Setting the record straight on Rachel Carson, malaria and DDT

The contemptible campaign of hoax and calumny against the work and memory of Rachel Carson continues. You should read more at the sites I cite near the end of this post.

The key false claim of the Carson critics is that, but for the ban on DDT, millions of lives would have been saved over the past 30 years. Chief problem with the claim is that national bans on DDT all preserve DDT use for essential mosquito eradication, especially if there are no other tools to fight the disease. But other problems with the claim include the fact that DDT had stopped being highly effective by the late 1960s; eradication was a pipe dream, and mosquitoes developed resistance to DDT.

That doesn’t stop the critics. So, Dear Reader, when you read criticisms of Rachel Carson and hear the pseudo-science whine that Carson alone has condemned millions to death by malaria, I want you to keep in mind this question: If DDT were such an effective tool against malaria, why didn’t the World Health Organization fight to keep it? Why didn’t the manufacturers fight to keep it? Why would more than 150 nations, tens of thousands of scientists, tens of thousands of health workers, and conservative “I-told-you-so” skeptics who hate environmentalists, all simultaneously fall asleep?

The answer is, Dear Reader, they didn’t all fall asleep. DDT stopped being effective, and malaria fighters realized there were other problems — the parasites that the mosquitoes spread also became resistant to anti-malaria drugs, a bigger problem than DDT resistance. People and organizations who fight malaria did ask that use of DDT be preserved for spraying to fight malaria; but they didn’t defend it against bans on other use because those bans help the malaria fighters.

Cover of Saving Lives, Buying Time: Economics of Malaria Drugs in an Age of Resistance (2004), from the National Academies Press

Below the fold, I offer two quotes from Saving Lives, Buying Time: Economics of Malaria Drugs in an Age of Resistance (2004) Board on Global Health (BGH) (available from the National Academy of Sciences). You can see that DDT is not the golden-egg-laying goose, and that consequently Rachel Carson is not the mindless ogre she is made out to be in recent invectives.

Check out these sites:

• Bug Girl’s Blog, “DDT, Junk Science, and the attack on Rachel Carson;” “DDT, Junk Science, and Malaria Resistance;” “Malarial Resistance: Exciting new development;” “Rachel Carson and Chemical News;” “New York Times, DDT, and an a–hole“
• Laelaps, “Something stinks over at National Geographic;”
• Deltoid, “Hundreds of Millions Killed by Rachel Carson;” “Creationists Claim Rachel Carson Killed Millions;” “The Rachel Carson Telephone Game;” “Reaction to Tierney’s Bad Science;” “John Tierney’s Bad Science;” “Raw Story Follows the Money on Rachel Carson Smears;” “Taking Aim at Rachel Carson” (describing the unsavory sources of the campaign against Carson)
• Rabbet Run, “Who Ordered That?“
• Obsidian Wings, “Junk Science: DDT“

From Saving Lives, Buying Time: Economics of Malaria Drugs in an Age of Resistance (2004) Board on Global Health (BGH), from pages 198-199:

Then came the golden days of DDT, a highly effective insecticide first used as a delousing agent at the end of World War II. During the 1950s and 1960s, indoor residual spraying with DDT was the centerpiece of global malaria eradication efforts. DDT’s months-long ability to kill or deter adult female mosquitoes resting on treated walls after feeding led to further declines in malaria in India, Sri Lanka, the former Soviet Union, and other countries. By 1966, campaigns using DDT spraying, elimination of mosquito breeding sites, and mass treatment had freed more than 500 million people (roughly one-third of the population previously living in malarious areas) from the threat of disease (Shiff, 2002). Unfortunately, eradication was not sustained due to high program costs, community resistance to repeated house spraying, and the emergence of resistance to DDT. By the late 1960s, the hope of eradicating malaria through vector control was finally abandoned (Guerin et al., 2002). In many countries, the pendulum then swung to overreliance on chloroquine, a widely available antimalarial drug.

Sub-Saharan Africa was always a special case. With the exception of a few pilot programs, no sustained malaria control efforts were ever mounted there (Greenwood and Mutabingwa, 2002). The biggest obstacle was the widespread distribution of Anopheles gambiae, a long-lived and aggressive malaria vector. The entomological inoculation rate (EIR) (which measures the frequency with which a human is bitten by an infectious mosquito) rarely exceeds five per year in Asia or South America. In contrast, EIRs of over 1,000 have been recorded in several parts of sub-Saharan Africa (Greenwood and Mutabingwa, 2002).

Today, the global burden of malaria is concentrated in sub-Saharan Africa where stable, endemic disease is linked to poverty and highly efficient vectors. The insecticide-treated bednet (ITN)—first shown in The Gambia to reduce overall childhood mortality by 60 percent when combined with malaria chemoprophylaxis (Alonso et al., 1991)—is the vector control tool with the greatest promise for Africa. At the Africa Summit on Roll Back Malaria in Abuja, Nigeria in 2000, leaders from 44 African countries set a target of 60 percent ITN coverage of pregnant women and infants in Africa by 2005, an ambitious goal requiring roughly 160 million ITNs at an estimated cost of US$1.12 billion (Nahlen et al., 2003). Sadly, the goal is still far from being met. At the same time, insecticide resistance (involving pyrethroids and DDT) is a growing problem in Africa, along with environmental change brought by agriculture and other types of development that foster mosquito breeding. International sponsors also have withdrawn support for DDT due to environmental concerns.

With respect to malaria’s human reservoir, the overriding challenge facing Africa is the development of drug resistance by Plasmodium falciparum to cheap and effective treatments (chloroquine and sulfadoxine-pyrimethamine [SP]), compounded by large and, in some cases, mobile infected populations.

From pages 201-202:

Levels of resistance in insect populations reflect the amount and frequency of insecticide contact as well as inherent characteristics of the target species. Thus far, DDT resistance has not developed in long-lived disease vectors such as tsetse flies or triatomid bugs (definitive hosts of African sleeping sickness and Chagas’ disease, respectively). Mosquitoes, in contrast, have several characteristics suited to rapid development of resistance, including a short life cycle and abundant progeny.

In 1946, only two species of malaria vector were resistant to DDT. However, by 1966 the emergence of resistance was clear: 15 species were resistant to DDT, and 36 species were resistant to dieldrin (WHO Expert Committee on Insecticides, 1970). By 1991, 55 anopheline vectors demonstrated resistance to one or more insecticides. Of these, 53 were resistant to DDT, 27 to organophosphates, 17 to carbamates, and 10 to pyrethroids (WHO, 1992a,b). A decade later, some form of pyrethroid resistance (either decreased mortality, or decreased excito-repellancy of mosquitoes by pyrethroid-impregnated ITNs) had been reported from countries in Asia, Africa, and South America (Takken, 2002).

Three major groups of inactivating enzymes (glutathione S-transferases, esterases, and monooxygenases) are responsible for metabolic resistance to DDT, pyrethroids, organophosphates, and carbamates in Anopheles mosquitoes. Knock-down resistance (kdr) is a separate resistance phenotype linked to a point mutation in sodium channels targeted by both pyrethroids and DDT. Although prevalent in A. gambiae in West Africa, kdr has not impaired ITN efficacy in the region (Sina and Aultman, 2001; Hemingway and Bates, 2003). In southern Africa, in contrast, the local vector A. funestus has acquired metabolic resistance to pyrethroids, rendering ITNs ineffective (Chandre et al., 1999; Brooke et al., 2001). A looming concern for the future is that A. gambiae in equatorial Africa will acquire the same metabolic resistance to pyrethroids seen in A. funestus in southern Africa. Currently, metabolic resistance to pyrethroids in A. gambiae is limited to focal areas of West Africa and Kenya (Ranson et al., 2002).

In our fight to save people from malaria, and to cure those cases we cannot prevent, calumny against Rachel Carson should not be a tool. Ranting, ignorantly, against a great woman, kills no mosquito, kills no Plasmodium. Let us honor her memory, and celebrate the disasters she prevented.

That’s one step. The record has been grossly distorted. This may take some time to fix.

Sen. Tom Coburn, R-Oklahoma — are you paying attention?