Environmental tobacco smoke in the workplace induces oxidative stress in employees, including increased production of 8-hydroxy-2'-deoxyguanosine

• Published in: Cancer epidemiology, biomarkers & prevention Vol. 7; no. 2; p. 141
• Main Authors: Howard, D J, Ota, R B, Briggs, L A, Hampton, M, Pritsos, C A
• Format: Journal Article
• Language: English
• Published: United States American Association for Cancer Research 01.02.1998
• Subjects: Adult; Air Pollution, Indoor - adverse effects; Ascorbic Acid - blood; beta Carotene; Catalase - blood; Coronary Disease - etiology; Cotinine - blood; Deoxyguanosine - analogs & derivatives; Deoxyguanosine - blood; Female; Glutathione Reductase - blood; Humans; Male; Middle Aged; Neoplasms - etiology; Oxidative Stress; Risk Factors; Superoxide Dismutase - blood; Tobacco Smoke Pollution - adverse effects; Vitamin E - blood; Workplace
• ISSN: 1055-9965; 1538-7755

Environmental tobacco smoke (ETS) is a pervasive contaminant in the workplace. Our objective was to determine the oxidative stress effects of ETS on employees who are exposed. The results provide information that is useful to the resolution of risk assessment questions associated with ETS. We analyzed two blood draws from volunteers in our control and exposed groups. The level of exposure to ETS was determined through plasma cotinine measurements, which showed a 65% increase from the control group to the exposed group. Exposure to ETS resulted in a statistically significant increase of 63% of the oxidative DNA mutagen 8-hydroxy-2'-deoxyguanosine in the blood of exposed subjects. This oxidative DNA damage has been linked to an increased risk of developing several degenerative chronic diseases, including coronary heart disease and cancer. The exposed subjects also had increased levels of superoxide dismutase, catalase, glutathione peroxidase (GPOX), and glutathione reductase. However, these increases were only statistically significant in catalase and GPOX. Catalase levels were 13% higher in the exposed group, and GPOX levels were 37% higher in exposed volunteers. The biochemical evidence suggests that exposure to ETS causes oxidative stress, resulting in DNA damage that may increase the risk of certain diseases.