Sublethal and Lethal Methods to Detect Recent Imidacloprid Exposure in Birds with Application to Field Studies

Abstract

We used domestic chickens (Gallus gallus domesticus) as a model for granivorous birds to identify methods to detect recent imidacloprid exposure in wild birds. We conducted dosing experiments of 1, 5, 10, and 20% of a reported median lethal dose for domestic chickens using repeated daily exposures over 7 d, at dosages equating to 1.04, 5.2, 10.4, and 20.8 mg/kg/d. We examined the parent compound and metabolites in serial collections of feces and blood during exposures and for 15 d after exposures. We also collected liver, kidney, brain, muscle, and spleen at the experiment end. Mean concentrations of parent compound at 15 d postexposure were highest in the feces and brain, followed by the liver, muscle, spleen, and kidney; but mean concentrations of metabolites 5‐OH‐imidacloprid and imidacloprid‐olefin were highest in feces; then liver, spleen, muscle, and kidney; and then brain. Imidacloprid was rapidly cleared from blood, with only one individual in any dose group having detectable concentrations after 48 h. In contrast, fecal pellets had the highest frequency of imidacloprid detection after 15 d. Concentrations of metabolites were higher than those of the parent compound at all sampling times examined but provided no information about time since exposure. Feces may provide a reliable nonlethal method for detection of recent imidacloprid exposure in wild birds. Additional work is needed to disentangle exposure dose concentration and time since exposure in field‐collected samples. Environ Toxicol Chem 2020;39:1355–1366. © 2020 SETAC

Deletion of Constitutive Androstane Receptor Led to Intestinal Alterations and Increased Imidacloprid in Murine Liver

“…Since IMI has been reported to have multi-organ adverse effects, organ weights (liver, small intestine, colon, kidney, and spleen) were analyzed with respect to the body weights ( Table 1 ). The kidney and spleen were examined for toxicity as they are additional sites of IMI accumulation [ 31 , 32 ]. Kidney and spleen weights were unaltered, although Car −/− mice exposed to IMI had a decreasing trend compared to vehicle control ( Table 1 ).…”

Inhibition of the Nrf2 signaling pathway involved in imidacloprid‐induced liver fibrosis in Coturnix japonica

“…[48][49][50][51] Previous studies have found that IMI is rapidly removed from the blood after exposure, but has higher residues in feces, brain, and liver. 52,53 The United States has stipulated that the maximum residue limit of IMI in poultry, fish, shellfish, and other foods is 0.05 mg/kg (http://www.tbtsps.cn). In our study, the results of HPLC-MS/MS confirmed the accumulation of IMI in quail liver tissue, which was much higher than the maximum residue limit of IMI in poultry in the United States, but Lut reduced the accumulation to a great extent.…”

“…IMI can enter the body through many ways to cause tissue injury, such as liver, kidney, brain, and muscle tissue 48–51 . Previous studies have found that IMI is rapidly removed from the blood after exposure, but has higher residues in feces, brain, and liver 52,53 . The United States has stipulated that the maximum residue limit of IMI in poultry, fish, shellfish, and other foods is 0.05 mg/kg (http://www.tbtsps.cn).…”