Risk assessment for children exposed to decabromodiphenyl (oxide) ether (Deca) in the United States.

Decabromodiphenyl (oxide) ether (Deca) is a widely used brominated flame retardant in the United States predominantly in the hard-plastic housings of consumer electronics and in flame-retarded backing on textiles used in furniture. A child-specific exposure assessment of Deca was performed for the US Environmental Protection Agency's Voluntary Children's Chemical Evaluation Program (VCCEP). The VCCEP guidance for a tier 1 exposure assessment requires that a screening-level assessment be conducted using currently available data and conservative assumptions. For Deca, relevant exposure pathways considered were general environmental exposures (e.g., exposures to contaminated soil, dust, air, and food), breast milk exposures, inhalation of Deca-containing particulates in air, and mouthing Deca-containing consumer products. For each of these scenarios, a mid-range and upper estimate of age-appropriate intakes were calculated. The calculated intakes indicate that, despite the uncertainties, children appear to be exposed to Deca at levels at least 1 order of magnitude, with most being several orders of magnitude, below the National Academy of Sciences reference dose for Deca of 4 mg/kg/d. This analysis indicates that, using the available data, current levels of Deca in the United States are unlikely to represent an adverse health risk for children.

Fatal poisoning by butachlor and chlornitrofen ingested from a bottle marked as nitrofen.

Nitrofen has been banned in Taiwan since January 1, 1983 due to its tetrogenicity. A 78-y-o female consumed about 500 ml of herbicide, labeled as nitrofen, in a suicide attempt. Consciousness disturbance occurred immediately. After 9 h, bloody-tarry stool was noted. Hematemesis occurred 19 h later. Hepatotoxicity and nephrotoxicity also developed. Twitching of head and both upper extremities lasting 20-30 sec and up to 5 min developed on day 3. Sometimes an upward gaze with the face turned to the right or a convulsion of the right upper extremity was observed. EEG showed alpha coma, generalized slow spike-and-wave complexes, and isolated generalized sharp waves mainly in the left occipital area. On day 7, endotracheal intubation was performed due to apnea; she expired on day 9. The pesticide was found to contain butachlor and chlornitrofen. The Agricultural Committee prohibited the marketing of chlornitrofen due to its generation of tumors in animals. The combination of butachlor and chlornitrofen can result in consciousness disturbance, leucocytosis, gastrointestinal hemorrhage, rhabdomyolysis, hypocalcemia, hypoalbuminemia, elevated amylase, nephrotoxicity, hepatotoxicity, seizures and death. The cytotoxicity of butachlor may be related to the patient's death. Active components of pesticides should be checked if the clinical course of a poisoned patient is unusual to allow appropriate interventions.

Problem-solving techniques in occupational medicine.

The diagnosis of occupational illnesses may be considerably more difficult than is the case with occupational injuries because of a variety of factors: an intervening latency period, uncertainty in identifying the most significant chemical or physical exposures, determination of exposure levels retrospectively, and coordination of the physician with regulatory and workers' compensation bureaucracies. Such problem-solving techniques as retrospective industrial hygiene and attention to in-situ chemistry can act as means of reducing the uncertainty in making the diagnosis of occupational illness. Advance familiarity with workers' compensation and state or federal regulatory agencies can further facilitate diagnosis and patient advocacy.

The prevention by sulphydryl compounds of the toxicity in the cat of 2,6-dimethoxyphenol and its morpholinopropionyl ester.

1 Intravenous (minus)-2,6-dimethoxyphenyl-2-morpholinopropionate hydrochloride (M&B 16,573) produced anaesthesia of short duration in the mouse, rat, rabbit, cat, dog and monkey. In the cat but not in other species, a severe and usually fatal toxic reaction was seen 1-2 h after administration. 2 This toxic reaction but not the anaesthetic properties of M&B 16,573 was prevented by the intravenous administration of cysteine or N-acetylcysteine. Cysteamine or dimercaprol were ineffective. 3 Intravenous administration of 2,6-dimethoxyphenol or 2,6-dimethoxyquinol in the cat produced a response similar to the delayed toxic effects of M&B 16,573 but not preceded by anaesthesia. The toxic effects of these compounds were prevented by cysteine. 4 Intravenous 4-allyl-2,6-dimethoxyphenyl-2-morpholinopropionate hydrochloride produced anaesthesia in the cat without the delayed toxic effects seen after M&B 16,573. 5 The acute toxicity of 2,6-dimethoxyquinol in mice was reduced by the administration of cysteine or N-acetylcysteine. 6 It is postulated that the delayed effects produced by M&B 16,573 in the cat are due to the formation of 2,6-dimethoxyquinol and 2,6-dimethoxybenzoquinone in this species, the toxicity of the latter being reduced by sulphydryl compounds.