Abstract
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…