Objective Waterpipe tobacco smoking (WTS) involves passing tobacco smoke through water prior to inhalation, and has spread worldwide. This spread becomes a public health concern if it is associated with tobacco-caused disease and if WTS supports tobacco/nicotine dependence. A growing literature demonstrates that WTS is associated with disability, disease and death. This narrative review examines if WTS supports nicotine/tobacco dependence, and is intended to help guide tobacco control efforts worldwide. Data sources PUBMED search using: ((“waterpipe” or “narghile” or “arghile” or “shisha” or “goza” or “narkeela” or “hookah” or “hubble bubble”)) AND (“dependence” or “addiction”). Study selection Excluded were articles not in English, without original data, and that were not topic-related. Thirty-two articles were included with others identified by inspecting reference lists and other sources. Data synthesis WTS and the delivery of the dependence-producing drug nicotine were examined, and then the extent to which the articles addressed WTS-induced nicotine/dependence explicitly, as well as implicitly with reference to criteria for dependence outlined by the WHO. Conclusions WTS supports nicotine/tobacco dependence because it is associated with nicotine delivery, and because some smokers experience withdrawal when they abstain from waterpipe, alter their behaviour in order to access a waterpipe and have difficulty quitting, even when motivated to do so. There is a strong need to support research investigating measurement of WTS-induced tobacco dependence, to inform the public of the risks of WTS, which include dependence, disability, disease and death, and to include WTS in the same public health policies that address tobacco cigarettes.

Electronic cigarettes (E-cigs) have been promoted as harm-free or less risky than smoking, even for women during pregnancy. These claims are made largely on E-cig aerosol having fewer number of toxic chemicals compared with cigarette smoke. Given that even low levels of smoking are found to produce adverse birth outcomes, we sought to test the hypothesis that vaping during pregnancy (with or without nicotine) would not be harm-free and would result in vascular dysfunction that would be evident in offspring during adolescent and/or adult life. Pregnant female Sprague Dawley rats were exposed to E-cig aerosol (1 h/day, 5 days/wk, starting on gestational day 2 until pups were weaned) using e-liquid with 0 mg/mL (E-cig0) or 18 mg/mL nicotine (E-cig18) and compared with ambient air-exposed controls. Body mass at birth and at weaning were not different between groups. Assessment of middle cerebral artery (MCA) reactivity revealed a 51%–56% reduction in endothelial-dependent dilation response to acetylcholine (ACh) for both E-cig0 and E-cig18 in 1-mo, 3-mo (adolescent), and 7-mo-old (adult) offspring (P < 0.05 compared with air, all time points). MCA responses to sodium nitroprusside (SNP) and myogenic tone were not different across groups, suggesting that endothelial-independent responses were not altered. The MCA vasoconstrictor response (5-hydroxytryptamine, 5-HT) was also not different across treatment and age groups. These data demonstrate that maternal vaping during pregnancy is not harm-free and confers significant cerebrovascular health risk/dysfunction to offspring that persists into adult life. NEW & NOTEWORTHY These data established that vaping electronic cigarettes during pregnancy, with or without nicotine, is not safe and confers significant risk potential to the cerebrovascular health of offspring in early and adult life. A key finding is that vaping without nicotine does not protect offspring from cerebrovascular dysfunction and results in the same level of cerebrovascular dysfunction (compared with maternal vaping with nicotine), indicating that the physical and/or chemical properties from the base solution (other than nicotine) are responsible for the cerebrovascular dysfunction that we observed. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/maternal-vaping-impairs-vascular-function-in-theoffspring/.

We observe a significant alteration in arterial structure and function in adolescent and adult offspring due to developmental exposure to toxicants resulting from perinatal maternal vaping. Taken together with previous work that described lasting dysfunction in cerebral microvasculature in offspring, these data underscore the adverse consequences of maternal exposure to electronic cigarette aerosol in conduit and resistance vessels alike, irrespective of nicotine content.

Despite claims of safety or harm reduction for electronic cigarettes (E-cig) use (also known as vaping), emerging evidence indicates that E-cigs are not likely safe, or necessarily safer than traditional cigarettes, when considering the user’s risk of developing vascular dysfunction/disease. E-cigs are different from regular cigarettes in that E-cig devices are highly customizable, and users can change the e-liquid composition (such as the base solution, flavors, and nicotine level). Since the effects of E-cigs on the microvascular responses in skeletal muscle are poorly understood, we used intravital microscopy with an acute (one-time 10 puff) exposure paradigm to evaluate the individual components of e-liquid on vascular tone and endothelial function in the arterioles of the gluteus maximus muscle of anesthetized C57Bl/6 mice. Consistent with the molecular responses seen with endothelial cells, we found that the peripheral vasoconstriction response was similar between mice exposed to E-cig aerosol or cigarette smoke (i.e., 3R4F reference cigarette); this response was not nicotine dependent, and endothelial cell-mediated vasodilation was not altered within this acute exposure paradigm. We also report that, regardless of the base solution component [i.e., vegetable glycerin (VG)-only or propylene glycol (PG)-only], the vasoconstriction responses were the same in mice with inhalation exposure to 3R4F cigarette smoke or E-cig aerosol. Key findings from this work reveal that some component other than nicotine, in inhaled smoke or aerosol, is responsible for triggering peripheral vasoconstriction in skeletal muscle, and that regardless of one’s preference for an E-cig base solution composition (i.e., ratio of VG-to-PG), the acute physiological response to blood vessels appears to be the same. The data suggest that vaping is not likely to be ‘safer’ than smoking towards blood vessels and can be expected to produce and/or result in the same adverse vascular health outcomes associated with smoking cigarettes.

Little is known regarding the impact of electronic cigarette (e‐cig) usage in the human body. However, emerging literature suggests that vaping results in endothelial cell mediated vascular impairments, altered thrombosis, and depressed immune function (similar to that observed with smoking). Since e‐cigs are marketed as a ‘safer’ alternative to traditional cigarettes, it is important to characterize mechanisms through which e‐cigs may induce cellular insult. It is known that traditional cigarette use results in systemic accumulation of biomolecular free radicals (BFR), thus we sought to determine whether exposure to e‐cig vapor will result in significant systemic increases in BFR. We hypothesize that vaping will increase the relative amount of BFR accumulation in vital tissues in a time‐dependent manner. To identify BFR in‐vivo, C57BL/7 mice were given IP 1.5 g/kg DMPO (5,5‐dimethyl‐l‐pyrroline‐l‐oxide) spin‐trap in 2 doses over 1 hour, and acutely exposed to french vanilla‐flavored e‐cig vapor (18 mg nicotine) for either 1 hour (n=3) or 4 hours (n=3). Sham mice were exposed to ambient air (n=3). Immediately following exposure, the mice were anesthetized, perfused with PBS via intra‐ventricular catheterization, organs/tissues were harvested and fixed in paraformaldehyde/sucrose, flash‐frozen in liquid nitrogen and then fixed in TFM. Imaging from fluorescent immunohistochemical labeling revealed significant increase BFR accumulation in the liver (223%, p<0.05) and to lesser extent in the heart (133%, p<0.05) in 1‐hour exposed animals. Similar trends for increased BFR (albeit not statistically significant) were found in the lung (236%) and brain (124%) in 4‐hour exposed group compared to air exposed controls. In summary, we found significant increase in the presence of BFR in the liver and heart of mice acutely exposed to 1‐hour of e‐cig vapor compared to controls, with similar trends in other tissue beds (lung, brain) after 4‐hours vape exposure. This is a pilot study which needs additional samples for further evaluation, but suggests that vaping induces BFR accumulation in multiple organs which could lead to cellular damage and tissue dysfunction. Support or Funding Information Support: WVU Cancer Institute Philip R Dino Innovative Research Grant (IMO); Transition Grant Support; Office of Research and Graduate Education (IMO), WVU Health Sciences Center APS STRIDE Fellowship (JO); NIHGMS 5U54GM104942‐03 (PDC) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .