Predisposing factors in occupational lung cancer: inorganic minerals and chromium.
Ding M; Shi X; Castranova V; Vallyathan V
J Environ Pathol Toxicol Oncol 2000 Jan; 19(1-2):129-138
Reactive oxygen species (ROS) have been implicated in the pathogenesis of cancer. Inhalation of inorganic minerals such as asbestos and crystalline silica, and metals such as arsenic, beryllium, chromium, nickel, and vanadium, may promote directly and indirectly enhanced generation of ROS at a persistent level in concert with chronic inflammation. Perpetual ROS generation can cause specific molecular changes resulting in the activation or inactivation of transcription factors that may alter gene expression leading to cell proliferation, differentiation, and carcinogenesis. The mechanisms involved in the signal transduction leading to these processes are the subject of intense investigation. In this review, some of the recent findings from our laboratories concerning key molecular events elicited by asbestos, crystalline silica, and chromium are presented. These include genotoxicity, DNA damage, lipid peroxidation, activation of transcription factors activator protein-1 (AP-1) or nuclear factor kappa B (NF-kappaB), and p53 or k-ras gene alterations. From these studies, it is evident that ROS signaling is critical for the responses of cytokines, growth factors, and activation or inactivation of transcription factors that promote carcinogenesis.
Occupational diseases; Occupational health; Lung cancer; Pulmonary system disorders; Respiratory system disorders; Inorganic compounds; Chromium compounds; Asbestos dust; Silica dusts; Silicates; Carcinogenesis; Gene mutation; Genotoxic effects; Mutagenesis;
Author Keywords: occupational cancer; lung cancer; cancer epidemiology; inorganic minerals; chromium; reactive oxygen species
Val Vallyathan, Ph.D., Professor of Pathology, Centers for Disease Control and Prevention, NIOSH, 1095 Willowdale Road, Morgantown, WV 26505-2888
7440-47-3; 14808-60-7; 7440-38-2; 7440-41-7; 7440-47-3; 7440-02-0; 7440-62-2
Journal of Environmental Pathology, Toxicology, and Oncology