Powerless Science?

Science and Politics in a Toxic World

Soraya Boudia, Nathalie Jas, Soraya Boudia, Nathalie Jas

• Publisher: Berghahn Books
• Year: 2014
• ISBN:
  9781782382379
• Edition: 1
• Topic: Politik & Internationale Beziehungen
• Subtopic: Umwelt- & Energiepolitik

In spite of decades of research on toxicants, along with the growing role of scientific expertise in public policy and the unprecedented rise in the number of national and international institutions dealing with environmental health issues, problems surrounding contaminants and their effects on health have never appeared so important, sometimes to the point of appearing insurmountable. This calls for a reconsideration of the roles of scientific knowledge and expertise in the definition and management of toxic issues, which this book seeks to do. It looks at complex historical, social, and political dynamics, made up of public controversies, environmental and health crises, economic interests, and political responses, and demonstrates how and to what extent scientific knowledge about toxicants has been caught between scientific, economic, and political imperatives.

PART I

Knowledge, Expertise, and the Transformations in Regulatory Systems

CHAPTER 1

Precaution and the History of Endocrine Disruptors

Nancy Langston

On 6 May 2010 the American President’s Cancer Panel released a bombshell in its annual report, stating that 41 percent of Americans will get cancer in their lifetimes. While efforts to fight cancer have focused on genetics, the report noted, “the true burden of environmentally induced cancers has been grossly underestimated.” Carcinogens and other toxic chemicals “needlessly increase health care costs, cripple our nation’s productivity, and devastate American lives.”¹ The report recommended a precautionary approach to environmental carcinogens that would shift the burden of proof to industry. Rather than requiring the government or consumer to prove harm after a chemical is on the market, industry would have to demonstrate that a chemical is safe before approval.

Within days of the report’s release, environmental groups applauded what they viewed as a new approach, while industry-supported voices rose in protest, claiming that no one can prove that any given case of cancer has been caused by an environmental exposure. According to some industry advocates, acting in a precautionary fashion would violate the scientific process. Because scientists have not proven that low-level exposure is the cause of reproductive problems in humans, too much scientific uncertainty remains for regulators to act. Above all, critics claimed, precaution is a novel, even radical idea, one likely to stifle innovation and destroy profits.²

Do these claims have any historical validity? Is precaution new, and will it destroy scientific process, innovation, and profit? This chapter explores debates over precaution in the context of endocrine disruptors, which are synthetic chemicals that alter hormone systems.

The Case of Diethylstilbestrol

Diethylstilbestrol (DES) offers a useful historical case study for understanding conflicting claims over the role of precaution in regulating synthetic chemicals. DES, synthesized in 1938 by the English biochemist Charles Dodds, was the first synthetic estrogen to be marketed and the first chemical known to act as an endocrine disruptor. Beginning in the 1940s, millions of American women were prescribed DES by their doctors, initially to treat the symptoms of menopause. In 1947 the Food and Drug Administration (FDA) approved DES for pregnant women with diabetes, and drug companies advertised it widely, promoting the use of DES in all pregnancies as a way to reduce the risk of miscarriage. Although no evidence ever supported this claim, millions of pregnant women took the drug. Meanwhile, millions of Americans were also being exposed to DES through their diet. Beginning in 1947, DES was approved in the United States to promote growth in livestock, first in poultry and then in cattle. At the peak of its use in the 1960s, DES was given to nearly 95 percent of feedlot cattle in the United States, and the estrogenic wastes from feedlots and human sewage made their way into aquatic ecosystems.

In 1939, when the American Food and Drug Administration first deliberated on whether to approve DES for human use, the agency was operating under new regulations that were fundamentally precautionary. The recently passed 1938 Food, Drug, and Cosmetic Act put the burden of proof on the industry to show safety, rather than on the consumer or government to show harm. Moreover, the agency and industry both knew of abundant research studies showing that the chemical was carcinogenic in laboratory animals. Three times, the FDA rejected new uses of DES, arguing that precaution suggested the drug was too risky for a particular use. Three times, however, the FDA quickly retreated from precaution and allowed the drug to make its way into human and livestock bodies, and from there, into broader ecosystems (Langston 2010). Why did these retreats from precaution happen? How did political pressures influence agency decision making?

When the FDA began to study DES in 1939, the Roosevelt administration had just weathered a bitter political battle over precaution and regulation. Industry had strenuously opposed the 1938 Food, Drug, and Cosmetic Act, claiming that it was an unwarranted expansion of government power into business, and industry’s efforts delayed the Act’s passage for nearly five years. In 1937, a drug manufacturer placed a tainted drug called Elixir Sulfanilamide on the market—legally—and over one hundred people died. Consumer outrage erupted, and that anger helped the Roosevelt administration finally push the Food, Drug, and Cosmetic Act through Congress a year later. DES was the first major test case for the FDA, and regulators felt they had to be extremely careful about how they proceeded with their new and contested authority (Hilts 2003: 72–102).

DES emerged during a larger debate going on in the 1920s and 1930s about the carcinogenic effects of estrogens. Nearly all researchers agreed that natural estrogens were carcinogenic, and that DES had the potential to be at least as carcinogenic, if not more so, because it was more potent at exciting “estrogenic effects.” Because of these concerns, and because of research on lab animals, in 1940 the FDA initially denied the drug companies’ new drug applications for DES. In rejecting DES, Commissioner Walter Campbell of the FDA argued that regulators must follow what he called the “conservative principle.” Given the scientific uncertainty over DES’s mechanisms of action and metabolism, and over the applicability of animal studies to women, the FDA refused to approve DES—not because scientists had any proof that the drug would harm women, but because they had no proof the drug would not harm women.³ FDA regulators essentially adopted the precautionary principle sixty years before that term came into common usage.

Within months, however, political pressures on the FDA forced the agency to reverse its decision against DES, and in 1941 the agency approved the use of DES in menopausal women. FDA staff had used scientific uncertainty as a justification for refusing to approve DES, but that strategy was not strong enough to resist court challenges and political pressures. A federal court decision against the American Medical Association (AMA) made the FDA wary of engaging with drug companies over the issues of scientific uncertainty—particularly the applicability of animal models to humans—as justification for stiff regulations on estrogens. In the late 1930s, a company named Hiresta had marketed a breast-enlarging estrogen cream. The AMA had been concerned enough about a possible increase in cancer risk from topical estrogen that it published an editorial decrying the dangers of this cream, and Hiresta sued the Association for defamation. The FDA used animal studies to support the AMA’s argument that estrogens were known carcinogens. The federal judge ruled against the AMA, arguing that animal studies failed to prove that estrogen cream would definitely lead to cancer in women—and that clear proof of actual harm to specific women was lacking. This court case led the FDA to abandon its planned campaign to regulate estrogen breast creams and made it wary of continuing to use animal studies in its case against new drug applications for DES.⁴

A similar pattern unfolded several years later when the FDA had to decide whether DES was safe to use during pregnancy. Soon after the initial approval of DES for menopause, drug companies and doctors began petitioning the FDA for approval to treat pregnant women with DES, even though experimental studies on lab animals had shown that DES could cause fetal death and could also harm a woman’s future fertility. Starting in 1939, a physician named Dr. Karl John Karnaky of Houston began experimenting with the use of DES in pregnant women, and he soon became an enthusiastic promoter of DES for all pregnancies. As he later recalled: “The drug companies came to Houston, … fed me and dined me… and I started using it” (Gillam and Bernstein 1987: 67). Research in the early 1940s by the physicians Priscilla White, George Smith, and Olive Smith encouraged the hope that DES might help to prevent miscarriages. Many physicians convinced themselves that DES was indeed a miracle drug for stopping “accidents of pregnancy.” Drug companies lobbied the FDA intensely to approve the drug for pregnancy, sending samples to doctors to create a consumer market for the drug, overwhelming the FDA with short-term data on human effects and ignoring data on animal experiments, and complaining about the safety limits constructed by the FDA.

Initially, FDA staff were quite cautious about DES use during pregnancy, and allowed it to be prescribed only for rare cases of diabetic pregnancies where the mother was almost certain to lose the child otherwise. But this degree of caution quickly faded. Widespread enthusiasm for children in the postwar years, combined with the frustration of the medical community that they had been so powerless to decrease miscarriage rates, helped to persuade much of the medical community that the synthetic estrogen might save babies. In 1947, after the FDA approved limited DES for pregnant women with diabetes, drug companies marketed the drug intensively, urging doctors to prescribe it even for “normal” women “to make a normal pregnancy more normal.” The FDA allowed these uses, and soon nearly one-tenth of pregnancies among American women were treated with the synthetic estrogen (Cody 2008: 232–end).

The retreat from precaution occurred a third time with DES, this time with livestock use. While drug manufacturers were promoting DES for pregnancy, the same companies were also looking for new markets in livestock production. During World War II, pharmaceutical companies requested that the FDA approve the use of diethylstilbestrol to treat certain veterinary conditions in livestock, but because of concern about the potential risks to soldiers who might consume estrogen residues, the FDA explicitly forbade DES treatment of livestock that might be eaten. When companies tried to push against wartime FDA restrictions on the use of synthetic hormones in livestock, the FDA insisted on precaution, arguing that the absence of evidence of harm did not prove safety.⁵

As the war came to an end, political pressures once again led the FDA to abandon its position of precaution. The wartime meat rationing had ended in the United States, but food shortages throughout Europe threatened to lead to famine, which many people were afraid might destroy the peace. Grain was being used to feed livestock rather than feed people, threatening shortages, but government officials worried that Americans would be unwilling to voluntarily reduce their meat consumption in order to make more grain available for human food. Rather than reinstitute rationing, the government encouraged research partnerships devoted to learning how to increase meat production while retaining enough grain to prevent famine. The answer appeared to be hormones, which promised more efficient feed utilization. Because animals treated with estrogen fattened up more quickly on less grain, science might allow Americans to eat more meat without guilt (Bentley 1998).

Poultry was the first target, for roosters and turkeys responded readily to DES implants. In February 1946, internal memos within the FDA showed that staff remained skeptical about the use of diethylstilbestrol in poultry. When one company insisted that the pellets were safe because they would be implanted in chicken necks, which middle-class housewives discarded, one staffer scribbled on a memo: “Some people do use the heads of poultry for food!”⁶ Throughout 1946, the FDA rejected New Drug Applications submitted for poultry, stating that “No information has been offered to show the amount of diethylstilbestrol remaining in the tissues of treated birds. Until it can be clearly shown that no significant quantity of the drug remains in the tissues which might be capable of producing undesirable effects in human consumers, we will not be disposed to consider any application for the diethylstilbestrol use with this purpose.”⁷ FDA staff initially insisted on a precautionary approach, telling companies that determining safety was the responsibility of the manufacturer, not the problem of the government.

But in January 1947 the agency reversed course and agreed to allow diethylstilbestrol to be used in poultry implants. None of the problems discussed in the correspondence from the previous several years had yet been fixed. The only research that drug companies offered in support of DES pellet safety actually showed the opposite, indicating that estrogen residues did migrate from the pellets into meat intended for human consumption.⁸

Why did the agency suddenly allow DES implants in livestock, when regulators had resisted for years? Pressures to increase meat production after the war were certainly great, but concerns about the risk of estrogens for men had initially led the FDA to resist these pressures. By 1947, however, DES began to seem much safer to the FDA. Because medical researchers had treated pregnant women with large doses of DES and no deaths had yet resulted, FDA staff began to argue that small doses presented little risk.⁹

Not all scientists or regulators agreed. Immediately after the FDA approved the chicken implants, Canadian regulators wrote to the federal government, urging the FDA to be extremely careful with the use of diethylstilbestrol in animals. A staff member from the Canadian Department of National Health and Welfare wrote: “We have been working on the problem with the poultry division of the Department of Agriculture and our results show that there is a residue of the estrogen in the cockerels, sufficient to change the vaginal smear of the menopausal woman. Of course this is not evidence of any harmful effects but it is possibly an undesirable reaction for some people. We were planning to publish these results and are wondering if any of the results from your division had been published and we had overlooked them.” The Canadians, in other words, had data showing that a synthetic estrogen implanted in chicken necks was so powerful that residues left in the meat could change the vaginal smears of the woman who ate that meat.¹⁰

After the Canadian researchers published their findings in the October 1947 issue of Endocrinology, the FDA forbade the use of DES in chicken feed, but continued to allow DES to be used in pellets that were implanted in chicken necks.¹¹ For decades the FDA insisted on something that made little scientific sense: that although diethylstilbestrol from chicken feed could accumulate in fatty tissues and pose a danger to humans, DES administered in pellets simply wouldn’t accumulate. When challenged by members of its own scientific staff, the FDA attempted to explain this logic by arguing that “it is possible to exercise a rigid control over the dosage in the [pellet] process and under these circumstances the estrogen does not accumulate in those portions of the treated bird which are consumed by human beings.”¹² A host of assumptions about the possibilities of scientific control are embedded in this statement. First, the statement assumes that technology can offer enough control to sidestep dilemmas posed by pollutants. Second, the statement assumes that people live in an ideal world, one designed by technicians: that no one ever sells a chicken head, that consumers eat what they’re supposed to eat, that companies do exactly what they promise to do, that pellets release a specific, measured, infallible dosage that can be carefully controlled. But none of these assumptions were based on empirical evidence. The FDA had never received or examined any data that showed that pellets did release a reliable and controllable dosage, or that this dosage did not accumulate in tissues, even if it were controllable and reliable. Even though the regulatory agencies tried to assure consumers that complete scientific control was possible over hormones, scientists within the agencies agreed that such control was imposs...