Anticoagulant rodenticides (ARs) are part of the near billion‐dollar rodenticide industry. Numerous studies have documented the presence of ARs in nontarget wildlife, with evidence of repeated exposure to second‐generation ARs. While birds are generally less sensitive to ARs than target rodent species, in some locations predatory and scavenging birds are exposed by consumption of such poisoned prey and, depending on dose and frequency of exposure, exhibit effects of intoxication that can result in death. Evidence of hemorrhage in conjunction with summed hepatic AR residues >0.1–0.2 mg kg−1 liver wet weight are often used as criteria to diagnose ARs as the likely cause of death. In this review focusing on birds of prey and scavengers, we discuss AR potency, coagulopathy, toxicokinetics and long‐lasting effects of residues, and the role of nutrition and vitamin K status on toxicity, and identify some research needs. A more complete understanding of the factors affecting AR toxicity in nontarget wildlife could enable regulators and natural resource managers to better predict and even mitigate risk. Published 2020. This article is a U.S. Government work and is in the public domain in the USA

Nitrate concentrations have been rising in surface waters over the last century and now frequently exceed drinking water standards and environmental safety benchmarks globally. Health‐wise, these trends are concerning because nitrate has been shown to disrupt endocrine function and developmental outcomes. The present study investigated potential sublethal effects of nitrate on developing fathead minnows. Fish were exposed from fertilization through 21 days postfertilization (dpf) to environmentally relevant concentrations of nitrate (0, 2, 5, 10, 25, or 100 mg/L NO3‐N as NaNO3). Nitrate effects on hatch timing, heart rate and rhythm at 3 dpf, growth through 21 dpf, swim bladder inflation timing and size, scoliosis, pericardial edema, and mortality were assessed. Because adding NaNO3 increases water conductivity, two conductivity controls were included to match the ionic strength of the 10‐ and 100‐mg/L NO3‐N treatments. Increasing nitrate delayed posterior swim bladder (PSB) inflation in a dose‐dependent manner, with possible inhibition of anterior swim bladder (ASB) inflation at higher doses, although nitrate did not affect swim bladder size. Conversely, nitrate did not affect hatch timing or cardiac endpoints at 3 dpf or induce pericardial edema or scoliosis, although there was a noted brood effect on these latter defects. As was observed with increasing nitrate, higher ion concentrations in the conductivity controls caused dose‐dependent increases in fish body size at 21 dpf. Increased ionic strength also hastened ASB inflation independently of nitrate. As in other published studies, the observed delay in PSB inflation suggests that nitrate disrupts the thyroid axis and warrants further investigation. In addition, the present study supports the need for conductivity controls in nitrate toxicity studies to distinguish nitrate‐specific effects. Environ Toxicol Chem 2023;42:1529–1541. Published 2023. This article is a U.S. Government work and is in the public domain in the USA.