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

Abderrahim Nemmar, Ahmed Al Hemeiri, Naser Al Hammadi, Priya Yuvaraju, Sumaya Beegam, Javed Yasin, Mohamed Elwasila, Badreldin H. Ali, Ernest Adeghate

Research output: Contribution to journalArticle

17 Citations (Scopus)

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.

Original languageEnglish
Article numbere12258
JournalPhysiological Reports
Volume3
Issue number3
DOIs
Publication statusPublished - 2015

Fingerprint

Nose
Smoking
Lung
Water
Endothelins
Oxidative Stress
Airway Resistance
Bronchoalveolar Lavage Fluid
Catalase
Lipid Peroxidation
Superoxide Dismutase
Reactive Oxygen Species
Pneumonia
Honey
L-Lactate Dehydrogenase
Smoke
Tobacco Products
Tobacco
Glutathione
Interleukin-6

Keywords

  • Airway resistance
  • Inflammation
  • Nose-only exposure
  • Oxidative stress
  • Water pipe smoking

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology

Cite this

Nemmar, A., Hemeiri, A. A., Hammadi, N. A., Yuvaraju, P., Beegam, S., Yasin, J., ... Adeghate, E. (2015). Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice. Physiological Reports, 3(3), [e12258]. https://doi.org/10.14814/phy2.12258

Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice. / Nemmar, Abderrahim; Hemeiri, Ahmed Al; Hammadi, Naser Al; Yuvaraju, Priya; Beegam, Sumaya; Yasin, Javed; Elwasila, Mohamed; Ali, Badreldin H.; Adeghate, Ernest.

In: Physiological Reports, Vol. 3, No. 3, e12258, 2015.

Research output: Contribution to journalArticle

Nemmar, A, Hemeiri, AA, Hammadi, NA, Yuvaraju, P, Beegam, S, Yasin, J, Elwasila, M, Ali, BH & Adeghate, E 2015, 'Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice', Physiological Reports, vol. 3, no. 3, e12258. https://doi.org/10.14814/phy2.12258
Nemmar A, Hemeiri AA, Hammadi NA, Yuvaraju P, Beegam S, Yasin J et al. Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice. Physiological Reports. 2015;3(3). e12258. https://doi.org/10.14814/phy2.12258
Nemmar, Abderrahim ; Hemeiri, Ahmed Al ; Hammadi, Naser Al ; Yuvaraju, Priya ; Beegam, Sumaya ; Yasin, Javed ; Elwasila, Mohamed ; Ali, Badreldin H. ; Adeghate, Ernest. / Early pulmonary events of nose-only water pipe (shisha) smoking exposure in mice. In: Physiological Reports. 2015 ; Vol. 3, No. 3.
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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.",
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N2 - 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.

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