Acrylamide is a chemical which is extensively used in research laboratories for the preparation of polyacrylamide gels for electrophoresis (PAGE). Blood samples were collected from laboratory personnel who were working with PAGE, from smokers, and from nonsmokers. Hemoglobin adducts of acrylamide, acrylonitrile, and ethylene oxide were determined using the modified Edman degradation procedure. Acrylamide adducts were detected in all persons. The PAGE workers (mean 54 pmol/g) had a significantly increased adduct level compared to nonsmoking controls (mean 31 pmol/g). The acrylamide adducts in smokers (mean 116 pmol/g) correlated with the number of cigarettes smoked per day. This confirms the presence of acrylamide in tobacco smoke and shows that it is an important source of acrylamide exposure. The increased level of acrylamide adducts in the PAGE workers corresponds to an uptake of acrylamide from about 3 cigarettes per day. It is not possible from this study to draw any conclusion as to which step in the working procedure is most critical for exposure. The PAGE workers are probably not at risk for neurotoxic damage to the peripheral nervous system. However, it needs to be investigated whether the exposure to acrylamide in PAGE workers represents a risk for genotoxic and reproductive effects. The high background of acrylamide adducts in nonsmoking controls was unexpected. The origin of this background is not known. Acrylonitrile adducts were below the detection limit (< 2 pmol/g) in nonsmoking controls. In the smokers (mean 106 pmol/g) this adduct correlated with cigarettes/day and with ethylene oxide adducts. Acrylonitrile adducts could be a better indicator of tobacco smoking than ethylene oxide adducts since the latter are showing a background of endogenous origin.

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Acrylamide is an important industrial chemical which is neurotoxic to experimental animals as well as humans and recently has been shown to be mutagenic and carcinogenic. Despite much research it is still unclear whether the parent compound or a metabolite is responsible for the observed toxic effects. Contradictory results as to the role of cytochrome P-450 mediated metabolism of acrylamide in the induction of neurotoxic effects prompted us to investigate the possible formation of glycidamide, a reactive epoxide metabolite. The formation of this epoxide was strongly indicated by the identification by means of gas chromatography-mass spectrometry of derivatized S-(2-carboxy-2-hydroxyethyl)cysteine in hydrolyzed hemoglobin samples from rats treated with acrylamide in vivo and in microsomal suspensions of acrylamide with cysteine in vitro. This amino acid was found to be present in uninduced and phenobarbital-induced Sprague-Dawley rats and absent in controls, but occurred in lower amounts than the adduct derived from the parent compound, S-(2-carboxyethyl)cysteine. This finding suggests that the possible role of glycidamide in the neurotoxicity and carcinogenicity of acrylamide should be evaluated further.