Toms River
Page 61
5. New Jersey Department of Health and Senior Services, Public Health Assessment: Reich Farm and Public Health Assessment: Ciba-Geigy Corporation (March 12, 2001). Said Bruce Molholt, whose work experience included four years at the EPA: “I’ve seen at least one hundred, maybe two hundred of these health consultations, and they never find anything. I was astounded when ATSDR came right out and said we do find reason to believe there was harm caused by both air and water contamination.”
6. U.S. Environmental Protection Agency, Final Source Control Remedial Investigation Report: Ciba-Geigy Site, Volume 4 (December 1994).
7. William P. Eckel, Disposal Safety Incorporated, Tentatively Identified Compounds at Ciba-Geigy Site, Toms River, NJ (May 28, 1997), 4. This report was produced by a consultant hired by the Ocean County Citizens for Clean Water, funded by Ciba to provide independent oversight of the factory cleanup.
8. Radiation is the only conclusively proven environmental risk factor for pediatric leukemia and nervous system cancers. For more about risk factors, see National Cancer Institute Cancer Statistics Branch, Cancer Incidence and Survival Among Children and Adolescents: United States SEER Program, 1975–1995 (1999).
9. The azo dye ingredient benzidine, for example, was not just a bladder carcinogen; it also caused nervous system cancers in mice. Acrylonitrile was one of the few chemicals known to cause brain tumors in rats, and factory studies suggested that it might cause brain cancer in humans, too, although there was conflicting evidence. Other research found that parents exposed to nitrobenzene were more likely to have children with brain cancer and that parental exposure to TCE and benzene raised the risk of childhood leukemia.
10. National Toxicology Program, Draft NTP Technical Report on the Toxicology and Carcinogenesis Study of Styrene-Acrylonitrile Trimer in F344/N Rats (December 2010), 22–24.
11. James Huff, “Long-Term Chemical Carcinogenesis Bioassays Predict Human Cancer Hazards: Issues, Controversies, and Uncertainties,” Annals of the New York Academy of Sciences 895 (December 1989): 56–79.
12. To be placed into the National Toxicology Program’s highest category (“clear evidence” of carcinogenicity in animals), a compound generally needed to cause tumors in multiple organs or in both mice and rats. Only about 25 percent of chemicals tested by the NTP met this higher standard. See Victor A. Fung et al., “Predictive Strategies for Selecting 379 NCI/NTP Chemicals Evaluated for Carcinogenic Potential: Scientific and Public Health Impact,” Fundamental and Applied Toxicology 20 (1993): 413–36.
13. In 1999, the National Toxicology Program was just completing a study of acrylonitrile that would find “clear evidence” that it caused cancer in mice. See National Toxicology Program, NTP Technical Report on the Toxicology and Carcinogenesis Studies of Acrylonitrile in B6C3F1 Mice (Gavage Studies), Report TR-506 (October 2001).
14. D. J. Caldwell, “Review of Mononuclear Cell Leukemia in F-344 Rat Bioassays and Its Significance to Human Cancer Risk: A Case Study Using Alkyl Phthalates,” Regulatory Toxicology and Pharmacology 30:1 (August 1999): 45–53.
15. Only a few chemicals had ever been found to trigger brain tumors in rats, but one was acrylonitrile, one of SAN trimer’s two ingredients, in a test involving Fisher 344 rats. See D. D. Bigner et al., “Primary Brain Tumors in Fischer 344 Rats Chronically Exposed to Acrylonitrile in Their Drinking Water,” Food and Chemical Toxicology 24:2 (1986): 129–37.
16. There was one fewer control family than planned, because one had been chosen errantly.
17. One of the only truly bizarre results from the Toms River interview study, almost certainly attributable to chance, was that children with brain cancer were 70 percent less likely to have been born to mothers who ate cured meat at least once a week during pregnancy, compared to mothers who followed their doctors’ advice and avoided foods that were high in sodium and nitrates. See New Jersey Department of Health and Senior Services, Case-Control Study of Childhood Cancers in Dover Township (Ocean County), New Jersey. Volume III: Technical Report Tables and Figures (January 2003), 14, table 34.
18. Childhood Cancers in Dover Township (Ocean County), New Jersey. Volume III: Technical Report Tables and Figures, 1–6, table 34.
19. In addition to Ciba, the class-action lawsuit, Kramer et al. vs. Ciba-Geigy et al. also named United Water and the two former Ciba employees who pleaded guilty to illegal dumping back in 1992, James McPherson and William Bobsein, as defendants. The lawsuit was resolved in August of 2002 without any admission of liability and with modest but undisclosed payments to the injured adults. For the uninjured, the companies agreed only to pay for ten years’ worth of screening for bladder cancer. Anyone who had drunk Toms River water in 1965 and 1966 was eligible. The settlement was the closest Ciba and United Water would ever come to acknowledging that their predecessors, Toms River Chemical and Toms River Water, had kept the public in the dark in 1965 and 1966 when dye chemicals seeped into the riverside wells on Holly Street and then into the homes of thousands of water customers in Oak Ridge and elsewhere. See Ana Alaya, “Toms River Families Press Fight,” Star-Ledger, December 18, 2002.
20. The property-damage class-action lawsuit, Janes et al. vs. Ciba-Geigy Corp. et al., stagnated in the court system for more than ten years before it was finally resolved in June of 2011. Under the terms of the court-approved settlement, Oak Ridge homeowners who bought their homes before March of 2000 and sold them before 2009 were awarded $4,000 each (up to a total of $900,000). Ciba also agreed to create a permanent, sixteen-acre buffer zone on the southeastern edge of the property (abutting homes along Cardinal Drive) and to spend $25,000 to landscape the buffer. By far the largest cash payment went to the plaintiffs’ attorneys; Ciba agreed to pay them $3 million.
21. For a mid-1990s overview of the progress and potential of molecular epidemiology, see Frederica P. Perera, “Molecular Epidemiology: Insights into Cancer Susceptibility, Risk Assessment, and Prevention,” Journal of the National Cancer Institute 88:8 (April 17, 1996): 496–509; and Frederica P. Perera et al., “Molecular Epidemiology in Environmental Carcinogenesis,” Environmental Health Perspectives 104, Supp. 3 (May 1996): 441–43.
Chapter Twenty-Two
1. B. A. Finette et al., “Gene Mutations with Characteristic Deletions in Cord Blood T Lymphocytes Associated with Passive Maternal Exposure to Tobacco Smoke,” Nature Medicine 4:10 (October 1998): 1144–51.
2. In an email to the author, Jack Mandel wrote that he “has no recollection of this discussion with Clapp. I can’t believe I would have said something like this.” For his part, Richard Clapp says he is certain that Mandel made the remark: “I’ll never forget it.”
3. For detailed accounts of how the water model was constructed, see Morris Maslia et al., Historical Reconstruction of the Water-Distribution System Serving the Dover Township Area, New Jersey: January 1962–December 1996 (Agency for Toxic Substances and Disease Registry, 2001), and also Morris Maslia et al., Analysis of the 1998 Water-Distribution System Serving the Dover Township Area, New Jersey: Field-Data Collection Activities and Water-Distribution System Modeling (Agency for Toxic Substances and Disease Registry, 2000).
4. Because there was so much uncertainty about when pollution from Reich Farm first reached the Parkway wells, the state’s case-control studies also included exposure scenarios that started as early as 1978 or as late as 1986, although the health department considered 1982 to be the best guess of when the first contamination occurred. In any case, moving the exposure window forward or back a few years did not materially change the results of the case-control studies (odds ratios were highest for a 1984 start date). For the Holly well contamination, which was assumed to have ended by 1975, the state also tested an alternate scenario in which the contamination did not end until 1980. Again, there was little change in the study results.
5. To quantify exposure to contamination from private wells, the state identified eleven neighborhoods where private wells had been contaminated by industrial chemicals, including Pleas
ant Plains and Oak Ridge Estates. A mother or child who lived in one of those eleven areas and relied on a private well during the months and years before diagnosis would be classified as highly exposed.
6. State cancer registries were crucial to identifying the forty-eight case children in the birth record study. Investigators looked for name and birth date matches between Toms River birth certificates and registries in New Jersey and nine other states. They then identified cancer-free children for the control group by looking for birth certificates that matched case children, in groups of ten, by age and sex.
7. Since they had no information about the birth record study children other than their birth certificate and diagnosis, investigators had to make two assumptions in order to estimate a mother’s exposure to contaminated air and water during pregnancy: first, that she had not changed addresses while pregnant and, second, that if she lived near a water line, she got her water from the public supply system, not from a backyard well or from bottled water.
8. To avoid potentially biasing his calculations, Morris Maslia did not know which addresses were for children with cancer and which were for healthy controls. He also did not know which months during the study period were relevant for each child.
9. A prenatal water exposure score of 50 percent or higher was classified as high, less than 10 percent was low, and everything in between was medium.
10. Twenty-five case children in the interview study were also in the birth record study, but the overlap was limited because the two studies defined cases differently. The interview study cases included only children diagnosed with leukemia, brain or nervous system cancers (the birth record study included any form of childhood cancer), and only children who lived in Toms River at the time of diagnosis (the birth record study included children who had moved away). In one way, the interview study was more inclusive: It included some children who were not born in Toms River, while the birth record study, based on birth certificates, included only natives.
11. As an example of how these adjustments worked, a boy who lived in a home that got an average of 30 percent of its water from the Parkway wells during his mother’s pregnancy and during his life before a cancer diagnosis would normally be classified as having a “medium” exposure to Parkway water, but if the boy’s mother reported that during her pregnancy she had drunk an unusually high number of glasses of water each day, the boy would be bumped up into the “high” category.
12. The total number of children—702—was fewer than 727 because of overlap between the 528 children in the birth record study and the 199 children in the interview study.
13. Frederica P. Perera and I. Bernard Weinstein, “Molecular Epidemiology and Carcinogen-DNA Adduct Detection: New Approaches to Studies of Human Cancer Causation,” Journal of Chronic Diseases 35 (1982): 581–600.
14. Frederica Perera and her collaborators found that mice and rabbits injected with benzo(a)pyrene had more DNA adducts than control animals did. But dogs exposed to cigarette smoke for twenty months did not. In humans, they found high adduct concentrations in the lung tissue of five lung cancer patients, all heavy smokers. But twenty-two other smokers did not have more adducts, and there was no dose-response pattern: Heavier smokers did not have more adducts. Frederica P. Perera et al., “A Pilot Project in Molecular Cancer Epidemiology: Determination of Benzo(a)pyrene-DNA Adducts in Animal and Human Tissues by Immunoassays,” Carcinogenesis 3:12 (1982): 1405–10.
15. Mutated TP53 genes are in about half of all cancers, including neuroblastomas, melanomas, and many other tumors. Timothy E. Baroni et al., “A Global Suppressor Motif for P53 Cancer Mutants,” Proceedings of the National Academy of Sciences 101:14 (April 6, 2004): 4930–35.
16. Richard Albertini and R. B. Hayes, “Somatic Cell Mutations in Cancer Epidemiology,” IARC Scientific Publications 142 (International Agency for Research on Cancer, 1997), 159–84.
17. Barry Finette’s mentor at the University of Vermont, Richard Albertini, had pioneered the use of the HPRT gene in cancer research in the late 1980s. One of the gene’s many advantages as a biomarker is that it is located on the X chromosome. Since there is normally only one active X chromosome in a human cell, just one mutation event is enough to guarantee a heritable mutation, which makes HPRT a more sensitive biomarker for genetic damage than genes on paired chromosomes. Albertini also identified mutational mechanisms in HPRT that seemed to apply to many other genes, supporting the idea that HPRT really was a good surrogate for genome-wide damage.
18. Barry Finette’s mutant frequency study was published as Pamela M. Vacek et al., “Somatic Mutant Frequency at the HPRT Locus in Children Associated with a Pediatric Cancer Cluster Linked to Exposure to Two Superfund Sites,” Environmental and Molecular Mutagenesis 34 (2005): 339–45.
Chapter Twenty-Three
1. To understand how Jerry Fagliano calculated adjusted odds ratios in the Toms River case-control studies, consider this example: Nine case children and twenty-three healthy controls in the interview study were in the “high” exposed category because their mothers had gotten more than 50 percent of their water during pregnancy from the Parkway well field. Twenty-six cases and 110 controls were in the “low” exposure category because their mothers had gotten less than 10 percent of their water from the Parkway wells during pregnancy. Calculating a “crude” odds ratio is simply a matter of comparing the odds that high-exposed women would have a child with cancer, versus low-exposed women. The simple equation looks like this: (exposed cases/unexposed cases)/(exposed controls/unexposed controls) = odds ratio. Applied to the Parkway data for high-exposure mothers, the math is (9/26)/(23/110), yielding an odds ratio of 1.66. Jerry Fagliano then adjusted that result in a way that helped to account for the influence of possible confounding factors such as the age and sex of each study child. After this final calculation, known as conditional logistical regression, the adjusted odds ratio is slightly higher: 1.68. In other words, the odds of a case child having been highly exposed to Parkway water were 68 percent greater than the odds that a healthy child had been exposed.
2. All of the odds ratios described in this chapter come from data tables in Case-Control Study of Childhood Cancers in Dover Township (Ocean County), New Jersey, Volume III: Technical Report Tables and Figures.
3. New Jersey Department of Health and Senior Services, Case-Control Study of Childhood Cancers in Dover Township (Ocean County), New Jersey, Volume II: Final Technical Report (January 2003), 23. Like many of the others in the study, this odds ratio fell short of statistical significance because the lower bound of its very wide confidence interval—0.79 to 274—was below 1.0.
4. The same small-numbers problem stymied the health department’s attempts to assess the consequences of the groundwater pollution that tainted hundreds of backyard wells in the neighborhoods like Oak Ridge Estates and Pleasant Plains in the 1960s and early 1970s, before water mains were fully extended to those areas. Eleven such neighborhoods had been identified by investigators, but so much time had passed that they could track down just two exposed cases from that era—too few to generate a credible odds ratio.
5. In order to create high-, medium-, and low-exposure categories for the air pollution model, its developers at Rutgers first analyzed air exposures for the residences of the control families. The family at the midpoint was assigned a 1.0 rating on a scale of “relative air impact units.” Under the same scale, the top 25 percent of controls in the interview study were at or above a rating of 2.18. They then applied the same scale to the case families, placing cases and controls into three categories: low (below 1.0), medium (1–2.17), and high (2.18 and above). For the birth record study, the “cut point” separating low from medium was 1.5; for separating medium from high exposure, the cut point was 3.04.
6. The size of the Toms River legal settlement has never been disclosed but, based on court filings, it is very likely that the total was somewhere between $35 and $40 million, before deductions for the lawyers’ 25 percent fee an
d other reimbursable expenses. Records from judicial hearings, held only for the twenty-nine families with children still under age eighteen, show that those families were awarded approximately $11.4 million in gross payments. The payments went to children and siblings and also to parents for reimbursable costs (such as lost wages, uninsured medical bills, and trips to distant hospitals). After deductions for legal fees and expenses, the net payout was about $8.4 million, or an average of about $290,000 per family. Assuming that those twenty-nine families were roughly representative of the forty families not subject to the judicial hearings, then the total gross payout was approximately $27.1 million. In addition, there was a “recurrence fund” of $5 million ($3.75 million after legal fees) to compensate any surviving children who relapsed before 2016, at which time the proceeds would be distributed to all the surviving children. There were also additional payments to parents beyond expense reimbursement. Thus, the gross amount of the settlement in 2001 (not including subsequent interest on funds held in trust for minors) was probably somewhere between $35 million and $40 million. The court records also show that some families with children under eighteen received as much as $501,570, after deductions for fees and expenses, while others got as little as $91,954. The lawyers donated $150,000 from their fees to TEACH, the environmental advocacy group formed by the families.