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Chapter 43 - Lead
Authors: Milton Friend.
Lead poisoning of waterfowl is neither a new disease nor a subject without controversy. The use of lead shot for waterfowl hunting within the United States has been prohibited and efforts are underway to ban the use of lead fishing sinkers and prohibit the use of lead shot for nonwaterfowl hunting. The first documented reports within the United States of lead-poisoned waterfowl were from Texas in 1874. Numerous other reports and studies added to those findings during the years and decades that followed. However, strong opposition to nontoxic shot requirements prevented full implementation of them until 1991. A full transition to nontoxic shot shells for all hunting and to nontoxic fishing sinkers and jig heads for fishing within the United States will not happen easily. The continued use of lead shot and lead fishing weights and the large amounts of these materials previously deposited in environments where birds feed assure that lead poisoning will remain a common bird disease for some time.
Lead poisoning is an intoxication resulting from absorption of hazardous levels of lead into body tissues. Lead pellets from shot shells, when ingested, are the most common source of lead poisoning in birds. Other far less common sources include lead fishing sinkers, mine wastes, paint pigments, bullets, and other lead objects that are swallowed.
Lead poisoning has affected every major species of waterfowl in North America and has also been reported in a wide variety of other birds. The annual magnitude of lead poisoning losses for individual species cannot be precisely determined. However, reasonable estimates of lead-poisoning losses in different waterfowl species can be made on the basis of mortality reports and gizzard analyses. Within the United States, annual losses from lead poisoning prior to the 1991 ban on the use of lead shot for waterfowl hunting were estimated at between 1.6 and 2.4 million waterfowl, based on a fall flight of 100 million birds. Followup studies have not been conducted since the ban on lead shot to determine current losses from lead poisoning. This disease still affects waterfowl and other species due to decades of residual lead shot in marsh sediments, continued deposition from allowable use of lead shot during harvest of other species, noncompliance with nontoxic shot regulations, target shooting over areas where birds may feed, and from other sources of lead.
Lead poisoning is common in mallard, northern pintail, redhead, and scaup ducks; Canada and snow geese; and tundra swan. The frequency of this disease decreases with increasing specialization of food habits and higher percentages of fish in the diet. Therefore, goldeneye and merganser ducks are seldom affected (Fig. 43.1). A surprising recent finding has been lead poisoning in spectacled and common eiders on their Alaskan breeding range, where the intensity of hunting is far less than in the contiguous 48 States. These findings demonstrate that lead poisoning can afflict birds even without heavy hunting pressure. Among land birds, eagles are most frequently reported dying from lead poisoning (Fig. 43.2). Lead poisoning in eagles and other raptors generally is a result of swallowing lead shot embedded in the flesh of their prey. With the exception of waterfowl and raptors, lead poisoning from ingesting lead shot is generally a minor finding for other species (Table 43.1). However, lead poisoning has been reported in partridge, grouse, and pheasants subjected to intensive shooting in uplands of Europe. Lead poisoning in pheasants in Great Britain was reported as early as 1875.
Lead poisoning due to ingesting lead fishing weights has been reported in numerous species. The greatest number of reports are from swans as a group, common loon, brown pelican, Canada goose, and mallard duck (Fig. 43.3). Laysan albatross chicks on Midway Atoll suffer high lead exposures and mortality from ingesting lead-laden paint chips flecking off of vacant military buildings (Fig. 43.4).
Losses occur coast-to-coast and border-to-border within the United States. Documented lead poisoning in birds varies widely between States and does not necessarily reflect true geographic differences in the frequency of occurrence of this condition. For example, although the geographic distribution of lead poisoning in bald eagles is closely associated with their wintering areas, the number of lead poisoning cases from Wisconsin and Minnesota is disproportionately high. Because submission of bald and golden eagles for examination from different areas is highly variable, no direct comparison can be made between States regarding the number of lead-poisoned eagles (Fig. 43.5A). The reported distribution of lead poisoning in eagles and waterfowl depends on the numbers of birds submitted for complete disease diagnostic evaluations. In areas where few birds are examined, the frequency of lead poisoning and other diseases will be underestimated. Even where many bird carcasses are adequately evaluated, the number of diagnoses made reflects minimum numbers of lead-poisoning cases. The general distribution of this disease in waterfowl on the basis of lead shot-ingestion surveys and documented mortality prior to nontoxic shot requirements is shown in Fig. 43.5B.
Lead poisoning has also been reported as a cause of migratory bird mortality in other countries (Fig. 43.6). Several of these countries have implemented nontoxic shot requirements and several others are beginning to address this issue.
Birds can die from lead poisoning throughout the year, although birds are most often poisoned by lead after the waterfowl hunting season has been completed in northern areas and during the later part of the season in southern areas of the United States. January and February are peak months for cases in tundra swans, Canada geese, and puddle ducks. Spring losses are more commonly reported for diving ducks. Tundra swans are also frequently lead poisoned during spring migration.
Lead-poisoned waterfowl are often mistaken for hunting season cripples. Special attention should be given to waterfowl that do not take flight when the flock is disturbed and to small groups of waterfowl that remain after most other birds of that species have migrated from the area. Lead-poisoned birds become reluctant to fly when approached and those that can still fly are often noticeably weak flyersunable to sustain flight for any distance or flying erratically and landing poorly. Birds that attempt to escape pursuit by running may exhibit an unsteady gait. In lead-poisoned Canada geese, the head and neck position may appear "crooked" or bent during flight; a marked change in the tone of call is also sometimes evident in this species. As the disease progresses and waterfowl become flightless, the wings are held in a characteristic "roof shaped" position (Fig. 43.7), which is followed by wing droop as the birds become increasingly moribund (Fig. 43.8). Fluid may discharge from the bill and often a bird may not attempt to escape in the presence of humans.
Lead-poisoned waterfowl are easily captured during advanced stages of intoxication (Fig. 43.9). Because severely affected birds generally seek isolation and protective cover, well-trained retrieving dogs can help greatly to locate and collect these birds. An abundance of bile-stained feces on an area used by waterfowl (Fig. 43.10) is suggestive of lead poisoning and warrants ground searches even if other field signs have not been observed. Green-colored feces can also result from feeding on green wheat and other plants, but the coloration is somewhat different.
Lead-poisoned waterfowl are often emaciated because of the prolonged course of the illness and its impact on essential body processes. Therefore, many affected birds appear to be starving; they are light in weight, have a "hatchet-breast" appearance (Fig. 43.11), and the undersurface of their skin is devoid of fat (Fig. 43.12). The vent area of these birds is often stained with a bright green diarrhea (Fig. 43.13). The heads of Canada geese may appear puffy or swollen because serum-like fluids accumulate in the tissues of the face (Fig. 43.14).
Less obvious pathological changes include wasting of internal organs such as the liver, kidneys, and spleen; areas of paleness in the heart muscle; a flabby-looking heart; and paler-than-normal-looking internal organs and muscle tissue.
The above field signs and gross lesions provide a basis for a presumptive diagnosis of lead poisoning. However, none of these signs or lesions is diagnostic by itself and all can result from other causes. Also, many of the above signs and lesions are absent in birds that die acutely following an overwhelming lead exposure.
Table 43.1 Documented North American cases of lead poisoning in free-ranging nonwaterfowl species.
A definitive diagnosis of lead poisoning as a cause of death is based on pathological and toxicological findings supplemented by clinical signs and field observations. The presence or absence of lead shot or lead particles in the gizzard contents is useful information and should be recorded, but it is not diagnostic. The liver or kidneys are the tissues of choice for toxicology analysis, with liver tissue being more commonly used. If you suspect lead poisoning and cannot submit whole birds to the diagnostic laboratory, remove the liver or kidney tissue, wrap the specimens separately in aluminum foil, and freeze them until they are submitted for analysis. Collect the entire liver or one entire kidney. However, because toxicology is but one aspect of reaching a lead-poisoning diagnosis, make every effort to submit whole birds for analysis. Liver lead values of 68 parts per million or higher on a wet-weight basis or 2030 parts per million on a dry-weight basis are suggestive of lead poisoning when other signs of lead poisoning are present.
Lead levels in populations of live birds can be evaluated by using whole blood. Collect a minimum of 25 milliliters of blood in lead-free tubes containing an anticoagulant such as sodium citrate or EDTA. Evidence of lead exposure can also be obtained through indirect measurements involving blood enzymes. Measurement of protoporphyrin IX in red blood cells is the most popular assay because only a few drops of blood are needed and testing is inexpensive once appropriate instrumentation is obtained. Elevated blood protoporphyrin levels are correlated with lead exposure and serve as a sensitive screening assay, but they do not provide direct measurement of the amount of lead in blood. This technique has its greatest value in identifying populations from which more direct measurements should be taken and for screening blood samples to determine which should be tested for blood lead concentrations. Confirm correct procedures for collecting blood samples for lead analysis with the diagnostic laboratory before collecting the samples. Keep blood samples chilled until submitting them for analysis, regardless of the assay that will be used. Write the date and time of collection on the tube along with the specimen number and other information identifying the sample and its origin.
The diagnosis of lead poisoning as a disease or poisoning syndrome, but not as a cause of death, can be made from tissue residues alone when there are sufficient residue data for the species in question or closely related species. The amount of tissue residue variability that exists between species can be considerable and it is also influenced by the route of lead exposure such as ingestion vs. inhalation (Fig. 43.19). For example, rock doves (pigeon) are highly resistant to high concentrations of lead when they are compared with other birds, but most lead exposure in rock doves is from automobile emissions in cities. Rock doves that have ingested lead shot have greatly increased tissue lead levels, can exhibit behavioral changes consistent with lead toxicity in other species, and can die from the toxic effects of lead.
Two actions can often be taken to reduce the magnitude of mortality from lead poisoning when die-offs occur: denying birds use of problem areas, and rigorous pickup and proper disposal of dead and moribund birds.
Denying birds use of problem areas requires knowing where the birds are picking up the lead. This is complicated by the fact that signs of intoxication may not appear until 1 week after lead ingestion, and birds may not start dying until 23 weeks after lead ingestion. Habitat modification of contaminated areas is also useful in some instances, but differences in feeding habits must be considered. For example, placing additional water on an area may protect puddle ducks from reaching lead shot on the bottom of wetlands, but this may create an attractive feeding area for diving ducks. Similarly, draining an area may prevent waterfowl from using an area and ingesting shot, but it may create an attractive feeding area for shorebirds or pheasants. Therefore, control plans must consider the broad spectrum of wildlife likely to use the area at the time action will be taken. Rigorous pickup and proper disposal of lead-contaminated waterfowl carcasses is required to prevent raptors and other scavenger species from ingesting them. The high percentage of waterfowl with embedded body shot provides a continual opportunity for lead exposure in raptors that far exceeds the opportunity for ingestion of shot present in waterfowl gizzards.
Other management practices that have been used to reduce losses from lead poisoning on site-specific areas include tillage programs to turn lead shot below the surface of soil so that shot is not readily available to birds, planting food crops other than corn and other grains that aggravate the effects of lead ingestion, and requiring the use of non-toxic shot in hunting areas. The potential contributions of the first two practices toward reducing lead-poisoning losses among birds are, at best, limited and temporary. Supplemental grit has also been placed in wetlands in the belief that birds intentionally ingest shot because grit is not available; as with tillage and food crops, any benefits are limited and temporary. The use of nontoxic shot is the only long-term solution for significantly reducing migratory bird losses from lead poisoning.
The strong correlation between exposure of waterfowl to lead and the use of lead shot for hunting waterfowl was vividly demonstrated by National Wildlife Health Center sponsored studies that compared tissue lead levels and gizzard analyses in a subpopulation of Canada geese as they migrated from their breeding grounds to their wintering grounds. Nontoxic shot requirements were in place at some sampling sites but not at others. Lead exposure was significantly less where nontoxic shot requirements existed.
Since lead shot has been banned for hunting waterfowl in the United States, attention has turned to regulating the use of lead fishing sinkers and lead jig heads. The Environmental Protection Agency has been petitioned to address the problem of bird mortality from these sources (Fig. 43.20). Prohibitions against using lead fishing weights below certain sizes have already been initiated on some Federal lands and other areas. The number of cases of lead poisoning in swans in the Thames Valley of England was reduced by 70 percent in 2 years following enactment of the 1987 ban on use of split lead shot and other fishing sinkers up to 1 ounce in size. Sizes larger than those that can be ingested by birds have not yet become a focus for concern.
The use of lead shot for target shooting and hunting on uplands is also receiving increased attention. In general, ingestion rates for lead shot in upland species are far less than those for waterfowl, even for doves (Table 43.2). The harvest of doves is somewhat analogous to waterfowl hunting in that large numbers of shells are often fired over the same location year after year (Fig. 43.21.). However, the duration of intense shooting on specific sites tends to be much less for doves than for waterfowl and the hunting area is generally tilled annually for agricultural purposes.
Veterinary treatment of lead-poisoned birds is generally not a reasonable approach. However, endangered species or other birds of high individual value that are lead poisoned may warrant treatment. In those instances, treatment should be done only by qualified persons familiar with and skilled in the proper use of lead-chelating chemicals. Under the best of circumstances, the results of treatment are unpredictable and the success rate low.
People do inadvertently consume lead-poisoned birds. Although this is not desirable, no appreciable risks to human health exist. Most lead present in the body of a lead-poisoned bird is in organs such as the liver and kidneys rather than in the flesh. The dose relation (milligrams of lead per kilogram of body weight) and lead excretion processes are such that a great number of lead-poisoned birds would need to be consumed in a relatively short time before toxic levels of lead could build up in the human body. Persons who eat the liver, kidneys, and other soft tissues from lead-poisoned birds would consume more lead than those who eat only the muscle tissue of these birds. Persons who consume waterfowl bones would be additionally exposed to lead, because lead is stored long-term in bone.
There are a few documented cases of humans developing lead poisoning after having accidentally ingested lead shot embedded in the meat they ate. This type of lead poisoning is rare, perhaps due to caution exercised when eating hunter-killed wildlife so as to avoid potential damage to teeth from biting into shot. Lead shot that is ingested can also become lodged in the appendix, resulting in appendicitis. This does not happen often, and it happens most in people who hunt waterfowl for subsistence. It is also possible that humans may ingest tiny fragments of lead that may be present in tissues of wildlife killed with lead shot.
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