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| Source of uncertainty | Risk of human illness due to insecticide exposure (examples) | Risk of nontarget insect mortality from transgenic insecticidal plants (examples) |
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| Body’s past exposures and synergistic effects | Prior exposure to common household cleaning agents not recorded or simultaneous exposure to so-called inert ingredients not available, but these substances could increase sensitivity to the toxin in question. | No prior exposure to secondary plant compounds when testing for the susceptibility of clean-cultured, non-target insects, reared on a diet with purified proteins, but substances in food derived from plants or herbivores could increase negative effects of the novel proteins [33]. |
| Dose-Response Relationships | Insecticides such as DDT are stored in the body fat, and thus are more likely to have cumulative effects than are organophosphates, which cause acute illness, and tend to have nonlinear, threshold level toxicity. | Dosages needed to cause lethal effects on non-targets are measured in standard tests on a small number of indicator species (e.g., [34], but exposure rates in the field are highly variable). Also, for insecticidal crops, high dose designations sufficient to delay resistance development in pest populations have been speculative [35]. |
| Etiological Uncertainty | Farm workers with exposure to low doses of an insecticidal nerve toxin experience respiratory distress that is over three times as severe when applying fungicides. It is difficult, if not impossible, to document conclusively that a specific disease is caused by exposure to a specific environmental effluent. | The rise in acreage of transgenic insecticidal crops accompanied the rise in colony collapse syndrome in honeybees, but so has the use of neonicotinoid insecticides, the number of cell phone towers, incidence of bee mites, virus infection, the distance commercial pollination hives were transported, and many other confounding factors [36]. |
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