Exposures to carbon nanotubes and asbestos induce related but distinct profiles of toxicologic lung pathology

Details

• Personal Author:
  Birch EM ; Carreira VS ; Frank E ; Yadav J
• Description:
  Carbon nanotubes (CNTs) are rapidly emerging as occupational and environmental lung toxicants. The increasing manufacture and applications of CNTs has prompted concerns surrounding their potential to cause adverse lung effects in light of asbestos-like characteristics such as high aspect ratio and biopersistance. Because of their novelty, the long-term health outcomes of CNT exposures in humans are unknown. CNTs may become agitated into aerosols in occupational settings, posing an inhalational threat to those who work in places of CNT manufacture, distribution, and usage. However, there are limited studies or inconsistent findings regarding CNT toxicology or their toxicological similarities to asbestos. In this study, we developed mouse models of exposure using repeated, low-dose oropharyngeal aspirations of multi-wall CNTs or crocidolite asbestos. Histopathological analysis of lung sections showed that while granulomatous inflammation was similarly induced in both exposures, CNTs caused type II pneumocyte (T2P) hyperplasia, while asbestos caused mixed-cell bronchoalveolar hyperplasia. Both exposures caused increases of fibrotic collagen as shown in Masson's trichrome stains. Fluorescent immunohistochemistry for T2P-specific proSPC showed that T2P number was substantially increased specifically in CNT-exposed lungs. These observations are significant considering that T2P cells are known to become hyperplastic in response to alveolar epithelial injury. Co-staining for proSPC and IL-1beta showed that while both exposures increased IL-beta+ cells in lung tissue, CNTinduced IL-1beta increases were largely specific to T2Ps. These results illustrate that CNT and asbestos exposures may induce related but reproducibly distinct profiles of toxicologic lung pathology, and that T2Ps may be sensitive to CNT-induced toxicity. This suggests that CNTs and asbestos may differ in their mechanisms of toxicity and resultant injury in the distal airway. [Description provided by NIOSH]
• Subjects:
  Environmental Monitoring Immune System Laboratories Lung Occupational Health Respiratory System Safety Toxicology
• Keywords:
  Alveolar-cells Carbon-compounds Cellular-reactions Connective-tissue Exposure-assessment Histopathology Immunochemistry Laboratory-animals Laboratory-testing Lung-cells Lung-fibrosis Lung-irritants Lung-tissue Models Nanotechnology Oropharynx

  More +
• ISSN:
  1096-6080
• Document Type:
  Text
• Genre:
  Abstract or Summary
• Place as Subject:
  California ; Ohio ; OSHA Region 5 ; OSHA Region 9
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  DART - Division of Applied Research and Technology
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  144
• Issue:
  1
• NIOSHTIC Number:
  nn:20045879
• Citation:
  Toxicologist 2015 Mar; 144(1):269
• CAS Registry Number:
  Asbestos (CAS RN 1332-21-4) ; Carbon (CAS RN 7440-44-0) ; Crocidolite asbestos (CAS RN 12001-28-4)
• Federal Fiscal Year:
  2015
• NORA Priority Area:
  Manufacturing
• Peer Reviewed:
  False
• Source Full Name:
  The Toxicologist. Society of Toxicology 54th Annual Meeting and ToxExpo, March 22-26, 2015, San Diego, California
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:01a2a2855f14092b9197a89fdbbdf77dcffa74958894ee34d3d642f2f7ab388ed798c4804986233c56c2948822e381105fe6212e314eea8966be3527971e752a
• Download URL:
  https://stacks.cdc.gov/view/cdc/201128/cdc_201128_DS1.pdf
• File Type:
  [PDF - 219.01 KB ]