Lead poisoning has been reported in most domestic animals and humans (20). This survey supports previous findings that cattle are the species most commonly affected by lead poisoning (22-29). Lead poisoning has been shown to be 10 times more common in cattle than in any other domesticated species (22). However, this laboratory also received substantial submissions for lead analyses from birds and horses. As the OMAFRA laboratory predominantly serves the agricultural community, there is a differential fee stucture for farm animals that may have been the reason for the low numbers of canine and feline samples. The large number of lead toxicoses in wild birds was expected; however, the number of positive equine samples was an unexpected finding, although this species appears to be quite susceptible to lead poisoning after chronic ingestion of lead (28). The clinical signs of chronic lead toxicity previously reported in horses located next to a smelter included laryngeal paralysis, colic, unthriftines, and respiratory distress (28). Six of the 8 horses in this present study consistently had clinical signs of anorexia, unthriftiness, weight loss, muscular weakness, laryngeal paralysis, and respiratory distress. The levels of lead in the liver ranged from 4 ppm to 10 ppm (tissue wet weight), which are compatible with the findings of others (25,26,28).
The most common sources of lead were old batteries, paint chips, and old asphalt shingles, which accounted for 42% of the bovine cases. However, the source of the lead could not be determined in 48% of the bovine cases. In earlier reports (24,25,27), a common source of lead for domestic species was identified as crankcase oil, with the lead derived from leaded gasolines. In the equine cases, no source could be identified. In birds, particularly ducks and loons, a common source of lead was fishing sinkers and lead shot.
Copper compounds are widely used in agriculture and veterinary practice as fungicides, bactericides, molluscicides, anthelmintics, and feed additives (31). The 280 sheep with liver and or kidney copper in the toxic range was expected. The clinical and pathological findings in these cases were similar to those previously reported (3,31). Both acute and chronic manifestations were noted; however, these terms are misleading, because "chronic" refers to a long cumulative poisoning that may suddenly develop into an acute hemolytic crisis (27). The ingestion and absorption of copper that is stored in the liver is termed "chronic copper poisoning" (3,5,6). In this study, the source of the copper was determined in 52% of the cases. Some of the more common sources were mineral mixes formulated for cattle, drinking water that had been treated with copper to control algae, and copper sulfate foot baths in 2 cases involving sheep. In a recent case involving 150 yearling ewes, 5 died after being lethargic and anorectic for 12 h prior to death. The copper and molybdenum concentrations in the liver were 1006 ,ug/g and
Of the 35 submissions for copper analysis from dogs, 15 had copper levels in the toxic range. Of these 15, 4 were Bedlington terriers, 2 were West Highland white terriers, and 3 were Doberman pinchers, all with copperassociated hepatitis. The Bedlington terrier and West Highland white terrier exhibit a genetically-linked liver storage disease that leads to copper poisoning (33). Doberman pinscher hepatic disease has been called "chronic active hepatitis" and "copper storage disease," although its pathogenesis is not yet clear (33). The other dogs came from a variety of breeds, including cocker spaniel, Labrador retriever, and 1 golden retriever. Of the 67 cases of high copper levels detected in cattle, 55 were calves and 12 were adult cattle. Calves have been shown to be more susceptible than adult cattle to high copper intake (31). There are areas in eastern Ontario known for peat soil that is high in molybdenum, which has resulted in copper deficiency problems and farmers routinely supplementing with copper. Three cases of copper toxicity in adult cattle were as a consequence of copper supplementation. Adult cattle, goats, deer, and pigs are considered tolerant, but they can also be affected (6,32).
The absence of domestic animal poisoning by mercury varies from previous reports of mercury toxicosis in domestic animals due to consumption of mercurial medicaments or seed grain treated with organic mercury (34,35,37) and may be due to to the recognition of the danger of these mercurial compounds, which lead to the discontinuance of their use in Ontario. All the cases of mercury poisoning were in raptors. These fish-eating birds were found weak or dead and no obvious cause of illness or death could be found at necropsy. Although paper mills and mines are reported to be the major sources of elemental mercury in Ontario, natural mercury contamination of lakes in Ontario does occur (37).
Elemental mercury is converted to methyl mercury in aquatic environments. Methyl mercury then accumulates to high concentrations in aquatic animals, particularily fish (15,18). The consumption of contaminated fish by raptors appears to be a primary source of the mercury toxicosis in the 83 birds examined in this study. Of interest was the 23 birds with tissue levels of both lead and mercury in the toxic range. Most of the birds were loons, and the tissue levels were in the lower part of the toxic range; the possibility of an additive effect of these toxic metals is possible with lower tissue levels having toxic effects. This could involve a greater number of water birds having heavy metal toxicosis than considered in previous estimates.
Industrial pollution with zinc is common (23,27). Toxicity has been documented in farm animals after treatment for lupinosis with zinc compounds or after feed supplementation (27). Zinc sulphate has also been used in the treatment of footrot (27). In the present study, 10 of the 77 birds with zinc levels in the toxic range were parrots and cockatoos that lived in metal cages, most of which had been recently galvanized. One case involved a young emu that was in contact with a galvanized fence. Several of the other birds with zinc levels in the toxic range were cormorants and great blue herons. No source of zinc could be identified in these cases. Of the 3 dogs with zinc toxicosis, 2 were young puppies that had swallowed metal objects with a high content of zinc. One was a zinc-coated nut and the other was an American penny, which after 1978 is known to contain abundant zinc (17). No source for the zinc was noted in the 16 cattle and 1 sheep with serum levels in the toxic range. Two typical selenium poisoning syndromes occur as a result of ingestion of selenium. A subacute form called "blind staggers" and a chronic form called "alkali disease" (27). In many areas of the world, soil is rich in selenium and certain plants are able to absorb selenium in quantities that are toxic to grazing animals (7-9). Therefore, it is easy to appreciate the significance of these diseases in selenium-rich regions. The OMAFRA toxicology laboratory is located in an area of selenium deficiency where supplementation is common. Only 4 cases of selenium excess was recorded in this period, 2 were in calves and 2 were in lambs. All had been injected with excess selenium. There were no reported cases of porcine focal symmetrical poliomylomalacia, a neurological disease in young feeder pigs receiving high dietary levels of selenium (7). From these findings, selenium toxicity due to supplementation does not appear to account for many losses in Ontario. Most of the 723 submissions from cattle for selenium analysis were because of concern about selenium deficiency.
Toxicity from large doses of iron administration is an uncommon finding in this laboratory. During the period from 1990 to 1995, 1 1 cases of iron toxicosis were diagnosed histologically. Only 3 of these cases were confirmed with serum or liver iron analysis. The 2 piglets and 1 calf with iron levels in the toxic range were due to overdosage of iron dextran.
No requests for arsenic analysis were received during the 5-year period of this study, although a diagnosis of organic arsenic toxicity was made 4 times using history and histopathologic lesions. During an 8-year period in the 1960s, 21 animals with arsenic toxicity were reported from this laboratory (2). The decreased occurrence in recent years may be due to the marked reduction in the use of arsenical pesticides (2). Nevertheless arsenic is still a constant source of poisoning in both man and animals (2). Chronic arsenic poisoning in animals is rare, because arsenic is rapidly excreted from the body (2).
No requests were made for cadmium, nickel, or chromium analysis. Cadmium and nickel are environmental contaminants, which could result in chronic low level ingestion (20). They have been shown to be carcinogenic (10,11). The chronic nature and lack of overt toxicity with these elements would make diagnosis difficult for veterinarians. Therefore, the lack of requests for analysis of cadmium and nickel does not preclude the possibility of subclinical effects or accumulation in liver or kidney of domestic animals.
Chromium is now being considered in Ontario as a feed additive for ruminants (18). The use of chromium in feed may result in formulation errors not uncommon with any feed additive. With newer technologies, such as Inductively Coupled Plasma Atomic Emission Spectrometry, samples can be screened for numerous metals simultaneously similar to serum biochemistry profiles. Such technology would provide a means to monitor for metal induced disease or residues. Public environmental concerns, as well as feed mixing errors, would make this a valuable addition to toxicological investigations in the future.
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