In the 1960s, DDT was a commonly used insecticide used to control malaria by targeting the mosquitoes that harbor the Plasmodia parasites. It functions by causing the insect nerve cells to repetitively fire, making them unable to activate specifically in response to signals. It does this by binding to a channel protein responsible for transporting the sodium ion (Na+) into the cell, which serves as the basis for signals to travel along neurons54. In a normal nervous system, a signal travels because the sodium channels are opened and closed at a specific time. DDT disrupts this rhythm, and the insect consequently dies due to the malfunction of its nervous system55. Significantly, studies suggest that the molecular structure of vertebrate and insect sodium channels are different enough that some insecticides might be insect-specific and unable to affect vertebrate channels54. Whether this might be the case with DDT is not clear, but it is probably not completely exclusive to insects.
Usually DDT is applied to the walls of homes in areas with a high prevalence of malaria or is used to coat bed nets that also serve to physically keep mosquitoes away55,56. However, 1962 spelled the end of the era of DDT, with the publication of Rachel Carson’s monumental Silent Spring57. While the contents of the book were perceived as somewhat alarmist at points, it led to wider awareness of pesticide toxicity. Besides DDT’s toxic properties, Carson also highlighted the growing numbers of insecticide resistant bugs in response to larger-scale spraying with increasingly toxic compounds57. Here is Darwinian natural selection on a time scale humans can appreciate: those insects that are naturally hardier will survive the insecticide to reproduce, leading to increasingly resistant populations. The more deadly the toxin, the tougher the bug must be to survive it. Thus, the problem only escalates as more “effective” pesticides are introduced. What causes this resistance? While Carson does note one instance of a molecular explanation – an insect enzyme degrading DDT to the less harmful compound DDE – in general the reasons have not been determined.
Besides insecticides, mosquito levels can also be regulated by destroying larva before they hatch. A number of strategies have been developed to do this: one is to use bio-degradable oils to suffocate developing mosquitoes in their watery habitat56. Another is to introduce into these environments bacteria or fungi that only infect mosquitoes56. Finally, mosquito-eating fish have proven effective at reducing the number of larvae in particularly large breeding grounds such as lakes56.
Beyond insecticides, scientists are now developing genetically-modified mosquitoes that can no longer effectively harbor malarial parasites. This is done by introducing foreign genes into the mosquito genome. Two examples of such genes are (1): a gene whose protein targets the parasites in the mosquito salivary gland, and (2): a gene whose protein prevents the plasmodia from adhering to the wall of the mosquito’s digestive system58.
1. What are the advantages of bed nets over other uses of insecticide?
2. What features of an environment are important for supporting mosquitoes?
3. Why might DTT spraying be cause for concern? For agriculture? For residential areas?