汽油车尾气排出物的致突变和致癌效应

本文概述了目前汽油车尾气的致突变及致癌性研究进展，研究表明汽油车尾气提物具有很强的致突变效应，可引起实验动物染毒部位发生肿瘤，然而吸入致癌实验未能得到肯定的结果，有限的人群调查结果尚不能证明汽油车尾气是使接触人群发生肺癌肿瘤的因素。     

汽车尾气提取物对哺乳动物细胞程序外DNA合成的影响

用大鼠原代肝细胞ＵＤＳ实验检测５种汽油车和一种柴油车尾气颗粒物及气体冷凝物的遗传毒性，均获阳性结果，表明颗粒物和气体部分中都含有损伤ＤＮＡ物质。颗粒物中，吉普、桑塔纳和公交车诱变性较强，气体部分以公交、解放和桑塔纳高。以每升排放物比较，柴油车颗粒排放量高，尾气总致突变作用最高，公交和吉普车稍次之．除柴油车和吉普外，其余车型尾气诱变性皆以气体部分为主。     

国产汽车尾气提取物的致突变性研究

采用ＴＡ９８和ＴＡ１００两种菌株检测汽车尾气中颗粒及气体冷凝提取物的致突变性，所有样品均有明显的致突变效应，以诱导ＴＡ９８菌株回变为主。综合比较，由于柴油车颗粒排放量高，每Ｌ排放物诱导的菌落回变数最高，除柴油车和吉普车外，其余汽油车尾气的间接诱变作用均以气体部分为主。     

铅暴露与致癌和致突变研究进展

铅是一种自然界广泛存在的有毒重金属物质,也是常见的环境和职业污染物。虽然多年来铅及其化合物对机体的各种组织毒效应研究很多,但其致癌、致突变相关研究仍存在争议。基于充分的动物实验和不充分的人群研究,IARC将铅列为可疑的人类致癌物(2B)。此外,虽然铅的生化和分子机制不清楚,但有研究显示,铅通过间接机制发挥其遗传毒性作用,如抑制DNA的修复或自由基的产生。作者就近年来动物致癌实验、人群流行病学调查、体内试验等,对铅的致癌、致突变相关研究予以综述。     

六种维生素和铜对亚硝化处理的酱油致突变性影响的研究

<正> 有关的流行病学调查发现酱油和消化道癌症的发病有密切相关。从酱油中可以分离出致突变性和致癌变性前体物质,用其饲喂动物,可以诱发肿瘤。酱油亚硝化后,其中的致突变性或致癌变性前体物质可形成很强的具有致癌变作用的亚硝胺。文献表明,多种食物和营养素可以阻断亚硝化的过程,防止亚硝胺的形成。国产酱油中存在微量的亚硝胺,我们检测了40种酱油亚硝化后对TA98和TA100的致突变作用,全部样品都表现出很强的致突变性。本文用体外试验,模拟体内的亚硝化过程,用维生素和铜阻断亚硝化过程,并观察处理后的酱油对TA100致突变性的影响。     

遗传毒理学生物实验现状——显性致死实验

显性致死实验是直接测定化学物对整体动物生殖细胞潜在致突变性的一种实验方法,其作用是证实在较低级的染色体畸变实验系统中检测到的阳性结果,以说明化学物进入生殖细胞,引起染色体损伤的可能性,但在致癌实验     

TNT远期效应的初步研究

关于三硝基甲苯(简称TNT)的致畸、致突变和致癌等远期效应,远未阐明。国外迄今未见TNT中毒致癌的人体和动物材料,致畸资料更完全空白。Won等曾用Ames法检测TNT的致突变性,发现浓度为0.5至10微克/毫     

杀虫脒生产工人劳动卫生学调查及其对人体致突变效应的观察

自从杀虫脒对动物的致癌性,经国内、外的小鼠致癌实验都得到证实后,关于杀虫脒对人体的健康影响及对人致突变、致癌的远期效应如何,必然地引起人们强烈的关注和讨论,极需积累职业流行病学方面的资料。为此,我们连续3天在无锡市电化厂杀虫脒车间进行了劳动卫生学现场调查,并作了包装工外周血淋巴细胞微核率测定和尿中致突变物的Ames试验,以期为研究杀虫脒的职业危害及其防护措施,为探讨杀虫脒对人体细胞致突变以及潜在致癌影响的可能性初步积累资料。     

尿中致突变物的浓缩、致突变性鉴定方法及吸烟者尿中致突变物的鉴定

本文应用XAD-2树脂对尿中已知致突变物浓缩分离后,进行了Ames试验,对检测尿中致突交物的实验条件进行了研究。并对吸烟者的尿样进行了致突变性鉴定。三种致突变物经XAD—2树脂吸附后的回收率如下:呋喃丙胺59.53～63.63％,4-基邻苯二胺71.87％,2—氨基芴32.38％。10个吸烟者的尿样,在加S—9的情况下对TA_(98)菌株均显示出致突变阳性结果,而10个非吸烟者的尿样,8个无致突变性,其它2个为弱致突变性。用XAD—2树脂吸附浓缩尿中致突变物的方法具有许多优点,适用于现场大量人群尿样的致突变性检测。此外在研究化学致癌的机理、毒理学研究、临床药物筛选等方面,都可通过人或动物的尿致突变性测定提供有价值的资料。     

苯乙烯致突变性致癌性评价

本研究选用Ames试验、骨髓染色体畸变分析和皮肤致癌实验优化组合,评价苯乙烯的致突变性和致癌性。结果表明苯乙烯经代谢活化后引起TA_(100)沙门氏突变株回复突变,证明苯乙烯属于碱基取代型致突变物。骨髓染色体畸变分析表明340mg/kg剂量下的苯乙烯引起明显的小鼠骨髓染色体畸变。小鼠皮肤致癌实验中最高剂量组只出现1例阳性。结果提示苯乙烯是致突变物和可疑致癌物。本研究为苯乙烯安全性评价,制定卫生标准提供了实验数据。     

含铅和无铅汽油汽车尾气成分和致突变性

为探讨含铅和无铅汽油汽车尾气成分和致突变性,使用含铅、无铅两种汽油,分别检测尾气中的一氧化碳（ＣＯ）和碳烃类化合物（ＨＣ）及颗粒物水平,同时利用气相色谱－质谱联用（ＧＣ／ＭＳ）对颗粒物吸附的有机物进行了分析并采用中国仓鼠肺组织（ＣＨＬ）体外微核实验检测了致突变性。结果显示无铅汽油能显著地减少ＣＯ、ＨＣ及颗粒物的排放,但两种汽油尾气颗粒物有机提取物均能诱导ＣＨＬ细胞微核率的升高,两种汽油一定量的颗粒     

Toxicity of prolonged exposure to ethanol and gasoline autoengine exhaust gases

A comparative chronic inhalation exposure study was performed to investigate the potential health effects of gasoline and ethanol engine exhaust fumes. Test atmospheres of gasoline and ethanol exhaust were given to Wistar rats and Balb C mice housed in inhalation chambers for a period of 5 weeks. Gas concentration and physical parameters were continually monitored during the exposure period. Several biological parameters were assessed after the exposure including pulmonary function, mutagenicity, and hematological, biochemical, and morphological examinations. The results demonstrated that the chronic toxicity of the gasoline-fueled engine is significantly higher than that of the ethanol engine.     

Oxidative Damage of the Extracts of Condensate,Particulate and Semivolatile Organic Compounds from Gasoline Engine Exhausts on Testicles of Rats

Oxidative damage induced by extracts of condensate, particulate matters and semivolatile organic compounds from gasoline engine exhausts were investigated in testicles of adult Sprague-Dawley rats. The results showed that gasoline engine exhaust could increase the contents of malondialdehyde and carbonyl protein, decrease activities of superoxide dismutase and glutathione peroxidase, and induce DNA damage in testicle of rat. Taking together, the gasoline engine exhaust could promote oxidative damage of bio-macromolecular in testicles of rat and oxidative stress might be an alternative mechanism for male reproductive function of male mammals.     

Public health aspects of air pollution fromdiesel vehicles

“To say that any source of air pollution is completely harmless would be utter folly. The exhaust products of petrol and diesel exhausts may yet be shown to contain some compound which has evil effects hitherto unrecognized. But it can be said with confidence that there has been no justification whatsoever for the attacks so frequently made against the diesel engine on the grounds of its supposed effects on health. The emission by diesel engines of large amounts of noisome black smoke is indefensible and is a great nuisance. Fortunately there is no good evidence at present that it is more than that. There can be no doubt that on evidence at present available from many studies, both epidemiological and experimental, that the diesel propelled vehicle is pollutionwise much safer than that propelled by petrol engines.Any review, however brief, of the health aspect of pollution by the exhaust products of diesel-powered vehicles must be prefaced by a firm statement that the diesel engine has been indicted by many authors, and by public opinion, on wholly inadequate evidence; frequently the grounds on which it has been blamed for causing ill-health have been based merely on emotional attitudes which may have been engendered in relation to the righteous indignation felt on witnessing the emission of black smoke from improperly functioning vehicles.Mortality and morbidity have been studied among carefully standardized populations of employees in large public transport undertakings, and, happily, there is no evidence from such studies that men who work in garages or on buses suffer more death or sickness absence than those who work in other branches of the transport industry” (W.H.O., 1967).     

Effects of exposure to vehicle exhaust on health

Exposure to combustion engine exhaust and its effect on crews of roll-on roll-off ships and car ferries and on bus garage staff were studied. The peak concentrations recorded for some of the substances studied were as follows: total particulates (diesel only) 1.0 mg/m3, benzene (diesel) 0.3 mg/m3, formaldehyde (gasoline and diesel) 0.8 mg/m3, and nitrogen dioxide (diesel) 1.2 mg/m3. The highest observed concentration of benzo(a)pyrene was 30 ng/m3 from gasoline and diesel exhaust. In an experimental study volunteers were exposed to diesel exhaust diluted with air to achieve a nitrogen dioxide concentration of 3.8 mg/m3. Pulmonary function was affected during a workday of occupational exposure to engine emissions, but it normalized after a few days with no exposure. The impairment of pulmonary function was judged to have no appreciable, adverse, short-term impact on individual work capacity. In the experimental exposure study, no effect on pulmonary function was observed. Analyses of urinary mutagenicity and thioether excretion showed no sign of exposure to genotoxic compounds among the occupationally exposed workers or among the subjects in the experimental study.     

汽油车尾气颗粒物中有机成分分析及对细胞免疫毒性研究

为了研究汽油车尾气颗粒物有机提取物中几种多环芳烃的含量及其对小鼠细胞功能的影响。「方法」采用大流量空气采样器采集汽油车尾气颗粒物,用高效液相色谱仪分析颗粒物有机提取物中６种多环芳烃（苯并（ａ）芘、苯并（ａ）蒽、Ｑｉ、芘、菲、晕苯）的含量。     

MTBE: recent carcinogenicity studies

MTBE, a gasoline oxygenate, has contaminated drinking water sources for many years. Carcinogenicity studies conducted in animals in the 1990s raised concerns of potential human health risks. Recent industry-sponsored studies have confirmed the carcinogenic effects of this agent and have identified additional sites of tumor induction (i.e., brain). However, the petroleum industry has attempted to portray these recent findings as demonstrating either no effect or no concern for humans. Our paper briefly summarizes the new findings and puts into perspective the totality of carcinogenic effects and health risks on this environmental chemical.     

Combustion of diesel fuel from a toxicological perspective

Epidemiological data and results of toxicity studies in experimental animals indicate the possible health risk of diesel exhaust exposure. Acute effects of this exposure include odor, eye irritations, lung function decrements, cardiovascular symptoms, and some non-specific effects. Most of these effects are reported among persons highly exposed to diesel exhaust. Lung function decrements are reported as chronic effects. Another chronic effect that has been studied extensively among occupationally exposed persons in lung cancer. In addition to lung cancer, but at a less frequent rate, an enhanced incidence of bladder cancer is reported. The carcinogenic action of diesel exhaust exposure is ascribed to effects of the soot particles, particle-associated organics, and/or gas phase compounds. Direct effects of the particle load may include retardation of lung clearance, inflammation, and increased cell proliferation. These effects were all demonstrated in rodents. The particles may also prolong the residence time of particulate organics or induce the generation of reactive oxygen species. These compounds are known to react with macromolecules, causing lipid peroxidation, DNA damage, and/or activation of other genotoxic substances such as polycyclic aromatic hydrocarbons (PAHs). However, these results have not yet been confirmed in mammals in vivo. A direct interaction of particles with lung tissue is also suggested as a cause of cancer but a mechanism for this interaction has not yet been proposed. Organics associated with the particles are known to contain genotoxic properties attributable to PAHs and their derivatives. A number of these compounds are also identified as carcinogens in animal studies. However, it is not clear whether parent PAHs, their nitro-, oxy-, alkylated, or heterocyclic derivatives, or possibly other compounds are principally responsible for inducing tumors in the lungs of animals after diesel exhaust exposure. Furthermore, the mechanism of the bioavailability of these organics is not completely understood. The effects of gas phase constituents on the carcinogenic properties of the particles and/or particle-associated organics either have not been investigated or the findings have been inconclusive.     

MTBE: recent carcinogenicity studies

Abstract

MTBE, a gasoline oxygenate, has contaminated drinking water sources for many years. Carcinogenicity studies conducted in animals in the 1990s raised concerns of potential human health risks. Recent industry-sponsored studies have confirmed the carcinogenic effects of this agent and have identified additional sites of tumor induction (i.e., brain). However, the petroleum industry has attempted to portray these recent findings as demonstrating either no effect or no concern for humans. Our paper briefly summarizes the new findings and puts into perspective the totality of carcinogenic effects and health risks on this environmental chemical.