Light at night (LAN) has received increasing attention for its potential health hazards to human and animals. However, to our knowledge, no study has explored the specific effects of bedroom nighttime light exposure on allostatic load (AL). To investigate the association between bedroom individual-level LAN exposure and AL among young adults, an integrative index manifests multiple system dysregulation. Using data from a cohort of 484 Chinese young adults aged 16–22 years. Bedroom light was objectively recorded at 1-min intervals for two nights using a portable illuminance meter. Fasting blood samples were collected at one-year follow-up for the detection of AL parameters. AL score was derived as sum of the top quartile of twelve physiological biomarkers in four systems: metabolic system (BMI, WC, TC, HDL, LDL, TG, HbA1c, INS, GLU); cardiovascular system (SBP, DBP); immune and inflammatory systems (hs-CRP), with HDL was lowest quartile. Univariate and multivariate linear regression models were used to evaluate the association between LAN intensity with AL score and separate AL parameters. The average age of subjects was 18.7 years, 64.3% were female. The mean AL score of LAN group (average LAN intensity ≥ 3lx) was significantly higher than Dim group (3.6 ± 2.6 vs. 2.7 ± 2.1; P = 0.007). For each 1 lx increase of LAN intensity was associated with 0.15-unit increase in AL score (95% CI: 0.06, 0.24; P = 0.001). Moreover, LAN group was associated with increased 1.01-unit in AL score (95% CI: 0.36–1.66; P = 0.003) compared to Dim group. Significant associations between bedroom LAN exposure with allostatic load and separate AL biomarkers were observed in our study. Keeping bedroom darkness at night may be a practicable option to reduce the wear of multiple body systems and improve human cardiometabolic health from early in life.

Cadmium (Cd) exposure is recognized as an important risk factor for psychological health, but suitable physical activity may relieve depression. However, it remains unknown whether physical activity (PA) can reduce the effect of cadmium exposure on depression. Therefore, a cross-sectional data from National Health and Nutrition Examination Survey (NHANES) 2015–2018 was used. The Nine-item Patient Health Questionnaire (PHQ-9) was used to assess depression among the participants. PA was calculated according to the metabolic equivalent (MET), weekly frequency, and duration of each activity. Logistic regression and restricted cubic spline models were used to examine the associations of Cd and depression. A total of 5560 adults aged 20 years and above were finally included in this study. The results indicated a positive correlation between blood Cd and depression. The multivariate-adjusted ORs (95% CI) of the highest quartile were 2.290 (1.754–2.990) for depression, which was still significant after controlling other heavy metals (P < 0.05). Under Cd exposure, the high intensity of physical activity group had the lowest risk of depression (OR = 2.226, 95%CI: 1.447–3.425), while the group with no physical activity had the highest risk (OR = 2.443, 95%CI: 1.382–4.318). Our results indicate that inner Cd exposure may be a risk factor for depression, and physical activity can moderate this relationship to some degree.

Four most concerned heavy metal pollutants, arsenic, cadmium, lead, and mercury may share common mechanisms to induce metabolic syndrome (MetS). However, recent studies exploring the relationships between MetS and metal exposure presented inconsistent findings. We aimed to clarify the relationship between heavy metal exposure biomarkers and MetS using a meta-analysis and systematic review approach. Literature search was conducted in international and the Chinese national databases up to June 2020. Of selected studies, we extracted the relevant data and evaluated the quality of each study’s methodology. We then calculated the pooled effect sizes (ESs), standardized mean differences (SMDs), and their 95% confidence intervals (CIs) using a random-effect meta-analysis approach followed by stratification analyses for control of potential confounders. Involving 55,536 participants, the included 22 articles covered 52 observational studies reporting ESs and/or metal concentrations on specific metal and gender. Our results show that participants with MetS had significantly higher levels of heavy metal exposure [pooled ES = 1.16, 95% CI: 1.09, 1.23; n = 42, heterogeneity I² = 75.6%; and SMD = 0.22, 95% CI: 0.15, 0.29; n = 32, I² = 94.2%] than those without MetS. Pooled ESs in the subgroups stratified by arsenic, cadmium, lead, and mercury were 1.04 (95% CI: 0.97, 1.10; n = 8, I² = 61.0%), 1.10 (0.95, 1.27; 11, 45.0%), 1.21 (1.00, 1.48; 12, 82.9%), and 1.26 (1.06, 1.48; 11, 67.7%), respectively. Pooled ESs in the subgroups stratified by blood, urine, and the other specimen were 1.22 (95% CI: 1.08, 1.38; n = 26, I² = 75.8%), 1.06 (1.00, 1.13; 14, 58.1%), and 2.41 (1.30, 4.43; 2, 0.0%), respectively. In conclusion, heavy metal exposure was positively associated with MetS. Further studies are warranted to examine the effects of individual metals and their interaction on the relationship between MetS and heavy metals.

Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with heart rate variability (HRV) reduction, a widely used marker of cardiovascular autonomic dysfunction. The role of DNA methylation in the relationship between PAHs exposure and decreased HRV is largely unknown. This study aims to explore epigenome-wide DNA methylation changes associated with PAHs exposure and further evaluate their associations with HRV alternations among non-current smokers. We measured 10 mono-hydroxylated PAHs (OH-PAHs) in urine and DNA methylation levels in blood leukocytes among participants from three panels of Chinese non-current smokers (152 in WHZH, 99 in SY, and 53 in COW). We conducted linear regression analyses between DNA methylation and OH-PAHs metabolites with adjustment for age, gender, body mass index, drinking, blood cell counts, and surrogate variables in each panel separately, and combined the results by using inverse-variance weighted fixed-effect meta-analysis to obtain estimates of effect size. The median value of total OH-PAHs ranged from 0.92 × 10⁻² in SY panel (62.6% men) to 13.82 × 10⁻² μmol/mmol creatinine in COW panel (43.4% men). The results showed that methylation levels of cg18223625 (COL20A1) and cg07805771 (SLC16A1) were significantly or marginally significantly associated with urinary 2-hydroxynaphthalene [β(SE) = 0.431(0.074) and 0.354(0.068), FDR = 0.016 and 0.056, respectively], while methylation level of cg09235308 (PLEC1) was positively associated with urinary total OH-PAHs [β(SE) = 0.478(0.079), FDR = 0.004]. Hypermethylations of cg18223625, cg07805771, and cg09235308 were inversely associated with HRV indices among the WHZH and COW non-current smokers. However, we did not observe significant epigenome-wide associations for the other 9 urinary OH-PAHs. These findings provide new evidence that PAHs exposure is linked to differential DNA methylation, which may help better understand the influences of PAHs exposure on HRV alternations.

Urban environments are characterized by multiple exposures that may influence body mass index (BMI) growth in early life. Previous studies are few, with inconsistent results and no evaluation of simultaneous exposures. Thus, this study aimed to assess the associations between exposure to air pollution, green spaces and built environment characteristics, and BMI growth trajectories from 0 to 5 years. This longitudinal study used data from an electronic primary care health record database in Catalonia (Spain), including 79,992 children born between January 01, 2011 and December 31, 2012 in urban areas and followed until 5 years of age. Height and weight were measured frequently during childhood and BMI (kg/m²) was calculated. Urban exposures were estimated at census tract level and included: air pollution (nitrogen dioxide (NO₂), particulate matter <10 μm (PM₁₀) and <2.5 μm (PM₂.₅₎), green spaces (Normalized Difference Vegetation Index (NDVI) and % green space) and built environment (population density, street connectivity, land use mix, walkability index). Individual BMI trajectories were estimated using linear spline multilevel models with several knot points. In single exposure models, NO₂, PM₁₀, PM₂.₅, and population density were associated with small increases in BMI growth (e.g. β per IQR PM₁₀ increase = 0.023 kg/m², 95%CI: 0.013, 0.033), and NDVI, % of green spaces and land use mix with small reductions in BMI growth (e.g. β per IQR % green spaces increase = −0.015 kg/m², 95%CI: −0.026, −0.005). These associations were strongest during the first two months of life. In multiple exposure models, most associations were attenuated, with only those for PM₁₀ and land use mix remaining statistically significant. This large longitudinal study suggests that early life exposure to air pollution, green space and built environment characteristics may be associated with small changes in BMI growth trajectories during the first years of life, and that it is important to account for multiple exposures in urban settings.

Mosaic loss of chromosome Y (mLOY) is the most common structure somatic event that related to increased risks of various diseases and mortality. Environmental pollution and genetic susceptibility were important contributors to mLOY. We aimed to explore the associations of polycyclic aromatic hydrocarbons (PAHs) exposure, as well as their joint effects with age, smoking, and genetic variants on peripheral blood mLOY. A total of 1005 male coke-oven workers were included in this study and their internal PAHs exposure levels of 10 urinary PAH metabolites and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts were measured. mLOY was defined by the median log R ratio(mLRR) of 1480 probes in male-specific region of chromosome-Y from genotyping array. We found that the PAHs exposure levels were linearly associated with mLOY. A 10-fold increase in urinary 1-hydroxynaphthalene (1-OHNa), 1-hydroxyphenanthrene (1-OHPh), 2-OHPh, 1-hydroxypyrene (1-OHP), ΣOH-PAHs, and plasma BPDE-Alb adducts could generate 0.0111, 0.0085, 0.0069, 0.0103, 0.0134, and 0.0152 decrease in mLRR-Y, respectively. Additionally, mLOY accelerated with age, smoking pack-years, and TCL1A rs1122138-C allele, and we observed the most severe mLOY among subjects carrying more than 3 of the above risk factors. Our results revealed the linear dose-effect associations between PAHs exposure and mLOY. Elder male smokers carrying rs1122138CC genotype were the most susceptible subpopulations to mLOY, who should be given protections for PAHs exposure induced chromosome-Y aberration.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.

The associations between bisphenol analogues (BPs) exposure and oxidative damage was explored in this 3-year longitudinal study of 275 school children in East China. Nine BPs in first morning urine samples were measured to assess BPs exposure, and 8-hydroxydeoxyguanosine (8-OHdG) and 8-oxo-7,8-dihydroguanosine (8-OHG) were measured as biomarkers of oxidative DNA and RNA damage. Linear mixed model (LMM) was used for repeated measures analysis. School children were mainly exposed to BPA, BPS, BPF, and BPAF (detection frequencies: 97.9%, 42.2%, 13.3%, and 12.8%) with median concentrations of 1.55, 0.355, 0.236 and 0.238 μg g⁻¹Cᵣₑ, respectively. An interquartile range (IQR) increase in urinary BPA was significantly associated with 12.9% (95% CI: 6.1%, 19.6%) increase in 8-OHdG and 19.4% (95% CI: 11.7%, 27.1%) increase in 8-OHG, and for total of BPs (the sum of BPA, BPS, BPF, and BPAF), they were 17.4% (95% CI: 8.9%, 26.0%) for 8-OHdG and 25.9% (95% CI: 16.1%, 35.7%) for 8-OHG, respectively. BPS was positively associated with 8-OHG, but not with 8-OHdG. The study found positive associations of urinary levels of BPA and total BPs with 8-OHdG and 8-OHG and indicated that BPs exposure might cause oxidative RNA damage.

Breast cancer is the most frequent tumor in women worldwide, although well-established risk factors account for 53%–55% of cases. Therefore, other risk factors, including environmental exposures, may explain the remaining variation. Our objective was to assess the relationship between risk of breast cancer and residential proximity to industries, according to categories of industrial groups and specific pollutants released, in the context of a population-based multicase-control study of incident cancer carried out in Spain (MCC-Spain). Using the current residence of cases and controls, this study was restricted to small administrative divisions, including both breast cancer cases (452) and controls (1511) in the 10 geographical areas recruiting breast cancer cases. Distances were calculated from the respective woman's residences to the 116 industries located in the study area. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (95%CIs) for categories of distance (between 1 km and 3 km) to industrial plants, adjusting for matching variables and other confounders. Excess risk (OR; 95%CI) of breast cancer was found near industries overall (1.30; 1.00–1.69 at 3 km), particularly organic chemical industry (2.12; 1.20–3.76 at 2.5 km), food/beverage sector (1.87; 1.26–2.78 at 3 km), ceramic (4.71; 1.62–13.66 at 1.5 km), surface treatment with organic solvents (2.00; 1.23–3.24 at 3 km), and surface treatment of plastic and metals (1.51; 1.06–2.14 at 3 km). By pollutants, the excess risk (OR; 95%CI) was detected near industries releasing pesticides (2.09; 1.14–3.82 at 2 km), and dichloromethane (2.09; 1.28–3.40 at 3 km). Our results suggest a possible increased risk of breast cancer in women living near specific industrial plants and support the need for more detailed exposure assessment of certain agents released by these plants.

The last decades have seen the increasing prevalence of thyroid disorders. These augmentations could be the consequence of the increasing contamination of the environment by chemicals that may disrupt the thyroid function. Indeed, in vitro studies have shown that many chemicals contaminating our environment and highlighted in human serum, are able to interfere with the thyroid function. Given the crucial importance of thyroid hormones on neurodevelopment in fetus and newborns, the influence of these pollutants on newborn thyroid homeostasis is a major health concern. Unfortunately, the overall evidence for a deleterious influence of environmental pollutants on thyroid remains poorly studied. Therefore, we assessed the contamination by polychlorinated biphenyls (PCBs), organochlorine pesticides and perfluorinated compounds (PFC) in 221 cord blood samples collected in Belgium between 2013 and 2016. Our results showed that compared to previous studies performed on newborns recruited in Belgium during the two last decades, the present pollutant contamination is declining. Multivariate statistical analyses pointed out a decrease of thyroid stimulating hormone (TSH) level in male newborns with detectable level of 4,4′- dichlorodiphenyldichloroethylene (4,4′-DDE) in comparison with those with no detectable level (p = 0.025). We also highlighted a negative association between perfluorononanoic acid (PFNA) concentration and TSH in male newborns (p = 0.018). Logistic regression showed increased odds ratio for presentation of hypothyroid in mother for each one unit augmentation of log natural concentration of PFOA (OR = 2.30, [1.18–4.5]) and PFOS (OR = 2.03 [1.08–3.83]). Our findings showed that the residual contamination by PFCs and organochlorine pollutants in cord blood are correlated with thyroid hormone in the newborns and the risk of hypothyroid in mothers.