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Although the Tasmanian lacewing Micromus tasmaniae (Walker) is a common aphid predator in New Zealand, information on effects of insecticides on this beneficial are rare. This study examined the acute and chronic toxicity of 6 insecticides (5 different classes), on M. tasmaniae with regard to its potential use in integrated pest management (IPM). Some experiments were carried out in parallel with the green lacewing Chrysoperla carnea (Steph.) to investigate the possibility to predict pesticide side-effects on M. tasmaniae from existing data for C. carnea. Acute toxicity testing (laboratory; contact exposure of third instars) revealed that stable (no further change) LC₅₀ values often can only be obtained using after-treatment periods of ≥72 h. The ecdysone agonist tebufenozide was the only compound that did not cause any mortality (within 360 h after initial exposure) in either of the two lacewing species. While methyl-parathion was the most toxic compound within a 48 h period after initial exposure, LC₅₀ and LC₉₀ estimates, determined after 360 h, produced similar values for methyl-parathion, azinphos-methyl, cypermethrin, fenoxycarb and diflubenzuron. Comparisons showed that C. caniea was far more resistant to the 2 organophosphates and the pyrethroid than M. tasmaniae. However, both species were equally sensitive to the 2 insect growth regulators fenoxycarb and diflubenzuron, with morphological effects being more severe in C. camea. In field experiments, fenoxycarb also proved to be harmful to both species (at a rate of 0.01% AI). Preliminary ultrastructural examinations could further underline the morphological defects that led to high mortalities after exposure to fenoxycarb (inability to pupate) or to diflubenzuron (disruption of the moulting process). Biochemical parameters (target and detoxifying enzymes) were assayed to gain an increased understanding of the functional toxicity of insecticides after sublethal exposure. It could be shown that the rate of acetylcholinesterase (AChE) inhibition after exposure to organophosphates was toxin specific, exponentially dose dependent and increased within 24 h after exposure. AChE activity was less inhibited in C.carnea compared with M. tasmaniae, which corroborated findings of the acute toxicity experiments. Base levels of glutathione-S-transferase (GST) were similar for both lacewing species. Changes observed in GST activity after insecticide treatment could not be correlated to levels of tolerance or susceptibility in the 2 species. Chronic effects after insecticide exposure of M. tasmaniae were assessed by the determination of life-table parameters (laboratory experiments). The most striking effects were recorded for diflubenzuron (shift in the sex ratio, reduced longevity, reduction of the oviposition rate and changes in various other fecundity parameters). Fecundity was also adversely affected in fenoxycarb treated lacewings and in the F1 generation of tebufenozide treated M. tasmaniae. Power analysis, when applied to the statistics, proved a useful tool to determine the sensitivity (percentage difference detectable) of the life-table parameter test for different numbers of replicates and for shortened evaluation periods. In view of the acute, functional and chronic effects observed in this study some recommendations were made on ways in which the M. tasmaniae could be used successfully as a biocontrol agent in IPM, in addition to some insecticides.