Background: While ECIGs are under scrutiny concerning safety, particularly in reference to the physiological impact that aerosolized ECIG liquid (E-liquid) may have on respiratory tissues, others believe that ECIGs are a “Harm Reduction” alternative to conventional cigarettes. Previous studies investigating ciliated respiratory epithelium indicate that smoking shortens cilia length, reduces cilia beat frequency and disrupts respiratory epithelium, which most likely contributes to the inhibition of mucocilliary clearance. Monitoring mucous clearance of respiratory tissues exposed to ECIG-generated aerosol or conventional cigarette smoke, as indexed by mucous transport velocity (MTV), is one way to gauge the impact aerosol and smoke have on the respiratory tract. Therefore, we designed an experiment to test the effect of ECIG-generated aerosol and smoke on MTV using the frog palate paradigm.Methods: Peristaltic pumps transport ECIG-generated aerosol and conventional cigarette smoke into custom-made chambers containing excised bullfrog palates. MTVs were determined before exposure, immediately after exposure and approximately 1 day following exposure. MTVs were also determined (at the same time points) for palates exposed to air (control). Surface and cross sectional SEM images of palates from all three groups were obtained to support MTV data.Results: The results indicate that ECIG-generated aerosol has a modest inhibitory effect (p < 0.05) on MTV 1 day post-exposure (0.09 ± 0.01) compared to control MTV (0.16 ± 0.03 mm/s). In contrast, smoke completely inhibits MTV from 0.14 ± 0.03 mm/s immediately before exposure to 0.00 mm/sec immediately after exposure and the MTV is unable to recover 1 day later. SEM images of control palates and palates exposed to ECIG-generated aerosol both show cilia throughout their epithelial surface, while some areas of palates exposed to smoke are completely devoid of cilia. Additionally, the epithelial thickness of aerosol-exposed palates appears thicker than control palates while smoke-exposed palates appear to be thinner due to epithelial disruption.Conclusions: These results indicate that ECIG-generated aerosol has only a modest effect on mucocilary clearance of bullfrog palates and aerosol sedimentation accounts for epithelial thickening. In accordance with the primary literature, conventional cigarette smoke dramatically inhibits mucociliary clearance and is, in part, due to decreased number of cilia and disruption of the smoke-exposed epithelium.

Thyroid peroxidase (TPO) is the enzyme involved in thyroid hormone synthesis. Arsenic trioxide (As2O3) is known to inhibit TPO activity in vitro. This inhibition is believed to occur when As2O3 binds to TPO's free sulfhydryl groups. Reduced glutathione (GSH) is also known to inhibit TPO activity in vitro. This inhibition may occur because GSH acts as a competitive substrate for hydrogen peroxide, or possibly reduce the oxidized form of iodide, requirements for TPO action. On the other hand, one could speculate that GSH reduces arsenic-induced TPO inhibition by interacting directly with arsenic or TPO, consequently limiting arsenic's ability to inhibit TPO activity. Since GSH is known to inhibit thyroid hormone synthesis while at the same time it is also known to be an important antioxidant preventing cellular damage induced by oxidative stress and protecting the thyroid gland from oxidative damage induced by arsenic, we wanted to determine if a combination of As2O3 and reduced GSH would either attenuate or augment the As2O3-induced inhibition on TPO activity. Using an in vitro system, TPO was assayed spectrophotometrically in the presence of As2O3 (0.01, 0.1, 1, and 10 ppm), GSH (0.1, 1, 5, and 10 ppm), and As2O3 (0.1 ppm) and GSH (0.01, 0.1, 1, or 10 ppm) combinations. Our results show that 0.1, 1.0, and 10 ppm As2O3 inhibit TPO activity. Similarly, 5 and 10 ppm GSH also inhibit TPO activity. When 0.1 ppm As2O3 (i.e., the lowest dose of arsenic able to partially inhibit TPO activity) is combined with 0.01, 0.1, 1.0, or 10 ppm GSH inhibition of in vitro TPO activity is augmented as indicated by complete inhibition of TPO. The mechanism of this augmentation and whether it translates to living systems remains unclear.