Report of a Study on the Toxicity of Several Food Preserving Agents

Abstract

The deterioration of some foods caused by the activity of microorganisms may be prevented and the keeping quality of the foods greatly improved by the addition of certain chemical compounds. It is obvious that preserva- tives which produce a marked toxic effect should not be used in food intended for human consumption. On the other hand, even when a marked toxicity is not shown, the consumption of food containing unusual quantities of pre- servatives may be dangerous and harmful because of the hidden cumulative effect. Definite proof of toxicity lies in knowing how the chemical agent is handled in the body. By tracing the chemical reactions of the preserving agent in the animal body and determining the method by which it is elimi- nated from the body, an accurate statement concerning its toxicity can be made. This experiment was designed to yield information that may contribute to the knowledge of the toxic properties of certain chemical substances used in human food, and a bactericidal material used for sterilizing utensils. The amount of gain made by growing white rats was used as an indication of the toxic effects. Individual feeding trials were conducted with diets to which were added calcium propionate, sodium propionate, sodium benzoate, zephiran, and sodium benzoate plus glycine. Propionates are used in the bread industry and to some extent in packaged cheese in order to control mold. Zephiran is a new germicide which may be used for disinfecting dairy utensils. Sodium benzoate has been used for some years as a preser- vative for various food products. Griffith (1) has shown that when 1.5 per cent or more sodium benzoate was in the diet, the rate of growth in young rats was decreased. The excre- tion of hippuric acid in the urine accounted for 66 to 95 per cent of the benzoic acid consumed as sodium benzoate. Small doses of sodium benzoate gave nearly perfect quantitative recovery of hippuric acid. As the amount of sodium benzoate was increased, the percentage recovered as hippuric acid decreased. It was assumed that this showed a lack of sufficient glycine in the animal for the detoxication of the benzoic acid. The addition of glycine