Inhaled benzene reduces aspects of cell-mediated tumor surveillance in mice.

Benzene is a potent bone marrow toxicant with particular activity against lymphocytes. Despite the recognized effects of benzene on lymphocyte populations, few data exist concerning the effects of benzene on in vivo immune responses. We have been conducting a series of studies concerning the effects of inhaled benzene on murine cell-mediated immune responses. The studies in this report involve the interaction of inhaled benzene with some of those cell-mediated immune responses associated with tumor surveillance. Exposures to 100 ppm benzene (5 days/week X 20 weeks) induced lethal tumor growth in 9/10 C57Bl/6 mice inoculated with 10(4) viable PYB6 tumor cells. Lethal tumor incidences in air controls and mice exposed to lower benzene concentrations were 3/10 or less. Exposures to 100 ppm benzene (5 days/week X 4 weeks) also reduced the tumor lytic abilities of cytotoxic T lymphocytes as determined by 51Cr-release assays. In addition, splenocytes taken from mice exposed to 10 or 100 ppm benzene (5 days/week X 4 weeks) exhibited delays in peak mixed leukocyte responses. Coculture experiments demonstrated that these delays were not due to an induction of suppressor cell activity by benzene. There were no alterations in the relative percentages of B cells, T cells, or T-cell subsets among splenocytes from animals exposed to any concentration of benzene tested. These results demonstrate that inhaled benzene can inhibit some of the processes associated with tumor surveillance, and that this inhibition is due, at least in part, to impairments of the functional abilities of some of the cells responsible for tumor surveillance.