Read The Big Ratchet: How Humanity Thrives in the Face of Natural Crisis Online
Authors: Ruth DeFries
DDT proved its power during World War II. Supplies of pyrethrum, the chrysanthemum-derived insecticide that protected Allied troops and civilians from diseases such as typhus (from lice) and malaria (from mosquitoes), were running low. Then typhus hit Naples in 1944. DDT powder dusted on louse-infested people stopped the typhus epidemic in its tracks for the first time in history. The insecticide sprayed from airplanes was equally effective in controlling
malaria during the war. Müller won a Nobel Prize in 1948 “for his discovery of the high efficiency of DDT as a contact
poison against several arthropods.”
After the war, DDT became another tool in the toolkit for public health campaigns to fight malaria in the southeastern United States, the Middle East, and southern Europe. In the United States, government programs had done much to reduce malaria: swamplands were drained to eliminate breeding grounds, larvicides such as Paris green were sprayed, and people were encouraged to put screens on their doors and windows to keep out mosquitoes. But malaria was still widespread in the southeastern states, where the mosquitoes were more plentiful than in other regions of the country and the people poorer. After the war, as veterans returned from overseas carrying new malaria strains that threatened to make the problem even worse, the government’s public health service decided to use the new DDT miracle on native soil. The indoors of millions of homes in the southeastern states were sprayed with DDT. Similar efforts elsewhere meant that by midcentury the disease was virtually eliminated from temperate climes, although it’s unclear how much DDT added to its death knell. Sadly, malaria still claims millions of lives a year in the tropics, where the
disease is more virulent.
After disease control, the chemical industry set its sights on agriculture as a new market. Advertisements claimed that DDT could kill every pest plaguing humanity, from weeds in home gardens to corn earworm across the prairies to flies on the livestock ranches of the western
states. Sales were brisk. Production of DDT increased nearly fivefold in the United States from the 1940s to the peak of DDT’s
popularity in the early 1960s. The chemical industry also synthesized scores of other pesticides similar in chemical composition to DDT, with names like aldrin, dieldrin, chlordane, heptachlor, and toxaphene. Hoskins’s goal, to reduce dependence on pesticides, was lost in the rush.
The US government was again a customer for the new miracle pesticides. Fire ants, known for their savagery and painful stings, had stowed away on a ship from South America and entered the United States through Mobile, Alabama, in the late 1910s. By the 1950s, they had spread across the South. Fire ants had a vicious sting. They had reportedly killed a young New Orleans boy and sent others to the hospital. Their foot-high mounds got in the way of tractors. They stung livestock that stepped into their mounds and ate seeds, crops, and young quail. In other words, the fire ants were
a frightening nuisance.
Exposed soil from the expansion of fields, cities, and suburbs across the south made conditions right for the ant’s march. Many entomologists were eager to use the new pesticides. They claimed in a Cold War–era press release that “Uncle Sam is ready to use a fleet of 60 planes to go to war against the dreaded fire ant. . . . Only the modern airplane, dropping insecticides on twenty million acres in the critical area, can hope to
stop the menace.” In 1957, the government spread potent chemical insecticides over 1 million acres in the South and
millions more acres after that. Ultimately, the eradication program backfired. The pesticides killed off the native ant species, which competed with the fire ant for space and food. With the natives gone, territory was wide open for the persistent fire ants to expand. The
problem became even worse. The world famous naturalist E. O. Wilson, who had studied the fire ants in his high-school years, later dubbed the expensive, unwinnable war as the “
Vietnam of entomology.” Fire ants remain a part of the insect community in the southern United States.
The gypsy moth has a similar story. In 1869, the moth accidently escaped from a yard in a Boston suburb into the forests of New England. A French immigrant, whose hobby was testing the potential of silkworms for the silk industry, had carried the insect to Boston from Europe, unaware of its devastating ability to strip trees bare of
leaves in his new homeland. Programs to rid the forests of the destructive pest began in 1890 with spraying Paris green from horse-drawn sprayers. A few years later, the sprayers were leveling a lead arsenite compound against the moths. In the 1940s, airplanes were spraying DDT followed later by more benign pesticides. Nothing worked, and today there’s little hope of
eradicating the moth. Likewise with the fungal Dutch Elm disease and the beetles that carry it.
These are just a few of many examples where the widespread use of DDT held out the false hope of a once-and-for-all solution. That was before the uphill battle against pests came into full view and the side effects became too alarming to ignore.
The decades following World War II were a pivot point from the perspective of pesticides. Before the pivot, some farmers tried to control pests with relatively small amounts of pesticides concocted from arsenic and other inorganic chemicals, or from plants with toxic properties. After the pivot, the cheap, widely available, and seemingly effective DDT set off a bonanza of new synthetic organic insecticides. These were termed “synthetic” because they were made in labs rather than nature, and “organic” for their carbon-containing molecules, which could attack the nervous systems of their victims. The bonanza added another notch to the ratcheting of food production. In this case, the hatchet was not far behind.
The same properties that make DDT and other synthetic organic pesticides effective poisons are the ones that make them dangerous. They do not dissolve readily in water, which made them attractive to farmers, because they remained on the field despite rain or dew. But that same
trait also meant they persisted for a long time in the environment without breaking down. The compounds dissolved in fat rather than water, and remained stored in the body fat of exposed animals. Attached to soil, they traveled through rivers and groundwater. Lofted in the air, they traveled long distances—as far as the poles. They caused convulsion, paralysis, and death. They did not discriminate. Sprays of DDT intended to kill mosquitoes, fire ants, or houseflies would also kill or sterilize birds and other animals as collateral damage. And then there was the issue of how effective the compounds really were over the long term, given the proclivity of organisms to evolve to fit their environment.
By the time Paul Müller walked onto the podium to collect the 1948 Nobel Prize for his discovery of DDT’s insecticidal properties, a problem with the miracle compound was already surfacing. Scientists had found that the chemical was becoming less effective against houseflies. The flies were becoming resistant to the pesticide.
The fact that pests might evolve to become resistant to the poison was not much on the minds of the manufacturers in the early days. In hindsight, it should have been obvious to anyone familiar with Darwin’s findings on short- and long-beaked finches. Pest species have coevolved with plants over long, long periods of time. Plants have had their own chemical defenses to ward off pests for eons—hence the early pesticides derived from tobacco leaves and chrysanthemum flowers. It’s to be expected that the gene pools of pest species will contain some individuals able to resist toxins, and that those hardy individuals might be able to withstand DDT or other pesticides. And it’s to be expected that these hardy individuals will go on to produce more offspring than their vulnerable rivals. Just as with the natural selection of the short- and long-beaked finches, over time the population will contain more of the hardy individuals than the susceptible individuals. With short generation times, it’s no surprise that populations of houseflies could develop the ability to weather the onslaught of DDT within a few years.
The phenomenon does not apply only to DDT. Insects and other organisms were becoming resistant to the inorganic and plant-derived pesticides that were being used even before the postwar boom in DDT. As the pace of spraying and dusting picked up with synthesized organic pesticides after the war, so did the pace of evolution for pests to become immune to the pesticides. When some pests didn’t die after being sprayed with a pesticide, it was logical to conclude that they had managed to survive because the dose of pesticide was too low. Ratcheting up the dose seemed to make sense. But, paradoxically, more pesticide means even faster selection for those individuals who can survive and pass on their genes to their offspring. The pesticide becomes even less effective, leading to even higher doses. It’s a runaway cycle.
By 1980, more than four hundred insect species and scores of pathogenic fungi and bacteria, weeds, and rodents were resistant to
one or more pesticides. For example, the Colorado potato beetle, by the early
1980s, was resistant to a barrage of different types of pesticides in Long Island, New York. Farmers returned to plant-derived pesticides that had been popular before the DDT boom. The resistance problem also threw a wrench into the once-promising fight against malaria. Malaria-carrying mosquitoes became resistant to DDT in Central America and South Asia, among other regions. Widespread spraying for monocultures of cotton, high-yield varieties of rice, and other crops where the threat of malaria once discouraged farming exacerbated the problem in tropical areas. Irrigation and drainage ditches, havens for breeding mosquitoes, made control of malaria even harder.
There’s no way to stop the process of natural selection. A pesticide might work for a decade or two. Beyond that, natural selection is likely to render the compound ineffective. Companies in the pesticide market need to continually synthesize new compounds to combat resistance. Many, many hundreds of different synthesized pesticides exist for this reason. It’s a costly endeavor with no endpoint. Resistance put a big dent in the premature optimism that DDT would once and for all make humanity the victor in the
battle against pests.
Pest resistance wrought by natural selection wasn’t the only problem with the DDT bonanza. The pesticide, when sprayed across fields and forests and inside homes, attacked all living organisms with which it came into contact. Again, this wasn’t new. Before DDT, strychnine to control rodents killed quail and songbirds, and arsenic to control tree
diseases killed deer. Once again, DDT hastened the impact, as pesticide-spraying planes left trails of dead animals in their wake. In the attack on the fire ant, biologists in Autauga County, Alabama, surveyed ten acres seven days after the chemical had been sprayed. Their report: “6 rabbits, 3 opossums, 1 Racoon, 3 Bobwhites, 1 Barred Owl, 10 Cardinals, 20 Song Sparrows, 2 Blue Jays, 1 Mockingbird, 1 Brown Thrasher, 1 warbler, 1 Red-bellied Woodpecker, 2 cotton rats and 1 white-footed mouse were found in a dead or dying condition. In a drainage ditch
which traversed the area numerous dead or dying fish and frogs were observed. . . . Laboratory analyses of these birds and animals revealed that hydrocarbons were present in sufficient
amounts to cause death.” Hydrocarbon pesticides like DDT were the culprit—one was mirex, an insecticide with harmful effects on the stomach, intestines, and other organs. This was not an isolated incident, and people were aware that it was happening elsewhere. Reports of the pesticides’ lethal effects on livestock and wildlife appeared in newspapers and scientific publications. “New Super Insect Killer Both Helps and Harms Farmer, Experts Find: Destroys Pests But Paralyzes Sheep,” read a
Wall Street Journal
headline
on February 7, 1945.
Moreover, it wasn’t only the direct effect of the pesticides that killed wildlife. The properties that made DDT and similar pesticides attractive—hydrophobia for not dissolving in water, and lipophilia for attaching to fats—meant that the concentrations of the chemical magnified up the food chain. Because DDT does not dissolve in water or break down easily, it persists on leaves and seeds. It remains for many years in sediments of lakes and rivers. From there, the DDT can easily make its way up the food chain. A caterpillar eats DDT-sprayed leaves, a small bird eats hundreds of caterpillars, and a predatory hawk or eagle eats dozens of the smaller birds. Or DDT attached to sediment runs off from a field into a lake. The DDT gets into the algae, then into the plankton that eat the algae, then into the small fish that eat the plankton, then into the larger fish who eat the small fish, then into the birds or humans who eat the fish. Each time, the concentration of DDT magnifies as it moves up the food chain. Being lipophilic, DDT is stored for the long term in fat tissue. By the time DDT reaches the top of the chain, concentrations can be magnified millions of times over.