n-Hexane is of low acute toxicity (Couri and Milks, 1982; IPCS, 1991), but in chronic exposure it may be the most toxic of the alkanes (Carreon, 2001). Peripheral neuropathy following chronic exposure to n-hexane was recognised from the mid 1960s (Spencer et al., 1980). The typical picture is insidious onset and slow progression (Spencer et al., 1980). Adverse effects from n-hexane in an industrial environment are now relatively rare (Harbison, 1998). However, when n-hexane neuropathy occurs, more than one worker may be affected (Herskowitz et al., 1971; Paulson and Waylonis, 1976; Scelsi et al., 1981; Wang et al., 1986; Huang et al., 1991; Chang et al., 1993). Cases of n-hexane-induced polyneuropathy reported in the older literature usually arose from ignorance of the hazards of a chemical originally thought to be non-hazardous. Now, an outbreak is usually associated with a change in working practice, e.g., a recent change to a product containing n-hexane (Huang et al., 1991), reduced ventilation or a combination of such factors (Wang et al., 1986). Polyneuropathy has occurred following exposure to n-hexane at a wide range of air concentrations (30-2,500 ppm); duration of exposure before onset has ranged from 2 months to 5 years (IPCS, 1991). However, long-term low level exposure may cause neuropathy (Barrgard et al., 1991).

Reports of polyneuropathy from abuse of n-hexane-containing glues first appeared in the mid 1970s (Goto et al., 1974; Shirabe et al., 1974; Korobkin et al., 1975; Towfighi et al., 1976; Griffin, 1981); but there have been more recent reports (Smith and Albers, 1997).

It is important to note that the metabolism of n-hexane varies between species and it is suggested that humans have a greater susceptibility to n-hexane-induced polyneuropathy than the rat (Perbellini et al., 1982). In many studies, it is unclear whether hexane or n-hexane was involved. Also, in industry many exposures are to solvent mixtures not to pure n-hexane.

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Peripheral Neuropathy Natural Treatment Options

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