Natl Toxicol Program Tech Rep Ser. 1990 Nov;279:1-341.
The term "asbestos" has a commercial/industrial derivation limited to naturally occurring fibrous minerals of the serpentine or amphibole series. Chrysotile is the only type of asbestos in the serpentine series, whereas the amphibole series is represented by actinolite, amosite, anthophyllite, crocidolite, and tremolite. The essential characteristic of asbestos minerals is their fibrous nature. Large portions of the population ingest asbestos through consumption of food and water. Asbestos or asbestos-like fibers may gain access to water supplies as a result of mining (Lake Superior), from the presence of natural serpentine or amphibole deposits in watersheds (Seattle, WA, and San Francisco, CA) or, under certain conditions, through the use of asbestos-cement pipes for municipal water supplies. For the latter, erosion of the pipe with release of fibers is associated with the "aggressiveness" of the water, a term representing a mathematical expression of pH, alkalinity, and calcium content. The EPA estimated that 68.5% of water systems in the United States utilize water that is potentially capable of eroding asbestos-cement pipe. Carcinogenesis studies of amosite asbestos alone or in combination with the intestinal carcinogen 1,2-dimethylhydrazine dihydrochloride (DMH) were conducted in male and female rats. Amosite asbestos was administered at a concentration of 1% in pelleted diet for the entire lifetime of the rats, starting with the dams of the study animals. One group of amosite asbestos-exposed rats (amosite preweaning gavage) also received chrysotile asbestos via gavage during lactation. Group sizes varied from 100 to 250. Litter size was the same, but the offspring from mothers exposed to amosite asbestos were smaller at weaning than those from nonexposed mothers and remained smaller throughout their life. The DMH was administered by gavage at a dose of 7.5 mg/kg for males and 15 mg/kg for females every 14 days, starting at 8 weeks of age, for a total of five doses. The administration of DMH did not affect body weight gain either in amosite-exposed or nonexposed animals. The amosite-exposed rats showed enhanced survival compared with that of the nonexposed rats. DMH exposure reduced survival by approximately 1 year, although the survival of the amosite plus DMH groups was slightly greater than that of the DMH group alone. Significant increases in the incidences of C-cell carcinomas of the thyroid gland (untreated control, 11/117; amosite, 50/246, P<0.05; amosite preweaning gavage, 14/100) and of leukemia (38/117; 106/249, P<0.05; 49/100, P<0.01) in male rats were observed in amosite-exposed groups. However, the biologic significance of the C-cell carcinomas in relation to amosite asbestos exposure is discounted because of a lack of significance when C-cell adenomas and carcinomas were combined and because the positive effect was not observed in the amosite preweaning gavage group. The biologic significance of an increased incidence of leukemia is questionable because of a lack of statistical significance in the amosite group when evaluated by life table analysis and because no toxic lesions were observed in the target organs, i.e., gastrointestinal tract and mesothelium. DMH caused a high incidence (62%-74%) of intestinal neoplasia in amosite-exposed and nonexposed groups. Neither an enhanced carcinogenic nor a protective effect was demonstrated by exposure to amosite asbestos. Conclusions: Under the conditions of these feed studies, amosite asbestos was not overtly toxic, did not affect survival, and was not carcinogenic when ingested at a concentration of 1% in the diet by male or female F344/N rats. The cocarcinogenic studies using DMH were considered inadequate because of the high incidence of DMH-induced intestinal neoplasia in both the amosite asbestos-exposed and nonexposed groups. Levels of Evidence of Carcinogenicity: Amosite Asbestos: Male Rats: Negative. Female Rats: Negative. Amosite Asbestos + DMH: Male Rats: Inadequate. Female Rats: Inadequate. Note: Amosite Asbestos was previously tested in Syrmosite Asbestos was previously tested in Syrian Golden Hamsters administered in feed (See TR-249, reported 1983).
“石棉”一词在商业/工业领域的定义仅限于蛇纹石或闪石系列的天然纤维状矿物。温石棉是蛇纹石系列中唯一的石棉类型，而闪石系列则包括阳起石、铁石棉、直闪石、青石棉和透闪石。石棉矿物的基本特征是其纤维性质。很大一部分人通过食物和水摄入石棉。由于采矿（苏必利尔湖）、流域中天然蛇纹石或闪石矿床的存在（华盛顿州西雅图市和加利福尼亚州旧金山），或者在某些情况下，通过使用石棉水泥管供应市政用水，石棉或类石棉纤维可能进入供水系统。对于后者，随着纤维的释放，管道的侵蚀与水的“侵蚀性”有关，“侵蚀性”是一个表示pH值、碱度和钙含量的数学表达式。美国环境保护局估计，美国68.5%的供水系统使用的水可能会侵蚀石棉水泥管。单独对铁石棉或与肠道致癌物二盐酸1,2 - 二甲基肼（DMH）联合进行了雄性和雌性大鼠的致癌研究。从研究动物的母鼠开始，在大鼠的整个生命周期内，以1%的浓度将铁石棉添加到颗粒饲料中。一组暴露于铁石棉的大鼠（断奶前经口灌胃给予铁石棉）在哺乳期还通过灌胃接受了温石棉。每组动物数量从100到250不等。窝仔数相同，但暴露于铁石棉的母鼠所生的后代在断奶时比未暴露母鼠所生的后代体型小，并且在其一生中都保持较小。从8周龄开始，每14天通过灌胃给雄性大鼠注射7.5 mg/kg、雌性大鼠注射15 mg/kg的DMH，共注射五剂。DMH的给药对暴露于铁石棉或未暴露的动物的体重增加均无影响。与未暴露的大鼠相比，暴露于铁石棉的大鼠存活率有所提高。DMH暴露使存活率降低约1年，尽管铁石棉加DMH组的存活率略高于单独的DMH组。在暴露于铁石棉的雄性大鼠组中，观察到甲状腺C细胞癌（未处理对照组，11/117；铁石棉组，50/246，P<0.05；断奶前经口灌胃给予铁石棉组，14/100）和白血病（38/117；106/249，P<0.05；49/100，P<0.01）的发生率显著增加。然而，由于C细胞腺瘤和癌合并时缺乏显著性，且在断奶前经口灌胃给予铁石棉组未观察到阳性效应，因此铁石棉暴露与C细胞癌的生物学意义被忽略。由于通过生命表分析评估时铁石棉组缺乏统计学显著性，且在靶器官即胃肠道和间皮中未观察到毒性损伤，白血病发生率增加的生物学意义值得怀疑。DMH在暴露于铁石棉和未暴露的组中均导致肠道肿瘤的高发生率（62% - 74%）。暴露于铁石棉既未显示出增强的致癌作用，也未显示出保护作用。结论：在这些饲料研究的条件下，雄性或雌性F344/N大鼠以1%的浓度摄入饲料中的铁石棉时，铁石棉没有明显毒性，不影响存活率，也不致癌。由于在暴露于铁石棉和未暴露的组中DMH诱导的肠道肿瘤发生率都很高，因此使用DMH进行的促癌研究被认为是不充分的。致癌性证据水平：铁石棉：雄性大鼠：阴性。雌性大鼠：阴性。铁石棉 + DMH：雄性大鼠：不充分。雌性大鼠：不充分。注意：铁石棉之前在叙利亚金仓鼠中进行过饲料给药测试（见1983年报告的TR - 249）。
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