Menthol Attenuates Respiratory Irritation and Elevates Blood Cotinine in Cigarette Smoke Exposed Mice
Fig 5
Effect of L-menthol on murine ventilation response to high concentration of cigarette smoke and on serum cotinine levels.
(A) Breathing patterns of a mouse at baseline (top), during exposure to 300 mg/m3 (>400 ppm carbon monoxide) side stream cigarette smoke (middle), and side stream smoke combined with 60 ppm L-menthol vapor (bottom). Shown are representative recordings of respiratory flow rate (inspiration downward, expiration upward). For the sake of clarity, the recordings are representative of minutes 6–9 of exposure when the effects of smoke and menthol were maximal and at equilibrium, see Fig. 5B. The prolonged braking at the onset of expiration during smoke exposure is readily apparent and is indicated by the heavy bars. This effect is measured as the duration of braking (DB) during each expiration. (B) Time course of the response to 300 mg/m3 smoke (>400 ppm carbon monoxide). Data are presented as the 1 minute average DB level during the baseline (-5 to 0 minute) or the exposure (0 to 20 minute) period, expressed a mean ± SEM (n = 7–8 mice per group). The response was significantly attenuated by 60 ppm L-menthol (repeated measures ANOVA, p value provided in the figure), particularly at the start of exposure. (C) Cotinine levels in blood drawn immediately after 20 minute exposure to 300 mg/m3 smoke or 300 mg/m3 smoke +60 ppm L-menthol. Data are expressed as mean ± SEM (n = 7–8 mice per group). These were the same mice whose breathing response is shown in (B) above. The two groups differed from each other (*) at p = 0.015 level (t-test). The airborne nicotine levels averaged 30 mg/m3 and were identical in the smoke-alone and smoke + L-menthol groups. Cotinine levels in control (non-exposed) mice averaged less than 1 ng/ml.