Banned

by Frederick Rowe Davis

  The ban on DDT and other organochlorines took effect in 1973. After paraffinic oil (60 million pounds) and the organochlorine, toxaphene (34 million pounds), the other top ten insecticides used by farmers were organophosphates and carbamates for total applications of more than 85 million pounds. Toxaphene topped the list of synthetic insecticides in 1976. Farmers typically applied this chlorinated hydrocarbon in mixtures with methyl parathion for insect control in cotton.34 Although methyl parathion and carbaryl/Sevin use slid to 23 million pounds and less than 16 million pounds, respectively, ethyl parathion use remained fairly constant at about 9 million pounds. Meanwhile, the application of phorate and disulfoton both rose to nearly 7 million pounds each. Like aldrin, both of these chemicals were applied to corn, and the increase more than offset the decline (by 7 million pounds) in the use of aldrin. Two new (and highly toxic) organophosphate insecticides, EPN (6 million pounds) and fonofos (5 million pounds), appeared in the list of the top ten insecticides used in agriculture. Economic entomologists compared EPN to parathion, but it was more persistent. Farmers applied fonofos, also highly toxic, to corn. Shifting the focus to acres rather than pounds, the decline in acres treated with aldrin and bufencarb (a total of more than 11 million acres) was more than offset by acres treated with carbofuran, fonofos, phorate, and terbofos (more than 16 million).35

  By 1982, use of organochlorines had dropped to such an extent that only toxaphene remained among the top ten insecticides by weight (6.6 million pounds). Several factors explain the precipitous fall in toxaphene applications (from more than 34 million pounds in 1976 to less than 7 million in 1982). First, the organochlorine (usually paired with methyl parathion) was becoming less effective due to the development of resistance in insects. Second, toxaphene use dropped as a result of the replacement of toxaphene and methyl parathion, typically applied to cotton in 1976 at the rate of 3 to 9 pounds per acre, with synthetic pyrethroids (fenvalerate and permethrin), which were applied at the rate of one half pound per acre in 1982. Finally, and perhaps most significant, the EPA banned the use of toxaphene in 1982.36 With the exception of paraffinic oil (50 million pounds), organophosphate insecticides dominated the list of insecticides applied at rate of more than 500,000 pounds per year. With that in mind, agricultural use of most of the well-known insecticides had fallen since 1976. Use of methyl parathion dropped more than 50 percent. Carbaryl and ethyl parathion applications fell more than 6 million pounds and nearly 3 million pounds, respectively. However, as in previous years, reductions were offset by significant increases in the use of such insecticides as terbufos (up 6 million pounds to 8.6 million pounds) and chlorpyrifos (5.4 million pounds). Registered in 1965, chlorpyrifos was applied to a variety of food and feed crops in agriculture especially corn. It was also popular for insect control on golf courses, wood treatment (nonstructural), and against adult mosquitoes. Over time, it became clear that single applications of chlorpyrifos posed risks to small mammals, birds, fish, and aquatic invertebrates for most outdoor uses. Risks to wildlife increased with multiple applications.37 Like many other organophosphate insecticides, terbufos was extremely toxic to birds, fish, and aquatic invertebrates. Farmers used it as an insecticide and nematicide on corn, sugar beets, and grain sorghum. Carbofuran and fonofos applications remained fairly consistent between 1976 and 1982. By 1982, some cotton farmers had begun to apply two synthetic pyrethroids in significant quantities: permethrin (1.5 million pounds) and fenvalerate (just under 1.3 million pounds). These ongoing trends are illustrated by the data in table 3.

  The year 1989 marked a major milestone. Aside from paraffinic oil (for which applications had fallen to 35 million pounds), organophosphate insecticides accounted for the rest of the insecticides in the top twenty agricultural insecticides applied for agriculture (for total applications that exceeded 90 million pounds). Organophosphates represented all but three of the insecticides of which more than 500,000 pounds were applied in 1989 (more than 100 million pounds in total). Specifically, agricultural use of chloripyrifos and terbufos rose to 11.3 million pounds and 10.2 million pounds, respectively. Malathion use rose to 6.3 million pounds, mainly because it was used in the program to eradicate cotton boll weevil.38 Meanwhile, applications of methyl parathion, carbofuran, and fonofos dropped considerably. Ethyl parathion and phorate use remained fairly consistent with 1982.

  Although 90 million pounds of potent insecticides is a vast quantity of chemicals, the number is misleading on several levels. First, it includes only those pesticides used in U.S. agriculture at a rate of 500,000 pounds per year or more in 1989. There were many other organophosphates used widely for which estimates fell short of 500,000 pounds. Second, the calculation includes only the active ingredients, for example, methyl parathion. Most insecticides require some sort of delivery medium, which are not included in calculations of pesticide use. Often the substances utilized for distributing the active ingredients add to the toxicological profile. Yet another source of underestimation stems from the simple fact that only a portion of pesticides are directed toward agriculture. Just as chemical companies sold chlorinated hydrocarbons widely, they also marketed organophosphates to consumers, who depended on them to replace banned chlorinated hydrocarbons. In addition, municipal public health organizations sprayed extensively for insect control. Just as farmers sought replacements for organochlorines like DDT, public health officials looked to organophosphate insecticides to fill the gap left by the ban on so many chlorinated hydrocarbons. Suffice it to say, 90 million pounds was a very conservative estimate for the quantity of insecticides deployed in 1989.

  Table 3

  Top Insecticides, 1966–1982 (1,000 pounds active ingredient/year)

  The details of the quantities and applications of insecticides in the decades after Silent Spring reveal several trends. First, as DDT and other chlorinated hydrocarbons underwent legislative and regulatory scrutiny, farmers turned to alternatives; first to another chlorinated hydrocarbon, toxaphene, but increasingly to organophosphates. Second, by 1976, organophosphates dominated insecticides in agricultural use. Finally, despite bans on DDT and other chlorinated hydrocarbons, total insecticide use remained at high levels, which suggests that most farmers continued to view insecticides as a major part of their effort to produce crops.

  After twenty-five years of considerable variability in the type and quantity of particular insecticides from 1966 to 1989, a few specific pesticides emerged as the preferred tools for insect control in agriculture. In 1992, 1997, and 2002, chlorpyrifos, terbufos, and methyl parathion topped the list of insecticides most used in agriculture. Several carbamates (carbaryl/Sevin, carbofuran, and aldicarb) remained popular. Demand remained high despite the initiation of a comprehensive review of the organophosphate and carbamate insecticides by EPA (see table 4).

  Meanwhile, the link between pesticides and cancer seemed evermore tenuous. In 1988, the Council on Scientific Affairs (CSA) of the American Medical Association reviewed the link between pesticides and cancer. After acknowledging the challenges of establishing such a link and the problems with animal models, the authors concluded that acute toxicity was the primary hazard of pesticide exposures and that no pesticides had been proven to be carcinogenic, despite evidence of carcinogenicity in animals: “A large number of pesticidal compounds have shown evidence of genotoxicity or carcinogenicity in animals and in vitro screening tests, but no pesticides—except arsenic and vinyl chloride (once used as an aerosol propellant)—have been proved definitely to be carcinogenic in man. Epidemiological studies offer only conjectural evidence at best that pesticides may be carcinogenic.”39 Nevertheless, the CSA recommended that the AMA urge the EPA to intensify its efforts at pesticide reregistration to determine the long-term health effects of pesticides especially carcinogenicity.

  Table 4

  Top Insecticides, 1989–2002 (1,000 pounds active ingredient/year)

  For the most part, organophosphate insecticides were not associated with carcinogenicity, so they pass
ed through the screen that was the regulatory emphasis on cancer. Since they typically did not bioaccumulate in the environment, they avoided one of the chief drawbacks of the organochlorines. Lost in these toxicological analyses was the damage that organophosphate insecticides wrought to humans and wildlife directly in the form of acute toxicity. As we have seen, with the exception of malathion, organophosphates were moderately to highly toxic to humans and wildlife, especially birds, fish, aquatic organisms, and non-target insects, including bees. To a degree that would have shocked and disappointed Carson, the “road traveled” was flooded with highly toxic organophosphate insecticides, which she had identified as some of the most toxic chemicals known to man.

  In the mid-1990s Theo Colborn, a World Wildlife Fund research scientist, pieced together evidence that pointed to a strikingly different concern. Drawing on hundreds of published studies, Colborn argued that environmental chemicals caused endocrine disruption in a wide range of animals and humans.40 Such a finding squared well with one of Rachel Carson’s greatest concerns in Silent Spring, namely, the decline of topline predators as a result of eggshell thinning due to the bioaccumulation of chlorinated hydrocarbons like DDT (and for that matter PCBs). Endocrine disruption, as Langston has shown, was a neglected element of risk assessment, with serious consequences.41

  Neither cancer nor endocrine disruption was on Kenneth DuBois’s mind when he expressed concern about the imminent ban on DDT. DuBois’s concern was neurotoxicity. With the DDT ban, DuBois worried that farmers and public health officials would turn to organophosphates to control insects, thereby exposing farm workers and others to extremely toxic chemicals. DDT was banned as were other chlorinated hydrocarbons, but it was many years before any of the organophosphates underwent the kind of scrutiny that could support a move to phase them out. In fact, most organophosphates were still in use as of 1996. As DuBois and others feared, organophosphate insecticides replaced DDT for many general uses. Between 1964 and 1994, pesticide use in the United States doubled from 500 million pounds to over 1 billion pounds.42 As we saw above, more than half of the pesticides in use through the 1990s were organophosphates.

  Wildlife continued to perish at phenomenal rates largely due to exposures to organophosphates. In 1997, Audubon (magazine) reported that more than 67 million birds were dying annually as a result of pesticide poisoning in the United States.43 Monocrotophos is one example of an organophosphate particularly toxic to birds. It was initially registered in the United States in 1965. Certain scientists believe that monocrotophos has been responsible for more avian mortality incidents than any other pesticide since 1965. EPA canceled all registered use of this chemical in 1991, and the largest U.S. manufacturer voluntarily began to phase out its production, but monocrotophos and many other organophosphates are still in use internationally, where they pose significant risks to humans and wildlife. One extreme example arose in Argentina in 1996 when thousands of Swainson’s hawks died at their core wintering site after monocrotophos spraying. As many as three thousand hawks at one site and perhaps twenty thousand in all perished.44 Argentina subsequently banned monocrotophos from agricultural use.

  As DuBois predicted, urban and suburban use of pesticides put humans and wildlife seriously at risk. Until its ban took effect in 2001, Americans used 6 million pounds annually of diazinon, 70 percent of it used by homeowners and professional applicators for structural and lawn pest control around residences and public buildings. Diazinon applications have caused the second largest number of total bird deaths of any pesticide.45 Birds are not alone in their susceptibility to organophosphates, although one of the legacies of Silent Spring is a particular public sensitivity to avian mortality. Populations of mammals, fish, reptiles, amphibians, as well as beneficial and nontarget insects, suffer from exposure to various pesticides, herbicides, and fungicides.

  As environmental historian Linda Nash elegantly argued, farm workers regularly faced exposures to these substances, in violation of state and federal regulations and at levels that can inhibit cholinesterase. In Our Children’s Toxic Legacy, Wargo noted that the other group most at risk is children who consume more of the liquids, fruits, and vegetables that may carry organophosphates. Children may also encounter organophosphates applied indoors. Animal studies continue to sharpen scientists’ understanding of the risks posed by organophosphates.46 For example, there is substantial toxicological evidence that repeated low-level exposure to organophosphate pesticides may affect neurodevelopment and growth in developing animals.47 At the peak of use during the 1990s, there may have been as many as ten thousand cases of organophosphate poisoning annually in the United States alone. Internationally, organophosphates still pose grave risks to children and farmworkers. In July 2013, twenty-three Indian children (aged five to twelve) died and dozens more were sickened after consuming free school lunches accidentally contaminated with the organophosphate monocrotophos at a school in the state of Bihar.48 Similar cases have been reported in China and Ecuador.

  In 1996, President Bill Clinton signed the Food Quality Protection Act (FQPA), which amended both FIFRA (1947) and the FFDCA (1938). The FQPA required the EPA to reassess all food tolerances established before August 3, 1996, giving priority to those pesticides posing the greatest risk. This act compelled the EPA to conduct an extensive cumulative risk assessment of the organophosphates. The forty or so organophosphates in use were among the first chemicals the EPA reviewed, followed by the other group of chemicals that induce cholinesterase inhibition: the carbamates. The deadline for the EPA to complete its review of all tolerances was August 2006.49 Although progress was slow, the EPA announced the phaseout of chlorpyrifos and diazinon based on toxicity and the risk they posed to children through contaminated food and drinking water, as well as their threat to birds and other wildlife.50 At the close of the 2006 cumulative risk assessment, the EPA announced the cancellation of many other organophosphates and carbamates.

  Recent studies have challenged conventional wisdom regarding the toxicity of organophosphates. Since DuBois and other researchers determined the very high neurotoxicity of organophosphates at very small exposure levels, few researchers pursued studies of chronic exposures to organophosphates. In 2011, three different research teams published on the neurotoxic effects of organophosphates in Environmental Health Perspectives, one of the leading journals of environmental health. Drawing on data from prenatal exposures to organophosphates resulting from spraying crops in Salinas, California, and from spraying roaches in New York City apartments, the studies reached similar conclusions: prenatal exposures to organophosphate insecticides impaired intellectual development in children. The researchers at the Mailman School of Public Health, Columbia University, found IQ declines of 1.4 percent on average in children with prenatal exposures to chlorpyrifos.51 Another group studying New York residents discovered that exposure to organophosphate pesticides was negatively associated with cognitive development, particularly perceptual reasoning.52 Even more striking, a third study of children exposed to organophosphates in agricultural areas in Salinas, California, showed that those in the group that suffered the highest exposures exhibited an average deficit of seven IQ points compared with children in the lowest exposure group.53 Even more surprising, yet another study revealed a possible association between low level exposures to organophosphate flame retardants (another common use of the chemicals) and two effects: altered hormone levels and decreased semen quality in men.54 Suffice it to say, current research has broadened the toxicological profile of organophosphates.

  The story of organophosphates and environmental risk continued to unfold up to and beyond 2006. Neither science nor regulation came to terms with this group of highly toxic chemicals until decades after restrictions and bans were placed on DDT and other chlorinated hydrocarbons. At the very least, Rachel Carson’s warning inspired grassroots environmental activism against DDT and other chlorinated hydrocarbons. The ban on DDT and protection under the Endangered Species Act (1973) has con
tributed to the recovery of numerous species of wildlife, most notably bald eagles, peregrines, brown pelicans, and ospreys. But more than three decades passed before the EPA completed its cumulative review of organophosphates. For most of that period, risk assessment focused on cancer, which reflected a public health priority dating back to World War II. Even when risk assessment broadened to include endocrine disruptors in the 1990s, most organophosphates slipped through the regulatory net. Only with the passage of the Food Quality Protection Act in 1996 and the cumulative review of organophosphates in 2006 did the organophosphates, some of the most toxic chemicals available, receive the careful scrutiny that led to the removal of these pesticides from the market. Introduced in the same time frame as DDT, the organophosphate insecticides, which were highly toxic nerve toxins, slipped through the cracks in the regulatory frameworks established in the wake of Silent Spring. Several recent studies have significantly broadened the toxicological profile of organophosphates to include cognitive impairment in children exposed prenatally and possible endocrine effects.

  CHAPTER 8

  Roads Taken

  What lessons might we draw from a century of pesticides, a hundred years of risk assessment? Despite the prodigious efforts of scientists, regulators, and legislators, simple solutions have not emerged. As we have seen, as the scale of agriculture developed to industrial proportions, farmers increasingly relied on chemical inputs—and particularly insecticides—to control crop damage as a result of insect infestations. A similar process of upscaling placed incredible distance between producers (of meat and other products) and consumers. When American consumers and legislators discovered the health risks that such distances entailed, Congress passed the 1906 Pure Food and Drug Act. The Insecticide Act of 1910 followed a few years later. Like the PFDA, the Insecticide Act was essentially a law for truth in labeling. Although these laws were groundbreaking at the time of passage, cracks soon appeared in the legislation that left consumers exposed to toxic substances. Several egregious cases that left thousands injured and worse and reports in popular books and articles accelerated the progress toward revised legislation in the form of the 1938 Federal Food, Drug, and Cosmetic Act. The efforts of University of Chicago pharmacologist E. M. K. Geiling and FDA scientists to develop rigorous quantitative methods revealed the value of toxicology in characterizing risks of chemicals in the marketplace. Contemporaneously, Alice Hamilton, researchers with the Harvard Lead Study, and W. C. Hueper, among others, initiated the study of industrial disease with important implications for the study of toxicology and carcinogenicity.