Static toxicity tests were used to assess the acute toxicity to third‐instar Aedes aegypti (L.) to short‐term exposures of five insecticides (technical permethrin, microencapsulated permethrin, fenitrothion, carbaryl, and carbofuran). Larvae were exposed to each insecticide for times of 0.25, 0.5, 1, 2, 4, 8, or 24 h, then transferred to clean water and reared to the adult stage. Technical permethrin was most toxic to Aedes aegypti, followed by fenitrothion, microencapsulated permethrin, carbofuran, and carbaryl (24 h LC50 values, based on survival to the adult stage, were 0.45, 3.1, 21.6, 90.0, and 510.0 μg/L, respectively). Acute toxicity increased with increasing exposure time to all five insecticides. However, the relationship between exposure time and acute toxicity differed among insecticides. The increase in acute toxicity was greater over short than over long exposures for technical permethrin, carbaryl, and carbofuran (LC50 values decreased 11.2 to 22.4‐fold over a 0.5‐ to 4‐h exposure, and 2.6‐ to 5.2‐fold over a 4‐ to 24‐h exposure). The opposite was true for microencapsulated permethrin (LC50 values decreased 3.6‐fold over a 0.5‐ to 4‐h exposure, and 6.2‐fold over a 4‐ to 24‐h exposure). Acute toxicity to fenitrothion increased proportionately with increasing exposure time. Some larvae recovered from immobilization following short (0.5‐ to 4‐h) exposures to technical permethrin, microencapsulated permethrin, carbaryl, and carbofuran (EC50 values based on immobilization immediately after exposure terminated were 0 to 15 times lower than corresponding LC50 values). However, ability to recover decreased with increasing exposure time such that no recovery from immobilization occurred after 8 or 24 h exposure. Larvae did not recover from immobilization following exposure to fenitrothion. These results indicate the need for a postexposure observational period to fully assess acute toxicity following exposure to insecticides.

The acute toxicity to third‐instar Aedes aegypti (L.) of two 1‐h exposures to each of five insecticides (technical permethrin, microencapsulated permethrin, fenitrothion, carbaryl, and carbofuran) was determined with static toxicity tests. The toxicity of two 1‐h exposures to these test compounds, separated by a 6‐h insecticide‐free period, was compared to that of continuous 2‐h exposures. Acute toxicity was expressed as LC50 values based on survival to the adult stage. The LC50 for two 1‐h exposures to microencapsulated permethrin (180 μg/L) was significantly lower than that for a continuous 2‐h exposure (250 μg/L). There was no significant difference between LC50 values for two 1‐h and continuous 2‐h exposures for each of technical permethrin (2.03–2.32 μg/L), fenitrothion (49.4–48.8 μg/L), carbaryl (3,040–3,470 μg/L, and carbofuran (1,590–2,130 μg/L). Increasing time between two 1‐h exposures to carbaryl from 6 to 24 h did not significantly affect acute toxicity (LC50 values were 3.0 mg/L and 3.8 mg/L, respectively). The LC50 for four 1‐h exposures to carbaryl each separated by a 12‐h period in clean water (LC50 = 1.7 mg/L) was not significantly different from that of a continuous 4‐h exposure (LC50 = 1.4 mg/L). These results suggest that there was no recovery from the effect of insecticide poisoning during the insecticide‐free period between exposures.

Two trials were conducted to determine whether deep stacking of contaminated corn with poultry litter destroys aflatoxin. Contaminated corn was ground and mixed with litter to carbon:nitrogen ratios of 30:1. Moistures were adjusted by adding tap water just prior to incubation or stacking. The initial laboratory trial included only broiler litter at 40% moisture, whereas the subsequent field trial involved a 2 x 2 factorial design with litter type (turkey or broiler) and moisture (20 or 40%) as main effects. Aflatoxin assays were reduced in the laboratory trial from 433 and 402 to 54 and 8 ppb in Containers 1 and 2, respectively, after 35 d of incubation at 28 C. In the field trial, aflatoxin disappeared from broiler and turkey litter mixtures with projected moistures of 20% after 10 and 6 wk of storage, respectively, whereas disappearance in mixtures containing projected moistures of 40% required 5 and 3 wk, respectively. Differences in moisture appear to account for differences in the ability of turkey and broiler litter to detoxify aflatoxin. Hence, turkey and broiler litter would appear equal with respect to the ability to detoxify aflatoxin-contaminated corn. Disappearance of aflatoxin during storage with litter could have occurred as a result of ammonia release during storage or microbial detoxification mechanisms. However, nitrogen values suggest that microbial action was responsible for much of the detoxification, as aflatoxin disappeared from mixtures with little apparent ammonia release.

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