The pathways of exposure to lead for humans and animals include ingestion, inhalation and dermal (i.e., skin) contact. Lead is common in the environment and exposure mainly comes from industrial lead products like leaded paint, gasoline and pesticides and the legacy remnants of those products that are found in soil, dust and water. These highly soluble forms of compounded lead can accumulate in an organism and can cause lead poisoning (toxicity).
Lead ingestion is the primary source of exposure and can cause two different types of lead poisoning, either acute or chronic. Acute lead poisoning may result from either a single ingestion of a soluble form of lead, or by multiple episodes within a short time period, causing a large spike in an organism’s blood-lead levels. The organism’s kidney and liver naturally filter and absorb some of the blood-lead, resulting in higher concentrations of lead within those organs. A real world example of acute lead poisoning is typically associated with cattle. Cattle are exposed to many sources of highly soluble forms of compounded lead in the environment, such as discarded lead sulfate containing batteries and old wood with peeling lead paint. After a cow inadvertently ingests a large amount of soluble forms of lead, blood-lead levels spike. The cow’s liver and kidneys attempt to filter out the lead, but ultimately the ingestion may lead to its death. The dead cow now lies in the field. Its organs contain a very high concentration of lead that has already been metabolized and is extremely soluble. Subsequently, a scavenger like vultures, California condors, ravens, bears or wolves may feed on the carcass before a rancher finds and removes the cow from the field. Consequently, the scavenger ingests significant levels of lead, and this soluble form of lead can easily cause lead poisoning in that animal.
Chronic lead poisoning can occur by ingesting sub-lethal amounts of soluble lead over a long period of time. When an organism consumes a lower amount of such lead, it can slowly sequester the lead from the blood and organs into skeletal tissue, effectively “locking” the lead away so it does not remain in the blood supply and harm the organism. Because chronic lead poisoning causes similar non-specific symptoms such as peripheral nerve damage, gastrointestinal disorders and diminished coordination, it can be very difficult to diagnose without accurate blood testing.
When an organism ingests metallic lead (insoluble lead), the lead resists breakdown under normal digestive conditions in the body and passes out of the organism relatively unchanged. When an organism ingests soluble forms of compounded lead found in industrial products, such as leaded paint, gasoline and pesticides, the lead is readily absorbed in the body and increases blood-lead levels significantly.
Inhalation of lead is mainly attributed to dust particles containing compounded industrial lead from leaded paint, gasoline and pesticides. These highly soluble legacy lead compounds remain in large quantities in the environment, and are deposited into the lungs when inhaled and are directly transmitted to the bloodstream.
Inhalation of lead can lead to elevated blood-lead levels in both humans and animals. Indeed, the California condor has been found to suffer from high rates of anthracosilicosis, which is a form of lung condition associated with the inhalation of dust particles. Because the condors inhale so much dust in their daily activities, the associated residual lead compounds in the soil may significantly contribute to their elevated blood-lead levels.
Dermal exposure to (aka skin contact with) lead is the least likely pathway of exposure to both humans and animals. Industrial lead compounds found in leaded gasoline (tetraethyl lead), which is still used in certain aviation gasolines, is easily absorbed through the skin. Once absorbed, the highly soluble form of lead is transmitted to the bloodstream and can cause elevated blood-lead levels.
Whether ingested, inhaled or absorbed through the skin, the effect of these lead substances on an organism depends upon the chemical properties of the substance, and how the organism retains, processes, and eliminates the substance. The time of retention of a substance is an important factor in how much of the substance ultimately is bioavailable to affect an organism. Also, whether a substance is retained in an organism’s body, and at what concentration, are likewise important factors in determining the potential effect of the lead substance on an organism.
When applied to the discussion of hunting with lead ammunition, the impact of ingesting insoluble metallic lead, in comparison to the impact of ingesting the highly soluble forms of industrial lead compounds, the effect on the organism is starkly contrasted.
Lead poisoning has very nonspecific symptoms, including abdominal pain, peripheral neuropathy, weight loss, and gastrointestinal problems. These symptoms are shared by other heavy metal poisonings, namely zinc and copper toxicosis, making diagnosis difficult without laboratory tests to determine the nature of the heavy metal poisoning.
Lead poisoning is clinically diagnosed in part by blood-lead level measurements. Other forms of diagnosis include x-ray to determine the extent lead has infiltrated the bone tissue, and histological examination.
Typically, when elevated blood lead-levels exceed 45 µg/dL in humans and 50 µg/dL in animals, chelation therapy is used for treatment. Chelation therapy is the administration of chelating agents to remove excessive heavy metals from the body and bloodstream. The chelation agent attaches itself to lead circulating in the blood and allows the kidneys to filter and remove the lead from the blood.
In humans, chelation is generally administered either orally or intravenously. Due to the propensity of chelating agents to remove all metals from humans and animals, chelation treatments should not be performed without direct supervision of qualified medical or veterinary personnel.
Notwithstanding the general preference for oral or intravenous chelation in the medical community, the Condor Recovery Team personnel have been discovered administering chelation treatment to California condors intra-muscularly. Evaluations are ongoing as to the extent of the harm to California condors caused by intra-muscular injections of Calcium EDTA by Condor Recovery Team personnel.
The most commonly used chelating agents are known to cause visceral gout and kidney damage in birds with impaired renal functions, and when improperly administered. Despite the known risks of this treatment, the Condor Recovery Team personnel routinely administered chelation therapy where lead fragments are not found in the condor and where the condor’s blood-lead level are well below clinical levels. As a result, numerous of California condors have been injured and some have died due to visceral gout. Nevertheless, condors continue to receive mis-applied chelation treatments administered by unlicensed individuals in the field, instead of being administered by a veterinarian in a clean, controlled environment.
Hunt for Truth is currently researching the extent of condor mortalities and harm related to the mis-application of chelation treatments by unlicensed and unqualified Condor Recovery Team personnel.
A necropsy (animal autopsy) is the examination of an animal carcass in order to determine the cause and manner of death and to diagnosis and evaluate any disease or injury that may have contributed to its mortality. Necropsies are typically performed by a veterinarian that specializes in the specific species being examined.
Condors atop Chalone Lookout Tower Picture from National Park Service
In evaluating the California condor necropsy reports, Hunt for Truth scientists have found necropsies that improperly conclude that the cause of death is lead poisoning, when the actual cause of death was visceral gout due to the mis-application of chelation treatment. Additionally, data contained in the condor necropsy reports indicate high blood lead-levels, but very few birds showed any evidence of ingesting lead ammunition. Despite the lack of evidence pointing to lead ammunition, lead poisoning from ingesting lead ammunition was determined to be the cause of death. Clearly the Condor Recovery Program (CRP) is ignoring alternative sources of lead exposure to California condors.
One such noted exposure to an alternative source of lead in the environment was discovered at Pinnacles National Monument, where condors 317 and 318 (all birds are numbered by the CRP) were observed ingesting lead paint fragments from the North Chalone Fire Lookout Tower. In turn, these parents fed the regurgitated lead paint fragments to their fledgling (550). Condors 317, 318 and 550 were all tested and found to have high blood-lead levels, and 550 had to be evacuated to the Los Angeles Zoo for intense treatment for lead poisoning.
This highly soluble form of industrial lead can easily cause acute lead poisoning in condors. Other alternative sources of compounded lead that are highly soluble and bioavailable include leaded gasoline, pesticides, mining waste and microtrash. All of these alternative sources need to be investigated and evaluated in order to determine the true cause of lead poisoning in the California condor and to ensure their long term survival.
Waterfowl in North America consist of ducks, geese and swans (Anitidae) that inhabit various fresh and salt water habitats across the continent. These are generally identified as “dabbling ducks,” “diving ducks,” “whistling ducks,” geese and swans.
Dabbling ducks are labeled for the way in which they feed by an inverted position on water plants in shallow waters. Dabbling ducks also feed on plant matter and certain insects out of water.
Diving ducks are those species that feed by diving deeper to feed on vegetation, certain insects and fish in larger bodies of water.
Geese consist of three distinct groups: gray, white and black.
Swans in North America consist of trumpeter, tundra and the non-native mute that was introduced from Europe.
Waterfowl hunting programs are primarily regulated by the U.S. Fish and Wildlife Service under the authority of the Migratory Bird Treaty Act (1918). Federal waterfowl hunting programs are run in conjunction with the state waterfowl hunting programs working in concert with four Flyway Councils: the Atlantic; the Mississippi; the Central, and; the Pacific Flyway Councils. Ultimate authority on the methods of taking waterfowl rests with the U.S. Fish and Wildlife Service.
Under the influence of the U.S. Fish and Wildlife Service and environmental activists, Flyway Councils started implementing lead shot restrictions and permitted methods of take regulations in the mid-1970s. States were not required to implement lead shot restrictions for waterfowl hunting absent federal funding in 1978 (the Stevens Amendment). Waterfowl lead shot bans were ultimately phased in across the United States by 1991, after a combination of litigation by the National Wildlife Federation and the lapse of the Steven’s Amendment in 1986.
Early use of replacement “nontoxic shot,” such as steel, has been noted for a higher crippling potential, which also had an early and negative effect on waterfowl populations. Modern versions of steel shot are still well known for crippling waterfowl.
Hunt for Truth is researching the potential for lead poisoning in various waterfowl.
Upland game differs both environmentally and physiologically from waterfowl. Upland game habitat is broader and is not concentrated over one particular area. Consequently, upland game hunting areas typically do not have places where lead shot tends to accumulate like it does in certain waterfowl hunting areas. Additionally, lead is not readily soluble in soil. Upland game, specifically upland birds, are more particular in their feeding preferences and will not select lead shot preferentially over food (seeds, plant matter, etc.) when foraging. Also, in the unlikely event that an upland bird mistakenly consumes a piece of shot, the food consumed by the animal will stimulate the digestive process such that the bolus of food is rapidly passed out of the stomach before any significant amount of lead can be absorbed. The ingestion of food buffers stomach acid and greatly reduces its already minimal ability to dissolve metallic lead.
Further, the ingestion of food causes the stomach to rapidly process its contents and to quickly expel those contents into the intestinal tract, where complete neutralization of the acid is accomplished. Once in the neutral conditions of the intestinal tract, there is no plausible mechanism whereby metallic lead can be absorbed by the organism. Thus, decreased exposure time in the stomach due to the presence of food makes dissolution of metallic lead extremely unlikely to lead to poisoning of wildlife or humans. In a study directly on point, researchers attempted to poison turkey vultures by continuously feeding six turkey vultures large amounts of lead shot with food. When the birds excreted the shot, the researchers cleaned and re-administered the shot to the birds, with the goal of determining the amount of time necessary for a turkey vulture to succumb to lead poisoning. After 211 days of being continuously fed significant amounts of metallic lead in their food, four of the six turkey vultures in the study showed few signs of lead poisoning. Only when very large amounts of lead were continuously administered for 143 days were the researchers able to induce a fatal lead poisoning in two of the six turkey vultures in the experiment. This experiment clearly shows how difficult it is for wildlife to be poisoned by food containing lead ammunition.