Grouped mixtures of air pollutants and seasonal temperature anomalies and cardiovascular hospitalizations among U.S. Residents.

BACKGROUND: Air pollution is a recognized risk factor for cardiovascular disease (CVD). Temperature is also linked to CVD, with a primary focus on acute effects. Despite the close relationship between air pollution and temperature, their health effects are often examined separately, potentially overlooking their synergistic effects. Moreover, fewer studies have performed mixture analysis for multiple co-exposures, essential for adjusting confounding effects among them and assessing both cumulative and individual effects. METHODS: We obtained hospitalization records for residents of 14 U.S. states, spanning 2000-2016, from the Health Cost and Utilization Project State Inpatient Databases. We used a grouped weighted quantile sum regression, a novel approach for mixture analysis, to simultaneously evaluate cumulative and individual associations of annual exposures to four grouped mixtures: air pollutants (elemental carbon, ammonium, nitrate, organic carbon, sulfate, nitrogen dioxide, ozone), differences between summer and winter temperature means and their long-term averages during the entire study period (i.e., summer and winter temperature mean anomalies), differences between summer and winter temperature standard deviations (SD) and their long-term averages during the entire study period (i.e., summer and winter temperature SD anomalies), and interaction terms between air pollutants and summer and winter temperature mean anomalies. The outcomes are hospitalization rates for four prevalent CVD subtypes: ischemic heart disease, cerebrovascular disease, heart failure, and arrhythmia. RESULTS: Chronic exposure to air pollutant mixtures was associated with increased hospitalization rates for all CVD subtypes, with heart failure being the most susceptible subtype. Sulfate, nitrate, nitrogen dioxide, and organic carbon posed the highest risks. Mixtures of the interaction terms between air pollutants and temperature mean anomalies were associated with increased hospitalization rates for all CVD subtypes. CONCLUSIONS: Our findings identified critical pollutants for targeted emission controls and suggested that abnormal temperature changes chronically affected cardiovascular health by interacting with air pollution, not directly.

Short term exposure to low level ambient fine particulate matter and natural cause, cardiovascular, and respiratory morbidity among US adults with health insurance: case time series study.

OBJECTIVE: To estimate the excess relative and absolute risks of hospital admissions and emergency department visits for natural causes, cardiovascular disease, and respiratory disease associated with daily exposure to fine particulate matter (PM2.5) at concentrations below the new World Health Organization air quality guideline limit among adults with health insurance in the contiguous US. DESIGN: Case time series study. SETTING: US national administrative healthcare claims database. PARTICIPANTS: 50.1 million commercial and Medicare Advantage beneficiaries aged ≥18 years between 1 January 2010 and 31 December 2016. MAIN OUTCOME MEASURES: Daily counts of hospital admissions and emergency department visits for natural causes, cardiovascular disease, and respiratory disease based on the primary diagnosis code. RESULTS: During the study period, 10.3 million hospital admissions and 24.1 million emergency department visits occurred for natural causes among 50.1 million adult enrollees across 2939 US counties. The daily PM2.5 levels were below the new WHO guideline limit of 15 µg/m3 for 92.6% of county days (7 360 725 out of 7 949 713). On days when daily PM2.5 levels were below the new WHO air quality guideline limit of 15 µg/m3, an increase of 10 µg/m3 in PM2.5 during the current and previous day was associated with higher risk of hospital admissions for natural causes, with an excess relative risk of 0.91% (95% confidence interval 0.55% to 1.26%), or 1.87 (95% confidence interval 1.14 to 2.59) excess hospital admissions per million enrollees per day. The increased risk of hospital admissions for natural causes was observed exclusively among adults aged ≥65 years and was not evident in younger adults. PM2.5 levels were also statistically significantly associated with relative risk of hospital admissions for cardiovascular and respiratory diseases. For emergency department visits, a 10 µg/m3 increase in PM2.5 during the current and previous day was associated with respiratory disease, with an excess relative risk of 1.34% (0.73% to 1.94%), or 0.93 (0.52 to 1.35) excess emergency department visits per million enrollees per day. This association was not found for natural causes or cardiovascular disease. The higher risk of emergency department visits for respiratory disease was strongest among middle aged and young adults. CONCLUSIONS: Among US adults with health insurance, exposure to ambient PM2.5 at concentrations below the new WHO air quality guideline limit is statistically significantly associated with higher rates of hospital admissions for natural causes, cardiovascular disease, and respiratory disease, and with emergency department visits for respiratory diseases. These findings constitute an important contribution to the debate about the revision of air quality limits, guidelines, and standards.

Exposure-response associations between chronic exposure to fine particulate matter and risks of hospital admission for major cardiovascular diseases: population based cohort study.

OBJECTIVE: To estimate exposure-response associations between chronic exposure to fine particulate matter (PM2.5) and risks of the first hospital admission for major cardiovascular disease (CVD) subtypes. DESIGN: Population based cohort study. SETTING: Contiguous US. PARTICIPANTS: 59 761 494 Medicare fee-for-service beneficiaries aged ≥65 years during 2000-16. Calibrated PM2.5 predictions were linked to each participant's residential zip code as proxy exposure measurements. MAIN OUTCOME MEASURES: Risk of the first hospital admission during follow-up for ischemic heart disease, cerebrovascular disease, heart failure, cardiomyopathy, arrhythmia, valvular heart disease, thoracic and abdominal aortic aneurysms, or a composite of these CVD subtypes. A causal framework robust against confounding bias and bias arising from errors in exposure measurements was developed for exposure-response estimations. RESULTS: Three year average PM2.5 exposure was associated with increased relative risks of first hospital admissions for ischemic heart disease, cerebrovascular disease, heart failure, cardiomyopathy, arrhythmia, and thoracic and abdominal aortic aneurysms. For composite CVD, the exposure-response curve showed monotonically increased risk associated with PM2.5: compared with exposures ≤5 µg/m3 (the World Health Organization air quality guideline), the relative risk at exposures between 9 and 10 µg/m3, which encompassed the US national average of 9.7 µg/m3 during the study period, was 1.29 (95% confidence interval 1.28 to 1.30). On an absolute scale, the risk of hospital admission for composite CVD increased from 2.59% with exposures ≤5 µg/m3 to 3.35% at exposures between 9 and 10 µg/m3. The effects persisted for at least three years after exposure to PM2.5. Age, education, accessibility to healthcare, and neighborhood deprivation level appeared to modify susceptibility to PM2.5. CONCLUSIONS: The findings of this study suggest that no safe threshold exists for the chronic effect of PM2.5 on overall cardiovascular health. Substantial benefits could be attained through adherence to the WHO air quality guideline.

Modification of the PM2.5- and extreme heat-mortality relationships by historical redlining: a case-crossover study in thirteen U.S. states.

BACKGROUND: Redlining has been associated with worse health outcomes and various environmental disparities, separately, but little is known of the interaction between these two factors, if any. We aimed to estimate whether living in a historically-redlined area modifies the effects of exposures to ambient PM2.5 and extreme heat on mortality by non-external causes. METHODS: We merged 8,884,733 adult mortality records from thirteen state departments of public health with scanned and georeferenced Home Owners Loan Corporation (HOLC) maps from the University of Richmond, daily average PM2.5 from a sophisticated prediction model on a 1-km grid, and daily temperature and vapor pressure from the Daymet V4 1-km grid. A case-crossover approach was used to assess modification of the effects of ambient PM2.5 and extreme heat exposures by redlining and control for all fixed and slow-varying factors by design. Multiple moving averages of PM2.5 and duration-aware analyses of extreme heat were used to assess the most vulnerable time windows. RESULTS: We found significant statistical interactions between living in a redlined area and exposures to both ambient PM2.5 and extreme heat. Individuals who lived in redlined areas had an interaction odds ratio for mortality of 1.0093 (95% confidence interval [CI]: 1.0084, 1.0101) for each 10 µg m-3 increase in same-day ambient PM2.5 compared to individuals who did not live in redlined areas. For extreme heat, the interaction odds ratio was 1.0218 (95% CI 1.0031, 1.0408). CONCLUSIONS: Living in areas that were historically-redlined in the 1930's increases the effects of exposures to both PM2.5 and extreme heat on mortality by non-external causes, suggesting that interventions to reduce environmental health disparities can be more effective by also considering the social context of an area and how to reduce disparities there. Further study is required to ascertain the specific pathways through which this effect modification operates and to develop interventions that can contribute to health equity for individuals living in these areas.

Impact of heatwaves on all-cause mortality in India: A comprehensive multi-city study.

BACKGROUND: Heatwaves are expected to increase with climate change, posing a significant threat to population health. In India, with the world's largest population, heatwaves occur annually but have not been comprehensively studied. Accordingly, we evaluated the association between heatwaves and all-cause mortality and quantifying the attributable mortality fraction in India. METHODS: We obtained all-cause mortality counts for ten cities in India (2008-2019) and estimated daily mean temperatures from satellite data. Our main extreme heatwave was defined as two-consecutive days with an intensity above the 97th annual percentile. We estimated city-specific heatwave associations through generalised additive Poisson regression models, and meta-analysed the associations. We reported effects as the percentage change in daily mortality, with 95% confidence intervals (CI), comparing heatwave vs non-heatwave days. We further evaluated heatwaves using different percentiles (95th, 97th, 99th) for one, two, three and five-consecutive days. We also evaluated the influence of heatwave duration, intensity and timing in the summer season on heatwave mortality, and estimated the number of heatwave-related deaths. FINDINGS: Among âˆ¼ 3.6 million deaths, we observed that temperatures above 97th percentile for 2-consecutive days was associated with a 14.7 % (95 %CI, 10.3; 19.3) increase in daily mortality. Alternative heatwave definitions with higher percentiles and longer duration resulted in stronger relative risks. Furthermore, we observed stronger associations between heatwaves and mortality with higher heatwave intensity. We estimated that around 1116 deaths annually (95 %CI, 861; 1361) were attributed to heatwaves. Shorter and less intense definitions of heatwaves resulted in a higher estimated burden of heatwave-related deaths. CONCLUSIONS: We found strong evidence of heatwave impacts on daily mortality. Longer and more intense heatwaves were linked to an increased mortality risk, however, resulted in a lower burden of heatwave-related deaths. Both definitions and the burden associated with each heatwave definition should be incorporated into planning and decision-making processes for policymakers.

Long-term exposure to ambient PM2.5, particulate constituents and hospital admissions from non-respiratory infection.

The association between PM2.5 and non-respiratory infections is unclear. Using data from Medicare beneficiaries and high-resolution datasets of PM2.5 and its constituents across 39,296 ZIP codes in the U.S between 2000 and 2016, we investigated the associations between annual PM2.5, PM2.5 constituents, source-specific PM2.5, and hospital admissions from non-respiratory infections. Each standard deviation (3.7-µg m-3) increase in PM2.5 was associated with a 10.8% (95%CI 10.8-11.2%) increase in rate of hospital admissions from non-respiratory infections. Sulfates (30.8%), Nickel (22.5%) and Copper (15.3%) contributed the largest weights in the observed associations. Each standard deviation increase in PM2.5 components sourced from oil combustion, coal burning, traffic, dirt, and regionally transported nitrates was associated with 14.5% (95%CI 7.6-21.8%), 18.2% (95%CI 7.2-30.2%), 20.6% (95%CI 5.6-37.9%), 8.9% (95%CI 0.3-18.4%) and 7.8% (95%CI 0.6-15.5%) increases in hospital admissions from non-respiratory infections. Our results suggested that non-respiratory infections are an under-appreciated health effect of PM2.5.

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.

Short-Term Increases in NO2 and O3 Concentrations during Pregnancy and Stillbirth Risk in the U.S.: A Time-Stratified Case-Crossover Study.

Associations between gaseous pollutant exposure and stillbirth have focused on exposures averaged over trimesters or gestation. We investigated the association between short-term increases in nitrogen dioxide (NO2) and ozone (O3) concentrations and stillbirth risk among a national sample of 116 788 Medicaid enrollees from 2000 to 2014. A time-stratified case-crossover design was used to estimate distributed (lag 0-lag 6) and cumulative lag effects, which were adjusted for PM2.5 concentration and temperature. Effect modification by race/ethnicity and proximity to hydraulic fracturing (fracking) wells was assessed. Short-term increases in the NO2 and O3 concentrations were not associated with stillbirth in the overall sample. Among American Indian individuals (n = 1694), a 10 ppb increase in NO2 concentrations was associated with increased stillbirth odds at lag 0 (5.66%, 95%CI: [0.57%, 11.01%], p = 0.03) and lag 1 (4.08%, 95%CI: [0.22%, 8.09%], p = 0.04) but not lag 0-6 (7.12%, 95%CI: [-9.83%, 27.27%], p = 0.43). Among participants living in zip codes within 15 km of active fracking wells (n = 9486), a 10 ppb increase in NO2 concentration was associated with increased stillbirth odds in single-day lags (2.42%, 95%CI: [0.37%, 4.52%], p = 0.02 for lag 0 and 1.83%, 95%CI: [0.25%, 3.43%], p = 0.03 for lag 1) but not the cumulative lag (lag 0-6) (4.62%, 95%CI: [-2.75%, 12.55%], p = 0.22). Odds ratios were close to the null in zip codes distant from fracking wells. Future studies should investigate the role of air pollutants emitted from fracking and potential racial disparities in the relationship between short-term increases in NO2 concentrations and stillbirth.

Long-Term Exposure to Air Pollution Below Regulatory Standards and Cardiovascular Diseases Among US Medicare Beneficiaries: A Double Negative Control Approach.

Growing evidence suggests that long-term air pollution exposure is a risk factor for cardiovascular mortality and morbidity. However, few studies have investigated air pollution below current regulatory limits, and causal evidence is limited. We used a double negative control approach to examine the association between long-term exposure to air pollution at low concentrations and three major cardiovascular events among Medicare beneficiaries aged ≥ 65 years across the contiguous United States between 2000 and 2016. We derived ZIP code-level estimates of ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and warm-season ozone (O3) from high-resolution spatiotemporal models. The outcomes of interest were hospitalizations for stroke, heart failure (HF), and atrial fibrillation and flutter (AF). The analyses were restricted to areas with consistently low pollutant levels on an annual basis (PM2.5 <10 µg/m3, NO2 < 45 or 40 ppb, warm-season O3 < 45 or 40 ppb). For each 1 µg/m3 increase in PM2.5, the hospitalization rates increased by 2.25% (95% confidence interval (CI): 1.96%, 2.54%) for stroke and 3.14% (95% CI: 2.80%, 3.94%) for HF. Each ppb increase in NO2 increased hospitalization rates for stroke, HF, and AF by 0.28% (95% CI: 0.25%, 0.31%), 0.56% (95% CI: 0.52%, 0.60%), and 0.45% (95% CI: 0.41%, 0.49%), respectively. For each ppb increase in warm-season O3, there was a 0.32% (95% CI: 0.21%, 0.44%) increase in hospitalization rate for stroke. The associations for NO2 and warm-season O3 became stronger under a more restrictive upper threshold. Using an approach robust to omitted confounders, we concluded that long-term exposure to low-level PM2.5, NO2, and warm-season O3 was associated with increased risks of cardiovascular diseases in the US elderly. Stricter national air quality standards should be considered.

Long-term association of air pollution and incidence of lung cancer among older Americans: A national study in the Medicare cohort.

BACKGROUND: Despite strong evidence of the association of fine particulate matter (PM2.5) exposure with an increased risk of lung cancer mortality, few studies had investigated associations of multiple pollutants simultaneously, or with incidence, or using causal methods. Disparities were also understudied. OBJECTIVES: We investigated long-term effects of PM2.5, nitrogen dioxide (NO2), warm-season ozone, and particle radioactivity (PR) exposures on lung cancer incidence in a nationwide cohort. METHODS: We conducted a cohort study with Medicare beneficiaries (aged ≥ 65 years) continuously enrolled in the fee-for-service program in the contiguous US from 2001 to 2016. Air pollution exposure was averaged across three years and assigned based on ZIP code of residence. We fitted Cox proportional hazards models to estimate the hazard ratio (HR) for lung cancer incidence, adjusted for individual- and neighborhood-level confounders. As a sensitivity analysis, we evaluated the causal relationships using inverse probability weights. We further assessed effect modifications by individual- and neighborhood-level covariates. RESULTS: We identified 166,860 lung cancer cases of 12,429,951 studied beneficiaries. In the multi-pollutant model, PM2.5 and NO2 exposures were statistically significantly associated with increased lung cancer incidence, while PR was marginally significantly associated. Specifically, the HR was 1.008 (95% confidence interval [CI]: 1.005, 1.011) per 1-µg/m3 increase in PM2.5, 1.013 (95% CI: 1.012, 1.013) per 1-ppb increase in NO2, and 1.005 (0.999, 1.012) per 1-mBq/m3 increase in PR. At low exposure levels, all pollutants were associated with increased lung cancer incidence. Men, older individuals, Blacks, and residents of low-income neighborhoods experienced larger effects of PM2.5 and PR. DISCUSSION: Long-term PM2.5, NO2, and PR exposures were independently associated with increased lung cancer incidence among the national elderly population. Low-exposure analysis indicated that current national standards for PM2.5 and NO2 were not restrictive enough to protect public health, underscoring the need for more stringent air quality regulations.

Long-Term Exposure to Ambient PM2.5 and Hospitalizations for Myocardial Infarction Among US Residents: A Difference-in-Differences Analysis.

Background Air pollution has been recognized as an untraditional risk factor for myocardial infarction (MI). However, the MI risk attributable to long-term exposure to fine particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5) is unclear, especially in younger populations, and few studies have represented the general population or had power to examine comorbidities. Methods and Results We applied the difference-in-differences approach to estimate the relationship between annual PM2.5 exposure and hospitalizations for MI among US residents and further identified potential susceptible subpopulations. All hospital admissions for MI in 10 US states over the period 2002 to 2016 were obtained from the Healthcare Cost and Utilization Project State Inpatient Database. In total, 1 914 684 MI hospital admissions from 8106 zip codes were included in this study. We observed a 1.35% (95% CI, 1.11-1.59) increase in MI hospitalization rate for 1-µg/m3 increase in annual PM2.5 exposure. The estimate was robust to adjustment for surface pressure, relative humidity, and copollutants. In the population exposed to ≤12 µg/m3, there was a larger increment of 2.17% (95% CI, 1.79-2.56) in hospitalization rate associated with 1-µg/m3 increase in PM2.5. Young people (0-34 years of age) and elderly people (≥75 years of age) were the 2 most susceptible age groups. Residents living in more densely populated or poorer areas and individuals with comorbidities were observed to be at a greater risk. Conclusions This study indicates long-term residential exposure to PM2.5 could increase risk of MI among the general US population, people with comorbidities, and poorer individuals. The association persists below current standards.

Additive effects of 10-year exposures to PM2.5 and NO2 and primary cancer incidence in American older adults.

Epidemiologic evidence on the relationships between air pollution and the risks of primary cancers other than lung cancer remained largely lacking. We aimed to examine associations of 10-year exposures to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) with risks of breast, prostate, colorectal, and endometrial cancers. Methods: For each cancer, we constructed a separate cohort among the national Medicare beneficiaries during 2000 to 2016. We simultaneously examined the additive associations of six exposures, namely, moving average exposures to PM2.5 and NO2 over the year of diagnosis and previous 2 years, previous 3 to 5 years, and previous 6 to 10 years, with the risk of first cancer diagnosis after 10 years of follow-up, during which there was no cancer diagnosis. Results: The cohorts included 2.2 to 6.5 million subjects for different cancers. Exposures to PM2.5 and NO2 were associated with increased risks of colorectal and prostate cancers but were not associated with endometrial cancer risk. NO2 was associated with a decreased risk of breast cancer, while the association for PM2.5 remained inconclusive. At exposure levels below the newly updated World Health Organization Air Quality Guideline, we observed substantially larger associations between most exposures and the risks of all cancers, which were translated to hundreds to thousands new cancer cases per year within the cohort per unit increase in each exposure. Conclusions: These findings suggested substantial cancer burden was associated with exposures to PM2.5 and NO2, emphasizing the urgent need for strategies to mitigate air pollution levels.

Long-term exposure to ambient fine particulate components and leukocyte epigenome-wide DNA Methylation in older men: the Normative Aging Study.

BACKGROUND: Epigenome-wide association studies of ambient fine particulate matter (PM2.5) have been reported. However, few have examined PM2.5 components (PMCs) and sources or included repeated measures. The lack of high-resolution exposure measurements is the key limitation. We hypothesized that significant changes in DNA methylation might vary by PMCs and the sources. METHODS: We predicted the annual average of 14 PMCs using novel high-resolution exposure models across the contiguous U.S., between 2000-2018. The resolution was 50 m × 50 m in the Greater Boston Area. We also identified PM2.5 sources using positive matrix factorization. We repeatedly collected blood samples and measured leukocyte DNAm with the Illumina HumanMethylation450K BeadChip in the Normative Aging Study. We then used median regression with subject-specific intercepts to estimate the associations between long-term (one-year) exposure to PMCs / PM2.5 sources and DNA methylation at individual cytosine-phosphate-guanine CpG sites. Significant probes were identified by the number of independent degrees of freedom approach, using the number of principal components explaining > 95% of the variation of the DNA methylation data. We also performed regional and pathway analyses to identify significant regions and pathways. RESULTS: We included 669 men with 1,178 visits between 2000-2013. The subjects had a mean age of 75 years. The identified probes, regions, and pathways varied by PMCs and their sources. For example, iron was associated with 6 probes and 6 regions, whereas nitrate was associated with 15 probes and 3 regions. The identified pathways from biomass burning, coal burning, and heavy fuel oil combustion sources were associated with cancer, inflammation, and cardiovascular diseases, whereas there were no pathways associated with all traffic. CONCLUSIONS: Our findings showed that the effects of PM2.5 on DNAm varied by its PMCs and sources.

Seasonal Temperature Variability and Mortality in the Medicare Population.

BACKGROUND: Seasonal temperature variability remains understudied and may be modified by climate change. Most temperature-mortality studies examine short-term exposures using time-series data. These studies are limited by regional adaptation, short-term mortality displacement, and an inability to observe longer-term relationships in temperature and mortality. Seasonal temperature and cohort analyses allow the long-term effects of regional climatic change on mortality to be analyzed. OBJECTIVES: We aimed to carry out one of the first investigations of seasonal temperature variability and mortality across the contiguous United States. We also investigated factors that modify this association. Using adapted quasi-experimental methods, we hoped to account for unobserved confounding and to investigate regional adaptation and acclimatization at the ZIP code level. METHODS: We examined the mean and standard deviation (SD) of daily temperature in the warm (April-September) and cold (October-March) season in the Medicare cohort from 2000 to 2016. This cohort comprised 622,427,230 y of person-time in all adults over the age of 65 y from 2000 to 2016. We used daily mean temperature obtained from gridMET to develop yearly seasonal temperature variables for each ZIP code. We used an adapted difference-in-difference approach model with a three-tiered clustering approach and meta-analysis to observe the relationship between temperature variability and mortality within ZIP codes. Effect modification was assessed with stratified analyses by race and population density. RESULTS: For every 1°C increase in the SD of warm and cold season temperature, the mortality rate increased by 1.54% [95% confidence interval (CI): 0.73%, 2.15%] and 0.69% (95% CI: 0.22%, 1.15%) respectively. We did not see significant effects for seasonal mean temperatures. Participants who were classified by Medicare into an "other" race group had smaller effects than those classified as White for Cold and Cold SD and areas with lower population density had larger effects for Warm SD. DISCUSSION: Warm and cold season temperature variability were significantly associated with increased mortality rates in U.S. individuals over the age of 65 y, even after controlling for seasonal temperature averages. Warm and cold season mean temperatures showed null effects on mortality. Cold SD had a larger effect size for those who were in the racial subgroup other, whereas Warm SD was more harmful for those living in lower population density areas. This study adds to the growing calls for urgent climate mitigation and environmental health adaptation and resiliency. https://doi.org/10.1289/EHP11588.

Effects of low-level air pollution exposures on hospital admission for myocardial infarction using multiple causal models.

Myocardial infarctions have been associated with PM2.5, and more recently with NO2 and O3, however counterfactual designs have been lacking and argument continues over the extent of confounding control. Here we introduce a doubly robust, counterfactual-based approach that deals with nonlinearity and interactions in associations between confounders and both outcome and exposure, as well as a double negative controls approach that capture omitted confounders. We used data from over 4 million admissions for myocardial infarction in the US Medicare population between 2000 and 2016 and linked them by ZIP code of residence to high resolution predictions of annual PM2.5, NO2, and O3. We computed the counts of admissions for each ZIP code-year. In the doubly robust approach, we divided each pollutant into deciles, and for each decile, we fitted a gradient boosting machine model to estimate the effects of covariates, including the co-pollutants, on the counts. We used these models to predict, for all ZIP code-years, the expected counts had everyone be exposed in that decile. We also estimated the probability of being in that decile given all covariates, again with a gradient boosting machine, and used inverse probability weights to compute the weighted average rate of MI admission in each decile. In the negative control approach, for each pollutant, we fitted a quasi-Poisson model to estimate the exposure effect, adjusting for covariates including the co-pollutants, and negative exposure and outcome controls to control for unmeasured confounding. Each 1-µg/m3 increase in annual PM2.5 increased the admission for MI by 1.37 cases per 10,000 person-years (95% CI: 1.20, 1.54) in the doubly robust approach, and by 0.69 cases (95% CI 0.60, 0.78) using the negative control approach. Elevated risks were seen even below annual PM2.5 level of 8 µg/m3. Results for NO2 and O3 were inconsistent.

Traffic-Related Air Pollution and Ultrasound Parameters of Fetal Growth in Eastern Massachusetts.

Previous studies have examined the association between prenatal nitrogen dioxide (NO2)-a traffic emissions tracer-and fetal growth based on ultrasound measures. Yet, most have used exposure assessment methods with low temporal resolution, which limits the identification of critical exposure windows given that pregnancy is relatively short. Here, we used NO2 data from an ensemble model linked to residential addresses at birth to fit distributed lag models that estimated the association between NO2 exposure (resolved weekly) and ultrasound biometric parameters in a Massachusetts-based cohort of 9,446 singleton births from 2011-2016. Ultrasound biometric parameters examined included biparietal diameter (BPD), head circumference, femur length, and abdominal circumference. All models adjusted for sociodemographic characteristics, time trends, and temperature. We found that higher NO2 was negatively associated with all ultrasound parameters. The critical window differed depending on the parameter and when it was assessed. For example, for BPD measured after week 31, the critical exposure window appeared to be weeks 15-25; 10-parts-per-billion higher NO2 sustained from conception to the time of measurement was associated with a lower mean z score of -0.11 (95% CI: -0.17, -0.05). Our findings indicate that reducing traffic emissions is one potential avenue to improving fetal and offspring health.

Association of Long-term Exposure to Air Pollution With Late-Life Depression in Older Adults in the US.

Importance: Emerging evidence has suggested harmful associations of air pollutants with neurodegenerative diseases among older adults. However, little is known about outcomes regarding late-life mental disorders, such as geriatric depression. Objective: To investigate if long-term exposure to air pollution is associated with increased risk of late-life depression diagnosis among older adults in the US. Design, Setting, and Participants: This population-based longitudinal cohort study consisted of US Medicare enrollees older than 64 years. Data were obtained from the US Centers for Medicare and Medicaid Services Chronic Conditions Warehouse. The participants were continuously enrolled in the Fee-for-Service program and both Medicare Part A and Part B. After the 5-year washout period at entry, a total of 8 907 422 unique individuals were covered over the study period of 2005 to 2016, who contributed to 1 526 690 late-onset depression diagnoses. Data analyses were performed between March 2022 and November 2022. Exposures: The exposures consisted of residential long-term exposure to fine particulate matter (PM2.5), measured in micrograms per cubic meter; nitrogen dioxide (NO2), measured in parts per billion; and ozone (O3), measured in parts per billion. Main Outcomes and Measures: Late-life depression diagnoses were identified via information from all available Medicare claims (ie, hospital inpatient, skilled nursing facility, home health agency, hospital outpatient, and physician visits). Date of the first occurrence was obtained. Hazard ratios and percentage change in risk were estimated via stratified Cox proportional hazards models accounting for climate coexposures, neighborhood greenness, socioeconomic conditions, health care access, and urbanicity level. Results: A total of 8 907 422 Medicare enrollees were included in this study with 56.8% being female individuals and 90.2% being White individuals. The mean (SD) age at entry (after washout period) was 73.7 (4.8) years. Each 5-unit increase in long-term mean exposure to PM2.5, NO2, and O3 was associated with an adjusted percentage increase in depression risk of 0.91% (95% CI, 0.02%-1.81%), 0.61% (95% CI, 0.31%- 0.92%), and 2.13% (95% CI, 1.63%-2.64%), respectively, based on a tripollutant model. Effect size heterogeneity was found among subpopulations by comorbidity condition and neighborhood contextual backgrounds. Conclusions and Relevance: In this cohort study among US Medicare enrollees, harmful associations were observed between long-term exposure to air pollution and increased risk of late-life depression diagnosis.

The role of short-term air pollution and temperature on arterial stiffness in a longitudinal closed cohort of elderly individuals.

BACKGROUND/AIMS: Our study adds to the sparse literature that examines whether arterial stiffness, related to cardiovascular risk, increases with exposure to air pollution. We assessed the associations between spatiotemporally resolved air pollutants and vascular and hemodynamic parameters in an elderly population-based in Eastern Massachusetts. METHODS: Among 397 men living in Eastern Massachusetts between 2007 and 2013, we utilized time-varying linear mixed-effects regressions to examine associations between central augmentation index (%) and central pulse pressure (mmHg) and short-term (0-7 days) exposure to air pollution concentrations (fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3)), and temperature adjusted for known cardiovascular risk factors. Central augmentation index (AIx) and pulse pressure (AP) were measured at each visit using radial artery applanation tonometry for pulse wave analysis. Each air pollutant and temperature were geocoded to the participant's residential address using validated ensemble and hybrid exposure models and gridMET predictions. RESULTS: We found consistent results that higher short-term PM2.5 concentrations (0-7 day moving averages) were associated with significantly higher measures of arterial stiffness. Each 4.52 µg/m3 interquartile range (IQR) increase in daily PM2.5 for a 3-day moving average was associated with a 0.63% (95% confidence interval (CI): 0.11, 1.15) increase in AIx and a 1.65 mmHg (95% CI: 0.42, 2.88) increase in pulse pressure. Furthermore, each 3.83 µg/m3 IQR increase in daily PM2.5 for a 7-day moving average was associated with a 0.57% (95% CI: -0.01, 1.14) increase in AIx and a 1.91 mmHg (95% CI: 0.54, 3.28) increase in pulse pressure. Smaller increases in AIx and AP were observed for the other short-term moving averages of PM2.5 exposure apart from days zero and five for AIx. We found no clear association between O3, NO2, temperature, and the outcomes. CONCLUSIONS: Short-term PM2.5 exposure was associated with markers of arterial stiffness and central hemodynamics.