燃汽油机动车尾气致核酸分子氧化损伤效应研究

目的：通过研究燃汽油机动车尾气成分，及其对DNA分子的氧化损伤，在分子生物学水平上探讨燃汽油机动车尾气污染物的遗传毒性效应与机制。方法：以DNA加合物8-羟基脱氧鸟苷(8-OHdG)作为DNA氧化损伤的生物学标志物，用高压液相色谱-电化学检测(HPLC-EC)法对污染物染毒后的DNA中8-OHdG进行定量检测，通过气质联用法(GC-MS)进行有机成分分析和原子吸收法(AAS)对其进行无机元素分析，并从化学组成成分的角度探讨DNA氧化损伤的分子机理。结果：在燃汽油机动车尾气的颗粒物和挥发性有机物中分别检出有机污染物85种和46种，无机元素7种和5种。燃汽油机动车尾气颗粒物和挥发性有机物均可在体外直接诱导DNA氧化损伤，尾气颗粒物还可诱导大鼠肺组织DNA氧化损伤，并呈现一定的剂量—反应关系。结论：污染物直接以及间接的氧化作用，源于含有醌类、多酚等具有自氧化作用的化合物，不需要任何生物活化系统，在体外就可产生大量的活性氧自由基，并在金属离子的催化作用下进攻DNA的碱基形成8-OHdG，产生遗传毒性效应，而8-OHdG是DNA氧化损伤的较好的效应标志物。     

汽油尾气对大鼠睾丸组织的氧化损伤和遗传毒性作用

目的探讨汽油尾气对大鼠睾丸的遗传毒性及氧化损伤作用。方法将汽油尾气的颗粒物、冷凝物和半挥发性有机物的二氯甲烷提取物以0、5.6、16.7和50.0L/kg的剂量经气管滴注染毒SD大鼠,每周一次,共4次。末次染毒24h后处死动物,测定睾丸脏器系数、睾丸组织内丙二醛(MDA)和羰基蛋白(CP)含量以及超氧化物岐化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性;并用彗星实验检测睾丸组织细胞中DNA的单链断裂水平。结果各剂量组体重增重和睾丸脏脏器系数与对照组相比差异无显著性(P>0.05);中、高剂量染毒组睾丸组织中MDA和CP含量显著升高;各剂量组SOD酶活力明显降低(P<0.05),而GSH-Px活性的下降仅在高剂量组具有显著性。在16.7L/kg和50.0L/kg组,睾丸组织细胞的拖尾率较对照组明显增加(P<0.05),但尾长的增加仅在50.0L/kg组具有统计学意义。结论汽油尾气可诱导大鼠睾丸组织生物大分子的氧化损伤和DNA单链断裂。     

汽车尾气对大鼠肺脏的氧化应激和遗传毒性作用

[目的]探讨汽车尾气对大鼠肺脏生物大分子的氧化损伤作用。[方法]将汽车尾气的颗粒物、冷凝物和半挥发性有机物的二氯甲烷提取物（extracts of gasoline engine exhaust,EGE）减压挥干后用二甲亚砜（dimethyl sulfoxide,DMSO）定容到200L／mL。将40只SD大鼠分为5组,每组8只。以DMSO为溶剂对照,以汽车尾气0、5．6、16．7、50．0L／kg的剂量经气管滴注染毒,每周1次,共4次,末次染毒24h后处死,测定肺脏脏器系数以及肺组织内丙二醛（malondialdehyde,MDA）和羰基蛋白（carbonyl protein,CP）含量以及超氧化物岐化酶（superoxide dismutase,SOD）、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH—Px）活力;并用彗星试验检测肺组织细胞中DNA的损伤程度。[结果]各组动物体重和肺脏脏器系数与对照组相比差异无统计学意义（P〉0．05）;16．7、50．0L／kg剂量组肺组织中MDA含量分别达到了4．57、4．48nmol／mg蛋白,故对照组明显升高（P〈0．05）;CP含量在50．0L／kg剂量组为8．91μmol／mg蛋白,较对照组明显增加（P〈0．05）;SOD和GSH—Px活力在50．0L／kg剂量组分别为1697．61NU／mg蛋白和14．80U／mg蛋白,与对照组比较均明显降低（P〈0．05）。在16．7L／kg和50．0L／kg组,肺组织细胞的拖尾率与对照组比较均明显增加（P〈0．05）,但各组尾长的增加无统计学意义。[结论]汽车尾气可诱导大鼠肺组织生物大分子的氧化损伤和DNA单链断裂。     

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     

汽油车尾气的致突变性和致癌性研究进展

该文主要对以汽油为燃料的汽车发动机尾气(简称汽油车尾气)的致突变性和致癌效应的实验研究和流行病学调查进展进行综述。研究表明汽油车尾气对细菌、动物和人均具有明显的遗传毒性和致突变性,但在致癌性方面,动物吸入致癌实验未见新的报道,而流行病学研究的结果仍缺乏一致性。     

汽车尾气的生殖毒性及对微量元素的影响

目的了解使用无铅化汽油后汽车尾气的生殖毒性效应。方法30只SD大鼠等分为实验和对照组,根据染毒时间4、6和8周不等各分为3个亚组,对照组用空白吸收液灌胃,实验组用汽车尾气吸收液灌胃,每周5 d,每天1次,灌胃量0.1 ml/L。观察大鼠生殖毒性及睾丸组织微量元素的变化。结果尾气吸收液染毒大鼠体重变化不明显;睾丸、附睾的脏器系数低于同时相对照组（P〈0.05）,且随时间呈下降趋势;精子含量和存活率显著降低,而畸形率增高（P〈0.05）;睾丸中Zn、Mn代谢紊乱,出现Zn低、Mn高,有时间-效应关系。结论汽车尾气具有明显的生殖毒性,微量元素代谢紊乱对生殖腺的损害起了重要作用。     

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.     

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。     

Occupational exposure to diesel and gasoline engine exhausts and risk of lung cancer among Finnish workers

BACKGROUND: Studies on engine exhausts and lung cancer have given inconsistent results. METHODS: Economically active Finns were followed-up for lung cancer during 1971-95 (33,664 cases). Their Census occupations in 1970 were converted to exposures to diesel and gasoline engine exhausts with a job-exposure matrix. The relative risks (RRs) for cumulative exposure (CE) were defined by Poisson regression, adjusted for smoking, asbestos, and quartz dust exposure, and socioeconomic status. RESULTS: RR for engine exhausts among men did not increase with increasing CE. In women, RR for gasoline engine exhaust was 1.58 (95% CI 1.10-2.26) in the CE-category of 1-99 mg/m(3)-y and 1.66 (1.11-2.50) among those with > or =100 mg/m(3)-y (lag 20 years). With a lag of 10 years RR for the middle/highest diesel exhaust category in women was 1.42 (0.94-2.13). CONCLUSIONS: Occupational exposure to engine exhausts was not consistently associated with lung cancer in this study, possibly due to low exposure levels.     

汽油尾气致慢性肺损伤的形态学改变研究

目的探讨汽油机尾气致肺脏慢性损伤的形态学改变。方法大鼠40只,随即分为8组,即对照组、1d、3d、1周、2周、4周、8周、12周,每组5只,将汽油机尾气通入装有实验大鼠的自制染毒容器中染毒,每天染毒2h,于1d、3d、1周、2周、4周、8周、12周分别处死实验大鼠,对肺组织进行HE染色、masson染色,显微镜下对肺组织进行观察。结果前2周以炎症反应为主,4周后可见肺组织开始出现成纤维细胞增生,随时间延长,纤维组织增生也越来越明显,但仍有慢性炎症反应。结论汽油机尾气长期染毒可致大鼠肺脏损伤,以纤维化和慢性炎症为主。     

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.     

Relationship between composition and toxicity of motor vehicle emission samples

In this study we investigated the statistical relationship between particle and semivolatile organic chemical constituents in gasoline and diesel vehicle exhaust samples, and toxicity as measured by inflammation and tissue damage in rat lungs and mutagenicity in bacteria. Exhaust samples were collected from "normal" and "high-emitting" gasoline and diesel light-duty vehicles. We employed a combination of principal component analysis (PCA) and partial least-squares regression (PLS; also known as projection to latent structures) to evaluate the relationships between chemical composition of vehicle exhaust and toxicity. The PLS analysis revealed the chemical constituents covarying most strongly with toxicity and produced models predicting the relative toxicity of the samples with good accuracy. The specific nitro-polycyclic aromatic hydrocarbons important for mutagenicity were the same chemicals that have been implicated by decades of bioassay-directed fractionation. These chemicals were not related to lung toxicity, which was associated with organic carbon and select organic compounds that are present in lubricating oil. The results demonstrate the utility of the PCA/PLS approach for evaluating composition-response relationships in complex mixture exposures and also provide a starting point for confirming causality and determining the mechanisms of the lung effects.     

以甲醇和汽油为燃料的汽车尾气对RAW 264.7细胞的细胞毒性及对其增殖和凋亡的影响

目的研究以甲醇和汽油为燃料的汽车尾气（以下简称甲醇车尾气和汽油车尾气）对小鼠RAW264．7细胞的细胞毒性及对其增殖和凋亡的影响。方法用甲醇车尾气和汽油车尾气对RAW264．7细胞染毒,用四甲基偶氮唑盐（MTT）比色法确定受试物的染毒剂量。RAW264．7细胞分甲醇车尾气组（分别用0．0078、0．0156、0．03125、0．0625、0．125L／ml的甲醇车尾气染毒）和汽油车尾气组（染毒剂量与甲醇车尾气组相同）,并分别设空白对照组。分别对各个组进行乳酸脱氢酶（LDH）活力测定、细胞形态学观察、检测细胞周期并计算细胞增殖指数及计算凋亡率。结果在MTT试验中,汽油车尾气组在0．125、0．5、1、2、4L/ml剂量组的光密度（OD）值低于对照组（P〈0．01）,甲醇车尾气组在0．5、1、2、4L／ml剂量组的OD值低于对照组（P〈0．01）。汽油车尾气组在0．1250．0625、0．03125L／ml剂量组的LDH活力高于对照组（P〈0．05）;汽油车尾气组0．03125、0．0625L／ml剂量组和甲醇车尾气组0．0625L／ml剂量组的细胞增殖指数低于对照组（P〈0．05）;甲醇车尾气组和汽油车尾气组在0．0156、0．03125、0．0625L／ml剂量组凋亡率均高于对照组（P〈0．05）。结论同等剂量下甲醇车尾气的细胞毒性明显大于汽油车尾气;汽油车尾气和甲醇车尾气对RAW264．7细胞株凋亡的影响相近;汽油车尾气对细胞增殖的抑制作用略大于甲醇车尾气。     

沙棘籽油对柴油机废气颗粒物染毒大鼠的肺泡灌洗液及血清生化指标的影响

目的研究沙棘籽油能否对柴油机汽车尾气颗粒物(DEP)所致大鼠肺组织损伤具有保护作用。方法健康成年雄性大鼠随机分为对照组、单纯染尘组和染尘低剂量(2 ml/kg)、中剂量(5 ml/kg)、高剂量(10 ml/kg)沙棘籽油干预组。对照组和单纯染尘组大鼠用生理盐水给予灌胃(1 ml/鼠),各染尘低、中、高剂量干预组大鼠用上述设定剂量的沙棘籽油分别给予灌胃,1次/d,连续2 d;灌胃48 h后,在乙醚麻醉下,对照组大鼠一次性气管注入生理盐水1 ml/鼠,单纯染尘组大鼠和染尘干预组一次性气管注入DEP生理盐水混悬液16 mg/ml。在各组大鼠染尘后24 h,腹主动脉采血收集血清,用生理盐水灌洗支气管肺泡,收集支气管肺泡灌洗液(BALF),测定支气管肺泡灌洗液和血清中乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)的活力及白蛋白的含量。结果BALF中,2,5,10 ml/kg沙棘籽油干预组大鼠白蛋白水平(6.38,3.78,6.23 g/L)均明显低于单纯染尘组(12.71 g/L,P<0.05);各实验干预组大鼠LDH水平(213.91,212.31,172.89 U/g蛋白)明显低于单纯染尘组(422.55 U/g蛋白,P<0.05);各实验干预组大鼠ACP水平(29.43,23.97,23.14 U/g蛋白)明显低于单纯染尘组(50.72 U/g蛋白,P<0.05)。血清中,各实验干预组白蛋白水平与单纯染尘组比较,差异无统计学意义(P>0.05);各组LDH变化不明显,差异无统计学意义(P>0.05);实验组大鼠ACP水平(2.33,2.35,2.09 U/ml)明显低于单纯染尘组(3.79 U/ml),差异有统计学意义(P<0.05)。结论沙棘籽油对柴油机汽车尾气颗粒物所致大鼠肺损伤具有一定的保护作用。     

汽油与甲醇燃烧汽车尾气致突变性的对比研究

目的　比较汽油与甲醇燃烧汽车尾气的致突变性 ,为甲醇代替汽油作为汽车燃料提供试验依据。方法　采用鼠伤寒沙门氏菌 哺乳动物微粒体酶试验 (Amesassay)和肺上皮A5 4 9细胞体外微核试验对汽油燃烧汽车尾气和甲醇燃烧汽车尾气的致突变性进行对比研究。结果　汽油燃烧汽车尾气在加与不加S9时对测试菌株TA98都具有致突变性 ,加S9时致突变性明显增加 ,其回变菌落数亦随剂量增加而增加 ;而甲醇燃烧汽车尾气在相同浓度下对TA98和TA10 0菌株都不具有致突变性。A5 4 9细胞体外微核试验中 ,在 0 . 0 2 5～0 . 2L ml浓度范围内 ,汽油燃烧汽车尾气具有诱导A5 4 9细胞微核细胞数增加的作用 ,并随剂量增加而增加 ,呈现良好的剂量效应关系 ,而甲醇燃烧汽车尾气在同样浓度下不具有诱导A5 4 9细胞微核增加的作用。结论　汽油尾气具有致突变性 ,甲醇尾气在两个试验中均未检测出致突变性 ,该研究为甲醇取代汽油作为汽车燃料提供了卫生学依据。     

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。     

Occupational exposure to diesel and gasoline emissions and lung cancer in Canadian men

The International Agency for Research on Cancer classifies diesel exhaust as a probable human carcinogen; this decision is based largely from lung cancer evidence. Gasoline exhaust is classified as a possible carcinogen. Epidemiological studies are needed that improve upon some of the limitations of previous research with respect to the characterization of exposure, and the control for the potential confounding influence of smoking and other occupational exposures. Our objective was to investigate associations between occupational exposure to diesel and gasoline engine emissions and lung cancer. We used a case-control study design that involved men 40 years of age and older at the time of interview. Analyses are based on 1681 incident cases of lung cancer and 2053 population controls. A self-reported questionnaire elicited a lifetime occupational history, including general tasks, and information on other potential risk factors. Occupational exposures to diesel and gasoline emissions, crystalline silica, and asbestos were assigned to each job held by study subjects by industrial hygienists who were blind to case-control status. Exposure metrics for diesel and gasoline emissions that were modeled included: ever exposure, cumulative exposure, and concentration of exposure. We found a dose–response relationship between cumulative occupational exposure to diesel engine emissions and lung cancer. This association was more pronounced for the squamous and large cell subtypes with adjusted odds ratios across the three increasing tertiles of cumulative lifetime exposure relative to those with no exposure of 0.99, 1.25, and 1.32 (p=0.04) for squamous cell carcinoma, and 1.06, 1.19, 1.68 (p=0.02) for large cell carcinoma. While the association with cumulative exposure to gasoline was weakly positive, it was not statistically significant. Our findings suggest that exposure to diesel engine emissions increases the risk of lung cancer particularly for squamous and large cell carcinoma subtypes.     

Influence of ethanol and methanol gasoline blends on the mutagenicity of particulate exhaust extracts

TheSalmonella mutagenicity test was used to evaluate the influence of alcohol fuel extenders on the genetic toxicity of particulate exhaust extracts. Four spark-ignition engine equipped vehicles were operated on gasoline alone, 10% blends of ethanol or methanol in gasoline, and a commercially available “gasohol.” The tests were conducted on a chassis dynomometer and the particulate exhaust was collected on high volume filters after dilution in a tunnel. The vehicles used were a 1980 Chevrolet Citation, a 1980 Mercury Monarch, a 1981 Ford Escort and a 1981 Oldsmobile Cutlass. Dichloromethane extracts of the exhaust particles from all tests were mutagenic inSalmonella typhimurium strains TA 100 and TA 98. The extracts were less mutagenic in the nitroreductase deficient strains TA 98NR and TA 98DNPR suggesting that nitro substituted polycyclic aromatic hydrocarbons may be responsible for part of the mutagenicity. In all the alcohol blended fuel tests, the mass of particle associated organics emitted from the exhaust was lower than that observed during the control tests using gasoline alone. Thus, in most cases, estimates of the emission of mutagenic combustion products from the exhaust were lower in the alcohol blend tests.     

汽车尾气诱导小鼠体内氧化损伤与遗传毒性的研究

目的 探讨汽车尾气导致小鼠体内氧化损伤与遗传毒性的关系。方法 将受试小鼠随机分为4组，即对照组与汽车尾气、：10，1：20，1：30稀释度染毒组，采用动式染毒装置，使小鼠暴露不同稀释度汽车尾气，每天暴露2h，连续暴露5d，测定受试组小鼠体内血、肝、肺、睾丸中活性氧族（ROS）、丙二醛（MDA）含量以及超氧化物歧化酶（SOD）活性与微核率的变化。结果 染毒组小鼠血、肝、肺、睾丸ROS与肺、睾丸DA含量和骨髓细胞微核率明显升高，与对照组比较，其差异均有显著性意义（P＜0.01），其中小鼠骨髓细胞微核率呈现一定剂量－效应关系。血、肝、肺ROS含量与微核率呈明显相关关系。结论 汽车尾气可导致机体氧化与抗氧化系统平衡紊乱；并能引起细胞染色体损伤。汽车尾气导致机体组织的氧化损伤可能在细胞遗传毒性作用中起重要作用。