The biopersistence of Canadian chrysotile asbestos following inhalation

The biopersistence of Canadian chrysotile asbestos following inhalation
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DOI:
10.1080/08958370390241713
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发表时间:
2003-11-01
影响因子:
2.1
通讯作者:
Smith, P
Smith, P
中科院分区:
医学4区
文献类型:
--
作者:
Bernstein, DM;Rogers, R;Smith, P

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温石棉常与其他石棉材料一起进行评估和分类。然而,温石棉是一种蛇纹石,与角闪石相比具有显着不同的物理和化学特征(例如,青石棉、铁石棉、透闪石)。闪石是固体棒状纤维,而温石棉则是由许多细原纤维组成的绳索,这些细原纤维往往会展开。为了量化温石棉从肺中去除的动力学和速率,对来自加拿大魁北克东部城镇地区的商用温石棉样品的生物持久性进行了研究,该样品被标记为QS 3-F级,这是用于纺织品的最长商用等级。由于长纤维已被证明具有最大的致病潜力,因此温石棉样品被特别选择为在暴露气溶胶中具有超过200根纤维/cm(3)的长度,超过20 μ m。本出版物提供了本研究至暴露后3个月的结果。研究设计包括:(1)纤维间隙(肺指):第1天、第2天、第7天、第14天、第1个月、第3个月和第12个月(待报告)吸入暴露5天(6小时/天)后,通过低温等离子体灰化消化来自动物组的肺,随后通过透射电子显微镜分析肺中的总温石棉纤维数和温石棉纤维尺寸(长度和直径)分布在肺部。(2)纤维分布(共聚焦显微镜):包括该程序以识别肺中纤维的位置。在暴露后1天、2天、7天、14天、1个月和3个月(待报告),通过共聚焦显微镜分析各组动物的肺,以确定沉积在气道和实质区域中的残留温石棉原纤维的解剖命运、方向和分布。发现温石棉可迅速从肺中清除。长于20 μ m的纤维在T-1/2 = 16天时被清除,最有可能是通过溶解和崩解成较短的纤维。较短的纤维也从肺中迅速清除,5-20 μ m的纤维比长度< 5 μm的纤维清除得更快(T-1/2 = 29.4天)。长度< 5 μ m的纤维以一定速率(T-1/2 = 107天)被清除,该速率在不溶性有害粉尘的清除范围内。较长纤维的断裂预计会增加短纤维池,因此可以解释清除率的差异。发现短纤维没有聚集在一起,而是作为单独的细原纤维出现,偶尔在一端解绕。肺泡隔角部可见短的游离纤维,肺泡巨噬细胞内可见纤维或纤维碎片。同样的情况也发生在淋巴细胞中,因为它们看起来是游离的或在吞噬淋巴细胞中。中性粒细胞介导的炎症反应没有发生在温石棉纤维的存在下,在检查的时间点。结合迄今为止的科学文献,本报告提供了新的可靠数据,明确支持流行病学上温石棉和闪石石棉之间的差异。
Chrysotile asbestos is often included with other asbestos materials in evaluation and classification. However, chrysotile is a serpentine with markedly different physical and chemical characteristics in comparison to amphiboles (e.g., crocidolite, amosite, tremolite). In contrast to amphiboles, which are solid, rodlike fibers, chrysotile is composed like a rope of many fine fibrils, which tend to unwind. In order to quantify the dynamics and rate by which chrysotile is removed from the lung, the biopersistence of a sample of commercial chrysotile from the Eastern Townships area of Quebec, Canada, labeled QS Grade 3-F, which is the longest commercial grade intended for textile use, was studied. As the long fibers have been shown to have the greatest potential for pathogenicity, the chrysotile samples were specifically chosen to have more than 200 fibers/cm(3) longer than 20 mum present in the exposure aerosol. This publication presents the results of this study through 3 mo postexposure. The study design included: (1) Fiber clearance (lung digestions): At 1 day, 2 days, 7 days, 14 days, 1 mo, 3 mo, and 12 mo (to be reported) following a 5-day (6 h/day) inhalation exposure, the lungs from groups of animals were digested by low-temperature plasma ashing and subsequently analyzed by transmission electron microscopy for total chrysotile fibers number in the lungs and chrysotile fiber size (length and diameter) distribution in the lungs. (2) Fiber distribution (confocal microscopy): This procedure was included in order to identify the location of the fibers in the lung. At 1 day, 2 days, 7 days, 14 days, 1 month, and 3 months (to be reported) postexposure, the lungs from groups of animals were analyzed by confocal microscopy to determine the anatomic fate, orientation, and distribution of the retained chrysotile fibrils deposited on airways and in the parenchymal region. Chrysotile was found to be rapidly removed from the lung. Fibers longer than 20 mum were cleared with T-1/2 = 16 days, most likely by dissolution and disintegration into shorter fibers. The shorter fibers were also rapidly cleared from the lung, with fibers 5-20 mum clearing even faster (T-1/2 = 29.4 days) than those < 5 μm in length. The fibers < 5 mum in length cleared at a rate (T-1/2 = 107 days) that is within the range of clearance for insoluble nuisance dusts. The breaking apart of the longer fibers would be expected to increase the short fiber pool and therefore could account for this difference in clearance rates. The short fibers were not found clumped together but appeared as separate, fine fibrils, occasionally unwound at one end. Short free fibers appeared in the corners of alveolar septa, and fibers or their fragments were found within alveolar macrophages. The same was true of fibers in lymphatics, as they appeared free or within phagocytic lymphocytes. Neutrophil-mediated inflammatory response did not occur in the presence of chrysotile fibers at the time points examined. Taken in context with the scientific literature to date, this report provides new robust data that clearly support the difference seen epidemiologically between chrysotile and amphibole asbestos.