The effects on platelet aggregation due to the insecticide, 2,2-bis-(p-chlorophenyl)-1,1-dichloroethylene (72559) (p,p'-DDE), and various mercury (7439976) compounds were studied. Platelet rich plasma was prepared from the blood of healthy human donors. The number of platelets was determined in a thrombocyte counter and adjusted to 250,000 platelets per microliter. Platelet aggregation was recorded in an aggregometer. Prostaglandin synthesis was determined by incubating homogenized platelet membranes with tritium labeled arachidonic-acid (AA) (506321) and by scintillation counting of the incorporated label. Compared to AA, both methyl-mercury (22967926) (MM) and thimerosal (54648) induced platelet aggregation were slower, and were inhibited by indomethacin, quinacrine, and p,p'-DDE. Mersalyl (492182), mercuric-chloride (7487947), and phenylmercuric-chloride (100561) failed to induce aggregation. Thromboxane-A2 (TxA2) synthesis was significantly inhibited by p,p'-DDE. MM probably inhibited TxA2 and stimulated phospholipase-A2 activity, while the thimerosal probably inhibited acylcoenzyme-A-synthetase and transferase. Quinacrine inhibited phospholipase-A2, but did not completely inhibit AA. Sufficient amounts of the latter were converted to TxA2 to induce aggregation. MM induced aggregation was totally inhibited by quinacrine. The calcium (Ca) ionophore, A-23187, induced aggregation in the presence of p,p'-DDE and quinacrine, indicating that the ability of platelets to respond to increased intracellular Ca was not interfered with. The authors conclude that hypercoagulability induced by mercury compounds is caused by changes in plasma factors.