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C H A P T ER 7 Good Citizens Every time we permit enlightened self-regulation to be replaced by forced regulation, all of us are diminished. Wealth, well-being, personal freedom, and the quality of our lives are inevitably diminished. —Cleve Goring, Dow’s director of agricultural products research1 I don’t want to be cynical, but are there any employees in the Department who don’t have chloracne already? —Emmet Kelly, Monsanto’s medical director2 Let us practice good citizenship. —V. K. Rowe, Dow’s chief toxicologist3 In 1964, George Lawton, a Navy lieutenant and medical resident, was assigned to the Public Health Service’s (PHS) Division of Occupational Health. Lawton spent a year in the dermatology section, run by Donald Birmingham and his assistant, Marcus Key. This PHS facility, based in Cincinnati, was small but important. The next generation of environmental agencies—the EPA, the National Institute of Environmental Health Sciences, and the National Institute for Occupational Safety and Health (NIOSH)—would rely heavily on its programs. NIOSH in particular never left Cincinnati and was staffed by many of the PHS people already there, including Marcus Key, who became its first director. The PHS had a reputation for either diluting or suppressing politically controversial findings. According to David Groth, an agency pathologist, “I was told that if you did something that made industry look bad, you would be transferred.”4 Birmingham and Key had already investigated the chloracne epidemics at the Monsanto and Diamond Alkali facilities. They understood that dioxin was responsible for the workers’ symptoms. But they assumed the risk inside the factory was 58 all anyone needed to worry about. If you supplied masks and protective clothing, installed showers, etc., then the problem could be kept under control. In 1964, two new incidents came to their attention, both demonstrating that dioxin was much more dangerous than they’d thought. Some of the Diamond T workers developed porphyria cutanea tarda (PCT), which is caused by the overproduction of porphyrins, the red-pigmented constituent of the blood. Found mostly in adult males, its symptoms include fragile skin, sensitivity to light, nerve damage, and impaired liver function, particularly if the patient is alcoholic. It’s usually hereditary, but can also be caused by toxic exposure.5 Apparently, chloracne could strike deeper into the human body than anyone knew. But this outbreak might still be an anomaly, not a true public health threat. The second incident, however, challenged some fundamental preconceptions about who was at risk. In the fall of 1962, a worker in the Ozark National Forest developed a rash on his face, arms, and back after spraying T. He was treated by Davis Goldstein, a dermatologist from Fort Smith, Arkansas. A few months later, Goldstein met Marcus Key at a scientific conference. They discussed the case, agreed that it was probably chloracne, and promised to share information. Goldstein had already informed the US Forest Service and the Arkansas dermatological association about his patient. But Key and Birmingham had a better grasp of how important this was: “So far as we know, yours is the first case of chloracne from a marketed herbicide.” Goldstein believed there were even more cases. “I questioned (the patient) about others having this same condition and he says they do have a few infected areas at times, but nothing like he has had.”6 Birmingham and Key decided to find out whether 2,4,5-T really was toxic. In April 1963, Key asked Goldstein for a sample of the offending product. Key applied a tiny amount to his forearm several times a week for the next three weeks. He later flippantly explained that he’d chosen himself as a subject because “We seldom had a supply of unused laboratory animals.” He had also assumed that this tiny amount of T wouldn’t cause him serious harm. He did develop a mild case of chloracne, but only at the exposed spot.7 Key familiarized himself with the scientific literature on T. He realized that despite Kimmig and Schulz’s research, no one really knew if the final product contained TCDD. Even the experiment he’d just conducted on himself proved only that this one particular batch of T was chloracnegenic, not whether dioxin was responsible . Part of the problem was TCDD’s almost unbelievable potency; only the best analytical technology of that time (none of it available to the PHS) could identify the infinitesimal levels capable of causing harm. As part of his...

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