Ambient Particulate Matter Air Pollution Research Articles

Penalized distributed lag interaction model: Air pollution, birth weight, and neighborhood vulnerability

AbstractMaternal exposure to air pollution during pregnancy has a substantial public health impact. Epidemiological evidence supports an association between maternal exposure to air pollution and low birth weight. A popular method to estimate this association while identifying windows of susceptibility is a distributed lag model (DLM), which regresses an outcome onto exposure history observed at multiple time points. However, the standard DLM framework does not allow for modification of the association between repeated measures of exposure and the outcome. We propose a distributed lag interaction model that allows modification of the exposure‐time‐response associations across individuals by including an interaction between a continuous modifying variable and the exposure history. Our model framework is an extension of a standard DLM that uses a cross‐basis, or bi‐dimensional function space, to simultaneously describe both the modification of the exposure‐response relationship and the temporal structure of the exposure data. Through simulations, we showed that our model with penalization out‐performs a standard DLM when the true exposure‐time‐response associations vary by a continuous variable. Using a Colorado, USA birth cohort, we estimated the association between birth weight and ambient fine particulate matter air pollution modified by an area‐level metric of health and social adversities from Colorado EnviroScreen.

Abstract 12441: Ambient Fine Particulate Matter Air Pollution but Not Ozone is Associated With Elevated Risk of All-Cause Hospitalization in Patients With a Prior Diagnosis of Atrial Fibrillation

Introduction: Short-term increases (days to weeks) in fine particulate matter (PM 2.5 ) air pollution are associated with atrial fibrillation (AF) episodes. We previously reported that PM 2.5 was not associated with severe AF measured as emergency or inpatient hospitalization for the primary diagnosis of AF. Mild AF, though, may influence all-cause hospitalizations. This study evaluated if short-term increases in PM 2.5 and ozone were associated with all-cause hospitalization at 11 Intermountain Health hospitals in patients with AF, and if this differed between wildfire (June-Oct.) and winter inversion (Nov.-March) seasons. Methods: Patients carrying an AF diagnosis (N=347,157) were evaluated for all-cause hospitalization and, secondarily, AF hospitalization (N=25,601) and first AF diagnosis (N=77,893). PM 2.5 levels were measured from January 1, 1999 to March 31, 2022 (ozone: 2006-2022) in subjects residing on Utah’s Wasatch Front. Using the case-crossover design that matched individual-level characteristics, Poisson regression also adjusted for weather variables. Results: Mean age was 72±15 years and 51.0% were female. Overall, PM 2.5 increases at a lag of 0 days, 1 day, 3-day moving average (mAvg) (days 0-2), and 7-day mAvg (days 0-6) were associated with all-cause hospitalization [respectively: odds ratio (OR)=1.010, 1.008, 1.011, 1.009 per +10 μg/m 3 ; p=0.0004, 0.006, 0.0004, 0.028]. Associations differed by seasons (Figure). Regressions entering both ozone and PM 2.5 mildly increased PM 2.5 ORs for all-cause hospitalization. PM 2.5 was not associated with first AF diagnosis. Increases in ozone were not associated with higher risk of any outcome. Conclusions: Short-term increases in PM 2.5 air pollution were associated with all-cause hospitalization in patients with a prior AF diagnosis. Lag structure varied for wildfire and inversion seasons, with greater effect sizes in wildfire season. Increases in ozone did not associate with elevated risk.

Abstract 12409: Ambient Fine Particulate Matter and Ozone Air Pollution Are Differentially Associated With Hospitalization for Unstable Angina and Acute Myocardial Infarction During Wildfire and Inversion Seasons

Background: Short-term increases (days to weeks) in fine particulate matter (PM 2.5 ) air pollution are associated with hospitalization for acute coronary syndromes (ACS). A changing climate is shifting sources of PM 2.5 toward summer wildfires in the western US. This study evaluated if short-term increases in PM 2.5 and ozone were associated with ACS risks in wildfire (June-October) and winter inversion (Nov.-March) seasons. Methods: Case-crossover analyses examined N=21,414 subjects with emergency or inpatient hospitalization at 11 Intermountain hospitals for ACS, including the primary diagnosis of myocardial infarction (AMI, n=20,287) or unstable angina (USA, n=1,127). PM 2.5 data were collected in January 1, 1999 to March 31, 2022 (ozone: 2006-2022) from community monitors on Utah’s Wasatch Front. Odds ratios (OR) and 95% confidence intervals (CI) were computed by Poisson regression with adjustment for weather data. Results: Subjects averaged 66±14 years of age and 31.0% were female. Overall PM 2.5 increases were associated with concurrent day (lag 0 days) ACS hospitalizations (OR=1.024 per +10 μg/m 3 , CI: 1.004, 1.043, p=0.019), driven by AMI (OR=1.025 per +10 μg/m 3 , CI: 1.004, 1.045, p=0.017). USA admissions were delayed to the second week [lag moving average (mAvg) days 7-13] after PM 2.5 increases (OR=1.090 per +10 μg/m 3 , CI: 1.024, 1.159, p=0.007) and PM 2.5 associations with USA were strengthened by adjustment for ozone. Analyzed by wildfire and inversion seasons, PM 2.5 associations differed for AMI and USA (Figure). Short-term increases in ozone in wildfire season were associated with lower USA risk at lag 1, lag 2, 3-day mAvg 0-2, and 1-week mAvg 0-6 and lower AMI risk at mAvg 7-13, but not with inversion season risks. Conclusions: Short-term increases in PM 2.5 air pollution were associated with ACS hospitalizations for AMI and USA, with patterns of risk differing between wildfire and inversion seasons. Ozone increases were not associated with greater risk.

Ambient particulate matter air pollution exposure and ovarian cancer incidence in the USA: An ecological study.

To investigate associations between air particulate matter of ≤2.5 μm in diameter (PM2.5 ) and ovarian cancer. County-level ecological study. Surveillance, epidemiology, and end results from a collection of state-level cancer registries across 744 counties. Data from the Environmental Protection Agency's network for PM2.5 monitoring was used to calculate trailing 5- and 10-year PM2.5 county-level values. County-level data on demographic characteristics were obtained from the American Community Survey. A total of 98 751 patients with histologically confirmed ovarian cancer as a primary malignancy from 2000 to 2016. Generalised linear regression models were developed to estimate the association between PM2.5 and PM10 levels, over 5- and 10-year periods of exposure, and ovarian cancer risk, after accounting for county-level covariates. Risk ratios for associations between ovarian cancer (both overall and specifically epithelial ovarian cancer) and PM2.5 levels. For the 744 counties included, the average PM2.5 level from 1990 through 2018 was 11.75 μg/m3 (SD = 3.7) and the average PM10 level was 22.7 μg/m3 (SD = 5.7). After adjusting for county-level covariates, the overall annualised ovarian cancer incidence was significantly associated with increases in 5-year PM2.5 (RR = 1.11 per 10 units (μg/m3 ) increase, 95% CI 1.06-1.16). Similarly, when the analysis was limited to epithelial cell tumours and adjusted for county-level covariates there was a significant association with trailing 5-year PM2.5 exposure models (RR = 1.12 per 10 units increase, 95% CI 1.08-1.17). Likewise, 10-year PM2.5 exposure was associated with ovarian cancer overall and with epithelial ovarian cancer. Higher county-level ambient PM2.5 levels are associated with 5- and 10-year incidences of ovarian cancer, as measurable in an ecological study.

Associations Between Hourly Ambient Particulate Matter Air Pollution and Ambulance Emergency Calls: Time-Stratified Case-Crossover Study.

Associations between short-term exposure to ambient particulate matter (PM) air pollutants and mortality or hospital admissions have been well-documented in previous studies. Less is known about the associations of hourly exposure to PM air pollutants with ambulance emergency calls (AECs) for all causes and specific causes by conducting a case-crossover study. In addition, different patterns of AECs may be attributed to different seasons and daytime or nighttime periods. In this study, we quantified the risk of all-cause and cause-specific AECs associated with hourly PM air pollutants between January 1, 2013, and December 31, 2019, in Shenzhen, China. We also examined whether the observed associations of PM air pollutants with AECs for all causes differed across strata defined by sex, age, season, and the time of day. We used ambulance emergency dispatch data and environmental data between January 1, 2013, and December 31, 2019, from the Shenzhen Ambulance Emergency Centre and the National Environmental Monitor Station to conduct a time-stratified case-crossover study to estimate the associations of air pollutants (ie, PM with an aerodynamic diameter less than 2.5 µm [PM2.5] or 10 µm [PM10]) with all-cause and cause-specific AECs. We generated a well-established, distributed lag nonlinear model for nonlinear concentration response and nonlinear lag-response functions. We used conditional logistic regression to estimate odds ratios with 95% CIs, adjusted for public holidays, season, the time of day, the day of the week, hourly temperature, and hourly humidity, to examine the association of all-cause and cause-specific AECs with hourly air pollutant concentrations. A total of 3,022,164 patients were identified during the study period in Shenzhen. Each IQR increase in PM2.5 (24.0 µg/m3) and PM10 (34.0 µg/m3) concentrations over 24 hours was associated with an increased risk of AECs (PM2.5: all-cause, 1.8%, 95% CI 0.8%-2.4%; PM10: all-cause, 2.0%, 95% CI 1.1%-2.9%). We observed a stronger association of all-cause AECs with PM2.5 and PM10 in the daytime than in the nighttime (PM2.5: daytime, 1.7%, 95% CI 0.5%-3.0%; nighttime, 1.4%, 95% CI 0.3%-2.6%; PM10: daytime, 2.1%, 95% CI 0.9%-3.4%; nighttime, 1.7%, 95% CI 0.6%-2.8%) and in the older group than in the younger group (PM2.5: 18-64 years, 1.4%, 95% CI 0.6%-2.1%; ≥65 years, 1.6%, 95% CI 0.6%-2.6%; PM10: 18-64 years, 1.8%, 95% CI 0.9%-2.6%; ≥65 years, 2.0%, 95% CI 1.1%-3.0%). The risk of all-cause AECs increased consistently with increasing concentrations of PM air pollutants, showing a nearly linear relationship with no apparent thresholds. PM air pollution increase was associated with a higher risk of all-cause AECs and cardiovascular diseases-, respiratory diseases-, and reproductive illnesses-related AECs. The results of this study may be valuable to air pollution attributable to the distribution of emergency resources and consistent air pollution control.

Fine particulate matter (PM2.5)-induced pulmonary oxidative stress contributes to increases in glucose intolerance and insulin resistance in a mouse model of circadian dyssynchrony

Results of human and animal studies independently suggest that either ambient fine particulate matter (PM2.5) air pollution exposure or a disturbed circadian rhythm (circadian dyssynchrony) are important contributing factors to the rapidly evolving type-2-diabetes (T2D) epidemic. The objective of this study is to investigate whether circadian dyssynchrony increases the susceptibility to PM2.5 and how PM2.5 affects metabolic health in circadian dyssynchrony. We examined systemic and organ-specific changes in glucose homeostasis and insulin sensitivity in mice maintained on a regular (12/12 h light/dark) or disrupted (18/6 h light/dark, light-induced circadian dyssynchrony, LICD) light cycle exposed to air or concentrated PM2.5 (CAP, 6 h/day, 30 days). Exposures during Zeitgeber ZT3–9 or ZT11–17 (Zeitgeber in circadian time, ZT0 = begin of light cycle) tested for time-of-day PM2.5 sensitivity (chronotoxicity). Mice transgenic for lung-specific overexpression of extracellular superoxide dismutase (ecSOD-Tg) were used to assess the contribution of CAP-induced pulmonary oxidative stress. Both, CAP exposure from ZT3–9 or ZT11–17, decreased glucose tolerance and insulin sensitivity in male mice with LICD, but not in female mice or in mice kept on a regular light cycle. Although changes in glucose homeostasis in CAP-exposed male mice with LICD were not associated with obesity, they were accompanied by white adipose tissue (WAT) inflammation, impaired insulin signaling in skeletal muscle and liver, and systemic and pulmonary oxidative stress. Preventing CAP-induced oxidative stress in the lungs mitigated the CAP-induced decrease in glucose tolerance and insulin sensitivity in LICD. Our results demonstrate that circadian dyssynchrony is a novel susceptibility state for PM2.5 and suggest that PM2.5 by inducing pulmonary oxidative stress increases glucose intolerance and insulin resistance in circadian dyssynchrony.

Long-term air pollution and risk of amyotrophic lateral sclerosis mortality in the Women's Health Initiative cohort

BackgroundAmyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder with no cure. Although the etiology of sporadic ALS is largely unknown, environmental exposures may affect ALS risk. ObjectiveWe investigated relationships between exposure to long-term ambient particulate matter (PM) and gaseous air pollution (AP) and ALS mortality. MethodsWithin the Women's Health Initiative (WHI) cohort of 161,808 postmenopausal women aged 50–79 years at baseline (1993–1998), we performed a nested case-control study of 256 ALS deaths and 2486 matched controls with emphasis on PM constituents (PM2.5, PM10, and coarse PM [PM10-2.5]) and gaseous pollutants (NOx, NO2, SO2, and ozone). Time-varying AP exposures estimates were averaged 5, 7.5, and 10 years prior to ALS death using both a GIS-based spatiotemporal generalized additive mixed model and ordinary kriging (empirical and multiple imputation, MI). Conditional logistic regression was used to estimate the relative risk of ALS death. ResultsIn general, PM2.5 and PM10-related risks were not significantly elevated using either method. However, for PM10-2.5, odds ratios (ORs) were >1.0 for both methods at all time periods using MI and empirical data for PM10-2.5 (coarse) except for 5 and 7.5 years using the kriging method with covariate adjustment. ConclusionThis investigation adds to the body of information on long-term ambient AP exposure and ALS mortality. Specifically, the 2019 US Environmental Protection Agency (EPA) Integrated Science Assessment summarized the neurotoxic effects of PM2.5, PM10, and PM10-2.5. The conclusion was that evidence of an effect of coarse PM is suggestive but the data is presently not sufficient to infer a causal relationship. Further research on AP and ALS is warranted. As time from symptom onset to death in ALS is ∼2–4 years, earlier AP measures may also be of interest to ALS development. This is the first study of ALS and AP in postmenopausal women controlling for individual-level confounders.

Ambient Air Pollution and Preeclampsia Onset in Massachusetts, United States

Background and Aim: Ambient particulate matter and gaseous air pollution have been linked to preeclampsia. However, despite the recognition that preeclampsia is likely a heterogenous syndrome with distinct pathogenic mechanisms, few studies have examined the association between air pollution and subtypes of preeclampsia. Our objective was to examine differential impacts of air pollution on early- vs. late-onset (i.e., diagnosed in or after 34th gestation week) preeclampsia among pregnant women in the Boston, Massachusetts based biorepository, LIFECODES. Methods: Preeclampsia was diagnosed according to the American College of Obstetrics and Gynecologists guidelines and each case was reviewed by a panel Maternal–Fetal Medicine–certified physicians. Women’s exposures to ozone and fine particulate matter (PM2.5) during pregnancy were estimated based on geocoded residential addresses using U.S. Environmental Protection Agency’s Fused Air Quality Surface Using Downscaling Files. Cox proportional hazards models and multinomial logistic regression were used to examine the associations of ozone and PM2.5 with preeclampsia and its onsets. Hazard ratio (HR), odds ratio (OR), and 95% confidence interval (95% CI) for each interquartile range increase in exposures were reported. Results: A total of 3,316 pregnant women were included. In the cox model, higher exposures to ozone during pregnancy were associated with higher hazard being diagnosed with preeclampsia (HR: 1.67, 95% CI: 1.16, 2.40). In the multinomial logistic regression model, ozone was significantly associated with early-onset preeclampsia (OR: 2.50, 95% CI: 1.48, 4.21) but not late-onset preeclampsia (OR: 1.34, 95% CI: 0.96, 1.88), and PM2.5 was significantly associated with both early- (OR: 1.62, 95% CI: 1.07, 2.45) and late-onset preeclampsia (OR: 1.32, 95% CI: 1.02, 1.71). Conclusions: Exposures to ozone and PM2.5 were significantly associated preeclampsia. This association was significant with respect to ozone exposure in the earlier onset, but not later onset, preeclampsia. This study highlights the importance of assessing the heterogeneity in preeclampsia.

Estimates, trends, and drivers of the global burden of type 2 diabetes attributable to PM2·5 air pollution, 1990–2019: an analysis of data from the Global Burden of Disease Study 2019

SummaryBackgroundExperimental and epidemiological studies indicate an association between exposure to particulate matter (PM) air pollution and increased risk of type 2 diabetes. In view of the high and increasing prevalence of diabetes, we aimed to quantify the burden of type 2 diabetes attributable to PM2·5 originating from ambient and household air pollution.MethodsWe systematically compiled all relevant cohort and case-control studies assessing the effect of exposure to household and ambient fine particulate matter (PM2·5) air pollution on type 2 diabetes incidence and mortality. We derived an exposure–response curve from the extracted relative risk estimates using the MR-BRT (meta-regression—Bayesian, regularised, trimmed) tool. The estimated curve was linked to ambient and household PM2·5 exposures from the Global Burden of Diseases, Injuries, and Risk Factors Study 2019, and estimates of the attributable burden (population attributable fractions and rates per 100 000 population of deaths and disability-adjusted life-years) for 204 countries from 1990 to 2019 were calculated. We also assessed the role of changes in exposure, population size, age, and type 2 diabetes incidence in the observed trend in PM2·5-attributable type 2 diabetes burden. All estimates are presented with 95% uncertainty intervals.FindingsIn 2019, approximately a fifth of the global burden of type 2 diabetes was attributable to PM2·5 exposure, with an estimated 3·78 (95% uncertainty interval 2·68–4·83) deaths per 100 000 population and 167 (117–223) disability-adjusted life-years (DALYs) per 100 000 population. Approximately 13·4% (9·49–17·5) of deaths and 13·6% (9·73–17·9) of DALYs due to type 2 diabetes were contributed by ambient PM2·5, and 6·50% (4·22–9·53) of deaths and 5·92% (3·81–8·64) of DALYs by household air pollution. High burdens, in terms of numbers as well as rates, were estimated in Asia, sub-Saharan Africa, and South America. Since 1990, the attributable burden has increased by 50%, driven largely by population growth and ageing. Globally, the impact of reductions in household air pollution was largely offset by increased ambient PM2·5.InterpretationAir pollution is a major risk factor for diabetes. We estimated that about a fifth of the global burden of type 2 diabetes is attributable PM2·5 pollution. Air pollution mitigation therefore might have an essential role in reducing the global disease burden resulting from type 2 diabetes.FundingBill & Melinda Gates Foundation.

Spatial environmental factors predict cardiovascular and all-cause mortality: Results of the SPACE study.

BackgroundEnvironmental exposures account for a growing proportion of global mortality. Large cohort studies are needed to characterize the independent impact of environmental exposures on mortality in low-income settings.MethodsWe collected data on individual and environmental risk factors for a multiethnic cohort of 50,045 individuals in a low-income region in Iran. Environmental risk factors included: ambient fine particular matter air pollution; household fuel use and ventilation; proximity to traffic; distance to percutaneous coronary intervention (PCI) center; socioeconomic environment; population density; local land use; and nighttime light exposure. We developed a spatial survival model to estimate the independent associations between these environmental exposures and all-cause and cardiovascular mortality.FindingsSeveral environmental factors demonstrated associations with mortality after adjusting for individual risk factors. Ambient fine particulate matter air pollution predicted all-cause mortality (per μg/m3, HR 1.20, 95% CI 1.07, 1.36) and cardiovascular mortality (HR 1.17, 95% CI 0.98, 1.39). Biomass fuel use without chimney predicted all-cause mortality (reference = gas, HR 1.23, 95% CI 0.99, 1.53) and cardiovascular mortality (HR 1.36, 95% CI 0.99, 1.87). Kerosene fuel use without chimney predicted all-cause mortality (reference = gas, HR 1.09, 95% CI 0.97, 1.23) and cardiovascular mortality (HR 1.19, 95% CI 1.01, 1.41). Distance to PCI center predicted all-cause mortality (per 10km, HR 1.01, 95% CI 1.004, 1.022) and cardiovascular mortality (HR 1.02, 95% CI 1.004, 1.031). Additionally, proximity to traffic predicted all-cause mortality (HR 1.13, 95% CI 1.01, 1.27). In a separate validation cohort, the multivariable model effectively predicted both all-cause mortality (AUC 0.76) and cardiovascular mortality (AUC 0.81). Population attributable fractions demonstrated a high mortality burden attributable to environmental exposures.InterpretationSeveral environmental factors predicted cardiovascular and all-cause mortality, independent of each other and of individual risk factors. Mortality attributable to environmental factors represents a critical opportunity for targeted policies and programs.

The dynamics of cardiovascular and respiratory deaths attributed to long-term PM2.5 exposures in global megacities

Exposure to ambient fine particulate matter (PM2.5) air pollution is a significant driver of premature deaths. We estimate the number of cardiovascular and respiratory (CR) premature deaths attributed to long-term exposure to PM2.5 in 33 global megacities based on long-term remotely sensed observations from 2000 to 2019. Our analysis uses high-resolution (0.01 degree) PM2.5 concentration data and cause-specific integrated exposure-response (IER) functions developed for the Global Burden of Disease Project. From 2000 to 2019, PM2.5-related CR death rates per 1000 people increased in 6 of 33 megacities, decreased in 9, and remained constant in 18 megacities. The increase in PM2.5-related CR mortality in 11 megacities located in South and East Asia during the period 2000–2019 can be attributed to the increases in PM2.5 concentrations. All 33 megacities could avoid 30,248 (9 %), 62,989 (20 %), 128,457 (40 %), 198,462 (62 %) and all of the estimated 322,515 CR deaths attributed to PM2.5 pollution in 2019 if they were to attain the World Health Organization's four interim PM2.5 targets (IT-1, IT-2, IT-3, and IT-4) and the new air quality guideline (AQG), respectively. Major improvements in air quality are needed to reduce the number of CR deaths attributed to PM2.5 in South and East Asia, in addition to ny reductions that would likely follow shifts in the population structures of these megacities moving forward.

Ambient particulate matter air pollution and stillbirth in Ghana: A difference-in-differences approach

Sub-Saharan African countries, including Ghana, are known hotspots for fine particulate matter air pollution (PM2.5) and stillbirths but lacked epidemiologic evidence. We investigated the association between PM2.5 and stillbirth in Ghana. District-level stillbirth data were obtained from the Ghana Health Service for all 260 local districts from 2012 to 2019 for a total of 5,229,338 births, including 81,611 stillbirths. Spatiotemporal datasets, including satellite-derived PM2.5, temperature, population density, and gross domestic product were linked with the birth data. We applied a variant difference-in-differences design with conditional quasi-Poisson regression to estimate the risk of stillbirth associated with annual PM2.5 concentrations. We adjusted for relevant environmental and sociodemographic factors and performed subgroup analyses by population density and household air pollution. The average district-level annual stillbirth incidence was 29 (standard deviation = 55) per 1000 births. The annual average PM2.5 concentration was 59.97 μg/m3 (standard deviation = 9.75). Every 10 μg/m3 increment in annual average PM2.5 was associated with a 3% risk of stillbirth (RR); 1.03 (95% CI: 0.97, 1.09) for all-source PM2.5 and 2% risk each for anthropogenic (RR = 1.02, 95% CI: 0.96, 1.07) and natural (RR = 1.02, 95% CI: 0.94, 1.11) sources. The association was higher for moderate or high subgroup, relative to low subgroup and higher in natural than anthropogenic sources of PM2.5 exposures. Thus, there was some evidence for an adverse association between PM2.5 exposure and stillbirth but estimates were less precise. Given that the district-level variation may be underpowered, stronger risk is expected in future high-quality individual-level longitudinal cohort studies in Ghana.

Ambient Air Pollution and Dysanapsis: Associations with Lung Function and Chronic Obstructive Pulmonary Disease in the Canadian Cohort Obstructive Lung Disease Study.

Rationale: Outdoor air pollution is a potential risk factor for lower lung function and chronic obstructive pulmonary disease (COPD). Little is known about how airway abnormalities and lung growth might modify this relationship. Objectives: To evaluate the associations of ambient air pollution exposure with lung function and COPD and examine possible interactions with dysanapsis. Methods: We made use of cross-sectional postbronchodilator spirometry data from 1,452 individuals enrolled in the CanCOLD (Canadian Cohort Obstructive Lung Disease) study with linked ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) air pollution estimates. Dysanapsis, or the ratio of the airway-to-lung volume calculated from thoracic computed tomography images, was used to examine possible interactions. Measurements and Main Results: In adjusted models, 101.7 ml (95% confidence interval [CI], -166.2 to -37.2) and 115.0 ml (95% CI, -196.5 to -33.4) lower FEV1 were demonstrated per increase of 2.4 ug/m3 PM2.5 and 9.2 ppb NO2, respectively. Interaction between air pollution and dysanapsis was not statistically significant when modeling the airway-to-lung ratio as a continuous variable. However, a 109.8 ml (95% CI, -209.0 to -10.5] lower FEV1 and an 87% (95% CI, 12% to 213%) higher odds of COPD were observed among individuals in the lowest, relative to highest, airway-to-lung ratio, per 2.4 μg/m3 increment of PM2.5. Conclusions: Ambient air pollution exposure was associated with lower lung function, even at relatively low concentrations. Individuals with dysanaptic lung growth might be particularly susceptible to inhaled ambient air pollutants, especially those at the extremes of dysanapsis.

Greenness alleviates the effects of ambient particulate matter on the risks of high blood pressure in children and adolescents

Both ambient particulate matter (PM) and decrease of greenness have been suggested as risk factors for high blood pressure (HBP) in children and adolescents. But most evidence were from cross-sectional studies with limited data from prospective cohorts. In this cohort study, we included 588,004 children and adolescents aged 7 to 18 years without HBP from 2005 to 2018 in Beijing (240,081) and Zhongshan (347,923) city of China. The cumulative incidence of HBP was 32.04%, and incidence rate was 14.86 per 100 person-year. After adjustment for confounders, the ten-unit increase in PM1, PM2.5, and PM10 exposure was significantly associated with 43%, 70%, and 43%- higher risks of HBP, respectively, but the 0.1-unit increase in NDVI exposure was significantly associated with a 25% lower risk of HBP. The HRs of PM1 on the HBP risk were 1.486 and 1.150 in the low and the high-level of greenness, and they were 2.635 and 2.507 for PM2.5, and for PM10 1.367 and 1.702 in the two groups. The attributable fraction (AFs) of PM1, PM2.5, and PM10 on HBP incidents were 13.74%, 40.08%, and 15.47% in the low-level of greenness, which simultaneously was higher than those in the high-level of greenness (AF = 4.62%, 17.28%, and 9.96%). The exposure to higher ambient PM air pollution and lower greenness around schools were associated with a higher risk of HBP in children and adolescents, but higher greenness alleviated the adverse effects of ambient PM1 and PM2.5 on the HBP risks. Our findings highlighted a synergic strategy in preventing childhood HBP by decreasing air pollution reduction and improving greenness concurrently.

Health impacts of air pollution exposure from 1990 to 2019 in 43 European countries

Air pollution is the fourth greatest overall risk factor for human health. Despite declining levels in Europe, air pollution still represents a major health and economic burden. We collected data from the Global Burden of Disease Study 2019 regarding overall, as well as ischemic heart disease (IHD), stroke, and tracheal, bronchus and lung cancer-specific disability adjusted life years (DALYs), years of life lost (YLL) and mortality attributable to air pollution for 43 European countries between 1990 and 2019. Concentrations of ambient particulate matter (aPM2.5), ozone, and household air pollution from solid fuels were obtained from State of Global Air 2020. We analysed changes in air pollution parameters, as well as DALYs, YLL, and mortality related to air pollution, also taking into account gross national income (GNI) and socio-demographic index (SDI). Using a novel calculation, aPM2.5 ratio (PMR) change and DALY rate ratio (DARR) change were used to assess each country’s ability to decrease its aPM2.5 pollution and DALYs to at least the extent of the European median decrease within the analysed period. Finally, we created a multiple regression model for reliably predicting YLL using aPM2.5 and household air pollution. The average annual population-weighted aPM2.5 exposure in Europe in 1990 was 20.8 μg/m3 (95% confidence interval (CI) 18.3–23.2), while in 2019 it was 33.7% lower at 13.8 μg/m3 (95% CI 12.0–15.6). There were in total 368 006 estimated deaths in Europe in 2019 attributable to air pollution, a 42.4% decrease compared to 639 052 in 1990. The majority (90.4%) of all deaths were associated with aPM2.5. IHD was the primary cause of death making up 44.6% of all deaths attributable to air pollution. The age-standardised DALY rate and YLL rate attributable to air pollution were more than 60% lower in 2019 compared to 1990. There was a strong positive correlation (r = 0.911) between YLL rate and aPM2.5 pollution in 2019 in Europe. Our multiple regression model predicts that for 10% increase in aPM2.5, YLL increases by 16.7%. Furthermore, 26 of 43 European countries had a positive DARR change. 31 of 43 European countries had a negative PMR change, thus not keeping up with the European median aPM2.5 concentration decrease. When categorising countries by SDI and GNI, countries in the higher brackets had significantly lower aPM2.5 concentration and DALY rate for IHD and stroke. Overall, air pollution levels, air pollution-related morbidity and mortality have decreased considerably in Europe in the last three decades. However, with the growing European population, air pollution remains an important public health and economic issue. Policies targeting air pollution reduction should continue to be strongly enforced to further reduce one of the greatest risk factors for human health.

Association of Ambient Fine Particulate Matter Air Pollution With Kidney Transplant Outcomes

Increased levels of ambient fine particulate matter (PM2.5) air pollution are associated with increased risks for detrimental health outcomes, but risks for patients with kidney transplants (KTs) remain unknown. To investigate the association of PM2.5 exposure with KT outcomes. This retrospective cohort study was conducted using data on patients who received KTs from 2004 to 2016 who were identified in the national US transplant registry and followed up through March 2021. Multiple databases were linked to obtain data on PM2.5 concentration, KT outcomes, and patient clinical, transplant, and contextual factors. Data were analyzed from April 2020 through July 2021. Exposures included post-KT time-dependent annual mean PM2.5 level (in 10 μg/m3) and mean PM2.5 level in the year before KT (ie, baseline levels) in quartiles, as well as baseline annual mean PM2.5 level (in 10 μg/m3). Acute kidney rejection (ie, rejection within 1 year after KT), time to death-censored graft failure, and time to all-cause death. Multivariable logistic regression for kidney rejection and Cox analyses with nonlinear assessment of exposure-response for death-censored graft failure and all-cause death were performed. The national burden of graft failure associated with PM2.5 levels greater than the Environmental Protection Agency recommended level of 12 μg/m3 was estimated. Among 112 098 patients with KTs, 70 522 individuals (62.9%) were older than age 50 years at the time of KT, 68 117 (60.8%) were men, and the median (IQR) follow-up was 6.0 (3.9-8.9) years. There were 37 265 Black patients (33.2%), 17 047 Hispanic patients (15.2%), 48 581 White patients [43.3%]), and 9205 patients (8.2%) of other race or ethnicity. The median (IQR) baseline PM2.5 level was 9.8 (8.3-11.9) μg/m3. Increased baseline PM2.5 level, compared with quartile 1 baseline PM2.5 level, was not associated with higher odds of acute kidney rejection for quartile 2 (adjusted odds ratio [aOR], 0.99; 95% CI, 0.92-1.06) but was associated with increased odds for quartile 3 (aOR, 1.11; 95% CI, 1.04-1.20) and quartile 4 (aOR, 1.13; 95% CI, 1.05-1.23). Nonlinear assessment of exposure-response for graft failure and death showed no evidence for nonlinearity. Increased PM2.5 levels were associated with increased risk of death-censored graft failure (adjusted hazard ratio [aHR] per 10 μg/m3 increase, 1.17; 95% CI, 1.09-1.25) and all-cause death (aHR per 10 μg/m3 increase, 1.21; 95% CI, 1.14-1.28). The national burden of death-censored graft failure associated with PM2.5 above 12 μg/m3 was 57 failures (95% uncertainty interval, 48-67 failures) per year among patients with KTs. This cohort study found that PM2.5 level was an independent risk factor associated with acute rejection, graft failure, and death among patients with KTs. These findings suggest that efforts toward decreasing levels of PM2.5 concentration may be associated with improved outcomes after KT.

Long-term particulate matter exposure and bone mineral density in the Women’s Health Initiative

BACKGROUND AND AIM: Ambient particulate matter air pollution 10 μm (PM10) concentrations have been associated with several outcomes, but few studies have examined their association with bone mineral density (BMD). Previous studies have suggested an effect of air pollution on bone health, but none has evaluated its impact in postmenopausal women. METHODS: We studied the longitudinal PM10-BMD association among 5,080 postmenopausal women in the Women’s Health Initiative Clinical Trials (WHI-CT). We used log-normal, ordinary kriging to estimate daily mean PM10 concentrations (μg/m3) at geocoded participant addresses. We averaged the means over 1-, 3-, and 5-year periods before triennial, dual energy X-ray absorptiometry (DXA) exams. We estimated total hip, lumbar spine, and total body BMD (in g/cm2) and their corresponding T-scores. We estimated the association of PM10 with BMD and T-scores using multivariable linear mixed models while controlling for correlation of repeated measures among participants and adjusting for age at DXA, race/ethnicity, income, body mass index (kg/m2), smoking status, coffee consumption, physical activity, CT randomization arm, US region of residence, and DXA equipment serial number. Multiple imputation was done for missing data. RESULTS:At baseline, women were aged 50-79 years, 78% were White, 40% were college graduates, and 71% earned $40,000/year. PM10 concentrations at baseline were cross-sectionally associated with both hip, lumbar spine, and whole-body BMD and T-scores (p 0.05). Longitudinally, lumbar spine BMD decreased 0.052 (95% confidence interval [95%CI]: 0.067, 0.037) g/cm2/year per 10% (2.21 ug/m3) increase in 5-year mean PM10 concentration. Lumbar spine T-scores also decreased with increasing duration of the 3- and 5-year mean PM10 concentrations: -0.362 Standard Deviations (SD) (-0.490, -0.235) and -0.512 SD (-0.649, -0.375), respectively. No association was seen with changes in hip or total body BMD. CONCLUSIONS:This is the first study suggesting an inverse association of ambient PM10 with BMD among postmenopausal women. KEYWORDS: Air pollution, long-term, PM10, bone mineral density, t-score, osteoporosis.

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.

Ambient particulate matter air pollution is associated with increased risk of papillary thyroid cancer

BackgroundThe association between exposure to air pollution and papillary thyroid carcinoma is unknown. We sought to estimate the relationship between long-term exposure to the fine (diameter ≤ 2.5 μm) particulate matter component of air pollution and the risk of papillary thyroid cancer. MethodsAdult (age ≥18) patients with newly diagnosed papillary thyroid carcinoma between January 1, 2013 and December 31, 2016 across a single health system were identified using electronic medical records. Data from 1,990 patients with papillary thyroid carcinoma were compared with 3,980 age- and sex-matched control subjects without any evidence of thyroid disease. Cumulative fine (diameter <2.5 μm) particulate matter exposure was estimated by incorporating patients’ residential zip codes into a deep learning neural networks model, which uses both meteorological and satellite-based measurements. Conditional logistic regression was performed to assess for association between papillary thyroid carcinoma and increasing fine (diameter ≤2.5 μm) particulate matter concentrations over 1, 2, and 3 years of cumulative exposure preceding papillary thyroid carcinoma diagnosis. ResultsIncreased odds of developing papillary thyroid carcinoma was associated with a 5 μg/m3 increase of fine (diameter ≤2.5 μm) particulate matter concentrations over 2 years (adjusted odds ratio = 1.18, 95% confidence interval: 1.00–1.40) and 3 years (adjusted odds ratio = 1.23, 95% confidence interval: 1.05–1.44) of exposure. This risk differed by smoking status (pinteraction = 0.04). Among current smokers (n = 623), the risk of developing papillary thyroid carcinoma was highest (adjusted odds ratio = 1.35, 95% confidence interval: 1.12–1.63). ConclusionIncreasing concentration of fine (diameter ≤2.5 μm) particulate matter in air pollution is significantly associated with the incidence of papillary thyroid carcinoma with 2 and 3 years of exposure. Our novel findings provide additional insight into the potential associations between risk factors and papillary thyroid carcinoma and warrant further investigation, specifically in areas with high levels of air pollution both nationally and internationally.

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.