Food additives the antioxidants butylated hydroxyanisole and butylated hydroxytoluene

101 Toxic Food Ingredients

101 Toxic Food Ingredients

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18.3.4.1 Introduction

To preserve quality and to prevent loss of nutritional value, the addition of antioxidants to food containing fatty acids has a long tradition. Two well-known antioxidant food additives are butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) (see Figure 18.2).

Although highly lipophilic, BHA and BHT do not accumulate in mammals. The reason for this is the efficient elimination of these chemicals from the body. In the case of BHA and BHT, the discussion on setting the dietary standards has focused on the question whether or not these food additives have to be considered as non-genotoxic carcinogens, and consequently, on whether or not safe human exposure levels for these substances can be established.

Figure 18.2 Structures of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT).

18.3.4.2 Toxicological risk assessment of BHA

In the rat, BHA induces epithelial hyperplasia and tumors in the forestomach. Since the forestomach is an organ specific to rodents (rat, mice, hamster) and not found in other animals, the question arises whether this effect can be used as the starting point for setting a dietary standard in man. To answer this question the Scientific Committee on Food of the European Commission Food-Science and Techniques asked in its 1983 evaluation of BHA for additional information on the following subjects:

1. the induction of hyperplasia by BHA in the part of the gastrointestinal tract immediately preceding the stomach, i.e., the esophagus, and the glandular stomach in species without a forestomach, and

2. the genotoxic properties of BHA.

On the basis of additional information from experimental studies, the Committee concluded in its reevaluation of BHA in 1989 that the effect of BHA on the forestomach epithelium is highly specific to rodents and does not occur in non-rodents. Furthermore, epithelial hyperplasia, qualified as a precancerous lesion, was found to be of a reversible nature and showed threshold characteristics, i.e., hyperplasia only occurred above a definite dietary BHA dose level. In species without a forestomach (guinea pig, dog, pig, monkey), BHA did not cause histopathological symptoms in the esophagus and the glandular stomach. All available mutagenicity data are negative, and BHA does not show any genotoxicity at all. Based on these data the Committee concluded that the induction of forestomach hyperplasia and tumors by BHA in rodents is of no significance in the assessment of human health risks from BHA exposure. Further, it was concluded that genotoxicity does not play a role in causing rodent forestomach tumors. Therefore, the Committee classified BHA as a rodent (and not human) carcinogen showing a threshold in the induction of effects. Consequently, the Committee accepted the calculation of an ADI for BHA to be relevant. In order to calculate this ADI, the NOAEL for the induction of hyperplasia in the rat forestomach was used as toxicity parameter for BHA. Experimentally, this NOAEL was found to be 50 mg/kg/day. Applying a standard safety factor of 100, this lead to an ADI of 0 to 0.5 mg BHA/kg/day for the safe chronic exposure level of the human population.

18.3.4.3 Toxicological risk assessment of BHT

As in the case of BHA, dietary standards for BHT were set at an expert meeting of the Scientific Committee on Food of the European Union. In its 1989 meeting, this Committee evaluated all available toxicity data on BHT. The toxicity profile of BHT was summarized as follows. In chronic toxicity studies, BHT induced liver carcinomas and adenomas in the rat at dose levels higher than 100 mg/kg/day. However, BHT was not found to be mutagenic or otherwise genotoxic. Therefore, the Committee considered BHT as a non-genotoxic carcinogen with a threshold in the induction of its carcinogenicity. In semi-chronic toxicity studies, BHT caused an increase in thyroid weight. In this type of study the lowest dose tested, 500 ppm BHT in the diet, still induced a significant increase in thyroid weight. However, the Committee concluded that "It is reasonable to assume that the likely NOAEL for thyroid weight change will be about 5 times lower than the lowest-observed-adverse effect level, i.e., 500 ppm." In subacute toxicity studies, BHT was found to interfere with blood clotting. The underlying mechanism is a reduction of the activity of vitamin K-dependent blood clotting factors. In the rat, the NOAEL for this effect was found to be 5 mg/kg/day. Taking all toxic effects into consideration, the Committee classified BHT as a non-genotoxic carcinogen in rodents. Likewise, the Committee recommended the determination of an ADI as a safe exposure measure for the human population. Since the NOAEL for the chronic toxicity (neoplasia in the liver) was about 50 times higher than the NOAEL for semi-chronic (increased thyroid weight) and subacute toxicity (hematological disorders), the latter parameter (5 mg/kg/day) was used for the calculation of the ADI of BHT. Applying a standard safety factor of 100, the Committee recommended an ADI of 0 to 0.05 mg/kg/day for BHT.

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