Determination of the major mercapturic acids of acrylamide and glycidamide in human urine by LC-ESI-MS/MS.

We developed a LC-MS/MS method for the quantitative determination of the mercapturic acid (MA) metabolites of acrylamide (AA) AAMA and of its oxidative metabolite glycidamide (GA) GAMA in urine samples from the general population. The method requires 4 mL of urine which is solid phase extracted prior to LC-MS/MS analysis. The metabolites are detected by ESI-tandem mass spectrometry in negative ionisation mode and quantified by isotope dilution. Detection limits ranged down to 1.5 microg/L urine for both AAMA and GAMA. The imprecision expressed as R.S.D. lay between 2% and 6% for both analytes (intra- and inter-assay). First results on a small group of 29 persons out of the general population ranged from 5 to 338 microg/L AAMA and

Encephalomyeloradiculoneuropathy following exposure to an industrial solvent.

A 19-year-old male developed complaints including weakness of the lower extremities and right hand, numbness, dysphagia and urinary difficulties following a 2 month exposure to an industrial solvent constituted mainly of 1-bromopropane, but also containing butylene oxide, 1,3 dioxolane, nitromethane, and other components. Nerve conduction studies revealed evidence of a primary, symmetric demyelinating polyneuropathy. Evidence of CNS involvement came from gadolinium enhanced MRI scans of the brain, showing patchy areas of increased T2 signal in the periventricular white matter, similar scans of the spinal cord revealing root enhancement at several lumbar levels, and SSEP studies. The patient's symptoms had started to resolve following the discontinuation of the exposure, before he was lost to follow-up. Similar findings have been reported following 1-bromopropane exposure in rats. I hypothesize that this patient's symptoms may have been due to 1-bromopropane-induced neurotoxicity.

Spatial variation of epoxyscillirosidine concentrations in Moraea pallida (yellow tulp) in South Africa.

Moraea pallida (yellow tulp) poisoning is economically the most important intoxication of livestock in South Africa. Poisoning varies according to locality, climatic conditions and growth stage of the plant. The primary objective of this study was to determine the concentration of the toxic principle, epoxyscillirosidine, in yellow tulp leaves and to ascertain the variability of epoxyscillirosidine concentrations within and between different locations. A secondary objective was to utilise Geographic Information Systems in an attempt to explain the variability in toxicity. Flowering yellow tulp plants were collected at 26 sampling points across 20 districts of South Africa. The leaves of five plants per sampling point were extracted and submitted for liquid chromatography/mass spectrometry analysis. A large variation in mean epoxyscillirosidine concentrations, ranging from 3.32 µg/g - 238.27 µg/g, occurred between different geographical regions. The epoxyscillirosidine concentrations also varied tremendously between individual plants (n = 5) collected at the same sampling point, with up to a 24 times difference between the lowest and highest concentration detected. No generalised correlation between epoxyscillirosidine concentrations and soil elemental concentrations could be established. However, samples obtained from the north-eastern part of the sampling region tended to have higher epoxyscillirosidine concentrations compared to samples obtained from the south-western part of the sampling region. Higher toxin concentrations in the north-east were associated with statistically significant higher soil concentrations of iron, bismuth, bromide, cadmium, chromium, rubidium, tellurium, thallium, titanium and zinc, whilst soil concentrations of strontium and soil pH, were significantly lower. This study corroborated the contention that epoxyscillirosidine concentration in yellow tulp fluctuates and may explain the variability in toxicity.

Polyneuropathy due to ethylene oxide, propylene oxide, and butylene oxide.

Axonal neuropathy occurs due to occupational ethylene oxide (EtO) exposure. The experimental model of human EtO neuropathy was established. In addition, the neurotoxic effects of propylene oxide (PpO) and butylene oxide (BtO) were demonstrated in rats. Although no human neuropathy due to PpO or BtO is reported, both chemicals must be considered to be neurotoxic, based on this study.