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PubMed1980

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

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.

Air Pollution↗
PubMed1995

Disturbances of potassium homeostasis in poisoning.

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.

Homeostasis↗