Welcome to another ongoing series on Our Modern Plagues: Better Know a Fix. It is the sister series to Better Know a Plague, which I introduced last week. The “fix” posts will explore the ways we use science and technology to thwart various modern plagues. Sometimes, I’ll line the posts up to match a specific plague I’ve already written about. Other times, that won’t be possible because there is no fix.
Fix is a funny word. To fix is to put something in order, or to make it more stable or permanent. Solving a problem fixes; it mends or repairs. But you can also be in a fix, which is akin to being in a quandary or a tight spot or hot water or any other such cliché.
Our first example is DDT, more formally dichloro-diphenyl-trichloroethane, which is widely credited with knocking down last week’s subject, the bed bug, after World War II.
DDT was the first modern synthetic pesticide. Paul Herman Müller, a Swiss chemist, discovered its insecticidal properties in 1939 after spending several years spritzing a glass box full of blue bottle flies with hundreds of chemicals. He was looking for a new insecticide with residual powers, which means that an insect that walked over or alit upon a treated surface would die. DDT worked so well that even after Müller washed his equipment, the chemical clung to the glass and continued to kill. Eventually, he had to dismantle the glass box, sanitize it, and air it out for a month to make it usable in new tests.
Müller’s main target was the Colorado potato beetle, an invasive species eating up crops on Swiss farms. His compound worked against this beetle. It also worked on houseflies and gnats. And since DDT’s discovery coincided with WWII, it wasn’t long before Allied forces were using it to control blood-sucking insect vectors, most famously malaria-carrying mosquitoes and typhus-carrying lice. Thanks in part to DDT, WWII was the first major engagement where fewer American troops died from disease than from weapons. Müller was subsequently awarded the Nobel Prize in Physiology or Medicine in 1948.
After the war, chemical companies offered DDT commercially, and soon we had DDT sprays, paints, wallpapers, dog powders, and more. DDT was on farmland and lawns, in orchards and homes.
To say we were overzealous with DDT is an understatment, and ultimately it caused long list of environmental and health problems, which you can read all about in Rachel Carson’s _Silent Spring _(although in retrospect, DDT was a relatively safe pesticide–its problems stemmed mostly from overuse). By 1972, the newly formed Environmental Protection Agency banned the use of DDT in the US, although we continued to manufacture and export it until 1982. The last American DDT plant, just outside of Los Angeles, is now a Superfund site.
Before its ban, the pesticide’s success was partly due to its novelty. Insects had never experienced such an assassin. Our previoulsy pesticides were mostly poisonous botanicals, or elements such as arsenic and mercury. None killed insects with such a pointed attack. DDT’s longevity was also an asset: it stayed on surfaces far longer than its predecessors, so was guaranteed to zap insects for a longer period of time.
How DDT works within an insect isn’t known for certain, but the best explanation is that it messes with proteins in the nervous system called sodium channels. These are the gates that open and close to let charged salts called sodium ions pass from one nerve cell to the other, and they are key to relaying the messages that zip through an organism’s body and allow it to move and to think. DDT basically holds the gate open so nerve signals can’t stop when they’re supposed to, which leads an insect to tremor to its death.
The thing about insects is that they exist in droves and they are very, very prolific. Some are apt to have genetic mutations that let them dodge a pesticide—perhaps one that changes the shape of the ion channel, for example, preventing DDT’s deadly grasp. Genetic mutations flow quickly through generations of insects, and thus those naturally resistant will beget more resistant insects, which will do the same, ad infinitum.
A major example for DDT resistance involves a mutation dubbed kdr, or knock-down resistance, named for the fact that such mutant insects are difficult or impossible to knock down. Bed bugs started showing resistance within a few years of DDT’s widespread use, as did a long list of other insects including lice, mosquitoes, houseflies, fruit flies, and cockroaches.
Environmental impact aside, DDT’s other unintended legacy is that it functions much in the same way as a modern class of pesticides called pyrethroids. Nearly every over-the-counter insecticide in your cabinet contains a pyrethroid, as do professional-grade sprays, topical lice and scabies creams, and pesticide-impregnated clothes and bedding. The genetic mutations that made bed bugs and other insects resistant to DDT are the same that have made them resistant to pyrethroids, which has contributed to the massive bed bug resurgence we experience today.
***
Additional reading
Paul Herman Müller biography, Nobel Prize website
DDT – A Brief History and Status, EPA website
Nobel Lectures in Physiology or Medicine: 1942-1962_,_ World Scientific Publishing Co.
DDT and the American Century, David Kinkela
Widespread distribution of knockdown resistance mutations in the bed bug, Cimex lectularius (Hemiptera: Cimicidae), populations in the United States, Zhu et al, Archives of Insect Physiology and Biochemistry, 2010
