Search

Exposure to the heavy metal cadmium has adverse effects on human health, including DNA methylation. This study aimed to investigate the effects of cadmium on liver and kidney functions and Klotho gene methylation and to explore the relationship of methylation level with indicators of liver and kidney functions. Graphite furnace atomic absorption spectrometry was conducted to determine urinary cadmium, and an automatic biochemical analyzer was used to detect indices of liver and kidney functions. PCR pyrosequencing was performed to detect the methylation rate of Klotho. One-way ANOVA was adopted to compare the differences between groups, and the linear correlation to variables was analyzed. Cadmium exposure was negatively correlated with albumin level (r=-0.143, p=0.021) and positively correlated with urinary β2-microglobulin level (r=0.229, p<0.001). However, the methylation levels of Klotho gene was decreased and increased by low and high doses of cadmium exposure, respectively. And Klothomethylation levels were negatively correlated with albumin levels and positively correlated with β2-microglobulin levels.In this study, cadmium exposure affects liver and kidney functions as well as Klotho methylation levels, but the effect on Klotho methylation levels is not linear. Klotho methylation levels also influence liver and kidney functions. [ABSTRACT FROM AUTHOR]

Few studies have reported on the effects of fixed and rotating shift systems on the prevalence of sleep disturbance. Thus, in this study, the relationships between different work schedules and sleep disturbance in Chinese workers were investigated. A total of 2180 workers aged 19–65 years responded to the self-report questionnaire on shift work schedule (fixed day-shift, fixed night-shift, two-shift or three-shift system), working hours a day, and working days a week, physical effort, subjective sleep quality and subjective mental state. It was found that the rotating shift workers, namely, two- and three-shift workers, exhibited higher risks of sleep disturbance than with the fixed day-shift workers did (OR 1.37; 95% CI 1.07to 1.74; and OR 2.19; 95% CI 1.52 to 3.15, respectively). The risk was particularly high among two- or three-shift workers who worked more than 8 hours a day or more than 5 days a week and among three-shift workers who reported both light and heavy physical effort at work. Moreover, the two- and three-shift workers (rotating shift workers) suffered from poorer sleep quality than the fixed night shift workers did (OR 1.84; 95% CI 1.01 to 3.32; and OR 2.94; 95% CI 1.53 to 5.64, respectively). Consequently, rotating shift work (two- and three-shift work) is a risk factor for sleep disturbance, and the fixed work rhythm may contribute to the quality of sleep. [ABSTRACT FROM PUBLISHER]

Poor sleep quality is an important symptom of many medical or psychiatric disorders. However, the impact of cooking oil fumes (COFs) on sleep quality has not been studied. This population-based cross-sectional study was conducted to examine the association between COFs of Chinese household cooking and sleep quality. Individual sleep quality assessment was completed in 2197 participants with an average age of 37.52 years, through Pittsburgh Sleep Quality Index (PSQI). Information about their cooking practice were also collected by self-reported questionnaire. As an internal biomarker of COFs, urinary 1-hydroxypyrene (1-HOP) (n = 562) was further measured using high-performance liquid chromatography. Binary logistic regression models were performed to evaluate the association between exposure to COFs and individual sleep quality. We found that, subjective poor kitchen ventilation, preheating oil to smoking, and cooking for over 30 minutes were positively associated with overall poor sleep quality (global PSQI score >5) [odds ratio (OR) = 1.75, 95% confidence interval (CI) = 1.43–2.16; 1.25, (1.03–1.52); 1.42, (1.15–1.76), respectively]. After adjusting for potential confounders, subjective poor kitchen ventilation still tend to increase the risk of long sleep latency, sleep disturbances, and daytime dysfunction [OR = 1.37, 95% CI = 1.09–1.73; 1.91, (1.39–2.61); 1.54, (1.23–1.93), respectively]. Similar results were observed in participants who preheated oil to smoking [OR = 1.36, 95% CI = 1.08–1.72; 1.55, (1.14–2.14); 1.25, (1.02–1.55), respectively] and cooked for over 30 minutes [OR = 1.34, 95% CI = 1.05–1.72; 1.46, (1.03–2.06); 1.36, (1.08–1.72), respectively]. Furthermore, high urinary 1-HOP level was also positively associated with overall poor sleep quality (OR = 2.30, 95% CI = 1.31–4.05). The results indicated that exposure to COFs from Chinese household cooking may be a risk factor for poor sleep quality among middle-aged Chinese population. [ABSTRACT FROM AUTHOR]

Some literature has documented ambient fine particulate matter (PM 2.5) pollution and corresponding health burden in China, however, the knowledge of spatial disequilibrium of PM 2.5 and PM 2.5 -induced disease burden is scarce. With the help of gravity center model, spatial autocorrelation analysis as well as the region-specific exposure-response coefficient and ground-based PM 2.5 daily concentrations over 336 cities in China from January 2016 to December 2017, this paper provides a completive assessment for spatial disequilibrium of PM 2.5 -induced health burden. Improving PM 2.5 concentrations and declining PM 2.5 -induced health burden were found in China. The 2-year city-average concentration of the 336 cities was 45 ± 17μg/m3 with a range from 11μg/m3 to 128μg/m3. PM 2.5 -related deaths from stroke, ischemic heart disease, chronic obstructive pulmonary disease, hypertensive heart disease and lower respiratory infection amounted to 0.766 million in 2016 and 0.720 million in 2017. Much higher but decreasing PM 2.5 -induced mortality happened in the west, while higher and increasing PM 2.5 -induced deaths existed in the south. Strong spatial autocorrelation of PM 2.5 and PM 2.5 -induced disease burden existed among cities, illustrated by high-high (HH) clusters with significant spatial homogeneity and spatial spillover effect. The cities included in PM 2.5 concentration HH cluster had average PM 2.5 concentration 68.5 μg/m3, about 1.5 times higher than the national average; the cities involved in combined mortality HH cluster had mortality 90.5/105, 1.8 times as much as the national city-average level; about 46.4% of PM 2.5 -induced combined deaths happened in HH cluster cities. The cities embraced in the HH clusters of PM 2.5 concentration, population, deaths and mortality simultaneously, mostly located in Hebei, Shandong and Henan provinces, should be the top priorities for joint air pollution control. This paper provides important implications for policymakers regarding priority areas of joint air pollution control in China. Image 1 • PM 2.5 pollution contributed to around 0.74 million premature deaths per year. • Improving PM 2.5 levels and declining PM 2.5 -induced health burden were found. • Strong spatial disequilibrium and autocorrelation existed. • Much higher but decreasing PM 2.5 -induced mortality happened in west. • Cities overlapped in HH clusters should be the top priorities for joint control. [ABSTRACT FROM AUTHOR]

Background: Elevated manganese (Mn) exposure impairs cognition in adults and children, but the association between Mn and cognitive function in elderly people is unclear. Previous studies have linked Mn neurotoxicity in AD to Aβ-dependent mechanisms. However, the association between Mn and plasma APP and Aβ in the general elderly population remains unknown. This study aimed to investigate the association between Mn exposure and cognitive function, plasma APP and plasma Aβ in older adults., Methods: Cognitive abilities in 375 men aged 60 and older in Guangxi, China were assessed using the Mini-Mental State Examination (MMSE) and cognitive impairment were identified using education-stratified cut-off points of MMSE scores. Urinary Mn levels and plasma APP, and Aβ levels were measured using ICP-MS and ELISA, respectively., Results: A total of 109 (29.07 %) older men were identified as having cognitive impairment. The median urinary Mn level was 0.22 μg/g creatinine. Urinary Mn levels were negatively correlated with MMSE scores (β = -1.35, 95 % CI: -2.65 to -0.06; p = 0.041). In addition, higher concentrations of urinary manganese were associated with a greater risk of cognitive impairment (OR = 2.03, 95 % CI: 1.14-3.59; comparing the highest and lowest manganese; p = 0.025). Moreover, plasma APP levels were inversely associated with urinary Mn levels (r = -0.123, p = 0.020), and positively associated with MMSE scores (r = 0.158, p = 0.002). Surprisingly, no correlations were observed between plasma Aβ42, Aβ40, Aβ40/Aβ42, or Aβ42/Aβ40 and urinary Mn levels and MMSE scores., Conclusion: These results suggested that Mn exposure is negatively associated with older men's cognition and plasma APP levels, but not plasma Aβ levels., (Copyright © 2021 Elsevier GmbH. All rights reserved.)

Cadmium (Cd) is a known neurotoxicant and its relation with cognition has been well studied in children. However, evidence linking Cd and cognitive function among older individuals is limited. To evaluate the association between Cd exposure and cognitive function in older age, we conducted a cross-sectional study involving 375 older men aged 60-74 years (mean age: 66.0 years) in Guangxi, China. Urinary Cd concentrations were measured. Cognitive function was assessed by the Chinese version of Mini-Mental State Examination (MMSE) and cognitive impairment was identified using education-specific cutoff points of MMSE scores. General linear regression and logistic regression models were applied to evaluate the associations of urinary Cd concentrations with MMSE scores and the risk of cognitive impairment, respectively. The median urinary Cd concentration of all participants was 1.58 μg/g creatinine. Urinary Cd levels were inversely associated with MMSE scores [β = -0.76; 95% confidence interval (CI): -1.28 to -0.23 for a 2-fold increase in urinary Cd]. A 2-fold increase in urinary Cd was associated with increased risk of cognitive impairment [adjusted odds ratio (OR) = 1.46; 95% CI: 1.14 to 1.86]. When urinary Cd levels were analyzed as quartiles, higher urinary Cd levels were also significantly associated with increased risk of cognitive impairment in a dose-response manner (adjusted OR = 2.68; 95% CI: 1.33 to 5.38 for the highest vs. lowest quartile; p for trend = 0.002). Our findings suggest that long-term exposure to Cd may have adverse consequences for older men's cognitive function, but these results need further confirmation., (Copyright © 2020. Published by Elsevier Ltd.)

Studies assessing body burden of polybrominated diphenyl ethers (PBDEs) exposure have been conducted in the United States and Europe. However, the long-term assessment that is associated with multimedia exposure of PBDEs for the Chinese population is not available. The current study estimated the health risks using large PBDEs data to quantify the contributions of various media from different regions and distinguished the most vulnerable periods in life. We summarized media-specific (soil, dust, outdoor and indoor air, human milk and food) concentration of PBDEs in China from 2005 to 2016. Probabilistic risk assessment was adopted to estimate the health risks of infants, toddlers, children, teenagers and adults through ingestion, inhalation and dermal absorption. Monte Carlo simulation and sensitivity analysis were performed to quantify risk estimates uncertainties. E-waste areas had the highest PBDEs concentration, which was at least an order of magnitude higher than in other areas. BDE209 was the primary congener, accounting for 38-99% of the estimated daily intake. The dominant exposure pathway for infants was dietary intake through human milk, whereas dust ingestion was a higher contributing factor for toddlers, children, teenagers and adults. The 95th percentile of hazard index for infants and toddlers from e-waste areas of Guangdong and Zhejiang provinces exceeded one. Our estimates also suggested that infants may have the highest body burdens of PBDEs compared to other age groups. Sensitivity analyses indicated that PBDEs concentrations and ingestion rates contributed to major variances in the risk model. In this study, e-waste was found as a significant source of PBDEs, and PBDEs-containing e-waste are likely to be a threat to human health especially during early period of life. Risk strategies for better managing environmental PBDEs-exposure and human health are needed, due to the high intake of PBDEs and their persistence in the environment., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Levels of methyl tertiary-butyl ether (MTBE) in occupational air, ambient air, and drinking water in Nanning, South China, were investigated, and then their potential health risks to occupational workers and the general public were evaluated. Results show that the MTBE concentration in occupational air from 13 service stations was significantly higher than that in ambient air from residential areas (p<0.0001); both are far lower than the threshold limit value-time weighted average of MTBE regulated in the United States (US). The drinking water samples from household taps yielded detectable MTBE in the range of 0.04-0.33 μg/L, which is below the US drinking water standard of 20-40 μg/L. The non-carcinogenic risk of MTBE from air inhalation may be negligible because the calculated hazard quotient was less than 1. The mean MTBE lifetime cancer risk was within the acceptable limit of 1 × 10(-6) to 1 × 10(-4), but the lifetime cancer risk of refueling workers in the urban service station at the 95th percentile slightly exceeded the maximum acceptable carcinogen risk (1 × 10(-4)), indicating the potential carcinogenic health effects on the population highly exposed to MTBE in this region. The hazard index and carcinogenic risk of MTBE in drinking water were significantly lower than the safe limit of US Environmental Protection Agency, suggesting that drinking water unlikely poses significant health risks to the residents in Nanning., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Epidemiological studies have shown that air pollution particulate matter (PM) is associated with increased respiratory morbidity and mortality. However, the mechanisms are not fully understood. Oxidative stress-mediated apoptosis plays an important role in the occurrence of respiratory diseases. In this study, human bronchial epithelial (16-HBE) cells were exposed to different concentrations (16-128 µg/ml) of PM(2.5) for 24 h to investigate the apoptosis induced by PM(2.5). The results showed that PM(2.5) exposure significantly induced apoptosis, DNA strand breaks, and oxidative damage in a dose-dependent manner in 16-HBE cells. The expression of p53 and p73 increased significantly along with the dose of PM(2.5) in 16-HBE cells, whereas the expression of p21(Cip1/WAF1) decreased; the expression of mdm2 increased and then decreased, but not significantly. Taken together, these observations indicate that PM(2.5) may lead to oxidative damage and induce apoptosis through the p53-dependent pathway in 16-HBE cells. p53-Dependent apoptosis mediated by DNA strand breaks may be an important mechanism of PM(2.5)-induced apoptosis in 16-HBE cells.