RESUMEN

Fine particulate matter (PM2.5) constituents are greatly affected by site-specific emission sources and are one of the main reasons for oxidative stress that leads to cardiovascular ailments. This study investigated the temporal, seasonal, and episodic variations in the oxidative potential (OP) of PM2.5 and its association with chemical components. Additionally, we have also examined the effect of filter substrates on OP. Dithiothreitol (DTT) and ascorbic acid (AA) acellular assays were used to estimate the formation of reactive oxygen species (ROS) in PM2.5 samples collected over a year from a regional site in India. PM2.5 morphology and functional groups were also analyzed. Results showed that OPDTTv was at the highest in winter (2.56 ±â€¯0.84 nmol min-1 m-3) and at the lowest during monsoon (0.79 ±â€¯0.65 nmol min-1 m-3). OPAAv exhibited the highest activity in post-monsoon (0.09 ±â€¯0.04 nmol min-1 m-3) and least in summer (0.05 ±â€¯0.04 nmol min-1 m-3). Biomass burning (BB) and open-field burning of crop residue during the rabi and kharif harvesting seasons were associated with significantly elevated PM2.5 toxicity, which is indicative of the contribution of combustion-derived particles. OPDTTv and OPAAv levels from BB in post-monsoon were 21 % and 67 % higher than the levels observed during BB in summer. Flaky irregular agglomerates and porous structures were observed during the BB period. Fourier-transformed infrared spectroscopy revealed that traffic-emitted organic hydrocarbons CH functional group was dominant across the season. Further, chemical species such as organics (OC and EC fractions) and ions (SO42-, NH4+, Cl-, NO3-) were found to be significantly associated with OP. Among the three filter substrates, the Teflon showed higher OP variability for both assays. This study emphasizes the impact of regional toxic aerosols across seasons and during episodic events. It contributes to our understanding of the toxicity of ambient PM2.5, which is crucial for developing targeted air-quality management strategies.

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Extensive research has established the link between PM2.5 exposure and blood pressure (BP) levels among normal individuals. However, the association between PM2.5 components and BP levels in hypertensive patients has not been fully explored. In this study, 12 971 hypertensive cases from Jinchang cohort (in Jinchang City, China) with nearly 9 years of follow-up were enrolled. Based on the linear mixed-effect model, the effects of fine particulate matter (PM2.5) and five major components [sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), black carbon (BC) and organic matter (OM)]on BP [systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP)]were evaluated by single-component model, component-joint model and component-residual model, respectively. A positive correlation was found between PM2.5 as well as its components (SO42-, NO3-, NH4+, BC and OM) exposure and BP levels. The effects of SO42-, BC and OM on BP were observed to be the most robust among the three models. Based on the results of interaction effects and stratified analysis, the effect of BC exposure on SBP, and the effect of PM2.5 and its five components on PP were greater in female than in males. Compared with elderly hypertensive patients, OM had more significant effects on SBP, DBP and MAP in young and (or) middle-aged hypertensive patients. During the heating season, the effect of PM2.5 and its components on BP was grater compared to the non-heating season. Meanwhile, PM2.5 and its components have a greater influence on BP in patients with hypertension combined with diabetes. Therefore, the findings suggested that both PM2.5 exposure and its components had a significant effect on BP in patients with hypertension. Women and young and middle-aged hypertensive patient were the sensitive population. The implementation of source control and reduction of PM2.5 emission (mainly for SO42-, BC and OM) may be of great significance to control BP level and could reduce the risk of cardiovascular disease in patients with hypertension.

RESUMEN

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.

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Air pollution is one of the major environmental threats contributing to the global burden of disease. Among diverse air pollutants, fine particulate matter (PM2.5) poses a significant adverse health impact and causes multi-system damage. As a highly dynamic organelle, mitochondria are essential for cellular energy metabolism and vital for cellular homeostasis and body fitness. Moreover, mitochondria are vulnerable to external insults and common targets for PM2.5-induced cellular damage. The resultant impairment of mitochondrial structure and function initiates the pathogenesis of diverse human diseases. This review mainly summarizes the in vivo and in vitro findings of PM2.5-induced mitochondrial dysfunction and its implication in PM2.5-induced health effects. Furthermore, recent advances toward the underlying mechanisms of PM2.5 and its components-induced mitochondrial dysfunction are also discussed, with an attempt to provide insights into the toxicity of PM2.5 and basic information for devising appropriate intervention strategies.

RESUMEN

We examined the association between walkability and blood lipids in a nationally representative sample of 29,649 participants aged 3-79 years who participated in the Canadian Health Measures Survey (CHMS) cycles 1 to 6. We focused on seven lipid biomarkers: apolipoprotein A (Apo A), apolipoprotein B (Apo B), triglycerides (TG), high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), total cholesterol (TC), and TC/HDL. Cross-sectional associations were analyzed using generalized linear mixed models incorporating survey-specific sampling weights. An increase in the Canadian Active Living Environments Index, a measure of neighborhood walkability, equivalent to the magnitude of its interquartile range (IQR) was associated with the following percentage (95% confidence intervals (CI)) changes in lipids: decreased TG, -2.85 (-4.77, -0.93) and TC/HDL, -1.68 (-2.80, -0.56), and increased HDL, 1.68 (0.93, 2.42). Significant effects were largely restricted to adults (aged 17 to 79). In the younger age group there were no significant associations between walkability and lipids in the fully adjusted model. Significant associations were more frequently seen in females than males. For females, fully adjusted significant inverse associations were observed for TG, LDL, and TC/HDL, and there were positive associations with HDL and Apo A. Canadians living in more walkable neighborhoods have more favorable lipid profiles, suggesting that the built environment has the potential to influence the risk profile for cardiovascular health, especially among adults and females.

Asunto(s)

Características de la Residencia , Triglicéridos , Caminata , Humanos , Persona de Mediana Edad , Masculino , Femenino , Adulto , Anciano , Canadá/epidemiología , Adolescente , Triglicéridos/sangre , Niño , Estudios Transversales , Adulto Joven , HDL-Colesterol/sangre , LDL-Colesterol/sangre , Preescolar , Apolipoproteínas B/sangre , Lípidos/sangre , Apolipoproteínas A/sangre , Biomarcadores/sangre

RESUMEN

BACKGROUND: Uncertainty remains about the long-term effects of air pollutants (AP) on multiple diseases, especially subtypes of cardiovascular disease (CVD). We aimed to assess the individual and joint associations of fine particulate matter (PM2.5), along with its chemical components, nitrogen dioxide (NO2) and ozone (O3), with risks of 32 health conditions. METHODS: A total of 17,566 participants in Sichuan Province, China, were included in 2018 and followed until 2022, with an average follow-up period of 4.2 years. The concentrations of AP were measured using a machine-learning approach. The Cox proportional hazards model and quantile g-computation were applied to assess the associations between AP and CVD. RESULTS: Per interquartile range (IQR) increase in PM2.5 mass, NO2, O3, nitrate, ammonium, organic matter (OM), black carbon (BC), chloride, and sulfate were significantly associated with increased risks of various conditions, with hazard ratios (HRs) ranging from 1.06 to 2.48. Exposure to multiple air pollutants was associated with total cardiovascular disease (HR 1.75, 95% confidence intervals (CIs) 1.62-1.89), hypertensive diseases (1.49, 1.38-1.62), cardiac arrests (1.52, 1.30-1.77), arrhythmia (1.76, 1.44-2.15), cerebrovascular diseases (1.86, 1.65-2.10), stroke (1.77, 1.54-2.03), ischemic stroke (1.85, 1.61-2.12), atherosclerosis (1.77, 1.57-1.99), diseases of veins, lymphatic vessels, and lymph nodes (1.32, 1.15-1.51), pneumonia (1.37, 1.16-1.61), inflammatory bowel diseases (1.34, 1.16-1.55), liver diseases (1.59, 1.43-1.77), type 2 diabetes (1.48, 1.26-1.73), lipoprotein metabolism disorders (2.20, 1.96-2.47), purine metabolism disorders (1.61, 1.38-1.88), anemia (1.29, 1.15-1.45), sleep disorders (1.54, 1.33-1.78), renal failure (1.44, 1.21-1.72), kidney stone (1.27, 1.13-1.43), osteoarthritis (2.18, 2.00-2.39), osteoporosis (1.36, 1.14-1.61). OM had max weights for joint effects of AP on many conditions. CONCLUSIONS: Long-term exposure to increased levels of multiple air pollutants was associated with risks of multiple health conditions. OM accounted for substantial weight for these increased risks, suggesting it may play an important role in these associations.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Enfermedades Cardiovasculares , Material Particulado , Humanos , China/epidemiología , Contaminación del Aire/efectos adversos , Masculino , Femenino , Persona de Mediana Edad , Estudios Prospectivos , Material Particulado/efectos adversos , Material Particulado/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Enfermedades Cardiovasculares/epidemiología , Adulto , Ozono/efectos adversos , Ozono/análisis , Anciano , Exposición a Riesgos Ambientales/efectos adversos , Factores de Riesgo , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis

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Fine particulate matter (PM2.5) exposure has been extensively linked to reproductive and developmental dysfunctions, yet the underlying mechanisms remain elusive. This study employed single-cell RNA sequencing (scRNA-seq) to investigate PM2.5-induced changes in uterine cell populations and gene expression profiles in mice during estrus and early pregnancy. Methodologically, we intranasally inoculated mice with 20 µL of 4.0 mg/mL PM2.5 suspension during their estrus and early pregnancy periods. Utilizing scRNA-seq analysis, we revealed significant alterations in cell type composition following PM2.5 exposure. Notably, we observed a marked decrease in the proportion of natural killer (NK) cells in PM2.5-exposed mice (2.00 % vs. 8.97 % in controls). Further functional enrichment analysis identified suppression of the IL-17 signaling pathway in NK cells as a key mechanism of PM2.5-induced toxicity. GSEA analysis showed in-depth details of the downregulated genes in this pathway, including Fosb, S100a8, Tnfaip3, IL-17a, and S100a9. PM2.5 exposure also disrupted intercellular communication within the uterine microenvironment, with the number of cell interactions decreasing from 483 to 315 and interaction strength reducing from 12.43 to 6.78 compared to controls. Histological examination revealed that PM2.5 exposure led to thinning of the endometrium and less prominent main branches in uterine tissues, and immunofluorescence assays corroborated the altered expression of IL-17 pathway components, showing enhanced Hsp90ab1 expression and reduced FOSB, S100A8, and S100A9 expression in PM2.5-exposed uterine tissues. These findings provide novel insights into the cellular mechanisms of PM2.5-induced reproductive toxicity, highlighting the IL-17 signaling pathway in uterine NK cells as a potential target for therapeutic interventions. Our results underscore the need for air quality regulations and open new avenues for developing biomarkers and targeted therapies to mitigate the reproductive risks associated with PM2.5 exposure.

RESUMEN

Fine particulate matter (PM2.5) can damage airway epithelial barriers. The anion transport system plays a crucial role in airway epithelial barriers. However, the detrimental effect and mechanism of PM2.5 on the anion transport system are still unclear. In this study, airway epithelial cells and ovalbumin (OVA)-induced asthmatic mice were used. In transwell model, the adenosine triphosphate (ATP)-induced transepithelial anion short-circuit current (Isc) and airway surface liquid (ASL) significantly decreased after PM2.5 exposure. In addition, PM2.5 exposure decreased the expression levels of P2Y2R, CFTR and cytoplasmic free-calcium, but ATP can increase the expressions of these proteins. PM2.5 exposure increased the levels of Th2-related cytokines of bronchoalveolar lavage fluid, lung inflammation, collagen deposition and hyperplasisa of goblet cells. Interestingly, the administration of ATP showed an inhibitory effect on lung inflammation induced by PM2.5. Together, our study reveals that PM2.5 impairs the ATP-induced transepithelial anion Isc through downregulating P2Y2R/CFTR pathway, and this process may participate in aggravating airway hyperresponsiveness and airway inflammation. These findings may provide important insights on PM2.5-mediated airway epithelial injury.

Asunto(s)

Asma , Regulador de Conductancia de Transmembrana de Fibrosis Quística , Material Particulado , Receptores Purinérgicos P2Y2 , Animales , Ratones , Receptores Purinérgicos P2Y2/metabolismo , Receptores Purinérgicos P2Y2/genética , Asma/metabolismo , Asma/patología , Asma/tratamiento farmacológico , Asma/inducido químicamente , Asma/inmunología , Material Particulado/efectos adversos , Material Particulado/toxicidad , Regulador de Conductancia de Transmembrana de Fibrosis Quística/metabolismo , Regulador de Conductancia de Transmembrana de Fibrosis Quística/genética , Humanos , Adenosina Trifosfato/metabolismo , Ovalbúmina/inmunología , Transducción de Señal/efectos de los fármacos , Células Epiteliales/efectos de los fármacos , Células Epiteliales/metabolismo , Regulación hacia Abajo/efectos de los fármacos , Mucosa Respiratoria/metabolismo , Mucosa Respiratoria/efectos de los fármacos , Mucosa Respiratoria/patología , Líquido del Lavado Bronquioalveolar/citología , Líquido del Lavado Bronquioalveolar/química , Líquido del Lavado Bronquioalveolar/inmunología

RESUMEN

BACKGROUND: Enhanced cardiovascular health (CVH) is linked to reduced mortality risks, whereas long-term exposure to fine particulate matter (PM2.5), elevates these risks. Whether long-term exposure to PM2.5 counteracts the health benefits of high CVH is unknown. The study aims to evaluate whether the association of CVH assessed by Life's Essential 8 (LE8) with death was consistent between participants with different PM2.5 exposures. METHODS: We included 134,727 participants in the field survey of China Chronic Disease and Risk Factor Surveillance which was conducted from August 2013 to June 2014. The deaths of participants were obtained by linking to the National Mortality Surveillance System (2013-2018). The environmental data is obtained by satellite inversion. The participants' CVH scores were calculated using the LE8 method. Hazard ratio (HR) and 95% confidence intervals (95%CI) for mortality were calculated using Cox regression models. RESULTS: A total of 2,936 all-cause deaths and 1,158 cardiovascular disease (CVD) deaths were recorded. Compared to those with low CVH, adults with high CVH demonstrated a reduced risk of all-cause mortality, irrespective of their PM2.5 exposure levels (P < 0.05, all P for interaction >0.05). Furthermore, in comparison to those with low CVH and highest PM2.5 exposure, adults with high CVH and lowest PM2.5 exposure exhibited HR of 0.18 (95%CI, 0.12-0.25) for all-cause mortality and 0.13 (95%CI, 0.08-0.22) for CVD mortality. CONCLUSIONS: High CVH is associated with reduced all-cause mortality risk, regardless of PM2.5 exposure levels. For Chinese adults, sustaining high CVH is advisable, irrespective of their residential location.

Asunto(s)

Enfermedades Cardiovasculares , Exposición a Riesgos Ambientales , Material Particulado , Humanos , Material Particulado/efectos adversos , Material Particulado/análisis , China/epidemiología , Masculino , Femenino , Persona de Mediana Edad , Enfermedades Cardiovasculares/mortalidad , Estudios Retrospectivos , Exposición a Riesgos Ambientales/efectos adversos , Adulto , Anciano , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminación del Aire/efectos adversos , Factores de Riesgo , Causas de Muerte

RESUMEN

BACKGROUND: There is increasing evidence that exposure to PM2.5 and its constituents is associated with an increased risk of gestational diabetes mellitus (GDM), but studies on the relationship between exposure to PM2.5 constituents and the risk of GDM are still limited. METHODS: A total of 17,855 pregnant women in Guangzhou were recruited for this retrospective cohort study, and the time-varying average concentration method was used to estimate individual exposure to PM2.5 and its constituents during pregnancy. Logistic regression was used to assess the relationship between exposure to PM2.5 and its constituents and the risk of GDM, and the expected inflection point between exposure to PM2.5 and its constituents and the risk of GDM was estimated using logistic regression combined with restricted cubic spline curves. Stratified analyses and interaction tests were performed. RESULTS: After adjustment for confounders, exposure to PM2.5 and its constituents (NO3-, NH4+, and OM) was positively associated with the risk of GDM during pregnancy, especially when exposure to NO3- and NH4+ occurred in the first to second trimester, with each interquartile range increase the risk of GDM by 20.2% (95% CI: 1.118-1.293) and 18.2% (95% CI. 1.107-1.263), respectively. The lowest inflection points between PM2.5, SO42-, NO3-, NH4+, OM, and BC concentrations and GDM risk throughout the gestation period were 18.96, 5.80, 3.22, 2.67, 4.77 and 0.97 µg/m3, respectively. In the first trimester, an age interaction effect between exposure to SO42-, OM, and BC and the risk of GDM was observed. CONCLUSIONS: This study demonstrates a positive association between exposure to PM2.5 and its constituents and the risk of GDM. Specifically, exposure to NO3-, NH4+, and OM was particularly associated with an increased risk of GDM. The present study contributes to a better understanding of the effects of exposure to PM2.5 and its constituents on the risk of GDM.

Asunto(s)

Diabetes Gestacional , Material Particulado , Humanos , Diabetes Gestacional/epidemiología , Femenino , Embarazo , Estudios Retrospectivos , Material Particulado/análisis , Material Particulado/efectos adversos , Adulto , China/epidemiología , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición Materna/efectos adversos , Factores de Riesgo , Modelos Logísticos

RESUMEN

Air pollution in India is a foremost environmental risk factor that affects human health. This study first investigates the geographical distribution of ambient and household air pollution (HAP) and then examines the associated mortality risk. Data on fine particulate matter (PM2.5) concentration has been extracted from the Greenhouse Gas Air Pollution Interactions and Synergies (GAINS) model. HAP, mortality and socio-demographic data were extracted from the National Family and Health Survey-5, India, 2019-2021. Regression models were applied to see the difference in age-group mortality by different pollution parameters. The districts with PM2.5 concentration above the National Ambient Air Quality Standard (NAAQS) level of 40 µg/m3 show a higher risk of neonatal (OR-1.86, CI 1.418-2.433), postneonatal (OR-2.04, CI 1.399-2.971), child (OR-2.19, CI 0.999-4.803) and adult death (OR-1.13, CI 1.060-1.208). The absence of a separate kitchen shows a higher probability of neonatal (OR: 1.18, CI 1.074-1.306) and adult death (OR-1.06, CI 1.027-1.088). The interaction between PM2.5 levels above NAAQS and HAP leads to a substantial rise in mortality observed for neonatal (OR 1.19 CI 1.051-1.337), child (OR 1.17 CI 1.054-1.289), and adult (OR 1.13 CI 1.096-1.168) age groups. This study advocates that there is a strong positive association between ambient and HAP and mortality risk. PM2.5 pollution significantly contributes to the mortality risk in all age groups. Children are more vulnerable to HAP than adults. In India, policymakers should focus on reducing the anthropogenic PM2.5 emission at least to reach the NAAQS, which can substantially reduce disease burden and, more precisely, mortality.

RESUMEN

BACKGROUND: There are a few reports on the associations between fine particulate matter (PM2.5)-bound heavy metals and lung function. OBJECTIVES: To evaluate the associations of single and mixed PM2.5-bound heavy metals with lung function. METHODS: This study included 316 observations of 224 Chinese adults from the Wuhan-Zhuhai cohort over two study periods, and measured participants' personal PM2.5-bound heavy metals and lung function. Three linear mixed models, including the single constituent model, the PM2.5-adjusted constituent model, and the constituent residual model were used to evaluate the association between single metal and lung function. Mixed exposure models including Bayesian kernel machine regression (BKMR) model, weighted quantile sum (WQS) model, and Explainable Machine Learning model were used to assess the relationship between PM2.5-bound heavy metal mixtures and lung function. RESULTS: In the single exposure analyses, significant negative associations of PM2.5-bound lead, antimony, and cadmium with peak expiratory flow (PEF) were observed. In the mixed exposure analyses, significant decreases in forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC), maximal mid-expiratory flow (MMF), and forced expiratory flow at 75% of the pulmonary volume (FEF75) were associated with the increased PM2.5-bound heavy metal mixture. The BKMR models suggested negative associations of PM2.5-bound lead and antimony with lung function. In addition, PM2.5-bound copper was positively associated with FEV1/FVC, MMF, and FEF75. The Explainable Machine Learning models suggested that FEV1/FVC, MMF, and FEF75 decreased with the elevated PM2.5-bound lead, manganese, and vanadium, and increased with the elevated PM2.5-bound copper. CONCLUSIONS: The negative relationships were detected between PM2.5-bound heavy metal mixture and FEV1/FVC, MMF, as well as FEF75. Among the PM2.5-bound heavy metal mixture, PM2.5-bound lead, antimony, manganese, and vanadium were negatively associated with FEV1/FVC, MMF, and FEF75, while PM2.5-bound copper was positively associated with FEV1/FVC, MMF, and FEF75.

RESUMEN

BACKGROUND: Many climate mitigation policies to reduce transportation emissions have public health benefits related to ambient air pollution. However, few health analyses consider the equity implications of alternative policies. Equity can be conceptualized in many different ways that may be relevant to communities, decision-makers, and other stakeholders. OBJECTIVES: To evaluate alternative transportation emissions reduction scenarios across the northeastern United States considering population exposure reductions and multiple equity constructs. METHODS: We developed four quantitative indicators reflecting equity constructs that aligned with stakeholder perspectives, including racial/ethnic exposure inequities, proportion of benefits in environmental justice communities, distribution of benefits among participating states, and rural/urban share of benefits. We analyzed numerous transportation emissions reduction scenarios for directly emitted fine particulate matter (primary PM2.5) covering 12 Northeast states and the District of Columbia. We used the Community Multiscale Air Quality model with the decoupled direct method to estimate the reduction in population-weighted primary PM2.5 exposure and the impact on equity for each scenario. RESULTS: Scenarios that yielded greater reductions in population-weighted primary PM2.5 exposure generally emphasized emissions reductions in urban areas or states with large urban centers, with a more than threefold difference in benefits across scenarios. The higher exposure-benefit scenarios typically also had greater reductions in racial/ethnic exposure inequities but led to higher between-state or rural/urban inequality. Scenarios that targeted uniform percentage emission reductions from light or heavy-duty trucks best addressed rural/urban inequalities but led to the smallest reductions in racial/ethnic inequity. CONCLUSION: There are intrinsic tradeoffs among equity constructs, where focusing resources on distributing benefits across states or between urban and rural populations could come at the expense of less reduction in racial/ethnic exposure inequities or in environmental justice communities. Future health benefits analyses should incorporate multiple equity indicators that reflect different stakeholder perspectives and articulate the underlying constructs and tradeoffs.

RESUMEN

Short-term ambient fine particulate matter (PM2.5) exposure has been related to an increased risk of myocardial infarction (MI) death, but which PM2.5 constituents are associated with MI death and to what extent remain unclear. We aimed to explore the associations of short-term exposure to PM2.5 constituents with MI death and evaluate excess mortality. We conducted a time-stratified case-crossover study on 237,492 MI decedents in Jiangsu province, China during 2015-2021. Utilizing a validated PM2.5 constituents grid dataset at 1 km spatial resolution, we estimated black carbon (BC), organic carbon (OC), sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), and chloride (Cl-) exposure by extracting daily concentrations grounding on the home address of each subject. We employed conditional logistic regression models to evaluate the exposure-response relationship between PM2.5 constituents and MI death. Overall, per interquartile range (IQR) increase of BC (lag 06-day; IQR: 1.75 µg/m3) and SO42- (lag 04-day; IQR: 5.06 µg/m3) exposures were significantly associated with a 3.91% and 2.94% increase in odds of MI death, respectively, and no significant departure from linearity was identified in the exposure-response curves for BC and SO42-. If BC and SO42- exposures were reduced to theoretical minimal risk exposure concentration (0.89 µg/m3 and 1.51 µg/m3), an estimate of 4.55% and 4.80% MI deaths would be avoided, respectively. We did not find robust associations of OC, NO3-, NH4+, and Cl- exposures with MI death. Individuals aged ≥80 years were more vulnerable to PM2.5 constituent exposures in MI death (p for difference <0.05). In conclusion, short-term exposure to PM2.5-bound BC and SO42- was significantly associated with increased odds of MI death and resulted in extensive excess mortality, notably in older adults. Our findings emphasized the necessity of reducing toxic PM2.5 constituent exposures to prevent deaths from MI and warranted further studies on the relative contribution of specific constituents.

RESUMEN

Air purifier use, shift work, and long-term exposure to fine particulate matter (PM2.5) are linked to platelet abnormality. However, the role of air purifier use and shift work in the individual or joint associations of PM2.5 and its components with platelet indices are largely unknown. A total of 8772 participants were recruited from a population of subway workers in China. PM2.5 and its component data were obtained from the Tracking Air Pollution in China dataset. The role of air purifier use and shift work in the association between PM2.5 and its components and platelet indices were analyzed. Among shift workers without air purifier use, positive associations of PM2.5 and each component in PM2.5 with the mean platelet volume (MPV) or platelet counts (PLT) were observed, whereas negative associations of PM2.5 and each component in PM2.5 with the platelet distribution width (PDW) were observed. Furthermore, estimated changes (95%CIs) in PLT, MPV, and PDW in response to each 10th percentile increment in the mixture of PM2.5 and its components were 0.8657 (0.2496, 1.4819), 0.0192 (0.0054, 0.0329), and -0.0648 (-0.0945, -0.0351), respectively, and sulfate in PM2.5 was the major contributor to those associations. Long-term exposure to PM2.5 and its components was related to increased platelet disorders among shift workers without air purifier use, and those associations were mainly attributed to sulfate in PM2.5.

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Accurate long-term PM2.5 prediction is crucial for environmental management and public health. However, previous studies have mainly focused on short-term air quality point predictions, neglecting the importance of accurately predicting the long-term trends of PM2.5 and studying the uncertainty of PM2.5 concentration changes. The traditional approaches have limitations in capturing nonlinear relationships and complex dynamic patterns in time series, and they often overlook the credibility of prediction results in practical applications. Therefore, there is still much room for improvement in long-term prediction of PM2.5. This study proposes a novel long-term point and interval prediction framework for urban air quality based on multi-source spatial and temporal data, which further quantifies the uncertainty and volatility of the prediction based on the accurate PM2.5 point prediction. In this model, firstly, multi-source datasets from multiple monitoring stations are preprocessed. Subsequently, spatial clustering of stations based on POI data is performed to filter out strongly correlated stations, and feature selection is performed to eliminate redundant features. In this paper, the ConvFormer-KDE model is presented, whereby local patterns and short-term dependencies among multivariate variables are mined through a convolutional neural network (CNN), long-term dependencies among time-series data are extracted using the Transformer model, and a direct multi-output strategy is employed to realize the long-term point prediction of PM2.5 concentration. KDE is utilized to derive prediction intervals for PM2.5 concentration at confidence levels of 85%, 90%, and 95%, respectively, reflecting the uncertainty inherent in long-term trends of PM2.5. The performance of ConvFormer-KDE was compared with a list of advanced models. Experimental results showed that ConvFormer-KDE outperformed baseline models in long-term point- and interval-prediction tasks for PM2.5. The ConvFormer-KDE can provide a valuable early warning basis for future PM2.5 changes from the aspects of point and interval prediction.

RESUMEN

Ambient particulate matter (PM2.5) is a potential risk factor for metabolic damage to the liver. Epidemiological studies suggest that elevated PM2.5 concentrations cause changes in hepatic metabolism, but there is a lack of laboratory evidence. Here, we aimed to evaluate the effects of PM2.5 exposure on liver metabolism in C57BL/6j female mice (10 months old) and to explore the mechanisms underlying metabolic alterations and differential gene expressions by combining metabolomics and transcriptomics analyses. The metabolomics results showed that PM2.5 exposure notably affected the metabolism of amino acids and organic acids and caused hepatic lipid and bile acid accumulation. The transcriptomic analyses revealed that PM2.5 exposure led to a series of metabolic pathway abnormalities, including steroid biosynthesis, steroid hormone biosynthesis, primary bile acid biosynthesis, etc. Among them, the changes in the bile acid pathway might be one of the causes of liver damage in mice. In conclusion, this study clarified the changes in liver metabolism in mice caused by PM2.5 exposure through combined transcriptomic and metabolomic analyses, revealed that abnormal bile acid metabolism is the key regulatory mechanism leading to metabolic-associated fatty liver disease (MAFLD) in mice, and provided laboratory evidence for further clarifying the effects of PM2.5 on body metabolism.

RESUMEN

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 (PM 2.5). Methods: Joinpoint 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 PM 2.5 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 PM 2.5-attributable stroke burden in China during 1990-2019, highlighting the health effects of air quality improvement policies.

Asunto(s)

Contaminantes Atmosféricos , Material Particulado , Accidente Cerebrovascular , Material Particulado/efectos adversos , Material Particulado/análisis , China/epidemiología , Humanos , Accidente Cerebrovascular/epidemiología , Accidente Cerebrovascular/etiología , Persona de Mediana Edad , Anciano , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Masculino , Femenino , Contaminación del Aire/efectos adversos , Adulto , Anciano de 80 o más Años , Exposición a Riesgos Ambientales/efectos adversos

RESUMEN

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.

Asunto(s)

Contaminantes Atmosféricos , Material Particulado , Fenoles , Estaciones del Año , Material Particulado/análisis , Material Particulado/toxicidad , Fenoles/análisis , Fenoles/toxicidad , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , China , Antioxidantes/análisis , Antioxidantes/química , Especies Reactivas de Oxígeno/metabolismo , Monitoreo del Ambiente , Estrés Oxidativo/efectos de los fármacos , Oxidación-Reducción

RESUMEN

Climate change and air pollution are major challenges facing the world today. Cold waves and air pollution significantly impact ischemic heart disease (IHD), but the extent of these effects at different altitudes remains unclear, especially their interactions. We collected daily meteorological, pollutant, and IHD hospitalization data from Xining and Xinxiang from 2016 to 2021. Using a time-stratified case-crossover approach, we fitted conditional Poisson regression models to assess the association between cold waves, PM2.5, and IHD hospitalizations and quantified their interactions. Additionally, we calculated the attributable fraction (AF) and attributable number (AN) of hospitalizations due to exposure to cold waves and medium to high-level PM2.5. We also performed stratified analyses by altitude, gender, and age. Both cold waves and PM2.5 were positively associated with IHD hospitalization rates in Xining and Xinxiang, but the differences between the two regions were not significant. The relative risk of cold waves was 1.15 (1.07, 1.24) in Xining and 1.16 (1.11, 1.21) in Xinxiang. In Xining, there was an interaction between cold waves and different levels of PM2.5. We estimated the attributable fraction due to the joint exposure of cold waves and PM2.5 to be 0.14-0.49 in Xining and 0.26-0.36 in Xinxiang. Older adults and males faced higher risks. This study highlights the importance of reducing PM2.5 exposure and optimizing extreme weather warning systems and suggests further exploration of the impacts of individual behaviors and regional characteristics on IHD.

Asunto(s)

Contaminantes Atmosféricos , Contaminación del Aire , Altitud , Hospitalización , Isquemia Miocárdica , Material Particulado , Material Particulado/análisis , Material Particulado/toxicidad , Humanos , Hospitalización/estadística & datos numéricos , Masculino , Femenino , Persona de Mediana Edad , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/toxicidad , Anciano , China/epidemiología , Contaminación del Aire/estadística & datos numéricos , Contaminación del Aire/efectos adversos , Isquemia Miocárdica/epidemiología , Isquemia Miocárdica/inducido químicamente , Exposición a Riesgos Ambientales/estadística & datos numéricos , Exposición a Riesgos Ambientales/efectos adversos , Adulto , Cambio Climático , Frío/efectos adversos