OBJECTIVETo study the genotoxicity effect of environmental tobacco side-stream smokes (ETSS) on oxidative DNA damage and its molecular mechanism.

METHODSDNA adduct 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. The level of 8-OHdG in DNA exposed to ETSS was detected by high performance liquid chromatography with electrochemical detection. Organic and inorganic components in ETSS were analyzed by gas chromatography-mass spectrum and atomic absorption spectrum respectively.

RESULTSParticle matters (PMs) and volatile organic compounds (VOCs) in ETSS could directly induce oxidative DNA damage and formation of 8-OHdG. There were 123 and 84 kinds of organic components in PMs and VOCs respectively, and 7 kinds of inorganic components in ETSS. Some components, especially quinones and polyphenols in ETSS, could produce free radicals in vitro by auto-oxidation without any biological activity systems, and with the catalytic reaction of metals, the DNA adduct 8-OHdG was produced.

CONCLUSIONETSS have biological oxidative effect on DNA in vitro and in vivo, and expressed direct genotoxicity. 8-OHdG is a valuable biomarker of oxidative DNA damage.

Animals ; Biomarkers ; analysis ; Cattle ; DNA ; drug effects ; metabolism ; DNA Adducts ; analysis ; DNA Damage ; Deoxyguanosine ; analogs & derivatives ; analysis ; Female ; Lung ; chemistry ; metabolism ; Metals, Heavy ; analysis ; Organic Chemicals ; analysis ; Oxidation-Reduction ; Rats ; Tobacco Smoke Pollution ; adverse effects ; analysis

OBJECTIVES: Nitrogen dioxide (NO2) has been inconsistently associated with gradual decreases in lung function. Here, we studied the effects of NO2 exposure in asthmatics by examining the association between changes in lung function and concentrations of NO2 which were personally measured. METHODS: Peak expiratory flow (PEF) and daily personal exposures to NO2 were recorded on 28 patients with asthma (confirmed by methacholine provocation test) over 4 weeks. We used generalized estimating equations to assess the relationship between personal NO2 exposure and PEF, adjusting for potential confounders such as age, gender, outdoor particulate matter, temperature, humidity, and exposure to environmental tobacco smoke. RESULTS: The personal NO2 exposures were higher than the corresponding ambient levels. The mean personal: ambient ratio for NO2 was 1.48. The personal NO2 exposures were not associated with the morning PEF, evening PEF, or the diurnal PEF variability. However, environmental tobacco smoke was negatively associated with both the morning and evening PEF. CONCLUSIONS: Among the asthmatic adults who participated in this study, we found no apparent impact of personal NO2 exposures on the peak expiratory flow.
Tobacco Smoke Pollution/adverse effects/analysis ; Time Factors ; Peak Expiratory Flow Rate/*drug effects ; Nitrogen Dioxide/*adverse effects ; Male ; Lung/*drug effects/physiology ; Korea/epidemiology ; Inhalation Exposure/*adverse effects/analysis ; Humans ; Female ; Asthma/epidemiology/*physiopathology ; Air Pollution, Indoor/adverse effects/analysis