Abstract
We explored the relationship of respiratory symptoms and lung function to exposure to ambient air pollution consisting of particulate and gaseous fluorides. The subjects were 253 North American Indian children 11 to 17 yr of age living on the Akwasasne reserve, which is adjacent to an aluminum smelter. Among boys, closing volume (CV/VC%) was increased in those raised closest to the smelter as opposed to those having lived most of their lives farthest from this source of air pollution. In both sexes, there was a significant linear relationship between increasing CV/VC% and the amount of fluoride contained in a spot urine sample. We conclude that exposure to fluoride air pollution in the community may be associated with abnormalities in small airways. The implication of these abnormalities for future respiratory health is unknown.
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Allergen sensitization and exposure to irritants in infancy
We investigated the relationship between residence in the neighbourhood of an aluminium smelter and the prevalence of atopy in schoolchildren (7-13 years of age). Atopy was assessed in 556 of the 620 participants by a skin prick test with eight common aeroallergens. The median exposures to sulphur dioxide and fluoride
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Fluoride-induced changes in 60 retired aluminum workers
Orthopedic, radiological and analytical examinations were performed in a group of 60 retired disabled workers of an aluminum factory. Occupational disease had previously been recognized in this group because of disturbances in the respiratory and circulatory systems. The age of those examined averaged 49.6 years; the duration of exposure averaged
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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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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 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 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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