Toms River

by Dan Fagin

  This was, of course, a very old story. Bladder tumors had been linked to dye manufacturing ever since Ludwig Rehn reported on three cases in Frankfurt dye workers in 1895. By 1925, so many cases had accumulated that the Swiss government officially recognized bladder cancer as an occupational disease in the dye industry, making the stricken workers eligible for special compensation. British dye workers (though not their American counterparts) received similar benefits starting in 1938 after a cluster of bladder cancer cases appeared at a Ciba-owned dye factory in Manchester.16

  The cause was almost certainly exposure to benzidine and beta-naphthylamine, or BNA. Thanks to Wilhelm Hueper’s dog studies, the case against BNA was so strong that by the 1950s DuPont and the Swiss had stopped using it at all of their plants, including in the United States. The discovery of cheaper substitutes made the decision to abandon BNA a relatively easy one. Benzidine, however, was a very different case; there were no similarly inexpensive alternatives. It was used in much greater volumes than BNA ever was, yet when dye workers at the Chambers Works kept getting bladder cancer in the 1940s and 1950s, DuPont scientists blamed past exposure to BNA, not the ongoing inhalation of benzidine dust.17 DuPont stuck to its position even after researchers at a Ciba plant in England reported in 1951 that twenty-one of the sixty-six workers who had developed bladder cancer there worked only with benzidine, not BNA.18 Dye makers also benefited from growing skepticism about the relevance of animal experiments. In a study published in 1950, for example, researchers at Allied Chemical and Dye Corporation acknowledged benzidine was carcinogenic in rats but noted that the tumors occurred in other organs, not the bladder. They also pointed out that rabbits and monkeys exposed to benzidine did not develop bladder tumors and that only one of seven dogs did.19

  The Cincinnati Chemical Works had been a national center of benzidine production since 1929, producing about three thousand pounds per day. There were large, uncovered piles of benzidine powder at the company’s St. Bernard factory, and the dust was everywhere. Workers shoveled benzidine by hand, often with no protection other than gloves and sometimes masks. In the late 1940s, there was a flurry of urinary tract tumors among workers there; the company blamed BNA and instituted stricter rules for handling it. But the Swiss owners, despite the evidence from their own factories in Europe, did not mandate similar controls on the much more important benzidine. In fact, benzidine production increased in Cincinnati after 1952, after vat dye production shifted to Toms River and freed up more space in the overcrowded St. Bernard plant to make benzidine-based azo dyes. As a result, workers at the aging St. Bernard factory throughout the 1950s continued to shovel piles of benzidine powder by hand and also used their hands to clean the powder off filter presses in the open air.20

  So when Arthur Wendel diagnosed a fourth case of bladder cancer among workers at the St. Bernard plant in January of 1958, alarms went off in the executive offices of the Cincinnati Chemical Works and its parent companies in Basel. They looked for help from the department of environmental health at the University of Cincinnati, which was housed in the independent Kettering Laboratory, a unique arrangement. Named for a longtime director of research at General Motors, the Kettering Lab was heavily funded by manufacturers and had a reputation for research that tended not to challenge industry interests. Mitchell Zavon, a Kettering physician who headed the team summoned to assist, arranged for Wendel to examine all twenty-five men who handled benzidine at St. Bernard. Despite all of the evidence from Europe about bladder cancer and dye chemicals, the Cincinnati Chemical Works had never encouraged its workers to get yearly bladder exams (a standard practice in Europe), and its medical record keeping was poor. Now Wendel and his cystoscope would begin filling in the record.

  By the summer of 1958, Wendel had completed his examinations of the twenty-five men. They were as young as thirty and as old as fifty-nine and had spent anywhere from three to twenty-eight years working on the factory floor in St. Bernard. Nine of them—36 percent—had bladder cancer, including five previously undiscovered cases. It was a staggeringly high percentage. Among the nineteen men who had handled benzidine for at least seven years, the rate was even higher: 47 percent.

  “It was just unbelievable how much cancer there was in that plant,” remembered Eula Bingham, a young biologist at the University of Cincinnati who was part of the research team summoned by the company to assess the situation. Bingham would go on to a distinguished fifty-year career as an environmental cancer researcher, including a stint as the director of the Occupational Safety and Health Administration in the late 1970s, but the extremely high case count at the Cincinnati Chemical Works made an indelible impression on her. Years later, she even invited a retired worker from the plant to visit an industrial hygiene class she taught at the University of Cincinnati to demonstrate how he used to shovel benzidine by hand. “In my entire career, I never saw anything else like that again,” Bingham recalled. “I never saw so many people get cancer in one place. Even back in 1958, there were enough cases to know that something terrible was going on.”

  Later in 1958, a protégé of Wilhelm Hueper’s named Thomas Mancuso, who worked for the Ohio State Health Department, confirmed Wendel’s findings in a more sophisticated study that included a control group. He found that plant workers were fourteen times more likely to die of bladder cancer, six times more likely to die of kidney cancer, and four times more likely to die of pancreatic cancer than typical Ohio men. The overall cancer death rate was 23 percent higher than the statewide rate.21

  The evidence was irrefutable: The Cincinnati Chemical Works had a major cancer problem. This time, the company could not ignore it. In 1958, soon after Arthur Wendel finished his examinations, the company halted manufacturing of benzidine in Cincinnati and belatedly instituted improved protections for workers handling the chemical. But the plant’s Swiss owners, who had already stopped using benzidine in many of their European plants, did not stop using it in Cincinnati. It was too economically important to abandon. Instead, they began shipping in benzidine via railcar from Allied Chemical’s huge factory in Buffalo, New York, where it had been made for more than forty years.

  Soon after, in 1959, the Cincinnati Chemical Works closed down, and azo dye production moved to Toms River. A few of the benzidine workers, including two with bladder cancer, transferred to New Jersey. Most, however, stayed in Ohio. Benzidine itself made the transfer, of course. The powder-laden railcars from Buffalo were re-routed to Toms River, where a new generation of employees began working with the carcinogenic chemical. Most knew nothing about what had happened in Cincinnati. Medical researchers around the world did not know either, because Mitchell Zavon, the consultant hired by the Cincinnati Chemical Works, did not publish the stunning results of Wendel’s examinations. After all, those embarrassing findings were mere case reports, not a massive, Richard Doll–style case-control study.22

  Fifteen years later, Zavon had a change of heart and decided to update the case count among the twenty-five workers who had been exposed to benzidine in Cincinnati. He discovered four more bladder cancer cases, raising the total to thirteen out of twenty-five long-term benzidine workers. This time, Zavon and Richard Wendel, Arthur’s son, wrote up the updated results and published two journal articles, in 1973 and 1974.23 By then, though, it was largely a moot point. The freight cars from Buffalo had made their last trip to New Jersey in 1971, when Toms River Chemical finally stopped using benzidine. The company had little choice. Animal tests had at last definitively shown that benzidine was a carcinogen, and the newly formed Occupational Safety and Health Administration was cracking down hard on its use.24 Allied Chemical, the last benzidine maker in the United States, ceased production in 1976, the same year it finally revealed the bladder cancer toll from six decades of production in Buffalo: one hundred and fifty one cases, and probably many more because record keeping in the early years was poor.25

  What about at Toms River Chemical? Benzidine was just one of many known or suspected car
cinogens—including epichlorohydrin, anthraquinone, trichloroethylene, and naphthalene—used in huge quantities at the plant at various times during the 1950s, 1960s, and 1970s. Were cancer cases piling up there as well? No one tried to find out. After the shocking study results in Cincinnati, Ciba was not eager to stir up more anxiety by bringing in another set of outsiders to study cancer in its Toms River workforce. There was little interest from outside researchers anyway, since most of them were now focusing on lifestyle risks like smoking and diet. In the absence of authoritative information, younger workers like George Woolley and the Talty brothers gradually developed their own ideas about possible cancer hotspots at Toms River Chemical, but their theories were based solely on unsubstantiated chatter around the plant.

  It was as if the events in Cincinnati had never happened—no stunning cluster of bladder cancer cases, no investigations, no irrefutable scientific confirmation. The workers and residents of Toms River were still on their own.

  The realization that there might be a cancer problem at the Toms River chemical plant was slow to take hold among the workforce, but once established it could not be shaken. The tipping point came in the summer of 1985, after more than a year of ceaseless pummeling in the newspapers over the toxic content of the waste that the factory was sending into the ground and ocean. The level of anxiety among employees who handled those chemicals every day grew so high that George Woolley and other union leaders felt that they had to ask Ciba-Geigy for a health study—even at the risk of generating more bad publicity that could threaten the company’s future in Toms River. “We didn’t necessarily demand a study, but we felt it had to be done, even if it couldn’t prove anything one way or the other,” Woolley said.

  Ciba-Geigy agreed to take the first step, authorizing a search of the plant’s personnel records to count the number of cancer cases. To interpret the results, the company hired Philip Cole, a predictable choice. The Harvard-trained Cole was the chairman of the epidemiology department of the University of Alabama at Birmingham, where he was building a long roster of chemical industry clients for whom he consulted on health controversies and testified in court cases. Cole was a forceful critic of what he considered overreaching by researchers like Eula Bingham and Thomas Mancuso who were close to labor unions and believed, as Wilhelm Hueper did, that workplace chemicals were important causes of cancer. Instead, Cole endorsed Doll’s view that occupational exposures were responsible for just 4 percent of cancers. In fact, in an interview many years later, Cole said, “My estimate would be two or three percent.”

  Cole had equally strong opinions on the kinds of studies that were scientifically meaningful. Like many of his peers, he believed that case series studies, such as the one Arthur Wendel conducted in Cincinnati, were of little value in identifying potential causes of workplace cancer because they lacked control groups for comparison. And even case-control studies were not very helpful, he believed, unless they included rigorous efforts to account for the confounding influences of luck and lifestyle. Philip Cole was, in short, an occupational cancer epidemiologist who was highly skeptical of the tools of occupational cancer epidemiology. One of his frequent antagonists, Richard Clapp of Boston University, called him “the father of the negative study.”

  When Cole traveled to Toms River in the summer of 1985 to meet with the plant managers, he learned that the company had found a few anomalies in its search of employee medical records. While there was nothing as obvious or dramatic as the cluster of bladder tumors Wendel had found in Cincinnati in 1958, one number did leap out: There were five fatal cases of brain cancer—seven if you counted two men who worked at the Toms River factory but died in Europe. There also seemed to be a surprisingly high number of deaths from bladder cancer and lung cancer. Were those case totals truly high? It was not an easy question to answer. Lung cancers were not particularly rare, but brain and bladder cancers were. On the other hand, more than sixteen hundred men, and a few women, had worked in the production areas of the sprawling factory at one time or another since 1952. Among such a large group, perhaps those cancer totals were not so high after all. “I told them that based on the information they had given me, it was not possible to decide whether or not Ciba-Geigy had a problem with cancer in Toms River,” Cole recalled years later. “The only way to find out would be to do a formal study.” Company officials told him that they would think it over.

  Ciba-Geigy and its employees had yet another reason to be jittery that summer about cancers at the factory: A federal investigator was in town to scrutinize the safety of the azo dye operation. Bruce Hills worked for the National Institute for Occupational Safety and Health, whose research was frequently used by the Occupational Safety and Health Administration to set workplace rules. Hills was there because of two suspect chemicals: ortho-tolidine and ortho-dianisidine. Both were closely related to benzidine, and Ciba-Geigy had depended on them since the mid-1970s, after OSHA’s crackdown on benzidine. The problem was, the two benzidine derivatives appeared to be almost as carcinogenic as their parent compound, which is why OSHA in 1980 had urged dye manufacturers to stop using them.26 In Toms River, that advice was not followed. By 1985, despite the overall decline of Ciba-Geigy’s dye business, the factory was still on track to make more than thirty million pounds of dyes, many of them black, blue, or deep red azos made from ortho-tolidine or ortho-dianisidine.

  Bruce Hills was not shocked by what he saw on his first visit to Ciba-Geigy. The production areas were cleaner than some other dye plants he had visited, where the air was so thick with colored particles that “you would think you were wearing tinted glasses.” He told company managers that he would return in a few weeks to test the factory air for ortho-tolidine and ortho-dianisidine, and he made a request: He wanted to collect urine samples from azo workers to test for dye chemicals. “I asked, and the company told me they’d talk to the union about it, and that it wouldn’t be a problem,” Hills recalled.

  Word that a federal cancer researcher was visiting spread quickly around the factory, generating more anxiety for workers who were already upset about all the bad news of the previous months. Benzidine had already been taken away as a dye ingredient because of previous cancer scares. If they lost ortho-tolidine and ortho-dianisidine, too, there would be no way left to make azo dyes. Ciba-Geigy’s most important remaining product—and all the jobs that went along with it—would disappear. Even more chilling than the economic threat was the sense that perhaps Greenpeace and the plant’s other critics were right. Maybe there really was a cancer problem at Ciba-Geigy.

  Three days after Bruce Hills completed his first visit and left town, plant manager Victor Baker gathered the factory’s employees together and announced that Ciba-Geigy would cooperate with Hills and would also launch its own cancer study. Philip Cole’s protégé at the University of Alabama, Elizabeth Delzell, would conduct a case-control epidemiological study of the company’s past and present workers in Toms River, with a special focus on brain cancer, and the results would be published in a medical journal. Ciba-Geigy’s new official spokesman, Thomas Chizmadia, told reporters that the company’s actions were spurred solely by a desire to assure its workers and neighbors that the plant was safe. The company had not found “anything of an emergency nature,” he said.27

  The low-key news coverage of the decision belied its significance. For a company that had suffered through so many unwanted “firsts” since the discovery of the pipeline leak sixteen months earlier—protests, sabotage, a record fine, a criminal investigation, slashing news coverage, and public scorn—here was another one. For the first time in its thirty-two-year history in Toms River, Ciba-Geigy was acknowledging the legitimacy of the longstanding worries of its workers and neighbors. No one had ever done a health study in Toms River; talk of cancer had always been confined to anxious exchanges over back fences and lunchroom tables. Now, at last, modern epidemiology—with its blazing controversies, tantalizing ambiguities, and frightening implications—was coming to t
own.

  There were limits to the company’s new openness, however. When Bruce Hills returned at the end of September to take air samples and collect urine, George Woolley told him that the union had instructed its members not to participate. “I was shocked and taken aback that the union said no,” Hills remembered. “I mean, if you were a worker, why wouldn’t you want this?” Woolley did not want it because the company had convinced him that the study design was flawed. Hills wanted to find out whether dye chemicals in the workers’ urine were mutagens capable of altering DNA—an indication that they might also be carcinogenic. But company officials argued that if the urine tested positive for mutagenicity, it could be due to a chemical exposure from one of those “lifestyle” exposures Richard Doll and Philip Cole considered so important: smoking, alcohol, or even diet soda or barbecued meat. Since there would be no control group for comparison, there was no way to know if dyes were truly at fault.

  Hills thought the objection was spurious—if the workers’ urine turned out to be mutagenic, then he could do a more extensive study to assess other potential causes. If it were not mutagenic, then the workers would have one fewer thing to worry about. But to Woolley, who knew how tense the workers were and how endangered their jobs were, the company’s objections made sense. “If we had been a part of that study, you’d wind up telling people they had mutagens in their urine but you wouldn’t be able to tell them why,” he recalled. “I just couldn’t see putting people through that, considering how much stress everyone was already under.” There was another reason, too, he acknowledged. “We didn’t want to have any more bad press and make the situation worse for the company and for the workers, especially for a study that wouldn’t prove anything.”