• Sükrü Oztürk, Sezai Vatansever, Kivanç Cefle, Sükrü Palanduz, Kerim Güler, Nilgün Erten, Osman Erk, M Akif Karan, and Cemil Taşcioğlu.
• Branch of Medical Genetics, Istanbul Medical Faculty, Istanbul University, Turkey. sozturk@istanbul.edu.tr
• J. Toxicol. Clin. Toxicol. 2002 Jan 1; 40 (2): 115-20.

ObjectiveThe object of this study was to investigate the genotoxic effect of acute overexposure to combustion products originating from coal or wood stoves in patients presenting with acute carbon monoxide intoxication.Study DesignIn a prospective study, we analyzed the frequency of sister chromatid exchange and the carboxyhemoglobin concentration in 20 consecutive patients without a history of smoking or drug use who had been treated in the Emergency Care Unit of Istanbul Medical Faculty due to acute carbon monoxide intoxication. All of these cases were domestic accidents due to dysfunctioning coal or wood stoves. The results were compared with a control group of 20 nonsmoking, nondrug-using healthy individuals matched for age, sex, and absence of other chemical exposure.ResultsThe mean sister chromatid exchange frequency per metaphase was significantly higher in the study group compared to the control group: 8.11 +/- 2.39 vs. 6.33 +/- 1.60 (p = 0.008). We found that there was no positive correlation between the blood carboxyhemoglobin concentration and sister chromatid exchange frequency.ConclusionsThese results suggest that acute exposure to combustion products of wood or coal is genotoxic to DNA. Potential causes of genotoxicity include known mutagenic compounds present in coal or wood smoke and ash, oxygen radicals formed during combustion, as well as hypoxic and reperfusion injury mechanisms initiated by carbon monoxide intoxication. Additional studies on separate carbon monoxide exposure from smoke and ash are needed to understand individual genotoxic contributions and mechanisms.

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