Widely used personal care product (PCP) chemicals can disrupt the function of thyroid hormones. Pregnancy-induced vulnerability heightens the risk of PCPs on maternal thyroid health, but their individual, joint, and longitudinal impacts have been underexplored. Moreover, the risk assessment regarding maternal thyroid-impairing effects of PCPs has been lacking from epidemiological and mechanistic insights. In this study, we conducted an integrated risk assessment of PCPs on maternal thyroid functions, synthesizing evidence from 47 epidemiological, 18 in vivo, and 19 in vitro evidences from four major databases. Besides, a separate cohort analysis was prospectively performed among 803 pregnant women to explore associations between real-world PCP exposure and thyroid function. Serum samples in the second trimester (T2) were analyzed for PCP profiles by liquid chromatography-tandem mass spectrometry (LC-MS/MS). Anti-thyroid peroxidase antibodies (ATPO), thyroid stimulating hormone (TSH), and free thyroxine (FT4) during T2 and the third trimester (T3) were measured using immunoassays. The targeted risk assessment of environmental chemicals (TRAEC) strategy yielded a middle-level risk score of 5.01 for PCPs, with category-specific scores of 5.47 for phthalates, 4.85 for per- and polyfluoroalkyl substances (PFASs), and 4.12 for bisphenols. The cohort results revealed significant associations between bisphenol S (BPS), monobutyl phthalate (MEHP), dimethyl phthalate (DMP), di-n-pentyl phthalate (DnPP), dicyclohexyl phthalate (DCHP) , Sodium perfluoro-1-octanesulfonate (L-PFOS), and perfluoro-n-undecanoic acid (PFUdA) with thyroid function markers during T2 and T3. Mixed-exposure models showed negative associations of PCPs with TSH during T2, with PFUdA, DMP, DCHP, and BPS identified as key contributors. These findings highlighted the potential risk of PCP exposure as determined by the TRAEC strategy. In conclusion, PCP exposure may contribute to maternal thyroid dysfunction with trimester-specific effects. Our findings highlighted the need to mitigate PCP-related exposures during pregnancy and improve maternal thyroid health.

Background:Prenatal metal mixtures exposure was associated with child growth. However, long-term impact of maternal metal mixture exposure on offspring's overweight or obesity (OWO) in childhood and the potential role of metabolites remain poorly understood. Methods:Based on a prospective cohort study, ten metals were measured and metabolomics profiling was conducted in maternal serum during pregnancy. Children's anthropometric parameters were measured at school age and OWO was defined according to the international World Health Organization (WHO) reference data. A combination of multiple regression models, variable selection models and exposome models were conducted to explore the effects of prenatal metal mixture exposure on child OWO and BMI z-score. A meet-in-the-middle (MITM) approach was employed to examine metabolites' potential role in mediating this association. Results:Maternal metals exposure such as Cu and V was found to be positively associated with OWO risk based on single-metal models, with ORs being 24.171 (95% CI: 2.351-403.256) and 2.534 (95% CI: 1.273-5.623), respectively. Similarly, prenatal exposure to V was also positively associated with BMI z-scores in school-aged children (β: 0.293, 95% CI: 0.015-0.572). Marginal association was found between Cu exposure and BMI z-scores (β: 0.758, 95% CI: -0.001-1.517). Metabolites such as glycerophosphocholine and glycine played potential intermediate roles in the association between maternal Cu levels and OWO risk. Conclusion:Prenatal Cu and V exposure may have an adverse effect on school-aged childhood's OWO risk, and metabolites may play an important intermediate role. By further examining metabolite profiles, our findings offer insight into potential metabolic pathways through which prenatal metal exposure may influence childhood obesity risk, thereby extending existing epidemiological evidence with a mechanistic perspective. Multi-center population studies and in vivo studies in future are needed to validate the results.

Pregnancy-triggered shifts in maternal serum elements and gut microbiota may disrupt metabolic balance; yet, their interplay in lipid regulation remains elusive. This study aimed to decode how metal elements and gut microbiota across mid-to-late pregnancy contribute to dyslipidemia and enable early risk prediction. In 689 pregnant women, we measured serum metals and profiled gut microbiota using 16S rRNA sequencing, applying interpretable machine learning and causal inference to unravel element-microbiota-dyslipidemia interactions. Higher serum levels of copper and zinc were linked to adverse lipid profiles, while cobalt showed inverse associations. Metals were also associated with broad alterations in microbial composition and diversity, including shifts in alpha diversity and over 30 significant taxa-level associations, primarily within Firmicutes and Bacteroidota. Microbiota features across pregnancy exhibited extensive associations with lipid metabolism, with reduced alpha diversity linked to elevated levels of triglycerides. Finally, a CatBoost model integrating midpregnancy metals and microbiota robustly predicted late gestational dyslipidemia (AUC = 0.91; AP = 0.94), with SHAP analysis revealing risk-defining microbial thresholds and taxa specific nonlinear effects. These findings demonstrate that maternal elements and microbiota jointly contribute to the development of dyslipidemia, supporting potential strategies for the early identification and prevention of gestational dyslipidemia.

Male fertility has declined rapidly in recent decades, a trend coinciding with increased environmental exposure pressures. Among these, perfluorinated and polyfluorinated alkyl substances (PFAS) have been reported to exert male reproductive toxicity, yet comparative risks across individual PFAS remain unclear. In this study, we employed an innovative systematic review strategy, the Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy, integrating all available evidence from 25 epidemiological studies, 75 in vivo, and 43 in vitro experiments, alongside independent experiments, to assess the effects of multiple PFAS on semen quality and sex hormone levels. The integrated evidence indicated that PFAS exposure posed a moderate risk level to male reproductive health with a comprehensive risk score of 6.47. Among individual PFAS, exposure to perfluorooctanesulfonic acid (PFOS, risk score: 7.43) and perfluorononanoic acid (PFNA, risk score: 6.38) presented the highest risk of sperm abnormalities, followed by perfluorodecanoic acid (PFDoA, risk score: 6.29), perfluorooctanoic acid (PFOA, risk score: 5.83), and perfluorohexyl sulfonic acid (risk score: 4.87), all of which are at moderate risk levels. And the risk of these PFAS compounds causing reproductive hormone abnormalities was at a low to moderate level, with the risk scores ranging from 3.79 (PFOA) to 6.74 (PFDoA). Additionally, PFAS exposure showed a relatively high risk of adversely affecting sperm progressive motility (risk score range: 5.23-5.62), particularly for PFOS (risk score: 5.57) and PFNA (risk score: 5.62). Risk for other sperm parameters was relatively lower (risk score range: 4.01-5.49). Notably, independent in vivo experiments confirmed that PFNA exposure significantly impaired sperm routine parameters and sperm dynamics across multiple mouse strains (including C57BL/6J, CC002, CC037, and CC057 strains). Our study identified PFOS and PFNA as particularly detrimental to male reproductive health across multiple dimensions, underscoring the urgent need for measures to reduce PFAS exposure and mitigate risks to male fertility.

Maternal exposure to exogenous microparticles (EMP) during pregnancy is associated with multiple adverse birth outcomes, yet evidence for its accumulation in early placental tissues remains limited. This study investigates the accumulation of EMP in early placental villi and decidua, exploring its association with miscarriage. A total of 40 pregnant women undergoing abortion (20 spontaneous and 20 induced) were enrolled. Placental villi and decidual tissues were collected under strict quality control, subjected to digestion and filtration, and analyzed using Raman spectroscopy. In addition, combined spectroscopic and electron microscopy techniques were employed for in situ detection of particles within the placental villi. Among 174 identified EMP, 68.4% were found in placental villi, primarily consisting of carbon-rich and iron-rich particles, with three microplastics also detected. Notably, EMP in villi exhibited larger mean size (11.37 ± 9.39 μm) and greater abundance (19.3 ± 19.4 items/g) compared to decidua. Additionally, in situ images of EMP in placental villi and their chemical composition were revealed. Despite no significant differences in EMP accumulation characteristics between the two groups, placental EMP abundance was significantly correlated with maternal platelet count and serum β‑hCG levels (P < 0.05). This study demonstrates that EMP from ambient can translocate to placental villi and decidua, thereby directly exposing the placenta and fetus. Given the established associations between air pollution and adverse birth outcomes, the effects of such exposures on placental function and fetal development remain to be fully elucidated.

The type VI secretion system (T6SS) is a specific protein secretion apparatus that contributes to bacterial virulence. Enterohemorrhagic Escherichia coli O157:H7 (EHEC) harbors multiple prophages and can cause severe human diseases worldwide. Here, we compared the EHEC T6SS main gene cluster with its ancestral strain E. coli O55:H7 (aEPEC) and predicted 26 mutation loci in protein-coding regions. Sequence analysis of these mutation loci indicated a degenerative trend in T6SS function in EHEC. Notably, a 28-bp tandem repeat insertion in the T6SS core gene tssM significantly compromised T6SS secretion activity. Inactivation of the T6SS significantly enhanced EHEC cytotoxicity and accelerated epithelial cell death. Mechanistically, inactivation of T6SS promotes EHEC Stx2-converting prophage (Φstx2) expression, and deletion of Φstx2 weakens the T6SS-deficient strain's cytotoxicity. Analysis of EHEC evolutionary path revealed that tssM mutation may occur after Φstx2 integration, and this mutation is widely distributed in E. coli bearing Φstx2 (E. coliΦstx2), suggesting T6SS degeneration may be closely associated with Φstx2 integration in E. coliΦstx2. Crucially, degenerative T6SS could render Φstx2 more sensitive to activation, and in turn activate EHEC major virulence factors such as Shiga toxin and type III secretion system. Taken together, our findings suggest that the ancestral aEPEC strain acquired Φstx2 and underwent T6SS degeneration, ultimately evolving into a highly cytotoxic EHEC lineage.

Trace elements have been recognized as the modifiers of the gut microbiota. However, population-based evidence about their effects on maternal gut microbiota dynamics, as well as the intergenerational impacts on neonatal gut microbiota, has been lacking. We examined the longitudinal microbiota data from mother-infant dyads and demonstrated that maternal trace element exposure played a pivotal role in shaping the composition and similarity of the mother-infant gut microbiota. Specifically, serum levels of cobalt (Co), molybdenum (Mo), and rubidium (Rb) were identified to cause further fluctuation in the shift of the maternal gut microbiota. Antibiotic usage shortly before or on the delivery day, as well as maternal zinc (Zn) exposure, affected the gut microbiota similarity within mother-infant dyads. Rb demonstrated an intergenerational effect on meconium Bifidobacterium abundance by altering its abundance in the maternal gut. Notably, this effect was strengthened in the vaginal delivery group without antibiotic usage, while it was attenuated in the c-section delivery group. Our results suggest that maternal trace element exposure has a persistent influence on perinatal gut microbiota, which offers novel insights into promoting mother and infant health.

Previous studies have suggested that pesticide exposure and gut microbiome alterations are associated with gestational diabetes mellitus (GDM) risk. Understanding the complex interactive effect of these factors on GDM is essential. In a cohort of 852 pregnant women, we assessed pesticide levels in serum and analyzed the gut microbiota using 16S rRNA and shotgun metagenomic sequencing. We explored the interactions between pesticides and gut microbiota, assessed their roles in GDM development, and proposed a predictive model based on identified biomarkers. We identified an environmental risk score (ERS), denoting the pesticide mixture level significantly associated with GDM, with the gut microbiota, particularly involving the Dorea branch, playing a crucial mediating role. In addition, we found an interactive effect of pesticide exposure and gut microbiota on GDM risk. Notably, low Prevotella enrichment combined with high ERS arisen from pesticide levels led to a 10.36-fold increased GDM risk. The identified pesticide and gut microbial biomarkers achieved high predictive accuracy for GDM (AUC: 0.833, 95% CI: 0.748-0.918). Collectively, maternal pesticide exposure may induce disrupted microbiome-dependent glycemic alteration, necessitating future assessment of clinical implications. Potential GDM markers can serve as targets for therapeutic intervention caused by pesticides, leading to prevention.

Background: Bisphenols (BPs) are present in medical instruments, plastic containers, and personal care products (PCPs). Bisphenol A has been replaced by its alternatives, bisphenol S, F, AF, and B. Due to the awareness of their toxicity, mixed exposure to these alternatives at the regional level has been given less attention; there is a need to study this area of research. This meta-analysis examined the exposure of urinary bisphenol A and its metabolites to blood Hypothalamic–Pituitary–Thyroid axis hormones (HPT axis hormones) in pregnant women and adult males and females. We searched Embase, PubMed, Web of Science, Cochrane Library, and CINAHL until 8 January 2025, yielding 4588 articles using the PECO framework. Quality assessment was done using AHRQ: Agency for Healthcare Research and Quality for cross-sectional and NOS: Newcastle Ottawa Scale for cohort studies, with combined exposure evaluated using random and fixed-effect models. The I2 test assessed heterogeneity. We included eighteen studies for the final analysis. Fixed-effect model estimates revealed that BPA is negatively associated with thyroid-stimulating hormone (TSH) in female and male adults (β = −0.02; 95% CI = −0.04 to −0.01); (β = −0.08; 95% CI = −0.14 to −0.02). In Females, BPA was positively associated with free thyroxine, FT4 (β = 0.001, 95% CI, 0.001 to 0.001). In the male group, BPA was negatively associated with FT4 (β = −0.001, 95% CI, −0.001 to −0.001). As per pregnant women, there was no association found between exposure to bisphenols and total Thyroxine (TT4), FT4, and TSH in both trimesters (β = 0.010, 95% CI = −0.030 to 0.050); (β = 0.001, 95% CI = −0.010 to 0.010); (β = −0.001, 95% CI = −0.010 to 0.001), respectively, for early pregnancy. Bisphenols can significantly influence HPT axis hormones in adult males, females, and pregnant women. Gender-based studies were observed, concluding that adult females are more affected by bisphenol exposures than adult males. The subgroup analysis based on the regions did not reveal any associations.

Pesticides play an essential role in modern agricultural systems by enhancing crop yields and controlling pest-related losses and are applied extensively across the globe. However, their pervasive use has led to widespread environmental contamination, including accumulation in household and environmental dust, a significant yet understudied pathway of human exposure. Despite growing evidence that dust ingestion serves as a critical route for pesticide uptake, the associated health hazards remain poorly quantified and understood. We developed a Reverse Dosimetry Evaluation System (RDES) to estimate internal exposure levels from urine (EDIu) and dust (EDId) samples and analyzed their association across various populations and seasons. Our study focused on eight key pesticides with high exposure risks through dust ingestion and identified risks to 12 human body systems. Notably, cypermethrin and deltamethrin were related to increased risks of asthma, lung injury, pulmonary fibrosis, and lung tumors, particularly affecting the respiratory system. A cross-regional analysis involving 13 countries using RDES and databases such as Tox21 and CTD, revealed that exposure-based health risks were highest in Korea, followed by Costa Rica/South Africa, China, Belgium, Poland, and the USA. This study introduced a standardized framework for Exposure Source identification-Internal Exposure assessment-Health Risk prediction (ESIEHR), for assessing emerging pollutants and highlights the necessity for targeted interventions to reduce health impacts.

Micro- and nano-plastics (MNPs) are emerging pollutants, with growing evidence suggesting the presence of MNPs in human tissues. However, there is a notable lack of quantitative data regarding the maternal-embryonic transfer of MNPs. In this study, rats were utilized as model animals and were orally exposed to europium-labeled nanoplastics (Eu-NPs, 0.2 μm) and microplastics (Eu-MPs, 2 μm) over 18 days, from gestation day 0.5 to day 18.5. High-angle annular dark-field scanning transmission electron microscopy and inductively coupled plasma mass spectrometry were employed to qualitatively and quantitatively track the maternal-fetal transfer of MNPs. The results indicate that the transfer of MNPs from the placenta to the fetus exhibits size-dependent. Specifically, the transfer rate from the placenta to fetus reached 0.48 %, significantly higher than that of Eu-MPs. Notably, MNPs underwent deformation and fragmentation during in vivo transfer. The study also demonstrated that MNPs primarily accumulated in the rat decidua, where they compressed capillaries, potentially impairing fetal growth. These findings provide new insights into the maternal-fetal transfer of MNPs and offer a novel perspective for further investigating the impact of MNPs on maternal and fetal health.

As a mitochondrial complex I inhibitor, pyridaben has been found to have the adverse effects on spermatogenesis, embryonic development and neurons. However, the effects of pyridaben exposure on offspring neurodevelopment are still insufficient. In this study, the risk of pyridaben exposure on the neurodevelopment of offspring was assessed by one novel strategy called Targeted Risk Assessment of Environmental Chemicals (TRAEC), which give a comprehensive assessment based on four dimensions (the reliability, correlation, outcome fitness and integrity) of published and researchers' own evidences. Six studies (one epidemiological study, two in vivo studies and three in vitro studies) and our supplementary evidences were finally enrolled for a final scoring system. After the evidence scoring, a composite risk score of 5.64 was gotten, indicating a medium-level risk of pyridaben on the neurodevelopmental in offspring. In our study, a supplement about the neurodevelopmental toxicity of pyridaben was conducted by using constructed NE-4C stem cells models. The results showed that pyridaben inhibited the viability and proliferation capacity of neural stem cells with an IC50 value of 0.58 mu M. After treatment with pyridaben for 24 h, the cell cycle of NE-4C cells was significantly increased in the S phase but decreased in the G2 phase, and its apoptosis had a significant increase in the total percentage of early apoptotic cells. Moreover, we found that pyridaben could change different neurons and glial cell markers such as Dnmt3b, Kmt1a and Kdm6a. Taken together, our study gives a comprehensive evaluation of the neurodevelopmental toxicity of pyridaben by using TRAEC strategy and highlights the necessity of enhancing the risk management measures for pyridaben.

Gut microbiota regulates host hematopoiesis, with notable alterations observed in individuals with gestational anemia (GA). Pregnancy-induced susceptibility to environmental stressors, including widespread pesticide residuals, may disrupt gut microbiota, further contributing to the development of GA. This study sought to investigate population-level associations between pesticide exposure and GA, with a focus on the mediating role of gut microbiota. Pregnant women were prospectively recruited with blood and stool samples collected in the second trimester. Red blood cell (RBC) count and hemoglobin (Hb) were assessed in the second and third trimesters. GA was diagnosed in 22.7 % of participants during the second trimester and 29.8 % during the third trimester. Robust associations were found between serum pesticides, such as atrazine and clomazone, and an increased risk of GA and reduced Hb and RBC count, both at a single time point and longitudinally. Pesticide exposure was linked to altered microbial Shannon index, with 24 significant associations identified between pesticides and individual taxa, nearly half of which involved Roseburia. Furthermore, both Shannon index and the Firmicutes/Bacteroidetes (F/B) ratio were negatively associated with RBC count. A total of 20 taxa showed associations with GA and hematological parameters. Finally, mediation analysis demonstrated that Shannon index and Roseburia mediated the relationships of pesticide exposure with RBC count and GA, respectively. These findings not only highlight the anemia-inducing effects of pesticides, but also inform microbiota-based interventions for managing GA and maternal health.

The environment dominates over host genetics in shaping the gut microbiome, which plays a pivotal role in modulating human health. Experimental evidence supports the notion that exposure to pesticides could perturb the gut microbiome, and the toxicant-induced dysbiosis may affect host homeostasis. However, the field of human studies, especially in early life, is still in its infancy. We aimed to evaluate the effects of landscape pesticide exposure on the maternal gut microbiome. Here, we assessed the blood levels of a broad array of pesticides in 405 pregnant women. Gut microbial compositions and functional profiles were assessed by using both 16S rRNA gene amplicon sequencing and shotgun metagenomic sequencing. Microbial alpha diversity indices were regressed on host and environmental factors using linear models. Differences in overall microbial compositions were evaluated by using univariable permutational multivariate analyses of variance (PERMANOVA) with Bray-Curtis dissimilarities. All pesticides, as well as other host and environmental factors, were correlated to the gut microbiome at the phylum, genus, species, and pathway levels employing the multivariable regression models adjusted for the potential covariates, respectively. The joint effects of the mixture of pesticide exposure on the gut microbiome were investigated using quantile g-computation. Microbial ecological networks were constructed via Spearman correlations to explore species co-occurrence patterns related to pesticide exposure. Significant associations were observed between exposure to various pesticides individually or as a mixture and maternal gut microbiome features. Specific taxa and pathways were enriched or depleted in response to varying pesticide concentrations, indicating the potential exposure-response relationships. Notably, mirex exposure showed a positive correlation with both the relative abundance of Blautia_wexlerae and the sucrose biosynthesis II pathway. Microbial co-occurrence network analyses revealed marked shifts in species interactions associated with increasing levels of pesticide exposure. Mediation analyses further identified a greater number of microbial taxa, particularly Blautia_wexlerae, as significant mediators linking pesticide exposure to alterations in microbial functional pathways. Our large-scale amplicon and metagenomic analyses unraveled the extensive impacts of landscape-level pesticides on the maternal gut microbiome. Further observational and experimental research is warranted to validate our findings as well as to elucidate whether and how these microbial changes affect maternal and offspring health.

Early risk detection and management are essential for cognitive preservation. While particulate matter with a diameter smaller than 2.5 mu m (PM2.5) is considered harmful to cognition, the effect of smaller, more penetrative particulate matter with a diameter smaller than 1 mu m (PM1) requires further evidence and explicit safety thresholds. In this study, we explored the effects of long-term PM1 exposure on early cognitive impairment and longitudinal cognitive changes in middle-aged and older populations. This study assessed data from two large-scale longitudinal surveys: the China Health and Retirement Longitudinal Study (CHARLS) and UK Biobank (UKB). Cross-sectional, longitudinal, and trajectory analyses were conducted to investigate the association between long-term PM1 exposure and cognition. Additionally, the exposure-response curves were fitted to determine the customized thresholds. The findings indicated that sustained PM1 exposure may lead to mild cognitive impairment, particularly at concentrations exceeding 30 and 5.6 mu g.m-3 in CHARLS and UKB participants, respectively. Furthermore, we found that long-term PM1 exposure can contribute to rapid cognitive decline at concentrations exceeding 23 and 5.5 mu g.m-3 in CHARLS and UKB participants, respectively. In conclusion, reducing PM1 exposure can improve the cognitive health of middle-aged and older adults. (c) 2024 THE AUTHORS. Published by Elsevier LTD on behalf of Chinese Academy of Engineering and Higher Education Press Limited Company. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Although emerging evidence on the association between per- and polyfluoroalkyl substances (PFASs) and neurodevelopment have been investigated, there is no consensus on the effect of maternal PFASs on neurodevelopment in offspring. Here, we assessed the risk of maternal PFASs exposure on the neurodevelopment of offspring using a novel Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy based on multiple evidence. The evidence from five online databases were analyzed the effect of PFASs on neurodevelopment. The potential neurodevelopment risk of PFASs was evaluated by the TRAEC strategy, which was conducted on a comprehensive scoring system with reliability, correlation, outcome fitness and integrity. The studies from five databases and additional researchers' experiments were included the present study to proceed following risk assessment. Based on the framework with TRAEC strategy, the comprehensive evaluation of health risks was classified as low (absolute value 0-4), medium (absolute value 4-8), high (absolute value 8-10). In the present study, the effect of PFASs exposure on neurodevelopment was a medium-risk level with 5.61 overall riskscore. The population-attributable risk (PAR) was 8.26 % for maternal PFASs exposure. The study identified a low-risk effect of prenatal PFASs exposure on ASD and behavioral disabilities. The chain length, type of PFASs and neurodevelopmental trajectories contributed to the risk of maternal PFASs on the neurodevelopment of offspring. Consistent with results of four criteria-based tools (ToxRTool, SciRAP, OHAT and IRIS), health risk assessment based on the TRAEC strategy demonstrated robustness and reliability in the present study. These results illustrated a medium-risk effect of maternal PFASs exposure on neurodevelopmental disorders of offspring. In addition, the TRAEC strategy provided a scientific and structured method for effect evaluation between prenatal PFASs and neurodevelopmental disorders, promoting the consistency and validation in risk assessment.

Micro/nanoplastics (MNPs), as emerging pollutants, have been detected in both the maternal and fetal sides of the placenta in pregnant women, and their reproductive toxicity has been demonstrated in in vivo and in vitro experimental models. The Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy has been innovatively devised to facilitate valid risk assessment, encompassing a comprehensive evaluation of reliability, correlation, outcome fitness, and integrity across four dimensions based on the included published evidence and our own findings. This study serves as an application case of TRAEC, with 40 items of research evidence on the toxicity of MNPs to the placenta, which were rigorously screened and incorporated into the final scoring system. The final score for this TRAEC case study is 5.63, suggesting a moderate-to-low risk of reproductive toxicity associated with MNPs in the placenta, which may potentially increase with decreasing particle size. It is essential to emphasize that the findings also report original data from assays indicating that exposure to high-dose groups (100 μg/mL, 200 μg/mL) of 50 nm and 200 nm polystyrene nanoplastics (PS-NPs) induces HTR8/SVneo cell cycle arrest and cell apoptosis, which lead to reproductive toxicity in the placenta by disrupting mitochondrial function. Overall, this study employed the TRAEC strategy to provide comprehensive insight into the potential reproductive health effects of ubiquitous MNPs.

Obtaining clean energy is of prime importance for planetary health and sustainable development. We aimed to assess the association between residential energy transition and the risk of chronic respiratory diseases. Using data from the Global Health Observatory and Global Burden of Diseases, Injuries, and Risk Factors Study, we delineated the spatial distribution and temporal trends of the population using clean fuels for cooking at a global scale. In the China Health and Retirement Longitudinal Study, we performed rigorous and well-structured multistage analyses incorporating both cross-sectional and prospective data analyses to examine the associations between solid fuel use, residential energy transition, duration of solid fuel use, and the risk of chronic respiratory diseases. Despite great progress, huge disparities in access to clean energy persist globally. Residential energy transition was associated with a lower risk of chronic respiratory diseases. In the period of 2011–2013, compared with persistent solid fuel users, both participants who switched from solid to clean fuels (adjusted risk ratio [RR] 0.78, 95% confidence interval [CI] 0.62–0.98) and persistent clean fuel users (adjusted RR 0.71, 95% CI 0.57–0.89) had significantly lower risk of chronic respiratory diseases (p < 0.001 for trend). Consistent associations were observed in the period of 2011–2015 and 2011–2018. Household energy transition from solid to clean fuels could reduce the risk of chronic respiratory diseases. This is a valuable lesson for policy-makers and the general public to accelerate energy switching to alleviate the burden of chronic respiratory diseases and achieve health benefits, particularly in low- and middle-income countries.