E-cigarettes May Worsen COPD

September 1, 2019

E-cigarette vapor may worsen COPD. A new study demonstrates exposure-related death of human airway smooth muscle cells and other toxic effects.

A new study, summarized in the slides above, extends this inquiry to the effect ECs may have on individuals who have COPD. Results suggest that e-cigarette vapor is associated with death of human airway smooth muscle cells and increased levels of interleukin 8 (CXCL8), a pro-inflammatory chemokine found in airway smooth muscles. Both processes could worsen COPD.⁵

Airway Smooth Muscle Cells Vulnerable in COPD. In COPD patients, ASMCs are increaed in bulk and secrete increased amounts of inflammatory cells; they are hyerresponsive to smoke from combustilbe cigarettes and have been found vulnerable to toxic byproducts at high vaporization temperatures found in ECs.

EC Impact on COPD. A small preliminary study simuating physiologic conditions looked at how EC vapor affects ASMCs. ASMCs collected from 22 patients (9 with COPD) were stimulated with increasing concentrations of tobacco- & menthol-flavored EC extract vapor and O or 18 mg nicotine; study measured cytotoxicity and interleukin-8 (CXCL8) production.

Cell Death, Inflammation Linked to ECs. Tobacco-flavored vapor with/without nicotine : no effect at high temperatures. Menthol-flavored vapor with nicotine: more cytotoxic at high temperatures
Overall increase in response to EC vapor, regardless of flavor or nicotine concentration.

Clinical Implications: EC and COPD: ECs may cause lung inflammation, cell death in COPD. Advise patients with COPD against substituting combustible cigarettes with ECs. May damage lungs in a similar way as cigarettes. May cause more rapid COPD progression

Authors' Cautions. Poor understanding of harms linked to EC should not be interpreted as meaning they are safe. Currently there is no universal experimental model to evaluate exposure, thus findings are contradictory and can be related to: Differences in device generation, vaporization temperature, e-liquids used, concentration of EC vapor used.

______________________________________________
References

1. Ween MP, Whittall JJ, Hamon R,et al. Phagocytosis and inflammation: exploring the effects of the components of e-cigarette vapor on macrophages. Physiol Rep 2017; 5: e13370.
2. Sussan TE, Gajghate S, Thimmulappa RK, et al. Exposure to electronic cigarettes impairs pulmonary anti-bacterial and anti-viral defenses in a mouse model. PLos One2015; 10: e0116861.
3. Garcia-Arcos I, Geraghty P, Baumlin N,et al. Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner. Thorax 2016; 71: 1119–1129.
4. Higham A, Rattray NJW, Dewhurst JA,et al. Electronic cigarette exposure triggers neutrophil inflammatory responses. Respir Res 2016; 17: 56.
5. Bozier J, Rutting S, Xenaki D, et al. Heightened response to e-cigarettes in COPD. ERJ Open Res. 2019 Feb 26;5(1). pii: 00192-2018. doi: 10.1183/23120541.00192-2018.

Because e-cigarettes (ECs) have generally been thought to be safer than combustible cigarettes, people with COPD may switch to them in an effort to curtail or quit smoking. As of yet, however, there are no data demonstrating that ECs are a less harmful alternative to smoking. In fact, preliminary research suggests that ECs may lead to inflammation, emphysema, and increase the risk for COPD and infection.1-4Â (Continued below)