Comparative immunomodulatory effects of chronic exposure to imidacloprid and thiamethoxam on the respiratory burst response in zebrafish and fathead minnow larvae.

Widespread use of neonicotinoid pesticides has resulted in their ubiquitous presence within aquatic ecosystems. Designed as nicotinic acetylcholine receptor (nAChR) agonists, they are generally classified as neurotoxicants. Neonicotinoids have been linked to suppression of the immune response in terrestrial species, but the potential for these pesticides to modulate the innate immune response in larval fish is not understood. In this study, the potential for chronic exposure to two neonicotinoid pesticides to disrupt the innate immune response was compared in two species of larval fish. Zebrafish and fathead minnows were exposed to 0, 0.02, 0.2, 2, 20, or 200 μg/L of imidacloprid (IM) or thiamethoxam (TM) beginning just after fertilization through the free-swimming larval stages (5 days for zebrafish and 8 days for fathead minnow). The in vivo respiratory burst response was used to evaluate the impact of exposure to these pesticides on the production of reactive oxygen species (ROS) by neutrophils as part of the innate immune response. While imidacloprid suppressed ROS production in both species, fathead minnow larvae appear more sensitive. Thiamethoxam also suppressed ROS production in fathead minnow larvae, but a non-monotonic response was observed in zebrafish. These species-specific modulatory effects appear independent of activation of the nAChR. This study highlights that neonicotinoid pesticides can impact non-target vertebrates by modulating the immune response as found for other species, and that further studies are needed to identify the risks that they pose to the integrity of aquatic ecosystems and potential for species-specific sensitivities.