National Institute for Occupational Health and Poison Control

BACKGROUND: Controlling childhood overweight/obesity would help early prevention on children from getting chronic noncommunicable diseases, exposing to screen for long periods may increase the risk of overweight/obesity due to lack of physical activity and tend to intake too much energy, and the relationship between screen time and overweight/obesity is inconsistent. Thus, the object of the present study was to estimate the relationship between screen time and overweight/obesity in children (<18 years) by systematically review prevalence studies. METHODS: We collected data from relevant studies published up to May 2019 using predefined inclusion/exclusion criteria. And all the literatures were searched in PubMed, ScienceDirect, Embase, and Web of Science. RESULTS: A total of 16 studies met the criteria and were included in the meta-analysis. When compared with the screen time <2 hr/day, an increased overweight/obesity risk among children was shown in the screen time ≥2 hr/day (OR = 1.67; 95% CI [1.48, 1.88], P < .0001). The subgroup analysis showed a positive association between the different types of screen time and overweight/obesity among children. CONCLUSION: Based on our study, increasing screen time could be a risk factor for being overweight/obesity in children and adolescents.

BACKGROUND: in a well established Chinese cohort of older adults. METHODS: exposure in the population aged 65 years and older in China in 2010. FINDINGS: exposure. INTERPRETATION: increases. FUNDING: National Natural Science Foundation of China, National High-Level Talents Special Support Plan of China for Young Talents, US National Aeronautics and Space Administration, and the Columbia University Global Policy Initiative.

Polycyclic aromatic hydrocarbons (PAHs) are a class of mutagenic and tumorigenic environmental contaminants. Although the mechanisms by which PAHs induce cancer in experimental animals have been extensively studied and the metabolic activation pathways have been determined, the environmental fate of PAHs and the phototoxicity exerted by PAHs, as well as their photoreaction products formed in the environment, have received much less attention. In this review, the formation of oxygenated PAHs, PAH quinones, nitro-PAHs, and halogenated PAHs from photoreaction of environmental PAHs are addressed. Upon light irradiation, PAHs and all PAH photoreaction products can absorb light energy to reach photo-excited states, which react with molecular oxygen, medium, and coexisting chemicals to produce reactive oxygen species (ROS) and other reactive intermediates, such as oxygenated PAHs and free radicals. These intermediates, including ROS, induce lipid peroxidation, and DNA damage including DNA strand breakage, oxidation to 8-oxo-2'-deoxyguanosine, and DNA-adducts. Since these toxicological endpoints are associated with age-related diseases, including cancer, environmental PAHs concomitantly exposed to sunlight may potentially promote human skin damage, leading to ageing and skin cancers. Thus, we suggest that (i) in addition to the widely recognized metabolic pathways, more attention must be paid to photoreaction as an important activation pathway for PAHs, (ii) risk assessment of environmental PAHs should take into consideration the complex photochemical reactions leading to mixtures of products that are also phototoxic; and (iii) the study of structure-toxicity relationships should be expanded to cover the complex photoreactions and extrinsic factors that affect phototoxicity endpoints.

Polyporaceae is one of the most important families of Basidiomycota. Investigations on the species diversity, taxonomy and phylogeny of Polyporaceae in China are carried out. So far 217 species belonging to 42 genera are reported from China. Two new genera: Amylosporia gen. nov. and Murinicarpus gen. nov., twelve new species: Coriolopsis dendriformis sp. nov., C. hainanensis sp. nov., Funalia cystidiata sp. nov., Haploporus microsporus sp. nov., Perenniporia citrinoalba sp. nov., P. yinggelingensis sp. nov., Picipes hainanensis sp. nov., P. jiajinensis sp. nov., P. pseudovarius sp. nov., Trametes duplexa sp. nov., T. ellipsoidea sp. nov. and T. stiptica sp. nov., and six new combinations, Amylosporia hattorii comb. nov., Hornodermoporus latissimus comb. nov., Murinicarpus subadustus comb. nov., Picipes pumilus comb. nov., Vanderbylia delavayi comb. nov. and Vanderbylia robiniophila comb. nov., are proposed. All the species are described based on the Chinese collections. Keys to genera of Polyporaceae occurring in China and keys to species of each genus are provided. This monograph provides a revised classification of Polyporaceae in China according to the modern taxonomy. The phylogeny of Polyporaceae from China are reconstructed based on DNA sequences of multiple loci including the internal transcribed spacer (ITS) regions, the large subunit nuclear ribosomal RNA gene (nLSU), the small subunit nuclear ribosomal RNA gene (nSSU), the small subunit mitochondrial rRNA gene sequences (mtSSU), the translation elongation factor 1-α gene (TEF1), the β-tubulin gene (TBB1), the RNA polymerase II largest subunit (RPB1) and second largest subunit (RPB2) genes. In addition, full morphological descriptions, illustrations, color photographs, taxonomic notes, ecology and all the available sequences of Polyporaceae species found from China are provided.

Amorpha-4,11-diene synthase (ADS) and Cyt P450 monooxygenase (CYP71AV1) in Artemisia annua L. are two key enzymes involved in the biosynthesis of artemisinin. The promoters of ADS and CYP71AV1 contain E-box elements, which are putative binding sites for basic helix-loop-helix (bHLH) transcription factors. This study successfully isolated a bHLH transcription factor gene from A. annua, designated as AabHLH1, from a cDNA library of the glandular secretory trichomes (GSTs) in which artemisinin is synthesized and sequestered. AabHLH1 encodes a protein of 650 amino acids containing one putative bHLH domain. AabHLH1 and ADS genes were strongly induced by ABA and the fungal elicitor, chitosan. The transient expression analysis of the AabHLH1-green fluorescent protein (GFP) reporter gene revealed that AabHLH1 was targeted to nuclei. Biochemical analysis demonstrated that the AabHLH1 protein was capable of binding to the E-box cis-elements, present in both ADS and CYP71AV1 promoters, and possessed transactivation activity in yeast. In addition, transient co-transformation of AabHLH1 and CYP71AV1Pro::GUS in A. annua leaves showed a significant activation of the expression of the GUS (β-glucuronidase) gene in transformed A. annua, but mutation of the E-boxes resulted in abolition of activation, suggesting that the E-box is important for the CYP71AV1 promoter activity. Furthermore, transient expression of AabHLH1 in A. annua leaves increased transcript levels of the genes involved in artemisinin biosynthesis, such as ADS, CYP71AV1 and HMGR. These results suggest that AabHLH1 can positively regulate the biosynthesis of artemisinin.

BACKGROUND: The improvement of life expectancy is one of the aims of the Healthy China 2030 blueprint. We aimed to investigate the extent to which healthy lifestyles are associated with life expectancy in Chinese adults. METHODS: We used the prospective China Kadoorie Biobank (CKB) study to examine the relative risk of mortality associated with individual and combined lifestyle factors (never smoking or quitting not for illness, no excessive alcohol use, being physically active, healthy eating habits, and healthy body shape). Participants with coronary heart disease, stroke, cancer, or missing values for body-mass index were excluded. For analysis of chronic respiratory diseases, participants with chronic obstructive pulmonary disease or asthma were excluded. We estimated the national prevalence of lifestyle factors using data from the China Nutrition and Health Surveillance (CNHS; 2015) and derived mortality rates from the Global Burden of Diseases, Injuries, and Risk Factors Study (2015). All three data sources were combined to estimate the life expectancy of individuals at age 30 years following different levels of lifestyle factors by using the life table method. The cause-specific decomposition of the life expectancy differences was analysed using Arriaga's method. FINDINGS: After the exclusion of CKB participants with coronary heart disease, stroke, cancer, or missing BMI data at baseline, 487 209 were included in the primary analysis. Participants with COPD or asthma at baseline were additionally excluded for chronic respiratory disease-related analysis, leaving 451 233 participants with data available for analysis. Data from 171 127 adults aged 30-84 years from the CNHS 2015 were used to estimate the sex-specific and age-specific prevalence of lifestyle-related factors. There were 42 496 deaths documented over a median follow-up of 11·1 years (IQR 10·2-12·1) in CKB. The adjusted hazard ratios (aHRs) of participants adopting five versus 0-1 low-risk factors was 0·38 (95% CI 0·34-0·43) for all-cause mortality, aHR 0·37 (0·30-0·46) for cardiovascular disease mortality, aHR 0·47 (0·39-0·56) for cancer mortality, and aHR 0·30 (0·14-0·64) for chronic respiratory disease mortality. The life expectancy at age 30 years for individuals with 0-1 low-risk factors was on average 41·7 years (95% CI 41·5-42·0) for men and 47·3 years (46·6-48·0) for women. For individuals with all five low-risk factors, the life expectancy at age 30 was 50·5 years (95% CI 48·5-52·4) for men and 55·4 years (53·5-57·4) for women; meaning a difference of 8·8 years (95% CI 6·8-10·7) for men and 8·1 years (6·5-9·9) for women. The estimated extended life expectancy for men and women was mainly attributable to reduced death from cardiovascular disease (2·4 years [27% of the total extended life expectancy] for men and 3·7 years [46%] for women), cancer (2·6 years [30%] for men and 0·9 years [11%] for women), and chronic respiratory disease (0·6 years [7%] for men and 1·2 years [15%] for women). INTERPRETATION: Our findings suggest that increasing the adoption of these five healthy lifestyle factors through public health interventions could be associated with substantial gains in life expectancy in the Chinese population. FUNDING: National Natural Science Foundation of China, National Key Research and Development Program of China, Kadoorie Charitable Foundation, UK Wellcome Trust.

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BACKGROUND: Although major concerns exist regarding the potential consequences of human exposures to nanoscale carbon black (CB) particles, limited human toxicological data is currently available. The purpose of this study was to evaluate if nanoscale CB particles could be responsible, at least partially, for the altered lung function and inflammation observed in CB workers exposed to nanoscale CB particles. METHODS: Scanning Electron Microscopy (SEM), Transmission Electron Microscopy (TEM), and Brunauer-Emmett-Teller were used to characterize CB. Eighty-one CB-exposed male workers and 104 non-exposed male workers were recruited. The pulmonary function test was performed and pro-inflammatory cytokines were evaluated. To further assess the deposition and pulmonary damage induced by CB nanoparticles, male BALB/c mice were exposed to CB for 6 hours per day for 7 or 14 days. The deposition of CB and the pathological changes of the lung tissue in mice were evaluated by paraffin sections and TEM. The cytokines levels in serum and lung tissue of mice were evaluated by ELISA and immunohistochemical staining (IHC). RESULTS: SEM and TEM images showed that the CB particles were 30 to 50 nm in size. In the CB workplace, the concentration of CB was 14.90 mg/m³. Among these CB particles, 50.77% were less than 0.523 micrometer, and 99.55% were less than 2.5 micrometer in aerodynamic diameter. The reduction of lung function parameters including FEV1%, FEV/FVC, MMF%, and PEF% in CB workers was observed, and the IL-1β, IL-6, IL-8, MIP-1beta, and TNF- alpha had 2.86-, 6.85-, 1.49-, 3.35-, and 4.87-folds increase in serum of CB workers, respectively. In mice exposed to the aerosol CB, particles were deposited in the lung. The alveolar wall thickened and a large amount of inflammatory cells were observed in lung tissues after CB exposure. IL-6 and IL-8 levels were increased in both serum and lung homogenate. CONCLUSIONS: The data strongly suggests that nanoscale CB particles could be responsible for the lung function reduction and pro-inflammatory cytokines secretion in CB workers. These results, therefore, provide the first evidence of a link between human exposure to CB and long-term pulmonary effects.

AIMS: To further investigate the antineuroblastoma effect of rutin which is a type of flavonoid. METHODS: The antiproliferation of rutin in human neuroblastoma cells LAN-5 were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Chemotaxis of LAN-5 cells was assessed using transwell migration chambers and scratch wound migration assay. The cell cycle arrest and apoptosis in a dose-dependent manner was measured by flow cytometric and fluorescent microscopy analyses. The apoptosis-related proteins BAX and BCL2 as well as MYCN mRNA express were determined by RT-PCR analysis. Secreted TNF- α level were determined using specific enzyme-linked immunosorbent assay kits. RESULTS: Rutin significantly inhibited the growth of LAN-5 cells and chemotactic ability. Flow cytometric analysis revealed that rutin induced G2/M arrest in the cell cycle progression and induced cell apoptosis. The RT-PCR showed that rutin could decrease BCL2 expression and BCL2/BAX ratio. In the meantime, the MYCN mRNA level and the secretion of TNF- α were inhibited. CONCLUSION: These results suggest that rutin produces obvious antineuroblastoma effects via induced G2/M arrest in the cell cycle progression and induced cell apoptosis as well as regulating the expression of gene related to apoptosis and so on. It supports the viability of developing rutin as a novel therapeutic prodrug for neuroblastoma treatment, as well as providing a new path on anticancer effect of Chinese traditional drug.

Benzene is an industrial chemical and component of gasoline that is an established cause of leukemia. To better understand the risk benzene poses, we examined the effect of benzene exposure on peripheral blood mononuclear cell (PBMC) gene expression in a population of shoe-factory workers with well-characterized occupational exposures using microarrays and real-time polymerase chain reaction (PCR). PBMC RNA was stabilized in the field and analyzed using a comprehensive human array, the U133A/B Affymetrix GeneChip set. A matched analysis of six exposed-control pairs was performed. A combination of robust multiarray analysis and ordering of genes using paired t-statistics, along with bootstrapping to control for a 5% familywise error rate, was used to identify differentially expressed genes in a global analysis. This resulted in a set of 29 known genes being identified that were highly likely to be differentially expressed. We also repeated these analyses on a smaller subset of 508 cytokine probe sets and found that the expression of 19 known cytokine genes was significantly different between the exposed and the control subjects. Six genes were selected for confirmation by real-time PCR, and of these, CXCL16, ZNF331, JUN, and PF4 were the most significantly affected by benzene exposure, a finding that was confirmed in a larger data set from 28 subjects. The altered expression was not caused by changes in the makeup of the PBMC fraction. Thus, microarray analysis along with real-time PCR confirmation reveals that altered expressions of CXCL16, ZNF331, JUN, and PF4 are potential biomarkers of benzene exposure.

We used natural spline (NS) models to investigate nonlinear relationships between levels of benzene metabolites (E,E-muconic acid, S-phenylmercapturic acid, phenol, hydroquinone, and catechol) and benzene exposure among 386 exposed and control workers in Tianjin, China. After adjusting for background levels (estimated from the 60 control subjects with the lowest benzene exposures), expected mean trends of all metabolite levels increased with benzene air concentrations from 0.03 to 88.9 ppm. Molar fractions for phenol, hydroquinone, and E,E-muconic acid changed continuously with increasing air concentrations, suggesting that competing CYP-mediated metabolic pathways favored E,E-muconic acid and hydroquinone below 20 ppm and favored phenol above 20 ppm. Mean trends of dose-specific levels (micromol/L/ppm benzene) of E,E-muconic acid, phenol, hydroquinone, and catechol all decreased with increasing benzene exposure, with an overall 9-fold reduction of total metabolites. Surprisingly, about 90% of the reductions in dose-specific levels occurred below about 3 ppm for each major metabolite. Using generalized linear models with NS-smoothing functions (GLM + NS models), we detected significant effects upon metabolite levels of gender, age, and smoking status. Metabolite levels were about 20% higher in females and decreased between 1% and 2% per year of life. In addition, levels of hydroquinone and catechol were greater in smoking subjects. Overall, our results indicate that benzene metabolism is highly nonlinear with increasing benzene exposure above 0.03 ppm, and that current human toxicokinetic models do not accurately predict benzene metabolism below 3 ppm. Our results also suggest that GLM + NS models are ideal for evaluating nonlinear relationships between environmental exposures and levels of human biomarkers.

BackgroundAir pollution and its adverse effects on public health remain a considerable problem in China, where policies have been implemented to improve the situation. We aimed to estimate the disease burden associated with particulate matter (PM)2·5 across China for 2020 and 2030 to identify the populations and regions most at risk, quantify the health benefits of air quality improvement targets, and determine the effect of population growth and ageing on this disease burden.MethodsIn this modelling study, we investigated premature deaths associated with PM2·5 across China on the basis of air quality scenarios proposed by the expert group involved in the formulation of the 13th Five-Year Plan for Eco-Environmental Protection and population scenarios based on the Shared Socioeconomic Pathways of the Intergovernmental Panel on Climate Change. We used the integrated exposure–response model used for the Global Burden of Disease Study to estimate the number of PM2·5-related premature deaths under each scenario.FindingsThe projected health benefits of the air-quality-improving targets are substantial, and could reduce the number of PM2.5-related premature deaths in China by approximately 129 278 by 2020 and 217 988 by 2030, compared with 2010. However, since China's population is increasing and ageing, the number of PM2.5-related premature deaths was estimated to increase by 84 102 by 2020 and by 244 191 by 2030, indicating that the health benefits induced by air quality improvements could be offset by the effect of the population increasing in size and ageing.InterpretationTo reduce the future disease burden in China, targets that are stricter than the interim target and stringent policies to improve air quality and protect public health are needed, especially for at-risk population groups, such as older individuals (aged >55 years) and patients with cardiovascular diseases, particularly in regions with a high disease burden.FundingNational Key Research and Development Program of China, National Natural Science Foundation of China, Beijing Natural Science Foundation, National High-level Talents Special Support Plan of China for Young Talents, and Special Foundation of Basic Science and Technology Resources Survey of Ministry of Science and Technology of China.

BACKGROUND: Benzene, an established cause of acute myeloid leukemia (AML), may also cause one or more lymphoid malignancies in humans. Previously, we identified genes and pathways associated with exposure to high (> 10 ppm) levels of benzene through transcriptomic analyses of blood cells from a small number of occupationally exposed workers. OBJECTIVES: The goals of this study were to identify potential biomarkers of benzene exposure and/or early effects and to elucidate mechanisms relevant to risk of hematotoxicity, leukemia, and lymphoid malignancy in occupationally exposed individuals, many of whom were exposed to benzene levels < 1 ppm, the current U.S. occupational standard. METHODS: We analyzed global gene expression in the peripheral blood mononuclear cells of 125 workers exposed to benzene levels ranging from < 1 ppm to > 10 ppm. Study design and analysis with a mixed-effects model minimized potential confounding and experimental variability. RESULTS: We observed highly significant widespread perturbation of gene expression at all exposure levels. The AML pathway was among the pathways most significantly associated with benzene exposure. Immune response pathways were associated with most exposure levels, potentially providing biological plausibility for an association between lymphoma and benzene exposure. We identified a 16-gene expression signature associated with all levels of benzene exposure. CONCLUSIONS: Our findings suggest that chronic benzene exposure, even at levels below the current U.S. occupational standard, perturbs many genes, biological processes, and pathways. These findings expand our understanding of the mechanisms by which benzene may induce hematotoxicity, leukemia, and lymphoma and reveal relevant potential biomarkers associated with a range of exposures.

Background The 2019-nCoV outbreak in Wuhan, China has attracted world-wide attention. As of February 11, 2020, a total of 44730 cases of novel coronavirus-infected pneumonia associated with COVID-19 were confirmed by the National Health Commission of China. Methods Three approaches, namely Poisson likelihood-based method (ML), exponential growth rate-based method (EGR) and stochastic Susceptible-Infected-Removed dynamic model-based method (SIR), were implemented to estimate the basic and controlled reproduction numbers. Results A total of 71 chains of transmission together with dates of symptoms onset and 67 dates of infections were identified among 5405 confirmed cases outside Hubei as reported by February 2, 2020. Based on this information, we find the serial interval having an average of 4.41 days with a standard deviation of 3.17 days and the infectious period having an average of 10.91 days with a standard deviation of 3.95 days. Conclusions The controlled reproduction number is declining. It is lower than one in most regions of China, but is still larger than one in Hubei Province. Sustained efforts are needed to further reduce the R c to below one in order to end the current epidemic.

BACKGROUND: Recent evidence has shown that humans metabolize benzene more efficiently at environmental air concentrations than at concentrations > 1 ppm. This led us to speculate that an unidentified metabolic pathway was mainly responsible for benzene metabolism at ambient levels. OBJECTIVE: We statistically tested whether human metabolism of benzene is better fitted by a kinetic model having two pathways rather than one. METHODS: We fit Michaelis-Menten-like models to levels of urinary benzene metabolites and the corresponding air concentrations for 263 nonsmoking Chinese females. Estimated benzene concentrations ranged from less than 0.001 ppm to 299 ppm, with 10th and 90th percentile values of 0.002 ppm and 8.97 ppm, respectively. RESULTS: Using values of Akaike's information criterion obtained under the two models, we found strong statistical evidence favoring two metabolic pathways, with respective affinities (benzene air concentrations analogous to K(m) values) of 301 ppm for the low-affinity pathway (probably dominated by cytochrome P450 enzyme 2E1) and 0.594 ppm for the high-affinity pathway (unknown). The exposure-specific metabolite level predicted by our two-pathway model at nonsaturating concentrations was 184 muM/ppm of benzene, a value close to an independent estimate of 194 muM/ppm for a typical nonsmoking Chinese female. Our results indicate that a nonsmoking woman would metabolize about three times more benzene from the ambient environment under the two-pathway model (184 muM/ppm) than under the one-pathway model (68.6 muM/ppm). In fact, 73% of the ambient benzene dose would be metabolized via the unidentified high-affinity pathway. CONCLUSION: Because regulatory risk assessments have assumed nonsaturating metabolism of benzene in persons exposed to air concentrations well above 10 ppm, our findings suggest that the true leukemia risks could be substantially greater than currently thought at ambient levels of exposure-about 3-fold higher among nonsmoking females in the general population.

Iodoacetic acid (IAA) and iodoform (IF) are unregulated iodinated disinfection byproducts (DBPs) found in drinking water. Their presence in the drinking water of China has not been documented. Recently, the carcinogenic potential of IAA and IF has been a concern because of their mutagenicity in bacteria and genotoxicity in mammalian cells. Therefore, we measured their concentrations in Shanghai drinking water and assessed their cytotoxicity, genotoxicity, and ability to transform NIH3T3 cells to tumorigenic lines. The concentrations of IAA and IF in Shanghai drinking water varied between summer and winter with maximum winter levels of 2.18 μg/L IAA and 0.86 μg/L IF. IAA with a lethal concentration 50 (LC50) of 2.77 μM exhibited more potent cytotoxicity in NIH3T3 cells than IF (LC50 = 83.37 μM). IAA, but not IF, induced a concentration-dependent DNA damage measured by γ-H2AX staining and increased tail moment in single-cell gel electrophoresis. Neither IAA nor IF increased micronucleus frequency. Prolonged exposure of NIH3T3 cells to IAA increased the frequencies of transformed cells with anchorage-independent growth and agglutination with concanavalin A. IAA-transformed cells formed aggressive fibrosarcomas after inoculation into Balb/c nude mice. This study demonstrated that IAA has a biological activity that is consistent with a carcinogen and human exposure should be of concern.

BACKGROUND: Lifestyle and longevity genes have different and important roles in the human lifespan; however, the association between a healthy lifestyle in late-life and life expectancy mediated by genetic risk is yet to be elucidated. We aimed to investigate the associations of healthy lifestyle in late-life and genetic risk with life expectancy among older adults. METHODS: A weighted healthy lifestyle score was constructed from the following variables: current non-smoking, non-harmful alcohol consumption, regular physical activity, and a healthy diet. Participants were recruited from the Chinese Longitudinal Healthy Longevity Survey, a prospective community-based cohort study that took place between 1998 and 2018. Eligible participants were aged 65 years and older with available information on lifestyle factors at baseline, and then were categorised into unhealthy (bottom tertile of the weighted healthy lifestyle score), intermediate (middle tertile), and healthy (top tertile) lifestyle groups. A genetic risk score was constructed based on 11 lifespan loci among 9633 participants, divided by the median and classified into low and high genetic risk groups. Stratified Cox proportional hazard regression was used to estimate the interaction between genetic and lifestyle factors on all-cause mortality risk. FINDINGS: Between Jan 13, 1998, and Dec 31, 2018, 36 164 adults aged 65 years and older were recruited, among whom a total of 27 462 deaths were documented during a median follow-up of 3·12 years (IQR 1·62-5·94) and included in the lifestyle association analysis. Compared with the unhealthy lifestyle category, participants in the healthy lifestyle group had a lower all-cause mortality risk (hazard ratio [HR] 0·56 [95% CI 0·54-0·57]; p<0·0001). The highest mortality risk was observed in individuals in the high genetic risk and unhealthy lifestyle group (HR 1·80 [95% CI 1·63-1·98]; p<0·0001). The absolute risk reduction was greater for participants in the high genetic risk group. A healthy lifestyle was associated with a gain of 3·84 years (95% CI 3·05-4·64) at the age of 65 years in the low genetic risk group, and 4·35 years (3·70-5·06) in the high genetic risk group. INTERPRETATION: A healthy lifestyle, even in late-life, was associated with lower mortality risk and longer life expectancy among Chinese older adults, highlighting the importance of a healthy lifestyle in extending the lifespan, especially for individuals with high genetic risk. FUNDING: National Natural Science Foundation of China. TRANSLATION: For the Mandarin translation of the abstract see Supplementary Materials section.

Benzene is a recognized hematotoxicant and carcinogen that produces genotoxic damage. Benzene metabolites can produce reactive oxidative species. Mitochondrial DNA (mtDNA) copy number may be increased in response to oxidative stress to compensate for damaged mitochondria. We carried out a cross-sectional study of 40 benzene-exposed workers and 40 controls to evaluate the association between benzene exposure and mtDNA copy number. Copy number of mtDNA in leukocyte DNA was determined by real-time PCR. Compared with controls, the copy number of mtDNA increased by 4% and by 15% in workers exposed to < or =10 ppm (n = 20) and >10 ppm (n = 20) benzene, respectively. After adjusting for recent infection, the factor that was significantly correlated with mtDNA, the increase of mtDNA was statistically significant in the high exposed group (P = 0.016) with a significant linear trend (P = 0.024). To our best knowledge, this is the first report that benzene exposure was associated with increased mitochondria DNA copy number. Benzene exposure may induce mtDNA amplification, possibly in response to oxidative stress caused by benzene. The finding needs to be replicated by other studies.

BACKGROUND: Cognitive impairment is a major contributor to mortality among the elderly. However, the relationship between cognitive impairment evaluated by educational levels and mortality and the trend between cognitive impairment and mortality with time are unclear. We aim to evaluate the differences in associations of cognitive impairment, taking the stratification by educational levels into account, with all-cause mortality and further explore the relationship of cognitive impairment with mortality in different age and sex groups in two cohorts ascertained 6 years apart in China. METHODS: A total of 13,906 and 13,873 Chinese elderly aged 65 years and older were included in the 2002-2008 and 2008-2014 cohorts from the Chinese Longitudinal Healthy Longevity Survey (CLHLS). Mortality data was ascertained from interviews with family members or relatives of participants. Cognitive function, evaluated by the Mini-Mental State Examination (MMSE), were defined by different cut-offs taking educational background into account. Cox models were used to explore the relationship of cognitive impairment with mortality. RESULTS: For the 2002-2008 and 2008-2014 cohorts, 55,277 and 53,267 person-years were followed up, and the mean (SD) age were 86.5 (11.6) and 87.2 (11.3) years, respectively. Compared to normal cognition, cognitive impairment was independently associated with higher mortality risk after controlling for potential confounders, with hazard ratios (HRs) of 1.32 (95% confidence interval [CI], 1.25-1.39) in 2002-2008 cohort and 1.26 (95% CI, 1.19-1.32) in 2008-2014 cohort, stratified by educational levels. The trend of cognitive impairment with all-cause mortality risk decreased from 2002 to 2008 to 2008-2014 cohort, while no significant interaction of cognitive impairment with cohort for all-cause mortality was observed. The associations of cognitive impairment and mortality were decreased with age in the two cohorts. CONCLUSIONS: Cognitive impairment evaluated by different cut-offs were associated with increased risk of mortality, especially among those aged 65-79 years in the two cohorts; this advocates that periodic screening for cognitive impairment among the elderly is warranted.

<sec> <b> <b>What is already known about this topic?</b> </b> Acute liver failure, rhabdomyolysis, acute renal failure, and hemolysis caused by poisonous mushrooms are the most important mushroom poisoning threats to the Chinese population. The most notorious lethal mushrooms are the species from genera <i>Amanita</i>, <i>Lepiota</i>, and <i>Galerina</i> that cause acute liver failure, and <i>Russula subnigricans</i> that leads to rhabdomyolysis. </sec><sec> <b> <b>What is added by this report?</b> </b> In 2020, the total number of investigations reached 676, involving an estimated 102 species of poisonous mushrooms, 24 of which were newly recorded in China. <i>Gyromitra venenata</i> was newly discovered in incidents in Yunnan and Guizhou provinces and were the first reported poisonings due to gyromitrins in China since 2000. The rare poisoning Shiitake mushroom dermatitis was recorded in China. Hemolysis poisoning caused by <i>Paxillus involutus</i> was recorded for the second time since the beginning of the new century, resulting in one death in Inner Mongolia Autonomous Region. </sec><sec> <b> <b>What are the implications for public health practice?</b> </b> Promoting knowledge about safe consumption of mushrooms is essential to reduce mushroom poisonings. It is not wise to collect and eat wild mushrooms. For southwestern provinces such as Yunnan, especially, caution must be exercised with unfamiliar mushroom species. </sec>