Effects of environmental synthetic chemicals on thyroid function.

Synthetic chemicals are released into the environment by design (pesticides) or as a result of industrial activity. It is well known that natural environmental chemicals can cause goiter or thyroid imbalance. However, the effects of synthetic chemicals on thyroid function have received little attention, and there is much controversy over their potential clinical impact, because few studies have been conducted in humans. This article reviews the literature on possible thyroid disruption in wildlife, humans, and experimental animals and focuses on the most studied chemicals: the pesticides DDT, amitrole, and the thiocarbamate family, including ethylenethiourea, and the industrial chemicals polyhalogenated hydrocarbons, phenol derivatives, and phthalates. Wildlife observations in polluted areas clearly demonstrate a significant incidence of goiter and/or thyroid imbalance in several species. Experimental evidence in rodents, fish, and primates confirms the potentiality for thyroid disruption of several chemicals and illustrates the mechanisms involved. In adult humans, however, exposure to background levels of chemicals does not seem to have a significant negative effect on thyroid function, while exposure at higher levels, occupational or accidental, may produce mild thyroid changes. The impact of transgenerational, background exposure in utero on fetal neurodevelopment and later childhood cognitive function is now under scrutiny. There are several studies linking a lack of optimal neurological function in infants and children with high background levels of exposure to polychlorinated biphenyls (PCBs), dioxins, and/or co-contaminants, but it is unclear if the effects are caused by thyroid disruption in utero or direct neurotoxicity.

Herbicide: fatal ammonium thiocyanate and aminotriazole poisoning.

OBJECTIVE: To describe fatal herbicide poisoning with Radoxone TL composed of aminotriazole and ammonium thiocyanate. CASE REPORT: A 54-year-old man was hospitalized because of unexplained coma with myoclonic jerks and vascular collapse. Despite symptomatic treatment with mechanical ventilation and vascular filling, life-threatening shock occurred with oliguria, profound metabolic acidosis and cardiac arrest. Hyperchloremia (141 mmol/L) with reversed anion gap (-19) suggested interference with chloride measurement caused by halogens (Br,F,I) or other anions such as thiocyanate. Eventually a weed killer, Radoxone TL containing ammonium thiocyanate, was found at the patient's house. Thiocyanate and aminotriazole blood levels were 750 mg/L and 138 mg/L respectively more than 12 hours after ingestion. After prolonged cardiopulmonary resuscitation, continuous venovenous hemodiafiltration was performed. Despite hemodynamic recovery the patient died 48 hours later of postanoxic coma. CONCLUSION: Aminotriazole, a systemic nonselective herbicide, is often associated with ammonium thiocyanate which enhances its activity. Experimental studies and previous fatal cases suggest a predominant toxicity of thiocyanate. Early diagnosis is important.

Atrazine in plasma and tissue following atrazine-aminotriazole-ethylene glycol-formaldehyde poisoning.

A high performance liquid chromatography method has been used to study the plasma kinetics of atrazine in a human fatality after ingestion of a herbicide mix containing atrazine, aminotriazole, ethylene glycol and formaldehyde. A hemodialysis was performed in an effort to eliminate these toxic substances. The mean atrazine clearance over 4 h was 250 mL/min and the dialysance of atrazine was calculated as 76%. On autopsy, the kidney showed the highest concentration of atrazine (97.62 micrograms/g-1 wet tissue) with lesser concentrations in the lung, small intestine and liver, and the lowest concentration in the heart.

[Characteristics of the development of cataract models against a background of poisoning]. / Osobennosti razvitiia modelirovannykh katarakt na fone intoksikatsii.

Biomicroscopic studies of lenses of 300 rabbits subjected to the action of various cataractogenic factors have shown that a combined action of cataractogenic factors (3-aminotriazole and light) as well as of cataractogenic and syncataractogenic factors (carbon tetrachloride) possess a much stronger action, that the isolated effect of such factors, as light of high intensity and 3-aminotriazole. It is shown that under combined action of 3-aminotriazole and carbon tetrachloride ripe cataract develops by the 42nd week and under combined action of light, aminotriazole and carbon tetrachloride--by the 30th week. The isolated action of aminotriazole and light doesn't induce ripe cataract. Aminotriazole produces pronounced cataractous changes 50-60 weeks after administration, the light--80 weeks after the action. A conclusion is made that opacification of the lens is a result of complex causes with many factors and is conditioned not only by photochemical processes in the lens itself and disturbances in the processes of detoxification of free radicals in the tissues of the eye as a whole and in the lens, in particular, but also by changes in the antiradical status of the body as a whole.