Reconsidering gas as clean energy: Switching to electricity for household cooking to reduce NO2-attributed disease burden.

Nitrogen dioxide (NO2) is a prevalent air pollutant in urban areas, originating from outdoor sources, household gas consumption, and secondhand smoke. The limited evaluation of the disease burden attributable to NO2, encompassing different health effects and contributions from various sources, impedes our understanding from a public health perspective. Based on modeled NO2 exposure concentrations, their exposure-response relationships with lung cancer, chronic obstructive pulmonary disease, and diabetes mellitus, and baseline disability-adjusted life years (DALYs), we estimated that 1,675 (655-2,624) thousand DALYs were attributable to NO2 in urban China in 2019 [138 (54-216) billion Chinese yuan (CNY) economic losses]. The transition from gas to electricity for household cooking was estimated to reduce the attributable economic losses by 35%. This reduction falls within the range of reductions achieved when outdoor air meets the World Health Organization interim target 3 and air quality guidelines for annual NO2, highlighting the significance of raising awareness of gas as a polluting household energy for cooking. These findings align with global sustainable development initiatives, providing a sustainable solution to promote public health while potentially mitigating climate change.

Associations between home environmental factors and childhood eczema and related symptoms in different cities in China.

Previous studies have shown significant associations between home environmental factors and childhood eczema. However, few studies have compared how associations differ in different regions. This study investigated associations between home environmental factors and childhood eczema ever, and related symptoms including itchy rash (IR) and being awakened by itchy rash at night (awake by IR) in 4 cities located in different regions of China, based on cross-sectional investigations during 2010-2012. We used two-step analysis to explore the associations between influencing factors and eczema/related symptoms: first, group Least Absolute Shrinkage and Selection Operator (LASSO) was conducted to identify important factors among a list of candidates; then, the associations in total study population and in each city were estimated using logistic regression. We found these home environmental factors to be risk factors for eczema or related symptoms: large residence size, shared room, air cleaner at home, abnormal smell, perceived dry air, visible mold or damp stains, cooking with coal or wood, painted wall, incense, mice, new furniture during pregnancy, abnormal smell at birth, window condensation at birth and environmental tobacco smoke at birth. Environmental protective factors were rural house location and window ventilation. Associations of factors with eczema/related symptoms differed across cities. For example, air conditioning was protective for eczema in Beijing and awakening by IR in Shanghai with ORs of 0.70 (95%CI: 0.52, 0.95) and 0.33 (95%CI: 0.14, 0.81) respectively, but not significant in other cities. Our results have implications for improving home environments to reduce the risk of childhood eczema/related symptoms in different regions of China.

The Role of Indoor Microbiome and Metabolites in Shaping Children's Nasal and Oral Microbiota: A Pilot Multi-Omic Analysis.

Maintaining a diverse and well-balanced nasal and oral microbiota is vital for human health. However, the impact of indoor microbiome and metabolites on nasal and oral microbiota remains largely unknown. Fifty-six children in Shanghai were surveyed to complete a questionnaire about their personal and environmental characteristics. The indoor microbiome and metabolites from vacuumed indoor dust were profiled via shotgun metagenomics and untargeted liquid chromatography-mass spectrometry (LC-MS). The nasal and oral microbiota in children was characterized using full-length 16S rRNA sequencing from PacBio. Associations between personal/environmental characteristics and the nasal/oral microbiota were calculated using PERMANOVA and regression analyses. We identified 6247, 431, and 342 microbial species in the indoor dust, nasal, and oral cavities, respectively. The overall nasal and oral microbial composition showed significant associations with environmental tobacco smoke (ETS) exposure during pregnancy and early childhood (p = 0.005 and 0.03, respectively), and the abundance of total indoor flavonoids and two mycotoxins (deoxynivalenol and nivalenol) (p = 0.01, 0.02, and 0.03, respectively). Notably, the abundance of several flavonoids, such as baicalein, eupatilin, isoliquiritigenin, tangeritin, and hesperidin, showed positive correlations with alpha diversity and the abundance of protective microbial taxa in nasal and oral cavities (p < 0.02), suggesting their potential beneficial roles in promoting nasal/oral health. Conversely, high carbohydrate/fat food intake and ETS exposure diminished protective microorganisms while augmenting risky microorganisms in the nasal/oral cavities. Further, potential microbial transfer was observed from the indoor environment to the childhood oral cavity (Moraxella catarrhalis, Streptococcus mitis, and Streptococcus salivarius), which could potentially increase virulence factors related to adherence and immune modulation and vancomycin resistance genes in children. This is the first study to reveal the association between the indoor microbiome/metabolites and nasal/oral microbiota using multi-omic approaches. These findings reveal potential protective and risk factors related to the indoor microbial environment.

Prevalence, risk factors, impact and management of pneumonia among preschool children in Chinese seven cities: a cross-sectional study with interrupted time series analysis.

BACKGROUND: Pneumonia is a common disease worldwide in preschool children. Despite its large population size, China has had no comprehensive study of the national prevalence, risk factors, and management of pneumonia among preschool children. We therefore investigated the prevalence of pneumonia among preschool children in Chinese seven representative cities, and explore the possible risk factors of pneumonia on children, with a view to calling the world's attention to childhood pneumonia to reduce the prevalence of childhood pneumonia. METHODS: Two group samples of 63,663 and 52,812 preschool children were recruited from 2011 and 2019 surveys, respectively. Which were derived from the cross-sectional China, Children, Homes, Health (CCHH) study using a multi-stage stratified sampling method. This survey was conducted in kindergartens in seven representative cities. Exclusion criteria were younger than 2 years old or older than 8 years old, non-permanent population, basic information such as gender, date of birth and breast feeding is incomplete. Pneumonia was determined on the basis of parents reported history of clearly diagnosed by the physician. All participants were assessed with a standard questionnaire. Risk factors for pneumonia, and association between pneumonia and other respiratory diseases were examined by multivariable-adjusted analyses done in all participants for whom data on the variables of interest were available. Disease management was evaluated by the parents' reported history of physician diagnosis, longitudinal comparison of risk factors in 2011 and 2019. RESULTS: In 2011 and 2019, 31,277 (16,152 boys and 15,125 girls) and 32,016 (16,621 boys and 15,395 girls) preschool children aged at 2-8 of permanent population completed the questionnaire, respectively, and were thus included in the final analysis. The findings showed that the age-adjusted prevalence of pneumonia in children was 32.7% in 2011 and 26.4% in 2019. In 2011, girls (odds ratio [OR] 0.91, 95%CI [confidence interval]0.87-0.96; p = 0.0002), rural (0.85, 0.73-0.99; p = 0.0387), duration of breastfeeding ≥ 6 months(0.83, 0.79-0.88; p < 0.0001), birth weight (g) ≥ 4000 (0.88, 0.80-0.97; p = 0.0125), frequency of putting bedding to sunshine (Often) (0.82, 0.71-0.94; p = 0.0049), cooking fuel type (electricity) (0.87, 0.80-0.94; p = 0.0005), indoor use air-conditioning (0.85, 0.80-0.90; p < 0.0001) were associated with a reduced risk of childhood pneumonia. Age (4-6) (1.11, 1.03-1.20; p = 0.0052), parental smoking (one) (1.12, 1.07-1.18; p < 0.0001), used antibiotics (2.71, 2.52-2.90; p < 0.0001), history of parental allergy (one and two) (1.21, 1.12-1.32; p < 0.0001 and 1.33, 1.04-1.69; p = 0.0203), indoor dampness (1.24, 1.15-1.33; p < 0.0001), home interior decoration (1.11, 1.04-1.19; p = 0.0013), Wall painting materials (Paint) (1.16, 1.04-1.29; p = 0.0084), flooring materials (Laminate / Composite wood) (1.08, 1.02-1.16; p = 0.0126), indoor heating mode(Central heating)(1.18, 1.07-1.30, p = 0.0090), asthma (2.38, 2.17-2.61; p < 0.0001), allergic rhinitis (1.36, 1.25-1.47; p < 0.0001), wheezing (1.64, 1.55-1.74; p < 0.0001) were associated with an elevated risk of childhood pneumonia; pneumonia was associated with an elevated risk of childhood asthma (2.53, 2.31-2.78; p < 0.0001), allergic rhinitis (1.41, 1.29-1.53; p < 0.0001) and wheezing (1.64, 1.55-1.74; p < 0.0001). In 2019, girls (0.92, 0.87-0.97; p = 0.0019), duration of breastfeeding ≥ 6 months (0.92, 0.87-0.97; p = 0.0031), used antibiotics (0.22, 0.21-0.24; p < 0.0001), cooking fuel type (Other) (0.40, 0.23-0.63; p = 0.0003), indoor use air-conditioning (0.89, 0.83-0.95; p = 0.0009) were associated with a reduced risk of childhood pneumonia. Urbanisation (Suburb) (1.10, 1.02-1.18; p = 0.0093), premature birth (1.29, 1.08-1.55; p = 0.0051), birth weight (g) < 2500 (1.17, 1.02-1.35; p = 0.0284), parental smoking (1.30, 1.23-1.38; p < 0.0001), history of parental asthma (One) (1.23, 1.03-1.46; p = 0.0202), history of parental allergy (one and two) (1.20, 1.13-1.27; p < 0.0001 and 1.22, 1.08-1.37; p = 0.0014), cooking fuel type (Coal) (1.58, 1.02-2.52; p = 0.0356), indoor dampness (1.16, 1.08-1.24; p < 0.0001), asthma (1.88, 1.64-2.15; p < 0.0001), allergic rhinitis (1.57, 1.45-1.69; p < 0.0001), wheezing (2.43, 2.20-2.68; p < 0.0001) were associated with an elevated risk of childhood pneumonia; pneumonia was associated with an elevated risk of childhood asthma (1.96, 1.72-2.25; p < 0.0001), allergic rhinitis (1.60, 1.48-1.73; p < 0.0001) and wheezing (2.49, 2.25-2.75; p < 0.0001). CONCLUSIONS: Pneumonia is prevalent among preschool children in China, and it affects other childhood respiratory diseases. Although the prevalence of pneumonia in Chinese children shows a decreasing trend in 2019 compared to 2011, a well-established management system is still needed to further reduce the prevalence of pneumonia and reduce the burden of disease in children.

Prevalence and influencing factors of wheeze and asthma among preschool children in Urumqi city: a cross-sectional survey.

To investigate the prevalence and indoor environmental influencing factors of wheeze and asthma among preschool children in Urumqi, Xinjiang, China to provide a strong basis for prevention and control. In August 2019, a cross-sectional study involving 8153 preschool children was conducted in 60 kindergartens in Urumqi. The ALLHOME-2 questionnaire was used for childhood wheeze and asthma survey, and the dampness in buildings and health (DBH) questionnaire was used for the childhood home dwelling and living environment survey. Multivariate unconditional logistic regression was then used to analyze the potential influencing factors of childhood asthma and wheeze. The prevalence of wheeze and asthma in children was 4.7% and 2.0%, respectively. Multivariate unconditional logistic regression results suggested that ethnicity other than the Han Chinese (odds ratio (OR) 1.39, 95% confidence interval (CI) 1.05-1.84), caesarean section (OR 1.24, 95% CI 1.00-1.53), family history of asthma (OR 5.00, 95% CI 3.36-7.44), carpet or floor bedding at home (OR 1.40, 95% CI 1.05-1.87), purchasing new furniture in the mother's residence during pregnancy (OR 1.58, 95% CI 1.06-2.36), pet keeping in the residence at aged 0-1 year (OR 1.55, 95% CI 1.13-2.13), passive smoking by child in the current residence (OR 1.35, 95% CI 1.01-1.80), and having mould or hygroma in the child's residence at aged 0-1 year (OR 1.72, 95% CI 1.12-2.64) were risk factors for wheeze. In addition, Girls (OR 0.73, 95% CI 0.59-0.90) was a protective factor for wheeze. Caesarean section (OR 1.46, 95% CI 1.06-2.00), family history of asthma (OR 7.06, 95% CI 4.33-11.53), carpet or floor bedding at home (OR 2.20, 95% CI 1.50-3.23), and pet keeping in the residence at aged 0-1 year (OR 1.64, 95% CI 1.04-1.83) were risk factors for asthma, whereas Girls (OR 0.58, 95% CI 0.42-0.80) was a protective factor for asthma. This survey indicates that the purchase of new furniture, the placement of carpet or floor bedding in the child's residence, the pets keeping, room dampness or moldy phenomena, and passive smoking may all contribute to an elevated risk of wheeze or asthma in children.

Coronarin A modulated hepatic glycogen synthesis and gluconeogenesis via inhibiting mTORC1/S6K1 signaling and ameliorated glucose homeostasis of diabetic mice.

Promotion of hepatic glycogen synthesis and inhibition of hepatic glucose production are effective strategies for controlling hyperglycemia in type 2 diabetes mellitus (T2DM), but agents with both properties were limited. Herein we report coronarin A, a natural compound isolated from rhizomes of Hedychium gardnerianum, which simultaneously stimulates glycogen synthesis and suppresses gluconeogenesis in rat primary hepatocytes. We showed that coronarin A (3, 10 µM) dose-dependently stimulated glycogen synthesis accompanied by increased Akt and GSK3ß phosphorylation in rat primary hepatocytes. Pretreatment with Akt inhibitor MK-2206 (2 µM) or PI3K inhibitor LY294002 (10 µM) blocked coronarin A-induced glycogen synthesis. Meanwhile, coronarin A (10 µM) significantly suppressed gluconeogenesis accompanied by increased phosphorylation of MEK, ERK1/2, ß-catenin and increased the gene expression of TCF7L2 in rat primary hepatocytes. Pretreatment with ß-catenin inhibitor IWR-1-endo (10 µM) or ERK inhibitor SCH772984 (1 µM) abolished the coronarin A-suppressed gluconeogenesis. More importantly, we revealed that coronarin A activated PI3K/Akt/GSK3ß and ERK/Wnt/ß-catenin signaling via regulation of a key upstream molecule IRS1. Coronarin A (10, 30 µM) decreased the phosphorylation of mTOR and S6K1, the downstream target of mTORC1, which further inhibited the serine phosphorylation of IRS1, and subsequently increased the tyrosine phosphorylation of IRS1. In type 2 diabetic ob/ob mice, chronic administration of coronarin A significantly reduced the non-fasting and fasting blood glucose levels and improved glucose tolerance, accompanied by the inhibited hepatic mTOR/S6K1 signaling and activated IRS1 along with enhanced PI3K/Akt/GSK3ß and ERK/Wnt/ß-catenin pathways. These results demonstrate the anti-hyperglycemic effect of coronarin A with a novel mechanism by inhibiting mTORC1/S6K1 to increase IRS1 activity, and highlighted coronarin A as a valuable lead compound for the treatment of T2DM.

Lung cancer as adverse health effect by indoor radon exposure in China from 2000 to 2020: A systematic review and meta-analysis.

Indoor radon exposure is thought to be associated with adverse health effect as lung cancer. Lung cancer incidences in China have been the highest worldwide during the past two decades. It is important to quantitively address indoor radon exposure and its health effect, especially in countries like China. In this paper, we have conducted a meta-analysis based on indoor radon and its health effect studies from a systematic review between 2000 and 2020. A total of 8 studies were included for lung cancer. We found that the relative risk (RR) was 1.01 (95% CI: 1.01-1.02) per 10 Bq/m3 increase of indoor radon for lung cancer in China. The subgroup analysis found no significant difference between the conclusions from the studies from China and other regions. The health effect of indoor radon exposure is relatively consistent for the low-exposure and high-exposure groups in the subgroup analysis. With a better understanding of exposure level of indoor radon, the outcomes and conclusions of this study will provide supports for next phase of researches on estimation of environmental burden of disease by indoor radon exposures in countries like China.

Health effects of exposure to sulfur dioxide, nitrogen dioxide, ozone, and carbon monoxide between 1980 and 2019: A systematic review and meta-analysis.

The burden of disease attributed to the indoor exposure to sulfur dioxide (SO2 ), nitrogen dioxide (NO2 ), ozone (O3 ), and carbon monoxide (CO) is not clear, and the quantitative concentration-response relationship is a prerequisite. This is a systematic review to summarize the quantitative concentration-response relationships by screening and analyzing the polled effects of population-based epidemiological studies. After collecting literature published between 1980 and 2019, a total of 19 health outcomes in 101 studies with 182 health risk estimates were recruited. By meta-analysis, the leave-one-out sensitivity analysis and Egger's test for publication bias, the robust and reliable effects were found for SO2 (per 10 µg/m3 ) with chronic obstructive pulmonary diseases (COPD) (pooled relative risks [RRs] 1.016, 95% CI: 1.012-1.021) and cardiovascular diseases (CVD) (RR 1.012, 95%CI: 007-1.018), respectively. NO2 (per 10 µg/m3 ) had the pooled RRs for childhood asthma, preterm birth, lung cancer, diabetes, and COPD by 1.134 (1.084-1.186), 1.079 (1.007-1.157), 1.055 (1.010-1.101), 1.019 (1.009-1.029), and 1.016 (1.012-1.120), respectively. CO (per 1 mg/m3 ) was significantly associated with Parkinson's disease (RR 1.574, 95% CI: 1.069-2.317) and CVD (RR 1.024, 95% CI: 1.011-1.038). No robust effects were observed for O3 . This study provided evidence and basis for further estimation of the health burden attributable to the four gaseous pollutants.

Walking and taking vitamin C alleviates oxidative stress and inflammation in overweight students, even in the short-term.

Objective: Obese or overweight is a risk factor for some chronic diseases, and oxidative stress and inflammation may be one of the molecular mechanisms leading to the persistence of these chronic diseases. Discovering interventions to alleviate oxidative stress and inflammation in the overweight/obese population, is very important for public health and health education. Methods: A two-week panel intervention study (Run 0-Run 1-Run 2) was conducted. The subjects were 77 overweight/obese undergraduates attending Dali University, with a BMI>24 kg/m2. The physical indices measured at the end of each run included BMI, waist circumference, serum ROS, TNF-α, IL-1ß and urinary 8-OHdG. Students were allocated to one of four intervention groups: No intervention (control); walking; taking vitamin C; and walking + taking vitamin C. Results: The results demonstrated (1) Walking significantly alleviated ROS levels, and this was consistent in Run 1 and Run 2; (2) During Run1, all three intervention modes reduced levels of 8-OHdG, but there was a statistically insignificant increase during Run 2; (3) No alleviating effects of the three intervention modes on TNF-α levels during Run 1 and Run 2 were observed; (4) The alleviating effects of the three intervention modes on IL-1ß levels during Run 1 and Run 2 were clear. Conclusion: Walking and taking vitamin C can reduce levels of ROS, 8-OHdG and IL-1ß, but not TNF-α, in overweight/obese participants. These interventions may become potential preventive measures for the overweight against obese-induced oxidative stress and inflammation.

Indoor formaldehyde levels in residences, schools, and offices in China in the past 30 years: A systematic review.

Exposure to formaldehyde causes a variety of adverse health outcomes, while the distributions of indoor formaldehyde in different building types are still not clear in China. In this study, based on the systematic review of previously published data and Monte Carlo simulation, we assessed geographical and temporal distributions of indoor formaldehyde concentrations in residences, schools, and offices across China. A total of 397 studies covered 34 provincial-level regions since 1986 were collected. The results showed that indoor formaldehyde concentrations in residences, schools, and offices in nationwide were decreasing over years due to the publishment of indoor air quality standards since 2002. During 2011 to 2015, the median concentrations of indoor formaldehyde in newly renovated residences, schools, and offices were 153 µg/m3 , 163 µg/m3 , and 94 µg/m3 , with an exceeding rate of 82%, 46%, and 91% considering a standard threshold of 100 µg/m3 at that time, while the exceeding rate was less than 5% for buildings that were renovated beyond one year. Our findings release the temporal trends and geographic distributions of indoor formaldehyde concentrations in residences, schools, and offices in China in the past 30 years, and provide basic data for the comprehensive evaluation of disease burden attributable to indoor formaldehyde exposure.

Associations of Early-Life Exposure to Submicron Particulate Matter With Childhood Asthma and Wheeze in China.

Importance: Exposure to particulate matter (PM) has been associated with childhood asthma and wheeze. However, the specific associations between asthma and PM with an aerodynamic equivalent diameter of 1 µm or less (ie, PM1), which is a contributor to PM2.5 and potentially more toxic than PM2.5, remain unclear. Objective: To investigate the association of early-life (prenatal and first year) exposure to size-segregated PM, including PM1, PM1-2.5, PM2.5, PM2.5-10, and PM10, with childhood asthma and wheeze. Design, Setting, and Participants: This cross-sectional study was based on a questionnaire administered between June 2019 and June 2020 to caregivers of children aged 3 to 6 years in 7 Chinese cities (Wuhan, Changsha, Taiyuan, Nanjing, Shanghai, Chongqing, and Urumqi) as the second phase of the China, Children, Homes, Health study. Exposures: Exposure to PM1, PM1-2.5, PM2.5, PM2.5-10, and PM10 during the prenatal period and first year of life. Main Outcomes and Measures: The main outcomes were caregiver-reported childhood asthma and wheeze. A machine learning-based space-time model was applied to estimate early-life PM1, PM2.5, and PM10 exposure at 1 × 1-km resolution. Concentrations of PM1-2.5 and PM2.5-10 were calculated by subtracting PM1 from PM2.5 and PM2.5 from PM10, respectively. Multilevel (city and child) logistic regression models were applied to assess associations. Results: Of 29 418 children whose caregivers completed the survey (15 320 boys [52.1%]; mean [SD] age, 4.9 [0.9] years), 2524 (8.6%) ever had wheeze and 1161 (3.9%) were diagnosed with asthma. Among all children, 18 514 (62.9%) were breastfed for more than 6 months and 787 (2.7%) had parental history of atopy. A total of 22 250 children (75.6%) had a mother with an educational level of university or above. Of the 25 422 children for whom information about cigarette smoking exposure was collected, 576 (2.3%) had a mother who was a current or former smoker during pregnancy and 7525 (29.7%) had passive household cigarette smoke exposure in early life. Early-life PM1, PM2.5, and PM10 exposure were significantly associated with increased risk of childhood asthma, with higher estimates per 10-µg/m3 increase in PM1 (OR, 1.55; 95% CI, 1.27-1.89) than in PM2.5 (OR, 1.14; 95% CI, 1.03-1.26) and PM10 (OR, 1.11; 95% CI, 1.02-1.20). No association was observed between asthma and PM1-2.5 exposure, suggesting that PM1 rather than PM1-2.5 contributed to the association between PM2.5 and childhood asthma. There were significant associations between childhood wheeze and early-life PM1 exposure (OR, 1.23; 95% CI, 1.07-1.41) and PM2.5 exposure (OR, 1.08; 95% CI, 1.01-1.16) per 10-µg/m3 increase in PM1 and PM2.5, respectively. Conclusions and Relevance: In this cross-sectional study, higher estimates were observed for the association between PM with smaller particles, such as PM1, vs PM with larger particles and childhood asthma. The results suggest that the association between PM2.5 and childhood asthma was mainly attributable to PM1.

Indoor exposure levels and risk assessment of volatile organic compounds in residences, schools, and offices in China from 2000 to 2021: A systematic review.

The last two decades have witnessed rapid urbanization and economic growth accompanied by severe indoor air pollution of volatile organic compounds (VOCs) in China. However, indoor VOC pollution across China has not been well characterized and documented. This study is a systematic review of field measurements of eight target VOCs (benzene, toluene, xylenes, acetaldehyde, p-dichlorobenzene, butadiene, trichloroethylene, and tetrachloroethylene) in residences, offices, and schools in China from 2000 to 2021. The results show that indoor pollution of benzene, toluene, and xylenes has been more serious in China than in other countries. Spatiotemporal distribution shows lower indoor VOC levels in east and south-east regions and a declining trend from 2000 to 2021. Moving into a dwelling more than 1 year after decoration and improving ventilation could significantly reduce exposure to indoor VOCs. Reducing benzene exposure is urgently needed because it is associated with greater health risks (4.5 × 10-4 for lifetime cancer risk and 8.3 for hazard quotient) than any other VOCs. The present study enriches the database of indoor VOC levels and provides scientific evidence for improving national indoor air quality standards as well as estimating the attributable disease burden caused by VOCs in China.

Associations between indoor environment and lifestyles and sick building syndrome symptoms among adults in Taiyuan and Urumqi of China.

The complex and uncertain causes of sick building syndrome (SBS) have become one of the most challenging and hot issues worldwide. Studies on the correlation between indoor environment and SBS based on local characteristics are relatively limited in China. We studied typical SBS risk factors related to the indoor environment and lifestyle in two northern Chinese cities. The study population was drawn from parents of pre-school children in randomized daycare centers in Taiyuan, Shanxi, and Urumqi, Xinjiang, China (N = 6838). Data on SBS and indoor environment were obtained from cross-sectional questionnaires. Odds ratios (OR) were estimated by multilevel logistic regression and adjusted using gender, atopy, own smoking, home size, and dampness index. Results showed that location, homeownership, year of construction completion, changes in the indoor environment (new furniture and decorations), and changes in indoor air (smoking, burning mosquito repellent and incense, cooking fuels including electricity, natural gas, coal, and wood) might contribute to different levels of SBS in Chinese adults, including eye, nasal, throat, dermal symptoms, and headache and tiredness. The results of the subgroup analysis suggest city and gender differences in susceptibility. Daily cleaning, window opening, and improved ventilation effectively improved SBS. People should improve their indoor environment and lifestyles based on sensitivity factors, gender, and geographic characteristics to reduce SBS risks.

Maternal exposure to PM2.5/BC during pregnancy predisposes children to allergic rhinitis which varies by regions and exclusive breastfeeding.

BACKGROUND: Increasing prevalence of childhood allergic rhinitis(AR) needs a deeper understanding on the potential adverse effects of early life exposure to air pollution. OBJECTIVES: The main aim was to evaluate the effects of maternal exposure to PM2.5 and chemical constituents during pregnancy on preschool children's AR, and further to explore the modification effects of regions and exclusive breastfeeding. METHODS: A multi-center population-based study was performed in 6 cities from 3 regions of China in 2011-2012. Maternal exposure to ambient PM2.5 and main chemical constituents(BC, OM, SO42-, NO3-, NH4+) during pregnancy was assessed and a longitudinal prospective analysis was applied on preschool children's AR. The modification effects of regions and exclusive breastfeeding were investigated. RESULTS: A total of 8.8% and 9.8% of children reported doctor-diagnosed allergic rhinitis(DDAR) and current hay fever, respectively, and 48.6% had less than 6 months of exclusive breastfeeding. The means of PM2.5 during pregnancy were 52.7 µg/m3, 70.3 µg/m3 and 76.4 µg/m3 in the east, north and central south of China, respectively. Multilevel log-binomial model regression showed that each interquartile range(IQR) increase of PM2.5 during pregnancy was associated with an average increase in prevalence ratio (PR) of DDAR by 1.43(95% confidence interval(CI): 1.11, 1.84) and current hay fever by 1.79(95% CI: 1.26, 2.55), respectively. Among chemical constituents, black carbon (BC) had the strongest associations. Across 3 regions, the eastern cities had the highest associations, followed by those in the central south and the north. For those equal to or longer than 6 months of exclusive breastfeeding, the associations were significantly reduced. CONCLUSIONS: Children in east of China had the highest risks of developing AR per unit increase of maternal exposure to PM2.5 during pregnancy, especially BC constituent. Remarkable decline was found in association with an increase in breastfeeding for ≥6 months, in particular in east of China.

Health effects of exposure to indoor volatile organic compounds from 1980 to 2017: A systematic review and meta-analysis.

Exposure to volatile organic compounds (VOCs) indoors is thought to be associated with several adverse health effects. However, we still lack concentration-response (C-R) relationships between VOC levels in civil buildings and various health outcomes. For this paper, we conducted a systematic review and meta-analysis of observational studies to summarize related associations and C-R relationships. Four databases were searched to collect all relevant studies published between January 1980 and December 2017. A total of 39 studies were identified in the systematic review, and 32 of these were included in the meta-analysis. We found that the pooled relative risk (RR) for leukemia was 1.03 (95% CI: 1.01-1.05) per 1 µg/m3 increase of benzene and 1.25 (95%CI: 1.14-1.37) per 0.1 µg/m3 increase of butadiene. The pooled RRs for asthma were 1.08 (95% CI: 1.02-1.14), 1.02 (95% CI: 1.00-1.04), and 1.04 (95% CI: 1.02-1.06) per 1 µg/m3 increase of benzene, toluene, and p-dichlorobenzene, respectively. The pooled RR for low birth weight was 1.12 (95% CI: 1.05-1.19) per 1 µg/m3 increase of benzene. Our findings provide robust evidence for associations between benzene and leukemia, asthma, and low birth weight, as well as for health effects of some other VOCs.

A new mechanism of obeticholic acid on NASH treatment by inhibiting NLRP3 inflammasome activation in macrophage.

OBJECTIVE: Obeticholic acid (OCA) has been proved to play potential therapeutic effect on nonalcoholic steatohepatitis (NASH). Up to now, the study of OCA on NLRP3 inflammasome activation in macrophage is still blank and merits great attention. Here, we aimed to better characterize the role and mechanism of OCA on NASH treatment focusing on NLRP3 inflammasome activation in macrophages. METHODS: The effects of OCA on inflammasome activation were investigated in BMDM, Kupffer cell, BMDC and LX2 cell. Preconditioned media from BMDM culture was used to treat primary hepatocytes to explore the effects of macrophage NLRP3 inflammasome activation on the function of hepatocytes. In vivo, high fat diet plus CCl4 (DIO + CCl4) induced murine NASH model and choline-deficient and amino acid-defined (CDA) diet-induced NASH mice were used to verify the inhibitory effect of OCA on inflammasome activation in liver macrophages and recapitulate its protective role on NASH progressing. To clear up the effect of OCA on macrophage is FXR dependent or not, FXR siRNA was introduced into BMDMs. RESULTS: OCA blockaded NLRP3 inflammasome in BMDMs by impacting on the activation stage and disrupting ASC oligomerization. Preconditioned supernatant from LPS + ATP treated BMDMs increased mRNA expression of lipogenic enzymes and lipid content, whereas preconditioned supernatant from OCA treated BMDM blocked these effects in both normal and the FXR knockdown hepatocytes. In DIO + CCl4 mice, the population of inflammatory myeloid lineage cells in livers was decreased upon OCA treatment. Accordingly, the level of IL-1ß and IL-18 in liver, the hepatic expression of ASC, pro-caspase-1 and active caspase-1, the expression of caspase 1 p20 in liver macrophages were also reduced. Similar results were obtained in CDA diet-fed mice. Furthermore, OCA maintained the inhibition on NLRP3 inflammasome activation in FXR knockdown BMDMs, suggesting FXR could be dispensable in this effect. CONCLUSIONS: This finding brings up a new mechanism of OCA on NASH treatment, suggested by direct inhibition on NLRP3 inflammasome activation in macrophage, further suppression on inflammasome activation-elicited hepatic lipid accumulation, and contributing to the amelioration of NASH.

Necessity of personal sampling for exposure assessment on specific constituents of PM2.5: Results of a panel study in Shanghai, China.

Many epidemiological studies have evaluated the health risks of ambient fine particulate matter (PM2.5). However, few studies have investigated the potential exposure misclassification caused by using ambient PM2.5 concentrations as proxy for individual exposure to PM2.5 in regions with high-level of air pollution. This study aimed to compare the differences between personal and ambient PM2.5 constituent concentrations, and to predict the personal exposure of sixteen PM2.5 constituents. We collected 141 72-h personal exposure filter samples from a panel of 36 healthy non-smoking college students in Shanghai, China. We then used the liner mixed effects models to predict personal constituent-specific exposure using ambient observations and several possible influencing factors including time-activity patterns, temporal variables, and meteorological conditions. The final model of each component was further evaluated by determination coefficient (R2) and root mean square error (RMSE) from leave-one-out-cross-validation (LOOCV). We observed ambient concentrations were higher than personal concentrations for all PM2.5 components except for Mn, Fe, Ca, and V. Especially, ambient NH4+, As, and NO3- concentrations were 3.65, 5.65 and 7.33-fold higher than their corresponding personal concentrations, respectively. The ambient level was the strongest predictor of their corresponding personal PM2.5 components with the highest marginal R2 (RM2: 0.081 ~ 0.901), meteorological conditions (RM2: 0.000 ~ 0.357), time-activity pattern (RM2: 0.000 ~ 0.083) and temporal indicators (RM2: 0.031 ~ 0.562) were also important predictors. Our final models predicted at least 50% of the variance of all personal PM2.5 constituents and even over 90% for K, Pb, and SO42-. LOOCV analysis showed that R2 and RMSE ranged from 0.251 to 0.907 and 0.000 to 0.092 µg/m3, respectively. Our results showed that ambient concentration of most PM2.5 constituents along with time-activity patterns, temporal variables, and meteorological conditions, could adequately predict personal exposure concentration. Prediction models of individual PM2.5 constituent may help to improve the accuracy of exposure measurement in future epidemiological studies.

Effects of parental smoking and indoor tobacco smoke exposure on respiratory outcomes in children.

The extensive literature has reported adverse effects on environmental tobacco smoke (ETS) on children's health. We aim to analyze associations of ETS with dry night cough, croup, pneumonia, and frequent common cold and to disentangle the effects of prenatal, infancy and childhood exposure by multilevel logistic regression. A cross-sectional study was conducted among 41,176 children aged 3-8 years in 8 major cities of China during 2010-2011, and obtained demographic information, smoke exposure information, and respiratory outcomes. Parents' smoking habit and indoor tobacco smoke odor were considered as two indicators of ETS. The prevalences of respiratory outcomes were 6.0% for croup, 9.5% for frequency common cold, 17.1% for dry night cough and 32.3% for pneumonia respectively in the study. The associations between respiratory outcomes and parental smoking were not obvious, while indoor tobacco smoke odor was clearly and strongly associated with most respiratory outcomes, with adjusted odds ratios ranging from 1.06 to 1.95. Both infancy and childhood exposure to tobacco smoke odor were independent risk factors, but infancy exposure had a higher risk. The results explore that ETS increased the risk of respiratory outcomes in children, highlighting the need for raising awareness about the detrimental effects of tobacco smoke exposure.

Onset of respiratory symptoms among Chinese students: associations with dampness and redecoration, PM10, NO2, SO2 and inadequate ventilation in the school.

Objective: To study onset of respiratory symptoms among students in China in relation to the school and the home environment. Methods: A two-year prospective cohort study among 1325 students in eight schools. Air pollution was measured at baseline in the schools. Respiratory symptoms and the home environment were assessed by a questionnaire. Results: The 2-year onset was 14.3%, 23.2%, 15.4%, 4.7% and 37.3% for wheeze, daytime attacks of breathlessness, nocturnal cough, nocturnal wheeze/breathlessness and respiratory infections, respectively. The mean concentrations of PM10, SO2, NO2, ozone and CO2 in the classrooms were 129 µg/m3, 68.0 µg/m3, 43.2 µg/m3, 8.6 µg/m3 and 1208 ppm, respectively. Environmental tobacco smoke (ETS), dampness/mold at home and ozone in the classroom were associated with onset of wheeze. Onset of daytime breathlessness was associated with redecoration and dampness/mold at home and CO2 and relative air humidity (RH) in the classrooms. Dampness/mold at home, PM10, CO2 and RH in the classrooms and outdoor PM10, SO2 and NO2 were associated with onset of nocturnal cough. Onset of nocturnal wheeze/breathlessness was associated with dampness/mold at home and RH and PM10 in the classrooms. Respiratory infections were more common at higher levels of outdoor PM10. Conclusions: Air pollution (PM10, ozone, SO2 and NO2) and inadequate ventilation flow in the classrooms (indicated by CO2 > 1000 ppm) and ETS, dampness or mold and chemical emissions from redecoration at home can increase onset of respiratory symptoms.

Personal Fine Particulate Matter Constituents, Increased Systemic Inflammation, and the Role of DNA Hypomethylation.

Limited evidence is available on the effects of various fine particulate matter (PM2.5) components on inflammatory cytokines and DNA methylation. We examined whether 16 PM2.5 components are associated with changes in four blood biomarkers, that is, tumor necrosis factor-α (TNF-α), soluble cluster of differentiation 40 ligand (sCD40L), soluble intercellular adhesion molecule-1 (sICAM-1), and fibrinogen, as well as their corresponding DNA methylation levels in a panel of 36 healthy college students in Shanghai, China. We used linear mixed-effect models to evaluate the associations, with controls of potential confounders. We further conducted mediation analysis to evaluate the potential mediation effects of components on inflammatory markers through change in DNA methylation. We observed that several components were consistently associated with TNF-α and fibrinogen as well as their DNA hypomethylation. For example, an interquartile range increase in personal exposure to PM2.5-lead (Pb) was associated with 65.20% (95% CI: 37.07, 99.10) increase in TNF-α and 2.66 (95% CI: 37.07, 99.10) decrease in TNF-α methylation, 30.51% (95% CI: 0.72, 69.11) increase in fibrinogen and 1.25 (95% CI: 0.67, 1.83) decrease in F3 methylation. PM2.5 components were significantly associated with sICAM-1 methylation but not with sICAM-1 protein. DNA methylation mediated 19.89%-41.75% of the elevation in TNF-α expression by various PM2.5 constituents. Our findings provide clues that personal PM2.5 constituents exposure may contribute to increased systemic inflammation through DNA hypomethylation.