Associations of fine particulate matter with incident cardiovascular disease; comparing models using ZIP code-level and individual-level fine particulate matter and confounders.

BACKGROUND: PM2.5 has been positively associated with cardiovascular disease (CVD) incidence. Most evidence has come from cohorts and administrative databases. Cohorts typically have extensive information on potential confounders and residential-level exposures. Administrative databases are usually more representative but typically lack information on potential confounders and often only have exposures at coarser geographies (e.g., ZIP code). The weaknesses in both types of studies have been criticized for potentially jeopardizing the validity of their findings for regulatory purposes. METHODS: We followed 101,870 participants from the US-based Nurses' Health Study (2000-2016) and linked residential-level PM2.5 and individual-level confounders, and ZIP code-level PM2.5 and confounders. We used time-varying Cox proportional hazards models to examine associations with CVD incidence. We specified basic models (adjusted for individual-level age, race and calendar year), individual-level confounder models, and ZIP code-level confounder models. RESULTS: Residential- and ZIP code-level PM2.5 were strongly correlated (Pearson r = 0.88). For residential-level PM2.5, the hazard ratio (HR, 95 % confidence interval) per 5 µg/m3 increase was 1.06 (1.01, 1.11) in the basic and 1.04 (0.99, 1.10) in the individual-level confounder model. For ZIP code-level PM2.5, the HR per 5 µg/m3 was 1.04 (0.99, 1.08) in the basic and 1.02 (0.97, 1.08) in the ZIP code-level confounder model. CONCLUSION: We observed suggestive positive, but not statistically significant, associations between long-term PM2.5 and CVD incidence, regardless of the exposure or confounding model. Although differences were small, associations from models with individual-level confounders and residential-level PM2.5 were slightly stronger than associations from models with ZIP code-level confounders and PM2.5.

Early-Life Exposure to Air Pollution and Childhood Asthma Cumulative Incidence in the ECHO CREW Consortium.

Importance: Exposure to outdoor air pollution contributes to childhood asthma development, but many studies lack the geographic, racial and ethnic, and socioeconomic diversity to evaluate susceptibility by individual-level and community-level contextual factors. Objective: To examine early life exposure to fine particulate matter (PM2.5) and nitrogen oxide (NO2) air pollution and asthma risk by early and middle childhood, and whether individual and community-level characteristics modify associations between air pollution exposure and asthma. Design, Setting, and Participants: This cohort study included children enrolled in cohorts participating in the Children's Respiratory and Environmental Workgroup consortium. The birth cohorts were located throughout the US, recruited between 1987 and 2007, and followed up through age 11 years. The survival analysis was adjusted for mother's education, parental asthma, smoking during pregnancy, child's race and ethnicity, sex, neighborhood characteristics, and cohort. Statistical analysis was performed from February 2022 to December 2023. Exposure: Early-life exposures to PM2.5 and NO2 according to participants' birth address. Main Outcomes and Measures: Caregiver report of physician-diagnosed asthma through early (age 4 years) and middle (age 11 years) childhood. Results: Among 5279 children included, 1659 (31.4%) were Black, 835 (15.8%) were Hispanic, 2555 (48.4%) where White, and 229 (4.3%) were other race or ethnicity; 2721 (51.5%) were male and 2596 (49.2%) were female; 1305 children (24.7%) had asthma by 11 years of age and 954 (18.1%) had asthma by 4 years of age. Mean values of pollutants over the first 3 years of life were associated with asthma incidence. A 1 IQR increase in NO2 (6.1 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.25 [95% CI, 1.03-1.52]) and children younger than 11 years (HR, 1.22 [95% CI, 1.04-1.44]). A 1 IQR increase in PM2.5 (3.4 µg/m3) was associated with increased asthma incidence among children younger than 5 years (HR, 1.31 [95% CI, 1.04-1.66]) and children younger than 11 years (OR, 1.23 [95% CI, 1.01-1.50]). Associations of PM2.5 or NO2 with asthma were increased when mothers had less than a high school diploma, among Black children, in communities with fewer child opportunities, and in census tracts with higher percentage Black population and population density; for example, there was a significantly higher association between PM2.5 and asthma incidence by younger than 5 years of age in Black children (HR, 1.60 [95% CI, 1.15-2.22]) compared with White children (HR, 1.17 [95% CI, 0.90-1.52]). Conclusions and Relevance: In this cohort study, early life air pollution was associated with increased asthma incidence by early and middle childhood, with higher risk among minoritized families living in urban communities characterized by fewer opportunities and resources and multiple environmental coexposures. Reducing asthma risk in the US requires air pollution regulation and reduction combined with greater environmental, educational, and health equity at the community level.

Ozone-related acute excess mortality projected to increase in the absence of climate and air quality controls consistent with the Paris Agreement.

Short-term exposure to ground-level ozone in cities is associated with increased mortality and is expected to worsen with climate and emission changes. However, no study has yet comprehensively assessed future ozone-related acute mortality across diverse geographic areas, various climate scenarios, and using CMIP6 multi-model ensembles, limiting our knowledge on future changes in global ozone-related acute mortality and our ability to design targeted health policies. Here, we combine CMIP6 simulations and epidemiological data from 406 cities in 20 countries or regions. We find that ozone-related deaths in 406 cities will increase by 45 to 6,200 deaths/year between 2010 and 2014 and between 2050 and 2054, with attributable fractions increasing in all climate scenarios (from 0.17% to 0.22% total deaths), except the single scenario consistent with the Paris Climate Agreement (declines from 0.17% to 0.15% total deaths). These findings stress the need for more stringent air quality regulations, as current standards in many countries are inadequate.

Applying a multistate survival model to explore the role of fine particles in promoting frailty in the Medicare cohort.

Fine particle pollution is a well-established risk to human health. Observational epidemiology generally treats events as though they are independent of one another and so do not examine the role air pollution may play in promoting the progression of disease. Multistate survival models account for the complex pathway of disease to death. We employ a multistate survival model to characterize the role of chronic exposure to PM2.5 in affecting the rate at which Medicare beneficiaries transition to first hospitalization for cardiovascular disease and then subsequently death. We use an open cohort of Medicare beneficiaries and PM2.5 concentrations estimated with photochemical model predictions, satellite-based observations, land-use data, and meteorological variables. The multistate model included three transitions: (1) entry to cardiovascular hospital admission; (2) entry to death; and (3) cardiovascular hospital admission to death. The transition intensity was modeled using a Cox proportional hazards model. For a 1 µg/m3 increase in annual mean PM2.5, we estimate a nationally pooled hazard ratio of 1.022 (95% confidence interval [CI] = 1.018, 1.025) for the transition from entry to first cardiovascular hospital admission; 1.054 (95% CI = 1.039, 1.068) for the transition from entry to death; 1.036 (95% CI = 1.027, 1.044) for the transition from first cardiovascular hospital admission to death. The hazard ratios exhibited some heterogeneity within each of nine climatological regions and for each of the three transitions. We find evidence for the role of PM in both promoting chronic illness and increasing the subsequent risk of death.

Interactive effects of ambient fine particulate matter and ozone on daily mortality in 372 cities: two stage time series analysis.

OBJECTIVE: To investigate potential interactive effects of fine particulate matter (PM2.5) and ozone (O3) on daily mortality at global level. DESIGN: Two stage time series analysis. SETTING: 372 cities across 19 countries and regions. POPULATION: Daily counts of deaths from all causes, cardiovascular disease, and respiratory disease. MAIN OUTCOME MEASURE: Daily mortality data during 1994-2020. Stratified analyses by co-pollutant exposures and synergy index (>1 denotes the combined effect of pollutants is greater than individual effects) were applied to explore the interaction between PM2.5 and O3 in association with mortality. RESULTS: During the study period across the 372 cities, 19.3 million deaths were attributable to all causes, 5.3 million to cardiovascular disease, and 1.9 million to respiratory disease. The risk of total mortality for a 10 µg/m3 increment in PM2.5 (lag 0-1 days) ranged from 0.47% (95% confidence interval 0.26% to 0.67%) to 1.25% (1.02% to 1.48%) from the lowest to highest fourths of O3 concentration; and for a 10 µg/m3 increase in O3 ranged from 0.04% (-0.09% to 0.16%) to 0.29% (0.18% to 0.39%) from the lowest to highest fourths of PM2.5 concentration, with significant differences between strata (P for interaction <0.001). A significant synergistic interaction was also identified between PM2.5 and O3 for total mortality, with a synergy index of 1.93 (95% confidence interval 1.47 to 3.34). Subgroup analyses showed that interactions between PM2.5 and O3 on all three mortality endpoints were more prominent in high latitude regions and during cold seasons. CONCLUSION: The findings of this study suggest a synergistic effect of PM2.5 and O3 on total, cardiovascular, and respiratory mortality, indicating the benefit of coordinated control strategies for both pollutants.

Long-term exposure to summer specific humidity and cardiovascular disease hospitalizations in the US Medicare population.

INTRODUCTION: Most climate-health studies focus on temperature; however, less is known about health effects of exposure to atmospheric moisture. Humid air limits sweat evaporation from the body and can in turn exert strain on the cardiovascular system. We evaluated associations of long-term exposure to summer specific humidity with cardiovascular disease (CVD), coronary heart disease (CHD) and cerebrovascular disease (CBV) hospitalization. METHODS: We built an open cohort consisting of âˆ¼63 million fee-for-service Medicare beneficiaries, aged ≥65, living in the contiguous US (2000-2016). We assessed zip code level summer average specific humidity and specific humidity variability, based on daily estimates from the Gridded Surface Meteorological dataset (∼4km spatial resolution). To estimate associations of summer specific humidity with first CVD, CHD, and CBV hospitalization, we used Cox-equivalent Poisson models adjusted for individual and area-level socioeconomic status indicators, temperature, and winter specific humidity. RESULTS: Higher summer average specific humidity was associated with an increased risk of CVD, CHD, and CBV hospitalization. We found hazard ratios (HRs) of 1.07 (95%CI: 1.07, 1.08) for CVD hospitalization, 1.08 (95%CI: 1.08, 1.09) for CHD hospitalization, and 1.07 (95%CI: 1.07, 1.08) for CBV hospitalization per IQR increase (4.0 g of water vapor/kg of dry air) in summer average specific humidity. Associations of summer average specific humidity were strongest for beneficiaries eligible for Medicaid and for beneficiaries with an unknown or other race. Higher summer specific humidity variability was also associated with increased risk of CVD, CHD, and CBV hospitalization. Associations were not affected by adjustment for temperature and regions of the US, as well as exclusion of potentially prevalent cases. CONCLUSION: Long-term exposure to higher summer average specific humidity and specific humidity variability were positively associated with CVD hospitalization. As global warming could increase humidity levels, our findings are important to assess potential health impacts of climate change.

Global short-term mortality risk and burden associated with tropical cyclones from 1980 to 2019: a multi-country time-series study.

BACKGROUND: The global spatiotemporal pattern of mortality risk and burden attributable to tropical cyclones is unclear. We aimed to evaluate the global short-term mortality risk and burden associated with tropical cyclones from 1980 to 2019. METHODS: The wind speed associated with cyclones from 1980 to 2019 was estimated globally through a parametric wind field model at a grid resolution of 0·5°â€ˆ× 0·5°. A total of 341 locations with daily mortality and temperature data from 14 countries that experienced at least one tropical cyclone day (a day with maximum sustained wind speed associated with cyclones ≥17·5 m/s) during the study period were included. A conditional quasi-Poisson regression with distributed lag non-linear model was applied to assess the tropical cyclone-mortality association. A meta-regression model was fitted to evaluate potential contributing factors and estimate grid cell-specific tropical cyclone effects. FINDINGS: Tropical cyclone exposure was associated with an overall 6% (95% CI 4-8) increase in mortality in the first 2 weeks following exposure. Globally, an estimate of 97 430 excess deaths (95% empirical CI [eCI] 71 651-126 438) per decade were observed over the 2 weeks following exposure to tropical cyclones, accounting for 20·7 (95% eCI 15·2-26·9) excess deaths per 100 000 residents (excess death rate) and 3·3 (95% eCI 2·4-4·3) excess deaths per 1000 deaths (excess death ratio) over 1980-2019. The mortality burden exhibited substantial temporal and spatial variation. East Asia and south Asia had the highest number of excess deaths during 1980-2019: 28 744 (95% eCI 16 863-42 188) and 27 267 (21 157-34 058) excess deaths per decade, respectively. In contrast, the regions with the highest excess death ratios and rates were southeast Asia and Latin America and the Caribbean. From 1980-99 to 2000-19, marked increases in tropical cyclone-related excess death numbers were observed globally, especially for Latin America and the Caribbean and south Asia. Grid cell-level and country-level results revealed further heterogeneous spatiotemporal patterns such as the high and increasing tropical cyclone-related mortality burden in Caribbean countries or regions. INTERPRETATION: Globally, short-term exposure to tropical cyclones was associated with a significant mortality burden, with highly heterogeneous spatiotemporal patterns. In-depth exploration of tropical cyclone epidemiology for those countries and regions estimated to have the highest and increasing tropical cyclone-related mortality burdens is urgently needed to help inform the development of targeted actions against the increasing adverse health impacts of tropical cyclones under a changing climate. FUNDING: Australian Research Council and Australian National Health and Medical Research Council.

The risk of being bitten by a dog is higher on hot, sunny, and smoggy days.

Humans commit more violent crimes when temperature and air pollution is higher. Here, we investigate if also the day-to-day rates of dogs biting humans is influenced by environmental factors. 69,525 reports of dogs biting humans, sourced from public records on animal control requests and from ER records, were analyzed. The impact of temperature and air pollutants were evaluated with a zero-inflated Poisson generalized additive model, while controlling for regional and calendar effects. Exposure-response curves were used to assess the association between outcome and major exposure variables. We find that the rates of dogs biting humans increases with increasing temperature and ozone, but not PM2.5 exposure. We also observed that higher UV irradiation levels were related to higher rats of dog bites. We conclude that dogs, or the interactions between humans and dogs, are more hostile on hot, sunny, and smoggy days, indicating that the societal burden of extreme heat and air pollution also includes the costs of animal aggression.

Heat-related cardiorespiratory mortality: Effect modification by air pollution across 482 cities from 24 countries.

BACKGROUND: Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations. OBJECTIVES: We investigated the effects of heat on cardiovascular and respiratory mortality and its modification by air pollution during summer months (six consecutive hottest months) in 482 locations across 24 countries. METHODS: Location-specific daily death counts and exposure data (e.g., particulate matter with diameters ≤ 2.5 µm [PM2.5]) were obtained from 2000 to 2018. We used location-specific confounder-adjusted Quasi-Poisson regression with a tensor product between air temperature and the air pollutant. We extracted heat effects at low, medium, and high levels of pollutants, defined as the 5th, 50th, and 95th percentile of the location-specific pollutant concentrations. Country-specific and overall estimates were derived using a random-effects multilevel meta-analytical model. RESULTS: Heat was associated with increased cardiorespiratory mortality. Moreover, the heat effects were modified by elevated levels of all air pollutants in most locations, with stronger effects for respiratory than cardiovascular mortality. For example, the percent increase in respiratory mortality per increase in the 2-day average summer temperature from the 75th to the 99th percentile was 7.7% (95% Confidence Interval [CI] 7.6-7.7), 11.3% (95%CI 11.2-11.3), and 14.3% (95% CI 14.1-14.5) at low, medium, and high levels of PM2.5, respectively. Similarly, cardiovascular mortality increased by 1.6 (95%CI 1.5-1.6), 5.1 (95%CI 5.1-5.2), and 8.7 (95%CI 8.7-8.8) at low, medium, and high levels of O3, respectively. DISCUSSION: We observed considerable modification of the heat effects on cardiovascular and respiratory mortality by elevated levels of air pollutants. Therefore, mitigation measures following the new WHO Air Quality Guidelines are crucial to enhance better health and promote sustainable development.

Personal air pollution exposure and metals in the nasal epithelial lining fluid of COPD patients.

Sampling of the nasal epithelial lining fluid is a potential method to assess exposure to air pollution within the respiratory tract among high risk populations. We investigated associations of short- and long-term particulate matter exposure (PM) and pollution-related metals in the nasal fluid of people with chronic obstructive pulmonary disease (COPD). This study included 20 participants with moderate-to-severe COPD from a larger study who measured long-term personal exposure to PM2.5 using portable air monitors and short-term PM2.5 and black carbon (BC) using in-home samplers for the seven days preceding nasal fluid collection. Nasal fluid was sampled from both nares by nasosorption, and inductively coupled plasma mass spectrometry was used to determine the concentration of metals with major airborne sources. Correlations of selected elements (Fe, Ba, Ni, Pb, V, Zn, Cu) were determined within the nasal fluid. Associations between personal long-term PM2.5 and seven day home PM2.5 and BC exposure and nasal fluid metal concentrations were determined by linear regression. Within nasal fluid samples, concentrations of vanadium and nickel (r = 0.8) and lead and zinc (r = 0.7) were correlated. Seven day and long-term PM2.5 exposure were both associated with higher levels of copper, lead, and vanadium in the nasal fluid. BC exposure was associated with higher levels of nickel in the nasal fluid. Levels of certain metals in the nasal fluid may serve as biomarkers of air pollution exposure in the upper respiratory tract.

Incidence rates of childhood asthma with recurrent exacerbations in the US Environmental influences on Child Health Outcomes (ECHO) program.

BACKGROUND: Descriptive epidemiological data on incidence rates (IRs) of asthma with recurrent exacerbations (ARE) are sparse. OBJECTIVES: This study hypothesized that IRs for ARE would vary by time, geography, age, and race and ethnicity, irrespective of parental asthma history. METHODS: The investigators leveraged data from 17,246 children born after 1990 enrolled in 59 US with 1 Puerto Rican cohort in the Environmental Influences on Child Health Outcomes (ECHO) consortium to estimate IRs for ARE. RESULTS: The overall crude IR for ARE was 6.07 per 1000 person-years (95% CI: 5.63-6.51) and was highest for children aged 2-4 years, for Hispanic Black and non-Hispanic Black children, and for those with a parental history of asthma. ARE IRs were higher for 2- to 4-year-olds in each race and ethnicity category and for both sexes. Multivariable analysis confirmed higher adjusted ARE IRs (aIRRs) for children born 2000-2009 compared with those born 1990-1999 and 2010-2017, 2-4 versus 10-19 years old (aIRR = 15.36; 95% CI: 12.09-19.52), and for males versus females (aIRR = 1.34; 95% CI 1.16-1.55). Black children (non-Hispanic and Hispanic) had higher rates than non-Hispanic White children (aIRR = 2.51; 95% CI 2.10-2.99; and aIRR = 2.04; 95% CI: 1.22-3.39, respectively). Children born in the Midwest, Northeast and South had higher rates than those born in the West (P < .01 for each comparison). Children with a parental history of asthma had rates nearly 3 times higher than those without such history (aIRR = 2.90; 95% CI: 2.43-3.46). CONCLUSIONS: Factors associated with time, geography, age, race and ethnicity, sex, and parental history appear to influence the inception of ARE among children and adolescents.

Heat-related mortality in U.S. state and private prisons: A case-crossover analysis.

Rising temperatures and heatwaves increase mortality. Many of the subpopulations most vulnerable to heat-related mortality are in prisons, facilities that may exacerbate temperature exposures. Yet, there is scare literature on the impacts of heat among incarcerated populations. We analyzed data on mortality in U.S. state and private prisons from 2001-2019 linked to daily maximum temperature data for the months of June, July, and August. Using a case-crossover approach and distributed lag models, we estimated the association of increasing temperatures with total mortality, heart disease-related mortality, and suicides. We also examined the association with extreme heat and heatwaves (days above the 90th percentile for the prison location) and assessed effect modification by personal, facility, and regional characteristics. There were 12,836 deaths during summer months. The majority were male (96%) and housed in a state-operated prison (97%). A 10°F increase was associated with a 5.2% (95% CI: 1.5%, 9.0%) increase in total mortality and a 6.7% (95% CI: -0.6%, 14.0%) increase in heart disease mortality. The association between temperature and suicides was delayed, peaking around lag 3 (exposure at three days prior death). Two- and three-day heatwaves were associated with increased total mortality of 5.5% (95% CI: 0.3%, 10.9%) and 7.4% (95% CI: 1.6%, 13.5%), respectively. The cumulative effect (lags 1-3) of an extreme heat day was associated with a 22.8% (95% CI: 3.3%, 46.0%) increase in suicides. We found the greatest increase in mortality among people ≥ 65 years old, incarcerated less than one year, held in the Northeast region, and in urban or rural counties. These findings suggest that warm temperatures are associated with increased mortality in prisons, yet this vulnerable population's risk has largely been overlooked.

The association of COVID-19 incidence with temperature, humidity, and UV radiation - A global multi-city analysis.

BACKGROUND AND AIM: The associations between COVID-19 transmission and meteorological factors are scientifically debated. Several studies have been conducted worldwide, with inconsistent findings. However, often these studies had methodological issues, e.g., did not exclude important confounding factors, or had limited geographic or temporal resolution. Our aim was to quantify associations between temporal variations in COVID-19 incidence and meteorological variables globally. METHODS: We analysed data from 455 cities across 20 countries from 3 February to 31 October 2020. We used a time-series analysis that assumes a quasi-Poisson distribution of the cases and incorporates distributed lag non-linear modelling for the exposure associations at the city-level while considering effects of autocorrelation, long-term trends, and day of the week. The confounding by governmental measures was accounted for by incorporating the Oxford Governmental Stringency Index. The effects of daily mean air temperature, relative and absolute humidity, and UV radiation were estimated by applying a meta-regression of local estimates with multi-level random effects for location, country, and climatic zone. RESULTS: We found that air temperature and absolute humidity influenced the spread of COVID-19 over a lag period of 15 days. Pooling the estimates globally showed that overall low temperatures (7.5 °C compared to 17.0 °C) and low absolute humidity (6.0 g/m3 compared to 11.0 g/m3) were associated with higher COVID-19 incidence (RR temp =1.33 with 95%CI: 1.08; 1.64 and RR AH =1.33 with 95%CI: 1.12; 1.57). RH revealed no significant trend and for UV some evidence of a positive association was found. These results were robust to sensitivity analysis. However, the study results also emphasise the heterogeneity of these associations in different countries. CONCLUSION: Globally, our results suggest that comparatively low temperatures and low absolute humidity were associated with increased risks of COVID-19 incidence. However, this study underlines regional heterogeneity of weather-related effects on COVID-19 transmission.

Critical windows of susceptibility for the effects of prenatal exposure to heat and heat variability on gestational growth.

BACKGROUND: Studies have shown that prenatal heat exposure may impact fetal growth, but few studies have examined the critical windows of susceptibility. As extreme heat events and within season temperature variability is expected to increase in frequency, it is important to understand how this may impact gestational growth. OBJECTIVES: We investigated associations between various measures of weekly prenatal heat exposure (mean and standard deviation (SD) of temperature and heat index (HI), derived using temperature in °C and dew point) and term birthweight or odds of being born small for gestational age (SGA) to identify critical windows of susceptibility. METHODS: We analyzed data from mother-child dyads (n = 4442) in the Boston-based Children's HealthWatch cohort. Birthweights were collected from survey data and electronic health records. Daily temperature and HI values were obtained from 800 m gridded spatial climate datasets aggregated by the PRISM Climate Group. Distributed lag-nonlinear models were used to assess the effect of the four weekly heat metrics on measures of gestational growth (birthweight, SGA, and birthweight z-scores). Analyses were stratified by child sex and maternal homelessness status during pregnancy. RESULTS: HI variability was significantly associated with decreased term birthweight during gestational weeks 10-29 and with SGA for weeks 9-26. Cumulative effects for these time periods were -287.4 g (95% CI: -474.1 g, -100.8 g for birthweight and 4.7 (95% CI: 1.6, 14.1) for SGA. Temperature variability was also significantly associated with decreased birthweight between weeks 15 and 26. The effects for mean heat measures on term birthweight and SGA were not significant for any gestational week. Stratification by sex revealed a significant effect on term birthweight in females between weeks 23-28 and in males between weeks 9-26. Strongest effects of HI variability on term birthweight were found in children of mothers who experienced homelessness during pregnancy. Weekly HI variability was the heat metric most strongly associated with measures of gestational growth. The effects observed were largest in males and those who experienced homelessness during pregnancy. DISCUSSION: Given the impact of heat variability on birthweight and risk of SGA, it is important for future heat warnings to incorporate measure of heat index and temperature variability.

Time-lagged relationships between a decade of air pollution exposure and first hospitalization with Alzheimer's disease and related dementias.

Alzheimer's disease and related dementias (ADRD) poses substantial health challenges among an aging population. One of the primary challenges in studying ADRD is that biological processes underlying these ailments begin decades prior to diagnosis. Previous studies indicate a relationship between ADRD and air pollution exposure to both fine particulate matter (PM2.5) and nitrogen dioxide (NO2) but are limited in their interpretation because they consider exposure measurements at a single time point. Our retrospective cohort study considered 27 + million Medicare enrollees in the United States followed up to 17 years and matched with highly accurate annual air pollution exposure measurements for PM2.5, NO2, and summer ozone. We applied distributed lag models and estimated the lagged associations between air pollution and odds of first hospitalization with ADRD. We found significantly increased odds due to overall PM2.5 and NO2 exposure and time-lagged exposure 10 and 8 years prior to admission, respectively. Furthermore, we found the connection between air pollution exposure and increased odds of first hospitalization with ADRD exists at air pollution levels below current National Ambient Air Quality Standards set by the US Environmental Protection Agency, with the steepest increase in odds occurring at low concentrations of PM2.5. Our findings are the first to show that air pollution exposures from as many as 10 years prior to the admission are related to increased odds of hospitalizations with ADRD. As there are no clear treatments available for ADRD, identifying modifiable risk factors such as air pollution exposure may make significant contributions towards prevention or delayed disease progression.

Associations Between Extreme Temperatures and Cardiovascular Cause-Specific Mortality: Results From 27 Countries.

BACKGROUND: Cardiovascular disease is the leading cause of death worldwide. Existing studies on the association between temperatures and cardiovascular deaths have been limited in geographic zones and have generally considered associations with total cardiovascular deaths rather than cause-specific cardiovascular deaths. METHODS: We used unified data collection protocols within the Multi-Country Multi-City Collaborative Network to assemble a database of daily counts of specific cardiovascular causes of death from 567 cities in 27 countries across 5 continents in overlapping periods ranging from 1979 to 2019. City-specific daily ambient temperatures were obtained from weather stations and climate reanalysis models. To investigate cardiovascular mortality associations with extreme hot and cold temperatures, we fit case-crossover models in each city and then used a mixed-effects meta-analytic framework to pool individual city estimates. Extreme temperature percentiles were compared with the minimum mortality temperature in each location. Excess deaths were calculated for a range of extreme temperature days. RESULTS: The analyses included deaths from any cardiovascular cause (32 154 935), ischemic heart disease (11 745 880), stroke (9 351 312), heart failure (3 673 723), and arrhythmia (670 859). At extreme temperature percentiles, heat (99th percentile) and cold (1st percentile) were associated with higher risk of dying from any cardiovascular cause, ischemic heart disease, stroke, and heart failure as compared to the minimum mortality temperature, which is the temperature associated with least mortality. Across a range of extreme temperatures, hot days (above 97.5th percentile) and cold days (below 2.5th percentile) accounted for 2.2 (95% empirical CI [eCI], 2.1-2.3) and 9.1 (95% eCI, 8.9-9.2) excess deaths for every 1000 cardiovascular deaths, respectively. Heart failure was associated with the highest excess deaths proportion from extreme hot and cold days with 2.6 (95% eCI, 2.4-2.8) and 12.8 (95% eCI, 12.2-13.1) for every 1000 heart failure deaths, respectively. CONCLUSIONS: Across a large, multinational sample, exposure to extreme hot and cold temperatures was associated with a greater risk of mortality from multiple common cardiovascular conditions. The intersections between extreme temperatures and cardiovascular health need to be thoroughly characterized in the present day-and especially under a changing climate.

Effects of long-term average temperature on cardiovascular disease hospitalizations in an American elderly population.

BACKGROUND: Short-term exposure to high or low temperatures is associated with increased mortality and morbidity. Less is known about effects of long-term exposure to high or low temperatures. Prolonged exposure to high or low temperatures might contribute to pathophysiological mechanisms, thereby influencing the development of diseases. Our aim was to evaluate associations of long-term temperature exposure with cardiovascular disease (CVD) hospitalizations. METHODS: We constructed an open cohort consisting of all fee-for-service Medicare beneficiaries, aged ≥65, living in the contiguous US from 2000 through 2016 (∼61.6 million individuals). We used data from the 4 km Gridded Surface Meteorological dataset to assess the summer (June-August) and winter (December-February) average daily maximum temperature for each year for each zip code. Cox-equivalent Poisson models were used to estimate associations with first CVD hospitalization, after adjustment for potential confounders. We performed stratified analyses to assess potential effect modification by sex, age, race, Medicaid eligibility and relative humidity. RESULTS: Higher summer average and lower winter average temperatures were associated with an increased risk of CVD hospitalization. We found a HR of 1.068 (95% CI: 1.063, 1.074) per IQR increase (5.2 °C) for summer average temperature and a HR of 1.022 (95% CI: 1.017, 1.028) per IQR decrease (11.7 °C) for winter average temperature. Positive associations of higher summer average temperatures were strongest for individuals aged <75 years, Medicaid eligible, and White individuals. Positive associations of lower winter average temperatures were strongest for individuals aged <75 years and Black individuals, and individuals living in low relative humidity areas. CONCLUSIONS: Living in areas with high summer average temperatures or low winter average temperatures could increase the risk of CVD hospitalizations. The magnitude of the associations of summer and winter average temperatures differs by demographics and relative humidity levels.