Association between Exposure to Volatile Organic Compounds and the Prevalence of Sleep Problems in US Adults.

BACKGROUND: While mounting evidence suggests a connection between environmental contaminants and sleep problems, it remains uncertain whether exposure to volatile organic compounds (VOCs) specifically is associated with such problems. METHODS: Data from the National Health and Nutrition Examination Survey program's five survey cycles (2005-2006, 2011-2018) were used to conduct cross-sectional research. Data on short sleep duration (SSD) and self-reported trouble sleeping were collected from questionnaire data. Data on urine VOCs were gathered from laboratory data. The association between urinary VOCs and sleep problems was examined using weighted generalized linear models and the restricted cubic spline (RCS), weighted quantile sum (WQS), and quantile-based g-calculation (QGC) methods. RESULTS: In all, a total of 4131 general adult individuals were included in this study. The prevalence of SSD and self-reported trouble sleeping was 34.11% and 25.03%, respectively. 3,4-MHA, AAMA, AMCC, SBMA, and MA were risk factors for SSD after adjusting several covariates, with the largest effect being AMCC (OR = 1.47, 95% CI: 1.08, 2.02). Risk factors for sleep issues included AAMA, AMCC, CEMA, CYMA, DGBMA, 2HPMA, 3HPMA, MA, and PGA, with AMCC having the highest impact with an OR of 1.69 (95% CI: 1.28, 2.22). Both the WQS model and the QGC model showed that the co-exposure to VOCs was positively associated with SSD and self-reported trouble sleeping, with AMCC being the most influential VOC. CONCLUSIONS: According to our research, high levels of single or mixed urine VOCs are linked to a higher prevalence of SSD and self-reported trouble sleeping in the general adult population of the United States. Further prospective and experimental studies are needed in the future to validate these potential relationships and explore the underlying mechanisms.

Self-harm and interpersonal violence due to high temperature from the global burden of disease study 2019: A 30-year assessment.

BACKGROUND: The impact of global warming on health due to climate change is increasingly studied, but the global burden of self-harm and interpersonal violence attributable to high temperature is still limited. This study aimed to systematically assess the burden of self-harm and interpersonal violence attributable to high temperature globally or by region and climate zone from 1990 to 2019. METHODS: We obtained the global, regional, and national deaths, disability-adjusted life years (DALYs), age-standardized mortality rates (ASMR), and age-standardized disability-adjusted life year rates (ASDR) of self-harm and interpersonal violence due to high temperature from 1990 to 2019 through the Global Burden of Disease Study (GBD) 2019. The burden of self-harm and interpersonal violence due to high temperature was estimated by age, sex, climate zone, the socio-demographic index (SDI), and the healthcare access and quality index (HAQ). Average annual percentage changes (AAPCs) in ASMR and ASDR were calculated for 1990-2019 using the Joinpoint model. RESULTS: From 1990 to 2019, the global deaths and DALYs related to self-harm and interpersonal violence due to high temperature increased from 20,002 (95% UI, 9243 to 41,928) and 1,107,216 (95% UI, 512,062 to 2,319,477) to 26,459 (95% UI, 13,574 to 47,265) and 1,382,487 (95% UI, 722,060 to 2,474,441), respectively. However, the ASMR and ASDR showed varying degrees of decreasing trends, with decreases of 13.36% and 12.66%, respectively. The ASMR was high and declining in low and low-middle SDI regions, particularly in tropical and subtropical regions. In addition, SDI and HAQ index were negatively correlated with ASMR in 204 countries and regions. CONCLUSIONS: The global burden of self-harm and interpersonal violence attributed to high temperature has decreased over the past 30 years, but the number of deaths and DALYs continues to rise. Climate change continues to make heat stress a significant risk factor for self-harm and interpersonal violence worldwide.

Disease burden of chronic kidney disease attributable to lead exposure: A global analysis of 30 years since 1990.

BACKGROUND: Exposure to lead (Pb) is associated with an increased risk of chronic kidney disease (CKD). However, limited studies explored the global burden of CKD attributable to Pb exposure, especially in countries with different development levels. This study aimed to comprehensively evaluate the temporal and spatial trend in the disease burden of CKD attributable to Pb exposure in 204 countries and territories from 1990 to 2019. METHODS: We used the data from Global Burden of Disease Study (GBD) 2019 to estimate annual deaths, disability-adjusted life years (DALYs), age-standardized mortality rates (ASMR), and age-standardized DALYs rate (ASDR) of CKD attributable to Pb exposure. The annual average percentage change (AAPCs) was calculated using the Joinpoint model to evaluate the changing trend of CKD ASMR and ASDR attributable to Pb exposure from 1990 to 2019. Meanwhile, age-period-cohort (APC) model was used to assess changes in the mortality of CKD attributable to Pb exposure from 1990 to 2019. RESULTS: Global ASMR for CKD attributable to Pb exposure trended upward from 1990 to 2019. ASMR and ASDR were the highest in low and low-middle SDI regions. With the APC model, we found that global mortality rates for CKD attributable to Pb exposure increased with age. The global period rate ratio showed the highest value in 2000-2004 and the lowest in 2015-2019, while the global cohort rate ratio showed the highest value in 1941-1949 and the lowest during 1986-1994. CONCLUSIONS: From 1990 to 2019, the global burden of CKD attributable to Pb exposure increased globally, especially in low and low-middle SDI regions, as well as the elderly. Pb exposure is still a great threat to the global burden of CKD, and the implementation of effective prevention measures to reduce Pb exposure in the environment should be continually strengthened.

Nano-selenium attenuates mitochondrial-associated apoptosis via the PI3K/AKT pathway in nickel-induced hepatotoxicity in vivo and in vitro.

The aim of this study was to investigate the protective effects of Nano-Se against nickel (Ni)-induced hepatotoxicity and the potential mechanism. Hence, we constructed in vivo and in vitro models of Ni-induced hepatotoxicity. Sprague-Dawley (SD) rats were exposed to nickel sulfate (NiSO4 , 5.0 mg/kg, i.p.) with or without Nano-Se (0.5, 1, and 2 mg/kg, oral gavage) co-administration for 14 days, and HepG2 cells were exposed to NiSO4 (1500 µM) with or without Nano-Se (20 µM) for 24 h. Nano-Se obviously prevented Ni-induced hepatotoxicity indicated by ameliorating pathological change and decreasing Ni accumulation in rat livers. Ni induced a significant increase in hepatic activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSH-Px), and malondialdehyde (MDA) level, decreased the glutathione (GSH) content while compared to those in the control group. Nano-Se administration improved the hepatic antioxidant capacity through increase hepatic GSH contents and GSH-Px activity, decrease the activities of SOD, CAT, and MDA level. Nano-Se improved the cell viability, decreased active oxygen (ROS) generation and ameliorated morphological changes of nuclear structures in Ni-treated HepG2 cells. In addition, Nano-Se inhibited the Ni-induced increases of cytochrome c, caspase-9, cleaved caspase-3, increased PI3K and AKT phosphorylation both in vivo and in vitro. Besides, the PI3K inhibitor Y294002 could inhibit the protective effects of Nano-Se on apoptosis. Thus, Nano-Se significantly activates PI3K/AKT signaling to ameliorate apoptosis in Ni-induced hepatotoxicity.

Association of interleukin-23 receptor gene polymorphisms with risk of bladder cancer in Chinese.

To assess whether polymorphisms of the interleukin-23 receptor (IL23R) gene are associated with bladder transitional cell carcinoma because chronic inflammation contributes to bladder cancer and the IL23R is known to be critically involved in the carcinogenesis of various malignant tumors. 226 patients with bladder cancer and 270 age-matched controls were involved in the study. Polymerase chain reaction-restriction fragment length polymorphism was used for genotyping. Genotype distribution and allelic frequencies between patients and controls were compared. In all three single nucleotide polymorphisms of IL23R studied, the distribution of genotype and allele frequencies of rs10889677 differed significantly between patients and controls. The frequency of allele C of rs10889677 was significantly increased in cases compared with controls (0.2898 vs. 0.1833, odds ratio 1.818, 95 % confidence interval 1.349-2.449). The result indicates that IL23R may play an important role in the susceptibility of bladder cancer in Chinese population.