Bisphenol S is an endocrine disruptor exhibiting metabolic disturbances, especially following perinatal exposures. To date, no data are available on the obesogen effects of BPS in a mutligenerational issue.We investigated obesogen effects of BPS in a multigenerational study by focusing on body weight, adipose tissue and plasma parameters in male and female mice.Pregnant C57BL6/J mice were exposed to BPS (1.5 μg/kg bw/day ie a human equivalent dose of 0.12 μg/kg bw/day) by drinking water from gestational day 0 to post natal day 21. All offsprings were fed with a high fat diet during 15 weeks. Body weight was monitored weekly and fat mass was measured before euthanasia. At euthanasia, blood glucose, insuline, triglyceride, cholesterol and no esterified fatty acid plasma levels were determined and gene expressions in visceral adipose tissue were assessed. F1 males and females were mated to obtain the F2 generation. Likewise, the F2 mice were cross-bred to obtain F3. The same analyses were performed.In F1 BPS induced an overweight in male mice associated to lipolysis gene expressions upregulation. In F1 females, dyslipidemia was observed. In F2, BPS exposure was associated to an increase in body weight, fat and VAT masses in males and females. Several plasma parameters were increased but with a sex related pattern (blood glucose, triglycerides and cholesterol in males and NEFA in females). We observed a down-regulation in mRNA expression of gene involved in lipogenesis and in lipolysis for females but only in the lipogenesis for males. In F3, a decrease in VAT mass and an upregulation of lipogenesis gene expression occurred only in females.BPS perinatal exposure induced sex-dependent obesogen multigenerational effects, the F2 generation being the most impacted. Transgenerational disturbances persisted only in females.

Organochlorine pesticides (OCPs), including dichlorodiphenyltrichloroethane (DDT) and its metabolites [dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane], hexachlorocyclohexanes (HCHs), and hexachlorobenzene (HCB), are widely detected in humans despite the considerable decline in environmental concentrations. To understand the placental transfer of OCPs and the possible maternal influence on them, we measured the concentrations of DDTs, HCHs, and HCB in 102 paired samples of maternal and cord sera, and placentas collected in Shanghai, China. The median concentrations of DDTs and HCHs were the highest in maternal sera (601, 188 ng g⁻¹ lipid), followed by umbilical cord sera (389, 131 ng g⁻¹ lipid), and placentas (65, 37 ng g⁻¹ lipid). 4,4′-DDE, β-HCH, and HCB were the predominant contaminants in the three matrices. The ubiquitous existence of OCPs, and the significant concentration relationships of DDTs, HCHs, and OCPs in the three matrices suggested placental transfer from mother to fetus. The lipid-based concentration ratios of 4,4′-DDE, β-HCH, and HCB in umbilical cord serum to those in maternal serum (F/M), and ratios of placenta to maternal serum (P/M) ranged from 0.66 to 1.01, and 0.12 to 0.25, respectively. Maternal variables affected the levels of fetal contamination. For primiparous women, significant correlations between maternal age and maternal HCHs, and between pre-pregnancy body mass index (BMI) and maternal HCHs were found. The negative effect of parity, and the positive effect of food consumption on maternal OCP concentrations were also observed, although there were no significant differences. The possible influence of parity on F/M and P/M of 4,4′-DDE suggested borderline significant differences between primiparous and multiparous women. Also, slight group differences were observed between elder and younger women, and between overweight and normal/underweight women. Parity seems to have a potential influence on transfer ratios of some OCP pollutants.

Few studies have investigated the effect of personal PM₂.₅ and PM₁ exposures on heart rate variability (HRV) for a community-based population, especially in Asia. This study evaluates the effects of personal PM₂.₅ and PM₁ exposure on HRV during two seasons for 35 healthy adults living in an urban community in Taiwan. The low-cost sensing (LCS) devices were used to monitor the PM levels and HRV, respectively, for two consecutive days. The mean PM₂.₅ and PM₁ concentrations were 13.7 ± 11.4 and 12.7 ± 10.5 μg/m³ (mean ± standard deviation), respectively. Incense burning was the source that contributed most to the PM₂.₅ and PM₁ concentrations, around 9.2 μg/m³, while environmental tobacco smoke exposure had the greatest impacts on HRV indices, being associated with the highest decrease of 20.2% for high-frequency power (HF). The results indicate that an increase in PM₂.₅ concentrations of one interquartile range (8.7 μg/m³) was associated with a change of −1.92% in HF and 1.60% in ratio of LF to HF power (LF/HF). Impacts on HRV for PM₁ were similar to those for PM₂.₅. An increase in PM₁ concentrations of one interquartile range (8.7 μg/m³) was associated with a change of −0.645% in SDNN, −1.82% in HF and 1.54% in LF/HF. Stronger immediate and lag effects of PM₂.₅ exposure on HRV were observed in overweight/obese subjects (body mass index (BMI) ≥24 kg/m²) compared to the normal-weight group (BMI <24 kg/m²). These results indicate that even low-level PM concentrations can still cause changes in HRV, especially for the overweight/obese population.

This study aims to examine the association between short-term exposure to ambient PM₁, PM₁₋₂.₅, and PM₂.₅ and forced vital capacity (FVC). Population data were obtained from a school-based cross-sectional survey in Shandong in 2014. Distributed lag non-linear models were used to examine the association between exposure to PM₁, PM₁–₂.₅, and PM₂.₅ and FVC at the day of FVC measurement and the previous 6 days (lag 0 to 6 days). A total of 35,334 students aged 9 to 18 years were included in the study, and the mean exposure concentrations of ambient PM₁, PM₁–₂.₅, and PM₂.₅ for them were 47.4 (standard deviation [SD] = 21.3) μg/m³, 32.8 (SD = 32.2) μg/m³, and 80.1 (SD = 47.7) μg/m³, respectively. An inter-quartile range (IQR, 24 μg/m³) increment in exposure to PM₁ was significantly associated with a lower FVC at lag 0 and lag 1 day (β = − 80 mL, 95% CI = − 119, − 42, and β = − 37 mL, 95% CI = − 59, − 16, respectively), and an IQR (54 μg/m³) increment in exposure to PM₂.₅ was significantly associated with a lower FVC at lag 0 and lag 1 day (β = − 57 mL, 95% CI = − 89, − 18, and β = − 34 mL, 95% CI = − 56, − 12, respectively) after adjustment for gender, age, body mass index category, residence, month of the survey, intake of eggs, intake of milk, physical activity, and screen time. No significant associations were observed for PM₁–₂.₅. The inverse associations of PM₁ and PM₂.₅ with FVC were larger in males, younger children, those overweight or obese, and those with insufficient physical activity levels. Short-term exposure to ambient PM₁ and PM₂.₅ was associated with decreased FVC, and PM₁ may be the primary fraction of PM₂.₅ causing the adverse pulmonary effects. Our findings emphasize the need to address ambient PM, especially PM₁, pollution for affecting pulmonary health in children and adolescents.

The production and emission of short-chain perfluoroalkyl acids (PFAAs) has increased over the years to replace long-chain PFAAs, leading to frequent detection in the environment and raising global concerns about the potential impacts on human health. In this study, the specific urine levels of 10 PFAAs were obtained from 189 children (age 8–12 years) from two primary schools located in urban and suburban areas of Shanghai in 2019, and the contributions of dietary factors were investigated. Perfluorohexanoic acid (PFHxA), perfluoroheptanoic acid (PFHpA), and perfluorobutane sulfonate (PFBS) were detected in 100%, 99.5%, and 87.3% of the samples, with median concentrations of 20.20 ng/L, 46.50 ng/L, and 20.95 ng/L, respectively. The most abundant PFAA was perfluorooctanoic acid (PFOA), with a median concentration of 78.90 ng/L. The concentration of ∑PFAAs ranged from 61.10 to 4108.93 ng/L, with a median concentration of 253.12 ng/L. Children aged 8–9 years had higher median levels of PFBS, perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS) than children aged 10–12 years. Obese/overweight children had lower levels of PFHpA, PFBS, and PFOS. The intake of red meats, tubers, sugared beverages, fish and seafood, and eggs contributed to higher concentrations of PFAAs, while frequent intake of poultry and soy milk was associated with lower PFAA concentrations.

Animal studies indicated that bisphenol A (BPA) exposure during pregnancy may disrupt thyroid function which is critical for fetal development. However, few epidemiological studies have examined this topic and the results were inconsistent. We aimed to evaluate whether prenatal BPA exposure is associated with thyroid hormone levels in Chinese mothers and newborns with stratification by maternal body mass index (BMI). BPA concentration were measured in urine samples collected from 555 women at late pregnancy. Maternal serum free thyroxin (FT4), thyroid-stimulating hormone (TSH) and thyroid peroxidase antibody (TPO-Ab) concentrations at the third trimester were abstracted from medical records. Cord serum-free triiodothyronine (FT3), FT4, TSH, and TPO-Ab levels were measured in 398 newborns. Prenatal urinary BPA was detected in 98.5% of mothers with a geometric mean of 1.32 ng/mL (95% CI 1.17–1.49 ng/mL). With each 10-fold increase in BPA concentrations, maternal log10_(TSH) mIU/L was 0.10 lowered (95% CI − 0.20, − 0.005, p < 0.05) among pre-pregnancy BMI > 23 kg/m², with adjustment for maternal age, maternal education, gestation diabetes mellitus (GDM), husband smoking during pregnancy, parity, and gestational age at thyroid parameters measured, but no association was observed in pre-pregnancy BMI < 18.5, or 18.5–22.9 kg/m² stratum. No BPA-associated changes were observed in maternal FT4 level or odds of positive TPO-Ab in all BMI stratum. Also, no associations were observed between prenatal urinary BPA concentration and cord serum FT4, FT3, TSH levels, and odds of positive TPO-Ab in both male and female newborns among pre-pregnancy BMI < 18.5, 18.5–22.9 or > 23 kg/m² stratum. In this study, prenatal urinary BPA concentration was associated with lower maternal TSH among women with overweight, but not associated with other maternal thyroid parameters or cord serum thyroid parameters across maternal BMI categories. More research on pregnant women and newborns cohort with BPA exposure are warranted.

Several negative health effects have been associated with environmental pollution. Coal mining activities are related to DNA damage. However, the impact of lifestyle as well as environmental exposure must be considered when evaluating the extent of DNA damage. The aim of this cross-sectional study was to analyze nutritional status, dietary patterns, and the prevalence of non-communicable diseases (CNCDs) among coal miners as well as to investigate the correlation of these variables with DNA damage. We used a questionnaire to assess demographics, health, and dietary habits. The nutritional status was measured in terms of BMI (body mass index) and DNA damage was assessed by the comet assay. The sample population was composed of 158 coal miners from the largest coal mining company in South of Brazil, and majority of them were classified as overweight (51.3%) or obese (28.5%). Hypertension was the most common CNCD (50.6%) and a majority of these workers consumed all groups of foods three or more times a week. There was a significant positive correlation between BMI and DNA damage (r = 0.1646, p = 0.04) and this association was stronger (r = 0.2556, p = 0.04) in coal miners with some CNCD. There was no significant correlation between dietary patterns and DNA damage in coal miners. These results suggest that the nutritional status and CNCD increase the extent of DNA damage in coal miners. Since this population is at high occupational risk, specific strategies should be designed to improve the health of these workers, aiming to achieve health equity.

Diabetics may be more vulnerable to the harmful effects of ambient air pollutants than healthy individuals. But, the risk factors that lead to susceptibility to air pollution in diabetics have not yet been identified. We examined the effect of exposure to ambient PM₁₀ on chronic symptoms and the pulmonary function tests (PFT) in diabetic and non-diabetic subjects. Also, to investigate possible determinants of susceptibility, we recruited 400 type 2 diabetic and 465 healthy subjects who were investigated for chronic respiratory symptoms (CRSs) and then underwent measurement of forced vital capacity (FVC) and forced expiratory volume 1 (FEV1) according to standard protocol. Percent predicted FEV1 and FVC (FEV1% and FVC%, respectively) for each subject were calculated. Particulate matter (PM₁₀) concentrations at residence place of subjects were estimated using AERMOD dispersion model. The association between PM₁₀ and CRSs was explored using logistic regression. We also used linear regression models controlling for potential confounders to study the association between chronic exposure to PM₁₀ and FEV1% and FVC%. Prevalence of current wheezing, allergy symptom, chest tightness, FEV1/FVC <70%, and physician-diagnosed asthma and COPD was significantly higher among diabetic subjects than non-diabetics. There was no significant difference between percent predicted value of PFT among diabetic and non-diabetic subjects (P < 0.05). We estimated that 1 SD increase in PM₁₀ concentration was associated with a greater risk of having dyspnea by 1.50-fold (95% CI, 1.12–2.01). Higher exposure to PM₁₀ concentration was also significantly associated with lower FVC%. The size of effect for 1 SD μg/m³ (=98.38) increase in PM₁₀ concentration was 3.71% (95% CI, 0.48–4.99) decrease in FVC%. In addition, we indicated that strength of these associations was higher in overweight, smoker, and aged persons. We demonstrated a possible contribution of air pollution to reduced lung function independent of diabetes status. This study suggests that decline in exposure may significantly reduce disease manifestation as dyspnea and impaired lung function. We conduct that higher BMI, smoking, and older age were associated with higher levels of air pollution effects.

Bisphenol A (BPA) is an ubiquitous chemical, which is an endocrine disruptor. Recent epidemiological studies have suggested a relationship between BPA exposure and body weight. However, most of these studies were cross-sectional and not on elderly people. We conducted a panel study with repeated measurements to evaluate the relationship between BPA and overweight in elderly people. A total of 560 elderly participants aged ≥60 years were recruited in Seoul from 2008 to 2010. Urinary BPA levels and body mass index (BMI, kg/m²) were measured at every visit. We defined a BMI ≥25 as overweight and examined the relations between urinary BPA and BMI or overweight. Repeated measures analysis was performed after adjusting for age, sex, low-density lipoprotein cholesterol levels, alcohol consumption, regular exercise, total calorie intake, fatty acid intake, urinary cotinine levels, and the status of diabetes mellitus. The geometric mean of BPA was 0.67 μg/g creatinine. The odds ratio (OR) of overweight was 1.17 (95 % confidence interval [CI] 1.04–1.32) per interquartile range increase of log-transformed BPA. When stratified based on sex, we observed a significant association in women (OR 1.25; 95 % CI 1.09–1.45) but not in men (OR 0.97; 95 % CI 0.77–1.22). The ORs of overweight increased with quartiles of BPA in women (quartile 2 vs 1: OR 1.54; 95 % CI 1.02–2.32, 3 vs 1: OR 1.70; 95 % CI 1.10–2.62, and 4 vs 1: OR 1.81; 95 % CI 1.13–2.92). Our results suggest that urinary BPA levels are significantly associated with overweight in elderly women but not elderly men.