[Background]Studies have shown that benzo(a)pyrene(BaP)exhibits neurotoxicity and can induce cognitive dysfunction.Olfactory dysfunction is an early marker of mild cognitive impairment;however,the mechanism by which BaP exposure causes this impairment is still unclear. [Objective]To investigate the effects of BaP exposure on olfactory function in mice. [Methods]Thirty 5-month-old male C57BL/6 mice were randomly assigned to five groups(n=6 per group):blank control,solvent control(olive oil),and low,medium and high doses(0.72,1.44,and 2.89 mg·kg-1,respectively).Following one week of acclimatization,BaP was administered in-tranasally every other day.Behavioral changes were assessed using the buried food test and Morris water maze(MWM).Olfactory bulb tissues were subsequently harvested for analysis.Hematoxylin-eosin(HE)staining was used to evaluate pathological changes,while immunofluo-rescence and quantitative polymerase chain reaction(qPCR)were employed to examine the ex-pression and distribution of protein and mRNA expressions and distributions of olfactory marker protein(OMP),membrane-spanning 4-pass A1(MS4A1),trace amine-associated receptor1(TAAR1). [Results]The buried food test revealed that BaP exposure significantly prolonged the time taken to find food in a dose-dependent manner(F=56.753,P<0.01).MWM results showed significant main effects for both time(F=128.5,P<0.01)and dose(F=3.889,P<0.05),with a sig-nificant interaction effect between them(F=2.128,P<0.05).HE staining showed that in the 2.89 mg·kg-1 group,although granule remained abundant,mitral cell layer neurons exhibited structural atrophy and deep staining.Immunofluorescence demonstrated a decreased dis-tribution of OMP,MS4A1,and TAAR1 in the olfactory nerve layer and glomerular layers in the 2.89 mg·kg-1 group compared with the blank control group(F=11.590,P<0.01;F=12.807,P<0.01;F=7.436,P<0.01).Furthermore,mRNA expression levels of OMP,MS4A1,and TAAR1 in the 2.89 mg·kg-1 group were also significantly downregulated compared to the control group(F=6.720,P<0.01;F=16.931,P<0.01;F=48.060,P<0.01). [Conclusion]BaP exposure leads to olfactory dysfunction in mice by inducing pathological damage to mitral cells and reducing the ex-pression of key olfactory receptors and markers in the olfactory bulb.

BACKGROUND:Benzo[a]pyrene (B[a]P) is both a carcinogen and a potent neurotoxic pollutant. Despite growing evidence linking B[a]P to neurological dysfunction, the responsible mechanisms have not been elucidated. METHODS:Here, we employed human apolipoprotein E4 (hAPOE4) transgenic mice and APOE knockout (APOE-KO) mice to evaluate the influence of APOE on B[a]P-mediated neurotoxicity. hAPOE4 mice overexpress the human APOE4 isoform, whereas APOE-KO mice lack APOE expression; wild-type C57BL/6 J mice served as controls. Animals received intraperitoneal injections of B[a]P at 0, 2.5, or 6.25 mg/kg on alternate days for 3 months. Spatial memory and learning were examined via Morris Water Maze (MWM). Neuronal morphology, including dendritic branching and spine density in the CA1 region of the hippocampus and dentate gyrus (DG), was assessed using Golgi-Cox staining. Neurofibrillary tangles were detected by silver glycine staining. Tau, phosphorylated Tau (Ser199 and Ser396), and LRP1 were evaluated using Western blot and immunohistochemical analyses. Chromatin immunoprecipitation PCR (ChIP-PCR) was undertaken to examine the regulation of APOE4 expression by the aryl hydrocarbon receptor (AHR). In addition, both untargeted metabolomics and lipidomics analyses were conducted following B[a]P exposure. RESULTS:B[a]P led to pronounced impairments in mouse spatial memory and learning, shown by greater escape latency, less time in the target quadrant, and a decreased number of platform crossings in MWM tests. Structural analyses revealed a significant reduction in dendritic branching within the hippocampal CA1 and DG regions. These neurobehavioral and morphological deficits were most severe in hAPOE4 mice, which displayed greater cognitive impairment and more extensive dendritic loss than B[a]P-treated wild-type mice, indicating that APOE4 amplifies B[a]P-induced neurotoxicity. ChIP assays demonstrated that B[a]P modulates APOE4 transcription through AHR-dependent mechanisms. Additionally, metabolomics and lipidomics analyses revealed widespread B[a]P-induced metabolic remodeling, suggesting that disrupted lipid metabolism and altered neuronal membrane integrity may contribute to the observed neurotoxicity and cognitive dysfunction. CONCLUSION:Collectively, the results indicate that B[a]P-mediated neurotoxicity may be facilitated, at least in part, by APOE4-dependent dysregulation of lipid metabolic pathways.

To elucidate the molecular mechanisms underlying Benzo[a]pyrene (BaP)-induced lung carcinogenesis, we constructed lung organoid and BaP-induced malignant transformation cell model (16HBE-T). Single-cell sequencing analysis confirmed that organoids were primarily composed of basal cells and secretory cells. Following BaP exposure, the lung organoids exhibited G1-phase cell cycle arrest. The expression of CYP1A1 (Log2FC = 10.24) and CYP1B1 (Log2FC = 6.27) were significantly upregulated, while that of SCGB1A1 (Log2FC = -0.26) was downregulated, indicating early-stage lung epithelial injury. Mfuzz soft clustering analysis and FindMarker function were employed to characterize gene expression patterns and identify differentially expressed genes (DEGs). GO, KEGG, GSEA and WikiPathway enrichment analyses revealed that these DEGs were enriched in redox-related metabolic processes (including cysteine/glutamate metabolism and glutathione biosynthesis), NRF2 signaling pathways, and carcinogenesis-associated pathways. Among the DEGs, 9 DEGs were associated with oxidative stress and amino acid metabolism, with SLC7A11 showing the most prominent upregulation (Log2FC = 3.40). The AddModuleScore function indicated that NRF2 exhibited the most significant transcriptional activity. In 16HBE-T cells, the protein expression of SLC7A11 and NRF2 increased by 35.74% and 82.85%, respectively. Knockdown of SLC7A11 significantly inhibited the migration, invasion, and colony-forming abilities of 16HBE-T cells. Meanwhile, intracellular glutamate and cysteine levels decreased, whereas glutamine levels increased. ChIP-PCR verified that NRF2 could directly bind to two specific regions (460-565 bp and 1488-1623 bp) within the SLC7A11 promoter to regulate amino acid metabolism. Collectively, our findings demonstrate that NRF2-regulated SLC7A11-mediated amino acid metabolic reprogramming plays a pivotal role in BaP-induced cellular malignant transformation.

Organophosphate esters (OPEs), commonly employed as flame retardants and plasticizers, have raised increasing concern due to their potential impacts on human health. Despite their widespread use, population-based evidence regarding their relationship with sleep health remains scarce. In this research, we examined data from the 2013-2016 cycles of the U.S. National Health and Nutrition Examination Survey (NHANES) to investigate the relationship between urinary OPE metabolites and sleep outcomes. The analysis included 2,606 participants who had complete data on both exposure and outcomes. Multivariable linear and logistic regression models were applied to examine associations, while restricted cubic spline models were used to test for potential nonlinear dose-response patterns. To account for combined exposure, we further conducted Bayesian kernel machine regression and weighted quantile sum regression. Our findings showed that dibutyl phosphate (DBUP) was inversely related to sleep duration and exhibited nonlinear associations with sleep indicators. Mixed-exposure analyses indicated that higher cumulative levels of OPEs were linked to shorter sleep duration. Additionally, bis(1-chloro-2-propyl) phosphate (BCPP) was positively related to self-reported sleep problems, particularly among older participants. In general, the findings indicate that exposure to OPEs, particularly DBUP (which originates from tri-n-butyl phosphate, TNBP) and BCPP [derived from tris(2-chloro-isopropyl) phosphate, TCPP], may be associated with sleep disturbances among the U.S. population. Additional mechanistic and long-term studies are needed to validate these associations.

OBJECTIVE:To evaluate whether targeted plasma phospholipidomics identifies an externally validated blood panel for pneumoconiosis triage across dust-exposed and nonexposed worker cohorts. METHODS:We quantified 53 plasma phospholipids by UPLC-MS/MS in discovery (n=392) and external (n=221) cohorts comprising pneumoconiosis, dust-exposed noncase, and nonexposed healthy control participants. Candidate lipids were selected by covariate-adjusted screening and LASSO, then tested with clinical covariates. RESULTS:A five-lipid panel was retained. In the external cohort, Firth logistic regression achieved AUC 0.983, sensitivity 0.923, and specificity 0.955. Cytokine-lipid correlations supported inflammatory plausibility. CONCLUSIONS:This panel may support occupational triage for confirmatory imaging, pending prospective multicenter validation.

Environmental pollution has become a global public health crisis, posing profound threats to human reproductive stability and fetal developmental homeostasis [...]

Hydroquinone (HQ) is a toxic phenolic pollutant that requires rapid and selective detection strategies for environmental monitoring. Herein, a mesoporous Fe-doped polydopamine (Fe-PDA) nanozyme was synthesized via a facile one-step soft-template strategy and employed to construct a colorimetric sensing platform for HQ detection. The Fe-PDA nanozyme exhibited enhanced peroxidase (POD)-like activity toward H2O2-mediated oxidation of 3,3 ',5,5 '-tetramethylbenzidine (TMB), benefiting from its mesoporous structure and abundant exposed catalytic sites. HQ effectively suppressed TMB oxidation through dual mechanisms, including reactive oxygen species (ROS) scavenging and direct reduction of oxidized TMB (oxTMB), producing a concentrationdependent colorimetric response. Under optimized conditions, the sensing platform exhibited a linear detection range of 1-20 & micro;M with a detection limit of 0.67 & micro;M (S/N = 3). By integrating a smartphone-assisted RGB analysis module, the detection limit was further reduced to 0.05 & micro;& Mcy;. The system demonstrated high selectivity toward HQ against structurally similar phenolic compounds. Moreover, principal component analysis (PCA) enabled reliable differentiation of HQ, trichlorophenol (TCP), and 4-aminophenol (4-AP) at concentrations as low as 5 & micro;M. Practical applicability was validated in spiked environmental water samples, yielding recovery rates ranging from 93.4% to 107.7% with relative standard deviations below 5.43%. This work presents a low-cost, portable, and intelligent nanozyme-based sensing strategy for sensitive HQ detection, offering a promising platform for selective phenolic pollutant monitoring in complex environmental systems.

Bisphenol A (BPA), a pervasive environmental endocrine disruptor, poses significant risks to liver health. Conventional detoxification strategies often lack specificity and efficacy. This study developed a novel targeted therapeutic approach using engineered postbiotics derived from Lactococcus lactis. We genetically modified L. lactis to express a surface-anchored human estrogen-related receptor gamma ligand-binding domain (ERR gamma-LBD), enabling specific recognition and binding of BPA and its analogues. This engineered postbiotic system was designed for the targeted transportation and sequestration of BPA within the gastrointestinal tract, thereby preventing its systemic absorption and subsequent hepatic accumulation. In murine models of BPA-induced hepatic injury, oral administration of these engineered postbiotics significantly mitigated liver damage. Histopathological analysis revealed a marked reduction in key pathological features, including extensive hepatocyte necrosis, structural disorganization of hepatic lobules, and inflammatory infiltration. Biochemical assays confirmed decreased serum levels of liver injury markers (ALT, AST) and inflammatory cytokines in treated mice compared to BPA-exposed controls. Furthermore, the treatment group exhibited restored expression levels of hepatic antioxidant enzymes. Our findings demonstrate that surface-displayed ERR gamma-LBD on L. lactis postbiotics effectively facilitates the targeted binding and removal of BPA in vivo. This strategy significantly alleviates BPAinduced hepatic injury by reducing oxidative stress and inflammation. This study presents the first proof-of-concept for using engineered postbiotics as precision interceptors of environmental toxins, offering a promising, specific, and safe therapeutic avenue for mitigating chemical-induced organ damage.

People spend the majority of their time indoors; however, most previous studies on the health effects of particulate matter (PM) and ozone (O3) have used outdoor concentrations as a proxy for personal exposure, which may introduce misclassification bias. Since indoor PM and O3 originate primarily from outdoors, estimating their indoor infiltration levels provides a closer approximation of true personal exposure. This study used data on approximately four million deaths occurring over an eight-year period in Jiangsu Province, China. The infiltration factor method and time-series analysis were employed to assess the linear and nonlinear associations of short-term indoor exposure to outdoor-origin PM1, PM2.5, PM10, and O3 with all-cause, cardiovascular, and respiratory mortality. In addition, the interactions between indoor PM and O3 were investigated. The results indicate that indoor exposure to outdoor-origin PM and O3 was positively associated with mortality, and these associations were stronger than those observed for direct outdoor exposure. Each 10 μg/m3 increase in the 2-day moving average concentration of indoor PM1, PM2.5, PM10, and O3 was associated with a 1.82% (95% confidence interval [CI]: 1.64, 2.01), 1.02% (95% CI: 0.91, 1.13), 0.69% (95% CI: 0.62, 0.77), and 1.79% (95% CI: 1.60, 1.99) increase in all-cause mortality, respectively. No threshold was observed in the exposure-response associations. Furthermore, significant multiplicative and additive interactions were identified between infiltrated PM and O3. Consequently, greater attention should be directed toward indoor air quality, particularly the coordinated management of combined exposure to indoor PM and O3, in order to better protect public health.

PurposeNon-communicable diseases (NCDs) are an important public health concern among coal miners, who may experience occupational hazards, demanding working conditions, and unhealthy lifestyles. The Guangdong Pharmaceutical University Occupational Health Cohort in Xishan Coal Electricity Group (GDPU-OHC) is an ambispective occupational cohort established to characterize NCD burden, identify high-risk occupational groups, support future longitudinal analyses, and inform occupational health management in China.ParticipantsGDPU-OHC was conducted in Shanxi Province, China, with a retrospective component covering 2009–2022 and a prospective component initiated in May 2023. Among 36,577 workers with routine health examination records in 2023, 25,597 eligible employees (median age: 41.00 years, IQR: 35.00–50.00; 89.19% male) were recruited into the prospective cohort. All baseline participants were asked to provide fasting blood and urine samples. The main cohort is scheduled for follow-up every 3–5 years. Planned sub-studies include occupational protection improvement (N = 200), work pattern optimization (N = 600), dietary optimization (N = 600), and a gut microbiota modulation pilot study (N = 50).Findings to dateAmong baseline participants, the crude prevalence of obesity, hypertension, type 2 diabetes, hyperuricemia, and hyperlipidemia was 22.64, 23.18, 13.89, 27.87, and 47.93%, respectively. Occupational hazards, including dust, noise, toxic gasses, and shift work, and lifestyle factors, including high oil/salt intake, smoking, and alcohol consumption, were common in this cohort and will serve as key exposures for future longitudinal analyses of NCD risks. These findings are descriptive; temporal trends and exposure-outcome associations were not assessed in the present cohort profile.Future plansThe GDPU-OHC will continue prospective follow-up to capture long-term NCD outcomes and repeated occupational health information. Future studies will evaluate longitudinal associations between occupational/lifestyle exposures and NCD risks, develop planned sub-studies, and conduct mechanistic analyses involving oxidative stress, inflammatory markers, metabolomics, and gene–environment interactions. Study findings will be disseminated through serial publications.

Long-term effects of occupational polycyclic aromatic hydrocarbons (PAHs) on biological aging are unclear. A prospective cohort study was conducted from 2019 to 2023, involving 610 coke oven workers and 454 control workers from a water treatment plant. Biological age was calculated using the Klemera and Doubal method (KDM-BA) based on 12 clinical biomarkers, and aging acceleration (KDM-Accel) was derived. Group-based trajectory modeling (GBTM) was employed to identify distinct aging trajectories over five time points. The associations between eleven urinary mono-hydroxylated PAH metabolites (measured via HPLC-MS) and both KDM-Accel and aging trajectories were assessed using multiple linear regression and multivariable logistic regression, respectively. GBTM identified three distinct aging trajectories: slow aging (14.86

Hypertension and subjective cognitive decline (SCD) frequently co-occur, consistent with broader multimorbidity patterns observed in aging populations and highlighting the need for targeted assessment of associated factors. This study aimed to test the hypothesis that multi-level factors across the five Health Ecological Model (HEM) layers are independently associated with SCD among hypertensive patients in rural China, and to identify specific associated factors within each layer. We conducted a cross-sectional study from May to August 2024 with 860 hypertensive patients selected from three rural counties in Shanxi Province, China (Daning and Yonghe counties in Linfen City, and Yangqu County in Taiyuan City) via multi-stage cluster random sampling. Participants were categorized into non-SCD (SCD-Q9 score < 5) and SCD (≥ 5) groups based on self-reported cognitive symptoms.Variables were classified into five HEM layers, and logistic regression was employed to identify associated factors. Based on self-reported screening, 80.58% of participants met the criteria for SCD. Multi-level factors were significantly associated with SCD. In the Individual Characteristics Layer, advanced age (OR = 1.042, 95% CI 1.010 ~ 1.074), family history of hypertension (OR = 2.352, 95% CI 1.550 ~ 3.570), hypertensive complications (OR = 3.049, 95% CI 1.680 ~ 5.534) and moderate hypertension risk level (OR = 1.847, 95% CI 1.149 ~ 2.968) were associated with higher odds of SCD. Within the Behavior and Lifestyle Layer, lack of physical exercise (OR = 1.611, 95% CI 1.075 ~ 2.412) and fairly good and fairly poor sleep quality (fairly good: OR = 1.644, 95% CI 1.063 ~ 2.543; fairly poor: OR = 1.939, 95% CI 1.017 ~ 3.698) were associated with SCD, while former drinker was associated with lower odds of SCD (OR = 0.294, 95% CI 0.107 ~ 0.809), although this association may reflect residual confounding and should not be interpreted causally. In the Working and Living Conditions Layer, lower household income (< 1000 CNY: OR = 3.282, 95% CI 1.647 ~ 6.540), utilization of county-level hospitals (OR = 1.697, 95% CI 1.077 ~ 2.676), and mild depression (OR = 2.068, 95% CI 1.215 ~ 3.519) were associated with SCD. In the Policy Environment Layer, no significant associations were observed. These findings identify multi-level factors associated with SCD in this population, highlighting potential areas for integrated prevention strategies, though longitudinal studies are needed to establish their predictive value.

Air quality in China has markedly improved over the past decade, yet pollution levels remain high and continue to threaten public health. This study analyzed the spatiotemporal variations in six air pollutants (PM2.5, PM10, SO2, NO2, O3, CO) across seven regions in China (2015–2024) using Kriging interpolation. The performance of Recurrent Neural Network (RNN), Long Short-term Memory (LSTM), and Convolutional Neural Network-Long Short-term Memory (CNN-LSTM) models was assessed using the Root Mean Square Error (RMSE), Mean Absolute Error (MAE), and Coefficient of Determination (R2) metrics. Results showed that all pollutants exhibited overall declining trends, with SO2 depicting the largest reduction (69.53%), while O3 displayed intermittent increases from 2017 to 2024. North China recorded both the highest concentrations and the greatest reductions in PM2.5, SO2, and CO, whereas Southwest and South China maintained the lowest overall levels. Among the predictive models, LSTM achieved the highest overall accuracy (mean RMSE = 1.802, mean MAE = 0.915, R2 > 0.99). These findings provide a comprehensive depiction of China’s air pollution evolution and highlight the potential of deep learning for region-specific air quality prediction and policy design. The results offer a quantitative foundation for optimizing differentiated control strategies and advancing precision air quality management.

Objective To investigate the relationship between the metabolites of polycyclic aromatic hydrocarbons(PAHs)in urine and the changes in cognitive function of steel mill workers.Methods In 2019,960 workers from a coking plant in Shanxi province were selected to undergo basic information investigations,cognitive function tests,and detection for hydroxylated metabolites of polycyclic aromatic hydrocarbons(OH-PAHs)in urine.During the follow-up in 2023,a total of 567 workers completed the cognitive function tests.The Beijing version of the Montreal Cognitive Assessment(MoCA)was employed to test the cognitive function of the workers.High performance liquid chroma-tography with tandem mass spectrometry(HPLC-MS/MS)was utilized to detect OH-PAHs in urine.The generalized linear model and the generalized estimation equation were adopted to analyze the relationship between urinary OH-PAHs and the cognitive function of the workers.Results Subjects were 49(46,53)years old at baseline,with 91.7%being the male.In the longitudinal study,the high exposure groups of 2-hydroxynaphthalene(2-OHNAP)and 1-hydroxypyrene(1-OHPYR)showed decreases in attention(β=-0.338,95%CI:-0.454 to-0.222,P<0.001;β=-0.450,95%CI:-0.557 to-0.343,P<0.001),abstract thinking(β=-0.463,95%CI:-0.549 to-0.377,P<0.001;β=-0.360,95%CI:-0.450 to-0.269,P<0.001)and the total score(β=-0.863,95%CI:-1.284 to-0.443,P<0.001;β=-0.548,95%CI:-0.987 to-0.108,P=0.015).Conclusions Long-term exposure to high concentrations of PAHs can lead to reduced cognitive function in steel mill workers.

Drug-induced liver injury (DILI) remains a persistent and unavoidable challenge in biomedicine, significantly impacting preclinical drug development and early clinical trials. The liver, as the primary site for endogenous antioxidant production, is particularly sensitive to acute damage mediated by reactive oxygen species (ROS) and reactive nitrogen species (RNS). The ratiometric and near-infrared (NIR) detection of peroxynitrite (ONOO-), as potential biomarker for DILI, is crucial for enhancing the imaging effectiveness of liver damage. Thus, an ONOO- activated endoplasmic reticulum (ER)-targeted fluorescent probe, named DSA, was easily designed and synthesized using dicyanoisophorone, syringaldehyde and arylboronate, which featured dicyanoisophorone as the fluorophore and an arylboronate group as the ONOO- recognition group. The probe DSA was converted into a long-wavelength DSA-ONOO- fluorophore in the presence of ONOO- with large Stokes shift (172 nm), high selectivity, and low detection limit (98 nM). The ratiometric response to ONOO- provided a more accurate intracellular analysis through a built-in internal reference calibration, successfully enabling sensitive detection of ONOO- in living cells. Additionally, leveraging the optical characteristics of NIR fluorescence imaging, DSA not only detected the ER-phagy process induced by starvation and ONOO- but also accurately monitored minor fluctuations in ONOO- levels during acetaminophen (APAP)-induced hepatotoxicity in mice, aiding in the diagnosis of DILI and the development of therapeutic drugs.

ABSTRACT Benzo[a]pyrene (B[a]P) is a carcinogenic contaminant widely present in the environment. Recently, increasing studies have paid attention to the developmental neurotoxicity of B[a]P in offspring in their early life stages; however, the underlying molecular mechanisms have not been clearly elucidated. In this study, we aimed to evaluate the effects of prenatal B[a]P exposure on neurobehavior of pups during their brain growth spurt (BGS) period and also explore the potential underlying mechanisms. Pregnant Sprague‐Dawley (SD) rats were intraperitoneally exposed to 0, 10, 20, or 40 mg/kg‐bw B[a]P for three consecutive days during embryonic days 17–19. The physiological development index of pups was observed, and a series of neurobehavioral tests assessing sensory and motor maturation were performed. The complexity of dendritic branches and the basal dendritic spine density of CA1 pyramidal neurons were examined using Golgi‐Cox staining during PND 1–14. In addition, the mRNA and protein expression levels of hippocampal BDNF, SYP, Arc, PSD‐95, DNMT1, and DNMT3a, and the level of 5‐mC were detected using RT‐qPCR, Western blotting, or immunohistochemical staining, respectively. We noted that prenatal B[a]P exposure induced body weight loss and neurobehavioral impairments in the early life stages. Furthermore, this study firstly revealed that maternal exposure to B[a]P impaired the dendritic arborization and complexity of pyramidal neurons in the hippocampus CA1 subfield in offspring during the early postnatal period, and the damage of B[a]P to basal dendritic spine density was also observed in a dose‐dependent manner. Correspondingly, maternal exposure to B[a]P markedly reduced BDNF, Arc, SYP, and PSD‐95 mRNA and protein levels in the offspring hippocampus. Meanwhile, the levels of hippocampal DNMT1, DNMT3a, and 5‐mC significantly increased in the offspring prenatally exposed to B[a]P. In summary, this study firstly demonstrated that maternal B[a]P exposure induced neurobehavioral deficits by destroying the hippocampal synaptic ultrastructure, which was possibly associated with the downregulation of BDNF, Arc, SYP, and PSD95 in the hippocampus through increased DNMTs‐mediated DNA methylation in offspring during the BGS period.

Li exposure is becoming a new prominent major issue in energy-environment-health field. However, its reproductive health risk has been less explored. In this study, we find that exposure to 28-fold REED (really environmental exposure dose) of Li is enough to induce mouse miscarriage by altering the structures and functions of placenta. Exposure to ≥ 5.6-fold REED of Li is enough to alter the structure and functions of ovary and placenta, and exposure to ≥ 28-fold REED of Li alters fetus morphology and uterus functions, showing a susceptibility to Li exposure as the order ovary > placenta > fetus > uterus. Some characteristics (such as AMH (anti-müllerian hormone) levels in serum, the mRNA levels of Pgr (progesterone receptor) and Nr2f2 in placenta, and the mRNA levels of Cyp19A1 and Sohlh2 in Ovary) are significantly altered with exposure to 5.6-fold REED of Li, which could be used as sensitive targets to predict reproductive health risk with Li exposure. Moreover, the doses of Li in clinical Li treatment (28- or 56-fold REED of Li) should be more cautious, especially for women. Collectively, this study identifies Li exposure as a new risk factor for female reproductive healthy in energy-environment-health field, which deserves the critical attention by governments, enterprises, and hospitals.

Grey hair, a common ageing-associated phenomenon in humans, is mainly attributed to the damage of melanocytes and the absence of melanin. Grey hair has long been treated with traditional medicine, and new research has shown that various plant-derived monomers can increase tyrosinase activity and melanogenesis, indicating that they may have therapeutic value in curing grey hair. In this study, we outlined the role of melanin and pigmentation during hair growth and collected various medicinal plant monomers with the potential value of grey hair reversal. Many active ingredients from medicinal plants, such as fraxinol, tribuloside, morin and naringenin, can upregulate melanogenesis and tyrosinase activity through different signalling pathways. Some of them can promote melanosome quantity, maturation and transportation as well. Monomers isolated from medicinal plants may act as stimulators of melanogenesis. Many plant-derived monomers perform as activators that upregulate melanin synthesis and tyrosinase activity through different signalling pathways. They are of great research value for the treatment of hair greying. Moreover, to further improve experimental effect, safety and reliability, a systematic and comprehensive evaluation system needs to be established in the future before studying their clinical efficacy.

Background: Long-term effects of occupational polycyclic aromatic hydrocarbons (PAHs) on biological aging are unclear. Methods: A prospective cohort study was conducted from 2019 to 2023, involving 610 coke oven workers and 454 control workers from a water treatment plant. Biological age was calculated using the Klemera and Doubal method (KDM-BA) based on 12 clinical biomarkers, and aging acceleration (KDM-Accel) was derived. Group-based trajectory modeling (GBTM) was employed to identify distinct aging trajectories over five time points. The associations between eleven urinary mono-hydroxylated PAH metabolites (measured via HPLC-MS) and both KDM-Accel and aging trajectories were assessed using multiple linear regression and multivariable logistic regression, respectively. Results: GBTM identified three distinct aging trajectories: slow aging (14.86%), moderately accelerated aging (59.14%), and rapidly accelerated aging (26%). Higher concentrations of urinary Σ-OHPAHs (sum of all metabolites), 1-hydroxypyrene (1-OHPyr), and 2-hydroxyphenanthrene (2-OHPhe) were significantly associated with increased KDM-Accel. A natural log-unit increase in Σ-OHPAHs and 1-OHPyr was associated with a 0.029-year and 0.028-year increase in KDM-Accel, respectively. Workers in the highest tertile (T3) of Σ-OHPAHs exposure had a 61.2% increased odds (OR = 1.612, 95% CI: 1.093–2.376) of being in the rapidly accelerated aging trajectory compared to those in the lowest tertile (T1). Similar positive dose-response relationships were observed. Conclusion: Occupational PAH exposure accelerates biological aging ; enhanced protection and early intervention are warranted.

Pneumoconiosis is a widespread occupational pulmonary disease caused by inhalation and retention of dust particles in the lungs, is characterized by chronic pulmonary inflammation and progressive fibrosis, potentially leading to respiratory and/or heart failure. Workers exposed to dust, such as coal miners, foundry workers, and construction workers, are at risk of pneumoconiosis. This review synthesizes the international and national classifications, epidemiological characteristics, strategies for prevention, clinical manifestations, diagnosis, pathogenesis, and treatment of pneumoconiosis. Current research on the pathogenesis of pneumoconiosis focuses on the influence of autophagy, apoptosis, and pyroptosis on the progression of the disease. In addition, factors such as lipopolysaccharide and nicotine have been found to play crucial roles in the development of pneumoconiosis. This review provides a comprehensive summary of the most fundamental achievements in the treatment of pneumoconiosis with the purpose of indicating the future direction of its treatment and control. New technologies of integrative omics, artificial intelligence, systemic administration of mesenchymal stromal cells have proved useful in solving the conundrum of pneumoconiosis. These directional studies will provide novel therapeutic targets for the treatment of pneumoconiosis.