Volatile Organic Compounds as Breath Biomarkers for Active and Passive Smoking. (Research Articles)

Article excerpt

We used real-time breath measurement technology to investigate the suitability of some volatile organic compounds (VOCs) as breath biomarkers for active and passive smoking and to measure actual exposures and resulting breath concentrations for persons exposed to tobacco smoke. Experiments were conducted with five smoker/nonsmoker pairs. The target VOCs included benzene, 1,3-butadiene, and the cigarette smoke biomarker 2,5-dimethylfuran. This study includes what we believe to be the first measurements of 1,3-butadiene in smokers' and nonsmokers' breath. The 1,3-butadiene and 2,5-dimethylfuran peak levels in the smokers' breath were similar (360 and 376 [micro] g/[m.sup.3], respectively); the average benzene peak level was 522 [micro] g/[m.sup.3]. We found higher peak values of the target chemicals and shorter residence times in the body than previously reported, probably because of the improved time resolution made possible by the continuous breath measurement method. The real-time breath analyzer also showed the presence of the chemicals after exposure in the breath of the nonsmokers, but at greatly reduced levels. Single breath samples collected in evacuated canisters and analyzed independently with gas chromatography/mass spectrometry confirmed the presence of the target compounds in the postexposure breath of the nonsmokers but indicated that there was some contamination of the breath analyzer measurements. This was likely caused by desorption of organics from condensed tar in the analyzer tubing and on the quartz fiber filter used to remove particles. We used the decay data from the smokers to estimate residence times for the target chemicals. A two-compartment exponential model generally gave a better fit to the experimental decay data from the smokers than a single-compartment model. Residence times for benzene, 1,3-butadiene, and 2,5-dimethylfuran ranged from 0.5 (1,3-butadiene) to 0.9 min (benzene) for [[tau].sub.1] and were essentially constant (14 min) for [[tau].sub.2]. These findings will be useful in models of environmental tobacco smoke exposure and risk. Key words: active smoking, benzene, 1,3-butadiene, decay, 2,5-dimethylfuran, environmental tobacco smoke, exhaled breath, passive smoking, pharmacokinetics, real time, uptake.


Tobacco smoke causes lung cancer and has been classified as a group A carcinogen under the U.S. Environmental Protection Agency's (EPA) carcinogen assessment guidelines (1). Various studies have shown that tobacco smoke is an important source of several well-established carcinogens, including benzene, 1,3-butadiene, and N-nitrosamines (2-11).

Exposure to tobacco smoke-related chemicals is widely believed to pose significant health risks. Studies suggest, for example, that prenatal or childhood passive exposure to parents' smoking significantly increases the risk of childhood and adult cancers (12-15), and nonsmoking spouses of smokers have an increased risk of lung and nasal sinus cancers compared to spouses of nonsmokers (1,16,17). According to Wallace (18,19) and Krause et al. (20), indoor benzene concentrations are, respectively, about 50% and 69% higher in smokers' homes than in the homes of nonsmokers. Furthermore, tobacco smoke is responsible for 5% of the total exposure to benzene in the United States. Smokers receive 89% of their benzene exposure directly from smoking; nonsmokers derive about 10% of their exposure from environmental tobacco smoke (ETS) (21). Benzene is a hematotoxic substance that can cause acute myeloid leukemia and has been classified as a group A human carcinogen by EPA (22).

Cigarette smoke and engine exhausts are the major sources of exposure of the general population, through inhalation, to 1,3-butadiene. EPA has identified 1,3-butadiene as a group B2 probable human carcinogen (23) based on evidence of carcinogenicity from studies in humans, which indicate a causal relationship between occupational exposure to 1,3-butadiene and excess mortality from lymphatic and/or hematopoietic cancers (23,24). …