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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Inflammatory markers in bronchoalveolar lavage fluid from human volunteers 2 hours after hydrogen fluoride exposure
Fluoride has been in focus as a possible causal agent for respiratory symptoms amongst aluminium potroom workers for several decades. Previously, using bronchoalveolar lavage (BAL), we demonstrated airway inflammation in healthy volunteers 24 hours after exposure to hydrogen fluoride (HF). The objective of the present study was to examine early
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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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Studies on the toxicology of fluorine compounds. I. Histological and histochemical investigations on the liver, heart, lungs, and stomach of rats exposed to hydrogen fluoride
The liver, heart, lungs, and stomach of rats exposed to hydrogen fluoride were studied. Histological examination showed partial liver necrosis and emphysema. Using histochemical methods the effect of fluorine ions was found in: a reduction of the activity of succinic and beta-hydroxybutyric dehydrogenases in the liver, heart muscle, superficial and
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Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.
An extensive body of research has demonstrated that pulmonary toxicity induced by fluoride is related to cell apoptosis. Although induction of death receptor-initiated extrinsic apoptosis by sodium fluoride (NaF) has been reported, its mechanism of action is still not clearly defined. Herein, we found that NaF treatment induced activation of
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Inflammatory responses of rat alveolar macrophages following exposure to fluoride
Inhalation exposure to fluoride compounds has been associated with respiratory failure. We have addressed effects of fluoride on alveolar macrophages and lung responses to intratracheally (i.t.) instilled fluoride in rats. I.t. instillation of fluoride at doses of 200 and 400 microg F/rat caused significant polymorphonuclear leukocyte (PMN) infiltration in the
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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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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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