Effects of particulate matter and antioxidant dietary intake on blood pressure.

OBJECTIVES: We assessed 2 pathways through which dietary antioxidants may counter adverse effects of exposure to particulate matter less than 2.5 micrometers in diameter (PM2.5) on blood pressure (BP): main (compensatory) and modifying (protective) models. METHODS: We used 2002 to 2003 data from the Detroit Healthy Environments Partnership community survey conducted with a multiethnic sample of adults (n = 347) in low- to moderate-income, predominantly Hispanic and non-Hispanic Black neighborhoods in Detroit, Michigan. We used generalized estimating equations to test the effects of ambient exposure to PM2.5 and dietary antioxidant intake on BP, with adjustment for multiple confounders. RESULTS: Dietary antioxidant intake was inversely associated with systolic BP (b = -0.5; P < .05) and pulse pressure (b = -0.6; P < .05) in neighborhoods closest to major sources of air pollutants. Adverse effects of PM2.5 remained significant after accounting for antioxidant intakes. Exploratory analyses suggested potential modifying effects of antioxidant intake on associations between ambient PM2.5 exposure and BP. CONCLUSIONS: Interventions to improve access to antioxidant-rich foods in polluted urban areas may be protective of cardiovascular health. However, efforts to reduce PM2.5 exposure remain critical for cardiovascular health promotion.

Fine particulate matter air pollution and blood pressure: the modifying role of psychosocial stress.

BACKGROUND: Consensus is growing on the need to investigate the joint effects of psychosocial stress and environmental hazards on health. Some evidence suggests that psychosocial stress may be an important modifier of the association between air pollution respiratory outcomes, but few have examined cardiovascular outcomes. OBJECTIVES: We examined the modifying effect of psychosocial stress on the association between fine particulate matter air pollution (PM2.5) and blood pressure (BP). METHODS: Our data came from the Detroit Healthy Environments Partnership (HEP) 2002-2003 survey. Of 919 participants, BP was collected at two time points in a subset of 347. Building on previous work reporting associations between PM2.5 and BP in this sample, we regressed systolic (SBP) and diastolic (DBP) BP and pulse pressure (PP), in separate linear models, on the interaction among psychosocial stress, PM2.5, and HEP neighborhood (Southwest, Eastside, Northwest). RESULTS: The association between PM2.5 and SBP was stronger for those who reported high levels of stress, but this interaction was significant only in the Southwest Detroit neighborhood. Southwest Detroit residents who reported low stress showed 2.94 mmHg (95% CI: -0.85, 6.72) increase in SBP for each 10 µg/m(3) increase in 2-day prior PM2.5 exposure. Those who reported high stress showed 9.05 mmHg (95% CI: 3.29, 14.81) increase in SBP for each 10 µg/m(3) increase in PM2.5 exposure. CONCLUSIONS: These results suggest that psychosocial stress may increase vulnerability to the hypertensive effects of PM2.5. This work contributes to an understanding of the ways in which the social and physical environments may jointly contribute to poor health and to health disparities.

PM2.5-induced cardiovascular dysregulation in rats is associated with elemental carbon and temperature-resolved carbon subfractions.

BACKGROUND: We tested the hypothesis that cardiovascular responses to PM2.5 exposure will be enhanced in hypertensive rats and linked to specific carbonaceous pollutants in an urban industrial setting. METHODS: Spontaneously hypertensive rats were exposed by inhalation to concentrated PM2.5 in an industrial area of Dearborn, Michigan, for four consecutive summer days. Blood pressure (BP), heart rate (HR) and HR variability (HRV) metrics (SDNN, RMSSD) were assessed by radiotelemetry and compared to 1 h- and 8 h-averaged fluctuations in PM2.5 composition, with a focus on elemental and organic carbon (EC and OC, respectively), and temperature-resolved subfractions (EC1-EC5, PC (pyrolized carbon), and OC1-OC4), as well as other major and minor PM components. RESULTS: Mean HR and BP were increased, while HRV was decreased over 4 days of exposure. Using 1 h averages, EC (1 µg/m3 increase) was associated with increased HR of 11-32 bpm (4-11% increase), 1.2-1.5 ms (22-27%) decreases in SDNN, 3-14 mmHg (1.5-8%) increases in systolic BP, and 5-12 mmHg (4-9%) increases in diastolic BP. By comparison, associations with OC were negligible. Using 8 h averages, EC subfractions were linked with increased heart rate (EC1: 13 bpm; EC2, EC3, PC: <5 bpm) and SDNN (EC1> > EC2 > EC3, EC4, PC), but with decreased RMSSD (EC2, EC5 > EC3, EC4). Minimal effects were associated with OC and OC1. Associations between carbon subfractions and BP were negligible. Associations with non-carbonaceous components and trace elements were generally non-significant or of negligible effect size. CONCLUSIONS: These findings are the first to describe associations between acute cardiovascular responses and thermally resolved carbon subfractions. We report that cardiovascular responses to PM2.5 carbonaceous materials appear to be driven by EC and its EC1 fraction.

No effect of acute exposure to coarse particulate matter air pollution in a rural location on high-density lipoprotein function.

CONTEXT: High-density lipoprotein (HDL) particles perform numerous vascular-protective functions. Animal studies demonstrate that exposure to fine or ultrafine particulate matter (PM) can promote HDL dysfunction. However, the impact of PM on humans remains unknown. OBJECTIVE: We aimed to determine the effect of exposure to coarse concentrated ambient particles (CAP) on several metrics of HDL function in healthy humans. METHODS: Thirty-two adults (25.9 ± 6.6 years) were exposed to coarse CAP [76.2 ± 51.5 µg·m(-3)] in a rural location and filtered air (FA) for 2 h in a randomized double-blind crossover study. Venous blood collected 2- and 20-h post-exposures was measured for HDL-mediated efflux of [(3)H]-cholesterol from cells and 20-h exposures for HDL anti-oxidant capacity by a fluorescent assay and paraoxonase activity. The changes [median (first, third quartiles)] between exposures among 29 subjects with available results were compared by matched Wilcoxon tests. RESULTS: HDL-mediated cholesterol efflux capacity did not differ between exposures at either time point [16.60% (15.17, 19.19) 2-h post-CAP versus 17.56% (13.43, 20.98) post-FA, p = 0.768 and 14.90% (12.47, 19.15) 20-h post-CAP versus 17.75% (13.22, 23.95) post-FA, p = 0.216]. HOI [0.26 (0.24, 0.35) versus 0.28 (0.25, 0.40), p = 0.198] and paraoxonase activity [0.54 (0.39, 0.82) versus 0.60 µmol·min(-1 )ml plasma(-1) (0.40, 0.85), p = 0.137] did not differ 20-h post-CAP versus FA, respectively. CONCLUSIONS: Brief inhalation of coarse PM from a rural location did not acutely impair several facets of HDL functionality. Whether coarse PM derived from urban sites, fine particles or longer term PM exposures can promote HDL dysfunction warrant future investigations.

Promotion of myofibroblast differentiation through repeated treatment of fibroblasts to low concentrations of PM2.5.

Exposure to particulate matter ≤ 2.5 µm (PM2.5) is a risk factor for many lung diseases. Although the toxicologic effects of PM2.5 on airway epithelium are well-described, the effects of PM2.5 on fibroblasts in the lung are less studied. Here, we sought to examine the effects of PM2.5 on the differentiation of fibroblasts into myofibroblasts. Although a single treatment of fibroblasts did not result in a change in collagen or the myofibroblast marker α-SMA, exposing fibroblasts to sequential treatments with PM2.5 at low concentrations caused a robust increase in these proteins. Treatment of fibroblasts with IMD0354, an inhibitor to nuclear factor κB, but not with an antagonist to aryl hydrocarbon receptor, abolished the ability of PM2.5 to induce myofibroblast differentiation. These data demonstrate that potential impact of PM2.5 to fibroblast activation and fibrosis and support the importance of utilizing low concentrations and varying exposure protocols to toxicologic studies.

Ambient fine particulate matter and ozone exposures induce inflammation in epicardial and perirenal adipose tissues in rats fed a high fructose diet.

BACKGROUND: Inflammation and oxidative stress play critical roles in the pathogenesis of inhaled air pollutant-mediated metabolic disease. Inflammation in the adipose tissues niches are widely believed to exert important effects on organ dysfunction. Recent data from both human and animal models suggest a role for inflammation and oxidative stress in epicardial adipose tissue (EAT) as a risk factor for the development of cardiovascular disease. We hypothesized that inhalational exposure to concentrated ambient fine particulates (CAPs) and ozone (O3) exaggerates inflammation and oxidative stress in EAT and perirenal adipose tissue (PAT). METHODS: Eight- week-old Male Sprague-Dawley rats were fed a normal diet (ND) or high fructose diet (HFr) for 8 weeks, and then exposed to ambient AIR, CAPs at a mean of 356 µg/m3, O3 at 0.485 ppm, or CAPs (441 µg/m3) + O3 (0.497 ppm) in Dearborn, MI, 8 hours/day, 5 days/week, for 9 days over 2 weeks. RESULTS: EAT and PAT showed whitish color in gross, and less mitochondria, higher mRNA expression of white adipose specific and lower brown adipose specific genes than in brown adipose tissues. Exposure to CAPs and O3 resulted in the increase of macrophage infiltration in both EAT and PAT of HFr groups. Proinflammatory genes of Tnf-α, Mcp-1 and leptin were significantly upregulated while IL-10 and adiponectin, known as antiinflammatory genes, were reduced after the exposures. CAPs and O3 exposures also induced an increase in inducible nitric oxide synthase (iNOS) protein expression, and decrease in mitochondrial area in EAT and PAT. We also found significant increases in macrophages of HFr-O3 rats. The synergetic interaction of HFr and dirty air exposure on the inflammation was found in most of the experiments. Surprisingly, exposure to CAPs or O3 induced more significant inflammation and oxidative stress than co-exposure of CAPs and O3 in EAT and PAT. CONCLUSION: EAT and PAT are both white adipose tissues. Short-term exposure to CAPs and O3, especially with high fructose diet, induced inflammation and oxidative stress in EAT and PAT in rats. These findings may provide a link between air-pollution exposure and accelerated susceptibility to cardiovascular disease and metabolic complications.

The effect of acute exposure to coarse particulate matter air pollution in a rural location on circulating endothelial progenitor cells: results from a randomized controlled study.

CONTEXT: Fine particulate matter (PM) air pollution has been associated with alterations in circulating endothelial progenitor cell (EPC) levels, which may be one mechanism whereby exposures promote cardiovascular diseases. However, the impact of coarse PM on EPCs is unknown. OBJECTIVE: We aimed to determine the effect of acute exposure to coarse concentrated ambient particles (CAP) on circulating EPC levels. METHODS: Thirty-two adults (25.9 ± 6.6 years) were exposed to coarse CAP (76.2 ± 51.5 µg m(-3)) in a rural location and filtered air (FA) for 2 h in a randomized double-blind crossover study. Peripheral venous blood was collected 2 and 20 h post-exposures for circulating EPC (n = 21), white blood cell (n = 24) and vascular endothelial growth factor (VEGF) (n = 16-19) levels. The changes between exposures were compared by matched Wilcoxon signed-rank tests. RESULTS: Circulating EPC levels were elevated 2 [108.29 (6.24-249.71) EPC mL(-1); median (25th-75th percentiles), p = 0.052] and 20 h [106.86 (52.91-278.35) EPC mL(-1), p = 0.008] post-CAP exposure compared to the same time points following FA [38.47 (0.00-84.83) and 50.16 (0.00-104.79) EPC mL(-1)]. VEGF and white blood cell (WBC) levels did not differ between exposures. CONCLUSIONS: Brief inhalation of coarse PM from a rural location elicited an increase in EPCs that persisted for at least 20 h. The underlying mechanism responsible may reflect a systemic reaction to an acute "endothelial injury" and/or a circulating EPC response to sympathetic nervous system activation.

Atmospheric Dry and Wet Deposition of Total Phosphorus to the Great Lakes.

Quantifying atmospheric loadings of total phosphorus (TP) to freshwater environments is essential to improve understanding of its fate and transport, and to mitigate the effects of excessive levels in freshwater ecosystems. To date, atmospheric deposition of TP in the U.S. is poorly characterized due to the lack of long-term deposition observations. Here, we integrate several historical datasets to develop an estimate of dry and wet deposition to the Great Lakes region. For dry deposition, we use TP concentrations in fine particulate matter (PM2.5) samples from fourteen land-based IMPROVE sites (2013-2020) upwind of the Great Lakes to provide new fine particle phosphorus dry deposition estimates. For wet deposition, we use TP concentrations in wet-only precipitation samples collected at eleven land-based sites (2001-2009) in the Great Lakes region. For both wet and dry deposition, a seasonal cycle is evident with higher concentrations in warmer and wetter months when compared to colder months. Additionally, there is an increasing gradient from north to south in wet deposition, likely driven by both higher precipitation and increased emissions near southern sites. Despite different sampling time periods, these updated observations can provide further constraints on the TP loadings to each of the five Great Lakes. We estimate annual deposition of TP to Lakes Superior, Michigan, Huron, Erie and Ontario at 526, 702, 495, 212, and 185 MTA per year, which is lower than prior estimates for Lakes Superior, Erie and Ontario, comparable for Lake Huron, and about two times greater for Lake Michigan. When considering only the contribution of fine particulate PM to the dry deposition, wet deposition dominated over dry at all lakes except for Lake Huron. However, prior global estimates suggest greater contributions from larger particles (PM10 and PM100), yet observations to validate these estimates over the Great Lakes are not available. Our findings indicate that dry deposition of a range of particle sizes are needed to constrain the total atmospheric deposition of TP over the Great Lakes.

Investigation of local mercury deposition from a coal-fired power plant using mercury isotopes.

Coal combustion accounts for approximately two-thirds of global anthropogenic mercury (Hg) emissions. Enhanced deposition of Hg can occur close to coal-fired utility boilers (CFUBs), but it is difficult to link specific point sources with local deposition. Measurement of Hg stable isotope ratios in precipitation holds promise as a tool to assist in the identification of local Hg deposition related to anthropogenic emissions. We collected daily event precipitation samples in close proximity to a large CFUB in Crystal River, Florida. Precipitation samples collected in Crystal River were isotopically distinct and displayed large negative δ(202)Hg values (mean = -2.56‰, 1 SD = 1.10‰, n = 28). In contrast, precipitation samples collected at other sites in FL that were not greatly impacted by local coal combustion were characterized by δ(202)Hg values close to 0‰ (mean = 0.07‰, 1 SD = 0.17‰, n = 13). These results indicate that, depending on factors such as powdered coal isotopic composition and efficiency of Hg removal from flue gas, Hg deposited near CFUBs can be isotopically distinct. As this tool is further refined through future studies, Hg stable isotopes may eventually be used to quantify local deposition of Hg emitted by large CFUBs.

Climate change and health: indoor heat exposure in vulnerable populations.

INTRODUCTION: Climate change is increasing the frequency of heat waves and hot weather in many urban environments. Older people are more vulnerable to heat exposure but spend most of their time indoors. Few published studies have addressed indoor heat exposure in residences occupied by an elderly population. The purpose of this study is to explore the relationship between outdoor and indoor temperatures in homes occupied by the elderly and determine other predictors of indoor temperature. MATERIALS AND METHODS: We collected hourly indoor temperature measurements of 30 different homes; outdoor temperature, dewpoint temperature, and solar radiation data during summer 2009 in Detroit, MI. We used mixed linear regression to model indoor temperatures' responsiveness to weather, housing and environmental characteristics, and evaluated our ability to predict indoor heat exposures based on outdoor conditions. RESULTS: Average maximum indoor temperature for all locations was 34.85°C, 13.8°C higher than average maximum outdoor temperature. Indoor temperatures of single family homes constructed of vinyl paneling or wood siding were more sensitive than brick homes to outdoor temperature changes and internal heat gains. Outdoor temperature, solar radiation, and dewpoint temperature predicted 38% of the variability of indoor temperatures. CONCLUSIONS: Indoor exposures to heat in Detroit exceed the comfort range among elderly occupants, and can be predicted using outdoor temperatures, characteristics of the housing stock and surroundings to improve heat exposure assessment for epidemiological investigations. Weatherizing homes and modifying home surroundings could mitigate indoor heat exposure among the elderly.

Monitoring SARS-CoV-2 in air and on surfaces and estimating infection risk in buildings and buses on a university campus.

BACKGROUND: Evidence is needed on the presence of SARS-CoV-2 in various types of environmental samples and on the estimated transmission risks in non-healthcare settings on campus. OBJECTIVES: The objective of this research was to collect data on SARS-CoV-2 viral load and to examine potential infection risks of people exposed to the virus in publicly accessible non-healthcare environments on a university campus. METHODS: Air and surface samples were collected using wetted wall cyclone bioaerosol samplers and swab kits, respectively, in a longitudinal environmental surveillance program from August 2020 until April 2021 on the University of Michigan Ann Arbor campus. Quantitative rRT-PCR with primers and probes targeting gene N1 were used for SARS-CoV-2 RNA quantification. The RNA concentrations were used to estimate the probability of infection by quantitative microbial risk assessment modeling and Monte-Carlo simulation. RESULTS: In total, 256 air samples and 517 surface samples were collected during the study period, among which positive rates were 1.6% and 1.4%, respectively. Point-biserial correlation showed that the total case number on campus was significantly higher in weeks with positive environmental samples than in non-positive weeks (p = 0.001). The estimated probability of infection was about 1 per 100 exposures to SARS-CoV-2-laden aerosols through inhalation and as high as 1 per 100,000 exposures from contacting contaminated surfaces in simulated scenarios. SIGNIFICANCE: Viral shedding was demonstrated by the detection of viral RNA in multiple air and surface samples on a university campus. The low overall positivity rate indicated that the risk of exposure to SARS-CoV-2 at monitored locations was low. Risk modeling results suggest that inhalation is the predominant route of exposure compared to surface contact, which emphasizes the importance of protecting individuals from airborne transmission of SARS-CoV-2 and potentially other respiratory infectious diseases. IMPACT: Given the reoccurring epidemics caused by highly infectious respiratory viruses in recent years, our manuscript reinforces the importance of monitoring environmental transmission by the simultaneous sampling and integration of multiple environmental surveillance matrices for modeling and risk assessment.

Ambient air pollution and risk for ischemic stroke and transient ischemic attack.

OBJECTIVE: Data on the association between air pollution and cerebrovascular disease in the United States are limited. The objective of this study was to investigate the association between short-term exposure to ambient air pollution and risk for ischemic cerebrovascular events in a US community. METHODS: Daily counts of ischemic strokes/transient ischemic attacks (TIAs) (2001-2005) were obtained from the population-based Brain Attack Surveillance in Corpus Christi (BASIC) Project. Daily particulate matter less than 2.5microm in diameter (PM(2.5)), ozone (O(3)), and meteorological data were obtained from Texas Commission on Environmental Quality. To examine the association between PM(2.5) and stroke/TIA risk, we used Poisson regression. Separate models included same-day PM(2.5), PM(2.5) lagged 1 to 5 days, and an averaged lag effect. All models were adjusted for temperature, day of week, and temporal trends in stroke/TIA. The effects of O(3) were also investigated. RESULTS: Median PM(2.5) was 7.0microg/m(3) (interquartile range, 4.8-10.0microg/m(3)). There were borderline significant associations between same-day (relative risk [RR], 1.03; 95% confidence interval [CI], 0.99-1.07 for an interquartile range increase in PM(2.5)) and previous-day (RR, 1.03; 95% CI, 1.00-1.07) PM(2.5) and stroke/TIA risk. These associations were independent of O(3), which demonstrated similar associations with stroke/TIA risk (same-day RR, 1.02; 95% CI, 0.97-1.08; previous-day RR, 1.04; 95% CI, 0.99-1.09). INTERPRETATION: We observed associations between recent PM(2.5) and O(3) exposure and ischemic stroke/TIA risk even in this community with relatively low pollutant levels. This study provides data on environmental exposures and stroke risk in the United States, and suggests future research on ambient air pollution and stroke is warranted.

Associations between recent exposure to ambient fine particulate matter and blood pressure in the Multi-ethnic Study of Atherosclerosis (MESA).

BACKGROUND: Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter

Airborne particulate matter exposure and urinary albumin excretion: the Multi-Ethnic Study of Atherosclerosis.

OBJECTIVES: Understanding mechanistic pathways linking airborne particle exposure to cardiovascular health is important for causal inference and setting environmental standards. We evaluated whether urinary albumin excretion, a subclinical marker of microvascular function which predicts cardiovascular events, was associated with ambient particle exposure. METHODS: Urinary albumin and creatinine were measured among members of the Multi-Ethnic Study of Atherosclerosis at three visits during 2000-2004. Exposure to PM(2.5) and PM(10) (microg/m(3)) was estimated from ambient monitors for 1 month, 2 months and two decades before visit one. We regressed recent and chronic (20 year) particulate matter (PM) exposure on urinary albumin/creatinine ratio (UACR, mg/g) and microalbuminuria at first examination, controlling for age, race/ethnicity, sex, smoking, second-hand smoke exposure, body mass index and dietary protein (n = 3901). We also evaluated UACR changes and development of microalbuminuria between the first, and second and third visits which took place at 1.5- to 2-year intervals in relation to chronic PM exposure prior to baseline using mixed models. RESULTS: Chronic and recent particle exposures were not associated with current UACR or microalbuminuria (per 10 microg/m(3) increment of chronic PM(10) exposure, mean difference in log UACR = -0.02 (95% CI -0.07 to 0.03) and relative probability of having microalbuminuria = 0.92 (95% CI 0.77 to 1.08)) We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 microg/m(3) increment in chronic PM(10) exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3-4 years, although 95% confidence intervals included the null (95% CI 0.96 to 1.36). CONCLUSIONS: UACR is not a strong mechanistic marker for the possible influence of air pollution on cardiovascular health in this sample.

Independent and Joint Contributions of Fine Particulate Matter Exposure and Population Vulnerability to Mortality in the Detroit Metropolitan Area.

Fine particulate matter is associated with adverse health outcomes. Exposure to fine particulate matter may disproportionately affect urban communities with larger numbers of vulnerable residents. We used multilevel logistic regression models to estimate the joint effects of fine particulate matter (PM2.5) and population vulnerabilities on cardiopulmonary mortality (CPM). We estimated the health benefits of reductions in PM2.5 across census tracts in the Detroit metropolitan area with varying levels of population vulnerability, using cluster-specific odds ratios scaled to reflect PM2.5-attributable cardiopulmonary risk. PM2.5 and population vulnerability were independently associated with odds of CPM. Odds of CPM and the number of deaths attributable to PM2.5 were greatest in census tracts with both high PM2.5 exposures and population vulnerability. Reducing PM2.5 in census tracts with high PM2.5 would lead to an estimated 18% annual reduction in PM2.5-attributable CPM. Between 78⁻79% of those reductions in CPM would occur within census tracts with high population vulnerabilities. These health benefits of reductions in PM2.5 occurred at levels below current U.S. reference concentrations. Focusing efforts to reduce PM2.5 in the Detroit metropolitan area in census tracts with currently high levels would also lead to greater benefits for residents of census tracts with high population vulnerabilities.

Effects of Airborne Particulate Matter on Respiratory Health in a Community near a Cement Factory in Chilanga, Zambia: Results from a Panel Study.

We conducted a panel study to investigate seasonal variations in concentrations of airborne PM2.5 and PM10 and the effects on respiratory health in a community near a cement factory; in Chilanga; Zambia. A panel of 63 and 55 participants aged 21 to 59 years from a community located at the edge of the factory within 1 km and a control community located 18 km from the factory respectively; were followed up for three climatic seasons July 2015 to February 2016. Symptom diary questionnaires were completed and lung function measurements taken daily for 14 days in each of the three climatic seasons. Simultaneously, PM2.5 and PM10 concentrations in ambient air were monitored at a fixed site for each community. Mean seasonal concentrations of PM2.5 and PM10 ranged from 2.39-24.93 µg/m3 and 7.03-68.28 µg/m³ respectively in the exposed compared to the control community 1.69-6.03 µg/m³ and 2.26-8.86 µg/m³. The incident rates of reported respiratory symptoms were higher in the exposed compared to the control community: 46.3 vs. 13.8 for cough; 41.2 vs. 9.6 for phlegm; 49.0 vs.12.5 for nose; and 13.9 vs. 3.9 for wheeze per 100 person-days. There was a lower performance on all lung indices in the exposed community compared to the control; overall the mean FEV1 (forced expiratory volume in one second) and FVC (forced vital capacity) predicted percentage for the exposed was six and four percentage points lower than the control. Restriction of industrial emissions coupled with on-going monitoring and regulatory enforcement are needed to ensure that PM (airborne particulate matter) levels in the ambient air are kept within recommended levels to safeguard the respiratory health of nearby community residents.

Combustion-Related Organic Species in Temporally Resolved Urban Airborne Particulate Matter.

Accurate characterization of the chemical composition of particulate matter (PM) is essential for improved understanding of source attribution and resultant health impacts. To explore this we conducted ambient monitoring of a suite of 15 combustion-related organic species in temporally resolved PM 2.5 samples during an ongoing animal exposure study in a near source environment in Detroit, MI. All of the 15 species detected were above the method detection limit in 8 hour samples. This study focused on two molecular classes: Polycyclic Aromatic Hydrocarbons (PAHs) and Hopanes measured in samples. Of the 12 PAHs studied, benzo[b]fluoranthene (169 pg m-3), benzo[g,h,i]perylene (124 pg m-3), and benzo[e]pyrene (118, pg m-3) exhibited the three highest mean concentrations while 17α(H),21ß(H)-Hopane (189 pg m-3) and 17α(H),21ß(H)-30-Norhopane (145 pg m-3) had the highest mean concentrations of the 3 Hopanes analyzed in samples. Ratios of individual compound concentrations to total compound concentrations (∑ 15 compounds) showed the greatest daily variation for 17α(H),21ß(H)-Hopane (11-28%) and 17α(H),21ß(H)-30-Norhopane (8-20%). Diagnostic PAH concentration ratios ([IP]/[IP + BP] (range 0.30 - 0.45), [BaP]/[BaP+BeP] (range 0.26 - 0.44), [BaP]/[BP] (range 0.41 - 0.82), [Bb]/[Bk] (range 2.07 - 2.66), in samples reflected impacts froma mixture of combustion sources consistent with greater prevalence of petroleum combustion source emissions (gasoline, diesel, kerosene, and crude oil) compared to coal or wood combustion emissions impacts at this urban site. Results from this study demonstrate that short duration sampling for organic speciation provides temporally relevant exposure information.

Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential effect modification by nutrition.

OBJECTIVES: The specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. METHODS: We propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. CONCLUSIONS: Protecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.

Acute increase in blood pressure during inhalation of coarse particulate matter air pollution from an urban location.

Particulate matter (PM) air pollution is a leading global risk factor for cardiovascular mortality. Although exposure to fine PM <2.5 µm raises arterial blood pressure (BP), few studies have evaluated the impact of coarse PM which differs in size (2.5-10 µm), sources, and chemistry. Twenty-nine healthy adults (30.4 ± 8.2 years) underwent a randomized double-blind crossover study involving 2-hour exposures to concentrated ambient coarse PM (164.2 ± 80.4 µg/m(3)) at an urban location (Dearborn, Michigan) versus filtered air. Cardiovascular outcomes were measured during, immediately, and 2 hours after exposures. Both systolic (1.9 mm Hg; 95% confidence interval: 0.96, 2.8; P < .001) and diastolic (1.9 mm Hg; 95% confidence interval: 1.1, 2.7; P < .001) BP levels were higher throughout coarse PM compared with filtered air exposures by mixed-model analyses. Heart rate variability, endothelial function, and arterial compliance were not significantly affected. Brief exposure to coarse PM in an urban environment raises arterial BP. These findings add mechanistic support to the contention that coarse PM may be capable of promoting cardiovascular events.

Social and physical environments and disparities in risk for cardiovascular disease: the healthy environments partnership conceptual model.

The Healthy Environments Partnership (HEP) is a community-based participatory research effort investigating variations in cardiovascular disease risk, and the contributions of social and physical environments to those variations, among non-Hispanic black, non-Hispanic white, and Hispanic residents in three areas of Detroit, Michigan. Initiated in October 2000 as a part of the National Institute of Environmental Health Sciences' Health Disparities Initiative, HEP is affiliated with the Detroit Community-Academic Urban Research Center. The study is guided by a conceptual model that considers race-based residential segregation and associated concentrations of poverty and wealth to be fundamental factors influencing multiple, more proximate predictors of cardiovascular risk. Within this model, physical and social environments are identified as intermediate factors that mediate relationships between fundamental factors and more proximate factors such as physical activity and dietary practices that ultimately influence anthropomorphic and physiologic indicators of cardiovascular risk. The study design and data collection methods were jointly developed and implemented by a research team based in community-based organizations, health service organizations, and academic institutions. These efforts include collecting and analyzing airborne particulate matter over a 3-year period; census and administrative data; neighborhood observation checklist data to assess aspects of the physical and social environment; household survey data including information on perceived stressors, access to social support, and health-related behaviors; and anthropometric, biomarker, and self-report data as indicators of cardiovascular health. Through these collaborative efforts, HEP seeks to contribute to an understanding of factors that contribute to racial and socioeconomic health inequities, and develop a foundation for efforts to eliminate these disparities in Detroit.