铅与癌症——有联系还是因果关系

铅与癌症——有联系还是因果关系１９８７年国际癌症研究机构（ＩＡＲＣ）承认铅及其无机化合物对人类是可能的致癌物，属２Ｂ组。即对实验动物的致癌性有足够证据，而对人的致癌性证据不充分。Ｆｕ和Ｂｕｆｅｔｔａ（１９９５）将可收集到的关于铅接触与癌症发生之间联系...     

自然界中的致癌物质

自然界存在的致癌因子除放射性,致癌性烃类化合物、激素等外,最近的资料表明还有下列几类致癌物质(1)微生物产生的致癌物(2)植物来源的致癌物(3)食品烹调加热过程中产生的致癌物(4)生物体内和食品中生成N-亚硝基致癌物。在微生物产生的致癌物中,最为人们所熟知的是真菌毒素,尤其是黄曲霉毒素。黄曲霉毒素有B_1、G、M等数种,就其毒性而言以B_1、M最强,G次之。动物试验证明,它们可诱发从鱼至猿类等多种动物发生肝癌。致癌性以B_1最强,有人认为大鼠只要经口摄入1ppb的黄曲霉毒素B_1就可以诱发肝癌。在泰国和印度等地有由于黄曲霉毒素引起人中毒死亡的报告。有人认为泰国和东非各地的肝癌发病率高与当地食品中的黄曲霉毒素含量高有关。     

食品中挥发性N-亚硝胺的分析方法

N-亚硝胺是一类致癌性物质,能引起多种动物各种器官组织的肿瘤。大量的实验证明某些食品中存在一定量的亚硝胺,人类可经消化道、呼吸道等途径接触这些致癌物。但迄今尚未得到 N-亚硝胺与人的肿瘤发病的直接证据,需做大量的研究来证实。鉴于人类     

职业性肿癌的药物治疗

1　致癌因素[1]1.1　经动物实验和流行病学调查证实对人有确切致癌作用 ,已肯定的致癌物　多环芳烃中的苯并 (α)芘 ;烷化剂的氯甲甲醚和芥子气 ;芳香胺中的 4 -氨基联苯、联苯胺和β-萘胺 ;异丙基油、苯、氯乙稀等有机化合物 ;无机化合物中的砷、铬、镍、石棉等 ;氡、镭、钍等放射性因素 ,X射线、紫外线等。1.2　对实验动物有致癌作用 ,对人致癌可能性大 ,但未被流行病学调查证实的能致癌物　有镉、铍、氧化铁、多氯联苯等。1.3　经动物实验有致癌性 ,但对人致癌性还不肯定的潜在致癌物　有钴、锌、铅、汞和四氯化碳等。2　职业性肿癌的特…     

日常生活中的化学致癌物

在五光十色的生活中,化学物质比比皆是。而化学致癌物是指在一定的条件下,使正常细胞转化为肿瘤细胞,且发展为癌的化学物。在动物实验中显示有致癌作用的化学物称为动物致癌物,它们是人类的潜在致癌物。９０年代国际癌症研究机构对７７５种化学物及其生产过程或环境对人致癌性作了综合评价,其中对人肯定是致癌的化学物和生产过程共有６３种之多,它们当中的一些最常见的化学致癌物,人们在生活和生产环境中都可有所接触,必须引起重视。日常生活中的致癌物举例：氯乙烯致肝血管肉瘤１９７０年首次发现长期吸入氯乙烯可诱发肝血管肉瘤,…     

致癌物质知多少

目前,癌症已成为一种严重危害人类健康的常见病,每年全世界死于癌症的人约占世界死亡总人口数的四分之一。难怪很多人都有一种恐癌心理。癌症患者在逐年增多,其病因是多方面的,但一般认为,有80—85％的癌症是由于化学因素引起的。那么具有致癌性的化学物质到底有多少种呢? 国际癌症研究机构(IARC)根据化学物质对动物致癌实验结果及对人类致癌性的流行病学资料,把化学致癌物分为三类:即确认致癌物、可疑致癌物和潜在性致癌物。     

对5种萘基呋喃化合物致癌性的预测

本文报告使用CPBS法(致癌性预测与选择试验组合的方法),对巴黎居里研究所新合成的5种萘基呋喃化合物致癌性的预测结果:其中A、B、C 3种化合物可能是潜在致癌物的概率相当高,D、E 2种化合物可能是非致癌物的概率也相当高,这与动物体内的试验结果十分相符。作者认为,此法可广泛用于分析短期筛选试验结果,以预测遗传毒性物质的致癌性。     

染毒动物血中羟乙基半胱氨酸的GC／MS分析

染毒动物血中羟乙基半胱氨酸的ＧＣ／ＭＳ分析刘峁子庞吉海沈惠麒王立秋氯乙烯是聚氯乙烯的单体，在低浓度下，长时间接触后可引起肝、肾损坏。已经证实氯乙烯对动物和人均有致癌作用，并已被列入对人类有致癌性的肯定致癌物［１］。氯乙烯进入人体后，经活化其中间代谢物...     

监测尿中N-亚硝基氨基酸作为内源性亚硝化的指标

自Magee和Barnes发现二甲基亚硝胺(NDMA)能引起大鼠肝癌以来,N-亚硝基化合物的致癌性得以广泛研究。已知N-亚硝基化合物是一类强致癌物。目前已对300多种这类化合物进行了研究,其中90％以上已被证明对多种动物有致癌作用。在所试动物中(包括灵长类在内),尚未见对N-亚硝基化合物致癌作用有抵抗力的报道,因而尽管目前尚无N-亚硝基化合物对人致癌的直接证据,但人们对N-亚硝基化合物在人类肿瘤病因中所起的     

石油与肿瘤

随着我国石油工业的蓬勃发展 ,不仅从事该行业的职工人数不断增加 ,而且使石油工业中存在的职业性有害因素也日趋复杂 ,石油工人在生产过程中经常接触多种职业性有害因素 ,这些职业性有害因素包括许多已被确认的职业性致癌物和一些可疑的潜在致癌物 ,有关石油致癌危险性的问题已引起人们日益关注 ,国内外学者对此进行了广泛探讨。1　石油对实验动物的致癌性有关石油及其组分对实验动物的致癌性文献早有报道 ,L eitch(1992 )采用苏格兰页岩油进行小鼠皮肤涂抹试验成功地诱发皮肤癌 ,最先用动物实验证实了石油的致癌性。 Holland[1 ]等 (1979…     

Follow-up of a group of workers intoxicated with 4,4′-methylenedianiline

4,4′-Methylenedianiline (MDA), an aromatic amine, is a known human hepatotoxin and an animal carcinogen but there is little information regarding its chronic effects in humans. Between 1967 and 1976, 10 workers at a plant in Ontario that used MDA as an epoxy hardener developed acute jaundice. We followed this group from the date of intoxication through to the end of 1991 for cancer incidence by matching with the Ontario Cancer Registry. To date, one cancer, a pathologically confirmed bladder cancer has developed (expected number based on provincial incidence rates: 0.64 for all cancers, 0.05 for bladder cancer). This finding may be important because bladder cancer was a site of interest a priori; bladder cancers have been observed in two other occupationally exposed groups (significantly higher than expected in one of these); in the National Toxicology Program bioassay, urinary bladder tumors occurred in exposed animals but not in controls; and MDA has structural similarity to known human bladder carcinogens such as benzidine.     

Lead and cancer in humans: where are we now?

BACKGROUND: Lead is only weakly mutagenic, but in vitro it inhibits DNA repair and acts synergistically with other mutagens. Lead acetate administered orally, cutaneously, or intraperitoneally causes kidney cancer, brain cancer (gliomas), and lung cancer in rodents, and acts synergistically with other carcinogens. Most cytogenetic studies of exposed workers have shown increases in chromosome aberrations or sister chromatid exchange, including some studies with positive-exposure response trends. There are eight studies of cancer mortality or incidence among highly exposed workers; most are cohort studies of lead smelter or battery workers exposed decades ago. METHODS: We reviewed the epidemologic studies with regard to cancer. RESULTS: These studies provide some evidence of increased risk of lung cancer (RR = 1.30, 1.15-1.46, 675 observed deaths) and stomach cancer (combined RR = 1.34, 1.14-1.57, 181 observed). However, the lung cancer findings are not consistent across studies, and confounding by arsenic may affect the study with the highest lung cancer RR. Exclusion of that study yields a combined lung cancer RR of 1.14 (1.04-1.73). There is little evidence of increased risk of kidney cancer (combined RR = 1.01, 0. 72-1.42, 40 observed) or brain cancer (combined RR = 1.06, 0.81-1.40, 69 observed). However, two studies show a two-fold increase in kidney cancer, and one study shows a significant excess of gliomas. IARC classified lead as a "possible human carcinogen" based on sufficient animal data and insufficient human data in 1987. Six of the eight studies cited above have been published since 1987. CONCLUSIONS: Overall, there is only weak evidence associating lead with cancer; the most likely candidates are lung cancer, stomach cancer, and gliomas.     

Application of benzo(a)pyrene and coal tar tumor dose-response data to a modified benchmark dose method of guideline development

Assessment of cancer risk from exposure to polycyclic aromatic hydrocarbons (PAHs) has been traditionally conducted by applying the conservative linearized multistage (LMS) model to animal tumor data for benzo(a)pyrene (BaP), considered the most potent carcinogen in PAH mixtures. Because it has been argued that LMS use of 95% lower confidence limits on dose is unnecessarily conservative, that assumptions of low-dose linearity to zero in the dose response imply clear mechanistic understanding, and that "acceptable" cancer risk rests on a policy decision, an alternative cancer risk assessment approach has been developed. Based in part on the emerging benchmark dose (BMD) method, the modified BMD method we used involves applying a suite of conventional mathematical models to tumor dose-response data. This permits derivation of the average dose corresponding to 5% extra tumor incidence (BMD0.05) to which a number of modifying factors are applied to achieve a guideline dose, that is, a daily dose considered safe for human lifetime exposure. Application of the modified BMD method to recent forestomach tumor data from BaP ingestion studies in mice suggests a guideline dose of 0.08 microg/kg/day. Based on this and an understanding of dietary BaP, and considering that BaP is a common contaminant in soil and therefore poses human health risk via soil ingestion, we propose a BaP soil guideline value of 5 ppm (milligrams per kilogram). Mouse tumor data from ingestion of coal tar mixtures containing PAHs and BaP show that lung and not forestomach tumors are most prevalent and that BaP content cannot explain the lung tumors. This calls into question the common use of toxicity equivalence factors based on BaP for assessing risk from complex PAH mixtures. Emerging data point to another PAH compound--H-benzo(c)fluorene--as the possible lung tumorigen.     

环境铅污染及其毒性的研究进展

铅是一种常见的环境污染物，给人类健康带来了巨大的损害。人类对铅的毒性研究已有上千年的历史，但近些年来伴随着现代生物技术的飞速发展，铅的毒性机制得到了深入的研究，同时也发现了一系列的敏感标志物。本文从铅的致癌性、认知能力和行为功能改变、遗传物质损伤、诱导细胞凋亡等方面进行综述。     

Respiratory effects of diesel exhaust emission

Adverse effects of diesel exhaust is being now a subject of many recent studies. These various outcomes and especially respiratory changes are due to high concentration of different polluants within diesel exhaust particles. To date, it have been demonstrated that diesel emission increase the airway allergic reaction as rhinitis and asthma. In addition, to those side effects, it is proved that diesel exhaust is a probable human carcinogen based on evidence. Many epidémiologic evidence found a significant increase in lung cancer risk. However, some studies have provided contradictory results due to concomittant exposure to other polluants, tobacco exposure and difficulties to extrapolate findings in animal models into humans.     

砷中毒对体外实验细胞损伤的分子生物学机制研究进展

摘要：砷是确认的人类致癌物,但由于无机砷的致癌动物模型较难复制,使体外细胞实验成为砷致癌机制研究的必要手段。随着分子生物学技术的快速发展,体外细胞实验在揭示砷致细胞损伤的分子生物学作用、增强人们对砷致癌机制的认识上提供了有价值、可信的成果,对砷致癌机制研究的深入开展有重要的推动作用。然而,由于体外细胞实验自身的特点,以及砷在生物体内的甲基化代谢模式,使体外细胞实验在砷致癌机制的研究上也存在一定的局限性。     

二氧化硅致癌作用研究进展

石英粉尘是一种危害较为严重的粉尘,可导致肺组织损伤和纤维化。石英近年被IARC宣布由动物致癌物升级为人类致癌物,同时指出尚需人类DNA水平的直接证据。本文将从动物实验、人群流行病学调查及可能的致癌机制几个方面对石英致癌作用的研究进展作一综述。     

Continued epidemic of bladder cancer in workers exposed to ortho-toluidine in a chemical factory

Ortho-toluidine (o-toluidine), an aromatic amine, is classified by the International Agency for Research on Cancer as a probable human carcinogen. A cohort study published in 1991 reported a 6.5-fold excess incidence of bladder cancer in a chemical plant that used o-toluidine. We report 19 additional cases of bladder cancer among workers in this cohort, yielding a total of 34 cases of bladder cancer in the cohort to date. The number of bladder cancers diagnosed in the recent period has increased. The timing of onset of exposure to o-toluidine of numerous cases of bladder cancer after 1968, and especially 1975, suggests that potentially confounding occupational exposures other than o-toluidine were not responsible for the observed excess bladder cancer. A formal cohort update is strongly indicated. This study further supports the human bladder carcinogenicity of o-toluidine.     

Agricultural chemicals and endocrine-mediated chronic toxicity or carcinogenicity

This brief review summarizes information on the endocrine effects and mechanisms of action of certain pesticides and considers whether exposure to pesticides with endocrine activity may play a role in human endocrine-related tumors of the breast, testis, prostate, and endometrium. Both animal and human data are considered. If animal data are to be used effectively for predicting human risk, a thorough understanding of comparative endocrinology and the underlying endocrine and pathological mechanisms contained in the animal model is needed. It is concluded that the evidence does not support an association between organochlorine pesticides and breast cancer, while the evidence on other tumor sites is too sparse to draw any conclusions concerning pesticides.     

Asbestos and kidney cancer: the evidence supports a causal association

The role of asbestos in the etiology of lung cancer and of mesothelioma of the pleura and peritoneum has been well documented. The evidence for a causal association between asbestos and other human cancers is not as extensive but suggests that asbestos may be carcinogenic at several different sites. This paper is concerned specifically with a possible causal association between asbestos and human kidney cancer. A review of the evidence to date indicates that only three human studies have sufficient statistical power to detect an excess mortality from kidney cancer among workers exposed to asbestos. All three were occupational cohort studies, and two of these gave strong direct evidence for such an excess; a study of U.S. insulators (kidney cancer SMR = 2.22, 90% CI 1.44-3.30), and a study of U.S. asbestos products company workers (kidney cancer SMR = 2.76, 90% CI 1.29-5.18). The third study, of Italian shipyard workers, reported excess mortality from "cancers of the kidney, urinary bladder, and other urinary organs" (SMR = 1.98, 90% CI 1.42-2.70). Further support for a causal association includes studies finding asbestos fibers in human kidneys and urine, as well as reports of kidney tumors in two animal bioassays. It is concluded that asbestos should be regarded as a probable cause of human kidney cancer.