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Environ Health Perspect. 1998 Oct;106 Suppl 5:1151-5.

Reactive oxygen species: their relation to pneumoconiosis and carcinogenesis.

Author information

1
Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, West Virginia 26505, USA. vav1@cdc.gov

Erratum in

  • Environ Health Perspect 1998 Dec;106 Suppl 6:1595.

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.

PMID:
9788890
PMCID:
PMC1533374
DOI:
10.1289/ehp.98106s51151
[Indexed for MEDLINE]
Free PMC Article

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