Reactive oxygen species: Their relation to pneumoconiosis and carcinogenesis

Val Vallyathan, Xianglin Shi, Vincent Castranova

Research output: Contribution to journalArticlepeer-review

103 Scopus citations

Abstract

Occupational exposures to mineral particles cause pneumoconiosis and other diseases, including cancer. Recent studies have suggested that reactive oxygen species (ROS) may play a key role in the mechanisms of disease initiation and progression following exposure to these particles. ROS-induced primary stimuli result in the increased secretion of proinflammatory cytokines and other mediators, promoting events that appear to be important in the progression of cell injury and pulmonary disease. We have provided evidence supporting the hypothesis that inhalation of insoluble particles such as asbestos, agricultural dusts, coal, crystalline silica, and inorganic dust can be involved in facilitating multiple pathways for persistent generation of ROS, which may lead to a continuum of inflammation leading to progression of disease. This article briefly summarizes some of the recent findings from our laboratories with emphasis on the molecular events by which ROS are involved in promoting pneumoconiosis and carcinogenesis.

Original languageEnglish
Pages (from-to)1151-1155
Number of pages5
JournalEnvironmental Health Perspectives
Volume106
Issue numberSUPPL. 5
DOIs
StatePublished - 1998

Keywords

  • Lung cancer
  • Occupational dust
  • Pneumoconiosis
  • Reactive oxygen species

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

Fingerprint

Dive into the research topics of 'Reactive oxygen species: Their relation to pneumoconiosis and carcinogenesis'. Together they form a unique fingerprint.

Cite this