Lead is both a heavy and a soft metal, and in a tough, mobile, grinding gizzard, the exterior roughness of the sinker's poured factory mould is rubbed off, leaving a very smooth surface. This produces quite a different kind of erosion than a piece of lead in a soft, stretchy stomach that does not grind. A bullet, most likely scavenged from a dead mammal, that I removed from a the stomach of a Bald Eagle was a large misshapen, sharp-edged thing, eroded yet rough, because the gastric acids had an etching action and the thin, stretchy stomach had no grinding muscle.
In a loon's grinding gizzard, the matte, slate-coloured lead sinker becomes rounded, much smoother than its usual fellow pebbles; the colourful paint on a jig disappears, and the lead body underneath gets smaller and smaller. Those studying lead poisoning in loons have told me they too have seen cases where a jig or sinker was used up completely, and we have seen this ourselves. It doesn't take much to permanently disable; even the smallest splitshot, less than a gram, is fatal for a loon.
Unexpected were several of those “used," smoothed sinkers in the glandular proventriculus. This suggests that the mobility of the whole alimentary tract juggles items up and down during digestion. The proventriculus, though stretchy and not strongly muscular, often has pebbles in it as well.
Other lead characteristics: A scratch with a fingernail on the lead leaves a bright silver line25 on the matte finish, and if the lead is rubbed on a hard, pale surface such as a countertop, it draws a dark mark like a coarse pencil. On X-ray, it stands sharply, brightly out among the pebbles, which though opaque, look softer-edged. Once or twice, though, a small piece of lead has been hidden behind a big pebble, unseen until a second X-ray. And of course, sometimes there is none left to see-- it has all been rubbed away and absorbed.
When the soft lead enters the gastro-intestinal system, it descends to the active digestive area where the combination of acid26 and gizzard and pebble grinding quickly wears off lead, which is then absorbed into the red blood cells in the bloodstream as soluble salts and transported around the body, accumulating in, and damaging, the brain, the liver and kidneys.
Because lead and calcium have properties in common, about 90% of the lead is stored in the bones along with calcium. In the body, things are never stationary, always in flux, in transition. Minerals such as calcium are hourly being either stored in, or taken from, bone in order to maintain essential levels in the circulation. While stored in the bone, the lead is temporarily not toxic, but when calcium demand is increased, calcium and lead together are mobilized from the bone, resulting in lead poisoning “from within"27.
The presence of the lead not only damages parts of the nervous system, especially causing swelling in the brain, but it interferes with the oxygen in the haemoglobin of the red blood cells, causing anaemia. Pb poisoned blood cells show basophilic stippling. In the kidneys, normal reabsorption of important nutrients from the fluid that is becoming urine is inhibited, causing their loss. Healthy kidney tissue finally becomes fibrous, leading to kidney failure and death.
Lead only poisons the organism when it enters the circulation, usually by being swallowed and getting eroded by gizzard and stomach acid. Small, stealthy but permanent effects are also caused by inhalation or absorption through the skin. When lodged in other tissue such as muscle, it rests in relatively neutral tissue, where scar tissue forms around the bullet; lots of people, mammals and birds (including loons) carry old lead shot in their bodies for years. This is why surgeons usually leave bullets in situ unless they are causing trauma that is detrimental to life of the person or animal.
There are rare exceptions. On an American medical TV documentary there was a woman who, over a five-month period, was being chronically poisoned by a lead bullet in her knee, where the strong alkaline synovial fluid of the bursa was slowly eroding the lead which was then being absorbed into her system. She died, mainly from brain swelling, before the cause was found.
# 2878, adult male, November. Beached. Thinnish. Gasping, dying. Euthanasia. Lead sinker weighing 3g in gizzard. Also two very large shots in soft tissue, one in thorax, another in a wing, though neither looked fresh or related to critical condition.
#3652 adult male, August. DOA. Thin. Some loss of waterproofing but good soles. Alimentary tract stuffed full; bulge evident on X-ray, and there were delicate outlines of snails and crayfish even in neck. Post-mortem showed a trace fat under abdominal skin. Esophagus crammed with partly digested fishy-smelling matter and many crayfish bits already reddening. Gizzard only contained a few pebbles, the end of a small black and shiny fish-hook not yet rusted, a frizzle of fishline, and a sinker, like a thick large coin-22mm diameter, 5mm thick, 21g.
# 3680 adult male, September. Beached. Gasping desperately. Thin. Dying. Euthanasia. Though quite rolled on the cassette, the unusual aspect of the X-ray was that the proventriculus and the gizzard were defined by crayfish, pebbles and a sinker. Usually only one part or the other is the container at the time of the X-ray, though as I mentioned before, they are all part of the same mobile digestive tube.
#5042 adult male August. Very weak, cuts from line and blood in the mouth, gasping. Thin. X-ray showed a 30mm straight length of metal in abdomen, and fishing gear in gizzard. Post-mortem revealed leader 25mm long, two bell sinkers of different shapes 19mm x 9mm, 5g, and 10mm x 6mm, 2g, plus half a clip (the brass crosspiece going green) attached to a swivel, along with a few fishbones and scales. Scattered in airsacs through the abdominal cavity were blackened pebbles and an old greenish hook, proof of a rupture. Liver not very healthy. Fair amount of fluid in pericardial sac. Whitish testes, about 15mm, mature. Some flukes in mouth.
Post hoc. I didn't find the long piece of metal, so it must have ended up like the piece rammed into the sternum of # 6032 (please see column called Common Loons, Some Surprising Results from Hook-swallowing; at that time it never occurred to me to look there.
#6328 adult female, June. Had been beached; dying. Eyes slitted, deep gasping about one a minute causing mouth to gape at corners with effort. In pool, beak hung limply underwater and blew bubbles. Waterproofing loss slight and even all over body.
On post-mortem there was a large Fallopian tube, large receding ovary, no fat, organs relatively healthy except for gizzard which was dark and slimy green internally; the pebbles, clip, and lead bell sinker were saved. Small tissue-wrapped amounts of debris were in mesentery outside the proventriculus. Upper half of broken hook turned out to be resting in mesentery too, among the intestines, and it was a sturdy, shiny half that didn't look as if it would break easily. No sign of the barbed end.
Note: the os pubis ends were overriding and very flexible, easily widened with fingers; so this is how those large eggs get through that narrow gap.
#5069 adult male, September. Lifted into boat with very little protest. Gasping, sides of mouth grey with saliva, eyes half open. Very large heavy loon just starting moult- sprinkle of head feathers beginning to escape and body plumage loose. Good waterproofing: first time in 13 lead-poisoned loons (1994). Euthanasia. Blood then taken. Post-mortem showed reasonably healthy interior. No fat. White testes. Gizzard was green and blackish, hardened, with many pebbles and a leader as well as a worn, small ovate lead sinker 5mm x 10mm, 1g. Half a hook-the barbed half, clean and sharp-was among the intestinal coils, neatly bundled in tissue like a spider's fly. Rest must have broken off and been hauled out with the line.
A fishing guide's opinion : “# 2 long shank, #7 swivel wire leader. Setup for pike. 8-lb test monofilament." ALA-d ratio 3.75, lead-poisoned. Of course.
#6382 adult male, August. Reported run over by jet ski, but not injured by it-already dying. Deeply gasping, eyes slitted with nictitating membrane closing often, head hanging, dry gray foam collected at gape. Dreadfully weak. Euthanasia. Bird in fine condition with good waterproofing and soles undamaged. On post-mortem the gizzard was empty except for pebbles and a capsule-shaped sinker. Airsacs opaque and rather tough, and one small white spot near lung suggestive of aspergillosis starting. Lungs reasonable. Testes oval, bluish. Liver looked a good, dark colour. Pancreas obvious.
Here I want to share with you a surprise I accidentally discovered during the three years I had a contract to provide histories, blood and/or bodies to Dr.Anthony Scheuhammer, a researcher then doing lead, mercury and selenium studies at the Canadian government's National Wildlife Research Centre. I had to learn to take the blood samples from loons whether they were strong and healthy or weak and dying, and though instructed to use the brachial vein I soon found the bare tarsus a much more manageable site-loons desperately don't want to be turned on their backs-and the loon could just rest belly-down on the treatment table with a leg hanging over the edge and let me get on with it; if he had to be held it was an easy position, but if the stick did not hurt I have managed by myself. So there was bare skin, little argument, less blood being spilled that was mine (healthy beak-stabs really penetrate; one even once went right through my rubber boot.) But there was always the bird's pain and fear caused by the needle-jabs, which I hated, so that whenever possible I took the sample while the bird was losing consciousness during the course of euthanasia.
One day, about to begin the usual loon-wrestling, I tried an off-the-wall idea. I prepared two syringes and two tubes identically, rinsing all four thoroughly with the same fresh heparin solution and labelling them “A" and “B". I then inflicted one last painful indignity on a loon dying of lead poisoning, taking sample “A", and later during the post-mortem, I much more easily took sample “B" from the very large hepatic vein leading up into the right lobe of the liver.
The lab results: “A" had clotted uselessly as often happened, but “B" from the dead bird was perfect! The lab scolded me over wasting a sample (and their time testing it, I suppose) but they missed the exciting point: usable blood samples can be drawn from birds freshly dead-maybe even deader than that-thus avoiding the pain and struggle for both taker and takee. Everyone working with living creatures should be constantly aware of the terror and hurt that such tests inflict on them, and try to avoid it whenever possible.
The implications have great application for studies involving blood taking. And this is a really big vein in loons, often tensely full: the first time I came upon it, I thought it was a giant aneurysm. It is an ideal site because it isn't necessary to hack one's way up the long bony sternum to find the big vessels of the heart.
Some time later, I found some other researchers taking dead bloods too, even in raptors.
The diagnosis of lead-poisoning may prompt a grab for a bottle of neutralizing compound such as EDTA. This is intended to neutralize the lead that is circulating in the blood stream, but there are dangers. If the state of health is uncertain (as in a creature with which one is unfamiliar) Pb poisoning should be proven first, which takes money and time. I know little about aggressive medical treatments that are used for waterfowl, but I am quite sure that for loons, only caught when they are already critically damaged by the toxin, trying to treat them would be useless and cause much suffering. If, as in the case of the 32 lead-poisoned loons we have seen and autopsied so far, there was a sinker or jig seen on X-ray and the bird was obviously very ill, it was too late for treatment. (NOTE: so far no sinker has ever turned out to be non-toxic material; if it was, the loon would not have become disabled and would not have been caught anyway.)
With our first Pb-poisoned loon we were instructed to give an injection of EDTA, and the loon died immediately. In humans, “[A brand].is capable of producing toxic and potentially fatal effects" mainly by further damaging the kidneys, reads the Compendium of Pharaceuticals and Specialities, 1991. When an early-poisoning-stage creature is treated with these chelating injections, usually EDTA30 any improvement in signs and symptoms is due to a temporary respite caused by the reduction of that 10% circulating lead in the blood, but the lead still in the bones is unaffected. There it is stored, sometimes for long periods, without provoking new symptoms. Pb poisoning recurs again and again over months and years because all the lead is never mopped up.
In the brain, some lead has been stored too, where it cannot recirculate back into the main bloodstream and so is 'trapped' resulting in long-lasting or permanent signs and symptoms. In industry, lead-affected workers, clumsy and lethargic, often get a pension; in homes, children's IQs shrink31; in the wild, brain-slowed loons just die.
.... and certain aggressive treatment regièmes developed for dabbling ducks and swans are, in my view, simply not applicable to loons. Studies have been done involving deliberate lead-poisoning followed by attempts at treatments using penned waterfowl-hardy, relatively tame, at home on land, easy to feed, easy to care for, easy to study. Some veterinarian articles have encouraged the treatment of lead poisoning and advocate aggressive therapy, and it may be appropriate in certain species. One of the therapies32 took up to six weeks and included both lots of i/m and i/v injections, tubing and a gastric lavage-colonoscope procedure, yet no statistics were given to indicate its outcome or whether the birds were ever released.
None of this applies to loons. It is unimaginable to consider trying to capture healthy loons for experimentation, and hopeless, even cruel, to inflict aggressive treatments on those dying from Pb toxicity, whose brains, systems and organs are already permanently damaged. Much of this damage can be found on autopsy.
When confronted with the one deadly aspect that they could wipe out altogether, the lead sinkers, the reaction of the anglers has been a curious combination of disbelief, dismissiveness and denial. One fishing-camp manager told me that if I could prove that fish were being poisoned by lead sinkers, then the fishermen would take interest! Outdoor sport TV programs and magazines rarely give it mention, and though the Canadian government passed a bill some years ago it was a feeble, piecemeal approach, banning sinkers “50g or less in Federal Parks," which allows all the larger sinkers for trolling for walleye etc, and knowledgeable fishermen say that not much fishing is done in Federal parks anyway.
Though some anglers have agreed that a few simple changes in fishing practices would make a great difference to wildlife, the majority do not see themselves in the frame at all and the greatest devotees wax passionate, even angry, when culpability is inferred. One sickly fisherman has been writing whining letters everywhere for years trying to make groups like ours out to be the culprits-- printing such nasty lies and spoiling their fun. I am left with the impression that fishermen want to go on with their pleasures without any interference, especially from the regulations of the government or the urgings of non-fishing laywomen.
So for three years I teamed up (the government prefers the more cautious term “collaborating," which sounds like spy stuff to me) with Dr. Scheuhammer, as I mentioned. His papers, published by a male, lab-coated PhD, are sure to have more impact, though their dryness made them [the ones I read] slow going, and government follow-up avoided taking a stand on the issue despite the evidence.
Though we never met, we once saw each other on a short lead-sinker documentary on the CBC TV's The National; my bit was in our clinic, showing X-rays and gizzard contents, with a dead loon on my treatment table, and Tony's bit was in his laboratory, showing the assay techniques, with a dead loon on his treatment table (one of mine-I recognized the toe-tag.)
Then the interviewer, who had the most expansive segment in the documentary, chatted with three fishermen. The first was disbelieving: “Such a remote chance, like a needle in a haystack." The second was dismissive: “The chance of it happening maybe what, two to three times a year?" And the third was disputing: “Yeah, but there are all kinds of pollutants in the water that are as bad or worse." These are direct quotes from the video-taping done in August, 1996.
Here is the commonest defence we all hear from anglers: “But the statistics show that only a few loons die of lead poisoning." They are correct is pointing out that even the most productive and well-done studies produce only two-digit figures. But the anglers are looking at the problem back to front. No one can argue that lead is fatal when swallowed and anglers use sinkers made of lead. It has and is being repeatedly proven that loons swallow fish with lead sinkers and die of it. The statistics look feeble because so few loons are garnered to be checked at all; researchers who don't get much, can't give much. The scarcity of evidence is caused by the tiny number of people who respond correctly to a dead or dying loon. And the anglers are in the best position to observe-out on the lake for hours-and to help-with a boat and nets-if they care to do so. But we don't see them at our door.
Every year, just at our rural centre amid dozens of lakes, we log many distressing reports from people who have seen sick loons on their lake. They won't, don't or can't, act. The loon gives up the ghost and disappears. Another invisible death. No body. No evidence. No proof.
Since our first proven lead-poisoned loon in 1987, I have worked hard digging into corpses to provide proof so that statistics can be produced to convince anglers of the simple solution they can provide - just don't use lead sinkers!- and for influential groups such as government bodies to publish and act on; the simple solution they can provide- just ban the sale, import and use of lead sinkers.
Besides the federal lab contract, I gave over sixty lectures (before getting tired of preaching to the converted) wrote and published dozens of loon articles and dying-loon and X-ray photographs in venues varying from local newspapers and lake associations newsletters to glossy Ontario Out of Doors and Fly Fisherman and Cottage Life magazines, as well as a fair number of 'loon' columns during my eleven and a half years as a freelance columnist in the Kingston Whig-Standard, the city's (then) only daily newspaper. I quizzed every visitor about lead use in their family or friends, gave away signs to post at popular fishing sites, newsletters about loon-lead mortalities, free packets of nontoxic sinkers, and information where they can be bought (very few places, even today). Bait shops say no one asks for them, that they would have to be specially ordered, that they cost four times as much.
I have dutifully appeared on TV and radio repeatedly, sometimes lugging my loon skeleton and precious gizzard-bags, clear plastic envelopes containing the laundered contents of each dead loon's gizzard. As those bags were pushed into the hands of reluctant fishermen or passed from person to person in an audience, it was obvious that those contents had a greater impact than anything I said. There, in their hands, they held the small gray instrument of death, often with its accompanying tackle, and they recognized it.
Yet even those anglers that nod and give lip-service are evasive, saying it is hard to understand how a hook could get in a loon, that lines don't break, especially not after a fish has been hooked, and certainly not their lines; and lead sinkers are a puzzle too, but they suppose they are grubbed up off the lake floor. If that were so, I'd like to ask who put them there!
This is a reminder to all those working with birds, and with lead-poisoned loons in particular, to make a routine of physically saving the findings. Ideally, all that has to be done is to have the loon X-rayed first to prove the presence and location of the sinker and other gear. If no X-ray is available, just do the post-mortem anyway; check the gonads, snip out the gizzard and proventriculus, open and empty the contents into a sieve at the sink, rinse, dry, pour into ziplock bag and label. Fishermen have been surprised to recognize fishing “setups," both US and Canadian government committees have requested exact weights and measurements of our sinkers, and photographs of bags have been circulated. If each of us contributes such proof, who knows? It may finally have a positive outcome.
After being compassionate to the dying loon, this is the most positive thing we loon-workers can do to make up for that needless death.
25 Fingernails are included in the Mohs Hardness Scale for minerals. On a scale of 1 (talc) to 10 (diamond) they have a value of 2. J.Burke, “Connections," (Scientific American Aug. 1999)
26 pH 2.5 in the digestive juice in the gizzard of ducks and geese. J.C. George, “Impact of Environmental Lead Pollution on the Physiology of Birds," Pavo 36, (1998): 1-14
27 From A Primer of Environmental Toxicology. Unfortunately, neither the author's name nor date was on the printout
28 unless it has been used up, see Pb Poisoning
29 Erythrocyte delta-aminolevulinic acid dehydratase in birds, and the effects of lead exposure in vivo. A.M. Scheuhammer, Toxicology 45: 165-175
30 CaNa2 edetate calcium disodium. Chelating agents bind lead as a water-soluble chelate for excretion in the urine
31 D. Franklin, “Lead Still Poisons After All These Years," In Health, Sausalito, CA,1991: 39
32 L Degernes, “Diagnosis and Treatment of Lead Poisoning in Trumpeter Swans," Wildlife Veterinary Report, ed. Ken Langelier, DVM, Vancouver,1989
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