Residential greenspace and major depression among older adults living in urban and suburban areas with different climates across the United States.

BACKGROUND AND AIM: Residential greenspace could alleviate depression - a leading cause of disability. Fewer studies of depression and greenspace have considered major depression, and, to our knowledge, none have considered how climate, which determines vegetation abundance and type, may change the impacts of greenspace. Our aim was to investigate whether residential greenspace is associated with major depression among older adults and explore effect modification by climate. METHODS: We used biennial interviews between 2008 and 2016 from the Health and Retirement Study. We calculated greenness within walking distance of home addresses as the maximum NDVI for the year of each participant interview averaged within a 1 km buffer. Reflecting clinical criteria, a score of ≥5 on the CIDI-SF indicated major depression in the preceding 12-months. We characterized climate using Köppen-Geiger classifications. To estimate prevalence ratios, we used Poisson regression. Our models adjusted for sociodemographic characteristics, geography, annual sunshine, and bluespace. RESULTS: The 21,611 eligible participants were 65 ± 10 years old on average, 55% female, 81% White, 12% Black, 10% Hispanic/Latino, and 31% had at least a 4-year college degree. The 12-month prevalence of a major depression was 8%. In adjusted models, more residential greenspace was associated with a lower prevalence of major depression (prevalence ratio per IQR, 0.91; 95% CI, 0.84 to 0.98). There was evidence of effect modification by climate (P forinteraction, 0.062). We observed stronger associations in tropical (prevalence ratio per IQR 0.69; 95% CI, 0.47 to 1.01) and cold (prevalence ratio per IQR, 0.83; 95% CI, 0.74 to 0.93) climates compared to arid (prevalence ratio per IQR 0.99; 95% CI, 0.90 to 1.09) and temperate (prevalence ratio per IQR 0.98; 95% CI, 0.86 to 1.11) climates. CONCLUSIONS: Residential greenspace may help reduce major depression. However, climate may influence how people benefit from greenspace.

Exposure to Primary Air Pollutants Generated by Highway Traffic and Daily Mortality Risk in Near-Road Communities: A Case-Crossover Study.

Most epidemiologic studies fail to capture the impact of spatiotemporal fluctuations in traffic on exposure to traffic-related air pollutants in the near-road population. Using a case-crossover design and the Research LINE source (R-LINE) dispersion model with spatiotemporally resolved highway traffic data, we quantified associations between primary pollutants generated by highway traffic-particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5), oxides of nitrogen (NOx), and black carbon (BC)-and daily nonaccidental, respiratory, cardiovascular, and cerebrovascular mortality among persons who had resided within 1 km (0.6 mile) of major highways in the Puget Sound area of Washington State between 2009 and 2013. We estimated these associations using conditional logistic regression, adjusting for time-varying covariates. Although highly resolved modeled concentrations of PM2.5, NOx, and BC from highway traffic in the hours before death were used, we found no evidence of an association between mortality and the preceding 24-hour average PM2.5 exposure (odds ratio = 0.99, 95% confidence interval: 0.96, 1.02) or exposure during shorter averaging periods. This work did not support the hypothesis that mortality risk was meaningfully higher with greater exposures to PM2.5, NOx, and BC from highways in near-road populations, though we did incorporate a novel approach to estimate exposure to traffic-generated air pollution based on detailed traffic congestion data.

Long-term community noise exposure in relation to dementia, cognition, and cognitive decline in older adults.

INTRODUCTION: Exposure to noise might influence risk of Alzheimer's disease (AD) dementia. METHODS: Participants of the Chicago Health and Aging Project (≥65 years) underwent triennial cognitive assessments. For the 5 years preceding each assessment, we estimated 5227 participants' residential level of noise from the community using a spatial prediction model, and estimated associations of noise level with prevalent mild cognitive impairment (MCI) and AD, cognitive performance, and rate of cognitive decline. RESULTS: Among these participants, an increment of 10 A-weighted decibels (dBA) in noise corresponded to 36% and 29% higher odds of prevalent MCI (odds ratio [OR] = 1.36; 95% confidence interval [CI], 1.15 to 1.62) and AD (OR = 1.29, 95% CI, 1.08 to 1.55). Noise level was associated with worse global cognitive performance, principally in perceptual speed (-0.09 standard deviation per 10 dBA, 95% CI: -0.16 to -0.03), but not consistently associated with cognitive decline. DISCUSSION: These results join emerging evidence suggesting that noise may influence late-life cognition and risk of dementia.

Ambient air pollution as a mediator in the pathway linking race/ethnicity to blood pressure elevation: The multi-ethnic study of atherosclerosis (MESA).

BACKGROUND: Racial/ethnic disparities in blood pressure and hypertension have been evident in previous studies, as were associations between race/ethnicity with ambient air pollution and those between air pollution with hypertension. The role of air pollution exposure to racial/ethnic differences in hypertension has not been explored. OBJECTIVE: To assess the potential mediating effects of ambient air pollution on the association between race/ethnicity and blood pressure levels. METHODS: We studied 6,463 White, Black, Hispanic and Chinese adults enrolled across 6 US cities. Systolic (SBP) and diastolic blood pressure (DBP) were measured at Exam 1 (2000-2002) and Exam 2 (2002-2004). Household-level annual average concentrations of fine particulate matter (PM2.5), oxides of nitrogen (NOX), and ozone (O3) for the year 2000 were estimated for participants. RESULTS: The difference in SBP levels by race/ethnicity that was related to higher PM2.5 concentrations compared with White men ("indirect associations") was 0.3 (95% CI: 0.1, 0.6) mmHg for Black men, 0.3 (95% CI: 0.1, 0.6) mmHg for Hispanic men and 1.0 (95% CI: 0.2, 1.8) mmHg for Chinese men. Findings were similar although not statistically significant for women. PM2.5 did not mediate racial/ethnic differences in DBP. Indirect associations were significant for O3 for SBP among women and men and for DBP among men. In contrast, racial/ethnic disparities were attenuated due to exposure to NOX. CONCLUSION: Racial disparities in blood pressure were reduced after accounting for PM2.5 and ozone while increased after accounting for NOX.

Robust distributed lag models using data adaptive shrinkage.

Distributed lag models (DLMs) have been widely used in environmental epidemiology to quantify the lagged effects of air pollution on an outcome of interest such as mortality or cardiovascular events. Generally speaking, DLMs can be applied to time-series data where the current measure of an independent variable and its lagged measures collectively affect the current measure of a dependent variable. The corresponding distributed lag (DL) function represents the relationship between the lags and the coefficients of the lagged exposure variables. Common choices include polynomials and splines. On one hand, such a constrained DLM specifies the coefficients as a function of lags and reduces the number of parameters to be estimated; hence, higher efficiency can be achieved. On the other hand, under violation of the assumption about the DL function, effect estimates can be severely biased. In this article, we propose a general framework for shrinking coefficient estimates from an unconstrained DLM, that are unbiased but potentially inefficient, toward the coefficient estimates from a constrained DLM to achieve a bias-variance trade-off. The amount of shrinkage can be determined in various ways, and we explore several such methods: empirical Bayes-type shrinkage, a hierarchical Bayes approach, and generalized ridge regression. We also consider a two-stage shrinkage approach that enforces the effect estimates to approach zero as lags increase. We contrast the various methods via an extensive simulation study and show that the shrinkage methods have better average performance across different scenarios in terms of mean squared error (MSE).We illustrate the methods by using data from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS) to explore the association between PM$_{10}$, O$_3$, and SO$_2$ on three types of disease event counts in Chicago, IL, from 1987 to 2000.

Association Between Long-term Exposure to Ambient Air Pollution and Change in Quantitatively Assessed Emphysema and Lung Function.

Importance: While air pollutants at historical levels have been associated with cardiovascular and respiratory diseases, it is not known whether exposure to contemporary air pollutant concentrations is associated with progression of emphysema. Objective: To assess the longitudinal association of ambient ozone (O3), fine particulate matter (PM2.5), oxides of nitrogen (NOx), and black carbon exposure with change in percent emphysema assessed via computed tomographic (CT) imaging and lung function. Design, Setting, and Participants: This cohort study included participants from the Multi-Ethnic Study of Atherosclerosis (MESA) Air and Lung Studies conducted in 6 metropolitan regions of the United States, which included 6814 adults aged 45 to 84 years recruited between July 2000 and August 2002, and an additional 257 participants recruited from February 2005 to May 2007, with follow-up through November 2018. Exposures: Residence-specific air pollutant concentrations (O3, PM2.5, NOx, and black carbon) were estimated by validated spatiotemporal models incorporating cohort-specific monitoring, determined from 1999 through the end of follow-up. Main Outcomes and Measures: Percent emphysema, defined as the percent of lung pixels less than -950 Hounsfield units, was assessed up to 5 times per participant via cardiac CT scan (2000-2007) and equivalent regions on lung CT scans (2010-2018). Spirometry was performed up to 3 times per participant (2004-2018). Results: Among 7071 study participants (mean [range] age at recruitment, 60 [45-84] years; 3330 [47.1%] were men), 5780 were assigned outdoor residential air pollution concentrations in the year of their baseline examination and during the follow-up period and had at least 1 follow-up CT scan, and 2772 had at least 1 follow-up spirometric assessment, over a median of 10 years. Median percent emphysema was 3% at baseline and increased a mean of 0.58 percentage points per 10 years. Mean ambient concentrations of PM2.5 and NOx, but not O3, decreased substantially during follow-up. Ambient concentrations of O3, PM2.5, NOx, and black carbon at study baseline were significantly associated with greater increases in percent emphysema per 10 years (O3: 0.13 per 3 parts per billion [95% CI, 0.03-0.24]; PM2.5: 0.11 per 2 µg/m3 [95% CI, 0.03-0.19]; NOx: 0.06 per 10 parts per billion [95% CI, 0.01-0.12]; black carbon: 0.10 per 0.2 µg/m3 [95% CI, 0.01-0.18]). Ambient O3 and NOx concentrations, but not PM2.5 concentrations, during follow-up were also significantly associated with greater increases in percent emphysema. Ambient O3 concentrations, but not other pollutants, at baseline and during follow-up were significantly associated with a greater decline in forced expiratory volume in 1 second per 10 years (baseline: 13.41 mL per 3 parts per billion [95% CI, 0.7-26.1]; follow-up: 18.15 mL per 3 parts per billion [95% CI, 1.59-34.71]). Conclusions and Relevance: In this cohort study conducted between 2000 and 2018 in 6 US metropolitan regions, long-term exposure to ambient air pollutants was significantly associated with increasing emphysema assessed quantitatively using CT imaging and lung function.

Vulnerability to the Cardiovascular Effects of Ambient Heat in Six US Cities: Results from the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: With climate change, temperatures are increasing. Heat-associated health events disproportionately affect certain subpopulations. However, prior research has often lacked information on individual-level health and air conditioning and neighborhood stressors/protections. OBJECTIVES: To assess whether (1) heat (2-day mean temperature above local 75th percentiles) is associated with increased heart rate and decreased blood pressure, controlling for age, time, season, daily ozone, and daily particulate matter (PM2.5) and (2) associations differ by antihypertensive medication use, renal function, fasting glucose, emotional support, air conditioning ownership and use, normalized difference vegetation index, neighborhood safety, and residence- specific oxides of nitrogen and PM2.5. METHODS: Health and behavioral characteristics were obtained repeatedly on participants of the Multi-Ethnic Study of Atherosclerosis in six US sites (2000-2010). These were linked with airport temperature, air quality, and satellite- and survey-derived neighborhood characteristics. We used a fixed-effects design, regressing health outcomes on linear temperature splines with knots at the 75th percentiles, interaction terms for each characteristic, and adjustment for month of year, age, PM2.5, and ozone. RESULTS: Overall, heat was not associated with heart rate. However, for a 2°C increase in heat, systolic blood pressure decreased by 1.1 mmHg (95% CI = -1.6, -0.6) and diastolic blood pressure by 0.3 mmHg (95% CI = -0.6, -0.1). Among nonusers of antihypertensive medications, heat-associated decreases in SBP were 2.1 mmHg greater among individuals with central air conditioning versus those without. Confidence intervals around the remaining modifiers were wide after multiple-comparisons corrections or sensitivity analyses. CONCLUSIONS: Outdoor heat is associated with decreasing blood pressure, and cardiovascular vulnerability may vary primarily by ownership of central air conditioning.

Change in Neighborhood Characteristics and Change in Coronary Artery Calcium: A Longitudinal Investigation in the MESA (Multi-Ethnic Study of Atherosclerosis) Cohort.

BACKGROUND: Although some evidence shows that neighborhood deprivation is associated with greater subclinical atherosclerosis, prior studies have not identified what aspects of deprived neighborhoods were driving the association. METHODS: We investigated whether social and physical neighborhood characteristics are related to the progression of subclinical atherosclerosis in 5950 adult participants of the MESA (Multi-Ethnic Study of Atherosclerosis) during a 12-year follow-up period. We assessed subclinical disease using coronary artery calcium (CAC). Neighborhood features examined included density of recreational facilities, density of healthy food stores, and survey-based measures of availability of healthy foods, walking environment, and social environment. We used econometric fixed-effects models to investigate how change in a given neighborhood exposure is related to simultaneous change in subclinical atherosclerosis. RESULTS: Increases in density of neighborhood healthy food stores were associated with decreases in CAC (mean changes in CAC Agatston units per 1-SD increase in neighborhood exposures, -19.99; 95% confidence interval, -35.21 to -4.78) after adjustment for time-varying demographic confounders and computed tomography scanner type. This association remained similar in magnitude after additional adjustment for time-varying behavioral risk factors and depression. The addition of time-varying biomedical factors attenuated associations with CAC slightly (mean changes in CAC per 1-SD increase in neighborhood exposures, -17.60; 95% confidence interval, -32.71 to -2.49). Changes across time in other neighborhood measures were not significantly associated with within-person change in CAC. CONCLUSIONS: Results from this longitudinal study provide suggestive evidence that greater access to neighborhood healthy food resources may slow the development of coronary atherosclerosis in middle-aged and older adults.

Synergism of Short-Term Air Pollution Exposures and Neighborhood Disadvantage on Initial Stroke Severity.

BACKGROUND AND PURPOSE: Little is known about the relation between environment and stroke severity. We investigated associations between environmental exposures, including neighborhood socioeconomic disadvantage and short-term exposure to airborne particulate matter <2.5 µm and ozone, and their interactions with initial stroke severity. METHODS: First-ever ischemic stroke cases were identified from the Brain Attack Surveillance in Corpus Christi project (2000-2012). Associations between pollutants, disadvantage, and National Institutes of Health Stroke Scale were modeled using linear and logistic regression with adjustment for demographics and risk factors. Pollutants and disadvantage were modeled individually, jointly, and with interactions. RESULTS: Higher disadvantage scores and previous-day ozone concentrations were associated with higher odds of severe stroke. Higher levels of particulate matter <2.5 µm were associated with higher odds of severe stroke among those in higher disadvantage areas (odds ratio, 1.24; 95% confidence interval, 1.00-1.55) but not in lower disadvantage areas (odds ratio, 0.82; 95% confidence interval, 0.56-1.22; P interaction =0.097). CONCLUSIONS: Air pollution exposures and neighborhood socioeconomic status may be important in understanding stroke severity. Future work should consider the multiple levels of influence on this important stroke outcome.

Traffic Congestion as a Risk Factor for Mortality in Near-Road Communities: A Case-Crossover Study.

Existing epidemiologic research on traffic largely neglects localized fluctuations. We leveraged finely resolved congestion data to investigate short-term associations with mortality in communities near roadways. We identified all nonaccidental, cardiovascular, cerebrovascular, and respiratory deaths (2009-2013) within 1 km of a highway in the Puget Sound region of Washington State. Using a case-crossover design, we examined the association of congestion 0-150 m, 151-300 m, and 301-1,000 m upwind of a decedent's home with mortality, adjusting for meteorology, holidays, and influenza activity. Among 9,449 deaths, we observed higher odds of cerebrovascular and respiratory mortality with greater upwind congestion, especially congestion near the decedent's home. For each 10-minute-km increase in upwind congestion within 150 m, the odds of cerebrovascular mortality were 1.08 (95% confidence interval (CI): 0.88, 1.33); within 151-300 m, the odds of cerebrovascular mortality were 1.05 (95% CI: 0.98, 1.12) times higher. We observed similar patterns for respiratory mortality, with 1.06 (95% CI: 0.76, 1.50) times higher odds of death with greater upwind congestion within 150 m and 1.02 (95% CI: 0.95, 1.10) times higher odds within 151-300 m. No increased odds of mortality were observed at greater distances, for overall mortality, or with downwind congestion. Unexpectedly, lower odds of cardiovascular mortality were suggested with greater congestion. This work demonstrates the use of nontraditional data to characterize the impacts of near-road exposures.

Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study.

BACKGROUND: Long-term exposure to fine particulate matter less than 2.5 µm in diameter (PM2.5) and traffic-related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness. METHODS: In this prospective 10-year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45-84 years enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010-12 for 3459 participants. Residence-specific spatio-temporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM2.5 and nitrogen oxides (NOX) between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PM2.5, NOX, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology. FINDINGS: In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima-media thickness by 12 µm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the years 2000-10 ranged from 9.2-22.6 µg PM2.5/m(3) and 7.2-139.2 parts per billion (ppb) NOX. For each 5 µg PM2.5/m(3) increase, coronary calcium progressed by 4.1 Agatston units per year (95% CI 1.4-6.8) and for each 40 ppb NOX coronary calcium progressed by 4.8 Agatston units per year (0.9-8.7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 µg/m(3) higher long-term exposure to PM2.5 in intima-media thickness was -0.9 µm per year (95% CI -3.0 to 1.3). For 40 ppb higher NOX, the estimate was 0.2 µm per year (-1.9 to 2.4). INTERPRETATION: Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases. FUNDING: US Environmental Protection Agency and US National Institutes of Health.

Short-term exposures to ambient air pollution and risk of recurrent ischemic stroke.

OBJECTIVE: To investigate the association between short-term changes in ambient pollution (particulate matter <2.5µm in aerodynamic diameter (PM2.5) and ozone (O3)) and the risk of recurrent ischemic stroke among individuals living in a bi-ethnic community. METHODS: We identified recurrent ischemic stroke cases from the population-based Brain Attack Surveillance in Corpus Christi (BASIC) project between 2000 and 2012. Associations between PM2.5 (mean 24-h) and O3 (maximal 8-h) levels, measured on the previous day, and odds of ischemic stroke were assessed using a time-stratified case-crossover design and modeled using conditional logistic regression. RESULTS: There were 317 recurrent ischemic strokes after excluding 41 strokes that occurred on days with missing air pollution data. Mean age was 72 years (SD=12) and median time to stroke recurrence was 1.1 years (IQR: 0.2-2.8 years). Median levels of PM2.5 and O3 over the study period were 7.7µg/m3 (IQR: 5.6-10.7µg/m3) and 35.2 ppb (IQR: 25.0-46.1 ppb), respectively. We observed no associations between previous-day PM2.5 and O3 and odds of recurrent stroke (OR=0.95 per 10µg/m3 of PM2.5, 95% CI: 0.71-1.28 and OR=0.97 per 10ppb of O3, 95% CI: 0.87-1.07) after adjusting for ambient temperature and relative humidity. Co-adjustment of both pollutants did not change the results. CONCLUSION: We found no evidence of associations between previous-day air pollution levels and recurrent ischemic stroke. Research on the influence of air pollutants on risk of stroke recurrence is still in its infancy, and more research is necessary in studies that are adequately powered to understand the relation.

Neighborhood Environments and Incident Hypertension in the Multi-Ethnic Study of Atherosclerosis.

We examined relationships between neighborhood physical and social environments and incidence of hypertension in a cohort of 3,382 adults at 6 sites in the United States over 10 years of follow-up (2000-2011), using data from the Multi-Ethnic Study of Atherosclerosis. The sample was aged 45-84 years (mean = 59 years) and free of clinical cardiovascular disease and hypertension at baseline. Of the participants, 51% were female, 44% white, 23% Hispanic, 21% black, and 13% Chinese-American; 39% of participants developed hypertension during an average of 7.2 years of follow-up. Cox models were used to estimate associations of time-varying cumulative average neighborhood features (survey-based healthy food availability, walking environment, social cohesion, safety, and geographic information system-based density of favorable food stores and recreational resources) with incident hypertension. After adjustment for individual and neighborhood-level covariates, a 1-standard-deviation increase in healthy food availability was associated with a 12% lower rate of hypertension (hazard ratio = 0.88, 95% confidence interval: 0.82, 0.95). Other neighborhood features were not related to incidence of hypertension. The neighborhood food environment is related to the risk of hypertension.

Air Pollution, Cardiovascular Outcomes, and Social Disadvantage: The Multi-ethnic Study of Atherosclerosis.

BACKGROUND: Social factors may enhance health effects of air pollution, yet empirical support is inconsistent. The interaction of social and environmental factors may only be evident with long-term exposures and outcomes that reflect long-term disease development. METHODS: We used cardiac magnetic resonance imaging data from the Multi-Ethnic Study of Atherosclerosis to assess left-ventricular mass index (LVMI) and left-ventricular ejection fraction (LVEF). We assigned residential concentrations of fine particulate matter (PM2.5), oxides of nitrogen, and nitrogen dioxide in the year 2000 to each participant in 2000 using prediction models. We examined modifying roles of four measures of adversity: race/ethnicity, racial/ethnic residential segregation, and socioeconomic status and psychosocial adversity as composite indices on the association between air pollution and LVMI or LVEF. RESULTS: Compared with whites, blacks showed a stronger adjusted association between air pollution and LVMI. For example, for each 5 µg/m greater PM2.5 level, whites showed a 1.0 g/m greater LVMI (95% confidence interval = -1.3, 3.1), while blacks showed an additional 4.0 g/m greater LVMI (95% confidence interval = 0.3, 8.2). Results were similar for oxides of nitrogen and nitrogen dioxide with regard to black race and LVMI. However, we found no evidence of a modifying role of other social factors or ethnic groups. Furthermore, we found no evidence of a modifying role for any social factors or racial/ethnic groups on the association between air pollution and LVEF. CONCLUSIONS: Our results suggest that racial group membership may modify the association between air pollution and cardiovascular disease.

Adopting Clean Fuels and Technologies on School Buses. Pollution and Health Impacts in Children.

RATIONALE: More than 25 million American children breathe polluted air on diesel school buses. Emission reduction policies exist, but the health impacts to individual children have not been evaluated. METHODS: Using a natural experiment, we characterized the exposures and health of 275 school bus riders before, during, and after the adoption of clean technologies and fuels between 2005 and 2009. Air pollution was measured during 597 trips on 188 school buses. Repeated measures of exhaled nitric oxide (FeNO), lung function (FEV1, FVC), and absenteeism were also collected monthly (1,768 visits). Mixed-effects models longitudinally related the adoption of diesel oxidation catalysts (DOCs), closed crankcase ventilation systems (CCVs), ultralow-sulfur diesel (ULSD), or biodiesel with exposures and health. MEASUREMENTS AND MAIN RESULTS: Fine and ultrafine particle concentrations were 10-50% lower on buses using ULSD, DOCs, and/or CCVs. ULSD adoption was also associated with reduced FeNO (-16% [95% confidence interval (CI), -21 to -10%]), greater changes in FVC and FEV1 (0.02 [95% CI, 0.003 to 0.05] and 0.01 [95% CI, -0.006 to 0.03] L/yr, respectively), and lower absenteeism (-8% [95% CI, -16.0 to -0.7%]), with stronger associations among patients with asthma. DOCs, and to a lesser extent CCVs, also were associated with improved FeNO, FVC growth, and absenteeism, but these findings were primarily restricted to patients with persistent asthma and were often sensitive to control for ULSD. No health benefits were noted for biodiesel. Extrapolating to the U.S. population, changed fuel/technologies likely reduced absenteeism by more than 14 million/yr. CONCLUSIONS: National and local diesel policies appear to have reduced children's exposures and improved health.

Racial and Ethnic Differences in Self-Reported Periodontal Disease in the Multi-Ethnic Study of Atherosclerosis (MESA).

PURPOSE: Racial and ethnic disparities in periodontal disease exist in the United States. This study examined the prevalence of self-reported periodontal disease, and the extent to which racial/ethnic disparities in the reported disease were reduced or eliminated after controlling for various risk factors in a multi-ethnic study population of older adults. MATERIALS AND METHODS: Information from the baseline examination (July 2000-August 2002) of the Multi-Ethnic Study of Atherosclerosis (MESA) was used. Study participants (N = 6256) were age 45-84 years and identified themselves as either: white, black, Hispanic or Chinese. Periodontal disease was assessed by self-report; demographic and socioeconomic status (SES) indicators, biomedical risk factors and psychosocial stress factors were used as predictors of self-reported periodontal disease. RESULTS: Chinese displayed the highest prevalence of self-reported periodontal disease (39.8%), followed by blacks (32.0%) and whites (26.0%), with Hispanics displaying the lowest prevalence (17.4%). Chinese and black participants had a significantly higher prevalence of disease compared to whites that persisted after adjusting for demographic and SES indicators, biomedical risk factors and psychosocial stress factors. After such adjustment, Hispanics did not differ significantly from whites in their reporting of disease. CONCLUSION: Racial/ethnic disparities in self-reported periodontal disease persisted after adjusting for all study covariates. This study highlights the need for continued research into the determinants of racial/ethnic disparities in periodontal disease in order to better target interventions aimed at reducing the burden of disease in all segments of the U.S. population.

Long-term exposure to air pollution and type 2 diabetes mellitus in a multiethnic cohort.

Although air pollution has been suggested as a possible risk factor for type 2 diabetes mellitus (DM), results from existing epidemiologic studies have been inconsistent. We investigated the associations of prevalence and incidence of DM with long-term exposure to air pollution as estimated using annual average concentrations of particulate matter with an aerodynamic diameter of 2.5 µm or less (PM2.5) and nitrogen oxides at baseline (2000) in the Multi-Ethnic Study of Atherosclerosis. All participants were aged 45-84 years at baseline and were recruited from 6 US sites. There were 5,839 participants included in the study of prevalent DM and 5,135 participants without DM at baseline in whom we studied incident DM. After adjustment for potential confounders, we found significant associations of prevalent DM with PM2.5 (odds ratio (OR) = 1.09, 95% confidence interval (CI): 1.00, 1.17) and nitrogen oxides (OR = 1.18, 95% CI: 1.01, 1.38) per each interquartile-range increase (2.43 µg/m(3) and 47.1 ppb, respectively). Larger but nonsignificant associations were observed after further adjustment for study site (for PM2.5, OR = 1.16, 95% CI: 0.94, 1.42; for nitrogen oxides, OR = 1.29, 95% CI: 0.94, 1.76). No air pollution measures were significantly associated with incident DM over the course of the 9-year follow-up period. Results were partly consistent with a link between long-term exposure to air pollution and the risk of type 2 DM. Additional studies with a longer follow-up time and a greater range of air pollution exposures, including high levels, are warranted to evaluate the hypothesized association.

Ethnic differences in ambient air pollution and risk of acute ischemic stroke.

OBJECTIVES: To investigate the association between short-term changes in ambient pollution (particulate matter <2.5 µm in aerodynamic diameter (PM2.5) and ozone (O3)) and the risk of ischemic stroke among individuals living in a bi-ethnic community and whether this association is modified by ethnicity. METHODS: We identified incident ischemic stroke cases from the population-based Brain Attack Surveillance in Corpus Christi (BASIC) project between 2000 and 2012. Associations between PM2.5 (mean 24-h) and O3 (maximal 8-h) levels, measured on the same-day and lags of 1-3 days, and odds of ischemic stroke were assessed using a time-stratified case-crossover design and modeled using conditional logistic regression. We explored race/ethnicity (Mexican American versus non-Hispanic white) as a modifier by including interaction terms in the models. RESULTS: There were 2948 ischemic strokes with median age 71 years (IQR: 59-80). We observed no overall associations between the air pollutants and odds of ischemic stroke at any lag. When stratified by ethnicity, higher O3 was consistently associated with greater odds of ischemic stroke for non-Hispanic whites, but not for Mexican Americans. Higher PM2.5 was generally associated with lower odds of ischemic stroke for non-Hispanic whites but modestly greater odds for Mexican Americans. CONCLUSION: Ethnic differences in the associations between ischemic stroke and short-term exposures to O3 and PM2.5 were suggested indicating that further study in diverse populations may be warranted.