Abstract
Communities across the United States are examining the manufacture, use, transport, and storage of hydrogen fluoride (HF) near residential areas as a consequence of a major release of HF in Texas in 1987. Reference exposure levels for routine and accidental HF emissions are calculated using existing animal and human data. The approach employs a log-probit extrapolation of concentration-response data to the 95% lower confidence limit on the toxic concentration producing a “benchmark dose” of 1% response (TC01), called a practical threshold. Species-specific and chemical-specific adjustment factors are applied to develop exposure levels applicable to the general public. Using this method, the 1-hr reference exposure level to protect the public against any irritation from a routine emission (REL-1) is 0.7 ppm and the level to protect against severe irritation from a once-in-a-lifetime (REL-2) release is 2 ppm. This approach is compared to a modified “uncertainty factor” approach.
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Effects of fluoride exposure on mitochondrial function: Energy metabolism, dynamics, biogenesis and mitophagy.
Fluoride is ubiquitous in the environment. Furthermore, drinking water represents the main source of exposure to fluoride for humans. Interestingly, low fluoride concentrations have beneficial effects on bone and teeth development; however, chronic fluoride exposure has harmful effects on human health. Besides, preclinical studies associate fluoride toxicity with oxidative stress,
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Fluoride exposure and respiratory symptoms in welders
Welders inhale gases and respirable particles. To investigate the relationship between fluoride exposure and respiratory symptoms in welders using basic electrodes containing calcium fluoride, 63 railroad track welders were interviewed. Fluoride was measured in post-shift urine samples. Seventeen welders reported respiratory symptoms related to welding fume exposures. Respiratory symptoms were
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Mitochondrial respiratory chain damage and mitochondrial fusion disorder are involved in liver dysfunction of fluoride-induced mice.
Highlights Excessive fluoride intake resulted in liver dysfunction. Fluoride increased ROS production and decreased ATP content in the liver tissue. Fluoride damaged the liver tissue ultrastructure. Fluoride induced mitochondrial respiratory chain damaged. Fluoride induced mitochondrial fusion disorder. Our previous study showed that excessive fluoride (F) intake can induce liver dysfunction. The
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Mortality and cancer morbidity after heavy occupational fluoride exposure
A cohort of 431 male cryolite workers employed for at least six months between 1924 and 1961 was identified from personnel records at the Copenhagen cryolite factory. During this period, heavy fluoride exposure resulted in at least 74 cases of skeletal fluorosis. All workmen in the cohort were followed up
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Respiratory symptoms and lung-function changes with exposure to five substances in aluminium smelters
OBJECTIVES: To determine whether exposure to five different occupational substances contributes to respiratory symptoms in aluminium smelter workers. METHODS: A cross-sectional survey of 1,615 male employees of two Australian aluminium smelters was conducted in 1995. Subjects underwent spirometry and were asked about respiratory symptoms and the relationship of those symptoms to
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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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