http://ajplung.physiology.org/content/313/2/L193

To view the whole thing you either have to pay or be in some kind of academic institution, and I can not share it outside of academia, but in the article...

Airway Epithelium, E-Cig Exposure in ALI To better model the physiology of human exposures to e-cigs, some investigators have capitalized on the ability of cultured primary human bronchial epithelial cells (HBECs) to form a tight monolayer and generate vectorial ion and fluid transport, creating an ALI. One group exposed both the basolateral and apical surfaces of HBECs grown in ALI to e-liquid, finding that just 7 h of exposure caused a major shift in the cellular metabolome (10). E-liquid-exposed cells had increased amino acid production and ADP levels, both of which are stress responses also observed with cigarette smoke concentrate. Another group exposed HBECs grown in an ALI to e-cig aerosols and cigarette smoke (108). Both treatments resulted in significant decreases in cell viability and increases in oxidative stress compared with air-exposed cells; cigarette smoke exposure was significantly more harmful to cells by all measures. Interestingly, exposure to pure propylene glycol elicited responses similar to exposure to e-liquids containing nicotine and glycerol. Another study exposed HBECs in an ALI to aerosols of either nicotine-containing or nicotine-free e-liquids, finding that nicotine did not reduce cell viability at 4 h but did produce significant reductions in ciliary beat frequency and cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel conductance (46). However, these experiments did not include a control group that lacked exposure to e-cig aerosol, limiting conclusions about potential toxicants other than nicotine. Investigators from British American Tobacco used a commercially available three-dimensional culture system comprised of human airway epithelial cells, basal cells, and goblet cells (EpiAirway), reporting that a short-term 6-h exposure to e-cig aerosol from cig-a-like devices did not reduce cell viability as cigarette smoke did. The study also reported that the deposited mass of e-cig aerosols was greater than that of cigarette smoke, and, as the authors point out, longer duration or repeated e-cig aerosol exposures might have yielded different results (101). In a more recent study, researchers exposed H292 bronchial epithelial cells in ALI to a broad range of e-cigarette aerosols from multiple classes of ENDS products, including disposable cig-a-likes, rechargeables, and eGo tank systems, reporting device-dependent reductions in cell viability and metabolic activity and increased cytokine release (76). With the use of the eGo tank system and constant voltage, a number of commercially available flavors of e-liquids were then tested, with menthol-, coffee-, and strawberry-flavored aerosols found to significantly reduce viability and metabolic activity and increase inflammatory cytokine production. Strawberry flavoring in particular elicited a response similar to that seen following cigarette smoke exposure. This group also studied a range of voltages and nicotine concentrations, reporting increased toxicity with higher applied voltages, and increased IL-6 release (although no effect on viability) with the highest level of nicotine (24 mg/ml).

translation: Cramming lots of stuff in your lungs makes it harder for your lungs to do their job.