Long-term exposure to ambient particulate matter is associated with prognosis in people living with HIV/AIDS: Evidence from a longitudinal study.

BACKGROUND: Evidence on the association between particulate matter (PM) exposure and prognosis in people living with HIV/AIDS (PWHA) is scarce. We aim to investigate the associations of long-term exposure to PM with AIDS-related deaths and complications. METHODS: We collected follow-up information on 7444 PWHAs from 2000 to 2021 from the HIV/AIDS Comprehensive Response Information Management System of the Wuhan Center for Disease Control and Prevention. The AIDS-related deaths and complications were assessed by physicians every 3 to 6 months, and the monthly average PM concentrations for each PWHA were extracted from the China High Air Pollutants dataset. We employed time-varying Cox regression models to evaluate the associations of the average cumulative PM exposure concentrations with AIDS-related deaths and complications, as well as the mediating effects of AIDS-related complications in PM-induced AIDS-related deaths. RESULTS: For each 1 µg/m3 increase in PM1, PM2.5, and PM10, the adjusted hazard ratios (HRs) for AIDS-related deaths were 1.021 (1.009, 1.033), 1.012 (1.005, 1.020), and 1.010 (1.005, 1.015), respectively; and the HRs for AIDS-related complications were 1.049 (1.034, 1.064), 1.029 (1.020, 1.038), and 1.031 (1.024, 1.037), respectively. AIDS-related complications mediated 18.38 % and 18.68 % of the association of exposure to PM1 and PM2.5 with AIDS-related deaths, respectively. The association of PM exposure with AIDS-related deaths was more significant in older PWHA. Meanwhile, the association between PM exposure and AIDS-related complications was stronger in PWHA with a BMI ≥ 24 kg/m2. CONCLUSION: Long-term exposure to PM is positively associated with AIDS-related deaths and complications, and AIDS-related complications have mediating effects in PM-induced AIDS-related deaths. Our evidence emphasizes that enhanced protection against PM exposure for PWHAs is an additional mitigation strategy to reduce AIDS-related deaths and complications.

The joint effects of prenatal exposure to PM2.5 constituents and reduced fetal growth on children's accelerated growth in the first 3 years: a birth cohort study.

BACKGROUND: Prenatal fine particulate matter (PM2.5) constituents exposure and reduced fetal growth may be risk factors for accelerated growth in early childhood, an important indicator for lifelong health. OBJECTIVE: The study investigated whether the joint effects are present between PM2.5 constituents and reduced fetal growth. METHODS: The study was embedded in a birth cohort in China, including 5424 mother-child pairs. Prenatal PM2.5 and its constituents' [organic carbon (OC), elementary carbon (EC), ammonium (NH4+), nitrate (NO3-), and sulfate (SO42-)] concentrations were estimated based on maternal residential addresses. Fetal growth was evaluated by fetal growth trajectory in utero and preterm birth (PTB), low birth weight (LBW), and small for gestational age (SGA). Children's accelerated growth was defined as body mass index (BMI) Z-score change of >0.67 between birth and 3 years. Generalized logistic regression was used to analyze the effects of prenatal PM2.5 constituents exposure and fetal growth on children's accelerated growth. Joint effect was tested on multiplicative scale and additive scale with the relative excess risk due to interaction (RERI). RESULTS: Children with lower fetal growth trajectory, PTB, LBW, and SGA had increased odds of children's accelerated growth, with odds ratios (ORs) ranging from 1.704 to 11.605. Compared with lower exposure (≤median), higher exposure (>median) of PM2.5, OC, and SO42- were significantly associated with increased odds of children's accelerated growth, varying in ORs from 1.163 to 1.478. Prenatal exposure to OC had joint effects with lower fetal growth on children's accelerated growth. We observed that the interaction was statistically significant on an additive scale in OC and lower fetal growth trajectory (RERI: 0.497, 95% CI: 0.033,0.962). IMPACT: Fine particulate matter (PM2.5) is a huge threat to human health worldwide, causing 6.7 million death globally in 2019. According to the theory of DOHaD, prenatal PM2.5 exposure could influence early childhood growth, which is important for lifelong health. We found that prenatal exposure to PM2.5, OC, and SO42- was associated with higher risk of accelerated childhood growth in the first 3 years. More importantly, reduced fetal growth moderated these associations. Our findings highlight the need for policies and interventions on PM2.5 constituents to improve lifelong health, especially for those vulnerable populations with reduced fetal growth.

DNA methylation mediates the effects of PM2.5 and O3 on ceramide metabolism: A novel mechanistic link between air pollution and insulin resistance.

Insulin resistance (IR), linked to air pollution, is an initial stage of early-onset Type 2 diabetes mellitus (T2DM). While ceramide metabolism plays an important role in IR pathogenesis, the effects of air pollution on this process and its mechanisms remain unclear. We recruited young adults aged 18-30 years to a panel study in Wuhan, China. Using personal portable devices and stationary monitoring stations, we tracked particulate matter with aerodynamic diameters≤ 2.5 µm (PM2.5) and Ozone (O3) levels. Liquid chromatography/mass spectrometry (LC-MS) based metabolomics quantified ceramide metabolism, and Illumina Infinium Human Methylation 850 kBeadChip assay measured deoxyribonucleic acid (DNA) methylation. Linear mixed-effects models assessed relationships of air pollution with i) IR indexes, ii) ceramide metabolism, and iii) DNA methylation. Mediation analysis was subsequently performed to evaluate the potential mediating effect of DNA methylation in the association between air pollution and ceramide metabolism. PM2.5 and O3 were associated with elevated IR. Specifically, each 10 µg/m3 increase in PM2.5 and O3 at lag0-12 h significantly increased triglyceride­glucose index (TyG index) and TyG-BMI (TyG - Body mass index) by 0.88%, 0.89% and 0.26%, 0.26%, respectively. Furthermore, levels of eight ceramides were altered by air pollution exposure, and nine methylated CpG sites in inflammation genes mediated the effects of air pollution on ceramide metabolism. Our findings imply the existence of a novel mechanism connecting air pollution to IR.

Cohort profile: China undergraduate cohort for environmental health study.

The China Undergraduate Cohort (CUC) is an ambispective cohort study with its major purpose to better understand the effects of lifetime environmental exposures on health outcomes. We recruited 5322 college students with an average age of 18.3 ± 0.7 years in China from August 23, 2019 to October 28, 2019. Follow-up surveys were conducted annually. The dataset comprises individual demographic data (e.g. age, sex, height, weight, birth date, race, home address, annual family income, contact information), health-related behavior data (smoking status, smoking cessation, passive smoking exposure, drinking habit, physical activity, dietary status), lifestyle data (physical exercise, dietary habit, length of time spent outdoors), disease history (respiratory disease history, cardiovascular disease history, urinary system disease history, etc.), mental health status data (sleep quality, self-reported stress, anxiety and depression symptoms), lung function and blood samples data. Preliminary results from our cohort have found the association between air pollution, summer heat and mercury exposure and lung function among young adults in China.

Association between ambient PM1 and the prevalence of chronic kidney disease in China: A nationwide study.

Particulate of diameter ≤ 1 µm (PM1) presents a novel risk factor of adverse health effects. Nevertheless, the association of PM1 with the risk of chronic kidney disease (CKD) in the general population is not well understood, particularly in regions with high PM1 levels like China. Based on a nationwide representative survey involving 47,204 adults and multi-source ambient air pollution inversion data, the present study evaluated the association of PM1 with CKD prevalence in China. The two-year average PM1, particulate of diameter ≤ 2.5 µm (PM2.5), and PM1-2.5 values were accessed using a satellite-based random forest approach. CKD was defined as estimated glomerular filtration rate < 60 ml/min/1.73 m2 or albuminuria. The results suggested that a 10 µg/m3 rise in PM1 was related to a higher CKD risk (odds ratio [OR], 1.13; 95% confidence interval [CI] 1.08-1.18) and albuminuria (OR, 1.11; 95% CI, 1.05-1.17). The association between PM1 and CKD was more evident among urban populations, older adults, and those without comorbidities such as diabetes or hypertension. Every 1% increase in the PM1/PM2.5 ratio was related to the prevalence of CKD (OR, 1.03; 95% CI, 1.03-1.04), but no significant relationship was found for PM1-2.5. In conclusion, the present study demonstrated long-term exposure to PM1 was associated with an increased risk of CKD in the general population and PM1 might play a leading role in the observed relationship of PM2.5 with the risk of CKD. These findings provide crucial evidence for developing air pollution control strategies to reduce the burden of CKD.

Association Between Home Renovation and Sleeping Problems Among Children Aged 6-18 Years: A Nationwide Survey in China.

BACKGROUND: Although the indoor environment has been proposed to be associated with childhood sleep health, to our knowledge no study has investigated the association between home renovation and childhood sleep problems. METHODS: The study included 186,470 children aged 6-18 years from the National Chinese Children Health Study (2012-2018). We measured childhood sleeping problems via the Chinese version of the Sleep Disturbance Scale for Children (C-SDSC). Information on home renovation exposure within the recent 2 years was collected via parent report. We estimated associations between home renovation and various sleeping problems, defined using both continuous and categorized (binary) C-SDSC t-scores, using generalized mixed models. We fitted models with city as a random effect variable, and other covariates as fixed effects. RESULTS: Out of the overall participants, 89,732 (48%) were exposed to recent home renovations. Compared to the unexposed group, children exposed to home renovations had higher odds of total sleep disorder (odd ratios [OR] = 1.3; 95% confidence interval [CI] = 1.2, 1.4). Associations varied when we considered different types of home renovation materials. Children exposed to multiple types of home renovation had higher odds of sleeping problems. We observed similar findings when considering continuous C-SDSC t-scores. Additionally, sex and age of children modified the associations of home renovation exposure with some of the sleeping problem subtypes. CONCLUSIONS: We found that home renovation was associated with higher odds of having sleeping problems and that they varied when considering the type of renovation, cumulative exposure, sex, and age differences.

Urban greenspace and visual acuity in schoolchildren: a large prospective cohort study in China.

BACKGROUND: Greenspace is known to have a positive impact on human health and well-being, but its potential effects on visual acuity have not been extensively studied. OBJECTIVES: Our aim was to examine the relationship between long-term greenspace exposure and visual acuity in children, while also exploring the potential mechanisms in this association. METHODS: We conducted this prospective cohort study based on the Children's growth environment, lifestyle, physical, and mental health development project (COHERENCE), which screened 286,801 schoolchildren in Guangzhou, China, starting in the 2016/17 academic year and followed them up for three academic years (2017/18-2019/20). Visual acuity was measured using a standardized logarithmic chart, and visual impairment was defined as visual acuity worse than 0.0 logarithm of the minimum angle of resolution (LogMAR) units in the better eye. We used the Normalized Difference Vegetation Index (NDVI), the Soil-Adjusted Vegetation Index (SAVI), and the Enhanced Vegetation Index (EVI) to assess the greenspace surrounding child's geocoded home and school at each visit. RESULTS: Our analysis indicated that higher greenspace exposure was associated with greater visual acuity z-score at baseline and with slower decline in visual acuity z-score during the 3-year follow-up. An interquartile range increase in home-school-based NDVI 300m was associated with a 7% decrease [hazard ratios (HRs): 0.93, 95% confidence interval (CI): 0.92, 0.94] in the risk of visual impairment. We also found that air pollution, physical activity, outdoor time, and recreational screen time partially mediated the greenspace-visual acuity association. CONCLUSION: Our findings suggest that increasing greenspace exposure could benefit children's visual acuity development and reduce the risk of visual impairment by reducing air pollution and recreational screen time while increasing physical activity and outdoor time. All results could have potential policy implications, given the individual and societal burdens associated with visual impairment.

Health Impacts of Wildfire Smoke on Children and Adolescents: A Systematic Review and Meta-analysis.

PURPOSE OF REVIEW: Wildfire smoke is associated with human health, becoming an increasing public health concern. However, a comprehensive synthesis of the current evidence on the health impacts of ambient wildfire smoke on children and adolescents, an exceptionally vulnerable population, is lacking. We conduct a systematic review of peer-reviewed epidemiological studies on the association between wildfire smoke and health of children and adolescents. RECENT FINDINGS: We searched for studies available in MEDLINE, EMBASE, and Scopus from database inception up to October 11, 2022. Of 4926 studies initially identified, 59 studies from 14 countries were ultimately eligible. Over 33.3% of the studies were conducted in the USA, and two focused on multi-countries. The exposure assessment of wildfire smoke was heterogenous, with wildfire-specific particulate matters with diameters ≤ 2.5 µm (PM2.5, 22.0%) and all-source (22.0%) PM2.5 during wildfire period most frequently used. Over half of studies (50.6%) focused on respiratory-related morbidities/mortalities. Wildfire smoke exposure was consistently associated with enhanced risks of adverse health outcomes in children/adolescents. Meta-analysis results presented a pooled relative risk (RR) of 1.04 (95% confidence interval [CI], 0.96-1.12) for all-cause respiratory morbidity, 1.11 (95% Ci: 0.93-1.32) for asthma, 0.93 (95% CI, 0.85-1.03) for bronchitis, and 1.13 (95% CI, 1.05-1.23) for upper respiratory infection, whilst - 21.71 g for birth weight (95% CI, - 32.92 to - 10.50) per 10 µg/m3 increment in wildfire-specific PM2.5/all-source PM2.5 during wildfire event. The majority of studies found that wildfire smoke was associated with multiple adverse health outcomes among children and adolescents, with respiratory morbidities of significant concern. In-utero exposure to wildfire smoke may increase the risk of adverse birth outcomes and have long-term impacts on height. Higher maternal baseline exposure to wildfire smoke and poor family-level baseline birthweight respectively elevated risks in preterm birth and low birth weight associated with wildfire smoke. More studies in low- and middle-income countries and focusing on extremely young children are needed. Despite technological progress, wildfire smoke exposure measurements remain uncertain, demanding improved methodologies to have more precise assessment of wildfire smoke levels and thus quantify the corresponding health impacts and guide public mitigation actions.

Outdoor light at night and depressive symptoms in male veterans: a multicenter cross-sectional study in China.

Previous studies have indicated depression was associated with environmental exposures, but evidence is limited for the association between outdoor light at night (LAN) and depression. This study aims to examine the association between long-term outdoor LAN exposure and depressive symptoms using data from the Chinese Veteran Clinical Research platform. A total of 6445 male veterans were selected from 277 veteran communities in 18 cities of China during 2009‒2011. Depressive symptoms were evaluated using the Chinese version of the Center for Epidemiological Studies Depression scale. Outdoor LAN was estimated using the Global Radiance Calibrated Nighttime Lights data. The odds ratio and 95% confidence intervals of depressive symptoms at the high level of outdoor LAN exposure against the low level during the 1 years before the investigation was 1.49 (1.15, 1.92) with p-value for trend < 0.01, and those associated with per interquartile range increase in LAN exposure was 1.22 (1.06, 1.40).

The association between outdoor light at night exposure and adult obesity in Northeastern China.

Previous studies have linked exposure to light at night (LAN) with various health outcomes, but evidence is limited for the LAN-obesity association. Thestudy analysed data from 24,845 participants of the 33 Communities Chinese Health Study and obesity (BMI ≥28 kg/m2) was defined according to the Working Group on Obesity in China. The Global Radiance Calibrated Nighttime Lights data were used to estimate participants' LAN exposure. The mixed-effect regression models examined the LAN-BMI and LAN-obesity association. We found that higher LAN exposure was significantly associated with greater BMI and higher risk of obesity. Changes of BMI and the odds ratios (ORs) of obesity and 95% confidence intervals (CIs) for 2nd, 3rd, and 4th against the 1st quartile of LAN exposure were 0.363 (0.208, 0.519), 0.364 (0.211, 0.516) and 0.217 (0.051, 0.383); 1.228 (1.099, 1.371), 1.356 (1.196, 1.538) and 1.269 (1.124, 1.433), respectively. Age and regular exercise showed significant modification effects on the LAN-obesity association.

Extreme temperature events and dementia mortality in Chinese adults: a population-based, case-crossover study.

BACKGROUND: The effect of exposure to extreme temperature events (ETEs) on dementia mortality remains largely unknown. We aimed to quantify the association of ETE exposure with dementia mortality. METHODS: We conducted a population-based, case-crossover study among 57 791 dementia deaths in Jiangsu province, China, during 2015-20. Daily mean temperatures were extracted from a validated grid dataset at each subject's residential address, and grid-specific exposures to heat wave and cold spell were assessed with a combination of their intensity and duration. We applied conditional logistic regression models to investigate cumulative and lag effects for ETE exposures. RESULTS: Exposure to ETE with each of all 24 definitions was associated with an increased odds of dementia mortality, which was higher when exposed to heat wave. Exposure to heat wave (daily mean temperature ≥95th percentile, duration ≥3 days (d); P95_3d) and cold spell (≤5th percentile, duration ≥3 d; P5_3d) was associated with a 75% (95% CI: 61%, 90%) and 30% (19%, 43%) increase in odds of dementia mortality, respectively. Definitions with higher intensity were generally associated with a higher odds of dementia mortality. We estimated that 6.14% of dementia deaths were attributable to exposure to heat wave (P90_2d) and cold spell (P10_2d). No effect modifications were observed by sex or age, except that the association for heat wave was stronger among women. CONCLUSIONS: Exposure to both heat wave and cold spell was associated with an increased odds of dementia mortality. Our findings highlight that reducing individual ETE exposures may be helpful in preventing deaths from dementia, especially among women in summer.

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

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

Urban greenspaces and child blood pressure in China: Evidence from a large population-based cohort study.

BACKGROUND: With the world's population steadily shifting toward urban living, children's engagement with the natural environment seems to be diminishing. This raises significant concerns about the influence of urban greenspaces on the cardiovascular health of children. OBJECTIVE: To assess the association between urban greenspaces exposure and blood pressure (BP) in Chinese primary schoolchildren. METHODS: This prospective cohort study used data from the Children's growth environment, lifestyle, physical, and mental health development (COHERENCE) project in Guangzhou, China. Participants included 164,853 primary schoolchildren starting from 2016/17 to 2019/20 academic year. We assessed the surrounding greenspaces at home and school by using Sentinel-2 satellite data on the normalized difference vegetation index. Prehypertension and hypertension status were defined with BP above 90th to less than the 95th percentile, at or above the 95th percentile, respectively. The association of surrounding greenness with children's BP levels and risk of prehypertension/hypertension were examined using linear mixed-effects models and Cox proportional hazards model. RESULTS: Among 164,853 eligible children aged 7.21 (0.74) years, 89,190 (54.1%) were boys. Our results showed that average systolic and diastolic BP increased by 0.48 and 0.42 standard deviations, respectively, over the 3-year follow-up. We identified 23,225 new cases of prehypertension and 35,067 of hypertension status. An interquartile range increase both in home-, school- and home-school NDVI100m was significantly associated with a reduction of 0.018-0.037 in BP z-scores and a 2.7%-7.6% lower risk of hypertension. Additionally, family socioeconomic status modified the impact of home-school greenness on BP levels. Air pollution exhibited mediating effects solely in school-greenness-BP associations, while physical activity and children's BMI mainly mediated the relationships between home-greenness and BP. CONCLUSION: The findings of this large cohort study suggest that surrounding greenspaces are associated with lower BP levels and a decreased risk of prehypertension and hypertension in Chinese schoolchildren.

Mediation of metabolic syndrome in the association between long-term exposure to particulate matter and incident cardiovascular disease: Evidence from a population-based cohort in Chengdu.

BACKGROUND: Particulate matter (PM) exposure has been linked with cardiovascular disease (CVD) and metabolic syndrome (MetS), the latter characterized by concurrent multiple metabolic disorders. As a result, the mechanisms assumption from PM to CVD through MetS have emerged, thus requiring further epidemiological evidence. This cohort study aimed to assess whether MetS mediates the associations of PM with CVD risk. METHODS: This study included 14,195 participants from the Chengdu cohort of the China Multi-Ethnic Cohort (CMEC) study in 2018. The primary outcome of incident CVD diagnoses was identified using matched hospital records from the Health Information Center of Sichuan Province. Residence-specific levels of PM with aerodynamic diameters of ≤ 1 µm (PM1), ≤ 2.5 µm (PM2.5), and ≤ 10 µm (PM10) were estimated by spatiotemporal models. Causal mediation analyses were applied to evaluate the indirect effect of MetS. RESULTS: Increased exposure levels to PM were significantly associated with MetS and CVD. Mediation analyses indicated that the associations between PM exposure and CVD were mediated by MetS, with the proportion of multiple mediations being 19.3%, 12.1%, and 13.5% for PM1, PM2.5, and PM10, respectively. Further moderated mediation analyses suggested that male, overweight individuals, alcohol drinkers, and those suffering from indoor air pollution may experience more significant adverse effects from PM exposure on CVD via MetS than others. CONCLUSIONS: Our findings suggest that MetS partially mediates the association between long-term exposure to PM and CVD. These mediation effects appear to be amplified by demographic characteristics and unhealthy lifestyles.

Climate change, environmental extremes, and human health in Australia: challenges, adaptation strategies, and policy gaps.

Climate change presents a major public health concern in Australia, marked by unprecedented wildfires, heatwaves, floods, droughts, and the spread of climate-sensitive infectious diseases. Despite these challenges, Australia's response to the climate crisis has been inadequate and subject to change by politics, public sentiment, and global developments. This study illustrates the spatiotemporal patterns of selected climate-related environmental extremes (heatwaves, wildfires, floods, and droughts) across Australia during the past two decades, and summarizes climate adaptation measures and actions that have been taken by the national, state/territory, and local governments. Our findings reveal significant impacts of climate-related environmental extremes on the health and well-being of Australians. While governments have implemented various adaptation strategies, these plans must be further developed to yield concrete actions. Moreover, Indigenous Australians should not be left out in these adaptation efforts. A collaborative, comprehensive approach involving all levels of government is urgently needed to prevent, mitigate, and adapt to the health impacts of climate change.

Long-term exposure to PM2.5 compositions and O3 and their interactive effects on DNA methylation of peripheral brain-derived neurotrophic factor promoter.

This study examined the associations of long-term exposure to ambient fine particulate matter (PM2.5) compositions/ozone with methylation of peripheral brain-derived neurotrophic factor (BDNF) promoters. A total of 101 participants were recruited from a cohort in Shijiazhuang, Hebei province, China. They underwent baseline and follow-up surveys in 2011 and 2015. DNA methylation levels were detected by bisulfite-PCR amplification and pyrosequencing. Participants' three-year average levels of PM2.5 compositions and ozone were estimated. Bayesian kernel machine regression (BKMR) models were used to examine the joint effects of pollutants on methylation levels. Exposure to PM2.5 compositions and ozone mixtures at the 75th percentile was associated with increased methylation levels at CpG2 of BDNF promoter (203%, 95% CI: 89, 316) than the lowest level of exposure, and sulfate dominated the effect in the BKMR models.Our findings provide clues to the epigenetic mechanisms for the associations of PM2.5 compositions and ozone with BDNF.

Residential greenness alleviated the adverse associations of long-term exposure to ambient PM1 with cardiac conduction abnormalities in rural adults.

BACKGROUND: Ambient air pollution was linked to elevated risks of adverse cardiovascular events, and alterations in electrophysiological properties of the heart might be potential pathways. However, there is still lacking research exploring the associations between PM1 exposure and cardiac conduction parameters. Additionally, the interactive effects of PM1 and residential greenness on cardiac conduction parameters in resource-limited areas remain unknown. METHODS: A total of 27483 individuals were enrolled from the Henan Rural Cohort study. Cardiac conduction parameters were tested by 12-lead electrocardiograms. Concentrations of PM1 were evaluated by satellite-based spatiotemporal models. Levels of residential greenness were assessed using Enhanced Vegetation Index (EVI) and Normalized difference vegetation index (NDVI). Logistic regression models and restricted cubic splines were fitted to explore the associations of PM1 and residential greenness exposure with cardiac conduction abnormalities risk, and the interaction plot method was performed to visualize their interaction effects. RESULTS: The 3-year median concentration of PM1 was 56.47 (2.55) µg/m3, the adjusted odds rate (ORs) and 95% confidence intervals (CIs) for abnormal HR, PR, QRS, and QTc interval risk in response to 1 µg/m3 increase in PM1 were 1.064 (1.044, 1.085), 1.037 (1.002, 1.074), 1.061 (1.044, 1.077) and 1.046 (1.028, 1.065), respectively. Participants exposure to higher levels of PM1 had increased risks of abnormal HR (OR = 1.221, 95%CI: 1.144, 1.303), PR (OR = 1.061, 95%CI: 0.940, 1.196), QRS (OR = 1.225, 95%CI: 1.161, 1.294) and QTc interval (OR = 1.193, 95%CI: 1.121, 1.271) compared with lower levels of PM1. Negative interactive effects of exposure to PM1 and residential greenness on abnormal HR, QRS, and QTc intervals were observed (Pfor interaction < 0.05). CONCLUSION: Long-term PM1 exposure was associated with elevated cardiac conduction abnormalities risks, and this adverse association might be mitigated by residential greenness to some extent. These findings emphasize that controlling PM1 pollution and increasing greenness levels might be effective strategies to reduce cardiovascular disease burdens in resource-limited areas.

Long-term exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons and cancer mortality: A difference-in-differences approach.

The association of ambient fine particulate matter (PM2.5) exposure with cancer mortality was controversial, which may ascribe to the difference in PM2.5 constituents. Polycyclic aromatic hydrocarbons (PAHs) are carcinogenic constituents in PM2.5, which are suspected to account for PM2.5-induced cancer mortality but are yet to be investigated. We aimed to assess the association between long-term exposure to PM2.5-bound PAHs and cancer mortality and estimate the attributable mortality. A difference-in-differences approach was used to investigate the causal effect of long-term exposure to PM2.5-bound PAHs on cancer mortality. We divided Jiangsu province, China into 53 spatial units and summarized the annual number of cancer deaths in each spatial unit during 2016-2020. Annual population-weighted exposure to PM2.5-bound PAHs of each spatial unit was assessed by an inverse distance weighting method. The association between PM2.5-bound PAHs exposures and cancer mortality was evaluated by controlling spatial differences, temporal trends, PM2.5 mass exposures, temperatures, and socioeconomic status. Records of 793,269 cancer deaths were identified among 84.7 million population. Each ln-unit increase of exposure to total benzo[a]pyrene equivalents (∑BaPeq), total carcinogenic PAHs (∑PAH7c), and total PAHs (∑PAHs) was significantly associated with a 3.21%, 3.48%, and 2.64% increased risk of cancer mortality, respectively; the risk increased monotonically at low-level exposures but attenuated or flattened afterward (all p for nonlinearity <0.05). Similar exposure-response associations were identified for specific PAHs except that the associations for both fluoranthene and benzo[a]anthracene were linear. We estimated that exposure to ∑BaPeq, ∑PAH7c, and ∑PAHs contributed to 5.73%, 8.73%, and 7.33% of cancer deaths, respectively. In conclusion, long-term exposure to PM2.5-bound PAHs was associated with an increased risk of cancer mortality and contributed to substantial cancer deaths. Our findings highlight the importance to prevent deaths from cancer by reducing PM2.5-bound PAHs exposures and the necessity to take into consideration specific constituents in particulate pollution management in future.

The mediation role of blood lipids on the path from air pollution exposure to MAFLD: A longitudinal cohort study.

BACKGROUND & AIMS: Recent cross-sectional studies found that exposure to ambient air pollution (AP) was associated with an increased risk of metabolic dysfunction-associated fatty liver disease (MAFLD). The alternation of blood lipids may explain the association, but epidemiological evidence is lacking. We aimed to examine whether and to what extent the association between long-term exposure to AP and incident MAFLD is mediated by blood lipids and dyslipidemia in a prospective cohort. METHODS: We included 6350 participants from the China Multi-Ethnic Cohort (CMEC, baseline 2018-2019, follow-up 2020-2021). Three-year average (2016-2018) of AP (PM1, PM2.5, PM10, NO2), blood lipids (TC, LDL-C, HDL-C, TG with their combinations) and incident MAFLD for each individual were assessed chronologically. Linear and logistic regression was used to assess the associations among AP, blood lipids, and MAFLD, and the potential mediation effects of blood lipids were evaluated using causal mediation analysis. RESULTS: A total of 744 participants were newly diagnosed with MAFLD at follow-up. The odds ratios of MAFLD associated with a 10 µm increase in PM1, PM2.5, and NO2 were 1.35 (95 % CI: 1.14, 1.58), 1.34 (1.10, 1.65) and 1.28 (1.14, 1.44), respectively. Blood lipids are important mediators between AP and incident MAFLD. LDL-C (Proportion Mediated: 6.9 %), non-HDL (13.4 %), HDL-C (20.7 %), LDL/HDL (30.1 %), and dyslipidemia (6.5 %) significantly mediated the association between PM2.5 and MAFLD. For PM1, the indirect effects were similar to those for PM2.5, with a larger value for the direct effect, and the mediation proportion by blood lipids was less for NO2. CONCLUSION: Blood lipids are important mediators between AP and MAFLD, and can explain 5 %-30 % of the association between AP and incident MAFLD, particularly cholesterol-related variables, indicating that AP could lead to MAFLD through the alternation of blood lipids. These findings provided mechanical evidence of AP leading to MAFLD in epidemiological studies.

Joint Effects of Long-Term Exposure to Ambient Fine Particulate Matter and Ozone on Asthmatic Symptoms: Prospective Cohort Study.

BACKGROUND: The associations of long-term exposure to air pollutants in the presence of asthmatic symptoms remain inconclusive and the joint effects of air pollutants as a mixture are unclear. OBJECTIVE: We aimed to investigate the individual and joint associations of long-term exposure to ambient fine particulate matter (PM2.5) and daily 8-hour maximum ozone concentrations (MDA8 O3) in the presence of asthmatic symptoms in Chinese adults. METHODS: Data were derived from the World Health Organization Study on Global Ageing and Adult Health (WHO SAGE) cohort study among adults aged 50 years or older, which was implemented in 1 municipality and 7 provinces across China during 2007-2018. Annual average MDA8 O3 and PM2.5 at individual residential addresses were estimated by an iterative random forest model and a satellite-based spatiotemporal model, respectively. Participants who were diagnosed with asthma by a doctor or taking asthma-related therapies or experiencing related conditions within the past 12 months were recorded as having asthmatic symptoms. The individual associations of PM2.5 and MDA8 O3 with asthmatic symptoms were estimated by a Cox proportional hazards regression model, and the joint association was estimated by a quantile g-computation model. A series of subgroup analyses was applied to examine the potential modifications of some characteristics. We also calculated the population-attributable fraction (PAF) of asthmatic symptoms attributed to PM2.5 and MDA8 O3. RESULTS: A total of 8490 adults older than 50 years were included, and the average follow-up duration was 6.9 years. During the follow-up periods, 586 (6.9%) participants reported asthmatic symptoms. Individual effect analyses showed that the risk of asthmatic symptoms was positively associated with MDA8 O3 (hazard ratio [HR] 1.12, 95% CI 1.01-1.24, for per quantile) and PM2.5 (HR 1.18, 95% CI 1.05-1.31, for per quantile). Joint effect analyses showed that per equal quantile increment of MDA8 O3 and PM2.5 was associated with an 18% (HR 1.18, 95% CI 1.05-1.33) increase in the risk of asthmatic symptoms, and PM2.5 contributed more (68%) in the joint effects. The individual PAFs of asthmatic symptoms attributable to PM2.5 and MDA8 O3 were 2.86% (95% CI 0.17%-5.50%) and 4.83% (95% CI 1.42%-7.25%), respectively, while the joint PAF of asthmatic symptoms attributable to exposure mixture was 4.32% (95% CI 1.10%-7.46%). The joint associations were greater in participants with obesity, in urban areas, with lower family income, and who used unclean household cooking fuel. CONCLUSIONS: Long-term exposure to PM2.5 and MDA8 O3 may individually and jointly increase the risk of asthmatic symptoms, and the joint effects were smaller than the sum of individual effects. These findings informed the importance of joint associations of long-term exposure to air pollutants with asthma.