Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms.

BACKGROUND: Pathophysiology of rhinitis in older adults is largely unknown. We tested whether air pollution is associated with this condition and how immune mechanisms may play a role in this relationship. METHODS: We analyzed cross-sectional data from the National Social Life, Health, and Aging Project, a nationally representative study of older adults born between 1920 and 1947. Particulate matter ≤2.5 µm (PM2.5 ) air pollution exposure estimates were generated using validated spatiotemporal models. Presence of rhinitis was defined based on medication use (≥1: intranasal medications: steroids, antihistamines, lubricants, and/or decongestants, and/or oral medications: antihistamines and/or decongestants). K-means cluster analysis (Jaccard method) was used to group 13 peripheral blood cytokines into 3 clusters to facilitate functional determination. We fitted multivariate logistic regressions to correlate PM2.5 exposure with presence of rhinitis, controlling for confounders, and then determined the role of cytokines in this relationship. RESULTS: Long- (but not short-) term exposure to PM2.5 was associated with presence of rhinitis: 3-year exposure window, odds ratio (OR) = 1.32, 95% confidence interval (CI): 0.98, 1.80, per 1 standard deviation (SD) PM2.5 increase. Inclusion of cytokine cluster in the model led to a modestly stronger effect of PM2.5 exposure on rhinitis (OR = 1.37; 95% CI: 1.00, 1.87; 3-year exposure window). The particular immune profile responsible for this result was composed of elevated IL-3, IL-12, and IFN-γ (OR = 4.86, 95% CI: 1.10, 21.58, immune profile-PM2.5 exposure interaction term). CONCLUSION: We show for the first time that IL-3, IL-12, and IFN-γ explain in part the relationship between PM2.5 exposure and rhinitis in older US adults. If confirmed, these immune pathways may be used as therapeutic targets.

Long-term measurement study of urban environmental low frequency noise.

BACKGROUND: Environmental low frequency noise (LFN < 125 Hz), ubiquitous in urban areas, is an understudied area of exposure science and an overlooked threat to population health. Environmental noise has historically been measured and regulated by A-weighted decibel (dBA) metrics, which more heavily weight frequencies between 2000 and 5000 Hz. Limited research has been conducted to measure and characterize the LFN components of urban environmental noise. OBJECTIVES: We characterized LFN noise at two urban sites in Greater Boston, Massachusetts (USA) using dBA and full spectrum noise measurements with aims to (1.) analyze spatio-temporal differences in the two datasets; (2.) compare and contrast LFN metrics with dBA noise metrics in the two sites; and (3.) assess meteorological covariate contributions to LFN in the dataset. METHODS: We measured A- and C-weighted, and flat, unweighted noise levels and 1/3-octave band continuously for 5 months using sound level meters sampling at f = 1 Hz and we recorded sound samples at 44.1 kHz. Our measurement sites were located in two urban, densely populated communities, burdened by close proximity to bus, rail, and aircraft routes. RESULTS: We found that (1.) LFN does not follow the same seasonal trends as A-weighted dBA loudness; there are spatial differences in LFN and its very low frequency noise components (VLFN) between two urban sites; (2.) VLFN and LFN are statistically significant drivers of LCeq (nearly independent of frequency) minus LAeq, (LCeq-LAeq) >10 dB, an accepted LFN metric; and (3.) LFN was minimally affected by high wind speeds at either Site. IMPACT STATEMENT: Environmental low-frequency noise (LFN < 125 Hz), ubiquitous in urban areas, is an understudied area of exposure science and an overlooked risk to population health. We measured environmental noise across the full spectrum of frequencies continuously for five months at two urban sites located in Environmental Justice communities. We found that LFN did not follow the same seasonal trends as A-weighted (dBA) loudness, and we observed spatial differences in LFN and very low frequency noise (VLFN < 20 Hz) at the two sites. Not characterizing LFN and basing noise regulations only on A-weightings, a poor predictor of LFN, may expose populations to LFN levels of concern.

The Impact of Long-Term Air Pollution Exposure on Type 1 Diabetes Mellitus-Related Mortality among U.S. Medicare Beneficiaries.

BACKGROUND: Little of the previous literature has investigated associations between air pollution exposure and type 1 diabetes mellitus (T1DM)-related mortality, despite a well-established link between air pollution exposure and other autoimmune diseases. METHODS: In a cohort of 53 million Medicare beneficiaries living across the conterminous United States, we used Cox proportional hazard models to assess the association of long-term PM2.5 and NO2 exposures on T1DM-related mortality from 2000 to 2008. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socioeconomic status (SES); we additionally investigated associations in two-pollutant models, and whether associations were modified by participant demographics. RESULTS: A 10 µg/m3 increase in 12-month average PM2.5 (HR: 1.183; 95% CI: 1.037-1.349) and a 10 ppb increase in NO2 (HR: 1.248; 95% CI: 1.089-1.431) was associated with an increased risk of T1DM-related mortality in age-, sex-, race-, ZIP code-, and SES-adjusted models. Associations for both pollutants were consistently stronger among Black (PM2.5: HR:1.877, 95% CI: 1.386-2.542; NO2: HR: 1.586, 95% CI: 1.258-2.001) and female (PM2.5: HR:1.297, 95% CI: 1.101-1.529; NO2: HR: 1.390, 95% CI: 1.187-1.627) beneficiaries. CONCLUSIONS: Long-term NO2 and, to a lesser extent, PM2.5 exposure is associated with statistically significant elevations in T1DM-related mortality risk.

Long-term PM2.5 exposure and sepsis mortality in a US medicare cohort.

BACKGROUND: Risk factors contributing to sepsis-related mortality include clinical conditions such as cardiovascular disease, chronic lung disease, and diabetes, all of which have also been shown to be associated with air pollution exposure. However, the impact of chronic exposure to air pollution on sepsis-related mortality has been little studied.  METHODS: In a cohort of 53 million Medicare beneficiaries (228,439 sepsis-related deaths) living across the conterminous United States between 2000 and 2008, we examined the association of long-term PM2.5 exposure and sepsis-related mortality. For each Medicare beneficiary (ages 65-120), we estimated the 12-month moving average PM2.5 concentration for the 12 month before death, for their ZIP code of residence using well validated GIS-based spatio-temporal models. Deaths were categorized as sepsis-related if they have ICD-10 codes for bacterial or other sepsis. We used Cox proportional hazard models to assess the association of long-term PM2.5 exposure on sepsis-related mortality. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES). We also evaluated confounding through adjustment of neighborhood behavioral covariates. RESULTS: A 10 µg/m3 increase in 12-month moving average PM2.5 was associated with a 9.1% increased risk of sepsis mortality (95% CI: 3.6-14.9) in models adjusted for age, sex, race, ZIP code, and SES. HRs for PM2.5 were higher and statistically significant for older (> 75), Black, and urban beneficiaries. In stratified analyses, null associations were found for younger beneficiaries (65-75), beneficiaries who lived in non-urban ZIP codes, and those residing in low-SES urban ZIP codes. CONCLUSIONS: Long-term PM2.5 exposure is associated with elevated risks of sepsis-related mortality.

The impact of Long-Term PM2.5 constituents and their sources on specific causes of death in a US Medicare cohort.

BACKGROUND: Our understanding of the impact of long-term exposures to PM2.5 constituents and sources on mortality is limited. OBJECTIVES: To examine associations between long-term exposures to PM2.5 constituents and sources and cause-specific mortality in US older adults. METHODS: We obtained demographic and mortality data for 15.4 million Medicare beneficiaries living within the conterminous United States (US) between 2000 and 2008. We assessed PM2.5 constituents exposures for each beneficiary and used factor analysis and residual-based methods to characterize PM2.5 sources and mixtures, respectively. In age-, sex-, race- and site- stratified Cox proportional hazard models adjusted for neighborhood socio-economic status (SES), we assessed associations of individual PM2.5 constituents, sources, and mixtures and cause-specific mortality and examined modification of these associations by participant demographics and location of residence. We assessed the robustness of our findings to additional adjustment for behavioral risk factors and to alternate exposure definitions and exposure windows. RESULTS: Hazard ratios (HR) were highest for all causes of death, except COPD, for PM2.5 constituents and the coal combustion-related PM2.5 components, with no evidence of confounding by behavioral covariates. We further found Pb and metal-related PM2.5 components to be significantly associated with increased HR of all causes of death, except COPD and lung cancer mortality, and nitrate (NO3-) and silicon (Si) and associated source-related PM2.5 components (traffic and soil, respectively) to be significantly associated with increased all-cause, CVD, respiratory and all cancer-related mortality HR. Associations for other examined constituents and mortality were inconsistent or largely null. Our analyses of mixtures were generally consistent with these findings. Mortality HRs were greatest for minority, especially Black, low-income urban, younger, and male beneficiaries. DISCUSSION: PM2.5 components related to coal combustion, traffic, and to a lesser extent, soil were strongly associated with mortality from CVD, respiratory disease, and cancer.

Non-pharmaceutical interventions and COVID-19 cases in US summer camps: results from an American Camp Association survey.

BACKGROUND: Most camps remained closed during Summer 2020, due to concerns regarding child transmission of SARS-CoV-2 and limited information about the effectiveness of non-pharmaceutical interventions (NPIs) within child congregate settings. METHODS: We surveyed US camps about on-site operations, camper and staff demographics, COVID-19 cases among campers and staff, and NPI usage as related to pre-camp quarantine, facial coverings, physical distancing, cleaning and facility modifications. For all NPIs, save quarantine, responses were provided on a 5-point Likert scale format. RESULTS: Within 486 on-site camps, a range of NPIs were instituted, most often related to reduced camper interactions, staff face coverings, cleaning and hand hygiene. Camper facial coverings were less common, with campers always wearing masks at ~34% of the camps. Approximately 15% of camps reported 1+ confirmed COVID-19 case in either campers or staff, with three camps reporting a COVID-19 outbreak. In both single and multi-NPI analyses, the risk of COVID-19 cases was lowest when campers always wore facial coverings. Constant use of staff facial coverings and targeted physical distancing measures, but not pre-camp quarantine, also reduced COVID-19 risks. CONCLUSIONS: We found constant facial coverings, especially for campers, and targeted physical distancing measures to reduce risks of SARS-CoV-2 transmission within summer camps. Our findings provide valuable insights for future operations of summer camps and other child congregate settings regarding the use of NPIs to reduce the risk of SARS-CoV-2 infection.

Long-term nitrogen dioxide exposure and cause-specific mortality in the U.S. Medicare population.

BACKGROUND: Since 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO2) has remained at 53 ppb, the impact of long-term NO2 exposure on mortality is poorly understood. OBJECTIVES: We examined associations between long-term NO2 exposure (12-month moving average of NO2) below the annual NAAQS and cause-specific mortality among the older adults in the U.S. METHODS: Cox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001 to 2008. RESULTS: A 10 ppb increase in NO2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05-1.06), cardiovascular (HR: 1.10; 95% CI: 1.10-1.11), respiratory disease (HR: 1.09; 95% CI: 1.08-1.11), and cancer (HR: 1.01; 95% CI: 1.00-1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM2.5 exposure using a 2-stage approach. NO2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries. CONCLUSIONS: Long-term NO2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO2.

Non-nutritive suck and airborne metal exposures among Puerto Rican infants.

Air pollution has been shown to impact multiple measures of neurodevelopment in young children. Its effects on particularly vulnerable populations, such as ethnic minorities, however, is less studied. To address this gap in the literature, we assess the associations between infant non-nutritive suck (NNS), an early indicator of central nervous system integrity, and air pollution exposures in Puerto Rico. Among infants aged 0-3 months enrolled in the Center for Research on Early Childhood Exposure and Development (CRECE) cohort from 2017 to 2019, we examined associations between exposure to fine particulate matter (PM2.5) and its components on infant NNS in Puerto Rico. NNS was assessed using a pacifier attached to a pressure transducer, allowing for real-time visualization of NNS amplitude, frequency, duration, cycles/burst, cycles/min and bursts/min. These data were linked to 9-month average prenatal concentrations of PM2.5 and components, measured at three community monitoring sites. We used linear regression to examine the PM2.5-NNS association in single pollutant models, controlling for infant sex, maternal age, gestational age, and season of birth in base and additionally for household smoke exposure, age at testing, and NNS duration in full models. Among 198 infants, the average NNS amplitude and burst duration was 17.1 cmH2O and 6.1 s, respectively. Decreased NNS amplitude was consistently and significantly associated with 9-month average exposure to sulfur (-1.026 ± 0.507), zinc (-1.091 ± 0.503), copper (-1.096 ± 0.535) vanadium (-1.157 ± 0.537), and nickel (-1.530 ± 0.501). Decrements in NNS frequency were associated with sulfur exposure (0.036 ± 0.018), but not other examined PM components. Our findings provide new evidence that prenatal maternal exposure to specific PM components are associated with impaired neurodevelopment in Puerto Rican infants soon after birth.

Preterm birth and PM2.5 in Puerto Rico: evidence from the PROTECT birth cohort.

BACKGROUND: Preterm birth (PTB, birth before 37 weeks of gestation) has been associated with adverse health outcomes across the lifespan. Evidence on the association between PTB and prenatal exposure to air pollutants is inconsistent, and is especially lacking for ethnic/racial minority populations. METHODS: We obtained data on maternal characteristics and behaviors and PTB and other birth outcomes for women participating in the Puerto Rico Testsite for Exploring Contamination Threats (PROTECT) cohort, who lived in municipalities located along the North Coast of Puerto Rico. We assessed pre-natal PM2.5 exposures for each infant based on the nearest US Environmental Protection Agency monitor. We estimated prenatal phthalate exposures as the geometric mean of urinary measurements obtained during pregnancy. We then examined the association between PM2.5 and PTB using modified Poisson regression and assessed modification of the association by phthalate exposure levels and sociodemographic factors such as maternal age and infant gender. RESULTS: Among 1092 singleton births, 9.1% of infants were born preterm and 92.9% of mothers had at least a high school education. Mothers had a mean (standard deviation) age of 26.9 (5.5) years and a median (range) of 2.0 (1.0-8.0) pregnancies. Nearly all women were Hispanic white, black, or mixed race. Median (range) prenatal PM2.5 concentrations were 6.0 (3.1-19.8) µ g/m3. Median (interquartile range) prenatal phthalate levels were 14.9 (8.9-26.0) and 14.5 (8.4-26.0), respectively, for di-n-butyl phthalate (DBP) and di-isobutyl phthalate (DiBP). An interquartile range increase in PM2.5 was associated with a 1.2% (95% CI 0.4, 2.1%) higher risk of PTB. There was little difference in PTB risk in strata of infant sex, mother's age, family income, history of adverse birth outcome, parity, and pre-pregnancy body mass index. Pregnancy urinary phthalate metabolite levels did not modify the PM2.5-PTB association. CONCLUSION: Among ethnic minority women in Puerto Rico, prenatal PM2.5 exposure is associated with a small but significant increase in risk of PTB.

Cohort profile: Center for Research on Early Childhood Exposure and Development in Puerto Rico.

PURPOSE: Puerto Rican children experience high rates of asthma and obesity. Further, infants born in Puerto Rico are more at risk for being born prematurely compared with infants on the mainland USA. Environmental exposures from multiple sources during critical periods of child development, potentially modified by psychosocial factors, may contribute to these adverse health outcomes. To date, most studies investigating the health effects of environmental factors on infant and child health have focused on single or individual exposures. PARTICIPANTS: Infants currently in gestation whose mother is enrolled in Puerto Rico Testsite for Exploring Contamination Threats (PROTECT) cohort, and infants and children already born to mothers who participated in the PROTECT study. FINDINGS TO DATE: Data collection and processing remains ongoing. Demographic data have been collected on 437 mother-child pairs. Birth outcomes are available for 420 infants, neurodevelopmental outcomes have been collected on 319 children. Concentrations of parabens and phenols in maternal spot urine samples have been measured from 386 mothers. Center for Research on Early Childhood Exposure and Development mothers have significantly higher urinary concentrations of dichlorophenols, triclosan and triclocarban, but lower levels of several parabens compared with reference values from a similar population drawn from the National Health and Nutrition Examination Survey. FUTURE PLANS: Data will continue to be collected through recruitment of new births with a target of 600 children. Seven scheduled follow-up visits with existing and new participants are planned. Further, our research team continues to work with healthcare providers, paediatricians and early intervention providers to support parent's ability to access early intervention services for participants.

The impact of long-term PM2.5 exposure on specific causes of death: exposure-response curves and effect modification among 53 million U.S. Medicare beneficiaries.

BACKGROUND: The shape of the exposure-response curve for long-term ambient fine particulate (PM2.5) exposure and cause-specific mortality is poorly understood, especially for rural populations and underrepresented minorities. METHODS: We used hybrid machine learning and Cox proportional hazard models to assess the association of long-term PM2.5 exposures on specific causes of death for 53 million U.S. Medicare beneficiaries (aged ≥65) from 2000 to 2008. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES) in our main analyses, with approximately 4 billion person-months of follow-up, and additionally for warm season average of 1-h daily maximum ozone exposures in a sensitivity analysis. The impact of non-traffic PM2.5 on mortality was examined using two stage models of PM2.5 and nitrogen dioxide (NO2). RESULTS: A 10 µg /m3 increase in 12-month average PM2.5 prior to death was associated with a 5% increase in all-cause mortality, as well as an 8.8, 5.6, and 2.5% increase in all cardiovascular disease (CVD)-, all respiratory-, and all cancer deaths, respectively, in age, gender, race, ZIP code, and SES-adjusted models. PM2.5 exposures, however, were not associated with lung cancer mortality. Results were not sensitive to control for ozone exposures. PM2.5-mortality associations for CVD- and respiratory-related causes were positive and significant for beneficiaries irrespective of their sex, race, age, SES and urbanicity, with no evidence of a lower threshold for response or of lower Risk Ratios (RRs) at low PM2.5 levels. Associations between PM2.5 and CVD and respiratory mortality were linear and were higher for younger, Black and urban beneficiaries, but were largely similar by SES. Risks associated with non-traffic PM2.5 were lower than that for all PM2.5 and were null for respiratory and lung cancer-related deaths. CONCLUSIONS: PM2.5 was associated with mortality from CVD, respiratory, and all cancer, but not lung cancer. PM2.5-associated risks of CVD and respiratory mortality were similar across PM2.5 levels, with no evidence of a threshold. Blacks, urban, and younger beneficiaries were most vulnerable to the long-term impacts of PM2.5 on mortality.

Long-term ozone exposures and cause-specific mortality in a US Medicare cohort.

We examined the association of long-term, daily 1-h maximum O3 (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000-2008. We modeled the association between O3 and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM2.5 (particles with aerodynamic diameters <2.5 µm) and NO2 (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O3 into its temporal and spatio-temporal components and comparing estimated risk ratios. We also examined sensitivity of our results to alternate exposure measures based on warm-season 8-h daily maximum and 24-h average exposures. We found increased risks from long-term O3 exposures to be strongest and most consistent for mortality from respiratory disease (1.030, 95% CI: 1.027, 1.034) (including COPD (chronic obstructive pulmonary disease)), CHF (congestive heart failure), and lung cancer (1.015, 95% CI: 1.010, 1.020), with no evidence of confounding by PM2.5, NO2, and temperature and with results similar across O3 exposure measures. While significant, associations between long-term O3 exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM2.5 and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O3 was used to assess exposures. In this large study, we provide strong evidence that O3 exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O3-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.

Daily ambient temperature is associated with biomarkers of kidney injury in older Americans.

BACKGROUND: Increases in ambient temperature have recently been associated with increased emergency department visits and hospital admissions for acute renal failure. However, potential biological mechanisms through which short-term ambient temperature affects kidney function are not known. METHODS: We used multiple regression models to evaluate the association between 1- and 3-day average, ambient temperature levels and two biomarkers of kidney injury (neutrophil gelatinase-associated lipocalin (NGAL) and adiponectin), among 3377 individuals over 57 years of age enrolled in the National Social Life, Health, and Aging Project. Ambient temperature was estimated on a 6-km grid covering the conterminous United States using ambient temperature measurements obtained from the National Climatic Data Center (NCDC). NGAL and adiponectin levels were measured from whole blood collected for each participant. All health effect models were adjusted for a number of demographics, socioeconomic, health behavior, medical history variables, with non-linear exposure-response relationships examined using natural cubic splines. RESULTS: The relationship between 1- and 3-day average temperature and both NGAL and adiponectin levels was significant and non-linear, with largely null associations below 10 °C, and positive association for temperatures >10 °C. In fully adjusted, linear multiple regression models restricted to >10 °C, NGAL and adiponectin levels increased by 1.89% (95% CI: 0.77, 3.91) and 2.51% (95% CI: 1.34, 3.69), respectively, for a 1 °C increase in daily average temperature. Additionally, every 1 °C increase in temperature over 10 °C was associated with a 1.83% increased odds of having plasma NGAL levels consistent with acute kidney injury (>150 µg/L). CONCLUSIONS: In a cohort of older men and women in the United States, our study is the first to observe that short-term ambient temperature exposures were significantly associated with biomarkers of kidney injury. These associations suggest that ambient temperature exposures could be an important risk factor for renal pathology.

Synthesis of Harvard Environmental Protection Agency (EPA) Center studies on traffic-related particulate pollution and cardiovascular outcomes in the Greater Boston Area.

The association between particulate pollution and cardiovascular morbidity and mortality is well established. While the cardiovascular effects of nationally regulated criteria pollutants (e.g., fine particulate matter [PM2.5] and nitrogen dioxide) have been well documented, there are fewer studies on particulate pollutants that are more specific for traffic, such as black carbon (BC) and particle number (PN). In this paper, we synthesized studies conducted in the Greater Boston Area on cardiovascular health effects of traffic exposure, specifically defined by BC or PN exposure or proximity to major roadways. Large cohort studies demonstrate that exposure to traffic-related particles adversely affect cardiac autonomic function, increase systemic cytokine-mediated inflammation and pro-thrombotic activity, and elevate the risk of hypertension and ischemic stroke. Key patterns emerged when directly comparing studies with overlapping exposure metrics and population cohorts. Most notably, cardiovascular risk estimates of PN and BC exposures were larger in magnitude or more often statistically significant compared to those of PM2.5 exposures. Across multiple exposure metrics (e.g., short-term vs. long-term; observed vs. modeled) and different population cohorts (e.g., elderly, individuals with co-morbidities, young healthy individuals), there is compelling evidence that BC and PN represent traffic-related particles that are especially harmful to cardiovascular health. Further research is needed to validate these findings in other geographic locations, characterize exposure errors associated with using monitored and modeled traffic pollutant levels, and elucidate pathophysiological mechanisms underlying the cardiovascular effects of traffic-related particulate pollutants. Implications: Traffic emissions are an important source of particles harmful to cardiovascular health. Traffic-related particles, specifically BC and PN, adversely affect cardiac autonomic function, increase systemic inflammation and thrombotic activity, elevate BP, and increase the risk of ischemic stroke. There is evidence that BC and PN are associated with greater cardiovascular risk compared to PM2.5. Further research is needed to elucidate other health effects of traffic-related particles and assess the feasibility of regulating BC and PN or their regional and local sources.

Long-term NO2 exposures and cause-specific mortality in American older adults.

BACKGROUND: The impact of long-term exposure to nitrogen dioxide (NO2) on cause-specific mortality is poorly understood. OBJECTIVE: To assess mortality risks associated with long-term NO2 exposure and evaluate confounding of this association. METHODS: We examined the association between 12-month moving average NO2 exposure and cause-specific mortality in 14.1 million US Medicare beneficiaries between 2000 and 2008. Associations were examined using age, gender, and race-stratified and state-adjusted Poisson regression models. We assessed the potential for confounding by PM2.5 and behavioral covariates and unmeasured confounding by decomposing NO2 into its spatial and spatio-temporal components. RESULTS: We found significant associations between 12-month NO2 exposure and increased mortality from all-causes [risk ratio (RR): 1.052; 95% CI: 1.051, 1.054; per 10 ppb], cardiovascular (CVD) (1.133; 95% CI: 1.130, 1.137) and respiratory disease (1.050; 95% CI: 1.044, 1.056), all cancers (1.021; 95% CI: 1.017, 1.025), ischemic heart disease (IHD) (1.221; 95% CI: 1.217, 1.226), cerebrovascular (CBV) disease (1.092; 95% CI: 1.085, 1.100), and for the first time pneumonia (1.275; 95% CI: 1.263, 1.287). Associations generally remained positive and statistically significant after adjustment for PM2.5 and behavioral factors. CONCLUSIONS: Our findings provide additional evidence of the increased risk posed by long-term NO2 exposures on increased mortality from all-causes, CVD, respiratory disease, IHD, CBV, and cancer and provide new evidence of their impact on mortality from pneumonia. Unmeasured confounding of these associations was present, however, demonstrating the need to understand sources of this confounding.

Low birth weight and PM2.5 in Puerto Rico.

BACKGROUND: Low birth weight (LBW) has been associated with adverse health outcomes across the lifespan. Among ethnic/racial minority populations, few studies have examined the association between LBW (<2,500 or ≥2,500 g) and prenatal exposure to air pollution, a key modifiable environmental risk factor. METHODS: We examined the association between LBW and prenatal exposure to PM2.5 in a Hispanic and black population in Puerto Rico between 1999 and 2013, adjusting for individual and municipality-level confounders. We used modified Poisson regression to estimate the association and performed sensitivity analyses treating birth weight as continuous or polychotomous. In secondary analyses, we applied a 2-stage mixed effects model suitable for longitudinally measured exposures and binary outcomes. RESULTS: Among 332,129 total and 275,814 term births, 12.2% and 6.3% of infants had LBW, respectively. Eighty-eight percent of mothers were Hispanic. Mean (SD) PM2.5 concentrations declined from 9.9 (1.7) µg/m3 in 1999 to 6.1 (1.1) µg/m3 in 2013. Mean birth weights dropped to 3,044 g in 2010 and rose steadily afterward. Among term births, a SD increase in PM2.5 was associated with a 3.2% (95% CI = -1.0%, 6.3%) higher risk of LBW. First (risk ratio, 1.02; 95% CI = 1.00, 1.04) and second (1.02; 95% CI = 1.01, 1.05) trimester exposures were associated with increased LBW risk. In a 2-stage approach that longitudinally modeled monthly prenatal exposure levels, a standard deviation increase in average PM2.5 was associated with higher risk of LBW (odds ratio, 1.04; 95% CI = 1.01, 1.08). CONCLUSIONS: In Puerto Rico, LBW is associated with prenatal PM2.5 exposure.

Close proximity to roadway and urbanicity associated with mental ill-health in older adults.

Evidence for the association between built environment and mental ill health, especially in older population where mental ill health is common, remains inconclusive. We examined the association of roadway distance and urbanicity, measured as percentage of urban land use within 1 km from participants' residence, with mental ill-health in a longitudinal study of community-dwelling older adults in the United States between 2005 and 2006 and 2011-2012. We evaluated perceived stress, depression and anxiety symptoms using the Cohen's Perceived Stress Scale, the Center for Epidemiological Studies - Depression, and the Hospital Anxiety and Depression Scale - anxiety subscale, respectively. Increment in roadway distance was significantly associated with -0.03 point (95% CI: -0.05, -0.01) change in depressive score, with loneliness and PM2.5 partially mediating the observed associations. Age, gender, race/ethnicity, and physical activity significantly modified the distance-depression association. Anxiety was inversely associated with roadway distance (-0.02; 95% CI: -0.03, 0.00), though the associations became insignificant upon adjusting for road traffic or noise. Urbanicity was significantly associated with 0.29 (95% CI: 0.10, 0.57) point increase in depressive symptoms in multivariable model; the association was partly mediated by loneliness, physical activity, social support and air pollution. No association was found between roadway distance and perceived stress, and between urbanicity, and anxiety and perceived stress. Built environment was associated with mental ill health, partially through pathways related to air pollution and certain individual characteristics (e.g. loneliness). Our study warrants further examination of the mediation and interaction of the built environment-mental health association.

Fine Particle Sources and Cognitive Function in An Older Puerto Rican Cohort in Greater Boston.

BACKGROUND: Puerto Ricans living in the mainland US have substantially higher rates of impairment to cognitive performance as compared to non-Hispanic Whites, with air pollutant exposures a potential risk factor. We investigated whether exposures to specific air pollution sources were associated with performance across several cognitive domains in a cohort of Puerto Rican older adults. OBJECTIVES: To investigate the association between sources of PM2.5 and cognitive performance in each of five cognitive domains. METHODS: We obtained demographic, health, and cognitive function data for 1500 elderly participants of the Boston Puerto Rican Health Study (BPRHS). Cognitive function was assessed in each of two waves for five domains: verbal memory, recognition, mental processing, and executive and visuospatial function. To these data, we linked concentrations of fine particulate matter (PM2.5) and its components, black carbon (BC), nickel, sulfur, and silicon, as tracers for PM2.5 from traffic, oil combustion, coal combustion, and resuspended dust, respectively. Associations between each PM2.5 component and cognitive domain were examined using linear mixed models. RESULTS: One year moving average exposures to BC were significantly associated with decreased verbal memory (-0.38;95% CI: -0.46,-0.30), recognition (-0.35; 95% CI: -0.46,-0.25), mental processing (-1.14; 95% CI: -1.55,-0.74), and executive function (-0.94; 95% CI: -1.31,-0.56). Similar associations were found for nickel. Associations for sulfur, and silicon, and PM2.5 were generally null, although sulfur (-0.51; 95% CI -0.75,-0.28) silicon (-0.25; 95% CI: -0.36,-0.13) and PM2.5 (-0.35; 95% CI: -0.57,-0.12) were associated with decreased recognition. CONCLUSION: Long-term exposures to BC and nickel, tracers of traffic and oil combustion, respectively, were associated with decreased cognitive function across all domains, except visuospatial function.

Association of neighborhood greenness with self-perceived stress, depression and anxiety symptoms in older U.S adults.

BACKGROUND: Neighborhood environment, such as green vegetation, has been shown to play a role in coping with stress and mental ill health. Yet, epidemiological evidence of the association between greenness and mental health is inconsistent. METHODS: We examined whether living in green space is associated with self-perceived stress, depressive and anxiety symptoms in a nationally representative, longitudinal sample of community-dwelling older adults (N = 4118; aged 57-85 years) in the United States. We evaluated perceived stress, depression and anxiety symptoms using the Cohen's Perceived Stress Scale, the Center for Epidemiological Studies - Depression, and the Hospital Anxiety and Depression Scale - anxiety subscale, respectively. Greenness was assessed for each participant using the Normalized Difference Vegetation Index at 250-m resolution, as well as a buffer of 1000-m. We conducted longitudinal analyses to assess the associations between greenness and mental health upon adjusting for confounders (e.g., education), and to examine potential mediation and effect modification. RESULTS: An interquartile range (0.25 point) increase in contemporaneous greenness was significantly associated with 0.238 unit (95% CI: - 0.346, - 0.130) and 0.162 unit (95% CI: - 0.271, - 0.054) decrease in the perceived stress in base and multivariable models, respectively. The magnitude of the association was similar or even stronger when examining summer (- 0.161; 95% CI: - 0.295, - 0.027) and annual average of greenness (- 0.188; 95% CI: - 0.337, - 0.038), as well as greenness buffer of 1000-m. The greenness-stress association was partially mediated by physical activity (15.1% mediated), where increased greenness led to increased physical activity and less stress, and by history of respiratory diseases (- 3.8% mediated), where increased greenness led to increased respiratory disease and more stress. The association was also significantly modified by race, social support, physical function, socioeconomic status, and region. While greenness was not significantly associated with anxiety and depressive scores across all participants, significant inverse associations were found for Whites participants, and for individuals with higher socioeconomic status, who were physically active, as compared to their counterparts. CONCLUSION: We found a direct association of greenness with perceived stress among older adults, and an indirect association mediated through physical activity and respiratory disease history. Our study findings warrant further examination of the mediation and modification of the greenness-mental health association.