Toxicology and metabolism of chloromethiuron in Boophilus microplus larvae

The toxicity of the acaricide chloromethiuron, 3-(4-chloro-o-tolyl)-1,1-dimethyl- (thiourea), and of nine related compounds to Boophilus microplus larvae was determined by a spray-tower method. Four of these compounds were toxic but only chloromethiuron and its N-demethyl derivative were of practical importance. Metabolism of [14C]chloromethiuron, in the formamidine-susceptible but organo-phosphorus-resistant Mt. Alford strain, was compared with that in a chlordimeform-selected Mt. Alford strain, which in laboratory tests was two to three times resistant to chloromethiuron, chlordimeform and amitraz. The latter strain produced smaller quantities of the toxic N-demethyl derivative than the Mt. Alford strain; this was the only resistance mechanism determined. Rates of degradation of chloromethiuron were the same in both strains. Piperonyl butoxide strongly antagonised the toxicity of chloromethiuron by 18 to 33 times and depressed the production of the N-demethyl derivative in both strains (0.3 times that of the control), while degradation rates of chloromethiuron itself were halved by piperonyl butoxide in both strains. These results indicated that the parent material was not toxic until oxidised to the N-demethyl derivative. As, in addition, some symptoms of chloromethiuron toxicosis in larvae were similar to those caused by formamidine acaricides, a common mode of lethal action is suggested.