ABSTRACT
A substantial amount of traffic-related particle emissions is released by gasoline cars, since most diesel cars are now equipped with particle filters that reduce particle emissions. Little is known about adverse health effects of gasoline particles, and particularly, whether a gasoline particle filter (GPF) influences the toxicity of gasoline exhaust emissions. We drove a dynamic test cycle with a gasoline car and studied the effect of a GPF on exhaust composition and airway toxicity. We exposed human bronchial epithelial cells (ECs) for 6 hours, and compared results with and without GPF. Two hours later, primary human natural killer cells (NKs) were added to ECs to form cocultures, while some ECs were grown as monocultures. The following day, cells were analyzed for cytotoxicity, cell surface receptor expression, intracellular markers, oxidative DNA damage, gene expression, and oxidative stress. The particle amount was significantly reduced due to GPF application. While most biological endpoints did not differ, oxidative DNA damage was significantly reduced in EC monocultures exposed to GPF compared to reference exhaust. Our findings indicate that a GPF has beneficial effects on exhaust composition and airway toxicity. Further studies are needed to assess long-term effects, also in other cell types of the lung.
Subject(s)
Air Pollutants/toxicity , Carcinogens, Environmental/toxicity , DNA Damage/drug effects , Epithelial Cells/drug effects , Epithelial Cells/physiology , Filtration , Gasoline/toxicity , Cells, Cultured , Coculture Techniques , Humans , Killer Cells, Natural/physiology , Oxidative StressABSTRACT
Air pollution exposure, including passenger car emissions, may cause substantial respiratory health effects and cancer death. In western countries, the majority of passenger cars are driven by gasoline fuel. Recently, new motor technologies and ethanol fuels have been introduced to the market, but potential health effects have not been thoroughly investigated. We developed and verified a coculture model composed of bronchial epithelial cells (ECs) and natural killer cells (NKs) mimicking the human airways to compare toxic effects between pure gasoline (E0) and ethanol-gasoline-blend (E85, 85% ethanol, 15% gasoline) exhaust emitted from a flexfuel gasoline car. We drove a steady state cycle, exposed ECs for 6h and added NKs. We assessed exhaust effects in ECs alone and in cocultures by RT-PCR, flow cytometry, and oxidative stress assay. We found no toxic effects after exposure to E0 or E85 compared to air controls. Comparison between E0 and E85 exposure showed a weak association for less oxidative DNA damage after E85 exposure compared to E0. Our results indicate that short-term exposure to gasoline exhaust may have no major toxic effects in ECs and NKs and that ethanol as part of fuel for gasoline cars may be favorable.
Subject(s)
Air Pollution , Ethanol/toxicity , Gasoline/toxicity , Vehicle Emissions/toxicity , Air Pollutants , Bronchi , Coculture Techniques , Epithelial Cells , Humans , Killer Cells, NaturalSubject(s)
Air Pollutants/analysis , Particle Size , Particulate Matter/analysis , Acute Lung Injury/chemically induced , Acute Lung Injury/physiopathology , Air Pollutants/chemistry , Air Pollutants/toxicity , Animals , Inhalation Exposure/adverse effects , Mice , Particulate Matter/chemistry , Particulate Matter/toxicity , Vehicle Emissions/toxicityABSTRACT
A constantly growing number of scooters produce an increasing amount of potentially harmful emissions. Due to their engine technology, two-stroke scooters emit huge amounts of adverse substances, which can induce adverse pulmonary and cardiovascular health effects. The aim of this study was to develop a system to expose a characterized triple cell coculture model of the human epithelial airway barrier, to freshly produced and characterized total scooter exhaust emissions. In exposure chambers, cell cultures were exposed for 1 and 2 h to 1:100 diluted exhaust emissions and in the reference chamber to filtered ambient air, both controlled at 5% CO(2), 85% relative humidity, and 37 degrees C. The postexposure time was 0-24 h. Cytotoxicity, used to validate the exposure system, was significantly increased in exposed cell cultures after 8 h postexposure time. (Pro-) inflammatory chemo- and cytokine concentrations in the medium of exposed cells were significantly higher at the 12 h postexposure time point. It was shown that the described exposure system (with 2 h exposure duration, 8 and 24 h postexposure time, dilution of 1:100, flow of 2 L/min as optimal exposure conditions) can be used to evaluate the toxic potential of total exhaust emissions.
