Interaction between Extreme Temperature Events and Fine Particulate Matter on Cardiometabolic Multimorbidity: Evidence from Four National Cohort Studies.

Accumulating evidence linked extreme temperature events (ETEs) and fine particulate matter (PM2.5) to cardiometabolic multimorbidity (CMM); however, it remained unknown if and how ETEs and PM2.5 interact to trigger CMM occurrence. Merging four Chinese national cohorts with 64,140 free-CMM adults, we provided strong evidence among ETEs, PM2.5 exposure, and CMM occurrence. Performing Cox hazards regression models along with additive interaction analyses, we found that the hazards ratio (HRs) of CMM occurrence associated with heatwave and cold spell were 1.006-1.019 and 1.063-1.091, respectively. Each 10 µg/m3 increment of PM2.5 concentration was associated with 17.9% (95% confidence interval: 13.9-22.0%) increased risk of CMM. Similar adverse effects were also found among PM2.5 constituents of nitrate, organic matter, sulfate, ammonium, and black carbon. We observed a synergetic interaction of heatwave and PM2.5 pollution on CMM occurrence with relative excess risk due to the interaction of 0.999 (0.663-1.334). Our study provides novel evidence that both ETEs and PM2.5 exposure were positively associated with CMM occurrence, and the heatwave interacts synergistically with PM2.5 to trigger CMM.

Assessing the spatiotemporal evolution and socioeconomic determinants of PM2.5-related premature deaths in China from 2000 to 2021.

China's swift socioeconomic development has led to extremely severe ambient PM2.5 levels, the associated negative health outcomes of which include premature death. However, a comprehensive explanation of the socioeconomic mechanism contributing to PM2.5-related premature deaths has not yet to be fully elucidated through long-term spatial panel data. Here, we employed a global exposure mortality model (GEMM) and the system generalized method of moments (Sys-GMM) to examine the primary determinants contributing to premature deaths in Chinese provinces from 2000 to 2021. We found that in the research period, premature deaths in China increased by 46 %, reaching 1.87 million, a figure that decreased somewhat after the COVID-19 outbreak. 62 thousand premature deaths were avoided in 2020 and 2021 compared to 2019, primarily due to the decline in PM2.5 concentrations. Premature deaths have increased across all provinces, particularly in North China, and a discernible spatial agglomeration effect was observed, highlighting effects on nearby provinces. The findings also underscored the significance of determinants such as urbanization, import and export trade, and energy consumption in exacerbating premature deaths, while energy intensity exerted a mitigating influence. Importantly, a U-shaped relationship between premature deaths and economic development was unveiled for the first time, implying the need for vigilance regarding potential health impact deterioration and the implementation of countermeasures as the per capita GDP increases in China. Our findings deserve attention from policymakers as they shed fresh insights into atmospheric control and Health China action.

Atmospheric emissions of particulate matter-bound heavy metals from industrial sources.

Although industrial activities are significant contributors to atmospheric releases of particulate matter (PM) and associated toxic substances that lead to adverse human health effects, a knowledge gap exists concerning the human health risk resulting from such activities owing to lack of evaluation of industrial emissions. Here, we comprehensively characterized and quantified PM from 118 full-scale industrial plants. The dominant (97.9 %) PM showed diameters of <2.5 µm; 79.0 % had diameters below 1 µm. Annual atmospheric releases of Fe and heavy metals (As, Cd, Cr, Cu, Ni, Pb, Zn) contained in fine PM from these global industrial activities are estimated to be 51,161 t and 69,591 t, respectively. Emissions of heavy metals from these industries cause increased cancer risk, estimated to range from 1461 % to 50,752 %. Five crystalline compounds (ZnO, PbSO4, Mn3O4, Fe3O4, Fe2O3) that can indicate specific industrial sources are identified. Global annual emissions of these toxic compounds in fine PM from the industrial sources are estimated to be 78,635 t. The Global South displayed higher emissions than the Global North. These results are significant for recognizing regional health risks of industrial emissions.

Year-long and seasonal differences of PM2.5 chemical characteristics and their role in the viability of human lung epithelial cells (A549).

Fine particulate matters-PM2.5 in the air can have considerable negative effects on human health and the environment. Various human cell-based studies examined the effect of PM2.5 on human health in different cities of the world using various chemical parameters. Unfortunately, limited information is available regarding the relationship between toxicity and chemical characteristics of PM2.5 collected in Istanbul, Türkiye, located in one of the most populated cities in the world. To investigate the chemical characteristics and cytotoxicity of PM2.5 in Istanbul, samples were collected for 12 months, then potentially toxic metals, oxidative potential, and particle indicators (e.g., functional groups and elements) were determined, and the cytotoxicity of PM2.5 on human A549 lung alveolar epithelial cells was examined. The mean PM2.5 mass concentration was 24.0 ± 17.4 µg m-3 and higher in cold months compared to other seasons. Moreover, the results of the metals, elemental, and functional groups indicated that seasonal and monthly characteristics were influenced by the regional anthropogenic sources and photochemistry input. The cytotoxicity results also showed that the viability of A549 cells was reduced with the exposure of PM2.5 (30-53%) and higher cytotoxicity was obtained in summer compared to the other seasons due to the impact of the metals, elements, and oxidative characteristics of PM2.5.

Residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and incident breast cancer among young women in Ontario, Canada.

BACKGROUND: Air pollution has been classified as a human carcinogen based largely on findings for respiratory cancers. Emerging, but limited, evidence suggests that it increases the risk of breast cancer, particularly among younger women. We characterized associations between residential exposure to ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and breast cancer. Analyses were performed using data collected in the Ontario Environmental Health Study (OEHS). METHODS: The OEHS, a population-based case-control study, identified incident cases of breast cancer in Ontario, Canada among women aged 18-45 between 2013 and 2015. A total of 465 pathologically confirmed primary breast cancer cases were identified from the Ontario Cancer Registry, while 242 population-based controls were recruited using random-digit dialing. Self-reported questionnaires were used to collect risk factor data and residential histories. Land-use regression and remote-sensing estimates of NO2 and PM2.5, respectively, were assigned to the residential addresses at interview, five years earlier, and at menarche. Logistic regression was used to estimate odds ratios (OR) and their 95 % confidence intervals (CI) in relation to an interquartile range (IQR) increase in air pollution, adjusting for possible confounders. RESULTS: PM2.5 and NO2 were positively correlated with each other (r = 0.57). An IQR increase of PM2.5 (1.9 µg/m3) and NO2 (6.6 ppb) at interview residence were associated with higher odds of breast cancer and the adjusted ORs and 95 % CIs were 1.37 (95 % CI = 0.98-1.91) and 2.33 (95 % CI = 1.53-3.53), respectively. An increased odds of breast cancer was observed with an IQR increase in NO2 at residence five years earlier (OR = 2.16, 95 % CI: 1.41-3.31), while no association was observed with PM2.5 (OR = 0.96, 95 % CI 0.64-1.42). CONCLUSIONS: Our findings support the hypothesis that exposure to ambient air pollution, especially those from traffic sources (i.e., NO2), increases the risk of breast cancer in young women.

Improving residential wood burning emission inventories with the integration of readily available data sources.

Residential wood burning (RWB) is the largest anthropogenic source of PM2.5 in many North American and European cities in the winter. The current lack of information on the locations, types, and intensity of use of wood burning appliances limits the ability to accurately assess the exposure of the population to RWB emissions. In this study, we generated a high spatial resolution emission inventory for RWB in the province of Quebec, Canada using a novel data driven approach. The method first combines real estate and socioeconomic census data through machine learning models to estimate ownership rates of fireplaces and wood stoves. These ownership rates are then combined with household survey data (on wood consumption and types of appliances), emission factors and building registry data to generate the emission inventory at a 1Km2 resolution. Our proposed approach was able to capture spatial patterns in RWB appliance ownership and intensity of use, which may be overlooked by using simple urban vs rural or population based spatial proxies. The machine learning models explained 80.3 % and 63 % of the variability in wood stove and fireplace ownership rates with each appliance type exhibiting different spatial trends. Wood stoves were common in rural areas and among lower income households, whereas fireplaces were more common in urban areas. Additionally, we observed large spatial and regional variability in emissions per residence due to differences in wood consumption, appliance ownership rates, and appliance mixes (e.g. conventional vs certified). Our results suggest that using simple spatial proxies based on population, urbanization levels or residence type are not enough to explain the spatial distribution of RWB emissions as they might overlook other factors such as socioeconomic factors or regional heating preferences. Finally, our spatially distributed emissions were strongly correlated (r = 0.86) with the increase in PM2.5 concentrations during peak-RWB hours on winter weekends at 42 reference stations across the province of Quebec.

Fine particulate matter components associated with exacerbated depressive symptoms among middle-aged and older adults in China.

Growing awareness acknowledges ambient fine particulate matter (PM2.5) as an environmental risk factor for mental disorders, especially among older people. However, there remains limited evidence regarding which specific chemical components of PM2.5 may be more detrimental. This nationwide prospective cohort study included 22,126 middle-aged and older adult participants of the China Health and Retirement Longitudinal Study (CHARLS, 2011-2016), to explore the individual and joint associations between long-term exposure to various PM2.5 components (sulfate, nitrate, ammonium, organic matter, and black carbon) and depressive symptoms. The depressive symptoms were assessed using the 10-item Center for Epidemiological Studies-Depression Scale (CES-D-10). Using the novel quantile-based g-computation for multi-pollutant mixture analysis, we found that exposure to the mixture of major PM2.5 components was significantly associated with aggravating depressive symptoms, with the exposure-response curve exhibiting consistent linear or supra-linear shape without a lower threshold. The estimated weight index indicated that, among major PM2.5 components, only nitrate, sulfate, and black carbon significantly contributed to the exacerbation of depressive symptoms. Given the expanding aging population, stricter regulation on the emissions of particularly toxic PM2.5 components may mitigate the escalating disease burden of depression.

Exploring the Burden of PM2.5-Related Deaths and Economic Health Losses in Beijing.

Air pollution is one of the major global public health challenges. Using annual fine particulate matter (PM2.5) concentration data from 2016 to 2021, along with the global exposure mortality model (GEMM), we estimated the multi-year PM2.5-pollution-related deaths divided by different age groups and diseases. Then, using the VSL (value of statistical life) method, we assessed corresponding economic losses and values. The number of deaths attributed to PM2.5 in Beijing in 2021 fell by 33.74 percent from 2016, while health economic losses would increase by USD 4.4 billion as per capita disposable income increases year by year. In 2021, the average annual concentration of PM2.5 in half of Beijing's municipal administrative districts is less than China's secondary ambient air quality standard (35 µg/m3), but it can still cause 48,969 deaths and corresponding health and economic losses of USD 16.31 billion, equivalent to 7.9 percent of Beijing's GDP. Therefore, it is suggested that more stringent local air quality standards should be designated to protect public health in Beijing.

TBHQ Alleviates Particulate Matter-Induced Pyroptosis in Human Nasal Epithelial Cells.

Pyroptosis represents a type of cell death mechanism notable for its cell membrane disruption and the subsequent release of proinflammatory cytokines. The Nod-like receptor family pyrin domain containing inflammasome 3 (NLRP3) plays a critical role in the pyroptosis mechanism associated with various diseases resulting from particulate matter (PM) exposure. Tert-butylhydroquinone (tBHQ) is a synthetic antioxidant commonly used in a variety of foods and products. The aim of this study is to examine the potential of tBHQ as a therapeutic agent for managing sinonasal diseases induced by PM exposure. The occurrence of NLRP3 inflammasome-dependent pyroptosis in RPMI 2650 cells treated with PM < 4 µm in size was confirmed using Western blot analysis and enzyme-linked immunosorbent assay results for the pyroptosis metabolites IL-1ß and IL-18. In addition, the inhibitory effect of tBHQ on PM-induced pyroptosis was confirmed using Western blot and immunofluorescence techniques. The inhibition of tBHQ-mediated pyroptosis was abolished upon nuclear factor erythroid 2-related factor 2 (Nrf2) knockdown, indicating its involvement in the antioxidant mechanism. tBHQ showed potential as a therapeutic agent for sinonasal diseases induced by PM because NLRP3 inflammasome activation was effectively suppressed via the Nrf2 pathway.

The Impact of Fine Particulate Matter on Embryonic Development.

Airborne fine particulate matter (PM2.5) in air pollution has become a significant global public health concern related to allergic diseases. Previous research indicates that PM2.5 not only affects the respiratory system but may also induce systemic inflammation in various tissues. Moreover, its impact may vary among different populations, with potential consequences during pregnancy and in newborns. However, the precise mechanisms through which PM2.5 induces inflammatory reactions remain unclear. This study aims to explore potential pathways of inflammatory responses induced by PM2.5 through animal models and zebrafish embryo experiments. In this study, zebrafish embryo experiments were conducted to analyze the effects of PM2.5 on embryo development and survival, and mouse experimental models were employed to assess the impact of PM2.5 stimulation on various aspects of mice. Wild-type zebrafish embryos were exposed to a PM2.5 environment of 25-400 µg/mL starting at 6 h after fertilization (6 hpf). At 6 days post-fertilization, the survival rates of the 25, 50, 100, and 200 µg/mL groups were 100%, 80, 40%, and 40%, respectively. Zebrafish embryos stimulated with 25 µg/mL of PM2.5 still exhibited successful development and hatching. Additionally, zebrafish subjected to doses of 25-200 µg/mL displayed abnormalities such as spinal curvature and internal swelling after hatching, indicating a significant impact of PM2.5 stimulation on embryo development. In the mouse model, mice exposed to PM2.5 exhibited apparent respiratory overreaction, infiltration of inflammatory cells into the lungs, elevated levels of inflammatory response-related cytokines, and inflammation in various organs, including the liver, lungs, and uterus. Blood tests on experimental mice revealed increased expression of inflammatory and chemotactic cytokines, and GSEA indicated the induction of various inflammatory responses and an upregulation of the TNF-α/NFκB pathway by PM2.5. Our results provide insights into the harmful effects of PM2.5 on embryos and organs. The induced inflammatory responses by PM2.5 may be mediated through the TNF-α/NFκB pathway, leading to systemic organ inflammation. However, whether PM2.5-induced inflammatory responses in various organs and abnormal embryo development are generated through different pathways requires further study to comprehensively clarify and identify potential treatment and prevention methods.

Ambient exposure to fine particulate matter with oxidative potential affects oxidative stress biomarkers in pregnancy.

Prenatal exposures to ambient particulate matter (PM2.5) from traffic may generate oxidative stress, and thus contribute to adverse birth outcomes. We investigated whether PM2.5 constituents from brake and tire wear affect levels of oxidative stress biomarkers (malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG)) using urine samples collected up to three times during pregnancy in 156 women recruited from antenatal clinics at the University of California Los Angeles. Land use regression models with co-kriging were employed to estimate average residential outdoor concentrations of black carbon (BC), PM2.5 mass, PM2.5 metal components, and three PM2.5 oxidative potential metrics during the 4-weeks prior to urine sample collection. 8-OHdG concentrations in mid-pregnancy increased by 24.8% (95% CI: 9.0, 42.8) and 14.3% (95% CI: 0.4%, 30.0%) per interquartile range (IQR) increase in PM2.5 mass and BC, respectively. The brake wear marker (barium) and the oxidative potential metrics were associated with increased MDA concentration in the 1st sample collected (10-17 gestational week), but 95% CIs included the null. Traffic-related air pollution contributed in early to mid-pregnancy to oxidative stress generation previously linked to adverse birth outcomes.

An exploration of meteorological effects on PM2.5 air quality in several provinces and cities in Vietnam.

Linking meteorology and air pollutants is a key challenge. The study investigated meteorological effects on PM2.5 concentration using the advanced convergent cross mapping method, utilizing hourly PM2.5 concentration and six meteorological factors across eight provinces and cities in Vietnam. Results demonstrated that temperature (ρ = 0.30) and radiation (ρ = 0.30) produced the highest effects, followed by humidity (ρ = 0.28) and wind speed (ρ = 0.24), while pressure (ρ = 0.22) and wind direction (ρ = 0.17) produced the weakest effects on PM2.5 concentration. Comparing the ρ values showed that temperature, wind speed, and wind direction had greater impacts on PM2.5 concentration during the dry season whereas radiation had a more influence during the wet season; Southern stations experienced larger meteorological effects. Temperature, humidity, pressure, and wind direction had both positive and negative influences on PM2.5 concentration, while radiation and wind speed mostly had negative influences. During PM2.5 pollution episodes, there was more contribution of meteorological effects on PM2.5 concentration indicated by ρ values. At contaminated levels, humidity (ρ = 0.45) was the most dominant factor affecting PM2.5 concentration, followed by temperature (ρ = 0.41) and radiation (ρ = 0.40). Pollution episodes were pointed out to be more prevalent under higher humidity, higher pressure, lower temperature, lower radiation, and lower wind speed. The ρ calculation also revealed that lower temperature, lower radiation, and higher humidity greatly accelerated each other under pollution episodes, further enhancing PM2.5 concentration. The findings contributed to the literature on meteorology and air pollution interaction.

Reduced human fecundity attributable to ambient fine particles in low- and middle-income countries.

BACKGROUND: Exposure to ambient fine particulate matter (PM2.5) has been associated with reduced human fecundity. However, the attributable burden has not been estimated for low- and middle-income countries (LMICs), where the exposure-response function between PM2.5 and the infertility rate has been insufficiently studied. OBJECTIVE: This study examined the associations between long-term exposure to PM2.5 and human fecundity indicators, namely the expected time to pregnancy (TTP) and 12-month infertility rate (IR), and then estimated PM2.5-attributable burden of infertility in LMICs. METHODS: We analyzed 164,593 eligible women from 100 Demographic and Health Surveys conducted in 49 LMICs between 1999 and 2021. We assessed PM2.5 exposures during the 12 months before a pregnancy attempt using the global satellite-derived PM2.5 estimates produced by Atmospheric Composition Analysis Group (ACAG). First, we created a series of pseudo-populations with balanced covariates, given different levels of PM2.5 exposure, using a matching approach based on the generalized propensity score. For each pseudo-population, we used 2-stage generalized Gamma models to derive TTP or IR from the probability distribution of the questionnaire-based duration time for the pregnancy attempt before the interview. Second, we used spline regressions to generate nonlinear PM2.5 exposure-response functions for each of the two fecundity indicators. Finally, we applied the exposure-response functions to estimate number of infertile couples attributable to PM2.5 exposure in 118 LMICs. RESULTS: Based on the Gamma models, each 10 µg/m3 increment in PM2.5 exposure was associated with a TTP increase by 1.7 % (95 % confidence interval [CI]: -2.3 %-6.0 %) and an IR increase by 2.3 % (95 %CI: 0.6 %-3.9 %). The nonlinear exposure-response function suggested a robust effect of an increased IR for high-concentration PM2.5 exposure (>75 µg/m3). Based on the PM2.5-IR function, across the 118 LMICs, the number of infertile couples attributable to PM2.5 exposure exceeding 35 µg/m3 (the first-stage interim target recommended by the World Health Organization global air quality guidelines) was 0.66 million (95 %CI: 0.061-1.43), accounting for 2.25 % (95 %CI: 0.20 %-4.84 %) of all couples affected by infertility. Among the 0.66 million, 66.5 % were within the top 10 % high-exposure infertile couples, mainly from South Asia, East Asia, and West Africa. CONCLUSION: PM2.5 contributes significantly to human infertility in places with high levels of air pollution. PM2.5-pollution control is imperative to protect human fecundity in LMICs.

[Association between exposure to PM_(2.5) and chronic kidney disease in a population with metabolic syndrome].

OBJECTIVE: To investigate the association between long-term fine particulate matter(PM_(2.5)) exposure and the risk of chronic kidney disease(CKD) in people with abnormal metabolism syndrome(MS) components. METHODS: Based on health checkup data from a hospital in Beijing, a retrospective cohort study was used to collect annual checkup data from 2013-2019. A questionnaire was used to obtain information on demographic characteristics and lifestyle habits. We measured blood pressure, height, weight, waist circumference, concentrations of triglycerides(TG), fasting glucose, and high-density lipoprotein cholesterol(HDL-C). Longitude and latitude were also extracted from the addresses of the study subjects for pollutant exposure data estimation. Logistic regression models were used to explore the estimated effect of long-term PM_(2.5) exposure on the risk of CKD prevalence in people with abnormal MS components. Two-pollutant and multi-pollutant models were developed to test the stability of these result. Subgroup analysis was conducted based on age, the presence of MS, individual MS component abnormalities, and dual-component MS abnormalities. RESULTS: The study included 1540 study subjects with abnormal MS components at baseline, 206 with CKD during the study period. The association between long-term PM_(2.5) exposure and increased risk of CKD in people with abnormal MS fractions was statistically significant, with a 2.26-fold increase in risk of CKD for every 10 µg/m~3 increase in PM_(2.5) exposure(OR=3.26, 95% CI 2.72-3.90). The result in the dual-pollutant models and multi-pollutant models suggested that the association between long-term PM_(2.5) exposure and increased risk of CKD in people with abnormal MS fractions remained stable after controlling for contemporaneous confounding by other air pollutants. The result of subgroup analysis revealed that individuals aged 45 or older, without MS, with TG<1.7 mmol/L, HDL-C≥1.04 mmol/L, without hypertension, and with central obesity and high blood sugar had a stronger association between PM_(2.5) exposure and CKD-related health effects. CONCLUSION: Long-term exposure to PM_(2.5) may increase the risk of CKD in people with abnormal MS components. More attention should be paid to middle-aged and elderly people aged ≥45 years, people with central obesity and hyperglycemia.

Characterization of airborne endotoxin in personal exposure to fine particulate matter (PM2.5) and bioreactivity for elderly residents in Hong Kong.

The heavy metals and bioreactivity properties of endotoxin in personal exposure to fine particulate matter (PM2.5) were characterized in the analysis. The average personal exposure concentrations to PM2.5 were ranged from 6.8 to 96.6 µg/m3. The mean personal PM2.5 concentrations in spring, summer, autumn, and winter were 32.1±15.8, 22.4±11.8, 35.3±11.9, and 50.2±19.9 µg/m3, respectively. There were 85 % of study targets exceeded the World Health Organization (WHO) PM2.5 threshold (24 hours). The mean endotoxin concentrations ranged from 1.086 ± 0.384-1.912 ± 0.419 EU/m3, with a geometric mean (GM) varied from 1.034 to 1.869. The concentration of iron (Fe) (0.008-1.16 µg/m3) was one of the most abundant transition metals in the samples that could affect endotoxin toxicity under Toll-Like Receptor 4 (TLR4) stimulation. In summer, the interleukin 6 (IL-6) levels showed statistically significant differences compared to other seasons. Spearman correlation analysis showed endotoxin concentrations were positively correlated with chromium (Cr) and nickel (Ni), implying possible roles as nutrients and further transport via adhering to the surface of fine inorganic particles. Mixed-effects model analysis demonstrated that Tumor necrosis factor-α (TNF-α) production was positively associated with endotoxin concentration and Cr as a combined exposure factor. The Cr contained the highest combined effect (0.205-0.262), suggesting that Cr can potentially exacerbate the effect of endotoxin on inflammation and oxidative stress. The findings will be useful for practical policies for mitigating air pollution to protect the public health of the citizens.

Exposure memory and susceptibility to ambient PM2.5: A perspective from hepatic cholesterol and bile acid metabolism.

Both epidemiological and experimental studies increasingly show that exposure to ambient fine particulate matter (PM2.5) is related to the occurrence and development of chronic diseases, such as metabolic diseases. However, whether PM2.5 has "exposure memory" and how these memories affect chronic disease development like hepatic metabolic homeostasis are unknown. Therefore, we aimed to explore the effects of exposure transition on liver cholesterol and bile acids (BAs) metabolism in mice. In this study, C57BL/6 mice were exposed to concentrated ambient PM2.5 or filtered air (FA) in a whole-body exposure facility for an initial period of 10 weeks, followed by another 8 weeks of exposure switch (PM2.5 to FA and FA to PM2.5) comparing to non-switch groups (FA to FA and PM2.5 to PM2.5), which were finally divided into four groups (FF of FA to FA, PP of PM2.5 to PM2.5, PF of PM2.5 to FA, and FP of FA to PM2.5). Our results showed no significant difference in food intake, body composition, glucose homeostasis, and lipid metabolism between FA and PM2.5 groups after the initial exposure before the exposure switch. At the end of the exposure switch, the mice switched from FA to PM2.5 exposure exhibited a high sensitivity to late-onset PM2.5 exposure, as indicated by significantly elevated hepatic cholesterol levels and disturbed BAs metabolism. However, the mice switched from PM2.5 to FA exposure retained a certain memorial effects of previous PM2.5 exposure in hepatic cholesterol levels, cholesterol metabolism, and BAs metabolism. Furthermore, 18-week PM2.5 exposure significantly increased hepatic free BAs levels, which were completely reversed by the FA exposure switch. Finally, the changes in small heterodimeric partner (SHP) and nuclear receptor subfamily 5 group A member 2 (LRH1) in response to exposure switch mechanistically explained the above alterations. Therefore, mice switching from PM2.5 exposure to FA showed only a weak memory of prior PM2.5 exposure. In contrast, the early FA caused mice to be more susceptible to subsequent PM2.5 exposure.

The association between the Canadian active living environments index and glucose metabolism in a Canadian national population study.

Biomarkers of glucose metabolism may reflect insulin resistance, a risk factor for diabetes and cardiovascular disease (CVD). Neighborhoods conducive to a physically active lifestyle have the potential to improve these biomarkers. We examined cross-sectional associations between walkability and blood biomarkers of glucose metabolism in 29,649 Canadian Health Measures Survey (CHMS) participants. We used generalized linear mixed models with sampling weights adjusted for province, participants' age, sex, annual household income and educational attainment, cigarette smoking, environmental tobacco smoke, alcohol consumption, and exposure to ambient fine particulate air pollution (PM2.5). A higher value of the Canadian Active Living Environments Index, a measure of neighborhood walkability, equivalent to the magnitude of its interquartile range (IQR) of 2.4 was significantly associated with percentage differences of -0.48 (95% confidence interval (CI): 0.63, -0.32), -3.17 (95%CI: 5.27, -1.08), -3.88 (95%CI: 6.38, -1.38), and -3.36 (95%CI: 5.25, -1.47) in HbA1C, fasting insulin, HOMA-IR, and HOMA-ß, respectively, for all CHMS participants. No significant effects were observed in those ≤16 years old. Canadians living in neighborhoods that facilitate active living have more favorable biomarkers of glucose metabolism, suggesting that the built environment has the potential to improve risk factors for diabetes and CVD in adults.

Association of short-term exposure to ambient fine particulate matter and ozone with outpatient visits for anxiety disorders: A hospital-based case-crossover study in South China.

BACKGROUND: The short-term adverse effects of ambient fine particulate matter (PM2.5) and ozone (O3) on anxiety disorders (ADs) remained inconclusive. METHODS: We applied an individual-level time-stratified case-crossover study, which including 126,112 outpatient visits for ADs during 2019-2021 in Guangdong province, China, to investigate the association of short-term exposure to PM2.5 and O3 with outpatient visits for ADs, and estimate excess outpatient visits in South China. Daily residential air pollutant exposure assessments were performed by extracting grid data (spatial resolution: 1 km × 1 km) from validated datasets. We employed the conditional logistic regression model to quantify the associations and excess outpatient visits. RESULTS: The results of the single-pollutant models showed that each 10 µg/m3 increase of PM2.5 and O3 exposures was significantly associated with a 3.14 % (95 % confidence interval: 2.47 %, 3.81 %) and 0.88 % (0.49 %, 1.26 %) increase in odds of outpatient visits for ADs, respectively. These associations remained robust in 2-pollutant models. The proportion of outpatient visits attributable to PM2.5 and O3 exposures was up to 7.20 % and 8.93 %, respectively. Older adults appeared to be more susceptible to PM2.5 exposure, especially in cool season, and subjects with recurrent outpatient visits were more susceptible to O3 exposure. LIMITATION: As our study subjects were from one single hospital in China, it should be cautious when generalizing our findings to other regions. CONCLUSION: Short-term exposure to ambient PM2.5 and O3 was significantly associated with a higher odds of outpatient visits for ADs, which can contribute to considerable excess outpatient visits.

High-Resolution Spatiotemporal Modeling for PM2.5 Major Components in the Pearl River Delta and Its Implications for Epidemiological Studies.

Distinguishing the effects of different fine particulate matter components (PMCs) is crucial for mitigating their effects on human health. However, the sparse distribution of locations where PM is collected for component analysis makes it challenging to investigate the relevant health effects. This study aimed to investigate the agreement between data-fusion-enhanced exposure assessment and site monitoring data in estimating the effects of PMCs on gestational diabetes mellitus (GDM). We first improved the spatial resolution and accuracy of exposure assessment for five major PMCs (EC, OM, NO3-, NH4+, and SO42-) in the Pearl River Delta region by a data fusion model that combined inputs from multiple sources using a random forest model (10-fold cross-validation R2: 0.52 to 0.61; root mean square error: 0.55 to 2.26 µg/m3). Next, we compared the associations between exposures to PMCs during pregnancy and GDM in a hospital-based cohort of 1148 pregnant women in Heshan, China, using both site monitoring data and data-fusion model estimates. The comparative analysis showed that the data-fusion-based exposure generated stronger estimates of identifying statistical disparities. This study suggests that data-fusion-enhanced estimates can improve exposure assessment and potentially mitigate the misclassification of population exposure arising from the utilization of site monitoring data.

Potential causal links of long-term exposure to PM2.5 and its chemical components with the risk of nasopharyngeal carcinoma recurrence: A 10-year cohort study in South China.

There is a lack of evidence from cohort studies on the causal association of long-term exposure to ambient fine particulate matter (PM2.5) and its chemical components with the risk of nasopharyngeal carcinoma (NPC) recurrence. Based on a 10-year prospective cohort of 1184 newly diagnosed NPC patients, we comprehensively evaluated the potential causal links of ambient PM2.5 and its chemical components including black carbon (BC), organic matter (OM), sulfate (SO4 2-), nitrate (NO3 -), and ammonium (NH4 +) with the recurrence risk of NPC using a marginal structural Cox model adjusted with inverse probability weighting. We observed 291 NPC patients experiencing recurrence during the 10-year follow-up and estimated a 33% increased risk of NPC recurrence (hazard ratio [HR]: 1.33, 95% confidence interval [CI]: 1.02-1.74) following each interquartile range (IQR) increase in PM2.5 exposure. Each IQR increment in BC, NH4 +, OM, NO3 -, and SO4 2- was associated with HRs of 1.36 (95%CI: 1.13-1.65), 1.35 (95%CI: 1.07-1.70), 1.33 (95%CI: 1.11-1.59), 1.32 (95%CI: 1.06-1.64), 1.31 (95%CI: 1.08-1.57). The elderly, patients with no family history of cancer, no smoking history, no drinking history, and those with severe conditions may exhibit a greater likelihood of NPC recurrence following exposure to PM2.5 and its chemical components. Additionally, the effect estimates of the five components are greater among patients who were exposed to high concentration than in the full cohort of patients. Our study provides solid evidence for a potential relationship between long-term exposure to PM2.5 and its components and the risk of NPC recurrence.