LAUSR

E-cigarettes (eCig)-vaping is considered as a safer cigarette smoke-replacement during pregnancy while their long-term safety and effect on lung pathophysiology are not known. Combining mouse models of maternal vaping and allergic asthma in vivo and human airway smooth muscle cells (ASM) in vitro we tested whether maternal eCig vaping enhances features of allergic asthma in the offspring. Female BALB/c mice were vaped with either eCig vapour (±nicotine) or room air (control). eCig vaping was started prior to mating and continued during gestation and lactation. Female offspring were then subjected to an ovalbumin (OVA)-induced allergic asthma model. 24h after the last aerosolized OVA or saline challenge, key parameters of allergic asthma: airway inflammation, airway remodeling and airway hyperresponsiveness (AHR) were measured. Human ASM cells were treated with varying concentrations of eCig liquid condensate and key parameters of mitochondrial function were measured. Allergen-exposure induced Th2-driven inflammation in OVA-exposed mice, characterized by massive influx of eosinophils which was further enhanced in the eCig (+Nic)-exposed group when compared with eCig (-Nic) or OVA-only animals. We found increase in features of airway remodeling and AHR (flexiVent) in eCig (+Nic) group with OVA when compared with eCig (-Nic) or OVA-only animals. Mehcanistically we found that eCig (±Nic) dose-dependently decreased cell viability, reduced mitochondrial transmembrane potential (JC10) and respiration (oxygen consumption rate; seahorse). Collectievelly, maternal eCig-vaping enhanced features of allergic asthma in the offspring and this could be attributed to aberrant mitochondrial function.