Lead Poisoning: The Lessons of the Birds of Esperance
By Jennifer Modrall and Mark Pokras, D.V.M. Tufts Cummings School of Veterinary Medicine
At first, it was just an unnatural morning quiet that residents noticed. Then birds were found dead by the hundreds. Some people said they saw them dropping from the sky. Locals reported that, "virtually the entire local song bird populations died out in only a few weeks." This was not a scene from a new horror movie about a mysterious plague. The birds died from lead poisoning.
This wasn’t decades ago or in a third world country with no environmental regulation. It was in Esperance, Australia starting at the end of 2006. Lead carbonate (cerrusite ore) from a local mine had been transported through the town for shipment. No one realized that lead dust was escaping at the port until the birds started dying. In the end, officials estimated that more than 9,000 birds died. The dying birds were the sentinel event that forced agencies to investigate, like the proverbial canary in the mine. Once officials investigated, they found an environmental and wildlife catastrophe and narrowly averted a human public health disaster - thanks to the claxon early warning of the birds’ deaths.
Australian officials discovered that lead dust from the ore had contaminated drinking water, soil, harbor sediments, shellfish, and house dust, and found elevated blood lead levels in people, including young children. The birds apparently got the lead poisoning from eating nectar and foods contaminated with lead dust, and from preening the dust off their feathers. Due to their small sizes, sensitivity to toxins, eating habits, and high visibility, birds are all too often environmental sentinels.
Lead poisoning is not a new problem. We’ve known of the dangers of lead for thousands of years. Although human blood lead levels in the U.S. and other developed countries have consistently decreased since regulations removed lead from many gasolines and paints in the 1970s, blood lead levels are still orders of magnitude above "natural" (i.e.: before humans started mining, smelting and using lead).
Acute lead poisoning of humans is still a large problem in many parts of the world, as recent episodes in Nigeria and China have highlighted. In the U.S., it is estimated that 25- 30 percent of children in New Orleans are still poisoned by hazardous levels of lead, mainly from old paints and soils contaminated from years of deposition from leaded gasoline and industrial pollution. Also, dangerously high blood lead levels are still common among certain occupations. Beyond the obviously risky occupations of mining and smelting, other at-risk workers include: painters, carpenters, car mechanics, plumbers, ceramic glazers, and people working in facilities that produce certain electronics and batteries. Workers can inadvertently bring lead dust home, and unwittingly expose their families, especially vulnerable children. Pets often share children’s risks. All these activities, which present lead poisoning hazards for humans, pose similar or greater risks for animals by contaminating their living environment. Simply living around human habitation and activities increases the risk of lead poisoning for animals. Wild animals who live around human habitations or industrial activity can have elevated (sometimes toxic) lead levels. Examples include: Nepalese monkeys living around temples in Kathmandu, Pacific island albatross chicks living near buildings, and urban (versus rural) dogs in India.
In the Esperance lead disaster, thousands of birds died of acute lead poisoning. But, if thousands of birds died, how many other animals suffered from sub-lethal lead poisoning? And, what are the consequences to wildlife of sub-lethal lead exposure? There is a growing body of research indicating that exposure to lower levels of lead once considered "safe," especially chronic exposure, has serious adverse health effects. Once in the body, lead affects virtually every physiological system - cardiovascular, renal, reproductive, and especially the central nervous system. In fact, many sub-lethal negative effects have been found in both humans and animals. These include increased aggressive behavior in humans, cats, and other species; hypertension in people and dogs; learning and behavioral deficits in humans and gulls; and hearing loss in humans and monkeys. Other sub-lethal effects of lead exposure that have been found in people and other species include: decreased reproductive success, decreased IQ in children, cognitive impairment in the elderly, behavioral and psychiatric disorders, and altered immunological, physiological and biochemical processes.
As in humans, some of the most dramatic effects of lead poisoning in animals are found in the young, such as: impaired development of the brain, anemia, decreased growth rates, and increased mortality in hatchling birds. The cognitive and behavioral effects of lead seen in humans can similarly alter wild animals’ physiology and behaviors, potentially in ways that negatively impact their ability to reproduce, migrate, feed, survive, and ultimately maintain stable populations. Such effects would be particularly deleterious for marginalized or endangered species or populations already "stressed" from other pressures.
The effects of acute mortality due to lead poisoning of wildlife should not be dismissed either. The largest impediment to the recovery of the California condor in the wild is arguably death by lead poisoning. Condors and other scavengers eat the discarded carcass waste from animals hunted with lead ammunition, and this source of lead is regularly implicated in elevated blood lead levels or deaths due to lead poisoning. And bald eagles, while no longer a federally endangered species, are reported poisoned and dying by ingested lead ammunition in increasing numbers. What would be the consequences of an Esperance type disaster for an endangered population such as the California condor? Notably, lead ingestion and poisoning have been documented in at least 63 avian species, including 10 globally threatened or near threatened species.
There is also a humane aspect to the issue of lead poisoning in wildlife. Using humans as a "reverse" animal model, we know that lead poisoning, even sub-lethal, is painful, causing colic, nausea, constipation or diarrhea, gastrointestinal pain, joint pain, persistent headaches, and seizures. Sub-lethal levels of lead have been documented in many animals. Is it a big leap to assume they suffer?
Spent lead ammunition also presents problems for other birds, which inadvertently consume lead shot or bullet fragments that have settled in soils and water sediments. Some birds consume soil while foraging, others deliberately eat small stones to aid with the grinding of food within their gizzards. Both groups may concurrently consume lead. It can take as little as one ingested lead shotgun pellet to poison and kill a bird. Wildlife cannot shop for lead-free food or know whether they drink lead-free water.
Humans have amassed vast knowledge about lead’s toxic effects, pervasive environmental contamination, presence in both humans and wildlife, and increasing evidence of adverse health effects at lower exposure levels. However, lead is regulated differently than most other environmental and physiological poisons. (The reasons behind this discrepancy are beyond the scope of this article and perhaps best left to sociologists, economists and historians.) In the case of other environmental threats, such as PCBs and DDT, the necessary proof for banning their use in the U.S. was that the substance was present and persistent in the environment or animals, and that it caused harm to animals or humans. Anthropogenic lead is also known to be present and persistent in the environment, humans and wildlife, and it does cause serious, often irreversible harmful effects.
All aspects of lead production, use, and disposal produce pollution and health risks. The entire life cycle of lead - from mining and smelting, to production of goods, to recycling and disposal - all contribute to lead getting into air, water, and living organisms. Yet, lead is inadequately regulated. Regulations are piecemeal and do not address the breadth of the problem. There are some limits on lead exposure: it is banned in some products (e.g., most gasoline and food cans), its maximum content is limited in others (e.g., children's toys and drinking water), and it is restricted for certain uses (e.g., hunting waterfowl). Additionally, industrial and health regulations vary greatly between countries, even though air and water contamination from mining and smelting, manufacturing, and disposal easily cross international borders. In the U.S., lead is still allowed in some paints (such as for bridges and other industrial uses), lead ammunition and sinkers continue to be used in hunting, fishing, and shooting sports, and occupationally allowable lead levels are still above those recommended by some health experts. Currently, there are only a few uses of lead for which alternatives do not exist, such as certain batteries and electronic components. But where there are viable alternatives to lead use, we should ask ourselves and our policymakers, "Why not switch to less toxic alternatives?"
How do we solve this problem? Regulations help, careful recycling helps, but perhaps the best answer is to stop using lead. There are non-toxic alternatives for almost every use of lead. Some are a bit more expensive than lead, but with a little determination and innovation, we can undoubtedly substantially reduce our lead use and pollution. The lessons of the birds of Esperance are, at a minimum, that lead "escapes," and that the health and environmental consequences of lead are far ranging, difficult to remediate and may be irreversible. Will these lessons be learned, or will, the birds of Esperance be forgotten, and will we allow the problem of lead to persist for millennia more?
Mark Pokras, D.V.M. is an Associate Professor and Wildlife Veterinarian at Tufts Cummings School of Veterinary Medicine’s Wildlife Clinic. Jennifer Modrall is a Project/Research Assistant at Tufts Cummings School of Veterinary Medicine.
What You Can Do
Although the problem of lead is vast, there are actions individuals can take. Educating yourself is key to protecting your family, animals and yourself. Lead enters our lives via many insidious routes, and is present in seemingly innocuous items. Lead paint in older houses and during remodels still presents hazards for many families and animals. What is less well known is that many brass fixtures contain lead that can leach into water, and brass fixtures are often present in homes and water fountains in schools. Lead can be found in many items you might not suspect, such as: bird cages, ceramic glazes on pet bowls, herbal remedies, child and pet toys, and cosmetics, which are not required to list many ingredients, including lead. Seemingly innocent hobbies, such as stained glass, jewelry making, and fishing with lead sinkers, present exposure hazards to the hobbyist, and/or their families and wild animals. Lead fishing tackle and hunting ammunition present serious problems for wildlife and are arguably some of the easiest lead contamination sources to reduce. We must remember that anglers and hunters cannot fix the problem by themselves; they need the assistance of industry and coordinated government agencies. Beyond avoiding lead, the next necessary action is getting lead out of our lives and products, and this will require local, national and international changes in policy and regulations. We can educate ourselves and do our best to avoid lead. Remember, however, that merely making choices to avoid lead does not solve the problems. Wild animals, meanwhile, do not have the luxury of choice.
The web can provide you with both educational information and links to lead-related policy issues and actions. Below is a list of some useful websites, and all U.S. State public health websites have sections on lead poisoning and prevention, and sometimes local lead related issues.
Burger, J. and Gochfeld, M. 2005. Effects of Lead on Learning in Herring Gulls: An Avian Wildlife Model for Neurobehavioral Deficits. NeuroToxicology 26: 615–624. doi:10.1016/j.neuro.2005.01.005
Burger, J. 1995. A risk assessment for lead in birds. Journal of Toxicology and Environmental Health Part A 45: 369 – 396. DOI: 10.1080/15287399509532003
Gulson, B., et al. 2009. Windblown Lead Carbonate as the Main Source of Lead in Blood of Children from a Seaside Community: An Example of Local Birds as "Canaries in the Mine." Environmental Health Perspectives 117:148–154. Available via: http://www.ncbi.nlm.nih. gov/pmc/articles/PMC2627859/pdf/EHP-117-148.pdf
Jusko, T .A., et al. 2008. Blood Lead Concentrations < 10 micrograms/dL and Child Intelligence at 6 Years of Age. Environmental Health Perspectives, 116:243-248. Available via: http://ehp03. niehs.nih.gov/article/info%3Adoi%2F10.1 289%2Fehp.10424
Navas-Acien, A., et al. 2007. Lead Exposure and Cardiovascular Disease—A systemic review. Environmental Health Perspectives, 115(3): p. 472-482. Available via: http://ehp03.niehs.nih.gov/article/ info%3Adoi%2F10.1289%2Fehp.9785
Needleman, H. 2004. Lead Poisoning. Annual Review of Medicine 55:209 -222.
Nriagu, J. 1983. Lead and Lead Poisoning in Antiquity. New York. John Wiley & Sons. 437 pp.
Shih, R.A., et al. 2007. Cumulative lead dose and cognitive function in adults: a review of studies that measured both blood lead and bone lead. Environmental Health Perspectives, 115(3): p. 483-492. Available via: http://ehp03.niehs.nih.gov/article/ info%3Adoi%2F10.1289%2Fehp.9786
Watson, R.T.M., Fuller M., Pokras M, and Hunt W.G. (eds). 2009. Ingestion of spent lead ammunition: Implications for wildlife and humans. The Peregrine Fund, Boise, Idaho. Available via: http://www.peregrinefund.org/Lead_ conference/2008PbConf_Proceedings.htm