Hazard identification of exhausts from gasoline-ethanol fuel blends using a multi-cellular human lung model

Abstract

Ethanol can be produced from biomass and as such is renewable, unlike petroleum-based fuel. Almost all gasoline cars can drive with fuel containing 10% ethanol (E10), flex-fuel cars can even use 85% ethanol (E85). Brazil and the USA already include 10-27% ethanol in their standard fuel by law. Most health effect studies on car emissions are however performed with diesel exhausts, and only few data exists for other fuels. In this work we investigated possible toxic effects of exhaust aerosols from ethanol-gasoline blends using a multi-cellular model of the human lung. A flex-fuel passenger car was driven on a chassis dynamometer and fueled with E10, E85, or pure gasoline (E0). Exhausts obtained from a steady state cycle were directly applied for 6h at a dilution of 1:10 onto a multi-cellular human lung model mimicking the bronchial compartment composed of human bronchial cells (16HBE14o-), supplemented with human monocyte-derived dendritic cells and monocyte-derived macrophages, cultured at the air-liquid interface. Biological endpoints were assessed after 6h post incubation and included cytotoxicity, pro-inflammation, oxidative stress, and DNA damage. Filtered air was applied to control cells in parallel to the different exhausts; for comparison an exposure to diesel exhaust was also included in the study. No differences were measured for the volatile compounds, i.e. CO, NO, and T.HC for the different ethanol supplemented exhausts. Average particle number were 6×10 #/cm (E0), 1×10 #/cm (E10), 3×10 #/cm (E85), and 2.8×10 #/cm (diesel). In ethanol-gasoline exposure conditions no cytotoxicity and no morphological changes were observed in the lung cell cultures, in addition no oxidative stress - as analyzed with the glutathione assay - was measured. Gene expression analysis also shows no induction in any of the tested genes, including mRNA levels of genes related to oxidative stress and pro-inflammation, as well as indoleamine 2,3-dioxygenase 1 (IDO-1), transcription factor NFE2-related factor 2 (NFE2L2), and NAD(P)H dehydrogenase [quinone] 1 (NQO1). Finally, no DNA damage was observed with the OxyDNA assay. On the other hand, cell death, oxidative stress, as well as an increase in pro-inflammatory cytokines was observed for cells exposed to diesel exhaust, confirming the results of other studies and the applicability of our exposure system. In conclusion, the tested exhausts from a flex-fuel gasoline vehicle using different ethanol-gasoline blends did not induce adverse cell responses in this acute exposure. So far ethanol-gasoline blends can promptly be used, though further studies, e.g. chronic and in vivo studies, are needed.

Gasoline particle filter reduces oxidative DNA damage in bronchial epithelial cells after whole gasoline exhaust exposure in vitro

“…Overall, the acute exposure to reference and GPF gasoline exhaust did not induce strong toxicity in our cell models, and, in fact, the toxicity seemed to be much lower compared to diesel exhaust exposure 27 , 28 . This is in accordance with previous studies showing only minor toxic effects of gasoline exhaust emissions 16 , 22 , 27 , 28 . Gasoline exhaust, however, contains high numbers of particles with metal oxides, so we expected to see an effect of the GPF.…”

“…The car was either driven without (reference) or with a coated GPF (cordierite substrate, 55% porosity, pore size of 14 µm, 200 cells per square inch, coated with palladium and rhodamine), mounted approximately 60 cm downstream of the three-way catalyst. For exhaust characterization, particle number (PN) concentration, carbon monoxide (CO), NO x , and total hydrocarbon (T.HC) were analyzed by the Laboratory for IC-Engines and Exhaust Emission Control at the Bern University of Applied Sciences, as described previously 27 , 28 . The particle size distribution was measured with a scanning mobility particle sizer consisting of a differential mobility analyzer (TSI, DMA model 3081 (long tube)) and a condensation particle counter (TSI, model 3772).…”

Traffic-Related Particulate Matter and Cardiometabolic Syndrome: A Review

“…Figure 2 presents a conceptual diagram of the induction of cardiometabolic syndrome by traffic-related PM, which bridges the connections among the PM sources, exposure routes, and biological perturbations (at molecular and cellular levels). Inhalation exposure to traffic-related PM first induces inflammatory cytokines and chemokines (e.g., IL-6, TNF-α, and CCL2) [3,9,14,15,50,75] by the activation of the TLR2/4-NF-κB signaling pathways, triggering the expression of cytokine genes [3,9]. These cytokines further cause systemic inflammation and oxidative stress, leading to the development of cardiometabolic disorders, including obesity and CVD.…”

“…The chemical and physical properties of traffic-related PM vary, depending on the type of fuels, engine efficiency, and exhaust technologies [13][14][15][16]. Diesel and gasoline engine exhausts have been recognized as carcinogenic (Group 1 for diesel) and possibly carcinogenic (Group 2B for gasoline) to humans, by the International Agency for Research on Cancer [17,18].…”

Biomass Energy Technological Paradigm (BETP): Trends in This Sector

“…As the development of renewable energy technological applications have progressed, ethanol has become a viable alternative fuel [99]. Almost all gasoline cars can drive with fuel containing 10% ethanol (E10), flex-fuel cars can even use 85% ethanol (E85), and Brazil and the USA already include 10%-27% ethanol in their standard fuel by law [100]. Ethanol has been proved to be a promising alternative fuel for the internal combustion engine.…”