Lead Exposure to Animals and Plants

As water and wind sculpt the face of the earth or as a result of volcanic activity, a very small amount of lead enters the atmosphere or is released from rock and soil. Thus, organisms have always been exposed to at least tiny amounts of lead throughout evolutionary time. The activities of humans vastly increased the concentrations of lead on the surface of earth -- putting our own species at risk and poisoning plants and animals in the process. Contamination of aquatic ecosystems occurs through extensive mining and industrial use of lead. Substantial amounts of gasoline derived lead are deposited from the atmosphere into streams and other water bodies and affects the animals and plants in these environments. Terrestrial plants and animals, some of whom share our households, are also at great risk from contaminated soil.

Exposures to Pets

Because cats and dogs lick their fur, they are very susceptible to lead exposure from soil and dust. Cats routinely dig in soil to dispose of their wastes; dogs often dig in the yard to bury bones or other objects, to get under fences, to make a cooler spot to lie in, or apparently just for enjoyment. Dogs also often lick their fur, although not in the stereotypical bathing fashion of cats.

In the three years between 1968 and 1972, according to a study of veterinary medicine colleges in the U.S. and Canada, more than 45 dogs were treated for lead-poisoning. The University of Pennsylvania Veterinary Hospital alone treated 27 dogs for lead poising over a ten year period during that time, and more than 500 dogs suffering from lead poisoning were admitted to the Angell Memorial Animal Hospital in Boston, between 1961 and 1971. Most of the dogs came from houses undergoing remodeling and renovation, where they had access to chips, plaster, and paint scraps. One dog had an extremely elevated blood lead level, 530 mg/dL. As with humans, chelation therapy is successful with dogs and cats. In the early 1980s sheepdogs were poisoned from lead in dust traced to old painted wood used to build their kennel in Australia. The dogs were taken to the vet after exhibiting fits, clearly a sign of neurological disorder. A study that focused on dogs and children within the same household concluded that an elevated blood-lead concentration in a dog increased by six-fold the likelihood of a child being lead poisoned. Researchers in Japan measured lead in hair from pet dogs. There were no differences between male and female dogs in the concentration of lead, but they found that age of the dogs made a difference in lead levels. Lead levels in the dog's hair increased as they aged to seven or eight years of age and then levels declined slightly. This is not much different from the pattern found in people. Thus measuring lead in dog hair is a good surrogate for or indicator of human lead exposure. A study done by the University of Illinois Department of Public Health, seven years after a smelter was closed revealed significant associations between soil lead, dust lead and blood-lead concentration in both the pets and humans. Blood of pets and children were tested for lead in 77 households with a total of 198 humans, 83 dogs and 24 cats. The relationships between environmental lead and lead levels in the pets were much stronger than those found in pet owners. This study and a subsequent study found that more pets become poisoned than do pet owners in the same leaded environment. The most significant association was found between indoor animals and younger children. Having at least one pet at home with a high blood-lead increased the likelihood of finding at least one person with a similar conditions. The studies indicate that pets can serve as reliable monitors of potential lead exposure, especially to young children in the household, even though the pets had higher lead levels and were thus more at risk than their owners when exposed to the same contaminated environment. In a case in Australia, a cat was brought to a veterinarian suffering a loss of appetite, diarrhea, and intermittent vomiting. From a physical examination the vet was unable to diagnose the problem, but when blood tests came back they indicated that the cat was lead poisoned. The blood-lead level in the cat was above 115 mg/dL. The cat underwent chelation therapy and recovered. It was found that the pet's home was undergoing renovation. One of the women in the house, who had been burning and sanding old paint off the outside of the house suffered abdominal pains during the previous month. Tests found a level of lead in her blood of almost 80 mg/dL. Another cat from the house had a blood lead level of 57 mg/dL. Two other cats, two dogs, and one additional person in the house had some evidence of lead exposure, although their blood-lead levels were not as elevated.

Various researchers have tried to determine the chronic toxic level of lead for dogs. In a recent study, a concentration of 10 mg/dL, the Center for Disease Control and Prevention standard for children, was used to define a case of lead exposure in the animal population. The range of blood-lead concentrations ranged from 5 to 28 mg/dL in the dogs and cats studied. The highest levels were below the 35 mg/dL concentration at which clinical signs had previously been observed in these species. Although no adverse health effect were observed in any animal, changes in biochemical markers associated with lead exposure were found. The enzyme, delta-amino-levulinic acid dehydratase (ALAD), involved in hemoglobin formation was inhibited. There was a linear relationship between the logarithm of ALAD activity and the logarithm of the blood-lead concentration. In addition, higher white blood cell counts and lower hemoglobin concentrations were found in both dogs and cats with a lead concentration in the blood equal to or greater than 10 mg/dL. Although the lead had measurable effects, the physiological values measured were within normal ranges; the biological significance of such changes remains unknown.

Effects of Lead in Ecosystems

Lead can concentrate in various kinds of plants, including single-celled algae in aquatic ecosystems, vegetables, grains and fruit eaten by humans and domesticated animals. Fortunately, however, lead does not appear to biomagnify up through the food chain. Other contaminants, such as PCBs or methyl mercury, do build up in increasing concentrations in organisms that eat plants or animals below them in the food chain. The opposite seems to be true for lead; top predators usually tend to have substantially lower lead levels than their prey. Raptors typically have lower take-up levels. This may result from regurgitating indigestible material such as bones of their prey where lead often accumulates. An exception may be the poisoning that occurs in carrion eaters, raptors, and other birds of prey when they eat something that contains lead shot.


Lead Uptake and Effects in Plants

The effects of lead on plants, especially at high concentrations, are harmful. They include inhibition of growth, interference with cell division and with water absorption and balance, and reduction of photosynthesis, the vital process whereby plants use the energy from sunlight to convert carbon dioxide and water into sugars, protein, fats and other products. The by-products of photosynthesis are useful in promoting growth and provide sustenance for the animal kingdom including humans. Thus a reduction in the process of photosynthesis can cause harmful effects at multiple levels in the food chain.

Algae, including single-cell plankton in aquatic systems, seem to be fairly resistant to toxic effects of lead. Studies have shown that these aquatic plants can concentrate lead. The resistance may be due to the lead being held within cell walls or other parts of the cell and make it less available to poison reactions of enzymes or other sensitive biochemical processes in the single-celled organism. The bioavailability of lead in fresh water ecosystems is influenced by the pH of the water.

Animals seem to be much more sensitive to lead than do the single celled plants discussed in the paragraghs above. Laboratory experiments of lead exposure carried out over a 28-day period in aquatic invertebrates (animals without backbones) including insects, snails, and amphipod crustaceans showed that in these animals the lead caused significant toxic effects.

More complex aquatic plants, such as the submerged aquatic vegetation that have roots and a multi-celled structure, appear to take up more lead than plants without roots; this may be related to their absorption of lead from sediments. Uptake of lead in aquatic systems varies with many different factors including the pH of the water, the presence of other minerals in the water, and the availability of organic compounds or other chemicals that may bind up the lead, making it less available for uptake on the one hand, or on the other, actually facilitating its uptake by the organism. In some aquatic plants, rooted in sediments, lead taken up by the roots can be translocated or moved to the shoot, although lead can also be directly absorbed from the water especially if the lead concentration is high there. Lead measured in aquatic plants may also include that adsorbed at the surface or taken up by bacteria that reside on the surface of the plant. In one study, 46% of the lead measured from the plants was actually in the epiphytic (surface-resident) bacteria. Certain bacteria can increase the toxicity of lead to aquatic plants by synthesizing methyl- or other alkyl-lead compounds. These are organic compounds consisting of one or more carbon atoms and associated hydrogen atoms; the organic compounds are more soluble in the fatty membranes of plant and animal cells and more readily taken up. Although these methyl-lead complexes are not nearly as important in food chain contamination as comparable organic mercury compounds, they can be as much as twenty times more toxic than an equivalent weight of inorganic lead.

Among land-based plants, mosses appear to take up higher concentrations than more advanced plants. The uptake factors for mosses have been measured from 3100 to 5300, whereas uptake factors in higher plants are estimated to range from about 180 to 720. Just as in aquatic plants, uptake of lead by land-based plants is influenced by many factors such as: soil acidity, positively-charged ion binding potential, organic content, soil type and composition, contaminant concentration, amount of precipitation, the temperature, and the amount of light. Toxic effects in plants can vary considerably with lead concentration, depending on such variables. For example, in one study 50% growth inhibition did not occur until the lead concentration in the water surrounding the plants reached 10 parts per million, whereas in phosphate deficient water, 50% inhibition occurred at a lead level as low as 0.5 ppm.

Because lead is more soluble at an intermediate pH range, its availability can be reduced by adding lime or phosphate to soil normally in the neutral range on the acid-base continuum, making lead less soluble by raising the pH as well as converting it to hydroxide, carbonate, or phosphate compounds of very low solubility. Presumably one could also add acid to bring the soil pH to lower lead solubility levels on that side of the curve. However, most plants do not tolerate acid conditions. Organic compounds in soil also have a tendency to bind lead, making it less available for uptake by plants. Even when lead in soil is at natural background concentrations in the range of 16 to 20 ppm, only 0.05 to 5 ppm may actually be available for uptake into plants. Contaminated soils tend to have higher percentages of lead available for uptake into plants. Since lead tends not to migrate readily in soil, it can build up in surface layers. Thus shallow rooted plants, such as garden plants and especially root crops such as carrots and radishes are more likely to become lead contaminated. Lead is likely to be at least 2 to 20 times greater in roots than shoots of plants. On the other hand, tests showo very little lead uptake into plants grown on soil to which sewage sludge was added as fertilizer and soil conditioner. Apparently the high organic content of such sludge acts to bind lead making it much less available to the plants. For many plants, much more lead remains in soil than is taken up by plants. With lettuce for example, a plant that more readily takes up lead than many others, experimental soil lead measurements were 200 ppm when lead in the plants was 3 ppm, giving a soil to plant ratio of 66.7. In general greenhouse tests, soil levels ranging from 76 to 164 ppm lead resulted in plants with lead concentrations in edible portions ranging from 1.3 to 16 ppm. One should remember, however, that portions of plants not eaten by humans may serve as fodder for animals, and that such portions could have higher lead levels than those we eat. A relatively new technique for cleaning up contaminated sites, phytoremediation, uses plants whose ability to take up lead has been enhanced through bioengineering and genetic manipulation. This technology is discussed in Chapter 7, on pollution control and cleanup.

The effects of lead in plants vary because plants differ in uptake and sensitivity to lead. Soil levels of lead exceeded 1000 ppm before adverse effects were seen in apples or grapes, for example. In fact, for many years lead-arsenate was used as a pesticide to protect apple orchards. In some experiments at 1000 ppm lettuce yields were reduced, but not those of oats. Multicellular plants, like their algal relatives, apparently have mechanisms, not available in animals, for holding lead away from the more sensitive parts of their cellular machinery, thus minimizing the toxic effects of this element. These binding mechanisms help to exclude or limit lead from the sensitive sites in the cell nucleus, plastids, and mitochondria. The genetic material DNA resides in the nucleus; the plastids make compounds for the plant by using the energy of sunlight, and mitochondria are the energy factories of the plant cell.

Although land plants can apparently take up some lead deposited on their leaves or other above-ground parts from the atmosphere, most lead is taken up from the soil by the root system where it remains. Lead absorbed in the above ground parts of the plant is also not readily translocated. It has been estimated that airborne lead, even when atmospheric levels are high, contribute only 0.5 to 1.5% of lead directly to the diet. However, atmospheric lead deposited on soil can later be available for uptake through the roots. Lead content of fruits and vegetables in the U.S. measured in 1968 ranged from 0.01 to 0.71 ppm in edible plant tissue. Exposure of red spruce seedlings to lead in the soil during one growing season brought about significantly elevated concentrations of lead in above ground tissues such as the xylem, growing tissue near the surface, and the bark during the following growing seasons. In these trees, lead that was temporarily stored in the roots could later be mobilized to other tissues.

Lead Effects in Aquatic Animals

A number of studies have shown the ability of marine organisms, especially invertebrates (animals without backbones), to take up metals. Bivalve mollusks such as clams, oysters, mussels, and scallops, perhaps more than any other group, are pre-eminent concentrators of heavy metals. Blue mussels, Mytilus edulis, because they are so widely occurring in marine and estuarine environments on both the East and West coasts of the U.S., have served as an indicator of pollution in the National Oceanic and Atmospheric Administration's "mussel watch" program. Very recently we learned that what was thought to be a single wide ranging species, M. edulis is actually three different species; how this will affect the mussel watch data base is still unclear. Radio labeled metal uptake studies in a related mussel, Mytilus galloprovincialis, carried out both in the laboratory and the field, showed similar absorption efficiencies of about 60% for lead, whether it was in the dissolved phase or associated with food. Dissolved lead was more likely to concentrate initially in the gill and then end up in the shell whereas lead in food, as might be expected, initially concentrated in the digestive gland. In laboratory experiments, researchers found a lead uptake of 277 ppm over a period of 20 weeks in oysters. Another determination in oysters showed a concentration ratio, in the animals compared to the water, of 6,600. In the Singapore River in southeast Asia the highest lead levels were found in invertebrate animals, such as polychaets, living in sediments. Fish had the lowest levels. This is consistent with previous determinations, for example, of rainbow trout with concentration ratios, compared to their watery environment, in the range of 700 to 800, much lower than those for invertebrates cited above.

Toxic effects of lead are readily apparent in mine drainage areas or other heavily polluted locations where few animals and plants are left compared to other parts of their ecosystem. Populations of aquatic invertebrates and fish have been severely decimated by mining waste containing lead deposited in streams. High lead levels kill the animals directly; lower concentrations act over a period of time with subtle detrimental effects on behavior and/or reproduction that may eliminate populations. In addition to the effects of lead, changes in pH brought about by the mining discharges, or other contaminants contained therein may be factors in loss of the animals. Poisoning of prey species may be another way of causing the death of a population dependent on that source of food.

Species of invertebrate aquatic animals, those without backbones such as worms and insects, species vary in sensitivity to effects of lead. The uptake and toxicity of lead vary with the type of lead (i.e., whether in an organic compound or in ionic form) , how much of it is dissolved in water, or water hardness or other mineral content. Embryos of an aquatic snail were all killed at lead levels between 1 ppm and 500 ppb. At 100 ppb, 41% hatched but only after a 37-day delay in development. After an additional 15 days, all the hatched snails had died. Adult animals are usually much more tolerant than young.

Apparently some more complex and larger invertebrates, such as crabs or adult molluscs (clams, oysters, snails, squid, etc.) may be able to adapt to high concentrations of lead. (end note*)

The inorganic, or metallic forms of lead apparently do not biomagnify up food chains as do DDT, PCBs, methyl mercury, and the organic forms of lead. A number of researchers, including some at Oklahoma State University who studied distribution of lead throughout the ecosystem of a pond on their university campus, have confirmed that inorganic lead apparently does not concentrate at increasing levels in higher trophic levels. In the pond, the top layer of sediment contained 529 parts per million (ppm) lead, almost 40,000 times the concentration of lead in the water that was 13 parts per billion (ppb). The average level of lead measured in plankton was 281 ppm (dry weight); in bottom-dwelling invertebrate animals the level was 37 ppm, and in mosquito fish, 11.5 ppm. Thus while lead certainly was taken up by plants and animals, in which plankton and in turn are eaten by the mosquito fish, amounts of lead didn't multiply up the food chain.

Organic lead compounds (tetraethyl- or tetramethyl-lead) are extremely toxic to aquatic animals. Scientists at the Canada Centre for Inland Waters measuring effects in juvenile rainbow trout; they found that uptake of these organic forms of lead was very rapid. In contrast to inorganic forms of lead, the organic forms may, like methyl-mercury, be more likely to biomagnify in the food web.

A variety of sublethal effects in fish have been observed at lead concentrations down to 7 ppb. While gross contamination may result in fish kills, sublethal toxicity may exert subtle damage to populations of fish over longer time-periods and over wider areas of the ecosystem as the lead concentrations spread and are diluted out. As with invertebrates, different species, sizes, life stages of fish show a wide range of sensitivity to lead concentrations. Water quality, which influences bioavailability of lead, also plays a substantial role.

Even at lead concentrations at or below the 50 parts per billion previously considered safe in drinking water for human consumption, chronic lead exposure to fish may bring about increased mortality rates, reduced hatching success and indications of neurotoxicity as indicated by higher incidences of black tails (darkening of the caudal area) and spinal curvatures. In a Colorado stream that received contaminants after a dam holding back tailings from a mining site broke, rainbow trout exhibited neurological damage, including spinal curvatures and blackening of the tail. The stream contained up to 50 ppb of lead per liter of water. Because of the sensitivity of these fish, a Maximum Acceptable Toxicant Concentration (MACT) of 7.2 mg/l (ppb) has been suggested for rainbow trout. Brook trout also showed scoliosis (bilateral spinal curvatures), an abnormality of the spine, and reduced growth after long term exposure to lead. These effects lasted over several generations.

Some of the same biochemical lesions occur in fish as have been observed in humans - for example, anemia and red blood cell stippling, hemolytic anemia, and neurotoxicity. Observations on behavioral changes include lowered stamina and decreased swimming capacity. This perhaps results from decreased oxygen exchange at gill surfaces and reduced oxygen transport. Ion exchange capacity, critical for osmoregulation (the maintenance of mineral and water balance), has been found diminished in some species after exposure to lead. On the other hand, decreased swimming capacity may result from toxicity to neural structures or pathways controlling movement. Lead has produced prolonged states of hyperactivity in fish; this may result from interference with brain neurotransmitter activity underlying circadian rhythms.

However, unique to fish, lead exposure may cause excessive mucus secretion; this may interfere with the role of the gill in diffusion of gases - the uptake of oxygen from water and expulsion of carbon dioxide. By interacting directly with the glycoproteins (proteins with sugar groups attached) in the mucus, lead may actually alter the physical properties of this material; such changes may affect the protective and hydrodynamic resistance functions of the mucus and thus could have an effect on the survival of the fish.

Effects of lead depend on such water characteristics such as hardness. Studies in water of hardness between 25 and 40 mg/l (as calcium carbonate), showed that lead at a concentration of 0.48 ppm caused inhibition of egg hatching in several species of fish. Fish tested included rainbow and lake trout, channel catfish, bluegill, and white sucker. Mortality in the larvae after hatch, occurred at concentrations as low as 0.12 ppm lead. After transfer to clean water, the clearance time of lead in fish is much shorter than that for humans, a half time of 3 to 4 weeks in fish compared to years in people. Even after transfer to clean water, however, some effects of lead exposure may linger. Researchers have shown that treatment with a chelating agent, dimercaptosuccinic acid, hastened recovery of the rainbow trout, with which they were experimenting with.

Lead in water causes changes in behavior in bullfrog tadpoles. By measuring the learning ability of the tadpoles in a discriminate avoidance test, and carrying out biochemical assays of neurotransmitters, researchers implicated lead effects on monoamine brain signaling chemicals. Further work with bullfrog tadpoles as a model to examine and understand mechanisms of lead neurotoxicity looks promising.

The Michigan Department of Public Health, concerned that lead may be a risk to sports anglers who typically eat greater amounts of locally caught fish from the Great Lakes , tested blood and found that the anglers had more than 40% greater lead concentrations than people who did not regularly eat locally caught fish.

Lead in Waterfowl

Until changes in regulations requiring replacement of shot made from lead, by non-toxic alternatives, it had been estimated that over one million wildfowl in North America died each year from picking up lead shot, mistaking it for grain or for the gravel which they use to grind up their food. Waterfowl that are active bottom feeders are most likely to be poisoned by ingesting or taking lead shot into their gizzards. G.B. Grinnel published observations of waterfowl poisoning by lead shot ingestion as early as 1894, in the wildlife magazine, Forest and Stream. Other countries have also reported poisoning from lead shot. An investigation of swan deaths in England revealed that half may have been from lead-poisoning as determined from the correlation of blood-lead to the amount of lead shot in their gizzards.

Chronic lead poisoning is associated with starvation and weight loss. Before death, birds may lose up to 60% of their body weight. On the other hand, acute lead poisoning in ducks, swans, and geese may leave them so weak as to be unable to fly, even before much loss in body weight has occurred. Observations in the early 1900s, in which remains of lead pellets were found in birds' gizzards, described waterfowl having a rattling in the throat, with the bill held open much of the time and dribbling a yellowish fluid. Often the birds couldn=t fly or walk because of progressive wing and leg muscle paralysis. On land the tips of the primaries dragged the ground and on water the wings floated loosely on the surface. One study in the 1950s found that after the fall and early winter hunting season, 12 percent of ducks had gizzards containing lead. Ingested lead pellets usually disappear from the gizzard in about 20 days, either by eroding or passing through the digestive tract. But even if the bird doesn=t die during that initial period, the chronic effects of poisoning may last.

In a 1989 paper, Dr. Douglas Roscoe and colleagues from New Jersey's Division of Fish, Game, and Wildlife, NJDEP, detailed their investigation of lead-poisoning of Northern Pintail ducks feeding in a tidal meadow that was contaminated with lead shot from a trap and skeet range. Shiny lead shot may look very much like seeds the birds like to eat for food. In follow-up studies, published in 1995 and 96, these researchers detailed adverse effects of trap and skeet range lead on small mammals and frogs. Elevated tissue lead levels were found in shrews, voles, mice, and frogs. Exposure was high enough to depress enzyme levels in white-footed mice and in green frogs; hemoglobin concentrations were reduced in the mice and hematological and histopathological lesions associated with lead toxicosis were observed in some animals. In their study of development in frogs, Pickerel frogs (Rana palustris), exposed to water from the range exhibited substantial mortality. Mortality was total for tadpoles exposed to undiluted range water and 98% for range water diluted to a 75% level. Autopsy showed tadpoles that died had stunted tail growth, curvature of the spine, hydropsy, and reduced body size.

The U.S. Fish and Wildlife Service has estimated that from 1965 to 1971 approximately 3000 tons of spent lead shotgun pellets were released into the environment by hunters. During this same time, approximately 1500 tons went into the environment annually in Canada. Ingestion of lead shot has had a substantial effect on some populations of ducks particularly in the Atlantic flyway. Lead shot from hunters can be a special exposure hazard to birds of prey. The National Wildlife Health Center of the U.S. Fish and Wildlife Service has documented lead-poisonings of many bald eagles; the eagle=s prey had been waterfowl that had ingested lead shot.

Wild birds are also vulnerable to lead-poisoning from lead fishing sinkers or split shot, the slotted weights fisherman use on their lines. Between 1984 and 1990, 17% of common loons, found dead or dying, collected in Minnesota were shown to have been killed by lead-poisoning. Fishing sinkers can be easily lost or discarded into the environment where they may end up in bottom sediments of lakes, ponds, or other water bodies, or along shorelines, piers, embankments, or rock jetties. If an angler's hook or line were to get tangled in weeds or other obstructions, the sinkers may be lost in the water where they could easily be ingested by water birds feeding on seeds or other food. Sinkers may also be dropped or discarded on land close by the water bodies; here they also could easily be picked up by waterfowl. In shallow water areas discarded or lost fishing sinkers are extremely persistent and thus may be available to waterbirds for hundreds of years. Natural deposition and sedimentation processes may eventually cover the discarded sinkers; but activities such as boating or dredging may disturb sediments and uncover the lead sinkers again. Receding water levels due to drought, tidal effects, natural subsidence, or to intentional drawdowns in reservoirs also could make sinkers readily available again.

Due to adverse effects on breeding adults, lead poisoning may be an important factor in limiting loon populations in some areas. This was borne out by data from New Hampshire, Wisconsin, Maine, and Minnesota submitted to the USEPA by environmental groups petitioning for a ban on use of lead sinkers. Scientists in New England found that lead toxicity from ingested fishing sinkers was the most typical cause of death in adult breeding common loons. Levels of lead found in the blood of loons that had ingested sinkers averaged 1.4 ppm, substantially greater than the 0.35 to 0.60 ppm lead in the blood scientists consider indicative of lead poisoning in many species. Results from necropsies conducted on 222 common loon carcasses from 18 States submitted to the National Wildlife Health Research Center from 1975 through 1991 showed that eleven of these birds had fishing sinkers in their gizzards and that lead poisoning was responsible for 6 percent of common loon deaths. These data also revealed that two common loons had ingested what appeared to be lead jigs, weighted hooks used for fishing. While not listed as a threatened or endangered species under the Federal Endangered Species Act, common loons are listed as an endangered or threatened species in some New England States. In the western United States lead poisoning from ingestion of lead pellets or fishing sinkers accounted for approximately 20 percent of the known deaths of trumpeter swans in Idaho, Montana, and Wyoming, and nearly 50 percent in western Washington. Tumpeter swans are particularly susceptible to lead poisoning because they feed by digging up large amounts of bottom sediments of streams and lakes, and ingesting large amounts of plant material in this manner.

In upstate New York, for example, a study that focused on lead shot in a lake dredging project, reported that for five months in 1990, an average of 4.2 fishing weights per day was found in sediment of the lake during the dredging process. Approximately 1225 cubic meters of sediment were dredged each day in the 60-acre lake. Mute swans were found poisoned in England, along a popular fishing section of the river Trent that was heavily contaminated with lead sinkers. In a one hour period, 1,100 lead split shot sinkers were collected by two people along a 100-meter stretch of riverbank. Another study in South Wales and in England of the loss of lead split shot by anglers found a range of 5 to 300 sinkers per square meter in the water along the shore line and along the banks of several lakes and small ponds. Each person fishing dropped 4 to 7 sinkers per visit to the water body, the authors of the study calculated.

The accumulation of lead shot over the years can be enormous; the Lincoln Park Skeet and Trap Club, a Chicago gun club located on the shores of Lake Michigan, since 1912, have shot 400 tons of lead shot into the lake. After intervention by regulatory agencies, the club had to hire a dredge company to clean up the lead contaminated sediments. In another case, 4 million pounds of lead shot were found in sediments along approximately 650,000 yards of shoreline of the confluence of the Housatonic River and Long Island Sound, in Southern Connecticut. Here the Remington Gun Club was ordered by the Connecticut Department of Environmental Protection to stop using lead shot by the end of 1986, to shut down the club, and to pay for analysis of the harm to the environment. According to an April 1991 article in Hazmat World, the site=s owner, Remington Arms. Co, had to pay to dredge the sediment up, remove the lead shot and return the cleaned sediment to the river and sound.

Waterbirds may intentionally pick up sinkers, mistaking them for seeds. Birds may inadvertently ingest the sinkers to use as grit in their gizzards. (Because birds have no teeth they use small pebbles to grind up food items as an aid in digestion.) Lead dissolves in the acid environment of the bird's digestive system and thereby is mobilized to various tissues where it causes biochemical damage. A single sinker or split shot or two swallowed with food or taken up as grit in the gizzard of birds may introduce enough lead into the bloodstream to be fatal. In a 1959 study, it was found that 7% of mallards in a sample of 17,000 contained 1 or more lead shot. In another national and state survey of hunting areas, 8.9% of gizzards from waterfowl in a sample of 2,734 animals contained at least one shot. Researchers from the U.S. Fish and Wildlife Service at Patuxent Wildlife Research Center in Maryland and at their Pesticide Research Laboratory in Columbia, Missouri, measured blood-lead in ducks; 12% of the sample exhibited over 500 ppb blood-lead and greater than 50% ALAD enzyme inhibition.

As reported in the New York Times, February 14, 1989, veterinarians at the Raptor Rehabilitation Center at the University of Minnesota in St. Paul, were using techniques developed for treating human cancer patients to save trumpeter swans. A drought in 1989 had lowered water levels in lakes and ponds; the swans gained access to lake bottom areas filled with lead shot. Using endoscopes, the vets were able to see into the gizzards of the birds and extract lead shot with tiny tweezers. Although these birds have never been officially declared endangered animals, they came close to extinction in the early part of the 20th century. Magnificent in their snowy white plumage, trumpeter swans once were common across much of North America, but they suffered from loss of habitat and from hunters eager for their meat and feathers. By the 1930s only a small group remained in the lower 48 states, near Yellowstone Park, although there was a large population in Alaska. In 1994, it was reported that Canada was slowly moving toward a ban on lead shot for hunting, even though of five trumpeter swans recently reintroduced into the Wye Marsh Wildlife Center in Ontario, three had died and two survivor's throats were so damaged that their trumpet calls became high-pitched barks. Although the Canadian Wildlife Service banned the use of lead shot in the 1,100 hectares of the Wye Marsh reserve, they were reluctant to impose a general ban because of the difficulties and unpopularity with hunters of the ban imposed in the U.S. However, a large-scale study published in 1996, involving almost 9500 juvenile ducks, showed wide ranging exposure to lead shot. It resulted in a change of policy, as Canada has now instituted a more general ban on hunting with lead shot.

Lead Effects in Other Birds

A study looking at lead levels in feathers of several species of birds found the highest lead levels were found in cattle egrets in Cairo, Egypt. There, the nesting grounds in the middle of the city were exposed to large amounts of lead in automobile exhaust from leaded gasoline. Researchers have examined feathers of California condors and compared them to turkey vultures whose populations are stable. Elevated levels in the condor feathers directed researchers to analyze lead levels in the birds' foods to determine possible contamination sources. In the northeastern United States, a study of common terns' feathers between 1978 and 1992 found high lead levels in the feathers in the late 1970s, with levels decreasing significantly by 1985, but increasing again in 1992. The phase-out of lead in gasoline during the 1980s was thought to have contributed to the decrease. The more recent increase may have been due to removal of leaded paint on bridges, which occurred in the 1990s.

Lead is neither essential nor beneficial to animals. In birds, studies show adverse metabolic effects. Lead may cause several sublethal effects including changes in the production and development of blood cells and modifications in the function and structure of the central nervous system, kidney, and bone. Severe damage to the central nervous system results in stupor, convulsions, coma, and death. Lead can cause changes in behavior, in the ability to reproduce, and the development of the chick within the egg. Studies in mallards have shown that ingested lead can impair the immune system by altering antibody production and lowering numbers of white blood cells and spleen plaque-forming cells. Lead-poisoning symptoms in birds also include loss of appetite with resulting weight loss, lethargy, weakness, emaciation, drooped wings, diarrhea, impaired balance and depth perception, impaired locomotion and an inability to fly. Lead exposure depletes fat deposits in the body and atrophies the bird's pectoral muscles. The progression of symptoms ends in the bird's death.

Younger birds are more susceptible to lead exposure than older animals. EPA scientists consider the toxic level of lead in the blood of waterbirds to be on the order of 500 ppb; toxic symptoms may begin to appear at 200 ppb lead. The level of lead in the liver considered lethal in waterbirds is 5000 ppb or more. After exposure to lethal amounts of lead, birds become less mobile, are limited in their ability to forage for food and to seek cover, tend to avoid other birds, and become increasingly susceptible to adverse climate changes and to predators. Death follows exposure in an average of 2 to 3 weeks. The behavior of lead-injected herring gull and common tern chicks was investigated by Dr. Burger and Dr. Michael Gochfeld who found behavioral changes related to survival and growth in the wild. The lead injected chicks begged as vociferously as control chicks, but were less able to compete for food, their growth was depressed, and were slower than the controls in recognizing their parents.

Poisoning of a particular species of bird or other animal may cause perturbations of food webs or other indirect effects in ecosystems. The health of one population is often dependent upon other populations within a natural community. Thus adverse effects of contaminant exposure on the total environment need to be considered in addition to effects on a specific population or species.

Lead Effects in Mammals

Mammals are exposed to environmental lead and are affected by this neurotoxin in much the same ways. A study in 1985 found neurotoxicity in monkeys exposed at levels that CDC is now calling dangerous to children. After exposure and initial high levels of 25 mg/dL blood, stabilizing at a maximum of 13 mg/dL blood, the monkeys when tested responded differently to controls to learning tasks, had impaired ability to learn a task involving reversal of discrimination. Other researchers have observed similar decrements in learning ability in laboratory rats exposed to lead.

Marine mammals may be exposed to lead in food they eat. A study of teeth of sea otters from the waters off Amchitka Island in Alaska, comparing contemporary animals to those approximately 2000 years old showed the results of contamination of the marine food chain in the modern animals. Analysis of the isotopic ratios of lead allowed researchers to distinguish anthropogenic lead from Asia and western Canada found in the modern animals from the natural lead sources measured in the remains of teeth from preindustrial otters.

Squirrels have been poisoned when they chew on urns, statuary and other garden fixtures made of lead. Squirrels seem to really like the soft metal, sometimes gnawing until the fixtures are virtually unrecognizable. Animals in zoos are susceptible to lead poisoning from both leaded paint on their cages and their location in heavily trafficked urban areas.

Accidental poisonings of domestic animals by lead are common because lead-containing materials are so often found around farms and houses, that is old paint cans, batteries, discarded oil filters, crankcase oil, for example. In some cases lead exposure has resulted in some degree of impairment of the normal functions of the animal's central nervous system, gastrointestinal tract, muscular system and blood-forming system, contributing eventually to the death of domestic animals. In less severe cases of lead-poisoning, the symptoms in cattle and other domestic animals include maniacal excitement, depression, anorexia, colic, ataxia, diarrhea, blindness, grinding of teeth, circular movement and pushing against objects. Poisoning of horses from grazing on contaminated soil and of cattle from ingestion of silage contaminated with lead shot from trap shooting have been documented in the U.S., the United Kingdom and Ireland. The age of the animal, the form of the lead, the condition of the animal, the amount and rate of lead ingestion, may make a difference in the uptake and effect on the animal.

Ewes grazing in areas of lead mining have suffered spontaneous abortions. The lethal dose of lead appears to be smaller in pregnant than in non-pregnant ewes. Horses have been accidentally poisoned with lead by drinking contaminated spring or stream water or eating grasses contaminated with lead. Lead can be passed into milk from cows poisoned by lead. According to a 1991 report, tissues from sheep and lambs bred near a lead smelter and mining area in Sardinia, Italy, had significantly elevated lead concentrations, approaching or exceeding threshold toxicity levels. Liver samples of sheep grazing in the mining area contained 30 times the lead levels of animals reared in less exposed conditions, implicating contaminated forage as the route of uptake for bioaccumulation of the toxic metal.

When lead is taken up in livestock, it accumulates mostly in bone, which is a lead storage site and may contain 90 to 98% of the total body burden. People eating meat thus are not necessarily exposed to high lead levels; however, as discussed in Chapter 2, bone-meal is often added to other foods to increase phosphorus and calcium. Clinical lead-poisoning has occurred in humans who have consumed such contaminated bone-meal as a food supplement.

Animals as Environmental Monitors

Measuring lead in animals provides a means of monitoring potential sources and anticipating environmental risks. Use of feathers to ascertain lead exposure in birds is very effective since approximately 60% of the body burden of this metal goes into the feathers.

Animals poisoned in the wild ought to alert us to the imperative to control lead emissions in the environment. Simple monitoring if blood-lead concentrations in dogs or cats can be easily and inexpensively done. The results can predict human risk without testing young children. This monitoring procedure could also be used even before a child is brought into the home, to determine the risk of lead exposure. Too often, we as a society have been careless with our industrial activities and uses of materials. The adverse effects of chemicals like lead on plants, animals, and ecosystems act as a warning beacon. The poisoning of animals which are closer to home, as domestic pets and farm animals to warn us of hazards to ourselves. The next chapter reviews effects of lead in humans.


Buck, W.B., L-M. Cote, & P Berny. 1994. Household Pets as Monitors of Lead Exposure to Humans. Hazardous Waste Research and Information Center. Champaign, IL.:Illinois Dept. Energy and Natural Resources.

Burger, J. 1995. A risk assessment for lead in birds. Journal of Toxicology & Environmentla Health 45:369-396.

Burger, J. 1993. Metals in Avian Feathers: Bioindicators of Environmental Pollution. Rev. Environmental Toxicology. 5: 203-311.

Burger, J., M. Gochfeld. 1993. Lead and Cadmium Accumulation in Eggs and Fledgling Seabirds in the New York Bight. Environ. Toxicol. Chem. 12: 261-267.

Burger, J., K. Parsons, T. Benson, T. Shukla, D. Rothstein, M. Gochfeld. 1992. Heavy Metal and Selenium Levels in Young Cattle Egrets from Nesting Colonies in the Northeastern United States, Puerto Rico, and Egypt. Archives Environ. Cont. Toxicol. 23: 435-439.

Burger, J., I.C.T. Nisbet, M. Gochfeld. 1992. Metal Levels in Regrown Feathers: Assessment of Contamination on the Wintering and Breeding Grounds in the Same Individuals. Journal of Toxicolology and Environmental Health. 37: 363-374.

Cooke, S. W. 1998. Lead poisoning in swans. Veterinary Record 142:228.

Crist, R.H., K. Oberholser, J. McGarrity, D.R. Crist, J.K. Johnson, & J.M. Brittsan. 1992. Interaction of Metals and Protons with Algae. 3. Marine Algae, with Emphasis on Lead and Aluminum. Environ. Sci. Technol. 26: 496-502.

Demayo, A., M.C. Taylor, K.W. Taylor, & P.V. Hodson. 1982. Toxic Effects of Lead and Lead Compounds on Human Health, Aquatic Life, Wildlife Plants, and Livestock. CRC Critical Reviews in Environmental Control. 12: 257-305.

De Pieri, L. A., W.T. Buckley, C.G. Kowalenko. Cadmium and lead concentrations of commercially grown vegetables and of soils in the Lower Fraser Valley of British Columbia. Canadian Journal of Soil Science 77:51-57.

Flint, P.L., M.R. Petersen, J.B. Grand. 1997. Exposure of Spectacled Eiders and other diving ducks to lead in western Alaska. Canadian Journal of Zoology 75:439-443.

Fisher, N.S., J.-L. Teyssie, S.W. Fowler, & W.-X. Wang. 1996. Accumulation and Retention of Metals in Mussels from Food and Water: A Comparison under Field and Laboratory Conditions. Environ. Sci. Technol. 30: 3232-3242.

Franson, J.C., M.R. Petersen, C.U. Meteyer, M.R. Smith. 1995. Lead poisoning of spectacled eiders (Somateria fischeri) and of a common eider (Somateria mollissima) in Alaska. Journal of Wildlife Diseases 31:268-271.


Kuzirian, A.M., F.M. Child, H.T. Epstein. 1996. Lead affects learning by Hermissenda crassicornis. Biological Bulletin 191:260-261.

MacLean, R.S., U. Borgmann, D.G. Dixon. 1996. Bioaccumulation kinetics and toxicity of lead in Hyalella azteca (Crustacea, Amphipoda). Canadian Journal of Fisheries & Aquatic Sciences 53:2212-2220.

Marinussen, M.P., J. C. van der Zee, E.A. Sjoerd, T. M. de Haan, A.M.Frans. 1997. Heavy metal (copper, lead, and zinc) accumulation and excretion by the earthworm, Dendrobaena veneta. Journal of Environmental Quality 26:278-284.

Mautino, M. 1997. Lead and zinc intoxication in zoological medicine: a review. Journal of Zoo and Wildlife Medicine 28:28-35.

Moore, Joseph L. Hohman, William L. Stark, Timothy M. 1998. Shot prevalences and diets of diving ducks five years after ban on use of lead shotshells at Catahoula Lake, Louisiana. J. Wildlife Man. 62; 564-569.

Nixdorf, W.L., D.H. Taylor, & L.G. Isaacson. 1997. Use of Bullfrog Tadpoles (Rana catesbeiana) to Examine the Mechanisms of Lead Neurotoxicity. American Zoology. 37:363-368.

Phinney, J.T. and K.W. Bruland. 1994. Uptake of Lipophillic Organic Cu, Cd, and Pb Complexes in the Coastal Diatom Thalassiosira weissflogil. Environ. Sci. Technol. 28: 1781-1790

Ramsey, D.T., S.W. Casteel, A.M. Faggella, C.B. Chastain, J.W. Nunn, D.J. Schaeffer. 1996. Use of orally administered succimer (meso-2,3-dimercaptosuccinic acid) for treatment of lead poisoning in dogs. Journal of the American Veterinary Medical Association 208:371-375.

Rice, D.C. 1996. Effect of long-term lead exposure on hematology, blood biochemistry, and growth curves in monkeys. Neurotoxicology. 18:1, 221-236.

Rocke, T.E., C.J. Brand, J.G. Mensik. 1997. Site-specific lead exposure from lead pellet ingestion in sentinel mallards. Journal of Wildlife Management 61:228-234.

Scheuhammer, A.M. and K.M. Dickson. 1996. Patterns of Environmental Lead Exposure in Waterfowl in Eastern Canada. Ambio 25 (1): 14-20.

Schmitt, N., G. Brown, E.L. Devlin, A.A. Larsen, E.D. McCausland, & J.M. Saville. 1971. Lead Poisoning in horses. An environmental health hazard. Archives of Environmental Health. 23: 185-195.

Shlosberg, A., M. Bellaiche, S. Regev, R. Gal, M. Brizzi, V. Hanji, L. Zaidel, A Nyska. 1997. Lead toxicosis in a captive bottlenose dolphin Tursiops truncatus) consequent to ingestin of air gun pellets. Journal of Wildlife Diseases 33:1325-139.

Smith, D.R., S. Niemeyer, J.A. Estes, & A.R. Flegal. 1990. Stable Lead Isotopes Evidence Anthropogenic Contamination in Alaskan Sea Otters. Environ. Sci. Technol. 24: 1517-1521.

Stair, E.L., J.G. Kirkpatrick, D.L. Whitenack. 1995. Lead arsenate poisoning in a herd of beef cattle. Journal of the American Veterinary Medical Association 207:341-343.

Stansley, W., D.E Roscoe. The uptake and effects of lead in small mammals and frogs at a trap and skeet range. Archives of Environmental Contamination & Toxicology 30:220-226.

Thomas, V.G., M. Owen. 1966. Preventing lead toxicosis of European waterfowl by regulatory and non-regulatory means. Environmental Conservation 23:358-364.

Tucker, R.K. and A. Matte. 1980. In vitro effects of cadmium and lead on ATPases in the gill of the rock crab, Cancer irroratus. Bull. Environ. Contam. Toxicol. 24:847-852.

Van Den Berg, K.J., J.H.C.M. Lammers, E.M.G. Hoogendijk, B.M. Kulig. 1996. Changes in regional brain GFAP levels and behavioral functinoing following subchronic lead acetate expsure in adult rats. NeuroToxicology. 17:3, 725-734.

Weber, D.N., W.M. Dingel. 1997. Alterations in Neurobehavioral Responses in Fishes Exposed to Lead and Lead-chelating Agents. American Zoology 37:354-362.

Weber, D.N., W.M. Dingel, J.J. Panos. 1997. Alterations in neurobehavioral responses in fishes exposed to lead and lead-chelating agents. American Zoologist 37:354-362.

Work, T. M., M.R. Smith. 1996. Lead exposure in Laysan albatross adults and chicks in Hawaii: prevalence, risk factors, and biochemical effects. Archives of Environmental Contamination & Toxicology 31:115-119.