Toms River (61 page)

The first, very preliminary results of the Toms River case-control studies were released in December of 1999, and they were tantalizing. Under pressure to show progress after three years, Jerry Fagliano and his colleagues had finished analyzing the questionnaire, looking for differences in the responses of the forty case families compared to the 159 healthy controls.
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Interview-only studies were a weak form of epidemiology because they depended on fallible memories. If everyone’s memory were equally unreliable, this might not be a major problem. But families struck by traumatic illness tended to have much more detailed memories about past exposures than control-group families who had been spared. This well-known phenomenon was known as recall bias. The air and water distribution models, which were still under construction in 1999, would minimize the distorting effects of recall bias because their exposure estimates were based not on memories but on reconstructions of historical emissions patterns. Since the models were not ready, Fagliano warned the families not to make too much of the interview results.

Still, the results were intriguing. The case and control families had been asked more than two hundred questions, on topics ranging from miscarriage history to hot dog consumption. They were asked about so many possible risk factors that it was likely that for a few of those questions the differences between the cases and controls were going to look significant even if they were really due to nothing but chance. As it turned out, though, there were only a few examples of these flukes.
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Instead, almost all of the potential nonenvironmental causes explored
in the interviews—including prominent theories such as maternal smoking, alcohol consumption, and family history of cancer—were no more common in case families than in control families. Case and control families tended to have similar diets and were similarly likely to have used nail polish, pesticides, and paint thinner, among many other possible risks. By process of elimination, water and air pollution now loomed larger than ever as possible explanations for the cluster. This was especially true because when the interviewers asked the study families whether they drank tap or bottled water, children who later developed cancer were 8 percent more likely to have drunk tap water and 60 percent more likely to have been born to mothers who drank tap water during their pregnancies. In fact, for both mothers and kids, there was a dose-response relationship: Cancer risk was highest for those who drank more than five glasses of tap water per day, lowest for those who drank none, and in between for those who had just a few glasses.
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As usual, Fagliano kept his feelings to himself, but he could not help being excited about this preliminary finding, even if it was influenced by recall bias. “It suggested we were on the right track,” he later explained.

The lawyers for the families were excited too; the drinking water correlation was another bit of leverage they could use in possible settlement negotiations. By early 2000, the tone of their meetings in Princeton had shifted again. No longer just exchanging information, the opposing attorneys were now focused on convincing each other of the correctness of their arguments. The stridency of their initial meetings was gone for good—as Schlichtmann had hoped, the lawyers knew each other too well now for overt hostility—but both sides also knew that the time for casual research was ending, especially because the case-control study was at last approaching completion. Fagliano had told Gillick’s committee that the study results would be available by the end of 2001—almost six years after the rowdy public meeting that had launched the investigation.

From the start, the case-control study (now two studies: the interview study and the birth record study) had loomed over the lawyers’ meetings as an omnipotent, if seldom discussed, presence. If, in the end, the study results linked the cluster to air pollution from Ciba or
to water pollution from Reich Farm and Ciba via United Water’s pipes, then the families would obviously have a very strong case for a huge payout, either from a settlement or—years later—a jury verdict. On the other hand, if the study did not find an association between pollution and cancer, the companies would surely offer nothing more than a token amount, and the families would have to decide whether to take it or risk a court battle premised on a greatly weakened case. A crucial question for both sides, then, was whether to take an all-or-nothing gamble by waiting for the case-control study results or instead try to negotiate a settlement before the study was completed.

“It got to the point where it was clear that the case-control study really was going to come to an end, and that we on the plaintiff’s side were not going to go away,” said lawyer Mark Cuker. “So the discussion became, how do we resolve this?” William Warren, a lawyer for Union Carbide, made it clear that his client would not settle the case merely out of sympathy for the families or to avoid bad publicity. He and his counterparts at Ciba and United Water hinted that a settlement was possible, but first the families’ lawyers would have to show that they could present a legitimate case for causation.

Essentially, what the companies wanted was a mini-trial that would be a surrogate for the real thing, but with no judge or jury—not even a mediator. Union Carbide, in particular, had resisted mediation because it implied that a settlement was in the offing. However, the company’s combative general counsel, Robert Butler, did have a soft spot for Eric Green, a law professor at Boston University and one of the best-known mediators in the United States. (He would soon achieve even more notoriety for brokering the massive 2001 antitrust settlement between Microsoft and federal prosecutors.) So when Schlichtmann heard that Green was going to be in Princeton for a different case on the same day the Toms River lawyers were meeting there, he convinced Butler and a few others to interrupt Green in the middle of a solitary lunch at the Forrestal Hotel (he had a napkin under his chin and was busy tucking into a steak) to see if he would be willing to consider getting involved in the Toms River case.

They were not looking for a mediator to engineer a settlement, the lawyers told Green. Instead, they wanted a “facilitator” to organize
and oversee a series of meetings at which experts from each side would present information and opinions about the key issues, just as they would do if they were witnesses at a trial. Instead of trying to persuade a judge, jury, or mediator, however, the lawyers and their experts would be trying to convince their counterparts on the other side that they could present a winning case if there ever were a trial. Later on, the lawyers told him, Green might play a more formal role in brokering a settlement—but that would depend on the persuasiveness of the expert presentations. Each side would first have to be convinced that a deal was preferable to the risk of waiting for the case-control study results or going to trial. Though irritated at having his lunch interrupted by the ever-pushy Schlichtmann, Green was intrigued; he had never been involved with anything quite like this. The lawyers agreed to hire him, splitting his fee, which would ultimately top $100,000.

Almost immediately, there were complications. In May of 2000, four other lawyers sued Ciba on behalf of six hundred residents, mostly of Oak Ridge, who lived downwind from the factory’s smokestacks or atop its groundwater plumes. About two hundred had cancer or other health issues they blamed on the factory.
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(A second class-action suit, seeking compensation from Ciba for diminished property values in Oak Ridge, was filed eight months later on behalf of about seven hundred homeowners.)
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Cuker, Berezofsky, and Schlichtmann had been dreading the prospect of other lawyers entering the fray because they feared that it would shut down the ongoing exchange of information and end any chance of a settlement. Union Carbide was already considering pulling out of the talks because it was being acquired by Dow Chemical, which had a history of taking a hard line in lawsuits. After a tense few weeks of uncertainty, the company lawyers said that they would keep participating while reserving the right to drop out at any time.

The expert presentations in front of Eric Green were shaping up as critical; they were perhaps the last time the attorneys would control the fate of their own case, since the case-control studies would be completed soon after. Both sides prepared intensively. Cuker pushed his experts to prepare a visual demonstration showing how contamination
and cancer washed across Toms River in successive waves. He envisioned a series of maps that would serve as a sort of time-lapse movie documenting the cluster over time as well as in space. They would show how Union Carbide’s plume spread south from Reich Farm, reached the Parkway wells, and was then distributed all over town, year by year. For each cancer diagnosis, meanwhile, a dot representing the affected child’s home address would be added; by the 1996 map, there would be dozens of dots.

The maps neatly summarized the families’ powerful but circumstantial case. Toms River had an extraordinary amount of toxic pollution and a discernible cluster of childhood cancer, and the two seemed to line up, roughly, in what looked like a cause-and-effect relationship. But the families’ case was based on epidemiology, and epidemiology was a science of probability, not certainty. Its practitioners looked for correlations between exposure and disease and then tried to assess the likelihood that they were causal. Even with all the pollution and cancer in Toms River, the apparent association could never be confirmed definitively because of the unanswerable questions about long ago exposures and also because of the enigmatic nature of cancer, which struck so unpredictably and had so many possible causes. If the case ever went to trial, a jury might be persuaded by Cuker’s maps, but the lawyer would have to make an indirect argument on the families’ behalf, one that relied on surrogacy and correlation—and plenty of emotion, too.

Bruce Molholt, lawyer Mark Cuker’s volunteer toxicologist, thought that there might be a more direct way to link the children’s cancers to local pollution. His training was in molecular genetics, and he was accustomed to assessing the impact of pollutants on individual cells and genes, not on large groups of people, the traditional domain of epidemiologists. Molholt no longer did research, but he kept up with the field. He knew that by the mid-1990s, scientists all over the world were looking for—and finding—distinctive changes in genes that seemed to be associated with exposure to specific environmental pollutants. In moments of enthusiasm, the new field’s practitioners sometimes claimed that these genetic biomarkers, as they were called,
were like fingerprints—unique identifiers of specific chemical exposures. They were not. Very few biomarkers were caused by only one chemical, and not everyone who was exposed to a particular compound carried the associated biomarker in his or her DNA. Lacking this one-to-one correspondence, researchers instead looked for patterns, probabilistic associations between biomarkers and exposures, which is why the new field was called molecular epidemiology.

The new discoveries were exciting, even if their meaning was unclear. New analytical tools were allowing scientists to peer into the architecture of the double helix, where they could see how certain industrial chemicals wreaked genetic havoc. Some pollutants slipped in between the tightly coiled base pairs of DNA like playing cards in a door spring; others fused with DNA and formed adducts that disrupted cell replication. No one was sure exactly what this meant for cancer causation, though it certainly seemed significant, in light of what Alfred Knudson and others had already proved about the importance of multiple “hits” on DNA in triggering cancer. If biomarkers proved to be sufficiently reliable—a big if—they might even save lives by serving as early indicators of cancer, long before tumors could be detected by conventional means, and by identifying populations that were particularly susceptible to cancer.
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What particularly excited Bruce Molholt about molecular epidemiology were its obvious implications for investigations of cancer hotspots like Toms River. So far, the research projects undertaken in the town were squarely within the twin realms of classical toxicology and epidemiology, fields that could trace their lineage back to Paracelsus. At the end of the National Toxicology Program’s two-year rat bioassay, pathologists would look for physical evidence of tumors, just as Katsusaburo Yamagiwa had done with his rabbits almost a century earlier. Similarly, Jerry Fagliano and his team were conducting a textbook epidemiological study, using exposure mapping and case-counting techniques that were much more sophisticated yet essentially similar to what John Snow had utilized during the London cholera epidemic of 1854. Fagliano identified his forty cases solely on the basis of a diagnosable tumor, not a genetic mutation or other biomarker. But tumors were only one way to document past exposure,
and not a very accurate one, since most cancers had many possible causes, and most exposed people did not get cancer.

A biomarker study of the Toms River children, Molholt thought, held out the hope of uncovering clearer evidence of exposure—not quite a fingerprint, but something more convincing than the correlative evidence of Mark Cuker’s maps. It would also be a way of expanding the focus of the investigation beyond SAN trimer, which Molholt worried was getting too much attention compared to other compounds in the town’s air and water. He thought that many of the chemicals dumped in Toms River—especially benzidine and anthraquinone dyes—were good candidates for a biomarker study. The dyes, he thought, were probably intercalators, which meant that they could damage genes by slipping between two base pairs of DNA. Several carcinogenic pollutants had already been shown to intercalate, including benzo(a)pyrene, the coal tar ingredient that Ernest Kennaway in 1932 had confirmed as the first known synthetic carcinogen. Benzidine and anthraquinone were excellent clothing dyes because they were highly reactive, binding tightly to fibers, and because they did not dissolve in water. Those same qualities, Molholt thought, probably made them DNA intercalators. They would be attracted to the hydrophobic environment of the inner surface of the double helix, binding there and, perhaps, triggering cancer-promoting mutations.