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.

Associations of Ambient Particulate Matter with Maternal Thyroid Autoimmunity and Thyroid Function in Early Pregnancy.

This prospective birth cohort study evaluated the association of exposure to PM2.5 (diameter ≤2.5 µm), PM1-2.5 (1-2.5 µm), and PM1 (≤1 µm) with maternal thyroid autoimmunity and function during early pregnancy. A total of 15,664 pregnant women were included at 6 to 13+6 gestation weeks in China from 2018 to 2020. Single-pollutant models using generalized linear models (GLMs) showed that each 10 µg/m3 increase in PM2.5 and PM1-2.5 was related with 6% (odds ratio [OR] = 1.06, 95% confidence interval [CI]: 1.01, 1.12) and 15% (OR = 1.15, 95% CI: 1.08, 1.22) increases in the risk of thyroid autoimmunity, respectively. The odds of thyroid autoimmunity significantly increased with each interquartile range increase in PM2.5 and PM1-2.5 exposure (P for trend <0.001). PM1 exposure was not significantly associated with thyroid autoimmunity. GLM with natural cubic splines demonstrated that increases in PM2.5 and PM1-2.5 exposure were associated with lower maternal FT4 levels, while a negative association between PM1 and FT4 levels was found when exposure exceeded 32.13 µg/m3. Only PM2.5 exposure was positively associated with thyrotropin (TSH) levels. Our findings suggest that high PM exposure is associated with maternal thyroid disruption during the early pregnancy.

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.

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.

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.

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.

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.

Long-term exposure to fine particulate matter and site-specific cancer mortality: A difference-in-differences analysis in Jiangsu province, China.

BACKGROUND: Accumulating studies have reported that chronic exposure to ambient fine particulate matter (PM2.5) can lead to adverse effects on lung cancer mortality; however, such chronic effects are less clear for mortality from other site-specific cancers. OBJECTIVE: To explore the causal effect of long-term PM2.5 exposure on mortality from all-site and a variety of site-specific cancers in Jiangsu province, China during 2015-2020 using a difference-in-differences analysis. METHODS: For each of 53 county-based spatial units in Jiangsu province, we calculated annual death counts for all-site cancer and 23 site-specific cancers. Using a validated high-resolution PM2.5 grid dataset, long-term PM2.5 exposure of a spatial unit within a given year was evaluated as the average of population-weighted annual concentrations during recent 10 years. Conditional Poisson regression models were employed to evaluate exposure-response associations adjusting for spatial and temporal variables, seasonal temperatures, relative humidity, and gross domestic product (GDP). RESULTS: During the study period, we identified 947,337 adult cancer deaths in Jiangsu province. Each 1 µg/m3 increment in PM2.5 exposure was significantly associated with a 2.7% increase in the risk of all-site cancer mortality. PM2.5-mortality associations were also observed in cancer of lip, oral cavity and pharynx, stomach, colorectum, pancreas, lung, bone and joints, ovary, prostate, and lymphoma (all adjusted P < 0.05), with the relative risks ranging from 1.028 (95% confidence interval [CI]: 1.011, 1.046) for stomach cancer to 1.201 (95% CI: 1.120, 1.308) for bone and joints cancers. Exposure-response curves showed that these associations were close to linearity, though most of them had increasing slopes at high exposure levels. Overall, women and subjects in low GDP regions were more vulnerable to PM2.5 exposures. CONCLUSIONS: Long-term exposure to ambient PM2.5 contributes to a higher risk of mortality from multiple site-specific cancers.

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.

Air pollution exposure and ovarian reserve impairment in Shandong province, China: The effects of particulate matter size and exposure window.

BACKGROUND: Lack of evidence exists on whether air pollution exposure may affect ovarian reserve, especially for Chinese women. OBJECTIVES: To explore the association between exposure to various air pollutants and anti-Müllerian hormone (AMH), a predictor of ovarian reserve, over different exposure windows in Shandong Province, China. METHODS: We enrolled 18,878 women who had AMH measurements in the Center for Reproductive Medicine, Shandong University during 2010-2019. Daily average concentrations of ambient particulate matter with diameters ≤1 µm/2.5 µm/10 µm (PM1, PM2.5, and PM10), nitrogen dioxide (NO2) and ozone (O3) were developed at a spatial resolution of 0.01° × 0.01°, and assigned to the residential addresses. Three exposure windows were considered, i.e., the process from primary to small antral follicle stage (W1), from primary to secondary follicle stage (W2), and from secondary to small antral follicle stage (W3). The air pollution-AMH association was fitted using the multivariable linear mixed effect model with adjustment for potential confounders. Stratified analyses were performed by age group, overweight status, residential region, and educational level. RESULTS: The level of AMH changed by -8.8% (95% confidence interval (CI): -12.1%, -5.3%), -2.1% (95% CI: -3.5%, -0.6%), -1.9% (95% CI: -3.3%, -0.5%), and -4.5% (95% CI: -7.1%, -1.9%) per 10 µg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively, during W1. The effect estimates were significant during W2 for PM1, PM2.5 and NO2 while minimal association was observed in W3. Greater vulnerability for certain air pollutants were observed for women who lived in inland areas and were less educated. CONCLUSIONS: We found that ovarian reserve was negatively associated with air pollution exposure for women, particularly from the primary to secondary follicle stage. The effect estimate increased by the reduction in the diameter of PMs, which also varied across population sub-groups.

Association between long-term ambient ozone exposure and attention-deficit/hyperactivity disorder symptoms among Chinese children.

BACKGROUND: Although ozone exposure has neurological toxicity, it remains unclear whether it was associated with an increased risk of attention-deficit/hyperactivity disorders (ADHD) among childhood. METHODS: We matched the four-year average ozone concentration with questionnaire data for 35,103 children aged 3-12 years from seven cities in Liaoning, China, 2012-2013. Using mixed-effect logistic regression models, we assessed the association of ozone concentration with multiple ADHD indicators using the Conners Abbreviated Symptom Questionnaire (C-ASQ), including explicit attention-deficit/hyperactivity symptoms (ADHD; score ≥15), attention-deficit/hyperactivity disorder tendencies (ADHD-T; 11 ≤ score ≤14), and attention-deficit/hyperactivity problems (ADHP; score ≥11). Results were also stratified by sociodemongraphics. RESULTS: After adjusting for covariates, we found that each interquartile range (IQR) increase in ozone concentration was associated with an increased risk of ADHD, ADHD-T, and ADHP (P < 0.001) with an odds ratio of 1.12 (95% confidence interval, 1.04-1.21), 1.08 (1.03-1.13), and 1.09 (1.05-1.14), respectively. Additionally, we found greater effect estimates in children who reported longer exercise time (vs those with limited exercise time) with odds ratio of 1.18 (1.07-1.31) vs 1.06 (0.96-1.17) for ADHD, 1.13 (1.06-1.21) vs 1.03 (0.96-1.10) for ADHD-T, and 1.15 (1.08-1.21) vs 1.04 (0.98-1.10) for ADHP. Non-breastfed children were also shown to be more vulnerable to ADHD with an odds ratio of 1.22 (1.09-1.36) compared with 1.06 (0.96-1.16) among the rest. CONCLUSIONS: Long-term ozone exposure may be associated with increased ADHD among children. Additional studies are needed to validate our findings and support policies and interventions to address this growing public health concern.

Association of long-term exposure to ambient air pollutants with cardiac structure and cardiovascular function in Chinese adults.

Epidemiological evidence increasingly suggests that air pollutants are intimately associated with the incidence and mortality of cardiovascular diseases (CVDs). However, studies on the association between chronic exposure to air pollutants and changes in left cardiac function and structure are limited. In our cross-sectional study, 3145 participants were enrolled from 6 provinces to explore the relationship between long-term air pollutants, cardiac structure, and cardiovascular function (e.g., blood lipids, blood pressure and pulse) in Chinese adults. Our study showed that exposure to five pollutants (NO2, O3, PM1, PM2.5 and PM10) was associated with reduced left ventricular systolic function based on EF and SV parameters. These pollutants were also associated with increased pulses, where smaller particle sizes correlated significantly with pulses. Second, except for O3, four pollutants were associated with decreased left ventricular diastolic parameters LVIDd and EDV and increased cardiac structural parameter IVSd. In addition, exposures to NO2, O3 and PM10 were positively correlated with triglycerides in blood lipids. Overall, this study showed that chronic pollutant exposure is strongly associated with impaired left ventricular function in Chinese adults.

Residential greenness associated with decreased risk of metabolic- dysfunction-associated fatty liver disease: Evidence from a large population-based epidemiological study.

BACKGROUND: Numerous studies have shown that residential greenness positively correlates with enhanced health. Metabolic dysfunction-associated fatty liver disease (MAFLD) affects about a quarter of the population while lacking specific treatments. Given that the association between green space and MAFLD is still unknown, we explored the association between residential greenness and MAFLD as well as the potential mechanisms based on the baseline survey of the China Multi-Ethnic Cohort (CMEC). METHODS: Residential greenness was expressed as normalized difference vegetation index (NDVI) and enhanced vegetation index (EVI). MAFLD was assessed through hepatic steatosis, the presence of overweight/obesity, type 2 diabetes mellitus, and evidence of metabolic dysregulation. We used logistic regression to examine the association between NDVI/EVI and the prevalence of MAFLD. Moreover, we utilized causal mediation analyses to explore the role of physical activity and ambient particulate matters (PM1, PM2.5, and PM10) on the association between residential greenness and MAFLD. RESULTS: We included 72,368 participants from the CMEC and found that residential greenness was negatively associated with the prevalence of MAFLD. For an interquartile range (IQR) increase in NDVI500 m and EVI500 m, the odds ratio (OR) of MAFLD were 0.78 (95 %CI: 0.75, 0.81) and 0.81 (95 %CI: 0.78, 0.84), respectively. Greater association between residential greenness and MAFLD was observed among males. Air pollutants and physical activity could mediate a partial effect (8.5-22.9 %) of residential greenness on MAFLD. CONCLUSION: Higher residential greenness was associated with decreased risk of MAFLD. Moreover, the association was greater among males. The protective effects of residential greenness may be achieved by mitigating the hazardous effects of air pollutants and encouraging physical activity.

Exposure to ambient particulate matter and hyperuricemia: An eight-year prospective cohort study on male traffic officers in China.

BACKGROUND AND OBJECTIVES: Studies on the effects of airborne particulates of diameter ≤ 1 µm (PM1), airborne particulates of diameter ≤ 2.5 µm (PM2.5) and airborne particulates of diameter ranges from 1 to 2.5 µm (PM1-2.5) on incidence of hyperuricemia are limited. We aimed to investigate the associations between PM1, PM2.5, and PM1-2.5 and hyperuricemia among male traffic officers. METHODS: We conducted a prospective cohort study of 1460 traffic officers without hyperuricemia in Guangzhou, China from 2009 to 2016. Exposures of PM1 and PM2.5 were estimated with a spatiotemporal model. PM1-2.5 concentrations were calculated by subtracting PM1 from PM2.5 concentrations. Cox's proportional hazards regressions models were used to examine the association between PM1, PM2.5, and PM1-2.5 and hyperuricemia, adjusted for potential confounders. Associations between PM1, PM2.5, and PM1-2.5 and serum uric acid (SUA) levels were evaluated with multiple linear regression models. RESULTS: Hazard ratios (HRs) and 95% confidence intervals (CIs) of hyperuricemia associated with 10 µg/m3 increment in PM1, PM2.5, and PM1-2.5 were 1.67 (95% CI:1.30-2.36), 1.49 (95% CI: 1.27-1.75), and 2.18 (95% CI: 1.58-3.02), respectively. The SUA concentrations increased by 12.23 µmol/L (95% CI: 5.91-18.56), 6.93 µmol/L (95% CI: 3.02-10.84), and 8.72 µmol/L (95% CI: 0.76-16.68) per 10 µg/m3 increase in PM1, PM2.5, and PM1-2.5, respectively. Stratified analyses indicated the positive associations of PM2.5 and PM1-2.5 with SUA levels were stronger in non-smokers, and PM1, PM2.5, and PM1-2.5 with SUA levels were stronger in non-drinkers. CONCLUSION: Long-term PM1, PM2.5, and PM1-2.5 exposures may increase the risk of hyperuricemia and elevate SUA levels among male traffic officers, especially in non-smokers and non-drinkers.

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.

Exposure to wildfire-related PM2.5 and site-specific cancer mortality in Brazil from 2010 to 2016: A retrospective study.

BACKGROUND: Long-term exposure to fine particles ≤2.5 µm in diameter (PM2.5) has been linked to cancer mortality. However, the effect of wildfire-related PM2.5 exposure on cancer mortality risk is unknown. This study evaluates the association between wildfire-related PM2.5 and site-specific cancer mortality in Brazil, from 2010 to 2016. METHODS AND FINDINGS: Nationwide cancer death records were collected during 2010-2016 from the Brazilian Mortality Information System. Death records were linked with municipal-level wildfire- and non-wildfire-related PM2.5 concentrations, at a resolution of 2.0° latitude by 2.5° longitude. We applied a variant difference-in-differences approach with quasi-Poisson regression, adjusting for seasonal temperature and gross domestic product (GDP) per capita. Relative risks (RRs) and 95% confidence intervals (CIs) for the exposure for specific cancer sites were estimated. Attributable fractions and cancer deaths were also calculated. In total, 1,332,526 adult cancer deaths (age ≥ 20 years), from 5,565 Brazilian municipalities, covering 136 million adults were included. The mean annual wildfire-related PM2.5 concentration was 2.38 µg/m3, and the annual non-wildfire-related PM2.5 concentration was 8.20 µg/m3. The RR for mortality from all cancers was 1.02 (95% CI 1.01-1.03, p < 0.001) per 1-µg/m3 increase of wildfire-related PM2.5 concentration, which was higher than the RR per 1-µg/m3 increase of non-wildfire-related PM2.5 (1.01 [95% CI 1.00-1.01], p = 0.007, with p for difference = 0.003). Wildfire-related PM2.5 was associated with mortality from cancers of the nasopharynx (1.10 [95% CI 1.04-1.16], p = 0.002), esophagus (1.05 [95% CI 1.01-1.08], p = 0.012), stomach (1.03 [95% CI 1.01-1.06], p = 0.017), colon/rectum (1.08 [95% CI 1.05-1.11], p < 0.001), larynx (1.06 [95% CI 1.02-1.11], p = 0.003), skin (1.06 [95% CI 1.00-1.12], p = 0.003), breast (1.04 [95% CI 1.01-1.06], p = 0.007), prostate (1.03 [95% CI 1.01-1.06], p = 0.019), and testis (1.10 [95% CI 1.03-1.17], p = 0.002). For all cancers combined, the attributable deaths were 37 per 100,000 population and ranged from 18/100,000 in the Northeast Region of Brazil to 71/100,000 in the Central-West Region. Study limitations included a potential lack of assessment of the joint effects of gaseous pollutants, an inability to capture the migration of residents, and an inability to adjust for some potential confounders. CONCLUSIONS: Exposure to wildfire-related PM2.5 can increase the risks of cancer mortality for many cancer sites, and the effect for wildfire-related PM2.5 was higher than for PM2.5 from non-wildfire sources.

Exposure to air pollution is associated with an increased risk of metabolic dysfunction-associated fatty liver disease.

BACKGROUND & AIMS: Accumulating animal studies have demonstrated the harmful contribution of ambient air pollution (AP) to metabolic dysfunction-associated fatty liver disease (MAFLD), but corresponding epidemiological evidence is limited. We examined the associations between long-term AP exposure and MAFLD prevalence in a Chinese population. METHODS: We conducted a cross-sectional study of 90,086 participants recruited in China from 2018 to 2019. MAFLD was assessed based on radiologically diagnosed hepatic steatosis and the presence of overweight/obese status, diabetes mellitus, or metabolic dysregulation. Residence-specific levels of air pollutants, including particulate matter with aerodynamic diameters of ≤1 µm (PM1), ≤2.5 µm (PM2.5), and ≤10 µm (PM10), and nitrogen dioxide (NO2), were estimated by validated spatiotemporal models. We used logistic regression models to examine the AP-MAFLD associations and further evaluated potential effect modifications by demographics, lifestyle, central obesity, and diabetes status. RESULTS: Increased exposure levels to all 4 air pollutants were significantly associated with increased odds of MAFLD, with odds ratios (ORs) of 1.13 (95% CI 1.10-1.17), 1.29 (1.25-1.34), 1.11 (1.09-1.14), and 1.15 (1.12-1.17) for each 10 µg/m3 increase in PM1, PM2.5, PM10, and NO2, respectively. Further stratified analyses revealed that individuals who are male, alcohol drinkers, and current and previous smokers, those who consume a high-fat diet, and those with central obesity experience more significant adverse effects from AP exposure than other individuals. CONCLUSIONS: This study provides evidence that long-term exposure to ambient PM1, PM2.5, PM10, and NO2 may increase the odds of MAFLD in the real world. These effects may be exacerbated by unhealthy lifestyle habits and central obesity. LAY SUMMARY: We conducted an epidemiological study on the potential effect of ambient air pollution on the risk of metabolic dysfunction-associated fatty liver disease (MAFLD) in approximately 90 thousand adults in China. We found that long-term exposure to ambient air pollution may increase the odds of MAFLD, especially in individuals who are male, smokers, and alcohol drinkers, those who consume a high-fat diet, and those with central obesity.

Aging biomarkers: Potential mediators of association between long-term ozone exposure and risk of atherosclerosis.

BACKGROUND: Long-term exposure to ambient ozone links to aging biomarkers and increased risk for atherosclerotic cardiovascular diseases (ASCVD). However, the roles of aging biomarkers in the association of long-term exposure to ambient ozone with ASCVD are unclear. METHODS: A total of 5298 participants completed the questionnaire and physical examination and provided biological specimens. Aging biomarkers (telomere length [TL] and mitochondrial copy number [mtDNA-CN]) were measured by using a real-time polymerase chain reaction method. The concentration of ambient ozone was assessed using a random forest model. Associations of ambient ozone or aging biomarkers with 10-year ASCVD risk were analyzed using logistic regression models. The roles of aging biomarkers in the association of ambient ozone exposure with 10-year ASCVD risk were explored by mediation analysis. RESULTS: The adjusted odds ratios and 95% confidence interval of high 10-year ASCVD risk were 1.16 (1.08, 1.25), 0.71 (0.60, 0.85), and 0.78 (0.64, 0.96) in association with each 1-unit increment in ambient ozone (1 µg/m3 ) concentration, relative TL, and mtDNA-CN, respectively. The mediated proportion of the association between ambient ozone exposure and high 10-year ASCVD risk by TL or mtDNA-CN was 21.13% or 7.75%, respectively. The total proportion of association between ambient ozone exposure and high 10-year ASCVD risk mediated by TL plus mtDNA-CN was 21.02%. CONCLUSIONS: Long-term exposure to ambient ozone was associated with increased 10-year ASCVD risk, and the association was partially mediated by aging biomarkers (shortened TL and decreased mtDNA-CN). This study indicated that ambient ozone pollution-related ASCVD risk might be partially explained by the telomere-mitochondrial axis of aging.

Association of short-term exposure to ambient air pollution with mortality from ischemic and hemorrhagic stroke.

BACKGROUND: Short-term exposure to ambient air pollution has been linked to increased risk of stroke mortality, but its adverse effects on mortality from specific types of stroke including ischemic stroke and hemorrhagic stroke remain poorly understood. METHODS: Using the China National Mortality Surveillance System, we conducted a time-stratified case-crossover study among 412,567 stroke deaths in Jiangsu province, China during 2015-2019. Residential daily PM2.5 , PM10 , SO2 , NO2 , CO, and O3 exposure concentrations were extracted from the ChinaHighAirPollutants dataset for each subject. Conditional logistic regression models were performed to conduct exposure-response analyses. RESULTS: Each 10 µg/m3 increase of PM2.5 , PM10 , SO2 , NO2 , CO, and O3 was respectively associated with a 1.44%, 0.93%, 5.55%, 2.90%, 0.148%, and 0.54% increase in odds of mortality from ischemic stroke, which was significantly stronger than that from hemorrhagic stroke (percent change in odds: 0.74%, 0.51%, 3.11%, 1.15%, 0.090%, and 0.10%). The excess fraction of ischemic stroke mortality associated with PM2.5 , PM10 , SO2 , NO2 , CO, and O3 exposure was 6.90%, 6.48%, 8.21%, 8.61%, 9.67%, and 4.76%, respectively, which was also significantly higher than that of hemorrhagic stroke mortality (excess fraction: 3.49%, 3.48%, 4.69%, 3.48%, 5.86%, and 0.88%). These differences in adverse effects generally remained across sex, age, and season. CONCLUSIONS: Short-term exposure to ambient air pollution was significantly associated with increased risk of both ischemic and hemorrhagic stroke mortality and posed considerable excess mortality. Our results suggest that air pollution exposure may lead to substantially greater adverse effects on mortality from ischemic stroke than that from hemorrhagic stroke.