Fipronil

Fipronil is not a neonicotinoid, but like many neonicotinoids, it is often used as an acaricide to control ticks and mites as well as other insects¹. Its activity is based on blocking the g-aminobutryic acid (GABA) receptor site on GABA-gated chloride channels. Fipronil binds more tightly to this receptor in insects than in vertebrate², making it an attractive pesticide for use in flea and tick collars, especially in areas where Lyme disease is endemic. Contact with pets treated with fipronil is one of the primary reasons for elevated levels of fipronil in indoor environments, and elevated levels of human exposure in non-agricultural workers.  For this reason, government researchers are studying human exposure to fipronil.

Unfortunately, GABA-gated chloride channels are present in birds and aquatic species, including fish and a host of aquatic insects and other invertebrates, which may lead to biomagnification. Fipronil will bioaccumulate in mammals as well, and since it is used as a systemic pesticide for household pets, human exposure and indoor exposure can be much higher than with conventional pesticides. A further problem is increased toxicity of some of the metabolites, including MB 46136 (fipronil sulfone) and MB 45950 (fipronil sulfide)³.  As with neonicotinoids, it has been implicated without conclusive proof in colony collapse disorder (CCD).

Production of this compound is on the order of thousands of tons per year, which is not a large amount in the world of pesticides, but the potential for widespread exposure to humans and the environment has become a concern to many organizations throughout the world. Concerns about the effect on humans, bees, fish and birds have led to restrictions and outright bans for use of fipronil in some countries.

The availability of these fipronil and metabolite standards will enable a more accurate assessment of these chemicals in human exposure and the environment.