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[The status of the teeth and periodontal tissues of children living in an area polluted by the wastes from an aluminum plant].

The author compares dental, periodontal, and bone system status of children living in two regions characterized by different degrees and patterns of environmental pollution. Children living in regions polluted by aluminum plant waste (sulfur dioxide, nitrogen dioxide, carbon monoxide, dust, hydrogen fluoride) developed specific abnormalities because of body poisoning with fluorides, namely, dental fluorosis, osteoporosis and osteosclerosis of the bones; periodontal diseases in these children were more incident than in controls. These findings prompted the development of a complex of sanitary, technologic, health, therapeutic and prophylactic measures aimed at reduction of fluorine levels in the environment to the normal level and of dental diseases incidence among children living near the Tajik aluminum plant.

Adolescent↗

[Death from fluoro-silicate in floor polish].

A fatal case of poisoning due to ingestion of an apparently innocuous household product is described. A healthy 28-year-old man accidentally drank floor polish (Cristalizador, a Spanish import). On arrival at the emergency room a few hours later he passed large amounts of bloody stool and lost consciousness. A call to the Spanish Poison Center revealed that although not indicated on the label, the polish contained a highly poisonous salt, fluoro-silicate. Blood gas analysis revealed severe metabolic acidosis. Serum calcium was 3.8 mg/dL. The post-resuscitation ECG showed subendocardial ischemia and ST-elevation in the anteroseptal wall and prolonged QT-interval. In the intensive care unit he received large amounts of fluids, dopamine, sodium bicarbonate and calcium. Despite the treatment, his condition continued to deteriorate: VPB's appeared, there was a short run of ventricular tachycardia and then atrial fibrillation developed. Further treatment included lidocaine, verapamil, amiodarone, and electrical cardioversion. Blood pressure remained low and 11 hours after admission he died of myocardial infarction, severe arrhythmia and multi-organ failure.

Adult↗

[Regularity of flourine release from fluorine-rich coal combustion in the fluorine poisoning area].

Laboratory experiments and in situ measurements inside farmer's houses indicate that the fluorine concentration of indoor air was positively related with the fluorine content in the consumed coal (R = 0.612, P<0.01), but fluorine content in the coal had no effect on the release rate of coal fluorine under the usual combustion temperature of about 1000 degrees C. The release rate of coal fluorine varied versus combustion temperature ranging from 200 to 1200 degrees C, following a "S" curve pattern, increasing slowly under 300 to 700 degrees C, but quickly under 700 to 1000 degrees C, and then slowly again before finally reaching 100% under 1100 to 1200 degrees C, this curve can be fit by Logistic equation. The release rate of coal fluorine usually depends upon the existence status of fluorine and the chemical and mineral components of the coal. The fluorine in soft coal or anthracite from Guizhou is released more quickly than in bone coal from Southern Shanxi, with the former almost completely released under 1100 degrees C but the later almost completely released under 1200 degrees C. The combustion temperature of civil stoves is at most 1000 degrees C, under which averagely 86.9% of the fluorine in coal from Guizhou and 80.6% of that in bone coal from Southern Shanxi is released.

Air Pollution, Indoor↗

Sudden cardiac death from acute fluoride intoxication: the role of potassium.

The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.

Animals↗

Syndrome of endemic arsenism and fluorosis. A clinical study.

Sixty-five patients in Xinjiang with syndrome of endemic arsenism and fluorosis (SEAF) were investigated clinically from March 1982 to August 1989. SEAF is a kind of chronic syndrome resulting from the combined, harmful effects of two trace elements, arsenic and fluorine. Peripheral neuritis and cardiovascular changes were observed in this syndrome more often than in simple arsenism or simple fluorosis. The excessive quantities of these two trace elements in blood might have a synergic, harmful effect on the nervous and circulatory systems. No definite conclusion could be reached with regard to the morbidity of skin and visceral tumors in this series. The incidence of associated skin cancer was found to be 7.7% and an associated Grade II squamous cell carcinoma of the esophagus was encountered in one patient.

Adolescent↗

Serum sialic acid and ceruloplasmin levels in experimental fluorosis.

The present study describes the effect of fluoride (10 mg NaF/kg body weight/day) on the total protein-bound sialic acid and ceruloplasmin levels in rabbit serum after receiving sodium fluoride intragastrically for 3, 5, 8 and 10 months. The total protein-bound sialic acid and ceruloplasmin levels in serum were reduced, whereas the fluoride levels were increased showing a cumulative effect. It is suggested that the decreased circulatory sialic acid and ceruloplasmin levels with increased serum fluoride may be used in an early detection of fluorosis.

Animals↗