RESUMO
Gasoline is an essential petroleum-derived product powering the automotive economy worldwide. This research focused on the Volatile Organic Component (VOC) cocktail resulting from gasoline evaporation. Petroleum fugitive VOC inhalation by petrol station attendants have been widely associated with toxicological and health risks concerns. Another unusual practice in poor nations is gasoline sniffing to get high which can lead to intoxication and organ damages. In this study, a static air/liquid interface methodology was designed to emulate acute human lung-derived cell exposure to all the gasoline-derived generated VOCs. The research investigated the cytotoxic and genotoxic end points resulting from whole gasoline fumes in vitro exposure using A549 cells. Petroleum-derived VOCs were identified and characterized by GC-MS. VOCs exposure was emulated in a controlled environment by evaporating spiked crude gasoline (1 to 100 µl) in a closed exposure chamber. In the chamber, A549 cultured cells on snapwell inserts were exposed on their apical side to various concentrations of generated vapors for one hour at 37 °C to mimic lung exposure. The results indicated that acute gasoline whole VOCs exposure reduced cell viability (IC50 = 485 ppm immediately and IC50 = 516 ppm 24 h post-exposure), disrupted cell membrane integrity though LDH leakage and induced DNA damages. Furthermore, VOC exposure triggered caspase-independent apoptosis in exposed cells through upregulation of apoptotic pathways. Overall, the presented findings generated by the static exposure technique showed a practical and reproducible model that can be used to assess acute crude VOCs mixture toxicity endpoints and cell death pathways.