Fine Particulate Air Pollution Research Articles

Short-term and Intermediate-term Fine Particulate Air Pollution are Synergistically Associated with Habitual Sleep Variability in Adolescents

BACKGROUND AND AIM: While both fine particulate (PM2.5) exposure and high sleep variability are potential risk factors for cardiovascular diseases (CVD), the association between PM2.5 and sleep variability remains unclear. Our study aimed at investigating the association between PM2.5 exposure and habitual sleep variability (HSV) in a population-based sample of U.S. adolescents. METHODS: Data obtained from 421 adolescents, who participated in the Penn State Child Cohort follow-up examination, were analyzed. For each participant, we collected 24-hour (i.e. short-term) individual-level PM2.5 exposure by using a personal nephelometer. We further estimated their residential-level PM2.5, during the 60-day period prior to the examination (i.e. intermediate-term), by utilizing a GIS-based kriging approach. Actigraphy was used to collect participants’ total sleep time (TST) for 7 consecutive nights. HSV was calculated as the standard deviation (SD) of the 7-night TST. Multivariable-adjusted linear regression was used to assess the association between PM2.5 exposures and HSV. An interaction between the short- and intermediate-term PM2.5 was created to test their potential synergistic impact on HSV. RESULTS:Both short-term and intermediate-term PM2.5 exposure were significantly (both p0.01) associated with HSV. There was a marginally significant (p=0.08) synergistic interaction between short-term and intermediate-term PM2.5. Specifically, the association between intermediate-term PM2.5 and HSV became stronger as short-term PM2.5 increased, and vice versa. For example, the regression coefficients (SE) between 1 SD (2.2 µg/m3) increase in intermediate-term PM2.5 and HSV were 3.5 (2.7, p=0.21), 5.1 (2.3, p=0.03), and 10.5 (3.4, p0.01) minutes, when short-term PM2.5 were at its 10th percentile (1.7 µg/m3), median (9.7 µg/m3), and 90th percentile (35.3 µg/m3), respectively. CONCLUSIONS:Both short-term and intermediate-term PM2.5 exposure were associated with higher sleep variability among adolescents. More importantly, short-term and intermediate-term PM2.5 exposure may impact sleep variability in a synergistic manner, which highlighted the importance of PM2.5 reduction in the early prevention of CVD. KEYWORDS: Particulate Matter, Sleep Variability, Adolescents

28163 Exposure of fine particulate matter air pollution and incident atopic dermatitis in the general population: A national population-based retrospective cohort study

Background: Atopic dermatitis(AD) is chronic recurrent inflammatory skin disease associated with various environmental factors. For decades, environmental pollutants have been known to play a major role in occur of AD. However, few population-based cohort studies has assessed the relationship between outdoor air pollutants and occurrence of AD, in short term exposure.

Association between Fine Particulate Air Pollution and the Onset of Uveitis in Mainland China

ABSTRACT Purpose Although it has long been recognized that air pollution can affect the immune system and human ocular symptoms, it is uncertain whether air pollutants may also contribute to the development of uveitis. This study aimed to quantify the association of particulate matters less than 2.5 μm (PM2.5) with uveitis onset. Methods We combined monthly averages of PM2.5 concentrations, with data from the largest database of uveitis cases to assess the association between PM2.5 and uveitis onset. We further estimated the uveitis burden that was attributed to PM2.5 exposure and used choropleth maps to precisely characterize geographical variations. Results We found that a 10 μg/m3 increase in PM2.5 concentration was associated with a one-case per 10 individuals increase in uveitis onset across the dataset. Our results further suggest that PM2.5 concentrations above the level of the minimum exposure are responsible for 13% of novel uveitis cases in our cohort. Conclusion: These findings provide evidence supporting the association between fine particulate air pollution and uveitis onset.

Fine particulate matter air pollution and aortic perivascular adipose tissue: Oxidative stress, leptin, and vascular dysfunction.

Exposure to fine particulate matter (PM2.5) air pollution increases blood pressure, induces vascular inflammation and dysfunction, and augments atherosclerosis in humans and rodents; however, the understanding of early changes that foster chronic vascular disease is incomplete. Because perivascular adipose tissue (PVAT) inflammation is implicated in chronic vascular diseases, we investigated changes in aortic PVAT following short‐term air pollution exposure. Mice were exposed to HEPA‐filtered or concentrated ambient PM2.5 (CAP) for 9 consecutive days, and the abundance of inflammatory, adipogenic, and adipokine gene mRNAs was measured by gene array and qRT‐PCR in thoracic aortic PVAT. Responses of the isolated aorta with and without PVAT to contractile (phenylephrine, PE) and relaxant agonists (acetylcholine, ACh; sodium nitroprusside, SNP) were measured. Exposure to CAP significantly increased the urinary excretion of acrolein metabolite (3HPMA) as well as the abundance of protein–acrolein adducts (a marker of oxidative stress) in PVAT and aorta, upregulated PVAT leptin mRNA expression without changing mRNA levels of several proinflammatory genes, and induced PVAT insulin resistance. In control mice, PVAT significantly depressed PE‐induced contractions—an effect that was dampened by CAP exposure. Pulmonary overexpression of extracellular dismutase (ecSOD‐Tg) prevented CAP‐induced effects on urinary 3HPMA levels, PVAT Lep mRNA, and alterations in PVAT and aortic function, reflecting a necessary role of pulmonary oxidative stress in all of these deleterious CAP‐induced changes. More research is needed to address how exactly short‐term exposure to PM2.5 perturbs PVAT and aortic function, and how these specific genes and functional changes in PVAT could lead over time to chronic inflammation, endothelial dysfunction, and atherosclerosis.

Association of Cardiovascular Disease and Long-Term Exposure to Fine Particulate Matter (PM2.5) in the Southeastern United States

There is a well-documented association between ambient fine particulate matter air pollution (PM2.5) and cardiovascular disease (CVD) morbidity and mortality. Exposure to PM2.5 can cause premature death and harmful and chronic health effects such as heart attack, diabetes, and stroke. The Environmental Protection Agency sets annual PM2.5 standards to reduce these negative health effects. Currently above an annual average level of 12.0 µg/m is considered unhealthy. Methods. We examined the association of long-term exposure to PM2.5 and CVD in a cohort of 44,610 individuals who resided in 12 states recruited into the Southern Community Cohort Study (SCCS). The SCCS was designed to recruit Black and White participants who received care from Federally Qualified Health Centers; hence, they represent vulnerable individuals from low-income families across this vast region. This study tests whether SCCS participants who lived in locations exposed to elevated ambient levels of PM2.5 concentrations were more likely to report a history of CVD at enrollment (2002–2009). Remotely sensed satellite data integrated with ground monitoring data provide an assessment of the average annual PM2.5 in urban and rural locations where the SCCS participants resided. We used multilevel logistic regression to estimate the associations between self-reported CVD and exposure to elevated ambient levels of PM2.5. Results. We found a 13.4 percent increase in the odds of reported CVD with exposure to unhealthy levels of PM2.5 exposure at enrollment. The SCCS participants with medical histories of hypertension, hypercholesterolemia, and smoking had, overall, 385 percent higher odds of reported CVD than those without these clinical risk factors. Additionally, Black participants were more likely to live in locations with higher ambient PM2.5 concentrations and report high levels of clinical risk factors, thus, they may be at a greater future risk of CVD. Conclusions: In the SCCS participants, we found a strong relation between exposures to high ambient levels of PM2.5 and self-reported CVD at enrollment.

Exposure to Fine Particulate Matter Air Pollution Alters mRNA and miRNA Expression in Bone Marrow-Derived Endothelial Progenitor Cells from Mice.

Exposure to fine particulate matter (PM2.5) air pollution is associated with quantitative deficits of circulating endothelial progenitor cells (EPCs) in humans. Related exposures of mice to concentrated ambient PM2.5 (CAP) likewise reduces levels of circulating EPCs and induces defects in their proliferation and angiogenic potential as well. These changes in EPC number or function are predictive of larger cardiovascular dysfunction. To identify global, PM2.5-dependent mRNA and miRNA expression changes that may contribute to these defects, we performed a transcriptomic analysis of cells isolated from exposed mice. Compared with control samples, we identified 122 upregulated genes and 44 downregulated genes in EPCs derived from CAP-exposed animals. Functions most impacted by these gene expression changes included regulation of cell movement, cell and tissue development, and cellular assembly and organization. With respect to miRNA changes, we found that 55 were upregulated while 53 were downregulated in EPCs from CAP-exposed mice. The top functions impacted by these miRNA changes included cell movement, cell death and survival, cellular development, and cell growth and proliferation. A subset of these mRNA and miRNA changes were confirmed by qRT-PCR, including some reciprocal relationships. These results suggest that PM2.5-induced changes in gene expression may contribute to EPC dysfunction and that such changes may contribute to the adverse cardiovascular outcomes of air pollution exposure.

Predicting Spatial Variations in Multiple Measures of Oxidative Burden for Outdoor Fine Particulate Air Pollution across Canada.

Fine particulate air pollution (PM2.5) is a leading contributor to the overall global burden of disease. Traditionally, outdoor PM2.5 has been characterized using mass concentrations which treat all particles as equally harmful. Oxidative potential (OP) (per μg) and oxidative burden (OB) (per m3) are complementary metrics that estimate the ability of PM2.5 to cause oxidative stress, which is an important mechanism in air pollution health effects. Here, we provide the first national estimates of spatial variations in multiple measures (glutathione, ascorbate, and dithiothreitol depletion) of annual median outdoor PM2.5 OB across Canada. To do this, we combined a large database of ground-level OB measurements collected monthly prospectively across Canada for 2 years (2016-2018) with PM2.5 components estimated using a chemical transport model (GEOS-Chem) and satellite aerosol observations. Our predicted ground-level OB values of all three methods were consistent with ground-level observations (cross-validation R2 = 0.63-0.74). We found that forested regions and urban areas had the highest OB, predicted primarily by black carbon and organic carbon from wildfires and transportation sources. Importantly, the dominant components associated with OB were different than those contributing to PM2.5 mass concentrations (secondary inorganic aerosol); thus, OB metrics may better indicate harmful components and sources on health than the bulk PM2.5 mass, reinforcing that OB estimates can complement the existing PM2.5 data in future national-level epidemiological studies.

Ambient fine particulate matter air pollution and the risk of preterm birth: A multicenter birth cohort study in China

Preterm birth (PTB), defined as live birth before the 37th week of gestation, is believed to have profound impacts on the infant's health in later life. Air pollution has been suggested to be a potential risk factor of PTB, but the evidence was inconsistent. In this multicenter birth cohort study, we aimed to examine the association between fine particulate matter (PM2.5) exposure during pregnancy and PTB in China. A total of 5976 live births were identified between Jan. 2009 and Feb. 2011 from 8 provinces in China. Residential exposures to PM2.5 were assigned based on satellite remote sensing estimates. Cox proportional hazards regressions were employed to explore the correlation for each trimester as well as the entire pregnancy. A total of 443 (7.4%) preterm births were observed. The average PM2.5 during pregnancy was 57.2 ± 8.8 μg/m3. We found exposure to PM2.5 during the whole pregnancy (hazard ratio, HR = 1.262; 95% CI: 1.087–1.465) and in the first trimester (HR = 1.114; 95% CI: 1.007–1.232) was associated with higher risk of PTB. The associations of PM2.5 were stronger for subjects with older maternal or paternal age, lower maternal pre-pregnancy BMI, and lower family income. This study adds supports to the cumulating evidence linking PM2.5 exposure and elevated PTB risk. Measures of air pollution reduction are needed during pregnancy, especially at early stage of pregnancy to prevent adverse birth outcomes.

Air pollution and retinal vessel diameter and blood pressure in school-aged children in a region impacted by residential biomass burning

Little is known about the early-life cardiovascular health impacts of fine particulate air pollution (PM2.5) and oxidant gases. A repeated-measures panel study was used to evaluate associations between outdoor PM2.5 and the combined oxidant capacity of O3 and NO2 (using a redox-weighted average, Ox) and retinal vessel diameter and blood pressure in children living in a region impacted by residential biomass burning. A median of 6 retinal vessel and blood pressure measurements were collected from 64 children (ages 4–12 years), for a total of 344 retinal measurements and 432 blood pressure measurements. Linear mixed-effect models were used to estimate associations between PM2.5 or Ox (same-day, 3-day, 7-day, and 21-day means) and retinal vessel diameter and blood pressure. Interactions between PM2.5 and Ox were also examined. Ox was inversely associated with retinal arteriolar diameter; the strongest association was observed for 7-day mean exposures, where each 10 ppb increase in Ox was associated with a 2.63 μm (95% CI − 4.63, − 0.63) decrease in arteriolar diameter. Moreover, Ox modified associations between PM2.5 and arteriolar diameter, with weak inverse associations observed between PM2.5 and arteriolar diameter only at higher concentrations of Ox. Our results suggest that outdoor air pollution impacts the retinal microvasculature of children and interactions between PM2.5 and Ox may play an important role in determining the magnitude and direction of these associations.

Commuter types identified using clustering and their associations with source-specific PM2.5

Traffic-related fine particulate matter air pollution (tr-PM2.5) has been associated with adverse health outcomes such as cardiopulmonary morbidity and mortality, with in-vehicle tr-PM2.5 exposure contributing to total personal pollution exposure. Trip characteristics, including time of day, day of the week, and traffic congestion, are associated with in-vehicle PM2.5 exposures. We hypothesized that some commuter characteristics, such as whether commuters travel primarily during rush hour, would also be associated with increased tr-PM2.5 exposures. The commute data consisted of unscripted personal vehicle trips of 46 commuters in the Washington, D.C. metro area over 48-h, with a total of 320 trips. We identified commuter types using sparse K-means clustering, which identifies the hours throughout the day important for clustering commuters. Source-specific PM2.5 over 48 h was estimated using Positive Matrix Factorization. Linear regression was used to estimate differences in source-specific PM2.5 by commuter cluster. Two commuter clusters were identified using the clustering approach: rush hour commuters, who primarily travelled during rush hour, and sporadic commuters, who travelled throughout the day. The hours given the largest weights by sparse K-means were 7–8 a.m. and 6–7 p.m., corresponding to peak travel times. Integrated black carbon (BC) was higher for rush hour commuters (median = 3.1 μg/m3 (IQR = 1.5)) compared to sporadic commuters (2.0 μg/m3 (IQR = 1.9)). Mobile PM2.5, consisting primarily of tailpipe emissions and brake/tire wear, was also higher for rush hour commuters (2.9 μg/m3 (IQR = 1.6)) compared to sporadic commuters (2.1 μg/m3 (IQR = 2.4)), though this difference was not statistically significant in regression models. Estimated differences between commuter types for secondary/mixed PM2.5 and road salt PM2.5 were smaller. Further research may elucidate whether commuter characteristics are an efficient way to identify individuals with highest tr-PM2.5 exposures associated with commuting and to develop effective mitigation strategies.

Relationship between fine particulate air pollution and hospital admissions for depression: a case-crossover study in Taipei

ABSTRACT There are few apparent studies regarding the association between fine particulate matter (PM2.5) air pollution and development of depression. Data obtained from epidemiological studies are inconsistent and controversial. The aim of this case-crossover study was to examine the association between short-term exposure to PM2.5 alone and in combination with other pollutants and frequency of hospitalizations for depression from 2009 to 2013 in Taipei, Taiwan. In the single pollutant model without adjustment for other pollutants, 17% and 4% increase in admissions attributed to depression correlated with interquartile range (IQR) rise in PM2.5 levels was noted on warm and cool days, respectively. Data were also analyzed using two-pollutant models and it was found that on warm days, the association continued to be significant after including one of the following pollutants: sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3) or carbon monoxide (CO). On cool days, the significance was lost. In conclusion, the relationship between ambient outdoor PM2.5 exposure and rates of hospitalization for depression appeared to be temperature dependent in Taipei. Further research is needed to verify these observations as well as to distinguish the relative contributions of PM2.5 and temperature to development for hospital admissions for depression.

Abstract MP70: Short-term Fine Particulate Air Pollution Is Associated With Shorter Sleep Duration And Higher Sleep Variability In Adolescents

Introduction: Sleep deprivation and large sleep variability are potential risk factors for obesity and cardiovascular diseases. While it is plausible that particulate air pollution may contribute to these unfavorable sleep patterns, very few studies have been conducted to assess the association between fine particulate (PM 2.5 ) air pollution and objectively measured sleep duration and its variability in an adolescent U.S. population. Hypothesis: We tested the hypothesis that higher individual-level short-term PM 2.5 exposure is associated with shorter sleep duration and higher sleep variability among adolescents. Methods: We analyzed the available data collected from 421 adolescents who participated in the follow-up examination of the population-based Penn State Child Cohort (PSCC) study. To estimate individual-level short-term PM 2.5 exposure, a personal nephelometer (Thermo pDR-1200) was used to measure real-time PM 2.5 concentration for 24 hours from the study participants. The 24-hour mean PM 2.5 concentration was used to quantify the short-term PM 2.5 exposure. To obtain objectively-measured habitual sleep duration (HSD) and habitual sleep variability (HSV), an actigraphy (GT3X+) was used to collect sleep data for 7 consecutive nights, including 1 night in parallel with the PM 2.5 monitoring and 6 nights thereafter. HSD and HSV were calculated as the intra-individual mean and standard deviation (SD) of the 7-night sleep duration, respectively. Participants with < 5 nights (70% of 7 nights) of data were excluded from the analyses. The associations between the individual-level PM 2.5 exposure and HSD/HSV were evaluated by using multi-variable adjusted linear regression models, controlling for age, race, sex, BMI percentile, environmental temperature, and relative humidity. Results: The mean (SD) age of the study population was 16.9 (2.2) years. The study sample consisted of 54% males and 78% whites. The 24-hour mean (SD) of PM 2.5 concentration was 16.9 (26.8) μg/m 3 , while the average HSD and HSV were 7.0 (0.9) hours and 1.2 (0.6) hours, respectively. We observed that a 10 μg/m 3 increase in the 24-hour mean PM 2.5 was associated with significantly lower HSD [β (SE): -0.06 (0.03) hours, p=0.02] and larger HSV [β (SE): 0.04 (0.02) hours, p=0.04]. The effect sizes were approximately 7% of their respective SDs. Conclusion: Individual-level short-term PM 2.5 exposure is associated with objective-measured shorter sleep duration and higher night-to-night sleep variability among U.S. adolescents. These observed associations suggest that particulate air pollution exposure in early life may impact habitual sleep pattern, which may in turn be associated with the risks of obesity and cardiovascular diseases in later life.

The association of in-utero exposure to ambient fine particulate air pollution with low birth weight in India

A growing body of research indicates that in-utero exposure to ambient fine particulate matter (PM2.5) is a risk factor for low birth weight (LBW). However, research on India, where the high and rising level of ambient air pollution is a significant health concern, is limited. In this study, we analyze the association between ambient PM2.5 and LBW in India. We match data on birth weight from the National Family and Health Survey (NFHS) conducted in India in 2015–16 with high-resolution spatial data on annual ambient PM2.5 concentration to calculate in-utero exposure based on the residential location of each child. We estimate the association of in-utero exposure to ambient PM2.5 with birth weight and LBW, after adjusting for child level, maternal, and household level characteristics that predict birth weight. In our sample (n = 149 416), in comparison to the reference category of in-utero PM2.5 level less than 26.7 µg m−3, the adjusted OR of LBW increases non-linearly from 1.098 (95% CI: 0.954, 1.263) for children in the exposure band 39.3–44.7 µg m−3 (i.e., the fourth octile) to 1.241 (95% CI: 1.065, 1.447) for those in the exposure band 44.7–51.6 µg m−3 (i.e., the fifth octile) and 1.405 (95% CI: 1.126,1.753) for those with in-utero PM2.5 level greater than 77.3 µg m−3 (i.e., the last octile). Our findings show that exposure to ambient PM2.5 is strongly associated with LBW in India and suggest that policies that improve air quality may be necessary for achieving the World Health Assembly target of 30% reduction in LBW by 2025.

Control of particulate nitrate air pollution in China

The concentration of fine particulate matter (PM2.5) across China has decreased by 30–50% over the period 2013–2018 due to stringent emission controls. However, the nitrate component of PM2.5 has not responded effectively to decreasing emissions of nitrogen oxides and has actually increased during winter haze pollution events in the North China Plain. Here, we show that the GEOS-Chem atmospheric chemistry model successfully simulates the nitrate concentrations and trends. We find that winter mean nitrate would have increased over 2013–2018 were it not for favourable meteorology. The principal cause of this nitrate increase is weaker deposition. The fraction of total inorganic nitrate as particulate nitrate instead of gaseous nitric acid over the North China Plain in winter increased from 90% in 2013 to 98% in 2017, as emissions of nitrogen oxides and sulfur dioxide decreased while ammonia emissions remained high. This small increase in the particulate fraction greatly slows down deposition of total inorganic nitrate and hence drives the particulate nitrate increase. Our results suggest that decreasing ammonia emissions would decrease particulate nitrate by driving faster deposition of total inorganic nitrate. Decreasing nitrogen oxide emissions is less effective because it drives faster oxidation of nitrogen oxides and slower deposition of total inorganic nitrate. Reduction of ammonia emissions may be effective in reducing the nitrate component of fine particulate matter air pollution across the North China Plain, according to the simulation of nitrate trends using the GEOS-Chem atmospheric chemistry model.

Ambient fine particulate matter air pollution and the risk of hospitalization among COVID-19 positive individuals: Cohort study

BackgroundEcologic analyses suggest that living in areas with higher levels of ambient fine particulate matter air pollution (PM2.5) is associated with higher risk of adverse COVID-19 outcomes. Studies accounting for individual-level health characteristics are lacking. MethodsWe leveraged the breadth and depth of the US Department of Veterans Affairs national healthcare databases and built a national cohort of 169,102 COVID-19 positive United States Veterans, enrolled between March 2, 2020 and January 31, 2021, and followed them through February 15, 2021. Annual average 2018 PM2.5 exposure, at an approximately 1 km2 resolution, was linked with residential street address at the year prior to COVID-19 positive test. COVID-19 hospitalization was defined as first hospital admission between 7 days prior to, and 15 days after, the first COVID-19 positive date. Adjusted Poisson regression assessed the association of PM2.5 with risk of hospitalization. ResultsThere were 25,422 (15.0%) hospitalizations; 5,448 (11.9%), 5,056 (13.0%), 7,159 (16.1%), and 7,759 (19.4%) were in the lowest to highest PM2.5 quartile, respectively. In models adjusted for State, demographic and behavioral factors, contextual characteristics, and characteristics of the pandemic a one interquartile range increase in PM2.5 (1.9 µg/m3) was associated with a 10% (95% CI: 8%–12%) increase in risk of hospitalization. The association of PM2.5 and risk of hospitalization among COVID-19 individuals was present in each wave of the pandemic. Models of non-linear exposure–response suggested increased risk at PM2.5 concentrations below the national standard 12 µg/m3. Formal effect modification analyses suggested higher risk of hospitalization associated with PM2.5 in Black people compared to White people (p = 0.045), and in those living in socioeconomically disadvantaged neighborhoods (p < 0.001). ConclusionsExposure to higher levels of PM2.5 was associated with increased risk of hospitalization among COVID-19 infected individuals. The risk was evident at PM2.5 levels below the regulatory standards. The analysis identified those of Black race and those living in disadvantaged neighborhoods as population groups that may be more susceptible to the untoward effect of PM2.5 on risk of hospitalization in the setting of COVID-19.

Within-City Variation in Reactive Oxygen Species from Fine Particle Air Pollution and COVID-19

Rationale: Evidence linking outdoor air pollution with coronavirus disease (COVID-19) incidence and mortality is largely based on ecological comparisons between regions that may differ in factors such as access to testing and control measures that may not be independent of air pollution concentrations. Moreover, studies have yet to focus on key mechanisms of air pollution toxicity such as oxidative stress.Objectives: To conduct a within-city analysis of spatial variations in COVID-19 incidence and the estimated generation of reactive oxygen species (ROS) in lung lining fluid attributable to fine particulate matter (particulate matter with an aerodynamic diameter ⩽2.5 μm [PM2.5]).Methods: Sporadic and outbreak-related COVID-19 case counts, testing data, population data, and sociodemographic data for 140 neighborhoods were obtained from the City of Toronto. ROS estimates were based on a mathematical model of ROS generation in lung lining fluid in response to iron and copper in PM2.5. Spatial variations in long-term average ROS were predicted using a land-use regression model derived from measurements of iron and copper in PM2.5. Data were analyzed using negative binomial regression models adjusting for covariates identified using a directed acyclic graph and accounting for spatial autocorrelation.Measurements and Main Results: A significant positive association was observed between neighborhood-level ROS and COVID-19 incidence (incidence rate ratio = 1.07; 95% confidence interval, 1.01–1.15 per interquartile range ROS). Effect modification by neighborhood-level measures of racialized group membership and socioeconomic status was also identified.Conclusions: Examination of neighborhood characteristics associated with COVID-19 incidence can identify inequalities and generate hypotheses for future studies.

Ambient Fine Particulate Matter Air Pollution and Risk of Weight Gain and Obesity in United States Veterans: An Observational Cohort Study.

Background:Experimental evidence and studies of children and adolescents suggest that ambient fine particulate matter [particulate matter in aerodynamic diameter ()] air pollution may be obesogenic, but the relationship between and the risk of body weight gain and obesity in adults is uncertain.Objectives:Our goal was to characterize the association between and the risks of weight gain and obesity.Methods:We followed 3,902,440 U.S. Veterans from 2010 to 2018 (median 8.1 y, interquartile range: 7.3–8.4) and assigned time-updated exposures by linking geocoded residential street addresses with satellite-based estimates of surface-level mass (at resolution). Associations with were estimated using Cox proportional hazards models for incident obesity [body mass index (] and a increase in weight relative to baseline and linear mixed models for associations with intra-individual changes in BMI and weight.Results:A higher average annual concentration was associated with risk of incident obesity [; (95% CI: 1.06, 1.11)] and the risk of a () increase in weight [ (95% CI: 1.06, 1.08)] and with higher intra-individual changes in BMI [ (95% CI: 0.139, 0.142)] and weight [ (95% CI: 0.955, 0.981)]. Nonlinear exposure–response models indicated associations at concentrations below the national standard of . As expected, a negative exposure control (ambient air sodium) was not associated with obesity or weight gain. Associations were consistent in direction and magnitude across sensitivity analyses that included alternative outcomes and exposures assigned at different spatial resolutions.Discussion: air pollution was associated with the risk of obesity and weight gain in a large predominantly male cohort of U.S. Veterans. Discussions about health effects of should include its association with obesity, and deliberations about the epidemiology of obesity should consider its association with . Investigation in other cohorts will deepen our understanding of the relationship between and weight gain and obesity. https://doi.org/10.1289/EHP7944

A Population-Based Cohort Study of Respiratory Disease and Long-Term Exposure to Iron and Copper in Fine Particulate Air Pollution and Their Combined Impact on Reactive Oxygen Species Generation in Human Lungs.

Metal components in fine particulate matter (PM2.5) from nontailpipe emissions may play an important role in underlying the adverse respiratory effects of PM2.5. We investigated the associations between long-term exposure to iron (Fe) and copper (Cu) in PM2.5 and their combined impact on reactive oxygen species (ROS) generation in human lungs, and the incidence of asthma, chronic obstructive pulmonary disease (COPD), COPD mortality, pneumonia mortality, and respiratory mortality. We conducted a population-based cohort study of ∼0.8 million adults in Toronto, Canada. Land-use regression models were used to estimate the concentrations of Fe, Cu, and ROS. Outcomes were ascertained using validated health administrative databases. We found positive associations between long-term exposure to Fe, Cu, and ROS and the risks of all five respiratory outcomes. The associations were more robust for COPD, pneumonia mortality, and respiratory mortality than for asthma incidence and COPD mortality. Stronger associations were observed for ROS than for either Fe or Cu. In two-pollutant models, adjustment for nitrogen dioxide somewhat attenuated the associations while adjustment for PM2.5 had little influence. Long-term exposure to Fe and Cu in PM2.5 and estimated ROS concentration in lung fluid was associated with increased incidence of respiratory diseases, suggesting the adverse respiratory effects of nontailpipe emissions.

Fine particulate matter concentration and composition and the incidence of childhood asthma

BackgroundSeveral studies have found positive associations between outdoor fine particulate air pollution (≤2.5 μm, PM2.5) and childhood asthma incidence. However, the impact of PM2.5 composition on children’s respiratory health remains uncertain. ObjectiveWe examined whether joint exposure to PM2.5 mass concentrations and its major chemical components was associated with childhood asthma development. MethodsWe conducted a population-based cohort study by identifying 1,130,855 singleton live births occurring between 2006 and 2014 in the province of Ontario, Canada. Concentrations of PM2.5 and its seven major chemical components were assigned to participants based on their postal codes using chemical transport models and remote sensing. The joint impact of outdoor PM2.5 concentrations and its major components and childhood asthma incidence (up to age 6) were estimated using Cox proportional hazards models, allowing for potential nonlinearity. ResultsWe identified 167,080 children who developed asthma before age 6. In adjusted models, outdoor PM2.5 mass concentrations during childhood were associated with increased incidence of childhood asthma (Hazard Ratio (HR) for each 1 μg/m3 increase = 1.026, 95% CI: 1.021–1.031). We found that the joint effects of PM2.5 and its components on childhood asthma incidence may be 24% higher than the conventional approach. Specific components/source markers such as black carbon, ammonium, and nitrate appeared to play an important role. ConclusionsEarly life exposure to PM2.5 and its chemical components is associated with an increased risk of asthma development in children. The heterogeneous nature of PM2.5 should be considered in future health risk assessments.

The Benefits of Intensive Versus Standard Blood Pressure Treatment According to Fine Particulate Matter Air Pollution Exposure: A Post Hoc Analysis of SPRINT.

Fine particulate matter <2.5 µm (PM2.5) air pollution is implicated in global mortality, especially from cardiovascular causes. A large body of evidence suggests a link between PM2.5 and elevation in blood pressure (BP), with the latter implicated as a potential mediator of cardiovascular events. We sought to determine if the outcomes of intensive BP lowering (systolic BP <120 mm Hg) on cardiovascular events are modified by PM2.5 exposure in the SPRINT (Systolic BP Intervention Trial). We linked annual PM2.5 exposure estimates derived from an integrated model to subjects participating in SPRINT. We evaluated the effect of intensive BP lowering by PM2.5 exposure on the primary outcome in SPRINT using cox-proportional hazard models. A total of 9286 participants were linked to PM2.5 levels (mean age 68±9 years). Intensive BP-lowering decreased risk of the primary outcome more among patients exposed to higher PM2.5 (Pinteraction=0.047). The estimate for lowering of primary outcome was numerically lower in the highest than in the lower quintiles. The benefits of intensive BP-lowering were larger among patients chronically exposed to PM2.5 levels above US National Ambient Air Quality Standards of 12 µg/m3 (hazard ratio, 0.47 [95% CI, 0.29-0.74]) compared with those living in cleaner locations (hazard ratio, 0.81 [95% CI, 0.68-0.97]), Pinteraction=0.037. This exploratory nonprespecified post hoc analysis of SPRINT suggests that the benefits of intensive BP lowering on the primary outcome was greater in patients exposed to higher PM2.5, suggesting that the magnitude of benefit may depend upon the magnitude of antecedent PM2.5 exposure.