heightened response to e-cigarettes in COPD

Introduction:
This text is a summary of an original research letter examining the effects of e-cigarette stimulation on primary airway smooth muscle cells (aSMCs) from people with and without Chronic Obstructive Pulmonary Disease (COPD). The study aims to evaluate dose-response relationships and investigate if lung cells from people with COPD are hyperresponsive to e-cigarettes. The key points of the study design, major findings, and main message are summarized below.

Key Points:

* The study included primary aSMCs from 22 patients, of which nine had a diagnosis of COPD.
* E-cigarette vapor extract (EVE) was made by bubbling e-vapour through DMEM supplemented with 0.1% Fetal Bovine Serum and antibiotics.
* CXCL8 release was measured in supernatant using ELISa, and cytotoxicity was determined post-stimulation using an MTT assay.
* Both tobacco EVEs induced greater CXCL8 production in COPD cells compared with non-COPD cells.
* Menthol EVEs did not induce greater CXCL8 production in COPD cells compared with non-COPD cells.
* Menthol EVE containing nicotine was more cytotoxic when generated at 60 W, with a trend towards increased toxicity with menthol flavoured nicotine-free EVE.
* Tobacco-flavoured EVE had no effect on cytotoxicity when generated at higher temperatures.
* The study suggests that e-cigarettes would stimulate lung neutrophilic inflammation and have a similar ability to stimulate inflammation and lung damage as cigarette smoke, potentially accelerating disease progression in COPD patients.

Main Message:
The study suggests that e-cigarette use may not be a safer alternative to smoking for individuals with COPD. Both tobacco and menthol-flavored e-cigarette vapor extracts induced greater CXCL8 production in COPD cells compared with non-COPD cells. additionally, menthol-flavored e-cigarette vapor extract containing nicotine was more cytotoxic when generated at higher temperatures. The study's findings suggest that e-cigarettes could stimulate lung neutrophilic inflammation and have a similar ability to stimulate inflammation and lung damage as cigarette smoke, potentially accelerating disease progression in COPD patients. Therefore, individuals with COPD should avoid using e-cigarettes as a smoking cessation aid.

Bozier, Jack, Sandra Rutting, Dia Xenaki, Matthew Peters, Ian adcock, and Brian G. Oliver. “heightened Response to E-Cigarettes in COPD.” ERJ Open Research 5, no. 1 (February 2019): 00192–02018. https://doi.org/10.1183/23120541.00192-2018.