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Baseline data on susceptibility levels to azinphosmethyl and permethrin were generated on five field-collected populations of the pink bollworm, Pectinophora gossypiella (Saunders), from Arizona and Southern California, relative to a standard susceptible laboratory strain. The field strains showed less than 2-fold resistance to azinphosmethyl but exhibited variable levels (1.3- to 18.3-fold) of resistance to permethrin. Resistance of pink bollworms to permethrin seems to be correlated with the pattern of insecticide-use prevalent in the localities studied. Strains from Yuma, Phoenix and Westmoreland exhibited highest levels of resistance to permethrin. Synergism of permethrin with an oxidase inhibitor, piperonyl butoxide (PBO), and an esterase inhibitor, S,S,S-tributyl phosphorotrithioate (DEF), produced less than 2-fold synergism in the Yuma strain. Results suggest that nonmetabolic factor(s) may be involved in permethrin resistance of the Yuma field strain since neither PBO nor PBO/DEF combination suppressed resistance completely. It is possible that pink bollworm resistance is at least partially conferred by the khr-gene. Rearing of two field strains collected from Marana and Yuma under insecticide-free conditions resulted in reversion of resistance in four and five generations, respectively, to levels close to that found in the susceptible laboratory strain. Permethrin-resistance in these field strains is unstable and is apparently in its early phase of development. Monitoring of resistance in field strains should be performed preferably in the F₁ generation. Subsequently, selection studies were performed on both larval and adult stages to investigate the capacity of the pink bollworm to develop resistance in both life-stages. Selection of larvae with both azinphosmethyl and permethrin resulted in higher levels of resistance in larvae than in adults. Results suggest that azinphosmethyl possesses a low degree of selectivity for development of resistance in pink bollworm adults. Fourteen to 16 generations of selection with azinphosmethyl and permethrin produced ca. 2- and 9-fold resistance, respectively, in the adult stage. A laboratory-selected strain showing ca. 13-fold resistance was used in reciprocal crosses with a susceptible laboratory strain. The F₁ results suggested that inheritance of permethrin resistance was autosomal and partially dominant. Chi-square analysis of responses of backcross progeny indicated that resistance seems to be conferred by a major gene under the influence of minor gene(s).

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