title: Developmental toxicity of lead-contaminated sediment to mallard ducklings.
abstract: 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.
authors.affiliation: U.S. Geological Survey, Patuxent Wildlife Research Center, 12011 Beech Forest Road, Laurel, Maryland 20708-4041, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Hoffman
authors.forename: G H
authors.initials: GH
authors.lastname: Heinz
authors.forename: L
authors.initials: L
authors.lastname: Sileo
authors.forename: D J
authors.initials: DJ
authors.lastname: Audet
authors.forename: J K
authors.initials: JK
authors.lastname: Campbell
authors.forename: L J
authors.initials: LJ
authors.lastname: LeCaptain
mesh_terms: D000622:Aminolevulinic Acid / Q000378:metabolism; D000821:Animal Feed; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development; D001774:Blood Chemical Analysis; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000473:pathology; D004372:Ducks / Q000254:growth & development*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D005618:Fresh Water; D019015:Geologic Sediments / Q000032:analysis; D005978:Glutathione / Q000378:metabolism; D006400:Hematocrit; D007061:Idaho; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007854:Lead / Q000097:blood / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011166:Porphyrins / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000633:toxicity*; D003313:Zea mays
chemical_list: D011166:Porphyrins; D014874:Water Pollutants, Chemical; D007854:Lead; D000622:Aminolevulinic Acid; D005978:Glutathione