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Exhaled ethanol and acetaldehyde in human subjects exposed to low levels of ethanol.

With the increased use of ethanol-blend gasoline as an alternative to gasoline, there is a demand for new data to assess the potential health risk of ethanol exposure. Currently, there is very limited information from the scientific database on the adverse effects of inhaled low doses of ethanol (ETOH). The aim of this study was to determine the concentration of ETOH and acetaldehyde (ACTDH), a toxic metabolite of ETOH, in the alveolar air (AA) of subjects exposed to low ETOH vapor concentrations by inhalation. Five healthy adults (2 women, 3 men), nonsmoking, 25-55 yr of age, were exposed for 6 consecutive hours to 25, 100, or 1000 ppm ETOH and were asked to provide AA samples at various intervals during and after each exposure session, for ETOH and ACTDH measurements. Results showed that the concentrations of ACTDH and ETOH in AA measured after 2 h of exposure at 25 ppm were 0.06 ppm and 7.5 ppm, respectively. Overall, there was a significant correlation between ETOH exposure and ETOH (R(2) =.92, p <.001) and ACTDH (R(2) =.99, p <.001) in AA. The ratios between ACTDH and ETOH in AA after 4 h of exposure to 25.9 ppm, 101.7 ppm, and 990.8 ppm ETOH were 0.005, 0.008, and 0.006, respectively. In conclusion, this study showed that inhalation of ETOH at low concentrations resulted in measurable levels of ACTDH in AA and suggests that ACTDH may be used, with good toxicological relevance, as an indicator of exposure to low levels of ETOH in air.

Acetaldehyde↗

Exhaled markers of oxidative stress in idiopathic pulmonary fibrosis.

BACKGROUND: Expired breath condensate (EBC) has never been used to explore the level of oxidative stress in idiopathic pulmonary fibrosis (IPF). Therefore, the aim of this study was to measure the levels of H2O2 and 8-isoprostane, as biomarkers of oxidative stress, in the EBC of patients with IPF. MATERIALS AND METHODS: We investigated 16 patients with IPF and 15 healthy subjects as the control group. The levels of H2O2 and 8-isoprostane were measured in the EBC of all subjects and were compared between the IPF and control groups. In patients with IPF, H2O2 and 8-isoprostane were further correlated with pulmonary function tests (PFTs), the resting pO2 and the differential cell count from the bronchoalveolar lavage fluid (BALF). RESULTS: The mean (95%CI) concentration of H2O2 was increased in the patients with IPF compared with the normal subjects (0.36, 0.24-0.47 microM vs. 0.16, 0.10-0.23 microM, P=0.003). The mean (95%CI) concentration of 8-isoprostane was also increased in the patients with IPF compared with the controls (74, 38-110 pg mL-1 vs. 33, 28-39 pg mL-1, P=0.02). In the patients with IPF, the diffusing capacity of the lung for carbon monoxide was negatively correlated with the levels of H2O2 in EBC (P=0.03, r=-0.58). No other correlation was found between the oxidative stress markers in the EBC and PFT values, pO2 or BALF cell count. CONCLUSIONS: Our data suggest that H2O2 and 8-isoprostane are increased in the EBC of patients with IPF. H2O2 may be correlated with the severity of the disease in IPF.

Adult↗