Abstract
1. Pyrethroids are neurotoxic and parent pyrethroid appears to be toxic entity. This study evaluated the oral disposition and bioavailability of bifenthrin in the adult male Long-Evans rat.
2. In the disposition study, rats were administered bifenthrin (0.3 or 3 mg/kg) by oral gavage and serially sacrificed (0.25 h to 21 days). Blood, liver, brain and adipose tissue were removed. In the bioavailability study, blood was collected serially from jugular vein cannulated rats (0.25 to 24 h) following oral (0.3 or 3 mg/kg) or intravenous (0.3 mg/kg) administration of bifenthrin. Tissues were extracted and analyzed for bifenthrin by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS).
3. Bifenthrin concentration in blood and liver peaked 1–2-h postoral administration and were approximately 90 ng/ml (or g) and 1000 ng/ml (or g) for both tissues at 0.3 and 3 mg/kg, respectively. Bifenthrin was rapidly cleared from both blood and liver. Brain concentrations peaked at 4–6 h and were lower than in blood at both doses (12 and 143 ng/g). Bifenthrin in adipose tissue peaked at the collected time points of 8 (157 ng/g) and 24 (1145 ng/g) h for the 0.3 and 3 mg/kg doses, respectively and was retained 21 days postoral administration. Following intravenous administration, the blood bifenthrin concentration decreased bi-exponentially, with a distribution half-life of 0.2 h and an elimination half-life of 8 h. Bifenthrin bioavailability was approximately 30%. These disposition and kinetic bifenthrin data may decrease uncertainties in the risk assessment for this pyrethroid insecticide.
Acknowledgements
The authors gratefully acknowledge Drs. E. Kenyon, J.E. Simmons and M. Tornero-Velez for their comments on a previous version of this manuscript. The authors thank Ms. J. Hutchison for her technical assistance in this study. All research was funded internally by the U.S. Environmental Protection Agency.
Declaration of interest
The authors declare that there is no conflict of interest. This article is reviewed in accordance with the policy of the National Health and Environmental Effects Research laboratory, U.S. Environmental Protection Agency and the National Institute of Environmental Health Sciences and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency, nor does mention of trade names or commercial products constitute endorsement or recommendation for use. This article may be the work product of an employee of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH); however, the statements opinions or conclusions contained therein do not necessarily represent the statements, opinions or conclusions of NIEHS, NIH or the United States government.
Supplementary materials available online
Supplemental Figures 1--5