From Coal Mine Dust to Quartz: Mechanisms of Pulmonary Pathogenicity

Details

• Personal Author:
  Castranova, Vincent
• Description:
  Exposure to coal mine dust or crystalline silica can result in the initiation and progression of interstitial lung disease. Pathogenesis is the consequence of damage to lung cells and resulting lung scarring associated with activation of fibrotic processes. This review presents the radiologic and histologic characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathological indices of acute and chronic silicosis. This presentation also reviews the results of in vitro, animal, and human investigations that elucidate mechanisms involved in the development of these pneumoconioses. Results support the involvement of four basic mechanisms in the etiology of CWP and silicosis: 1. Direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring. 2. Activation of oxidant production by pulmonary phagocytes, such as alveolar macrophages. When oxidant production exceeds antioxidant defenses, lipid peroxidation and protein nitrosation occur, resulting in tissue injury and consequent scarring. 3. Activation of mediator release from alveolar macrophages and alveolar epithelial cells. Chemokines recruit polymorphonuclear leukocytes and macrophages from the pulmonary capillaries into the air spaces. Once within the air spaces, these leukocytes are activated by proinflammatory cytokines to produce reactive species, which increase oxidant injury and lung scarring. 4. Secretion of growth factors from alveolar macrophages and alveolar epithelial cells. Release of such mediators stimulates fibroblast proliferation and induces fibrosis. In conclusion, results of in vitro and animal studies have provided the basis for proposing mechanisms that may lead to the initiation and progression of CWP and silicosis. Data obtained from exposed workers has lent support to these proposals. The mechanistic understanding obtained for the development of CWP and silicosis should be useful in elucidating the possible pathogenicity of other inhaled particles. [Description provided by NIOSH]
• Subjects:
  Coal Coal Mining Dust Environmental Exposure Fibrosis Lung Lung Diseases Mining Occupational Health Quartz Respiratory System Respiratory Tract Diseases Safety Silicon Dioxide

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• Keywords:
  Coal Dust Coal Mining Exposure Levels In Vitro Studies Lung Disease Lung Fibrosis Pathogenicity Pneumoconiosis Pulmonary System Disorders Quartz Dust Respirable Dust Respiratory System Disorders Silica Dusts Silicosis

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• ISSN:
  0895-8378
• Document Type:
  Text
• Genre:
  Journal Article
• Place as Subject:
  OSHA Region 3 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  7-14
• Volume:
  12
• NIOSHTIC Number:
  nn:20020627
• Citation:
  Inhal Toxicol 2000 Sep; 12(Suppl 2):7-14
• Contact Point Address:
  Vincent Castranova, NIOSH/HELD/PPRB, Mail Stop L-2015, 1095 Willowdale Road, Morgantown, WV 26505, USA
• Email:
  VIC1@cdc.gov
• CAS Registry Number:
  Quartz (SiO2) (CAS RN 14808-60-7)
• Federal Fiscal Year:
  2000
• Peer Reviewed:
  True
• Source Full Name:
  Inhalation Toxicology
• Supplement:
  2
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:bb108578f159fc8a9552e5b1d592a804e51903428419a0ab288c9cf874b9bd75cf394245f97a91247266128a2edb8e631b0bab315590e0881d2bb517adc529aa
• Download URL:
  https://stacks.cdc.gov/view/cdc/198322/cdc_198322_DS1.pdf
• File Type:
  [PDF - 2.96 MB ]