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Acetone treatment of rats (1 or 5% in drinking water for 7-12 days) was shown to induce oxidative stress and lipid peroxidation in liver, plasma and erythrocytes (weight of evidence approach: Armutcu et al., 2005; Orellana et al., 2001; Puntarolo and Cederbaum, 1988).

Sensory irritation

Studies using objective measures of sensory irritation tended to show that acetone is an extremely weak sensory irritant for humans with a sensory irritation threshold (nasal pungency) between 10,000 to 40,000 ppm. The odor detection threshold of acetone is much lower ranging from about 20 - 400 ppm based on reliable studies. Loss of sensitivity due to adaptation and/or habituation to the odor of acetone may occur, as was shown in studies comparing occupationally exposed workers with unexposed subjects. An evaluation of studies on subjectively reported irritation symptoms at acetone concentrations below 1000 ppm showed that perception of odor intensity, information bias, and habituation by exposure to acetone are confounding factors in the reporting of irritation thresholds and health symptoms (Arts et al., 2002; Cometto-Muniz and Cain, 1993, 1995; Dalton et al., 1997a, b; Morgott, 2001; Wysocki et al., 1997).

In the Alarie test with Swiss-Webster mice (N = 4/group) sensory irritation was observed with RD50 values of 77,516 ppm acetone ( 95% confidence interval: 59,004-115,366 ppm) for a 10 min-exposure (Alarie and Luo, 1986; Kane et al., 1980), and 23,480 ppm acetone for a 5 min-exposure (De Ceaurizz et al., 1981).

Local dermal effects

Acetone was shown to be a defatting agent at contact with mouse skin. Defatting of the epidermis lead to a substantial reduction in residual stratum corneum lipids and subsequently to disturbation of the epidermal permeability barrier and to transepidermal water loss. These effects were reversible within 48 hours by de novo lipid biosynthesis. Restoration of the permeability barrier was retarded as long as an occlusive impermeable membrane was present. After removal, the permeability barrier function of the epidermis was fully restored within 24 hours (Weight of evidence approach: Grubauer et al., 1989a, b).

The sequelae of the fat solubilizing property of acetone was also investigated in the skin of human volunteers after permanent contact with a glass reservoir filled with acetone for 30 or 90 min. Acetone induced local cellular changes, mainly in the stratum corneum and the stratum spinosum. Microscopic and ultrastructural examination indicated intracellular edematous lesions with e.g. vacuolation and swollen mitochondria, and rupture of cell membranes and desmosomes. After the 90 min-exposure, a significant reduction of protein synthesis was measured while collagen synthesis was unaffected. DNA synthesis was moderately but significantly increased. Within 72 hrs after discontinuation of exposure, a high degree of restoring activity was demonstrated. The application of a protective gel (composition: 50% water, 25% glycerin, 10-15% cellulose methasol gum, 2-3% preservative) prior to acetone exposure substantially reduced the ultrastructural changes of the epidermal cells. This protection presumably resulted from blocking the absorption and migration of the lipid solvent acetone through the epidermis (Weight of evidence approach: Lupulescu and Birmingham, 1972, 1973, 1975, 1976). Wearing appropriate gloves will avoid this effect.

A local, short-lasting proliferative response in epidermal cells of mouse skin was induced up to 12 hrs after a single dermal application of 0.2 mL. The mechanism is not known. The authors discussed a very weak skin irritating activity of acetone as a possible trigger (Weight of evidence approach: Iversen et al., 1988).