Fluoride Action Network


Fluorosis from excessive exposure to fluoride can result in inflammatory reactions involving macrophages and their differentiation, a process that is rapidly followed by generation of prostanoids—products of arachidonic acid metabolism, including the pro-inflammatory factors prostaglandin PGE2 and thromboxane TXA2, which are implicated in atherogenesis and rapidly increase during acute inflammation. This paper examines the effect of fluoride at concentrations found in the blood of individuals environmentally exposed to fluorine compounds as the production of PGE2 and TXA2 is affected. Peripheral blood mononuclear cells (PBMCs) used in the present study were isolated from the blood of donors and incubated with 1, 3, 6, and 10 µM NaF. Secretory phospholipase A2 (sPLA2) activity and the concentrations of prostaglandin E2 (PGE2) and thromboxane A2 (TXA2) were measured by enzyme immunoassay kits, arachidonic acid (AA) release by gas chromatography, and apoptosis by flow cytometry. Incubation of macrophages with NaF caused increased concentrations of PGE2, TXA2, sPLA2, and AA in the cells and increased the number of macrophages in early-stage apoptosis in a dose-dependent manner. The results indicate that NaF, even in small concentrations, may induce an inflammatory process and an apoptotic effect in macrophages through the stimulation of the metabolism of prostanoids and increased synthesis of PGE2 and TXA2.