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Abstract
Aim: With the invention of electronic cigarettes (ECIG), many questions have been raised regarding their safety as an alternative to smoking conventional cigarettes. Conventional cigarette smoke contains a variety of toxicants including heavy metals. However, ECIG-generated aerosol contains only trace amounts of metals, adding to the argument for it being a safer alternative. In response to heavy metal exposure, metallothioneins are induced in cells to help store the metal, detoxify the body, and are also known responders to oxidative stress. In an attempt to add to the evaluation of the safety of ECIGs, metallothionein expression was quantified using the nematode Caenorhabditis elegans as an assessment of stress induced cellular damage caused by exposure.Methods: Adult nematodes were exposed to either ECIG aerosol or conventional cigarette smoke at doses of 15, 30, and 45 puffs, the equivalent of one, two, and three cigarettes, respectively. Movement, survival, and stress-induced sleep were assessed for up to 24 h after exposure. Relative expression levels for mtl-1 and mtl-2, C. elegans metallothionein genes, were analyzed after 1, 5, and 24 h post exposure using quantitative RT-PCR.Results: Nematodes exposed to conventional cigarette smoke underwent stress-induced sleep in a dose dependent manner with animals recovering to values within the range of air control after 5 h post exposure. Those exposed to ECIG aerosol did not undergo stress-induced sleep and were indistinguishable from controls. The expression of mtl-1 increased in a dose and time dependent manner in C. elegans exposed to conventional cigarette smoke, with a maximum expression observed at 5 h post exposure of 45 puffs. No induction of mtl-2 was observed in any animals. Additionally, ECIG aerosol did not induce expression of mtl-1 and mtl-2 at levels different than those of untreated.Conclusion: ECIG aerosol failed to induce a stress response in C. elegans. In contrast, conventional cigarette smoke induced the production of mtl-1 in a manner that correlates with the induction of stress-induced sleep suggesting a stress response to damage. The lack of cellular stress response to ECIG aerosol suggests it may be a safer alternative to conventional cigarettes.
Highlights
Cigarette smoking is responsible for hundreds of thousands of deaths per year and increases the risk of cardiovascular disease, stroke, respiratory disease, and cancer
Trace amounts of metals in Electronic cigarettes (ECIGs) aerosol have been reported at levels significantly lower than those found in conventional cigarette smoke (Williams et al, 2013, 2017; Czoli et al, 2015; Palazzolo et al, 2017a)
Exposure to conventional cigarette smoke caused an initial shock response in the animals, followed by a delayed recovery period, whereas exposure to ECIG aerosol had little to no effect on movement and responsiveness (Table 1)
Summary
Cigarette smoking is responsible for hundreds of thousands of deaths per year and increases the risk of cardiovascular disease, stroke, respiratory disease, and cancer. Trace amounts of metals in ECIG aerosol have been reported at levels significantly lower than those found in conventional cigarette smoke (Williams et al, 2013, 2017; Czoli et al, 2015; Palazzolo et al, 2017a). These metals are hypothesized to originate from the metal components of the atomizer and include: aluminum (Al), arsenic (As), cadmium (Cd), copper (Cu), iron (Fe), manganese (Mn), nickel (Ni), lead (Pb), and zinc (Zn) (Williams et al, 2013, 2017; Palazzolo et al, 2017a). While Aherrera et al (2017) very recently reported positive associations of Ni and Chromium (Cr) aerosol concentrations with corresponding Ni and Cr biomarker levels in urine and saliva, their results (along with the aforementioned studies) suggest absorption of these metals from cigarette smoke would present a greater physiological problem
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