Dietary exposure Subject

The foUowing sections deal in detail only with processing contaminants whose occurrence (and amount) in foods is either regulated by EU legislation (for which MRL are set), or with processing contaminants the evaluation of which is subject to various monitoring studies. The aim of these studies is to collect sufficient information to estimate dietary exposure to these substances and evaluate the associated health risks. 

Phytochemicals have been the subject of many studies evaluating their effects in relation to common chronic human illnesses such as cancer and cardiovascular diseases. These studies encounter difficulties in using this information to influence the dietary patterns of consumers because in the past they have used models or experiments with animals. However, in the last decade, researchers have moved away from animal studies in favour of human cell models or human intervention studies. Scientists still need to determine the likely incidence of illness from exposure to known amounts of a given natural compound in the diet and specifically in relation to the complex matrices of whole foods. Therefore, it is inevitable that some animal studies have to be continued for toxicological studies. 

A number of dietary deficiencies may increase the risk of deleterious cyanide effects. Iodine deficiency is involved in the etiology of such thyroid disorders as goiter and cretinism. These disorders may be exacerbated by excess exposure to cyanide (Delange and Ermans 1971 Ermans et al. 1972). Protein deficiencies and vitamin B12, riboflavin and other vitamins and elemental deficiencies may subject people... 

Neither TDG or TDGO are ideal biological markers of exposure because of the very low concentrations present in the urine and blood of normal subjects. TDG appears to be present in urine usually at levels < 1 ng/ml, but higher concentrations (up to 16 ng/ml) have been detected in blood (20). TDGO was detected at concentrations mainly in the range 1-10 ng/ml in normal human urine, but in one subject it was as high as 36 ng/ml (28). The source of these background levels is unknown but may be dietary. 

Treatment of tardive dyskinesia is often unsatisfactory, especially in severe cases. A large number of treatments have been proposed (SEDA-20,40), including antiparkinsonian drugs, benzodiazepines, baclofen, hormones, calcium channel blockers, valproate, propranolol, opiates, cyproheptadine, tryptophan, lithium, manganese, niacin, botulinum toxin, ECT, dietary control, and biofeedback training. In an open study, 20 patients (mean age 65 years) with severe unresponsive tardive dyskinesia (mean duration 44 months, mean exposure 52 months) were treated with tetrabenazine (mean dose 58 mg/day) (310). The mean score on the AIMS motor subset, determined from videotapes, improved by 54%. Sedation was the only subjective complaint. 

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