Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9036568 | Toxicology Letters | 2005 | 10 Pages |
Abstract
There is much data implicating environmental tobacco smoke (ETS) in the development and progression of disease, notably cancer, yet the mechanisms for this remain unclear. As ETS is both a pro-oxidant stressor and carcinogen, we investigated the relationship of ETS exposure to intracellular and serum levels of DNA-damage, both oxidative 8-hydroxy-2-deoxyguanosine (8OHdG) and general, in non-smokers from non-smoking households, occupationally exposed to ETS. General DNA-damage consisting of single and double strand breaks, alkali-labile sites and incomplete base-excision repair, increased significantly in a dose-dependent manner with ETS exposure in men (P = 0.015, n = 32, Pearson) but not women (P = 0.736, n = 17). Intracellular 8OHdG-DNA-damage and general DNA-damage were both greater in men than women (P = 0.0005 and 0.016, respectively) but 8OHdG serum levels did not differ between the genders. Neither 8OHdG-DNA-damage nor serum levels correlated with increasing ETS exposure. This is the first study to demonstrate dose-dependent increases in DNA-damage from workplace ETS exposure. Perhaps most interesting was that despite equivalent ETS exposure, significantly greater DNA-damage occurred in men than women. These data may begin to provide a mechanistic rationale for the generally higher incidence of some diseases in males due to tobacco smoke and/or other genotoxic stressors.
Keywords
Related Topics
Life Sciences
Environmental Science
Health, Toxicology and Mutagenesis
Authors
Abby C. Collier, Sachin D. Dandge, James E. Woodrow, Chris A. Pritsos,