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OBJECTIVE: This study aimed to explore the associations of tobacco smoke exposure (TSE) and heavy metal exposure on sex hormones and the joint effects between them in adult males. METHODS: The study used data of 2244 adult males from the National Health and Nutrition Examination Survey (NHANES, 2013-2016). Weighted linear regression models were used to calculate their beta (ß) coefficients and corresponding confidence interval (95% CI), which assessed the joint effects of TSE and heavy metals on sex hormones. RESULTS: Sex hormone-binding globulin (SHBG) showed a positive association with increased per standard deviation (SD) for cotinine (ß=0.024 [0.004, 0.043]; P<0.001), lead (ß=0.021 [0.002, 0.039]; P=0.028), and cadmium (ß=0.034 [0.015, 0.053]; P<0.001). Manganese was positively associated with estradiol (E2) (ß=0.025 [0.009, 0.042]; P=0.002). The subjects with higher cadmium levels were more likely to have higher total testosterone (TT) (ß=0.042 [0.023, 0.062]; P<0.001). TSE and lead exerted synergistic effects on TT (p for interaction = 0.015) and E2 (p for interaction = 0.009), as also did TSE and cadmium on SHBG (p for interaction = 0.037). Compared with the reference group, TSE participants who were exposed to high concentrations of lead, cadmium, mercury, and manganese had significantly elevated TT levels, but these high levels presented no significant association with E2 levels. A significantly higher level of SHBG among TSE participants was detected in high concentrations for lead, cadmium, and mercury. CONCLUSION: TSE exacerbated sex hormone imbalances when combined with high levels of metal exposure. Smoking cessation is crucial, especially in the case of high levels of occupational exposure to heavy metals.

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BACKGROUND: Epidemiological evidence regarding the association between air pollutants and cardiopulmonary disease, mortality in individuals with preserved ratio impaired spirometry (PRISm), and their combined effects remains unclear. METHODS: We followed 36,149 participants with PRISm in the UK Biobank study. Annual concentrations of PM2.5, PM10, NO2, NOx, and SO2 at residential addresses were determined using a bilinear interpolation method, accounting for address changes. A multistate model assessed the dynamic associations between air pollutants and cardiopulmonary diseases and mortality in PRISm. Quantile g-computation was used to investigate the joint effects of air pollutants. RESULTS: Long-term exposure to PM2.5, PM10, NO2, NOx, and SO2 was significantly associated with the risk of cardiopulmonary disease in PRISm. The corresponding hazard ratios (HRs) [95 % confidence intervals (95 % CIs)] per interquartile range (IQR) were 1.49 (1.43, 1.54), 1.52 (1.46, 1.57), 1.34 (1.30, 1.39), 1.30 (1.26, 1.34), and 1.44 (1.41, 1.48), respectively. For mortality, the corresponding HRs (95 % CIs) per IQR were 1.36 (1.25, 1.47), 1.35 (1.24, 1.46), 1.27 (1.18, 1.36), 1.23 (1.15, 1.31), and 1.29 (1.20, 1.39), respectively. In PRISm, quantile g-computation analysis demonstrated that a quartile increase in exposure to a mixture of all air pollutants was positively associated with the risk of cardiopulmonary disease and mortality, with HRs (95 % CIs) of 1.84 (1.76, 3.84) and 1.45 (1.32, 1.57), respectively. CONCLUSION: Long-term individual and joint exposure to air pollutants (PM2.5, PM10, NO2, NOx, and SO2) might be an important risk factor for cardiopulmonary disease and mortality in high-risk populations with PRISm.

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The present study examines the extent and direction of horizontal, backward and forward spillover effects of FDIs on firms' productivity. It also shows how the mediating factors (firm's age, export and import intensity, R&D and advertisement intensity) contribute to the firms' productivity. Further, the study also uncovers the importance of the ownership patterns of the firms that affect the spillovers. It uses a balanced firm-level panel data set from the Indian manufacturing industries over the available period 2003 to 2016 to examine the inter- and intra-industry spillovers of the FDIs. The estimation methods used in this study are the fixed effects approach and the generalised method of moments. The study also applies the Levinsohn-Petrin method to compute firm-level productivity. It finds a significant positive spillover backward effect and confirms the supportive role of the mediating factors in augmenting the spillover channels. However, the results do not support the existence of horizontal and forward FDI spillover effects for the overall manufacturing industries. They suggest that a comprehensive policy package approach be used, thereby underlining the importance of all channels of the FDI spillover effects and their relations to the downstream sector, particularly by keeping the performance of the firms and their external links in perspective.

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INTRODUCTION: Racial and ethnic disparities in gynecologic cancer care have been documented. Treatment at academic facilities is associated with improved survival, yet no study has examined independent associations between race and ethnicity with facility type among gynecologic cancer patients. MATERIALS & METHODS: We used the National Cancer Database and identified 484,455 gynecologic cancer (cervix, ovarian, uterine) patients diagnosed between 2004 and 2020. Facility type was dichotomized as academic vs. non-academic, and we used logistic regression to estimate multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) between race and ethnicity and facility type. Secondarily, we examined joint effects of race and ethnicity and facility type on overall survival using Cox proportional hazards regression. RESULTS: We observed higher odds of treatment at academic (vs. non-academic) facilities among American Indian/Alaska Native (OR = 1.42, 95% CI = 1.28-1.57), Asian (OR = 1.64, 95% CI = 1.59-1.70), Black (OR = 1.69, 95% CI = 1.65-1.72), Hispanic (OR = 1.70, 95% CI = 1.66-1.75), Native Hawaiian/Pacific Islander (OR = 1.74, 95% CI = 1.57-1.93), and other race (OR = 1.29, 95% CI = 1.20-1.40) patients compared with White patients. In the joint effects survival analysis with White, academic facility-treated patients as the reference group, Asian, Hispanic, and other race patients treated at academic or non-academic facilities had improved overall survival. Conversely, Black patients treated at academic facilities [Hazard Ratio (HR) = 1.10, 95% CI = 1.07-1.12] or non-academic facilities (HR = 1.19, 95% CI = 1.16-1.21) had worse survival. DISCUSSION: Minoritized gynecologic cancer patients were more likely than White patients to receive treatment at academic facilities. Importantly, survival outcomes among patients receiving care at academic institutions differed by race, requiring research to investigate intra-facility survival disparities.

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BACKGROUND: Concerns remain about the neurotoxic properties of the ubiquitous organophosphate esters (OPEs), the replacement of the toxicant polybrominated diphenyl ethers. OBJECTIVES: We examined the associations of prenatal exposure to OPEs and their mixtures with early-life neurodevelopment trajectories. METHODS: Totally 1276 mother-child pairs were recruited from the Shanghai Maternal-Child Pairs Cohort. A high-performance liquid chromatography-triple quadrupole mass spectrometer was used to measure the levels of 7 OPEs in cord serum. Ages and Stages Questionnaires was used to examine children's neuropsychological development at 2, 6, 12, and 24 months of age. Group-based trajectory models were applied to derive the neurodevelopmental trajectories. Multiple linear regression and logistic regression model were performed to assess the relationships between OPEs exposure and neurodevelopment and trajectories. Mixtures for widely detected OPEs (n = 4) were investigated using quantile-based g-computation. RESULTS: Tributyl phosphate (TBP), tris (2-butoxy ethyl) phosphate (TBEP), tris(1,3-dichloro-2-propyl) phosphate (TDCPP), and 2-ethylhexyl diphenyl phosphate (EHDPP), had detection rates >50 %. TDCPP had the highest median concentration (1.02 µg/L) in cord serum. EHDPP concentrations were negatively associated with scores in most domains at 12 months of age, with effect values (ß) ranging from -1.89 to -0.57. EHDPP could negatively affect the total ASQ (OR = 1.07, 95 % CI: 1, 1.15) and gross-motor (OR = 1.09, 95 % CI: 1.02, 1.17) trajectory in infancy. Joint exposure to OPEs was associated with decreased scores in the total ASQ, gross-motor, fine-motor and problem-solving domain of 12-month-old infants, with ß ranging from -5.93 to -1.25. In addition, the qgcomp models indicated significant positive associations between the concentrations of OPEs mixtures and risks of the persistently low group of the total ASQ, gross-motor and fine-motor development in early childhood. The impact of OPEs was more pronounced in boys. DISCUSSION: Our findings suggested OPEs, especially EHDPP, had a persistently negative effect on neurodevelopment during the first 2 years.

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The joint toxicity effects of mixtures, particularly reproductive toxicity, one of the main causes of aquatic ecosystem degradation, are often overlooked as it is impractical to test all mixtures. This study developed and evaluated the following models to predict the concentration response curve concerning the joint reproductive toxicity of mixtures of three bisphenol analogues (BPA, BPF, BPAF) on the rotifer Brachionus calyciflorus: concentration addition (CA), independent action (IA), and two deep neural network (DNN) models. One applied mixture molecular descriptors as input variables (DNN-QSAR), while the other applied the ratios of chemicals in the mixtures (DNN-Ratio). Descriptors related to molecular mass were found to be of greater importance and exhibited a proportional relationship with toxic effects. The results indicate that the range of correlation coefficients (R2) between predicted and measured values for various mixture rays by CA and IA models is 0.372 to 0.974 and - 0.970 to 0.586, respectively. The R2 values for DNN-Ratio and DNN-QSAR were 0.841 to 0.984 and 0.834 to 0.991, respectively, demonstrating that models developed by DNN significantly outperform traditional models in predicting the joint toxicity of mixtures. Furthermore, DNN-QSAR not only predicts mixture toxicity but also provides accurate toxicity predictions for BPA, BPF, and BPAF, with R2 values of 0.990, 0.616, and 0.887, respectively, while DNN-Ratio yields values of 0.920, 0.355, and - 0.495. The study also found that the joint effects of mixtures are primarily influenced by the total concentration of the mixtures, and an increase in total concentration shifts the joint effects towards addition. This study introduces a novel approach to predict joint toxicity and analyze the influencing factors of joint effects, providing a more comprehensive assessment of the ecological risk posed by mixtures.

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Air pollution and neighborhood socioeconomic status (N-SES) are associated with adverse cardiovascular health and neuropsychiatric functioning in older adults. This study examines the degree to which the joint effects of air pollution and N-SES on the cognitive decline are mediated by high cholesterol levels, high blood pressure (HBP), and depression. In the Emory Healthy Aging Study, 14,390 participants aged 50+ years from Metro Atlanta, GA, were assessed for subjective cognitive decline using the cognitive function instrument (CFI). Information on the prior diagnosis of high cholesterol, HBP, and depression was collected through the Health History Questionnaire. Participants' census tracts were assigned 3-year average concentrations of 12 air pollutants and 16 N-SES characteristics. We used the unsupervised clustering algorithm Self-Organizing Maps (SOM) to create 6 exposure clusters based on the joint distribution of air pollution and N-SES in each census tract. Linear regression analysis was used to estimate the effects of the SOM cluster indicator on CFI, adjusting for age, race/ethnicity, education, and neighborhood residential stability. The proportion of the association mediated by high cholesterol levels, HBP, and depression was calculated by comparing the total and direct effects of SOM clusters on CFI. Depression mediated up to 87 % of the association between SOM clusters and CFI. For example, participants living in the high N-SES and high air pollution cluster had CFI scores 0.05 (95 %-CI:0.01,0.09) points higher on average compared to those from the high N-SES and low air pollution cluster; after adjusting for depression, this association was attenuated to 0.01 (95 %-CI:-0.04,0.05). HBP mediated up to 8 % of the association between SOM clusters and CFI and high cholesterol up to 5 %. Air pollution and N-SES associated cognitive decline was partially mediated by depression. Only a small portion (<10 %) of the association was mediated by HBP and high cholesterol.

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BACKGROUND: Co-exposure to air pollution and neighborhood disadvantage may influence cognition decline. We tested these associations in the context of dementia risk. METHODS: We leveraged a cohort of adults ≥65 years (n = 5397) enrolled from 2011 to 2018 in the National Health and Aging Trends Study (NHATS). Particulate matter (PM) ≤ 10 µm in diameter, PM ≤ 2.5 µm in diameter, carbon monoxide, nitric oxide, and nitrogen dioxide - and neighborhood disadvantage were tested for joint associations with dementia risk. Pollutant concentrations at the 2010 census tract level were assigned using the US Environmental Protection Agency's Community Multiscale Air Quality Modeling System. Neighborhood disadvantage was defined using the tract Social Deprivation Index (SDI). Dementia was determined through self- or proxy-report or scores indicative of "probable dementia" according to NHATS screening tools. Joint effects of air pollutants and SDI were tested using quantile g-computation Cox proportional hazards models. We also stratified joint air pollution effects across SDI tertiles. Analyses adjusted for age at enrollment, sex, education, partner status, urbanicity, income, race and ethnicity, years at residence, census segregation, and census region. RESULTS: SDI score (aHR = 1.08; 95% CI 0.96, 1.22), joint air pollution (aHR = 1.03, 95% CI 0.92, 1.16) and joint SDI with air pollution (aHR = 1.04, 95% CI 0.89, 1.22) were not associated with dementia risk. After accounting for competing risk of death, joint SDI with air pollution was not associated with dementia risk (aHR = 1.06; 95% CI 0.87, 1.29). In stratified models, joint air pollution was associated with greater risk of dementia at high (aHR = 1.19; 95% CI 0.87, 1.63), but not at medium or low SDI. CONCLUSION: Air pollution was associated with greater dementia risk in disadvantaged areas after accounting for competing risks. Air pollution associations with dementia incidence may be attenuated when other risk factors are more prominent in disadvantaged neighborhoods.

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The interaction between pesticides and microplastics (MPs) can lead to changes in their mode of action and biological toxicity, creating substantial uncertainty in risk assessments. Succinate dehydrogenase inhibitor (SDHI) fungicides, a common fungicide type, are widely used. However, little is known about how penthiopyrad (PTH), a member of the SDHI fungicide group, interacts with polyethylene microplastics (PE-MPs). This study primarily investigates the individual and combined effects of virgin or aged PE-MPs and penthiopyrad on zebrafish (Danio rerio), including acute toxicity, bioaccumulation, tissue pathology, enzyme activities, gut microbiota, and gene expression. Short-term exposure revealed that PE-MPs enhance the acute toxicity of penthiopyrad. Long-term exposure demonstrated that PE-MPs, to some extent, enhance the accumulation of penthiopyrad in zebrafish, leading to increased oxidative stress injury in their intestines by the 7th day. Furthermore, exposure to penthiopyrad and/or PE-MPs did not result in histopathological damage to intestinal tissue but altered the gut flora at the phylum level. Regarding gene transcription, penthiopyrad exposure significantly modified the expression of pro-inflammatory genes in the zebrafish gut, with these effects being mitigated when VPE or APE was introduced. These findings offer a novel perspective on environmental behavior and underscore the importance of assessing the combined toxicity of PE-MPs and fungicides on organisms.

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Per- and polyfluoroalkyl substances (PFASs) are known to be linked with dyslipidemia. Between March and June 2022, we collected 575 fasting serum samples from individuals without occupational exposure in Jinan, China. Eighteen PFASs were analyzed using UHPLC-Orbitrap MS. Multiple linear regression (MLR), Bayesian kernel machine regression (BKMR), and Quantile g-computation (QGC) models were utilized to assess the effects of both individual PFAS and PFAS mixtures on serum lipid levels, including triglycerides (TG), cholesterol (CHO), high-density lipoprotein (HDL), and low-density lipoprotein (LDL). The PFAS mixture, composed of perfluoroheptanoic acid (PFHpA), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), perfluorodecanoic acid (PFDA), perfluoroundecanoic acid (PFUnDA), perfluorododecanoic acid (PFDoDA), perfluorotridecanoic acid (PFTrDA), perfluorohexane sulfonate (PFHxS), perfluoroheptane sulfonic acid (PFHpS), perfluorooctane sulfonate (PFOS), and 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA), showed a positive association with CHO and LDL levels, while no distinct trend was noted in HDL and TG levels about changes in PFAS mixtures levels in BKMR and QGC models, adjusted for gender, age, BMI, occupation, and educational level. The effects of individual PFASs on lipid levels were in general consistent across MLR, BKMR and QGC models. PFUnDA and PFTrDA demonstrated greater impacts on blood lipid levels compared to other PFAS, albeit with varied directional effects. Age-stratified analysis revealed PFAS mixture effect was more pronounced in participants aged higher than 40. No obvious trend in lipid levels with changes in PFAS mixture levels in participants with age ranged from 18 to 40, while positive association between PFAS mixture and CHO and LDL was detected in participants aged higher than 40.

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This study was to assess the individual effects of serum copper levels and environmental tobacco exposure and their joint effects on the risk of overweight and obesity among children and adolescents of 6 to 19 year olds. We analyzed cross-sectional data from 1849 children and adolescents participating in the National Health and Nutrition Examination Survey (NHANES) collected between 2011 and 2016. Environmental tobacco exposure was determined by cotinine levels. The serum copper level was divided into < median group and ≥ median groups according to the median of 109.81 µg/dL. The outcome was overweight/obese in children and adolescents. Weighted multinomial multivariate logistic regression models were used to assess the association of serum copper and cotinine levels, with the risk of overweight/obesity, and the joint effects on the risk of overweight and obesity among children and adolescents. The subgroup analyses based on age, gender, and household smoking status were conducted. Among 1849 children and adolescents, 332 children and adolescents had overweight BMI, and 450 children and adolescents had obese BMI. Higher serum copper levels were associated with the risk of obesity in children and adolescents (odds ratio (OR) 2.96, 95% confidence interval (CI) 1.39-6.31, P = 0.006). A positive association between increasing levels of cotinine levels and the risk of overweight (OR 1.83, 95% CI 1.16-2.87, P = 0.010) and obesity (OR 2.56, 95% CI 1.03-6.40, P = 0.044) in children and adolescents was observed. A remarkable association was found between higher serum copper in combination with higher cotinine levels and the risk of overweight (OR 3.23, 95% CI 1.19-8.83, P = 0.023) and obesity (OR 8.76, 95% CI 2.14-35.87, P = 0.003) in children and adolescents. The subgroup analyses revealed positive associations between high serum copper levels in combination with high cotinine levels and overweight and obesity in children and adolescents aged ≥ 12 years, of female sex, and without smoking family members. There may exist a joint effect of serum copper levels and environmental tobacco exposure on overweight/obesity among children and adolescents. These findings offer an insight that early weight control and reduction of tobacco exposure and the detection of serum copper levels may be important in reducing the risk of obesity in children.

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BACKGROUND: Studies from Finland and Taiwan have shown that walking against traffic was beneficial for reducing pedestrian crashes and fatalities. This study examined whether such beneficial effects are consistent across various circumstances. METHODS: This study aimed to investigate pedestrian fatalities in walking-against or with-traffic crashes by analysing the UK STATS19 crash data for the period between 1991 and 2020. We firstly employed Chi-square tests to examine risk factors for pedestrian injury severity. These variables were then incorporated into stepwise logistic regression models with multiple variables. We subsequently conducted joint effect analysis to investigate whether the beneficial effects of walking against traffic on injury severity vary across different situations. RESULTS: Our data contained 44,488 pedestrian crashes, of which 16,889 and 27,599 involved pedestrians walking against and with traffic, respectively. Pedestrians involved in with-traffic crashes were more likely to sustain fatalities (adjusted odds ratio [AOR] = 1.542; confidence interval [CI] = 1.139-1.927) compared with those in walking against-traffic crashes. The detrimental effect of walking with traffic on fatalities appeared to be more pronounced in darkness-unlit conditions (AOR = 1.48; CI = 1.29-1.70), during midnight hours (00:00-06:59 am) (AOR = 1.60; CI = 1.37-1.87), in rural areas (AOR = 2.20; CI = 1.92-2.51), when pedestrians were elderly (≥ 65 years old) (AOR = 2.65, CI = 2.16-3.26), and when heavy goods vehicles were crash partners (AOR = 1.51, CI = 1.28-1.78). CONCLUSIONS: Walking against traffic was beneficial in reducing pedestrian fatalities compared with walking with traffic. Furthermore, such a beneficial effect was more pronounced in darkness-unlit conditions, at midnights (00:00-06:59 am), in rural areas, when pedestrians were elderly, and when heavy goods vehicles struck pedestrians.

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OBJECTIVE: To explore the independent and combined effects of smoking and passive smoking during pregnancy on maternal depression, anxiety and depressive anxiety comorbidities. METHODS: From August 2020 to February 2022, women who underwent 42-day postpartum examination in Changfeng Women's Center and Shuangfeng Hospital of Hefei were recruited. Their depression and anxiety symptoms were assessed using EPDS Scale and GAD Scale, respectively, and smoking and passive smoking status during pregnancy were collected. Multivariate Logistic regression was used to analyze the independent and combined effects of smoking and passive smoking during pregnancy on postpartum depression, anxiety and depression and anxiety comorbidities. RESULTS: A total of 2 447 parturients were included, whose mean age was(29.23±4.20) years old.58.6% of parturients lived in urban areas.97.2% parturients had unassisted reproduction and 73.5% pregnancy intention was spontaneous. Among them, 362(14.8%) had depression, 523(21.4%) had anxiety, and 270(11.0%) had depression and anxiety comorbidities. In an independent analysis of effects, maternal smoking during pregnancy was statistically associated with postpartum depression(OR=3.86, 95%CI 2.37-6.28), anxiety(OR =2.58, 95%CI 1.60-4.17) and depressive anxiety comorbidity(OR = 3.34, 95%CI 2.00-5.71). Maternal passive smoking during pregnancy was also positively associated with the risk of postpartum depression(OR = 1.56, 95%CI 2.00-5.71), anxiety(OR=1.71, 95%CI 1.24-2.37) and depression and anxiety comorbidities(OR = 1.52, 95%CI 1.02-2.28), and the higher the frequency of exposure to passive smoking, the higher risk of depression, anxiety, and depressive and anxiety comorbidities. No interaction between smoking during pregnancy and passive smoking exposure on postpartum depression(RERI = 0.69, 95%CI-4.62-6.00; AP = 10.84, 95%CI-73.37-95.04; S= 0.58, 95%CI 0.02-15.18), anxiety(RERI=0.27, 95%CI 0.05-0.49; AP=4.02, 95%CI-0.52-8.57; S=0.78, 95%CI 0.64-0.94) and depression and anxiety comorbidities(RERI = 0.07, 95%CI-0.25-0.39; AP=1.74, 95%CI-6.03-9.52; S=0.93, 95%CI 0.68-1.27)was observed. CONCLUSION: Both smoking and passive smoking during pregnancy were positively associated with the risk of postpartum depression, anxiety and depressive anxiety comorbidity.

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Increasing studies have linked air pollution to kidney dysfunction, however, the associations between the mixture of air pollutants and kidney function and potential effect modifiers remain unclear. We aimed to investigate whether obese adults were more susceptible than normal-weight ones to the joint effects of multiple air pollutants on kidney function and further to explore effect modification by free fatty acids (FFAs). Forty obese and 49 normal-weight adults were recruited from a panel study (252 follow-up visits). Individual exposure levels of air pollutants (PM2.5, PM10, O3, NO2, SO2 and CO) were estimated. Glomerular function (cystatin C (CysC) and estimated glomerular filtration rate (eGFR)) and tubular function (neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1) were evaluated. Plasma levels of FFAs including trans fatty acids (TFAs) and essential fatty acids (EFAs) were quantified using targeted metabolomics. Bayesian kernel machine regression model was applied to estimate the associations between the mixture of air pollutants and kidney function. The results showed significant joint effects of air pollutants on kidney function indicators. In the normal-weight group, the mixture of air pollutants was significantly associated with CysC and eGFRcr-cys when the mixture was at or above its 70 percentile compared with the median, where O3 was identified as the key pollutant. In the obese group, a significantly positive association between the pollutant mixture and NGAL was observed in addition to trends in CysC and eGFRcr-cys, mainly driven by SO2. Interaction analysis suggested that the associations of air pollutants with kidney function were augmented by TFAs in both groups and weakened by EFAs in the normal-weight group. This study highlighted the renal adverse effects of air pollutants and modification of FFAs, which has implications for target prevention for kidney dysfunction associated with air pollution, especially among vulnerable populations.

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Per- and polyfluoroalkyl substances (PFAS) are persistent, ubiquitous pollutants, and the current epidemiological evidence regarding the impact of in utero exposure to PFAS on anogenital distance (AGD) is limited and inconclusive. The primary aim of this study was to investigate the potential associations between maternal exposure to PFAS during pregnancy and AGD in newborns. A total of 2273 mother-child pairs were recruited for this study, and both PFAS levels and AGD were measured. Multiple linear regression models were utilized to explore the relationships between individual PFAS and AGD. Additionally, quantile-based g-computation (QGC) was employed to assess the joint effects of mixtures of PFAS on AGD. Our findings showed that maternal exposure to PFOS (ß = 0.518, 95% CI: 0.093, 0.942), PFNA (ß = 0.487, 95% CI: 0.037, 0.937), PFDA (ß = 0.443, 95% CI: 0.048, 0.838), PFUA (ß = 0.434, 95% CI: 0.031, 0.838), and PFBS (ß = 0.444, 95% CI: 0.124, 0.763) during early pregnancy had a significant positive association with AGD in boys. Similarly, in girls, maternal exposure to PFOS (ß = 0.423, 95% CI: 0.006, 0.841), PFNA (ß = 0.641, 95% CI: 0.207, 1.074), PFDA (ß = 0.670, 95% CI: 0.306, 1.033), PFUA (ß = 0.895, 95% CI: 0.509, 1.281), and PFBS (ß = 0.474, 95% CI: 0.178, 0.770) had a positive association with AGD, while PFOA (ß = -1.254, 95% CI: -1.786, -0.723) had a negative association. QGC models further confirmed that PFAS mixtures were positively associated with AGD. Moreover, PFBS was the primary contributor to the joint effects of PFAS mixtures on AGD. In summary, our study has provided further corroboration for the possibility that PFAS exposure can have an impact on AGD in both boys and girls. The use of AGD as a promising biomarker for endocrine disruption highlights the significance of our findings, which may have valuable clinical implications for reproductive diseases.

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Introduction: In recent years, air pollution caused by co-occurring PM2.5 and O3, named combined air pollution (CAP), has been observed in Beijing, China, although the health effects of CAP on population mortality are unclear. Methods: We employed Poisson generalized additive models (GAMs) to evaluate the individual and joint effects of PM2.5 and O3 on mortality (nonaccidental, respiratory, and cardiovascular mortality) in Beijing, China, during the whole period (2014-2016) and the CAP period. Adverse health effects were assessed for percentage increases (%) in the three mortality categories with each 10-µg/m3 increase in PM2.5 and O3. The cumulative risk index (CRI) was adopted as a novel approach to quantify the joint effects. Results: The results suggested that both PM2.5 and O3 exhibited the greatest individual effects on the three mortality categories with cumulative lag day 01. Increases in the nonaccidental, cardiovascular, and respiratory mortality categories were 0.32%, 0.36%, and 0.43% for PM2.5 (lag day 01) and 0.22%, 0.37%, and 0.25% for O3 (lag day 01), respectively. There were remarkably synergistic interactions between PM2.5 and O3 on the three mortality categories. The study showed that the combined effects of PM2.5 and O3 on nonaccidental, cardiovascular, and respiratory mortality were 0.34%, 0.43%, and 0.46%, respectively, during the whole period and 0.58%, 0.79%, and 0.75%, respectively, during the CAP period. Our findings suggest that combined exposure to PM2.5 and O3, particularly during CAP periods, could further exacerbate their single-pollutant health risks. Conclusion: These findings provide essential scientific evidence for the possible creation and implementation of environmental protection strategies by policymakers.

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BACKGROUND: Ambient particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5) consists of various toxic constituents. However, the health effect of PM2.5 may differ depending on its constituents, but the joint effect of PM2.5 constituents remains incompletely understood. OBJECTIVE: Our goal was to evaluate the joint effect of long-term PM2.5 constituent exposures on dyslipidemia and identify the most hazardous chemical constituent. METHODS: This study included 67,015 participants from the China Multi-Ethnic Cohort study. The average yearly levels of PM2.5 constituents for all individuals at their residences were assessed through satellite remote sensing and chemical transport modeling. Dyslipidemia was defined as one or more following abnormal blood lipid concentrations: total cholesterol (TC) ≥ 6.22 mmol/L, triglycerides (TG) ≥ 2.26 mmol/L, high-density lipoprotein cholesterol (HDL-C) < 1.04 mmol/L, and low-density lipoprotein cholesterol (LDL-C) ≥ 4.14 mmol/L. The logistic regression model was utilized to examine the single effect of PM2.5 constituents on dyslipidemia, while the weighted quantile sum regression model for the joint effect. RESULTS: The odds ratio with a 95 % confidence interval for dyslipidemia positively related to per-SD increase in the three-year average was 1.29 (1.20-1.38) for PM2.5 mass, 1.25 (1.17-1.34) for black carbon, 1.24 (1.16-1.33) for ammonium, 1.33 (1.24-1.43) for nitrate, 1.34 (1.25-1.44) for organic matter, 1.15 (1.08-1.23) for sulfate, 1.30 (1.22-1.38) for soil particles, and 1.12 (1.05-1.92) for sea salt. Stronger associations were observed in individuals < 65 years of age, males, and those with low physical activity. Joint exposure to PM2.5 constituents was positively related to dyslipidemia (OR: 1.09, 95 %CI: 1.05-1.14). Nitrate was identified as the constituent with the largest weight (weighted at 0.387). CONCLUSIONS: Long-term exposure to PM2.5 constituents poses a significant risk to dyslipidemia and nitrate might be the most responsible for the risk. These findings indicate that reducing PM2.5 constituent exposures, especially nitrate, could be beneficial to alleviate the burden of disease attributed to PM2.5-related dyslipidemia.

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A higher dietary diversity score (DDS) and a lower energy-adjusted dietary inflammatory index (E-DII) may be associated with lower risks of type 2 diabetes (T2D) and mortality. This cohort study aimed to investigate the associations of DDS and E-DII with all-cause mortality, incidence of T2D, and mortality of T2D, as well as the joint effects of these two dietary factors. A total of 181,360 participants without all types of diabetes at baseline from the UK Biobank and 42,139 participants from the US NHANES were included. Cox proportional hazards models were used to assess the associations of DDS and E-DII with outcomes. In the UK Biobank data, 8338 deaths, 3416 incident T2D cases, and 353 T2D deaths occurred during a median follow-up of 12.5 years. In the US NHANES data, 6803 all-cause deaths and 248 T2D-specific deaths were recorded during a median follow-up of 9.6 years. We observed that higher DDS and lower E-DII were significantly associated with lower risks of total mortality and incident T2D. Compared with low DDS, the hazard ratios (HRs) and 95% confidence intervals (CIs) of high DDS were 0.69 (0.64, 0.74) for all-cause mortality, 0.79 (0.70, 0.88) for incident T2D in the UK Biobank, and 0.69 (0.61, 0.78) for all-cause mortality in the US NHANES. Compared with participants in tertile 3 of E-DII, those in tertile 1 had a lower risk of overall death [HR 0.86 (95% CI: 0.81, 0.91) in UK Biobank; 0.83 (0.77, 0.88) in US NHANES] and incident T2D [0.86 (0.79, 0.94)] in UK Biobank. No evidence was observed of the interactive effects of DDS and E-DII on either all-cause mortality or the incidence and mortality of T2D. There was no significant association found between any exposure and T2D mortality in this study. In conclusion, our results revealed that higher DDS and lower E-DII were associated with both total mortality and incident T2D in UK and US adults.

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Some plant species tolerate and accumulate high levels of metals or metalloids in their tissues. The elemental defence hypothesis posits that metal(loid) hyperaccumulation by these plants can serve as protection against antagonists. Numerous studies support this hypothesis. In addition, as other plant species, hyperaccumulators synthesise specialised metabolites that can act as organic defences. In principle, the composition and concentration of plant-specialised metabolites vary pronouncedly not only among species, but also within species and within individuals. This variation is called chemodiversity. Surprisingly, the role of chemodiversity has received little attention in elemental defence. Thus, we advocate that the concept of the elemental defence hypothesis should be extended and linked to the multifunctionality of plant chemodiversity to better understand the eco-evolutionary dynamics and maintenance of metal(loid) hyperaccumulation. Comprehensive literature studies revealed that both metal(loid)s and specialised metabolites acting as defences are highly diverse in some hyperaccumulators and the biosynthetic pathways of these two types of defences are partly intertwined. Several edaphic-, population-, temporal- and spatial-related factors were found to influence metal(loid) diversity, which should be considered in the elemental defence hypothesis. We thus present a novel synthesis and outlook to extend the elemental defence hypothesis in the light of chemodiversity.

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Epidemiological studies have reported potential effects of individual paraben or bisphenol exposure on lung function, but few studies have estimated their joint effects. We conducted a cross sectional survey to investigate the associations of parabens and bisphenols exposure with lung function in 205 children aged 5-12 years from Shanghai, China. Urinary concentrations of six parabens [methyl-, ethyl-, propyl-, butyl-, benzyl-, and heptyl-paraben (MeP, EtP, PrP, BuP, BzP, and HeP)] and seven bisphenols [bisphenol A (BPA), bisphenol AF (BPAF), bisphenol AP (BPAP), bisphenol B (BPB), bisphenol P (BPP), bisphenol S (BPS), and bisphenol Z (BPZ)] were assessed by the high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Lung function, including forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC), FEV1/FVC, peak expiratory flow (PEF), and forced expiratory flow between 25% and 75% of forced vital capacity (FEF25-75%), was further measured. Linear regression, bayesian kernel machine regression (BKMR), and weighted quantile sum regression (WQS) evaluated the individual and joint relationships of the parabens and bisphenols with the lung function parameters. Further, the analysis was stratified by child sex. Parabens (MeP, EtP, PrP, and BuP) and bisphenols (BPA, BPAP, BPB, and BPS) with detection rates >75% were included for analyses. In linear regressions, parabens (MeP, PrP, and BuP) were generally negatively associated with FEV1, FVC, PEF, and FEF25-75%, but no associations for bisphenols were found. The association of parabens with lung function was more pronounced in girls. The aforementioned negative associations between parabens and lung function were confirmed by both the BKMR and WQS, with MeP being considered most heavily weighing chemical. Our findings suggested that exposure to parabens, either individuals or as a mixture, were associated with decreased lung function in children aged 5-12 years, and these associations were stronger among girls. Considering the cross-sectional study design, large longitudinal studies are warranted to confirm our findings.

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