Xiaoming Lou

Background/Objectives: Vitamin A (VA), which is fat-soluble, belongs to the group of carotenoids, a class of highly effective antioxidant and genoprotective compounds (including astaxanthine, zeaxanthine, luteine). It plays a critical role in cellular growth, differentiation, and oxidative stress regulation, but prospective evidence linking childhood VA to subsequent genomic stability is scarce. This study investigated whether baseline VA levels were associated with later measurements of relative telomere length (RTL), four ribosomal DNA copy numbers (rDNA-CN: 5S, 18S, 28S, and 45S), and mitochondrial DNA copy number (mtDNA-CN) in children over a 4-year follow-up. Methods: Baseline VA levels were measured in 2021. In 2025, peripheral blood genomic DNA was extracted, and RTL, rDNA-CNs, and mtDNA-CN were quantified using qPCR. Multivariable linear regression and restricted cubic spline regression (RCS) were employed to examine the associations and dose–response shapes. Sex-stratified analyses with interaction tests were performed to evaluate effect modification by sex. Results: Among 215 children, baseline VA was positively associated with RTL, 5S rDNA-CN, 18S rDNA-CN, and 45S rDNA-CN after covariate adjustment. RCS analyses revealed strictly monotonic positive dose–response curves between VA and RTL, 5S rDNA-CN, and 18S rDNA-CN, with no statistically significant sex interaction (all p for interaction > 0.05). Conclusions: Higher childhood VA levels are positively associated with longer telomeres and higher rDNA-CN in later childhood, suggesting that adequate early-life VA may confer long-term benefits for ribosomal genomic stability and cellular aging. These observations expand our understanding of nutrition-related modulators of child genomic homeostasis and support further investigation into nutritional interventions targeting genomic protection in early life.

Background: The health risks of noise pollution have attracted global attention, especially the potential cardiovascular effects of occupational noise exposure. Our study aimed to investigate the associations of occupational noise with cardiovascular disease risk factors [fasting blood glucose (FBG), systolic blood pressure (SBP), diastolic blood pressure (DBP), and electrocardiogram (ECG) abnormality], and further evaluate the possible mediating role of hearing loss in the associations. Methods: This cross-sectional study included 64,382 participants exposed to occupational noise in China. Individual level of noise exposure with an 8-h equivalent A-sound level (L _{Aeq, 8h} ) was measured by personal noise dosimeter. And the noise exposure level of workers was approximated using the average of measured individual noise values within each enterprise. Generalized linear models and logistic regression models were used to analyze the associations of noise exposure with cardiovascular disease risk factors. Mediation analyses were performed to assess the mediating roles of hearing loss on above associations. Results: L _{Aeq, 8h} was positively associated with FBG (β = 0.006, 95% CI: 0.001–0.011), SBP (β = 0.036, 95% CI: 0.003–0.068), and risk of ECG abnormality (OR = 1.014, 95% CI: 1.009–1.019). We observed positive linear dose-response associations of noise exposure with blood pressure, as well as non-linear relationships with FBG and ECG abnormality risk [L _{Aeq, 8h} exceeded around 82 dB(A) as a turning point]. Age, dust exposure, high temperature, and length of service significantly modified above associations ( P modification < 0.05), and the effects were more obvious in participants >43 years, workers with dust or high temperature exposure, and workers with length of service >5 years. Hearing loss mediated 3.7%−10.9% of the associations of noise exposure with elevated blood pressure and risk of ECG abnormality. Conclusions: Occupational noise exposure was associated with adverse changes in FBG, blood pressure, and risk of ECG abnormality. Older people, workers exposed to dust or high temperature, and those with longer working duration were more susceptible. Hearing loss might play potential role in cardiovascular damage induced by noise exposure. Efficient strategies for reducing occupational noise exposure should be enhanced to control the cardiovascular threat from occupational noise pollution.

Previous epidemiological studies have established associations between fine particulate matter (PM_2.5) exposure and maternal thyroid hormone suppression. However, as PM_2.5 is a complex chemical mixture, the specific contribution of metallic constituents to PM_2.5-induced thyroid disruption remains poorly characterized. This study aimed to evaluate the relationship between maternal thyroid function and exposure to metallic and metalloid components of PM_2.5 during pregnancy. In a longitudinal study of 847 pregnant women recruited from three maternal and child healthcare hospitals, we collected fasting blood samples at 10, 17, and 32 weeks of gestation for thyroid hormone assessment. Concurrently, ambient PM_2.5 monitoring stations near participating hospitals quantified 11 metallic/metalloid elements. Linear mixed-effects regression models assessed individual element associations with thyroid parameters, while weighted quantile sum (WQS) regression evaluated combined effects of metal mixtures. Significant inverse associations were observed between lead (Pb) exposure and serum thyroid stimulating hormone (TSH) levels. Multiple elements - including aluminum (Al), arsenic (As), cadmium (Cd), lead (Pb), antimony (Sb), selenium (Se) and thallium (Tl) - demonstrated negative correlations with free thyroxine (FT₄) and free triiodothyronine (FT₃) concentrations. WQS analysis revealed that each inter-decile rise in mixed metal exposure was associated with a 0.52% decrease in TSH (95% CI: -3.84%, 2.91%), a 1.52% reduction in FT₄ (95% CI: -1.95%, -1.09%), and a 1.18% decline in FT₃ (95% CI: -1.60%, -0.77%). Tl, Al, and As emerged as primary contributors to these effects, collectively accounting for 86%- 97% of the weighted mixture impact. These findings demonstrate that metallic components of PM_2.5, particularly Tl, Al and As are significantly associated with suppressed maternal thyroid function during pregnancy. This highlights the importance of metal-specific toxicity in PM_2.5-related endocrine disruption.

Background: Iodine nutrition requires continued surveillance after changes in salt iodization policy. This study evaluated iodine status and associated factors among children and adolescents in Zhejiang Province, ten years after the national salt iodization standard was lowered. Methods: A cross-sectional survey employing a stratified, multistage cluster sampling design was conducted in 2022. A total of 688 participants aged 6–17 years with complete data on urinary iodine concentration, household salt iodine concentration, geographic classification, and key questionnaire variables were included in the analysis. Multivariate logistic regression analysis was performed to identify factors independently associated with iodine sufficiency. Results: Among 688 participants, the median household salt iodine concentration was 21.50 mg/kg, and iodized salt coverage was 64.68%. The median urinary iodine concentration (UIC) was 191.4 μg/L; however, 15.26% of participants had UIC < 100 μg/L. Participants in coastal areas had lower UIC levels and lower household iodized salt coverage than those in inland areas. Multivariate logistic regression analysis identified age, geographic region, and household use of iodized salt as factors significantly associated with iodine sufficiency. Conclusions: The overall iodine nutritional status among children and adolescents aged 6–17 years in Zhejiang Province is adequate. However, a certain proportion of iodine deficiency persists. Continued, targeted monitoring and health education on the appropriate use of qualified iodized salt are warranted, particularly in coastal areas and among younger children.

The association between tobacco exposure and obesity remains controversial, with the potential modifying role of cadmium (Cd) unclear. Childhood population

Microplastics, as emerging pollutants, are ubiquitously present globally and pose significant threats to both ecosystems and human health. These pollutants not only exert direct toxicity on the environment and living organisms but also influence the toxicity of other pollutants through mechanisms such as adsorption and carrier effects. The health risks of microplastics are multifaceted and complex, involving cellular toxicity, immune dysfunction, and impairments to neurological, endocrine, and reproductive systems. This review summarizes the combined toxic effects of microplastics and heavy metals, organic pollutants, plastic additives, antibiotics, and viruses, exploring their potential mechanisms and influencing factors. The paper suggests that future research should focus on simulating exposure scenarios, examining the long‐term effects of exposure, and understanding the health consequences of combined exposures. This will provide new perspectives on the toxic effects of microplastics on the environment and organisms, enhance public awareness of their potential harm, and better address the impact of microplastic pollution on ecosystems.

Micro(nano)plastics (MNPs), as a globally emerging environmental pollutant, are now ubiquitous in natural environments and can continuously enter the human body through ingestion, inhalation, and dermal contact. This widespread exposure has raised significant concerns regarding the potential health risks posed by MNPs. Although epidemiological studies are still in the early stages, accumulating in vitro cellular experiments have provided key evidence suggesting that nano- to micro-sized plastic particles can cross physiological barriers in the human body. These particles enter cells via endocytosis or direct penetration through the cell membrane, triggering toxic effects such as oxidative stress, immune responses, mitochondrial dysfunction, and DNA damage, which can potentially lead to cell apoptosis. These findings highlight that the direct interaction between MNPs and human cells could be a core mechanism underlying their potential health hazards. This review systematically summarizes the toxic effects of MNPs exposure on various human cell types, exploring the underlying molecular mechanisms and providing insights for future research into the toxicological impacts of MNPs and their implications for human health risk assessment.

Background: Despite escalating global pollution from microplastics (MPs) and the concurrent surge in high-fat food consumption, the health impacts of MP exposure on individuals under different dietary patterns remain poorly understood. Methods: This study investigated the differential effects of environmentally relevant concentrations of polystyrene microplastics (5 μm, 8 mg/kg) on gut barrier function in mice fed either a normal chow diet (CD) or a high-fat diet (HFD). Results: Key findings revealed that, in HFD-fed mice, MP exposure significantly reduced (p < 0.05) the transcriptional levels of genes encoding the tight junction proteins (ZO-1, Occludin, and Claudin-1), as well as the mucin protein Muc-2, accompanied by decreased protein expression levels of these markers in both colonic and ileal tissues. In contrast, no significant differences were observed in CD-fed mice exposed to MPs. Analysis of the gut microbiota and measurement of short-chain fatty acid (SCFA) metabolites showed that MPs induced significant alterations in the composition and diversity indices of the gut microbiota, along with a marked decrease (p < 0.05) in the levels of the characteristic metabolite butyrate in HFD-fed mice. Conversely, butyrate levels remained unchanged in CD-fed mice following MP exposure. Quantitative PCR (qPCR) and immunofluorescence staining of colonic tissues demonstrated that MP exposure significantly downregulated (p < 0.05) both the transcription and protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in HFD-fed mice. Again, no significant changes were detected in CD-fed mice. Conclusions: These results collectively indicate that the impact of microplastics on the intestinal barrier differs significantly between mice fed normal and high-fat diets. The gut microbiota and its metabolites, particularly butyrate, may play a critical role, possibly through modulating PPARγ signaling. This study contributes valuable insights into understanding the toxicity profiles of microplastics and establishing crucial links between dietary patterns and the health effects of emerging pollutants.