24 Apr Will chronic e-cigarette use cause lung disease?
Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. The effects of tobacco smoke, in particular nicotine, have been extensively investigated and found to be a significant contributing factor in the development of lung cancers and COPD. Furthermore, much emphasis has been placed on the development of cessation of smoking programs and public education. Whilst tobacco smoking has continued to decline since the 1950’s, the use of E-cigarettes (E-Cigs)/vaping units has worryingly increased, attracting both former tobacco smokers and never smokers.
E-Cig liquids contain nicotine in a glycerol/propylene glycol vehicle which is vaporised and inhaled. Given the bitter taste of nicotine E-Cigs often contain flavourings, however, to date, neither E-Cigs nor E-Cig liquids are regulated by the Food and Drug Administration (FDA), therefore they have not undergone toxicological evaluation. In fact, the frightening reality is that no safety data from either humans or animals exits for many of the chemicals and information regarding clinical evaluation of biomarkers of harm (e.g., inflammatory and cytotoxic markers) is scarce at best. What is marketed as a safe alternative to tobacco smoking is potentially a ticking bomb.
A study by Vardavas et. al. showed that 5 minutes E-cig use was sufficient to lead to an increase in lung flow resistance over a range of frequencies and was related to a decrease in Fractional Expired Nitric Oxide (FeNO). NO has a number of functions in the lung, and changes in NO levels can affect ciliary beating frequency, inflammation and airway smooth muscle tone. NO is altered in many disease, including asthma (increased), cystic fibrosis (decreased), primary ciliary dyskinesia (decreased) and COPD (may be increased). Thus, it is possible that E-cig exposure has the potential to contribute to different lung diseases other than COPD.
Nicotine in vaping has been shown to alter many aspects of airway physiology such as increasing a cough reflex via nicotinic acetylcholine receptors expressed in pulmonary afferent neurons, as well as the proinflammatory effect on neutrophils. A further compounding factor to this is the potential for the flavoured constituents (sweet and bitter) in E-cig liquids to stimulate taste receptor signalling pathways that could alter airway physiology with chronic use. For example, the buttery flavour often added to E-cig liquids contains diacetyl which, when inhaled, is known to cause bronchiolitis obliterans or “popcorn” lung. This causes a range of symptoms from mild reversible respiratory impairment to more severe non-reversible lung obstruction from extensive scarring in the small airways. Further to this, T2R bitter receptors play a role in detection of noxious inhalants and expelling them from the airways by indirectly influencing mucociliary clearance. T2R’s are expressed in nasal mucosa along with T1R sweet receptors therefore, may play a role in causing persistent airway infections and chronic rhinitis.
With so many factors to consider it is essential that at-risk patients are closely monitored for changes in airway physiology. The Wesley Lung Function Lab recommend Complex Lung Function, FeNO and Rhinomanometry testing as standard. This allows close monitoring of both upper and lower respiratory physiology in conjunction with bronchial and paranasal inflammation.
For more information: https://www.qld.gov.au/health/staying-healthy/atods/smoking/devices