The Animal Disease and Parasite Research Division currently has a contract for 
research on one small phase of lead poisoning. There are extreme variances in the liter- 
ature regarding susceptibility, tissue residues, chronic poisoning, and the lead levels of 
industrial contamination of livestock feeds. The relationship of levels of lead, which 
livestock ingest, to the amount required to produce residues in meat and milk and 
symptoms in the animals is an area of needed research. Binns and Beeson (1959) report 
that there may be effects from a nonlethal dose of lead at a certain period of gestation. 
The diagnosis of lead poisoning with certainty is difficult even with chemical analyses, 
It is generally considered that for evidence of diagnosis of lead poisoning, findings in the 
undried tissues should be 40 p.p.m. in the kidney cortex or 20 p.p.m. in the liver. Lead 
is retained by the organs for a long time and abnormally high blood levels have been 
seen 6 months after ingestion of a single sub-lethal dose (Allcroft, 1951). However, 
deaths occurred from unquestioned lead poisoning in calves in which the liver contained 
from 9.5 to 182 p.p.m. and the kidneys from 0.5 to 300 p.p.m. (White, et al., 1948). 
Cows have experimentally tolerated 2 gms. each daily for 2 years without apparent harm 
(Allcroft, 1951). Calves up to 4 months of age are usually killed by ingestion in 1 day of 
200 to 400 mg./kg. of the acetate, oxide, or carbonate. With cattle and sheep, it is ex- 
tremely unlikely that cumulative poisonings occur naturally to produce the chronic 
poisoning, possibly due to the low 1 to 2 percent absorption of the lead ingested (Blaxter, 
1950). We should expect little actual lead poisoning of cattle and sheep from industrial 
contamination of livestock feeds from air pollution or from the greases and lubricants 
that get into feeds, particularly pellets. 
Arsenic also contaminated livestock feeds by air pollution from various industrial 
processes, such as smelter fumes or coal containing arsenic as an impurity. Grain dried 
by direct contact with flue gases has been reported to have an arsenic content of 0.2 
Ppepem., when the coke used to produce the flue gases contained 80 p.p.m. of arsenic 
(Phillips, 1956), Chronic poisoning occurred inanimals grazing on land over 6 miles from 
precipitated fumes from smelters and blast furnaces using ores containing arsenic. 
Toxicity from spray and dust contaminations of livestock feeds have been reported, Many 
factors involved make it impossible to state the toxic dose to any one species. The average 
lethal dose according to Garner (1957) for sodium arsenite for the cow is 1 to 4 gms. and 
0.2 to 0.5 gms. for the sheep. Cattle have been reported to sicken on alfalfa containing 
40 to 45 p.p.m. arsenic (Phillips, 1956). Arsenic is chemically rather indestructible. It 
can be detected in the liver and other tissue years after death and burial (Smith and 
Jones, 1957). 
After lead, arsenic constitutes the most important toxicological hazard to farm 
animals. In the roasting of many metallic ores,arsenic may be carried as a dust with the 
smoke to contaminate neighboring livestock feed (Garner, 1957). 
The relationship of the ingestion of arsenic inits various soluble, insoluble, organic, 
and inorganic forms by farm animals in various livestock feeds to the p.p.m. in the tissues 
and milk of dairy cows needs research and evaluation. Jones (1954) reported quantities 
of arsenic toxic to man in the milk of cows feeding on vegetation that had been sprayed 
with an arsenical weedkiller. Scheidy, et al., (1953) have shown that arsenic accumulates 
in the liver and is gradually distributed to other tissues. These workers found 2.1 
pep-m. in the liver of swine 7 days following the oral administration of 104 mg. of sodium 
arsanilate. 
Fluorine is an important industrial contaminant of livestock feeds. Contamination is 
due to industrial air pollution settling on vegetables or to use of raw or nondefluorinated 
rock phosphate in mineral feeds. 
During 1956, damage in court cases in the United States because of losses from 
fluorine amounted to over $50 million (Butler, 1958). It was a national problem involving 
many States of the Nation. In July 1959, the Utah State University sponsored a research 
seminar on the effects of fluorides on animals and man. In April 1960, the University 
of Wisconsin held a meeting on ‘‘The Review of the Research Work on Bovine Fluorosis."" 
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