White spirit is a complex mixture of aliphatic, alicyclic and aromatic hydrocarbons, comprising over 200 compounds (Pfaffli et al., 1985; IPCS, 1996). With such solvent mixtures it is difficult to identify the causative agents of occupational diseases (Pedersen et al, 1980). From kinetic studies in humans, white spirit has a long redistribution phase, a large volume of distribution, slow total body clearance, and a long mean residence time (Pedersen et al., 1987). This means that even when exposure has ceased, adipose tissue continues to release white spirit into the blood, and hence the brain. Pedersen et al. (1987) suggested that this uninterrupted concentration of white spirit may be one of the explanations of the toxic encephalopathy reported after white spirit exposure (Arlien-Soborg et al., 1993).
All hydrocarbons may cause CNS depression, however the straight chain hydrocarbons that predominate in white spirit are poorly absorbed across the gastrointestinal tract. The aspiration toxicity of white spirit is due to the physical characteristics of the compound rather than any particular constituent. The risk of aspiration of a chemical depends upon its viscosity and surface tension. The lower the viscosity, the greater the penetration into the distal airway, and the lower the surface tension the more the product spreads across the lung tissue. White spirit has an extremely low viscosity that enables it to be easily aspirated into the lungs. Once in the lungs, small amounts of low viscosity material can spread over large portions of the pulmonary bed resulting in chemical pneumonitis.
Metabolism of the small percentage of polyaromatic hydrocarbons (e.g., benzene and naphthalene) in white spirit may produce active metabolites. Benzene is metabolised to reactive benzoquinones (IPCS, 1996) and 1,4-benzoquinone, for example, has been shown to inhibit topoisomerase II (Chen and Eastmond, 1995). Topoisomerase II is believed to play a role in genomic stability, and interference with topoisomerase II activity at critical stages of the cell cycle could cause chromosome breakage, aneuploidy or cell death (Chen and Eastmond, 1995).
Cumulative oxidative damage may be an underlying mechanism of white spirit induced neurotoxicity (Lam et al. 1994; Bondy et al., 1995). Following inhalation exposure of rats to white spirit (14-21% aromatic hydrocarbons) there was depression of glutamine synthetase concentrations in the P2 fraction of the liver and kidney. This suggested that prolonged inhalation of white spirit elevated pro-oxidant events in liver and kidney tissue (Bondy et al., 1995).
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