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Cardiovascular disease (CVD) and depression are the leading causes of disability in the U.S. Using five cycles (2009-2018) of the U.S. National Health and Nutrition Examination Survey, we examined the cross-sectional association between CVD risk factor burden and depression severity in nonpregnant adults with no history of CVD events.With at least 3000 participants per cycle, the overall N was 18,175. CVD risk factors were ascertained through self-report, lab tests, or medications. The sum of hypertension, diabetes, dyslipidemia, and current smoking represented a CVD risk score variable (range: 0-4). Depression severity was assessed using scores on the 9-item patient health questionnaire: 0-9 (none-mild) and 10-27 (moderate-to-severe). Logistic regression models were performed to investigate the association between CVD risk score categories and moderate-to-severe depression. Cycle-specific odds ratios (OR) were meta-analyzed to obtain a pooled OR (95 % CI) (Q-statistic p 0.05).Compared to participants with no CVD risk factors, participants with risk scores of 1, 2, 3, and 4, had 1.28 (0.92-1.77), 2.18 (1.62-2.94), 2.53 (1.86-3.49), 2.97 (1.67-5.31) times higher odds of moderate-to-severe depression, respectively, after adjusting for socio-demographics and antidepressant use (linear trend p 0.0001). This relationship persisted after additionally adjusting for lifestyle variables.NHANES data is cross-sectional and self-reported, thus preventing causal assessments and leading to potential recall bias.Among U.S. adults, CVD risk factor burden was associated with worsened depression symptoms. Integrated mental and physical healthcare services could improve risk stratification among persons with CVD and depression, possibly reducing long-term disability and healthcare costs.

Motor synergies, i.e., neural mechanisms that organize multiple motor elements to ensure stability of actions, are affected by several neurological condition. Asymptomatic welders showed impaired synergy controlling the stability of multi-finger action compared to non-welders and this impairment was associated with microstructural damage in the globus pallidus. We further explored the effect of welding-related metal exposure on multi-finger synergy and extended our investigation to posture-stabilizing synergy during a standing task. Occupational, MRI, and performance-stabilizing synergies during multi-finger accurate force production and load releasing while standing were obtained from 29 welders and 19 age- and sex-matched controls. R2* and R1 relaxation rate values were used to estimate brain iron and manganese content, respectively, and diffusion tensor imaging was used to reflect brain microstructural integrity. Associations of brain MRI (caudate, putamen, globus pallidus, and red nucleus), and motor synergy were explored by group status. The results revealed that welders had higher R2* values in the caudate (p = 0.03), putamen (p = 0.01), and red nucleus (p = 0.08, trend) than controls. No group effect was revealed on multi-finger synergy index during steady-state phase of action (ΔV

Lead is a nonessential metal and may be a coexposure in welding fumes. Preclinical data indicate lead may affect iron regulation. The current study investigated blood lead concentrations and their association with brain iron accumulation in workers with chronic welding fume exposure, with a focus on iron-rich subcortical regions of the cerebellum and basal ganglia. Occupational exposure, whole blood metal, and brain MRI data were obtained from 29 controls and 42 welders. R2* (1/T2*) and R1 (T1 relaxation rate) values were used to estimate brain iron and manganese content, respectively. Blood metals and brain R2* (in the red nucleus [RN], dentate nucleus, caudate, putamen, globus pallidus, and substantia nigra) were compared between groups. Associations between brain R2* values and exposure metrics were tested within each group, and analyses were adjusted for potential confounders. Welders had significantly higher levels of whole blood lead, manganese, iron, and copper. Welders also had higher R2* RN (p = .002), but not R1. A 2nd-order polynomial modeled the association between R2* RN and a long-term welding exposure metric. In welders, but not controls, R2* RN was associated positively with whole blood lead (r = 0.54, p = .003), and negatively with whole blood manganese (r = −0.43, p = .02). Higher blood Pb and lower blood Mn independently accounted for variance in high RN R2*. Together, these data suggest that higher RN R2* values may mark lead exposure in welders. Because lead is a known neurotoxicant, additional studies are warranted to confirm this finding, and ascertain its scientific and public/occupational health implications.

IntroductionMetal exposure has been associated with higher risk of neurodegenerative disorders such as Alzheimer’s disease (AD). We examined the potential link between welding-related metal co-exposure (e.g., Fe, Mn, Pb) and AD-related structural and neurobehavioral metrics.MethodsSubjects with (welders; n=42) or without (controls; n=31) a history of welding were examined. Metal exposure was estimated by exposure questionnaires and whole blood metal levels. Brain metal accumulations were estimated by MRI R1 (Mn) and R2* (Fe) in the caudate, putamen, globus pallidus, red nucleus (RN), and hippocampus. AD-related structural differences were assessed by volume and diffusion tensor imaging metrics in the hippocampus, and neurobehavioral aspects by learning/memory task scores.ResultsCompared to controls, welders displayed higher blood metal levels (p’s Story Recall scores (p=0.049), but no difference in volume or domain-wise learning/memory performance (p’s>0.117). Group differences in hippocampal MD and Story Recall scores were greater with higher RN R2* values (p’sDiscussionWelders had hippocampal structural and learning/memory performance differences similar to those in AD-at-risk populations. These AD-like differences in welders may, in part, be linked to Pb exposure reflected by higher RN R2* levels at the brain level.

The aim of this study was to determine whether long-standing racial disparities in lead exposure still exists for children age 1–5 years old. We examined if blood lead levels were higher among non-Hispanic Black children and others compared to non-Hispanic White children. Data from the National Health and Nutrition Examination Survey (NHANES) from 1999-2016 were used. Geometric mean blood lead levels (BLLs) were compared by race/ethnicity using log-transformed simple linear regression. Associations between race and elevated BLL were assessed using weighted Chi-square tests. Log-transformed multiple weighted linear regression was used to assess what factors affected BLLs. A total of 6772 children were included in this study. In 1999–2000, the geometric mean BLL for non-Hispanic Black children was 3.08 μg/dL, compared to 2.03 μg/dL for non-Hispanic White children (p = 0.01). The difference in geometric mean BLL between non-Hispanic Black children and non-Hispanic White children continued to be statistically significant in later years (all p < 0.05) until 2015-2016 (0.89 μg/dL vs 0.74 μg/dL, p = 0.17). Log-transformed linear regression showed that being non-Hispanic Black and having low family income were independently associated with higher BLL. Although lead exposure in the general population continued to decline for all racial/ethnic groups, non-Hispanic Black children still had higher BLL than non-Hispanic White children. In more recent years, the racial/ethnic gap was lesser but persisted. Racial/ethnic disparity in childhood BLL could be partially explained by socio-economic factors.

The aim of this study was to investigate the association between blood lead level (BLL) and hypertension in adults when lead exposure for the general population is low. The study used data from the US National Health and Nutrition Examination Survey (NHANES) 1999–2016. Participants aged 20 to 79 years were included in our study. Weighted multiple linear regression and logistic regression were conducted to test the association between BLL and systolic/diastolic blood pressure and hypertension status, respectively, while controlling for age, gender, race/ethnicity, body mass index, income level, and education. A total of 30,467 participants were included in this study. There was no association between BLL and hypertension status for the overall sample. Among those who were not taking antihypertensive medication, after adjusting for covariates, systolic blood pressure was positively correlated with BLL in non-Hispanic Whites (P = 0.004) and non-Hispanic Blacks (P = 0.0005), but not Hispanics (P = 0.07) nor Others (P = 0.37). The relationship between diastolic blood pressure and lead levels was also significant in non-Hispanic Whites and non-Hispanic Blacks. This study showed that higher BLL was associated with higher systolic and diastolic blood pressure in some population groups, but not associated with hypertension status.

BACKGROUND AND OBJECTIVES: Exposure to particulate matter (PM)

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no cure. Although the etiology of sporadic ALS is largely unknown, environmental exposures may affect ALS risk.We investigated relationships between exposure to long-term ambient particulate matter (PM) and gaseous air pollution (AP) and ALS mortality.Within the Women's Health Initiative (WHI) cohort of 161,808 postmenopausal women aged 50-79 years at baseline (1993-1998), we performed a nested case-control study of 256 ALS deaths and 2486 matched controls with emphasis on PM constituents (PMIn general, PMThis investigation adds to the body of information on long-term ambient AP exposure and ALS mortality. Specifically, the 2019 US Environmental Protection Agency (EPA) Integrated Science Assessment summarized the neurotoxic effects of PM

Objective: To examine the association between prevalent cardiovascular diseases (CVDs) and CVD risk factors and depression symptoms in a US general population sample. Methods: US adults in the 2013-14 and 2015-16 National Health and Nutrition Examination Survey were included. CVDs (coronary heart disease [CHD], congestive heart failure [CHF], stroke) and CVD risk factors: current smoking; hypertension [HTN]; diabetes mellitus [DM]; and dyslipidemia; systolic BP (SBP), HbA1C, fasting plasma glucose (FPG), serum cholesterol (C), triglycerides (TG), HDL-C, and LDL-C were based on patient-report or lab tests, or medication prescriptions. The sum of HTN, DM, dyslipidemia, and current smoking represented a CVD risk score variable (range: 0-4). Depression symptoms were assessed using the 9-item Patient Health Questionnaire (PHQ-9): 0-9 (none-mild); 10-27 (moderate-to-severe). Logistic regression models were used to assess the association between CVDs and moderate-to-severe depression. Results: A total of 12,105 participants (52% females, 64% Caucasians) of mean (SE) age of 46.8 (0.3) years and BMI of 29.2 (0.1) kg/m 2 were included. Moderate-to-severe depression was prevalent among 8.1% of participants. The proportions (%) of CVD risk score categories of 0-4 were: 20.5; 31.4; 32.1; 14.6; 1.5. After adjusting for age, race, sex, BMI, marital and educational status, participants with risk scores of 1; 2; 3; and 4 had 1.3 (95% CI: 0.8-2.1); 2.4 (1.5-3.7); 5.0 (3.2-7.8); and 5.5 (2.9-10.4) times higher odds of having moderate-to-severe depression, compared to those without CVD risk. One percent higher HbA1C and a five mg/dl decrease in HDL-C were associated with 1.1 (95% CI: 1.1-1.2) and 1.0 (95% CI: 1.0-1.1) times higher odds of having moderate-to-severe depression, respectively. Self-reported CHD; stroke; CHF; and any CVD were associated with 3.5 (1.8-6.7); 1.7 (0.7-3.9); 2.1 (1.3-3.4); and 2.1 (1.2-3.6) times higher odds of having moderate-to-severe depression, after additional adjustment for current smoking, LDL-C, SBP, and FPG. Conclusions: Prevalent CVDs and CVD risk factors are significantly associated with depression symptoms in the US general population, underscoring the need to integrate mental and physical healthcare services.

BackgroundShort-term variations in particulate matter (PM) and traffic-related air pollutants (e.g., nitrogen dioxide, NO2) have been associated with daily mortality and cardiovascular health outcomes in previous studies. We aimed to evaluate whether short-term changes in PM in three size fractions (PM2.5 , PM2.5-10 , and PM10) and NO2 were associated with systolic and diastolic arterial blood pressure (SBP and DBP, respectively) in the Women’s Health Initiative Observational Study (OS) and Clinical Trials (CT). MethodsWe used linear mixed-effect models to estimate the association between short-term air pollution concentrations and repeated measures of arterial blood pressure. ResultsWe found statistically significant positive associations between short-term measures (lag days 3-5) of PM2.5 as well as NO2 for both SBP and DBP in fully adjusted models when not controlling for calendar time. Also, in only the CT, PM10 and PM2.5-10 were associated with DBP but not SBP. In fully adjusted models controlling for calendar time, associations with PM2.5-10 and NO2 remained statistically significant for DBP (except for PM2.5-10 in the OS). Specifically, in the CT group, each IQR increase in lag 3-5 NO2 exposure (9.88 ppb) was associated with a 0.13 mm Hg increase in DBP. Also, each IQR increase in lag 3-5 PM2.5-10 exposure (8.46 µg m -3) was associated with a 0.05 mm Hg increase in DBP. Effect modification was found for body mass index (BMI), socioeconomic position (SEP), diabetes, dietary sodium intake, combined fruit and vegetable consumption, and long-term PM2.5 for PM2.5 , PM10 , and NO2 . Shorter lag periods (lag 0 through lag 2) typically exhibited lesser and, especially for SBP, sometimes negative associations. In two-pollutant models of exposures lagged over 3-5 days, NO2 associations with DBP were stronger (0.20 mm Hg per IQR), but those for PM2.5-10 were attenuated to null, as compared to single-pollutant models. ConclusionsOur findings are consistent with short-term (lag days 3-5) PM2.5-10 and NO2 levels as risk factors for acute cardiovascular outcomes and cardiovascular disease, though two-pollutant model results suggest NO2 is more likely responsible for the observed effects.

Background: Dementia is a devastating neurologic condition that is common in older adults. We previously reviewed the epidemiological evidence examining the hypothesis that long-term exposure to air pollution affects dementia risk. Since then, the evidence base has expanded rapidly. Objectives: With this update, we collectively review new and previously identified epidemiological studies on air pollution and late-life cognitive health, highlighting new developments and critically discussing the merits of the evidence. Methods: Using a registered protocol (PROSPERO 2020 CRD42020152943), we updated our literature review to capture studies published through 31 December 2020, extracted data, and conducted a bias assessment. Results: We identified 66 papers (49 new) for inclusion in this review. Cognitive level remained the most commonly considered outcome, and particulate matter (PM) remained the most commonly considered air pollutant. Since our prior review, exposure estimation methods in this research have improved, and more papers have looked at cognitive change, neuroimaging, and incident cognitive impairment/dementia, though methodological concerns remain common. Many studies continue to rely on administrative records to ascertain dementia, have high potential for selection bias, and adjust for putative mediating factors in primary models. A subset of 35 studies met strict quality criteria. Although high-quality studies of fine particulate matter with aerodynamic diameter ≤2.5μm (PM2.5) and cognitive decline generally supported an adverse association, other findings related to PM2.5 and findings related to particulate matter with aerodynamic diameter ≤10μm (PM10, NO2, and NOx) were inconclusive, and too few papers reported findings with ozone to comment on the likely direction of association. Notably, only a few findings on dementia were included for consideration on the basis of quality criteria. Discussion: Strong conclusions remain elusive, although the weight of the evidence suggests an adverse association between PM2.5 and cognitive decline. However, we note a continued need to confront methodological challenges in this line of research. https://doi.org/10.1289/EHP8716

Systemic inflammation may serve as a biological mechanism linking air pollution to poor health but supporting evidence from studies of long-term pollutant exposure and inflammatory cytokines is inconsistent.We studied associations between multiple particulate matter (PM) and gaseous air pollutants and pro- and anti-inflammatory cytokines within two nationwide cohorts of men and women.Data were obtained from 16,151 women in the Nurses' Health Study and 7,930 men in the Health Professionals' Follow-up Study with at least one measure of circulating adiponectin, C-Reactive Protein (CRP), Interleukin-6 (IL-6) or soluble tumor necrosis-factor receptor-2 (sTNFR-2). Exposure to PM with aerodynamic diameter ≤2.5, 2.5-10, and ≤10 μm (PMIn adjusted models, we observed a 2.72% (95% CI: 0.43%, 5.95%), 3.11% (-0.12%, 6.45%), and 3.67% (0.19%, 7.26%) increase in CRP associated with a 10 μg/mAcross multiple long-term pollutant exposures and inflammatory markers, associations were generally weak. Focusing on specific pollutant-inflammatory mechanisms may clarify pathways.

Epigenetic mechanisms may underlie air pollution-health outcome associations. We estimated gaseous air pollutant-DNA methylation (DNAm) associations using twelve subpopulations within Women's Health Initiative (WHI) and Atherosclerosis Risk in Communities (ARIC) cohorts (n = 8397; mean age 61.3 years; 83% female; 46% African-American, 46% European-American, 8% Hispanic/Latino). We used geocoded participant address-specific mean ambient carbon monoxide (CO), nitrogen oxides (NO2; NOx), ozone (O3), and sulfur dioxide (SO2) concentrations estimated over the 2-, 7-, 28-, and 365-day periods before collection of blood samples used to generate Illumina 450 k array leukocyte DNAm measurements. We estimated methylome-wide, subpopulation- and race/ethnicity-stratified pollutant-DNAm associations in multi-level, linear mixed-effects models adjusted for sociodemographic, behavioral, meteorological, and technical covariates. We combined stratum-specific estimates in inverse variance-weighted meta-analyses and characterized significant associations (false discovery rate; FDR 0.05). We attempted replication in the Cooperative Health Research in Region of Augsburg (KORA) study and Normative Aging Study (NAS). We observed a -0.3 (95% CI: -0.4, -0.2) unit decrease in percent DNAm per interquartile range (IQR, 7.3 ppb) increase in 28-day mean NO2 concentration at cg01885635 (chromosome 3; regulatory region 290 bp upstream from ZNF621; FDR = 0.03). At intragenic sites cg21849932 (chromosome 20; LIME1; intron 3) and cg05353869 (chromosome 11; KLHL35; exon 2), we observed a -0.3 (95% CI: -0.4, -0.2) unit decrease (FDR = 0.04) and a 1.2 (95% CI: 0.7, 1.7) unit increase (FDR = 0.04), respectively, in percent DNAm per IQR (17.6 ppb) increase in 7-day mean ozone concentration. Results were not fully replicated in KORA and NAS. We identified three CpG sites potentially susceptible to gaseous air pollution-induced DNAm changes near genes relevant for cardiovascular and lung disease. Further harmonized investigations with a range of gaseous pollutants and averaging durations are needed to determine the effect of gaseous air pollutants on DNA methylation and ultimately gene expression.

Purpose: Stroke is a leading cause of mortality worldwide, and air pollution is the third largest contributor to global stroke burden. Existing studies investigating the association between long-term exposure to particulate matter (PM) and stroke incidence have been mixed and very little is known about the associations with medium-term exposures. Therefore, we wanted to evaluate these associations in an cohort of male health professionals. Methods: We assessed the association of PM exposures in the previous 1 and 12 months with incident total, ischemic, and hemorrhagic stroke in 49,603 men in the prospective US-based Health Professionals’ Follow-up Study 1988–2007. We used spatiotemporal prediction models to estimate monthly PM less than 10 (PM10) and less than 2.5 (PM2.5), and PM2.5–10 at all mailing addresses. We used time-varying Cox proportional hazards models adjusted for potential confounders based on previous literature to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for each 10-μg/m3 increase in exposure in the preceding 1 and 12 months. We explored possible effect modification by age, obesity, smoking, aspirin use, diet quality, physical activity, diabetes, and Census region. Results: We observed 1,467 cases of incident stroke. Average levels of 12-month PM10, PM2.5–10, and PM2.5 were 20.7, 8.4, and 12.3 µg/m3, respectively. In multivariable adjusted models, we did not observe consistent associations between PM and overall or ischemic stroke. There was a suggestion of increased risk of hemorrhagic stroke (12-month PM10 multivariable HR: 1.13 [0.86, 1.48]; PM2.5–10: 1.12 [0.78, 1.62]; PM2.5:1.17 [0.76, 1.81], all per 10 µg/m3). There was little evidence of effect modification. Conclusions: We observed only weak evidence of an association between long-term exposure to PM and risks of overall incident stroke. There was a suggestion of increasing hemorrhagic stroke risk., In this US-wide study of male health professionals, particulate matter was only weakly associated with increased risk of stroke. Supplemental Digital Content is available in the text.

PURPOSE OF REVIEW We identified 24 publications from January 2010 until September 2018 in the peer-reviewed literature addressing the relationship of long-term air pollution exposures and type 2 diabetes-related morbidity and mortality among adults. We examine key methodological issues, synthesize findings, and address study strengths and limitations. We also discuss biological mechanisms, policy implications, and future research needed to address existing knowledge gaps. RECENT FINDINGS In general, the studies included in this review employed rigorous methodology with large sample sizes, appropriate study designs to maximize available cohort study or administrative data sources, and exposure modeling that accounted for spatial patterns in air pollution levels. Overall, studies suggested increased risks of type 2 diabetes-related morbidity and mortality among adults associated with increased exposures; however, findings were not uniformly positive nor statistically significant. SUMMARY Current research is particularly limited regarding the biological mechanisms involved and the relationship between ozone and diabetes. Additionally, more research is needed to distinguish clearly the effects of nitrogen oxides from those of other pollutants and to identify potential subpopulations with greater susceptibility for certain pollutant exposures. A better understanding of the potential link between long-term ambient air pollution exposures and type 2 diabetes may provide opportunities for the reduction of health risks and inform future interventions for environmental protection and diabetes management.

Chronic high-level manganese (Mn)-induced neurotoxicity has been associated with Mn accumulation in the basal ganglia and higher risk for developing parkinsonism. Recent studies in Mn-exposed animals revealed Mn accumulation in the hippocampus, the presence of Aβ diffuse plaques, and deficits in associative learning, the latter being hallmarks of Alzheimer’s disease (AD) or related disorders. This and recent evidence of hippocampal Mn accumulation in welders prompted us to test the hypothesis that welders with chronic Mn exposure would display changes in the hippocampus. Subjects with (welders; n = 42) or without (controls; n = 31) welding history were studied. Mn exposure was estimated by occupational questionnaires, whole blood Mn, and R1 imaging (estimate of short-term brain Mn accumulation). Hippocampal diffusion tensor imaging (DTI; estimate of microstructural brain changes) and volume were determined. Compared with controls, welders displayed no significant difference in hippocampal volume (p = .165). Welders, however, exhibited higher DTI hippocampal mean diffusivity (MD) values compared with controls (p = .035) that was evident particularly in older welders (>50 years, p = .002). Hippocampal MD was associated significantly with age in welders (R = 0.59; p

Introduction: Fine particulate (PM 2.5 ) exposure has been related to higher propensity of arrhythmias in adults. However, the association between PM 2.5 exposure and arrhythmia in adolescents remains unclear. Hypothesis: PM 2.5 exposure is related to an acute increase in numbers of arrhythmic heartbeats in adolescents. Methods: We used data collected from 421 adolescents in the Penn State Child Cohort (PSCC) follow-up examination for this report. From each participant, we obtained 24-hour beat-to-beat ECG data using a 12-lead Holter ECG. From which, arrhythmias, including premature ventricular contraction (PVC) and premature atrial contraction (PAC), were identified. The number of PVCs and PACs every 30 minutes were analyzed with individual-level 30-minute average PM 2.5 concentrations obtained by using a personal minute-by-minute PM 2.5 monitor for 24 hours in parallel to the ECG. Thus, each participant contributed 48 30-minute segments of arrhythmia and PM 2.5 data. Polynomial distributed lag models within a framework of a negative binomial model were used to assess the segment-specific and cumulative effect of PM 2.5 concentration on numbers of PVC and PAC, adjusting for age, race, sex, BMI percentile, temperature, and humidity. Results: The mean (SD) age of PSCC was 16.9 (2.2) years, with 54% males, and 78% whites. The 30-minute mean (SD) of PM 2.5 concentration was 14.4 (45.4) μg/m 3 , while PVC and PAC counts were 0.2 (2.0) and 0.5 (4.0). As shown in the table, 10 μg/m 3 increases in PM 2.5 concentration 0.5-2.0 hours prior to the ECG measures (lags 1-3) each were associated with 2% increase in PVC counts (all p3 increment in PM 2.5 was associated with a 5% (1% - 10%) increase in PVC counts within 2 hours after exposure. PM 2.5 was not related to PAC counts. Conclusion: Individual-level exposure to PM 2.5 is associated with an acute increased number of ventricular arrhythmia in population-based adolescents. The time course of the effect of PM 2.5 on ventricular arrhythmia is within 2 hours after exposure.

Introduction: Sleep deprivation and large sleep variability are potential risk factors for obesity and cardiovascular diseases. While it is plausible that particulate air pollution may contribute to these unfavorable sleep patterns, very few studies have been conducted to assess the association between fine particulate (PM 2.5 ) air pollution and objectively measured sleep duration and its variability in an adolescent U.S. population. Hypothesis: We tested the hypothesis that higher individual-level short-term PM 2.5 exposure is associated with shorter sleep duration and higher sleep variability among adolescents. Methods: We analyzed the available data collected from 421 adolescents who participated in the follow-up examination of the population-based Penn State Child Cohort (PSCC) study. To estimate individual-level short-term PM 2.5 exposure, a personal nephelometer (Thermo pDR-1200) was used to measure real-time PM 2.5 concentration for 24 hours from the study participants. The 24-hour mean PM 2.5 concentration was used to quantify the short-term PM 2.5 exposure. To obtain objectively-measured habitual sleep duration (HSD) and habitual sleep variability (HSV), an actigraphy (GT3X+) was used to collect sleep data for 7 consecutive nights, including 1 night in parallel with the PM 2.5 monitoring and 6 nights thereafter. HSD and HSV were calculated as the intra-individual mean and standard deviation (SD) of the 7-night sleep duration, respectively. Participants with < 5 nights (70% of 7 nights) of data were excluded from the analyses. The associations between the individual-level PM 2.5 exposure and HSD/HSV were evaluated by using multi-variable adjusted linear regression models, controlling for age, race, sex, BMI percentile, environmental temperature, and relative humidity. Results: The mean (SD) age of the study population was 16.9 (2.2) years. The study sample consisted of 54% males and 78% whites. The 24-hour mean (SD) of PM 2.5 concentration was 16.9 (26.8) μg/m 3 , while the average HSD and HSV were 7.0 (0.9) hours and 1.2 (0.6) hours, respectively. We observed that a 10 μg/m 3 increase in the 24-hour mean PM 2.5 was associated with significantly lower HSD [β (SE): -0.06 (0.03) hours, p=0.02] and larger HSV [β (SE): 0.04 (0.02) hours, p=0.04]. The effect sizes were approximately 7% of their respective SDs. Conclusion: Individual-level short-term PM 2.5 exposure is associated with objective-measured shorter sleep duration and higher night-to-night sleep variability among U.S. adolescents. These observed associations suggest that particulate air pollution exposure in early life may impact habitual sleep pattern, which may in turn be associated with the risks of obesity and cardiovascular diseases in later life.

Background/Aim: Since our prior review in 2016, the epidemiologic evidence examining the association between long-term exposure to air pollution and dementia and dementia-related outcomes has grown...

Background Atmospheric particulate matter (PM) has been associated with endothelial dysfunction, an early marker of cardiovascular risk. Our aim was to extend this research to a genetically homogenous, geographically stable rural population using location-specific moving-average air pollution exposure estimates indexed to the date of endothelial function measurement. Methods We measured endothelial function using brachial artery flow-mediated dilation (FMD) in 615 community-dwelling healthy Amish participants. Exposures to PM

The aim of this study was to investigate the association between blood lead level (BLL) and hypertension in adults when lead exposure for the general population is low. The study used data from the US National Health and Nutrition Examination Survey (NHANES) 1999-2016. Participants aged 20 to 79 years were included in our study. Weighted multiple linear regression and logistic regression were conducted to test the association between BLL and systolic/diastolic blood pressure and hypertension status, respectively, while controlling for age, gender, race/ethnicity, body mass index, income level, and education. A total of 30,467 participants were included in this study. There was no association between BLL and hypertension status for the overall sample. Among those who were not taking antihypertensive medication, after adjusting for covariates, systolic blood pressure was positively correlated with BLL in non-Hispanic Whites (P = 0.004) and non-Hispanic Blacks (P = 0.0005), but not Hispanics (P = 0.07) nor Others (P = 0.37). The relationship between diastolic blood pressure and lead levels was also significant in non-Hispanic Whites and non-Hispanic Blacks. This study showed that higher BLL was associated with higher systolic and diastolic blood pressure in some population groups, but not associated with hypertension status.

The aim of this study was to determine whether long-standing racial disparities in lead exposure still exists for children age 1-5 years old. We examined if blood lead levels were higher among non-Hispanic Black children and others compared to non-Hispanic White children.Data from the National Health and Nutrition Examination Survey (NHANES) from 1999-2016 were used. Geometric mean blood lead levels (BLLs) were compared by race/ethnicity using log-transformed simple linear regression. Associations between race and elevated BLL were assessed using weighted Chi-square tests. Log-transformed multiple weighted linear regression was used to assess what factors affected BLLs.A total of 6772 children were included in this study. In 1999-2000, the geometric mean BLL for non-Hispanic Black children was 3.08 μg/dL, compared to 2.03 μg/dL for non-Hispanic White children (p = 0.01). The difference in geometric mean BLL between non-Hispanic Black children and non-Hispanic White children continued to be statistically significant in later years (all p0.05) until 2015-2016 (0.89 μg/dL vs 0.74 μg/dL, p = 0.17). Log-transformed linear regression showed that being non-Hispanic Black and having low family income were independently associated with higher BLL.Although lead exposure in the general population continued to decline for all racial/ethnic groups, non-Hispanic Black children still had higher BLL than non-Hispanic White children. In more recent years, the racial/ethnic gap was lesser but persisted. Racial/ethnic disparity in childhood BLL could be partially explained by socio-economic factors.

Background: Inflammatory effects of ambient particulate matter (PM) air pollution exposures may underlie PM-related increases in cardiovascular disease risk and mortality, although evidence of PM-associated leukocytosis is inconsistent and largely based on small, cross-sectional, and/or unrepresentative study populations. Objectives: Our objective was to estimate PM–leukocyte associations among U.S. women and men in the Women’s Health Initiative and Atherosclerosis Risk in Communities study (n=165,675). Methods: We based the PM–leukocyte estimations on up to four study visits per participant, at which peripheral blood leukocytes and geocoded address-specific concentrations of PM≤10, ≤2.5, and 2.5–10μm in diameter (PM10, PM2.5, and PM2.5–10, respectively) were available. We multiply imputed missing data using chained equations and estimated PM–leukocyte count associations over daily to yearly PM exposure averaging periods using center-specific, linear, mixed, longitudinal models weighted for attrition and adjusted for sociodemographic, behavioral, meteorological, and geographic covariates. In a subset of participants with available data (n=8,457), we also estimated PM–leukocyte proportion associations in compositional data analyses. Results: We found a 12 cells/μL (95% confidence interval: −9, 33) higher leukocyte count, a 1.2% (0.6%, 1.8%) higher granulocyte proportion, and a −1.1% (−1.9%, −0.3%) lower CD8+ T-cell proportion per 10-μg/m3 increase in 1-month mean PM2.5. However, shorter-duration PM10 exposures were inversely and only modestly associated with leukocyte count. Discussion: The PM2.5–leukocyte estimates, albeit imprecise, suggest that among racially, ethnically, and environmentally diverse U.S. populations, sustained, ambient exposure to fine PM may induce subclinical, but epidemiologically important, inflammatory effects. https://doi.org/10.1289/EHP5360

Background: Domestic violence is a prevalent global health issue that causes incredibly adverse consequences for an individual’s physical and psychological health. The rates of physical and sexual violence in developing countries are thought to be some of the highest in the world, where up to 44% of women in Sub-Saharan Africa have experienced domestic violence. However, this has not been explored systematically. We present the first study to estimate the incidence and prevalence of physical and sexual violence across Africa. Methods: Poisson meta-regression analysis on demographic health survey data from 482,670 women from 442,507 households in 30 countries across Africa. Hotspot analysis using the Getis-ORD Gi approach at the sub-regional level. Findings: Of 482,670 women, those who were divorced or separated were approximately 7 times more likely to experience physical violence and 6 times more likely to experience sexual violence compared to those who were never married (Risk Ratio: RRs:7.35, 95%CI 7.16-7.54 and 5.89, 95%CI 5.75-6.02 respectively). Likewise, wealth index and education level were inversely related to the incidence and prevalence of sexual and physical violence. Hotspots of sexual and physical violence were identified in Congo and surrounding areas. Interpretation: Interventions should be designed to address the high levels of physical and sexual violence in Congo and surrounding areas, especially in those who are less educated, have lower wealth indices, and are divorced or separated. Funding: The USAID funded the Demographic and Health Survey collection. However, the funders played no role in the conceptualization, data analysis, or writing of this manuscript. Declaration of Interests: The authors report no competing interest. Ethics Approval Statement: Each country’s ethical review committee and institutional review board of OCF International, USA reviewed and approved the DHS protocol and guideline. Informed consent was collected prior to the survey being given. Data were de-identified and are publically available upon request; therefore, the authors did not need to seek any further clearance.

Numerous studies document increased health risks from exposure to traffic and traffic-related particulate matter (PM). However, many studies use simple exposure metrics to represent traffic-related PM, and/or are limited to small geographic areas over relatively short (e.g., 1 year) time periods. We developed a modeling approach for the conterminous US from 1999 to 2011 that applies a line-source Gaussian plume dispersion model using several spatially and/or temporally varying inputs (including daily meteorology) to produce high spatial resolution estimates of primary near-road traffic-related PM levels. We compared two methods of spatially averaging traffic counts: spatial smoothing generalized additive models and kernel density. Also, we evaluated and validated the output from the line-source dispersion modeling approach in a spatio-temporal model of 24-h average PM

OBJECTIVE: We investigated the effects of chronic exposures to particulate and traffic-related air pollution on allostatic load (AL) score, a marker of cumulative biological risk, among youth with type 1 diabetes. RESEARCH DESIGN AND METHODS: Participants were drawn from five clinical sites of the SEARCH for Diabetes in Youth (SEARCH) study (n=2,338). Baseline questionnaires, anthropometric measures, and a fasting blood test were taken at a clinic visit between 2001 and 2005. AL was operationalized using 10 biomarkers reflecting cardiovascular, metabolic, and inflammatory risk. Annual residential exposures to PM(2.5) and proximity to heavily-trafficked major roadways were estimated for each participant. Poisson regression models adjusted for sociodemographic and lifestyle factors were conducted for each exposure. RESULTS: No significant associations were observed between exposures to PM(2.5) or proximity to traffic and AL score, however analyses were suggestive of effect modification by race for residential distance to heavily-trafficked major roadways (p=0.02). In stratified analyses, residing

Background: Evidence of the association between daily variation in air pollution and risk of stroke is inconsistent, potentially due to the heterogeneity in stroke etiology. Objectives: To estimate the associations between daily variation in ambient air pollution and risk of stroke and its subtypes among participants of the Women's Health Initiative, a large prospective cohort study in the United States. Methods: We used national-scale, log-normal ordinary kriging models to estimate daily concentrations of fine particulate matter (PM2.5), respirable particulate matter (PM10), nitrogen dioxide (NO2), nitrogen oxides (NOx), sulphur dioxide, and ozone at participant addresses. Stroke was adjudicated by trained neurologists and classified as ischemic or hemorrhagic. Ischemic strokes were further classified according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) classification. We used a time-stratified case-crossover approach to estimate the odds ratio (OR) of the risk of stroke associated with an interquartile range (IQR) increase in concentrations of each air pollutant. We performed stratified analysis to examine whether associations varied across subgroups defined by age at stroke onset, US census region, smoking status, body mass index, and prior history of diabetes mellitus, hypertension, heart or circulation problems, or arterial fibrillation at enrollment. Results: Among 5417 confirmed strokes between 1993 and 2012, 4300 (79.4%) were classified as ischemic and 924 (17.1%) as hemorrhagic. No association was observed between day-to-day variation in any pollutant and risk of total stroke, ischemic stroke, or specific etiologies of ischemic stroke. We observed a positive association between risk of hemorrhagic stroke and NO2 and NOx in the 3 days prior to stroke with OR of 1.24 (95% CI: 1.01, 1.52) and 1.18 (95% CI: 1.03, 1.34) per IQR increase, respectively. The observed associations with hemorrhagic stroke were more pronounced among non-obese participants. Conclusions: In this large cohort of post-menopausal US women, daily NO2 and NOx were associated with higher risk of hemorrhagic stroke, but ambient levels of four other air pollutants were not associated with higher risk of total stroke, ischemic stroke, or ischemic stroke subtypes. Keywords: Air pollution, Hemorrhagic stroke, Ischemic stroke, Case-crossover, United States

Background: Emerging studies suggest that ambient temperature during pregnancy may be associated with fetal growth, but the existing evidence is limited and inconsistent. Objectives: We aimed to evaluate the association of trimester-specific temperature with risk of being born small for gestational age (SGA) and birth weight—markers of fetal growth—among term births in the contiguous United States. Methods: We included data on 29,597,735 live singleton births between 1989 and 2002 across 403 U.S. counties. We estimated daily county-level population-weighted mean temperature using a spatially refined gridded climate data set. We used logistic regression to estimate the association between trimester-specific temperature and risk of SGA and linear regression to evaluate the association between trimester-specific temperature and term birth weight z-score, adjusting for parity, maternal demographics, smoking or drinking during pregnancy, chronic hypertension, and year and month of conception. We then pooled results overall and by geographic regions and climate zones. Results: High ambient temperatures (>90th percentile) during the entire pregnancy were associated with higher risk of term SGA {odds ratio [OR] = 1.041 [95% confidence interval (CI): 1.029, 1.054]} and lower term birth weight [standardized to −15g (95% CI: −17g, −13g) reduction in birth weight for infants born at 40 weeks of gestation]. Low temperatures (≤10th percentile) during the entire pregnancy were not associated with SGA [OR = 1.003 (95% CI: 0.991, 1.015)] but were associated with a small decrement in term birth weight [standardized to −6g (95% CI: −8g, −4g)]. Risks of term SGA and birth weight were more strongly associated with temperature averaged across the second and third trimesters, in areas the Northeast, and in areas with cold or very cold climates. Conclusions: Above-average temperatures during pregnancy were associated with lower fetal growth. Our findings provide evidence that temperature may be a novel risk factor for reduced fetal growth. https://doi.org/10.1289/EHP4648