The antagonistic activity of coal dust (bituminous coal from the Pittsburgh seam, Cambria County, Pennsylvania) on interferon induction by influenza virus was studied. Such activity was noticeably reduced when either coal dust or Rhesus-monkey kidney (LLC-MK2) cell monolayers were pretreated with poly(4-vinylpyridine- N-oxide) (PVPNO). The polymer alone had a minimal effect on the interferon system or host cells. The polymer neither induced interferon synthesis, inhibited viral induction of interferon, nor affected cellular induced resistance by interferon against virus. Maximal polymer adsorption to coal dust was achieved more rapidly than to cell monolayers and less polymer was needed to pretreat coal dust than cell monolayers to achieve similar levels of interferon synthesis. The depressive activity of coal dust was markedly reduced, independently from dust particle size. The level of virus increase in the presence of coal dust treated cell monolayers was two times higher than that observed with either polymer pretreated coal dust or polymer pretreated cell monolayers. While interferon production was effectively inhibited in the presence of coal dust particles, pretreating the particles or cells with the polymer negated this effect of coal dust. It appears that the particles of coal dust per se interact with cell membranes to suppress interferon production and that the polymer produces an adsorbed layer on the dust cell complex to subvert their interaction.