Biodiesel fuels: A greener diesel? A review from a health perspective.

Biodiesels have been promoted as a greener alternative to diesel with decreased emissions and health effects. To investigate the scientific basis of the suggested environmental and health benefits offered by biodiesel, this review examines the current state of knowledge and key uncertainties of pollutant profiles of biodiesel engine exhaust and the associated the respiratory and cardiovascular outcomes. The ease and low cost of biodiesel production has facilitated greater distribution and commercial use. The pollutant profile of biodiesel engine exhaust is distinct from diesel, characterised by increased NOx and aldehyde emissions but decreased CO and CO2. Lower engine-out particulate matter mass concentrations have also been observed over a range of feedstocks. However, these reduced emissions have been attributable to a shift towards smaller sized particulate emissions. The toxicity of biodiesel engine exhaust has been investigated in vitro using various lung cell, in vivo evaluating responses induced in animals and through several human exposure studies. Discrepancies exist across results reported by in vitro and in vivo studies, which may be attributable to differences in biodiesel feedstocks, engine characteristics, operating conditions or use of aftertreatment systems across test scenarios. The limited human testing further suggests short-term exposure to biodiesel engine exhaust is associated with cardiopulmonary outcomes that are comparable to diesel. Additional information about the health effects of biodiesel engine exhaust exposure is required for effective public health policy.

Carbonaceous aerosol sampling of gasoline direct injection engine exhaust with an integrated organic gas and particle sampler.

Positive and negative artifacts of particle-phase organic carbon (p-OC) and the polycyclic aromatic hydrocarbons (PAHs) in gasoline direct injection (GDI) engine exhaust particulate matter (PM) were assessed using an integrated organic gas and particle sampler (IOGAPS). Three configurations (denuder + sorbent impregnated filters (SIFs), upstream Zefluor filter + denuder + SIFs, and standard filter pack + SIFs) were used to collect GDI exhaust samples at cold start and highway cruise operating conditions with no aftertreatment. Approximately 35% of the measured GDI p-OC was attributed to positive artifacts; negative artifacts were not detectable due to low overall SVOC concentrations. GDI engine exhaust PAH concentrations were approximately 10 times higher during cold start than highway cruise. At highway cruise, pyrene and fluoranthene were the dominant PAHs in the undenuded filter pack; downstream of the denuder benzo(a)anthracene was the dominant PAH. From a comparison of our findings to published PAH emission factors we estimate that three-way catalyst conversion efficiencies of PAHs were approximately 80% for 3 of the 15 PAHs measured during highway cruise operation. These conversion efficiencies may be considerably lower during cold start operation when the three-way catalyst has not reached its operating temperature. Our previous work showed that adverse biological responses to GDI engine exhaust exposure may be dominated by the particle phase when measured downstream of a Teflon filter. Understanding the partitioning characteristics of PAHs may help elucidate specific PAHs contributing to this effect.

Murine precision-cut lung slices exhibit acute responses following exposure to gasoline direct injection engine emissions.

Gasoline direct injection (GDI) engines are increasingly prevalent in the global vehicle fleet. Particulate matter emissions from GDI engines are elevated compared to conventional gasoline engines. The pulmonary effects of these higher particulate emissions are unclear. This study investigated the pulmonary responses induced by GDI engine exhaust using an ex vivo model. The physiochemical properties of GDI engine exhaust were assessed. Precision cut lung slices were prepared using Balb/c mice to evaluate the pulmonary response induced by one-hour exposure to engine-out exhaust from a laboratory GDI engine operated at conditions equivalent to vehicle highway cruise conditions. Lung slices were exposed at an air-liquid interface using an electrostatic aerosol in vitro exposure system. Particulate and gaseous exhaust was fractionated to contrast mRNA production related to polycyclic aromatic hydrocarbon (PAH) metabolism and oxidative stress. Exposure to GDI engine exhaust upregulated genes involved in PAH metabolism, including Cyp1a1 (2.71, SE=0.22), and Cyp1b1 (3.24, SE=0.12) compared to HEPA filtered air (p<0.05). GDI engine exhaust further increased Cyp1b1 expression compared to filtered GDI engine exhaust (i.e., gas fraction only), suggesting this response was associated with the particulate fraction. Exhaust particulate was dominated by high molecular weight PAHs. Hmox1, an oxidative stress marker, exhibited increased expression after exposure to GDI (1.63, SE=0.03) and filtered GDI (1.55, SE=0.04) engine exhaust compared to HEPA filtered air (p<0.05), likely attributable to a combination of the gas and particulate fractions. Exposure to GDI engine exhaust contributes to upregulation of genes related to the metabolism of PAHs and oxidative stress.