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accumulative metabolic poison that affects behavior, as well as the
<br />hematopoietic, vascular, nervous, renal, and reproductive systems. In humans,
<br />Pb causes stillbirths, miscarriages, inhibited development of fetuses,
<br />decreased male fertility, and abnormal sperm. Severe damage to the central
<br />nervous system from exposure to large amounts of Pb may result in stupor,
<br />convulsions, coma, and death. Children that survive Pb poisoning are often
<br />permanently retarded or have permanent neurological handicaps. At subclinical
<br />injury levels, Pb causes slight, but irreversible, damage to the brain
<br />development of growing children.
<br />Natural resources are also affected by environmental Pb contamination,
<br />and some wildlife species numbers may be reduced as a result. For example,
<br />waterfowl deaths resulting from the ingestion of spent Pb shot pellets from
<br />shotgun shells were discovered more than 100 years ago in Italy and in the
<br />United States; since then Pb poisoning of waterfowl has occurred in 15
<br />countries (Street 1983). In North America alone, approximately 3,000 tons of
<br />Pb shot are expended annually into lakes, marshes, and estuaries by several
<br />million waterfowl hunters (FWS 1986, 1987). Spent pellets are eaten by
<br />waterfowl and other birds, either in mistake for seeds or as pieces of grit.
<br />These pellets may be retained in the gizzard for weeks, where they are reduced
<br />chemically and mechanically, form soluble toxic salts, and cause
<br />characteristic signs of Pb intoxication--especially lethargy and emaciation
<br />(Street 1983). At least 2% of all North American waterfowl--or about 2
<br />million ducks and geese (Lumeij 1985)--die each year as a direct result of
<br />ingestion of Pb shot (Bellrose 1959). These deaths contribute to the decline
<br />of some species, such as the canvasback, Aythya valisineria (Dieter 1979),
<br />pintail, Anas acuta (White and Stendell 1977), and black duck, Anas rubripes
<br />(Pain and Rattner 1988). Up to 7X more waterfowl died from Pb toxicosis as a
<br />result of ingesting spent pellets than from wounding by hunters (Zwank et al.
<br />1985). In addition, Pb-poisoned waterfowl show delayed mortality from
<br />Pb-induced starvation, are readily captured by predators, are susceptibile to
<br />disease, and reproduce poorly (Dieter 1979). Susceptibility is markedly
<br />influenced by species, by the number and size of shot ingested, and by the
<br />types of foods eaten (White and Stendell 1977). Swans are among the more
<br />vulnerable waterfowl. In England, Pb poisoning through the ingestion of
<br />discarded Pb fishing sinkers is the major cause of death in the mute swan,
<br />Cygnus olor (Birkhead 1983); for all species of swans in England, about half
<br />died as a direct result of Pb poisoning (Demayo et al. 1982). In Washington
<br />State, 30% of the endangered trumpeter swans (Cygnus buccinator) found dead
<br />had died of Pb poisoning from ingestion of Pb shot (Kendall and Driver 1982).
<br />Lead toxicosis caused by ingestion of spent shot and other Pb objects has also
<br />been reported for sandhill crane, Grus canadensis (Windingstad et al. 1984);
<br />Canada goose, Branta canadensis (Szymczak and Adrian 1978); mourning dove,
<br />Zenaidura macroura (Locke and Bagley 1967); and wild turkey, Meleagris
<br />gallopavo (Stone and Butkas 1978). Secondary poisoning has been documented in
<br />at least five species of raptors that ate food containing Pb shot (especially
<br />hunter-wounded animals): Andean condor, Vultur r hus (Locke et al. 1969);
<br />bald eagle, Haliaeetus leucocephalus (Pattee and Hennes 1983); honey buzzard,
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