Associations between long-term exposure to air pollution and kidney function utilizing electronic healthcare records: a cross-sectional study.

BACKGROUND: Chronic kidney disease (CKD) affects more than 38 million people in the United States, predominantly those over 65 years of age. While CKD etiology is complex, recent research suggests associations with environmental exposures. METHODS: Our primary objective is to examine creatinine-based estimated glomerular filtration rate (eGFRcr) and diagnosis of CKD and potential associations with fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) using a random sample of North Carolina electronic healthcare records (EHRs) from 2004 to 2016. We estimated eGFRcr using the serum creatinine-based 2021 CKD-EPI equation. PM2.5 and NO2 data come from a hybrid model using 1 km2 grids and O3 data from 12 km2 CMAQ grids. Exposure concentrations were 1-year averages. We used linear mixed models to estimate eGFRcr per IQR increase of pollutants. We used multiple logistic regression to estimate associations between pollutants and first appearance of CKD. We adjusted for patient sex, race, age, comorbidities, temporality, and 2010 census block group variables. RESULTS: We found 44,872 serum creatinine measurements among 7,722 patients. An IQR increase in PM2.5 was associated with a 1.63 mL/min/1.73m2 (95% CI: -1.96, -1.31) reduction in eGFRcr, with O3 and NO2 showing positive associations. There were 1,015 patients identified with CKD through e-phenotyping and ICD codes. None of the environmental exposures were positively associated with a first-time measure of eGFRcr < 60 mL/min/1.73m2. NO2 was inversely associated with a first-time diagnosis of CKD with aOR of 0.77 (95% CI: 0.66, 0.90). CONCLUSIONS: One-year average PM2.5 was associated with reduced eGFRcr, while O3 and NO2 were inversely associated. Neither PM2.5 or O3 were associated with a first-time identification of CKD, NO2 was inversely associated. We recommend future research examining the relationship between air pollution and impaired renal function.

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.

Longitudinal associations between ambient PM2.5 exposure and lipid levels in two Indian cities.

Background: Exposure to ambient PM2.5 is known to affect lipid metabolism through systemic inflammation and oxidative stress. Evidence from developing countries, such as India with high levels of ambient PM2.5 and distinct lipid profiles, is sparse. Methods: Longitudinal nonlinear mixed-effects analysis was conducted on >10,000 participants of Centre for cArdiometabolic Risk Reduction in South Asia (CARRS) cohort in Chennai and Delhi, India. We examined associations between 1-month and 1-year average ambient PM2.5 exposure derived from the spatiotemporal model and lipid levels (total cholesterol [TC], triglycerides [TRIG], high-density lipoprotein cholesterol [HDL-C], and low-density lipoprotein cholesterol [LDL-C]) measured longitudinally, adjusting for residential and neighborhood-level confounders. Results: The mean annual exposure in Chennai and Delhi was 40 and 102 µg/m3 respectively. Elevated ambient PM2.5 levels were associated with an increase in LDL-C and TC at levels up to 100 µg/m3 in both cities and beyond 125 µg/m3 in Delhi. TRIG levels in Chennai increased until 40 µg/m3 for both short- and long-term exposures, then stabilized or declined, while in Delhi, there was a consistent rise with increasing annual exposures. HDL-C showed an increase in both cities against monthly average exposure. HDL-C decreased slightly in Chennai with an increase in long-term exposure, whereas it decreased beyond 130 µg/m3 in Delhi. Conclusion: These findings demonstrate diverse associations between a wide range of ambient PM2.5 and lipid levels in an understudied South Asian population. Further research is needed to establish causality and develop targeted interventions to mitigate the impact of air pollution on lipid metabolism and cardiovascular health.

Nationwide estimation of daily ambient PM2.5 from 2008 to 2020 at 1 km2 in India using an ensemble approach.

High-resolution assessment of historical levels is essential for assessing the health effects of ambient air pollution in the large Indian population. The diversity of geography, weather patterns, and progressive urbanization, combined with a sparse ground monitoring network makes it challenging to accurately capture the spatiotemporal patterns of ambient fine particulate matter (PM2.5) pollution in India. We developed a model for daily average ambient PM2.5 between 2008 and 2020 based on monitoring data, meteorology, land use, satellite observations, and emissions inventories. Daily average predictions at each 1 km × 1 km grid from each learner were ensembled using a Gaussian process regression with anisotropic smoothing over spatial coordinates, and regression calibration was used to account for exposure error. Cross-validating by leaving monitors out, the ensemble model had an R2 of 0.86 at the daily level in the validation data and outperformed each component learner (by 5-18%). Annual average levels in different zones ranged between 39.7 µg/m3 (interquartile range: 29.8-46.8) in 2008 and 30.4 µg/m3 (interquartile range: 22.7-37.2) in 2020, with a cross-validated (CV)-R2 of 0.94 at the annual level. Overall mean absolute daily errors (MAE) across the 13 years were between 14.4 and 25.4 µg/m3. We obtained high spatial accuracy with spatial R2 greater than 90% and spatial MAE ranging between 7.3-16.5 µg/m3 with relatively better performance in urban areas at low and moderate elevation. We have developed an important validated resource for studying PM2.5 at a very fine spatiotemporal resolution, which allows us to study the health effects of PM2.5 across India and to identify areas with exceedingly high levels.

Indoor and ambient black carbon and fine particulate matter associations with blood biomarkers in COPD patients.

BACKGROUND: Systemic inflammation contributes to cardiovascular risk and chronic obstructive pulmonary disease (COPD) pathophysiology. Associations between systemic inflammation and exposure to ambient fine particulate matter (PM ≤ 2.5 µm diameter; PM2.5), and black carbon (BC), a PM2.5 component attributable to traffic and other sources of combustion, infiltrating indoors are not well described. METHODS: Between 2012 and 2017, COPD patients completed in-home air sampling over one-week intervals, up to four times (seasonally), followed by measurement of plasma biomarkers of systemic inflammation, C-reactive protein (CRP) and interleukin-6 (IL-6), and endothelial activation, soluble vascular adhesion molecule-1 (sVCAM-1). Ambient PM2.5, BC and sulfur were measured at a central site. The ratio of indoor/ambient sulfur in PM2.5, a surrogate for fine particle infiltration, was used to estimate indoor BC and PM2.5 of ambient origin. Linear mixed effects regression with a random intercept for each participant was used to assess associations between indoor and indoor of ambient origin PM2.5 and BC with each biomarker. RESULTS: 144 participants resulting in 482 observations were included in the analysis. There were significant positive associations between indoor BC and indoor BC of ambient origin with CRP [%-increase per interquartile range (IQR);95 % CI (13.2 %;5.2-21.8 and 11.4 %;1.7-22.1, respectively)]. Associations with indoor PM2.5 and indoor PM2.5 of ambient origin were weaker. There were no associations with IL-6 or sVCAM-1. CONCLUSIONS: In homes of patients with COPD without major sources of combustion, indoor BC is mainly attributable to the infiltration of ambient sources of combustion indoors. Indoor BC of ambient origin is associated with increases in systemic inflammation in patients with COPD, even when staying indoors.

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.

Harnessing AI to unmask Copenhagen's invisible air pollutants: A study on three ultrafine particle metrics.

Ultrafine particles (UFPs) are airborne particles with a diameter of less than 100 nm. They are emitted from various sources, such as traffic, combustion, and industrial processes, and can have adverse effects on human health. Long-term mean ambient average particle size (APS) in the UFP range varies over space within cities, with locations near UFP sources having typically smaller APS. Spatial models for lung deposited surface area (LDSA) within urban areas are limited and currently there is no model for APS in any European city. We collected particle number concentration (PNC), LDSA, and APS data over one-year monitoring campaign from May 2021 to May 2022 across 27 locations and estimated annual mean in Copenhagen, Denmark, and obtained additionally annual mean PNC data from 6 state-owned continuous monitors. We developed 94 predictor variables, and machine learning models (random forest and bagged tree) were developed for PNC, LDSA, and APS. The annual mean PNC, LDSA, and APS were, respectively, 5523 pt/cm3, 12.0 µm2/cm3, and 46.1 nm. The final R2 values by random forest (RF) model were 0.93 for PNC, 0.88 for LDSA, and 0.85 for APS. The 10-fold, repeated 10-times cross-validation R2 values were 0.65, 0.67, and 0.60 for PNC, LDSA, and APS, respectively. The root mean square error for final RF models were 296 pt/cm3, 0.48 µm2/cm3, and 1.60 nm for PNC, LDSA, and APS, respectively. Traffic-related variables, such as length of major roads within buffers 100-150 m and distance to streets with various speed limits were amongst the highly-ranked predictors for our models. Overall, our ML models achieved high R2 values and low errors, providing insights into UFP exposure in a European city where average PNC is quite low. These hyperlocal predictions can be used to study health effects of UFPs in the Danish Capital.

Warm season ambient ozone and children's health in the USA.

BACKGROUND: Over 120 million people in the USA live in areas with unsafe ozone (O3) levels. Studies among adults have linked exposure to worse lung function and higher risk of asthma and chronic obstructive pulmonary disease (COPD). However, few studies have examined the effects of O3 in children, and existing studies are limited in terms of their geographic scope or outcomes considered. METHODS: We leveraged a dataset of encounters at 42 US children's hospitals from 2004-2015. We used a one-stage case-crossover design to quantify the association between daily maximum 8-hour O3 in the county in which the hospital is located and risk of emergency department (ED) visits for any cause and for respiratory disorders, asthma, respiratory infections, allergies and ear disorders. RESULTS: Approximately 28 million visits were available during this period. Per 10 ppb increase, warm-season (May through September) O3 levels over the past three days were associated with higher risk of ED visits for all causes (risk ratio [RR]: 0.3% [95% confidence interval (CI): 0.2%, 0.4%]), allergies (4.1% [2.5%, 5.7%]), ear disorders (0.8% [0.3%, 1.3%]) and asthma (1.3% [0.8%, 1.9%]). When restricting to levels below the current regulatory standard (70 ppb), O3 was still associated with risk of ED visits for all-cause, allergies, ear disorders and asthma. Stratified analyses suggest that the risk of O3-related all-cause ED visits may be higher in older children. CONCLUSIONS: Results from this national study extend prior research on the impacts of daily O3 on children's health and reinforce the presence of important adverse health impacts even at levels below the current regulatory standard in the USA.

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.

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.

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.

Enrichment of polycyclic aromatic hydrocarbon metabolizing microorganisms on the oral mucosa of tobacco users.

Certain soil microbes resist and metabolize polycyclic aromatic hydrocarbons (PAHs). The same is true for a subset of skin microbes. In the human mouth, oral microbes have the potential to oxidize tobacco PAHs, thereby increasing these chemicals' ability to cause cancer of adjacent epithelium. We hypothesized that we could identify, in smokers, the oral mucosal microbes that can metabolize PAH. We isolated bacteria and fungi that survived long-term in minimal media with PAHs as the sole carbon source, under aerobic conditions, from the oral mucosa in 17 of 26 smokers and two of 14 nonsmokers. Of bacteria genera that survived harsh PAH exposure in vitro, most were found at trace levels, except for Staphylococcus, Actinomyces, and Kingella, which were more abundant. Two PAH-resistant strains of Candida albicans (C. albicans) were isolated from smokers. C. albicans was a prime candidate to contribute to carcinogenesis in tobacco users as it is found orally at high levels in tobacco users on the mucosa, and some Candida species can metabolize PAHs. However, when C. albicans isolates were tested for metabolism of two model PAH substrates, pyrene and phenanthrene, they were not capable, suggesting they cannot metabolize PAH under the conditions used. In conclusion, evidence for large scale microbial degradation of tobacco PAHs under aerobic conditions on the oral mucosa remains lacking, though nonabundant PAH metabolizers are certainly present.

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 noise exposures and cardiovascular diseases mortality: A study in 5 U.S. states.

BACKGROUND: Previous studies have linked noise exposure with adverse cardiovascular events. However, evidence remains inconsistent, and most previous studies only focused on traffic noise, excluding other anthropogenic sources like constructions, industrial process and commercial activities. Additionally, few studies have been conducted in the U.S. or evaluated the non-linear exposure-response relationships. METHODS: We conducted a relative incidence analysis study using all cardiovascular diseases mortality as cases (n = 936,019) and external causes mortality (n = 232,491) as contrast outcomes. Mortality records geocoded at residential addresses were obtained from five U.S. states (Indiana, 2007; Kansas, 2007-2009, Missouri, 2010-2019, Ohio, 2007-2013, Texas, 2007-2016). Time-invariant long-term noise exposure was obtained from a validated model developed based on acoustical measurements across 2000-2014. Noises from both natural sources (natural activities, including animals, insects, winds, water flows, thunder, etc.) and anthropogenic sources (human activities, including transportation, industrial activities, community facilities & infrastructures, commercial activities, entertainments, etc.) were included. We used daytime and nighttime total anthropogenic noise & day-night average sound pressure level combining natural and anthropogenic sources as exposures. Logistic regression models were fit controlling for Census tract-level & individual-level characteristics. We examined potential modification by sex by interaction terms and potential non-linear associations by thin plate spline terms. RESULTS: We observed positive associations for daytime anthropogenic L50 (sound level exceeded 50% of time) noise (10-dBA OR = 1.047, 95%CI 1.025-1.069), nighttime anthropogenic L50 noise (10-dBA OR = 1.061, 95%CI 1.033-1.091) in a two-exposure-term model, and overall Ldn (day-night average) sound pressure level (10-dBA OR = 1.064, 95%CI 1.040-1.089) in single-exposure-term model. Females were more susceptible to all three exposures. All exposures showed monotonic positive associations with cardiovascular mortality up to certain thresholds around 45-55 dBA, with a generally flattened or decreasing trend beyond those thresholds. CONCLUSIONS: Both daytime anthropogenic and nighttime anthropogenic noises were associated with cardiovascular disease mortality, and associations were stronger in females.