[Suspected azodicarbonamide poisoning in a patient with acute hemorrhaging pancreatitis]. / Podejrzenie zatrucia azodikarbonamidem u pacjenta z ostrym krwotocznym zapaleniem trzustki.

The report describes the case of death of a 22-year old man due to acute hemorrhaging pancreatitis. Azodicarbonamide poisoning was suspected in this patient. Autopsy results, data from the literature and the knowledge about mechanisms of azodicarbonamide toxicity allowed for excluding poisoning with this substance as the cause of death.

Chemical monitoring of urine from workers potentially exposed to benzidine-derived azo dyes.

Benzidine (Bzd) and monoacetylbenzidine (MoAcBzd) were found in the urine of workers exposed to benzidine-based azo dyes. A colorimetric screening method, based on the reaction of extracted free aromatic amines with 2,4,6-trinitrobenzene-sulfonic acid (TNBS), was used with a specific electron-capture gas chromatographic (EC-GC) method. Alkaline hydrolyzable conjugates of Bzd and 2,4-diaminoazobenzene (DiAmAzBz) were found together with free DiAmAzBz and traces of 3,3'-dimethylbenzidine (DiMeBzd) and 3,3'-dimethoxybenzidine (DiMxBzd). The presence of a known human bladder carcinogen (Bzd) and its metabolites in the urine of workers exposed to benzidine-based azo dyes is a cause for concern.

Acquired toxic methaemoglobinaemia.

Eighty Six adult males presented with central cyanosis and constitutional symptoms 2 to 4 hours following ingestion of meal from a common kitchen. On spectrometry methaemoglobin was detected. All recovered fully in 12 to 36 hours on symptomatic treatment. Epidemiological study and toxicological examination revealed that metanil yellow used for colouring the rice was responsible.

Haemolytic anaemia associated with Nigerian barbecued meat (red suya).

Five cases of haemolytic anaemia occurring in male Nigerians following the ingestion of spiced barbecued meat (suya) are described. Although suya is a popular food item in various parts of Nigeria, all five patients described in this report had consumed a special brand, called red suya, purchased from vendors at a popular road junction between the cities of Lagos and Ibadan. Ingestion of the culprit suya sample was followed within 24 h by malaise and fever, while passage of dark-coloured urine and jaundice followed 1-3 days thereafter. Glucose-6-phosphate dehydrogenase (G6PD) deficiency was demonstrated by a fluorescent screening test in all cases, while the enzyme phenotype was shown to be GdA- in all four cases studied by starch-gel electrophoresis, thus suggesting that G6PD deficiency was a predisposing factor in the cases reported in this series. The haemolytic disease was self-limiting and full recovery followed in all cases. In view of the markedly circumscribed range from where the patients originated, the culprit agent responsible for the haemolytic disease is believed to be a recently introduced food additive that is probably accessible only to a limited number of suya vendors.

Measuring histological form change with finite element methods: an application using diazo-oxo-norleucine (DON)-treated rats.

Analyses of drug-induced anatomical malformations routinely rely on linear measurements as a data base. Morphometric approaches utilizing these measures become inappropriate at the histological level at which a constant external referencing system is impossible to achieve. The purpose of this study was to quantify anatomical form change in the craniofacial region of late embryonic rats induced by a known teratogen, diazo-oxo-norleucine (DON), independent of any global referencing system. A sample of 17 untreated specimens of 17-day gestation served as the control. A second group, equivalent in number and age, received 2.0 mg DON on day 15. Homologous landmarks were identified in each specimen and craniofacial regions were partitioned with respect to these bounding nodes into nasal, oral, and mandibular elements. Form change was viewed as the continuous deformation of a reference craniofacial region from a 15-day untreated specimen into each final 17-day geometry. An interactive graphics program generated spatially invariant measures of form change through finite element methods. A local coordinate system was established for each element. A point within each region of the 15-day reference specimen was selected and the spatial relationship between this point and bounding nodes was quantified through interpolation functions. Size and shape variables were derived from a Lagrangian strain tensor, and values were compared between groups. Results showed that all three craniofacial regions were smaller in size among DON-treated specimens, but only oral and mandibular region shapes were different from controls. The finite element approach was considered superior to other histological morphometric techniques since an entire geometry was described and a visual description of form change as well as spatially invariant measures of size and shape change were derived.

Neurologic dysfunction from exposure to 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH): a new occupational neuropathy.

Seven cases of subacute central and peripheral neurologic dysfunction developed in 18 workers employed in the manufacture of reinforced plastic bathtubs. Cases were characterized by weight loss, dizziness, paresthesias, muscle weakness, incontinence, memory loss, and loss of peripheral, color, and night vision. Neuropathies began distally, involved both sensory and motor function, and were associated with prolonged sensory latency, muscle fibrillation, and reduced numbers of functioning motor units. One patient developed posterior lenticular cataracts. Slow improvement occurred on removal from exposure, but residual neuropathies persisted for as long as two years. Epidemiologic investigation disclosed that the first case developed approximately two weeks after introduction of a new plastic foaming agent, 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH). All cases occurred in workers exposed directly to BHMH. No new cases developed after use of BHMH was discontinued. A survey of the firm which produced BHMH and of 68 user firms found two additional clusters of mild neuropathy which may have been caused by BHMH. BHMH was withdrawn from distribution following discovery of these cases. Subsequently, BHMH has been shown in rats to be a potent neurotoxin. Adequate premarket testing could have averted this outbreak.

[Rhythmicity in the structure-functional changes in hepatocytes following exposure to pesticides]. / Ritmichnost' strukturno-funktsional'nykh izmenenii gepatotsitov pri vozdeistvii pestitsidov

The processes of dursban biotransformation during the liver perfusion in rats exposed to CCl4 and milbex for 4, 8 and 15 days (microsomal enzyme inhibitor and inducer, respectively) were studied. The ultrastructure of hepatocytes was examined in the animals treated with the mentioned poisons. Three stages of the structural and functional changes were revealed. Reconstruction of the dursban biotransformation ways occurred from the 8th day, i.e. the dialkylation processes were intensified, resulting in production of less toxic metabolites.