High-wattage electronic cigarette use in large amounts may lead to sustained tissue hypoxia, airway epithelial injury, and small airway constriction, according to an article published in the American Journal of Respiratory Critical Care Medicine.

The article reported the preliminary results from an ongoing randomized, placebo-controlled, crossover study evaluating the cardiorespiratory effects of e-cigarettes. The purpose of the study is to determine the effects of a 50:50 mix of propylene glycol and glycerol, when acutely vaporized under intense conditions, on the lung and skin microvascular function by way of the oxidative stress pathway.

Researchers recruited 23 individuals and assigned them to receive 25 puffs of propylene glycol/glycerol mix (50:50) vaporized at 60 watts, followed by 25 puffs of the same mix with the e-cigarette turned off (sham-vaping) 7 days after the first 25 puffs.

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The study participants experienced 60 minutes of skin tissue hypoxia after being exposed to the high-wattage e-cigarettes (84±2 mm Hg to 70±4 mm Hg; P <.001 vs baseline). No changes or modifications in transcutaneous CO 2 tensions were noted (analysis of covariance group × period interaction P >.05); however, changes in serum club cell protein 16 (CC16) from baseline were noted, possibly indicative of lower airway injury.

Researchers observed an overall decrease of forced expiratory flow-50%, forced expiratory flow-25%, and forced mild expiratory flow rate (L×s−1, median, 4.8 [interquartile range (IQR), 4-6.1] to 4.2 [IQR, 3.7-5.5]; P =.002 vs baseline; L×s−1, median, 2.5 [IQR, 1.7-2.6] to 2 [IQR, 1.4-2.3]; P =.005 vs baseline; and L×s-1, median, 4.2 [IQR, 3.5-5.4] to 3.7 [IQR, 3.1-4.9], P =.005 vs baseline, respectively). The same changes were observed when the sessions were compared with each other (P <.004).

Interestingly, no modifications in baseline skin continuous microcirculatory flow were observed during the study (P >.1), in addition to no increase in plasma oxidative stress biomarkers and superoxide anion production in human umbilical vein endothelial cells incubated with study participants’ sera.

Researchers concluded that vaping causes lung gas exchange perturbations that decrease the partial pressure of arterial O 2 , causing a state of hypoxia researchers state could not explained by oxidative stress imbalance or microvascular dysfunction. Vaping may cause deep lung inflammation and, with long-term exposure, could potentially lead to impairment of epithelial thickening and mucociliary clearance.

Clinicians should encourage individuals to decrease or avoid smoking high-wattage e-cigarettes, as it has severe negative short- and long-term effects on pulmonary health.

Reference

Chaumont M, Bernard A, Pochet S, et al. High wattage e-cigarettes induce tissue hypoxia and lower airway injury: a randomized trial [published online February 16, 2018]. Am J Respire Crit Care Med. doi:10.1164/rccm.201711-2198LE