Electronic cigarettes (e-cig) and heated tobacco products (HTP) are often used as smoking cessation aids, while the harm reduction effects of these alternatives to cigarettes are still the subject of controversial debate, in particular regarding their carcinogenic potential. The objective of this study is to compare the effects of e-cig, HTP and conventional cigarette emissions on the generation of oxidative stress and genetic and epigenetic lesions in human bronchial epithelial BEAS-2B cells. Our results show that HTP were less cytotoxic than conventional cigarettes while e-cig were not substantially cytotoxic in BEAS-2B cells. E-cig had no significant effect on the Nrf2 pathway, whereas HTP and cigarettes increased the binding activity of Nrf2 to antioxidant response elements and the expression of its downstream targets HMOX1 and NQO1. Concordantly, only HTP and cigarettes induced oxidative DNA damage and significantly increased DNA strand breaks and chromosomal aberrations. Neither histone modulations nor global DNA methylation changes were found after acute exposure, regardless of the type of emissions. In conclusion, this study reveals that HTP, unlike e-cig, elicit a biological response very similar to that of cigarettes, but only after a more intensive exposure: both tobacco products induce cytotoxicity, Nrf2-dependent oxidative stress and genetic lesions in human epithelial pulmonary cells. Therefore, the health risk of HTP should not be underestimated and animal studies are required in order to determine the tumorigenic potential of these emerging products.

Fine particles (PM_2.5) have generally been reported as the major contributor to the adverse health effects of air pollution. Lebanon is characterized by a high density of transport, the production of electricity by generators, and a problem of uncontrolled incineration of household waste. For the purpose of this paper, the physico-chemical properties of fine (PM_2.5-0.3) and quasi-ultrafine (PM_0.3) particulate matter sampled in Southern Lebanon, were studied. Then, an evaluation and comparison of the toxicity of the different extracted fractions from PM (i.e., native PM_2.5-0.3 vs. organic extractable matter fraction (OEM_2.5-0.3), and non-extractable matter fraction (NEM_2.5-0.3)) was performed. Also, an examination of the toxicity of PM_0.3 was conducted indirectly through the evaluation of the OEM_0.3 harmfulness. The physico-chemical analysis showed that PM_0.3 was much more concentrated than PM_2.5-0.3 in organic compounds such as polycyclic aromatic hydrocarbons (PAHs) (28-fold) and their nitrated (N-PAHs, 14-fold) and oxygenated (O-PAHs, 10-fold) derivatives. Normal human bronchial epithelial cells (BEAS-2B) were exposed to PM_2.5-0.3, its derived fractions (i.e., OEM_2.5-0.3 and NEM_2.5-0.3), and OEM_0.3 before evaluating the global cytotoxicity, metabolic activation of organic compounds, genotoxicity, and inflammatory response. Different responses were observed depending on the considered fraction of particles. The global cytotoxicity showed a pronounced response related to ATP and LDH activities after exposure to the quasi-ultrafine organic extractable matter fraction (OEM_0.3). There was no significant induction of the AhR cell-signaling pathway by NEM_2.5-0.3. Despite the apparent difference in the kinetics of induction of the toxicological endpoints under study, OEM_0.3 provoked a higher overall cytotoxicity and genotoxicity than OEM_2.5-0.3 and total PM_2.5-0.3. Taken together, these results clearly showed that the finest particles are more damaging to BEAS-2B cells than PM_2.5-0.3 because they are richer in organic compounds, thereby inducing more remarkable toxic effects.