A REVIEW OF THE TOXICOLOGY OF PERMETHRIN WITH REFERENCE TO DRINKING WATER
Report No FR0098

May 1990

SUMMARY

I OBJECTIVES

To review the information on the toxicity of permethrin with reference to drinking water and to discuss the setting of a drinking water guide level for the compound.

II REASONS

Permethrin is widely used in agriculture and also in the disinfection of water mains. There is a need to provide water suppliers with sound guidance on the maximum levels of toxic substances that should be permitted in drinking water. The WHO is undertaking a review of drinking water guidelines for a number of substances. This review is part of the UK water industry's contribution to that process of establishing new guidelines based on a sound scientific assessment of the latest available data.

III CONCLUSIONS

There are no data on the occurrence of permethrin in treated water. The major source of exposure for the general population is the diet and the contribution from drinking water is minimal. Permethrin is of low to moderate acute and chronic toxicity. There is no evidence of carcinogenicity in rats and only limited evidence for a weak carcinogenic potential in female mice of one strain. The absence of positive mutagenic results suggests this is probably an epigenetic mechanism. Permethrin is not teratogenic in test animals.

IV RECOMMENDATIONS

The FAO/WHO Joint Meeting on Pesticide Research (JMPR) have recommended a maximum acceptable daily intake (ADI) of 0.05 mg/kg body weight for permethrin. The ADI can be used to calculate the drinking water guideline, allocating 1% of the ADI to water.

V RESUME OF CONTENTS

Permethrin is widely used in agriculture and in the disinfection of water mains. Levels have not been reported for drinking water but it is generally considered that permethrin is readily removed by conventional treatment methods. It does not react with chlorine under conditions similar to those found during the disinfection of water.

Permethrin is of low to moderate acute and chronic toxicity. There is weak evidence for a carcinogenic potential in female mice of one strain but the mechanism is probably epigenetic. The ADI approach can therefore be used to calculate a guideline value, allocating 1% of the ADI to water. The calculated value compares favourably with analytical limits of detection and reported taste and odour values.

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