Disparities in ambient nitrogen dioxide pollution in the United States.

Average ambient concentrations of nitrogen dioxide (NO2), an important air pollutant, have declined in the United States since the enactment of the Clean Air Act. Despite evidence that NO2 disproportionately affects racial/ethnic minority groups, it remains unclear what drives the exposure disparities and how they have changed over time. Here, we provide evidence by integrating high-resolution (1 km × 1 km) ground-level NO2 estimates, sociodemographic information, and source-specific emission intensity and location for 217,740 block groups across the contiguous United States from 2000 to 2016. We show that racial/ethnic minorities are disproportionately exposed to higher levels of NO2 pollution compared with Whites across the United States and within major metropolitan areas. These inequities persisted over time and have worsened in many cases, despite a significant decrease in the national average NO2 concentration over the 17-y study period. Overall, traffic contributes the largest fraction of NO2 disparity. Contributions of other emission sources to exposure disparities vary by location. Our analyses offer insights into policies aimed at reducing air pollution exposure disparities among races/ethnicities and locations.

Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States.

Growing evidence suggests that fine particulate matter (PM2.5) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO3-), sulfate (SO42-), ammonium (NH4+), and soil dust (DUST). To investigate the impact of long-term exposure to PM2.5 constituents on incident all-cause dementia and Alzheimer's disease (AD), hazard ratios for dementia and AD were estimated using Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration-response (C-R) relationships. Results using two exposure datasets consistently indicated higher rates of incident dementia and AD for an increased exposure to PM2.5 and its major constituents. An interquartile range increase in PM2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM2.5 constituents, associations remained significant for BC, OM, SO42-, and NH4+ for both end points (even after adjustments of other constituents), among which BC and SO42- showed the strongest associations. All constituents had largely linear C-R relationships in the low exposure range, but most tailed off at higher exposure concentrations. Our findings suggest that long-term exposure to PM2.5 is significantly associated with higher rates of incident dementia and AD and that SO42-, BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

Long-term exposure to PM2.5 species and all-cause mortality among Medicare patients using mixtures analyses.

BACKGROUND: The relationship between long-term exposure to PM2.5 and mortality is well-established; however, the role of individual species is less understood. OBJECTIVES: In this study, we assess the overall effect of long-term exposure to PM2.5 as a mixture of species and identify the most harmful of those species while controlling for the others. METHODS: We looked at changes in mortality among Medicare participants 65 years of age or older from 2000 to 2018 in response to changes in annual levels of 15 PM2.5 components, namely: organic carbon, elemental carbon, nickel, lead, zinc, sulfate, potassium, vanadium, nitrate, silicon, copper, iron, ammonium, calcium, and bromine. Data on exposure were derived from high-resolution, spatio-temporal models which were then aggregated to ZIP code. We used the rate of deaths in each ZIP code per year as the outcome of interest. Covariates included demographic, temperature, socioeconomic, and access-to-care variables. We used a mixtures approach, a weighted quantile sum, to analyze the joint effects of PM2.5 species on mortality. We further looked at the effects of the components when PM2.5 mass levels were at concentrations below 8 µg/m3, and effect modification by sex, race, Medicaid status, and Census division. RESULTS: We found that for each decile increase in the levels of the PM2.5 mixture, the rate of all-cause mortality increased by 1.4% (95% CI: 1.3%-1.4%), the rate of cardiovascular mortality increased by 2.1% (95% CI: 2.0%-2.2%), and the rate of respiratory mortality increased by 1.7% (95% CI: 1.5%-1.9%). These effects estimates remained significant and slightly higher when we restricted to lower concentrations. The highest weights for harmful effects were due to organic carbon, nickel, zinc, sulfate, and vanadium. CONCLUSIONS: Long-term exposure to PM2.5 species, as a mixture, increased the risk of all-cause, cardiovascular, and respiratory mortality.

National Cohort Study of Long-Term Exposure to PM2.5 Components and Mortality in Medicare American Older Adults.

There is increasing evidence linking long-term fine particulate matter (PM2.5) exposure to negative health effects. However, the relative influence of each component of PM2.5 on health risk is poorly understood. In a cohort study in the contiguous United States between 2000 and 2017, we examined the effect of long-term exposure to PM2.5 main components and all-cause mortality in older adults who had to be at least 65 years old and enrolled in Medicare. We estimated the yearly mean concentrations of six key PM2.5 compounds, including black carbon (BC), organic matter (OM), soil dust (DUST), nitrate (NO3-), sulfate (SO42-), and ammonium (NH4+), using two independently sourced well-validated prediction models. We applied Cox proportional hazard models to evaluate the hazard ratios for mortality and penalized splines for assessing potential nonlinear concentration-response associations. Results suggested that increased exposure to PM2.5 mass and its six main constituents were significantly linked to elevated all-cause mortality. All components showed linear concentration-response relationships in the low exposure concentration ranges. Our research indicates that long-term exposure to PM2.5 mass and its essential compounds are strongly connected to increased mortality risk. Reductions of fossil fuel burning may yield significant air quality and public health benefit.

Short-term associations between warm-season ambient temperature and emergency department visits for Alzheimer's disease and related dementia in five US states.

BACKGROUND: Ambient temperatures are projected to increase in the future due to climate change. Alzheimer's disease (AD) and Alzheimer's disease-related dementia (ADRD) affect millions of individuals and represent substantial health burdens in the US. High temperature may be a risk factor for AD/ADRD outcomes with several recent studies reporting associations between temperature and AD mortality. However, the link between heat and AD morbidity is poorly understood. METHODS: We examined short-term associations between warm-season daily ambient temperature and AD/ADRD emergency department (ED) visits for individuals aged 45 years or above during the warm season (May to October) for up to 14 years (2005-2018) in five US states: California, Missouri, North Carolina, New Jersey, and New York. Daily ZIP code-level maximum, average and minimum temperature exposures were derived from 1 km gridded Daymet products. Associations are assessed using a time-stratified case-crossover design using conditional logistic regression. RESULTS: We found consistent positive short-term effects of ambient temperature among 3.4 million AD/ADRD ED visits across five states. An increase of the 3-day cumulative temperature exposure of daily average temperature from the 50th to the 95th percentile was associated with a pooled odds ratio of 1.042 (95% CI: 1.034, 1.051) for AD/ADRD ED visits. We observed evidence of the association being stronger for patients 65-74 years of age and for ED visits that led to hospital admissions. Temperature associations were also stronger among AD/ADRD ED visits compared to ED visits for other reasons, particularly among patients aged 65-74 years. CONCLUSION: People with AD/ADRD may represent a vulnerable population affected by short-term exposure to high temperature. Our results support the development of targeted strategies to reduce heat-related AD/ADRD morbidity in the context of global warming.

Long-term effects of ambient PM2.5 constituents on metabolic syndrome in Chinese children and adolescents.

Metabolic syndrome (MetS) is considered a main public health issue as it remarkably adds the risk of cardiovascular disease, leading to a heavy burden of disease. There is growing evidence linking fine particulate matter (PM2.5) exposure to MetS. However, the influences of PM2.5 constituents, especially in children and adolescents, remain unclear. Our study was according to a national analysis among Chinese children and adolescents to examine the associations between long-term exposure to PM2.5 main constituents and MetS. A total of 10,066 children and adolescents aged 10-18 years were recruited in 7 provinces in China, with blood tests, health exams, and questionnaire surveys. We estimated long-term exposures to PM2.5 mass and its five constituents, containing black carbon (BC), organic matter (OM), inorganic nitrate (NO3-), sulfate (SO42-), and soil particles (SOIL) from multi-source data fusion models. Mixed-effects logistic regression models were used with the adjustment of a variety of covariates. In the surveyed populations, 2.9% were classified as MetS. From the single-pollutant models, we discovered that long-term exposures to PM2.5 mass, BC, OM, NO3-, as well as SO42-, were significantly associated with the prevalence of MetS, with odds ratios (ORs) per 1 µg/m3 that were 1.02 (95% confidence interval (CI): 1.01, 1.03) for PM2.5 mass, 1.24 (95% CI: 1.14, 1.35) for BC, 1.07 (95% CI: 1.04, 1.11) for OM, 1.09 (95% CI: 1.04, 1.13) for NO3-, and 1.14 (95% CI:1.04, 1.24) for SO42-. The influence of BC on the prevalence of MetS was robust in both the multi-pollutant model and the PM2.5-constituent joint model. The paper indicates long-term exposure to PM2.5 mass and specific PM2.5 constituents, particularly for BC, was significantly associated with a higher MetS prevalence among children and adolescents in China. Our results highlight the significance of establishing further regulations on PM2.5 constituents.

Air pollution, climate conditions and risk of hospital admissions for psychotic disorders in U.S. residents.

BACKGROUND: The physical environmental risk factors for psychotic disorders are poorly understood. This study aimed to examine the associations between exposure to ambient air pollution, climate measures and risk of hospitalization for psychotic disorders and uncover potential disparities by demographic, community factors. METHODS: Using Health Cost and Utilization Project (HCUP) State Inpatient Databases (SIDs), we applied zero-inflated negative binomial regression to obtain relative risks of hospitalization due to psychotic disorders associated with increases in residential exposure to ambient air pollution (fine particulate matter, PM2.5; nitrogen dioxide, NO2), temperature and cumulative precipitation. The analysis covered all-age residents in eight U.S. states over the period of 2002-2016. We additionally investigated modification by age, sex and area-level poverty, percent of blacks and Hispanics. RESULTS: Over the study period and among the covered areas, we identified 1,211,100 admissions due to psychotic disorders. For each interquartile (IQR) increase in exposure to PM2.5 and NO2, we observed a relative risk (RR) of 1.11 (95% confidence interval (CI) = 1.09, 1.13) and 1.27 (95% CI = 1.24, 1.31), respectively. For each 1 °C increase of temperature, the RR was 1.03 (95% CI = 1.03, 1.04). Males were more affected by NO2. Older age residents (≥30 yrs) were more sensitive to PM2.5 and temperature. Population living in economically disadvantaged areas were more affected by air pollution. CONCLUSIONS: The study suggests that living in areas with higher levels of air pollutants and ambient temperature could contribute to additional risk of inpatient care for individuals with psychotic disorders.

Socioeconomic and racial disparities in source-apportioned PM2.5 levels across urban areas in the contiguous US, 2010.

Fine particulate matter (PM2.5) air pollution exposure is associated with short and long-term health effects. Several studies found differences in PM2.5 exposure associated with neighborhood racial and socioeconomic composition. However, most focused on total PM2.5 mass rather than its chemical components and their sources. In this study, we describe the ZIP code characteristics that drive the disparities in exposure to PM2.5 chemical components attributed to source categories both nationally and regionally. We obtained annual mean predictions of PM2.5 and fourteen of its chemical components from spatiotemporal models and socioeconomic and racial predictor variables from the 2010 US Census, and the American Community Survey 5-year estimates. We used non-negative matrix factorization to attribute the chemical components to five source categories. We fit generalized nonlinear models to assess the associations between the neighborhood predictors and each PM2.5 source category in urban areas in the United States in 2010 (n=25,790 zip codes). We observed higher PM2.5 levels in ZIP codes with higher proportions of Black individuals and lower socioeconomic status. Racial exposure disparities were mainly attributed to Heavy Fuel, Oil and Industrial, Metal Processing Industry and Agricultural, and Motor Vehicle sources. Economic disparities were mainly attributed to Soil and Crustal Dust, Heavy Fuel Oil and Industrial, Metal Processing Industry and Agricultural, and Motor Vehicle sources. Upon further analysis through stratifying by regions within the United States, we found that the associations between ZIP code characteristics and source-attributed PM2.5 levels were generally greater in Western states. In conclusion, racial, socioeconomic, and geographic inequalities in exposure to PM2.5 and its components are driven by systematic differences in component sources that can inform air quality improvement strategies.

The effect of race and co-morbidities on Alzheimer's disease based on Medicare data.

INTRODUCTION: Alzheimer's disease (AD) incidence is thought to be higher among Black than White individuals. METHODS: We studied the US Medicare population from 2000 to 2018. Cox regression was used to determine the roles of race and co-morbidities for AD incidence. RESULTS: We studied 11,880,906 Medicare beneficiaries, with 774,548 AD cases. Hazard ratios (HRs) by increasing numbers of co-morbidities (1-7) were 1.51, 2.00, 2.55, 3.16, 2.89, 4.77, and 5.65. Among those with no co-morbidities, Black individuals had a lower rate than those who are White (HR = 0.69), while among those with one more co-morbidities, Black individuals had a higher rate (HR = 1.19). The presence of hypertension increased AD rates by 14% for White individuals, but 69% for those who are Black. DISCUSSION: More co-morbidities was strongly associated with higher AD rates. The higher rates for Black versus White individuals was apparent only for those with co-morbidities and appears driven both by more co-morbidities, and the greater effect of hypertension. HIGHLIGHTS: Black individuals have been shown to have higher Alzheimer's disease (AD) rates than those who are White. Some co-morbidities are known to increase AD risk. Among those In Medicare data with no co-morbidities, Black individuals have less risk than those who are White. Among those with co-morbidities, Black individuals have higher rates than those who are White. Hypertension results in a much stronger increase in AD risk for Black versus White individuals.

Long-Term Association of Air Pollution and Hospital Admissions Among Medicare Participants Using a Doubly Robust Additive Model.

BACKGROUND: Studies examining the nonfatal health outcomes of exposure to air pollution have been limited by the number of pollutants studied and focus on short-term exposures. METHODS: We examined the relationship between long-term exposure to fine particulate matter with an aerodynamic diameter <2.5 micrometers (PM2.5), NO2, and tropospheric ozone and hospital admissions for 4 cardiovascular and respiratory outcomes (myocardial infarction, ischemic stroke, atrial fibrillation and flutter, and pneumonia) among the Medicare population of the United States. We used a doubly robust method for our statistical analysis, which relies on both inverse probability weighting and adjustment in the outcome model to account for confounding. The results from this regression are on an additive scale. We further looked at this relationship at lower pollutant concentrations, which are consistent with typical exposure levels in the United States, and among potentially susceptible subgroups. RESULTS: Long-term exposure to fine PM2.5 was associated with an increased risk of all outcomes with the highest effect seen for stroke with a 0.0091% (95% CI, 0.0086-0.0097) increase in the risk of stroke for each 1-µg/m3 increase in annual levels. This translated to 2536 (95% CI, 2383-2691) cases of hospital admissions with ischemic stroke per year, which can be attributed to each 1-unit increase in fine particulate matter levels among the study population. NO2 was associated with an increase in the risk of admission with stroke by 0.00059% (95% CI, 0.00039-0.00075) and atrial fibrillation by 0.00129% (95% CI, 0.00114-0.00148) per ppb and tropospheric ozone was associated with an increase in the risk of admission with pneumonia by 0.00413% (95% CI, 0.00376-0.00447) per parts per billion. At lower concentrations, all pollutants were consistently associated with an increased risk for all our studied outcomes. CONCLUSIONS: Long-term exposure to air pollutants poses a significant risk to cardiovascular and respiratory health among the elderly population in the United States, with the greatest increase in the association per unit of exposure occurring at lower concentrations.

Global Emissions of Hydrogen Chloride and Particulate Chloride from Continental Sources.

Gaseous and particulate chlorine species play an important role in modulating tropospheric oxidation capacity, aerosol water uptake, visibility degradation, and human health. The lack of recent global continental chlorine emissions has hindered modeling studies of the role of chlorine in the atmosphere. Here, we develop a comprehensive global emission inventory of gaseous HCl and particulate Cl- (pCl), including 35 sources categorized in six source sectors based on published up-to-date activity data and emission factors. These emissions are gridded at a spatial resolution of 0.1° × 0.1° for the years 1960 to 2014. The estimated emissions of HCl and pCl in 2014 are 2354 (1661-3201) and 2321 (930-3264) Gg Cl a-1, respectively. Emissions of HCl are mostly from open waste burning (38%), open biomass burning (19%), energy (19%), and residential (13%) sectors, and the major sources classified by fuel type are combustion of waste (43%), biomass (32%), and coal (25%). Emissions of pCl are mostly from biofuel (29%) and open biomass burning processes (44%). The sectoral and spatial distributions of HCl and pCl emissions are very heterogeneous along the study period, and the temporal trends are mainly driven by the changes in emission factors, energy intensity, economy, and population.

Low-Concentration Air Pollution and Mortality in American Older Adults: A National Cohort Analysis (2001-2017).

Mounting epidemiological evidence has documented the associations between long-term exposure to multiple air pollutants and increased mortality. There is a pressing need to determine whether risks persist at low concentrations including below current national standards. Air pollution levels have decreased in the United States, and better understanding of the health effects of low-level air pollution is essential for the amendment of National Ambient Air Quality Standards (NAAQS). A nationwide, population-based, open cohort study was conducted to estimate the association between long-term exposure to low-level PM2.5, NO2, O3, and all-cause mortality. The study population included all Medicare enrollees (ages 65 years or older) in the contiguous U.S. from 2001 to 2017. We further defined three low-exposure subcohorts comprised of Medicare enrollees who were always exposed to low-level PM2.5 (annual mean ≤12-µg/m3), NO2 (annual mean ≤53-ppb), and O3 (warm-season mean ≤50-ppb), respectively, over the study period. Of the 68.7-million Medicare enrollees, 33.1% (22.8-million, mean age 75.9 years), 93.8% (64.5-million, mean age 76.2 years), and 65.0% (44.7-million, mean age 75.6 years) were always exposed to low-level annual PM2.5, annual NO2, and warm-season O3 over the study period, respectively. Among the low-exposure cohorts, a 10-µg/m3 increase in PM2.5, 10-ppb increase in NO2, and 10-ppb increase in warm-season O3, were, respectively, associated with an increase in mortality rate ranging between 10 and 13%, 2 and 4%, and 12 and 14% in single-pollutant models, and between 6 and 8%, 1 and 3%, and 9 and 11% in tripollutant models, using three statistical approaches. There was strong evidence of linearity in concentration-response relationships for PM2.5 and NO2 at levels below the current NAAQS, suggesting that no safe threshold exists for health-harmful pollution levels. For O3, the concentration-response relationship shows an increasingly positive association at levels above 40-ppb. In conclusion, exposure to low levels of PM2.5, NO2, and warm-season O3 was associated with an increased risk of all-cause mortality.

Associations between long-term exposures to airborne PM2.5 components and mortality in Massachusetts: mixture analysis exploration.

BACKGROUND: Numerous studies have documented PM2.5's links with adverse health outcomes. Comparatively fewer studies have evaluated specific PM2.5 components. The lack of exposure measurements and high correlation among different PM2.5 components are two limitations. METHODS: We applied a novel exposure prediction model to obtain annual Census tract-level concentrations of 15 PM2.5 components (Zn, V, Si, Pb, Ni, K, Fe, Cu, Ca, Br, SO42-, NO3-, NH4+, OC, EC) in Massachusetts from 2000 to 2015, to which we matched geocoded deaths. All non-accidental mortality, cardiovascular mortality, and respiratory mortality were examined for the population aged 18 or over. Weighted quantile sum (WQS) regression models were used to examine the cumulative associations between PM2.5 components mixture and outcomes and each component's contributions to the cumulative associations. We have fit WQS models on 15 PM2.5 components and a priori identified source groups (heavy fuel oil combustion, biomass burning, crustal matter, non-tailpipe traffic source, tailpipe traffic source, secondary particles from power plants, secondary particles from agriculture, unclear source) for the 15 PM2.5 components. Total PM2.5 mass analysis and single component associations were also conducted through quasi-Poisson regression models. RESULTS: Positive cumulative associations between the components mixture and all three outcomes were observed from the WQS models. Components with large contribution to the cumulative associations included K, OC, and Fe. Biomass burning, traffic emissions, and secondary particles from power plants were identified as important source contributing to the cumulative associations. Mortality rate ratios for cardiovascular mortality were of greater magnitude than all non-accidental mortality and respiratory mortality, which is also observed in cumulative associations estimated from WQS, total PM2.5 mass analysis, and single component associations. CONCLUSION: We have found positive associations between the mixture of 15 PM2.5 components and all non-accidental mortality, cardiovascular mortality, and respiratory mortality. Among these components, Fe, K, and OC have been identified as having important contribution to the cumulative associations. The WQS results also suggests potential source effects from biomass burning, traffic emissions, and secondary particles from power plants.

Tracking the impacts of climate change on human health via indicators: lessons from the Lancet Countdown.

BACKGROUND: In the past decades, climate change has been impacting human lives and health via extreme weather and climate events and alterations in labour capacity, food security, and the prevalence and geographical distribution of infectious diseases across the globe. Climate change and health indicators (CCHIs) are workable tools designed to capture the complex set of interdependent interactions through which climate change is affecting human health. Since 2015, a novel sub-set of CCHIs, focusing on climate change impacts, exposures, and vulnerability indicators (CCIEVIs) has been developed, refined, and integrated by Working Group 1 of the "Lancet Countdown: Tracking Progress on Health and Climate Change", an international collaboration across disciplines that include climate, geography, epidemiology, occupation health, and economics. DISCUSSION: This research in practice article is a reflective narrative documenting how we have developed CCIEVIs as a discrete set of quantifiable indicators that are updated annually to provide the most recent picture of climate change's impacts on human health. In our experience, the main challenge was to define globally relevant indicators that also have local relevance and as such can support decision making across multiple spatial scales. We found a hazard, exposure, and vulnerability framework to be effective in this regard. We here describe how we used such a framework to define CCIEVIs based on both data availability and the indicators' relevance to climate change and human health. We also report on how CCIEVIs have been improved and added to, detailing the underlying data and methods, and in doing so provide the defining quality criteria for Lancet Countdown CCIEVIs. CONCLUSIONS: Our experience shows that CCIEVIs can effectively contribute to a world-wide monitoring system that aims to track, communicate, and harness evidence on climate-induced health impacts towards effective intervention strategies. An ongoing challenge is how to improve CCIEVIs so that the description of the linkages between climate change and human health can become more and more comprehensive.

The association between polymorphisms in miRNA and the cholinesterase activity of workers in an omethoate-exposed environment.

To explore the association between polymorphisms in microRNAs (miRNAs) and the cholinesterase (ChE) activity in omethoate-exposed workers, we recruited 180 omethoate-exposed workers and 115 controls to measure their ChE activity using acetylcholine and dithio-bis-(nitrobenzoic acid) and genotype susceptible SNPs in their miRNA by time-of-flight mass spectrometry. ChE activity in the exposure group was lower than that in the control group (P < 0.001). The analysis of covariance result showed that ChE activity was lower in the (- -/- T) genotype in miR-30a rs111456995 (1.97 ± 0.47) than in the TT genotype (2.23 ± 0.59) of the exposure group (P = 0.004). Multivariate linear regression was performed to find influencing factors on ChE activity, and variables kept in the model included omethoate exposure (b = -1.094, P < 0.001), gender (b = -0.381, P < 0.001), miR-30a rs111456995 (- -/- T)(b = -0.248, P < 0.001), and drinking (b = 0.258, P =0.019). The results suggest that individuals carrying a (- -/- T) genotype in miR-30a rs111456995 were more susceptible to damage in their cholinesterase induced by omethoate exposure.

Short-term exposure to nitrogen dioxide and mortality: A systematic review and meta-analysis.

BACKGROUND: Ambient air pollution has been characterized as a leading cause of mortality worldwide and has been associated with cardiovascular and respiratory diseases. There is increasing evidence that short-term exposure to nitrogen dioxide (NO2), is related to adverse health effects and mortality. METHODS: We conducted a systematic review of short-term NO2 and daily mortality, which were indexed in PubMed and Embase up to June 2021. We calculated random-effects estimates by different continents and globally, and tested for heterogeneity and publication bias. RESULTS: We included 87 articles in our quantitative analysis. NO2 and all-cause as well as cause-specific mortality were positively associated in the main analysis. For all-cause mortality, a 10 ppb increase in NO2 was associated with a 1.58% (95%CI 1.28%-1.88%, I2 = 96.3%, Eggers' test p < 0.01, N = 57) increase in the risk of death. For cause-specific mortality, a 10 ppb increase in NO2 was associated with a 1.72% (95%CI 1.41%-2.04%, I2 = 87.4%, Eggers' test p < 0.01, N = 42) increase in cardiovascular mortality and a 2.05% (95%CI 1.52%-2.59%, I2 = 78.5%, Eggers' test p < 0.01, N = 38) increase in respiratory mortality. In the sensitivity analysis, the meta-estimates for all-cause mortality, cardiovascular and respiratory mortality were nearly identical. The heterogeneity would decline to varying degrees through regional and study-design stratification. CONCLUSIONS: This study provides evidence of an association between short-term exposure to NO2, a proxy for traffic-sourced air pollutants, and all-cause, cardiovascular and respiratory mortality.

A Co-Twin control study of fine particulate matter and the prevalence of metabolic syndrome risk factors.

The relationship between ambient fine particulate matter (PM2.5) and metabolic syndrome (MetS) is understudied. It also remains unknown whether familial factors play a role in this relationship. In a study of 566 middle-aged twins, we examined the association of PM2.5 with MetS risk factors, measured by a MetS score as a summation of individual risk factors (range, 0 to 5). High-resolution PM2.5 estimates were obtained through previously validated models that incorporated monitor and satellite derived data. We estimated two-year average PM2.5 concentrations based on the ZIP code of each twin's residence. We used ordinal response models adapted for twin studies. When treating twins as individuals, the odds ratio of having 1-point higher MetS score was 1.78 for each 10 µg/m3-increase in exposure to PM2.5 (confidence interval [CI]: 1.01, 3.15), after adjusting for potential confounders. This association was mainly between pairs; the odds ratio was 1.97 (CI: 1.01, 3.84) for each 10 µg/m3-increase in the average pairwise exposure level. We found no significant difference in MetS scores within pairs who were discordant for PM2.5 exposure. In conclusion, higher PM2.5 in residence area is associated with more MetS risk factors. This association, however, is confounded by shared familial factors.

Associations of single and multiple per- and polyfluoroalkyl substance (PFAS) exposure with vitamin D biomarkers in African American women during pregnancy.

Vitamin D has been linked to various physiological functions in pregnant women and their fetuses. Previous studies have suggested that some per- and polyfluoroalkyl substances (PFAS) may alter serum vitamin D concentrations. However, no study has investigated the relationship between PFAS and vitamin D in pregnant women. This study aims to evaluate the associations of serum PFAS with serum total and free 25-hydroxyvitamin D (25(OH)D) during pregnancy in a cohort of African American women in Atlanta, GA. Blood samples from 442 participants were collected in early pregnancy (8-14 weeks of gestation) for PFAS and 25(OH)D measurements, and additional samples were collected in late pregnancy (24-30 weeks) for the second 25(OH)D measurements. We fit multivariable linear regressions and weighted quantile sum (WQS) regressions to estimate the associations of individual PFAS and their mixtures with 25(OH)D concentrations. We found mostly positive associations of total 25(OH)D with PFHxS (perfluorohexane sulfonic acid), PFOS (perfluorooctane sulfonic acid), PFDA (perfluorodecanoic acid), and NMeFOSAA (N-methyl perfluorooctane sulfonamido acetic acid), and negative associations with PFPeA (perfluoropentanoic acid). For free 25(OH)D, positive associations were observed with PFHxS, PFOS, PFOA (perfluorooctanoic acid), and PFDA, and a negative association with PFPeA among the women with male fetuses in the models using 25(OH)D measured in late pregnancy. In mixture models, a quartile increase in WQS index was associated with 2.88 ng/mL (95%CI 1.14-4.59) and 5.68 ng/mL (95%CI 3.31-8.04) increases in total 25(OH)D measured in the early and late pregnancy, respectively. NMeFOSAA, PFDA, and PFOS contributed the most to the overall effects among the eight PFAS. No association was found between free 25(OH)D and the PFAS mixture. These results suggest that PFAS may affect vitamin D biomarker concentrations in pregnant African American women, and some of the associations were modified by fetal sex.

The association between long-term exposure to low-level PM2.5 and mortality in the state of Queensland, Australia: A modelling study with the difference-in-differences approach.

BACKGROUND: To date, few studies have investigated the causal relationship between mortality and long-term exposure to a low level of fine particulate matter (PM2.5) concentrations. METHODS AND FINDINGS: We studied 242,320 registered deaths in Queensland between January 1, 1998, and December 31, 2013, with satellite-retrieved annual average PM2.5 concentrations to each postcode. A variant of difference-in-differences (DID) approach was used to investigate the association of long-term PM2.5 exposure with total mortality and cause-specific (cardiovascular, respiratory, and non-accidental) mortality. We observed 217,510 non-accidental deaths, 133,661 cardiovascular deaths, and 30,748 respiratory deaths in Queensland during the study period. The annual average PM2.5 concentrations ranged from 1.6 to 9.0 µg/m3, which were well below the current World Health Organization (WHO) annual standard (10 µg/m3). Long-term exposure to PM2.5 was associated with increased total mortality and cause-specific mortality. For each 1 µg/m3 increase in annual PM2.5, we found a 2.02% (95% CI 1.41%-2.63%; p < 0.01) increase in total mortality. Higher effect estimates were observed in Brisbane than those in Queensland for all types of mortality. A major limitation of our study is that the DID design is under the assumption that no predictors other than seasonal temperature exhibit different spatial-temporal variations in relation to PM2.5 exposure. However, if this assumption is violated (e.g., socioeconomic status [SES] and outdoor physical activities), the DID design is still subject to confounding. CONCLUSIONS: Long-term exposure to PM2.5 was associated with total, non-accidental, cardiovascular, and respiratory mortality in Queensland, Australia, where PM2.5 levels were measured well below the WHO air quality standard.

Causal Effects of Air Pollution on Mortality Rate in Massachusetts.

Air pollution epidemiology studies have primarily investigated long- and short-term exposures separately, have used multiplicative models, and have been associational studies. Implementing a generalized propensity score adjustment approach with 3.8 billion person-days of follow-up, we simultaneously assessed causal associations of long-term (1-year moving average) and short-term (2-day moving average) exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 µm (PM2.5), ozone, and nitrogen dioxide with all-cause mortality on an additive scale among Medicare beneficiaries in Massachusetts (2000-2012). We found that long- and short-term PM2.5, ozone, and nitrogen dioxide exposures were all associated with increased mortality risk. Specifically, per 10 million person-days, each 1-µg/m3 increase in long- and short-term PM2.5 exposure was associated with 35.4 (95% confidence interval (CI): 33.4, 37.6) and 3.04 (95% CI: 2.17, 3.94) excess deaths, respectively; each 1-part per billion (ppb) increase in long- and short-term ozone exposure was associated with 2.35 (95% CI: 1.08, 3.61) and 2.41 (95% CI: 1.81, 2.91) excess deaths, respectively; and each 1-ppb increase in long- and short-term nitrogen dioxide exposure was associated with 3.24 (95% CI: 2.75, 3.77) and 5.60 (95% CI: 5.24, 5.98) excess deaths, respectively. Mortality associated with long-term PM2.5 and ozone exposure increased substantially at low levels. The findings suggested that air pollution was causally associated with mortality, even at levels below national standards.