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Akwesasne Cow Population Impacted from Reynolds Fluoride Pollution  

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Cornell Vet 1980 Apr;70(2):183-92

New York State and U.S. Federal fluoride pollution standards do not protect cattle health.

Crissman JW, Maylin GA, Krook L

Fluoride emissions from an aluminum plant in New York State just west to the bridge to Cornwall, Ontario, Canada, are in compliance with New York State and U.S. Federal standards. Ambient air fluoride virtually never exceeds New York State standards. In a New York State dairy farm, downwind from the aluminum plant about 40% of the time and with the fields within 1300 to 2800 m from the plant, fluoride contamination of forage ranged from 13 to 25 ppm, well below the 40 ppm which is the "tolerance" level by National Academy of Sciences. Sixty-three of 82 dairy cattle on that farm were slaughtered in 1979 because of chronic fluoride poisoning. In the 19 cattle left on the farm in June, 1979, there was no dental fluorosis in calves less than 4 months of age, mild to moderate dental fluorosis in older calves and heifers and severe dental fluorosis in the 4 young adult cattle. Ash fluoride in a stillborn calf was 280 ppm and in the oldest cattle 2800; the increase was significantly correlated to age. It is concluded that New York State and U.S. Federal standards for fluoride emissions, New York State standards for ambient air fluoride and National Academy of Sciences "tolerance" levels for ingestion of fluoride do not protect cattle health.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=
Retrieve&db=PubMed&list_uids=7408498&dopt=Abstract

PMID: 7408498, UI: 81002874


Cornell Vet 1979 Apr;69 Suppl 8:suppl 1-70

Industrial fluoride pollution. Chronic fluoride poisoning in Cornwall Island cattle.

Krook L, Maylin GA

An aluminum plant on the south bank of the St. Lawrence river, southwest of Cornwall Island, Ontario, Canada, has emitted 0.816 metric tons of fluoride daily since 1973; considerably higher amounts were emitted from 1959 to 1973. The plant has been designated as the "major source of fluoride emissions impacting on Cornwall Island." Chronic fluoride poisoning in Cornwall island cattle was manifested clinically by stunted growth and dental fluorosis to a degree of severe interference with drinking and mastication. Cows died at or were slaughtered after the third pregnancy. The deterioration of cows did not allow further pregnancies. Fluoride concentrations in ash of biopsied coccygeal vertebrae increased significantly with age and were dependent on distance from and direction to the aluminum plant. Fluoride in bone ash of a 7-month old-fetus exceeded 500 ppm; fluoride thus was passed transplacentally. Analyses of fluoride in ash of bones obtained at necropsy of cattle from 4 months of age to 4 to 5 years of age showed increased amounts with age. Cancellous bone retained far higher amounts than cortical bone, a reflection of the normally higher metabolic rate of cancellous bone. Concentrations exceeding 10,000 ppm fluoride were recorded in cancellous bone of a 4-to 5-year-old cow. The target cells for fluoride in chronic fluorosis were shown to be the ameloblasts, the dental pulp cells and the odontoblasts and, in bone, primarily the resorbing osteocytes and also the osteoblasts. Atrophy and necrosis of the ameloblasts were responsible for enamel defects. The existing enamel showed brown discoloration from fluoride deposits. The pulp cells underwent fibrous and osseous metaplasia and necrosis of the ectopic bone occurred. The odontoblasts were atrophic and the dentin showed brown discoloration. The resorbing osteocytes were inactive and osteosclerosis resulted. This was especially pronounced in areas of normally great apposition, i.e. in the metaphyses. The epiphyseal plate became squeezed between petrotic bone and growth was stunted. Resorption of alveolar bone surrounding the deciduous teeth was severely retarded or arrested. A delay in eruption of permanent teeth occurred; it was up to 3.5 years in incisor teeth. Interference with the resorbing osteocytes in fluorotic bone was also demonstrated by loss of collagen birefringency in such bone. Failure of bone resorption also caused retention of trabecular bone in the cortices; this was observed even in a 4-t0-5-year-old cow. In areas where modeling into osteonic bone had begun, fluoride deposits were extremely heavy but this bone showed numerous soft osteons in microradiographs. The toxic effect of fluoride on osteocytes also resulted in the death of the cells. Such osteonecrosis occurred mainly in gnathic bone. There was atrophy of the osteoblasts. Osteopenia thus resulted from osteonecrosis and osteoporosis. Subperiosteal exostoses were not observed in long bones. The degree of fluorosis in Cornwall Island cattle was severe.

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=
Retrieve&db=PubMed&list_uids=467082&dopt=Abstract

PMID: 467082, UI: 79235525


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