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Transnational immigration has increased since the 1950s. In countries such as the United States, immigrants now account forWe summarized current knowledge comparing immigrants' and nonimmigrants' exposure to and health effects of environmental exposures.We conducted a title and abstract review on articles identified through PubMed and selected those that assessed environmental exposures or health effects separately for immigrants and nonimmigrants. After a full text review, we extracted the main findings from eligible studies and categorized each article as exposure-focused, health-focused, or both. We also noted each study's exposure of interest, study location, exposure and statistical methods, immigrant and comparison groups, and the intersecting socioeconomic characteristics controlled for.We conducted a title and abstract review on 3,705 articles, a full text review on 84, and extracted findings from 50 studies. There were 43 studies that investigated exposure (e.g., metals, organic compounds, fine particulate matter, hazardous air pollutants) disparities, but only 12 studies that assessed health disparities (e.g., mortality, select morbidities). Multiple studies reported higher exposures in immigrants compared with nonimmigrants. Among immigrants, studies sometimes observed exposure disparities by country of origin and time since immigration. Of the 50 studies, 43 were conducted in North America.The environmental health of immigrants remains an understudied area, especially outside of North America. Although most identified studies explored potential exposure disparities, few investigated subsequent differences in health effects. Future research should investigate environmental health disparities of immigrants, especially outside North America. Additional research gaps include the role of immigrants' country of origin and time since immigration, as well as the combined effects of immigrant status with intersecting socioeconomic characteristics, such as race/ethnicity, income, and education attainment. https://doi.org/10.1289/EHP9855.

Particulate matter with aerodynamic diameter no larger than 2.5 µm (PM2.5) has been linked to cardiovascular diseases (CVDs) but evidence for vulnerability by sex remains unclear. We performed systematic review and meta-analysis to synthesize the state of scientific evidence on whether cardiovascular risks from PM2.5 differ for men compared to women. The databases Pubmed, Scopus, Embase, and GreenFILE were searched for studies published January 1995 to February 2020. Observational studies conducting subgroup analysis by sex for impacts of short-term or long-term exposure to PM2.5 on target CVDs were included. Data were independently extracted in duplicate and pooled with random-effects meta-regression. Risk ratios (RRs) for long-term exposure and percent changes in outcomes for short-term exposure were calculated per 10 µg m−3 PM2.5 increase. Quality of evidence of risk differences by sex was rated following Grading of Recommendations Assessment, Development and Evaluation (GRADE). A total of 12 502 articles were screened, with 61 meeting inclusion criteria. An additional 32 studies were added from citation chaining. RRs of all CVD mortality for long-term PM2.5 for men and women were the same (1.14; 95% CI: 1.09, 1.22) indicating no statistically different risks. Men and women did not have statistically different risks of daily CVD mortality, hospitalizations from all CVD, ischemic heart disease, cardiac arrest, acute myocardial infarction, and heart failure from short-term PM2.5 exposure (difference in % change in risk per 10 µg m−3 PM2.5: 0.04 (95% CI, −0.42–0.51); −0.05 (−0.47–0.38); 0.17 (−0.90, 1.24); 1.42 (−1.06, 3.97); 1.33 (−0.05, 2.73); and −0.48 (−1.94, 1.01), respectively). Analysis using GRADE found low or very low quality of evidence for sex differences for PM2.5-CVD risks. In conclusion, this meta-analysis and quality of evidence assessment of current observational studies found very limited evidence of the effect modification by sex for effects of PM2.5 on CVD outcomes in adults, which can inform clinical approaches and policies.

Greenhouse gas emissions are changing the Earth's climate, most directly by modifying temperatures and temperature variability (TV). Residents of low- and middle-income countries (LMICs) are likely more adversely affected, due to lack of air conditioning to compensate. To date, there is no local epidemiological evidence documenting the cardio-respiratory health effects of TV in Dhaka, Bangladesh, one of the most climate change vulnerable cities in the world.We assessed short-term TV associations with daily cardiovascular disease (CVD) and respiratory emergency department (ED) visits, as well as effect modification by age and season.TV was calculated from the standard deviations of the daily minimum and maximum temperatures over exposure days. Time-series regression modeling was applied to daily ED visits for respiratory and CVD from January 2014 through December 2017. TV effect sizes were estimated after controlling for long-term trends and seasonality, day-of-week, holidays, and daily mean relative humidity and ambient temperature.A 1 °C increase in TV was associated with a 1.00% (95 %CI: 0.05%, 1.96%) increase in CVD ED visits at lag 0-1 days (TVThis study provided novel and important evidence that cardio-pulmonary health in Dhaka is adversely affected year-round by day-to-day increases in TV, especially among older adults. TV is a key factor that should be considered in evaluating the potential human health impacts of climate change induced temperature changes.

Background Ambient air pollution is a modifiable risk factor for cardiovascular disease, yet uncertainty remains about the size of risks at lower levels of fine particulate matter (PM2.5) exposure which now occur in the USA and elsewhere. Methods We investigated the relationship of ambient PM2.5 exposure with cause-specific cardiovascular disease mortality in 565 477 men and women, aged 50 to 71 years, from the National Institutes of Health-AARP Diet and Health Study. During 7.5 x 106 person-years of follow up, 41 286 cardiovascular disease deaths, including 23 328 ischaemic heart disease (IHD) and 5894 stroke deaths, were ascertained using the National Death Index. PM2.5 was estimated using a hybrid land use regression (LUR) geostatistical model. Multivariate Cox regression models were used to estimate relative risks (RRs) and 95% confidence intervals (CI). Results Each increase of 10 μg/m3 PM2.5 (overall range, 2.9–28.0 μg/m3) was associated, in fully adjusted models, with a 16% increase in mortality from ischaemic heart disease [hazard ratio (HR) 1.16; 95% CI 1.09-1.22] and a 14% increase in mortality from stroke (HR 1.14; CI 1.02-1.27). Compared with PM2.5 exposure Conclusions Long-term exposure to fine particulate air pollution is associated with ischaemic heart disease and stroke mortality, with excess risks occurring in the range of and below the present US long-term standard for ambient exposure to PM2.5 (12 µg/m3), indicating the need for continued improvements in air pollution abatement for CVD prevention.

Human mobility is a significant factor for disease transmission. Little is known about how the environment influences mobility during a pandemic. The aim of this study was to investigate an effect of green space on mobility reductions during the early stage of the COVID-19 pandemic in Maryland and California, USA. For 230 minor civil divisions (MCD) in Maryland and 341 census county divisions (CCD) in California, we obtained mobility data from Facebook Data for Good aggregating information of people using the Facebook app on their mobile phones with location history active. The users’ movement between two locations was used to calculate the number of users that traveled into an MCD (or CCD) for each day in the daytime hours between 11 March and 26 April 2020. Each MCD’s (CCD’s) vegetation level was estimated as the average Enhanced Vegetation Index (EVI) level for 1 January through 31 March 2020. We calculated the number of state and local parks, food retail establishments, and hospitals for each MCD (CCD). Results showed that the daily percent changes in the number of travels declined during the study period. This mobility reduction was significantly lower in Maryland MCDs with state parks (p-value = 0.045), in California CCDs with local-scale parks (p-value = 0.048). EVI showed no association with mobility in both states. This finding has implications for the potential impacts of green space on mobility under an outbreak. Future studies are needed to explore these findings and to investigate changes in health effects of green space during a pandemic.

Ubiquitin mediated signaling contributes critically to host cell defenses during pathogen infection. Many pathogens manipulate the ubiquitin system to evade these defenses. Here we characterize a likely effector protein bearing a deubiquitylase (DUB) domain from the obligate intracellular bacterium Orientia tsutsugamushi, the causative agent of scrub typhus. The Ulp1-like DUB prefers ubiquitin substrates over ubiquitin-like proteins and efficiently cleaves polyubiquitin chains of three or more ubiquitins. The co-crystal structure of the DUB (OtDUB) domain with ubiquitin revealed three bound ubiquitins: one engages the S1 site, the second binds an S2 site contributing to chain specificity and the third binds a unique ubiquitin-binding domain (UBD). The UBD modulates OtDUB activity, undergoes a pronounced structural transition upon binding ubiquitin, and binds monoubiquitin with an unprecedented ~5 nM dissociation constant. The characterization and high-resolution structure determination of this enzyme should aid in its development as a drug target to counter Orientia infections., Many pathogens manipulate ubiquitin-mediated signaling to evade host cell defense. Here, the authors characterize the structure and enzymatic activity of a deubiquitylase domain from the causative pathogen of scrub typhus, providing evidence for a distinct mechanism of ubiquitin chain selectivity.

While a growing body of literature suggests beneficial impacts of greenness on several health outcomes, relatively few studies have examined greenness as an effect modifier to impacts of air pollution on health outcomes, and results from the existing studies are inconclusive. We performed a comprehensive, systematic review of previous literature on greenness as a potential effect modifier for associations between particulate matter air pollution and health. After initial screening of 7814 studies, we identified 20 eligible studies. We summarized findings on study characteristics based on several criteria: health outcome, air pollution exposure, source of air pollution data, study location, study period, and median year of the study period. We evaluated characteristics of effect modification by greenness on air pollution and health associations based on the number of greenness metrics applied, type of greenness metric (e.g. normalized difference vegetation index, land use), data source for greenness, and spatial resolution and buffer size. We also summarized evidence for effect modification by greenness based on strength and direction of evidence for each study and overall evidence of effect modification by greenness by several study characteristics. Our systematic review showed that only a limited number of studies have been conducted on greenness as an effect modifier for air pollution-health associations. We found differences in several study characteristics such as greenness assessment (e.g. greenness metrics applied, spatial resolution, and data sources) across studies. Collectively, the studies provide suggestive evidence for the hypothesis that areas with high greenness have lower impacts of air pollution on health, although some studies reported inconsistent findings. The findings from our review provide valuable knowledge on how greenness affects associations between air pollution and health and could help identify critical areas for future study.

Background The predictive coding framework of perception postulates that we automatically infer what is around us by combining our sensory input with our prior beliefs. Mathematical models based in Bayesian statistics can describe this process, elucidating both typical as well as atypical brain processes, such as emergence of hallucinations. A previous study using a Pavlovian conditioning task showed that hallucinations are a result of over-weighting of prior beliefs over incoming sensory evidence. Participants with Auditory Verbal Hallucinations (AVH) were more susceptible to auditory conditioned hallucinations (ACH) than individuals without AVH, regardless of a diagnosis of psychosis. This suggests a common underlying mechanism for the emergence of hallucinations irrespective of functional status. To further investigate these mechanisms, we developed a visual conditioned hallucinations (VCH) task, modeled after the original ACH task. Together, these tasks can elucidate the specificity of conditioned hallucinations with regards to sensory modality. In addition to the deployment of the VCH, we also tested the feasibility of the first known online deployment of QUEST, an adaptive psychometric thresholding method, in a targeted population. Methods Task Methodology. Individual trials of the task consist of simultaneous presentation of a faintly-presented (low-contrast) visual stimulus (Gaussian stripes embedded in visual white noise) and a salient auditory stimulus (loud tone). An association between visual and auditory stimuli is established, followed by testing of the strength of this association by presenting the auditory stimulus alone. Trials where the visual stimulus is not presented, but nevertheless reported to be perceived are considered as CH trials. Data Collection and Analysis. Subjects were recruited on two platforms, the Amazon-powered Mechanical Turk (MTurk) and the COPE Project an initiative targeted at individuals with unusual experiences. Analyses were conducted by pooling across the four groups and grouping based on presence of visual or auditory hallucinations, creating four groups: AH+/VH+, AH+/VH-, AH-/VH+, AH-/VH-. Between-group differences were analyzed using two-sample t-tests. Results The responses of participants across the board, both in the control sample and in those with perceptual experiences, validates the efficacy of using the QUEST thresholding paradigm to predict response to threshold levels. Participants who were assigned VH+ groups showed a significantly higher rate of reporting CHs, compared to the control group with no hallucinatory experiences (p < 0.01). Similarly, participants assigned to AH+ groups also showed a significantly higher rate of reporting CHs (p < 0.01). Differential parameter values for a computational model assessing perceptual inference were computational signatures of CH were also examined between groups, as were neural signatures encoding visual versus auditory-mediated conditioned hallucinations. Discussion In this study, we show the feasibility of psychometric experiments in a targeted online sample of individuals with unusual experiences. We also demonstrate that the differential parameter values of the computational modeling of visually conditioned hallucinations differentiate between individuals with and without hallucinations, leading to better understanding of the neural signatures of hallucinations and potential therapeutic targets in clinical populations.

The cellular protein SERINC5 inhibits the infectivity of diverse retroviruses, and its activity is counteracted by the glycosylated Gag (glycoGag) protein of murine leukemia virus (MLV), the S2 protein of equine infectious anemia virus (EIAV), and the Nef protein of human immunodeficiency virus type 1 (HIV-1). Determining the regions within SERINC5 that provide restrictive activity or Nef sensitivity should inform mechanistic models of the SERINC5/HIV-1 relationship. Here, we report that deletion of the conserved sequence EDTEE, which is located within a cytoplasmic loop of SERINC5 and which is reminiscent of an acidic-cluster membrane trafficking signal, increases the sensitivity of SERINC5 to antagonism by Nef, while it has no effect on the intrinsic activity of the protein as an inhibitor of infectivity. These effects correlated with enhanced removal of the ΔEDTEE mutant relative to that of wild-type SERINC5 from the cell surface and with enhanced exclusion of the mutant protein from virions by Nef. Mutational analysis indicated that the acidic residues, but not the threonine, within the EDTEE motif are important for the relative resistance to Nef. Deletion of the EDTEE sequence did not increase the sensitivity of SERINC5 to antagonism by the glycoGag protein of MLV, suggesting that its virologic role is Nef specific. These results are consistent with the reported mapping of the cytoplasmic loop that contains the EDTEE sequence as a general determinant of Nef responsiveness, but they further indicate that sequences inhibitory to as well as supportive of Nef activity reside in this region. We speculate that the EDTEE motif might have evolved to mediate resistance against retroviruses that use Nef-like proteins to antagonize SERINC5. IMPORTANCE Cellular membrane proteins in the SERINC family, especially SERINC5, inhibit the infectivity of retroviral virions. This inhibition is counteracted by retroviral proteins, specifically, HIV-1 Nef, MLV glycoGag, and EIAV S2. One consequence of such a host-pathogen “arms race” is a compensatory change in the host antiviral protein as it evolves to escape the effects of viral antagonists. This is often reflected in a genetic signature, positive selection, which is conspicuously missing in SERINC5. Here we show that despite this lack of genetic evidence, a sequence in SERINC5 nonetheless provides relative resistance to antagonism by HIV-1 Nef.

PURPOSE OF REVIEW: Ambient air pollution is strongly linked to cardiovascular and respiratory diseases. We summarize available published evidence regarding similar associations with diabetes across the life course. RECENT FINDINGS: We performed a life-course survey of the recent literature, including prenatal, gestational, childhood/adolescence, and adult exposures to air pollution. Oxidative stress is identified as a key factor in both metabolic dysfunction and the effects of air pollution exposure, especially from fossil fuel combustion products, providing a plausible mechanism for air pollution-diabetes associations. The global burden of diabetes attributed to air pollution exposure is substantial, with a recent estimate that ambient fine particulate matter (PM(2.5)) exposure contributes to more than 200,000 deaths from diabetes annually. SUMMARY: There is a growing body of literature linking air pollution exposure during childhood and adulthood with diabetes etiology and related cardiometabolic biomarkers. A small number of studies found that exposure to air pollution during pregnancy is associated with elevated gestational diabetes risk among mothers. Studies examining prenatal air pollution exposure and diabetes risk among the offspring, as well as potential transgenerational effects of air pollution exposure, are very limited thus far. This review provides insight into how air pollutants affect diabetes and other metabolic dysfunction-related diseases across the different life stages.

Rationale: Many studies have linked short-term exposure to ozone (O3) with morbidity and mortality, but epidemiologic evidence of associations between long-term O3 exposure and mortality is more li...

Background: Recent experimental evidence suggests that nutritional supplementation can blunt adverse cardiopulmonary effects induced by acute air pollution exposure. However, whether usual individual dietary patterns can modify the association between long-term air pollution exposure and health outcomes has not been previously investigated. We assessed, in a large cohort with detailed diet information at the individual level, whether a Mediterranean diet modifies the association between long-term exposure to ambient air pollution and cardiovascular disease mortality risk. Methods: The National Institutes of Health–American Association for Retired Persons Diet and Health Study, a prospective cohort (N=548 845) across 6 states and 2 cities in the United States and with a follow-up period of 17 years (1995–2011), was linked to estimates of annual average exposures to fine particulate matter and nitrogen dioxide at the residential census-tract level. The alternative Mediterranean Diet Index, which uses a 9-point scale to assess conformity with a Mediterranean-style diet, was constructed for each participant from information in cohort baseline dietary questionnaires. We evaluated mortality risks for cardiovascular disease, ischemic heart disease, cerebrovascular disease, or cardiac arrest associated with long-term air pollution exposure. Effect modification of the associations between exposure and the mortality outcomes by alternative Mediterranean Diet Index was examined via interaction terms. Results: For fine particulate matter, we observed elevated and significant associations with cardiovascular disease (hazard ratio [HR] per 10 μg/m 3 , 1.13; 95% CI, 1.08–1.18), ischemic heart disease (HR, 1.16; 95% CI, 1.10–1.23), and cerebrovascular disease (HR, 1.15; 95% CI, 1.03–1.28). For nitrogen dioxide, we found significant associations with cardiovascular disease (HR per 10 ppb, 1.06; 95% CI, 1.04–1.08) and ischemic heart disease (HR, 1.08; 95% CI, 1.05–1.11). Analyses indicated that Mediterranean diet modified these relationships, as those with a higher alternative Mediterranean Diet Index score had significantly lower rates of cardiovascular disease mortality associated with long-term air pollution exposure ( P -interaction Conclusions: A Mediterranean diet reduced cardiovascular disease mortality risk related to long-term exposure to air pollutants in a large prospective US cohort. Increased consumption of foods rich in antioxidant compounds may aid in reducing the considerable disease burden associated with ambient air pollution.

Awareness of the human health impacts of exposure to air pollution is growing rapidly. For example, it has become evident that the adverse health effects of air pollution are more pronounced in disadvantaged populations. Policymakers in many jurisdictions have responded to this evidence by enacting initiatives that lead to lower concentrations of air pollutants, such as urban traffic restrictions. In this review, we focus on the interplay between advances in environmental exposure assessment and developments in policy. We highlight recent progress in the granular measurement of air pollutants and individual-level exposures, and how this has enabled focused local policy actions. Finally, we detail an illustrative study designed to link individual-level health-relevant exposures with economic, behavioral, biological, familial, and environmental variables., How can scientists and policymakers work together to reduce the health impacts of air pollution? In this review paper, the authors discuss the interplay between advances in environmental exposure assessment and policy advances to tackle pollution in a focused way.

To control the novel coronavirus disease (COVID-19) outbreak, state and local governments in the United States have implemented several mitigation efforts that resulted in lower emissions of traffic-related air pollutants. This study examined the impacts of COVID-19 mitigation measures on air pollution levels and the subsequent reductions in mortality for urban areas in 10 US states and the District of Columbia. We calculated changes in levels of particulate matter with aerodynamic diameter no larger than 2.5 μm (PM2.5) during mitigation period versus the baseline period (pre-mitigation measure) using the difference-in-difference approach and the estimated avoided total and cause-specific mortality attributable to these changes in PM2.5 by state and district. We found that PM2.5 concentration during the mitigation period decreased for most states (except for 3 states) and the capital. Decreases of average PM2.5 concentration ranged from 0.25 μg/m3 (4.3%) in Maryland to 4.20 μg/m3 (45.1%) in California. On average, PM2.5 levels across 7 states and the capital reduced by 12.8%. We estimated that PM2.5 reduction during the mitigation period lowered air pollution-related total and cause-specific deaths. An estimated 483 (95% CI: 307, 665) PM2.5-related deaths was avoided in the urban areas of California. Our findings have implications for the effects of mitigation efforts and provide insight into the mortality reductions can be achieved from reduced air pollution levels., Graphical abstract Unlabelled Image, Highlights • PM2.5 levels during COVID-19 mitigation decreased across 7 states and the capital. • PM2.5 reduction during COVID-19 mitigation is estimated to lowered air pollution-related deaths. • Findings have implications for the indirect health effects of mitigation efforts. • Results have implications for potential health benefits from air pollution policy.

Background With the number of annual global travellers reaching 1.2 billion, many individuals encounter greater levels of air pollution when they travel abroad to megacities around the world. This study’s objective was to determine if visits to cities abroad with greater levels of air pollution adversely impact cardiopulmonary health. Methods A total of 34 non-smoking healthy adult participants who travelled abroad to selected cities from the New York City (NYC) metropolitan area were pre-trained to measure lung function, blood pressure and heart rate (HR)/HR variability (HRV) and record symptoms before, during and after travelling abroad. Outdoor particulate matter (PM)2.5 concentrations were obtained from central monitors in each city. Associations between PM exposure concentrations and cardiopulmonary health endpoints were analysed using a mixed effects statistical design. Results East and South Asian cities had significantly higher PM2.5 concentrations compared with pre-travel NYC PM2.5 levels, with maximum concentrations reaching 503 μg/m3. PM exposure–related associations for lung function were statistically significant and strongest between evening Forced Expiratory Volume in the first second (FEV1) and same-day morning PM2.5 concentrations; a 10-μg/m3 increase in outdoor PM2.5 was associated with a mean decrease of 7 mL. Travel to a highly polluted city (PM2.5 > 100 μg/m3) was associated with a 209-ml reduction in evening FEV1 compared with a low polluted city (PM2.5 Conclusions Exposure to increased levels of PM2.5 in cities abroad caused small but statistically significant acute changes in cardiopulmonary function and respiratory symptoms in healthy young adults. These data suggest that travel-related exposure to increased PM2.5 adversely impacts cardiopulmonary health, which may be particularly important for travellers with pre-existing respiratory or cardiac disease.

Introduction: Recent development of both portable air pollution particle sensors and wearable technologies offers unique opportunities to study the real-time association between exposure and cardio...

Exposure to ambient fine particulate matter (PM 2.5 ) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM 2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM 2.5 -mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM 2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM 2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Objective Recent mechanistic and epidemiological evidence implicates air pollution as a potential risk factor for diabetes; however, mortality risks have not been evaluated in a large US cohort assessing exposures to multiple pollutants with detailed consideration of personal risk factors for diabetes. Research design and methods We assessed the effects of long-term ambient air pollution exposures on diabetes mortality in the NIH-AARP Diet and Health Study, a cohort of approximately a half million subjects across the contiguous U.S. The cohort, with a follow-up period between 1995 and 2011, was linked to residential census tract estimates for annual mean concentration levels of PM2.5, NO2, and O3. Associations between the air pollutants and the risk of diabetes mortality (N = 3598) were evaluated using multivariate Cox proportional hazards models adjusted for both individual-level and census-level contextual covariates. Results Diabetes mortality was significantly associated with increasing levels of both PM2.5 (HR = 1.19; 95% CI: 1.03–1.39 per 10 μg/m3) and NO2 (HR = 1.09; 95% CI: 1.01–1.18 per 10 ppb). The strength of the relationship was robust to alternate exposure assessments and model specifications. We also observed significant effect modification, with elevated mortality risks observed among those with higher BMI and lower levels of fruit consumption. Conclusions We found that long-term exposure to PM2.5 and NO2, but not O3, is related to increased risk of diabetes mortality in the U.S, with attenuation of adverse effects by lower BMI and higher fruit consumption, suggesting that air pollution is involved in the etiology and/or control of diabetes.

Background/Aim: Oxidative stress and systemic inflammation are suggested pathways for air pollution-mediated adverse health outcomes. Recent evidence from dietary supplementation intervention studi...

Background: Outdoor fine particulate matter (≤ 2.5 μm; PM2.5) has been identified as a global health threat, but the number of large U.S. prospective cohort studies with individual participant data remains limited, especially at lower recent exposures. Objectives: We aimed to test the relationship between long-term exposure PM2.5 and death risk from all nonaccidental causes, cardiovascular (CVD), and respiratory diseases in 517,041 men and women enrolled in the National Institutes of Health-AARP cohort. Methods: Individual participant data were linked with residence PM2.5 exposure estimates across the continental United States for a 2000–2009 follow-up period when matching census tract–level PM2.5 exposure data were available. Participants enrolled ranged from 50 to 71 years of age, residing in six U.S. states and two cities. Cox proportional hazard models yielded hazard ratio (HR) estimates per 10 μg/m3 of PM2.5 exposure. Results: PM2.5 exposure was significantly associated with total mortality (HR = 1.03; 95% CI: 1.00, 1.05) and CVD mortality (HR = 1.10; 95% CI: 1.05, 1.15), but the association with respiratory mortality was not statistically significant (HR = 1.05; 95% CI: 0.98, 1.13). A significant association was found with respiratory mortality only among never smokers (HR = 1.27; 95% CI: 1.03, 1.56). Associations with 10-μg/m3 PM2.5 exposures in yearly participant residential annual mean, or in metropolitan area-wide mean, were consistent with baseline exposure model results. Associations with PM2.5 were similar when adjusted for ozone exposures. Analyses of California residents alone also yielded statistically significant PM2.5 mortality HRs for total and CVD mortality. Conclusions: Long-term exposure to PM2.5 air pollution was associated with an increased risk of total and CVD mortality, providing an independent test of the PM2.5–mortality relationship in a new large U.S. prospective cohort experiencing lower post-2000 PM2.5 exposure levels. Citation: Thurston GD, Ahn J, Cromar KR, Shao Y, Reynolds HR, Jerrett M, Lim CC, Shanley R, Park Y, Hayes RB. 2016. Ambient particulate matter air pollution exposure and mortality in the NIH-AARP Diet and Health cohort. Environ Health Perspect 124:484–490; http://dx.doi.org/10.1289/ehp.1509676

Recent epidemiological evidence suggests that exposure to particulates may be a factor in the etiology of metabolic syndrome (MetS). In this novel study, we investigated the relationship between particulate levels and prevalence of MetS component abnormalities (hypertension, hyperglycemia, obesity) in a recruited cohort (N = 2025) in Jeddah, Saudi Arabia. We observed significant associations between a 10 μg/m3 increase in PM2.5 and increased risks for MetS (Risk Ratio (RR): 1.12; 95% Confidence Interval (CI): 1.06–1.19), hyperglycemia (RR: 1.08; 95% CI: 1.03–1.14), and hypertension (RR: 1.09; 95% CI: 1.04–1.14). PM2.5 from soil/road dust was found to be associated with hyperglycemia (RR: 1.12; 95% CI: 1.06–1.19) and hypertension (RR: 1.11; 95% CI: 1.05–1.18), while PM2.5 from traffic was associated with hyperglycemia (RR: 1.33; 95% CI: 1.05–1.71). We did not observe any health associations with source-specific mass exposures. Our findings suggest that exposure to specific elemental components of PM2.5, especially Ni, may contribute to the development of cardiometabolic disorders.

This study provides the first comprehensive analysis of the seasonal variations and weekday/weekend differences in fine (PM2.5) and coarse (PM2.5–10) particulate matter mass concentrations, elemental constituents, and potential source origins in Jeddah, Saudi Arabia. Air quality samples were collected over one year, from June 2011 to May 2012 at a frequency of three times per week, and analyzed. The average mass concentrations of PM2.5 (21.9 µg/m3) and PM10 (107.8 µg/m3) during the sampling period exceeded the recommended annual average levels by the World Health Organization (WHO) for PM2.5 (10 µg/m3) and PM10 (20 µg/m3), respectively. Similar to other Middle Eastern locales, PM2.5–10 is the prevailing mass component of atmospheric particulate matter at Jeddah, accounting for approximately 80% of the PM10 mass. Considerations of enrichment factors, absolute principal component analysis (APCA), concentration roses, and backward trajectories identified the following source categories for both PM2.5 and PM2.5–10: 1) soil/road dust; 2) incineration; and 3) traffic; and for PM2.5 only, 4) residual oil burning. Soil/road dust accounted for a major portion of both the PM2.5 (27%) and PM2.5–10 (77%) mass, and the largest source contributor for PM2.5 was from residual oil burning (63%). Temporal variations of PM2.5–10 and PM2.5 were observed, with the elevated concentration levels observed for mass during the spring (due to increased dust storm frequency), and on weekdays (due to increased traffic). The predominant role of windblown soil and road dust in both the PM2.5 and PM2.5–10 masses in this city may have implications regarding the toxicity of these particles versus those in the western world where most PM health assessments have been made in the past. These results support the need for region-specific epidemiological investigations to be conducted and considered in future PM standard setting.

Background— Stroke in female first-degree relatives (FDRs) is a powerful risk factor for ischemic stroke in women, but its association with acute coronary syndromes (ACS) is unknown. Family history (FH) of stroke is omitted from existing myocardial infarction risk prediction tools, which perform less well in women than in men. Our objective was to study the sex-of-parent and sex-of-proband interactions for FH of stroke in ACS patients. Methods and Results— In a prospective, population-based study (Oxford Vascular Study) of all patients with ACS or stroke/transient ischemic attack, FH data for stroke and myocardial infarction were analyzed by sex of proband and FDRs, and coronary angiograms were reviewed, where available; 942 of 1058 ACS probands and 1015 of 1152 stroke/transient ischemic attack probands had complete FH data; 24.1% of ACS probands and 24.3% of stroke/transient ischemic attack probands had history of stroke in ≥1 FDR. Maternal stroke was more common than paternal stroke in female ACS probands (odds ration [OR], 2.53; 1.39 to 4.61) but not in male probands (OR, 0.92; 0.64 to 1.32) (difference- P =0.004). Overall, female ACS probands were more likely to have female than male FDRs with stroke (OR, 2.09; 1.29 to 3.37), whereas the opposite trend was seen in male ACS probands (OR, 0.69; 0.50 to 0.97) (difference- P =0.0002). However, there was no association between parental history of stroke and disease localization or presence of multivessel disease on coronary angiography. Conclusions— FH of stroke is as common in ACS patients as in stroke/transient ischemic attack patients and sex-of-parent/sex-of-proband interactions are similar. Stroke in female FDRs may help to identify women at increased risk of ACS as well as ischemic stroke.

At least 18 different drug-eluting balloons are being developed by medical device companies for treatment of either de novo or restenotic coronary artery disease. This re-emergence of enthusiasm for balloon-only treatment rather then stent implantation, might be considered surprising by those cardiologists who experienced the vagaries of ‘stentless’ coronary intervention in the late 1980s. Plain old balloon angioplasty (POBA) was unpredictable because of its tendency to create eccentric, potentially occlusive dissection flaps and the impact of early vessel recoil within the first few hours of the procedure. Restenosis after POBA was common and it reflected adverse vessel remodelling and some neointimal proliferation and extracellular matrix production by vascular smooth muscle cells.1 The advent of stent implantation provided the opportunity to scaffold dissection, optimising acute lumen gain and preventing early recoil and late remodelling. However, for stenting to be successful in the long term these gains in lumen area had to exceed the inevitable increase in neointima formation caused by the presence of the stent. Using polymer technology to bind antiproliferative drugs to stents has significantly improved the likelihood that drug-eluting stent (DES) implantation will be beneficial, by reducing the volume of neointima that is generated by the presence of the stent. However, DES implantation necessarily attenuates the vessel's healing processes, resulting in delayed and sometimes incomplete endothelialisation and a risk of catastrophic stent thrombosis, particularly if antiplatelet therapy is …

Prasad et al. ([1][1]) present valuable insights into the prognostic influence of spontaneous myocardial infarction (SMI) and periprocedural myocardial infarction (PMI) following stent insertion in the ACUITY (Acute Catheterization and Urgent Intervention Triage Strategy) trial. They concluded that

Periprocedural myocardial injury (PMI) is common after percutaneous coronary intervention (PCI). Periprocedural infarction (myocardial infarction type 4a) occurs after at least 10% of PCI procedures and has an impact on long-term prognosis. Measurement of biomarkers to allow assessment of PMI is an important tool for clinical and research purposes and should be routine after every PCI (troponin I or T and CK-MB). The importance of oral and intravenous antiplatelet agents and other drugs which have been proven to reduce PMI is discussed.

Background: Long-term PM2.5 exposure is associated with an increased mortality risk. Effect modification of this relationship by gaseous pollutants needs further investigation in a multi-pollutant ...

Background— Absolute quantification of perfusion with cardiovascular magnetic resonance has not previously been applied in patients with coronary artery bypass grafting (CABG). Owing to increased contrast bolus dispersion due to the greater distance of travel through a bypass graft, this approach may result in systematic underestimation of myocardial blood flow (MBF). As resting MBF remains normal in segments supplied by noncritical coronary stenosis ( Methods and Results— The study population comprised 28 patients undergoing elective CABG for treatment of multivessel coronary artery disease. Eligible patients had angiographic evidence of at least 1 myocardial segment subtended by a noncritically stenosed coronary artery (P =0.57). In the latter, MBF after revascularization did not change significantly from baseline (0.86±0.20 mL/min/g, P =0.82). Conclusions— Model-independent deconvolution analysis does not systematically underestimate blood flow in graft-subtended territories, justifying the use of this methodology to evaluate myocardial perfusion in patients with CABG.