This research was initiated to determine the mechanism(s) of action that could explain increased weight gain and decreased milk production i n dairy cattle fed corn silage containing residues of certain organophosphate pesticides. It was proposed that the mode of action involved and alteration of thyroid physiology by the metabolites of the pesticides, namely halogenated phenols. Studies were carried out to determine the effect of tri-halogenated phenols and pyridinols upon T4-binding to bovine serum albumin (BSA) and to liver mitochondria isolated from male rats. Using the rat as a model, feeding trials were performed to determine the effect of halogenated phenols and pyridinols on rate of gain, relative thyroid weight, thyroid histology, and serum- T 4 levels. In vitro results with BSA indicated that the mechanism could have involved competition between T4 and the phenol for the T4 -binding site(s) of serum proteins, thus possibly lowering the serum-T4 level. This was not well substantiated by in vivo measurements of serum-T4 levels from rats fed varying concentrations of halogenated phenols. The methods employed to determine the effect of halophenols upon r4 binding to mitochondria indicated that these compounds are poor competitors for the T4 -binding site on mitochondria. At the dose levels employed, there appeared to be no uniform dose response relationship between the various halogenated phenols and pyridinols and thyroid histology, relative thyroid weight and feed efficiency.