One hundred goitrous school children received 475 mg iodized oil by mouth, while 100 controls received mineral oil, on a double-blind basis. On follow-up 22 months later the urinary iodine had increased and goiter size had decreased in both groups, more strikingly in the iodine-treated children. There were no consistent differences between the two treatment groups in rate of somatic growth or performance on the Stanford-Binet and Bender tests. Because of the complexities introduced by increases in urinary iodine in the controls, we compared goiter reduction with improvement in IQ score in all children, regardless of group, and found a significant relationship (p = 0.014), particularly in girls (p = 0.029). We conclude that oral iodized oil is an attractive alternative to its injection but we recommend an approximate doubling of the dose used here for more effective control. Also, while our data are not conclusive, they support the possibility that correction of iodine deficiency may improve mental performance in school age children, particularly girls.

Abstract. UV irradiation of four non-fluorescent phenylurea herbicides including linuron, diuron, isoproturon and neburon is shown to yield fluorescent photoproducts. The photochemically-induced fluorescence (PIF) properties of these herbicides in several media (water, 2-propanol and their mixtures) and aqueous micellar solutions of sodium dodecyl sulfate (SDS), and cetyltrimethylammonium chloride (CTAC) are reported. The use of micellar media enhances significantly the PIF signal relative to an aqueous solution. A PIF method is developed for the determination of the four herbicides under study, with linear dynamic ranges over about one order of magnitude, and limits of detection (LOD) between 410 and 640 ng mL -1 , according to the compound. Applications to the analysis of tap water and river water samples yield satisfactory recoveries (86-115 %).

BackgroundDietary supplement use in both human and animals to augment overall health continues to increase and represents a potential health risk due to the lack of safety regulations imposed on the manufacturers. Because there are no requirements for demonstrating safety and efficacy prior to marketing, dietary supplements may contain potentially toxic contaminants such as hepatotoxic microcystins produced by several species of blue-green algae.Case presentationAn 11-year-old female spayed 8.95 kg Pug dog was initially presented for poor appetite, lethargy polyuria, polydipsia, and an inability to get comfortable. Markedly increased liver enzyme activities were detected with no corresponding abnormalities evident on abdominal ultrasound. A few days later the liver enzyme activities were persistently increased and the dog was coagulopathic indicating substantial liver dysfunction. The dog was hospitalized for further care consisting of oral S-adenosylmethionine, silybin, vitamin K, and ursodeoxycholic acid, as well as intravenous ampicillin sodium/sulbactam sodium, dolasetron, N-acetylcysteine, metoclopramide, and intravenous fluids. Improvement of the hepatopathy and the dog’s clinical status was noted over the next three days. Assessment of the dog’s diet revealed the use of a commercially available blue-green algae dietary supplement for three-and-a-half weeks prior to hospitalization. The supplement was submitted for toxicology testing and revealed the presence of hepatotoxic microcystins (MCs), MC-LR and MC-LA. Use of the supplement was discontinued and follow-up evaluation over the next few weeks revealed a complete resolution of the hepatopathy.ConclusionsTo the authors’ knowledge, this is the first case report of microcystin intoxication in a dog after using a commercially available blue-green algae dietary supplement. Veterinarians should recognize the potential harm that these supplements may cause and know that with intervention, recovery is possible. In addition, more prudent oversight of dietary supplement use is recommended for our companion animals to prevent adverse events/intoxications.

Submission of a raccoon (Procyon lotor) for necropsy following exhaustion at a California wildlife care center revealed minimal gross pathologic changes and only mild vacuolar changes in the white matter of the brain. Turquoise granular material was noted in the gastrointestinal tract and was submitted for toxicological testing along with portions of the brain, liver, kidney, and mesenteric and perirenal adipose tissues. Testing of the turquoise material for 7 anticoagulant rodenticides, strychnine, 4-aminopyridine, starlicide, and salts revealed none of these compounds; however, desmethylbromethalin was detected by high-performance liquid chromatography-tandem mass spectrometry. Other tissues were subsequently analyzed; the mesenteric and perirenal adipose tissues contained desmethylbromethalin. Desmethylbromethalin is the active metabolite of bromethalin, uncouples oxidative phosphorylation, and results in cerebral edema. Bromethalin is a rodenticide that is visually indistinguishable from many other rodenticides, making identification of poisonings by appearance alone nearly impossible. Based on the pathological and toxicological findings, a diagnosis of bromethalin toxicosis was established. In cases of wildlife species with unknown deaths or inconsistent clinical signs with normal or minimal histological findings, bromethalin toxicosis should be considered as a differential. Adipose tissue is the tissue of choice and can be easily harvested from a live or deceased animal to help confirm or rule out bromethalin exposure or intoxication.

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