Ambient Fine Particulate Matter Research Articles

Prenatal exposure to ambient fine particulate matter and child lung function in the CANDLE cohort

Background Ambient fine particulate matter (PM2.5) exposure adversely impacts child airway health; however, research on prenatal PM2.5 exposure, and child lung function is limited. We investigated these associations in the ECHO-PATHWAYS Consortium, focusing on the role of exposure timing during different phases of fetal lung development. Methods We included 675 children in the CANDLE cohort born between 2007 and 2011 in Memphis, TN, USA. Prenatal exposure to ambient PM2.5 was estimated using a spatiotemporal model based on maternal residential history and averaged over established prenatal periods of lung development. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) were measured by spirometry at age 8–9 years. We used linear regression and Bayesian Distributed Lag Interaction Models (BDLIM) to estimate associations between exposure and lung function z-scores, adjusting for maternal/child characteristics, prenatal/postnatal tobacco exposure, and birth year/season, and evaluating effect modification by child sex and allergic sensitization. Results The average ambient concentration of PM2.5 during pregnancy was 11.1 µg/m3 (standard deviation:1.0 µg/m3). In the adjusted linear regression and BDLIM models, adverse, but not statistically significant, associations were observed between exposure during the pseudoglandular (5–16 weeks of gestation) and saccular (24–36 weeks) phases of lung development and FEV1 and FVC. The strongest association was between a 2 μg/m3 higher concentration of PM2.5 during the saccular phase and FEV1 z-score (−0.176, 95% Confidence Interval [CI]: −0.361, 0.010). The FEV1/FVC ratio was not associated with PM2.5 in any exposure window. No effect modification by child sex or allergic sensitization was observed. Conclusions We did not find strong evidence of associations between prenatal ambient PM2.5 exposure and child lung function in a large, well-characterized study sample. However, there was a suggested adverse association between FEV1 and exposure during late pregnancy. The saccular phase of lung development might be an important window for exposure to PM2.5.

The coupling model of random forest and interpretable method quantifies the response relationship between PM2.5 and influencing factors

Ambient fine particulate matter (PM2.5) is affected by many factors, such as source emissions, meteorological conditions, and chemical reactions. Revealing the effects of these factors on PM2.5 is essential to understand the causes of PM2.5 pollution. The machine learning method can establish the non-linear relationship between influencing factors and PM2.5. Here, a coupling model of machine learning and interpretation method was constructed to comprehensively quantify the importance of influencing factors to PM2.5 from multiple dimensions and analyze the sensitivity of influencing factors. Among the primary indicators of influencing factors, the importance of emission, meteorological conditions, and atmospheric chemical reaction to PM2.5 is 49%, 29%, and 22%, respectively. In the secondary indicator of influencing factors, the transmission effect is the most important meteorological condition, with an important degree of 15%. The liquid phase reaction is the most important atmospheric chemical reaction, with an importance of 7%. Among the three levels of influencing factors, emission, transport distance, liquid phase reaction coefficient, aerosol acidity, and accumulation promotion coefficient are important factors. The sensitivity of a single factor is complex and changeable, and the interaction between emission and other important factors is the strongest among the two factors. Of which the interaction between transmission distance and emission during the observation period is the strongest, and the interaction coefficient is 1.82. Our study focuses on the effect of influencing factors on PM2.5, provides a basis for the analysis of the causes of PM2.5 pollution, and technical support for the treatment of PM2.5.

Underappreciated roles of soil nitrogen oxide emissions on global acute health burden

The recognized importance of ambient fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) on human health has prompted the world to enact increasingly strict regulations on anthropogenic nitrogen oxides (NOx) emissions. However, the health concerns from soil NOx, potentially driven by fertilizer input but conventionally categorized as natural sources, remain less studied. Here, we emphasize the underappreciated roles of soil NOx emissions on health burden attributable to short-term PM2.5, O3, and NO2 exposure. Globally, we quantify acute health effects using machine-learning-based daily exposure estimates and identify influences of soil NOx emissions based on chemical transport model simulations. We find that 72.3% of the globe is affected by soil NOx emissions, whose contributions to short-term PM2.5, O3, and NO2 pollution lead to 13.9 (95% Confidence Interval [CI]: 9.1-18.8), 26.0 (18.2-34.2), and 13.9 (10.3-17.5) thousand premature mortality, respectively, in 2019. With distinct variations in regions, seasons, and pollutants, soil NOx-originated air pollution poses a global health concern, particularly for developing regions and intensively agricultural areas. In response to the intensive fertilizer use, South Asia, Southern Sub-Saharan Africa, and Central Europe witness the largest soil NOx-related health burden of up to 1.6 (95% CI: 1.1-2.1) mortality per 100k population. The overall health risk peaks in May, with O3 pollution typically dominating the soil NOx-attributable health burden during warm seasons and NO2 or PM2.5 during cold months. Our study highlights the necessity of dynamically adapted agricultural strategies for health-oriented multi-pollutant control, among which the improved use of synthetic fertilizers deserves priority under the ever-changing climate.

Critical periods of maternal exposure to ambient fine particulate matter and the risks of stillbirth and spontaneous preterm birth in Western Australia

Few studies have investigated weekly or monthly exposure-lag-response association between fine particulate matter (PM2.5) and preterm birth, and there has been no known such study for stillbirth. We aimed to identify potential critical susceptible periods of the association between monthly PM2.5 exposure during pregnancy and stillbirth and spontaneous preterm birth (sPTB). A total of 414,771 singleton births, of which 0.5% and 3.9% were stillbirth and sPTB respectively, between 1st January 2000 and 31st December 2015 in Western Australia were linked to fine spatiotemporal monthly PM2.5 concentrations. Monthly distributed lag linear and non-linear Cox regressions were performed to investigate PM2.5 exposure during pregnancy and covariate-adjusted hazards of stillbirth and sPTB. The mean PM2.5 exposure during pregnancy was 8.1 μg/m3. Pregnancy PM2.5 exposure showed small dose-response associations with stillbirth and sPTB with critical susceptible periods spanning the 3rd–6th gestational months. Relative to 5 μg/m3, the strongest hazards of PM2.5 exposure were 1.04 (95% CI 0.99, 1.08) and 1.03 (95% CI 1.02, 1.05) during the 4th gestational month for stillbirth and sPTB, respectively. Monthly exposures at late pregnancy were associated with lower hazards. The average pregnancy exposure hazards were 1.08 (95% CI 0.88, 1.32) and 1.07 (95% CI 0.99, 1.15) per 5 μg/m3 increment for stillbirth and sPTB, respectively. The average entire pregnancy exposure showed potential attributable burden, synergistic interaction effects with biothermal stress, and comparatively higher hazards for female births and births to mothers who were Caucasian, < 35 years old, high SES, nulliparous, and smoked during pregnancy.

Life course cumulative PM2.5 exposure since childhood and albuminuria in midlife: a 30-year prospective cohort study

Abstract Background Previous studies have confirmed the adverse effect of ambient fine particulate matter (PM2.5) on kidney and cardiovascular diseases. However, the effects of long-term cumulative PM2.5 exposure on albuminuria, particularly from childhood to middle age, remains uncertain. Purposes We aimed to investigate the association between cumulative PM2.5 exposure and albuminuria across three distinct time frames using data from the 30-year population-based cohort study. Methods Using data from the ongoing cohort of Hanzhong Adolescent Hypertension study, 1643 children and adolescents were followed with 6 visits over 30 years. The annual mean PM2.5 concentration for the period 1987-2017, at the address of each participant, was obtained from the MERRA-2 and CHAP datasets in China. We assessed cumulative PM2.5 exposure as the area under the curve (AUC) and used the linear regression models to estimate the association between cumulative PM2.5 exposure and urinary albumin-to-creatinine ratio (uACR) in 2017. Results In full adjustment for potential confounders, childhood and life course cumulative PM2.5 exposure was positively associated with uACR in midlife [childhood: β=0.103 (95%CI: 0.003, 0.202); life course: β=0.078 (95%CI: 0.004, 0.153)]. However, the relationship between adulthood cumulative PM2.5 exposure and uACR in middle age was not statistically significant. In addition, the associations of adulthood and life course cumulative PM2.5 exposure with uACR in middle age were only observed in non-smokers [β=0.109 (95% CI: 0.002, 0.216)], but not in smokers. Conclusions Cumulative PM2.5 exposure during childhood and over the life course is associated with higher uACR in midlife, especially for children and non-smokers. Lowering PM2.5 pollution early in life could prevent the development of renal dysfunction and cardiovascular disease in later life.

Heart rate variability, electrodermal activity and cognition in adults: Association with short-term indoor PM2.5 exposure in a real-world intervention study

BackgroundLong-term effects of ambient fine particulate matter (PM2.5) exposure on mortality and morbidity are well established. The study aims to evaluate how short-term indoor PM2.5 exposure affects physiological responses and understand potential mechanisms mediating the cognitive outcomes in working-age adults. MethodsThis real-world randomized single-blind crossover intervention study was conducted in an urban office setting, with desk-based air purifiers used as the intervention. Participants (N = 40) were exposed to average PM2.5 levels of 18.0 μg/m3 in control and 3.7 μg/m3 in intervention conditions. Cognitive tests, heart rate variability (HRV), and electrodermal activity (EDA) measures were conducted after 5 h of exposure. Self-reported mental effort, exhaustion, and task difficulty were collected after the cognitive tests. ResultsParticipants in the intervention condition had significantly higher HRV during cognitive testing, particularly in the standard deviation of normal-to-normal intervals (SDNN), root mean square of successive differences (RMSSD), and high-frequency power (HF) indices. Mediation analysis revealed that elevated PM2.5 exposure reduced HRV indices, which mediated the effect on two executive function-related cognitive skills out of 16 assessed skills. No significant differences were found in EDA, self-reported task difficulty, or exhaustion, but self-reported mental effort was higher in the control condition. ConclusionsLower indoor PM2.5 level was associated with reduced mental effort and higher HRV during cognitive testing. Furthermore, the association between indoor PM2.5 exposure and executive function might be mediated through cardiovagal responses. These findings provide insights on the mechanisms through which fine particle exposure adversely affects the autonomic nervous system and how this in turn affects cognition. The potential cardiovascular and cognitive health benefits of PM2.5 reduction warrants further research.

Co-existing ambient fine particulate matter exacerbated electronic cigarette toxicity on human respiratory cells.

Respiratory co-exposure to ambient PM2.5 and electronic cigarettes (e-cigarettes) frequently occurs in public. However, the combined effects on human respiratory health have not been well documented. To discuss potential co-effects and possible biological mechanisms, A549/THP-1 co-cultures and BEAS-2B cells were exposed to unvapedtobacco or mint-flavored e-liquids (0-7.2% v/v), e-cigarette aerosol extract (ECE, 0-50% v/v), PM2.5 (60 μg/mL), or PM2.5 + ECE for 24 h. Cell viability assessments on e-liquids, ECE, PM2.5 + ECE showed that the mint flavor exhibited higher cytotoxicity compared to the tobacco flavor in both A549/THP-1 and BEAS-2B. However, the influence of flavors on ROS levels and mRNA expression of inflammatory markers (IL-6, TNF-α, IL-8, IL-1β) after ECE exposure demonstrated inconsistency in the two cell models. PM2.5 + ECE treatment notably elevated ROS production and inflammation responses compared to ECE alone exposure. Only co-exposure induced a significant increase in nuclear transcription factor-κB p65 (NF-κB p65) and NOD-like receptor 3 (NLRP3) protein expression regardless of flavors. Our results indicate that PM2.5-treated cells exacerbate the adverse effects induced by ECE in both A549/THP-1 and BEAS-2B cells. Flavors in unvaped e-liquids affect cytotoxicity, oxidative stress and inflammation response, but these effects vary depending on the vaping process and the specific cell line.

Importance of aerosol composition and aerosol vertical profiles in global spatial variation in the relationship between PM2.5 and aerosol optical depth

Abstract. Ambient fine particulate matter (PM2.5) is the leading global environmental determinant of mortality. However, large gaps exist in ground-based PM2.5 monitoring. Satellite remote sensing of aerosol optical depth (AOD) offers information to help fill these gaps worldwide when augmented with a modeled PM2.5–AOD relationship. This study aims to understand the spatial pattern and driving factors of this relationship by examining η (PM2.5AOD) using both observations and modeling. A global observational estimate of η for the year 2019 is inferred from 6870 ground-based PM2.5 measurement sites and satellite-retrieved AOD. The global chemical transport model GEOS-Chem, in its high-performance configuration (GCHP), is used to interpret the observed spatial pattern of annual mean η. Measurements and the GCHP simulation consistently identify a global population-weighted mean η value of 96–98 µg m−3, with regional values ranging from 59.8 µg m−3 in North America to more than 190 µg m−3 in Africa. The highest η value is found in arid regions, where aerosols are less hygroscopic due to mineral dust, followed by regions strongly influenced by surface aerosol sources. Relatively low η values are found over regions distant from strong aerosol sources. The spatial correlation of observed η values with meteorological fields, aerosol vertical profiles, and aerosol chemical composition reveals that spatial variation in η is strongly influenced by aerosol composition and aerosol vertical profiles. Sensitivity tests with globally uniform parameters quantify the effects of aerosol composition and aerosol vertical profiles on spatial variability in η, exhibiting a population-weighted mean difference in aerosol composition of 12.3 µg m−3, which reflects the determinant effects of composition on aerosol hygroscopicity and aerosol optical properties, and a population-weighted mean difference in the aerosol vertical profile of 8.4 µg m−3, which reflects spatial variation in the column–surface relationship.

Involvement of autophagy and gut dysbiosis in ambient particulate matter-induced colonic inflammation

Ambient fine particulate matter (PM2.5), a vital environmental toxicant, not only adversely affects the cardiovascular and respiratory systems but also potentially exhibits an association with intestinal inflammation and colorectal cancer (CRC). The underlying molecular mechanisms of PM2.5 impacts on CRC are still unclear. In this study, we utilized collected ambient PM2.5 and standard reference material SRM2786 to investigate the toxic effects on the colon through in vivo chronic exposure mouse and in vitro cell culture models. We employed a chronic mouse exposure model to clarify the colonic injury and gut microbiome biomarkers. Prolonged exposure to PM2.5 via oropharyngeal aspiration led to a significant rise in colonic epithelial proliferation and reduced colon length in mice. It triggered characteristics indicative of gut microbiota dysbiosis linked to inflammatory bowel disease. The gut microbiome alternations may serve as a biomarker indicating the colonic health impacts of PM2.5 exposure. PM2.5 and SRM2786-induced cytotoxicity manifested as autophagy dysregulation-mediated abnormal proliferation, IL-8 production, p62/SQSTM1 accumulation, and lysosomal membrane damage in human colon cells WiDr and Caco-2. Both PM2.5 and SRM2786 exposures led to the accumulation of p62/SQSTM1 and compromised lysosomal membrane integrity, showing impaired autophagic flux in WiDr and Caco-2 cells. Finally, we examined the correlations between atmospheric PM2.5 data and biomarkers of colonic inflammation in human population. The serum level of IL-8 was significantly correlated with regional anthropogenic pollutants. In conclusion, our findings elucidate that ambient PM2.5 exhibits adverse effects on colon health manifested as inflammation, aberrant proliferation, and gut dysbiosis, potentially mediated through autophagy dysregulation, thereby highlighting the importance of further research on the impact of environmental pollutants on gastrointestinal health.

Temperature variability and influenza incidence in China: Effect modification by ambient fine particulate matter

This study aims to examine the association between temperature variabilit (TV) exposure and influenza incidence in China, and the modification effect of PM2.5 levels. Data on daily influenza cases, weather conditions, and PM2.5 concentrations were collected from 339 cities across mainland China from 2014 to 2019. TV was computed as the standard deviation of daily maximum and minimum temperatures for the current day and the previous several days (i.e., TV0–1 to TV0–7). A space-time-stratified case-crossover design with conditional Poisson regression was employed. Overall, each 1 °C increase in TV0–6 was linked to 3.3 % (95 % CI: 3.1 %, 3.5 %) rise in influenza incidence, potentially attributing 14.73 % (95 % CI: 14.08 %, 15.37 %) of cases to this exposure. PM2.5 concentration showed substantial modification effect on the association, such that the relative risk (RR) of influenza incidence grew from 1.027 (95 % CI: 1.025, 1.029) to 1.040 (95 % CI: 1.038, 1.042) as PM2.5 levels increased from 15 to 75 μg/m³ . Females and individuals over 65 years old were more susceptible to TV exposure and the PM2.5 modification. Stronger effects were observed during cold season and in North region. The findings highlight the integrating considerations of TV and PM2.5 exposures into public health measures for influenza prevention and control.

Simultaneous comparison of the chemical composition and attributable source of PM2.5 during 2014–2018 in major metropolitan cities in South Korea: impacts of policy interventions

Abstract Ambient fine particulate matter (PM2.5) is one of the most concerning pollutants, characterized by its diverse chemical composition. Although various studies have revealed PM2.5 chemical components, there is limited knowledge on how to reduce PM2.5 concentrations through administrative policies focusing on source management. We compared PM2.5 compositional characteristics and performed source apportionment using the positive matrix factorization in four metropolitan cities (Seoul, Daejeon, Gwangju, and Ulsan) in South Korea from 2014 to 2018. The annual average of PM2.5 concentrations exceeded the annual national ambient air quality standard of 15 μg m−3 in all areas while secondary inorganic aerosols constituted the largest fraction of PM2.5. This implies that secondary formation from gaseous precursors in the atmosphere was the main factor contributing to ambient PM2.5. However, the concentrations of PM2.5 constituents varied significantly across cities, suggesting that PM2.5 is a heterogeneous pollutant considerably influenced by region-specific conditions. In line with the chemical composition, secondary nitrate, secondary sulfate, and mobile-related sources were found to be significant contributors of PM2.5. Additionally, the extent of contribution from each source varied across the study regions. We also evaluated the impacts of policy interventions by comparing the PM2.5 composition and source apportionment before and after the policies for improving air quality. Intensive programs focused on the vehicle sector in Seoul led to a considerable decrease in the concentrations of carbonaceous compounds and mobile-related sources. In addition, strengthened regulations on coal-fired power plants (CFPPs) since 2016 have influenced the contributions of coal combustion sources in two cities adjacent to the west coastal area, where approximately half of the CFPPs of the country are densely distributed. Overall, the study’s findings indicate that region-specific PM2.5 chemical constituents and source contributions should be considered for establishing PM2.5-related policies, considering the high heterogeneity of PM2.5.

Modifying factors and temporal trends of adverse health effects of short-term exposure to PM2.5 in Canada (2001–2018)

Considerable evidence has been accumulated on serious acute health outcomes associated with short-term exposure to ambient fine particulate matter (PM2.5). Modifying factors of those associations, however, have been less explored and need further analyses. In this national study, we investigated whether short-term effects of PM2.5 are modified according to region, cause of mortality/hospitalization, season, age, and sex. PM2.5-related adverse health effects were estimated by an ecological time-series study, covering about 80 % of the Canadian population for 18 years (2001–2018). We estimated city-specific associations using daily averages of PM2.5 and temperature, and daily counts of hospitalizations and mortality (non-accidental all-cause, circulatory, and respiratory). National and regional associations were then estimated with a 2-stage model. We considered potential modifying factors of PM2.5-related adverse health effects, and examined linear trends in the annual associations. Nationally, PM2.5 exposure was associated with both hospitalizations and mortality, and there was evidence of differences by the modifying factors. Of the various causes, circulatory mortality and respiratory hospitalization were more attributable to PM2.5 exposure. We found regional differences for both all-cause hospitalization and all-cause mortality, and seasonal differences for respiratory hospitalization (warm season) and circulatory hospitalization (cold season). Circulatory mortality risk was significant for seniors and females. All-cause hospitalizations appeared to gradually decrease over time, but annual all-cause mortality remained constant at 0.6 % of the population. Adverse health effects of PM2.5 exposures may depend on not only PM2.5 concentration, but also other factors (region, cause, season, age, sex). National estimates for the baseline (age ≥ 1 year, both sexes) risk cannot be interpreted without consideration of the differences by modifying factors. Study findings can be used by seniors, women, and those who have pre-existing health conditions to make informed decisions regarding their health risks from daily exposure to ambient PM2.5.

Ambient Air Pollution Exposure and Outcomes in Patients Receiving Lung Transplant

Elevated ambient fine particulate matter (PM2.5) air pollution exposure has been associated with poor health outcomes across several domains, but its associated outcomes among lung transplant recipients are poorly understood. To investigate whether greater PM2.5 exposure at the zip code of residence is associated with a higher hazard for mortality and graft failure in patients with lung transplants. This retrospective cohort study used panel data provided by the United Network for Organ Sharing, which includes patients receiving transplants across all active US lung transplant programs. Adult patients who received lung transplants between May 2005 and December 2016 were included, with a last follow-up of September 10, 2020. Data were analyzed from September 2022 to May 2023. Zip code-level annual PM2.5 exposure was constructed using previously published North American estimates. The primary outcome was time to death or lung allograft failure after lung transplant. A gamma shared frailty Cox proportional hazards model was used to produce unadjusted and adjusted hazard ratios (HRs) to estimate the association of zip code PM2.5 exposure at the time of transplant with graft failure or mortality. Among 18 265 lung transplant recipients (mean [SD] age, 55.3 [13.2] years; 7328 female [40.2%]), the resident zip code's annual PM2.5 exposure level was greater than or equal to the Environmental Protection Agency (EPA) standard of 12μg/m3 for 1790 patients (9.8%) and less than the standard for 16 475 patients (90.2%). In unadjusted analysis, median graft survival was 4.87 years (95% CI, 4.57-5.23 years) for recipients living in high PM2.5 areas and 5.84 years (95% CI, 5.71-5.96 years) for recipients in the low PM2.5 group. Having an annual PM2.5 exposure level greater than or equal to the EPA standard 12 μg/m3 was associated with an increase in the hazard of death or graft failure (HR, 1.11; 95% CI, 1.05-1.18; P < .001) in the unadjusted analysis and after adjusting for covariates (HR, 1.08; 95% CI, 1.01-1.15; P = .02). Each 1 μg/m3 increase in exposure was associated with an increase in the hazard of death or graft failure (adjusted HR, 1.01; 95% CI, 1.00-1.02; P = .004) when treating PM2.5 exposure as a continuous variable. In this study, elevated zip code-level ambient PM2.5 exposure was associated with an increased hazard of death or graft failure in lung transplant recipients. Further study is needed to better understand this association, which may help guide risk modification strategies at individual and population levels.

Ambient fine particulate matter and its constituents may exacerbate the acceleration of aging in adults

Both ambient fine particulate matter (PM2.5) and aging are important urban concerns. However, the associations between PM2.5 constituents and the acceleration of aging (AA) remain unclear. We included 16,051 adults (aged 25–80 years) with 19,252 medical observations in Taiwan during 2008−2017. 2-year average PM2.5 and its five major constituents were assessed using a two-stage machine learning model at a resolution of 1 km2. AA was determined by the difference between the Klemera–Doubal biological age and chronological age. A linear mixed model (LMM) with inverse probability weights was used to examine the associations between AA and air pollution. In a semi-randomized study design, we applied a post-matching LMM to assess the impacts of changes in air pollution exposure on AA. Each interquartile range increase in ambient PM2.5, SO4-2, NO3–, NH4+, organic matters (OM), and black carbon (BC) was associated with a 0.20 (95 %confidence interval [CI]: 0.17–0.24), 0.19 (0.15–0.23), 0.14 (0.11–0.18), 0.21 (0.17–0.24), 0.22 (0.19–0.26) and 0.25 (0.21–0.28) year increase in AA, respectively. BC was generally associated with the greatest increase in AA as compared to other constituents. We did not find evident thresholds in their concentration–response associations. Participants exposed to increased levels of PM2.5, SO4-2, NO3–, NH4+, OM, and BC experienced an increase in AA of 0.11 (−0.07–0.29), 0.20 (0.02–0.39), 0.15 (−0.02–0.33), 0.12 (−0.07–0.31), 0.24 (0.07–0.41), and 0.30 (0.07–0.52) years, respectively, compared to those exposed to decreased/unchanged levels. Long-term exposure to ambient PM2.5 and its constituents may accelerate biological aging among Chinese adults. Exposed to increased levels may further aggregate the aging process. This study suggests that reducing exposure to air pollution is beneficial, even for residents within moderately-to-highly polluted regions, such as Taiwan. Rigorous regulation of PM2.5 and its constituents may prevent the acceleration of biological age.

Study of condensable particulate matter from stationary combustion sources: Source profiles, emissions, and impact on ambient fine particulate matter

Although significant progress has been made in controlling emissions from stationary combustion sources in China over the past decade, understanding of condensable particulate matter (CPM) emissions from these sources and their impact on ambient PM2.5 remains limited. In this study, we established the source profiles and emission inventories of CPM from coal-fired industrial boilers (CFIBs), coal-fired power plants (CFPPs), and iron and steel industry (ISIs) for the Yangtze River Delta (YRD) region of China; furthermore, the air quality model (Community Multiscale Air Quality, CMAQ) was used to evaluate the impact of CPM emissions from these three types of stationary combustion sources on ambient PM2.5 during Feb. 2018, a month characterized by elevated PM2.5 concentrations. The results indicated that CPM emissions from these three sources in the YRD region before and after the implementation of the ultra-low emissions (ULE) policy amounted to 109,839 and 43,338 tons, respectively, with particularly high emission intensity along the Yangtze River. The implementation of CFPPs ULE policy was shown to reduce the impact of CPM emissions from these three stationary sources on monthly PM2.5 concentrations from 0.92 μg/m3 to 0.41 μg/m3 (with a maximum of 5.35 μg/m3). This reduction exceeded the 0.31 μg/m3 decrease in PM2.5 concentrations resulting from the emission reductions of conventional pollutants (FPM, SO2 and NOx). CPM emissions from these three stationary sources were found to increase the PM2.5 by 0.68 μg/m3 during pollution periods. The largest components of PM2.5 contributed by CPM emissions from stationary combustion sources were sulfate, organic carbon, and nitrate, accounting for 21.4 %, 21.1 %, and 18.2 %, respectively. Particularly, contributions from CPM emissions to PM2.5 varied by altitude, with a relatively large impact at altitudes between 220 and 460 m. Attention should be given to CPM emission control, with particular priority placed on implementing ULE measures for ISIs and CFIBs.

Impact of Model Spatial Resolution on Global Geophysical Satellite-Derived Fine Particulate Matter.

Global geophysical satellite-derived ambient fine particulate matter (PM2.5) inference relies upon a geophysical relationship (η) from a chemical transport model to relate satellite retrievals of aerosol optical depth (AOD) to surface PM2.5. The resolution dependence of simulated η warrants further investigation. In this study, we calculate geophysical PM2.5 with simulated η from the GEOS-Chem model in its high-performance configuration (GCHP) at cubed-sphere resolutions of C360 (∼25 km) and C48 (∼200 km) and satellite AOD at 0.01° (∼1 km). Annual geophysical PM2.5 concentrations inferred from satellite AOD and GCHP simulations at ∼25 km and ∼200 km resolutions exhibit remarkable similarity (R 2 = 0.96, slope = 1.03). This similarity in part reflects opposite resolution responses across components with population-weighted normalized mean difference (PW-NMD) increasing by 5% to 11% for primary species while decreasing by -30% to -5% for secondary species at finer resolution. Despite global similarity, our results also identify larger resolution sensitivities of η over isolated pollution sources and mountainous regions, where spatial contrast of aerosol concentration and composition is better represented at fine resolution. Our results highlight the resolution dependence of representing near-surface concentrations and the vertical distribution of chemically different species with implications for inferring ground-level PM2.5 from columnar AOD.

Burden of disease in Germany attributed to ambient particulate matter pollution : Findings from the Global Burden of Disease Study 2019.

Ambient fine particulate matter pollution with adiameter less than 2.5micrometers (PM2.5) is asignificant risk factor for chronic noncommunicable diseases (NCDs), leading to asubstantial disease burden, decreased quality of life, and deaths globally. This study aimed to investigate the disease and mortality burdens attributed to PM2.5 in Germany in 2019. Data from the Global Burden of Disease (GBD) Study 2019 were used to investigate disability-adjusted life-years (DALYs), years of life lost (YLLs), years lived with disability (YLDs), and deaths attributed to ambient PM2.5 pollution in Germany. In 2019, ambient PM2.5 pollution in Germany was associated with significant health impacts, contributing to 27,040 deaths (2.82% of total deaths), 568,784 DALYs (2.09% of total DALYs), 135,725 YLDs (1.09% of total YLDs), and 433,058 YLLs (2.92% of total YLLs). The analysis further revealed that cardiometabolic and respiratory conditions, such as ischemic heart disease, stroke, chronic obstructive pulmonary disease, lung cancer, and diabetes mellitus, were the leading causes of mortality and disease burden associated with ambient PM2.5 pollution in Germany from 1990-2019. Comparative assessments between 1990 and 2019 underscored ambient PM2.5 as aconsistent prominent risk factor, ranking closely with traditional factors like smoking, arterial hypertension, and alcohol use contributing to deaths, DALYs, YLDs, and YLLs. Ambient PM2.5 pollution is one of the major health risk factors contributing significantly to the burden of disease and mortality in Germany, emphasizing the urgent need for targeted interventions to address its substantial contribution to chronic NCDs.

PM2.5 chemical components are associated with in-hospital case fatality among acute myocardial infarction patients in China

Recent studies have linked the cardiovascular events with the exposure to ambient fine particulate matter (PM2.5); however, the impact of PM2.5 chemical components on acute myocardial infarction (AMI) case fatality remains poorly understood. To address this gap, we included 178,340 hospitalised patients with AMI utilising the inpatient discharge database from Sichuan, Shanxi, Guangxi, and Guangdong, China spanning 2014–2019. We evaluated exposure to PM2.5 and its components (black carbon (BC), organic matter (OM), sulphate (SO42−), nitrate (NO3−), and ammonium (NH4+)) using bilinear interpolation based on the patient’s residential address. We used mixed-effects logistic regression models to investigate the associations of PM2.5 and its five components with in-hospital AMI case fatality. Per interquartile range (IQR) increment in short-term exposure (7-day average) to overall PM2.5 (odds ratio (OR): 1.086, 95 % confidence interval (CI): 1.045–1.128), SO42−(1.063, 1.024–1.104), BC (1.055, 1.023–1.089), OM (1.052, 1.019–1.086, and NO3− (1.045, 1.003–1.089) were significantly associated with high risk of in-hospital AMI case fatality. The ORs per IQR increment in long-term exposure (annual average) were 1.323 (95 % CI: 1.255–1.394) for PM2.5, followed by BC (1.271, 1.210–1.335), OM (1.243, 1.188–1.300), SO42− (1.212, 1.157–1.270), NO3− (1.116, 1.075–1.159), and NH4+ (1.068, 1.031–1.106). Our study suggests that PM2.5 chemical components might be important risk factors for in-hospital AMI case fatality, highlighting the importance of targeted reduction of PM2.5 emissions, particularly BC, OM, and SO42−.

Seasonal variations and the prevalence of phenolic profiles in ambient fine particulate matter and their impact on oxidative potential

Exposure to fine particulate matter (PM2.5) poses numerous health risks, with oxidative potential (OP) serving as a critical marker of its toxicity. Synthetic phenolic antioxidants (SPAs) and bisphenols (BPs) influence reactive oxygen species (ROS) levels in PM2.5, and exposure to these compounds induces oxidative stress in organisms, thereby potentially affecting the OP of PM2.5. We detected 26 phenols (including 12 SPAs, 5 transformation products (TPs), and 9 BPs) in PM2.5 sample collected from October 2018 to September 2021 in Wuhan, China. Among them, 19 substances were detected at a detection frequency greater than 50 % in PM2.5 sample. AO 2246 and BHT were the main components of SPAs, and BHT-Q and BPA had the highest concentrations in TPs and BPs, respectively. PM2.5 mass concentrations and phenolic levels were higher in winter and autumn. Substances within groups were strongly correlated, suggesting the same or similar source of exposure. This finding aid in more precise pollution source identification and is crucial for comprehensively evaluating their combined health effects. Furthermore, we determined the OP of PM2.5 and found that BPs were related to increased OP and ROS. This suggests that the toxicity of PM2.5 is influenced not only by its concentration but also by its chemical composition, with BPs potentially enhancing its toxic effects. These factors should be fully considered when assessing the health impacts of PM2.5.

Changes on Stroke Burden Attributable to Ambient Fine Particulate Matter in China

Objective In recent decades, China has implemented a series of policies to address air pollution. We aimed to assess the health effects of these policies on stroke burden attributable to ambient fine particulate matter (PM2.5).MethodsJoinpoint regression was applied to explore the temporal tendency of stroke burden based on data from the Global Burden of Disease 2019 study.Results The age-standardized rates of disability-adjusted life year (DALY) for stroke attributable to ambient PM2.5 in China, increased dramatically during 1990–2012, subsequently decreased at an annual percentage change (APC) of –1.98 [95% confidence interval (CI): –2.26, –1.71] during 2012–2019. For ischemic stroke (IS), the age-standardized DALY rates doubled from 1990 to 2014, and decreased at an APC of –0.83 (95% CI: –1.33, –0.33) during 2014–2019. Intracerebral hemorrhage (ICH) showed a substantial increase in age-standardized DALY rates from 1990 to 2003, followed by declining trends, with APCs of –1.46 (95% CI: –2.74, –0.16) during 2003–2007 and –3.33 (95% CI: –3.61, –3.06) during 2011–2019, respectively. Conversely, the age-standardized DALY rates for subarachnoid hemorrhage (SAH) generally declined during 1990–2019.Conclusion Our results clarified the dynamic changes of the ambient PM2.5–attributable stroke burden in China during 1990–2019, highlighting the health effects of air quality improvement policies.