Journal Article

Analysis of the tidocaine Metabolite 2,6-Dimethylaniline in Bovine and Human Milk

Neil W. Puente and P. David Josephy

in Journal of Analytical Toxicology

Volume 25, issue 8, pages 711-715
Published in print November 2001 | ISSN: 0146-4760
Published online November 2001 | e-ISSN: 1945-2403 | DOI:
Analysis of the tidocaine Metabolite 2,6-Dimethylaniline in Bovine and Human Milk

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2,6-Dimethylaniline (2,6-xylidine; 2,6-DMA) is a nasal carcinogen in rats. Humans may be exposed to this compound via several routes: 2,6-DMA is found in cigarette smoke; it is a pharmacologically inactive metabolite of some drugs (e.g., the local anesthetic lidocaine) and pesticides (e.g., metalaxyl); and it is an impurity in technical grade metalaxyl. The potential transfer of 2,6-DMA from mother to nursing infant via milk is of toxicological concern. Solid-phase microextraction with separation and detection using gas chromatography-mass spectrometry was optimized and used for the analysis of 2,6-DMA in milk. 2,6-DMA-d9 was synthesized and used for quantitation by the isotope ratio method. At a concentration of 5 ppb 2,6-DMA, the method detection limit was 0.20 ppb, and the relative standard deviation was 3.6%. Samples of milk were obtained from bovines administered lidocaine (2.9–3.9 mg/kg) during surgery. A breast milk sample was also obtained from a human donor who received 36 mg lidocaine during dental work. 2,6-DMA was present at levels ranging from 14.5 to 66.0 ppb in bovine milk and was detected at 1.6 ppb in the human milk sample. Our results demonstrate that 2,6-DMA, formed by the metabolism of lidocaine, is transferable to bovine and human milk.

Journal Article.  0 words. 

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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