A Civil Action (20 page)

Whatever its true merits or failings, the study created an immediate public sensation. The headline on the front page of
The Boston Globe—
WOBURN LEUKEMIA LINKED TO TAINTED WATER
—delighted Schlichtmann. As he saw it, the study confirmed to the world at large the legitimacy of the Woburn case, and it came with the imprimatur of Harvard upon it.

He wasn’t disturbed by the critics, but he also understood that as a piece of evidence the study had limitations. It had not addressed the biological causes of leukemia. It did not prove that the contaminated well water had caused the leukemias. It showed only that those children who drank water from Wells G and H were more likely to get leukemia than those who did not. Schlichtmann knew that he and Roisman would need more than this study to prove that TCE had caused leukemia in Jimmy Anderson and the other children.

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The Harvard Health Study also provoked response from another quarter—from Cheeseman. He had planned, in his methodical way, a longrange strategy for the Woburn case. After his disappointment with Rule 11, his strategy called for him to wait until Schlichtmann made the next move. Months had passed, and then a year, and Schlichtmann had done nothing. By then, Cheeseman felt he might have reason to hope that Woburn had become an orphan.

But the Harvard study dashed that hope. The day after its release Cheeseman started to prepare his next move, a motion for summary judgment. It took him several months. He had been working on it—had almost finished it, in fact—when he had that chance encounter on Milk Street with Schlichtmann. He was glad he’d gotten the tour of
Schlichtmann’s office and seen the Carney exhibits. If Woburn ever went to trial, Cheeseman told himself, at least he’d know what to expect.

Cheeseman’s summary judgment motion asked Judge Skinner to dismiss the Woburn case on the grounds that Schlichtmann would be unable to present any competent scientific evidence showing that TCE caused leukemia. Without such evidence, Cheeseman argued in his brief, the case, as a matter of law, could not go to a jury.

At first Cheeseman had figured his motion didn’t stand much of a chance. He’d regarded it mostly as a means of educating Judge Skinner to the real scientific issues in the case. But he’d found himself growing more optimistic as he worked on the motion. At the Harvard Medical School he visited the labs of two doctors, both world-renowned experts in the study of blood disorders. Between them, they had treated more than two thousand leukemia patients. One of the doctors, Dr. James Jandl, had just written a chapter on leukemic diseases for his latest book,
Blood: Textbook of Hematology
. Jandl had reviewed all of the medical and scientific literature on leukemogenesis and had found nothing at all to suggest that TCE played a role in the disease. He regarded the Woburn lawsuit with thinly veiled contempt.

The Environmental Protection Agency, it was true, had listed TCE as a “probable” carcinogen. But it had done so on the basis of animal tests—lab experiments in which mice, rats, and hamsters were fed enormous quantities of TCE over long periods. In one experiment, white mice had developed cancers of the lymph system, which manufactures white blood cells. But that particular strain of laboratory mouse, Jandl pointed out, was known to have a high incidence of “spontaneous” lymphosarcoma, and even the authors of the study had discounted the results. Furthermore, both Harvard doctors told Cheeseman they had little faith in extrapolating the results of animal studies to human beings. The life spans of animals, their chromosomal structures, and their metabolism were just too different.

Cheeseman called Facher to tell him of his work on summary judgment. He would have liked Facher to join the motion, but once again, as with Rule 11, Facher expressed no interest.

Cheeseman went on by himself. He asked the two doctors to sign lengthy affidavits stating that there existed no medically accepted evidence to support the opinion that TCE could cause leukemia in humans. In the absence of such evidence, Cheeseman wrote in his brief
to Judge Skinner, Schlichtmann could not make out a
prima facie
case on causation. “Summary judgment should therefore be entered, dismissing the claims.”

Cheeseman felt confident the judge would schedule a hearing for oral argument in a motion of this importance, but he wanted to make certain of that. He ended his motion by saying, “Grace believes that oral argument with respect to this matter may be of assistance to the Court and therefore requests such argument, and estimates one hour will be necessary for both sides to be heard.”

The arrival of Cheeseman’s summary judgment motion—only a week after the Carney verdict—dampened Schlichtmann’s spirits considerably. It was an excellent motion, well argued and supported by two illustrious doctors. Schlichtmann had hoped to take a vacation after the Carney trial, but now he and Roisman had only ten days in which to respond. They could ask Cheeseman for a thirty-day extension, but even so, that still wouldn’t allow much time to reply to a motion of this caliber. Because of the shortness of time, they agreed that Schlichtmann would handle the reply largely by himself.

Schlichtmann called Cheeseman to ask for an extension. “It’s a very good motion,” he added. “I think you’ve got a chance of winning.”

By now, Cheeseman thought so too, although it surprised him to hear Schlichtmann admit it. He didn’t object to a thirty-day extension.

Schlichtmann went to work. He met with an immunologist from California who had been recommended by Roisman. The immunologist, Dr. Alan Levin, was experienced in legal matters. He had served as an expert witness many times before in cases involving toxic substances. He told Schlichtmann that he regarded lawsuits as a useful vehicle for social change. Schlichtmann found this attitude most unusual in a doctor. The medical community, Levin explained, was far too slow in recognizing the perils of environmental toxins. “Twenty years ago we were using X rays to see if our shoes fit, and zapping our gonads in the process,” Levin said. “If you talk to any intelligent twenty-year-old today, he’d say nobody could be that stupid. Your children are going to ask you, ‘Did they really spray insecticides from airplanes?’ ”

Levin had a theory about the Woburn case. He believed that constant low-level exposure to TCE had damaged the immune systems of
all the members of the Woburn families. “These chemicals always do something,” he told Schlichtmann. “Most of the time they don’t do enough damage for us to notice. You might lose a few cells, but you won’t notice it because we’ve got a lot of extra cells.” A healthy, vigilant immune system will attack and kill aberrant cells. But if the immune system has been damaged, as Levin speculated, a malignant cell stands a far greater chance of surviving and proliferating.

All this made sense to Schlichtmann. But was there an objective way of testing for this damage? Levin said he knew of an immunopathologist at Harvard whose lab specialized in monitoring the immune systems of patients after organ transplant surgery. But the tests would be expensive, warned Levin, and he could not be certain what they would show.

Schlichtmann decided to go ahead anyway. Levin called the pathologist, whose name was Dr. Robert Colvin, and explained his interest in a series of blood tests. The working hypothesis, Levin told Colvin, was that exposure to chemicals in the drinking water had caused abnormalities in the immune systems of all the family members, not just those who had gotten leukemia.

Colvin had heard about the Harvard Health Study and the Woburn cluster. An interesting subject, he said to Levin. He asked what tests Levin wanted. A lymphocyte count, replied Levin, And a series of T cell assays.

The lymphocyte count—a simple count of white blood cells—was easy enough. Any lab could do that. The T cell assays were somewhat more difficult. All T cells look alike, but they perform different functions, and distinguishing one from another was a tricky business. The helper T cell, for instance, identifies foreign organisms—viruses, bacteria, cancerous cells—and summons killer T cells, which are equipped with cytotoxic enzymes. Another type of T cell, the suppressor, stops the attack of the killer T cells when the invading organism has been conquered.

Colvin used a technique for marking T cells with reagents to differentiate them, and then he counted them with a laser. But he had never heard of using T cell assays to document exposure to chemicals. Even if the tests did show something unusual, there would be no way of telling what had caused the abnormality. The assays would serve no diagnostic purpose, he told Levin.

Levin thought that Colvin might find an abnormality in the ratios of one set of T cells to another. He could not predict what sort of
abnormality, however. The assays would be somewhat of a fishing expedition, Levin allowed.

Colvin did not like fishing expeditions. His lab was in great demand. It was hard enough for him to find time to fulfill all his colleagues’ requests. Yet the idea intrigued him, and in the end he agreed to do the tests. “But,” he added, “I don’t think you’re going to find anything.”

Colvin suggested they start by testing just one family. The protocol was rigid: the blood could not be refrigerated, and it had to arrive in Colvin’s lab on the morning it was drawn. It would take a full day to do one run of blood in the machine, to agglutinate out the red cells, to fix and stain the white cells, and to perform the cell counts. Schlichtmann would have to make the arrangements to have the blood drawn and transported to the lab. It would cost about ten thousand dollars to have all the families tested. Schlichtmann readily agreed to the price. After all, he had spent more than that for a conference room table in his new office.

The Zonas were the first to have their blood drawn. When the tubes arrived at Colvin’s lab, a technician prepared the blood, marked the T cells with reagents, and ran the assays on the Spectrum 3 cytometer, the machine that counted cells by laser.

As Colvin began plotting the results on a graph, he knew immediately something was awry. To begin with, he saw far more white cells than he expected, a condition known as lymphocytosis, a sign of an immune system in a heightened state of alert. As he calculated the ratio of helper T cells to killer T cells, it became apparent there was another abnormality. The killer cells peaked sharply in all of the family members, particularly in two of the adolescent children. Colvin rarely saw such distinct peaks. He was not certain precisely what this meant. Perhaps their systems were reacting to a carcinogen, as Levin suspected. Whatever its significance, Colvin found it very unusual.

Colvin called Levin and described what he’d found. As a scientist, Colvin trusted results only if they could be replicated. “I think we ought to do the Zonas again, to make sure that this is something that persists,” Colvin said.

Before performing a second assay on the Zonas, Colvin tested the accuracy of the Spectrum 3 cytometer. He regularly sampled his own blood and that of people who worked in his lab, and compared those
results with the normal values reported by other labs. If the normals corresponded, Colvin felt confident that the machine was functioning accurately.

But when Colvin tested the new control group this time, he inadvertently included a lab employee who’d had skin cancer—a melanoma—several years earlier. Colvin saw at once that the killer T cell values for this employee were far outside the normal range, and he eliminated that individual from the control population. But those readings had looked, he thought, strikingly like the results for the Zonas.

Schlichtmann meanwhile got Cheeseman to agree to yet another thirty-day extension. In the weeks that followed, all twenty-eight living members of the Woburn families had blood drawn. Colvin tested the blood of each individual twice. By the time he finished he saw a distinct pattern. “The data are intriguing,” he wrote in a note to Levin on June 15, “because they suggest that there is an increased number of cells in these patients that have a phenotype compatible with killer cells. The implication is that this might be a compensatory response to resist the effects of a carcinogen.”

Levin flew in from California to meet with Schlichtmann. “Basically,” explained Levin, “Colvin thinks that these people might have a carcinogen on board and they’re constantly fighting it. The kids who developed leukemia have lost the fight.”

By now, Colvin felt he was onto something interesting and he wanted to keep pursuing it. He suggested to Levin that he run another series of tests—functional assays, more complicated and more expensive than the first. He and Levin came up with the idea of testing a control group of fifty Woburn residents who had not been exposed to the well water and comparing those results with the eight families. A study of that scope would cost at least fifty thousand dollars.

Schlichtmann was excited by the initial results. He was eager to do the big study, and he wasn’t daunted by the cost, but it would take months to set up, and he had no time for that now. The deadline for his reply to the summary judgment motion was only days away.

Levin had also been searching the scientific literature for studies of TCE. He’d found an epidemiological study of three hundred and thirty dry-cleaning workers, an occupation in which both TCE and perc, the other chemical in the Woburn wells, were commonly used.
The study reported significant increases of several different cancers, among them kidney, bladder, and cervix, and also found five leukemia victims where, statistically, only two had been expected. The author of the study considered the leukemia finding only marginally significant, however. And since the workers had been exposed to several chemicals—TCE, perc, and carbon tetrachloride—the study was unable to draw conclusions about the carcinogenic capacity of any single chemical.

Schlichtmann was beginning to feel slightly more confident. He still did not have any definitive medical evidence to show that TCE could cause leukemia in humans. But he did have the Harvard study; he had Colvin’s blood tests; and Levin had found two more animal studies, overlooked by Cheeseman’s Harvard doctors, suggesting that TCE had damaged blood-forming cells in the bone marrow. He and Levin worked on an affidavit in which Levin stated his belief, “to a reasonable medical certainty,” that the TCE in the wells had “caused or substantially contributed to serious illnesses, including immune dysfunction and leukemia” among the families.