The Riverside Division of the Academic Senate

University of California

is pleased to present the sixty-fifth annual

FACULTY RESEARCH LECTURE

Distinguished Professor Carl F. Cranor

Department of Philosophy, and

Faculty Member, Environmental Toxicology

“The Law’s Contribution to a Lifetime Arc of Good Health” The Greeks and Romans often viewed good health partly as an individual goal and partly as a cultural ideal, but community wide lifetimes of good health have remained elusive. That goal edged closer with the elimination of heavily polluted environments, the introduction of vaccines, better preventive medicine, and other medical advances that reduced infectious diseases in developed countries. Chronic diseases, including cancers, lung disorders, neurological dysfunctions, heart disease, diabetes, and immune system disorders, inter alia, now are major sources of mortality and morbidity that undermine and even truncate lifetime opportunities that good health provides. Maladies can result from bad luck, personal choices, unfortunate genes, and the actions of others. Toxic substances can cause chronic diseases and dysfunctions at different life stages. Some legal institutions could prevent many of these diseases, while others could provide resources to redress harm from them. Well-founded theories of distributive justice support the need for laws to prevent and reduce exposures to disease-causing substances or, less effectively, to redress harms from toxicants. Exposures of children to toxicants during development—in utero, in early childhood, and in the teenage years—are of special concern because of their vulnerability, under-developed defenses, and long futures. However, the initial conception and subsequent implementation of administrative environmental health laws have not protected well our and our children’s health from toxic substances. A major, but flawed, law has now been improved, but rectifying its legacies will take considerable time, resources, and strong commitment from legal administrators. Redress in the tort law has been limited for diseases and dysfunctions caused by toxicants because of how the law and science have been administered. While shortcomings of the relevant laws are apparent, recent modifications provide some hope going forward.

Friday, June 2, 2017

3:30 PM

Genomics Auditorium, Room 1102A

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Distinguished Professor Carl F. Cranor Carl F. Cranor is a Distinguished Professor of Philosophy and Faculty Member of the Environmental Toxicology Graduate Program at the University of California, Riverside. He has written widely on philosophic issues at the interface of philosophy, law, and science, leading to the publication of numerous books (6) and articles (80). Three recent books— Legally Poisoned: How the Law Puts Us at Risk from Toxicants (Harvard, 2011), Toxic Torts: Science, Law and the Possibility of Justice, 2d Ed. (Cambridge, 2016), and Tragic Failures: How and Why We are Harmed by Toxic Chemicals (Oxford, 2017)—develop concerns about legal failures to protect the public, including children, and about shortcomings in the use of science in legal venues. In 2014 he was named the national Romanell-Phi Beta Kappa Professor of Philosophy for distinguished achievement and substantial contributions to public understanding of philosophy. Tragic Failures is the publication of the Romanell lectures. Devoted to and enjoying teaching Professor Cranor held the Patricia McSweeny McCauley Chair in Teaching in Excellence, received the Academic Senate’s Distinguished Teaching Award, and is a member of the Academy of Distinguished Teachers. Having served as the chair for five different departments and for a decade as the HA&SS Associate Dean and Acting Dean, he received the Academic Senate’s Distinguished Campus Service Award for a “long history of extraordinary service … to his department, college, and the UCR campus at large.” He has been the HA&SS Distinguished Research Lecturer and an Honors Professor of the Year. Professor Cranor has been an American Council of Learned Societies Fellow, a Yale Master of Studies in Law Fellow, a Congressional Fellow, and is an elected Fellow of the American Association for the Advancement of Science and the Collegium Ramazzini, an international scientific society “dedicated to advancing the study of occupational and environmental health issues around the world.” Twice he was invited as a Gordon Research Conference speaker. NSF and UC’s Toxic Substances Research and Teaching Program supported his research. For four years he served on the team for the National Oceanic and Atmospheric Administration and the Department of Justice to redress damage that British Petroleum’s Deepwater Horizon explosion caused to the Gulf of Mexico; British Petroleum agreed to a $20.8 billion settlement. The state of California invited his service on science advisory panels for Proposition 65, the Electric and Magnetic Fields Program, the Nanotechnology Program, and the Scientific Guidance Panel of the California Environmental Contaminant Biomonitoring Program. He received his BA in mathematics (minor physics) from the University of Colorado, his doctorate from the University of California, Los Angeles, and a Masters of Studies in Law from Yale Law School.

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The Law’s Contribution to a Lifetime Arc of Good Health1

I. Some Historical Context

A Sketch of Early Views of the Importance of Good Health The Greeks among ancient civilizations suggested the importance of good human

health. Because they ‘put mankind at the center of the universe, … idealized the human body, [and] their art was motivated by a lust for life in the face of the tragic certainty of death…’” some writers recognized the importance of good health.2 “[B]asic concepts of health promotion … have [their] roots in ancient civilizations and in particular in Greek antiquity. Plato in the Timaeus taught that morality was not simply a matter of education; because the mind was influenced by the body, the doctor had a part to play in teaching virtue.”3 Thus, he urged, “[The soul and the body] … [should] be healthy and well balanced.” [Intellectuals should] practice gymnastics and [athletes] should practice music and all philosophy…” 4

Later the Roman poet Juvenal urged that one should “[P]ray for a healthy mind in a healthy body.”5 Plutarch, his approximate contemporary, urged physical training as part of education, “[because it] was seen as necessary for improving one's appearance, preparation for war, and good health at an old age.” 6

However, as western culture shifted from placing humans at the center of concerns to following monotheistic gods, particularly Christianity, an interest in having a healthy body tended to recede as a social concern. Some early Christian writers seemed to have an “attitude of indifference or even outright hostility toward the body” with a much greater emphasis on getting the soul into heaven or saving it from hell.7 Even in the 21st century there appears to be tension between two views: Some seem to regard the body separate from it’s sprit and “thus a cause of sin that must be controlled,” while others believe the two are connected and jointly sacred.8 Stephen Greenblatt in The Swerve: How the World Became Modern emphasizes that early Christians tended to reject Greek and Roman views of life and attitudes toward pain, targeting Epicureanism in particular. He suggests that an important strand of the religion encouraged flagellation and other physical abuses to mimic the suffering of Jesus on the cross.9 Such views are hardly those that embrace good human health.

Consequently, the Greek ideals of good health were deemphasized or even overturned for centuries for cultural reasons. At the same time humans, of course, were afflicted, even ravaged, by infectious diseases, plagues, and pandemics.

Gaining Control of Infectious Diseases At the turn of the 20th century in the U.S. public health officials began to take steps

that over time greatly reduced infectious diseases as a source of morbidity and mortality. They commenced removing horse manure from streets, greatly assisted by the

development of automobiles, and cleaning up sewage dumped into rivers, a source of drinking water and children’s recreational swimming These constituted substantial sources of diseases. Public health officers and physicians also chlorinated drinking water, developed antibiotics, and discovered and used vaccines to prevent diseases. This is represented in the following Figure.

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A major consequence of these actions is that chronic diseases are now the leading

causes of morbidity and mortality in developed countries.10 Examples include cancers, neurological disorders, immune dysfunctions, lung disorders, diabetes, and cardiovascular diseases.

Chronic diseases persist for a long time and are not “prevented by vaccines or cured by medication.” They are also “not communicable … and do not just disappear.11

Bad luck, unfortunate genes, voluntary behavior, and the actions of others can produce chronic diseases. My research has addressed how we should use science and the law to reduce chronic diseases caused by the actions or products of others.

A filthy New York City street in 1893; 2.5 million pounds of horse manure/day

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A major problem with chronic diseases is that they can also cause greater or lesser interference with a person’s life-long normal good health and flourishing. My particular research has focused on toxic substances that contribute to chronic diseases, such as those noted just above.

II. How does a philosopher become interested in such a topic? Typically moral philosophers study and write about actions, policies, or states of affairs that are, inter alia, right, wrong, just or unjust, and justifications for their rightness or wrongness, as well as more abstract related issues. Moral philosophy constituted my foundation, but for most of my career I have been interested in legal philosophy, which led to the study of laws and legal institutions, what they are, how they function in society, and specifically how they might be used to better protect the public.

While all of us are familiar with various means of inflicting harm with bullets, knives, or blunt objects, considerable harm to people exposed to chemical creations can occur and disrupt our biology, causing diseases and dysfunctions. However, diagnosing harm caused by molecular substances and reducing their effects is typically more difficult than identifying and reducing the effects of grosser forms of violence. For instance, a female fetus exposed to diethylstilbestrol, a potent synthetic estrogen, in utero has a substantial risk of developing cancer of the cervix and vagina as a young woman when she reaches about the age of 20. Twenty years after that she is at greater risk of breast cancer than women who did not have early life exposures to substantial doses of estrogen or other carcinogens.12 Invisible molecules often associated with substantial latency periods complicate tracing a disease from exposure to outcome. III. The Moral Case for Preventing Chronic Diseases Caused by Other Citizens

Because chronic diseases can arbitrarily interfere to a greater or lesser extent with lifelong normal good health and flourishing, what makes such interferences wrong? Of course, the mere fact of harm and suffering befalling a person presumptively is a wrong (although not all harms are wrongs). However, a powerful principle of justice—fair equality of opportunity—identifies more specific features of justice that make arbitrary interference with one’s good health an injustice. Let me explain.

While we might think that people have equal opportunities in a community, provided there are not legal barriers to their reaching, for example, educational or professional goals, this simplified idea fails to capture a deeper idea of fair opportunity. For instance, there may be no legal barriers for a talented poor person from a poor community achieving a Harvard or Yale education, but we understand that such a person likely must overcome barriers created by substandard educational systems in a poor communities or more subtle social pressures, such as family or church attitudes, that would poorly prepare her for the best educational institutions.

Fair equality of opportunity identifies two major institutions—educational along with health protection and health care institutions—that help counteract less visible barriers that subtly and unjustly reduce one’s chances of a good life. If we had good and equal primary and secondary education institutions in both the poorest communities and Beverly Hills it would be plausible that a person from the poor community would have a much fairer chance at receiving a Harvard education, as long as that person had abilities, talents, and motivations equal to those of a Beverly Hills student. Good and equal educational

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opportunities for similarly talented and motived persons correct for disadvantages that occur because of poverty, ethnic background, family education, or place of birth.13

Similarly diseases and biological dysfunctions over which humans largely lack control can disadvantage people. These can frustrate life-long opportunities to pursue careers or to change them,14 or, much more broadly, to develop life-plans, modify them, and pursue them beyond working years.15 Diseases can result from poverty or living in poor communities, inadequate prenatal or early life health care, lacking access to health care institutions, or the actions or products of others that cause disease.16 Serious chronic diseases that arise from such circumstances can easily undermine a lifetime of fair opportunities.

The justice point is not that some people in the community intentionally deprive others of health care, although that could certainly be the case. Instead, the issue is whether institutions in the community function sufficiently well for everyone to prevent diseases and to treat those who contract them.

Consider Brian Milward’s fate. Mr. Milward worked as a refrigerator repairman and in his work used a number of fluids that contained the well-known carcinogen benzene as a solvent. As a result of the benzene exposure from twenty-two different products at age 47 he contracted a quite rare form of leukemia, acute promyelocytic leukemia that occurs in only about one person per million in the U.S. population annually. However, because of his disease, chemotherapy, and associated diseases, he was left at age 57 “with ‘absolutely ridiculous’ fatigue.”17

Of course, he was harmed, but this idea fails to fully account for a more substantial injustice. His career was ended and lifetime opportunities were greatly diminished: he suffered substantially from his disease, its treatment, and associated diseases. Together they forced him to retire early and take disability. Moreover, in retirement he can’t do what he loves: repair racecars, work in his yard, play with his grandchildren. “It just sucks when you get a cancer like this.”18 The lifetime of opportunities he would have had if he not been harmed by benzene are gone.

Importantly, this disease and its treatment have not only truncated his life-long

opportunities, but other citizens in the community created the products containing benzene that led to his loss of opportunities. One might say he was treated doubly unjustly: his

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opportunities were unfairly reduced by disease and it had been triggered by a toxic substance in products created by other members of the community. Institutions permitted his harmful and opportunity-undermining disease: companies created the products likely with inadequate safeguards for their use, and preventive legal institutions likely did not sufficiently assess the risk from multiple benzene exposures.

In contrast we have sterling examples of people who have avoided serious chronic diseases, were able to modify their life plans, pursue their dreams beyond their working years, and continued to flourish even when others chose rocking chairs. These include the oldest people to climb Africa’s highest mountain, Kilimanjaro, or to climb Mt. Everest at the age of 73 (the oldest woman) or 80 (the oldest man). A 105-year-od cyclist is not only improving his cycling speed, but also increasing his capacity to utilize oxygen during a period of life when such capacities typically wane. Diana Nyad, the long-distance swimmer, swam the 90 miles from Cuba to Florida at age 64 and Kareem Abdul-Jabbar continued play professional basketball until he was 42, a ripe old age for an athlete in a highly demanding sport.

Of course, people do not have to be athletic to live long and healthy lives (but it helps19). Where they live, what they eat, even their personalities and habits can contribute to long, healthy lives. The important point is that good health fosters a full and robust human life.

In order to avoid the arbitrary interference with our life-long opportunities the principle of fair equality of opportunity endorses health protection and health care institutions to i) prevent diseases with medical interventions and environmental health protections, ii) treat diseases that undermine persons’ health by ensuring access to good medical care, and iii) maintain the chronically ill as close to normal functioning as their ages and conditions allow by providing medical treatment and accommodations, for example, for people with severed spines from car accidents.20 I build on the first two points.

IV. The Law’s Contribution to Just Health-Protection and Health-Care

The law can make a contribution to helping to secure just health protections and just health care to assist the life-long opportunities for a healthy and flourishing life. Administrative health laws can prevent (or at least substantially reduce) toxicity-caused chronic diseases. Personal injury (or the tort) law can support treatment and redress for diseases caused by others. These are not the only means by which laws can promote or assist health protections and health care, but they have been the objects of my research for more than thirty years.

This research has focused on how well these institutions and their use of science have functioned to prevent chronic diseases and assist in their treatment when others in the community have caused adverse effects.

Preventive Administrative Health Institutions Broadly speaking there have been two different legal strategies trying to prevent

diseases caused by exposures to molecules that may be toxic. 1) Under the laws for pharmaceuticals and pesticides Congress chose to place high priority on using science to test substances and understand any potential risks before people are exposed. These institutions require prudent testing for possible risks before the public is exposed to the products in question. These are premarket testing and approval laws.

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2) About the same time Congress chose postmarket laws to govern general chemical creations entering commerce. Accordingly there are no routinely required toxicity tests, no preparations, and no reasonable assurances of safety before products enter the market and the public and workforce are exposed. There are no careful assessments of safe exposures. There are no special safeguards for children, and the health and welfare of citizens are not of central concern in the same way they are under premarket toxicity testing laws. In short, there are no commitments to use science to identify adverse effects until well after exposures, risks and harms have occurred.21 Any prevention of diseases was thought to result from quick identification and reduction of risks before they materialized into harm. That thought turned out to be mistaken.

The premarket laws for pharmaceuticals and pesticides govern only about 10-20% of the chemical creations by manufacturers, while a single law, the 1976 Toxic Substances Control Act (that I dub “old” TSCA) governs about 90% to 80% of general chemical creations excluding comparatively small numbers of prescription drugs, pesticides, tobacco products, nuclear material, foods, new food additives, chemical mixtures, and cosmetic ingredients.22

For existing chemicals TSCA grandfathered as “safe” an inventory of about 62,000 “general” substances manufactured or imported into the United States. Any substances not on that inventory would be considered “new.” These would have to be submitted to the EPA under a premarket “notification” provision, but were not required to undergo any routine toxicity testing and would only undergo a cursory agency review (with little or no toxicity data). If the EPA could discern evidence of a toxic effect from minimal data submitted with the proposed chemical creation, it could require toxicity tests, but there was no requirement to conduct any testing on products before they were subject to approval.23

My first foray into understanding how well the law and science prevent exposures to toxic products came as a U.S. Congress Congressional Fellow in 1985-86. Because I was on a fellowship, I provided free help to the Congress’s Office of Technology Assessment (OTA) and this helped to make possible the OTA report, Identifying and Regulating Carcinogens (which I coauthored).24

The House Committee on Government Operations and its Subcommittee on Intergovernmental Relations and Human Resources requested that OTA examine federal activity in testing chemical creations for carcinogenicity and in reviewing the use of those results by administrative agencies under various federal laws passed in the late 1960s to late1970s.25

We found that federal agencies had “acted on” less than one-half of the substances within their purview.26 We also found that reducing exposures to carcinogens was slow, science-intensive, and post-harm, only occurring after there was evidence of risks or harm to the public.

These findings revealed several problems of justice with the regulation of carcinogens subject to postmarket laws. Slow assessments leave carcinogens in commerce, and with sufficient exposures they can cause cancers to the public, contrary to the aim of the laws in question.

Moreover, after reflecting on the OTA report and interviewing agency personnel I came to understand that rigid scientific norms could frustrate legal norms and health protections. This is most easily understood with regard to low powered human statistical epidemiological studies. These are studies that have too few participants in exposed and

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control groups accurately detect disease causation in an exposed population. In short, samples too small for the suspected diseases can result in studies that are too insensitive to detect a risk even if it is present.27

The justice issue is that with sufficient exposures sluggish regulation leads to more cancers in the general public. This occurred to hairdresser Sandy Guest, who used Brazilian Blowout that was “loaded with formaldehyde.”28 As a consequence she died of leukemia at age 55. This is particularly poignant because over a thirty-year period beginning in 1981 seventeen different studies ultimately revealed that formaldehyde exposure could cause nasopharyngeal, sinonasal, and myeloid cancers, along with other disorders. As of this date there are still no general protections from formaldehyde. Industry resistance and slow agency review likely led to her death. Two institutions—the company that made Brazilian Blowout and administrative institutions—failed her, leading to her death and eliminating her opportunities.

Analogous problems arose from public exposures to DuPont’s perfluorooctanoic acid (PFOA), also known as C8, the main ingredient in Teflon, Gore-Tex, and stain-resistant fabrics, inter alia. Individuals representing a broader group of plaintiffs won tort lawsuits for kidney cancer and two cases of testicular cancer, diseases known to be caused by C8.29 And, Wilbur Tennant’s cattle drank stream water contaminated by C8, became blind, developed tumors, and vomited blood, with most of them dying.30 This information resulted from jury verdicts or tort law settlements facilitated by a scientific panel formed as a result of litigation that identified these adverse effects.31 Ultimately, because of the outcomes in early cases DuPont settled for $670.7 million to cover damages affecting 3,550 plaintiffs and their communities.32

The justice issue is that DuPont, which created products it discovered were toxic, and preventive administrative law, which was too sluggish to protect the public, failed these people and thousands more that lived in nearby communities. The tort law redressed some of their harms. However, it is likely that numerous individuals have contracted cancers or other diseases that result from C8 exposures that have substantially reduced their opportunities.

When I wrote Regulating Toxic Substances (1993) after my stint as a Congressional Fellow, it seemed that both policy considerations and expediting some important steps in risk assessment could improve public health protections under postmarket laws. Policy considerations could substitute for long and irresolvable scientific disagreements about carcinogens, for example, how they behave in the lowest dose regions where theories could not be tested.33 Moreover, because such data would be effectively unattainable for many years, health protections should not wait for their resolution. Scientists from California Environmental Protection Agency, UC Berkeley, and I found that expediting carcinogen potency assessments, based on animal data, which previously had taken one-half to five-person years per substance, need only take one day. This would speed a critical risk assessment step and modestly speed up public health protections from carcinogens. These were both quick and accurate.34

The sluggishness of protecting the public from carcinogens led to considerations of the “precautionary principle” to improve health protections when there was sufficient data to justify taking action. Consequently, I explored various formulations of this idea and also suggested legal devices that could better and more quickly protect the public. 35

An Early Foray into the Tort Law

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Regulating Toxic Substances also addressed how science was being used in the tort law during the late 1980s and early 1990s. Some of the same ideas about science that plagued administrative law also hampered redress of diseases caused by others’ chemical creations.

In the tort law in order to receive redress for harms caused by others a plaintiff must show that a) the defendant violated the law, b) plaintiff suffered a legally recognized compensable injury, c) defendants product can cause the kind of harm plaintiff suffered, and d) the defendant’s product did cause plaintiff’s harm. Thus, scientific findings are needed to address c) and d) in a legal case. How well were judges utilizing science in the tort law?

Commentators and a few courts demanded “ideal” science—multiple lines of the “best” evidence. This temptation likely arose because of judicial unfamiliarity with science and because judges might wish to be quite certain that the science was appropriate for the case. However, the lure of ideal science would bar redress for virtually all injured parties simply because, while a plaintiff might have good evidence that he or she had been harmed by toxic exposures, he/she might not have all the lines of the best and fullest evidence.36 If judges demanded this, as a few did, this would preclude redress for nearly all plaintiffs. From previous writings on carcinogen risk assessments I could see that judges and some litigators poorly understood the science involved and that could be helpful.

In addition, many courts required human statistical data, even if they did not require ideal data. As Judge Weinstein of the Southern District of New York put it in the Agent Orange litigation, epidemiological studies are “the only [ones] having [a] bearing on causation.”37 This is mistaken, as I argue directly, and its consequence would have barred some or many plaintiffs from receiving redress for harms suffered.

Common scientific issues plagued both the administrative and tort law. Stringent scientific norms dominated legal values. This resulted in public health under-protection of citizens and the likely exclusion of meritorious plaintiffs in the tort law. Were legal administrators and judges gripped by a too-rigid scientific paradigm? That is how it seemed to me at the time, although later, as I present below, such arguments in either the administrative or the tort law became a deliberate strategy because it favored companies whose products were threatened in both venues. Regulating Toxic Substances sought to counter this tendency by recognizing the use of a wide range of data and the norms of the law. An official at the Federal Judicial Center recognized the significance of this theme: Regulating Toxic Substances “recognizes and integrates the values of two complex and disparate institutions.”38

V. A Tort Law Sea Change: The Daubert Trilogy 1993-1999

Regulating Toxic Substances was published the same year a U.S. Supreme Court decision made major changes in how science should be used and presented in the tort law. Consequently, my research turned to the ensuing debates. This was ultimately developed in Toxic Torts: Science, Law and the Possibility of Justice, and in numerous articles.39

The Court transformed the use of science in tort law litigation with three legal cases: Daubert v. Merrell-Dow Pharmaceutical, Inc. (1993), General Electric v. Joiner (1997), and Kumho Tire v. Carmichael (1999). The overall results of these cases pulled the law in different directions. On the one hand, they improved the scientific basis of legal decisions, but on the other hand, led to mistakes, hampered access to the law, and reduced

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success of injured parties in court. Consider each case in turn. Incompatibilities between law and science were not a surprise because of inherent tensions between the two institutions.40

Daubert v. Merrell-Dow Pharmaceuticals, Inc. The first case, like the Roman god Janus, seemed to have two faces. One visage

recognized that Congressional amendments of the Federal Rules of Evidence (FRE) “relaxed the traditional barriers to 'opinion' testimony.” 41 This made it easier for litigants to have their experts admitted to present testimony to juries, but the Court noted that the legal tools of “Vigorous cross-examination …presentation of contrary evidence, and judicial instruction on the burden of proof” could prevent juries from being overwhelmed and overly impressed with expert testimony.42

However, the Daubert opinion presented a second mien. Justice Blackman, discussing how judges should review expert testimony and its scientific foundation, appeared to conflate scientific studies with testimony about them. This tended to mislead lower courts, perhaps suggesting that they could exclude “reliable” and “relevant” testimony that did not satisfy standards for scientific studies. I personally have seen this in a few legal cases in which I served as an expert: defendants would ask whether the toxicologist in the case had had his testimony “peer-reviewed,” “published,” or whether or not it had an “error rate” and what was it? These considerations mentioned by the Court are quite appropriate for scientific studies, but quite out of place for testimony about the studies.

Apart from the Supreme Court’s possible misguidance in its opinion, many lower courts tended to demand human statistical (epidemiological) evidence to support expert testimony. In the Daubert litigation itself there had been myriad human studies addressing whether or not exposure to Bendectin could cause birth defects (somewhat resembling those caused by in utero exposure to the sedative Thalidomide). It is plausible that lower courts assumed that every allegation that exposure to a toxicant caused human harm could be or only could be identified by human statistical studies. This is a mistake, as I indicate below, but courts tended to demand such data. Insistence on such studies, what we might consider “excellent scientific evidence,” can make “bad law” because this can easily erect substantial barriers in the law where other sufficient science could support testimony about toxic substances.43

General Electric v. Joiner (1997) The legal and scientific issue in this case was whether exposure to PCBs could and

did contribute to Mr. Joiner’s lung cancer. As an electrician he worked with electrical capacitors containing liquid PCBs and sometimes burned PCBs when capacitors had been damaged by lightning strikes or electrical shocks.

The trial judge, following defendants’ arguments, individually examined four of thirteen epidemiological studies and two excellent animal studies on which Joiner’s experts’ testimony was based. She found each study to be individually insufficient to support the plaintiffs’ ultimate scientific conclusion. The Eleventh Circuit Court of Appeals, noting this and other errors, overturned her review of testimony and its scientific foundation. However, General Electric and other defendants appealed this to the Supreme Court. In 1997 the Court upheld the trial judge’s dismissal of the case and more importantly upheld the trial judge’s “atomistic,” or study-by-study, evaluation of each “piece” of evidence for whether it supported plaintiff’s ultimate causal conclusion. The

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Court did not analyze whether the total body of evidence Mr. Joiner’s team submitted could support the claim that PCB exposures could and did contribute to Mr. Joiner’s lung cancer.

The Federal Judicial Center (FJC), which provides a guide to courts in their review of scientific evidence and expert testimony, recognizing an argument developed in my research, correctly noted that this ‘atomistic approach’ … “[is contrary to] scientific inferences that require consideration of numerous [lines] of evidence” to support conclusions. 44 An official of the FJC noted, “As judges and the public develop a more thoughtful understanding of scientific evidence in legal institutions, Professor Cranor’s scholarship will be there to guide them. For this, I and others will be grateful.”45

Some Worrisome Consequences of Daubert and Joiner Following these two cases, lower courts struggled with scientific evidence. First, a

few courts required ideal evidence.46 However, when courts impose such scientific standard, they can become the enemy of sufficiently good evidence for legal purposes even though it may fall short of some ideal for other purposes.47

Second, early on many courts required and some commentators argued that human epidemiological studies are needed to show harm to humans.48 While this is relevant and can be quite good evidence from properly conducted studies, demanding such studies poses problems (more below). Later courts, perhaps beginning to understand the errors of their ways, did not require such studies for every tort case concerning toxic exposures.49 However, despite a generic recognition of this point, they didn’t always practice what they preached as revealed in a 2010 case for which I served as an expert witness. 50

Third, and related to the second point, some courts precluded other scientifically relevant studies that could help reveal human harm51—e.g., animal or mechanistic data—which would bar some plaintiffs, who, because of the absence of human statistical studies or rareness of disease, might not be able to find human data.

Fourth, even when courts recognized an appropriate methodology for inferring causation, they frequently either misinterpreted or distorted it to come to a legal view about causation. For example, too often courts and defendants misused Austin Bradford Hill’s viewpoints designed to guide causal inference, usually erecting unnecessary barriers to the presentation of evidence in a trial.52

The judicial decisions described above were, I submit, naïve choices that can produce mistaken legal outcomes and prevent just redress for wrongfully injured parties. In fact if one has familiarity with, or reads how distinguished national and international scientific committees assess evidence to determine whether chemical creations can harm people, many diverse lines of evidence can contribute to revealing toxicity: Human epidemiological studies, animal data, mechanistic data, various test tube studies, and human case reports, inter alia. Better court approaches toward the science would improve the possibility of just redress.

In fact when scientists seek to determine whether or not a substance is a hazard to human health, they consider all the scientifically relevant evidence. This is quite sharply illustrated in one of my favorite examples, the International Agency for Research on Cancer’s scientific review of the chemical MOCA (4,4'-Methylene-bis(2-chloroaniline)). MOCA is a curing agent in the plastics industry for epoxy resins. It is a known human carcinogen, but no human statistical studies support this finding. There is excellent animal data that MOCA causes cancerous tumors in animals. IARC found three humans (two under the age of 30) with asymptomatic bladder tumors after only a two-year exposure to

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MOCA. Where it had the data it found identical MOCA-DNA adducts in animals and in one man. This meant that MOCA was attaching to DNA, disrupting it, and potentially leading to cancers. Finally, it found that MOCA is “comprehensively genotoxic,” damaging the genome. 53This total body of evidence strongly supports the conclusion that MOCA is a known human carcinogen. However, MOCA is not an isolated example, as numerous IARC known or probable human carcinogens are identified without good human statistical evidence.54

The concern in Toxic Torts and related articles was that judges had mistakenly reviewed evidence and constrained what scientific studies and testimony could be presented in court. They were inadvertently (not deliberately, I hope) predisposing legal outcomes they were administering by mistakenly reviewing the science.

The Daubert and Joiner cases together had substantial consequences on litigation, but not merely because of scientific errors. Two legal scholars reviewed 4 million cases, finding that defendants sought out Daubert jurisdictions, while plaintiffs tried to avoid them.55 Because of more extensive scientific documentation of expert testimony required of experts prior to trial, injured parties could easily be precluded from a jury trial by judges. Following these decisions, “This forced many plaintiffs’ lawyers to buttress “their arguments with platoons of experts, and improv[e] their chances of winning by choosing only truly egregious cases involving the most seriously injured parties.”56 Craig Hilborn, a New York attorney noted, "If they're not a quadriplegic, a paraplegic or losing some part of their body, there's no way I'm going to take that case.”57 Somewhat similarly, an expert I know tended to reject 80 to 90% of the cases he was invited to participate in. In both instances—Hilborn and my friend—the extensive requirements for researching the science drove up legal costs for attorneys and greatly burdened experts in finding appropriate evidence for a case.

Kumho Tire v. Carmichael (1999) Kumho Tire v. Carmichael is the third decision in the Daubert Trilogy. This case

addressed a procedural issue tangential to my interests here. However, in rendering its opinion, the Court indicated that the Daubert line of cases sought to ensure that experts must exhibit “the same level of intellectual rigor” in court as in their professional fields.58 Based on this assertion one could easily imagine district court judges or defense attorneys asserting that the scientific evidence underlying an opposition expert’s testimony did not have sufficient “intellectual rigor.” Indeed, occasionally lawyers use this language.59 Like requirements for ideal evidence this could easily block experts from testifying to juries. However, to the Supreme Court’s credit, one page later it explained what this should mean in practice: expert testimony should fall within “the range where experts might reasonably differ [in a field] and where the jury must decide among the conflicting views of different experts, even though the evidence is ‘shaky.’”60

With this guidance the Court recognized that there could be respectable disagreement within scientific fields, that courts should permit testimony that is within this range, and that the testimony need not be based on the most certain evidence. In asserting the latter point the Court seemed to recognize that sometimes evidence on which an expert relies may not be highly certain. However, testimony based on this should be permitted but is also open to the traditional legal challenges of cross-examination, presentation of contrary evidence, and judicial rulings on the burden of proof.

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A significant consequence of this case is that the requirements for expert testimony winnow the testimony going to a jury to be within acceptable ranges where experts within the field could have reasonable disagreement. Thus, one might say the ultimate jury decision would fall broadly within acceptable scientific limits, giving it scientific legitimacy.

An Important Legal Development Following Kumho Tire: Milward v. Acuity Specialty Products

In a legal case explicitly developed from the legal findings of Kumho Tire, along with the Federal Rules of Civil Procedure, Milward v. Acuity Specialty Products (2011), the First Circuit Court of Appeals recognized the importance of a wider range of science and scientific arguments than other appellate courts had to date. However, the litigation did not start well at the trial court.

This case adjudicated the legal causes of Brian Milward’s acute promyelocytic leukemia (APL). He alleged his APL was caused by exposure to benzene (discussed above) in the products of twenty-two different companies. However, the district judge dismissed the case because of plaintiffs’ expert’s “unreliable” testimony. The judge objected to i) a widely accepted and nearly unanimous view about the mechanisms of leukemia, ii) UC Berkeley toxicologist Martyn Smith’s scientific presentation, iii) Smith’s weight-of-the-evidence or inference to the best explanation argument that benzene could cause APL, and iv) the absence of “statistically significant” human studies. The “trial” for Mr. Milward was dismissed after pretrial hearings. Plaintiffs appealed this decision to the First Circuit Court of Appeals where it had a different fate.

The Appellate Court ruled that the trial judge had “abused his discretion” according to the Federal Rules of Evidence. In a trial there is a division of responsibility between judges and juries, and trial Judge O’Toole had crossed that line. In reviewing expert testimony and its foundation a judge’s task is to assess the “reliability of scientific testimony,” but it is a jury’s task to assess its factual correctness.61 Judge O’Toole had usurped the jury’s task by adjudicating the correctness of the scientific testimony.

The First Circuit ruled on several other issues. 1) Human statistical evidence is not needed in every legal case; various lines of evidence can point to adverse effects. 2) The court rejected the trial court’s “atomistic analysis of evidence” that resulted from the trial judge ignoring Smith’s weight-of-the-evidence argument. It especially emphasized, “No serious argument can be made that weight-of-the-evidence arguments [or inferences to the best explanation] are inherently unreliable.” Instead, admissibility rests on how experts apply it.62

Moreover, the First Circuit noted, “As explained by Dr. Cranor, Distinguished Professor of Philosophy at the University of California, Riverside, inference to the best explanation [also known as weight-of-the-evidence arguments] can be thought of as involving six general steps, some of which may be implicit. The scientist must (1) identify an association between an exposure and a disease, (2) consider a range of plausible explanations for the association, (3) rank the rival explanations according to their plausibility, (4) seek additional evidence to separate the more plausible from the less plausible explanations, (5) consider all of the relevant available evidence, and (6) integrate the evidence using professional judgment to come to a conclusion about the best explanation.”63

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This case explicitly clarifies a judge’s responsibility in reviewing expert testimony and its foundation (compared with a jury’s) and permits a wider range of scientific evidence in support of testimony. It also evaluated scientific evidence more sensitively, which will foster better science in the law and increase the chances for just redress.

Defendants appealed the First Circuit decision to the Supreme Court; it was not accepted. Following this 21 of 22 companies settled with Mr. Milward or could show their products did not expose him to benzene. A new trial judge replaced Judge O’Toole at the First District of Massachusetts and found that one defendant did not contribute to Mr. Milward’s APL.

The Second Edition of Toxic Torts explains several consequences resulting from this case. It permits wider evidence and arguments (than many previous courts had recognized). This may increase redress of harms, improve deterrence of toxic products, increase authoritative determinations about toxicants in commerce, reduce some toxic ignorance, and foster a somewhat safer world. Michael A. Green, one of the foremost tort law scholars in the country, has said the Milward decision is ““One of the most significant toxic tort cases in recent memory.”64

Importantly, Brian Milward is alive! He has not succumbed to APL. However, chemotherapy, diabetes and a rare bowel disorder have produced “‘absolutely ridiculous’ fatigue.” Trying to work after contracting the disease, “he [napped] to endure an eight- hour shift. [And, given] … office duty, … he fell asleep at his desk.” He took disability and retired. However, he cannot do what he loves: He can’t repair racecars, work in his yard, or play with his grandchildren. “It just sucks when you get a cancer like this.”65

Returning to the justice themes of this lecture, companies and preventive administrative law failed Mr. Milward. The tort law redressed his harm as best it could. Yet this case shows the limits of tort law redress; he received compensation, which surely assisted his medical costs, loss of his job-based income, and likely funds for the suffering his benzene-caused disease imposed, but his good health was not restored. His life opportunities have been unjustly and substantially curtailed because of his disease caused by the products of others.

V. Return to Preventive Administrative Law (2007)

Up to this time in my research, changes in the law had led me to recommend how science might be better used to protect the public in the two legal venues. However, in 2007 the First International Conference on the Developmental Origins of Disease highlighted new scientific developments that forced a more radical and sensible reassessment of legal approaches to protect the public. The “developmental origins of disease” revealed even worse shortcomings of postmarket laws than many others and I had understood previously. Postmarket laws were already known to be inadequate to protect citizens from toxicants because any new protections occurred long after most citizens had been exposed and some likely had been harmed. However, the new science, focusing on how vulnerable children are to toxicants, raised the stakes. Children with long lives ahead of them are among the most vulnerable humans exposed to toxicants. Our largely postmarket laws are hopelessly inadequate to protect them.66

The Developmental Origins of Disease What is this new science of thedevelopmental basis of disease? The idea is that a

number of chronic diseases can originate from environmental toxic insults or in some

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instances from perturbations caused by nutrition during development—from embryos to fetuses to infants, and teenagers.67 One major mechanism by which adverse effects occur is through epigenetic phenomena that turn genes on or off, or alter protein regulation, but do not change DNA sequences.68 These modifications can alter biological pathways or tissue development sufficiently to produce organ dysfunctions.

Children are especially vulnerable to diseases from toxicants for several reasons. Their biology is more easily damaged by toxicants. They have greater exposures per body weight. They have lesser defenses against toxic invasions, and they have a longer lifespan for diseases to develop if diseases are triggered. Moreover, some of the adverse effects are irreversible.69

Catastrophes Alerting Scientists to Early Life Harms: Three major catastrophes presaged more extensive research into the developmental origins of disease: in utero exposures to methylmercury, thalidomide and diethylstilbestrol. Methylmercury, dumped into Minimata Bay in Japan, was absorbed by fish, people ate the fish, including pregnant women, and children were exposed to the methylmercury in utero (1950s). Some children were born with cerebral palsy, a crippling disease, but also many had neurological problems, auditory disturbance, limb deformities, and poor muscle control. Some died and some were stillborn.70

A second major catastrophe ensued when women in the first trimester of pregnancy

took the sedative Thalidomide (1960s). This led to children being born with shortened or displaced limbs, as well as perhaps having no ears, spinal malformations, kidney abnormalities, autism, and other learning disabilities, inter alia. These maladies affected about 5,000 to 7,000 children worldwide, but only about 40 in the U.S., thanks to the vigilance of Frances Oldham Kelsey, a physician at the U.S. Food and Drug Administration. She was suspicious of previous German and United Kingdom tests on Thalidomide and urged that the FDA stop approval of the drug before there was widespread exposure. Another 7,000-8,000 children worldwide aborted or were stillborn.71

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A third catastrophe occurred when doctors recommended that women take the synthetic estrogen diethylstilbestrol (DES) during pregnancy on the mistaken theory that this would assist in the prevention of miscarriages for women who had a history of such problems. Female children exposed in utero to a mother’s DES were at risk of contracting vaginal/cervical cancer after a twenty-year latency period.

A fourth, less visible, example of the developmental origins of disease resulted from women drinking alcohol during pregnancy. At the same dose fetal alcohol effects are worse for the developing child than for the mother who imbibed it.72 These children tended to have visible morphological problems along with vision, hearing, memory, and attention span disorders plus lesser abilities to learn and communicate.

In sum this body of research revealed how vulnerable developing children could be during the developmental period because they were growing quickly with rapid changes in

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cells and tissues that were comparatively easy to disturb and damage, and a long lifetime for diseases to develop.

Contamination: Moreover, researchers at the Centers for Disease Control and Prevention Biomonitoring Program along with California’s Biomonitoring Program have now identified that U.S. citizens are contaminated by 304+ manmade toxicants.73 Pregnant women can harbor up to 43 toxicants that would be shared with developing children in utero.74 And, confirming this effect, babies have been born with toxicants in their bodies.75

Some obvious contaminants include C8 in Teflon cookware, stain-resistant fabrics (including in sofas and carpets), food packaging, and Gore- Tex, now widespread in the environment; polybrominated flame retardants (PBDEs) in upholstery, plastic cases for electronic instruments, seat cushions, furniture, carpets, and draperies, as well as in the environment; polychlorinated biphenyls (PCBs) in foods, meats, the environment, air, and water; organochlorine pesticides on food and in the air; phthalates in cosmetics, linoleum flooring, and intravenous lines; polycyclic aromatic hydrocarbons (PAHs), the by-products of combustion; and perchlorate, a rocket fuel and fireworks component that is in groundwater, drinking water, and soil.76

The developmental basis of disease and our permeability to toxicants reveals the inadequacy of legal protections. We cannot prevent human permeability or developmental vulnerability to toxicants. A pregnant woman’s contamination is shared with developing children in utero. There is “no placental barrier per se: the vast majority of chemicals given the pregnant animal (or woman) reach the fetus in significant concentrations soon after administration.”77 New technologies are joining the invasions: plastic nanoparticles can move from mom to baby through the placenta.78

Developing children typically have larger toxic doses per body weight than the mother, via cord blood and breast milk.79 Methylmercury is concentrated 5 times higher in a fetal brain than in the mother’s blood.80 Lipophilic (fat loving) substances, such as PCBs, are present in breast milk at much higher concentrations than in the mother’s blood.81 Some phthalates are concentrated five times greater in children than in adults, but, surprisingly, perfluorinated compounds (C8) are much lower in breast milk than in blood serum.82 During development, lead is transferred from a mother’s bones to developing child via the “calcium stream” in utero or via breast milk in sufficient can damage developing brains. 83

After birth children continue to have greater exposures because they have higher metabolism, breathing, absorption, and circulation rates, along with higher fluid and food intake rates per body weight.84 Finally, as they become mobile they play close to ground/floor, “mouth” everything in sight, ingesting more dust and anything it is contaminated with, including lead in the environment.

Potential Sensitivity to Tiny Doses: Once children are contaminated they can be quite sensitive even to tiny doses of some toxicants. Mutagenic carcinogens have no threshold for toxicity for developing children or adults.85 There has been no identified threshold for lead toxicity. 86 Researchers found that a single Thalidomide pill caused malformations in at least one child,87 while a single dose of valproic acid (an anti-epileptic drug) in animals can cause autism-like behavior.88

Sometimes low doses cause greater harm than larger doses. High doses of tamoxifen inhibit breast cancer cell growth, lower concentrations stimulate breast cancer cells, and the highest doses are acutely toxic.89

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Moreover, developing children are more susceptible than adults to toxicants. Toxicants can disrupt differentiating cells and growing tissues that result in alterations in physiological functions.90

Children Have Lesser Defenses against Toxicants: They have less developed immune systems, blood brain barriers, livers, and detoxifying enzymes.91 Consequently, when they are contaminated by toxicants, their growing bodies can do less than adults’ bodies to protect them from diseases or dysfunctions that might be initiated.

Some Organ Systems Have “One Chance to Get It Right:” Some organ systems are “uniquely susceptible,” such as the developing brain and immune system. The developing brain has windows of “unique susceptibility” because it must grow from a single cell into billions following “precise pathways” in the “correct sequence” to function properly. While considerable growth occurs in utero and in the first six months of life, brain development is not fully complete until adulthood.92

The immune system is similarly sensitive; for both systems there seems to be “one chance to get it right.”93 For reproductive systems there may or may not be only one chance to “get it right.” However, Michael Skinner’s animal research at Washington State University has revealed that it is comparatively easy to get the reproductive system wrong, with very likely little chance to make it right later in life (brief discussion of this follows below).94

Genetic variability Increases Children’s Susceptibility: Individual genetic variation exacerbates children’s vulnerability. Researchers have identified particular genes that make subpopulations of individual children or adults more vulnerable to substances such as polycyclic aromatic hydrocarbons (by-products of combustion),95 organophosphate pesticides, 96 and methylmercury.97

VI. Chronic Diseases Arise from Exposures During Development

Recall that the greatest disease burdens today in developed countries come from chronic diseases. Toxic substances can cause a variety of chronic diseases.

Neurobehavioral diseases: For example, mental retardation, autism, and cerebral palsy are neurobehavioral disorders of environmental origin that had an annual cost of approximately $9.2 billion in 1997.98 Lead, a well-known neurotoxicant whose causes are all of environmental origin, had 1997 annual costs of $43.4 billion from pediatric lead poisoning.99 Exposures to lead cause lower IQs, motor skill problems, attention disorders [ADHD], violent behavior, and cardiovascular disease.100

Parkinson’s disease can have environmental origins and this source costs between $12 and 25 billion in 1997 dollars.101 An early manifestation occurred when five young heroin addicts (ages 26-42 years) were admitted to drug clinics or emergency rooms with symptoms of Parkinson’s disease. The oldest was so “frozen” that he could not move his body except for blinking his eyes, unless he was given dopamine to temporarily restore his voluntary movements.102 These addicts had taken heroin contaminated with MPTP (1-methyl-4-phenyl-1, 2,3,6-tetrahydropyridine), which targets neurons “that are involved in Parkinson’s disease.” 103

In addition, more recent studies have found that exposures to two pesticides, Paraquat and rotenone, both chemically similar to MPTP in structure, can contribute to Parkinson’s at consumer exposures. 104 Human studies of twins also reveal that exposures to several solvents increase risks of Parkinson’s disease: trichloroethylene (a six-fold risk),

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perchloroethylene (a 10.5 increase in risk) and carbon tetrachloride (a 2.3 risk increase). 105 The annual 1997 costs of Parkinson’s from environmental exposures were estimated to be $12-25 million. 106

Immunological disorders: Early life and adult exposures to toxicants can adversely affect the immune system. However, the immune system is not isolated from other organ systems, as it interacts with the respiratory, neurological, cardiovascular, dermal, and gastrointestinal organ systems. 107 For one example, asthma results from the interaction of the immune system and respiratory system. In 1997 the estimated costs of pediatric asthma resulting from environmental origin were about $2.0 billion (range $0.7-2.3 billion). As occurs with other toxic exposures, exposed infants are much more susceptible than adults, having greater dose-sensitivity, severity of effects, and persistence of effects. 108 Some substances can create invisible immunotoxic alternations until a person’s system is stressed with a second “hit.” 109 There are many immunotoxicants ranging from the heavy metals lead, mercury, and magnesium, to pesticides and some hormonal mimics. 110

Particularly worrisome is that early life immune dysfunctions carry some risk of reappearing as other but related diseases later in life. Consider this figure illustrating the relationship between childhood asthma and type I diabetes, respectively, resulting in some risk of later adult-onset diseases.111 Similar patterns are seen for childhood inflammatory bowel disease and infant respiratory infection/rhinitis.112

Dietert,

Pie Childhood cancer: Cancers can affect children and research suggests that many

childhood cancers begin in the womb, e.g., acute lymphoblastic (ALL) and acute myeloid childhood leukemias (AML).113 Pesticide exposures have been associated with ALL with an increased eleven-fold relative risk and AML with a fourteen-fold relative risk compared with non-exposed children.114 Both paternal and maternal exposures to other substances increase the risks of childhood cancers beyond pesticides.115

Interestingly, childhood cancers typically take 2 hits. An initial hit appears to be a characteristic chromosomal translocation in utero followed by some major immunological stress after birth.116

However, the initial cancer does not end suffering or loss of lifetime opportunities. For example, “serious, disabling, and life-threatening chronic health conditions … [cause] functional impairment and activity limitations.”117 The treatment of childhood cancer often leads to neurological problems, e.g., ADHD, reading and math difficulties, or other cognitive problems. It can also result in strokes, secondary cancers or other diseases, such

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as breast cancer, heart disorders, diabetes, and earlier mortality. It can even accelerate the aging process. In sum it results in a “failure to thrive.”118

The disease and resulting treatment-morbidities hamper a person’s opportunities, seemingly from a very early age. The social costs of childhood cancer are substantial with annual costs of environmental origin about $322 million in 1997.

Some effects of childhood cancer are illustrated by Jarrett McElheney’s cancer. Early in life this adventurous boy loved playing in water. After contracting “ALL (at age 4) [from benzene] he was pale, fatigued, had pain his knees and shoulders, screamed from spasms, and nearly died …” At age 20 he had “feebleness, and fatigue—… lingering fears … [and is at risk for] osteoporosis, cataracts, or even another cancer.” 119

The McElheneys settled a tort case with British Petroleum, among others, for benzene’s contribution to Jarrett’s disease. However the settlement was quite small; their lawyer earned only about $0.75 per hour on the case, substantially less than typical fees. Such a seemingly small settlement is hardly adequate to compensate the McElheneys for Jarrett’s disease, his suffering, their costs, and their agony. Compensation after the fact of harm also seems wholly inadequate to compensate him for opportunities he would have had without the childhood cancer. We might say the companies and the military that exposed him to benzene at Camp Lejeune marine base along with administrative law all failed him. The tort law somewhat assisted him, but his lifetime opportunities have been unjustly truncated.

Reproductive disorders: Recall that female offspring exposed to DES in utero had a substantial probability of contracting vaginal/cervical cancer about the age of 20. Analogous to childhood cancer a woman does not just contract the disease, cure it, and be done with it. Once she has contracted vaginal cancer, she would need an initial operation to electrically burn out the cancer. However, according to a conversation I had with a DES daughter, she has had multiple similar operations to burn out recurring cancers. She is not able to have children (or it may be unadvisable), may not take birth control pills, and may not take some post-menopausal drugs.120 Her lifetime opportunities have been substantially modified compared with a fully healthy woman because of the disease and its aftermath.

If we regard breast cancer as being in the generic category of reproductive disorders, young women exposed to toxicants such as radiation and DDT are at a higher risk of breast cancer than adults: radiation—3-5 times higher; DDT 5 times higher.121

Animal data showa much more worrisome possibility from exposures to toxicants in utero: transgenerational reproductive disorders. Pregnant rats exposed to an individual pesticide or a dose of BPA when reproductive organs are developing in male fetuses can cause sperm damage, sterility, and a host of cancers when the males become adults (first generation) and in their sons’ (second generation). Subsequent generations showed a wider range of diseases: prostrate disease, kidney disease, immune system abnormalities, testis abnormalities, and tumor development. Thus, a brief period of exposure in a pregnant rat can affect family lines for an indefinite period.122

Similar experiments with a range of substances revealed somewhat analogous effects in female offspring. Michael Skinner exposed pregnant rats to one of the following compounds— (1) vinclozolin, a pesticide, (2) a combination of the pesticides permethrin and DEET (N, N- Diethyl- meta- toluamide), (3) a plastics mixture, (4) dioxin, or (5) jet fuel— during gestation days 8-15 when female reproductive organs develop. The subsequent four generations of female offspring developed polycystic ovarian disease and

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primary ovarian insufficiency (POI). Polycystic ovarian disease consists of infrequent ovulation, high androgen levels, multiple persistent ovarian cysts, and often-related insulin resistance. These effects, demonstrated in rats, are seen in 6– 18% of women; thus, if chemical exposures caused similar effects in human populations, they would be quite significant and disturbing. POI is the acronym for a decreased primordial follicle pool of eggs, the precursors of fully developed eggs. When this pool is smaller, it tends to reduce the chances of pregnancy over a lifetime. Again, these results were demonstrated in rats, but in humans POI appears in about 1% of women.123

Obesity: A single dose of DES (or some other synthetic estrogens) is sufficient to cause obesity in mice that does not result from an energy imbalance. The two mice shown in the slide below have the same genome, same diet, same exercise, but had different in utero exposures to one dose of a synthetic estrogen in the obese mouse.124

Researchers understand that chemical exposures disrupt hormonal pathways that in

turn increase susceptibility “to obesity in the face of … waistline-challenging lifestyles.”125 A host of known toxicants has been shown to contribute to obesity in animal studies.126

Beyond causing obesity in immediate offspring, Michael Skinner’s lab has identified more worrisome effects from exposures to DDT. DDT exposures at consumer levels predispose animals to obesity two generations later. Moreover, this is of concern because it suggests that similar exposures may predispose people to obesity as well.127

“Contaminated Daddy” Factors: While it is well established that pregnant women exposed to certain toxicants during (or before) pregnancy can give birth to children with diseases or dysfunctions, contaminated fathers whose sperm is exposed to a variety of substances can also adversely influence their offspring. Men exposed to Paxil, anesthetic gases, morphine, lead, mercury, pesticides, solvents, dyes, and paints (each individually) can increase risks of miscarriages or other prenatal or neonatal problems.128 A father’s nutrition or stress can also affect the health of his future children. Thus, men need to understand that their “life experience [can also] leave biological traces on [their] children.”129

Contaminated Parents: Occupational and Developmental Issues: Since both contaminated men and women could contribute to their children’s diseases or dysfunctions, this is an important additional issue for occupational exposures, apart from harm to the

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adults. If either parent is contaminated with a toxicant at the wrong time, it could affect the future health of their children.

Workplaces in particular pose problems, despite early congressional passage of the Occupational Safety and Health Act (1970), which aimed to protect employees from toxicants. Under this statute, OSHA is charged with setting “the standard which most adequately assures … that no employee will suffer material impairment of health or functional capacity even if such employee has regular exposure to the hazard dealt with by such standard for the period of his working life.”130 However, the Center for Public Integrity reported that workers are “callously” unprotected.131 Moreover, OSHA has issued fewer than five workplace health protections in the last sixteen years.

As a result of in utero exposures to lead and other toxic substances Mark Flores was

born with “extensive cognitive impairment.” 132 Because Yvette Flores, his mother, worked in a poorly protected workplace in a Spectra-Physics electronic plant her body “was a ‘toxic warehouse before Mark was conceived.’”133Consequently, Mark’s diseases and dysfunctions could be traced to his mother’s contamination in the plant and the company settled a tort case for his injuries. It seems clear that Spectra-Physics and the Occupational Safety and Health Administration failed Yvette and Mark, who were both treated unjustly.

Mark (now 36) has clearly been harmed, but more importantly he has no opportunities during his lifetime that the rest of us consider routine. He cannot conduct daily living activities on his own and will need the assistance of an adult to supply his most basic needs the rest of his life.

The upshot of this short section and the example of Mark and Yvette Flores is that good workplace protections from toxicants better both the exposed adult and any children the adult may produce or even consider producing. This suggests that justice requires more stringent occupational protections for adults and their children in order to ensure a wide range of opportunities for both.

VII. Brief Exposures Can Endure Biologically

One other inference of substantial import is that tiny, even fleeting exposures to toxic molecules can become biologically embedded in individuals, in their children, grandchildren (multigenerational), or, with unlucky timing, in great grandchildren and

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beyond (transgenerational), causing adverse effects. This occurs because an initial or repeated exposure can damage biological processes at the cellular level that in turn develop into diseases or dysfunctions at some later time.134

The evidentiary picture that emerges from research into the developmental basis of disease is something like a pointillist painting: parts of the picture filled with numerous data points, others partially filled, some blank, but the general background reasonably solid. There is substantial scientific evidence that our children are among the most vulnerable of citizens, they are highly permeable to chemical invasions, and some in fact are harmed. We also know that portions of the population are at live risk on the basis of findings in animal data.135

VIII. What Should Be Done?

In 1976 Congress created what I now call “Old” TSCA to regulate 80-90% of chemical creations with postmarket laws. That legislation resulted in 62,000 substances being grandfathered as “safe” with another 22,000 entering commerce with little or no toxicity data because of the provisions of that law.

Both groups of substances remain in commerce until a health agency carries a difficult legal and scientific burden to reduce exposures. A postmarket law such as this (as well as other postmarket laws) is too late to protect many cohorts of children. That is, products enter commerce and remain there until they are removed or their risks are reduced. Yet if children are exposed in utero or shortly after birth to toxic products in sufficient amounts, they are at risk of contracting diseases or dysfunctions the exposures typically cause.

Postmarket laws simply cannot prevent diseases induced by toxic substances during development, because protections come too late. Moreover, even when conscientious, impartial scientists seek to develop good data showing risks or harm, delays frustrate reducing or removing risks because studies move at their own pace. Inadequately funded and understaffed public health institutions, obfuscating actions by affected companies, and less honorable intransigence substantially aggravate the problems.136

In addition, important features of postmarket laws frustratebetter health protections. The Environmental Protection Agency has the legal burden of proof to change the legal status quo, to identify exposures that pose risks or cause harm, and then to take appropriate legal action to reduce them. However, because of the allocation of the burden of proof, companies merely have to play “defense” to frustrate or discourage the agency from taking action. This is quite unlike laws under which pharmaceuticals or pesticides enter the market. Under these laws a company must have sufficient scientific data under the law to persuade an agency to permit its product into the market (although removing them under such laws remains difficult). Under postmarket laws companies have been given a free pass for their products to enter commerce without toxicity data, and they have learned to pressure EPA to have “doubt free” data before improving protections—a governmental agency must have very strong scientific data, even doubt free data, before removing a commercial product from commerce. Such efforts greatly burden and even thwart improved health protections.137

Even though the normal scientific and administrative procedures just described could and likely would be too slow to protect the public well, corporate phalanxes of “doubting experts” additionally frustrate health protections. While in the 1970s even into

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the 1980s legal actors in administrative law and the tort law might have been in the grip of the need for quite “rigorous” science before changing the legal status quo, now defendants whose products are legally at risk from legal action adopt deliberate strategies to mire improved health protections in scientific uncertainty. They have adopted the strategy used successfully for decades by the tobacco industry:

“Doubt is our product… the best means of competing with the ‘body of evidence that exits in the minds of the general public … [and] it also [establishes] a controversy.” 138

This strategy is permits a company to fully support health protections, but argue that the there is just too much doubt about the needed science to achieve them.

Such actions have had their effects. One indicator of this is the difficulty that the EPA has in establishing even partial risk estimates through its Integrated Risk Information System, or IRIS, which involves only the first two steps of a typical risk assessment. However, these two steps still proceed slothfully (my term), according to the Governmental Accountability Office (GAO). Without risk estimates, the EPA cannot begin to go through other regulatory steps to protect the public by reducing or removing adverse effects. These two steps of risk assessment had been delayed at IRIS for several substances for inordinate periods of time: trichloroethylene (TCE) (20+ years), dioxin (25+), perchloroethylene (18+), formaldehyde (19+), and naphthalene (9+).139 In May of 2017 the American Chemistry Council requested that the EPA reconsider its formaldehyde risk assessment because of a new study. This seems like yet another delaying tactic to postpone an already stalled assessment of a substance that caused Sandy Guest’s death.

Moreover, under TSCA the EPA has issued improved health protections for only five toxicants grandfathered as safe in 1979. Even to institute procedures to require additional testing of existing substances takes more than five years per compound. Once testing has begun it takes longer yet to obtain data.140 And, one major EPA attempt to eliminate all uses of asbestos under TSCA, with 45,000 pages of scientific and legal support, was vacated by the Fifth Circuit Court of Appeals.141 This extremely toxic substance could not be legally removed from the US market. The EPA has not used that TSCA provision again because it is so burdensome.

Postmarket Laws Are Unjust They cannot prevent chronic diseases and morbidity from occurring in children or

adults. They permit harms and undermine a variety of lifetime opportunities for some of us. Premarket testing and approval laws are much better in addressing new chemical

creations, but even these can miss adverse effects and tests need to be designed to better detect developmental toxicants in drugs and pesticides. For example, the FDA reports that most drugs are not tested for children yet are often prescribed.142

IX. What Can Be Done about Toxicity-Induced Chronic Diseases?

Vaccinations will not prevent toxicity-caused diseases143 and antibiotics won’t treat them. Like public health officials of the last century, we must “clean up” toxicants in our lives. However, now instead of cleaning up sewage, polluted water or contaminated air in the environment, although we still have some of this to do, we must use the law to clean up toxicants and prevent new contamination. For prevention we need a new legal paradigm to

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protect the public. However, examples have been before Congress since 1962 in the form of the Food, Drug, and Cosmetic Act amendments occasioned by the Thalidomide catastrophe and the pesticide amendments of 1968. Consequently, for many years I have argued in various publications for addressing general chemicals, previously covered by Old TSCA, with premarket testing and approval laws.144

As my Tragic Failures was in press in June of 2016 a previously “do nothing” Congress passed the Frank R. Lautenberg Chemical Safetyfor the 21st Century Act (2016) that has several attractive provisions and does require premarket review of general chemicals before they enter commerce.

1) The EPA “must make an affirmative finding on the safety of a new chemical or significant new use of an existing chemical before it is allowed into the marketplace.”428 It must “consider risks to susceptible and highly exposed populations [these may include infants, pregnant women, children and workers] and ensure a substance does not pose an ‘unreasonable risk.’” This is a major improvement. In order for it to function well, however, the agency must hold proposed new substances to good evidentiary standards and careful review to protect the public. How well EPA does this will be revealed as it implements the law. (Early results are not as promising as the Lautenberg Act foresaw.)145 An important point that follows from the science concerning the developmental origins of disease is that in some instances tiny concentrations of toxicants can cause harm, and, of course, genetic variation increases susceptibility for some diseases in some people. Administrators of the Lautenberg Act must be sensitive to these issues in order to adequately protect children during development.

2) If needed evidence is missing, the EPA can more easily demand it by an administrative order rather than using a time-consuming notice and rule-making, which in the past could take three years.146 Under the Lautenberg Act no specific toxicity tests appear to be required for identifying toxic effects, as there are for pharmaceuticals and pesticides. On the one hand, this appears to give EPA flexibility to decide on what kinds and amounts of data it needs for particular substances, but on the other hand, it may open the door for companies to pressure the agency not to require some data or to forego certain tests altogether.

3) The amendments mandate safety reviews for all chemicals currently in “active commerce,” namely those a company has manufactured in the last ten years. Within the first six months after the date of enactment the EPA must have 10 ongoing risk evaluations and must have “20 ongoing risk evaluations within 3.5 years.” 147

4) EPA must give priority to chemicals that are persistent, bioaccumulative, and are known human carcinogens or otherwise have high toxicity. This is an important addition.

5) In implementing these reviews, there are aggressive and judicially enforceable deadlines for EPA actions that many commentators applaud. These likely will face considerable litigation and other pressures and possibly be eroded over time. Public and administrative support for EPA’s efforts might help counterbalance manufacturers’ efforts to slow health protections.148

With a new strongly anti-regulatory administration implementing this statute, there are serious concerns. One is whether proposed new chemical creations will have to be supported by good toxicity testing and receive in-depth review before commercialization or whether they will be quickly approved with little testing and only cursory review by EPA from an administration committed to reducing regulatory burdens on companies. Early

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reports suggest that the second course of action is being followed. Since January 2017 the EPA has approved 600 new products to enter commerce.149 It seems unlikely they received careful review to prevent risks to developing children or adults.

Another issue is how quickly EPA will act under “aggressive and judicially enforceable” deadlines for removing unreasonably toxic substances already in commerce. A considerable distortion of the new law would be for the EPA to permit new products into the market with little or no testing and then to insist on quite detailed and certain evidence before removing them for health risks. Neither protects the public well. Will the agency continue to be plagued by delays and extensive industry lobbying in removing health risks, will it collaborate in delaying health protections, or will it commit to enforcing legally mandated deadlines? X. Some Conclusions

Toxic contamination is unavoidable; there is no place to hide. Routine premarket testing under “new” TSCA could contribute to an arc of good health by screening out toxicants among general chemicals that could harm children or adults alike, if it is properly implemented. This would importantly improve the justice of our chemical laws.

Unfortunately, for existing substances, despite aggressive and enforceable deadlines under the Lautenberg Act, removing existing toxicants will be slower than slothful simply because there is such a backlog of chemical creations in commerce that it will take the EPA decades to consider them and reduce any unreasonable risks they pose. These products will almost certainly linger for decades.

The tort law can support the treatment of chronic diseases caused by others and assist deterrence of other exposures. The legal cases of Kumho Tire and Milward will assist this effort, but unfortunately the public rarely uses the tort law.150

Both institutions will only serve justice goals—better protect our opportunities over a lifetime and provide redress for injuries that we suffer at the hands of others—if they are well administered and officials use science appropriate to the legal tasks. My research has proposed strategies for better protecting the public on these dimensions.

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Publications (Books only): U. S. Congress, Office of Technology Assessment, Identifying & Regulating Carcinogens (U.S. Government Printing Office, Nov. 1987) (251 pp.) (co-author, 40%). Eric Reichard, Carl Cranor, Robert Raucher, Giovanni Zapponi, Groundwater Risk Assessment: A Guide to Understanding and Managing Uncertainties (International Association of Hydrological Sciences, 1990) (204 pp.) (author of 25%). Regulating Toxic Substances: A Philosophy of Science and the Law (New York: Oxford University Press, 1993, 1997 (paperback)) (277 pp.). Valuing Health: Cost Effectiveness Analysis for Regulation, eds. Wilhelmine Miller, Lisa A. Robinson, and Robert S. Lawrence. Co-authors: Institute of Medicine Committee to Evaluate Measures of Health Benefits for Environmental, Health, and Safety Regulation: Robert S. Lawrence, Henry A. Anderson, Richard T. Burnett, Carl F. Cranor, Maureen Cropper, Norman Daniels, Dennis G. Fryback, Alan M. Garber, Marthe R. Gold, James K. Hammitt, Lisa I. Iezzoni, Peter D. Jacobson, Emmett Keeler, Willard G. Manning, Charles Poole, David A. Schkade, (Washington, D.C.: National Academies Press, 2006). Toxic Torts: Science, Law and the Possibility of Justice (Cambridge and New York: Cambridge University Press, 2006, 2007 (paperback) 411 pp.) Legally Poisoned: How the Law Puts Us at Risk from Toxicants (Harvard University Press, 2011, 2013 (paperback) 315 pp.). Toxic Torts: Science, Law and the Possibility of Justice, invited second edition (Cambridge and New York: Cambridge University Press, 2016, 2017 (paperback) 409 pp.) Tragic Failures: How and Why We Are Harmed by Toxic Chemicals [National Romanell lectures, Oxford University Press, 2017 (252 pp.)) Edited Book: Are Genes Us? The Social Consequences of the New Genetics, ed. C. Cranor. (New Brunswick, NJ: Rutgers University Press, 1994) (271 pp.)

Notes

1 Acknowledgements: Thank you Chancellor Wilcox. I am simultaneously deeply honored, humbled, and delighted to give this lecture, knowing of its history and significance in the UC system. I am delighted and humbled to join the 64 previous Faculty Research Lecturers in receiving this award because I know distinguished achievements of many of them.

29

I also wish to recognize several colleagues over many years who have helped improve much the

work I am about to describe. A comparatively new member of the department, Josef Muller, helped me find some writings of the Greeks that called early attention to the importance of good health.

My 46-year colleague, Larry Wright’s work on explanation and argument has been invaluable in teaching and in explaining scientific reasoning to judges in the tort law.

David Eastmond, Environmental Toxicology, has been most supportive in discussing toxicological issues, pointing to and sending me articles, lending books, educating me many matters of toxicology, and in being a co-author on several articles. Finally, thanks to Howard Friedman for his enthusiastic support of my work and for him setting up today’s lecture in his The Longevity Project: as he notes some things are reliably known to be directly and consistently bad for health: Toxins such as tobacco smoke, lead, heavy metals, pesticides, polluted air, radioactivity and virulent infectious diseases.1 All of these receive some mention in this lecture. 2 Jenkins, Defining Beauty: the Body in Ancient Greek Art,” Exhibition Catalog, British Museum, June 2015-

July 2015, 16, located at http://www.historytoday.com/alexia-petsalis-diomidis/defining-beauty-body-ancient-greek-art.

3 Yannis Tountas, “Historical Origins of the Basic Concepts of Health Promotion and Education: The Role of ancient Greek Philosophy and Medicine” Health Promotion International, 24.2: 190.

4 Plato, Timaeus, 360 BCE, 88a-c. 5 Juvenal (Decimus Iūnius Iuvenālis) , Tenth Satire, (Roman poet, 1st Century, CE). 6 Plutarch of Chaeronea in Boeotia, “The Training of Children,” 7. 7 “The Body and Christian Theology,” Present Truth Magazine, 29, Article 4: 1, quoting James N. Lapsley,

Salvation and Health, 39. 8 David Briggs, “This is my Body: How Christian Theology Affects Body Image,” Christianity Today,

October 26, 2016, located at http://www.christianitytoday.com/news/2016/october/how-christian-theology-affects-body-image-body-shaming.html.

9 Stephen Greenblatt’s, The Swerve: How the World Became Modern (New York: W.W. Norton, 2012), 103, 104-109. He notes, that Christians of the fifth and sixth centuries believed that “humans were by nature corrupt. Inheritors of the sins of Adam and Eve, they richly deserved every miserable catastrophe that befell them. The needed to be punished; they had coming to them an endless diet of pain. Indeed, it was only through this pain that a small number could find the narrow gate to salvation.” (105).

10 James F. Fries, “Aging, Natural Death, and the Compression of Morbidity,” New England Journal of Medicine, 808. 3, (1980): 132; Bruce P. Lanphear, “Origins and Evolution of Children’s Environmental Health,” in Special Issue: Essays on the Future of Environmental Health Research: A Tribute to Kenneth Olden, Environmental Health Perspectives 113 (August 2005): 2; Rodney R. Dietert, et al., “Breaking Patterns of Environmentally Influenced Disease for Health Risk Reduction: Immune Perspectives,” Environmental Health Perspectives, 118.8, (August 2010): 1091-1002.

11 http://www.medicinenet.com/script/main/art.asp?articlekey=33490 12 US National Institutes of Health, National Cancer Institute, “Diethylstilbestrol (DES) and Cancer,”

available at http:// www.cancer.gov/ cancertopics/ causes- prevention/ risk/ hormones/ des- fact- sheet. 13 John Rawls, A Theory of Justice, rev. ed. (Cambridge, MA: Belknap Press of Harvard University Press,

1999). 14 Ibid. 15 Normal Daniels, “Health Care Needs and Distributive Justice,” Philosophy &Public Affairs, 10.2 (Spring,

1981): 146-179; Carl F. Cranor, Legally Poisoned: How the Law Puts Us at Risk from Toxicants (Cambridge, MA: Harvard University Press, 2011); and Carl F. Cranor, Tragic Failures: How and Why We are Harmed by Toxic Substances (New York and Oxford: Oxford University Press, 2017)

16 Carl F. Cranor, “Risk Assessment, Susceptible Subpopulations and Environmental Justice,” in The Law of Environmental Justice, 2d Edition, ed. Michael B. Gerrard and Sheila Foster (The American Bar Association: 2008): 341-394.

17 Kristen Lombardi, “Benzene and Worker Cancers: An American Tragedy,” Center for Public Integrity, December 4, 2014, available at http://www.publicintegrity.org/2014/12/04/16320/benzene-and-worker-cancers-american-tragedy.

18 Id. and Carl F. Cranor, Toxic Torts: Science, Law, and the Possibility of Justice, 2nd ed. (New York: Cambridge University Press, 2016).

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19 James F. Fries, Bonnie Bruce, and Eliza Chakravarty, “Compression of Morbidity 1980–2011: A Focused

Review of Paradigms and Progress,” Journal of Aging Research, Vol. 2011 (2011), Article ID 261702. 20 Daniels, “Health Care Needs”; Cranor, Legally Poisoned; Cranor, Tragic Failures. 21 Cranor, Tragic Failures, 92. 22 U.S. General Accounting Office, Report to Congress: Toxic Substances Control Act, Legislative Changes

Could Make the Act More Effective, GAO/RCED-94-108 (Washington, DC: US General Accounting Office, September 1994): 4.

23 Ibid. 24 U.S. Congress, Office of Technology Assessment, Identifying and Regulating Carcinogens, (Washington,

D. C.: Office of Technology Assessment, 1987). 25 Ibid. 3. 26 Ibid. 3. The charge to OTA was not that administrative agencies necessarily had to reduce exposures to

carcinogens (because that might not be needed), but that they had to assess the seriousness of the cancer risk from exposures and act on those whose risks were sufficiently great to put the public at risk of cancer.

27 Moreover, this remains an issue even today. In May of 2017 I was invited to write an Amicus Brief for the 4th Circuit Court of Appeals on this issue because a trial judge had made this substantial statistical error. BRIEF FOR AMICI CURIAE CARL CRANOR, DIERDRE N. MCCLOSKEY, AND STEPHEN T. ZILIAK IN SUPPORT OF PLAINTIFFS-APPELLANTS FOR IN RE: LIPITOR (ATROVASTATIN CALCIUM) MARKETING, SALES PRACITCES AND PRODUCTS LIABILITY LITIGATION (NO II) MDL 2502 (April 28, 2017).

28 Jim Morris, “She Loved Making People Feel Great: Sandy Guest, 55, Hairdresser,” Center for Public Integrity, June 29, 2015, available at https://www.publicintegrity.org/2015/06/29/17533/she-loved-making-people-feel-great.

29 Stephanie J. Frisbee, A. Paul Brooks Jr., Arthur Maher, et al., “The C8 Health Project: Design, Methods, and Participants,” Environmental Health Perspectives, 117.12 (December 2009): 1873-1882.

30 Ken Ward Jr., “DuPont lawyers lose bid to keep jury in first C8 case from hearing about the Tennants’ cattle farm, Charleston Gazette-Mail, September 1, 2015, located at http://blogs.wvgazettemail.com/watchdog/2015/09/01/dupontlawyers-lose-bid-to-keep-jury-in-first-c8-case-from-hearing-aboutthe-tennants-cattle-farm/.

31 Frisbee, Brooks, Maher, et al., “The C8 Health Project: Design, Methods, and Participants,” Environmental Health Perspectives (2009).

32 Earl Rinehart, “DuPont to pay $670 million to settle C8 lawsuits,” The Columbus Dispatch, Feb 13, 2017, located at http://www.dispatch.com/news/20170213/dupont-to-pay-670-million-to-settle-c8-lawsuits; Ken Ward Jr., DuPont, Chemours Agree to $670.7M Settlement in C8 Cases,” Charleston Gazette-Mail, February 13, 2017, located at http://www.wvgazettemail.com/news/20170213/dupont-chemours-agree-to-6707m-settlement-in-c8-cases.

33 Carl F. Cranor, Regulating Toxic Substances: A Philosophy of Science and the Law (New York: Oxford University Press, 1993, 1997) and Carl F. Cranor, “Eggshell Skulls and Loss of Hair from Fright: Some Moral and Legal Principles that Protect Susceptible Subpopulations,” Environmental Toxicology and Pharmacology, 4 (1997): 239-245.

34 Sara M. Hoover, Lauren Zeise, William S. Pease, Louise E. Lee, Mark P. Henning, Laura B. Weiss, and Carl Cranor, "Improving the Regulation of Carcinogens by Expediting Cancer Potency Estimation," Risk Analysis, 15.2, (April, 1995): 267-280; Carl F. Cranor, “The Social Benefits of Expedited Risk Assessment,” Risk Analysis, 15.4 (June, 1995): 353-358.

35 Carl F. Cranor, "Asymmetric Information, the Precautionary Principle and Burdens of Proof in Environmental Health Protections," Protecting Public Health and the Environment: Implementing the Precautionary Principle, ed. Carolyn Raffensperger and Joel Tickner (Washington, D.C., Island Press: 1999): 74-99; "Learning from the Law to Address Uncertainty in the Precautionary Principle," Science and Engineering Ethics, 7 (2001): 313-326; “What Could Precautionary Science Be? Research for Early Warnings and a Better Future,” in Precaution: Environmental Science and Preventive Public Policy, ed. Joel A. Tickner (Washington, D.C.: Island Press, 2003): 305-320; “Toward Understanding Aspects of the Precautionary Principle,” the Journal of Medicine and Philosophy, 29.3 (2004): 259-279; “Some Legal Implications of the Precautionary Principle: Improving Information Generation and Legal Protections,” the European Journal of Oncology, Library. 2 (2003), 31-51 (Reprinted in the International Journal of Occupational Medicine and Environmental Health; 17(1) (2004): 17-34.)

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36 Bert Black and David E. Lilienfeld, “Epidemiologic Proof in Toxic Tort Litigation,” Fordham Law Review

52 (1984): 732, 769; Wade-Greaux v. Whitehall Lab., Inc., 874 F. Supp. at 1441 (D.V.I.), aff’d, 46 F.3d 1120 (3d Cir. 1994).

37 In re Agent Orange Product Liability Litigation, 611F. Supp. 1223 (E.D.N.Y. 1985). 38 Joe Cecil, Director of Research, Federal Judicial Center, letter in support of the nomination of Carl Cranor

for the Faculty Research Lecture, 2014. 39 Cranor, Toxic Torts: Science, Law, and the Possibility of Justice (New York: Cambridge University Press,

2006, 2008). 40 Ibid. 41 Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 589 (1993). 42 Ibid., 596. 43 Cranor, Regulating Toxic Substances; Carl F. Cranor, David A. Eastmond, and John G. Fischer, "Judicial

Boundary-Drawing and the Need for Context-Sensitive Science in Toxic Torts after Daubert v. Merrell-Dow Pharmaceutical," The Virginia Environmental Law Journal, 16 (1998): 1-77; Carl F. Cranor and David A. Eastmond, “Scientific Ignorance and Reliable Patterns of Evidence in Toxic Tort Causation: Is There a Need for Liability Reform?” Law and Contemporary Problems, 64.4 (Autumn 2001): 5-48; Carl F. Cranor, “A Framework for Assessing Scientific Arguments: Gaps, Relevance, and Integrated Evidence,” in the Journal of Law and Policy, XV.1 (2007): 7-58.

44 Margaret A. Berger, “The Admissibility of Expert Testimony,” in Reference Manual on Scientific Evidence, 3rd ed., ed. Federal Judicial Center (Washington, DC: National Academies Press, 2011): 19l. See also, Cranor and Eastmond, “Scientific Ignorance and Reliable Patterns of Evidence in Toxic Tort Causation” and Cranor, “A Framework for Assessing Scientific Arguments,” plus several other articles.

45 Cecil, letter in support of the nomination of Carl Cranor for the Faculty Research Lecture. 46 Wade-Greaux v. Whitehall Lab., Inc., 874 F. Supp. at 1441; Zoloft Products Liability Litigation, WL

3943916 (E.D.Pa, 2014). 47 Cranor, Toxic Torts, 2nd ed.: 217-219. 48 In Re Agent Orange Product Liability, 611 F. Supp. 1267 (E.D.N.Y. 1985), aff'd, 818 F.2d 187 (2d Cir.);

Lynch v. Fisher (1987); Brock v. Merrell-Dow, 874 F.2d 307 at 312 (5th Cir. 1989); Richardson v. Richardson-Merrell 857 F.2d 823, 825, 831 n.59 (D.C. Cir. 1988), cert. denied, 493 U.S. 882 (1989) (noting “epidemiological studies are of crucial significance”); Renaud v. Martin Marietta (1990); Chambers v. Exxon, 81F. Supp. 2d 661 (2000). For articles see, for instance, David E. Bernstein, “The Admissibility of Scientific Evidence After Daubert v. Merrell Dow Pharmaceuticals Inc.,” Cardozo Law Review 15 (1994): 2139, Harvard Law Review, 1995; Bert Black and David E. Lilienfeld, “Epidemiologic Proof in Toxic Tort Litigation,” Fordham Law Review 52 (1984): 732, 769.

49 Michael D. Green, Michal Freedman, and Leon Gordis, Reference Guide on Epidemiology,” in Reference Manual on Scientific Evidence (Federal Judicial Center and National Research Council, National Academies of Sciences, Washington, D.C., 2011): 610, citing the Restatement (Third) of Torts: Liability for Physical and Emotional Harm § 28 cmt. c(3) & rptrs. note (2010). See also, Westberry v. Gislaved Gummi AB, 178 F.2d 257 (4th Cir. 1999); Zuchowicz v. United States, 140 F.3d 381 (2d Cir. 1998); In re Heparin Prods Liab. Litig. 29971918 ((N.D. Ohio July 21, 2011). ????

50 Compare: Milward v. Acuity Specialty Products, Inc., 664 F.Supp. 2d 148 with Milward v. Acuity Specialty Products, 639 F.3d at 24.

51 Brock v. Merrell Dow Pharm., Inc., 874 F.2d 307, 312 (5th Cir. 1989), cert. denied, 494 U.S. 1046 (1990); In re Breast Implant Litigation, 11 F.Supp.2d 1217 (U.S. District Court, D. Colorado, 1998); Chambers v. Exxon, 81F. Supp. 2d 661, 665 (2000).

52 Austin Bradford Hill, Professor Emeritus of Med. Statistics, Univ. of London, “The Environment and Disease: Association or Causation?” President’s Address Before the Royal Society of Medicine (Jan. 14, 1965), in 58 PROC. ROYAL SOC’Y MED. 295 (1965). For some discussion see also Cranor, Toxic Torts, 2nd ed., 101-106, 222-230, 233-235. Currently, a more extensive paper, Raymond Neutra, Carl F. Cranor, David Gee, “The Use and Misuse of Bradford Hill in U.S. Tort Law,” forthcoming in Jurimeterics: the Journal of Science, Technolory and Law.

53 International Agency for Research on Cancer, “4,4′-Methylenebis(2-Chlorobenzenamine),” in Special Issue: Chemical Agents and Related Occupations, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans 100F (2012): 73–82.

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54 Carl F. Cranor, “Milward v. Acuity Specialty Products: Advances in General Causation Testimony in toxic

Tort Litigation,” Wake Forest Journal of Law and Policy, 3 (2013): 105, 114-115. 55 Andrew W. Jurs and Scott DeVito, “The Stricter Standard: An Empirical Assessment of Daubert’s Effect

on Civil Defendants,” Catholic University Law Review 62.3 (2013): 675–731; Andrew W. Jurs and Scott DeVito, “Et Tu, Plaintiffs? An Empirical Analysis of Daubert’s Effect on Plaintiffs, and Why Gatekeeping Standards Matter (a Lot),” Arkansas Law Review 66.4 (2013): 975–1006.

56 Greg Winter, “Jury Awards Soar as Lawsuits Decline on Defective Goods,” New York Times, January 30, 2001, available at http:// www.nytimes.com/ 2001/ 01/ 30/ business/ 30JURY.html?pagewanted=all.

57 Ibid. 58 Kumho Tire Co., Ltd. v. Carmichael, 526 U.S. 137, (1999) 59 OPPOSITION BRIEF OF DEFENDANTSAPPELLEES PFIZER INC., PFIZER INTERNATIONA LLC,

AND GREENSTONE LLC, In re Lipitor (Atorvastatin Calcium) Marketing, Sales Practices and Products Liability Litigation, June 30, 2017.

60 Kumho Tire Co., Ltd. v. Carmichael, 526 U.S. 153 (citing Daubert at 596). 61 Milward v. Acuity Specialty Products, 639 F.3d 11, 15 (citing Beaudette v. Louisville Ladder, Inc.462 F.3d

22, 25–26 (1st Cir.2006) (quoting Kumho Tire, 526 U.S. at 150). 62 Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 18-19. 63 Id. at 17-18. 64 Michael D. Green, “Introduction: Restatement of Torts as a Crystal Ball,” William Mitchell Law Review

993 (2011): 993 (discussing the Restatement (Third) of Torts in the “Liability for Physical and Emotional Harms”).

65 Lombardi, “Benzene and Worker Cancers.” 66 Carl F. Cranor, “(Almost) Equal Protection for Genetically Susceptible Subpopulations: A Hybrid

Regulatory-Compensation Proposal,” in Genomics and Environmental Policy, ed. Richard R. Sharp, Gary E. Marchant and Jamie A. Grodsky (Johns Hopkins University Press, 2008): 267-289; Carl F. Cranor “Do You Want to Bet Your Children’s Health on Post-Market Harm Principles? An Argument for A Trespass or Permission Model for Regulating Toxicants, Villanova Environmental Law Journal, XIX.2 (2008): 251-314; Cranor, Legally Poisoned.

67 Jerrold J. Heindel, “Animal Models for Probing the Developmental Basis of Disease and Dysfunction Paradigm,” Basic & Clinical Pharmacology & Toxicology 102.2 (2008): 76–81, 78.

68 Ibid. 77. 69 Cranor, Legally Poisoned, 81-132. 70 Masazumi Harada, “Minamata Disease: Methylmercury Poisoning in Japan Caused by Environmental

Pollution, Critical Reviews in Toxicology,” 25(1) (1995), 1-24, 3. For symptoms of MeHg poisoning see, J. McCurry, “Japan Remembers Minamata,” Lancet 367.9505 (2006): pp. 99–100.

71 James L. Schardein and Orest T. Macina, Human Developmental Toxicants: Aspects of Toxicology and Chemistry (Boca Raton, FL: Taylor & Francis, 2007): 13, 158.

72 Philippe Grandjean et al., “The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment,” Basic and Clinical Pharmacology and Toxicology 102 (2008): 73–75, esp. 74.

73 U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Environmental Health, National Report on Human Exposure to Environmental Chemicals, January, 2017.

74 Tracey J. Woodruff et al., “Environmental Chemicals in Pregnant Women in the United States: NHANES 2003–2004,” Environmental Health Perspectives 119.6 (2011): 878–85; American College of Obstetricians and Gynecologists Committee on Health Care for Underserved Women, American Society for Reproductive Medicine Practice Committee, with the assistance of the University of California at San Francisco (UCSF) Program on Reproductive Health and the Environment, “Committee Opinion: Exposure to Toxic Environmental Agents,” Committee Opinion 575 (October 2013).

75 Peter Fimrite, “Study: Chemicals, Pollutants Found in Newborns,” SFGate, December 3, 2009, available at http://www.sfgate.com/health/article/Study-Chemicals-pollutants-found-in-newborns-3207709.php

76 Cranor, Tragic Failures, 3, 48,49, 78, 93. 77 James L. Schardein, Chemically Induced Birth Defects, 3rd ed., rev. and expanded (New York: Marcel

Dekker, 2000), 5

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78 Peter Wick, et al.,”Barrier Capacity o fHuman Placenta for Naosized Materials,” Environmental Health

Perspectives, 118.3 (2010): 432-6. 79 Grandjean et al., “The Faroes Statement: 74. 80 Shun’ichi Honda et al., “Recent Advances in Evaluation of Health Effects on Mercury with Special

Reference to Methylmercury—a Minireview,” Environmental Health and Preventive Medicine 11.4 (2006): 171–6, at 176

81 Philippe Grandjean et al., “Elimination Half-Lives of Polychlorinated Biphenyl Congeners in Children,” Environmental Science & Technology 42.18 (2008): 6991–6, at 6991. Scientists note that breast milk contamination is not a reason to refrain from breastfeeding, because on balance it is desirable. However newborns’ contamination is worrisome. See also, Cranor, Tragic Failures, 71.

82 Birger G. J. Heinzow, “Endocrine Disruptors in Human Breast Milk and the Health-Related Issues of Breastfeeding,” in Endocrine-Disrupting Chemicals in Food, ed. Ian Shaw (Cambridge, UK: Woodhead, 2009): 322–55, at 324–5 and 322–47._

83 David Bellinger and Herbert L. Needleman, “The Neurotoxicity of Prenatal Exposure to Lead: Kinetics, Mechanisms and Expressions,” in Prenatal Exposure to Toxicants, ed. Herbert L. Needleman and David Bellinger (Baltimore: Johns Hopkins University Press 1994): 89–111, 92.

84 Mark D. Miller et al., “Differences between Children and Adults: Implications for Risk Assessment at California EPA,” International Journal of Toxicology 21.5 (2002): 403–18, 412.

85 David Eastmond, personal communication, UCR Environmental Toxicology, 2012. 86 Donald T. Wigle and Bruce P. Lanphear, “Human Health Risks from Low-Level Environmental

Exposures: No Apparent Safety Thresholds,” PLoS Medicine 2.12 (2005): e350; Richard L. Canfield et al., “Low-Level Lead Exposure, Executive Functioning, and Learning in Early Childhood,” Child Neuropsychology 9.1 (2003): 35–53; Ana Navas-Acien et al., “Lead Exposure and Cardiovascular Disease—a Systematic Review,” Environmental Health Perspectives 115.3 (2007): 472–82.

87 Luz Claudio et al., “Testing Methods for Developmental Neurotoxicity of Environmental Chemicals,” Toxicology and Applied Pharmacology 164.1 (2000): 1–14, 6.

88 Diane Dufour-Rainfray et al., “Fetal Exposure to Teratogens: Evidence of Genes Involved in Autism,” Neuroscience & Biobehavioral Reviews 35.5 (2011): 1254–65.

89 Laura N. Vandenberg et al., “Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses,” Endocrine Reviews 33.3 (2012): 378–455.

90 Ronald D. Hood, “Principles of Developmental Toxicology Revisited,” in Developmental and Reproductive Toxicology: A Practical Approach, 2nd ed., ed. Ronald D. Hood (Boca Raton, FL: Taylor & Francis, 2006): 3–17, 7.

91 Philippe Grandjean and Philip J. Landrigan, “Developmental Neurotoxicity of Industrial Chemicals,” The Lancet 368.9553 (2006): 2167; Dietert and Piepenbrink, “Perinatal Immunotoxicity,” Environmental Health Perspectives 114.4 (2006): 477–83; Rodney R. Dietert and Judith T. Zelikoff, “Identifying Patterns of Immune-Related Disease: Use in Disease Prevention and Management,” World Journal of Pediatrics 6.2 (2010): 111-18.

92 Ibid. 93 Grandjean & Landrigan, 2006; Philippe Grandjean, Only One Chance: How Environmental Pollution

Impairs Brain Development -- and How to Protect the Brains of the Next Generation, (New York: Oxford University Press, 2013).

94 Matthew D. Anway et al., “Endocrine Disruptor Vinclozolin Induced Epigenetic Transgenerational Adult-Onset Disease,” Endocrinology 147.12 (2006): 5515–23; Mohan Manikkam et al., “Transgenerational Actions of Environmental Compounds on Reproductive Disease and Identification of Epigenetic Biomarkers of Ancestral Exposures” PLoS ONE 7.2 (2012): e31901; and Mohan Manikkam et al., “Dioxin (TCDD) Induces Epigenetic Transgenerational Inheritance of Adult Onset Disease and Sperm Epimutations,” PLoS ONE 7.2 (2012): e31901.

95 Frederica P. Perera et al., “Molecular Epidemiologic Research on the Effects of Environmental Pollutants on the Fetus,” Environmental Health Perspectives 107.S3 (1999): 451–60.

96 Karen Huen, Kim Harley, Jordan Brooks, Alan Hubbard, Asa Bradman, Brenda Eskenazi, and Nina Holland, “Developmental Changes in PON1 Enzyme Activity in Young Children and Effects of PON1 Polymorphisms,” Environmental Health Perspectives, 117.10 (2009): 1632–1638, at 1638.

97 J. Julvez et al., “Prenatal Methylmercury Exposure and Genetic Predisposition to Cognitive Deficit at Age 8 Years,” Epidemiology 24.5 (2013): 643–50.

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98 Philip J. Landrigan, et al., “Environmental Pollutants and Disease in American Children: Estimates of

Morbidity, Mortality, and Costs for Lead Poisoning, Asthma, Cancer, and Developmental Disabilities, Environmental Health Perspectives, 110.7 (July 2002): 721-728.

99 Id. 100 Kim M. Cecil et al., “Decreased Brain Volume in Adults with Childhood Lead Exposure,” PLoS Medicine

5.5 (2008): 741–50; Ana Navas-Acien et al., “Lead Exposure and Cardiovascular Disease—a Systematic Review,” Environmental Health Perspectives 115.3 (2007): 472–82.

101 Philip J. Landrigan, et al., “Early Environmental Origins of Neurodegenerative Disease in Later Life,” Environmental Health Perspectives, 113. 9 (Sep., 2005): 1230-1233.

102 “The Case of the Frozen Addict,” NOVA, WGBH and BBC, February 18, 1986, www.pbs.org/wgbh/nova/listseason/13.html (accessed January 10, 2010); J. William Langston, Phillip Ballard, James W. Tetrud, and Ian Irwin, “Chronic Parkinsonism in Humans due to a Product of Meperidine-Analog Synthesis,” Science 219 (1983): 979–980.

103 J Sian, et al., “MPTP-Induced Parkinsonian Syndrome,” in Basic Neurochemistry: Molecular, Cellular and Medical Aspects, 6th edition, ed. Siegel GJ, Agranoff BW, Albers RW, et al., Philadelphia: Lippincott-Raven (1999).

104 Caroline M. Tanner, “Occupational and Environmental Causes of Parkinsonism,” in Occupational Medicine: State of the Art Reviews 7 (1992): 503–513, 506

105 Samuel M. Goldman et al., “Solvent Exposures and Parkinson Disease Risk in Twins,” Annals of Neurology 71.6 (2012): 776–84.

106 (Landrigan, et al., “Early Environmental Origins of Neurodegenerative Disease in Later Life.”) 107 Robert W. Luebke, et al., “The Comparative Immunotoxicity of Five Selected Compounds Following

Developmental or Adult Exposure,” Journal of Toxicology and Environmental Health, part B, 9 (2006), 1–26

108 Dietert and Piepenbrink, Environmental Health Perspectives 114.4: 477–83. 109 Id. 110 Id. 111 Dietert, Zellikoff, 2010, World Journal of Pediatrics, 6.2 (May 15, 2010). 112 Id. 113 M. F. Greaves and J. Wiemels, “Origins of Chromosome Translocations in Childhood Leukaemia,” Nature

Reviews Cancer 3 (2003): 639–649, cited by Martyn Smith, Professor of Toxicology, School of Public Health, University of California, Berkeley, personal email communication (May 7, 2009).

114 Julie A. Ross et al., “Epidemiology of Childhood Leukemia, with a Focus on Infants,” Epidemiological Reviews 16.2 (1994): 243–72.

115 Id. 116 Greaves and Wiemels, “Origins of Chromosome Translocations in Childhood Leukaemia,” 639–649; M.T.

Smith, “Prenatal Origin of Chromosomal Translocations in Acute Childhood Leukemia: Implications and Future Directions,” American Journal of Hematology, 75 (2004): 25425–25427.

117 National Cancer Institute, Childhood Cancers, “Late Effects of Treatment for Childhood Cancer (PDQ®) Health Professional Version, https://www.cancer.gov/types/childhood-cancers/late-effects-hp-pdq).

118 Laurie McGinley, “A New Urgency to Protect Survivors of Childhood Cancer, The Washington Post, December 25, 2016, located at https://www.washingtonpost.com/national/health-science/a-new-urgency-to-protect-survivors-of-childhood-cancer/2016/12/25/f29abb92-c0a8-11e6-afd9-f038f753dc29_story.html?utm_term=.a8a953beee8c.

119 Lombardi, “Benzene and Worker Cancers. 120 Interview with a DES daughter who will remain unnamed. 121 Miller et al., “Differences between Children and Adults: Implications for Risk Assessment at California

EPA,” 412 (citing NRC, Health Effects of Exposure to Low Levels of Ionizing Radiation: BEIR V [Washington, DC: National Academy Press, 1990]; Ronckers, 2004; Barbara A. Cohn, Mary S. Wolff, Piera M. Cirillo, and Robert I. Sholtz, “DDT and Breast Cancer in Young Women: New Data on the Significance of Age at Exposure,” Environmental Health Perspectives 115, no. 10 (October 2007): 1406–1414, at 1406; Cranor, Tragic Failures, 75-77.

122 Matthew D. Anway, et al., “Endocrine Disruptor Vinclozolin Induced Epigenetic transgenerational Adult-Onset Disease,” Endocrinology 147.1_2 (2006): 5515– 23; Mohan Manikkam et al., “Transgenerational Actions of Environmental Compounds on Reproductive Disease and Identification of Epigenetic

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Biomarkers of Ancestral Exposures;” and Mohan Manikkam et al., “Dioxin (TCDD) Induces Epigenetic Transgenerational Inheritance of Adult Onset Disease and Sperm Epimutations,” PLoS ONE 7.9 (2012): e46249.

123 Eric Nilsson et al., “Environmentally Induced Epigenetic Transgenerational Inheritance of Ovarian Disease,” PLoS ONE 7.5 (2012): e36129 and Rebecca Tracey et al., “Hydrocarbons (Jet Fuel JP-8) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations,” Reproductive Toxicology 36 (April 2013): 104–16.

124 Personal communication, Fred Vom Saal, University of Missouri, Columbia, 2011. 125 Kerry Grens, “Obesogens,” The Scientist, November 1, 2015, located at http://www.the-

scientist.com/?articles.view/articleNo/44278/title/Obesogens/. 126 Ibid. (These include organobromine flame retardants, DDT, PCBs, organophosphate insecticides,

bisphenol A, phthalates, C8 or PFOA, along with cadmium, arsenic, tributyltin.) 127 Michael K. Skinner et al., “Ancestral Dichlorodiphenyltrichloroethane (DDT) Exposure Promotes

Epigenetic Transgenerational Inheritance of Obesity,” BMC Medicine 11 (2013): 228–50, available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853586/.

128 Emily Anthes, “Hey Would-Be Daddies, How You Take Care of Yourself Plays into the Health of Your Future Children,” Miller-McCune (December 14, 2010): available at http://www.alternet.org/story/149200/hey_would-be_daddies%2C_how_you_take_care_of_yourself_plays_into_the_health_of_your_future_children.

129 Judith Shulevitz, “Why Fathers Really Matter,” Sunday Review, New York Times, September 8, 2012, available at http://nyti.ms/QavdtZ.

130 Occupational Safety and Health Act, 29 U.S. Code § 655(b) 5. 131 Morris, “She Loved Making People Feel Great.” 132 Id. 133 Id. 134 Martyn T. Smith, Kathryn Z. Guyton, Catherine F. Gibbons, Jason M. Fritz, Christopher J. Portier, et al.,

“Key Characteristics of Carcinogens as a Basis for Organizing Data on Mechanisms of Carcinogenesis,” Environmental Health Perspectives, 124.6 (June 2016): 713-721.

135 Cranor, Legally Poisoned, 4,8,11,38, 47, 48-49, 58, 65-74. 136 Cranor, Tragic Failures, 94. 137 Id., 182,184. 138 Brown and Williamson Tobacco Company, “Smoking and Health Proposal,” Brown and Williamson

document no. 680561778–1786, 1969, legacy.library.ucsf.edu/tid/nvs40f00 (accessed June 30, 2008). 139 U.S. Government Accountability Office, “Testimony Before the Committee on Environment and Public

Works, U.S. Senate: “Toxic Chemicals: EPA’s New Assessment Process Will Increase Challenges EPA Faces in Evaluating and Regulating Chemicals, GAO-08-743T.

140 U.S. Institute of Medicine, Identifying and Reducing Environmental Health Risks of Chemicals in Our Society (Washington, DC: National Academies Press, 2014), 27.

141 Corrosion Proof Fittings v. Environmental Protection Agency, 947 F.2d 1201 (Fifth Circuit, 1991). 142 U.S. Food and Drug Administration, “Drug Research and Children, located at

https://www.fda.gov/drugs/resourcesforyou/consumers/ucm143565.htm. 143 One counterexample to this claim is that some cervical cancers traceable to the human papillomavirus

(HPV) can be prevented by a vaccine, but that’s because the disease is caused by a virus, not a toxic chemical creation.

144 Cranor, Toxic Torts (2006); Toxic Torts, 2d Ed. (2016); Legally Poisoned (2011). 145 Loraine Chow, “Industry Friendly’ EPA Completes Review of 600 New Chemicals,” Eco Watch, August

8, 2017, located at https://www.ecowatch.com/epa-approves-chemicals-2470558970.html. 146 Richard Dennison, “Historic deal on TSCA reform reached, setting stage for a new law after 40 years of

waiting,” Environmental Defense Fund, located at blogs.edf.org/health/2016/05/23/historic-deal-on-tsca-reform-reached-setting-stage-for-a-new-law-after-40-years-of-waiting/#more-5276.

147Cranor, Tragic Failures, 153-155 148 Ibid., 156. 149 U.S. Environmental Protection Agency, News Release: EPA Eliminates New-Chemical Backlog,

Announces Improvements to New Chemical Safety Reviews: Administrator Pruitt Strengthens TSCA New

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Chemical Review Program to Ensure Safety, Transparency and Continuous Improvements, August 8, 2017, located at https://www.epa.gov/newsreleases/epa-eliminates-new-chemical-backlog-announces-improvements-new-chemical-safety-reviews.

150 Michael J. Saks, “Do We Really Know Anything about the Behavior of the Tort Litigation System—and Why Not?” Pennsylvania Law Review 140 (1992): 1147–1289.