Tobacco and Cannabis Studies
The harmful effects of tobacco smoke exposure are well documented. While smoking prevention and cessation are key to bringing an end to this epidemic, scientific research is needed both to understand smoke-induced pathophysiological mechanisms and to develop novel therapeutic agents to treat patients.
Given the extended time period needed to generate sound scientific evidence, research on tobacco or tobacco-related products requires a joint effort. SCIREQ is proud to be part of these efforts by offering state-of-the-art equipment for basic in vivo and in vitro studies. Learn what Dr. Wold, a researcher at the forefront of inhaled toxicology research, has to say about the current state and future of the field.
Additionally, with increasing legalization of recreational cannabis, there is an increased interest in research into both the pulmonary effects of inhaled cannabis, as well as improving our understanding of the endocannabinoid system.
For more information on our pulmonary equipment for E-cigarette exposure studies, please feel free to visit our E-cigarette Application page.
VERSATILE, PROGRAMMABLE, REPRODUCIBLE
The smoke composition is influenced by a number of technical factors. The constituents of smoke or their concentrations will differ whether the smoke is drawn from side-stream, main-stream, or environmental tobacco smoke. It will also vary with the smoke preparation (e.g. cigarette brand, water filtered smoke or hookah, cigars, or e-cigarette liquids) or the puff profile used. Since studies assessing the impact of smoke are typically conducted over a prolonged time period, it is therefore important to consistently and reproducibly introduce the same smoke composition for each experimental session.
The inExpose is a versatile, programmable, and compact exposure system that can be configured with smoke generation devices (e.g. cigarette smoking robot, single cigarette chamber, e-cigarettes), or nebulizers to generate a wide range of exposures consistently within and between studies, as well as across laboratories. Using the inExpose system, researchers create accurate and reproducible models of smoke exposure for tobacco and cannabis studies using the automated generation of vapor, customizable puffing volumes, and frequencies.
There are two different cigarette and marijuana accessories for the inExpose system, the integrated Cigarette Smoking Robot (CSRi) and Single Cigarette Chamber (SCC), which are described in the table below. Both systems can provide pre-defined and customizable puffing profiles.
- Acute neuroradiological, behavioral, and physiological effects of nose-only exposure to vaporized cannabis in C57BL/6 mice. Farra, Y., et al. (2020). Inhalation Toxicology. 1-18
- Synergistic effect of cigarette smoke and bacterial-induced chronic obstructive pulmonary disease type airway inflammation on promotion of K-ras mutant lung cancer. Ramos, M.A. et al. (2018). Cancer Research, 78(13)
- Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis. Yoshida, M., et al (2019). Nature Communications, 3145
- Smoke-induced neuromuscular junction degeneration precedes the fiber type shift and atrophy in chronic obstructive pulmonary disease. Kapchinsky, S., et al. (2018). The Journal of Physiology.
- Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension. Dikalov, S., et al. (2019). Vascular Biology and Microcirculation, 316(3): H639- H646
- Cigarette Smoke Triggers IL-33–associated Inflammation in a Model of Late-Stage Chronic Obstructive Pulmonary Disease. Lee, J.H., et al. (2019). American Journal of Respiratory Cell and Molecular Biology, 61(5): https://doi.org/10.1165/rcmb.2018-0402OC
- In utero tobacco smoke exposure alters lung inflammation, viral clearance, and CD8+ T-cell responses in neonatal mice infected with respiratory syncytial virus. Cheemarla, N.R., et al. (2019). American Journal of Physiology, 317(2): 212-221
- Dynamic changes in lung responses after single and repeated exposures to cigarette smoke in mice. Engle, M. L., et al. (2019). PLOS ONE, 14(2), e0212866. 2019.
- The expression profile of Claudin family members in the developing mouse lung and expression alterations resulting from exposure to secondhand smoke (SHS). Lewis, J. B., et al. (2018). Experimental Lung Research, 44(1), 13–24.
- Proline-Glycine-Proline Peptides Are Critical in the Development of Smoke-Induced Emphysema. Abdul Roda, M., et al. (2019). American Journal of Respiratory Cell and Molecular Biology.
- Dynamic changes in lung responses after single and repeated exposures to cigarette smoke in mice. Engle, M. L., et al. (2019). PLoS ONE, 14(2).
QUANTITATIVE, INTEGRATIVE AND TRANSLATIONAL OUTCOMES
The impact of smoke exposure on the respiratory system can best be captured by evaluating the changes in lung function. These measurements are quantitative and can capture the effect of several disease determinants (e.g. extent and pattern of tissue destruction). The flexiVent system combines a wide selection of lung function measurements within a single device while offering the sensitivity to capture small but significant changes. Overall and detailed respiratory mechanics, specific lung volumes, pressure-volume, or flow-volume loops are examples of measurements that can be used to characterize the respiratory system in tobacco or e-cigarette-related studies, with some outcomes (e.g. FEV, lung volumes) also having a translational value.
- Modelling the Impact of Chronic Cigarette Smoke Exposure in Obese Mice: Metabolic, Pulmonary, Intestinal, and Cardiac Issues. Dubois-Deruy, E., et al. (2020). Nutrients, 12(3): 827
- The role of miR-155 in cigarette smoke-induced pulmonary inflammation and COPD. De Smet, E.G., et al. (2020). MucosalImmunology, 13: 423-436
- Airway Resistance Caused by Sphingomyelin Synthase 2 Insufficiency in Response to Cigarette Smoke. Gupta, G., et al. (2019). American Journal of Respiratory Cell and Molecular Biology, 62(3). https://doi.org/10.1165/rcmb.2019-0133OC
- Cigarette Smoke Particles-Induced Airway Hyperreactivity in Vivo and in Vitro. Jia, M., et al. (2019). Pharm. Bull, 42: 703-711
- Protein Phosphatase 2A Reduces Cigarette Smoke–induced Cathepsin S and Loss of Lung Function. Doherty, D.F., et al. (2019). American Journal of Respiratory and Critical Care medicine, 200(1). https://doi.org/10.1164/rccm.201808-1518OC
- Bone morphogenetic protein 6 (BMP-6) modulates lung function, pulmonary iron levels and cigarette smoke-induced inflammation. Verhamme, F.M., et al. (2019). Mucosal Immunology, 12: 340-351
- Proline-Glycine-Proline Peptides Are Critical in the Development of Smoke-induced Emphysema. Abdul Roda, M., et al. (2019). American Journal of Respiratory Cell and Molecular Biology, 61(5): https://doi.org/10.1165/rcmb.2018-0216OC
CHRONIC STUDIES, VENTILATORY PARAMETERS
Smoke-related preclinical studies are often chronic studies involving repeated exposures over several months. During such studies, the harmful effects of smoke exposure on ventilation can be followed in a longitudinal manner using one of the plethysmography techniques (whole body, head-out, double-chamber). Parameters such as breathing frequency, tidal volume, or minute ventilation can be obtained non-invasively with these techniques, both under room air or altered atmospheric (e.g. hypoxia, hypercapnia) conditions. With the appropriate system configuration, the recording and computation of coughing events can also be achieved.
- Effects of cigarette smoke and chronic hypoxia on ventilation in guinea pigs. Clinical significance. – Olea, Elena et al. Adv Exp Med Biol. 2012;758:325-32. doi: 10.1007/978-94-007-4584-1_44.
- Cigarette smoke-induced pulmonary inflammation is TLR4/MyD88 and IL-1R1/MyD88 signaling dependent. – Doz, Emilie, et al. The Journal of Immunology 180.2 (2008): 1169-1178.
- Extracellular matrix defects in aneurysmal fibulin-4 mice predispose to lung emphysema. – PloS one 9.9 (2014): e106054.
- A ferret model of COPD-related chronic bronchitis. – JCI Insight 1.15 (2016): e87536.
CLASSIC, RELEVANT, TRANSLATIONAL
Smoking was established as a common determinant for smoke-related pulmonary and cardiovascular diseases. Exposures to smoke or its constituents can therefore affect airway and/or vascular smooth muscle contractility or relaxation. These effects can be directly addressed using tissue baths, a classic yet relevant and translational approach to study concentration-responses in isolated whole tissue preparations. The technique can be performed on contractile tissues from various sources or species under different conditions to simulate in vivo or clinical conditions (e.g. various oxygen concentrations).
- Structure and Function of Small Airways in Smokers: Relationship between Air Trapping at CT and Airway Inflammation 1. – Berger, Patrick, et al. Radiology 228.1 (2003): 85-94.
- Impairment of Pulmonary Vasoreactivity in Response to Endothelin-1 In Patients With Chronic Obstructive Pulmonary Disease (COPD). – J Vasc Med Surg 3.4 (2015): 213 doi:10.4172/2329-6925.1000213.
- Chronic nicotine treatment enhances vascular smooth muscle relaxation in rats. – Xu, Tian-ying, et al. Acta Pharmacologica Sinica 36.4 (2015): 429-439.
- Measurement of smooth muscle function in the isolated tissue bath applications to pharmacology research. – Jespersen, Brian, et al. J Vis Exp 95 (2015): 52334.
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