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Evidence increasingly suggests molybdenum exposure at environmental levels is still associated with adverse human health, emphasizing the necessity to establish a more protective reference dose (RfD). Herein, we conducted a study measuring 15 urinary metals and 30 clinical health indicators in 2267 participants residing near chemical enterprises across 11 Chinese provinces to investigate their relationships. The kidney and cystatin-C emerged as the most sensitive organ and critical effect indicator of molybdenum exposure, respectively. Odds of cystatin-C-defined chronic kidney disease (CKD) in the highest quantile of molybdenum exposure significantly increased by 133.5% (odds ratio [OR]: 2.34, 95% CI: 1.78, 3.11) and 75.8% (OR: 1.76, 95% CI: 1.24, 2.49) before and after adjusting for urinary 14 metals, respectively. Intriguingly, cystatin-C significantly mediated 15.9–89.5% of molybdenum's impacts on liver and lung function, suggesting nephrotoxicity from molybdenum exposure may trigger hepatotoxicity and pulmonary toxicity. We derived a new RfD for molybdenum exposure (0.87 μg/kg-day) based on cystatin-C-defined estimated glomerular filtration rate by employing Bayesian Benchmark Dose modeling analysis. This RfD is significantly lower than current exposure guidance values (5–30 μg/kg-day). Remarkably, >90% of participants exceeded the new RfD, underscoring the significant health impacts of environmental molybdenum exposure on populations in industrial regions of China. [Display omitted] • CYS-C was first identified as the critical effect indicator of Mo exposure. • CYS-C mediated 15.9–89.5% of molybdenum's impacts on liver and lung function. • Elevated Sr markedly attenuated the nephrotoxicity associated with Mo exposure. • The new RfD (0.87 μg/kg-day) was far lower than the current intake guidance values. • >90% participants faced non-carcinogenic risk from Mo exposure using the new RfD. [ABSTRACT FROM AUTHOR]

Recent evidences highlight the potential impact of outdoor Light at Night (LAN) on executive function. However, few studies have investigated the association between outdoor LAN exposure and executive function. We employed data from 48,502 Chinese children aged 5–12 years in a cross-sectional study conducted in Guangdong province during 2020–2021, to examine the association between outdoor LAN and executive function assessed using the validated parent-completed Behavior Rating Inventory of Executive Function. We assessed children's outdoor LAN exposure using the night-time satellite images based on the residential addresses. We used generalized linear mixed models to estimate the association between outdoor LAN exposure and executive function scores and executive dysfunction. After adjusting for potential covariates, higher quintiles of outdoor LAN exposure were associated with poorer executive function. Compared to the lowest quintile (Q1), all higher quintiles of exposure showed a significant increased global executive composite (GEC) score with β (95% confidence intervals, CI) of 0.58 (0.28, 0.88) in Q2, 0.59 (0.28, 0.9) in Q3, 0.85 (0.54, 1.16) in Q4, and 0.76 (0.43, 1.09) in Q5. Higher quintiles of exposure were also associated with higher risks for GEC dysfunction with odd ratios (ORs) (95% CI) of 1.34 (1.18, 1.52) in Q2, 1.40 (1.24, 1.59) in Q3, 1.40 (1.23, 1.59) in Q4, and 1.39 (1.22, 1.58) in Q5. And stronger associations were observed in children aged 10–12 years. Our study suggested that high outdoor LAN exposure was associated with poor executive function in children. These findings suggested that future studies should determine whether interventions to reduce outdoor LAN exposure can have a positive effect on executive function. [Display omitted] • A large study to examine the association of outdoor LAN and executive function in children aged 5–12 years. • Outdoor LAN exposure was associated with executive dysfunction in children. • Stronger associations were found among children aged 10–12 years. [ABSTRACT FROM AUTHOR]

Chlorinated polyfluorinated ether sulfonate (F–53B), a substitute of perfluorooctane sulfonic acid (PFOS), has attracted significant attention for its link to hepatotoxicity and enterotoxicity. Nevertheless, the underlying mechanisms of F–53B-induced enterohepatic toxicity remain incompletely understood. This study aimed to explore the role of F–53B exposure on enterohepatic injury based on the gut microbiota, pathological and molecular analysis in mice. Here, we exposed C57BL/6 mice to F–53B (0, 4, 40, and 400 μg/L) for 28 days. Our findings revealed a significant accumulation of F–53B in the liver, followed by small intestines, and feces. In addition, F–53B induced pathological collagen fiber deposition and lipoid degeneration, up-regulated the expression of fatty acid β-oxidation-related genes (PPARα and PPARγ , etc), while simultaneously down-regulating pro-inflammatory genes (Nlrp3 , IL-1β , and Mcp1) in the liver. Meanwhile, F–53B induced ileal mucosal barrier damage, and an up-regulation of pro-inflammatory genes and mucosal barrier-related genes (Muc1 , Muc2 , Claudin1 , Occludin , Mct1 , and ZO-1) in the ileum. Importantly, F–53B distinctly altered gut microbiota compositions by increasing the abundance of Akkermansia and decreasing the abundance of Prevotellaceae_NK3B31_group in the feces. F–53B-altered microbiota compositions were significantly associated with genes related to fatty acid β-oxidation, inflammation, and mucosal barrier. In summary, our results demonstrate that F–53B is capable of inducing hepatic injury, ileitis, and gut microbiota dysbiosis in mice, and the gut microbiota dysbiosis may play an important role in the F–53B-induced enterohepatic toxicity. [Display omitted] • F–53B that simulated human exposure levels is accumulated in the liver, intestines, and feces of mice. • F–53B led to hepatic deposition of collagen fibers, ileitis, and gut microbiota dysbiosis in mice. • F–53B-altered microbiota was associated with genes related to hepatic fatty acid β-oxidation and ileal mucosal barrier in mice. [ABSTRACT FROM AUTHOR]

Exposure to chemicals may affect liver enzyme to increase the risk of liver diseases. Perfluoroalkyl acids (PFAAs) are one kind of persistent organic pollutants with hepatotoxic effect in organism. However, data is scarce to characterize the hepatotoxic effects of specific structural PFAA isomers in general population. To address this data gap, we evaluated the association between serum PFAAs concentration and liver function biomarkers in the Isomers of C8 Health Project in China. High performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) was used to measure 18 serum PFAAs, except for linear and branched isomers of PFOA/PFOS, nine perfluorinated carboxylic acids (PFCAs) and two perfluorinated sulfonic acids (PFSAs) were also included, in 1605 adult residents of Shenyang, China. Values for nine serum liver function biomarkers were determined by full-automatic blood biochemical analyzer. Linear regression was used to evaluate associations between PFAAs and continuous liver function biomarkers and logistic regression to assess markers dichotomized per clinical reference intervals. Results indicated that serum PFAAs concentrations were associated with liver biomarker levels suggestive of hepatotoxicity, especially for liver cell injury. For example, a 1 ln-unit increase in total- perfluorooctanoic acid (PFOA) exposure was associated with a 7.4% [95% confidence interval (CI): 3.9%, 11.0%] higher alanine aminotransferase (ALT) level in serum. Interestingly, we observed association between branched PFAA isomers and liver biomarkers. For example, one ln-unit increase in branched perfluorooctane sulfonate (PFOS) isomers exposure was associated with a 4.3% increase in ALT level (95% CI: 1.2%, 7.4%) and a 33.0% increased odds of having abnormal ALT (95% CI: 5.0%, 67.0%). Also, we found that PFNA had positive association with ALT [(6.2%, 95% CI: 3.1%, 9.4%) and AST levels (2.5%, 95% CI: 0.5%, 4.5%)]. Logistic regression results showed that PFPeA, PFHxA, PFNA, PFDoDA, PFTrDA and PFTeDA had statistically association with abnormal prealbumin. Conclusively, our results support previous studies showing association between PFAAs exposure and liver function biomarkers. We found new evidence that branched PFAAs isomer exposure is associated with the risk of clinically relevant hepatocellular dysfunction. • Few human studies reported the associations of PFAA isomers with liver function. • A large population-based study was conducted in China to assess theses associations. • We found new evidence that branched PFOS isomers exposure is associated with the risk of clinically relevant hepatocellular dysfunction. [ABSTRACT FROM AUTHOR]

Abstract No evidence exists concerning the association between blood pressure and ambient particles with aerodynamic diameter ≤ 1.0 µm (PM 1), a major component of PM 2.5 (≤ 2.5 µm) particles, and potentially causing more hazardous health effects than PM 2.5. We aimed to examine the associations of blood pressure in adults with both PM 1 and PM 2.5 in China. In 2009, we randomly selected 24,845 participants aged 18–74 years from 33 communities in China. Using a standardized mercuric-column sphygmomanometer, we measured blood pressure. Long-term exposure (2006–08) to PM 1 and PM 2.5 were estimated using a spatial statistical model. Generalized linear mixed models were used to evaluate the associations between air pollutants and blood pressure and hypertension prevalence, controlling for multiple covariates. A 10-μg/m3 increase in PM 1 was significantly associated with an increase of 0.57 (95% CI 0.31–0.83) mmHg in systolic blood pressure (SBP), 0.19 (95% CI 0.03–0.35) mmHg increase in diastolic blood pressure (DBP), and a 5% (OR=1.05; 95% CI 1.01–1.10) increase in odds for hypertension. Similar associations were detected for PM 2.5. Furthermore, PM 1–2.5 showed no association with blood pressure or hypertension. In summary, both PM 1 and PM 2.5 exposures were associated with elevated blood pressure levels and hypertension prevalence in Chinese adults. In addition, most of the pro-hypertensive effects of PM 2.5 may come from PM 1. Further longitudinal designed studies are warranted to validate our findings. Highlights • Little information exists on pro-hypertensive effects of PM 1. • We investigated the topic in 24,845 Chinese adults. • Associations between PM 1 and PM 2.5 and blood pressure were examined. • Long-term PM 1 exposure was associated with higher blood pressure levels. • The pro-hypertensive effects of PM 2.5 were mainly come from PM 1. [ABSTRACT FROM AUTHOR]

Little evidence exists about the effects of long-term exposure to ambient air pollution on metabolic syndrome (MetS). This study aimed to determine the association between long-term ambient air pollution and MetS in China. A total of 15,477 adults who participated in the 33 Communities Chinese Health Study (33CCHS) in 2009 were evaluated. MetS was defined based on the recommendation by the Joint Interim Societies. Exposure to air pollutants was assessed using data from monitoring stations and a spatial statistical model (including particles with diameters ≤ 1.0 µm (PM 1 ), ≤ 2.5 µm (PM 2.5 ), and ≤ 10 µm (PM 10 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), and ozone (O 3 )). Two-level logistic regression analyses were utilized to assess the associations between air pollutants and MetS. The prevalence of MetS was 30.37%. The adjusted odds ratio of MetS per 10 µg/m 3 increase in PM 1 , PM 2.5 , PM 10 , SO 2 , NO 2 , and O 3 were 1.12 (95% CI = 1.00–1.24), 1.09 (95% CI = 1.00–1.18), 1.13 (95% CI = 1.08–1.19), 1.10 (95% CI = 1.02–1.18), 1.33 (95% CI = 1.12–1.57), and 1.10 (95% CI = 1.01–1.18), respectively. Stratified analyses indicated that the above associations were stronger in participants with the demographic variables of males, < 50 years of age, and higher income, as well as with the behavioral characteristics of smoking, drinking, and consuming sugar-sweetened soft drinks frequently. This study indicates that long-term exposure to ambient air pollutants may increase the risk of MetS, especially among males, the young to middle aged, those of low income, and those with unhealthy lifestyles. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated associations between serum levels of perfluoroalkyl substances (PFASs) and asthma or asthma related-biomarkers. However, no studies have reported a possible relationship between PFASs exposure and lung function among children. The objective of the present study is to test the association between PFASs exposure and lung function in children from a high exposure area by using a cross-sectional case-control study, which included 132 asthmatic children and 168 non-asthmatic controls recruited from 2009 to 2010 in the Genetic and Biomarkers study for Childhood Asthma. Structured questionnaires were administered face-to-face. Lung function was measured by spirometry. Linear regression models were used to examine the influence of PFASs on lung function. The results showed that asthmatics in our study had significantly higher serum PFAS concentrations than healthy controls. Logistic regression models showed a positive association between PFASs and asthma, with adjusted odds ratios (ORs) ranging from 0.99 (95% confidence interval [CI]: 0.80–1.21) to 2.76 (95% CI: 1.82–4.17). Linear regression modeling showed serum PFASs levels were significantly negatively associated with three pulmonary function measurements (forced vital capacity: FVC; forced expiratory volume in 1 s: FEV 1 ; forced expiratory flow 25–75%: FEF 25–75 ) among children with asthma, the adjusted coefficients between lung function and PFASs exposure ranged from −0.055 (95%CI: −0.100 to −0.010) for FVC and perfluorooctane sulfonate (PFOS) to −0.223 (95%CI: −0.400 to −0.045) for FEF 25–75 and perfluorooctanoic acid (PFOA). PFASs were not, however, significantly associated with pulmonary function among children without asthma. In conclusion, this study suggests that serum PFASs are associated with decreased lung function among children with asthma. [ABSTRACT FROM AUTHOR]

Previous studies have indicated that chlorinated polyfluorinated ether sulfonic acids (Cl-PFESAs), when used as an alternative to per- and polyfluoroalkyl substances (PFASs), result in kidney toxicity. However, their co-exposure with heavy metals, has not yet been described. To explore the joint effects of Cl-PFESAs and heavy metal exposure on renal health in Chinese adults, and identify specific pollutants driving the associations. Our sample consists of 1312 adults from a cross-sectional survey of general communities in Guangzhou, China. We measured Cl-PFESAs, legacy PFASs (perfluorooctanoic acid [PFOA] and perfluorooctane sulfonated [PFOS]), and heavy metals (arsenic, cadmium, and lead). The relationship between single pollutant and glomerular filtration rate (eGFR) and the odds ratio (OR) of chronic kidney disease (CKD) was studied using Generalized additive models (GAMs). Bayesian Kernel Machine Regression (BKMR) models were applied to assess joint effects of Cl-PFESAs and heavy metals. Additionally, we conducted a sex-specific analysis to determine the modification effect of this variable. In single pollutant models, CI-PFESAs, PFOA, PFOS and arsenic were negatively associated with eGFR. Additionally, PFOA and heavy metals were positively correlated with the OR of CKD. For example, the estimated change with 95% confidence intervals (CI) of eGFR at from the highest quantile of 6:2 Cl-PFESA versus the lowest quantile was −5.65 ng/mL (95% CI: −8.21, −3.10). Sex played a role in modifying the association between 8:2 Cl-PFESA, PFOS and eGFR. In BKMR models, pollutant mixtures had a negative joint association with eGFR and a positive joint effect on CKD, especially in women. Arsenic appeared to be the primary contributing pollutant. We provide epidemiological evidence that Cl-PFESAs independently and jointly with heavy metals impaired kidney health. More population-based human and animal studies are needed to confirm our results. [Display omitted] • We conducted a study of the general adult population of urban communities in southern China. • For the first time, Cl-PFESAs was reported to be associated with human kidney health. • Interactions exist between Cl-PFESAs and heavy metals. • Cl-PFESAs and heavy metals impaired kidney function, especially in women. [ABSTRACT FROM AUTHOR]

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. 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. 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. 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. [Display omitted] • Ozone was associated with children attention-deficit/hyperactivity disorders (ADHD). • Children with symptoms but not reaching the diagnostic criteria had similar results. • Non-breastfed children and those who exercise frequently are the most vulnerable. [ABSTRACT FROM AUTHOR]

Studies have investigated associations between maternal exposure to PFAS and preterm birth, but the impact of paternal and overall family exposure to PFAS mixtures on preterm birth remains unknown. To address this knowledge gap, a total of 355 preterm births and 481 controls were selected for a family-based birth cohort study in a coastal area of China, between 2016 and 2018. Seven PFAS, including perfluorobutanoic acid (PFBA), perfluorohexanoic acid (PFHxA), perfluorohexanesulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonic acid (PFOS), perfluorononanoic acid (PFNA) and perfluorodecanoic acid (PFDA), were quantified in maternal, paternal and neonatal sera. Preterm birth was defined as live delivery at <37 completed gestational weeks. Bayesian kernel machine regression (BKMR) model was used to inspect the combined effect of family PFAS mixtures. Latent class analysis was used to identify family-level PFAS exposure profiles. Multiple linear regression analysis showed higher odds of preterm birth in association with higher maternal PFBA (OR = 1.16, 95%CI:1.09, 1.25), PFOA (OR = 1.51, 95%CI:1.27, 1.80), PFOS (OR = 2.07, 95%CI:1.70, 2.52) and PFNA (OR = 1.36, 95%CI: 1.01, 1.83), and neonatal PFBA (OR = 1.16, 95%CI:1.05,1.29), PFHxA (OR = 1.46, 95%CI:1.32, 1.62), PFHxS (OR = 1.15, 95%CI:1.05, 1.26) and PFNA (OR = 1.30, 95%CI:1.09,1.56). The associations were reversed between individual paternal PFAS exposures and preterm birth. At the family level, higher PFAS mixture concentration was associated with higher odds of preterm birth. In particular, higher PFNA and PFDA exposure was associated with greater preterm birth risk (OR = 2.55, 95%CI:1.45, 4.50). The PFAS-preterm association was modified by family-level seafood consumption. Our results suggest that higher family-level PFNA and PFDA exposure was associated with greater preterm birth risk, although the results for individual paternal, maternal and neonatal PFAS exposures were contradictory. If replicated in other coastal areas, these findings highlight a need to focus on the family triad and to consider seafood consumption when assessing the reproductive toxicity of PFAS exposure. • Higher odds of preterm birth in association with higher maternal and neonatal PFASs exposure, and these associations reversed in paternal. • Higher perfluorononanoic acid (PFNA) and perfluorodecanoic acid (PFDA) exposure was associated with greater preterm birth risk at the family level. • The PFAS-preterm association was modified by family-level seafood consumption. [ABSTRACT FROM AUTHOR]

The widely used Air Quality Index (AQI) has been criticized due to its inaccuracy, leading to the development of the air quality health index (AQHI), an improvement on the AQI. However, there is currently no consensus on the most appropriate construction strategy for the AQHI. In this study, we aimed to evaluate the utility of AQHIs constructed by different models and health outcomes, and determine a better strategy. Based on the daily time-series outpatient visits and hospital admissions from 299 hospitals (January 2016–December 2018), and mortality (January 2017–December 2019) in Guangzhou, China, we utilized cumulative risk index (CRI) method, Bayesian multi-pollutant weighted (BMW) model and standard method to construct AQHIs for different health outcomes. The effectiveness of AQHIs constructed by different strategies was evaluated by a two-stage validation analysis and examined their exposure-response relationships with the cause-specific morbidity and mortality. Validation by different models showed that AQHI constructed with the BMW model (BMW-AQHI) had the strongest association with the health outcome either in the total population or subpopulation among air quality indexes, followed by AQHI constructed with the CRI method (CRI-AQHI), then common AQHI and AQI. Further validation by different health outcomes showed that AQHI constructed with the risk of outpatient visits generally exhibited the highest utility in presenting mortality and morbidity, followed by AQHI constructed with the risk of hospitalizations, then mortality-based AQHI and AQI. The contributions of NO 2 and O 3 to the final AQHI were prominent, while the contribution of SO 2 and PM 2.5 were relatively small. The BMW model is likely to be more effective for AQHI construction than CRI and standard methods. Based on the BMW model, the AQHI constructed with the outpatient data may be more effective in presenting short-term health risks associated with the co-exposure to air pollutants than the mortality-based AQHI and existing AQIs. [Display omitted] • Morbidity data from 299 hospitals in Guangzhou, China were used for the improved AQHI validation and construction. • The utility of AQHIs constructed with two updated multi-pollutant models and three health outcomes were compared. • AQHI constructed with BMW model and outpatient visit data exhibited relatively higher effectiveness in communicating risks. [ABSTRACT FROM AUTHOR]

Health effects of greenness perceived by residents at eye level has received increasing attention. However, the associations between eye-level greenness and respiratory health are unknown. The aim of the study was to investigate the associations between exposure to eye-level greenness and lung function in children. From 2012 to 2013, a total of 6740 school children in seven cities in northeast China were recruited into this cross-sectional study. Forced expiratory volume in 1 s (FEV 1), forced vital capacity (FVC), peak expiratory flow rate (PEF), and maximum mid expiratory flow rate (MMEF) were measured to evaluate lung function and to define lung impairment. Eye-level greenness was extracted from segmented Tencent Map street view images, and a corresponding green view index (GVI) was calculated. Higher GVIs mean more greenness coverage. Mixed-effects logistic regressions were used to estimate the health effects on lung impairment per interquartile range (IQR) increase in GVI. Linear regressions were used to estimate the associations between GVI and lung function. The health effects of ambient air pollutants were also assessed, including particulate matter with an aerodynamic diameter <1.0 μm (PM 1), <2.5 μm (PM 2.5), <10 μm (PM 10) as well as nitrogen dioxide (NO 2). An increase of GVI 800m was associated with lung impairment in FEV 1 , FVC, PEF and MMEF, with ORs ranging from 0.68 (95% CI: 0.59, 0.79) to 0.83 (95% CI: 0.74, 0.93). The associations between an IQR increase of GVI 800m and FEV 1 (48.15 ml, 95% CI: 30.33–65.97 ml), FVC (50.57 ml, 95% CI: 30.65–70.48 ml), PEF (149.59 ml/s, 95% CI: 109.79–189.38 ml/s), and MMEF (61.18 ml/s, 95% CI: 31.07–91.29 ml/s) were significant, and PM 1 , PM 2.5 , and PM 10 were found to be mediators of this relationship. More eye-level greenness was associated with better lung function and reduced impairment. However, eye-level greenness associations with lung function became non-significant once lower particulate matter air pollution exposures were considered. • More eye-level greenness exposure is associated with better lung function. • The associations became non-significant once lower particulate matter air pollution exposures were considered. • Greenness may serve as an index for a reduction of other factors in open space. [ABSTRACT FROM AUTHOR]

Urban greenness may protect against obesity, but very few studies have assessed 'street view' (SV) greenness metrics, which may better capture people's actual exposure to greenness compared to commonly-used satellite-derived metrics. We aimed to investigate these associations further in a Chinese adult study. Our analysis included 24,845 adults in the 33 Chinese Community Health Study in 2009. SV images from Tencent Map, segmented by machine learning algorithms, were used to determine the average proportion of green vegetation in SV images at community level in 800m road network buffer. Sensitivity analyses were performed with an alternative buffer size. Overall greenness was assessed as normalized difference vegetation index (NDVI) in 800 m buffer. We used predicted PM 2.5 and monitored NO 2 as proxies of air pollution. Body mass index (BMI), waist circumference (WC) and hip circumference (HC) were regressed on SV greenness by generalized linear mixed models, with adjustment for covariates. Mediation analyses were performed to assess the mediation effects of air pollution. Each interquartile range (IQR = 3.6%) increase in street view greenness was associated with a 0.15 kg/m2 (95% CI: −0.22, −0.09) decrease in BMI and 0.23 cm (95% CI: −0.35, −0.11) reduction in HC, and was associated with 7% lower odds of overweight (OR = 0.93, 95% CI:0.90, 0.96) and 18% lower odds of obesity (OR = 0.82, 95% CI:0.76, 0.89). Similar effect estimation was observed compared with commonly-used NDVI measures. PM 2.5 and NO 2 mediated 15.5% and 6.1% of the effects of SV greenness with BMI, respectively. Our findings suggest beneficial associations between community-level SV greenness and lower body weight in Chinese adults. The effects were observed in women but not in men. Air pollution may partially mediate the association. These findings may have implications to support efforts to promote greening in urban areas. [ABSTRACT FROM AUTHOR]

Exposure to perfluoroalkyl acids (PFAAs) is known to be associated with metabolic disorders. However, whether PFAAs isomers are associated with metabolic syndrome (MetS) still remains unknown. To explore the associations between serum PFAAs isomers and MetS. We recruited 1,501 adults from a cross-sectional study, the "Isomers of C8 Health Project in China" to investigate the associations between PFAAs isomers and MetS. A total of 20 PFAAs including the isomers of PFOS and PFOA were detected. Logistic regression models and restricted cubic spline models were used to evaluate the relationship of serum PFAAs isomers exposure with MetS and its components as well after adjusting for covariates. The MetS prevalence in our study was 43.0%. The serum levels of both PFOS and PFOA isomers were higher in participants with MetS than that with non-MetS (p < 0.05). We found positive associations for per natural log-transformed ng/mL of branched perfluorooctane sulfonate (br-PFOS) (odds ratio (OR) = 1.18, 95% confidence interval (CI): 1.01, 1.38)) linear perfluoronanoic acid (n-PFOA) (OR = 1.35, 95% CI: 1.16, 1.58) and perfluoro-6-methylpheptanoic acid (6 m-PFOA) (OR = 1.32, 95% CI: 1.11, 1.57) with higher odds of MetS after covariates adjustment, while null association was observed for linear isomers of PFOS (OR = 1.09, 95% CI: 0.94, 1.25). We found a nonlinear dose-response relationship with a "threshold" effect in serum br-PFOS isomers with MetS, in which the odds of MetS increased quickly with increasing serum br-PFOS isomers under low exposure (p for nonlinearity = 0.030). We report new evidence of associations between PFAAs isomers and MetS and the nonlinearity of dose-response relationship with br-PFOS isomers. Our findings indicate that more attention is needed to pay on the nonlinearity of dose-response relationship when investigate the association of PFAAs isomers with human health. • We provided evidence on isomeric-specific associations between serum PFAAs and metabolic syndrome in adults. • Branched PFOS isomers were associated with metabolic syndrome with an apparent "threshold" effect. • Both serum PFOS and PFOA were associated with elevated fasting blood glucose. [ABSTRACT FROM AUTHOR]

Ambient air pollution exposure and influenza virus infection have been documented to be independently associated with reduced lung function previously. Influenza vaccination plays an important role in protecting against influenza-induced severe diseases. However, no study to date has focused on whether influenza vaccination may modify the associations between ambient air pollution exposure and lung function. We undertook a cross-sectional study of 6740 children aged 7–14 years into Seven Northeast Cities (SNEC) Study in China during 2012–2013. We collected information from parents/guardians about sociodemographic factors and influenza vaccination status in the past three years. Lung function was measured using portable electronic spirometers. Machine learning methods were used to predict 4-year average ambient air pollutant exposures to nitrogen dioxide (NO 2) and particulate matter with an aerodynamic diameter <1 μm (PM 1), <2.5 μm (PM 2.5) and <10 μm (PM 10). Two-level linear and logistic regression models were used to assess interactions between influenza vaccination and long-term ambient air pollutants exposure on lung function reduction, controlling for potential confounding factors. Ambient air pollution were observed significantly associated with reductions in lung function among children. We found significant interactions between influenza vaccination and air pollutants on lung function, suggesting greater vulnerability to air pollution among unvaccinated children. For example, an interaction (p interaction = 0.002) indicated a −283.44 mL (95% CI: −327.04, −239.83) reduction in forced vital capacity (FVC) per interquartile range (IQR) increase in PM 1 concentrations among unvaccinated children, compared with the −108.24 mL (95%CI: −174.88, −41.60) reduction in FVC observed among vaccinated children. Results from logistic regression models also showed stronger associations between per IQR increase in PM 1 and lung function reduction measured by FVC and peak expiratory flow (PEF) among unvaccinated children than the according ORs among vaccinated children [i.e., Odds Ratio (OR) for PM 1 and impaired FVC: 2.33 (95%CI: 1.79, 3.03) vs 1.65 (95%CI: 1.20, 2.28); OR for PM 2.5 and impaired PEF: 1.45 (95%CI: 1.12,1.87) vs 1.04 (95%CI: 0.76,1.43)]. The heterogeneity of the modification by influenza vaccination of the associations between air pollution exposure and lung function reduction appeared to be more substantial in girls than in boys. Our results suggest that influenza vaccination may moderate the detrimental effects of ambient air pollution on lung function among children. This study provides new insights into the possible co-benefits of strengthening and promoting global influenza vaccination programs among children. Image 1 • No study on interactions between flu vaccine and air pollution on lung function. • Flu vaccine may mitigate the detrimental effects of air pollution on lung function. • The interactions appeared to be more substantial in girls than in boys. [ABSTRACT FROM AUTHOR]

There is a large body of evidence linking Environmental Tobacco Smoke (ETS) exposure with impaired lung function. However, it is not known whether exposure to pets modifies this relationship. To investigate if pet ownership changes the association between ETS exposure and lung function, a population-based sample of 7326 children, 7–14 years old, were randomly recruited from 24 districts in northeast China. Lung function including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV 1), peak expiratory flow (PEF), and maximal mid-expiratory flow (MMEF) was measured by spirometry, while pet ownership time periods and ETS exposure were collected by questionnaire. Two-level regression analysis was done, with covariates controlled for. The results showed pet exposure in certain early lifetime windows modified the associations of ETS exposure on decreased lung function in children. Among children exposed to current ETS, those exposed to pets in utero had greater reductions in lung function (for instance: OR for reduced FVC (<85% predicted) = 10.86; 95% CI: 3.80–30.97) than those not exposed to pets in utero (OR = 2.32; 95% CI: 1.76–3.05) (p interaction = 0.005). While, children exposed to current pet ownership reduced the lung function impairment induced by ETS exposure during the first 2 years of life and/or ETS exposure during pregnancy, especially for FVC impairment. For instance, OR (95%CI) for reduced FVC (<85% predicted) was 0.81 (0.56, 1.18) and 1.42 (1.15, 1.74), respectively, for children with or without current pet ownership exposed to ETS during the first 2 years of life (p interaction = 0.010). Furthermore, pet type or number of pets did not significantly modify associations between ETS exposure and lung function. In conclusion, the timing of pet ownership modified associations between ETS exposure and lung function, pet ownership in utero and during the first 2 years of life significantly worsened the adverse impacts of passive smoking on lung function. • Studies of joint effects of pet ownership and ETS on children's lung function are rare. • We explored this topic in 6740 Chinese children from 49 schools in 7 cites. • Pet exposure in certain early lifetime windows modified the associations of ETS exposure on decreased lung function. • Pet ownership in utero and during the first 2 years of life worsened the adverse impacts of ETS exposure on lung function. [ABSTRACT FROM AUTHOR]