There are no studies investigating the association of chlorinated drinking water with the risk of cardiovascular diseases (CVDs) among young and middle-aged adults. This study was aimed to assess the associations between trihalomethanes (THMs) in drinking water and the risk of CVDs in in the target group in Petropavlovsk, Kazakhstan. 448 dwellers of Petropavlovsk were asked about their demographic, socioeconomic, lifestyle, behavioural characteristics, and drinking water preferences. THMs exposure was assessed to each participant based on their residence address. We used multivariable logistic regression analysis to assess the risk of CVDs in young and middle-aged adults. The results showed that the risk of hypertension in the adjusted logistic regression model was increased by 68%   and a 2.7-fold   in the second and third THM tertiles, respectively. Participants in the second and third THM exposure tertiles had a 2.3-fold and a 4.8-fold increase in the risk of arrhythmia.

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Global industrialisation and urbanisation has led to an increased interest in the link between the environment and health. Stroke is a major cause of morbidity and mortality, and there is increased evidence that environmental factors may affect both the incidence and severity of stroke. This review summarises the evidence for relationship between green space exposure and stroke incidence and outcomes.

We conducted a literature search in Medline and Scopus until 1 August 2023, and screened references of relevant articles. Selected articles were appraised for their relevance, and critically reviewed. The findings were thematically categorised.

Of the 1342 papers identified, 27 were included. These involved a mix of study designs (cohort, cross-sectional, quasi-experimental, time stratified case crossover and ecological). There was consistent evidence indicating a protective association between green space exposure and disability and stroke-related death with mortality hazard ratios between 0.66 and 0.95. Most studies also showed that green space was inversely associated with stroke risk, with risk estimates from studies showing a protective effect ranging between 0.4 and 0.98; however, results were more mixed and some did not reach statistical significance. The moderating effects of green spaces on ambient temperatures, noise and air pollution, and psychosocial health plus greater enjoyment and opportunity for exercise and enrichment of the human microbiome may underly these associations.

There is likely some protective effect of green space on stroke, with the benefits most convincingly shown for post-stroke outcomes. More research is recommended to confirm the protective association between green space exposure and reduced stroke risk.

The health effects of traffic-related air pollution (TRAP) continue to be of important public health interest across the globe. Following its 2010 review, the Health Effects Institute appointed a new expert Panel to systematically evaluate the epidemiological evidence regarding the associations between long-term exposure to TRAP and selected health outcomes. This paper describes the main findings of the systematic review on non-accidental mortality.

The Panel used a systematic approach to conduct the review. An extensive search was conducted of literature published between 1980 and 2019. A new exposure framework was developed to determine whether a study was sufficiently specific to TRAP, which included studies beyond the near-roadway environment. We performed random-effects meta-analysis when at least three estimates were available of an association between a specific exposure and outcome. We evaluated confidence in the evidence using a modified Office of Health Assessment and Translation (OHAT) approach, supplemented with a broader narrative synthesis.

Thirty-six cohort studies were included. Virtually all studies adjusted for a large number of individual and area-level covariates-including smoking, body mass index, and individual and area-level socioeconomic status-and were judged at a low or moderate risk for bias. Most studies were conducted in North America and Europe, and a few were based in Asia and Australia. The meta-analytic summary estimates for nitrogen dioxide, elemental carbon and fine particulate matter-pollutants with more than 10 studies-were 1.04 (95% CI 1.01, 1.06), 1.02 (1.00, 1.04) and 1.03 (1.01, 1.05) per 10, 1 and 5 µg/m³, respectively. Effect estimates are interpreted as the relative risk of mortality when the exposure differs with the selected increment. The confidence in the evidence for these pollutants was judged as high, because of upgrades for monotonic exposure-response and consistency across populations. The consistent findings across geographical regions, exposure assessment methods and confounder adjustment resulted in a high confidence rating using a narrative approach as well.

The overall confidence in the evidence for a positive association between long-term exposure to TRAP and non-accidental mortality was high.

Both psychosocial and physical environmental stressors have been linked to chronic mental health and chronic medical conditions. The psycho-immune-neuroendocrine (PINE) network details metabolomic pathways which are responsive to varied stressors and link chronic medical conditions with mental disorders, such as major depressive disorder via a network of pathophysiological pathways. The primary objective of this review is to explore evidence of relationships between airborne particulate matter (PM, as a concrete example of a physical environmental stressor), the PINE network and chronic non-communicable diseases (NCDs), including mental health sequelae, with a view to supporting the assertion that physical environmental stressors (not only psychosocial stressors) disrupt the PINE network, leading to NCDs. Biological links have been established between PM exposure, key sub-networks of the PINE model and mental health sequelae, suggesting that in theory, long-term mental health impacts of PM exposure may exist, driven by the disruption of these biological networks. This disruption could trans-generationally influence health; however, long-term studies and information on chronic outcomes following acute exposure event are still lacking, limiting what is currently known beyond the acute exposure and all-cause mortality. More empirical evidence is needed, especially to link long-term mental health sequelae to PM exposure, arising from PINE pathophysiology. Relationships between physical and psychosocial stressors, and especially the concept of such stressors acting together to impact on PINE network function, leading to linked NCDs, evokes the concept of syndemics, and these are discussed in the context of the PINE network.

We conducted a study of the leaf-deposited particles and magnetism of plant leaves in different functional areas (traffic areas, parks, and residential areas) in Lanzhou, China. The saturation isothermal remanent magnetization (SIRM) of the washed and unwashed leaves of 23 plant species (including evergreen shrubs, deciduous shrubs, deciduous liana species, and deciduous trees) at three sampling heights (0.5 m, 1.5 m, and 2.5 m) was measured. In addition, the mass of the leaf-deposited particles was measured using the elution-filtration method and the leaf morphological characteristics were determined by scanning electronic microscope (SEM) analysis. The results revealed significant differences in particle retention capacity among the 23 plant species, with evergreen shrub species at the heights of 0.5 m and 1.5 m having higher particle concentrations. Buxus sinica, Buxus megistophylla, Prunus cerasifera, and Ligustrum×vicaryi were the most effective plant species for accumulating particles. The SEM results showed that leaves with a relatively complex adaxial surface (such as deep grooves and protrusions) were more effective at accumulating particles. The SIRM of washed leaves, unwashed leaves, and leaf-deposited particles were significantly higher in traffic areas than in parks and residential areas. In addition, significant correlations were found between SIRM of unwashed leaves and leaf-deposited particles and the mass of leaf-deposited particles, and therefore the leaf magnetic properties effectively reflect levels of PM pollution under different environmental conditions. Overall, our results provide a valuable reference for the selection of plant species with high particle retention capacity that is suitable for urban greening and pollution mitigation.

High surrounding road density could increase traffic-related air pollution, noise and the risk of traffic injuries, which are major public health concerns for children. We collected geographical data for all childcare centers (16,146) in Australia and provided the data on the road density surrounding them. The road density was represented by the child care center's nearest distance to main road and motorway, and the length of main road/motor way within 100~1000-meter buffer zone surrounding the child care center. We also got the data of PM2.5 concentration from 2013 to 2018 and standard Normalized Difference Vegetation Index (NDVI) data from 2013 to 2019 according to the longitude and latitude of the child care centers. This data might help researchers to evaluate the health impacts of road density on child health, and help policy makers to make transportation, educational and environmental planning decisions to protect children from exposure to traffic-related hazards in Australia.

Built-up environments limit air pollution dispersion in street canyons and lead to complex trade-offs between green infrastructure (GI) usage and its potential to reduce near-road exposure. This study evaluated the effects of an evergreen hedge on the distribution of particulate matter (PM₁, PM_2.5, PM₁₀), black carbon (BC) and particle number concentrations (PNCs) in a street canyon in West London. Instrumentation was deployed around the hedge at 13 fixed locations to assess the impact of the hedge on vertical and horizontal concentration distributions. Changes in concentrations behind the hedge were measured with reference to the corresponding sampling point in front of the hedge for all sets of measurements. Results showed a significant reduction in vertical concentrations between 1 and 1.7 m height, with maximum reductions of -16% (PM₁ and PM₁₀) and -17% (PM_2.5) at ∼1 m height. Horizontal concentrations revealed two zones between the building façade and the hedge, with opposite trends: (i) close to hedge (within 0.2 m), where a reduction of PM₁ and PM_2.5 was observed, possibly due to dilution, deposition and the barrier effect; and (ii) 0.2-3 m from the hedge, showing an increase of 13-37% (PM₁) and 7-21% (PM_2.5), possibly due to the blockage effect of the building, restricting dispersion. BC showed a significant reduction at breathing height (1.5 m) of between -7 and -50%, followed by -15% for PNCs in the 0.02-1 µm size range. The ELPI + analyser showed a peak of ∼30 nm. The presence of the hedge led to a ∼39 ± 32% decrease in total PNCs (0.006-10 µm), suggesting a greater removal in different modes, such as a 83 ± 12% reduction in nucleation mode (0.006-0.030 µm), 74 ± 15% in ultrafine (≤0.1 µm), and 34 ± 30% in accumulation mode (0.03-0.3 µm). These findings indicate graded filtering of particles by GI in a near-road street canyon environment. This insight will guide the improved design of GI barriers and the validation of microscale dispersion models.

Although many studies have evaluated the effects of ambient particulate matter with diameters of less than 2.5 μm (PM_2.5) on stroke mortality in the general population, little is known about the mortality effects of PM_2.5 in post-stroke populations. Therefore, a retrospective cohort was constructed using information from the health insurance database to evaluate whether exposure to PM_2.5 is associated with increased mortality in aged stroke survivors residing in seven Korean metropolitan cities. A total of 45,513 older adults (≥65 years) who visited emergency rooms due to stroke and who were discharged alive between 2008 and 2016 were followed up. By using district-level modeled PM_2.5 concentrations and a time-varying Cox proportional hazard model, associations between 1-month and 2-month moving average PM_2.5 exposures and mortality in stroke survivors were evaluated. The annual average concentration of PM_2.5 was 27.9 μg/m³ in the seven metropolitan cities, and 14,880 subjects died during the follow-up period. A 10 μg/m³ increase in the 1-month and 2-month moving average PM_2.5 exposures was associated with mortality hazard ratios of 1.07 (95% confidence interval: 1.05, 1.09) and 1.06 (95% confidence interval: 1.03, 1.08), respectively. The effects of PM_2.5 were similar across types of stroke (ischemic and hemorrhagic), age groups (65-74, 75-84, and ≥85), and income groups (low and high) but were greater in women than in men. This study highlights the adverse health effects of ambient PM_2.5 in post-stroke populations. Active avoidance behaviors against PM_2.5 are recommended for aged stroke survivors.

Background Previous studies have found associations between fine particulate matter <2.5 µm in diameter (PM2.5) and increased risk of cardiovascular disease (CVD) among populations with no CVD history. Less is understood about susceptibility of adults with a history of CVD and subsequent PM2.5-related CVD events and whether current regulation levels for PM2.5 are protective for this population. Methods and Results This retrospective cohort study included 96 582 Kaiser Permanente Northern California adults with a history of stroke or acute myocardial infarction. Outcome, covariate, and address data obtained from electronic health records were linked to time-varying 1-year mean PM2.5 exposure estimates based on residential locations. Cox proportional hazard models estimated risks of stroke, acute myocardial infarction, and cardiovascular mortality associated with PM2.5 exposure, adjusting for multiple covariates. Secondary analyses estimated risks below federal and state regulation levels (12 µg/m3 for 1-year mean PM2.5). A 10-µg/m3 increase in 1-year mean PM2.5 exposure was associated with an increase in risk of cardiovascular mortality (hazard ratio [HR], 1.20; 95% CI, 1.11-1.30), but no increase in risk of stroke or acute myocardial infarction. Analyses of <12 µg/m3 showed increased risk for CVD mortality (HR, 2.31; 95% CI, 1.96-2.71), stroke (HR, 1.41; 95% CI, 1.09-1.83]), and acute myocardial infarction (HR, 1.51; 95% CI, 1.21-1.89) per 10-µg/m3 increase in 1-year mean PM2.5. Conclusions Adults with a history of CVD are susceptible to the effects of PM2.5 exposure, particularly on CVD mortality. Increased risks observed at exposure levels <12 µg/m3 highlight that current PM2.5 regulation levels may not be protective for this susceptible population.

Since the publication of the last American Heart Association scientific statement on air pollution and cardiovascular disease in 2010, unequivocal evidence of the causal role of fine particulate matter air pollution (PM2.5, or particulate matter ≤2.5 μm in diameter) in cardiovascular disease has emerged. There is a compelling case to provide the public with practical personalized approaches to reduce the health effects of PM2.5. Such interventions would be applicable not only to individuals in heavily polluted countries, high-risk or susceptible individuals living in cleaner environments, and microenvironments with higher pollution exposures, but also to those traveling to locations with high levels of PM2.5. The overarching motivation for this document is to summarize the current evidence supporting personal-level strategies to prevent the adverse cardiovascular effects of PM2.5, guide the use of the most proven/viable approaches, obviate the use of ineffective measures, and avoid unwarranted interventions. The significance of this statement relates not only to the global importance of PM2.5, but also to its focus on the most tested interventions and viable approaches directed at particulate matter air pollution. The writing group sought to provide expert consensus opinions on personal-level measures recognizing the current uncertainty and limited evidence base for many interventions. In doing so, the writing group acknowledges that its intent is to assist other agencies charged with protecting public health, without minimizing the personal choice considerations of an individual who may decide to use these interventions in the face of ongoing air pollution exposure.

To evaluate the association between long-term exposure to ambient air pollution and cognitive decline in older adults residing in an urban area.

Data for this study were obtained from 2 prospective cohorts of residents in the northern Manhattan area of New York City: the Washington Heights-Inwood Community Aging Project (WHICAP) and the Northern Manhattan Study (NOMAS). Participants of both cohorts received in-depth neuropsychological testing at enrollment and during follow-up. In each cohort, we used inverse probability weighted linear mixed models to evaluate the cross-sectional and longitudinal associations between markers of average residential ambient air pollution (nitrogen dioxide [NO2], fine particulate matter [PM2.5], and respirable particulate matter [PM10]) levels in the year prior to enrollment and measures of global and domain-specific cognition, adjusting for sociodemographic factors, temporal trends, and censoring.

Among 5,330 participants in WHICAP, an increase in NO2 was associated with a 0.22 SD lower global cognitive score at enrollment (95% confidence interval [CI], -0.30, -0.14) and 0.06 SD (95% CI, -0.08, -0.04) more rapid decline in cognitive scores between visits. Results were similar for PM2.5 and PM10 and across functional cognitive domains. We found no evidence of an association between pollution and cognitive function in NOMAS.

WHICAP participants living in areas with higher levels of ambient air pollutants have lower cognitive scores at enrollment and more rapid rates of cognitive decline over time. In NOMAS, a smaller cohort with fewer repeat measurements, we found no statistically significant associations. These results add to the evidence regarding the adverse effect of air pollution on cognitive aging and brain health.

The association between particulate pollution and cardiovascular morbidity and mortality is well established. While the cardiovascular effects of nationally regulated criteria pollutants (e.g., fine particulate matter [PM_2.5] and nitrogen dioxide) have been well documented, there are fewer studies on particulate pollutants that are more specific for traffic, such as black carbon (BC) and particle number (PN). In this paper, we synthesized studies conducted in the Greater Boston Area on cardiovascular health effects of traffic exposure, specifically defined by BC or PN exposure or proximity to major roadways. Large cohort studies demonstrate that exposure to traffic-related particles adversely affect cardiac autonomic function, increase systemic cytokine-mediated inflammation and pro-thrombotic activity, and elevate the risk of hypertension and ischemic stroke. Key patterns emerged when directly comparing studies with overlapping exposure metrics and population cohorts. Most notably, cardiovascular risk estimates of PN and BC exposures were larger in magnitude or more often statistically significant compared to those of PM_2.5 exposures. Across multiple exposure metrics (e.g., short-term vs. long-term; observed vs. modeled) and different population cohorts (e.g., elderly, individuals with co-morbidities, young healthy individuals), there is compelling evidence that BC and PN represent traffic-related particles that are especially harmful to cardiovascular health. Further research is needed to validate these findings in other geographic locations, characterize exposure errors associated with using monitored and modeled traffic pollutant levels, and elucidate pathophysiological mechanisms underlying the cardiovascular effects of traffic-related particulate pollutants. Implications: Traffic emissions are an important source of particles harmful to cardiovascular health. Traffic-related particles, specifically BC and PN, adversely affect cardiac autonomic function, increase systemic inflammation and thrombotic activity, elevate BP, and increase the risk of ischemic stroke. There is evidence that BC and PN are associated with greater cardiovascular risk compared to PM_2.5. Further research is needed to elucidate other health effects of traffic-related particles and assess the feasibility of regulating BC and PN or their regional and local sources.

Evidence from epidemiological studies has demonstrated that outdoor air pollution is now a well-known major problem of public health, mainly in low and middle income countries. Contrasting with myocardial infarction, there are few data on the association of air pollution and stroke.

We propose a narrative literature review of the effects and the underlying biological mechanisms of short- and long-term exposure to air pollutants on stroke risk and mortality, using the following key-words: stroke, cerebrovascular events, ischemic and haemorrhage stroke, transient ischaemic attack, mortality, air pollution and air pollutants.

Twenty-one papers were selected. Air pollution, of which whose small particulate matter are the most toxic, contributes to about one-third of the global burden of stroke. We can identify vulnerable patients with classical neuro-vascular risk factors or a prior history of stroke or transient ischemic attack or persons living in low-income countries. Biological mechanisms of this new morbid association are discussed.

Air pollution should be recognized as a silent killer inducing stroke whose mortality rates remain elevated by its role as a new modifiable neurovascular risk factor, needing public health policies.

Although several air pollution studies have examined the relationship between people living close to roadways and human health, we are unaware of studies that have examined the distance-decay of this effect based on a snapshot of congestion and focused on a micro-level traffic emission inventory. In this paper we estimate the distance-decay of premature mortality risk related to PM_2.5 emitted by traffic congestion in Hamilton, Canada, in 2011 We employ the Stochastic User Equilibrium (SUE) traffic assignment algorithm to estimate congested travel times for each road link in our study area. Next, we used EPA's MOVES model to estimate mass of PM_2.5, and then R-line dispersion model to predict concentration of PM_2.5. Finally, we apply Integrated Exposure Response Function (IERF) to estimate PM_2.5-related premature mortality at 100 m × 100 m grid resolution. We estimated total premature mortality over Hamilton to be 73.10 (95%CI: 39.05; 82.11) deaths per year. We observed that the proximity to a roadway increases the risk of premature mortality and the strength of this risk decreases as buffer sizes are increased. For example, we estimated that the premature mortality risk within buffer 0-100 m is 29.5% higher than for the buffer 101-200 m, 179.3% higher than for the buffer 201-300 m, and 566% higher than for the buffer 301-400 m. Our study provides a new perspective on exposure increments from traffic congestion. In particular, our findings show health effects gradients across neighborhoods, capturing microscale near-road exposure up to 2000 m of the roadway. Results from this research can be useful for policymakers to develop new strategies for the challenges of regulating transportation, land use, and air pollution.

Exposure to traffic-related PM_2.5 mass and its components can affect human health. Meanwhile, indoor concentrations are better exposure predictors as compared to outdoor concentrations because individuals spend the majority of their time indoors. We estimated the impact of traffic emissions on indoor PM_2.5 mass and its species as a function of road proximity in Massachusetts. A linear regression model was built using 662 indoor samples and 580 ambient samples. Analysis shows that indoor exposures to traffic-related particles increased dramatically with road proximity. We defined relative concentration decrease, R(α), as the ratio of the indoor concentration at perpendicular distance α in meters from the closest major road to the indoor concentration at 1800 m from the major road. R(13) values for PM_2.5 mass and Black Carbon (BC) were 1.3 (95%CI: 1.4, 1.6) and 2.1 (95%CI: 1.3, 2.8) for A12 roads, and 1.3 (95%CI: 1.2, 1.4) and 1.2 (95%CI: 1.1, 1.3) for A3 roads. R(α) values were also estimated for Fe, Mn, Mo, Sr and Ti for A12 roads, and Ca, Cu, Fe, Mn, Mo, Ni, Si, Sr, V and Zn for A3 roads. R(α) values for species associated mainly with brakes, tires or road dust (e.g., Mn, Mo and Sr) were higher than others. For A12 roads, R(13) values for Mn and Mo were 10.9 (95%CI: 0.9, 20.9) and 6.5 (95%CI: 1.4, 11.5), and ranged from 1.3 to 2.1 for other species; for A3 roads, R(13) values for Mn, Mo and Sr were 1.9 (95%CI: 1.1, 2.9), 1.8 (95%CI: 1.1, 2.4), and 8.5 (95%CI: 5.9, 10.9), and ranged from 1.2 to 1.6 for others. Our results indicate a significant impact of local traffic emissions on indoor air, which depends on road proximity. Thus road proximity which has been used in many epidemiological studies is a reasonable exposure metric.

The evidence supporting the deleterious cardiovascular health effects of living near a major roadway is growing, although this association is not universal. In primary analyses, we hypothesized that residential proximity to a major roadway would be associated with incident ischemic stroke and that cardiovascular risk factors would modify that association.

NOMAS (The Northern Manhattan Study) is an ongoing, population-based cohort study designed to measure cardiovascular risk factors, stroke incidence, and other outcomes in a multiethnic urban population. Recruitment occurred from 1993 to 2001 and participants are followed-up annually by telephone. Residential addresses at baseline were geocoded and Euclidean distance to nearest major roadway was estimated and categorized as in prior studies. We used Cox proportional hazard models to calculate hazard ratios and 95% confidence intervals for the association of this distance to incidence of stroke and other outcomes, adjusting for sociodemographic and cardiovascular risk factors, year at baseline, and neighborhood socioeconomic status. We assessed whether these associations varied by age, sex, smoking status, diabetes mellitus, and hypertension.

During a median follow-up period of 15 years (n=3287), 11% of participants were diagnosed with ischemic stroke. Participants living <100 m from a roadway had a 42% (95% confidence interval, 1.01-2.02) higher rate of ischemic stroke versus those living >400 m away. This association was more pronounced among noncurrent smokers (hazard ratio, 1.54; 95% confidence interval, 1.05-2.26) and not evident among smokers (hazard ratio, 0.69; 95% confidence interval, 0.23-2.06). There was no clear pattern of association between proximity to major roadways and other cardiovascular events including myocardial infarction, all-cause death, or vascular death.

In this urban multiethnic cohort, we found evidence supporting that within-city variation in residential proximity to major roadway is associated with higher risk of ischemic stroke. An individual's smoking history modified this association, with the association remaining only among participants not currently smokers.

Stroke is a disease related to high mortality and morbidity, particularly in developing countries. Some studies have linked self-reported indoor and outdoor pollution to stroke and mini-stroke, while some others showed no association. Our objective was to assess this association in Lebanon, a Middle Eastern developing country. A national cross-sectional study was conducted all over Lebanon. In addition to self-reported items of pollution exposure, we assessed potential predictors of stroke and mini-stroke, including sociodemographic characteristics, self-reported health information, and biological measurements. Moreover, we assessed dose-effect relationship of pollution items in relation with stroke. Self-reported indoor pollution exposure was associated with stroke and mini-stroke, with or without taking biological values into account. Moreover, we found a dose-effect relationship of exposure with risk of disease, but this effect did not reach statistical significance after adjustment for sociodemographics and biological characteristics. No association was found for any outdoor pollution item. Although additional studies would be necessary to confirm these findings, sensitizing the population about the effect of pollution on chronic diseases, working on reducing pollution, and improving air quality should be implemented to decrease the burden of the disease on the population and health system.

Long-term exposure to ambient air pollution has been associated with impaired cognitive function and vascular disease in older adults, but little is known about these associations among people with concerns about memory loss.

To examine associations between exposures to fine particulate matter and residential proximity to major roads and markers of small vessel disease.

From 2004-2010, 236 participants in the Massachusetts Alzheimer's Disease Research Center Longitudinal Cohort participated in neuroimaging studies. Residential proximity to major roads and estimated 2003 residential annual average of fine particulate air pollution (PM2.5) were linked to measures of brain parenchymal fraction (BPF), white matter hyperintensities (WMH), and cerebral microbleeds. Associations were modeled using linear and logistic regression and adjusted for clinical and lifestyle factors.

In this population (median age [interquartile range] = 74 [12], 57% female) living in a region with median 2003 PM2.5 annual average below the current Environmental Protection Agency (EPA) standard, there were no associations between living closer to a major roadway or for a 2μg/m3 increment in PM2.5 and smaller BPF, greater WMH volume, or a higher odds of microbleeds. However, a 2μg/m3 increment in PM2.5 was associated with -0.19 (95% Confidence Interval (CI): -0.37, -0.005) lower natural log-transformed WMH volume. Other associations had wide confidence intervals.

In this population, where median 2003 estimated PM2.5 levels were below the current EPA standard, we observed no pattern of association between residential proximity to major roads or 2003 average PM2.5 and greater burden of small vessel disease or neurodegeneration.

We examined associations between ambient air pollution and hepatic steatosis among 2,513 participants from the Framingham (Massachusetts) Offspring Study and Third Generation Cohort who underwent a computed tomography scan (2002-2005), after excluding men who reported >21 drinks/week and women who reported >14 drinks/week. We calculated each participant's residential-based distance to a major roadway and used a spatiotemporal model to estimate the annual mean concentrations of fine particulate matter. Liver attenuation was measured by computed tomography, and liver-to-phantom ratio (LPR) was calculated. Lower values of LPR represent more liver fat. We estimated differences in continuous LPR using linear regression models and prevalence ratios for presence of hepatic steatosis (LPR ≤ 0.33) using generalized linear models, adjusting for demographics, individual and area-level measures of socioeconomic position, and clinical and lifestyle factors. Participants who lived 58 m (25th percentile) from major roadways had lower LPR (β = -0.003, 95% confidence interval: -0.006, -0.001) and higher prevalence of hepatic steatosis (prevalence ratio = 1.16, 95% confidence interval: 1.05, 1.28) than those who lived 416 m (75th percentile) away. The 2003 annual average fine particulate matter concentration was not associated with liver-fat measurements. Our findings suggest that living closer to major roadways was associated with more liver fat.

The purpose of this review is to describe recent clinical and epidemiological studies examining the adverse effects of urban air pollution on the central nervous system (CNS). Air pollution and particulate matter (PM) are associated with neuroinflammation and reactive oxygen species (ROS). These processes affect multiple CNS pathways. The conceptual framework of this review focuses on adverse effects of air pollution with respect to neurocognition, white matter disease, stroke, and carotid artery disease. Both children and older individuals exposed to air pollution exhibit signs of cognitive dysfunction. However, evidence on middle-aged cohorts is lacking. White matter injury secondary to air pollution exposure is a putative mechanism for neurocognitive decline. Air pollution is associated with exacerbations of neurodegenerative conditions such as Alzheimer's and Parkinson's diseases. Increases in stroke incidences and mortalities are seen in the setting of air pollution exposure and CNS pathology is robust. Large populations living in highly polluted environments are at risk. This review aims to outline current knowledge of air pollution exposure effects on neurological health.

Many features of the environment have been found to exert an important influence on cardiovascular disease (CVD) risk, progression, and severity. Changes in the environment because of migration to different geographic locations, modifications in lifestyle choices, and shifts in social policies and cultural practices alter CVD risk, even in the absence of genetic changes. Nevertheless, the cumulative impact of the environment on CVD risk has been difficult to assess and the mechanisms by which some environment factors influence CVD remain obscure. Human environments are complex, and their natural, social, and personal domains are highly variable because of diversity in human ecosystems, evolutionary histories, social structures, and individual choices. Accumulating evidence supports the notion that ecological features such as the diurnal cycles of light and day, sunlight exposure, seasons, and geographic characteristics of the natural environment such as altitude, latitude, and greenspaces are important determinants of cardiovascular health and CVD risk. In highly developed societies, the influence of the natural environment is moderated by the physical characteristics of the social environments such as the built environment and pollution, as well as by socioeconomic status and social networks. These attributes of the social environment shape lifestyle choices that significantly modify CVD risk. An understanding of how different domains of the environment, individually and collectively, affect CVD risk could lead to a better appraisal of CVD and aid in the development of new preventive and therapeutic strategies to limit the increasingly high global burden of heart disease and stroke.

Traffic and ambient air pollution exposure are positively associated with cardiovascular disease, potentially through atherosclerosis promotion. Few studies have assessed associations of these exposures with thoracic aortic calcium Agatston score (TAC) or abdominal aortic calcium Agatston score (AAC), systemic atherosclerosis correlates. We assessed whether living close to a major road and residential fine particulate matter (PM_2.5) exposure were associated with TAC and AAC in a Northeastern US cohort.

Cohort study.

Framingham Offspring and Third Generation participants residing in the Northeastern USA.

Among 3506 participants, mean age was 55.8 years; 50% female. TAC was measured from 2002 to 2005 and AAC up to two times (2002-2005; 2008-2011) among participants from the Framingham Offspring or Third Generation cohorts. We first assessed associations with detectable TAC (logistic regression) and AAC (generalised estimating equation regression, logit link). As aortic calcium scores were right skewed, we used linear regression models and mixed-effects models to assess associations with natural log-transformed TAC and AAC, respectively, among participants with detectable aortic calcium. We also assessed associations with AAC progression. Models were adjusted for demographic variables, socioeconomic position indicators and time.

There were no consistent associations of major roadway proximity or PM_2.5 with the presence or extent of TAC or AAC, or with AAC progression. Some estimates were in the opposite direction than expected.

In this cohort from a region with relatively low levels of and variation in PM_2.5, there were no strong associations of proximity to a major road or PM_2.5 with the presence or extent of aortic calcification, or with AAC progression.

Outdoor air pollution is a known risk factor for mortality and morbidity. The type of air pollutant most reliably associated with disease is particulate matter (PM), especially finer particulate matter that can reach deeper into the lungs like PM_2.5 (particulate matter diameter < 2.5 μm). Some subpopulations may be particularly vulnerable to PM pollution. This review focuses on one subgroup, long-term stroke survivors, and the emerging evidence suggesting that survivors of a stroke may be at a higher risk from the deleterious effects of PM pollution. While the mechanisms for mortality are still under debate, long-term stroke survivors may be vulnerable to similar mechanisms that underlie the well-established association between PM pollution and cardiovascular disease. The fact that long-term stroke survivors of ischemic, but not hemorrhagic, strokes appear to be more vulnerable to the risk of death from higher PM pollution may also bolster the connection to ischemic heart disease. Survivors of an ischemic stroke may be more vulnerable to dying from higher concentrations of PM pollution than the general population. The clinical implications of this association suggest that reduced exposure to PM pollution may result in fewer deaths amongst stroke survivors.

Higher traffic-related air pollution has been associated with higher body mass index (BMI) among children. However, few studies have assessed the associations among adults.

Participants (N = 2,372) from the Framingham Offspring and Third Generation cohorts who underwent multidetector-computed tomography scans (2002-2005) were included. Residential-based proximity to the nearest major roadway and 1-year average levels of fine particulate matter (PM_2.5 ) air pollution were estimated. BMI was measured at Offspring examination 7 (1998-2001) and Third Generation examination 1 (2002-2005); subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were measured using multidetector-computed tomography. Linear regression models were used for continuous BMI, SAT, and VAT and logistic models for the binary indicator of obesity (BMI ≥30 kg/m² ), adjusting for demographic variables, individual- and area-level measures of socioeconomic position, and clinical and lifestyle factors.

Participants who lived 60 m from a major roadway had 0.37 kg/m² higher BMI (95% CI: 0.10 to 0.65 kg/m² ), 78.4 cm³ higher SAT (95% CI: 4.5 to 152.3 cm³ ), and 41.8 cm³ higher VAT (95% CI: -4.7 to 88.2 cm³ ) than those who lived 440 m away.

Living closer to a major roadway was associated with higher overall and abdominal adiposity.

Outdoor air pollution represents a potentially modifiable risk factor for stroke. We examined the link between ambient pollution and mortality up to 5 years poststroke, especially for pollutants associated with vehicle exhaust.

Data from the South London Stroke Register, a population-based register covering an urban, multiethnic population, were used. Hazard ratios (HR) for a 1 interquartile range increase in particulate matter <2.5 µm diameter (PM_2.5) and PM <10 µm (PM₁₀) were estimated poststroke using Cox regression, overall and broken down into exhaust and nonexhaust components. Analysis was stratified for ischemic and hemorrhagic strokes and was further broken down by Oxford Community Stroke Project classification.

The hazard of death associated with PM_2.5 up to 5 years after stroke was significantly elevated (P=0.006) for all strokes (HR=1.28; 95% confidence interval [CI], 1.08-1.53) and ischemic strokes (HR, 1.32; 95% CI, 1.08-1.62). Within ischemic subtypes, PM_2.5 pollution increased mortality risk for total anterior circulation infarcts by 2-fold (HR, 2.01; 95% CI, 1.17-3.48; P=0.012) and by 78% for lacunar infarcts (HR, 1.78; 95% CI, 1.18-2.66; P=0.006). PM₁₀ pollution was associated with 45% increased mortality risk for lacunar infarct strokes (HR, 1.45; 95% CI, 1.06-2.00; P=0.022). Separating PM_2.5 and PM₁₀ into exhaust and nonexhaust components did not show increased mortality.

Exposure to certain outdoor PM pollution, particularly PM_2.5, increased mortality risk poststroke up to 5 years after the initial stroke.

Long-term exposure to traffic and particulate matter air pollution is associated with a higher risk of cardiovascular disease, potentially via atherosclerosis promotion. Prior research on associations of traffic and particulate matter with coronary artery calcium Agatston score (CAC), an atherosclerosis correlate, has yielded inconsistent findings. Given this background, we assessed whether residential proximity to major roadway or fine particulate matter were associated with CAC in a Northeastern US study.

We measured CAC ≤2 times from 2002 to 2005 and 2008 to 2011 among Framingham Offspring or Third-Generation Cohort participants. We assessed associations of residential distance to major roadway and residential fine particulate matter (2003 average; spatiotemporal model) with detectable CAC, using generalized estimating equation regression. We used linear mixed effects models to assess associations with loge(CAC). We also assessed associations with CAC progression. Models were adjusted for demographic variables, socioeconomic position markers, and time. Among 3399 participants, 51% had CAC measured twice. CAC was detectable in 47% of observations. At first scan, mean age was 52.2 years (standard deviation 11.7); 51% male. There were no consistent associations with detectable CAC, continuous CAC, or CAC progression. We observed heterogeneous associations of distance to major roadway with odds of detectable CAC by hypertensive status; interpretation of these findings is questionable.

Our findings add to prior work and support evidence against strong associations of traffic or fine particulate matter with the presence, extent, or progression of CAC in a region with relatively low levels of and little variation in fine particulate matter.

Air pollution is being increasingly recognized as a significant risk factor for stroke. There are numerous sources of air pollution including industry, road transport and domestic use of biomass and solid fuels. Early reports of the association between air pollution and stroke come from studies investigating health effects of severe pollution episodes. Several daily time series and case-crossover studies have reported associations with stroke. There is also evidence linking chronic air pollution exposure with stroke and with reduced survival after stroke. A conceptual framework linking air pollution exposure and stroke is proposed. It links acute and chronic exposure to air pollution with pathways to acute and chronic effects on stroke risk. Current evidence regarding potential mechanisms mainly relate to particulate air pollution. Whilst further evidence would be useful, there is already sufficient evidence to support consideration of reduction in air pollution as a preventative measure to reduce the stroke burden globally.

This study examines the effects of nano-size particulate matter (nPM) exposure in the setting of murine reperfused stroke. Particulate matter is a potent source of inflammation and oxidative stress. These processes are known to influence stroke progression through recruitment of marginally viable penumbral tissue into the ischemic core. nPM was collected in an urban area in central Los Angeles, impacted primarily by traffic emissions. Re-aerosolized nPM or filtered air was then administered to mice through whole body exposure chambers for forty-five cumulative hours. Exposed mice then underwent middle cerebral artery occlusion/ reperfusion. Following cerebral ischemia/ reperfusion, mice exposed to nPM exhibited significantly larger infarct volumes and less favorable neurological deficit scores when compared to mice exposed to filtered air. Mice exposed to nPM also demonstrated increases in markers of inflammation and oxidative stress in the region of the ischemic core. The findings suggest a detrimental effect of urban airborne particulate matter exposure in the setting of acute ischemic stroke.

Air quality exposure assessment using personal exposure sampling or direct measurement of spatiotemporal air pollutant concentrations has difficulty and limitations. Most statistical methods used for estimating spatiotemporal air quality do not account for the source characteristics (e.g. emissions). In this study, a prediction method, based on the lognormal probability distribution of hourly-average-spatial concentrations of carbon monoxide (CO) obtained by a CALINE4 model, has been developed and validated in an urban traffic corridor. The data on CO concentrations were collected at three locations and traffic and meteorology within the urban traffic corridor.(1) The method has been developed with the data of one location and validated at other two locations. The method estimated the CO concentrations reasonably well (correlation coefficient, r≥0.96). Later, the method has been applied to estimate the probability of occurrence [P(C≥Cstd] of the spatial CO concentrations in the corridor. The results have been promising and, therefore, may be useful to quantifying spatiotemporal air quality within an urban area.

Environmental exposure is an important but underappreciated risk factor contributing to the development and severity of cardiovascular disease (CVD). The heart and vascular system are highly vulnerable to a number of environmental agents--ambient air pollution and the metals arsenic, cadmium, and lead are widespread and the most-extensively studied. Like traditional risk factors, such as smoking and diabetes mellitus, these exposures advance disease and mortality via augmentation or initiation of pathophysiological processes associated with CVD, including blood-pressure control, carbohydrate and lipid metabolism, vascular function, and atherogenesis. Although residence in highly polluted areas is associated with high levels of cardiovascular risk, adverse effects on cardiovascular health also occur at exposure levels below current regulatory standards. Considering the widespread prevalence of exposure, even modest contributions to CVD risk can have a substantial effect on population health. Evidence-based clinical and public-health strategies aimed at reducing environmental exposures from current levels could substantially lower the burden of CVD-related death and disability worldwide.

Living near major roadways has been associated with increased risk of cardiovascular morbidity and mortality, presumably from exposure to elevated levels of traffic-related air and/or noise pollution. This association may potentially be mediated through increased risk of incident hypertension, but results from prior studies are equivocal. Using Cox proportional hazards models we examined residential proximity to major roadways and incident hypertension among 38,360 participants of the Women's Health Initiative (WHI) Clinical Trial cohorts free of hypertension at enrollment and followed for a median of 7.9 years. Adjusting for participant demographics and lifestyle, trial participation, and markers of individual and neighborhood socioeconomic status, the hazard ratios for incident hypertension were 1.13 (95% CI: 1.00, 1.28), 1.03 (0.95, 1.11), 1.05 (0.99, 1.11), and 1.05 (1.00, 1.10) for participants living ≤50, >50-200, >200-400, and >400-1000 m vs >1000 m from the nearest major roadway, respectively (ptrend=0.013). This association varied substantially by WHI study region with hazard ratios for women living ≤50 m from a major roadway of 1.61 (1.18, 2.20) in the West, 1.51 (1.22, 1.87) in the Northeast, 0.89 (0.70, 1.14) in the South, and 0.94 (0.75, 1.19) in the Midwest. In this large, national cohort of post-menopausal women, residential proximity to major roadways was associated with incident hypertension in selected regions of the U.S. If causal, these results suggest residential proximity to major roadways, as a marker for air, noise and other traffic-related pollution, may be a risk factor for hypertension.

Recent assessments have analyzed the health impacts of PM2.5 from emissions from different locations and sectors using simplified or reduced-form air quality models. Here we present an alternative approach using the adjoint of the Community Multiscale Air Quality (CMAQ) model, which provides source-receptor relationships at highly resolved sectoral, spatial, and temporal scales. While damage resulting from anthropogenic emissions of BC is strongly correlated with population and premature death, we found little correlation between damage and emission magnitude, suggesting that controls on the largest emissions may not be the most efficient means of reducing damage resulting from anthropogenic BC emissions. Rather, the best proxy for locations with damaging BC emissions is locations where premature deaths occur. Onroad diesel and nonroad vehicle emissions are the largest contributors to premature deaths attributed to exposure to BC, while onroad gasoline emissions cause the highest deaths per amount emitted. Emissions in fall and winter contribute to more premature deaths (and more per amount emitted) than emissions in spring and summer. Overall, these results show the value of the high-resolution source attribution for determining the locations, seasons, and sectors for which BC emission controls have the most effective health benefits.

This study investigated variations in perceptions of air quality as a function of residential proximity to busy highways, across two suburbs of South Auckland, New Zealand. While plenty is known about the spatial gradients of highway emissions, very little is known about variation of lay understanding at the fine spatial scale and whether there are gradients in severity of concerns. One-hundred and four near-highway residents agreed to participate in a semi-structured interview on their knowledge and attitudes towards highway traffic emissions. Proximity to the highway edge varied within 5-380 m at the predominantly downwind side of the highway and 13-483 m at the upwind side. Likert-type ordered response questions were analysed using multivariate regression. Inverse linear relationships were identified for distance from highway and measures of concern for health impacts, as well as for noise (p<0.05). Positive linear relationships were identified for distance from highway and ratings of both outdoor and indoor air quality (p<0.05). Measures of level of income had no conclusive statistically significant effect on perceptions. Additional discussion was made surrounding participant's open-ended responses, within the context of limited international research. Findings indicate that there may be quantifiable psychological benefits of separating residents just a short distance (40 m+) from highways and that living within such close proximity can be detrimental to wellbeing by restricting local outdoor activity. This work lends additional rationale for a residential separation buffer of ~100 m alongside major highways in the interests of protecting human health.

Living near major roadways has been linked with increased risk of cardiovascular events and worse prognosis. Residential proximity to major roadways may also be associated with increased risk of hypertension, but few studies have evaluated this hypothesis.

We examined the cross-sectional association between residential proximity to major roadways and prevalent hypertension among 5401 postmenopausal women enrolled into the San Diego cohort of the Women's Health Initiative. We used modified Poisson regression with robust error variance to estimate the association between prevalence of hypertension and residential distance to nearest major roadway, adjusting for participant demographics, medical history, indicators of individual and neighborhood socioeconomic status, and for local supermarket/grocery and fast food/convenience store density. The adjusted prevalence ratios for hypertension were 1.22 (95% CI: 1.07, 1.39), 1.13 (1.00, 1.27), and 1.05 (0.99, 1.12) for women living ≤100, >100 to 200, and >200 to 1000 versus >1000 m from a major roadway (P for trend=0.006). In a model treating the natural log of distance to major roadway as a continuous variable, a shift in distance from 1000 to 100 m from a major roadway was associated with a 9% (3%, 16%) higher prevalence of hypertension.

In this cohort of postmenopausal women, residential proximity to major roadways was positively associated with the prevalence of hypertension. If causal, these results suggest that living close to major roadways may be an important novel risk factor for hypertension.

Research links air pollution mostly to respiratory and cardiovascular disease. The effects of air pollution on the central nervous system (CNS) are not broadly recognized. Urban outdoor pollution is a global public health problem particularly severe in megacities and in underdeveloped countries, but large and small cities in the United States and the United Kingom are not spared. Fine and ultrafine particulate matter (UFPM) defined by aerodynamic diameter (<2.5-μm fine particles, PM2.5, and <100-nm UFPM) pose a special interest for the brain effects given the capability of very small particles to reach the brain. In adults, ambient pollution is associated to stroke and depression, whereas the emerging picture in children show significant systemic inflammation, immunodysregulation at systemic, intratechal and brain levels, neuroinflammation and brain oxidative stress, along with the main hallmarks of Alzheimer and Parkinson's diseases: hyperphosphorilated tau, amyloid plaques and misfolded α-synuclein. Animal models exposed to particulate matter components show markers of both neuroinflammation and neurodegeneration. Epidemiological, cognitive, behavioral and mechanistic studies into the association between air pollution exposures and the development of CNS damage particularly in children are of pressing importance for public health and quality of life. Primary health providers have to include a complete prenatal and postnatal environmental and occupational history to indoor and outdoor toxic hazards and measures should be taken to prevent or reduce further exposures.

Residential proximity to green space has been associated with physical and mental health benefits, but whether green space is associated with post-stroke survival has not been studied.

Patients ≥ 21 years of age admitted to the Beth Israel Deaconess Medical Center (BIDMC) between 1999 and 2008 with acute ischemic stroke were identified. Demographics, presenting symptoms, medical history and imaging results were abstracted from medical records at the time of hospitalization for stroke onset. Addresses were linked to average Normalized Difference Vegetation Index, distance to roadways with more than 10,000 cars/day, and US census block group. Deaths were identified through June 2012 using the Social Security Death Index.

There were 929 deaths among 1645 patients with complete data (median follow up: 5 years). In multivariable Cox models adjusted for indicators of medical history, demographic and socioeconomic factors, the hazard ratio for patients living in locations in the highest quartile of green space compared to the lowest quartile was 0.78 (95% Confidence Interval: 0.63-0.97) (p-trend = 0.009). This association remained statistically significant after adjustment for residential proximity to a high traffic road.

Residential proximity to green space is associated with higher survival rates after ischemic stroke in multivariable adjusted models. Further work is necessary to elucidate the underlying mechanisms for this association, and to better understand the exposure-response relationships and susceptibility factors that may contribute to higher mortality in low green space areas.