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A municipal waste incinerator (MWI) in Zhejiang, China, operating since 2008 was completely reconstructed from 2016 to 2019. In 2013, we conducted a cross-sectional study of breastfeeding mothers living near the MWI. We evaluated the concentrations of polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in the mothers' breast milk and their infants' estimated daily intake (EDI). To investigate the temporal variations of these pollutants, we conducted a cross-sectional study of 29 mothers in 2019. We assessed the levels of 18 PCB congeners, 17 PCDD/F congeners, and 21 per- and polyfluoroalkyl substance (PFAS) congeners in breast milk and estimated the EDI. The mean total concentrations of PCDD/Fs (ΣPCDD/Fs) and PCBs (ΣPCBs) were 81.2 and 4.90 ng/g lipid, respectively, while the toxic equivalent quantity (TEQ) levels of ΣPCDD/Fs and dioxin-like PCBs (ΣDL-PCBs) were 2.7 and 1.4 pg WHO-TEQ/g lipid, respectively. Compared to our 2013 measurements, the mass concentrations of ΣPCDD/Fs and ΣPCBs decreased by 13% and 35%, respectively (3.361 vs. 2.915 pg/g wet weight [ww] and 269.1 vs. 175.0 pg/g ww, respectively). The TEQ-ΣPCDD/F levels decreased by 67% (0.241 vs. 0.080 pg/g ww), but the TEQ-ΣDL-PCB levels increased by 11% (0.046 vs. 0.051 pg WHO-TEQ/g ww). The median concentration of PFASs was 0.250 ng/mL, ranging from 0.151 to 0.833 ng/mL. The infants' mean EDI of total PCDD/Fs and DL-PCBs was 17.7 pg TEQ/kg body weight [bw], representing a 20% decline compared to 2013. The average EDI levels of PFOS, PFOA, and PFNA were 5.8, 17.9, and 1.7 ng/kg bw, respectively. A comprehensive comparison of the results with studies from around the world showed that the potential health risks posed by legacy PCDD/F and PCB pollutants were not as grave for mothers and infants living near this MWI, but the emerging PFAS pollutants represented a new cause for concern. MAIN FINDINGS: The potential health risks posed by legacy PCDD/F and PCB pollutants were not particularly serious for mothers and infants living near the MWI, but the emerging PFAS pollutants raised new concerns.

This study aimed to evaluate the body burdens of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and their associated health impacts toward school-age children living near a municipal waste incinerator (MWI). A total of 82 children from the exposure area and 49 from the control area were recruited. We measured blood PCDD/F levels, conducted comet assays, calculated the percentage of 5-methylcytosine (%5-mC) and 5-hydroxymethylcytosine (%5-hmC), performed flow cytometry, measured hormonal levels, and analyzed hematological parameters. We also examined 17 congeners of PCDD/Fs in environmental samples, namely, eggs, rice, water, soil, and PM2.5. The mean blood levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs were statistically higher in the exposure group than in the control group (3.40 vs. 2.77 pg/g wet weight and 0.40 vs. 0.28 pg WHO-TEQ/g wet weight, respectively; p 0.05). Furthermore, the mean ΣPCDD/F levels in eggs and soil obtained from the exposure area were statistically higher than those of the samples obtained from the control area (31.08 vs. 4.32 pg/g dry weight and 1026.04 vs. 674.97 pg/g dry weight, respectively). In conclusion, children living near the MWI may suffer genetic and epigenetic modifications, such as DNA damage or global DNA hypomethylation due to the MWI-emitted PCDD/Fs and other contaminants.

To evaluate the body burdens of heavy metals correlated with health impact on school-age children living around a waste incinerator. A total of 81 children from the exposure area and 95 from the control area were recruited in our study. We measured the blood levels of chromium (Cr), cadmium (Cd) and lead (Pb) by an inductively coupled plasma mass spectrometer (ICP-MS), conducted comet assays, calculated the percentage of 5-methylcytosine (5 mC) and 5-hydroxymethylcytosine (5hmC) by MethylFlash methylated and a hydroxymethylated DNA quantification kit, and performed the flow cytometry to detect the expressions of surface antigens (including CD3+, CD19+, CD3+CD4+, CD3+CD8+, and CD3−CD16+ and/or CD56+) in peripheral lymphocytes. Besides, we measured hormonal levels, including triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH), and analyzed several regular hematological parameters. In addition, concentrations of heavy metals in environmental samples including rice, soils, vegetables, and drinking water were detected by ICP-MS. The mean blood levels of Cr, Cd, and Pb in the exposure group were all statistically higher than in the control group (2.57 vs. 0.79 μg/L; 1.83 vs. 1.81 μg/L; 44.00 vs. 32.31 μg/L, p

To monitor the body burden of persistent organic pollutants in mothers and infants living in proximity to a 10-year-old municipal waste incinerator (MWI), levels of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) in the breast milk of mothers were evaluated, and the estimated daily intake (EDI) level of these pollutants in infants was assessed. In total, 14 mothers from the exposure area and 18 mothers from a control area were recruited for this study. In addition, the levels of 17 PCDD/F congeners and 18 PCB congeners in the breast milk of the mothers were estimated, and risk assessment for their infants by calculating their EDI levels was performed. The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs in the breast milk of the exposure group were significantly greater than those of the control group (3.36 vs. 1.47 pg/g wet weight; and 0.24 vs. 0.12 pg TEQ/g wet weight, respectively; p 0.05). With respect to PCBs, the mean levels of the total PCBs (ΣPCBs) and non-dioxin like-PCBs (ΣNDL-PCBs) in the exposure group were significantly greater than those in the control group (269 vs. 141 pg/g wet weight; 230 vs. 115 pg/g wet weight, respectively; p 0.05). The mean levels of ΣPCDD/Fs and TEQ-ΣPCDD/Fs were positively correlated with the inhabit time of the exposure group (r = 0.636, r = 0.629, p 0.05, respectively). The mean EDI level of the exposure group in infants was significantly greater than that of the control group (22.0 vs. 13.0 pg TEQ/kg bw day; p 0.05). In conclusion, mothers and their breast-fed infants living in proximity to the 10-year-old MWI located in the Zhejiang Province of China exhibited a significantly higher body burden of PCDD/Fs and PCBs compared to those living in the control area.

Epidemiological evidence linking metals bound to ambient particulate matters with aerodynamic diameter less than 2.5 μm (PM

Air pollution could be a risk factor for the development of pterygium. This study aimed to investigate the potential associations between outpatient visits for pterygium and air pollutants. Using a time-stratified case-crossover design, the data of 3017 outpatients with pterygium visiting an eye center in Hangzhou, China, and the air pollution data of the Environmental Protection Department of Zhejiang Province between July 1, 2014, and November 30, 2019, were examined. The relationships between the air pollutants nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone, and fine particulate matter (PM) with median aerometric diameter

Previous studies have found that fine particulate matter (PM2.5) air pollution is associated with decreased lung function. However, most current research focuses on children with asthma, leading to small sample sizes and limited generalization of results. The current study aimed to measure the short-term and lag effects of PM2.5 among school-aged children using repeated measurements of lung function.This prospective panel study included 848 schoolchildren in Zhejiang Province, China. Each year from 2014–2017, two lung function tests were conducted from November 15th to December 31st. Daily air pollution data were derived from the monitoring stations nearest to the schools. A mixed-effects regression model was used to investigate the relationship between PM2.5 and lung function. The effect of PM2.5 on lung function reached its greatest at 1-day moving average PM2.5 exposure. For every 10 μg/m3 increase in the 1-day moving average PM2.5 concentration, Forced Vital Capacity (FVC) of children decreased by 33.74 mL (95% CI: 22.52, 44.96), 1-s Forced Expiratory Volume (FEV1) decreased by 32.56 mL (95% CI: 21.41, 43.70), and Peak Expiratory Flow (PEF) decreased by 67.45 mL/s (95% CI: 45.64, 89.25). Stronger associations were found in children living in homes with smokers. Short-term exposure to PM2.5 was associated with reductions in schoolchildren’s lung function. This finding indicates that short-term exposure to PM2.5 is harmful to children’s respiratory health, and appropriate protective measures should be taken to reduce the adverse effects of air pollution on children’s health.

To take an insight into the long-term accumulation of chromium (Cr) and cadmium (Cd) in school-age children living near an MWI and to assess their early renal impairment, we conducted a cross-sectional study in 2015. A total of 116 children from the exposure area and 122 from the control area were recruited. We measured the urinary levels of Cr (U-Cr) and Cd (U-Cd) by inductively coupled plasma mass spectrometry (ICP-MS), and detected three classic renal tubule indicators, including N-acetyl-β-d-glucosaminidase (NAG), β2-microglobulin (BMG), and retinol binding protein (RBP). The U-Cd and U-Cr levels in children living near the MWI were 0.11 and 1.57 μg/g creatinine, respectively. Both the U-Cd and U-Cr levels in the exposure group were lower than those in the control group, although only U-Cd showed a statistical difference (p < 0.01). The U-NAG and U-RBP levels in the exposure group were also statistically lower than those in the control group (0.80 vs. 1.74 IU/g creatinine, 0.26 vs. 0.48 mg/g creatinine, respectively). The U-Cd level in this study was positively correlated with the U-NAG level (r = 0.26, p < 0.01), as the U-Cr level was also positively correlated with the levels of U-NAG, U-RBP, and U-BMG (r = 0.21, 0.33, 0.18, p < 0.01, respectively). This study indicates that children living close to this particular MWI may not suffer considerable long-term accumulation of Cd or Cr, nor early renal impairment.

Enhanced osteoclast formation and function have essential roles during post‑menopausal osteoporosis. A number of cytokines have been reported to regulate osteoclastogenesis and to be involved during the pathogenesis of osteoporosis. However, the regulation of osteolysis by microRNAs (miRNAs) has remained to be fully elucidated. The present study used a microarray analysis to identify a variety of miRNAs that are differentially expressed during osteoclast formation. Six down‑regulated miRNAs, miR‑21a‑5p, miR‑27a‑3p, let‑7i‑5p, miR‑22‑3p, miR‑340‑5p and miR‑23a‑5p, whose molecular mechanisms during osteoclast differentiation have not been reported previously, were further assessed. Using an osteoclast formation assay and a mouse model of progressive osteoporosis, the downregulation of these miRNAs was validated in vitro and in vivo. Of note, the expression patterns of these six miRNAs were associated with the progression of osteoporosis. Therefore, these miRNAs are of potential diagnostic and therapeutic value for osteolytic diseases.

The objective of this study was to investigate the potential association between air pollutants and respiratory diseases (RDs). Generalized additive models were used to analyze the effect of air pollutants on mortalities or outpatient visits. The average concentrations of air pollutants in Hangzhou (HZ) were 1.6–2.8 times higher than those in Zhoushan (ZS), except for O3. In a single pollutant model, the increased concentrations of PM2.5, NO2, and SO2 were strongly associated with deaths caused by RD in HZ, while PM2.5 and O3 were associated with deaths caused by RD in ZS. All air pollutants (PM2.5, NO2, SO2, and O3) were strongly associated with outpatient visits for RD in both HZ and ZS. In multiple pollutant models, a significant association was only observed between PM2.5 and the mortality rate of RD patients in both HZ and in ZS. Moreover, strong associations between SO2, NO2, and outpatient visits for RD were observed in HZ and ZS. This study has provided evidence that both the mortality rates and outpatient visits for RD were significantly associated with air pollutants. Furthermore, the results showed that different air pollutant levels lead to regional differences between mortality rates and outpatient visits.

The purpose of this study is to investigate the potential associations between air pollution and dry eye disease (DED). Data of outdoor air pollutants and meteorology as well as outpatient visits for DED were collected. A time-stratified case-crossover approach was used to analyze the associations between ambient air pollutants and outpatient visits for DED. Among the 5062 DED patients studied, 65.45% were female and 34.55% were male. In the single-pollutant model, significant associations were observed between an increase of 10 μg/m3 in the concentrations of fine-particulate matter with a median aerometric diameter of less than 10 μm (PM10), fine-particulate matter with a median aerometric diameter of less than 2.5 μm (PM2.5), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO) and outpatient visits for DED. These results were consistent with those of the multipollutant model. The strongest associations between air pollutants and patient visits were observed during the cold season and in patients aged 21–40. The significant association between air pollutants (PM10, PM2.5, SO2, NO2, and CO) and DED outpatient visits indicates the importance of increased environmental protection.

BACKGROUND Conjunctivitis, one of the most common ocular surface diseases, can be caused by many factors. OBJECTIVES The objective of this study was to investigate the potential association between conjunctivitis and air pollutants. MATERIALS AND METHODS Data of 9737 outpatient visits for conjunctivitis from July 1, 2014 to June 30, 2016 were obtained from the Eye Center of the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China. The data were linked to data on the concentrations of carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and fine particulate matter with a median aerometric diameter of less than 10 and 2.5 μm (PM10 and PM2.5, respectively), which were obtained from the Environmental Protection Department of Zhejiang Province. A time-stratified case-crossover study design and conditional logistic regression were applied to analyze the association between air pollutants and outpatient visits for conjunctivitis. RESULTS A 10 μg/m3 increase in PM10, PM2.5, SO2, NO2, and CO concentrations on the same day as the hospital visit or on lag days before the hospital visit date was associated with outpatient visits for conjunctivitis. The strongest association was observed between SO2 and conjunctivitis patients aged 2–5 years. Variation occurs between warm and cold seasons, between genders, and among different age groups. CONCLUSIONS Our study provided evidence that outpatient visits for conjunctivitis were significantly associated with air pollution in Hangzhou, China.

Increased electronic waste (e-waste) has raised public concerns regarding exposure to numerous toxic contaminants, particularly polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs). In China, the body burdens of PCBs, PBDEs and PCDD/Fs are associated with thyroid hormones in populations from e-waste dismantling sites; however, it is unclear whether this association occurs in children. In this study, we determined the serum levels of PCBs, PBDEs and PCDD/Fs and the endocrine hormones including free triiodothyronine (FT3), total triiodothyronine (TT3), free thyroxine (FT4), total thyroxine (TT4), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), cortisol and growth hormone (GH) in 21 children from an e-waste dismantling area and 24 children from a control area. The results showed that the mean levels of ∑PCBs and ∑PBDEs in the exposure group were significantly higher than in the control group (40.56 and 32.09 ng g(-1) lipid vs. 20.69 and 8.43 ng g(-1) lipid, respectively, p0.01 for each), and the mean level of ∑PCDD/Fs in the exposure group was higher than in the control group, but the difference was not significant (206.17 vs. 160.27 pg g(-1) lipid, p0.05). For the endocrine hormones, we did not find significant differences between the exposed and control groups, although the mean levels of FT3, TT3, TT4, ACTH, cortisol and GH were higher, whereas the mean levels of FT4 and TSH were lower in the exposed group. The mean level of ∑PBDEs was positively correlated with the mean levels of ∑PCBs (r=0.60, p0.05) and ∑PCDD/Fs (r=0.61, p0.05). Furthermore, the mean level of ∑PBDEs was positively correlated with ACTH (r=0.61, p0.05). In conclusion, our data suggested that exposure to e-waste dismantling environment increased the body burdens of PCBs and PBDEs in local children and that these contaminants released from the e-waste might contribute to abnormal changes in hormone levels.

Non-small cell lung cancer (NSCLC) is related to the genetic and epigenetic factors. The goal of this study was to determine association of cigarette smoking and BPDE-DNA adducts with promoter methylations of several genes in NSCLC. Methylation of the promoters of p16, RARβ, DAPK, MGMT, and TIMP-3 genes of tumor tissues from 199 lung cancer patients was analyzed with methylation-specific PCR (MSP), and BPDE-DNA adduct level in lung cancer tissue was obtained by ELISA. Level of BPDE-DNA adduct increased significantly in males, aged people (over 60 years), and smokers; however, no significant difference was found while comparing the BPDE-DNA adduct levels among different tumor types, locations, and stages. Cigarette smoking was also associated with increased BPDE-DNA adducts level (OR = 2.43, p > .05) and increased methylation level in at least 1 gene (OR = 5.22, p < .01), both in dose-response manner. Similarly, cigarette smoking also significantly increase the risk of p16 or DAPK methylation (OR = 3.02, p < .05 for p16, and 3.66, p < .05 for DAPK). The highest risk of BPDE-DNA adducts was detected among individuals with cigarette smoking for more than 40 pack-years (OR = 4.21, p < .01). Furthermore, the present study did not show that BPDE-DNA adducts are significantly associated with abnormal TSGs methylations in NSCLC, including SCC and AdO, respectively. Conclusively, cigarette smoking is significantly associated with the increase of BPDE-DNA adduct level, promoter hypermethylation of p16 and DAPK genes, while BPDE-DNA adduct was not significantly related to abnormal promoter hypermethylation in TSGs, suggesting that BPDE-DNA adducts and TSGs methylations play independent roles in NSCLC.

Background Hypnotic susceptibility is one of the stable characteristics of individuals, but not closely related to the personality traits such as those measured by the five-factor model in the general population. Whether it is related to the personality disorder functioning styles remains unanswered. Methods In 77 patients with personality disorders and 154 healthy volunteers, we administered the Stanford Hypnotic Susceptibility Scale: Form C (SHSSC) and the Parker Personality Measure (PERM) tests. Results Patients with personality disorders showed higher passing rates on SHSSC Dream and Posthypnotic Amnesia items. No significant correlation was found in healthy volunteers. In the patients however, SHSSC Taste hallucination (β = 0.26) and Anosmia to Ammonia (β = -0.23) were significantly correlated with the PERM Borderline style; SHSSC Posthypnotic Amnesia was correlated with the PERM Schizoid style (β = 0.25) but negatively the PERM Narcissistic style (β = -0.23). Conclusions Our results provide limited evidence that could help to understand the abnormal cognitions in personality disorders, such as their hallucination and memory distortions.