.2.5], or N[O.sub.2] and PD risk. The suggestive evidence that exposures to [PM.sub.2.5] and [PM.sub.10] may increase PD risk among female never smokers warrants further investigation. http://dx.doi.org/10.1289/EHP135

Introduction Exposure to ambient particulate matter (PM) has been linked to the occurrence of cardiovascular events (Brook et al. 2010; Pope et al. 2004). Although the causal mechanisms remain unclear, [...], BACKGROUND: Particulate matter (PM) exposure may directly affect the pulmonary vasculature. Although the pulmonary vasculature is not easily measurable, differential associations for right ventricular (RV) and left ventricular (LV) mass may provide an indirect assessment of pulmonary vascular damage. OBJECTIVES: We tested whether long-term exposure to PM < 2.5 µm ([PM.sub.2.5]) is associated with greater RV mass and RV mass/end-diastolic volume ratio relative to the LV. Methods: The Multi-Ethnic Study of Atherosclerosis performed cardiac magnetic resonance (CMR) imaging among participants 45-84 years old without clinical cardiovascular disease in 2000-2002 in six U.S. cities. A fine-scale spatiotemporal model estimated ambient [PM.sub.2.5] exposure in the year before CMR; individually weighted estimates accounted for indoor exposure to ambient [PM.sub.2.5]. Linear regression models were adjusted for demographics, anthropometrics, smoking status, cardiac risk factors, and LV parameters, with additional adjustment for city. RESULTS: The 4,041 included participants had a mean age of 61.5 years, and 47% were never smokers. The mean ambient [PM.sub.2.5] was 16.4 µg/[m.sup.3] and individually weighted [PM.sub.2.5] was 11.0 µg/[m.sup.3]. [PM.sub.2.5] exposure was associated with greater RV mass [ambient: 0.11 g per 5 µg/[m.sup.3] (95% CI: -0.05, 0.27); individually weighted: 0.20 g per 5 µg/[m.sup.3] (95% CI: 0.04, 0.36)] and a greater RV mass/end-diastolic volume ratio conditional on LV parameters. City-adjusted results for RV mass were of greater magnitude and were statistically significant for both measures of [PM.sub.2.5], whereas those for RV mass/end-diastolic volume ratio were attenuated. CONCLUSIONS: Long-term [PM.sub.2.5] exposures were associated with greater RV mass and RV mass/ end-diastolic volume ratio conditional on the LV; however, additional adjustment for city attenuated the RV mass/end-diastolic volume findings. These findings suggest that [PM.sub.2.5] exposure may be associated with subclinical cardiopulmonary differences in this general population sample. http://dx.doi.org/10.1289/ehp.1409451

Introduction Aging-related physical disability has become a critical health concern because of its high associated health care costs and because of the rapidly growing number of older Americans (Administration on [...], BACKGROUND: Physical disability is common though not inevitable in older age and has direct bearing on a person's ability to perform activities essential for self-care and independent living. Air pollution appears to increase the risk of several chronic diseases that contribute to the progression of disability. OBJECTIVE: We evaluated long-term exposure to traffic-related air pollution (TRAP) in relation to progression in physical disability. METHODS: We conducted our investigation within the Chicago Health and Aging Project. We measured participants' exposures to TRAP using two surrogates: residential proximity to major roads (1993 onwards) and ambient concentrations of oxides of nitrogen (NO# 1999 onwards), predicted via a geographic information systems-based spatiotemporal smoothing model (cross-validation [R.sup.2] = 0.87) that incorporated community-based monitoring and resolved intraurban exposure gradients at a spatial scale of tens of meters. Participants' lower-extremity physical ability was assessed every 3 years (1993-2012) via tandem stand, chair stand, and timed walking speed. RESULTS: In multivariable-adjusted analyses (n = 5,708), higher long-term NO# exposure was associated with significantly faster progression in disability. Compared with the 5-year decline in physical ability score among participants in the lowest quartile of NO# exposure, decline among those in the highest exposure quartile was 1.14 units greater (95% confidence interval [CI]: -1.86, -0.42), equivalent to 3 additional years of decline among those in the lowest exposure quartile. The association was linear across the continuum of NO# exposure: per 10-ppb increment in exposure, the 5-year decline in physical ability score was 0.87 unit greater (95% CI: -1.35, -0.39). Proximity to a major road was not associated with disability progression (n = 9,994). CONCLUSIONS: These data join a growing body of evidence suggesting that TRAP exposures may accelerate aging-related declines in health. http://dx.doi.org/10.1289/ehp.1510089

Introduction There is a well-established relationship between combustion-related air pollution exposure-- especially particulate matter ≤ 2.5 µm in diameter ([PM.sub.2.5])--and cardiovascular disease (CVD) morbidity and mortality (Brook et al. 2010). [...], Background: Exposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution. OBJECTIVE: We examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes. METHODS: This analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (N[O.sub.2]) and fine particulate matter (≤ 2.5 µm; [PM.sub.2.5]) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding. RESULTS: A 10-µg/[m.sup.3] increase in [PM.sub.2.5] was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in N[O.sub.2] was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure. CONCLUSIONS: Long-term [PM.sub.2.5] and N[O.sub.2] exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies. http://dx.doi.org/10.1289/ehp.1408125

Introduction Evidence of the association between long-term exposure to ambient [PM.sub.2.5] (particulate matter with diameter < 2.5 [micro]m) and human health continues to accumulate (Laden et al. 2006; Miller et [...], BACKGROUND: Regulatory monitoring data have been the exposure data resource most commonly applied to studies of the association between long-term [PM.sub.2.5] components and health. However, data collected for regulatory purposes may not be compatible with epidemiological studies. OBJECTIVES: We studied three important features of the [PM.sub.2.5] component monitoring data to determine whether it would be appropriate to combine all available data from multiple sources for developing spatiotemporal prediction models in the National Particle Component and Toxicity (NPACT) study. METHODS: The NPACT monitoring data were collected in an extensive monitoring campaign targeting cohort participant residences. The regulatory monitoring data were obtained from the Chemical Speciation Network (CSN) and the Interagency Monitoring of Protected Visual Environments (IMPROVE). We performed exploratory analyses to examine features that could affect our approach to combining data: comprehensiveness of spatial coverage, comparability of analysis methods, and consistency in sampling protocols. In addition, we considered the viability of developing spatiotemporal prediction models given a) all available data, b) NPACT data only, and c) NPACT data with temporal trends estimated from other pollutants. RESULTS: The number of CSN/IMPROVE monitors was limited in all study areas. The different laboratory analysis methods and sampling protocols resulted in incompatible measurements between networks. Given these features we determined that it was preferable to develop our spatiotemporal models using only the NPACT data and under simplifying assumptions. CONCLUSIONS: Investigators conducting epidemiological studies of long-term [PM.sub.2.5] components need to be mindful of the features of the monitoring data and incorporate this understanding into the design of their monitoring campaigns and the development of their exposure prediction models. http://dx.doi.org/10.1289/ehp.1307744

Introduction Recent estimates suggest that ambient particulate matter exposures result in nearly 3.5 million deaths and 76 million disability-adjusted life years lost globally each year (Lim et al. 2013). Increased [...], BACKGROUND: Toxicological research suggests that coarse particles ([PM.sub.10-2.5]) are inflammatory, but responses are complex and may be best summarized by multiple inflammatory markers. Few human studies have investigated associations with [PM.sub.10-2.5] and, of those, none have explored long-term exposures. Here we examine long-term associations with inflammation and coagulation in the Multi-Ethnic Study of Atherosclerosis. METHODS: Participants included 3,295 adults (45-84 years of age) from three metropolitan areas. Site-specific spatial models were used to estimate 5-year concentrations of [PM.sub.10-2.5] mass and copper, zinc, phosphorus, silicon, and endotoxin found in [PM.sub.10-2.5]. Outcomes included interleukin-6, C-reactive protein, fibrinogen, total homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagulation scores. We used multivariable regression with multiply imputed data to estimate associations while controlling for potential confounders, including co-pollutants such as fine particulate matter. RESULTS: Some limited evidence was found of relationships between inflammation and coagulation and [PM.sub.10-2.5]. Endotoxin was the [PM.sub.10-2.5] component most strongly associated with inflammation, with an interquartile range (IQR) increase (0.08 EU/[m.sup.3]) associated with 0.15 (95% CI: 0.01, 0.28; p = 0.03) and 0.08 (95% CI: -0.07, 0.23; p = 0.28) higher inflammation scores before and after control for city, respectively. Copper was the component with the strongest association with coagulation, with a 4-ng/[m.sup.3] increase associated with 0.19 (95% CI: 0.08, 0.30; p = 0.0008) and 0.12 (95% CI: -0.05, 0.30; p = 0.16) unit higher coagulation scores before and after city adjustment, respectively. CONCLUSIONS: Our cross-sectional analysis provided some evidence that long-term [PM.sub.10-2.5] exposure was associated with inflammation and coagulation, but associations were modest and depended on particle composition. http://dx.doi.org/10.1289/ehp.1308069.

Introduction Organophosphate pesticides (OPs) have been the most commonly used insecticides in the United States for more than three decades. After the passage of the Food Quality Protection Act of [...], BACKGROUND: Organophosphate pesticide (OP) exposure to the U.S. population is dominated by dietary intake. The magnitude of exposure from diet depends partly on personal decisions such as which foods to eat and whether to choose organic food. Most studies of OP exposure rely on urinary biomarkers, which are limited by short half-lives and often lack specificity to parent compounds. A reliable means of estimating long-term dietary exposure to individual OPs is needed to assess the potential relationship with adverse health effects. OBJECTIVES: We assessed long-term dietary exposure to 14 OPs among 4,466 participants in the Multi-Ethnic Study of Atherosclerosis, and examined the influence of organic produce consumption on this exposure. METHODS: Individual-level exposure was estimated by combining information on typical intake of specific food items with average OP residue levels on those items. In an analysis restricted to a subset of participants who reported rarely or never eating organic produce ('conventional consumers'), we assessed urinary dialkylphosphate (DAP) levels across tertiles of estimated exposure (n = 480). In a second analysis, we compared DAP levels across subgroups with differing self-reported organic produce consumption habits (n = 240). RESULTS: Among conventional consumers, increasing tertile of estimated dietary OP exposure was associated with higher DAP concentrations (p < 0.05). DAP concentrations were also significantly lower in groups reporting more frequent consumption of organic produce (p < 0.02). CONCLUSIONS: Long-term dietary exposure to OPs was estimated from dietary intake data, and estimates were consistent with DAP measurements. More frequent consumption of organic produce was associated with lower DAPs. http://dx.doi.org/10.1289/ehp.140819

BACKGROUND: Previous studies suggest that certain dietary patterns and constituents may be beneficial to brain health. Airborne exposures to fine particulate matter [particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5)] are neurotoxic, but the combined effects of dietary patterns and PM2.5 have not been investigated. OBJECTIVES: We examined whether previously reported association between PM2.5 exposure and lower white matter volume (WMV) differed between women whose usual diet during the last 3 months before baseline was more or less consistent with a Mediterranean–DASH Intervention for Neurodegenerative Delay (MIND)-like diet, a dietary pattern that may slow neurodegenerative changes. METHODS: This study included 1,302 U.S. women who were 65–79 y old and free of dementia in the period 1996–1998 (baseline). In the period 2005–2006, structural brain magnetic resonance imaging (MRI) scans were performed to estimate normal-appearing brain volumes (excluding areas with evidence of small vessel ischemic disease). Baseline MIND diet scores were derived from a food frequency questionnaire. Three-year average PM2.5 exposure prior to MRI was estimated using geocoded participant addresses and a spatiotemporal model. RESULTS: Average total and temporal lobe WMVs were 0.74 cm³ [95% confidence interval (CI): 0.001, 1.48) and 0.19 cm³ (95% CI: 0.002, 0.37) higher, respectively, with each 0.5-point increase in the MIND score and were 4.16 cm³ (95% CI: -6.99, -1.33) and 1.46 cm³ (95% CI: -2.16, -0.76) lower, respectively, with each interquartile range (IQR) (IQR = 3.22 μg/m³) increase in PM2.5. The inverse association between PM2.5 per IQR and WMV was stronger (p-interaction <0.001) among women with MIND scores below the median (for total WMV, -12.47 cm³; 95% CI: -17.17, -7.78), but absent in women with scores above the median (0.16 cm³; 95% CI: -3.41, 3.72), with similar patterns for WMV in the frontal, parietal, and temporal lobes. For total cerebral and hippocampus brain volumes or WMV in the corpus callosum, the associations with PM2.5 were not significantly different for women with high MIND scores and women with low MIND scores. DISCUSSION: In this cohort of U.S. women, PM2.5 exposure was associated with lower MRI-based WMV, an indication of brain aging, only among women whose usual diet was less consistent with the MIND-like dietary pattern at baseline. [ABSTRACT FROM AUTHOR]

BACKGROUND: Episodic memory decline varies by age and underlying neuropathology. Whether ambient air pollution contributes to the heterogeneity of episodic memory decline in older populations remains unclear. OBJECTIVES: We estimated associations between air pollution exposures and episodic memory decline according to pollutant, exposure time window, age, and latent class subgroups defined by episodic memory trajectories. METHODS: Participants were from the Women's Health Initiative Memory Study-Epidemiology of Cognitive Health Outcomes. Older women (푛 = 2,056; 74-92 years of age) completed annual (2008-2018) episodic memory assessments using the telephone-based California Verbal Learning Test (CVLT). We estimated 3-y average fine particulate matter [PM with an aerodynamic diameter of = 2.5µm (PM2.5)] and nitrogen dioxide (NO2) exposures at baseline and 10 y earlier (recent and remote exposures, respectively), using regionalized national universal kriging. Separate latent class mixed models were used to estimate associations between interquartile range increases in exposures and CVLT trajectories in women ≤80 and >80 years of age, adjusting for covariates. RESULTS: Two latent classes were identified for women ≤80 years of age (푛 = 828), "slow-decliners" {slope=-0.12/y [95% confidence interval (CI): -0.23, -0.01] and "fast-decliners" [slope=-1.79/y (95% CI: -2.08, -1.50)]}. In the slow-decliner class, but not the fast-decliner class, PM2.5 exposures were associated with a greater decline in CVLT scores over time, with a stronger association for recent vs. remote exposures [-0.16/y (95% CI: -2.08, -0.03) per 2.88 μg/m³ and -0.11/y (95% CI: -0.22, 0.01) per 3.27μg/m³, respectively]. Among women ≥ 80 years of age (푛 = 1,128), the largest latent class comprised "steady-decliners" [slope=-1.35/y (95% CI: -1.53, -1.17)], whereas the second class, "cognitively resilient", had no decline in CVLT on average. PM2.5 was not associated with episodic memory decline in either class. A 6.25-ppb increase in recent NO2 was associated with nonsignificant acceleration of episodic memory decline in the = 80-y-old fast-decliner class [-0.21/y (95% CI: -0.45, 0.04)], and in the >80-y-old cognitively resilient class [-0.10/y (95% CI: -0.24, 0.03)] and steady-decliner class [-0.11/y (95% CI: -0.27, 0.05)]. Associations with recent NO2 exposure in women >80 years of age were stronger and statistically significant when 267 women with incident probable dementia were excluded [e.g., -0.12/y (95% CI: -0.22, -0.02) for the cognitively resilient class]. In contrast with changes in CVLT over time, there were no associations between exposures and CVLT scores during follow-up in any subgroup. DISCUSSION: In a community-dwelling U.S. population of older women, associations between late-life exposure to ambient air pollution and episodic memory decline varied by age-related cognitive trajectories, exposure time windows, and pollutants. [ABSTRACT FROM AUTHOR]

Introduction Chronic obstructive pulmonary disease (COPD) is one of the 10 most debilitating illnesses worldwide (Vos et al. 2012). In 2010, 329 million people were estimated to have COPD, with [...], Background: Air pollution is linked to low lung function and to respiratory events, yet little is known of associations with lung structure. Objectives: We examined associations of particulate matter ([PM.sub.2.5], [PM.sub.10]) and nitrogen oxides (N[O.sub.x]) with percent emphysema-like lung on computed tomography (CT). Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) recruited participants (45-84 years of age) in six U.S. states. Percent emphysema was defined as lung regions < -910 Hounsfield Units on cardiac CT scans acquired following a highly standardized protocol. Spirometry was also conducted on a subset. Individual-level 1- and 20-year average air pollution exposures were estimated using spatiotemporal models that included cohort-specific measurements. Multivariable regression was conducted to adjust for traditional risk factors and study location. RESULTS: Among 6,515 participants, we found evidence of an association between percent emphysema and long-term pollution concentrations in an analysis leveraging between-city exposure contrasts. Higher concentrations of [PM.sub.2.5] (5 µg/[m.sup.3]) and N[O.sub.x] (25 ppb) over the previous year were associated with 0.6 (95% CI: 0.1, 1.2%) and 0.5 (95% CI: 0.1, 0.9%) higher average percent emphysema, respectively. However, after adjustment for study site the associations were -0.6% (95% CI: -1.5, 0.3%) for [PM.sub.2.5] and -0.5% (95% CI: -1.1, 0.02%) for N[O.sub.x]. Lower lung function measures ([FEV.sub.1] and FVC) were associated with higher [PM.sub.2.5] and N[O.sub.x] levels in 3,791 participants before and after adjustment for study site, though most associations were not statistically significant. CONCLUSIONS: Associations between ambient air pollution and percentage of emphysema-like lung were inconclusive in this cross-sectional study, thus longitudinal analyses may better clarify these associations with percent emphysema. citation: Adar SD, Kaufman JD, Diez-Roux AV, Hoffman EA, D'Souza J, StukovskyKH, Rich SS, Rotter JI, Guo X, Raffel LJ, Sampson PD, Oron AP, Raghunathan T, Barr RG. 2015. Air pollution and percent emphysema identified by computed tomography in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:144-151; http://dx.doi.org/10.1289/ehp.1307951

Introduction A large body of observational studies has documented associations of air pollution with health outcomes including cardiovascular disease, pregnancy outcomes, and asthma and other respiratory problems in children (Brook [...], BACKGROUND: Although research has shown that low socioeconomic status (SES) and minority communities have higher exposure to air pollution, few studies have simultaneously investigated the associations of individual and neighborhood SES with pollutants across multiple sites. OBJECTIVES: We characterized the distribution of ambient air pollution by both individual and neighborhood SES using spatial regression methods. METHODS: The study population comprised 6,140 participants from the Multi-Ethnic Study of Atherosclerosis (MESA). Year 2000 annual average ambient [PM.sub.2.5] and N[O.sub.x] concentrations were calculated for each study participant's home address at baseline examination. We investigated individual and neighborhood (2000 U.S. Census tract level) SES measures corresponding to the domains of income, wealth, education, and occupation. We used a spatial intrinsic conditional autoregressive model for multivariable analysis and examined pooled and metropolitan area-- specific models. RESULTS: A 1-unit increase in the z-score for family income was associated with 0.03-µg/[m.sup.3] lower [PM.sub.2.5] (95% CI: -0.05, -0.01) and 0.93% lower N[O.sub.x] (95% CI: -1.33, - 0.53) after adjustment for covariates. A 1-SD--unit increase in the neighborhood's percentage of persons with at least a high school degree was associated with 0.47-µg/[m.sup.3] lower mean [PM.sub.2.5] (95% CI: -0.55, -0.40) and 9.61% lower N[O.sub.x] (95% CI: -10.85, -8.37). Metropolitan area--specific results exhibited considerable heterogeneity. For example, in New York, high-SES neighborhoods were associated with higher concentrations of pollution. CONCLUSIONS: We found statistically significant associations of SES measures with predicted air pollutant concentrations, demonstrating the importance of accounting for neighborhood- and individual-level SES in air pollution health effects research.

Introduction The relationship between air pollution and adverse health outcomes has been well documented (Pope et al. 2002; Samet et al. 2000). Many studies focus on particulate matter, specifically particulate [...], Background: Studies estimating health effects of long-term air pollution exposure often use a two-stage approach: building exposure models to assign individual-level exposures, which are then used in regression analyses. This requires accurate exposure modeling and careful treatment of exposure measurement error. Objective: To illustrate the importance of accounting for exposure model characteristics in two-stage air pollution studies, we considered a case study based on data from the Multi-Ethnic Study of Atherosclerosis (MESA). Methods: We built national spatial exposure models that used partial least squares and universal kriging to estimate annual average concentrations of four [PM.sub.2.5] components: elemental carbon (EC), organic carbon (OC), silicon (Si), and sulfur (S). We predicted [PM.sub.2.5] component exposures for the MESA cohort and estimated cross-sectional associations with carotid intima-media thickness (CIMT), adjusting for subject-specific covariates. We corrected for measurement error using recently developed methods that account for the spatial structure of predicted exposures. Results: Our models performed well, with cross-validated [R.sup.2] values ranging from 0.62 to 0.95. Naive analyses that did not account for measurement error indicated statistically significant associations between CIMT and exposure to OC, Si, and S. EC and OC exhibited little spatial correlation, and the corrected inference was unchanged from the naive analysis. The Si and S exposure surfaces displayed notable spatial correlation, resulting in corrected confidence intervals (CIs) that were 50% wider than the naive CIs, but that were still statistically significant. Conclusion: The impact of correcting for measurement error on health effect inference is concordant with the degree of spatial correlation in the exposure surfaces. Exposure model characteristics must be considered when performing two-stage air pollution epidemiologic analyses because naive health effect inference may be inappropriate. http://dx.doi.org/10.1289/ehp.1206010

Introduction Chronic bronchitis is a common clinical condition defined by chronic cough and sputum production for at least 3 mo in 2 or more consecutive years (American Thoracic Society 1995). [...], 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 Methods: We estimated annual average [PM.sub.2.5], [PM.sub.10, and N[O.sub.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.sub.10] [adjusted odds ratio (aOR) per interquartile range (IQR) difference (5.8 [micro]g/[m.sup.3]) = 1.07; 95% confidence interval (CI): 1.01, 1.13]. In never- smokers, [PM.sub.2.5] was associated with prevalent chronic bronchitis (aOR= 1.18 per IQR difference; 95% CI: 1.04, 1.34), and N[O.sub.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) Conclusions: [PM.sub.10] exposure was related to chronic bronchitis prevalence. Among never-smokers, [PM.sub.2.5] and N[O.sub.2] exposure was associated with chronic bronchitis and component symptoms. Results may have policy ramifications for [PM.sub.10] regulation by providing evidence for respiratory health effects related to long-term [PM.sub.10] exposure.