Cytochrome P450‐associated monooxygenase activities and cytochrome P450 proteins were measured in pipping black‐crowned night heron (Nycticorax nycticorax) embryos collected from a reference site (next to the Chincoteague National Wildlife Refuge, VA) and three polluted sites (Cat Island, Green Bay, Lake Michigan, WI; Bair Island, San Francisco Bay, CA; West Marin Island, San Francisco Bay, CA). In a laboratory study, artificially incubated night heron embryos from the reference site were treated with 3‐methylcholanthrene (200 μg administered into the air cell 2 d before pipping) or phenobarbital (2 mg daily for 2 d before pipping). Compared to controls (untreated + vehicle‐treated embryos), 3‐methylcholanthrene induced a greater than fivefold increase in activities of several monooxygenases (arylhydrocarbon hydroxylase, AHH; benzyloxyresorufin‐O‐dealkylase, BROD; ethoxyresorufin‐O‐dealkylase, EROD; pentoxyresorufin‐O‐dealkylase, PROD) and a greater than 100‐fold increase in the concentration of immunodetected cytochrome P450 1A (CYP1A). Phenobarbital treatment resulted in only a slight increase in BROD activity but induced proteins recognized by antibodies to cytochrome P450 2B (CYP2B) by 2,000‐fold. In a field study, activities of AHH, BROD, EROD, and ethoxycoumarin‐O‐dealkylase (ECOD) were up to 85‐fold higher in pipping black‐crowned night herons collected from Cat Island compared to other sites. Hepatic CYP1A and CYP2B cross‐reactive proteins were detected in significantly more individuals from Cat Island than from the reference site. Greatest burdens of total PCBs and p,p′‐DDE were detected in embryos from Cat Island. Cytochrome P450‐associated monooxygenase activities and cytochrome P450 proteins (AHH, BROD, EROD, ECOD, CYP1A, CYP2B) were significantly associated with total PCB burdens (r = 0.50‐0.72). These data indicate that cytochrome P450 may be a useful biomarker of exposure to some PCB mixtures in black‐crowned night heron embryos.

Feces from tundra swans [Cygnus columbianus (Ord)], Canada geese [Branta canadensis (L.)], and mallards [Arias platyrhynchos (L.)] were collected from the Coeur d'Alene River Basin and two reference areas in Idaho to estimate exposure to lead from mining activities and relate that exposure to the ingestion of contaminated sediments. The average acid‐insoluble ash content of the feces, a measure of sediment ingestion, was 18% for Canada geese and tundra swans, and 12% for ducks. The 18% value corresponded to an estimated 9% sediment ingestion rate (dry weight). The 90th percentile for acid‐insoluble ash in feces of tundra swans corresponded to an estimated 22% sediment in the diet. The average lead concentration (dry weight) of tundra swan feces from all Coeur d'Alene River Basin wetlands sampled was 880 mg/kg, compared to 2.1 mg kg−1 from reference areas. The 90th percentile of lead in tundra swan feces from the Coeur d'Alene River Basin sites was 2700 mg kg−1. Fecal lead concentrations of tundra swans were correlated (Spearman's rho = 0.74, P < 0.05) with the acid‐insoluble ash content of the feces. The very low lead concentrations in feces having low acid‐insoluble ash contents established that the sediment was the primary source of the lead ingested by waterfowl. Sediment lead concentrations at 11 wetland sites were closely correlated (r = 0.91, P < 0.05) with average fecal lead concentrations for all waterfowl, corrected for the average percent acid‐insoluble ash in the feces.

Two-year-old male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dose-dependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver injury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 8-32 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

Sediment ingestion has been identified as an important exposure route for toxicants in waterfowl. The toxicity of lead-contaminated sediment from the Coeur d'Alene River Basin (CDARB) in Idaho was examined on posthatching development of mallard (Anas platyrhynchos) ducklings for 6 weeks. Day-old ducklings received either untreated control diet, clean sediment (24%) supplemented control diet, CDARB sediment (3,449 microg/g lead) supplemented diets at 12% or 24%, or a positive control diet containing lead acetate equivalent to that found in 24% CDARB. The 12% CDARB diet resulted in a geometric mean blood lead concentration of 1.41 ppm (WW) with over 90% depression of red blood cell ALAD activity and over threefold elevation of free erythrocyte protoporphyrin concentration. The 24% CDARB diet resulted in blood lead of 2.56 ppm with over sixfold elevation of protoporphyrin and lower brain weight. In this group the liver lead concentration was 7.92 ppm (WW), and there was a 40% increase in hepatic reduced glutathione concentration. The kidney lead concentration in this group was 7.97 ppm, and acid-fast inclusion bodies were present in the kidneys of four of nine ducklings. The lead acetate positive control group was more adversely affected in most respects than the 24% CDARB group. With a less optimal diet (mixture of two thirds corn and one third standard diet), CDARB sediment was more toxic; blood lead levels were higher, body growth and liver biochemistry (TBARS) were more affected, and prevalence of acid-fast inclusion bodies increased. Lead from CDARB sediment accumulated more readily in duckling blood and liver than reported in goslings, but at given concentrations was generally less toxic to ducklings. Many of these effects are similar to ones reported in wild mallards and geese within the CDARB.

No abstract