The effects of hexabromocyclododecane on human natural killer cell function

This study investigates the effect of Hexabromocyclododecane (HBCD) on human natural killer (NK) cell lytic function, and whether a decrease in lytic function is cause by the inability of NK cells to bind to their targets (tumor cells). HBCD exposures that caused a loss of binding function were examined for effects on expression of key NK cell surface proteins needed for binding to targets. Additionally; this study investigates the effects of HBCD on ATP levels in NK cells. Human NK cells are a subset of lymphocytes that are capable of lysing tumor cells, virally infected cells, and antibody-coated cells. HBCD is a non-aromatic, brominated cyclic alkane used primarily as an additive flame retardant. If HBCD interferes with NK cell function, this could increase risk of tumor development and/or viral infection. NK cells were exposed to various concentrations of HBCD for 1 h, 24 h, 48 h, and/or 6 days before determining lytic function, binding function, cell-surface marker expression and ATP levels. ATP levels, binding function, cell-surface marker expression and lytic function were also determined in NK cells that were exposed to HBCD for 1 h followed by 24 h, 48 h, and 6 days in HBCD-free media. The results indicated that exposure of NK cells to 10 µM HBCD for 24 h causes a very significant decrease in NK cell lytic function, NK cells binding function, CD 16 and CD 56 cell-surface protein expression and ATP levels (93.5%, 70.9%, 57.8%, 24.6% and 90.5%, respectively). Exposure of NK cells to 10 µM HBCD for 1 h followed by 24 h in HBCD-free media also showed a very significant decrease in lytic function (89.3%), binding function (79.2%), CD 16 expression (48.1%) and a lesser decrease in ATP levels (46.1%). The results indicate that HBCD exposures decreased lytic function, binding function, cell-surface marker expression as well as ATP levels in NK cells