摘要：
We estimated associations between ambient air pollution, home environment and asthma as well as rhinitis among adults across China. A total of 40,279 young adults from eight Chinese cities participated in a questionnaire survey (participation rate 75%). There were questions on health and home environment. Information on city level gross domestic product (GDP) per capita, ambient temperature and PM10 and NO2 were collected from registers. Two-level logistic regression models were used to study health associations. Totally 1.6% reported asthma and 6.6% reported allergic rhinitis (AR). Higher temperature was associated with more asthma but less AR. Higher GDP was associated with less asthma but more AR. Higher degree of urbanization, higher level of NO2 and living near heavily trafficked road were risk factors for asthma and AR. Participants in older buildings reported more asthma. Redecoration and buying new furniture were related to more asthma and AR (OR = 1.15-1.91). Using natural gas (OR = 1.34) and biomass (OR = 1.35) for cooking were risk factors for AR. Burning mosquito coils and incense increased the risk of asthma and AR. Cat keeping (OR = 2.88), dog keeping (OR = 2.04), cockroaches (OR = 1.54) and rats or mice (OR = 1.46) were associated with asthma. Cockroaches increased the risk of AR (OR = 1.22). Air humidifier and air cleaner were linked to asthma and AR. Frequent cleaning and exposing bedding to sunshine were protective. In conclusion, urbanization, NO2 and traffic exhaust can increase the risk of adult asthma and AR. Higher ambient temperature was related to more asthma but less AR. Indoor animals such as cats, dogs, rats/mice and presence of cockroaches were associated with asthma or AR. Indoor chemical sources such as redecoration and new furniture were other risk factors. Cooking with natural gas or biomass and burning mosquito coils and incense were associated with asthma or AR. Frequent cleaning and exposing bedding to sunshine were protective. (C) 2020 The Authors. Published by Elsevier B.V.
作者：
Zhao, Yun;Magana, Laura C.;Cui, Haiyan;Huang, Jiawei;McHale, Cliona M.;...
期刊：
Archives of Toxicology,2021年95(2):693-701 ISSN：0340-5761
通讯作者：
Zhang, Luoping;Li, Rui
作者机构：
[Zhang, Luoping; McHale, Cliona M.; Zhao, Yun; Magana, Laura C.] Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;[Li, Rui; Yang, Xu; Zhao, Yun; Huang, Jiawei; Cui, Haiyan] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.;[Looney, Mark R.] Univ Calif San Francisco UCSF, Dept Med, San Francisco, CA USA.;[Looney, Mark R.] Univ Calif San Francisco UCSF, Dept Lab Med, San Francisco, CA USA.
通讯机构：
[Zhang, Luoping] U;[Li, Rui] C;Univ Calif Berkeley, Sch Publ Hlth, Div Environm Hlth Sci, Berkeley, CA 94720 USA.;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan, Peoples R China.
摘要：
BACKGROUND: As cooking is an essential part of people's daily life, cooking oil fumes (COF) has been recognized as one of the major indoor air pollutant. Mounting epidemiological evidence has indicated that COF exposure is significantly associated with an increased risk of various health effects including lung cancer, but toxicological studies are very limited. OBJECTIVES: We conduct a systematic study to provide toxicological evidence of COF exposure on the lungs, to examine the underlying toxicological mechanism, and to suggest intervention measures to mitigate this toxicity. METHODS: A total 96 female rats were randomly divided into control groups, COF exposure groups (0.2, 2, 20 mg/kg) and vitamin E protection groups, receiving appropriate treatment for 30 days. First we measured airway hyperresponsiveness (AHR) followed by a lung histological analysis to investigate the toxicological effects of COF. We next analyzed the biomarkers of oxidative stress, inflammation, and apoptosis to examine the underlying toxicological mechanism, and finally we investigated the protective effects of vitamin E against the toxicity of COF. RESULTS: AHR measurement indicated that the airway resistance increased with the COF dose and the lung histological assay showed narrowing of the airway lumen, which provided evidence of the toxicological effects of COF. The biomarkers of oxidative stress (ROS and MDA), pro-inflammation (TNF-α and IL-1β), and apoptosis (NF-κB and Caspase-3) were all significantly increased with COF dose. We observed that above toxicological effects and biomarker levels induced by COF were significantly ameliorated after administration of VE. CONCLUSION: The toxicity of cooking oil fumes on the lungs is clear from the evidence and mechanism, and can be ameliorated by vitamin E. We suggested that oxidative stress may be primarily responsible for the observed cooking oil fumes-induced toxicity.
关键词：
building materials;childhood rhinitis;household renovation;indoor air quality;renovation periods
摘要：
During 2010-2012, we surveyed 40,010 3- to 6-year-old children in seven Chinese cities (Beijing, Taiyuan, Urumqi, Shanghai, Nanjing, Changsha, and Chongqing). Their parents reported information on household renovation, including the timing of renovation and the choice of materials for walls and floors in the child's room, and the incidence of their child's rhinitis. Multivariate and two-level (city-child) logistic regression analyses yielding adjusted odds ratios (AOR) with 95% confidence intervals were performed. Sensitivity analyses stratifying data for location and economic level were also performed. About 48.0% of the children had ever had allergic rhinitis, 41.2% had current allergic rhinitis, and 9.0% had had doctor-diagnosed rhinitis. Exposure to household renovation during early lifetime (birth to 1-year-old) had an AOR of 1.43 (1.04-1.9) for allergic rhinitis. The incidence of allergic rhinitis was significantly different in children exposed to different floor and wall covering materials. Floor or wall covering material composed of organic materials significantly increased the risk of childhood allergic rhinitis compared with tile flooring or lime wall covering. Oil paint had an AOR of 1.66 (1.28-2.14) for diagnosed rhinitis compared with lime wall covering. Adding new furniture the year before pregnancy was associated with an AOR of 1.18 (1.10-1.27) and 1.18 (1.11-1.25) for lifetime and current rhinitis. Solid wood or tiles/ceramic as floor materials, and using wallpaper, oil paint, or emulsion panels as wall materials were risk factors for doctor-diagnosed rhinitis. Sensitivity analyses showed that children living in southern or higher economic level China cities were more likely to have allergic rhinitis with household renovation.
摘要：
Epidemiology suggests ambient temperature is the triggers and potential activator of asthma. The role of high and low temperatures on airway inflammation of asthma, and the underlying molecular mechanism are not yet understood. A mouse model of asthma was adopted in our experiment. The BALB/c mice were exposed at different temperature for 4h (2h in the morning and 2h in the afternoon) on weekday. The exposure temperatures were 10 degrees C, 24 degrees C and 40 degrees C. Ovalbumin (OVA) was used to sensitize the mice on days 14, 18, 22, 26, and 30, followed by an aerosol challenge for 30min from day 32-38. After the final OVA challenge, lung function, serum protein and pulmonary inflammation were assessed. Comparing the OVA with the saline group at 24 degrees C, we saw a significant increase in: serum Total-IgE (p<0.05); OVA-sIgE (p<0.01); IL-4 (p<0.05); IL-1beta (p<0.01); IL-6 (p<0.01); TNF-alpha (p<0.01); and the ratio of IL-4/IFN-gamma (p<0.01). At the same time, there was a significant decrease in IFN-gamma (p<0.01). As the temperature increase, there is a U shape for immune proteins and pro-inflammatory factors with a peak value at 24 degrees C, exception for IFN-gamma (inverted U-shape). After the high and low temperature exposure, the Ri and Re increased significantly, while Cldyn decreased significantly compared with the 24 degrees C group. Histopathological analysis of the OVA groups showed airway remodeling, airway wall thickening and deforming, and subepithelial fibrosis. More obvious changes were found in the high and low temperature exposure groups. The immunohistochemistry suggested that TRPs changed with temperatures. High and low temperatures can aggravate airway inflammation in a mouse model of asthma. TRPs play an important role in temperature aggravation of allergic asthma. The results suggest that asthmatics should avoid exposure to high and low temperatures for too long time.
摘要：
Dibutyl phthalate (DBP) is one of the most ubiquitous phthalate esters found in everyday products, and is receiving increased attention as an immunologic adjuvant. However, information regarding DBP-aggravated allergic asthma is still limited. This study used a mouse model sensitized with ovalbumin (OVA) to determine any adverse effects of DBP on allergic asthma. Our results reveal that allergic asthmatic mice exposed to DBP for an extended period had a significant increase in inflammatory cell infiltration; a significant increase in levels of serum immunoglobulin and T helper 2 cell (Th2) and T helper 17 cell (Th17) cytokines in lung tissue; and significant changes in lung histology and AHR, all of which are typical asthmatic symptoms. The levels of oxidative stress and levels of the neuropeptide, calcitonin gene related peptide (CGRP), were also elevated after DBP exposure. Interestingly, blocking oxidative stress by administering melatonin (MT) not only reduced oxidative stress and CGRP levels, but also ameliorated the asthmatic symptoms. Collectively, these results show that DBP exacerbates asthma-like pathologies by increasing the expression of CGRP mediated by oxidative stress.
作者机构：
[Hua Qian; Zheng, Xiaohong; Yang Zhuge] Southeast Univ, Sch Energy & Environm, Nanjing, Peoples R China.;[Chen Huang] Univ Shanghai Sci & Technol, Sch Environm & Architecture, Shanghai, Peoples R China.;[Sundell, Jan; Zhang, Yinping] Tsinghua Univ, Beijing Key Lab Indoor Air Qual Evaluat & Control, Beijing, Peoples R China.;[Li, Baizhan] Chongqing Univ, Key Lab Three Gorges Reservoir Reg Ecoenvironm, Chongqing, Peoples R China.;[Zhao, Zhuohui] Fudan Univ, Sch Publ Hlth, Shanghai, Peoples R China.
通讯机构：
[Hua Qian] S;Southeast Univ, Sch Energy & Environm, Nanjing, Peoples R China.
摘要：
<jats:title>Abstract</jats:title><jats:p>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.</jats:p>
摘要：
This paper studied associations between reported common cold and home dampness and mould, cleaning habits and ventilation, climate and outdoor air pollution in China among young adults without asthma or allergic rhinitis. Parents of children attending day care in eight Chinese cities answered a questionnaire on then health and home environment (75% response rate). We restricted the population to subject without asthma or allergic rhinitis (N 37,275). Temperature and air pollution data was obtained from monitoring stations. Associations were estimated by multilevel logistic regression. Totally 12.5% reported common cold (?"3 colds) and 1.6% frequent common cold (?5 colds) in the past 12 months. Female gender (OR 1.53; 95%01.37-1.71), residents in southern China (OR 1.89; 95% CII.16-3.07) and living in homes with water leakage (OR 1.32; 95% C11.16-1.50), mould odour (OR 1.48; 95% (11.28-172), indoor mould (OR 1.47; 95% Cl 1.28-1.70), condensation on window panes (OR 1.42; 95%01.32-1.52) and clamp bed clothing (OR 1.19; 95% C11.11-1.28) were associated with common cold. Having many signs of dampness increased ORs. Daily cleaning (OR 0.91; 95% C10.85-0.97) and mechanical ventilation in kitchen or bathroom (OR 0.75; 95%, CI 0.64-0.89) were protective. Higher mean ambient temperature (OR 1.11 per "C; 95%, CI 1.02-1.21), PM io (OR 1.17 per 10 iiglin3; 95% CI 1.14-1.21) and PM-2.5 (OR 1.28 per 10 figlm3; 95% CI 1.20-1.37) were associated with common cold. The association with particulate air pollution was stronger in southern China Similar associations were found for frequent common cold. In conclusion, indoor dampness and mould, a warmer climate and PM10 and PM25 can be associated wiLh reported common cold. further intervention and prospective studies are needed to verify causality of observed association in this cross-sectional study. (C) 2020 The Authors. Published by Elsevier B.V.
作者机构：
[Fei, Xuechao; Yue, Xiangpei; He, Rongqiao; Jiang, Wenjing; Mei, Yufei; Tong, Zhiqian; Ai, Li] Capital Med Univ, Collaborat Innovat Ctr Brain Disorders, Beijing Inst Brain Disorders, Lab Brain Disorders,Alzheimers Dis Ctr,Minist Sci, Beijing 100069, Peoples R China.;[Zhang, Yun; Song, Weihong] Capital Med Univ, Xuanwu Hosp, Adv Innovat Ctr Human Brain Protect, Natl Clin Res Ctr Geriatr Disorders, Beijing 100053, Peoples R China.;[Zhang, Yun; Song, Weihong] Univ British Columbia, Dept Psychiat, Townsend Family Labs, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.;[Mei, Yufei] Zhejiang Univ, Sch Basic Med Sci, Hangzhou 310058, Peoples R China.;[Lyv, Jihui; Jiang, Wenjing] Beijing Geriatr Hosp, Ctr Cognit Disorders, Beijing 100095, Peoples R China.
通讯机构：
[Tong, Zhiqian; Song, Weihong] C;[Song, Weihong] U;Capital Med Univ, Collaborat Innovat Ctr Brain Disorders, Beijing Inst Brain Disorders, Lab Brain Disorders,Alzheimers Dis Ctr,Minist Sci, Beijing 100069, Peoples R China.;Capital Med Univ, Xuanwu Hosp, Adv Innovat Ctr Human Brain Protect, Natl Clin Res Ctr Geriatr Disorders, Beijing 100053, Peoples R China.;Univ British Columbia, Dept Psychiat, Townsend Family Labs, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.
摘要：
Dysregulation of formaldehyde (FA) has been implicated in the development of Alzheimer's Disease (AD). Elevated FA levels in Alzheimer's patients and animal models are associated with impaired cognitive functions. However, the exact role of FA in AD remains unknown. We now identified that oxidative demethylation at serine(8/26) of amyloid-beta protein (A beta) induced FA generation and FA cross-linked with the lysine(28) residue in the beta-turn of A beta monomer to form A beta dimers, and then accelerated A beta oligomerization and fibrillogenesis in vitro. However, A beta 42 mutation in serine(8/26), lysine(28) abolished A beta self-aggregation. Furthermore, A beta inhibited the activity of formaldehyde dehydrogenase (FDH), the enzyme for FA degradation, resulting in FA accumulation. In turn, excess of FA stimulated A beta aggregation both in vitro and in vivo by increasing the formation of A beta oligomers and fibrils. We found that degradation of FA by formaldehyde scavenger-NaHSO3 or coenzyme Q10 reduced A beta aggregation and ameliorated the neurotoxicity, and improved the cognitive performance in APP/PS1 mice. Our study provides evidence that endogenous FA is essential for A beta self-aggregation and scavenging FA could be an effective strategy for treating AD.
摘要：
Circulating tumor DNA (ctDNA) as a class of liquid biopsy is a type of gene fragment that contains tumor-specific gene changes in body fluids such as human peripheral blood. More and more evidences show that ctDNA is an excellent tumor biomarker for diagnosis, prognosis, tumor heterogeneity and so on. ctDNA is a tumor code in the blood. Liquid biopsy of ctDNA is firstly summarized. Compared with the traditional detection technologies of ctDNA, the biosensor is an excellent choice for the detection of ctDNA because of its portability, sensitivity, specificity and ease of use. This review mainly evaluates various biosensors applied to the detection of ctDNA. We discuss the most commonly used bioreceptors to specifically identify and bind ctDNA, including complementary DNA (cDNA), peptide nucleic acid (PNA) and anti-5 MethylCytosines, and the biotransducers which convert biological signals to analysable signs. The review also discusses signal amplification strategies in biosensors to detect ctDNA.
作者机构：
[Yang, Xu; Zhang, Yuchao; Liu, Xudong] Moutai Inst, Dept Food Sci & Engn, Renhuai 564507, Peoples R China.;[Yang, Xu] Cent China Normal Univ, Coll Life Sci, Lab Environm Biomed, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Yang, Xu] M;[Yang, Xu] C;Moutai Inst, Dept Food Sci & Engn, Renhuai 564507, Peoples R China.;Cent China Normal Univ, Coll Life Sci, Lab Environm Biomed, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
摘要：
Neurodegenerative diseases (ND) affect a large and ever-growing population globally, resulting in heavy burdens for patients and their families. Though some specific genes related to ND have been identified, the genetic factors fail to fully account for the pathogenesis of ND. Therefore, the roles of the environment and life styles in the occurrence of ND are being actively probed. As a typical air pollutant, exposures to PM2.5 are linked to the occurrence of ND. However, there are still few studies on this exposure, particularly on the in vivo and molecular mechanisms of the ND-like lesions after PM2.5 exposure. To investigate this link further, C57BL/6J mice were exposed everyday to PM2.5 for one week. Then, resulting brain damage and upstream events were investigated. After acute PM2.5 exposure, several ND-like changes were detected, such as cognitive deficits, loss of neurons, protein aggregates etc. Oxidative stress and inflammation may be involved with these toxic mechanisms. These effects were blocked by concurrent administration of vitamin E (Vit E). Down-regulation of oxidative stress and inflammation were proposed to explain the antagonistic effects of Vit E.
摘要：
Around the globe, worsening air pollution is spawning major public health and environmental concerns, especially in the poorest and most populous cities. As a major secondary air pollutant, ozone is a potential risk factor for exacerbated asthma, although the underlying mechanisms remain uncertain. In this study, we aim to investigate the role of ozone on asthma exacerbation using a classic asthmatic model with allergic airway inflammation by treating Balb/c mice with ovalbumin (OVA). Our study shows ozone exposure significantly exacerbated OVA-induced asthmatic phenotypes, including serum immunoglobulin, Th cytokines, inflammatory cell counts, mucus production, airway remodeling, and airway hyper responsiveness (AHR). Interestingly, expression of transient receptor potential cation channel subfamily V memberl (TRPV1) was also significantly elevated in ozone-exacerbated asthmatic mice and that treatment with TRPVI antagonist effectively suppressed AHR, airway inflammation and remodeling. The underlying mechanisms of these effects may be associated with suppression of neuropeptide calcitonin gene-related peptide (CGRP) and thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine. Base on the role of TRPV1 in allergic asthma, this study further revealed that inhibition of TRPVI by TRPV1 antagonist has significant anti-inflammatory effects on ozone-induced asthma exacerbation in this study. Induction of TRPVI expression may be an important mechanism underlying the increased risks for asthma after exposure to environmental pollutants. (C) 2019 Elsevier Ltd. All rights reserved.
作者机构：
[Li, Yan; Wang, Pengcheng] Wuhan Polytech Univ, Key Lab Deep Proc Major Grain & Oil, Minist Educ, Coll Food Sci & Engn, Wuhan, Hubei, Peoples R China.;[Wu, Yang; Gong, Zhiyong] Wuhan Polytech Univ, Hubei Key Lab Proc & Transformat Agr Prod, Coll Food Sci & Engn, Wuhan, Hubei, Peoples R China.;[Yang, Xu] Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Coll Life Sci, Wuhan, Hubei, Peoples R China.
通讯机构：
[Wu, Yang] W;[Yang, Xu] C;Wuhan Polytech Univ, Hubei Key Lab Proc & Transformat Agr Prod, Coll Food Sci & Engn, Wuhan, Hubei, Peoples R China.;Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Coll Life Sci, Wuhan, Hubei, Peoples R China.
会议名称：
Joint Symposium of the 9th International Conference of th Chinese-Society-of-Micro-Nano-Technology (CSMNT) / Microsystems and Nanoengineering Summit (MAN)
会议时间：
AUG 17-20, 2018
会议地点：
Hohhot, PEOPLES R CHINA
会议主办单位：
[Li, Yan;Wang, Pengcheng] Wuhan Polytech Univ, Key Lab Deep Proc Major Grain & Oil, Minist Educ, Coll Food Sci & Engn, Wuhan, Hubei, Peoples R China.^[Gong, Zhiyong;Wu, Yang] Wuhan Polytech Univ, Hubei Key Lab Proc & Transformat Agr Prod, Coll Food Sci & Engn, Wuhan, Hubei, Peoples R China.^[Yang, Xu] Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Coll Life Sci, Wuhan, Hubei, Peoples R China.
关键词：
3D cell cuture;MnO2 nanowires;oxidative stress;vascular toxicity
作者机构：
[Fei, Xuechao; He, Rongqiao; Di, Yalan; Bai, Shangying; Tong, Zhiqian; Wang, Xiaoming; Ai, Li] Capital Med Univ, Beijing Inst Brain Disorders, Alzheimers Dis Ctr, Beijing 100069, Peoples R China.;[Fei, Xuechao; He, Rongqiao; Di, Yalan; Bai, Shangying; Tong, Zhiqian; Wang, Xiaoming; Ai, Li] Capital Med Univ, Ctr Brain Disorders Res, Beijing 100069, Peoples R China.;[Tan, Tao] SUNY Buffalo, Sch Med & Biomed Sci, Dept Physiol & Biophys, Buffalo, NY 14214 USA.;[Tan, Tao] Sichuan Prov Hosp Women & Children, Chengdu 610000, Sichuan, Peoples R China.;[Wang, Weishan; Lin, Weiying; Tang, Yonghe] Jinan Univ, Inst Fluorescent Probes Biol Imaging, Sch Chem & Chem Engn, Sch Mat Sci & Engn, Jinan 250022, Shandong, Peoples R China.
通讯机构：
[Tong, Zhiqian] C;Capital Med Univ, Beijing Inst Brain Disorders, Alzheimers Dis Ctr, Beijing 100069, Peoples R China.;Capital Med Univ, Ctr Brain Disorders Res, Beijing 100069, Peoples R China.
摘要：
Gaseous formaldehyde is an organic small molecule formed in the early stages of earth’s evolution. Although toxic in high concentrations, formaldehyde plays an important role in cellular metabolism and, unexpectedly, is found even in the healthy brain. However, its pathophysiological functions in the brain are unknown. Here, we report that under physiological conditions, spatial learning activity elicits rapid formaldehyde generation from mitochondrial sarcosine dehydrogenase (SARDH). We find that elevated formaldehyde levels facilitate spatial memory formation by enhancing N-methyl-D-aspartate (NMDA) currents via the C232 residue of the NMDA receptor, but that high formaldehyde concentrations gradually inactivate the receptor by cross-linking NR1 subunits to NR2B. We also report that in mice with aldehyde dehydrogenase-2 (ALDH2) knockout, formaldehyde accumulation due to hypofunctional ALDH2 impairs memory, consistent with observations of Alzheimerʼs disease patients. We also find that formaldehyde deficiency caused by mutation of the mitochondrial SARDH gene in children with sarcosinemia or in mice with Sardh deletion leads to cognitive deficits. Hence, we conclude that endogenous formaldehyde regulates learning and memory via the NMDA receptor. Ai et al. report that endogenous formaldehyde bidirectionally modulates cognition via the NMDA-R receptor, with both insufficiency and overabundance resulting in cognitive defects. The target site of formaldehyde enhancing NMDA-currents is cysteine C232 residue in amino terminal domain sequence of the NR2B subunit of NMDA-R and excessive formaldehyde suppresses NMDA-R activity by cross-linking NR1 to NR2B residues.
作者机构：
[Ai, Li; Fei, Xuechao; Di, Yalan; Wang, Xiaoming; Bai, Shangying; He, Rongqiao; Tong, Zhiqian] Alzheimer’s Disease Center, Beijing Institute for Brain Disorders;Center for Brain Disorders Research, Capital Medical University, Beijing, China;[Tang, Yonghe; Wang, Weishan; Lin, Weiying] Institute of Fluorescent Probes for Biological Imaging, School of Chemistry and Chemical Engineering, School of Materials Science and Engineering, University of Jinan, Shandong, China;[Cai, Xiang] Department of Physiology, Southern Illinois University School of Medicine, Carbondale, USA;[Yu, Yan; Zhao, Shengjie] Beijing Boai Hospital, China Rehabilitation Research Center, Beijing, China
通讯机构：
[Zhiqian Tong] A;Alzheimer’s Disease Center, Beijing Institute for Brain Disorders;Center for Brain Disorders Research, Capital Medical University, Beijing, China
关键词：
building materials;childhood eczema;China;home renovation;renovation periods
摘要：
We surveyed 40 010 three- to six-year-old children in seven Chinese cities (Beijing, Taiyuan, Urumqi, Shanghai, Nanjing, Changsha, and Chongqing) during 2010-2012 so as to investigate possible links between home renovation and childhood eczema. Their parents responded to questions on home renovation and childhood eczema. Multivariate and two-level (city-child) logistic regression analyses yielding odds ratios with 95% confidence intervals were performed. Sensitivity analyses stratifying data for region, climate, and income level were also performed. The prevalences of childhood eczema in children with different floor and wall covering materials were significantly different and were significantly higher with home renovation during early lifetime. Exposure to synthetic materials significantly increased the risk of childhood eczema by 20%-25%. The risks (AOR, 95% CI) of current eczema among children in families with solid wood flooring and oil paint wall covering were 1.25 (1.04-1.49) and 1.35 (1.14-1.60), respectively. Home renovation during pregnancy was related to children's lifetime and current eczema.
