Air pollutants and ovarian reserve: a systematic review of the evidence.

Background: Growing evidence indicates an association between ambient air pollution and decreased human reproductive potential. This study aims to systematically review the association between air pollutants and female ovarian reserve. Methods: The literature was searched in six electronic databases through June 2024. Screening the 136 articles retrieved for inclusion criteria resulted in the selection of 15 human observational studies that evaluated the effect of environmental pollutants on ovarian reserve markers. The study protocol was registered on the International Prospective Register of Systematic Reviews (PROSPERO, registration code: CRD42023474218). Results: The study design of the selected studies was found to be cross-sectional (2 of 15), retrospective cohort (10 of 15), prospective cohort (2 of 15), and case-control (1 of 15). The study population was distributed as follows: Asians (53%, eight studies), Americans (33%, five studies), and Europeans (14%, two studies). The main findings showed a higher body of evidence for the environmental pollutants PM2.5, PM10, and NO2, while a low body of evidence for PM1, O3, SO2, and a very low body of evidence for benzene, formaldehyde, and benzo(a)pyrene, yet consistently showing significant inverse association data. The overall methodological quality of the selected studies was rated moderated across the 14 domains of the National Institutes of Health (NIH) toolkit. Conclusion: The data suggest that increased exposure to air pollutants seems to be associated with reduced ovarian reserve, with the most substantial evidence for pollutants such as PM2.5, PM10, and NO2. However, more evidence is needed to draw conclusions about causality.

Association of specific PM2.5 chemical constituents and ozone exposure with pregnancy outcomes in women undergoing assisted reproductive technology treatment in central China.

The associations of air pollutants exposure with assisted reproductive technology (ART) pregnancy outcomes are mixed, and the effects of specific components of fine particulate matter (PM2.5) and ozone (O3) are not well understood. We conducted a retrospective longitudinal study to explore the association of PM2.5 constituents and O3 exposure with three ART outcomes among women undergoing ART treatment. The exposure window was segmented into five periods corresponding to the cycle of ovarian stimulation and oocyte retrieval procedure. Generalized linear mixed model (GLMM) was applied to explore the relationships between PM2.5 constituents, O3, Normalized Vegetation Index (NDVI) exposure and three ART outcomes. The combined effect of PM2.5 constituents was evaluated by the quantile g (qg)-computation. We also explored the modifying effect of different covariate. Elevated exposure level of PM2.5 (OR = 0.915, 95% CI: 0.859, 0.974) and its constituents (BC: 0.905, 95% CI: 0.840, 0.975; OM: 0.910, 95% CI: 0.848, 0.976; NO3-: 0.909, 95% CI: 0.850, 0.972, SO42-: 0.905, 95% CI: 0.846, 0.968, and NH4+: 0.902, 95% CI: 0.842, 0.966) exposure throughout the year before oocyte retrieval (period 1) was correlated with a reduced odds ratio (OR) of live birth with statistical significance. Similarly, for each interquartile range (IQR) increase in O3 exposure during periods 2 (85 days prior to oocyte retrieval), 3 (30 days prior to oocyte retrieval), 4 (oocyte retrieval to embryo transfer) and 5 (embryo transfer to hCG test) was significantly related to a decreased OR of live birth. Especially, participants who underwent fresh embryo transfer cycles and received two cleavage-stage embryo transfer, and were younger than 30 years old, showed a higher susceptibility to particulate matter. Findings from this study suggest that PM2.5 constituents and O3 exposure may have adverse effects on the ART outcomes, highlighting the importance of identifying critical exposure periods for various air pollutants and the need for meticulous management of particulate matter.

Research on the causal relationship between fine particulate matter and type 2 diabetes mellitus: A two-sample multivariable mendelian randomization study.

BACKGROUND AND AIMS: Previous research has suggested a correlation between fine particulate matter (PM2.5) and type 2 diabetes mellitus (T2DM). However, the causality was vulnerable to confounding variables. METHODS AND RESULTS: A two-sample multivariable mendelian randomization study was designed to examine the causal connection between PM2.5 and T2DM. PM2.5 trait was investigated as exposure while T2DM-related traits as outcomes. The summary data were obtained from the Finngen database and the open genome-wide association study database. The mendelian randomization estimates were obtained using the inverse-variance weighted approach, and multiple sensitivity analyses were conducted. There were potential causal relationships between PM2.5 and T2DM (OR = 2.418; P = 0.019), PM2.5 and glycated hemoglobin (HbA1c) (OR = 1.590; P = 0.041), and PM2.5 and insulin metabolism. PM2.5 was found to have no causal effect on fasting glucose and insulin, 2-h glucose, and insulin-like growth factor binding protein-1 (P > 0.05), while had a potential protective effect against some diabetes complications. CONCLUSIONS: Our findings indicated potential causal relationships among PM2.5 and T2DM, especially the causal relationship between PM2.5 and long-term glucose levels.

Higher risk of patients after stent(s) insertion with vessel bifurcation treated in the association between PM2.5 and cardiovascular hospital readmission.

Stent(s) insertion is a common form of surgery for patients with cardiovascular diseases, and is associated with a high rate of hospital readmission. This study aims to investigate the acute association between PM2.5 exposure and hospital readmission for patients with cardiovascular disease and a history of stent(s) insertion. The records of hospital admission were collected from the Beijing Municipal Commission of Health and Family Planning Information Center between 1st January 2013 and 31st December 2017. Subsequent hospital readmission records for patients with a history of stent(s) insertion or without any surgery were extracted. The conditional logistic regression model was applied to investigate the association between PM2.5 concentration and cardiovascular disease readmission in patients who had undergone stent(s) insertion or without any surgery. A total of 81,468 patients who had a history of stent(s) insertion were included in this study. Of these, 17,224 patients (21.1 % of the total number of patients) were readmitted 27,749 times due to cardiovascular disease. The median daily PM2.5 concentration was 62.8 µg/m3 with an interquartile range (IQR) of 71.5 µg/m3. The excess risk (ER) associated 10 µg/m3 increase in PM2.5 concentration for readmission due to cardiovascular disease was 0.48 % (95 % CI: 0.09 %, 0.87 %) in patients with a history of stent(s) insertion. Patients who had stent(s) insertion at the vessel bifurcation site showed the highest risk of readmission for cardiovascular disease when exposed to PM2.5; the ER was 4.12 % (95 % CI: 1.60 %, 6.70 %). PM2.5 was significantly associated with angina pectoris and readmission for chronic ischemic heart disease in patients with a history of stent(s) insertion. PM2.5 had a significant association with cardiovascular readmission among patients with a history of insertion of stent(s). Patients who had vessel bifurcation treated showed the highest risk of readmission.

Airborne antibiotic resistome from sludge dewatering systems: Mobility, pathogen accessibility, cross-media migration propensity, impacting factors, and risks.

Bioaerosol contamination was considered as a potential health threat in sludge dewatering systems (SDSs), while emission and risk of airborne antibiotic resistome remain largely unclear. Herein, seasonal investigations of fine particulate matter (PM2.5) were conducted using metagenomics-based methods within and around different SDSs, together with an analysis of sewage sludge. Featured with evident seasonality, antibiotic resistance genes (ARGs) in SDS-PM2.5 also possessed greater accumulation, transfer, and pathogen accessibility than those in ambient air PM2.5. Mobile ARGs in SDS-PM2.5 mainly encoded resistance to tetracycline, and most were flanked by integrase. Some pathogenic antibiotic resistant bacteria (PARB), including Enterobacter asburiae, Escherichia coli, Enterococcus faecium, and Staphylococcus aureus, also carried mobile genetic elements in SDS-PM2.5. Dewatering behavior actuated > 50.56% of ARG subtypes and > 42.86% of PARB in sewage sludge to aerosolize into air. Relative humidity, temperature, and PM2.5 concentration collectively drove the evolution of bacterial community and indirectly promoted the antibiotic resistance of SDS-PM2.5. SDS-PM2.5 posed more serious resistome risks than sewage sludge and ambient air PM2.5, and the highest levels were discovered in winter. These findings underline the role of dewatering behavior in facilitating resistome's aerosolization, and the need to mitigate this potential air pollution.

Variation in oxidative potential of fine particulate matter and its association with chemical constituents at a regional site in India.

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 ± 0.84 nmol min-1 m-3) and at the lowest during monsoon (0.79 ± 0.65 nmol min-1 m-3). OPAAv exhibited the highest activity in post-monsoon (0.09 ± 0.04 nmol min-1 m-3) and least in summer (0.05 ± 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.

Kidney Injury Evoked by Fine Particulate Matter: Risk Factor, Causation, Mechanism and Intervention Study.

Fine particulate matter (PM2.5) is suggested to pose a severe risk to the kidneys by inducing functional degradation and chronic kidney diseases (CKD). This study aims to explore the nephrotoxicity of PM2.5 exposure and the underlying mechanism. Herein, based on the UK Biobank, it is found that per interquartile range (IQR) increase in PM2.5 is associated with a 6% (95% CI: 1%-11%), 7% (95% CI: 3%-11%), 9% (95% CI: 4%-13%), 11% (95% CI: 9%-13%), and 10% (95% CI: 8%-12%) increase in the risk of nephritis, hydronephrosis, kidney stone, acute renal failure, and CKD, respectively. In experimental study, noticeable kidney injury, which is the initiation of kidney diseases, is observed with PM2.5 exposure in C57BL/6N mice (n = 8), accompanied with oxidative stress, autophagy and pyroptosis. In vitro, HK-2 cells with PM2.5-stimulation exhibit tubulopathy, increased reactive oxygen species (ROS) generation and activated pyroptosis and autophagy. All changes are abolished by ROS scavenger of N-acetyl-L-cysteine (NAC) both in vivo and in vitro. In conclusion, the study provides evidence showing that PM2.5 exposure is associated with 5 kinds of kidney diseases by directly inducing nephrotoxicity, in which ROS may be the potential target by triggering autophagy and pyroptosis.

The temporal trend and disparity in short-term health impacts of fine particulate matter in California (2006-2019).

Most epidemiological studies assume that the relationship between short-term air pollution exposure and health outcomes is constant over time, which ignores potential changes in population composition and particulate matter emission sources. Limited studies have assessed changes in the relationship between fine particulate matter (PM2.5) and adverse health outcomes over time, with mixed results. Additionally, there is a need to identify which subgroups are disproportionately impacted over time by PM2.5-related health consequences. Therefore, we aimed to examine whether temporal trends exist in the relationships between daily PM2.5 exposure and circulatory and respiratory acute care utilization in California from 2006 to 2019. We further assessed whether certain subpopulations are more susceptible to PM2.5 exposure by demographic characteristics and extreme wildfire frequency. Daily PM2.5 concentrations estimated from a stacked ensemble model and daily cause-specific acute care utilization and demographic data from the California Department of Health Care Access and Information. We analyzed this relationship using modified two-stage Bayesian hierarchical models, where we first did not consider temporal trends, then stratified by two periods, and finally flexibly considered non-linear changes over time. Increases in circulatory (0.56 %; 95 % credible interval (CI): 0.17 %, 0.96 %) and respiratory acute care utilization risk (2.61 %; 95%CI: 2.29 %, 2.94 %) were found with every 10 µg/m3 increase in PM2.5 on the same day and previous two days. These risks were found to increase over time, where 0.13 % (95%CI: 0.02 %, 0.22 %) and 1.40 % (95%CI: 1.24 %, 1.54 %) increases were identified for circulatory and respiratory acute care utilizations, respectively, from the first (2006-2012) to second period (2013-2019). Differences by age, sex, race/ethnicity, and extreme wildfire frequency were noted. These findings confirm that air pollution guidelines should consider the dynamic nature of epidemiological dose-response and can provide insight for targeted air pollution control and adaptation policies designed to reduce PM2.5 exposure, particularly for the most susceptible subpopulations.

Long-term exposure to wildland fire smoke PM2.5 and mortality in the contiguous United States.

Despite the substantial evidence on the health effects of short-term exposure to ambient fine particles (PM2.5), including increasing studies focusing on those from wildland fire smoke, the impacts of long-term wildland fire smoke PM2.5 exposure remain unclear. We investigated the association between long-term exposure to wildland fire smoke PM2.5 and nonaccidental mortality and mortality from a wide range of specific causes in all 3,108 counties in the contiguous United States, 2007 to 2020. Controlling for nonsmoke PM2.5, air temperature, and unmeasured spatial and temporal confounders, we found a nonlinear association between 12-mo moving average concentration of smoke PM2.5 and monthly nonaccidental mortality rate. Relative to a month with the long-term smoke PM2.5 exposure below 0.1 µg/m3, nonaccidental mortality increased by 0.16 to 0.63 and 2.11 deaths per 100,000 people per month when the 12-mo moving average of PM2.5 concentration was of 0.1 to 5 and 5+ µg/m3, respectively. Cardiovascular, ischemic heart disease, digestive, endocrine, diabetes, mental, and chronic kidney disease mortality were all found to be associated with long-term wildland fire smoke PM2.5 exposure. Smoke PM2.5 contributed to approximately 11,415 nonaccidental deaths/y (95% CI: 6,754, 16,075) in the contiguous United States. Higher smoke PM2.5-related increases in mortality rates were found for people aged 65 and above. Positive interaction effects with extreme heat were also observed. Our study identified the detrimental effects of long-term exposure to wildland fire smoke PM2.5 on a wide range of mortality outcomes, underscoring the need for public health actions and communications that span the health risks of both short- and long-term exposure.

Interactions between fibroblasts and monocyte-derived cells in chronic lung injuries induced by real-ambient particulate matter exposure.

Long-term exposure to fine particulate matter (PM2.5) can lead to chronic lung injury, including inflammation, idiopathic pulmonary fibrosis, and cancer. Mesenchymal cells, such as fibroblasts, myeloid-derived suppressor cells (MDSCs), and interstitial macrophages (IMs), contribute to immune regulation in lung, yet their diversity and functions upon long-term exposure to particulate matter (PM) remain inadequately characterized. In this study, we conducted a 16-week real-ambient PM exposure experiment on C57BL/6 J male mice in Shijiazhuang, China. We used single-cell RNA sequencing to analyze the cellular and molecular changes in lung tissues. Notably, we revealed a significant increase in specific fibroblast (ATX+, Col5a1+Meg3+, universal fibroblasts) and monocyte-derived cell subpopulations (monocytic-MDSCs (M-MDSCs), Lyve1loMHC-Ⅱhi IMs, Lyve1hiMHC-Ⅱlo IMs) that exhibited pro-inflammatory and pro-fibrotic functions. These cell subpopulations engaged in immunosuppressive signaling pathways and interactions with various cytokines, shaping a pulmonary microenvironment similar to those associated with cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs). This altered immune environment may promote the development of pulmonary fibrosis caused by PM exposure, underscoring the intricate roles of mesenchymal cells in chronic lung injury and highlighting the cancer-causing potential of PM2.5 exposure.

Air pollution and risk of 32 health conditions: outcome-wide analyses in a population-based prospective cohort in Southwest China.

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.

A longitudinal study on the effect of PM2.5 components on blood pressure in the hypertensive patients from 2011 to 2019.

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.

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.

The prevalent trajectory of early menopause associated with PM2.5 exposure across 1956-2018 extrapolated from LightGBM algorithm.

BACKGROUND: Fine particulate matter (PM2.5) is noxious to female reproductive development and facilitates the occurrence of subsequent diseases. Early menopause is initiative factor of female aging. But due to the lack of historical exposure of PM2.5, we could not gain insight into the linkage between ambient PM2.5 exposure and early menopause. METHODS: We conducted a community-based retrospective cross-sectional study and pooled 1173 postmenopausal women. The machine learning algorithm of LightGBM was processed to derive the historical concentrations of PM2.5 based on aerography of 1956-2022. The quantile g-computation and binary logistic regression were employed to estimate the mixed and single associations between PM2.5 and early menopause. RESULTS: The visibility topped the most important feature for derivations of historical PM2.5 concentrations. The R2 of 10-fold cross-validation and predictive capability during processing were all above 0.8. The prevalence of early menopause was 7.3 %. Each 10 µg/m3 PM2.5 increased the prevalence of early menopause during prior 2 years exposure (OR: 1.49, 95 %CI: 1.03-2.16) and spring and autumn (OR: 1.28, 95 %CI: 1.07-1.54). After adjusting the reverse effects of temperature, the prior 2 years exposure of PM2.5 remained positively associated with early menopause in the fourth quantile vs the first quantile (OR: 3.36, 95 %CI: 1.53-7.36) in the spring and autumn. The higher BMI (OR: 1.40, 95 %CI: 1.14-1.72), waistline (OR: 1.42, 95 %CI: 1.09-1.85) and unfavourable dietary habits of less meat (OR: 1.72, 95 %CI: 1.11-2.68), more fried food (OR: 2.39, 95 %CI: 1.15-4.99) elevated the prevalence of early menopause. CONCLUSIONS: The accurate environmental exposure assessment of historical PM2.5 vigorously promoted the researches on the relationship between PM2.5 and early menopause. It sounds the alarm on female infertility menace associated with particulate matter especially during the turbulent 2 years before menopause.

Single-cell RNA sequencing of estrual mice reveals PM2.5-induced uterine cell heterogeneity and reproductive toxicity.

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.

Mitochondrial dysfunction induced by ambient fine particulate matter and potential mechanisms.

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.

The association between neighbourhood walkability and blood lipids: a Canadian population study.

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.

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.

Associations of personal PM2.5-bound heavy metals and heavy metal mixture with lung function: Results from a panel study in Chinese urban residents.

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.

Short-term exposure to ambient fine particulate matter constituents and myocardial infarction mortality.

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.