Document 1g10qNgQ803yLn58xK85BpdVZ

APRiL?988L REP0RT 85<114) ArHlL 1988 CONTAMINANT HAZARD REVIEWS REPORT NO. 14 LEAD HAZARDS TO FISH, WILDLIFE, AND INVERTEBRATES: A SYNOPTIC REVIEW Fish and Wildlife Service U.S. Department of the Interior vr: ------ ---------------------------------------------- N 276X9 DUP040007944 Other publications in the "Hazards" series3 Subject - Publication date ... Hi rex March 1985 Cadmium July ' 1985 Carbofuran j ^ AugustSl985 Toxaphene ' - August-1985 Selenium --------- -------October 1985 Chromi urn - -- January 1986 Polychlorinated Biphenyls _ April. 1986 Dioxins May 1986 Diazinon August 1986 Mercury April 1987 Polycyclic~Aromatic"Hydrocarbo ns May 1987.... Arsenic . .......January. 1988 Chlorpyrifos - March 1988 Publication number 85(1,1) 85(1.2) 85(1.3) 85(1.4) 85(1.5) 85(1.6) 85(1.7) 85(1.8) 85(1.9) 85(1.10) 85(1.11) 85(1.12) 85(1.13) aCopies of individual reviews,if-available, can be obtained by writing the Section of Information Management, U.S. Fish and Wildlife Service, Patuxent Wildlife Research Center, Laurel", Maryland 20708. - DUP040007945 Biological Report 85(1.14) April 1988 Contaminant Hazard Reviews Report No. 14 LEAD HAZARDS TO FISH, WILDLIFE, AND INVERTEBRATES: A SYNOPTIC REVIEW by Ronald Eisler U.S. Fish and Wildlife Service Patuxent Wildlife Research Center Laurel, MD 20708 i Fish and Wildlife Service______ U.S. Department of the Interior DUP040007946 SUMMARY Lead (Pb) and its compounds have been known to man for about 7,000 years, and Pb poisoning has been recognized for at least 2,500 years* ATI credible evidence indicates that Pb is neither essential nor beneficial to living organisms, and that all measured effects are adverse-including those on survival, growth, reproduction, development, behavior, learning, and metabo lism. Various living resources are at increased risk from Pb: migratory waterfowl that frequent hunted areas and ingest shot; avian predators that eat game wounded by hunters; domestic livestock near smelters, refineries, and Pb battery recycling plants; captive zoo animals and domestic livestock held in enclosures coated with Pb-based paints; wildlife that forage extensively near heavily traveled roads; aquatic life in proximity to mining activities, areas where Pb arsenate pesticides are used, metal finishing industries, organolead industries, and areas of Pb aerosol fallout; and crops and invertebrates growing or living in Pb-contaminated soils. Adverse effects on aquatic biota reported at waterborne Pb concentrations of 1.0 to 5.1 ug/1 included reduced survival, impaired reproduction, reduced growth, and high bioconcentration from the medium. Among sensitive species of birds, survival was reduced at doses of 50 to 75 mg Pb^/kg body weight (BW) or 28 mg organolead/kg BW, reproduction was impaired at dietary levels of 50 mg IHr ykg, and signs of poisoning were evident at doses as low as 2.8 mg organolead/kg BW. In general, forms of Pb other than shot (or ingestible Pb objects), or routes of administration other than ingestion, are unlikely to cause clinical signs of Pb poisoning in birds. Data for toxic and sublethal effects of Pb on mammalian wildlife are missing. For sensitive species of domestic and laboratory animals, survival was reduced at acute oral Pb doses of 5 mg/kg BW (rat), at chronic oral doses of 5 mg/kg BW (dog), and at dietary levels of 1.7 mg/kg BW (horse). Sublethal effects were documented in monkeys exposed to doses as low as 0.1 mg Pb/kg BW daily (impaired learning at 2 years postadministration) or fed diets containing 0.5 mg Pb/kg (abnormal social behavior). Signs of Pb exposure were recorded in rabbits given 0.005 mg Pb/kg BW and in mice given 0.05 mg Pb/kg BW. Tissue Pb levels were elevated in mice given doses of 0.03 mg Pb/kg BW, and in sheep given 0.05 mg Pb/kg BW. In general, organolead compounds were more toxic than inorganic Pb compounds, food chain biomagnification of Pb was negligible, and younger organisms were most susceptible. More research seems merited on organolead toxicokinetics (including effects on behavior and learning), and on mammalian wildlife sensitivity to Pb and its compounds. iii DUP040007947 TABLES Number Page 1 World Pb production, consumption, and principal end uses (modified from Harrison and Laxen 1981; Demayo et al. 1982)....................................... ........................... 6 2 Use patterns for Pb in selected countries (from EPA 1979).................................................. ................... ... 7 3 Amounts of lead- in global reservoirs (modified from Nriagu 1978a). , . . ...................... , , 17 4 Lead concentrations in selected nonbiological materials...................................................................................... 18 5 Lead concentrations in field collections of selected species of flora and fauna. Values shown are in mg Pb/kg (ppm) fresh weight (FW), or dry weight (DW)................................................................................... 24 6 Lethal and sublethal effects of lead to selected species of aquaticorganisms. . . .. .......................... 58 7 Lethal and sublethal effects of lead to selected species of birds, .................... , .................... 75 8 Lethal and sublethal effects of lead to selected species of mammals. , .. .......................................... 88 9 Proposed lead criteria for the protection of natural resources and human health. ........................ ... 102 / vi DUP040007948 ACKNOWLEDGMENTS I thank Nancy A. Bushby, Lynda 0. Garrett, and Joyce E. Haber for technical services; Julia Armstrong and Jean Higgis for secretarial help; Louis N. Locke, Jerry R. Longcore, Keith A. Morehouse, Oliver H. Pattee, , Matthew C, Perry, and Christopher J. Schmitt for reviewing the manuscript; and Paul H. Eschmeyer and James R. Zuboy for editorial services. vi i DUP040007949 accumulative metabolic poison that affects behavior, as well as the hematopoietic, vascular, nervous, renal, and reproductive systems. In humans, Pb causes stillbirths, miscarriages, inhibited development of fetuses, decreased male fertility, and abnormal sperm. Severe damage to the central nervous system from exposure to large amounts of Pb may result in stupor, convulsions, coma, and death. Children that survive Pb poisoning are often/" permanently retarded or have permanent neurological handicaps. At subclinical injury levels, Pb causes slight, but irreversible, damage to the brain development of growing children. Natural resources are also affected by environmental Pb contamination, and some wildlife species numbers may be reduced as a result. For example, waterfowl deaths resulting from the ingestion of spent Pb shot pellets from shotgun shells were discovered more than 100 years ago in Italy and in the United States; since then Pb poisoning of waterfowl has occurred in 15 countries (Street 1983). In North America alone, approximately 3,000 tons of Pb shot are expended annually into lakes, marshes, and estuaries by several million waterfowl hunters (FWS 1986, 1987). Spent pellets are eaten by waterfowl and other birds, either in mistake for seeds or as pieces of grit. These pellets may be retained in the gizzard for weeks, where they are reduced chemically and mechanically, form soluble toxic salts, and cause characteristic signs of Pb intoxication--especially lethargy and emaciation (Street 1983), At least 2% of all North American waterfowl--or about 2 million ducks and geese (Lumeij 1985)--die each year as a direct result of ingestion of Pb shot (Bellrose 1959), These deaths contribute to the decline of some species, such as the canvasback, AvthyavaliSiberia (Dieter 1979), pintail, Anas acuta (White and Stendeil 1977), and black duck, Anas rubripes (Pain and Rattner 1988). Up to 7X more waterfowl died from Pb toxicosis as a result of ingesting spent pellets than from wounding by hunters (Zwank et al, 1985). In addition, Pb-poisoned waterfowl show delayed mortality from Pb-induced starvation, are readily captured by predators, are susceptibile to disease, and reproduce poorly (Dieter 1979). Susceptibility is markedly influenced by species, by the number and size of shot ingested, and by the types of foods eaten (White and Stendeil 1977). Swans are among the more vulnerable waterfowl. In England, Pb poisoning through the ingestion of discarded Pb fishing sinkers is the major cause of death in the mute swan, Cygnus olor (Birkhead 1983); for all species of swans in England, about half died as a direct result of Pb poisoning (Demayo et al. 1982), In Washington State, 30% of the endangered trumpeter swans (Cygnus buccinator) found dead had died of Pb poisoning from ingestion of Pb shot (Kendall and Driver 1982), Lead toxicosis caused by ingestion of spent shot and other Pb objects has also been reported for sandhill crane, Grus canadensis (Windingstad et al. 1984); Canada goose, Branta canadensis (Szymczak and Adrian 1978); mourning dove, Zenaidura macroura (Locke and Bagley 1967); and wild turkey, Meleaqris gallopavo (Stone and Butkas 1978). Secondary poisoning has been documented in at least five species of raptors that ate food containing Pb shot (especially hunter-wounded animals): Andean condor, Vultur qryphus (Locke et al. 1969); bald eagle, Hal 1aeetus 1eucocephalus (Patted and Hennes 1983); honey buzzard, 2 DUP040007950 In this reportj I summarize available data on lead in the environment, with emphasis on fishery and wildlife resources, and review current recommendations for the protection of sensitive species. This account is part of a continuing series of brief reviews prepared in response to requests for information from environmental specialists of the U.S. Fish and Wildlife Service. 4 1 DUP040007951 Table 1. World Pb production, consumption, and principal end uses (modified from Harrison and Laxen 1981; Demayo et al. 1982), Production, consumption, and use Metric tons, in thousands PRODUCTION, 1978 Mined Pb Refined Pb CONSUMPTION 1977 1980 PRINCIPAL END USES OF REFINED Pb 1977 Storage batteries Pigments and chemicals Tetraalkyllead Cable covering Pipe and sheeting Other 1980 Storage batteries Tetraethyllead Cable covering Solder Litharge Building construction Caulking Other 3,625 4,202 2,995 3,801 1,478 369 292 216 160 480 1,330 380 380 380 190 190 190 760 / 6 DUP0400079S2 atmospheric Pb concentrations increased sharply due to massive increases in Pb emissions from automobiles; since then, increased Pb emissions to the atmosphere have matched trends in gasoline Pb content and consumption (Eisenreich et al. 1986; Smith et al, 1987). In 1957, the United States was overtaken by Australia and the USSR in domestic mine production of Pb; however, in 1967, the opening of the "New Lead Belt" in Missouri revivedy mining in the United States, and subsequently Pb was produced at the annual rate of 450,000 to 550,000 metric tons (EPA 1979). In 1975, the United States was again the leading Pb producer from mine sources, accounting for 16% of the world total; at that time, about 70% of the world Pb production came from the USA, the USSR, Australia, Canada, Peru, Mexico, China, Yugoslavia, and ,:;t Bulgaria (Tsuchiya 1979). In 1986, world mine production of lead was 2,352,000 tons of which USA mine production was 353,000 tons, or 15% of the world total, and production in Missouri was 308,000 tons, or 87% of the USA total (personal communication, R. L. Amistadi, Doe Run Company, St. Louis, Missouri). 8 DUP040007953 naturally, and their rate of formation may be affected by man-made organoleads (Nriagu 1978a). In surface waters, Pb exists in three forms: dissolved labile (e.g., Pb > PbOHt, PbC03), dissolved bound (e.g., colloids or strong complexes), or as a particulate (Benes et al. 1985). The labile forms represent a significant part of the Pb input from washout of atmospheric deposits, whereas particulate and bound forms were common in urban runoff and ore-mining effluents (Benes et al. 1985). The solubility of Pb compounds in'" water is pH dependent, and ranges from about 10 g Pb/1 at pH 5.5, to less than 1 ug Pb/1 at pH 9.0 (EPA 1980); little detectable Pb remains in solution at pH >8.0 (Prause et al. 1985). At pH 6.5 and water alkalinity of 25 mg CaC03/l, elemental Pb is soluble to 330 ug/1; however, Pb4+ under the same conditions , is soluble to 1,000 ug/1 (Demayo et al. 1982), In acidic waters, the common forms of dissolved Pb are salts of PbSO. and PbCl2, ionic Pb, cationic forms of lead hydroxide, and (to a lesser extent) the ordinary hydroxide Pb(0H)2. In alkaline waters, common species include the anionic forms of Pb carbonate^ and hydroxide, and the hydroxide species present in acidic waters (NRCC 1973). Unfortunately, the little direct information available about the speciation of Pb in natural aqueous solutions has seriously limited our understanding of Pb transport and removal mechanisms (Nriagu 1978a). Most Pb entering natural waters is precipitated to the sediment bed as carbonates or hydroxides (May and McKinney 1981). Lead is readily precipitated by many common anions; desorption and replacement by other cations is extremely slow (Boggess 1977). In some acidic lakes, the deposition of particulate Pb was strongly correlated with the deposition of aluminum and carbon, especially during periods of increasing pH (White and Driscoll 1985). Precipitation of sparingly soluble Pb compounds is not a primary factor controlling the concentration of dissolved Pb in stream waters. Migration and speciation of Pb was strongly affected by water flow rate, increasing flow rate resulting in increased concentrations of particulate and labile Pb and a decrease in bound forms. At low stream flow, Pb was rapidly removed from the water column by sedimentation (Benes et al. 1985), In the sediments, Pb is mobilized and released when the pH decreases Suddenly or ionic composition changes (Demayo et al. 1982). However, there was no significant release of Pb from dredge spoils suspended in estuarine waters of different salinities for 4 weeks (Prause et al. 1985). Some Pa in sediments may be transformed to tetraalkyllead compounds, including TML, through chemical and microbial processes. There is also the possibility of methylation of ionic Pb in vivo by fish and other aquatic biota, but the mechanisms are unclear (May and McKinney 1981). Methylation of Pb in sediments was positively related to increasing temperatures, reduced pH, and microbial activity, but seemed to be independent of Pb concentration (Demayo et al, 1982). In general, the concentration of tetraalkylleads in sediments is low, representing less than 10% of total Pb (Chau et al. 1980). 10 DUP040007954 amino acid transport, uncouple oxidative phosphorylation, and inhibit cerebral glucose metabolism (Hong et al. 1983). Biochemically, Pb exerts deleterious effects on hematopoiesis through derangement of hemoglobin synthesis, resulting in a shortened life span of circulating erythrocytes, often resulting in anemia. Two essential enzymes in, heme formation that are extremely sensitive to Pb are delta aminolevulinic acid dehydratase (ALAD), which catalyzes the dehydration of delta amino levelinic acid (ALA) to form porphobilinogen (PBG), and ferrochelatase (- heme synthetase), which catalyzes the insertion of Fe- into protoporphyrin IX (PP). This second reaction requires the presence of glutathione and ascorbic acid. Some of the intermediates in heme follow sequentially: ALA, PBG, uroporphyrinogen III, coproporphyrinogen III, protoporphyrinogen IX, and PP. It is now well established that ALAD and ferrochelatase are the most sensitive biochemical indicators of Pb exposure, the net result being 1owered ALAD activity and elevated PP activity (Barth et al. 1973; Nriagu 1978b; EPA 1979, 1980; Tsuchiya 1979; Harrison and Laxen 1981; Hoffman et al. 1981; De Michele 1984; Schmitt et al. 1984; Lumeij 1985). Inhibition of blood ALAD activity after exposure to Pb has been documented in many species of freshwater and marine teleosts (Hodson 1976; Hodson et al. 1977, 1980; Johansson-Sjobeck and Larsson 1979; Krajnovic-Ozretic and Ozretic 1980; Demayo et al. 1982; Schmitt et al. 1984; Haux et al. 1986), in the freshwater cladoceran, Daphnia magna (Berglind et al. 1985), in ducks, quail, doves, swallows, raptors, and songbirds (Finley et al. 1976; Dieter and Finiey 1978; Dieter 1979; Hoffman et al. 1981; Franson and Custer 1982; Kendal1 et al. 1982; Kendall and Scanlon 1982; Eastin et al. 1983; Franson et al. 1983; Hoffman et al. 1985a, 1985b; Beyer et al. 1988), and in humans, sheep, mice, rats, rabbits, and calves (Barth et al. 1973; Boggess 1977; Nriagu 1978b; Tsuchiya 1979; Hejtmancik et al. 1982; Hayashi 1983; Peter and Strunc 1983; Schlick et al. 1983; Gietzen and Wooley 1984; Zmudzki et al. 1984). Lead-induced ALAD inhibition has been recorded not only in blood, but also in brain, spleen, liver, kidney, and bone marrow (Johansson-Sjobeck and Larsson 1979; Hoffman et al, 1981, 1985a, 1985b; Schlick et al, 1983; Friend 1985). Time for ALAD recovery to normal 1evels is dose dependent, organ specific, and usually directly correlated with blood Pb concentrations (Finley et al. 1976; Hodson et al. 1977; Dieter 1979; Hayashi 1983; Friend 1985). ALAD activity 1evels in Pb-stressed teleosts were normal 3 to 11.7 weeks postadministration (Hodson et al. 1977; Johansson-Sjobeck and Larsson 1979; Krajnovic-Ozretic and Ozretic 1980; Demayo et al. 1982); this range was 2 to 14 weeks in birds (Dieter and Finley 1978; Kendall et al. 1982; Kendal1 and Scanlon 1982; Friend 1985), and 3 to 12 weeks in mammals (Barth et al. 1973; Schlick et al. 1983). The physiological significance of depressed blood ALAD activity 1evels, except perhaps as an early indicator of Pb exposure, is debatable. Aside from a few instances of moderate anemia in workers at lead smelters, other abnormalities noted were not regarded as serious (Barth et al. 1973). Lead-induced depression in ALAD activity in mal1ard (Anas piatyrhynehos) ducklings and ring-necked pheasant (Phasianus 12 DUP040007955 number of difficulties for the usual multicompartmental loss-rate models. Some Pb in bones of high medullary content, such as the femur and sternum, have relatively long retention times--!,e., Tb 1/2 of >20 years in humans--whereas Pb stored in bones of low medullary content have Tb 1/2 values of 20 to 200T days, similar to the values for Pb in soft tissues and blood (Tsuchiya 1979; Marcus 1985). In birds, medullary bone undergoes sequences of bone formation and destruction associated with the storage and liberation of calcium during eggshell formation, indicating that sex and physiological condition primarily influence Pb kinetics in avian bone (Finley and Dieter 1978). Marcus (1985) endorsed the use of diffusion models based on the exchange of Pb between blood in canalicull and the crystalline bone of the ; osteon to account for retention and bioavailability. More research is needed on the role of bone in Pb kinetics. Lead damages nerve cells and ganglia, and alters cell structure and enzyme function. Axonal degenerative changes, especially in neuronal cell bodies, were recorded in Pb-poisoned freshwater snails (Viviparus ater), leading to altered protein synthesis (Fantin et al. 1985)1 Mallards dosed orally with Pb shot developed demyelinating lesions in vagal, branchial, and sciatic nerves, and,, showed vascular damage in the cerebellum; lesions were similar to those in Pb-Intoxicated guinea pigs (Cavia sp.), rats, and guinea hens, Gallos sp, (Hunter and Wobeser 1980). Crop stasis in birds, which is characterized by paralysis of the alimentary tract, Impaction of food in the gizzard and proventricuius, and regurgitation of crop fluid, has been produced by Pb shot or Pb acetate solutions, lead induces crop dysfunction by acting either directly on the smooth muscle or on associated nerve plexuses of crop tissue, depending on the route of administration (Clemens et al. 1975; Boyer et al. 1985; Boyer and Di Stefano 1985). Mammals, including humans, undergo similar alimentary distress following Intakes of lead (Boyer et al. 1985). Effects of Pb on the nervous system are both structural and functional, involving the cerebellum, spinal cord, and motor and sensory nerves; the result may be deterioration of intellectual, sensory, neuromuscular, and psychological functions (Nraigu 1978b). The pathogenesis of Pb-induced injury to the nervous system is poorly understood, but may be mediated through vascular damage, the direct action of Pb on neurons, or alterations in porphyrin metabolism (Hunter and Wobeser 1980). Retarded brain growth in prenatal guinea pigs has been recorded at subclinical levels of Pb (i.e., at concentrations producing no elevation in blood Pb and no change in body weight), and this effect Is potentiated at temperatures of 42 C (Edwards and Beatson 1984). Lead may cause a transient disturbance in the blood-brain barrier during early postnatal growth of rats. This effect is associated with the presence of hemorrhagic lesions, suggesting focal damage to the vessels as an important event in the pathogenesis of Pb encephalopathy to suckling rats (Sundstrom et al. 1985). Brain histopathology has been recorded in Pb-poisoned chickens (Narbaltz et al. 1985) and cattle (Osweiler and Van Gelder 1978), Brain Pb concentrations are usually among the lowest in body organs, but the brain is one of the main sites of action. During chronic Pb 14 DUP040007956 BACKGROUND CONCENTRATIONS GENERAL Lead concentrations were usually highest in ecosystems nearest Pb mining, smelting, and refining activities; Pb storage battery recycling plants; areas of high vehicular traffic; urban and industrialized areas; sewage and spoil disposal areas; dredging sites; and areas of heavy hunting pressure. In general, Pb does not biomagnify in food chains. Older organisms usually contain the greatest body burdens, and Pb accumulations are greatest in bony tissues. It seems that resources that are now at high risk (i.e., increased mortality, reduced growth, or impaired reproduction) from Pb include the following: migratory waterfowl that congregate at heavily-hunted areas; raptors that eat hunter-wounded game; domestic livestock near smelters, refineries, and recycling plants; wildlife that forage extensively near heavily traveled roads; aquatic life in proximity to mining activities, Pb arsenate pesticides, metal finishing industries, lead alkyl production, and Pb aerosol fallout; and crops and invertebrates growing or living in Pb-contaminated soils. Data on background concentrations in nonbiological and living resources are cited extensively in Bernhard and Zattera (1975), Nriagu (1978a,b), Wong et al. (1978), Branica and Konrad (1980), Jenkins (1980), Eisler (1981), Harrison and Laxen (1981), and Demayo et al. (1982). NONBIOLOGICAL SAMPLES Average Pb concentrations in nonbiological materials worldwide were much higher in sediments (47,000 ug/kg), soils (16,000), and sediment interstitial waters (36) than in atmospheric and other hydrospheric compartments (Table 3). Most of the lead discharged into surface waters is rapidly incorporated into suspended and bottom sediments, and most will ultimately be found in marine sediments (Harrison and Laxen 1981). Sediments now constitute the largest global reservoir of Pb; sediment interstitial waters and soils constitute secondary reservoirs (Table 3). Lead concentrations were elevated in certain nonbiological materials as a result of nonhunting human activities and natural processes (Table 4). In sediments, Pb concentrations ranged from 3 mg/kg in carbonate marls off the Florida coast to more than 11,000 mg/kg at Sorfjord, Norway, the site of massive discharges of Pb-containing industrial and domestic wastes (Nriagu 1978a). Lead contaminates sediments from sources as diverse as steelworks, shipyards, crude oil refineries, cement and ceramic factories, Pb storage 16 DUP040007957 Table 4. Lead concentrations in selected nonbiological materials. Material (units) AIR (ug/m3) Nonurban areas Urban areas Metropolitan areas Rural roads Heavy traffic Near industrial sources RAIN (ug/1) Minnesota 1979 Rural Urban 1983 Rural Urban ATMOSPHERIC DEPOSITION (g/ha) New Jersey Pine Barrens 1978-1979 1980-1982 ICE (ug/1) Greenland 800 BC 1750 1940 1973 SOILS {mg/kg dry weight) Near Pb smelter Missouri British Columbia Concentration9 Reference** 0.1 (0.3 - 2.5) (2 - 10) 6 40 May exceed 1,000 EPA 1980 NRCC 1973 EPA 1980 NRCC 1973 EPA 1980 / 6 29 2 4 350 140 0.001 0.01 0,07 >0.2 128 >1,000 Eisenreieh et al. 1986 Turner et al. 1985 NRCC 1973 Burrows 1981 18 DUP040007958 Table 4. (Continued) Material (units) Concentration3 SOLIDS ENTERING SURFACE WATERS (mg/kg dry weight) Street dust Urban Rural Highway runoff Suspended sediments Settleable solids Sewage sludge Suspended sediments in mineralized areas (1,000-4,000) 440 (3,100-5,800) 16,000 (100-1,400) (1,000-8,000) INTEGRATED STUDY (ug/kg) Tennessee stream Water Dissolved solids Coarse particles Colloidal particles (0.01-0.019) (30-84) (124-653) (62-2,820) SEDIMENTS (mg/kg dry weight) Egypt, Nile River Industrialized area Max. 1,800 Greece Near major industries Several km distant Preindustrial levels Norway Sorfjord Sweden Polluted lake Reference lake USA Chesapeake Bay, 1979-1981 (500-600) 40 10 Max. 11,000 (2,000-2,500) 110 (1-134) Upper Mississippi River Southeastern Missouri, Big River, 1979-1981 13 (0.4-86) Reference*5 -- Harrison and Laxen 1981 Demayo et al. 1982 Fayed and Abd-El-Shafy 1985 Seoul!os 1986 Nriagu 1978a Haux et al. 1986 Di Giulio and Scanlon 1985 Wiener et al. 1984 20 DUP040007959 battery recycling plants, and heavy traffic (Scorn ivfio). Mining activities are also important. High concentrations of Pb were measured in sediments (up to 2,200 mg/kg) and detritus (up to 7,000 mg/kg) of the Big River in southeastern Missouri (Czarneski 1985). The Big River drains what was once the largest Pb-mining district in the world; commercial mining was extensive between the early 1700's and 1972. During this period more than 20,Q metric tons of tailings accumulated within the Big River wate-rsbed as a result of seepage from tailings ponds, from erosion of tailings piles on the banks, and through accidental discharges (Niethammer et al. 1985). In soils, Pb concentrates in organic-rich surface horizons (Hk CC 1973).,. In one instance, only 17 mg of soluble Pb/kg was found in soils 3 days after the addition of 2,784 mg of Pb (as lead nitrate)/kg (NRCC 1973). The estimated residence time of Pb in soils is about 20 years; complete turnover in topsoil is expected every few decades (Nriagu 1978a). In forest litter, however, the mean residence time of Pb is lengthy; estimates range from 220 years (Turner et al. 1985) to more than 500 years (Friedland and Johnson 1985). Lead deposited on roadways is removed in drainage water, and later accumulated in roadside soils (Harrison et al. 1985). Amounts of Pb in roadside soils are increased as a direct result of the combustion of gasoline containing organolead additives. In general, the amounts of Pb were greatest along roads with the highest density of vehicular traffic, and amounts decreased rapidly with increasing distance from the roadway (Harrison and Dyer 1974; Boggess 1977; Chmiel and Harrison 1981; Way and Schroder 1982; Table 4), Elevated levels of Pb in soils also were recorded from the vicinity of storage battery reclamation plants, smelting activities, and mining ana milling operations (Boggess 1977; Burrows 1981; Kisseberth et al. 1984). Fly ash from coal burned in homes or privately hauled from power plants, which contains 100 to 450 mg Pb/kg and is frequently used to reclaim land for the growth of forage and pasture crops and as an alkaline amendment in the reclamation of strip mined areas (Nriagu 1978a), is considered another source of soil Pb. Two additional sources of Pb in soils are municipal sewage sludge and lead-arsenate pesticides (Nriagu 1978a). Sewage sludge, which contains up to 100 mg Pb/kg and is applied as a fertilizer and soil conditioner at the rate of 50 million tons annually, may increase top soil levels by as much as 25 mg Pb/kg. Lead arsenate, a pesticide used to reduce bird hazards near airport runways by controlling earthworm abundance, and also to control pests in fruit orchards, represents another local source of lead contamination to soils. Lead reaches the aquatic environment through industrial and municipal discharges, in atmospheric deposition, from weathering processes in areas of natural Pb mineralization, and in highway runoff (EPA 1980; Harrison and Laxen 1981; Birdsall et al. 1986). Industrial Pb input to aquatic environments is estimated at 10X that introduced by natural weathering processes (Seoul1 os 1986); sewage and aerosols are major sources (Harrison and Laxen 1981). 22 DUP040007960 Table 5. Lead concentrations in field collections of selected species of flora and fauna. Values shown are in mg Pb/kg (ppm) fresh weight (FW), or dry weight (DW). Taxonomic group, organism, tissue, and other variables Concentration9 Reference13 ^ FUNGI, MOSSES, AND LICHENS Fungi, 4 species Near metal smelter Control site Moss. Brachvthecium rivulare Near lead mines Moss. Hvonum cuDressiforme Sweden, museum specimens Year of Collection 1860 1880 1900 1920 1940 1960 1968 Vicinity urban industry 4 DW 2 DW (1,330 - 8,206) DW (18 - 27) DW (20 - 37) DW (40 - 70) DW (22 - 90) DW (15 - 70) DW (65 - 75) DW (70 - 90) DW Max. 11,61.1 DW Lichen. Parmelia baltimorensis Washington, DC 1938 1958 1970 Connecticut, 1971 106 DW 270 DW (950 - 1,371) DW 198 DW ALGAE AND MACROPHYTES Acorns and berries, 4 species Near metal smelter Control site Aquatic macrophytes, whole Nile River, Egypt Indus trialized area 4 DW 3 DW Max. 22 DW Aquatic plants, 7 species From lead shot seeded area Roots Shoots 19 DW 3 DW Beyer et al. 1985 McLean and Jones 1975 Ruhling and Tyler 1968 Goodman and Roberts 1971 Jenkins 1980 Beyer et al. 1985 Fayed and Abd-El-Shafy 1985 Behan et al. 1979 24 DUP040007961 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration3 Reference13 Foliage, 8 species Near metal smelter 21 DW Control site 10 DW Alda. Fucus distichus Distance from Pb deposit 1 km 1 DW 2 km 0.6 DW Alga* Focus vesiculosus Whole, Raritan Bay, New Jersey Water Pb content 0.002 mg/1 8 DW 0,01 mg/1 38 DW Lettuce. Lactuca sativa Pb-contaminated areas 71 FW Uncontaminated areas 0.5 FW Mule deer forage, Colorado, Roadside 1978 59 DW 1979 42 DW Rice. Orvza sativa Grown 10 m from highway Grain 0.2 DW Straw 5.8 DW Grown 230 m from highway Grain 0.2 DW Straw 2.1 DW SDruce. Picea abies. Germany. 1984 Declining spruce forest Litter 416 DW Needles 13 DW Nondeclining stand Litter 213 DW Needles 2 DW Short!eaf pine, Pinus echinata Missouri, leaf Distance from smelter,km 0.8 3,546 (42C1-11,750)I DW 0.8 1.6 497 (101 -1,475) DW 1.6 - 2.4 274 (52 -1,050) DW 2.4 - 3.2 142 (62 - 412) DW 3.2 123 (22 - 661) DW Beyer et al. 1985 Bohn 1979 Seeliger and Edwards. 1977 Demayo et al. 1982 Harrison and Dyer 1984 Ter Haar 1970 Backhaus and Backhaus 1986 Bolter et al. 1973 26 DUP040007962 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration* Foliage Wood Near roadway, UK 1979 Grass Grass seeds Hawthorn. Crataegus spp. Leaves Fruit Control site, UK 1979 Grass Grass seeds Hawthorn Leaves Fruit Grass Near factory 1,000 m distant Growing Dead and litter 1,700 m distant Growing Dead and litter Near Pb smelter, forage Missouri British Columbia Kansas, vegetation Near highway Distant site INVERTEBRATES Limpet, Aomafia digitalis California Near bridges Soft parts Shell Pb-free area Soft parts Shell 4 DW 0.5 DW 63 DW 99 DW 146 DW 4 DW 2 DW 4 DW 4 DW 2 DW (830 - 1,840) 1 (120 - 1,200) 1 (370 * 1,570) i (240 - 420) DW (170 - 1,970) 1 979 FW (100 - 200) FW 11 DW 3 DW 931 DW 108 DW 8 DW 9 DW Reference** Chmiel and Harrison 1981 Edwards and Clay 1977 Burrows 1981 Robel et al. 1981 Graham 1972 28 DUP040007963 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration3 Insects, various species Distance from highway 0-7 meters Sucking Chewing Predatory 13 - 20 meters Sucking Chewing Predatory >20 meters Sucking Chewing Predatory Kansas, 1978 Near roadway Control site Lepidopteran larvae, UK, 1979 Near roadway Control site Earthworm. Lumbricus terrestris Whole, Maryland Distance from highway, meters 3.0 6.1 12.2 24.4 48.8 Eastern tent caterpillar, Maiacosoma americanum Whole, 1978 Near roadway >10 m distant Millipedes, Diplopoda UK, 1979 Near roadway Control site 16 DW 27 DW 31 DW 9 DW 10 DW 20 DW 5 DW 5 DW 6 DW 50 DW 15 DW 118 DW <1 DW 269 DW 113 DW 80 DW 43 DW 52 DW 70 <5.3 D 162 DW 34 DW Reference^ Anderson 1977 Udevltz et al. 1980 Chmlel and Harrison 1981 Gish and Christensen 1973 Beyer and Moore 1980 Chmlel and Harrison 1981 30 DUP040007964 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration3 Near roadway Control site Spiders, Aranea, UK, 1979 Near roadway Control site Tubifield worms Rural streams Urban streams Wood!ice, Isopoda UK, 1979 Near roadway Control site USA Near highway 141 DW 27 DW 560 DW <1 DW 16 DW 367 DW 152 DW 19 DW (380 - 682) DW FISH Spotted wolffish, Anarhichas minor Near Pb mine, Greenland Liver Max. 1.8 FW Muse!e Max. 0.12 FW Coastal marine fishes, USA Liver 5 species (<0.1 - 0.2) FW 20 species (0.2 - 0.4) FW 33 species (0.4 - 0.6) FW 13 species (0.6 - 0.8) FW 6 species (0.8 - 1) FW 5 species (1 - 3) FW Muscle 5 species (0.1 - 0.3) FW 92 species (0.3 - 0.5) FW 51 species (0.5 - 0.7) FW 7 species (0.7 - 1) FW 4 species (1 - 3) FW Whitefish. Coreoonus s d d .. Sweden Liver Polluted lake (6 - 7) DW Reference lake <1 DW Reference1* Chmiel and Harrison 1981 Boggess 1977 Chmiel and Harrison 1981 Beyer and Moore 1980 Bollingberg and Johansen 1979 Hall et al. 1978 Haux et al, 1986 32 DUP040007965 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration Age 2+ Age 3+ Age 4+ Age 5+ 14 DW 16 DW 18 DW 19 DW INTEGRATED STUDIES Great Lakes, Lake Ontario PIankton 4 DW Zooplankton (1 - 5) DW Fish (0.1 - 0.13) FW Marine food chain, Central Pacific Seawater 0.006 FW Phytoplankton 0.05 FW Zooplankton 0.04 FW Carnivores, muse!e Intermediate (anchovy) 0.02 FW Top (tuna) 0.0003 FW Oklahoma pond Water 0.013 FW Sediments Surface 529 DW 12 cm depth 206 DW PIankton 281 DW Benthos 37 DW Mosauitofish. Gambusia so. 11 DW AMPHIBIANS AND REPTILES Amphibians, whole Near metal smelter No species found Control site, 5 species 12 DW Frog. Rapa sp.f tadpole, whole Missouri, tailings pond 4,139 DW Distance downstream from tailings pond 1 km 552 DW 25 km 37 DW Southeastern Missouri, 1981-1982, Big River Bullfroo. Rana catesbeiana. carcass Reference1* Demayo et al. 1982 Flegal 1985 Demayo et al. 1982 Beyer et al. 1985 Gale et al. 1976 34 DUP040007966 Table 5. (Continued) Taxonomic group, organism. tissue, and other variables Concentration* Reference^ Blood Chesapeake Bay, 1974 Normal Abnormal (17%) Wingbone La Crosse, Wisconsin 1976 Mai es Females Immatures Males Females 1977 Mai es Females Immatures Males Femal es Keokuk, Iowa 1976 Males Females Immatures Males Females 1977 Males Females Birds Galveston Bay, Texas, 1980-1981, 3 species, liver (0.059 - 0.064) FW 0.263 FW 18 (6-56) DW 5 (1-20) DW 0.8 (0.1 - 4) DW 1 (0-21) DW 11 (9 - 12) DW 8 (1 - 48) DW 0.8 (<0.1 - 7) DW <0.5 DW 6 (4 - 10) DW 5 (1 - 20) DW 0.5 (0.1 - 2) DW 1 (0.1 - 22) DW 2 (0.2 - 19) DW 4.(1 - 19) DW (0.1 - 0,5) FW Texas Probers with Pb shot in gizzards Bone II FW Feather 4 FW Liver 0.3 FW Probers without Pb shot in gizzards Bone 6 FW Feather 5 FW Dieter et al. 1976 Fleming 1981 King and Cromartie 1986 Hall and Fisher 1985 36 D U P040007967 Table 5, (Continued) Taxonomic group, organism, tissue, and other variables Concentration4 Juveniles 0.11(0.07-0. Peregrine falcon, Falco oerearinis Baltimore, Maryland, Age 7+ Liver 0.8 FW Kidney 1.4 FW Prey organism Rock dove Urban Blood 1 (0.3 - 17) Liver 3 FW . Kidney 9 FW Whole 5 FW Rural Blood <0.1 FW Liver 0.4 FW Kidney 0.5 FW Whole 0.3 FW Common loon. Gayle inffler. Pb poisoned Liver (21 - 39) FW Bald eagle. Haliaeetus 1eucoceohalus Nationwide, 1978 - 1981, found dead, suspected Pb poisoning Liver 28 (11-61) FW Liver Control 0.6 FW Pb-poisoned 21 FW Barn swallow. Hirundo rustica Near Baltimore-Washington Parkway 9 1979 Feather Male 67 (55-82) DW Female 54 (43-68) DW Nestling 2 (2 - 3) DW Carcass Male 5 (4 - 6) DW Female 9 (6 -12) DW Nestling 2 (1 - 2) DW Stomach contents Male 5 DW 38 Reference** De Went et al. 1986 Locke et al . 1982 Reichel et al. 1984 Bagley and Locke 1967 Mulhern et al. 1970 Grue et al. 1984 DUP040007968 Table 5. {Conti Taxonomic group, organism. tissue, and other variables Concentration Reference*5 1972 Georgia 0.1 FW Florida 0.1 FW 1973 South Carolina 0.3 FW Florida 0.2 FW Shot, 1970 Florida 0.1 FW South Carolina Sora rail. Porzana Carolina 0.1 FW Maryland Lead shot in gizzard Liver (0.1 - 17) FW Bone (1 - 127) DW No lead shot in gizzard Liver (<0.01 - 0.08) FW Bone (<0.4 - 42) DW Songbirds, carcass Near metal smelter, 10 species 56 (9 - 240) DW Control site, 9 species 15 (6 - 25) DW Southeastern Missouri, 1981-1982, Big River Green-backed heron, Butorides striatus Liver Upstream from mine site 0.1 (Max. 0.3) FW Downstream 0.5 (Max. 1.5) FW Northern rough-winged swallow, StelaidoDtervx serriDennis Carcass Upstream from mine site 0.5 (Max. 5) FW Downstream 1 (Max. 15) FW European starlino. Sturnus vuloaris Nesting near highway, Maryland Carcass (4 - 10) DW Feathers (7 - 52) DW Stomach contents (84 - 94) DW Control site Carcass Feathers (1 - 3) DW (3 - 14) DW Stomach contents (6 - 7) DW Stendel1 et al. 1980 Beyer et al. 1985 Niethammer et al. 1985 Grue et al. 1986 40 DUP040007969 Table 5. (Continued) Taxonomic group, organism. tissue, and other variables Concentration4 California Merced Sacramento Other Northern pintail, Anas acuta Adult Immature Mottled duck, Anas fulvioula Adult immature Canvasback Adult Immature Redhead, Avthva americana Adult Immature Lesser scaup, Avthva affinis Adult Immature Black duck, Anas rubrioes Adult MAMMALS Field mouse, Apodemus svlvaticus Near abandoned Pb mine Whole body Kidney Liver Bone Brain Muscle Control area Whole body Kidney Liver Bone Brain Muscle IS DM 38 DW 25 DW 7 DW 6 DW 48 DW 40 DW 17 DW 8 DW 26 DW 24 DW 3 DW 2 DW 8 DW (9 - 14} DW (39 - 46) DW (12 - 13) DW (189 - 352) DW (6 - 13) DW (7 - 10) DW 1 DW (9 - 13) DW (5 - 8) DW (11 - 21) DW (3 - 4) DW (5 - 6) DW Reference*1 Roberts et al. 1978 42 DUP040007970 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration3 Reference^ Dog, Canis familiaris Blood Heal thy (0.01 - 0.05) FW Pb-poisoned (0.06 - 0.15) FW Big brown bat, Eptesicus fuscus Whole, minus GI tract and large embryos Males 47 (20-90) FW Females 32 (20-56) FW Guano 61 DW Stomach contents 4 DW Horse, Eouus cabal!us Near smelter, British Columbia Liver 18 FW Kidney 16 FW Bone 88 FW Near Pb smelter (some deaths), California Liver (15 - 222) FW Kidney (14 - 80) FW Blood (0.4 - 0.5) FW Control areas Blood (0.1 - 0.3) FW Bank vole, Clethrionomvs olareolus Whole body Near abandoned Pb mine (16 - 21) DW Control area (2 - 3) DW Chipmunk, Eutamias townsendil Hair Roadside location 235 DW Control area 6 DW Prairie vole, Microtus ochrooaster Illinois, whole body Near heavy traffic 8 DW Control area 3 DW Little brown bat, Mvotis lucifuaus Whole Guano 17 (11-29) FW 65 DW Stomach contents 26 FW Bats, Mvotis spp., Florida 1981-1983 Guano (3 - 6) DW NRCC 1973 Clark 1979 Burrows 1981 Knight and Burau 1973 Jenkins 1980 Roberts et al. 1978 Raymond and Forbes 1975 Getz et al. 1977b Clark 1979 Clark et al. 1986 44 DUP040007971 Table 5. (Continued) Taxonomic group, organism, tissue, and other variables Concentration3 Kidney Liver Brain Feces Roadside locations Brain Liver Kidney Bone Hair Control areas Brain ' Liver Kidney Bone Hair Illinois, 1982 Distance from lead battery reclamation plant 100 m Liver Kidney Bone 1,000 m Liver Kidney Bone Whole, 1978-1979 Near Cu-Zn mine Juveniles Adults Control site Juveniles Adults Raccoon. Procvon lotor Connecticut, Pb-Intoxicated Liver, kidney Commensal rat. Rattus norveoicus Houston, Texas, 1978-1979 Urban 3 DM 1 DW 0.1 DW 7 DW (0.6 - 0.8) DW (0.9 - 3) DW (2 - 8) DW (14 - 52) DW 235 DW 0.1 DW 1 DW 3 DW 5 DW 6 DW 4 FW 13 FW 79 FW 1 FW 3 FW 2 FW 4 FW 5 FW 0.5 FW 0,7 FW >35 FW 46 Reference*3 Jenkins 1980 Kisseberth et al. 1984 Smith and Rongstad 1982 Diters and Nielsen 1978 DUP040007972 Damage to plants with elevated Pb contents is usually negligible, but varies widely among species. Atmospheric Pb may have contributed to the decline of European spruce forests. The mean Pb content of needles and Titter was significantly higher where tree decline was most pronounced than in areas where forests were unaffected (Backhaus and Backhaus 1986). Lead can have deleterious effects on plant growth processes at current Pb levels in urban areas and may similarly affect plants in rural areas in the future (Rolfe and Reinbold 1977). A reduction in yield of corn or soybeans is expected in low-binding capacity soils with Pb levels greater than 200 mg/kg (Rolfe and Reinbold 1977), Hay grown near roadsides may be toxic to horses and cattle (Rolfe and Reinbold 1977). In extreme cases, reforestration has been initiated in areas where forage is so heavily contaminated with Pb that it has become necessary to slaughter domestic livestock because the amounts of Pb in their livers and kidneys became unacceptably high (Edwards and Clay 1977). Typical area reforestration includes removal of contaminated forage by cutting, bailing, and burying native grasses; burning of stubble and litter; and adding of agricultural lime at the rate of 2,244 kg/ha (2,000 pounds/acre) to all soils within 1,525 m (5,000 feet) of sites where Pb levels exceed 175 mg/kg (Edwards and Clay 1977). TERRESTRIAL INVERTEBRATES In earthworms, lead levels were highest in those closest to highways and in areas with high volumes of traffic (Goldsmith and Scanlon 1977; Table 5). Various species of insects and soil invertebrates from roadsides, from areas receiving sewage sludge, and from metal smelter environs also contain high amounts of Pb (Table 5). Amounts of Pb in whole body were higher in earthworms, millipedes, and wood!ice collected from soil and plant litter near highways than away from highways; soil and litter seem to be major reservoirs of Pb in roadside communities (Beyer and Moore 1980). In contrast, Pb concentrations in the eastern tent caterpillar (Maiacosoma americanum) were lower than those reported for roadside soil and litter invertebrates, and were about 76% of that in leaves of its host, the black cherry Prunes serotina (Beyer and Moore 1980). The use of terrestrial invertebrates as sentinel organisms has been suggested for monitoring Pb. The spider Araneus umbricatus, for example, contained Pb body burdens that correlated with that in a lichen (Lecanora conizaeoides) that is currently used to monitor atmospheric Pb (Clausen 1984). Similarly, the woodlouse (Porcellio scaber) seems to reflect Pb 'concentrations in adjacent soil or leaf litter (Hopkin et al. 1986). AQUATIC BIOTA Freshwater algae, invertebrates, and fish had comparatively elevated Pb concentrations when collected near industrialized areas, ponds with high numbers of Pb shot, urban areas, Pb mines, and tailings ponds (Table 5). For 48 Whitefish, Coregonus spp., from Pb-contaminated Swedish lakes, showed depressed blood ALAD and blood chemistry derangement when compared to fish from a reference lake--suggesting that Pb affects natural populations of fish in a manner similar to that observed in laboratory studies (Haux et al. 1986). The significance of organolead residues in aquatic life is unknown, and merits additional research. In Ontario, Canada, about 16% of all fish sampled contained tetraalkyl1ead compounds, although none were recorded in water, vegetation, or sediments from the collection sites (Chau et al. 1980). Tetramethyllead reportedly was produced from biological and chemical methyl ation of several inorganic and organic Pb compounds in the aquatic environment, and has been detected at low concentrations in marine mussels, lobsters, and bony fishes (Wong et al. 1981). AMPHIBIANS AND REPTILES Tadpoles of bull frogs (Rana catesbeiana) and green frogs (R. cl ami tans) from drainages along highways with different daily average traffic volumes (4,272 to 108,800 vehicles per day) contained elevated amounts of Pb (up to 270 mg/kg dry weight), which were positively correlated with Pb in sediments and with average daily traffic volume. Lead in tadpoles living near highways may contribute to the Pb levels reported in wildlife that eat tadpoles. Diets with amounts of Pb similar to those in tadpoles collected near heavily traveled highways have caused adverse physiological and reproductive effects in some species of birds and mammals (Birdsall et al. 1986)., Elevated Pb concentrations also were recorded in various species of amphibians and reptiles collected near Pb smelters and mines (Table 5). BIRDS In general, Pb concentrations were highest in birds from urban locations (perhaps reflecting greater exposure to automotive and industrial contamination) and in birds near Pb mining and smelting facilities. Lead residues also are greatest in older birds (especially in bone, because of accumulation over time), in sexually mature females, and in waterfowl that have Ingested Pb shot pellets (Table 5). Continued deposition of Pb shot by hunters into wetlands habitats exposes birds to lead. Lead shot is a substantial localized source of contamination, especially in prime waterfowl habitat (Bellrose 1951, 1959; NRCC 1973; White and Stendell 1977; Stendell et al. 1979; Wobeser 1981; Clausen et al. 1982; Longcore et al. 1982; Mudge 1983; Driver and Kendall 1984; Hall and Fisher 1985). Several million hunters are estimated to deposit more than 6,000 metric tons of Pb shot annually into lakes, marshes, and estuaries; this represents about 6,440 pellets per bird bagged. Shot densities as great as 860,000 pellets/ha (2,124,000/acre) have been estimated in some locations (Wobeser 1981), although concentrations of 34,000 to 140,000/ha are more 50 DUP040007974 (Kirby et al, 1983). Lead in seeds and invertebrates within rights-of-way of major highways probably is not a hazard to adult ground-foraging songbirds, as judged from experiments with the European starling (Sturnus vulgaris). However, the effects of Pb on survival of fledglings are unknown, although Pb causes reductions in blood hemoglobin, hematocrit, ALAD activity, and brain weight (Grue et al. 1986). In another study, Pb concentrations in feather, carcass, and stomach contents of adult and nestling barn swallows (Hi rondo rustical were greater near a major U.S. highway than in a rural area; however, the number of eggs and nestlings, the body weight of nestlings at 17 days of age, and body weights of adults were similar in the two colonies, suggesting that contamination of roadsides with Pb from automobile emissions is not a major hazard to birds that feed on flying invertebrates (Grue et al. 1984). Signs of Pb poisoning, i.e., depressed blood ALAD activity or elevated blood Pb levels, were reported for birds near a metal smelter (Beyer et al. 1985), in 17% of canvasbacks from Chesapeake Bay in 1974 (Dieter et al. 1976), and in three species of waders from the Dutch Wadden Sea living in an urban postnuptial moulting area (Goede and de Voogt 1985). The decline in submerged aquatic vegetation in Chesapeake Bay and the later shift in diet of some waterfowl species of Chesapeake Bay from the vegetation (Pb content 2.2 to 18.9 mg/kg dry weight), to the softshell clam Mya arenaria (1.3 to 7.6 mg Pb/kg dry weight), or to other bivalve molluscs (0.8 to 20,4 mg Pb/kg dry weight), probably did not increase dietary Pb burdens in these species (Di Guilio and Scanlon 1985). The significance of trace amounts of organolead residues in birds is unknown. Trialkyllead seems to concentrate in avian kidney, but contributes less than 5% of the total amount of Pb in kidneys (Johnson et al. 1982). MAMMALS The highest body burdens of Pb reported in mammals were near urban areas of dense vehicular traffic, near metal mines and smelters, or near plants that reclaimed storage batteries; concentrations were higher in older organisms, especially in bone and hematopoietic tissues (Table 5; Goldsmith and Scanlon 1977; Way and Schroder 1982). A similar pattern of Pb occurrence and distribution was evident for human populations (Barth et al. 1973). Diet provides the major pathway for Pb exposure, and amounts in bone are indicative of estimated Pb exposure and metabolism (Chmiel and Harrison 1981). Amounts of whole body Pb and feeding habits of roadside rodents were correlated: body burdens were highest in insectivores such as shrews; intermediate in herbivores, and lowest in granivores (Boggess 1977; Getz et al. 1977c). Food chain biomagnification of Pb, although uncommon in terrestrial communities, may be important for carnivorous marine mammals, such as the California sea lion (Zalophus californianus); accumulations were 52 DUP040007975 The interaction effects of Pb components in smelter emissions with other components, such as zinc, cadmium, and arsenic, are unresolved (EPA 1972), and warrant additional research. 54 DUP040007976 TERRESTRIAL PLANTS AND INVERTEBRATES Fruits and vegetables acquire Pb by surface deposition from rainfall, dust, and soil, and by biological uptake through the root system (EPA 1980). Foliar absorption of Pb and transport to the root could account for a significant portion of the Pb in root tissues; however, this transport process varies widely among species. Dollard (1986) showed that this pathway accounted for 35% of the root Pb content in the radish (Raphanus sativus), but for <3% in carrots (Daucus carota) and beans (Phased us vulgaris). Corn (Zea mays) contained 30 mg Pb/kg dry weight when grown in soils containing Pb concentrations of 924 mg/kg, but only 17 mg/kg when grown in soils containing 786 mg Pb/kg. Sadiq (1985) concluded that contamination of soils with up to 800 mg Pb/kg probably does not elevate concentrations of Pb in corn plants. Within any plant species, however, there are Pb-resistant and Pb-sensitive breeds; some genetically fixed resistant species grow in soils containing up to 10,000 mg Pb/kg (HOll and Hampp 1975). PI ants readily accumulate Pb from soils of low pH or low organic content; however, uptake is significantly reduced after the application of lime or phosphate, which converts Pb to hydroxides, carbonates, or phosphates of relatively low solubility (Demayo et al. 1982). Lead persists for lengthy periods in forest litter; the estimated Tb 1/2 is 220 years (Turner et al. 1985). Lead seems to be tightly bound by most soils, and substantial amounts must accumulate before it affects the growth of higher plants (Boggess 1977). Although Pb is preferentially bound in soils by organics and oxides, interaction kinetics of Pb with other metals are complex and largely unknown (Bjerre and Schierup 1985). For example, uptake of Pb from soils by oat seeds (Avina sativa) was inhibited by cadmium salts, and reduced in loamy or organic soils; further, Pb in soils interfered with manganese uptake, and also increased the availability of cadmium and other heavy metals (Bjerre and Schierup 1985). Lead inhibits plant growth, reduces photosynthesis, and reduces mitosis and water absorption (Demayo et al. 1982). Inhibition of photosynthesis is attributed to the blocking of protein sulfhydryl groups and to changes in phosphate 1evels in living cells (Holl and Hampp 1975). For two species of roadside weeds (Cassia spp.), pollen germination was reduced by 90% and seed germination by 87% at Pb levels of about 500 mg/kg dry weight in soil and about 300 mg/kg dry weight in foliage (Krishnayya and Bedi 1986). Normal germination rates were recorded at Pb levels of 46 mg/kg in soil and 22 mg/kg dry weight in foliage; however, some adverse effects were evident at Pb levels of 12 to 312 mg/kg in soil, and 55 to 97 mg/kg dry weight in foliage (Krishnayya and Bedi 1986). Tetraethyllead from automobile exhaust fumes is known to react in the l ight to produce the highly phytotoxic triethyl lead cation (Backhaus and Backhaus 1986), which can freely permeate the plasma membranes of plant cells (Stournaras et al. 1984). Growth of cultures of soybean (Glycine max) cells exposed to 207 ug Pb/1 (as triethyl!ead salts) was inhibited before the cells died (Stournaras et al. 1984). There is no 56 DUP040007977 MATC L ife tim e Table 6. Lethal and sublethal e ffe c ts o f lead to selected species o f aquatic organisms. Uo0) sz 0> cc JQ P U 4O-) 4U4 o> c s- o 3 *<A p b id Q-S-. X3 LU "O pH iH CM CM pj ro JJppo0CVoaVVrCC>-)>)).' JJppGsvVVooCrC~)))s cl oooCcrMvr% OuCO. ootCoM OUCO. EOV) lCOM* * 4O**p0fCr--f*-.OCm0Mft UOCO-jtGc* UOCO- 4Qp* *Xx*pCCoprfrp*:)*i rPxpi(--d1z) Jp*Pp--rcoiNO--O*rd--*1 VJ v> V) V) V) >> >, s~ s- 5- <A m* <d id 3 3 .3 >> "O "P o O Q rd .JC xz -G "O CO 00 cSJ CSJ ro ro CO CM LO ro sOPai %IDa sVr-OaH fk A ^ 1+.sE5ina*TM"--=ujj '*S+arfcSsar--t_-)jfSa4cfs!aS--rl>"_*:j >tu X40?ooaSt-i3t>)I-n T*O4>o3oSkaap33>_A)"i X-O+>3aoUarai--SJ->Iia V) V) V) >>>> id rd rd -a *3 "D 0HJ1H rH r--1 <M 16.7 p Id SU.r-- *"% <P'N.S C XJ 3 P *oCi Ou. F- c end) 3S O*--* 3 JO O rd o> *s*-- a <>d sOr-- <i1-3 G -C XO Po rd P "cO f* rd S CL) ~ PV>>) *v0--)i V) O O 0) o a. LU vi LO o ooo LD -o o in CM o 1--1 XO O -H CO ooco rd v> P >t 3 JZ &- CO rd *3G O TJ i. s~ rd rd crd O a<d CD id p* oo WCO oa. P v> id id 0c) Q ">3O G CD V) .J3rCd O QIi OIi *C3 rd iCnsl Of E X<cJ9 a) a! JC CO tolo * L> * 'SZ <cdn Qid iod> rod* *1-- Ol ois: o 3 ** * S- rd CD CrdD rCdD rd p rsd- -p50Q*) "O "O "O S -- *r-- rr- <y C CC P j ac.-pc. -ac.3r id r-- y^ r- S- CP < << t<-- r<-^ o aCD id rd rd >q go UJ OS LL. 58 DUP040007978 Table 6, (Continued) o 03 U c 03 s. 03 tt03 oo j ci o 03 UJ in m io o o in (A > o o & <0 o 000 s0s 0. 0 m 1 o 0inI 0inI 0in13sa)- mo11ton Oin Om 11 OO CM Om (1> 3 O .3 Of) 4-4 0 to CL SX3 LU "O co <TJ 544 p--- #-S <1> -Q 3 OC Q- ID!0O p3> 03 (A t3 O 1--4 ddd (A S- &- S- d S- 01 3 3 .3 > 3 >> O O O <0 O <15 -C JC JS "O -C O "O 4-> 00 oo co 10 tr 0 -< 00 LO O00 Oo Oo Oo OoOoOo CM c m m 0 0 o m o CO r-4 1^ co *r r--I lO OJ c3OnJCiD-3o> r 5O 0) C -C O -M XO 4(O->"3 * 03 ** + d d a> 5S r dO 0 03 O a. Ui d u 03 > si <0 <u 10 o<u 03 ez +* to r* rtf > 0C0L in <0V) 3 -4-* V) d ntf cS- M :m 4-> C j z (Otf P+> > so * o c m Q> JQ f-- oa to-- ! O<u (A s-O* d p-- Q- *:>: P _ X> M *? coc Q. S~ -C -r- !- rd -O r* O 03 r-- T7 (a e s: O- P <0 3 Ord 0c0 <eC/> <cr dd s- s33 PO jC jC 00 CO ^ wf oo o0 oo #1 ft o 01 CO K CO <A s3 O JS CM K in to xX<cui- t. (0 D1 6 E <9 E CO J3 a) a. s_ r D) +> r-- S3 >i*-i OS- m J4c-Su -+Ca _ E an '3s tis 'f~ O i- (I) JO 4- * = O r- J--* nj a: 60 DUP040007979 Table 6. (Continued) o epu s- CO ioiAiDiA min ipmmm to p 4a>- a: , -a 4- P 0u w0} 4- S p to 4-3 .c i-- S. <0 +3 O r- -r-- to 4- P -o 4-> >, p EM O 4-3 r-- 4-3 S- O P (0 JQ -- o s_ 4- P P 44P QC.-Jt'--o-JE--OS- TJ .<= i--- OP3- c r-^ 3 <0 P 4- P >e> 4-> P nj *s--<c=n o o om m oo j Q flJ O fc o oixua -a i +a 3 Ctf -G C T* a> j c >> o <2 i i >- * w-- UO I ' S* (0 ; o) u 0 O 0 01 S- 4-3 4- > <Z< 01 G uo 3 *A +> om Q. i- X3 UJ "O V) 0 0 0 p E *r-- to V* P P s- J- I 3 3 -r- -r- 01 01 .G E EU f afMB G.JS JC + > -P 4-> ecc oi E r^ VI JtO S- s33 4- O O 4- 44 P+j Q oo 4- P -CjC P P 0) E EEE 01 -C JC 4- 4-4- 4-<+. 4- tO tO *r-- >r- " *r- CT> Ol 01O) r* * -J o> o --1 _J JJH i--1 rH .r--l CM CM 10 4-3 "V. 3 P O- -rO XJ ts end) ~ M0) CLr-- 3-Q O <9 $ *r" o> r- E Sop C JE 0 4-3 X 0 P 4- 3 6- Te103 01 ~ 4-> <A to a> >>*r" 1A U O 01 U CL UJ SO so cf to O CO SO H O' so SO CM CM CO I om 00 o o* CM l SO * CO in co 9 .*.* * o co N so c m o -h in JO -Q j O 0.0.0. > 4? S-.4- O T3 T3 jq p p p "' " > > f-- r-- 44 <S 0 . r-- o o o <0 VI M V) 4-> t/1 t/1 VI I 4-> P (/> O t- -f -- *-- s- o toco O O Q 00 a. a. co co to cm cm CO <0 CO 4-3 4= 3 3Cl rococo S- u to CM to 4-3 > CO CO p_ ^ rtJ n> c 62 Water hardness 44 Total Pb 58 - 119 3 generations MATO 3,5,18 DUP040007980 Reference E ffe c t cn cri to LO to >> D> *<00*0 0 p -4r->. C nj i < c O 0.0 --J *rO .*4 C J-- <t O o oooo CM CM CM CM 44 3. 0*0 s- o cn C -Q ' O 4O0-) *Co4f-c(p/?) 4o- x<0 o6 i0ni0ni0n 0XP3 JOC OI Oi O1 Oo iori> iooi co "-(l3MO0- to j4s4 GOE cS3o* tc><3o0> tcn t**o ge> 4r-> *PP_l 4sOC31Otcn V) <0 x) 3.Iso3f!-l4Ms3oS- XMs3o:- 4t3Soo1- 4VC3o1O oo tcoh t0ot VcrO> clOn VoO> Exposure Concentration Ecosystem, taxonomic group, >s. e JO 3 Cl . -i- cn ao) 3E CO P 3<0 i-- i<*0. > - P o C nj v> p o p o. to . CM o^> oo fH CO CM CO 00 <O O CO CO LO CM LO O 3</} c CO CO o oo<0 oo<0 o C3 CO <J cn-*s s C o r- o C X o >S*>U<0 P<0 co p-- 0) CM lO JC o C +cJ oo co toU ooCO U <0 CO o a*; cP pfP w 00 -o <0 Pc CcOn 0.1 XJ Q. s<0- 00 O) -Q 4P-i XI co 3 s- PV<0- r*^r--- 4S G V) 44 P 4= 5- -r- "O V) C *1-0 ip-sp-ato ip. o3 -44 q _O fc. p Pcn e s- CP -I- XJ XP (UP r- U -*- T~ 4-> (0 P CO i-- U 0LL Ou &. r-- >> O --5- ZX S- <0 0 *P O S O .6 CJ co v> ooco ooo oocn CM 00 LO C\JH W A *0 oo LO ooo co o CO P E O sP-l to p CO 34= oo <0 QO P E cn >>- E S- Q. w 4-- co I CO '> MOJO) 4s-- ccn noso oC"cO r** C S- dr*" 3 *P *0 3 S- C E-C I P to S do 3 5- 0 r** C 0)0POO 3* cn p c m co CO U- UJ --pC> 3P: (0 LU -as 64 Algae and macrophytes DUP040007981 0 0; BCF 1 0; BCF 2 aat a cat uat <a*-t ac JO +> uat aot st o u - 09 O VO 3 *- V) 44 CD O rtf CL S- X3 rd LU "O h- rt> co co co ro CM 04 CM CM in M3 CM CM r** r*. r>. r>. CM CM CM CSI 00 00 cm cm 00 00 CM CM CO CO CO CM CM CM UO l o O S- -4j i <r> n CM O --I i- p CMr-* ,rH M-- 10 <0 t3 O. Ob LULL. U_OC O - Oo CD uu CO CQ Oeo 0in0 <0 <4-+>. P>* *0 4- >> o c m at </> IX) V) o in o in o IX) o IX) oin i--i -cto s- CM J. i i I Li. *i-- O U. P o o <_> <_) O O X0 4- 0 4- _j m 00 00 a r-l pv IX) 00 IP CO MMC) CM Uuoa- yL0Ql_uLClQuU03. c_ h<- c .c op *r-- iJ +X uu 33 0X1 oo s- s- Sa)- a> TaJ> "a0i r" *r* -C J,CS HH HH oo IcX_ >I) IX) o--i 1 m m in Oji Pji?goi ti) co v) - v) c/i S, i- i, Jl S- o 3 3 3 3 3 >> P P P P P (0 J=X= J= J=x=-p CO CO co to CO ro 0)0)0) O) 0) CO (0 > "0 o in f4 vi u v i ia >,>,>>>) p p-p-OTJ CM CM 10- Pv 0- Wf t-H P r-- 4-> /-- --1 V) V) >> >> rtf rtf Xf "O CO CO CM CM <0 V) i- s33 PP J=x= co co O) CD co oo <n S- S* 3 33 ooo x:.- vo VO VO oi o> cn 10 +SJ-I JD =f CSL *ru T? c a> ai oo 3 s . va>t Q3.J<--3 O (0 t- -ro> S~ u ><0 is C -C X oO 4- as + *t3 c E- rtf fl> a V) V) 0) >>*" v u CD U QLU </> CO o o o o o N O O N 0h 0- i--1 IX) CM H -Q at x CL Xa.I <0 -Q CL r-- > a. >-- S<0- r-- .r>--V*-C> X->T "-+x>=j |XP*; P<E0 +) p + P S. SL4- CM ci-- *-- + * +XM Abl-PPA Q. (-- 1TM HTM O. o o m + CM JQ Cu CO oo H pH 1 oo oo ooo CM O o o o o o rtf l>M 4- r^H t- O co 00 pH rtf 4-> CO o I-'- IX) 00 IX) i--r ' t~~ C co CD *T3 O a> u rtf ao ua rtf I3E1, O-> rtf V) 50) o P o </> C 6 a) Q o _o rtf sr- (A 3 o -O Of o Q- . c a. U+i+JOONW-r <c r- L rtf *-H r-H CM CM tfl 4-i >irr f?---- 0Q. J0U) 5 ! I 3 X> S_ rtJ O -G >, U a> a. > in o o in o ^ P -l-> PEOOU)J * <0T r-4 CM CL-H CM f* P V> 4- Of H H*0 -H 3c E "SM <- Oh t * -cro 0) X) S- J- 4- CO V) cdl C S~ CL>-- I-- o >> ja| rtf <n -- OO OO 66 DUP040007982 u o= s<u- 4- Of X Po 44LxJ l*aoo> oc 3 E S- O 3 -i- tO V) P O rtf <X) at. X3 LU T3 Ca rtf pS--">r--*. e cCu Oa *3r-- Oer av-a OO s3-- E * Va>> 30.1--Q o S- r* o> O Sr>t-j p-- & S- o a> cj z O 4J +x<o-o3 c * rtf S0) * -VP) v<>u >>*i-- CO U o a> o a. UJ CO o in co 3 0 iOOl in --1 CO 3CO 3 oo xu uo Sr- -CP) sgu0e) xr - c fclp O - -- >P i-- C > S%- p 3S <n 3u p er rtf - O >JC O P *- P W C V* XVtl OX --J O r-> C O CD C * P * O 1# +r>tf 4-- -o-- S- 4~ T3 P SS --. p CO 3 p Pu 3> P vi Crtf S* .P.. EOCD X -- o cor o at -- c P p S-0 0 3 3 in p -a o a. o a. S- X P Q- p -o -pi-- S -P C 3 v O EV cOO CD XP 2E cO CD 0P p .c II P P 3S s- O S- 3 P <D 1--P- p -C gC :C 4- P P 4- -- C ID *o t.oa a> 0 0 3 PP p* O P P JO o in p 4- p S. "O -C O 3 c C Ot-O CD p* O p P XT P CO P E CO ID e S. PPtf c e c cd 3 pc .* P *r-- c -a .- u xi O C C3 a. P-r- Otf O pO i-- p S- P t- <s Ow o a P 3 o II 03 3 p O U. O S P V) UK CM < CO c JO 2E S-P P > A t tfk a> o ** ovco c j iHrtM CM Is 0 A ,4 ch <0 t^.O) to ** S CO Is* l*s, co co a) n qi o) ts a> O q> ^ o> ti iH rH r-- ,k e io bn o r- da n > c d -i- i r~. -I--< CD 3 NO) in J_ +J r-- r-l 00 _J 3 Ok J JC P P p *o P J= 4)30 CCD M e2 p o ~ > C P CD to -X r-- CVI XI p j c p o -a o rr i-- --x: Q.-Q tf- tf ID o -aa r^. c *r>co i o> O r- CD c M -H f"* . | |WM. oven C 3 CD - i~ OOO HIM V) oo p 1O C0 ao - id o> v i-- a> 00 C P p -03 p c d xr x: c m i at HOONN ON 1-- P m . o -- 3 t00 P - CD -C CO CD CO -l- p -r f H N CD ID 3 pC <c * -- - a. p - c m uj ecoor-Ntf C CD 00 X r-- - p CD > -- 3 CO g P -f-- CD a> cc h* <o -- J_ r-- < CD CO O O- --Pr -- 00 CO UJ P CD Ok P CM - CM r-i -- -- (-- 00 co - w - CDP CO tf1 r-- -- C 00 P CO co o .--ok ok NXIOfH P P Ok K C P -Ok iS CSI r--c r-- S- O P CD CD o oe 04 .--p-- 4J o -- tzo S-p p 00 -Ok sC IN N P P CO CM P - -- s. x: x> -- 00 CDCM C r--l D-- ID ID 3 00 Ok O *- CD P S- -r- O O XT P U. > 00 tA * --Ok *f-- r- p -O Op xr p c m as Ok P r-- p -- . -- S-- -- = -- lO 00 CO P 00 P CM CD CO Ok >> -- C CD ---r -- p O P -- l-- N 3i in p t>. > 00 C Ok -- i--- Ok 3 p id io pa. S- O --p -o C CM JC S P 00 Ok -X lD S- CD C 3 O -- P !- S- O UJ 4- P JJ (S3 CEEU OC p 0 3 Do u- oc x s: c m 68 DUP040007983 stippling of erythrocytes; elevated Pb concentrations in blood, bone, gill, liver, and kidney; muscular atrophy; paralysis; renal pathology; growth inhibition; retardation of sexual maturity; altered blood chemistry; testicular and ovarian histopathology; and death (Aronson 1971; NRCC 1973; Adams 1975; Davies et al. 1976; Holcombe et al. 1976; Hodson et alt 1977,, 1980, 1982; Johansson-Sjobeck and Larsson 1979; Reichert et al. 1979; Ozoh 1980; Demayo et al 1982; Kumar and Pant 1984; Rai and Qayyum 1984; Hodson and Spry 1985; Haux et al. 1986). The prevalence of signs is closely correlated with duration of exposure to Pb and to its uptake (Hodson et al 1982). Toxic effects of Pb uptake in fishes are increased under conditions favoring their rapid growth. Hodson et al. (1982) have shown that the rate of intoxication by Pb--as judged by uptake rates into tissues and incidence and prevalence of black tail--did not increase with fish size, but rather with growth rate. Rooted aquatic pi ants, such as wild rice (Zizania aquatica) , can accumulate up to 67 mg Pb/kg dry weight when cultured in tanks contaminated with high concentrations of powdered Pb (equivalent to 7,400 kg Pb/ha); however, this level is not considered hazardous to waterfowl feeding on wild rice (Behan et al. 1979). Lead content in plants collected from heavily hunted areas near refuges did not differ from those collected in the protected areas (Behan et al. 1979), which suggests that Pb bioavailability to rooted aquatics is substantially lower from shot than from powdered Pb. In another study with rooted macrophytes, Navicula sp. and nodea canadensis rapidly accumulated Pb from solutions containing 1.0 mg Pb1"*/T, 1.e., 70 mg Pb/kg dry weight per minute; the process was overwhelmingly passive (Everard and Denny 1985). Depuration was rapid; 90% of the Pb sorbed during the first hour by shoots of El odea was released within 14 days after transfer to clean water, though 10% seemed to be irreversibly bound (Everard and Denny 1985). High accumulations of Pb from ambient seawater by marine plants is well documented; concentration factors vary from 13,000 to 82,000 for algae from Raritan Bay, New Jersey (Seeliger and Edwards 1977), and from 1,200 to 26,000 for algae from Sorfjorden, Norway (Melhuus et al. 1978). Studies on the kinetics of lead uptake and retention in two species of marine algae (Phaeodactylum tricornutum. Piatymonas subcordiformes) showed that both species accumulated Pb from the medium at ambient concentrations of 20 ug/1, and higher (Schulz-Baldes and Lewin 1976). In the first phase, usually completed within minutes after addition of Pb, cells of Phaeodactylum became saturated when the Pb reached a remarkable 11,640 mg/kg dry weight. In the second phase, the lead content of PI atymonas continued to rise slowly, but that of Phaeodactylum declined after 2 or 3 days. In both species the content of bound Pb increased with increasing exposure time, suggesting that during prolonged exposure Pb is initially adsorbed to the cell surface, then translocated into the cell wall, the plasma membrane, and eventually the cytoplasm (Schulz-Baldes and Lewin 1976). Sediments are not only sinks for Pb but may act as a source of Pb to aquatic biota after contamination from the original source has subsided 70 to the guppy. Thus, in organisms held for 28 days in solutions containing 5 ug Pb/1, Pb content was 460 mg/kg dry weight in the alga, 23 mg/kg in the grazing daphnids, and 4 to 16 mg/kg in the guppies that fed on the daphnids (Vighi 1981). Concentrations of Pb in the freshwater snail, Lytnnaea peregra, collected near an abandoned Pb mine were positively correlated with the Pb content in its diet; the digestive glands contained up to 5,600 mg/kg dry weight (Everard and Denny 1984). The gut contents of eels (Anguilla anguilla) grazing on contaminated snails contained up to 4,350 mg Pb/kg, but the Pb was rapidly released; feces from both snails and eels return the Pb to the ecosystem as particulates and detritus (Everard and Denny 1984). As discussed earlier, Pb clearly inhibits the formation of heme at several points, adversely affects blood chemistry, and accumulates in hematopoietic organs of aquatic organisms. In addition, Pb interferes with chlorophyll formation in pi ants by inhibiting the conversion of coproporphyrinogen to proporphyrinogen by competing with iron, inhibits allantoise formation in annelids, inhibits alpha-glycerophosphate dehydrogenase activity in trout, increases glutamic oxalacetate transaminase activity in Daphnia, affects neural and hormonal systems that control activity and metabolic rates in fish, interacts with polar sites of glycoproteins in epidermal mucus of fish, and may inhibit vitamin C and tryptophan metabolism (Wong et al. 1978). Some populations of freshwater isopods are tolerant to Pb. Inasmuch as nontolerant isopods from an unpolluted site can be made tolerant by exposure to low levels, it is suggested that naturally occurring tolerance may be achieved by acclimatization (Fraser 1980). Research is needed on Pb transformation mechanisms, on toxic forms of Pb and interaction effects with other compounds, and on effects of Pb-contaminated sediments on benthos (Wong et al. 1978). AMPHIBIANS AND REPTILES Lead poisoning in adult leopard frogs (Rana pipiens) is indicated by a series of signs: sloughing of integument; sluggishness; decreased muscle tone; decreases in red blood cells, white blood cells, neutrophils, and monocytes; erosion of the gastric mucosa; and (before death) excitement, salivation, and muscular twitching. The 30-day LC-50 value for R. pipiens was 105 mg Pb/1, but some deaths and elevated liver residues were noted at water concentrations as low as 25 mg/1 (Kaplan et al. 1967). In soft water (99 mg CaC0^/l), some marbled salamanders (Amb.ystoma opacum) exposed to 1.4 mg Pb/1 died5 in 8 days (EPA 1985). At about 1.0 mg/1, Pb blocked synaptic transmission by competitive inhibition of calcium in the bullfrog, Rana catesbeiana (Kober and Cooper 1976). At 0.5 mg Pb/1, tadpoles of Rana utrlcularia required additional time to metamorphose; and at 1.5 mg Pb/1, thyroid histopathology was recorded and the delay in metamorphosis was more pronounced (Yeung 1978). 72 DUP040007985 from ingestion of Pb shot in food items (Custer et al. 1984). Some raptors ingest many shot in a short time. For example, the stomach of a bald eagle suspected of dying from Pb poisoning contained 75 shot (Jacobson et al. 1977). Results of experimental Pb shot poisoning of bald eagles (Table 7) confirmed results of nationwide monitoring showing that 5.4% of all dead/ eagles found in 1974-1975 died of Pb poisoning, as evidenced by liver Pb levels of 23 to 38 mg/kg fresh weight (Pattee et al. 1981). Ingestion of food containing biologically incorporated Pb, although contributing to the Pb burden of carnivorous birds, is unlikely in itself to cause clinical Pb poisoning (Custer et al. 1984). A similar case is made for powdered Pb / (Franson et al. 1983), and forms of Pb other than shot (Table 7); the strong indication is that the form in which Pb is ingested is crucial. Signs of Pb poisoning in birds have been extensively documented (Bellrose 1951, 1959; Jordan and Bell rose 1951; Clemens et al. 1975; Forbes and Sanderson 1978; Hunter and Wobeser 1980; Pattee et al. 1981; Wobeser 1981; Franson and Custer 1982; Johnson et al. 1982; Eastin et al. 1983; Kendall and Scanlon 1983; Street 1983; Di Giulio and Scanlon 1984; Fimreite 1984; Gjerstad and Hanssen 1984; Hudson et al. 1984; Anderson and Havera 1985; Burger and Gochfeld 1985; Carlson and Nielsen 1985; Friend 1985; Hoffman et al. 1985a; Lumeij 1985; Beyer et al. 1988). Outwardly, Pb-poisoned birds show the following signs: loss of appetite, lethargy, weakness, emaciation, tremors, drooped wings, green liquid feces, and impaired locomotion, balance, and depth perception. Internally, Pb-poisoned birds show microscopic lesions of the proventricular epithelium, pectoral muscles, brain, proximal tubular epithelium of the kidney, and bone medul1 ary osteocytes; an enlarged bile-filled gall bladder; anemia; elevated protoporphyrin IX levels in blood; decreased ALAD activity levels in blood, brain, and liver; reduced brain weight; abnormal skeletal development; cephalic edema; and esophageal impaction. Postmortem examination of Pb-poisoned birds may show edematous lungs; serous fluid in the pleural cavity; bile regurgitation; abnormal gizzard lining; a usually pale, emaciated, and dehydrated carcass; and elevated Pb levels in liver (>2 mg/kg fresh weight, >10 mg/kg dry weight), kidney (>6 mg/kg dry weight), and blood (> 0.2 mg/1). Toxic and sublethal effects of Pb and its compounds on birds held under controlled conditions vary widely with species, with age and sex, and with form and dose of administered Pb (Table 7). Several generalizations are possible: decreased blood ALAD and increased protoporphyrin IX activity levels are useful early indicators of Pb exposure; Pb shot and certain organolead compounds are the most toxic forms of Pb; nestlings are more sensitive than older stages; and tissue Pb concentrations and pathology both increase in birds given multiple doses over extended periods (Table 7). 74 DUP040007986 Table 7. (Continued) Species, route of administration, dose, and other variables Effects Reference3 Single oral dose of shot Single oral dose of tetraethyllead Fed diets containing 25 mg Pb/kg, as lead nitrate, for 12 weeks Fed diets containing. 100 mg Pb*7kg Fed diets containing metallic Pb for 42 days 100 mg/kg diet dry weight Dosed birds recaptured in significantly greater numbers than controls. LD-50 of 107 mg/kg BW. Signs of intoxication included excessive drinking, regur gitation, hypoactivity, muscular incoordination, fluffed feathers, eyelid drooping, tremors, and loss of appetite. Regur gitation within 7 minutes, other signs as soon as 20 minutes, and death usually between 1 and 4 days posttreatment. Remission took up to 8 No deaths; no pathology; no significant accumulations of Pb in liver, kidney, or bone; no changes in hemoglobin or hematocrit; decrease in blood ALAD activity, and increase in blood Pb levels--both returned to normal within 3 weeks on Pbfree diet. Elevated levels in bone (9.6 mg/kg fresh weight vs. 0.7 in controls) and egg (1.3 vs. 0.9 in controls). Elevated Pb levels (mg/kg dry weight) in kidney (23) liver (7), and bone (5). 7 7a 8 9 10 76 DUP040007987 Table 7. (Continued) Species, route of administration, dose, and other variables Effects Reference5 Rock dove, Columba 1ivla Intragastric administration of 6.25 mg Pb (as lead acetate)/kg 8W daily for 64 weeks Anemia, elevation in erythrocyte porphyrin, kidney pathology, residues (mg/kg fresh weight) of 603 in kidney, 501 in bone, 8 in liver, 2 in brain, 4.4 in blood, 0.8 in sciatic nerve, and 0.1 in crop. Intubation of 6.25 mg Pb (as lead acetate)/ kg BW, chronic exposure Interfered with four-step learning sequence; elevated blood Pb levels remained for 5 weeks after Pb exposure. Japanese quail, Coturnix .iaoonica Single oral dose of tetraethyllead LD-50 of 24.6 mg/kg BW. Fed diets containing different forms of Pb for 5 days 5,000 mg metallic Pb/kg No effect on survival or food consumption. 5,000 mg Pb (as lead nitrate)/kg No overt signs of toxicity. 5,000 mg Pb (as lead subacetate C4H10OgPb3)/kg No overt signs of toxicity. 2,761/mg Pb (as lead arsenate)/kg LD-50. 14 15 7a 16 16 16 16 Prairie falcon, Falco mexicanus Fed shotgun-killed pheasants and ducks Death, preceded by vomiting, ataxia, blindness, and SBSSSBfS 78 DUP040007988 Table 7. (Continued) Species, route of administration, dose, and other variables Effects Reference3 10 mg Pb/kg diet Nestlings dosed orally with metallic Pb powder daily for 10 days 625 mg/kg BW 125 mg/kg BW 25 mg/kg BW Fed 60 days with homogenized cockerels (Gallus sp.) containing up to 448 mg (biologically incor porated) Pb/kg dry weight Elevated Pb in bone (4 to 9 mg/kg dry weight vs. <0.8 in controls) and in liver (3 vs. <0.5 in controls). Mortality (40% in 6 days); reduced growth; reduced kidney and liver weight; abnormal skeletal development; ALAD depression in all tissues examined; elevated burdens (mg/kg fresh weight) in kidney (15), liver (6), and brain (3). Reduced growth, reduced brain weight, abnormal skeletal development, ALAD depressions in hematopoietic tissues, elevated burdens (mg/kg fresh weight) in kidney (7), and liver (4). ALAD depression in all tissues examined; burdens (mg/kg fresh weight) elevated in kidney (3) and in liver 1.4). No effect on survival, growth, hemoglobin, hematocrit, and erythrocyte number. Elevated burdens in kidney, liver, femur, brain, and blood. 20 21 21 21 22 80 DUP040007989 Table 7. (Continued) Species, route of administration. dose, and other variables Effects Reference3 3 No.6 shot (300 mg) Some deaths between days 8 and 15 posttreatment, reduced food intake, weight loss, lethargy, diarrhea; residues of 7.3 mg/kg fresh weight liver, 139 dry weight tibia. 6 No. 6 shot (600 mg) If shot retained in gizzard, death resulted; residues (mg/kg) 72 fresh weight in liver, 154 dry weight in tibia. ControlS Residues (mg/kg) 0.1 fresh weight in liver, 5 dry weight in tibia. Raptors, 4 spp. Fed rock doves (Columba livia) and brown hares (Lepus europaeusl containing Pb shot for 3 weeks to 6 months Death preceded by weight loss, convulsions, and inability to fly. Residues (mg/kg dry weight) at death ranged from 57 to 175 in liver, and 34 to 221 in kidney. Common tern, Sterna hirundo Single injection of 200 mg Pb^ Adverse effects on behavior (1ocomotion, balance, righting response, feeding tasks, behavioral thermoO regulation); most apparent within 5 days postinjection. Ringed turtle-dove, Streptooelia ri sorla Single oral dose of 2 pellets (220 mg) Blood Pb (mg/1) 4.69 at 24 hours, and 0.14 at 14 days (vs. control values of 0.004 to 0.012 mg/1); blood ALAD depressed from 24 hours through 14 days. y 25,26 25,26 25,26 27 28 29 82 DUP040007990 Table 7. (Continued) Species, route of administration, dose, and other variables Effects Reference* and feather in progeny of Pbtreated parents than in controls. 34 European starling, Sturnus vulgaris Oral administration (capsule) of triethyllead chloride at 2,000 ug daily (28 mg/kg BW) for 11 days, or until death Mortality 100% by day 6. Dying birds showed decreased respiration, squatting, fluffed feathers, and abnormal head posture. Average residues (mg/kg fresh weight) 6.0 in bone, 7.3 in brain 19.9 in kidney, 20.0 in muscle, and 40.2 in liver. 35 As above, but dose was 200 ug daily (2.8 mg/kg BW) No deaths, reduced food consumption. All tissue residues <2.0 mg/kg fresh weight (vs. <0.1 in controls). 35 Oral administration (capsule) of trimethyllead chloride at 2,000 ug daily (28 mg/kg BW) for 11 days, or until death Mortality 100% by day 6. Signs included impaired balance, tremors, fluffed feathers, uncoordinated feeding movements, weight loss, inability to fly. Residues (mg/kg fresh weight) averaged 4,3 in bone, 11.0 in muscle, 16.7 in brain, 30,2 in kidney, and 82.4 in liver. 35 As above, but dose was 200 ug daily (2.8 mg/kg BW) No deaths, survivors hyperactive. Average tissue residues (mg/kg fresh weight) 0.4 in bone, 3.1 in muscle, 3.5 in brain, 3.7 in liver, and 5,4 in kidney. 35 84 DUP040007991 Trialkyllead salts are 10 to 100X more toxic to birds than are inorganic Pb salts; they tend to accumulate in lipophilic soft tissues in the yolk and developing embryo, and have high potential as neurotoxicants (Forsyth et al. 1985); accordingly more research is needed on alkyl!ead toxicokinetics. Some alkyllead Compounds have been implicated in bird kills. In autumn 1979, about 2,400 birds of many species were found dead or disabled on the Mersey estuary, England, an important waterfowl and marsh bird wintering area; smaller kills were observed in 1980 and 1981 (Bull et al. 1983), Affected birds contained elevated Pb concentrations in liver (>7.5 mg/kg fresh weight), mostly as organolead. Bull et al. (1983) suggested that trialkyllead compounds were discharged from a petrochemical factory producing alkyl!eads, into the estuary where they were accumulated (up to 1.0 mg/kg fresh weight) by clams (Macoma balthica) and other invertebrates on which the birds could feed. Birds dosed" experimentally with trialkyl!ead compounds died with the same behavioral and internal signs found in Mersey casualties; tissue levels of trialkyllead were similar in the two groups of birds (Osborn et al. 1983). , Sublethal effects that might influence survival in the wild were found in both sublethally dosed and apparently healthy wild birds when tissue levels of trialkyl!ead compounds were matched in the two groups of birds. It was concluded that trialkyllead compounds were the main cause of the observed mortalities and that many apparently healthy birds were still at risk (Osborn et al. 1983). Nestlings of altricial species (those confined to the nest for some time after hatch) may be considerably more sensitive to Pb exposure than adults, and also more sensitive than hatchlings of many precocial species (Hoffman et al. 1985a). Hatchlings of precocial species, including chickens, Japanese quail (Coturnix coturnix), mallards, and pheasants, are relatively tolerant to moderate Pb exposure, i.e., there was no effect on growth at dietary levels of 500 mg Pb/kg, or survival at 2,000 mg Pb/kg (Hoffman et al. 1985a,b). Some species of domestic birds are resistant to Pb toxicosis, for example, blood Pb levels of 3.2 to 3.8 mg/1 in Pb-stressed cockerels (Gallus sp.) were much higher than residues considered diagnostic for Pb poisoning in most domestic mammals, except swine--which tolerated up to 143 mg Pb/1 blood (Franson and Custer 1982), MAMMALS Three stages of recognizable Pb poisoning, or plumbism, have been reported in humans (NRCC 1973): (1) mild or severe dysfunction of the alimentary tract as shown by loss of appetite, constipation, abdominal cramps, headaches, general weakness, and fatigue; (2) atrophy of forearm extensor muscles, or paralysis of these muscles and more striking atrophy; and (3) lead encephalopathy, which occurs frequently in Pb-poisoned infants and young children, but only rarely in industrial workers. In general, people with hepatitis, anemia, and nervous disorders were more susceptible to Pb poisoning (Barth et al. 1973). The transfer of Pb across the human placenta and its potential threat to the fetus have been recognized for more than 100 years; women occupationally exposed to Pb showed a comparatively high abortion rate (Tachon et al. 1983). Sensitivity of the brain to the toxic effects of Pb is 86 DUP040007992 Table 8. Lethal and sublethal effects of lead to selected species of mammals. Species, dose, and other variables Effects Reference3 Cattle, cows, Bos spp. Tissue Pb (mg/kg fresh weight) 0.81 in blood, 26.4 in liver, 50.3 in kidney, and 400 in rumen contents Calves given 2.7 mg Pb/kg body weight (BW), as Pb acetate, for 20 days; milk diet Signs of clinical Pb toxicosis observed. Death. 1 2 Calves given 3.0 to 3.5 mg Pb/kg BW daily for 3 months; grain and hay diet Calves given 5 mg Pb/kg BW, as Pb acetate, for 7 days; grain and hay diet Calves given 5 mg Pb/kg BW, as Pb acetate, for 7 days; milk diet Calves given 5 mg Pb/kg BW daily for 10 to 20 days Calves given foragecontaining 5 to 6 mg Pb/kg Calves given 5to 6 mg Pb/kg BW daily for 3 years Adults given 6mg Pb/kg BW daily for 3 years Calves given 6to 7 mg Pb/kg BW daily for 2 months No effect. Appeared normal. Signs of Pb poisoning; some deaths. Blindness, 16% mortality. Fatal in 2 months. Chronic toxicity. No deaths. Fatal. 2 3 3,4 4 1 2 5 2 88 DUP040007993 Table 8. (Continued) Species, dose, and other variables Effects Reference3 equivalent to about 3.5 mg Pb/kg BW Total dose of 10 to 25 grams Goat, Caora sp. Total dose of 20 to 25 grams Guinea pig, Cavia cobava Single intraperitoneal injection of 25 mg/kg BW, as Pb acetate Horse, Eauus cabal1 us Tissue Pb levels, in mg/kg fresh weight, of 0.39 in blood, 18 in liver, and 16 in kidney Ate forage containing 1.7 mg Pb/kg Consumed 2.4 mg Pb/kg BW daily Fed 6.25 mg Pb/kg BW daily for 105 days, as Pb acetate Tissue Pb levels (mg/kg fresh weight) 1,2 in brain, 1.7 in blood, 15.7 in spleen, 23.4 in liver, 32.2 in kidney, and 735 in bone. Toxic, 9 6 Toxic. 6 Reduced brain weight of newborn pigs. Effect synergized when dams were exposed to elevated (42 C) temperatures for 24 hours: 88% with microencephaly vs. 5% in group given 25 mg/kg without hyperthermia. 10 Signs of clinical Pb toxicosis observed, 1 Fatal in several months. Lethal, No deaths; blood Pb levels of 350 to 380 ug/1 at day 105. 1 4 6 90 DUP040007994 Table 8. (Continued) Species, dose, and other variables Effects Reference3 Mouse, Mus sp. 0.05 to 0.1 mg Pb/kg BW daily Tissue concentrations of 0.78 mg/kg femur bone marrow, 3.7 mg/1 blood, 15.8 mg/kg brain, or 43 mg/kg liver 1.5 mg Pb/kg BW daily, as tetraethyllead chloride 2.2 mg/kg BW or 3 mg/kg BW daily, as tetraethyllead Pregnant females given single intrauterine injection of 20 mg Pb/kg BW on day 8 of gestation 800 mg Pb/1, as lead acetate, in drinking water for 11 weeks 1,000 mg Pb/1 in drinking water for 9 months Sheep, Ovls aries lambs fed 50 ug Pb/kg daily (~ 3 mg) Lambs exposed to low levels (350 ug Pb/1 blood) in utero Irreversible inhibition of ALAD activity in bone marrow and red blood cells. 14 Inhibition of ALAD activity 50% within 10 minutes, 14 Reduction in success of implanted ova, 8 Frequency of pregnancy reduced when dose given 3 to 5 days after mating. 8 Smaller litters, increased fetal deaths. 15 Decrease in litter size, decreased survival of pups, and decreased birth weight, No effect on survival or fertility. 16 4 Tissue accumulations, 5 Impaired visual discrimination and learning behavior. 17 92 DUP040007995 Table 8. (Continued) Species, dose, and other variables Effects Reference3 Single oral dose of 600 mg Pb/kg Fatal. BW 9 Total dose of 20 to 25 grams Toxic. 6 Primates, various species Cynmolgus monkey, Macaca iris Intramuscular injection of 1.0 mg Pb/kg BW daily during pregnancy or lactation Fetus exposed to lead through placenta or maternal milk. 19 1.5 mg Pb/1 in drinking water as lead acetate, for 9 months (equivalent to 0.5 mg Pb/kg BW daily), or 6 mg/1 (2 mg/kg BW), or 15 mg/1 (5 mg/kg BW). Increasing blood Pb levels from third month, according to dose; kidney pathology. Effects more severe in animals on low calcium diets. 20 Intramuscular adminstration of 5 mg Pb^ykg BW daily during pregnancy or lactation Abortions and death in pregnant monkeys; cerebral pathology in newborns! 19 Cynmolgus monkey, Macaca fascicularls Dosed orally from birth to age 200 days with 100 ug Pb (as Pb acetate)/kg BW, 5X weekly, milk substitute diet Blood Pb concentration of 254 ug/1; declined to 131 ug/1 over next 100 to 150 days. At age 3 years, impaired ability to perform motor discrimination reversal tasks, 21 As above, except dose is 50 ug Pb/kg BW Blood Pb levels of 154 ug/1 (vs, 35 ug/1 in controls), declining to 109 ug/1 at day 150 post administration. At age 3 years, group showed impaired color discrimination. No overt signs of toxicity, normal blood chemistry (except Pb), normal growth and development skills. 21 94 DUP040007996 Table 8. (Continued) Species, dose, and other variables Effects Reference3 Weanling females given 0.0, 0.5, 5, 25, 50, or 250 mg Pb (as Pb acetate)/! drinking water for 6 to 7 weeks, then mated and exposed continuously through gestation and lactation Single intravenous injection (mg Pb/kg BW in parentheses) Tetramethyllead (80) Tetraethyllead (10) Trimethyl lead (20 to 25) Triethyllead (8) Single oral dose (mg Pb/kg BW) Tetramethyllead (108) Tetraethyllead (12) Single intraperitoneal injection (mg Pb/kg BW) Tetramethyllead (70 to 100) Tetraethyllead (10) Trimethyllead (17) Triethyl!ead (5) 5 mg Pb/1 drinking water, lifetime exposure Single intraperitoneal injection of 7 mg Pb/kg BW, as tetraethyllead Male weanlings exposed to age 50 days to drinking water containing 25 mg Pb/1, as Pb acetate At 25 mg/1 and higher, growth retardation and delayed vaginal opening observed; some maternal deaths occurred and were associated with blood Pb concentrations >200 ug/1. Some pup malformations and deaths in all groups. The 5 mg/1 group had elevated blood Pb levels. 23 LD-50. LD-50. LD-50. LD-50. LD-50. LD-50. 24 24 24 24 24 24 LD-50. LD-50. LD-50. LD-50. Lowered survival and reduced longevity. Depressed food intake, and hyperactivity. 24 24 24 24 4 25 At day 8$: behavioral deficits; blood Pb concentrations of 150 to 200 ug/1; brain Pb 1evels (ug/kg) 70 in treated group vs. 28 in controls. 26 96 DUP040007997 Table 8. (Concluded) Species, dose, and other variables Effects Reference Swine, Sus sp. Oral doses of 64 mg Pb/kg BW, as Pb acetate, 6X weekly for 13 weeks As above, except doses administered intraperitoneal1y Total dose of 10 to 25 grams No deaths, reduced blood ALAD activity, blood Pb concentration (a remarkable) 143 mg/1. All died. 5 Toxic. 32 32 6 References: 1, Osweiler and Van Gelder 1983; 2, Zmudzki et al. 1983; 3, Zmudzki et al. 1984 ; 4,'i'Demayo et al. 1982; 5, NRCC 1973; 6, Dollahite et al. 1978; 7, Kwatra et al. 1986; 8, Clark 1979; 9 Forbes and Sanderson 1978; 10, Edwards and Beatson 1984; 11, Burrows and Borchard 1982; 12, Gilraartin et al. 1985; 13, Barth et al. 1973; 14, Schlick et al. 1983; 15, Wide 1985; 16, Sharma and Kanwar 1985; 17, EPA 1980; 18,. Nriagu 1978b; 19 Tachon et at. 1983; 20, CoTle et al. 1980; 21, Rice 1985; 22, Hopkins 1970; 23, Kimmel et al. 1980; 24, Branica and Konrad 1980; 25, Czech and Hoium 1984; 26, Cory-Slechta et al. 1985; 27, Cory-Slechta et at. 1983; 28, Massaro et al. 1986; 29, Cory-Slechta et at. 1981; 30, Zirkin et al. 1985; 31, Barrett and Livesey 1985; 32, Lassen and Buck 1979. 98 DUP040007998 Although the use of lead arsenate as an insecticide in orchards is diminishing, residues of Pb still remain in the upper soil surface and will continue to remain bioavailable almost indefinitely (Gilmartin et al. 1985). Naturally occurring radiolead-210, which has a half-life of 22 years, is a significant contributor to the natural radiation dose in man; comparatively high levels have been reported in certain grasses and lichens, and their consumers, such as reindeer, caribou, and ptarmigan, as well as in lanternfishes (Nriagu 1978b). The implications of this finding to wildlife health are unknown. 100 DUP040007999 Table 9. Proposed lead criteria for the protection of natural resources and human health. Resource, (units), and other variables Criterion CROPS Irrigation water (mg/1) USA Neutral and alkaline soils Acidic soils Chronic use Short-term use Canada Continuous use. Intermittent use Australia AQUATIC LIFE Freshwater (ug total Pb/1) USA Water hardness, in mg CaCO,/l 50 4 100 200 Great Lakes Superior Huron Others England . Seawater (ug total Pb/1) Water (ug/1) Tetraalkyilead Trialkyllead Sewage effluent limits (ug/1) California Industrial discharge limits to surface waters (ug/1) Illinois USA Canada Switzer!and <10 <5 <5 <20 <5 <10 <5 1x. 3o.^ , 34c 3*2b> 82C 7.7D, 200c <100 <200 <250 <18 0.0 , <1 <100 <100 <500 <2,000 <5,000 uo 41-- ooo Reference3 ^ Demayo et al,, 1982 Abbasi and Soni 1986 Demayo et a). 1982 EPA 1985 Harrison and Laxen 1981 EPA 1985 Maddock and Taylor 1980 Harrison and Laxen 1981 102 DUP040008000 Table 9. (Continued) Resource, (units), and other variables Criterion Domestic livestock Drinking water (ug/1) USA <100 Australia <250 Canada Horse <500 Others <1,000 Forage (mg/kg fresh weight) Horse <80 Cattle <200 Tissue residues Unstressed (mg/kg fresh weight) B1 ood <0.2 Liver <1.1 Kidney <1.2 Mouse, Mus sp. Elevated (mg/kg body weight daily) Total intake >0.05 Mule deer. Odocoileus hemionus Excessive (mg/day) Total intake >3 Raccoon. Procvon lotor Elevated (mg/kg fresh weight) Liver >10 HUMAN HEALTH Drinking water (ug/T) USA 1975 1977 1980 <500 <250 <50 South Africa <500 Canada, Australia <50 USSR, Japan India <100 10 to <100 104 Reference3 Demayo et al. 1982 Edwards and Clay 1977 Osweiler and Van Gelder 19' Schlick et al 1983 Harrison and Dyer 1984 Diters and Nielsen 1978 Harrison and Laxen 1981 EPA 1980; NAS 1980 Harrison and Laxen 1981 Demayo et al. 1982 Abbasi and Soni 1986 DUP040008001 Table 9. (Concluded) Resource, (units), and other variables Life-threatening Target , Air (ug Pb/rtr ) Safe, USA Occupational, USA Proposed, worldwide Hazardous House paints {mg/1) Gasoline (mg/1) USA Recent Proposed UK 1972 1978 1981 Proposed West Germany Criterion >1,000 <150, maximum 300 <1.5 (3-month arithmetic mean) <50* <2 2,220 <600 A 473 to 658 131e 840 450 400 150 150 Reference / MAS 1980 EPA 1979; NAS 1980 Barrett and Howells 1984 Barth et al. 1973 EPA 1979 EPA 1979 Harrison and Laxen 1981 Barrett and Howells 1984 Harrison and Laxen 1981 a Each reference applies to the values in the same row, and in the rows that follow for which no other reference is indicated. ^Four-day average, not to be exceeded more than once every 3 years. c0ne-hour average, not to be exceeded more than once every 3 years. ^Equals 1.8 to 2.5 g/gallon. eEquals 0.5 g/gallon. f Average 8-hour period %lood Pb levels, usually expressed as ug/deciliter, have been converted to ug/liter, for uniformity, in the present work. 106 DUP040008002 1980, 1985; Rice 1985). Behavioral deficits have been reported for young rats when blood Pb levels exceeded 0.1 mg/1, and in children with bipod Pb concentrations of 0.4 to 0.5 mg/1 (EPA 1980; Rice 1985), and in birds when Pb was administered early in development (Burger and Gochfeld 1985). Recently, behavioral impairment was recorded in 3-year-old monkeys that received 50 or 100 ug Pb/kg BW from birth to age 200 days. Blood Pb levels immediately after, exposure, and at time of testing, were 0.15 to 0.25 mg/1 (age 200 days), and 0.11 to 0.13 mg/1 (age 3 years); this is the first report of behavioral impairment in a primate species at blood Pb concentrations that are considered to be well within the bounds of safety for children (Rice 1985). This subject appears to constitute a high priority research need for wildlife species of concern. 108 DUP040008003 Teratol. 5:557-563. Barrett, J., and P.J. Livesey. 1985. Low level lead effects on activity under varying stress conditions In the developing rat. 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MMt) Ronald Eisler 9. parfocmln* Orcanltatlon Nam. and Addr* U.S. Fish and Wildlife Service Patuxent Wildlife Research Center Laurel, MD 20708 12- Spon*oHo< Organlxstlon Homo and Address 15. Supplementary Note* 3* KtcipUflifs AeettaJM No. S. Report Oete April 1988 *- P.fomln Or*anli.(lon Raoi. No. la Project/Teeh/Wor* Unit No. 11. ContnctiC) or Grant(G) NO. CO (Cl 13. Typo of Report 4 Period Covered 14. 14. Abstract (Limit: 200 word*) Ecological and toxicological aspects of lead (Pb) in the environment are briefly reviewed, with emphasis on fish and wildlife, their predators, and prey. Subtopics include sources and uses, chemical properties, mode of action, background concentrations, lethal and sublethal effects, and current recommendations for the protection of sensitive living resources. Resources that are at increased risk from Pb include migratory waterfowl that congregate at heavily hunted staging areas and ingest shot, avian predators that consume hunter-wounded game, domestic livestock near smelters and Pb battery recycling plants, zoo animals and livestock held in enclosures coated with Pb-based paints, wildlife that forage near heavily traveled roads, aquatic life near mining activities and areas of Pb pesticide use or aerosol fallout, and crops and terrestrial invertebrates growing or living in Pb-contaminated soils. Recent legislation limiting the content of Pb in paints, reducing.the Pb content in gasoline, and (by 1991-1992) eliminating the use of Pb shot will substantially reduce environmental burdens of Pb. 17. Oocunwrt Aiwlyili . Descriptors Fish Birds Mammal $ Contaminants PI ants Natural Resources Toxicity Invertebrates b. IdentlfVer*/Op<vnded Teem* Lead Heavy metals Metabolism c. COSATI Field/Group ll> Availability Statement Lead shot Hunting Regulations Released unlimited (Sea ANSKZ39.U) Organolpads Sublethal effects 19. Security Obju (This Report) Unclassified 20. Security Class {This Fag*) Unclassified See ImtitwtiMy on Reverse 2U No. of Paces 134 22. Price OPTIONAL PORU 272 <4-77> (Formerly NT1S-35) Department of Commerce DUP040008017 PreserveOurNatural Resources -.As tha Nation'vprincipal-conservation agencyi tho Department of the Interior has respon. sibility;f6r most of our.natlonalhroWneri public lands and natural resources. This includes fosterin^thewisestuseofourJandLand water resources, protecting our fish and wildlife, irpresefvihgttherenvirorimentarandxulturarvalues of our national parks and historical places, and-pr6vidingIforIthe_enj6ymeht.of:life: through outdoor recreation. The Department as. sesses our energy'and, mineral resources and works to assure that their development Is in the best Interests of all our people; The Department"also has a major responsibility for American Indian reservation communities and for people who live in island territories under U.S.- administration.--". 'J'l T-""--:'..'"-""'.......... ,, DUP040008018--- REGION! REGION 2 Regional Director Regional Director U.S. Fish and Wildlife Service _ ____U^STEgh md WHaiiK]Sarvice Lloyd Five Hundred Building, Suite 1692 -~ " ~ -- P.Q.-Bo)rl306 ------- 500 N.E. Multnomah Street Portland, Oregon 97232 Aftuquerque, New Me>acp 87103 REGION 4 REGIONS Regional Director ' .............. ' RegionalDirector U.S. Fish and Wildlife Service ' ~ ` U;S. KsK and Wildlife Service Rickard B. Russell Building---.------ ------- -............. -- One Gateway Center 75 Spring Street,. S.W.----------- :------------------NewtonComer, Massachusetts 02158 Atlanta,Georgia30303 ....... .. .... - "REGION 7 r-- - ....... Regional Director-------- U.S. Fish and Wildlife Service lOil ErTudor Road " Ahdhiorage, Alaska 99503 T. L .. REGION! Regional Director U.S, Fish and Wildlife Service Federal Building, Fort Sneiling Twin Cities, Minnesota 55111 REGION 6 Regional Director U.S. Fish and Wildlife Service P.O. Box 25486 Denver Federal Center Denver, Colorado ,80225 r '? | DUP040008019