大气污染与人体健康

随着经济的较快增长，大气污染日趋严重，达到一定程度，就会影响人的身体健康。根据大气污染物的来源不同，可以将空气污染粗略地分为两类，一是以SO2和TSP(颗粒物)为主要污染物的煤烟型污染；二是以氮氧化物、一氧化碳、铅为主要污染物的交通型污染。由于污染物的成分不同，其对人体的影响也不同，现将污染物对人体的影响分析如下。     

微量元素与人体健康的关系

目前证实在人体内存在元素有七十余种,其中含量占人体总质量万分之一以下的元素人们称之为微量元素。微量元素又分人体必需和非必需两种。现在认识到人体必需微量元素有十七种,它们是 Fe、Cu、Zn、Cr、I、Se、Mn、Sn、Co、F、Mo、V、Si、Ni、Ge、B和 As 元素。微量元素在人体内含量虽少,但作用非     

碘与人体健康的关系及临床应用

碘是人体必需的微量元素，是合成甲状腺激素的重要成分。碘是一种稀有元素，属于强氧化剂，主要以I^2、I^0、I^或者IO3的形式存在。游离碘可与多种元素结合，不易溶于水，但可溶于碘化钾的水溶液和多种仃机溶媒（乙醇、氯仿，苯）中，在自然界中碘以化合物状态存在。     

硒与人体健康

在人体组织中,有20多种元素是构成人体组织、维持生理功能、生化代谢所必需的,其中含量〈0.01%者称之为微量元素。目前已检测出70多种人体微量元素,维持正常生命活动不可缺少的必需微量元素共有14种,硒元素就是其中一种。     

锌与人体健康

微量元素锌与一系列的代谢有关,人体中锌的缺乏将会导致一系列代谢紊乱和病理变化,致使DNA、RNA的合成减少,结缔组织蛋白、肠粘液蛋白的合成及维生素A的代谢过程受到干扰。又、锌参与了,核酸和蛋白质的代谢过程,在纤维细胞增殖和胶合过程中起关键作用,因而缺锌就会出现一系列与生长发育迟缓、性机能障碍等有关的症状。锌参与缺血缺氧肌肉中能量代谢,锌可改善血流灌注,因而与肢体动脉硬化性跛行有关。锌在眼含色素的组织中浓度很高,当维生素A醇转变成能制造视紫质的     

重金属-镍对人体健康的危害及预防

本文探讨了重金属镍对人体健康的危害（炎症、癌症、神经衰弱、系统紊乱,以及降低生育能力、致畸、致突变等）,以及对镍中毒的预防措施。     

大气污染对松江乡人体健康的影响

我们调查了松江小学(污染区)和郊区小学(对照区)的1100余名小学生的身高、体重、胸围、植物血凝素(PHA)皮疹、肺功能等项指标,污染区普遍低子对照区;还统计分析了污染区居民的病伤死亡原因,与对照区比较,总死亡率和50岁以上各年龄别死亡率污染区高于对照区。本文阐明了大气污染对人体健康的影响。     

月亮圆缺与人体健康

人们常说“月有阴晴圆缺，人有悲欢离合”，此语也形象地说明，我们的命运与月亮一样变化不定，人月同理。现在，科学家已经有了充分的依据证明，我们的身体与情绪确实随着月亮的阴晴圆缺发生着微妙的变化。     

兽药与人体健康的若干问题

介绍了兽药的特点，及其残留和危害，并总结了我国兽药残留的现状，揭示兽药对人体健康的严重影响。     

室内外空气污染对儿童呼吸健康的影响及相关因素研究

目的　探讨不同水平室内外空气污染对儿童呼吸系统的影响 ,并进行相关因素分析。方法　选取位于太原市城区中心的坝陵桥地区为重污染点 ,位于太原北郊的上兰村地区为轻污染点 ,分别抽取两地学龄儿童30 2人 ,通过问卷调查、肺功能检查结果比较以及进行肺功能主要参数的相关因素分析。结果　通过两地生活环境和个人一般情况比较发现 ,坝陵桥地区灶具以燃气灶为主 ,取暖以中心供暖为主 ,通风条件较好 ;上兰村地区主要以煤炉为灶具和以燃煤为主要供暖方式 ,且家庭通风条件差。两组肺功能参数比较 ,仅在用力肺活量 ( FVC)、第1秒量 ( FEV1 .0 )和 FVC50 %时流速 / FVC2 5%时流速 ( V5 0 / V2 5 )三项差异有显著的统计学意义 ,除 FVC外 ,FEV1 .0和 V5 0 / V2 5 坝陵桥组 (重污染点 )高于上兰村组 (轻污染点 ) ;同时问卷调查也显示轻污染点儿童呼吸系统疾病症状和发生多于重污染组。进一步选择坝陵桥燃气组与上兰村燃煤组儿童进行了比较 ,显示 FVC和 V5 0 / V2 5两项差异有显著的统计学意义 ,V5 0 / V2 5 值坝陵桥组仍高于上兰组。多元逐步回归分析结果显示儿童性别、家人吸烟量、家中取暖设备及通风条件与肺功能有关。结论　室内外空气污染对儿童大、小气道功能均有影响 ,室内小环境污染 (呼吸带水平 )对儿童?     

The toxicology of air pollution predicts its epidemiology

Abstract

The epidemiologic investigation has successively delineated associations of air pollution exposure with non-malignant and malignant lung disease, cardiovascular disease, cerebrovascular disease, pregnancy outcomes, perinatal effects and other extra-pulmonary disease including diabetes. Defining these relationships between air pollution exposure and human health closely parallels results of an earlier epidemiologic investigation into cigarette smoking and environmental tobacco smoke (ETS), two other particle-related exposures. Humic-like substances (HULIS) have been identified as a chemical component common to cigarette smoke and air pollution particles. Toxicology studies provide evidence that a disruption of iron homeostasis with sequestration of host metal by HULIS is a fundamental mechanistic pathway through which biological effects are initiated by cigarette smoke and air pollution particles. As a result of a common chemical component and a shared mechanistic pathway, it should be possible to extrapolate from the epidemiology of cigarette smoking and ETS to predict associations of air pollution exposure with human disease, which are currently unrecognized. Accordingly, it is anticipated that the forthcoming epidemiologic investigation will demonstrate relationships of air pollution with COPD causation, peripheral vascular disease, hypertension, renal disease, digestive disease, loss of bone mass/risk of fractures, dental disease, eye disease, fertility problems, and extrapulmonary malignancies.     

Black smoke air pollution and daily non-accidental mortality in Nis, Serbia

The short-term effects of ambient black smoke concentrations on total non-accidental, cardiovascular and respiratory mortalities in Nis, during the 2000-2003 period, were investigated. Daily measurements for black smoke (BS), as well as the daily number of deaths have been collected. Generalised linear models extending Poisson regression were applied. The e.ects of time trend, seasonal variations, days of the week, temperature, humidity and air pressure were adjusted. The per cent increase in the daily number of total deaths associated with a 10 μg/m³ increase in BS was 1.13% (0.08–2.20%). The e.ect size was slightly higher for cardiovascular mortality (1.25%, 95% CI: 0.53–1.97%). There was no signi.cant association between air pollution and respiratory mortality. These results indicate that current levels of ambient BS have signi.cant e.ects on total and cardiovascular mortalities in Nis.     

甲醛空气污染对桂花叶形态特征的急性损害

目的：观察室内甲醛污染对盆栽桂花成熟叶片的急性损害。方法：将盆栽培育的桂花放人自制染毒箱,分别用浓度为32．60mg／ml、3．260mg／ml、0．326mg／ml、0．0326mg/ml、0．00326mg／ml的甲醛溶液3．1ml以薰气法染毒桂花24h,放入实验棚内继续培养10d,每组每株随机采摘100张叶片,采用双盲法观察叶片的形态特征变化。结果：各染毒组间与阴性对照组比较差异有极显著性（P〈0．001）。当剂量达1．0mg/ml,叶中部及叶尖开始出现明显不规则斑块状损害,并有剂量一反应关系。结论：甲醛空气污染可以导致盆栽桂花叶片出现急性损害．并表现出明显的效应。     

不同环境压力下吸入气体与人体血压调节的关系

目的探讨环境压力对血压影响的作用机制。方法在高压仓内,施加0～0.5个大气压的环境压力,分别给予不同压力的氧气和加压空气,观察受试者血压的变化情况。结果在环境压力与吸入气体压力一致的情况下,血压变化与环境压力同步变化(P<0.001),吸入高压氧气与加压空气,血压改变无显著性差异(P>0.05);在环境压力与吸入氧气压力不一致的情况下,血压与环境压力同步变化(P<0.001),呼吸气体压力的改变小于血压变化值。结论正压状态下,人体血压的调节作用主要是通过环境压力来完成的,没有证据显示这一机制与呼吸气体的氧浓度和压力有关。     

Pre and post-natal exposure to ambient level of air pollution impairs memory of rats: the role of oxidative stress

The aims of this study were to evaluate whether air pollution during pre-natal and post-natal phases change habituation and short-term discriminative memories and if oxidants are involved in this process. As secondary objectives, it was to evaluate if the change of filtered to nonfiltered environment could protect the cortex of rats against oxidative stress as well as to modify the behavior of these animals. Wistar, male rats were divided into four groups (n?=?12/group): pre and post-natal exposure until adulthood to filtered air (FA); pre-natal period to nonfiltered air (NFA-FA); until (21st post-natal day) and post-natal to filtered air until adulthood (PND21); pre-natal to filtered air until PND21 and post-natal to nonfiltered air until adulthood (FA-NFA); pre and post-natal to nonfiltered air (NFA). After 150 days of air pollution exposure, animals were tested in the spontaneous object recognition test to evaluate short-term discriminative and habituation memories. Rats were euthanized; blood was collected for metal determination; cortex dissected for oxidative stress evaluation. There was a significant increase in malondialdehyde (MDA) levels in the NFA group when compared to other groups (FA: 1.730?±?0.217; NFA-FA: 1.101?±?0.217; FA-NFA: 1.014?±?0.300; NFA: 5.978?±?1.920?nmol MDA/mg total proteins; p?=?0.007). NFA group presented a significant decrease in short-term discriminative (FA: 0.603?±?0.106; NFA-FA: 0.669?±?0.0666; FA-NFA: 0.374?±?0.178; NFA: ?0.00631?±?0.106?sec; p?=?0.006) and an improvement in habituation memories when compared to other groups. Therefore, exposure to air pollution during both those periods impairs short-term discriminative memory and cortical oxidative stress may mediate this process.     

The effects of air pollution and smoking on placental cadmium, zinc concentration and metallothionein expression

This study is designed to determine the placental zinc (Zn) and cadmium (Cd) levels in mothers who were smokers, mothers who were thought to be exposed to air pollution, and mothers who were non-smokers and to investigate the relationship between the expression of placental metallothionein (MT) binding these metals and blood progesterone level. Placental Zn and Cd levels were measured by atomic absorption spectrometry. Presence of placental MT was determined immunohistochemically. Placental changes were examined by light microscope after H&E and PAS staining. Immunohistochemical MT staining of syncytiotrophoblastic and villous interstitial cells were scored as positive or negative. Among the 92 mothers included in the study, 33 were smokers (Group I), 29 had been exposed to air pollution (Group II) and 30 were non-smoker rural residents who had never been exposed to air pollution (Group III). Mean off-spring birth weight of 3198.62+/-380.01 g and mean placenta weight of 561.38+/-111.55 g of Group II were lower when compared with those of other two groups. In Group I, mean placental Cd and Zn were 0.063+/-0.022 microg/g and 39.84+/-15.5 microg/g, respectively, being higher than in other groups. In Group II, mean placental Cd and Zn levels were higher than those of Group III. Blood progesterone levels of subjects in Group I (121 ng/ml) were the lowest of all groups. While the mean count of villi was the highest in Group III; the highest mean count of syncytial knots was in Group II. Thickening of vasculo-syncytial membrane was most prominent in Group I. Similarly, MT staining was positive and very dense in 72.7% (24/33) of cases in Group I (p相似文献   

Alveolar macrophage cytokine response to air pollution particles: oxidant mechanisms

Alveolar macrophages (AMs) primed with LPS and treated with concentrated ambient air particles (CAPs) showed enhanced release of tumor necrosis factor (TNF) and provide an in vitro model for the amplified effects of air pollution particles seen in people with preexisting lung disease. To investigate the mechanism(s) by which CAPs mediate TNF release in primed rat AMs, we first tested the effect of a panel of antioxidants. N-Acetyl-l-cysteine (20 mM), dimethyl thiourea (20 mM) and catalase (5 microM) significantly inhibited TNF release by primed AMs incubated with CAPs. Conversely, when LPS-primed AMs were treated with CAPs in the presence of exogenous oxidants (H(2)O(2) generated by glucose oxidase, 10 microM/h), TNF release and cell toxicity was significantly increased. The soluble fraction of CAPs suspensions caused most of the increased bioactivity in the presence of exogenous H(2)O(2). The metal chelator deferoxamine (DFO) strongly inhibited the interaction of the soluble fraction with H(2)O(2) but had no effect on the bioactivity of the insoluble CAPs fraction. We conclude that CAPs can mediate their effects in primed AMs by acting on oxidant-sensitive cytokine release in at least two distinct ways. In the primed cell, insoluble components of PM mediate enhanced TNF production that is H(2)O(2)-dependent (catalase-sensitive) yet independent of iron (DFO-insensitive). In the presence of exogenous H(2)O(2) released by AMs, PMNs, or other lung cells within an inflamed alveolar milieu, soluble iron released from air particles can also mediate cytokine release and cell toxicity.     

Rat models of cardiometabolic diseases: baseline clinical chemistries,and rationale for their use in examining air pollution health effects

Abstract

Individuals with cardiovascular and metabolic diseases (CVD) are shown to be more susceptible to adverse health effects of pollutants. Rodent models of CVD are used for examining susceptibility variations. CVD models developed by selective inbreeding are shown to represent the etiology of human disease and metabolic dysfunction. The goal of this article was to review the origin and the pathobiological features of rat models of varying CVD with or without metabolic syndrome and healthy laboratory rat strains to allow better interpretation of the data regarding their susceptibility to air pollutant exposures. Age-matched healthy Sprague–Dawley (SD), Wistar (WIS) and Wistar Kyoto (WKY), and CVD-prone spontaneously hypertensive (SH), Fawn-Hooded hypertensive (FHH), SH stroke-prone (SHSP), SHHF/Mcc heart failure obese (SHHF) and insulin-resistant JCR:LA-cp obese (JCR) rat models were considered for this study. The genetics and the underlying pathologies differ between these models. Normalized heart weights correlated with underlying cardiac disease while wide differences exist in the number of white blood cells and platelets within healthy strains and those with CVD. High plasma fibrinogen and low angiotensin converting enzyme activity in FHH might relate to kidney disease and associated hypertension. However, other obese strains with known kidney lesions do not exhibit decreases in ACE activity. The increased activated partial thromboplastin time only in SHSP correlates with their hemorrhagic stroke susceptibility. Increases plasma lipid peroxidation in JCR might reflect their susceptibility to acquire atherosclerosis. These underlying pathologies involving CVD and metabolic dysfunction are critical in interpretation of findings related to susceptibility variations of air pollution health effects.     

Closing the gap between science and policy on air pollution and health

This paper discusses critical issues underlying the interface between air quality science, stakeholder participation, and policy development within the context of the European AIRNET Network multistakeholder project. The paper argues that it is not only the content of air pollution and health issues that stakeholders consider important, but also the process and mechanisms by which the interface operates. A visual representation of the interaction between science, society, and stakeholders in the development, dissemination, and evaluation of effective air quality policy strategies is provided. The paper discusses the role of AIRNET in supporting the Clean Air for Europe (CAFE) program and assesses the AIRNET experience in establishing a network to bridge the gap between air quality policy, stakeholders, the public, and scientific communities.