CONCOMITANT EXPOSURE TO CARBON-BLACK PARTICULATES ENHANCES OZONE-INDUCED LUNG INFLAMMATION AND SUPPRESSION OF ALVEOLAR MACROPHAGE PHAGOCYTOSIS
CONCOMITANT EXPOSURE TO CARBON-BLACK PARTICULATES ENHANCES OZONE-INDUCED LUNG INFLAMMATION AND SUPPRESSION OF ALVEOLAR MACROPHAGE PHAGOCYTOSIS
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DOI：
10.1080/15287399409531838
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发表时间：
1994-02-01
期刊：
影响因子：
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通讯作者：
HEMENWAY, DR
中科院分区：
文献类型：
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作者：
JAKAB, GJ;HEMENWAY, DR
本研究的目的是通过炎症反应和肺泡巨噬细胞(AM)吞噬功能的定量，研究炭黑和O-3联合暴露是否会导致肺部的毒理相互作用。这一目标是通过将瑞士小鼠吸入目标浓度为10 mg/m(3)的碳黑和1.5ppm的O-3或单独暴露于这两种介质中的4小时来实现的。作为共暴露实验的对照，小鼠也暴露在碳黑中4h，然后立即暴露在O-3中4h，反之亦然。染毒后24小时，取肺灌洗，计数细胞总数和分类细胞数，并测定AM Fc受体介导的吞噬功能。接触碳黑不会导致炎症反应，也不会对AM吞噬功能产生任何影响。臭氧暴露可引起肺部炎症反应，抑制AM吞噬功能。在联合暴露于颗粒物和气体后，这两个生物参数都显著提高。与单独接触O-3相比，在O-3之前或之后接触炭黑对AM吞噬功能没有显著影响。这些数据表明，在公认的生物标志物肺毒性上，共同暴露于惰性颗粒和O-3的毒理学相互作用。增强生物效应的机制可能是碳黑颗粒作为O-3的载体机制，使O-3在气相中到达O-3无法到达的肺远端区域，或者O-3将颗粒物的物理化学从无毒变为有毒。
The goal of this study was to investigate whether coexposures to carbon black and O-3 result in a toxicologic interaction in the lungs as quantitated by the inflammatory response and alveolar macrophage (AM) phagocytosis. This aim was accomplished through inhalation coexposures of Swiss mice for 4 h to target concentrations of 10 mg/m(3) of carbon black and 1.5 ppm O-3,, or exposure to either agent alone. As a control for the coexposure experiments, mice were also exposed for 4 h to carbon black, followed immediately thereafter by exposure for 4 h to O-3, or vice versa. At 24 h after exposure, the lungs of the animals were lavaged for quantitation of total and differential cell counts and assessment of AM Fc-receptor-mediated phagocytosis. Exposure to carbon black did not result in an inflammatory response, nor had it any effect on AM phagocytosis. Ozone exposure resulted in an inflammatory response in the lungs and suppression of AM phagocytosis. Both biologic parameters were significantly enhanced following combined exposure to the particle and the gas. Carbon black exposure either before or after O-3 had no significant effect on AM phagocytosis as compared to O-3 exposure alone. These data demonstrate the toxicologic interaction of coexposures to an inert particle and O-3 on well-accepted biologic markers pulmonary toxicity. The mechanism for the enhanced biologic effect may be that the carbon black particle acts as a carrier mechanism for O-3 to areas in the distal lung not accessible to O-3 in the gaseous phase or that O-3 alters the physicochemistry of the particulate from a nontoxic to a toxic form.