Combustion of diesel fuel from a toxicological perspective

Publisher Website
Google Scholar
Abstract
Epidemiological data and results of toxicity studies in experimental animals indicate the possible health risk of diesel exhaust exposure. Acute effects of this exposure include odor, eye irritations, lung function decrements, cardiovascular symptoms, and some nonspecific effects. Most of these effects are reported among persons highly exposed to diesel exhaust. Lung function decrements are reported as chronic effects. Another chronic effect that has been studied extensively among occupationally exposed persons is lung cancer. In addition to lung cancer, but at a less frequent rate, an enhanced incidence of bladder cancer is reported. The carcinogenic action of diesel exhaust exposure is ascribed to effects of the soot particles, particle-associated organics, and/or gas phase compounds. Direct effects of the particle load may include retardation of lung clearance, inflammation, and increased cell proliferation. These effects were all demonstrated in rodents. The particles may also prolong the residence time of particulate organics or induce the generation of reactive oxygen species. These compounds are known to react with macromolecules, causing lipid peroxidation, DNA damage, and/or activation of other genotoxic substances such as polycyclic aromatic hydrocarbons (PAHs). However, these results have not yet been confirmed in mammals in vivo. A direct interaction of particles with lung tissue is also suggested as a cause of cancer but a mechanism for this interaction has not yet been proposed. Organics associated with the particles are known to contain genotoxic properties attributable to PAHs and their derivatives. A number of these compounds are also identified as carcinogens in animal studies. However, it is not clear whether parent PAHs, their nitro-, oxy-, alkylated, or heterocyclic derivatives, or possibly other compounds are principally responsible for inducing tumors in the lungs of animals after diesel exhaust exposure. Furthermore, the mechanism of the bioavailability of these organics is not completely understood. The effects of gas phase constituents on the carcinogenic properties of the particles and/or particle-associated organics either have not been investigated or the findings have been inconclusive.