Abstract
Thirty-five subjects employed in a phosphoric acid producing plant were studied by the authors. The investigation included: history, according to the C.E.C.A. questionnaire for chronic bronchitis and emphysema; physical examination, chest X-ray spirometry and lung diffusing capacity for carbon monoxide by the steady state method (DLCOSS). High prevalence of chronic bronchitis (45.7%), obstructive spirometric impairment (37.1%), and decreased values of DlcoSS (31.4%) were detected. Two subjects were found to be affected with p 1/0 and 7 with p 0/1 pneumoconiosis. Such findings were significantly related to the lenght of working activity as well as to dust and gaseous fluoride (hydrofluoric acid, hexafluorosilicic acid and silicon tetrafluoride) exposure.
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Fluoride in low concentration modifies expression and activity of 15 lipoxygenase in human PBMC differentiated monocyte/macrophage
Epidemiological and experimental evidences demonstrate positive correlation between environmental and occupational fluoride exposure and risk to various cardio-respiratory disorders. Therefore we decided to examine the effect of fluorides on activity and expression of 15LOX enzyme which is implicated in biosynthesis of inflammatory mediators. Expression of 15LOX-1 and -2 enzymes mRNA
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Subchronic neurotoxicity in rats of the structural fumigant, sulfuryl fluoride
Inhalation exposure of male and female Fischer 344 rats to sulfuryl fluoride [Vikane (Dow Chemical Company) gas fumigant] at 300 ppm for 6 hr/day, 5 days week, for 13 weeks caused diminished weight gain, dental fluorosis, a slight decrease in grooming, decreased flicker fusion threshold, slowing of flash, auditory and
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Acute lethal effects and kinetics of fluoride in blood and BALF after inhalation exposure of rats to aerosolized hydrofluoric acid.
The purpose of this study was to reveal the mechanism of acute lethal accident after the exposure of human on face to a diluted solution of hydrofluoric acid (HFA). Particles of HFA solution and saline (50 µL) were intratracheally (i.t.) sprayed to rats using an aerosol generator as examples of
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Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health.
In this study, several lines of evidence are provided to show that Na+ , K+ -ATPase activity exerts vital roles in normal brain development and function and that loss of enzyme activity is implicated in neurodevelopmental, neuropsychiatric and neurodegenerative disorders, as well as increased risk of cancer, metabolic, pulmonary and
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Fluoride-induced cyclooxygenase-2 expression and prostaglandin E(2) production in A549 human pulmonary epithelial cells.
To clarify the mechanisms of fluoride-induced airway diseases, we examined the expression of cyclooxygenase-2 (COX-2), an important mediator of airway inflammation, in A549 human pulmonary epithelial cells treated with sodium fluoride (NaF). Following exposure to 5mM NaF, COX-2 protein and COX-2 transcript increased markedly. However, no change was observed in
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Respiratory Risks from Occupational Fluoride Exposure
Starting in the 1930s, scientists have observed that workers exposed to airborne fluorides suffer from an elevated rate of respiratory disorders. For over 50 years, however, US government and industry scientists made repeated assurances that the allowable level of fluoride dusts and gases in industrial workplaces would not cause any
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Fluoride Enhances Toxicity of Beryllium
Occupational exposure to beryllium is well-documented to put workers' health at risk. The two principal targets of beryllium poisoning are the respiratory system and the skin. Of all beryllium compounds, beryllium fluoride complexes (including beryllium fluoride and beryllium oxyfluoride) appear to be the most toxic. As shown below, studies dating back
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