Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice

Abstract

Water pipe smoking (WPS) is increasing in popularity and prevalence worldwide. Convincing data suggest that the toxicants in WPS are similar to that of cigarette smoke. However, the underlying pathophysiologic mechanisms related to the early pulmonary events of WPS exposure are not understood. Here, we evaluated the early pulmonary events of nose-only exposure to mainstream WPS generated by commercially available honey flavored “moasel” tobacco. BALB/c mice were exposed to WPS 30 min/day for 5 days. Control mice were exposed using the same protocol to atmospheric air only. We measured airway resistance using forced oscillation technique, and pulmonary inflammation was evaluated histopathologically and by biochemical analysis of bronchoalveolar lavage (BAL) fluid and lung tissue. Lung oxidative stress was evaluated biochemically by measuring the level of reactive oxygen species (ROS), lipid peroxidation (LPO), reduced glutathione (GSH), catalase, and superoxide dismutase (SOD). Mice exposed to WPS showed a significant increase in the number of neutrophils (P < 0.05) and lymphocytes (P < 0.001). Moreover, total protein (P < 0.05), lactate dehydrogenase (P < 0.005), and endothelin (P < 0.05) levels were augmented in bronchoalveolar lavage fluid. Tumor necrosis factor α (P < 0.005) and interleukin 6 (P < 0.05) concentrations were significantly increased in lung following the exposure to WPS. Both ROS (P < 0.05) and LPO (P < 0.005) in lung tissue were significantly increased, whereas the level and activity of antioxidants including GSH (P < 0.0001), catalase (P < 0.005), and SOD (P < 0.0001) were significantly decreased after WPS exposure, indicating the occurrence of oxidative stress. In contrast, airway resistance was not increased in WPS exposure. We conclude that subacute, nose-only exposure to WPS causes lung inflammation and oxidative stress without affecting pulmonary function suggesting that inflammation and oxidative stress are early markers of WPS exposure that precede airway dysfunction. Our data provide information on the initial steps involved in the respiratory effects of WPS, which constitute the underlying causal chain of reactions leading to the long-term effects of WPS.

Chronic Exposure to Water-Pipe Smoke Induces Alveolar Enlargement, DNA Damage and Impairment of Lung Function

“…Recent studies reported that acute exposure to WPS using whole body or nose-only WPS exposure systems caused an increase in proinflammatory cytokines and markers of oxidative stress [13,14]. We recently demonstrated that exposure to WPS for one month increased airway resistance, inflammation, and oxidative stress [15].…”

“…Following 1 week of acclimatization, animals were randomly divided into air (control) and WPS-exposed groups. Mice were placed in soft restrainers and connected to the exposure tower [13,[15][16][17][18]. They were exposed to WPS or air through their noses using a nose-only exposure system (InExpose System, Scireq, Canada).…”

“…The tobacco was lit with instant light charcoal disk (Star, 3.5 cm diameter and 1 cm width). A standard of one puff of 2-s duration was taken once a minute, followed by 58 s of fresh air at a rate of 6 ml/s was applied [13,15,17,19,20]. The duration of the session was 30 min/day and 5 days/week for 6 months (except during the days of Friday and Saturday each week).…”

“…Homogenates were centrifuged for 10 min at 3000xg at 4°C to remove cellular debris, and supernatants were used for further analysis. Protein content was measured by Bradford's method as described before [13,17].…”

Water-Pipe Smoke Exposure-Induced Circulatory Disturbances in Mice, and the Influence of Betaine Supplementation Thereon

“…The activity of SOD was measured according to the vendor's protocol (Cayman Chemicals, Michigan, USA). NADPH-dependent membrane lipid peroxidation was measured as thiobarbituric acid reactive substance using malonedialdehyde as standard (Sigma-Aldrich Fine Chemicals, St Louis, MO, USA) [27,36].…”