Ambient Fine Particulate Matter Research Articles

Interplay of Climate Change and Air Pollution- Projection of the under-5 mortality attributable to ambient particulate matter (PM2.5) in South Asia

Ambient fine particulate matter (PM2.5) pollution is a leading health risk factor for children under- 5 years, especially in developing countries. South Asia is a PM2.5 hotspot, where climate change, a potential factor affecting PM2.5 pollution, adds a major challenge. However, limited evidence is available on under-5 mortality attributable to PM2.5 under different climate change scenarios. This study aimed to project under-5 mortality attributable to long-term exposure to ambient PM2.5 under seven air pollution and climate change mitigation scenarios in South Asia. We used a concentration-risk function obtained from a previous review to project under-5 mortality attributable to ambient PM2.5. With a theoretical minimum risk exposure level of 2.4 μg/m3, this risk function was linked to gridded annual PM2.5 concentrations from atmospheric modeling to project under-5 mortality from 2010 to 2049 under different climate change mitigation scenarios. The scenarios were developed from the Aim/Endues global model based on end-of-pipe (removing the emission of air pollutants at the source, EoP) and 2 °C target measures. Our results showed that, in 2010–2014, about 306.8 thousand under-5 deaths attributable to PM2.5 occurred in South Asia under the Reference (business as usual) scenario. The number of deaths was projected to increase in 2045–2049 by 36.6% under the same scenario and 7.7% under the scenario where EoP measures would be partially implemented by developing countries (EoPmid), and was projected to decrease under other scenarios, with the most significant decrease (81.2%) under the scenario where EoP measures would be fully enhanced by all countries along with the measures to achieve 2 °C target (EoPmaxCCSBLD) across South Asia. Country-specific projections of under-5 mortality varied by country. The current emission control strategy would not be sufficient to reduce the number of deaths in South Asia. Robust climate change mitigation and air pollution control policy implementation is required.

Effects of long-term indoor air purification intervention on cardiovascular health in elderly: a parallel, double-blinded randomized controlled trial in Hong Kong

Ambient fine particulate matter (PM2.5) is a leading environmental risk factor globally, and over half of the associated disease burden are caused by cardiovascular disease. Numerous randomized controlled trials (RCT) have investigated the short-term cardiovascular benefits of indoor air purifiers (IAPs), but major knowledge gaps remain on their longer-term benefits. In this 1-year, randomized, double-blinded, parallel controlled trial of 47 elderly (ntrue-purification = 24; nsham-purification = 23) aged ≥70 years, true-purification reduced household PM2.5 levels by 28% and maintained lower exposure throughout the year compared to the sham-purification group. After 12 months of intervention, a significant reduction of diastolic blood pressure was found in the true-purification versus sham-purification group (-4.62 [95% CI: -7.28, -1.96] mmHg) compared to baseline measurement prior to the intervention, whereas systolic blood pressure showed directionally consistent but statistically non-significant effect (-2.49 [95% CI: -9.25, 4.28] mmHg). Qualitatively similar patterns of associations were observed for pulse pressure (-2.30 [95% CI: -6.57, 1.96] mmHg) and carotid intima-media thickness (-10.0% [95% CI: -24.8%, 4.7%]), but these were not statistically significant. Overall, we found suggestive evidence of cardiovascular benefits of long-term IAPs use, particularly on diastolic blood pressure. Evidence on other longer-term cardiovascular traits is less clear. Further trials with larger sample sizes and long-term follow-up are needed across diverse populations to evaluate the cardiovascular benefits of IAPs.

Autophagy alleviates hippocampal neuroinflammation by inhibiting the NLRP3 inflammasome in a juvenile rat model exposed particulate matter

Ambient fine particulate matter (PM) is a global public and environmental problem. PM is closely associated with several neurological diseases, which typically involve neuroinflammation. We investigated the impact of PM exposure on neuroinflammation using both in vivo (in a juvenile rat model with PM exposure concentrations of 1, 2, and 10 mg/kg for 28 days) and in vitro (in BV-2 and HT-22 cell models with PM concentrations of 50–200 μg/ml for 24 h). We observed that PM exposure induced the activation of the NLRP3 inflammasome, leading to the production of IL-1β and IL-18 in the rat hippocampus and BV-2 cells. Furthermore, inhibition of the NLRP3 inflammasome with MCC950 effectively reduced neuroinflammation and ameliorated hippocampal damage. In addition, autophagy activation was observed in the hippocampus of PM-exposed rats, and the promotion of autophagy by rapamycin (Rapa) effectively attenuated the NLRP3-mediated neuroinflammation induced by PM exposure. However, autophagic flow was blocked in BV-2 cells exposed to PM, and Rapa failed to ameliorate NLRP3 inflammasome activation. We found that autophagy was activated in HT-22 cells exposed to PM and that treatment with Rapa reduced the release of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as cell apoptosis. In a subsequent coculture model of BV-2 and HT-22 cells, we observed the activation of the NLRP3 inflammasome in BV-2 cells when the HT-22 cells were exposed to PM, and this activation was alleviated when PM-exposed HT-22 cells were pretreated with Rapa. Overall, our study revealed that PM exposure triggered hippocampal neuroinflammation by activating the NLRP3 inflammasome. Notably, autophagy mitigated NLRP3 inflammasome activation, potentially by reducing neuronal ROS and apoptosis. This research emphasized the importance of reducing PM exposure and provided valuable insight into its neurotoxicity.

Changing patterns for cardiovascular disease and subtypes mortality attributable to ambient fine particulate matter pollution between China and India during 1990 to 2019

Changing patterns for cardiovascular disease and subtypes mortality attributable to ambient fine particulate matter pollution between China and India during 1990 to 2019

Tree species classification improves the estimation of BVOCs from urban greenspace

Accurate estimation of biogenic volatile organic compounds (BVOCs) emissions from urban plants is important as BVOCs affect the formation of secondary pollutants and human health. However, uncertainties exist for the estimation of BVOCs emissions from urban greenspace due to the lack of tree species classification with high spatial resolution. Here, we generated a tree species classification dataset with 10 m resolution to estimate tree species-level BVOCs emissions and quantify their impact on air quality in Shenzhen in southern China. The results showed that for the entire city, the BVOCs emissions based on traditional plant functional types (PFTs) dataset were substantially underestimated compared with the tree species classification data (6.37 kt versus 8.23 kt, with 22.60 % difference). The underestimation is particularly prominent in urban built-up areas, where our estimation was 1.65 kt, nearly twice of that based on PFTs data (0.86 kt). BVOCs estimation in built-up areas contributed approximately 20.07 % to the total. These BVOCs contributed substantially to the increase of ambient O3, but had limited impacts to ambient fine particulate matter (PM2.5). Our results underscore the importance of high spatial resolution tree species-level classification in more accurate estimation of BVOCs, especially in highly developed urban areas. The enhanced understanding of the patterns of BVOCs emissions by urban trees and the impact on secondary pollutants can better support fine-scale tree planning and management for livable environments in urban areas.

Exposure to ambient fine particulate matter components during pregnancy and early childhood and its association with asthma, allergies, and sensitization in school-age children.

Exposure to fine particulate matter (PM2.5) has been associated with allergic diseases, including asthma. However, information about the effects of specific PM2.5 components is limited. This study aimed to investigate the relationship of exposure to chemical components of PM2.5 during pregnancy and early childhood with the development of asthma, allergies, and sensitization in school-age children. This study included 2,408 children in the second grade of elementary school. Questionnaire surveys of respiratory/allergic symptoms and measurements of serum total IgE and specific IgE levels to house dust mite (HDM) and animal proteins were conducted. Exposures to ambient PM2.5 mass, sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), elemental carbon (EC), and organic carbon (OC) of PM2.5 in participants' residences from conception to age six were estimated using predictive models. Multiple logistic regression analysis was used to analyze the association of respiratory/allergic symptoms and allergen sensitization with estimated exposure concentrations, after adjustment for survey year, sex, season of birth, feeding method during infancy, presence of siblings, history of lower respiratory tract infection, use of childcare facilities, passive smoking, presence of pets, mother's age, history of allergic diseases, smoking during pregnancy, and annual household income. No significant association was found between PM2.5 and its component concentrations and asthma. However, wheezing significantly increased with mean NO3- concentrations during pregnancy (odds ratio of 1.64 [95% confidence interval: 1.10, 2.47] for an interquartile range increase). Significant associations were also found between EC in the second trimester of pregnancy and PM2.5, NO3-, EC, and OC concentrations in early childhood. Higher PM2.5, SO4-, and NH4+ concentrations during the second trimester increased the risk of rhinitis. Sensitizations to HDM and animal proteins were significantly associated with exposure to components such as SO42- and NH4+ during pregnancy but not with postnatal exposure. Exposures to NO3-, EC, and OC during pregnancy and early childhood were associated with wheezing. SO42- and NH4+ exposures during pregnancy were associated with sensitization to HDM and animal proteins. Asthma was not associated with exposure to PM2.5 and its main components at any period.

High ambient air pollution erodes the benefits of using clean cooking fuel in preventing low birth weight in India

A large fraction of the population in rural India continues to use biomass fuel for cooking and heating. In-utero exposure to the resulting household air pollution (HAP), is known to increase the risk of low birth weight (LBW). Mitigating HAP, by shifting to clean cooking fuel (CCF), is expected to minimize the risk associated with LBW. However, India also has high levels of ambient air pollution (AAP). Whether exposure to AAP modifies the effect of reducing HAP by switching to CCF on LBW is not known. The present study addressed this knowledge gap by analyzing the National Family Health Survey (2019–21) data of the most recent full-term, singleton, live births from rural households born after 2017 (n = 56 000). In-utero exposure to AAP was calculated from satellite-derived ambient fine particulate matter (PM2.5) concentration at the level of the primary sampling unit for the pregnancy duration of the mothers. The moderation by ambient PM2.5 level on the odds of LBW among CCF users was examined by logistic regression analysis with interaction. The adjusted odds ratio (aOR) of LBW was 7% lower among users of CCF. At the lowest Decile (20–37 μg m−3) of ambient PM2.5 exposure, the aOR of LBW among CCF users was 0.83 (95% CI:0.81–0.85). At every 10th percentile increase in ambient PM2.5 exposure (in the range 21–144 μg m−3), aOR increased gradually, reaching the value of 1 at PM2.5 level of 93 μg m−3. Our results, therefore, suggest that the benefit of using CCF during pregnancy may be downgraded by moderate to high ambient PM2.5 exposure.

Desipramine ameliorates fine particulate matter-induced hepatic insulin resistance by modulating the ceramide metabolism in mice

Recent research has highlighted a correlation between exposure to ambient fine particulate matter (PM2.5) and the development of systemic insulin resistance (IR) along with an elevated risk of diabetes. Ceramide has emerged as one of the pathogenic mechanisms contributing to IR. The inhibition of acid sphingomyelinase (ASMase) activity by desipramine (DES) has been shown to effectively reduce ceramide levels. In the present study, 24 female C57BL/6 N mice were randomized into one of the four groups: the filtered air exposure (FA) group, the concentrated PM2.5 exposure (PM) group, the concentrated PM2.5 treated with low-dose DES (DL) group, and the concentrated PM2.5 treated with high-dose DES (DH) group. The PM, DL and DH groups were exposed to PM2.5 for an 8-week period within a whole-body exposure system. The study encompassed extensive examinations of glucose homeostasis, liver lipid profile, ceramide pathway, and insulin signaling pathway. Our results demonstrated that PM2.5 exposure caused impaired glucose tolerance, elevated ceramide levels, increased phosphorylation PP2A, reduced Akt phosphorylation, and hindered GLUT2 expression. Remarkably, DES administration mitigated PM2.5-induced IR by effectively lowering ceramide levels. In conclusion, the reduction of ceramide levels by DES may be a promising therapeutic strategy for coping PM2.5-induced IR.

Associations of exposure to ambient fine particulate matter constituents from different pollution sources with semen quality: Evidence from a prospective cohort

The association between ambient fine particulate matter (PM2.5) exposure and semen quality remains inconclusive, possibly due to variations in pollution sources and PM2.5 compositions. Studies investigating the constituents of PM2.5 have been hindered by small sample sizes, and research exploring the relationships between PM2.5 pollution sources and semen quality is lacking. To address this gap, we conducted a comprehensive study based on the Anhui prospective assisted reproduction cohort to evaluate the associations between semen quality and the constituents and pollution sources of PM2.5. This study included 9013 semen samples from 4417 males in the urban districts of Hefei. The median concentrations of PM2.5 constituents, including eight metals and four water-soluble ions (WSIs), were measured for seven days per month at two monitoring stations during the 0–90-day exposure window. A linear mixed-effects model, weighted quantile sum regression, and positive matrix factorisation were used to evaluate the associations of the constituents and pollution sources of PM2.5 with semen quality. The results showed that exposure to PM2.5-bound metals (antimony, arsenic, cadmium, lead, and thallium) and WSIs (sulphate and chloride) were negatively associated with semen quality parameters. Moreover, mixtures of PM2.5-bound metals and WSIs were negatively associated with semen quality. Additionally, PM2.5 derived from traffic emissions was negatively associated with semen quality. In summary, our study revealed that ambient PM2.5 and its constituents, especially metals, were negatively associated with semen quality. Antimony, lead, and thallium emerged as the primary contributors to toxicity, and PM2.5 from traffic emissions was associated with decreased semen quality. These findings have important public health implications for the management of PM2.5 pollution in the context of male reproductive health.

Role of metabolic risk factors in the relationship between ambient fine particulate matter and depressive symptoms: Evidence from a longitudinal population study

BackgroundThere is growing evidence indicating a connection between fine particulate matter (PM2.5) and depressive symptoms. Metabolic risk factors are critical determinants of depressive symptoms. However, the mediating role of these factors on the association between PM2.5 and depressive symptoms remains elusive. We aimed to investigate whether and to what extent metabolic risk factors mediated the link between long-term PM2.5 exposure and depressive symptoms. MethodsThis study comprised 7794 individuals aged between 30 and 79 years who participated in two waves of the on-site surveys in the China Multi-Ethnic Cohort. Ambient PM2.5 concentrations were assessed utilizing a random forest method based on satellite data. We employed the Patient Health Questionnaire-9 to assess depressive symptoms at wave 2, and the overall as well as three sub-domain symptom scores (emotional, neurovegetative, and neurocognitive symptoms) were calculated. Three metabolic risk factors, including hypertension, diabetes, and dyslipidemia, were considered. Mediation analyses were conducted to assess the indirect effects of PM2.5 on depressive symptoms through metabolic risk factors. ResultsWe found a positive association between chronic exposure to ambient PM2.5 and overall depressive symptoms as well as the three sub-domains. In mediation analyses, metabolic risk factors partially mediated the associations of PM2.5 on depressive symptoms. The natural indirect effects (RR, 95% CI) of PM2.5 on overall, emotional, neurovegetative, and neurocognitive symptoms mediated through metabolic risk factors were 1.004(1.001, 1.007), 1.004 (1.001, 1.008), 1.004 (1.001, 1.007), and 1.003(0.999, 1.007), respectively. Larger indirect effects were found in elderly participants (mediated proportion, 29.3%), females (13.3%), and people who did not consume alcohol (19.6%). ConclusionsMetabolic risk factors may act as mediators in the relationship between chronic PM2.5 exposure and depression. Treatment of metabolic risk factors may be an opportunity to reduce the burden of depression caused by long-term exposure to PM2.5.

Ambient fine particulate matter constituents and semen quality among adult men in China

Exposure to ambient fine particulate matter (PM2.5) was associated with decreased semen quality, but the relationship between PM2.5 constituents and semen quality was unclear. We recruited 27,824 adult men attending an infertility clinic in Wuhan, China, between 2014 and 2020. We used a four-dimensional spatiotemporal deep forest model to estimate concentrations of PM2.5 mass and its chemical constituents, including organic matter (OM), black carbon (BC), sulfate (SO42−), nitrate (NO3–), ammonium (NH4+), and chloride (Cl−). We employed linear regression models to estimate the association between PM2.5 mass and its constituents with various sperm parameters. Exposure to PM2.5 was associated with a reduction in sperm quality, with a percent change of − 5.69% (95% confidence interval [CI]: −8.53%, −2.85%) for sperm density, − 15.09% (95% CI: −22.24%, −7.94%) for sperm total count, − 1.63% (95% CI: −2.36%, −0.91%) for sperm progressive motility, and − 2.30% (95% CI: −3.04%, −1.55%) for sperm total motility. Among specific constituents, exposure to OM, BC, Cl−, or NO3– was associated with a reduction in these four semen quality parameters. The association was more pronounced among older men or individuals with lower levels of education. Our findings suggest that PM2.5 mass and each constituent were associated with decreased semen quality in adult men.

Modulatory effects of dietary saturated fatty acids on platelet mitochondrial function following short-term exposure to ambient Particulate Matter (PM2.5)

ABSTRACT Exposure to ambient fine particulate matter (PM2.5) was found to produce vascular injury, possibly by activating platelets within days after exposure. The aim of this study was to investigate the modulatory effects of dietary saturated fatty acids on platelet mitochondrial respiratory parameters following short-term inhalational exposure to PM2.5. A total of 22 healthy male volunteers were recruited from the Research Triangle area of North Carolina. Platelets were isolated from fresh whole blood samples and mitochondrial respiratory parameters were measured using an extracellular flux analyzer. Intake of saturated fat was averaged from multiple 24-hr dietary recalls. Daily ambient PM2.5 concentrations were obtained from ambient air quality monitoring stations. Correlation and ANOVA were used in data analyses, along with the pick-a-point method and the Johnson-Neyman technique for probing moderation. After controlling for age and omega-3 index, the intake of dietary saturated fatty acids after reaching 9.3% or higher of the total caloric intake significantly moderated the associations between PM2.5 exposure and several platelet mitochondrial respiratory parameters. In conclusion, dietary saturated fatty acids above 9.3% of total caloric intake influenced the relationship between short-term PM2.5 exposure and platelet mitochondrial respiration. Further research is needed to understand these associations and their implications for cardiovascular health.

Air quality sensors and distributional environmental justice: a case study of Salt Lake County, Utah

ABSTRACT Ambient fine particulate matter (PM2.5) causes health problems and is monitored by U.S. federal and state governments. Due to gaps in public monitoring, people rely on non-regulatory air quality monitoring networks (NAQMNs), comprised of low-cost PM2.5 sensors, to obtain air quality information. While environmental justice studies have examined social disparities in PM2.5 and sensor distribution, none have examined disparities in university-purchased vs. privately-purchased sensor distributions. This is important because who purchases sensors (and why) may impact sensor distribution equity. Using multivariable generalized estimating equations, we investigate university-purchased (n=68) and privately-purchased (n=230) sensors in the Salt Lake County, Utah NAQMN with a focus on socioeconomic status (SES), race/ethnicity/immigrant status, and PM2.5 at the census tract-level (n=208). Tracts with higher SES and PM2.5 concentrations had increased sensors per resident. Findings related to SES attenuate when predicting university-purchased vs. privately-purchased sensors. Tracts with greater Hispanic immigrant populations and higher PM2.5 concentrations had increased access to university-purchased sensors. Tracts with higher Asian concentrations were underserved regardless of sensor purchaser. This approach illuminates how university-purchased sensors may enhance distributional environmental justice. Findings have implications for enhancing equitable sensor distribution in NAQMNs.

Long-term exposure to ambient fine particulate matter constituents and mortality from total and site-specific gastrointestinal cancer

BackgroundAmbient fine particulate matter (PM2.5) exposure has been associated with an increased risk of gastrointestinal cancer mortality, but the attributable constituents remain unclear. ObjectivesTo investigate the association of long-term exposure to PM2.5 constituents with total and site-specific gastrointestinal cancer mortality using a difference-in-differences approach in Jiangsu province, China during 2015–2020. MethodsWe split Jiangsu into 53 spatial units and computed their yearly death number of total gastrointestinal, esophagus, stomach, colorectum, liver, and pancreas cancer. Utilizing a high-quality grid dataset on PM2.5 constituents, we estimated 10-year population-weighted exposure to black carbon (BC), organic carbon (OC), sulfate, nitrate, ammonium, and chloride in each spatial unit. The effect of constituents on gastrointestinal cancer mortality was assessed by controlling time trends, spatial differences, gross domestic product (GDP), and seasonal temperatures. ResultsOverall, 524,019 gastrointestinal cancer deaths were ascertained in 84.77 million population. Each interquartile range increment of BC (0.46 μg/m3), OC (4.56 μg/m3), and nitrate (1.41 μg/m3) was significantly associated with a 27%, 26%, and 34% increased risk of total gastrointestinal cancer mortality, respectively, and these associations remained significant in PM2.5-adjusted models and constituent-residual models. We also identified robust associations of BC, OC, and nitrate exposures with site-specific gastrointestinal cancer mortality. The mortality risk generally displayed increased trends across the total exposure range and rose steeper at higher levels. We did not identify robust associations for sulfate, ammonium, or chlorine exposure. Higher mortality risk ascribed to constituent exposures was identified in total gastrointestinal and liver cancer among women, stomach cancer among men, and total gastrointestinal and stomach cancer among low-GDP regions. ConclusionsThis study offers consistent evidence that long-term exposure to PM2.5-bound BC, OC, and nitrate is associated with total and site-specific gastrointestinal cancer mortality, indicating that these constituents need to be controlled to mitigate the adverse effect of PM2.5 on gastrointestinal cancer mortality.

Ultra-high-resolution mapping of ambient fine particulate matter to estimate human exposure in Beijing

With the decreasing regional-transported levels, the health risk assessment derived from fine particulate matter (PM2.5) has become insufficient to reflect the contribution of local source heterogeneity to the exposure differences. Here, we combined the both ultra-high-resolution PM2.5 concentration with population distribution to provide the personal daily PM2.5 internal dose considering the indoor/outdoor exposure difference. A 30-m PM2.5 assimilating method was developed fusing multiple auxiliary predictors, achieving higher accuracy (R2 = 0.78–0.82) than the chemical transport model outputs without any post-simulation data-oriented enhancement (R2 = 0.31–0.64). Weekly difference was identified from hourly mobile signaling data in 30-m resolution population distribution. The population-weighted ambient PM2.5 concentrations range among districts but fail to reflect exposure differences. Derived from the indoor/outdoor ratio, the average indoor PM2.5 concentration was 26.5 μg/m3. The internal dose based on the assimilated indoor/outdoor PM2.5 concentration shows high exposure diversity among sub-groups, and the attributed mortality increased by 24.0% than the coarser unassimilated model.

Associations of long-term exposure to PM2.5 constituents with serum uric acid and hyperuricemia in Chinese adults

ObjectiveLittle is known about the magnitude of the relation of ambient fine particulate matter (PM2.5) constituents with hyperuricemia and serum uric acid (SUA) levels. Therefore, we aimed to assess the associations and to identify the most hazardous constituent.MethodsThis study included 72,840 participants from the China Multi-Ethnic Cohort. Annual average concentrations of PM2.5 mass and its major 7 constituents were matched to individuals by residential address. SUA levels exceeding 7.0 mg/dL (417 μmol/L) for men and 6.0 mg/dL (357 μmol/L) for women were considered to be hyperuricemia. Multiple logistic and linear regressions were performed on the association of single exposure to PM2.5 constituents with hyperuricemia and SUA, separately. The weighted quantile sum method was applied to examine the joint effect of PM2.5 constituents on hyperuricemia/SUA.ResultsSignificant positive associations were discovered between PM2.5 constituents and SUA/hyperuricemia. For example, the odds ratio (95% confidence interval) of hyperuricemia for per standard deviation increase of PM2.5 mass, black carbon, organic matter, ammonium, and nitrate concentrations were 1.22 (1.12–1.32), 1.17 (1.08–1.27), 1.20 (1.10–1.31), 1.21 (1.11–1.31), and 1.28 (1.18–1.40), respectively. The joint exposure to PM2.5 constituents was significantly positively correlated with hyperuricemia (1.09, 1.05–1.14) and SUA (1.05, 1.03–1.06). And the weight of nitrate was the largest (0.668 for hyperuricemia, 0.586 for SUA).ConclusionsOur findings suggest that long-term exposure to PM2.5 constituents is associated with increased SUA levels and a higher risk of hyperuricemia. In particular, nitrate seems to be the main contributor. This study may help prevent hyperuricemia by promoting the introduction of precise preventive measures.Graphical

Global, regional, and national burden of ischemic heart disease attributable to ambient PM2.5 from 1990 to 2019: An analysis for the global burden of disease study 2019

Information on the spatio-temporal patterns of the burden of ischemic heart disease (IHD) caused by ambient ambient fine particulate matter (PM2.5) in the global level is needed to prioritize the control of ambient air pollution and prevent the burden of IHD. The Global Burden of Disease Study (GBD) 2019 provides data on IHD attributable to ambient PM2.5. The IHD burden and mortality attributable to ambient PM2.5 were analyzed by year, age, gender, socio-demographic index (SDI) level, geographical region and country. Estimated annual percentage change (EAPC) was calculated to estimate the temporal trends of age-standardized mortality rate (ASMR) and age-standardized disability-adjusted life years rate (ASDR) from 1990 to 2019. Globally, the ASMR and ASDR for ambient PM2.5-related IHD tended to level off generally, with EAPC of −0.03 (95% CI: −0.06, 0.12) and 0.3 (95% CI: 0.22, 0.37), respectively. In the past 30 years, there were obvious differences in the trend of burden change among different regions. A highest increased burden was estimated in low-middle SDI region (EAPC of ASMR: 3.73 [95% CI: 3.56, 3.9], EAPC of ASDR: 3.83 [95% CI: 3.64, 4.02]). In contrast, the burden in high SDI region (EAPC of ASMR: −4.48 [95% CI: −4.6, −4.35], EAPC of ASDR: −3.98 [95% CI: −4.12, −3.85]) has declined most significantly. Moreover, this burden was higher among men and older populations. EAPCs of the ASMR (R = −0.776, p < 0.001) and ASDR (R = −0.781, p < 0.001) of this burden had significant negative correlations with the countries’ SDI level. In summary, although trends in the global burden of IHD attributable to ambient PM2.5 are stabilizing, but this burden has shifted from high SDI countries to middle and low SDI countries, especially among men and elderly populations. To reduce this burden, the air pollution management prevention need to be further strengthened, especially among males, older populations, and middle and low SDI countries.

Atmospheric elemental carbon pollution and its regional health disparities in China

Previous studies have reported that atmospheric elemental carbon (EC) may pose potentially elevated toxicity when compared to total ambient fine particulate matter (PM2.5). However, most research on EC has been conducted in the US and Europe, whereas China experiences significantly higher EC pollution levels. Investigating the health impact of EC exposure in China presents considerable challenges due to the absence of a monitoring network to document long-term EC levels. Despite extensive studies on total PM2.5 in China over the past decade and a significant decrease in its concentration, changes in EC levels and the associated mortality burden remain largely unknown. In our study, we employed a combination of satellite remote sensing, available ground observations, machine learning techniques, and atmospheric big data to predict ground EC concentrations across China for the period 2005–2018, achieving a spatial resolution of 10 km. Our findings reveal that the national average annual mean EC concentration has remained relatively stable since 2005, even as total PM2.5 levels have substantially decreased. Furthermore, we calculated the all-cause non-accidental deaths attributed to long-term EC exposure in China using baseline mortality data and pooled mortality risk from a cohort study. This analysis unveiled significant regional disparities in the mortality burden resulting from long-term EC exposure in China. These variations can be attributed to varying levels of effectiveness in EC regulations across different regions. Specifically, our study highlights that these regulations have been effective in mitigating EC-related health risks in first-tier cities. However, in regions characterized by a highconcentration of coal-power plants and industrial facilities, additional efforts are necessary to control emissions. This observation underscores the importance of tailoring environmental policies and interventions to address the specific challenges posed by varying emission sources and regional contexts.

The effects of the COVID-19 pandemic on PICU admissions for severe asthma exacerbations: Asingle-center experience.

The incidence of severe asthma exacerbations (SAE)requiring a pediatric intensive care unit (PICU)admission during the coronavirus disease 2019 (COVID-19) pandemic (and its association with public restrictions) is largely unknown. We examined the trend of SAE requiring PICU admission before, during, and after COVID-19restrictions in Amsterdam, the Netherlands, and its relationship with features such as environmental triggers and changes in COVID-19restriction measures. In this single-center, retrospective cohort study, all PICU admissions of children aged ≥2 years for severe asthma at the Amsterdam UMC between 2018 and 2022 were included. The concentrations of ambient fine particulate matter (PM2.5 ) and pollen were obtained from official monitoring stations. Between January 2018 and December 2022, 228 children were admitted to the PICU of the Amsterdam UMC for SAE. While we observed a decrease in admissions during periods of more stringent restriction, there was an increase in the PICU admission rate for SAE in some periods following the lifting of restrictions. In particular, following the COVID-19restrictions in 2021, we observed a peak incidence of admissions from August to November, which was higher than any other peak during the indicated years. No association with air pollution or pollen was observed. We hypothesize that an increase in clinically diagnosed viral infections after lockdown periods was the reason for the altered incidence of SAE at the PICU in late 2021, rather than air pollution and pollen concentrations.

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.