Abstract
BackgroundMulti-walled carbon nanotubes and nanofibers (CNT/F) have been previously investigated for their potential toxicities; however, comparative studies of the broad material class are lacking, especially those with a larger diameter. Additionally, computational modeling correlating physicochemical characteristics and toxicity outcomes have been infrequently employed, and it is unclear if all CNT/F confer similar toxicity, including histopathology changes such as pulmonary fibrosis. Male C57BL/6 mice were exposed to 40 µg of one of nine CNT/F (MW #1–7 and CNF #1–2) commonly found in exposure assessment studies of U.S. facilities with diameters ranging from 6 to 150 nm. Human fibroblasts (0–20 µg/ml) were used to assess the predictive value of in vitro to in vivo modeling systems.ResultsAll materials induced histopathology changes, although the types and magnitude of the changes varied. In general, the larger diameter MWs (MW #5–7, including Mitsui-7) and CNF #1 induced greater histopathology changes compared to MW #1 and #3 while MW #4 and CNF #2 were intermediate in effect. Differences in individual alveolar or bronchiolar outcomes and severity correlated with physical dimensions and how the materials agglomerated. Human fibroblast monocultures were found to be insufficient to fully replicate in vivo fibrosis outcomes suggesting in vitro predictive potential depends upon more advanced cell culture in vitro models. Pleural penetrations were observed more consistently in CNT/F with larger lengths and diameters.ConclusionPhysicochemical characteristics, notably nominal CNT/F dimension and agglomerate size, predicted histopathologic changes and enabled grouping of materials by their toxicity profiles. Particles of greater nominal tube length were generally associated with increased severity of histopathology outcomes. Larger particle lengths and agglomerates were associated with more severe bronchi/bronchiolar outcomes. Spherical agglomerated particles of smaller nominal tube dimension were linked to granulomatous inflammation while a mixture of smaller and larger dimensional CNT/F resulted in more severe alveolar injury.
Highlights
Carbon nanotubes and nanofibers (CNT/F) are known to cause pathologic changes in the lung, both in the alveolar and bronchiolar regions [1,2,3,4,5,6]
The broad class of carbon nanotubes and nanofibers (CNT/F) exhibit a vast array of physicochemical characteristics including an extensive range of diameters and lengths in conjunction with functionalization, surface coatings, etc., which are critical for the applications of these particles for their engineered purposes, yet are critical for driving the toxicity of CNT/F
Male C57BL/6 J mice were exposed to 40 μg of CNT/F or dispersion medium (DM) via oropharyngeal aspiration and euthanized at 84 d post-exposure
Summary
Carbon nanotubes and nanofibers (CNT/F) are known to cause pathologic changes in the lung, both in the alveolar and bronchiolar regions [1,2,3,4,5,6]. The longer and thicker CNT/F, or rod-like materials, were more likely to impact non-cell mediated translocation and airway fibrosis compared to spherical agglomerating CNT/F [2, 3, 20,21,22]. This pattern was not entirely consistent as noted in several studies. Multi-walled carbon nanotubes and nanofibers (CNT/F) have been previously investigated for their potential toxicities; comparative studies of the broad material class are lacking, especially those with a larger diameter. Human fibroblasts (0–20 μg/ml) were used to assess the predictive value of in vitro to in vivo modeling systems
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