Here's the actual study if you're interested:

The results presented indicate that nicotine has dose-dependent deleterious pulmonary effects that result in loss of lung endothelial barrier function, acute lung inflammation, and decreased lung endothelial cell proliferation. These findings enhance our understanding of how CS exposure causes inflammation and define pulmonary effects of nicotine inhalation.

The preservation of an intact endothelial barrier is determined by a balance of contracting cytoskeletal forces and the integrity of cell-cell contacts, both of which can be affected by exposure to soluble components of CS extract (22). In this work, we identified that nicotine, which can be absorbed in the circulation as a component of CS or e-Cig disrupts endothelial barrier by increasing acto-myosin contractile signaling, primarily by Rho kinase-dependent phosphorylation and therefore inhibition of endothelial myosin phosphatase, causing increased MLC phosphorylation. Interestingly, although nicotine caused oxidative stress and activated p38 MAPK, similar to CS extract (22), neither p38 MAPK inhibition nor the ROS scavenger NAC were sufficient to restore barrier function following nicotine exposure, in contrast to their remarkable effect on CS-induced barrier dysfunction. These results suggest several possible explanations that include a threshold of MLC phosphorylation that is needed for barrier dysfunction which is achievable by Rho kinase activation but not by p38 MAPK alone. Such a concept is supported by a recent report in which Rho kinase was found, in certain conditions, to activate p38, but not vice versa (34). Alternatively, nicotine-activated Rho kinase may have additional targets that cause barrier dysfunction besides MLC phosphorylation, as supported by the recent finding of a critical role for Rho kinase isoform 2 in regulating cellular junctional tension (2). Finally, at least theoretically, nicotine-activated p38 MAPK may have additional unexpected barrier enhancing activities that counteract its MLC phosphorylation effects.
Either inhibition of Rho kinase, or enhancement of S1P to S1P1 signaling significantly counteracted the barrier disruptive effects of nicotine (Figure 8) and CS extract. The novel finding of a protective effect of S1P1 agonists on the CS/nicotine-disrupted endothelial barrier is not surprising, given reports of similar S1P1-dependent protective effects of FTY phosphonates against lung endothelial permeability during sepsis or acute lung injury (23, 31, 32), or during synergistic conditions of CFTR inhibition and CS extract exposure (3). FTY phosphonates acted at least in part by activating MYPT and inhibiting MLC phosphorylation, although additional effect on intercellular tethering cannot be ruled out. The fact that S1P augmentation did not recapitulate the effects of FTY phosphonates may be due to the short half-life of the molecule, or due to complementary, S1P385 pendent mechanisms of action of FTY phsosphonates (7).

Using various pharmacological inhibitors of nicotinic receptors to test their involvement in nicotine’s effects on the pulmonary endothelium, we could not identify a protective effect against barrier dysfunction (data not shown). However, it is possible that untested receptors and other mediators may regulate nicotine-altered endothelial barrier function. This may be true especially in response to high, cytotoxic nicotine exposure levels shown to inhibit prostaglandin and endothelin expression in bovine pulmonary endothelial cells (25), but were not tested in our work. The concentrations of nicotine used in our cell culture studies were derived from detailed dose response testing, were non-cytotoxic, and induced significant effects at levels higher than those absorbed in the circulation by smokers, but which may be achieved in tissue levels with high nicotine concentrations, such as the lung (6, 30). The effect of nicotine on barrier function may be organ dependent, since other studies have shown an improvement in the gut barrier function by cholinergic actions of nicotine on enteric glial cells (4).

While many of the nicotine effects on the lung endothelium were dose-dependent, nicotine399 pendent deleterious effects of e-Cig solutions were also noted. We have identified acrolein as putative mediator for nicotine-independent toxicity, based its presence in both e-Cig solution and vapor and on a large body of literature showing adverse pulmonary effects of acrolein, including on endothelial intercellular tethering molecules (12). The signaling effects on nicotine-free e-Cig vapors on the lung endothelial barrier remain to be investigated.

The noted dose-dependent anti-proliferative effects of nicotine on lung endothelial cells may have implications in angiogenesis and in lung injury repair. Our results on primary lung endothelial cells are in contrast to pro-proliferative effects of nicotine on human umbilical vascular endothelial cells (11), systemic vasculature, or on lung cancer cells (15), suggesting cell type-specific effects of low-dose nicotine.

Intra-vital lung microcopy in animals with intact circulation (no pump-perfusion) demonstrated that the in vitro finding of CS extracts causing decreased endothelial barrier function was paralleled by increased lung inflammation in vivo, measured by increased adherence of circulating leukocytes to the lung microvasculature within 20 minutes of CS inhalation without pulmonary edema (21). This previous work led us to complement our investigations of nicotine in cell culture models with in vivo studies of acute lung and systemic effects of nebulized nicotine and e-Cig extracts, mimicking the inhalation of e-Cig vapors by humans. We found that nicotine and e- Cig extracts caused rapid oxidative and nitroxidative stress observed in the BALF and plasma as well as a trend of increased neutrophil lung inflammation at 24h following inhalation, measured by the relatively less sensitive method of BALF cytospins, rather than intravital microscopy. Although future studies will determine how these acute inflammatory lung responses translate into long term effects of recurrent e-Cig exposures, we anticipate these will include dose-dependent sustained oxidative-stress and inflammatory lung damage with limitation of endothelial repair. In this context, ceramide/S1P balance may serve as an important rheostat of alveolar integrity, as seen in experimental models of COPD (5). By augmenting barrier enhancing and angiogenic S1P signaling via S1P1, such as shown here with pharmacological agonists, one may be able to improve barrier function in vivo and potentially attenuate the chronic damage caused by e-Cig inhalation.

The clinical implications of this work are related to the potential detrimental lung effects of exposure to inhaled e-Cig which may be dose-dependent, although further studies are needed to determine what are the usual levels of absorbed e-Cig vapor that are harmful to human lung health. Extrapolation of our results in primary human and murine lung endothelial cells and in animal models to human lungs, may indicate the need for further studies into the safety of e-Cig use.