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Fluorine toxicosis and industry.

The onset of chronic fluorosis is insidious and may be confused with chronic debilitating diseases such as osteoarthritis . . . * https://pubmed.ncbi.nlm.nih.gov/5463662/

The mutagenic activity of inorganic fluorine compounds.

... The present investigation concerns the influence of inorganic fluorine compounds on chromosomes in bone marrow and on the mytotic activity of epithelial cells of the cornea in female white rats. The animals were exposed 6 hours a day, six days a week, for 5 months, to the inhalation of cryolite (Na3AlF6) in concentrations of 3, 1, and 0.5 mg/m3 (calculated as fluoride ion), which is frequently encountered in the air of electrolysis areas of aluminum plants, and also of a mixture of 0.5 mg/m3

Clinical aspects of fluorosis in horses

These [fluorotic] changes first appear at sites of greatest metabolic activity and stress within a given bone and in bones that are under the greatest stress from weight bearing and locomotion.

Variations in the metabolism and maturation of collagen after fluoride ingestion

It is concluded that fluoride, ingested in excessive amounts, increases the solubility and degradation of collagen and reduces the collagen biosynthesis and cross-links. Therefore, the matured tissue collagen fibers would be abnormal due to inadequate cross-linking.

Effect of sodium fluoride on collagen cross-link precursors.

NaF [sodium fluoride] produces abnormal collagen fibres which provide an abnormal environment for calcification. The formation of defective collagen fibres during fluoride poisoning may explain the development of neobone in fluorosis. NaF is suggested to interfere with maturation of collegen fibres by exerting an adverse effect on cross-link precursors.

Fluorosis in dairy cattle

In 1934 there was a report from the United States (Phillips and others) of chronic fluorosis in cattle resulting from the use of rock phosphate. In Great Britain fluorsis arising from atmospheric pollution was reported by Blackmore and others in 1948 and Burns and Allcroft in 1964. Most of the references in the literature reported cases occurring as a result of industrial contamination of herbage, drinking water with a high fluorine content, or experimentally fed sources of fluorine (usually sod