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Background: Many studies have identified an inequitable distribution of exposure to PM2.5 (particulate matter less than 2.5 microns) by race. We investigated the association of PM2.5 and cardiovascular mortality considering both the decedents' race and neighborhood racial composition as potential modifiers. Methods: We obtained geocoded cardiovascular mortality records of all black and white decedents from urban block-groups in Massachusetts between 2001 and 2011 (n = 130,863). We examined the association between PM2.5 and cardiovascular mortality, and assessed effect modification by three types of racial modifiers: decedents' race, census block-group percent black and white, and two novel measures of racial segregation. The Racial Residential Segregation (RRS) quantifies the concentration of non-Hispanic blacks and whites in each block-group. The Index of Racial Dissimilarity measures dissimilarity in non-Hispanic black and white racial distribution between the smaller census block-group and larger tract. Results: We found a 2.35%(95%CI: 0.92%;3.79%) increase in mortality for each 10μg/m3 increase in two-day average exposure to PM2.5. The effect was modified by the block-group racial composition, with higher risks in block-groups with the highest percentage of black residents (interaction p-value = 0.04), and in block-groups with the lowest RRS (i.e. higher black to white resident ratio, interaction p-value = 0.072). Racial dissimilarity did not modify the associations. Conclusion: Current levels of PM2.5 are associated with increased cardiovascular deaths in Massachusetts, with different risks between areas with different racial composition and segregation. This suggests that pollution reductions in neighborhoods with the highest percentage of non-Hispanic blacks would be most beneficial in reducing cardiovascular mortality and disparities. [ABSTRACT FROM AUTHOR]

Traffic-related air pollution has been linked to higher risks of infertility and miscarriage. We evaluated whether folate intake modified the relationship between air pollution and livebirth among women using assisted reproductive technology (ART). Our study included 304 women (513 cycles) presenting to a fertility center in Boston, Massachusetts (2005–2015). Diet and supplements were assessed by food frequency questionnaire. Spatiotemporal models estimated residence-based daily nitrogen dioxide (NO2), ozone, fine particulate, and black carbon concentrations in the 3 months before ART. We used generalized linear mixed models with interaction terms to evaluate whether the associations between air pollutants and livebirth were modified by folate intake, adjusting for age, body mass index, race, smoking, education, infertility diagnosis, and ART cycle year. Supplemental folate intake significantly modified the association of NO2 exposure and livebirth (P = 0.01). Among women with supplemental folate intakes of <800 μg/day, the odds of livebirth were 24% (95% confidence interval: 2, 42) lower for every 20-parts-per-billion increase in NO2 exposure. There was no association among women with intakes of ≥800 μg/day. There was no effect modification of folate on the associations between other air pollutants and livebirth. High supplemental folate intake might protect against the adverse reproductive consequences of traffic-related air pollution. [ABSTRACT FROM AUTHOR]

BACKGROUND: Among nondiabetic individuals, higher fasting blood glucose (FBG) independently predicts diabetes risk, cardiovascular disease, and dementia. Ambient PM2.5 (particulate matter with aerodynamic diameter ≤ 2.5 μm) is an emerging determinant of glucose dysregulation. PM2.5 effects and mechanisms are understudied among nondiabetic individuals. OBJECTIVES: Our goals were to investigate whether PM2.5 is associated with an increase in FBG and to explore potential mediating roles of epigenetic gene regulation. METHODS: In 551 nondiabetic participants in the Normative Aging Study, we measured FBG, and DNA methylation of four inflammatory genes (IFN-γ, IL-6, ICAM-1, and TLR-2), up to four times between 2000 and 2011 (median = 2). We estimated short- and medium-term (1-, 7-, and 28-day preceding each clinical visit) ambient PM2.5 at each participant's address using a validated hybrid land-use regression satellite-based model. We fitted covariate-adjusted regression models accounting for repeated measures. RESULTS: Mean FBG was 99.8 mg/dL (SD = 10.7), 18% of the participants had impaired fasting glucose (IFG; i.e., 100-125 mg/dL FBG) at first visit. Interquartile increases in 1-, 7-, and 28-day PM2.5 were associated with 0.57 mg/dL (95% CI: 0.02, 1.11, p = 0.04), 1.02 mg/dL (95% CI: 0.41, 1.63, p = 0.001), and 0.89 mg/dL (95% CI: 0.32, 1.47, p = 0.003) higher FBG, respectively. The same PM2.5 metrics were associated with 13% (95% CI: -- 3%, 33%, p = 0.12), 27% (95% CI: 6%, 52%, p = 0.01) and 32% (95% CI: 10%, 58%, p = 0.003) higher odds of IFG, respectively. PM2.5 was negatively correlated with ICAM-1 methylation (p = 0.01), but not with other genes. Mediation analysis estimated that ICAM-1 methylation mediated 9% of the association of 28-day PM2.5 with FBG. CONCLUSIONS: Among nondiabetics, short- and medium-term PM2.5 were associated with higher FBG. Mediation analysis indicated that part of this association was mediated by ICAM-1 promoter methylation. Citation: Peng C, Bind MA, Colicino E, Kloog I, Byun HM, Cantone L, Trevisi L, Zhong J, Brennan K, Dereix AE, Vokonas PS, Coull BA, Schwartz JD, Baccarelli AA. 2016. Particulate air pollution and fasting blood glucose in nondiabetic individuals: associations and epigenetic mediation in the Normative Aging Study, 2000-2011. Environ Health Perspect 124:1715-1721; http://dx.doi.org/10.1289/EHP183 [ABSTRACT FROM AUTHOR]

BACKGROUND: It is unknown if ambient fine particulate matter (PM2.5) is associated with lower renal function, a cardiovascular risk factor. OBJECTIVE: We investigated whether long-term PM2.5 exposure was associated with estimated glomerular filtration rate (eGFR) in a cohort of older men living in the Boston Metropolitan area. METHODS: This longitudinal analysis included 669 participants from the Veterans Administration Normative Aging Study with up to four visits between 2000 and 2011 (n = 1,715 visits). Serum creatinine was measured at each visit, and eGFR was calculated according to the Chronic Kidney Disease Epidemiology Collaboration equation. One-year exposure to PM2.5 prior to each visit was assessed using a validated spatiotemporal model that utilized satellite remote-sensing aerosol optical depth data. eGFR was modeled in a time-varying linear mixed-effects regression model as a continuous function of 1-year PM2.5, adjusting for important covariates. RESULTS: One-year PM2.5 exposure was associated with lower eGFRs; a 2.1-µg/m³ interquartile range higher 1-year PM2.5 was associated with a 1.87 mL/min/1.73 m² lower eGFR [95% confidence interval (CI): -2.99, -0.76]. A 2.1 µg/m³-higher 1-year PM2.5 was also associated with an additional annual decrease in eGFR of 0.60 mL/min/1.73 m² per year (95% CI: -0.79, -0.40). CONCLUSIONS: In this longitudinal sample of older men, the findings supported the hypothesis that long-term PM2.5 exposure negatively affects renal function and increases renal function decline. [ABSTRACT FROM AUTHOR]

Background: Short-term fine particulate matter (PM2.5) exposure has been linked with increased QT interval duration, a marker of ventricular repolarization and a risk factor for cardiac arrhythmia and sudden death, in several studies. Only one previous study evaluated whether long-term PM exposure is related to the QT interval. We aim to evaluate whether subchronic and long-term exposure to PM2.5 at home is linked with QT duration in an elderly cohort.Methods: We measured heart-rate corrected QT interval duration among 404 participants from the Greater Boston area between 2003 and 2011. We modeled residential PM2.5 exposures using a hybrid satellite- and land use-based model. We evaluated associations between moving averages of short-term (1-2 days), subchronic (3-28 days), and long-term (1 year) pollutant exposures and corrected QT duration using linear mixed models. We also evaluated effect modification by oxidative stress genetic score using separated regression models and interaction terms.Results: We observed positive associations between subchronic and long-term PM2.5 exposure and corrected QT duration, with the strongest results for longer-term exposures. For example, a one standard deviation increase in 1-year PM2.5 was associated with a 6.3 ms increase in corrected QT (95% confidence interval: 1.8, 11). We observed somewhat greater effects among subjects with higher (8.5 ms) rather than lower (3.1 ms) oxidative stress allelic profiles (P interaction = 0.25).Conclusions: PM2.5 was associated with increased corrected QT duration in an elderly cohort. While most previous studies focused on short-term air pollution exposures, our results suggest that longer-term exposures are associated with cardiac repolarization. [ABSTRACT FROM AUTHOR]

Background: Rodent and human studies suggest an association between air pollution exposure and type 2 diabetes mellitus, but the extent to which air pollution is associated with gestational diabetes mellitus (GDM) is less clear.Methods: We used the Massachusetts Registry of Vital Records to study primiparous women pregnant from 2003-2008 without pre-existing diabetes. We used satellite-based spatiotemporal models to estimate first and second trimester residential particulate (PM2.5) exposure and geographic information systems to estimate neighborhood traffic density. We obtained GDM status from birth records. We performed logistic regression analyses adjusted for sociodemographics on the full cohort and after stratification by maternal age and smoking habits.Results: Of 159,373 women, 5,381 (3.4 %) developed GDM. Residential PM2.5 exposure ranged 1.3-19.3 μg/m(3) over the second trimester. None of the exposures were associated with GDM in the full cohort [e.g. OR 0.99 (95 % CI: 0.95, 1.03) for each interquartile range (IQR) increment in second trimester PM2.5]. There were also no consistent associations after stratification by smoking habits. When the cohort was stratified by maternal age, women less than 20 years had 1.36 higher odds of GDM (95 % CI: 1.08, 1.70) for each IQR increment in second trimester PM2.5 exposure.Conclusions: Although we found no evidence of an association between air pollution exposure and GDM among all women in our study, greater exposure to PM2.5 during the second trimester was associated with GDM in the youngest age stratum. [ABSTRACT FROM AUTHOR]

Background: Short-term particulate air pollution exposure is associated with reduced heart rate variability (HRV), a risk factor for cardiovascular morbidity and mortality, in many studies. Associations with sub-chronic or long-term exposures, however, have been sparsely investigated. We evaluated the effect of fine particulate matter (PM2.5) and black carbon (BC) exposures on HRV in an elderly cohort: the Normative Aging Study.Methods: We measured power in high frequency (HF) and low frequency (LF), standard deviation of normal-to-normal intervals (SDNN), and the LF:HF ratio among participants from the Greater Boston area. Residential BC exposures for 540 men (1161 study visits, 2000-2011) were estimated using a spatio-temporal land use regression model, and residential PM2.5 exposures for 475 men (992 visits, 2003-2011) were modeled using a hybrid satellite based and land-use model. We evaluated associations between moving averages of sub-chronic (3-84 day) and long-term (1 year) pollutant exposure estimates and HRV parameters using linear mixed models.Results: One-standard deviation increases in sub-chronic, but not long-term, BC were associated with reduced HF, LF, and SDNN and an increased LF:HF ratio (e.g., 28 day BC: -2.3% HF [95% CI:-4.6, -0.02]). Sub-chronic and long-term PM2.5 showed evidence of relations to an increased LF and LF:HF ratio (e.g., 1 year PM: 21.0% LF:HF [8.6, 34.8]), but not to HF or SDNN, though the effect estimates were very imprecise and mostly spanned the null.Conclusions: We observed some evidence of a relation between longer-term BC and PM2.5 exposures and changes in HRV in an elderly cohort. While previous studies focused on short-term air pollution exposures, our results suggest that longer-term exposures may influence cardiac autonomic function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Studies looking at air temperature (Ta) and birth outcomes are rare. OBJECTIVES: We investigated the association between birth outcomes and daily Ta during various prenatal exposure periods in Massachusetts (USA) using both traditional Ta stations and modeled addresses. METHODS: We evaluated birth outcomes and average daily Ta during various prenatal exposure periods in Massachusetts (USA) using both traditional Ta stations and modeled address Ta. We used linear and logistic mixed models and accelerated failure time models to estimate associations between Ta and the following outcomes among live births > 22 weeks: term birth weight (> 37 weeks), low birth weight (LBW; < 2,500 g at term), gestational age, and preterm delivery (PT; < 37 weeks). Models were adjusted for individual-level socioeconomic status, traffic density, particulate matter < 2.5 μm (PM2 5), random intercept for census tract, and mother's health. RESULTS: Predicted Ta during multiple time windows before birth was negatively associated with birth weight: Average birth weight was 16.7 g lower (95% CI: -29.7, -3.7) in association with an interquartile range increase (8.4°C) in Ta during the last trimester. Ta over the entire pregnancy was positively associated with PT [odds ratio (OR) = 1.02; 95% CI: 1.00, 1.05] and LBW (OR = 1.04; 95% CI: 0.96, 1.13). CONCLUSIONS: Ta during pregnancy was associated with lower birth weight and shorter gestational age in our study population. [ABSTRACT FROM AUTHOR]

BACKGROUND: Influences of prenatal and early-life exposures to air pollution on cognition are not well understood. OBJECTIVES: We examined associations of gestational and childhood exposure to traffic-related pollution with childhood cognition. METHODS: We studied 1,109 mother-child pairs in Project Viva, a prospective birth cohort study in eastern Massachusetts (USA). In mid-childhood (mean age, 8.0 years), we measured verbal and nonverbal intelligence, visual motor abilities, and visual memory. For periods in late pregnancy and childhood, we estimated spatially and temporally resolved black carbon (BC) and fine particulate matter (PM2.5) exposures, residential proximity to major roadways, and near-residence traffic density. We used linear regression models to examine associations of exposures with cognitive assessment scores, adjusted for potential confounders. RESULTS: Compared with children living ≥ 200 m from a major roadway at birth, those living < 50 m away had lower nonverbal IQ [-7.5 points; 95% confidence interval (CI): -13.1, -1.9], and somewhat lower verbal IQ (-3.8 points; 95% CI: -8.2, 0.6) and visual motor abilities (-5.3 points; 95% CI: -11.0, 0.4). Cross-sectional associations of major roadway proximity and cognition at mid-childhood were weaker. Prenatal and childhood exposure to traffic density and PM2.5 did not appear to be associated with poorer cognitive performance. Third-trimester and childhood BC exposures were associated with lower verbal IQ in minimally adjusted models; but after adjustment for socioeconomic covariates, associations were attenuated or reversed. CONCLUSIONS: Residential proximity to major roadways during gestation and early life may affect cognitive development. Influences of pollutants and socioeconomic conditions on cognition may be difficult to disentangle. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to fine particulate matter (PM with diameter ≤ 2.5 μm; PM2.5) has been linked to type 2 diabetes mellitus, but associations with hyperglycemia in pregnancy have not been well studied. METHODS: We studied Boston, Massachusetts–area pregnant women without known diabetes. We identified impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM) during pregnancy from clinical glucose tolerance tests at median 28.1 weeks gestation. We used residential addresses to estimate second-trimester PM2.5 and black carbon exposure via a central monitoring site and spatiotemporal models. We estimated residential traffic density and roadway proximity as surrogates for exposure to traffic-related air pollution. We performed multinomial logistic regression analyses adjusted for sociodemographic covariates, and used multiple imputation to account for missing data. RESULTS: Of 2,093 women, 65 (3%) had IGT and 118 (6%) had GDM. Second-trimester spatiotemporal exposures ranged from 8.5 to 15.9 μg/m3 for PM2.5 and from 0.1 to 1.7 μg/m3 for black carbon. Traffic density was 0–30,860 vehicles/day × length of road (kilometers) within 100 m; 281 (13%) women lived ≤ 200 m from a major road. The prevalence of IGT was elevated in the highest (vs. lowest) quartile of exposure to spatiotemporal PM2.5 [odds ratio (OR) = 2.63; 95% CI: 1.15, 6.01] and traffic density (OR = 2.66; 95% CI: 1.24, 5.71). IGT also was positively associated with other exposure measures, although associations were not statistically significant. No pollutant exposures were positively associated with GDM. CONCLUSIONS: Greater exposure to PM2.5 and other traffic-related pollutants during pregnancy was associated with IGT but not GDM. Air pollution may contribute to abnormal glycemia in pregnancy. [ABSTRACT FROM AUTHOR]

Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI). Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants. Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI. Results: An interquartile range (IQR) increase in area PM2.5 (0.59 μg/m3) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM2.5 (area + local, 1.05 μg/m3) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11). Conclusions: Residential exposure to PM2.5 may best be represented by a combination of area and local PM2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events. [ABSTRACT FROM AUTHOR]

Abstract: Although meteorological stations provide accurate air temperature observations, their spatial coverage is limited and thus often insufficient for epidemiological studies. Satellite data expand spatial coverage, enhancing our ability to estimate near surface air temperature (Ta). However, the derivation of Ta from surface temperature (Ts) measured by satellites is far from being straightforward. In this study, we present a novel approach that incorporates land use regression, meteorological variables and spatial smoothing to first calibrate between Ts and Ta on a daily basis and then predict Ta for days when satellite Ts data were not available. We applied mixed regression models with daily random slopes to calibrate Moderate Resolution Imaging Spectroradiometer (MODIS) Ts data with monitored Ta measurements for 2003. Then, we used a generalized additive mixed model with spatial smoothing to estimate Ta in days with missing Ts. Out-of-sample tenfold cross-validation was used to quantify the accuracy of our predictions. Our model performance was excellent for both days with available Ts and days without Ts observations (mean out-of-sample R2 =0.946 and R2 =0.941 respectively). Furthermore, based on the high quality predictions we investigated the spatial patterns of Ta within the study domain as they relate to urban vs. non-urban land uses. [Copyright &y& Elsevier]

• Heat and PM 2.5 exposure were independently associated with lower TBW. • Women are more susceptible to both exposures towards the end of pregnancy. • Susceptibility to heat was higher in the initial weeks of pregnancy as well. Birthweight is a strong predictor of normal growth, healthy development, and survival. Several studies have found associations between temperature, fine particulate matter (PM 2.5), and birth weight. However, the relevant timing of exposures varies between studies and is yet unclear. Therefore, we assessed the difference in term birthweight (TBW) associated with weekly exposure to temperature and PM 2.5 throughout 37 weeks of gestation. We included all singleton live term births in Massachusetts, U.S between 2004 and 2015 (n = 712,438). Weekly PM 2.5 and temperature predictions were estimated on a 1 km grid from satellite-based models. We utilized a distributed lag nonlinear model (DLNM) to estimate the difference in TBW associated with weekly exposures from the last menstrual period to 37 weeks of gestation. We found a nonlinear association with prenatal temperature exposure. Larger effects were observed in warmer temperatures, where higher temperatures were negatively associated with TBW. Temperature effects were larger in the first and final weeks of gestation. We observed a negative difference in TBW associated with PM 2.5 exposure. Overall, a 1 µg/m3 increase in prenatal exposure was associated with 3.9 g lower TBW (95% CI −5.0 g; −2.9 g). PM 2.5 effects were larger in the final weeks of gestation. We found heat and PM 2.5 exposure to be related to lower TBW. Our findings suggest that women are more susceptible to both exposures towards the end of pregnancy. Susceptibility to heat was higher in the initial weeks of pregnancy as well. These critical windows of susceptibility can be communicated to pregnant women during routine prenatal visits to increase awareness and target interventions to reduce exposures. [ABSTRACT FROM AUTHOR]