TORTINI

For your delectation and delight, desultory dicta on the law of delicts.

Acetaminophen – Partisan Politics Corrupts Scientific Assessments – Part 2

July 30th, 2026

Most medico-legal controversies over causation resolve in the pages of medical journals and within the walls of state and federal courthouses. The claim that pregnant women’s ingestion of acetaminophen causes their children to have an increased risk of autism, however, has become a flash point in American political drama.[1]

After the district court entered judgment against plaintiffs in the acetaminophen MDL, a sea change in the politicization of science occurred in the executive branch of the United States. In November 2024, the United States returned Donald Trump, its first fully post-modern president to office. For most of his life, Trump, in an homage to Michel Foucault, has seen no difference between assertions and truth. In the run up to the general election of 2024, Trump forged an alliance with independent candidate Robert F. Kennedy, Jr., whose disdain for evidence and truth has long made him a notorious source of misinformation on vaccines, autism, antidepressants, pesticides, glyphosate, among other things.

In August 2024, Kennedy quit his campaign and endorsed Trump, in return for a role in a future Trump Administration. After promising Kennedy a cabinet level position, Trump told his supporters that: “I’m going to let him go wild on health. I’m going to let him go wild on the food. I’m going to let him go wild on the medicines.”[2] Trump kept his promise of an appointment to Kennedy. On February 13, 2025, Robert F. Kennedy Jr. was confirmed by a narrow vote of the Senate, and sworn in as Secretary of Health and Human Services. President Trump immediately issued Executive Order 14211 to establish a “Make America Healthy Again [MAHA] Commission,” to be chaired by Secretary Kennedy.[3] One of the key objectives of the MAHA commission included investigating the causes of chronic childhood diseases and “assess[ing] the prevalence of and threat posed by the prescription of selective serotonin reuptake inhibitorsantipsychoticsmood stabilizers, stimulants, and weight-loss drugs.”

Two months later, at a press conference in April 2025, Kennedy asserted that environmental toxic substances were responsible for the increasing prevalence of autism. Only a day earlier, the Centers for Disease Control issued a report in which over 50 government scientists explained that evolving diagnostic criteria and improved awareness of parents and teachers (not to mention entitlements to social and educational support) were largely responsible for the changing patterns of diagnosis and assessment.[4]

Channeling his lawsuit industry practice in which Kennedy labeled any adverse evidence as a manufacturing industry conspiracy, the Secretary dismissed the CDC’s explanations as a (manufacturing) industry “canard” to deflect attention from possible environmental causes. Kennedy promised a massive research initiative to identify the environmental “culprit,” with results to be available by September 2025.[5]

The scientific community might well have been skeptical about how Kennedy was going to deliver answers to etiological questions surrounding autism in five months, when causal conclusions had eluded the scientific world for decades. In the fullness of the next five months, not much new research was done, but with the clock ticking, a conclusion was launched in the absence of evidence.

On September 22, 2025, President Trump, along with Secretary Kennedy, FDA Commissioner Marty Makary, Director of the National Institutes of Health Jay Bhattacharya, and Administrator of the Centers for Medicare & Medicaid Services Mehmet Oz, called a news conference to announce the “conclusion.”[6] Stumbling over the pronunciation of acetaminophen, Trump told women not to take the medication; it caused autism. Kennedy struck a more moderate note about acetaminophen, in describing a “potential” association between acetaminophen and ASD and ADHD. He acknowledged reviewing “contrary” studies showing no association, and announced that the FDA would issue a notice to physicians and begin a change in the medication label.

When Commissioner Makary spoke, he cited studies showing “consistent” associations between acetaminophen and autism. In a flourish, Makary stated that:

“four weeks ago, a Mount Sinai Harvard study [“Pada 2025”] reviewed all the existing literature and found the overwhelming body of evidence points to an association. Sure, you’ll be able to find a study to the contrary, that’s how science works, but to quote the dean of the Harvard School of Public Health, there is a causal relationship between prenatal acetaminophen use and neurodevelopmental disorders of ADHD and autism spectrum disorder.”[7]

The dean referenced by Makary was none other than Andrea Baccarelli, the key expert witness for plaintiffs’ in the acetaminophen MDL, who was excluded by Judge Denise Cote’s Rule 702 decision. Baccarelli has only recently moved from Columbia University to assume a new position at Harvard. The Mount Sinai study published four weeks earlier was a review by four authors, including Baccarelli.[8] Baccarelli and his co-authors, however, decidedly did not embrace a causal conclusion in their publication. In their statement of conclusions in the paper’s abstract, Baccarelli and his co-authors stated that their “analyses using the Navigation Guide thus support evidence consistent with an association between acetaminophen exposure during pregnancy and increased incidence of NDDs.” (emphasis added). In the discussion section of their paper, the authors explained that their “analysis demonstrated evidence consistent with an association between exposure to acetaminophen during pregnancy and offspring with NDDs, including ASD and ADHD, though observational limitations preclude definitive causation.”[9] In his press conference remarks, Makary was quoting not from a peer-reviewed article, but from Baccarelli’s expert witness report, written for litigation, and excluded from evidence by Judge Cote’s decision in 2023.

Makary’s reference to language from Baccarelli’s 2023 expert witness litigation report thus raises two interesting questions. First, given that expert witness reports do not generally find their way to the desks of the FDA Commissioner, how did Makary come by this plaintiffs’ litigation report? Second, and more troubling, why did Baccarelli defend his causal conclusion under oath, at an examination before trial in 2023,[10] when he was unwilling to embrace a causal conclusion two years later, in 2025? The first question raises at least the appearance of collusion between the lawsuit industry and political actors such as Secretary Kennedy and Commissioner Makary. The second question raises the issue of fraud on the court by a witness who is willing to assert a causal conclusion in legal proceedings, but is not willing to publish and defend the causal conclusion to his peers in a scientific journal.

In the wake of the news conference, the New York Times talked with  Baccarelli, and reported that he opined in the interview that “[f]urther research is needed to confirm the association and determine causality, but based on existing evidence, I believe that caution about acetaminophen use during pregnancy — especially heavy or prolonged use — is warranted.”[11] In essence, Baccarelli was offering a precautionary principle interpretation of the available evidence, not a causal conclusion. Baccarelli issued a statement on social media, the day of the news conference, to state that he and his colleagues “had conducted a rigorous review funded by a grant from the National Institutes of Health (NIH), of the potential risks of acetaminophen use during pregnancy.” Baccarelli disclaimed having reached a causal conclusion, describing his review as showing merely “evidence of an association between exposure to acetaminophen during pregnancy and increased incidence of neurodevelopmental disorders in children,” and that “[f]urther research is needed to confirm the association and determine causality….”[12] As we will see, Baccarelli’s claim that the Prada review was funded by an NIH grant was a bit of a tall tale, but his disclaiming a causal conclusion and explaining that his position was based upon the precautionary principle, not a showing of medical causation, was both candid and at odds with his litigation expert report.

The lead author of the Prada Review, Diddier Prada, an epidemiologist at Mount Sinai Hospital in New York, similarly told the Times that “[w]e cannot answer the question about causation — that is very important to clarify.”[13] A third author of the Prada Review was Ann Bauer, the lead author of the 2021 putative consensus paper that was instrumental in starting the acetaminophen mass tort. Bauer commented in advance of the September press conference. In anticipating the Administration’s embrace of a causal claim, Bauer noted that she was “a little concerned about how this message is going to come because I think they may be jumping the gun”; “I think those of us in the research community would like to see stronger evidence.”[14]

Scientific Community’s Reaction to Trump’s News Conference

Trump’s press conference on acetaminophen and vaccines was widely met with condemnation and disbelief.[15] Most medical organizations were appalled at the administration’s sloppy messaging. The day after the press conference, the American College of Medical Toxicology (ACMT) issued a statement in response, to affirm the safety of acetaminophen in pregnancy.  The ACMT noted that its position agreed with those of the American College of Obstetrics and Gynecologists, the Society for Maternal-Fetal Medicine, the American Academy of Pediatrics, and the Society for Developmental and Behavioral Pediatrics.[16]

In Europe, where pharmaceutical regulation is typically even more precautionary than in the United States, the European Medicines Agency (EMA) announced, a day after the Trump news conference, that using acetaminophen during pregnancy was safe, with no showing that it causes autism in offspring. The EMA announcement quoted Steffen Thirstrup, the EMA’s Chief Medical Officer, as stating that “[p]aracetamol remains an important option to treat pain or fever in pregnant women. Our advice is based on a rigorous assessment of the available scientific data and we have found no evidence that taking paracetamol during pregnancy causes autism in children.”[17] In the United Kingdom, the governmental Medicines & Healthcare Products Regulatory Agency issued a notice, on September 23, 2025, that acetaminophen was safe to take in pregnancy and that the medication has not been shown to cause autism in children.[18]

The day of the news conference, the Autism Science Foundation issued a statement of deep concern about Trump’s announcement. The Foundation observed that “[b]ased on the existing data, there is not sufficient evidence to support a link between acetaminophen and autism.”[19] Medical ethicist Dr. Professor Arthur Caplan, who is not given to hyperbole, called the conference “the saddest display of a lack of evidence, rumors, recycling old myths, lousy advice, outright lies, and dangerous advice I have ever witnessed by anyone in authority.”[20]

The official governmental messaging in the wake of Trump’s press conference was more circumspect. In her press release on the day of the news conference, Press Secretary Karoline Leavitt used the meaningless locution, “suggested link,” and cited the Prada review, which eschewed causal conclusions.[21] Leavitt gratuitously added that “[t]he Trump Administration does not believe popping more pills is always the answer for better health.” Unless of course, it is Propecia for Donald Trump, testosterone for Peter Hegseth, or ketamine for Elon Musk.

When the administration physicians communicated with the public, they said something very different from Trump’s presentation. Dr. Mehmet Oz, former surgeon and television talking head, who stood mute by Trump’s side, found his voice later in the week, when he acknowledged that pregnant women of course should take acetaminophen when physicians direct them to do so.[22]

When FDA Commissioner Makary issued a notice to physicians, the same day as the Trump news conference, he carefully avoided causal language:

“In recent years, evidence has accumulated suggesting that the use of acetaminophen by pregnant women may be associated with an increased risk of neurological conditions such as autism and ADHD in children.

           * * *

To be clear, while an association between acetaminophen and autism has been described in many studies, a causal relationship has not been established and there are contrary studies in the scientific literature.”[23]

An FDA news release, also on September 22, 2025, announced that the agency was beginning a change in safety labeling, but the agency press release spoke only in terms of association and correlation, and like the FDA notice to physicians, explicitly disavowed a causal conclusion.[24] The FDA also noted that it was undertaking a safety label change, but the official communication did not reveal the dodgy origins of this initiative. The impetus for the label change appears to have come not from FDA scientists, but from Aaron Siri, a plaintiff’s lawyer who worked in concert with Robert Kennedy for years in anti-vaccination litigation. In a remarkable coincidence, Siri filed a citizen’s petition with the FDA, the same day of Trump’s news conference to raise “exigent concerns” over a need for a label change.[25] The New York Times noted some of the troubling ethical concerns raised by Siri’s parallel activities. In 2023, Siri’s law firm recruited plaintiffs for acetaminophen mass tort litigation. In 2024, Siri represented Kennedy in his election campaign.[26] The week before the Trump news conference, Jill Schoff, an employee of Siri’s law firm, uploaded Baccarelli’s expert witness report from the acetaminophen MDL to the Internet Archive, which explains how Dr. Makary was able to quote from its conclusions at the September 22nd news conference.[27] Siri cited to Baccarelli’s for-litigation report, at the Internet Archive, in his citizen’s petition that plumped for a label change.

The politicization of the acetaminophen issue appeared to be complete, when a month after Trump’s press conference, Trump sycophant and Texas Attorney General Ken Paxton sued manufacturers of acetaminophen for “deceptively marketing Tylenol to pregnant mothers despite knowing that early exposure to acetaminophen, Tylenol’s only active ingredient, leads to a significantly increased risk of autism and other disorders.”[28] Only a month earlier, the FDA acknowledged in its press release and its notice to physicians, that causation was not known. Paxton filed the complaint in Panola County, Texas, where Trump received 81.4% of the counted votes in 2024.[29] In addition to lawyers at the Office of the Texas Attorney General, Ashley Keller and others from the Keller Postman LLC firm were listed as representing Texas in its epistemic and scientific overclaiming. Ashley Keller was the principal lawyer for plaintiffs in the MDL, which had been dismissed by Judge Cote in 2024.

(to be continued)


[1] I am indebted to, and thank, Barbara McIntyre for sharing some of the research for this series.

[2] Brett Samuels, Trump says he’ll let RFK Jr. ‘go wild’ on health and food in potential second term, THE HILL (Oct. 27, 2024), available at https://thehill.com/homenews/campaign/4956319-trump-says-hell-let-rfk-jr-go-wild-on-health-and-food-in-potential-second-term/.

[3] Executive Order 14211, Establishing the President’s Make America Healthy Again Commission”The White House (Feb. 13, 2025), available at https://www.whitehouse.gov/presidential-actions/2025/02/establishing-the-presidents-make-america-healthy-again-commission/.

[4] Kelly A. Shaw, et al., Prevalence and Early Identification of Autism Spectrum Disorder Among Children Aged 4 and 8 Years — Autism and Developmental Disabilities Monitoring Network, 16 Sites, United States, 2022, 74 MORBIDITY & MORTALITY WEEKLY REP. 1 (Apr. 17, 2025).

[5] Meredith Wadman, Claiming autism ‘epidemic,’ RFK Jr. describes NIH initiative to find environmental causes, SCIENCE (Apr. 16, 2025), available at https://www.science.org/content/article/claiming-autism-epidemic-rfk-jr-describes-nih-initiative-find-environmental-causes

[6] Transcript, News Conference – Remarks: Donald Trump Makes an Autism Announcement at the White House, ROLLCALL (Sept. 22, 2025), available at

https://rollcall.com/factbase/trump/transcript/donald-trump-remarks-health-autism-white-house-september-22-2025/ (Transcript).

[7] Transcript at 24:35.

[8] Diddier Prada, Beate Ritz, Ann Z. Bauer and Andrea A. Baccarelli, “Evaluation of the evidence on acetaminophen use and neurodevelopmental disorders using the Navigation Guide methodology,” 24 ENVT’L HEALTH 56 (2025) [Prada]

[9] Prada Review at 38.

[10] Notes of Testimony from Deposition of Andrea Baccarelli, In re Acetaminophen ASD-ADHD Prods. Liab. Litig., Case No. 1:22-md-03043-DLC (Aug. 14, 2023).

[11] Azeen Ghorayshi, Trump Issues Warning Based on Unproven Link Between Tylenol and Autism, N.Y. TIMES (Sept. 22, 2025), available at https://www.nytimes.com/2025/09/22/health/kennedy-autism-tylenol-trump.html?searchResultPosition=2

[12] Statement from Andrea Baccarelli on X (Sept. 22, 2025), available at https://x.com/RapidResponse47/status/197023187271541578.

[13] Id.

[14] Jon Hamilton, Yuki Noguchi & Nell Greenfieldboyce, Trump blames Tylenol for autism. Science doesn’t back him up, NAT. PUBLIC RADIO (Sept. 22, 2025) (quoting Dr. Bauer), available at https://www.npr.org/sections/shots-health-news/2025/09/22/nx-s1-5550153/trump-rfk-autism- tylenol-leucovorin- pregnancy#:~:text=Many%20physicians%20and%20autism%20advocacy,studies%20in%20the %20scientific%20literature.%22

[15] Jeff Mason, Ahmed Aboulenein, and Julie Steenhuysen, Trump Links Autism to Tylenol and Vaccines, Claims Not Backed by Science, REUTERS (Sept. 22, 2025) (quoting Britain’s health regulator as saying that using paracetamol was safe and that there is no evidence paracetamol caused autism in children; quoting Coalition of Autism Scientists as stating that “[t]he data cited do not support the claim that Tylenol causes autism … .”) available at https://www.reuters.com/business/healthcare-pharmaceuticals/trump-expected-link-autism-with-tylenol-experts-say-more-research-needed-2025-09-22/; Brianna Abbott & Andrea Petersen, The Trump administration said acetaminophen could cause autism. Doctors maintain it is safe during pregnancy, WALL ST. J. (Sept. 22, 2025) (“Doctors and medical societies say acetaminophen, the active ingredient in Tylenol, remains the best option for treating fever and pain during pregnancy”), available at https://www.wsj.com/politics/policy/tylenol-pregnancy-autism-trump-report-what-to-know-2873d8e1; Will Weissert, Dr. Trump? The president reprises his COVID era, this time sharing unproven medical advice on autism, ASSOC. PRESS NEWS (Sept. 23, 2025), available at https://apnews.com/article/trump-doctor-vaccines-autism-tylenol-covid-disinfectants-22f5bcfe2fd3c18fdd412419941541f8; Editorial Board, ‘I’m not a doctor’: This shoddy autism science helps no one; President Donald Trump’s rant on vaccines and Tylenol has no basis in fact, WASH. POST (Sept. 22, 2025), available at https://www.washingtonpost.com/opinions/2025/09/22/trump-autism-vaccines-tylenol-acetaminophen/; Vivian Ho & Karla Adam, WHO joins global health leaders rejecting U.S. acetaminophen warnings; The World Health Organization is the latest to criticize claims from President Donald Trump and Robert F. Kennedy Jr. linking autism to Tylenol use during pregnancy, WASH. POST (Sept. 24, 2025), available at https://www.washingtonpost.com/health/2025/09/24/paracetamol-acetaminophen-tylenol-autism-who-trump/; Ariana Eunjung Cha, Matt Viser & Dan Diamond, As Trump ties Tylenol to autism, doctors raise alarms; U.S. officials will issue a warning label for pregnant individuals — a move that contradicts the guidance from the major medical societies, WASH. POST (Sept. 23, 2025), available at https://www.washingtonpost.com/health/2025/09/22/tylenol-autism-trump-announcement/

[16] American College of Medical Toxicology, ACMT Position Statement: ACMT Supports the Safe Use of Acetaminophen in Pregnancy (Sept. 23, 2025), available at https://www.acmt.net/news/acmt-position-statement-acmt-supports-the-safe-use-of-acetaminophen-in-pregnancy/

[17] European Medicines Agency, Use of paracetamol during pregnancy unchanged in the EU (Sept. 23, 2025), available at https://www.ema.europa.eu/en/news/use-paracetamol-during-pregnancy-unchanged-eu

[18] Medicines & Healthcare Products Regulatory Agency, MHRA confirms taking paracetamol during pregnancy remains safe and there is no evidence it causes autism in children (Sept. 23, 2025), available at https://www.gov.uk/government/news/mhra-confirms-taking-paracetamol-during-pregnancy-remains-safe-and-there-is-no-evidence-it-causes-autism-in-children.

[19] Autism Science Foundation, Statement on White House Announcement on Autism (Sept. 22, 2025), available at

https://autismsciencefoundation.org/press_releases/asf-statement-wh-briefing/.

[20] Ali Swenson & Lauran Neergaard, “Trump makes unfounded claims about Tylenol and repeats discredited link between vaccines and autism,” ASSOC. PRESS (Sept. 23, 2025) (quoting Prof. Caplan), available at https://apnews.com/article/tylenol-cause-autism-trump-kennedy-0847ee76eedecbd5e9baa6888b567d66

[21] Karoline Leavitt, “FACT: Evidence Suggests Link Between Acetaminophen, Autism,” WHITE HOUSE (Sept. 22, 2025), available at https://www.whitehouse.gov/releases/2025/09/fact-evidence-suggests-link-between-acetaminophen-autism/

[22] Sara Moniuszko & Céline Gounder, Dr. Oz says “of course” pregnant women should take Tylenol if a doctor says so (Sept. 26, 2025), available at https://www.cbsnews.com/news/dr-oz-says-of-course-pregnant-women-should-take-tylenol-if-a-doctor-says-so/

[23] Martin A. Makary, Notice to Physicians on the Use of Acetaminophen During Pregnancy, (Sept. 22, 2025) (emphasis added), available at https://www.fda.gov/media/188843/download?attachment=&utm_medium=email&utm_source=govdelivery

[24] FDA News Release, FDA Responds to Evidence of Possible Association Between Autism and Acetaminophen Use During Pregnancy (Sept. 22, 2025), available at https://www.fda.gov/news-events/press-announcements/fda-responds-evidence-possible-association-between-autism-and-acetaminophen-use-during-pregnancy.

[25] Informed Consent Action Network, Citizen Petition regarding safety-related labeling changes for the use of over-the-counter acetaminophen drug products during pregnancy, (Sept. 22, 2025), available at https://static01.nyt.com/newsgraphics/documenttools/88fe67f3f222ab88/66655cc8-full.pdf

[26] Christina Jewett, Kennedy’s Ties to Ally Leading Vaccine Lawsuits Raise Ethical Concerns, N.Y. TIMES (Oct. 3, 2025), available at https://www.nytimes.com/2025/10/03/health/kennedy-aaron-siri-vaccines-lawsuits.html

[27] Andrea Baccarelli, Rule 26 Witness Report, In re Acetaminophen ASD-ADHD Prods. Liab. Litig., Case No. 1:22-md-03043-DLC (Oct. 10, 2023), uploaded to Internet Archive on Sept. 16, 2025, available at https://archive.org/details/baccarelli-expert-report-acetaminophen-asd-adhd.

[28] Office of Texas Attorney General, Press Release: Attorney General Paxton Sues Big Pharma Manufacturers for Deceptively Marketing Tylenol to Pregnant Mothers Despite Known Dangers to Unborn Children (Oct. 28, 2025) (emphasis added), available at https://www.texasattorneygeneral.gov/news/releases/attorney-general-paxton-sues-big-pharma-manufacturers-deceptively-marketing-tylenol-pregnant-mothers.

[29] Panola County, TX Voting, available at https://www.bestplaces.net/voting/county/texas/panola.

Acetaminophen – No Cure for Bad Jurisprudence – Part 1

July 28th, 2026

INTRODUCTION

Two weeks ago, the Second Circuit reversed the summary judgment entered by Judge Denise Cote, in the acetaminophen autism litigation. Judge Cote had excluded the plaintiffs’ expert witnesses on causation, under Rule 702, in a lengthy, careful opinion that found numerous deviations from the standard of scientific care by the challenged witnesses.[1] Rule 702 of the Federal Rules of Evidence cried out for application, especially subparts (b), (c), and (d):

(b) the testimony is based on sufficient facts or data;

(c) the testimony is the product of reliable principles and methods; and

(d) the expert’s opinion reflects a reliable application of the principles and methods to the facts of the case.

The Second Circuit, in an opinion by Judge Guido Calebresi, held that Judge Cote abused her discretion with respect to the most important of the plaintiffs’ witnesses.[2] Judge Calebresi’s opinion in turn failed to engage meaningfully with the science of causation, and abused both the facts and the law to reach its conclusions. Judge Calebresi cited opinions discredited by the 2023 amendment to Rule 702, and he failed to engage with the legal requirements of that amendment and controlling decisions of the Supreme Court.

The errors in Judge Calebresi’s opinion are symptomatic of a deep confusion between causation and precautionary policy. This confusion is prevalent in litigation and regulation, and it even infects what purport to be purely scientific determinations, such as the carcinogenicity determinations of the International Agency for Research on Cancer.[3] To appreciate the depth and extent of Judge Calebresi’s errors requires exploring the scientific record and an analysis of the appellate opinion’s errors and omissions.

BACKGROUND

Acetaminophen is a generic medication available for treating pain (analgesic) and fever (antipyretic), without a prescription in the United Sates. The chemical compound, N-acetyl-para-aminophenol (or APAP) was first prepared in 1878, and it was initially used in clinical practice in 1893.  Acetaminophen did not become commercially available in the United States until the 1950s. Starting in 1960, acetaminophen became available to consumers as an over-the-counter medication.[4]

The 1970s marked the discovery of potential harms to both pregnant women and fetuses from mothers’ use of aspirin as an analgesic or antipyretic medication. In the 1980s, scientists suspected that aspirin may cause Reyes syndrome in children.  Because untreated fevers in pregnant women can harm fetuses, including miscarriage and birth defects, fever presents a difficult clinical problem for women and their physicians.[5] Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with miscarriage and birth defects, and opioid pain medications are associated with birth defects and maternal and neonatal addiction.[6] Clinicians have thus considered acetaminophen the preferred analgesic and antipyretic medication for pregnant women because of its consistently reassuring safety profile, and the absence of alternatives.

In December 2021, a group of advocacy scientists published a self-proclaimed consensus that precautionary action should be taken to restrict the use of acetaminophen by pregnant women.[7] The authors included advocacy scientist Shanna Swan, who was a protagonist on behalf of plaintiffs in notorious litigations involving silicone gel implants[8] and bendectin, and David Kriebel, a zealous proponent of the precautionary principle.[9] Swan and co-authors manifestly did not conclude that the available scientific evidence supported a causal inference between maternal acetaminophen use and their children’s autism. Instead, the authors asserted a precautionary policy approach that acetaminophen “be used by pregnant women cautiously at the lowest effective dose for the shortest possible time.”[10] Although the authors appropriately stopped short of causal conclusions, they incoherently argued that they had a “professional and social responsibility” to argue for precaution “even in the face of uncertainty, in light of the serious consequences of inaction.”[11] Given that they were addressing an uncertain and undetermined causal nexus, the authors had no warrant for suggesting that there would be any benefits from their recommendations or any untoward consequences from their having taken no action at all.

The pretense of the self-proclaimed consensus was dispelled by spirited dissent in response to the Call for Precautionary Action. One letter to the editor chided the precautionists for their misleading analysis.[12] Another letter highly critical of the faux consensus, was submitted by 50 or so signatories, including members of the Organization of Teratology Information Specialists, the Society of Birth Defects Research and Prevention, and Anthony R. Scialli, a past president of the Teratology Society, and founder and editor-in-chief of the journal Reproductive Toxicology.[13]

The American College of Obstetricians and Gynecologists (ACOG) issued a strongly worded rebuttal statement to highlight that the precautionists had not cited any clear evidence to show that acetaminophen use during any trimester causes fetal developmental issues.[14] ACOG reiterated its identification of acetaminophen as the only safe analgesic and antipyretic medication for pregnant women. ACOG further pointed out that despite the fear-mongering language of the Call for Precautionary Action, ACOG’s clinical guidance has long emphasized that medications in pregnancy should be used only when needed, in moderation, and in consultation with physicians. Indeed, the Food & Drug Administration already required that all over-the-counter medications intended for systemic absorption, including acetaminophen, be labeled: “If pregnant or breast-feeding, ask a health professional before use.”[15] At best, the precautionists had not managed to say anything important; at worst, they had stoked serious and unnecessary anxiety and concern among families and their physicians.

The precautionists also stoked the lawsuit industry. True to form, that industry was unfazed by the lack of certainty and the inability to infer causation even by the advocacy scientists who called for precautionary action.  Within a few months of the 2021 opinion piece, the lawsuit industry started to file complaints, and the mass of litigation quickly led to consolidation and transfer to the Southern District of New York, for coordinated pre-trial procedures as a multi-district litigation (MDL).[16] A mass tort was born without scientific support for actual causation between the product and the harm, autism and other neurocognitive impairments.

Unsurprisingly, given the fragile and indeterminate scientific record on causation, the defense moved to exclude the plaintiffs’ causation expert witnesses, pursuant to Rule 702, at the close of discovery. Finding that the plaintiffs’ expert witnesses’ testimony failed to evidence a reliable application of epidemiologic method to reach the proffered conclusions, the district court excluded the challenged testimony,[17] and in August 2024, the district court dismissed over 500 cases in the MDL.[18]

(to be continued)


[1] In re Acetaminophen ASD-ADHD Prods. Liab. Litig., 707 F. Supp. 3d 309 (S.D.N.Y. 2023). Judge Cote addressed the admissibility of an additional expert witness in a subsequent opinion. In re Acetaminophen – ASD-ADHD Prods. Liab. Litig., 2024 WL 6 3874183 (S.D.N.Y. Aug. 20, 2024).

[2] Rutledge v. Walgreen Co., Nos. 24-916-cv(L), 24-1121(Con), 24-2360(Con); 24-2594-cv, Slip Op. (2nd Cir. July 13, 2026), available at https://scholar.google.com/scholar_case?case=13067399726798054350&q=rutledge+v.+walgreen&hl=en&as_sdt=2006.

[3] See Nathan Schachtman, IARC’s Precautionary Science: How the WHO Cancer Research Agency Misinforms Regulation and Litigation, Wash. Legal Found. Monograph (2026), available at https://www.wlf.org/wp-content/uploads/2026/04/WLF-Precautionary-Science-monograph.pdf

[4] Laurie F. Prescott. Paracetamol: past, present, and future, 7 AM. J.  THERAPEUTICS 143 (2000).

[5] See, e.g., Stephanie Antoun, Pierre Ellul, Hugo Peyre, Michelle Rosenzwajg, Pierre Gressens, David Klatzmann & Richard Delorme, Fever during pregnancy as a risk factor for neurodevelopmental disorders: results from a systematic review and meta-analysis, 12 MOLECULAR AUTISM 60 (2021).

[6] Rachela Smith &  Jonathan S. Zipursky, Safety of acetaminophen use in pregnancy: review of existing evidence, 8 AM. J. OBSTET. & GYN. 101925 (2025).

[7] Ann Z. Bauer, Shanna H. Swan, David Kriebel, Zeyan Liew, Hugh S. Taylor, Carl- Gustaf Bornehag, Anderson M. Andrade, Jørn Olsen, Rigmor H. Jensen, Rod T. Mitchell, Niels E. Skakkebaek, Bernard Jégou & David M. Kristensen, Paracetamol use during pregnancy — a call for precautionary action, 17 NATURE REV. ENDOCRINOL. 757 (2021). [Call for Precautionary Action]

[8] See Judge Jack B. Weinstein, Preliminary Reflections on Administration of Complex Litigation, 2009 CARDOZO L. REV. de novo 1, 14 (2009) (describing plaintiffs’ expert witnesses in silicone litigation as “charlatans”; “[t]he breast implant litigation was largely based on a litigation fraud. … Claims—supported by medical charlatans—that enormous damages to women’s systems resulted could not be supported.”).

[9] See, e.g., David Kriebel, Joel Tickner, Paul Epstein, John Lemons, Richard Levins, Edward L. Loechler, Margaret Quinn, Ruthann Rudel, Ted Schettler & Michael Stoto, The Precautionary Principle in Environmental Science, 109 ENVT’L HEALTH PERSP. 871 (2001).

[10] Call for Precautionary Action at 764.

[11] Call for Precautionary Action at 763 (emphasis added).

[12] Joseph O’Sullivan, Alexandra E. Cairns, Elena Plesca, Rebecca S. Black, Charlotte Frise, Manu Vatish and Ana Sofia Cerdeira, Paracetamol use in pregnancy — neglecting context promotes misinterpretation, 18 NATURE REV. ENDOCRINOL. 385 (2022) (noting that the Swan review, in the absence of conclusive evidence, was propagating a scare that acetaminophen use in pregnancy was unsafe and should be unduly restricted).

[13] Sura Alwan, Elizabeth A. Conover, Lorrie Harris-Sagaribay, Steven H. Lamm, Sharon V. Lavigne, Shari I. Lusskin, Sarah G. Obican, Alfred N. Romeo, Anthony R. Scialli & Katherine L. Wisner, Paracetamol Use in Pregnancy—Caution Over Causal Inference from Available Data, 18 NATURE REV. ENDOCRINOL. 190 (2022).

[14] American College of Obstetricians and Gynecologists, Response to Consensus Statement on Paracetamol Use During Pregnancy (Sept. 29, 2021), available at https://www.acog.org/news/news-articles/2021/09/response-to-consensus-statement-on-paracetamol-use-during-pregnancy.

[15] 21 C.F.R. § 201.63(a). See also Pregnant or Nursing Women, 47 Fed. Reg. at 54,751.

[16] 28 U.S.C. § 1407

[17] In re Acetaminophen – ASD-ADHD Prods. Liab. Litig., 707 F. Supp. 3d 309 (S.D.N.Y. 2023) (Cote, J.). Additional plaintiffs designated one other expert witness, who succumbed to a later Rule 702 challenge. In re Acetaminophen – ASD-ADHD Prods. Liab. Litig., No. 22md3043 (DLC), 2024 WL 3357608 (S.D.N.Y. Jul. 10, 2024).

[18] In re Acetaminophen – ASD-ADHD Prods. Liab. Litig., No. 22md3043 (DLC), Order & Opinion (Aug. 20, 2024).

The Recrudescence of Ferebee – Part Two

July 1st, 2026

In 2010, almost 30 years after Ferebee was decided, the Solicitor General cited the case in an amicus brief before the Supreme Court case, in Matrixx Iniatives, Inc. v. Siracusano. The case was a securities fraud class action, which was dismissed initially by the trial court on consideration of the defendant’s motion that the complaint failed to allege causation supported by statistically significant studies. The Supreme Court would go on unanimously to reject causation as a criterion for establishing a prima facie case of securities fraud, which made statistical significance irrelevant. Because the FDA could (and later did) require the company to recall its product upon a showing that material evidence suggested that there might be a possible causally induced harm, the Court held that the plaintiff class did not have to allege causation.[1] The harm to the shareholders came in the form of management’s bullish financial projections for a product that was later recalled for safety concerns, even if the recalled product never was shown to cause any harm. The Solicitor General’s amicus brief advanced the Ferebee case as an example of a causal relationship that could be established “through consideration of multiple factors independent of statistical significance.”[2] Although the government’s amicus brief correctly discerned that the causal connection between paraquat exposure and pulmonary fibrosis was established without analytical epidemiologic studies, and the necessary tools of statistical analysis for such studies, the brief mistakenly placed the allegations that Zycam caused anosmia in the same conceptual framework as paraquat. Unlike paraquat toxicity, millions of people used Zycam for relief from cold and flu symptoms, and the alleged harm, anosmia, commonly occurs in the aftermath of colds and flu. The Zycam personal injury claims fared poorly in litigation because of the dearth of supportive evidence that was appropriate to support causation, as opposed to materiality in securities law.[3]

The Ferebee case correctly observed that epidemiology was not necessary to establish the causal claim involving paraquat dermal exposure and lung toxicity and fibrosis. At the time that Mr. Ferebee sustained extensive paraquat exposure as a result of his governmental employer’s extreme negligence, the scientific community fully accepted that paraquat exposure, by ingestion, inhalation, or dermal exposure caused systemic toxicity and deleterious lung effects. This “general causation” had been established by case reports and case series, along with studies of paraquat’s metabolic fate and distribution in humans and non-human animals (including non-human primates), and assessment of mechanistic effects in cells and tissues of the target organs affected by paraquat when it became systemically distributed in the human body.

About the time of the Ferebee litigation, a textbook on agricultural chemicals described the toxic effects of dipyridyl compounds in humans, including paraquat:

“Human Toxicology Experience: A considerable amount of clinical experience has been reported in the literature with over 100 cases of illness and/or death. The chemical is unique in the sense that there is not only an acute toxicity syndrome but, in addition, it has the ability to produce a delayed fibroblastic response in the lungs. The latter is usually the principal mechanism of death.

For industrial workers, paraquat is not considered very dangerous. Inhalation hazard is extremely low due to the low vapor pressure of the chemical. Nevertheless, protective respiratory equipment should be used particularly when other atmospheric contamination might occur. * * * On no occasion should an applicator be allowed to walk through drifting spray.” [4]

This textbook cited studies that suggested that dermal and respiratory exposure to paraquat did not appear to be a hazard to field applicators, despite the demonstration of absorption, as long as precautions against overexposure are taken.[5] The premise of the textbook discussion, that appropriate, well-known safety measures and protective gear are employed, was an important part of its analysis.

This early textbook discussion also flagged delayed lung fibrosis as the main problem caused by all modes of paraquat exposure, including dermal absorption:

“Although the acute symptoms of paraquat intoxication are of concern and are dangerous, the principal problem relates to the unique delayed manifestations of this chemical’s ability to produce a fibroblastic change in the lung which begins a number of days after absorption. * * * Experiments then found that it was possible to induce respiratory failure as a result of both dermal and aerosol routes of absorption (Newhouse, 1978).”[6]

An early review by the World Health Organization also emphasized that paraquat exposure was not expected to pose a health risk as long as safe work practices are followed:

“Occupational exposure to paraquat does not pose a health risk if the recommendations for use are followed and there is adherence to safe working practices.

                   *     *     *

In the small number of reported cases of paraquat poisoning allegedly resulting from occupational exposure, the cause can be identified as one or a combination of a number of factors, viz contamination of the skin with concentrated products, use of inadequately diluted solutions, use of faulty equipment, misuse of equipment (e.g., blowing blocked spray jets) or failure to take action in the event of contamination of skin or clothing.”[7]

Cases of dermal exposure to undiluted paraquat (20%), especially when exposure involved dermal exposure to the scrotum, can produce serious systematic toxicity.[8]

Ferebee was not given an appropriate respirator even when exposed to intense atmospheric contamination. He was drenched in paraquat spray, and remained drenched for hours. The gross negligence of his employer ensured that there would not be many similar cases, and that the tools of analytical epidemiology would not be available.[9] Indeed, epidemiology was never involved in determining general causation of paraquat exposure and lung fibrosis. Given that the outcome of interest would likely occur only in the context of negligent or intentional over-exposure, epidemiology will never be available.

Revisiting the Ferebee decision and the unique facts of the case place the decision in a better perspective for judging how courts continue to cite the case. The facts of the case readily distinguish the case, the claimed harm, and the manner of showing causation, from the facts in cancer, birth defects, and other cases where epidemiology is essential. The principle of charity would require the frequently quoted language on expert witness admissibility to be taken as a statement of the appellate standard of review for the jury’s determination of medical causation. Most of the glib characterizations of the Ferebee turn out to be wrong on close inspection of the case.

a. Ferebee was not a precedent under the Federal Rules of Evidence

Chevron’s evidentiary arguments were posed under Maryland law. Neither Rule 702[10] nor Rule 703[11] was ever mentioned in the district court or the Court of Appeals decisions.

b. Ferebee does not support a false distinction between scientific and legal causation.

In a later Bendectin birth defects case, Richardson v. Richardson-Merrell, Inc., the Court of Appeals struggled to distinguish Ferebee and its holdings based upon the ample epidemiologic evidence involving Bendectin. The Court mischaracterized Ferebee as not pertinent because it was on the “frontier of current medical and epidemiological inquiry.”[12] The Richardson court was impressed by the 20 years of research on Bendectin, including multiple epidemiologic studies. Unfortunately, the court was apparently ignorant of the irrelevance of epidemiology to the Ferebee case, and the extensive research base for determining the lung toxicity of paraquat. This ignorance seems to have resulted from Judge Mikva’s generalizations and overstatements of the paucity of evidence in Ferebee.

c. Ferebee does not support the false distinction between scientific and legal certainty.

Courts and commentators have attempted to explain the result in Ferebee by invoking what is largely a false distinction between scientific and legal certainty (or sufficiency). The Ferebee decision itself provided the ammunition by asserting a distinction between the requirements of scientific and legal decision making:

“In a courtroom, the test for allowing a plaintiff to recover in a tort suit of this type is not scientific certainly but legal sufficiency.”[13]

This was a common approach in distinguishing Ferebee, in the Bendectin litigation,[14] but it was picked up and promulgated by scientists and legal commentators.[15] Invoking this alleged distinction has become a common rhetorical move to excuse inadequate or insufficient evidence to support an expert witness’s causation opinion in litigation. The generalization from the facts of Ferebee to all scientific and legal questions of causation was wrong from the inception, and citations to a single case, Ferebee, cannot make those generalizations true.[16]

d. Ferebee did not establish the irrelevance or the dispensability of epidemiologic evidence in cancer or birth defects cases.

The Ferebee case observed that “a cause-effect relationship need not be clearly established by animal or epidemiological studies before a doctor can testify that in his opinion such a relationship exists.”[17] The bit about animal studies certainly cannot be part of the holding because the plaintiffs’ expert witnesses relied extensively on animal studies, along with human case reports, and human clinical studies of the metabolic fate and distribution of paraquat in both animals and humans.

The Ferebee case does properly stand for the proposition that there is a subset of all health effect cases for which epidemiologic evidence is unavailable and unnecessary for an expert witness to have for a valid conclusion of general and specific causation. The case illustrates how the ill effects of paraquat were observed shortly after exposure, and were sufficiently unique to not have a meaningful base- or background- rate. Adding the studies of absorption, metabolic fate and distribution, and mechanism of action, the plaintiff’s expert witnesses had an ample scientific, and legal, basis to assess causality. 

The Ferebee case is sometimes mistakenly thought of as a cancer case, which would have required epidemiologic evidence.[18] This mistake may well result from later courts citing Ferebee in cancer cases, for the proposition that epidemiologic evidence is unnecessary to support plaintiff’s causal claim between some exposure and some cancer. Perhaps the Illinois Supreme Court has provided the most egregious example of this sort of mistake. In Donaldson, a case involving plaintiff’s exposure to coal tar and his later development of neuroblastoma, the Court confusedly found Ferebee to be “of particular significance.”[19] The Donaldson court affirmed the trial court’s admission of plaintiffs’ expert witness testimony about “a causal link causal link despite the lack of a statistical number of others with neuroblastoma and a history of coal tar exposure.”[20] The court rambled on about how the plaintiffs were not required to prove general or specific causation “with 100% certainty that neuroblastoma.” This assertion was a common strawman argument that channels a misreading of Ferebee. The defense in Donaldson did not argue that 100% certainty was required, and such a level of posterior probability has never been required in law or in science.

The Ferebee case also did not establish that statistical significance was not required in epidemiologic studies for expert witnesses to be able reasonably to rely upon such studies. Because epidemiologic evidence was not at issue, there was no holding about epidemiologic studies or statistical significance as a criterion of the validity of such studies.

e. Ferebee did not establish that a clinician can opine about causation without sufficient facts and data.

One of plaintiff’s expert witnesses in Ferebee was Dr. Crystal, who was both a physician and a research scientist. His opinion as an expert witness was hardly without supporting facts and data, and the facts and data were of the exact kind that led to the scientific acceptance of the causal connection between some paraquat exposures and lung fibrosis. Crystal’s opinion was certainly not proffered without any evidentiary basis, as some have suggested.[21] Nor was Ferebee a case in which expert witnesses opined without facts and data to support unprecedented opinions on general and specific causation.[22]

This overwrought, over-extended interpretation of Ferebee as permitting causation opinions based upon only clinical observations of the patient appeared in the first edition of the Reference Manual on Scientific Evidence, but disappeared in all subsequent editions. In the chapter by evidence law professor Margaret Berger, the Manual reported that Ferebee was frequently cited for a “holding that causation can be established by the testimony of treating physicians.”[23] Berger’s observation about frequent citation is correct, but the observation does nothing to validate the opinion cited. Berger offered no comments or analysis in critique of the frequent miscitation of Ferebee, leaving the reader to believe that citing Ferebee for the sufficiency of treating physician opinion without data was somehow appropriate. The citations to which Berger referred were erroneous in 1994, and they remain erroneous today.


[1] Matrixx Iniatives, Inc. v. Siracusano, 563 U.S. 27, 131 S.Ct. 1309, 1320 (2011).

[2] Brief for the United States as Amicus Curiae, in Matrixx Iniatives, Inc. v. Siracusano, No. 09-1156, 2010 WL 4624148, at *15 (Nov. 2010).

[3] See, e.g., Benkwith v. Matrixx Initiatives, Inc., 467 F. Supp. 2d 1316, 1326, 1330, 1332 (M.D. Ala. 2006) (granting defendant’s motion to exclude testimony of an expert in the field of epidemiology regarding Zicam nasal spray’s causing plaintiff’s anosmia, because the opinions had not been tested and a rate of error could not be provided).

[4] Sheldon L. Wagner, CLINICAL TOXICOLOGY OF AGRICULTURAL CHEMICALS 198, 199-200 (1983).

[5] Id. at 200 (citing “[s]tudies by Staiff and co-workers (1975)” on occupationally exposed persons).

[6] Id. at 201. See also A. J. Gardiner, Pulmonary oedema in paraquat poisoning, 27 THORAX 132 (1972).

[7] WORLD HEALTH ORGANIZATION, ENVIRONMENTAL HEALTH CRITERIA 39: PARAQUAT AND DIQUAT at § 1.1.5. Effects on man (1984).

[8] See K. Tungsanga, S. Chusilp, S. Iarasena & V. Sitprija, Paraquat poisoning: evidence of systemic toxicity after dermal exposure, 59 POSTGRAD. MED. J. 338, 338 (1983).

[9] Cf. Zuchowicz v. United States, 140 F.3d 381 (2nd Cir. 1998) (analyzing causation in the context of defendants clear negligence that resulted in undisputed overexposure to prescription medication Danocrine). Unlike Zuchowicz, however, the Ferebee case did provide a strong evidentiary base for causation.

[10] See Kenneth J. Chesebro, Taking Daubert’s “Focus” Seriously: The Methodology/Conclusion Distinction, 15 CARDOZO L. REV. 1745, 1747, 1753 (1994) (misciting Ferebee as a Rule 702 case).

[11] See Alani Golanski, Judicial Scrutiny of Expert Testimony in Environmental Tort Litigation, 9 PACE ENVT’L L. REV. 399, 406-07 (1992) (misrepresenting Ferebee as a case under Rule 703; “this evidentiary issue was resolved through examination of the facts or data underlying the proffered expert opinion only to the extent necessary to make a Rule 703 determination on whether they are of the type reasonably relied upon by experts in the field.”). See also Michael C. McCarthy, “Helpful” or “Reasonably Reliable”? Analyzing the Expert Witness’s Methodology Under Federal Rules of Evidence 702 and 703, 77 CORNELL L. REV. 350, 373 (1992) (discussing Ferebee as a Rule 702 and 703 decision).

[12] Richardson v. Richardson-Merrell, Inc., 857 F.2d 823, 831-832 (D.C. Cir. 1988).

[13] Ferebee, 736 F.2d at 1536.

[14] Id.

[15] Louis Lasagna & Sheila R. Shulman, Bendectin and the Language of Causation, chap. 5, at 111, in Kenneth R. Foster, David E. Bernstein & Peter W. Huber, eds., PHANTOM RISK: SCIENTIFIC INFERENCE AND THE LAW (1993)

[16] See Michael C. McCarthy, “Helpful” or “Reasonably Reliable”? Analyzing the Expert Witness’s Methodology Under Federal Rules of Evidence 702 and 703, 77 CORNELL L. REV. 350, 373 (1992) (“Essentially, the Ferebee decision distinguished between the level of certainty required by a scientific discipline-and the level of certainty required by a court in drawing conclusions regarding causation”: and “Ferebee stands for the proposition that courts, in determining whether a given substance more likely than not caused a plaintiff’s injury, cannot always wait for the sciences.”).

[17] Ferebee, 736 F.2d 1529, 1535 (D.C. Cir. 1984).

[18] David E. Bernstein, The Misbegotten Judicial Resistance to the Daubert Revolution, 89 NOTRE DAME L. REV. 27, 36 (2013); David E. Bernstein, Expert Witnesses, Adversarial Bias, and the (Partial) Failure of the Daubert Revolution, 93 IOWA L. REV. 451, 465 (2008) (“Ferebee involved a claim that exposure to an herbicide caused an individuals’ cancer.”).

[19] Donaldson v. Central Illinois Public Service Co., 313 Ill. App.3d 1061, 730 N.E.2d 68, 79 (2000).

[20] Id.

[21] Lee Loevinger, Evidentiary Framework Margaret A. Berger Reference Manual on Scientific Evidence, 36 JURIMETRICS J. 149, 153 & n.21 (1996) (discussing the before (Daubert) times when “mere qualification and the facial relevance of an opinion might suffice to let an expert testify in some jurisdictions.”).

[22] See Kenneth J. Chesebro, Taking Daubert’s “Focus: Seriously: The Methodology/Conclusion Distinction, 15 CARDOZO L. REV. 1745, 1747 & n.20 (1994) (incorrectly arguing that Ferebee involved an expert witness offered an “unprecedented expert factual conclusion which no published literature supported.”

[23] See Margaret A. Berger, Evidentiary Framework, 39, 81 & n.164, in FEDERAL JUDICIAL CENTER, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE (1st ed. 1994).

The Recrudescence of Ferebee – Part One

June 29th, 2026

The infamous Ferebee decision is certainly a contender to be a Dred Scott decision involving scientific evidence,[1] by declaring that science has no validity issues that the law is bound to respect.[2] The decision is often cited for its dictum, written with impressive rhetorical flourish, about how courts should not interfere with expert witness opinion testimony. The dictum, when written in 1984, was contrary to the law of Federal Rule of Evidence 702, and was relegated in 1993 to the trash bin of jurisprudential history by the Supreme Court’s 1993 decision in Daubert.[3]

Since 1993, scofflaw judges continued to cite Ferebee’s discredited dictum, without looking at the specific facts of the case. Indeed, even after Rule 702 was amended to clarify its meaning, courts have cited Ferebee as precedential for a let-it-all-in approach to expert witness testimony. As recently as February 2026, the Chief Judge of the Federal Circuit, of the United States Court of Appeals, cited Ferebee in derogation of Federal Rule of Evidence 702.[4] This recrudenscence of Ferebee warrants revisiting the case, what was actually decided, and whether it has any continuing jurisprudential relevance.

The Ferebee case was a personal injury case against the manufacturer of paraquat, a herbicide, for damages for severe pulmonary fibrosis. Interestingly, the case is sometimes erroneously cited as a cancer causation case, which may explain why some commentators criticize its dismissal of epidemiology and statistical significance.

Critics of Ferebee, as well as its acolytes, rarely describe the factual context of the case. The facts of a case are always germane to its holding, and Ferebee cannot be cited appropriately without a sane appreciation of its facts.

  1. Ferebee is a government negligence case.

The plaintiff worked for the federal government when he was exposed to paraquat. Richard Ferebee began working for the Department of Agriculture’s Beltsville Agricultural Research Center (BARC), in Beltsville, Maryland. He started spraying paraquat in the summer of 1977, and used the herbicide regularly through the time he was diagnosed with pulmonary fibrosis, in November 1979.[5] Mr. Ferebee sued Chevron Chemical Company, the supplier of the paraquat, for failing to warn. The important failure to warn, however, was committed by the federal governmental, which had actual knowledge of the hazard, and which owned the BARC facility, employed Ferebee, controlled and supervised his use of paraquat, and failed to comply with Chevron’s instructions. The federal government itself further regulated the sale and use of paraquat extensively, first by the Department of Agriculture, and later by the Environmental Protection Agency. [6]

  1. The exposure.

Ferebee filed his lawsuit in 1981; he died in 1982. His case was tried twice. In the first trial, the jury deadlocked. In the second trial, the jury returned a verdict in favor of his estate, and for his family, for $60,000. In his deposition testimony, Ferebee described how he sprayed paraquat, in the summer of 1977. The chemical was diluted for use, per Chevron’s instructions. There was no evidence that Ferebee ever had direct contact with undiluted paraquat, or that the paraquat he was exposed to was not diluted according to the proportions recommended on Chevron’s label.[7]

Crediting Ferebee’s testimony, the federal government was at best grossly negligent; at worst, the government was an intentional tortfeasor. In flagrant disregard of Chevron’s written instructions (as required by federal regulation), Ferebee frequently had the chemical on his ungloved hands.[8] Ferebee further described an occasion when he was drenched with paraquat as he walked behind a tractor that was spraying the chemical, and another incident when he used a defective sprayer that leaked paraquat “all over his pants.”[9]

On the occasions of Ferebee’s being exposed to paraquat without appropriate protective gear, the federal government deviated from its employer common law, statutory, and regulatory duties. Ferebee did not wash when he was dermally exposed to paraquat, and he went home contaminated, where he fell asleep, tired and dizzy, without showering.[10]  The exposure that Ferebee described would not have occurred had his federal employer followed the instructions on the label that the government itself mandated. In 1978, the federal Occupational Health & Safety Administration published Guidelines on the need for protective clothing, respirators, immediate washing of contaminated skin. Ferebee’s federal governmental employer recklessly disregarded the guidelines it mandated that Chevron provide.

  1. The warnings.

Paraquat could be sold in the United States only when labeled in accordance with EPA regulations, promulgated pursuant to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA).[11] The statute bars EPA from allowing sale of regulated herbicides, such as paraquat, unless the chemicals, as labeled, will not cause “unreasonable adverse effects on the environment.”[12] Such effects are in turn defined as any unreasonable risk to man or the environment, taking into account the economic, social, and environmental costs and benefits of the use of [the] pesticide.[13] FIFRA further requires the EPA to require labeling that is “adequate to protect health and the environment” and that is “likely to be read and understood.”[14]

In the Ferebee case, both the district and the circuit courts failed to provide the complete warning label and the material data safety sheets that Chevron supplied to the federal government employer, as required by the federal government. There are “snippets” of the warning communications in the published opinions, which make clear that the government was largely if not entirely to blame for failing to comply with the directions required under FIFRA. For instance, the district court, in a footnote, acknowledged:

“For example, the label advised the user spraying paraquat to wear waterproof clothing and goggles, to avoid working in spray mist, and to wash splashes on the skin or eyes immediately with water.”[15]

The Court of Appeals Ferebee opinion described the label,[16] as stating a warning in large bold letters:

DANGER

CAN KILL IF SWALLOWED

HARMFUL TO THE EYES AND SKIN

The label also informed users to wash any exposed areas immediately, and to remove contaminated clothing.[17]

  1. The Stipulation.

Essential to understanding the holding in Ferebee are the facts of the case, including the parties’ stipulation:

“that Mr. Ferebee’s only significant exposure to paraquat was on his intact skin; i.e., there was no evidence that Mr. Ferebee swallowed or inhaled paraquat, or that he spilled or sprayed it on an area of his skin upon which he had any apparent cuts or scrapes. The jury was not, of course, precluded from concluding that a person engaged in Mr. Ferebee’s line of work could have had some, or even many, minor cuts or abrasions not readily discernible to the naked eye or likely to be remembered some time later.”[18]

Why did the plaintiffs try to present their case solely as a dermal exposure cases? As we will see, this stratagem made their medical causation case a little more difficult, but it avoided defenses of serious misuse and lack of proximate cause. Ferebee had been instructed by his co-workers and supervisors that paraquat was extremely dangerous if swallowed or inhaled. The warning label was unequivocal in detailing the dangers and the need to avoid ingestion. (Without the full label, it is difficult to evaluate how well the label warned against inhalation, but the 1978 OSHA guidelines address the use of a proper respirator for situations in which paraquat may be inhaled.) On the other hand, the label had a weakness, which could be exploited, as long as the preemption defense could be held at bay: the label urged protective clothing, goggles, and immediate washing of contaminated skin, but it failed to describe the consequence of dermal exposure other than irritation. Ferebee could thus try to avoid his own culpable conduct, as well as a sophisticated intermediary defense, by claiming that his exposure was only dermal.

Why did Chevron agree to the stipulation? Ferebee surely had some inhalational exposure when he walking behind applicators and when he was drenched in paraquat. The Chevron warning label, per government-employer regulations, did not specify respirator usage for ordinary work exposures of applicators (as opposed to workers who handled undiluted paraquat, or who worked in confined spaces). The defendant probably felt sanguine about its preemption defense, and thus also about the adequacy of its warnings overall. The stipulation limited the plaintiff’s medical causation case to a route of exposure that put it into an arguable “first instance” case report. Chevron stood to gain a claim of “lack of notice,” and thus lack of actual or constructive knowledge of the risk of lung disease from dilute dermal exposure. The clinical presentation itself differed from many of the cases of known paraquat poisoning, and Chevron probably believed that it could deal with the medical causation claim better if exposure was limited to transdermal absorption on unbroken skin.

  1. Medical causation

Chevron stridently argued that there had been no previous documented cases of pulmonary fibrosis in workers exposed to diluted paraquat on unbroken skin. The manufacturer’s argument was clever by halves.  The following facts were uncontroverted as known at the time of Chevron’s sale of the product:

  • Paraquat causes pulmonary fibrosis in humans.
  • The evidence that established paraquat as a cause of pulmonary fibrosis was largely case series of acute onset of pulmonary fibrosis after ingestion.
  • Paraquat induces pulmonary fibrosis relatively rapidly.
  • Paraquat can be absorbed through the skin.
  • The parties agreed that any type of exposure – ingestion, inhalation, or dermal absorption – could cause lung damage.[19]
  • Once paraquat is ingested, inhaled, or absorbed, it can travel to the lungs.
  • Lung fibrosis caused by dermal absorption of paraquat had been described previously only with skin lesions before or after the injury.[20]
  • The lungs are the target organ for paraquat, regardless of route of administration.
  • There are numerous causes of pulmonary fibrosis (such as asbestosis, scleroderma, rheumatoid arthritis, etc.).
  • The variants of pulmonary fibrosis do not all look alike clinically or pathologically, present alike, or progress alike.
  • Ferebee had no known other disease or exposure that could account for his pulmonary fibrosis.
  • There are cases of pulmonary fibrosis with no identifiable cause, known as idiopathic pulmonary fibrosis (IPF).
  • IPF is relatively rare; it too has a rapid onset and progression, although arguably not as fast as the cases described after exposure to undiluted paraquat.
  • Ferebee’s medical history was largely unhelpful in explaining his clinical course.
  • Ferebee had some shortness of breath before starting to use paraquat.[21]
  • Ferebee used or was exposed to paraquat occasionally over three years before he was diagnosed with pulmonary fibrosis.

These stipulated facts are rarely acknowledged in the discussion of the Ferebee case. The legal implications of these facts are far reaching. General causation in a sense was not contested. Paraquat causes pulmonary fibrosis. The issue was whether diluted paraquat through dermal exposure over three years causes pulmonary fibrosis, and whether this exposure caused Ferebee’s pulmonary fibrosis. Chevron stridently asserted that the “scientific method” required controlled experimental or observational (epidemiologic) studies. The problem with Chevron’s position was that general causation had already been established, and not by analytical epidemiologic studies. General causation between paraquat exposure of any kind and pulmonary fibrosis had been established by case reports, based upon close temporal proximity between exposure and pulmonary toxicity and fibrosis. Animal toxicology and mechanistic studies confirmed the toxicity observed in clinical studies.[22]

Because idiopathic pulmonary fibrosis is rare, the appearance of this disease in a series of exposed workers soon after they were exposed to a specific toxic chemical really did not require the rigors of analytical epidemiology. The causal analysis between paraquat and lung fibrosis was more akin to the analysis that is used to attribute liver failure to herbal exposure than the epidemiologic approach to the relationship between smoking and lung cancer. At the time of Ferebee’s exposure and his litigation, there was no serious dispute that paraquat caused pulmonary fibrosis when inhaled or swallowed, or that paraquat was absorbed dermally, or that the lung was a target organ of paraquat exposure of any sort.

  1. The expert witnesses.

Ferebee was initially treated by Dr. Muhammed Yusuf, a pulmonary specialist, who diagnosed pulmonary fibrosis. Dr. Yusef referred Ferebee to the National Institutes of Health (NIH), where he came under the care of Dr. Ronald G. Crystal of the Heart, Lung, and Blood Institute. (Dr. Crystal is now Chairman of Genetic Medicine at Weill-Cornell Medical College, where he continues to practice pulmonary medicine.)

In the litigation, Chevron called Dr. Carrington, who diagnosed Ferebee with idiopathic pulmonary fibrosis. Dr. Carrington challenged the plaintiffs’ expert witnesses’ opinions for lacking reliance upon controlled observational or experimental studies.[23] Dr. Carrington, however, acknowledged that dermal cases are too rare for observational epidemiologic analysis, but emphasized that no animal studies of sufficient size had been done to support plaintiffs’ hypothesis. Chevron also called a Dr. Fisher, who presented a toxicokinetic (TK) analysis of Ferebee’s dermal absorption. Based upon his TK analysis, Dr. Fisher concluded that the maximal amount of paraquat absorbed by Ferebee was too small, based upon known cases and animal studies, to have caused paraquat toxicity with lung fibrosis.[24]

  1. Chevron’s challenge to plaintiffs’ expert witnesses’ causation opinion.

None of the defendant’s expert witnesses examined Ferebee. The courts thought this was relevant, but the judicial opinions never articulated what would have been observed on physical examination that was important to resolving the differential diagnosis of paraquat toxicity versus IPF. There was no dispute that Ferebee had rapidly progressing pulmonary fibrosis. The expert witnesses on both sides evaluated Ferebee’s clinical data, presentation, clinical course, and arrived at different diagnoses, either paraquat-induced lung fibrosis or IPF. The plaintiffs’ expert witnesses’ diagnosis involved a causal attribution to paraquat exposure; the defendant’s expert witness’s diagnosis of IPF ruled out any causal toxic exposure.

The Ferebee case was litigated under Maryland law because federal statutory law requires state law to control in a wrongful death action arising out of the neglect or wrongful act of another on a federal enclave.[25] The choice of law had implications both for procedural and substantive law. Chevron appears to have relied upon Maryland’s articulation of the Frye general acceptance doctrine, and the courts analyzed Chevron’s arguments as a Frye challenge.[26] Under the Erie doctrine, a federal court should have applied its own procedural law to the case at hand, including Rule 702 of the Federal Rules of Evidence.[27] The use of Maryland law to determine an evidentiary issue in federal court was error.

Chevron pressed its challenge in terms of Maryland’s version of Frye, and not under Federal Rule of Evidence 702. The oft-repeated infamous language used by both the district and the circuit courts was, therefore, not an interpretation of federal law. Rule 702 was never cited or discussed in either the trial or the appellate court’s opinion. This oddity has profound implications for how we evaluate the Ferebee decision, and how it can be cited. Before the Supreme Court decided the Daubert case, the epistemic implications of Rule 702 were largely ignored. Defendants sometimes attempted to press the Frye twilight-zone general acceptance test into a rule of decision that would reject an expert witness’s opinion testimony.[28] The Frye case was decided by a federal appellate court, but superseded by the enactment of Rule 702, in 1975. Ferebee was, of course, decided before the Supreme Court breathed life into Rule 702, but Rule 702 was nonetheless the law when the Ferebee case was litigated.

  1. The judicial resolution of  Chevron’s Frye challenge

The district court insightfully recognized that Chevron was demanding a level of evidence, which had never been required to establish paraquat’s generally accepted ability to cause pulmonary fibrosis. This recognition led to the district court’s rhetorical language:

“It is true that medical expert testimony must be grounded in proper scientific methodology, but the extremely stringent standard that defendant suggests is beyond reason. Product liability law, especially as it relates to relatively new products or those with a relatively rare yet significant danger, would be rendered next to meaningless if a plaintiff could prove he was injured by a product only after a ‘statistically significant’ number of other people were also injured. A civilized legal system does not require that much human sacrifice before it can intervene. The fact that this is the first case of this exact type – or at least the first of its exact type in which the involvement of paraquat was discovered by alert doctors – cannot be enough by itself to shield defendant from liability. Defendant’s experts were not able to fault Dr. Crystal for his basic diagnostic methodology; in fact, they used the same kinds of test results, consultations, and other tools that he did. What they disagreed with chiefly were his conclusions.”[29]

The important observation is that general causation had been established case series and reports of human exposure. There never was statistical evidence that had been evaluated for “significance,” to establish general causation for undiluted paraquat, and the trial court refused, under Maryland law, to require such evidence for general causation for diluted paraquat. In this context, we can see that the trial court’s suggestion that statistical significance was not required has little bearing upon cases in which general causation could only be established using epidemiologic evidence, with its attendant statistical inferences.

Of course, the matter only became worse when Chevron persisted in its argument and presented it to a panel of the D.C. Circuit. The litigants pulled a panel of what can be described as activist judges not known for their scientific acumen. Judge Mikva wrote the opinion for a panel that included Judge Wald, and Senior Judge Bazelon. The panel’s decision ratcheted up the district court’s rhetoric:

“Thus, a cause-effect relationship need not be clearly established by animal or epidemiological studies before a doctor can testify that, in his opinion, such a relationship exists. As long as the basic methodology employed to reach such a conclusion is sound, such as use of tissue samples, standard tests, and patient examination, product liability does not preclude recovery until a ‘statistically significant’ number of people have been injured or until science has had the time and resources to complete sophisticated laboratory studies of the chemical. In a courtroom, the test for allowing a plaintiff to recover is not scientific certainty, but legal sufficiency; if reasonable jurors could conclude from the expert testimony that paraquat more likely than not caused Ferebee’s injury, the fact that another jury might reach the opposite conclusion or that science would require more evidence before conclusively considering the causation question resolved is irrelevant. That Ferebee’s case may have been the first of its exact type, or that his doctors may have been the first alert enough to recognize such a case, does not mean that the testimony of those doctors, who are concededly well qualified in their fields, should not have been admitted.”[30]

Judge Mikva’s dichotomy between levels of certainty needed in science and in the law was false. On behalf of the plaintiff, Dr. Crystal had done much more than give a clinical diagnosis. His assessment of causality was informed by case series of exposure and lung fibrosis, along with physiological evidence of oral, inhalational, and dermal absorption and distribution to the lungs, with toxic effect soon after exposure.

The appellate court’s dismissive attitude towards statistically significant evidence is severely limited to the factual context of a causal analysis that had been made by scientists, to everyone’s satisfaction, for undiluted paraquat, without the need for epidemiologic, statistical evidence. Statistical significance was never really at issue. In this way, Ferebee resembles the untoward dictum on statistical significance from Matrixx Initiatives Inc. v. Siracusano,[31] where the Court held that causation was not at issue.

In Ferebee, causation was very much at issue, but it had been well established – and the subject of warnings – based upon clinical case reports of paraquat exposure and rapid development of lung fibrosis. Dermal absorption and systemic distribution with toxic effects in the lungs were well established, and not the stuff of epidemiologic proofs.

In both Ferebee and Matrixx Initiatives, statistical significance was never really at issue. In Ferebee, there was no statistical evidence needed or used to reach causal conclusions about paraquat’s ability to induce pulmonary fibrosis. In Matrixx Initiatives, allegations of statistical significance and causation were not necessary because the plaintiffs needed only to allege materiality of the facts suppressed by the company in order to plead a securities fraud case. The FDA could impose warnings or require a product recall on evidence that fell well short of establishing causality. Materiality thus could be established without causation, and neither causation nor statistical significance needed to be alleged.

As for Chevron’s Frye challenge, the district court rejected the implied call for a vote on the general acceptance of Dr. Crystal’s reasoning. Frye may require “vote counting” of some sort, but the process becomes irrelevant when virtually no one has registered to vote. Otherwise, both the defense and plaintiffs’ expert witnesses were indeed using the same technique of arguing by analogy to accepted cases of paraquat poisoning or IPF. Dr. Crystal opined that Ferebee’s case was “similar” to three other cases he had identified. Dr. Carrington argued that Ferebee’s case was more like IPF cases, although IPF cases themselves have some clinical heterogeneity as well. Most reported paraquat cases described onset of toxicity to death as a very rapid process. Ferebee did not present with significant symptoms for three years after his first exposure, and then he survived for another two plus years. Ferebee did not report skin lesions, which had been reported in previous cases of dermal exposure leading up to pulmonary fibrosis. On the other hand, there was no precise exposure assessment for Ferebee’s absorption of paraquat. The case presented, on the diagnostic level, with the implied causality, a difficult call, but it is easy to understand the courts’ impatience with the defendant’s insistence upon more stringent criteria and evidence than was used to establish the causal connection with undiluted paraquat. The ability of paraquat to cause pulmonary fibrosis had been well established based upon case reports, including case reports of dermal exposure to open sores, with documented systemic distribution with specific toxicity to the lung, regardless of the route of administration.

  1. Expert witness qualifications.

Chevron never challenged Dr. Yusuf’s or Dr. Crystal’s qualifications, both of whom were highly accomplished and respected clinicians and scientists. Neither was a “hired gun.” The oft-quoted comments about expert witness qualifications were made in the context of describing the appellate court’s standard of review, and the court’s role in not assessing credibility or weighing the evidence:

“These admonitions apply with special force in the context of the present action, in which an admittedly dangerous chemical is alleged through long-term exposure to have caused disease. Judges, both trial and appellate, have no special competence to resolve the complex and refractory causal issues raised by the attempt to link low-level exposure to toxic chemicals with human disease. On questions such as these, which stand at the frontier of current medical and epidemiological inquiry, if experts are willing to testify that such a link exists, it is for the jury to decide whether to credit such testimony.”[32]

Remarkably, this language has been mistakenly invoked as a standard for trial courts to use in determining the admissibility of expert witness opinion testimony. It is no such thing. Some other observations are in order. Although Ferebee worked with diluted paraquat, his exposures were hardly low level. He described himself as drenched in the herbicide, without protective gear, and without his governmental supervisors ever directing him to shower and change clothing.

  1. Preemption and Warnings Causation.

Ultimately, Chevron’s preemption defense was rejected by both the district and the circuit court. The defense’s claim of FIFRA preemption might have gone very differently today, after the Supreme Court’s decisive application of preemption to FIFRA labeling of glyphosate.[33]

Even more important in evaluating liability is the emphasis that both the district and the appellate courts gave to the important role of the employer in the case. The evidence showed that there was indeed a warning label that Ferebee had never read. The plaintiff’s case was thus in jeopardy of failing to show proximate causation between an allegedly inadequate warning and harm. The courts, however, emphasized the role that the employer, through its supervisors and responsible co-workers, play in the complex organizational situation of a modern workplace:

“Mr. Ferebee’s situation was quite different, however. He did not purchase paraquat for his personal use; rather, it was provided to him by his employer for use on the job. The evidence showed that his principal source of information about paraquat was the oral instructions of his supervisors and co-workers, not the written label. He learned from them how to mix the product and how to spray it. It was also from this source that he learned of the danger of getting the product in his mouth: one of his co-workers warned him that if he accidently swallowed paraquat, it would ‘get in his blood’ and poison him. This is a common pattern of instruction and use of occupational materials in the workplace. Learning by doing and learning by oral instruction are tried and true methods of educating manual workers in their jobs. Therefore, although it is crucial to plaintiff’s case that someone would have read the label, it was not necessary for Mr. Ferebee to have done so. And it is obvious that one or more employees at BARC did read the label, since information did reach Mr. Ferebee about the proportions for diluting the product and about the dangers about which the label did warn. It was appropriate for the jury to infer that a warning about the danger of fatal lung disease from dermal exposure would also have been communicated to Mr. Ferebee. See Restatement (Second) of Torts § 388 comment n (seller normally entitled to assume that adequate warning will be passed on by purchaser to ultimate user); cf. Chambers v. G.D. Searle & Co., 441 F.Supp. at 381 (in product liability case involving prescription drug, relevant warning is the one given to doctor, not patient).”[34]

There is significant irony in that the Ferebee case has been the subject of serious criticism from defense counsel, and yet it embraced Section 388, comment n, as well as applied the learned or sophisticated intermediary principles to a case not involving prescription drugs. The appellate court waxed enthusiastic about the principles of Section 388, and went so far as to cite the late Victor Schwartz in support:

“We live in an organizational society in which traditional common-law limitations on an actor’s duty must give way to the realities of society. *** In this case, Mr. Ferebee did not purchase the paraquat for his personal use, and there was substantial evidence that workplace communication about the dangers associated with various chemicals usually took the form of oral instructions from supervisors to workers, the latter of whom then retransmitted the information to co-workers. This, rather than individual reading of product warnings, is a typical method by which information is disseminated in the modern workplace. See Schwartz & Driver, “Warnings in the Workplace: The Need for a Synthesis of Law and Communication Theory,” 52 U. Cinn. L. Rev. 38, 66-83 (1983). The requirement that an improper warning proximately ‘cause’ the injury should be elaborated against this background. We believe Maryland would construe its tort law in this case to require only that someone in the workplace have read the label, not that Mr. Ferebee personally have read it. Because there is no dispute that one or more employees at BARC did read the label, we hold that the jury could properly have inferred that, had a warning about the danger of disease from dermal exposure been included on the label, that warning would have been communicated to Mr. Ferebee and that he would as a result have acted differently. Alternatively, the jury could have inferred that an adequate warning would have led Ferebee’s employers to undertake steps that would have protected him from paraquat poisoning-for example, provision of showers for use after spraying.”[35]

Judge Mikva’s prediction, of course, was accurate; Maryland tort law did, soon thereafter, embrace the sophisticated intermediary defense to exculpate the defendant in such remote supplier situations.[36] The principle invoked to excuse plaintiff from reading the warning label also works to exculpate the defendant when that warning label is otherwise adequate, or when the intermediary knows of the hazard in any event. Given that the employer was the federal government, including the scientists at EPA, OSHA, the National Institutes of Health, and the Public Health Service, as well as the plaintiff’s principal expert witness (Dr. Crystal), the employer had complete and superior knowledge to the seller about the known or knowable effects of diluted paraquat.[37]


[1]  Nathan Schachtman, Wells v. Ortho Pharmaceutical Corporation -A Dred Scott Case in Science Jurisprudence, ResearchGate (June 2026); DOI: 10.13140/RG.2.2.30242.18880

[2] Ferebee v. Chevron Chem. Co., 552 F. Supp. 1297 (D.D.C. 1982), aff’d, 736 F.2d 529 (D.C. Cir.), cert. denied, 469 U.S. 1062 (1984).

[3] Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993).

[4] Willis Electric Co., Ltd. v. Polygroup Ltd., 166 F. 4th 1363, 1379, 1380-81 (Fed. Cir. 2026) (citing Ferebee, and declaring that the validity of assumptions underlying an expert witness’s methodology were fact questions for the jury, and not a a proper basis for excluding the challenged expert witness testimony). See also Barry v. DePuy Synthes Cos., 164 F.4th 896, 912 (Fed. Cir. 2026) (characterizing expert witness challenges to “purported flaws” in methodology as objections that “go to the weight the jury might accord to that evidence and not to its admissibility.”)

[5] Ferebee, 736 F.2d at 1531-32.

[6] Id. at 1532.

[7] 552 F. Supp. at 1295 & n. 3.

[8] Ferebee, 552 F. Supp. at 1294-95

[9] Ferebee, 736 F.2d at 1532.

[10] Id.

[11] 7 U.S.C. § 136, et seq.

[12] 7 U.S.C. § 136a(c)(5)(C).

[13] 7 U.S.C. § 136(bb).

[14] 7 U.S.C. § 136(q)(1)(E). See Ferebee 736 F.2d at 1539-40.

[15] 552. F. Supp. at 1304 n.40.

[16] Ferebee, 736 F.2d at 1536.

[17] Id.

[18] 552. F. Supp. at 1295 & n. 3.

[19] Ferebee, 552. F. Supp. at 1300 & n.28.

[20] Ferebee, 736 F.2d at 1538.

[21] Ferebee, 552. F. Supp. at 1295.

[22] See generally Leah Utyasheva, Prabath Amarasinghe & Michael Eddleston, Paraquat at 63 – the story of a controversial herbicide and its regulations: It is time  to put people and public health first when regulating paraquat, 25 BMC PUB. HEALTH 3089 (2025).

[23]  Ferebee, 552. F. Supp. at 1301.

[24] Id.

[25] 16 U.S.C. § 457; Ferebee, 736 F.2d at 1533.

[26] Ferebee, 552 F. Supp. at 1301; 736 F.2d at 1535.

[27] Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 589 & n.6 (1993). See also Cavallo v. Star Enterprise, 100 F.3d 1150, 1157-58 (4th Cir. 1996); Amorgianos v. National Railroad Passenger Corp., 303 F.3d 256 (2d Cir. 2002); Legg v. Chopra, 286 F.3d 286, 289-92 (6th Cir. 2002). See Erie R.R. Co. v. Tompkins, 304 U.S. 64 (1938); Hanna v. Plumer, 380 U.S. 460, 470 (1965) (Erie does not displace the application of federal procedural rules in federal courts).

[28] Frye v. United States, 293 F. 1013, 1014 (D.C.Cir.1923).

[29] Ferebee, 552 F. Supp. at 1301.

[30] Ferebee, 736 F.2d at 1535-36 (emphasis in original).

[31] 563 U.S. 27 (2011). See Nathan Schachtman & David Venderbush, Matrixx Unbounded:  High Court’s Ruling Needlessly Complicates Scientific Evidence Principles, 26(4) WASH. LEG. FDTN. LEG. BACKGROUNDER (2011).

[32] Ferebee, 736 F.2d at 1534.

[33] Monsanto v. Durnell, ___ U.S. ___, Slip op. (June 25, 2026), available at https://www.supremecourt.gov/opinions/25pdf/24-1068_n7ip.pdf

[34] Ferebee, 552 F. Supp. at 1303-04 (internal citations omitted).

[35] Ferebee, 736 F.2d at 1539 (emphasis in original; internal citation omitted).

[36] See, e.g., Kennedy v. Mobay Corp., 84 Md. App. 397 (1990) (applying sophisticated user defense to bar claims against manufacturers of toluene diisocyanate), aff’d, 325 Md. 385 (1992); Higgins v. E.I. DuPont de Nemours, Inc., 671 F. Supp. 1055 (D. Md. 1987) (Maryland law; holding that manufacturer of paint was in better position than bulk supplier to communicate warnings to customers’ employees), aff’d, 863 F.2d 1162 (4th Cir. 1988).

[37] See Miller v. Diamond Shamrock Co., 275 F.3d 414, 422-23 (5th Cir. 2001) (“There can be no reasonable dispute that knowledge possessed by the United States Public Health Service, … [and] the Navy’s Bureau of Medicine and Surgery is the knowledge of the military.”).

The American Public Health Association – Lawsuit Industry Affiliate

June 14th, 2026

Over a decade ago, I wrote a post about the American Public Health Association (APHA) and its position papers opposing the Daubert regime of gatekeeping the validity of expert witness opinion testimony. I am updating the post, with some modifications, because the links to the APHA documents are broken. It appears that the APHA now keeps its meeting minutes and policy position statements as secrets for the cognoscenti, and so I have uploaded documents that once were publicly available to document the APHA’s tepid relationship with science.

The APHA was once a significant organization committed to the improvement of public health. The Association has many thousands of members, and it engages in the pretense that it represents the entire public health community. Among its many activities, the APHA publishes a journal, the American Journal of Public Health

Here is how the APHA described itself and its activities, in 2014, to advance public health:

“The American Public Health Association champions the health of all people and all communities. We strengthen the profession of public health, share the latest research and information, promote best practices and advocate for public health issues and policies grounded in research. We are the only organization that combines a 140-plus year perspective, a broad-based member community and the ability to influence federal policy to improve the public’s health.”

How could anyone be against the APHA? Let’s see.

The mission statement currently on the APHA’s website has added the ultimate social justice adjective, “equitable,” and emphasized the association’s advocacy roles:

“We champion optimal, equitable health and well-being for all. We speak out for public health issues and policies backed by science. We are the only organization that combines a 150-year perspective, a broad-based member community and the ability to influence federal policy to improve the public’s health.”

Somewhere along the way, the association was commandeered by revolutionaries who remade it in the “Spirit of 1848.[1]” The APHA evolved into a tool of the lawsuit industry and its putative scientist allies. In 2004, after several years of lobbying, agents of the lawsuit industry managed to push a policy statement past the Association’s leadership, to condemn the requirement of evidence-based reasoning in federal courts in the United States. The APHA has since proven itself an enemy of good science on many fronts.

The success of the lawsuit industry’s influence was dutifully memorialized in the “Final Minutes of Meetings of the APHA Governing Council,” held in November 2004. The lawsuit industry’s attack on evidence-based science and data transparency, known as “Policy Number: 2004-11 Threats to Public Health Science,” was adopted as an official APHA policy statement.

APHA 2004-11” was published in an American Journal of Public Health newsletter, but is now available only to members on the APHA website, as Policy Number: 2004-11:  Threats to Public Health Science. I have excerpted contentions and recommendations from the APHA policy, in the left column of the chart, below. The policy statement is typical of what comes out of precautionary principle NGOs and groups such as the Collegium Ramazzini, and passed off for scientific commentary. The APHA policy is parsed in the left-hand column; my comments to quoted language are in the right-hand column.

APHA Policy Comment
“Acknowledging that within science, absolute proof and perfect information are rare;” Note the false dichotomy between absolute proof and perfect information and the entire remaining spectrum of scientific information.  This dichotomization has been part of the litigation strategy of passing off hypotheses, preliminary conclusions, unreplicated findings, etc., as though they were acceptable bases for causal conclusions.
“Recognizing that special interests have exploited the nature of science, specifically scientific uncertainty, to delay protective legal and/or regulatory action;”  

Note the asymmetry of the accusations; the APHA apparently has no concern for the “special interests” that exploit science by passing off hypotheses as conclusions, and seeking to accelerate protective legal and regulatory action by manufacturing faux scientific consensuses and conclusions.

“Acknowledging that some public health decisions must be made in the absence of perfect scientific information;”  

Le mieux est l’ennemi du bien.” But isn’t the good also the enemy of the shabby, dodgy, and fraudulent? Note again the false dichotomy between “perfect” information and everything else, as though our failing to achieve the perfect opens the door to the worst. True, of course, that sometimes action is needed on incomplete records, but such action is rarely needed for compensation claims.

“Recognizing that special interests, under the guise of a call for “sound science” have sponsored and promoted changes in public policy that have weakened and continue to threaten public health protections;”  

If the call for sound science cannot be sustained, then this rhetorical gambit will blow back hard on those “special interests.”  Why are these putative scientists, at APHA, so afraid of sound science?

“Recognizing that special interests have challenged highly regarded public health research and researchers, and inappropriately characterized established scientific methods as ‘junk science’;”  

Mon Dieu! Highly regarded by whom? How cheeky of those special interests.  See the discussion of Dr. Barry S. Levy, below. Of course, special interests from the folks at Green Peace, and EWG, etc., are welcome. The claim that the challenges are inappropriate is a mere conclusion without evidence.

“Recognizing that the Daubert decision has propagated misinterpretations and misapplications of scientific principles relied upon throughout the public health sciences, such as insisting that any epidemiologic study that is relied on to support causation demonstrate a twofold increase in risk as well as a reliance on significance testing to determine which scientific findings are to be allowed as evidence;”  

This contention seriously misrepresents the basic nature of evidence law. Studies, whether they have statistically significant results, or not, are rarely admissible in evidence.  What is admissible, or not, are the opinions of duly qualified expert witnesses, who explain and show the epistemic warrant for their opinions.  With respect to general causation opinions, expert witnesses will often have to show, among other things, that they have relied upon studies that have ruled out chance, bias, and confounding to arrive at a causal conclusions.  Significance testing can be abused, in both directions, but the APHA ignores the need for having some quantitative assessment of  random variability and error. As for relative risks greater than two, the APHA is correct that general causation may often be found with small relative risks, but the attribution of causation in an individual claimant often can be made only on probabilistic inferences that will require relative risks greater than two, or even larger.

“Recognizing that special interests are engaged in a campaign to extend Daubert’s reach to those states that have not embraced prescriptive definitions of scientific reliability.”  

The APHA makes common cause with the rent-seeking and special pleading of “special interests” that would abolish all limits on the admissibility of expert witness opinions, and all normative assessments of scientific research. This position ignores the prescriptive aspect of methodology, and the nature of epistemic warrant in a methodology.

What follows from these contentions? 

“Therefore, APHA:”

“Opposes legislation or administrative policies that attempt to define the characteristics of valid public health science, or dictate prescriptive scientific methodologies; and”  

Admittedly, defining good science is very difficult, but the law often works like science as defining health as the absence of disease.  There are obviously some well-known pathologies of scientific method, and it hardly seems extravagant to urge courts to avoid flaws, fallacies, and fraud.  

“Supports the efforts of other scientific organizations to promote the government’s ability to utilize the best available science to protect the public’s health; and”  

Of course, sometimes the “best” available science is rather shabby. The science will only protect public health if it is valid and supports valid causal inferences.

“Urges friend of the court briefs that address the problem inherent in the adoption of Daubert and Daubert-like court rulings, the application of Daubert in regulatory proceedings, and when judges misinterpret scientific evidence in their implementation of the Daubert ruling.”  

There are no instances of the APHA’s deploring jury verdicts that offend scientific sensibilities; and so the APHA’s urging here is one-sided and partisan.  The fact, however, that judges’ misinterpretations of scientific evidence can be criticized publicly is one of the key differences that separates judicial gatekeeping from the black box of jury determinations.

In 2005, the APHA published, in its journal, APJH, a special supplement, “Scientific Evidence and Public Policy,” with

“academic analysis of the conflicts arising in the use of science in regulatory, civil and criminal proceedings. This special issue examines how recent developments in the legal and regulatory arenas have emboldened corporations involved in civil litigation and regulatory proceedings to accuse adversaries of practicing ‘junk science’.”

Apparently, the APHA was not, and is not, concerned with the emboldening the lawsuit industry and its efforts to subvert the truth-finding function of civil litigation. 

David Michaels served as the guest editor for the APJH special supplement.  Michaels repeated many of the contentions of the 2004 Policy Statement, above, and in an introductory essay,[2] he added some new dubious assertions:

  • Judges are no better than juries in assessing scientific evidence.
  • Scientists evaluate all the evidence by applying a “weight-of-the-evidence” approach.
  • Uncertainty in science is normal and does not mean the underlying science flawed.

These are all serious half truths.  Many judges are quite astute when evaluating scientific evidence, but even the lowest aptitude judges must give articulated reasons for their decisions, which opens up a public process of comment, correction, and criticism.  Juries vote in secret, without having to explain or justify their verdicts. Judges can review the actual studies relied upon; juries never read the entire studies that are cited by expert witnesses. The collective judgment of juries can, on occasion, be more insightful than that of a single judge. Juries can also be more emotive and less analytical than judges, and they can be seduced by the hyperbolic rhetoric, and evidence-free claims. It seems obvious what aspects of the jury system are being endorsed by the APHA.

Scientists, metaphorically speaking, weigh evidence, as do non-scientists, but this opaque metaphor hardly explicates the process of how scientists arrive at conclusions about causal relationships.  And uncertainty is a condition of many scientific fields, but the error lies in trying to pass off tentative, uncertain, preliminary observations and findings as knowledge.

Michaels sees the development of judicial gatekeeping as favoring “the powerful,” and hurting “the weak and vulnerable.”[3]  Michaels showed no compunction with having his editorial recommendations favoring the lawsuit industry and undermining the truth.  Michaels was the head of the Occupational Health & Safety Administration, where he squandered his tenure with a shambolic rulemaking on silica, which did little actually to protect workers.

As for self-righteousness, Michaels’ special issue of the American Journal of Public Health was itself funded by corrupt interests. Michaels and the APHA described the funding for the special AJPH supplement:

“Support for the supplement was provided through unrestricted funding to the Project on Scientific Knowledge and Public Policy (SKAPP) from the Common Benefit Litigation Trust, a fund established by court order in the Silicone Gel Breast Implant Products Liability Litigation. SKAPP is an initiative of scholars that examines the application of scientific evidence in the legal and regulatory arenas. SKAPP is based at the George Washington University School of Public Health and Health Services; more information is available at  www.DefendingScience.org.”[4]

This pseudo-disclosure provides a window of discovery into the fraudulent aspect of the entire APHA enterprise.  The Common Benefit Trust was a fund that was held back from settlement monies paid by defendants in the silicone gel breast implant litigation.  The Trust was nothing more than the Plaintiffs’ Steering Committee’s war chest, and “walking-around-money,” from which it could advance litigation goals within MDL 926 (silicone breast implant cases).  Ironically, the appointment of neutral, court-appointed expert witnesses led to the success of “sound science,” and the collapse of the plaintiffs’ counsel house of cards.  Rather than returning their litigation expense fund to the claimants, the plaintiffs’ counsel diverted the funds to an illegitimate recipient, SKAPP, to advance their litigation goals, not for MDL 926, but for the next MDL, and the next, and the next….[5]  

                                     * * * * * * *

The same year that the APHA published the SKAPP-inspired and funded challenges to Federal Rules of Evidence 702, the APHA awarded its most prestigious award, the Sedgwick Medal, to Barry S. Levy, a physician whose opinions had routinely been found to be unreliable and irrelevant in various litigation industry efforts.[6]

Perhaps the APHA had Levy in mind when it complained that “special interests have challenged highly regarded public health … researchers….”  Dr. Levy seems to have less favorable accolades from trial and appellate judges.[7]  For instance, one federal judge found Levy engaged in a dubious enterprise to manufacture silicosis claims in Mississippi.[8] Interestingly, Judge Jack’s opinion was not mentioned in the APHA press release for Dr. Levy’s award ceremony.

                                     * * * * * * *

The APHA is still at it. The July 2026 issue of the American Journal of Public Health features articles on ultra-processed foods and public health. The association, in its website, describes the issue as “[a] curated collection of peer-reviewed research on the health impacts of ultraprocessed food consumption, food marketing, regulatory policy, and community-level interventions.”[9] The casual observer will no doubt detect that this issue is a one-sided presentation of advocacy positions, including a sop to the lawsuit industry about how litigation is necessary to challenge the food industry’s “toxic practices.”[10] The APHA has become an unserious politicized organization, which contributes to the erosion of trust in science and scientists.


[1] See APHA, Spirit of 1848 Caucus, available at https://www.apha.org/apha-communities/caucuses/spirit-of-1848-caucus.

[2] David Michaels, Editorial: Scientific Evidence and Public Policy, 95 (Supp. 1) AM. J. PUB. HEALTH S5 (2005).

[3] Id.

[4] This press release had been available at the APHA website <http://www.apha.org/about/news/pressreleases/2005/05arenas.htm>, last visited on February 10, 2014, but alas is no longer available. The press release, Is Public Health Science Being Derailed in the Legal and Regulatory Arenas (July 20, 2005), is available here.

[5] See Schachtman, SKAPP A LOT, TORTINI (April 30, 2010), available at https://schachtmanlaw.com/2010/04/30/skapp-a-lot/; and Conflicted Public Interest Groups, TORTINI (Nov. 3, 2013), available at https://schachtmanlaw.com/2013/11/03/conflicted-public-interest-groups/.

[6]Barry Levy Wins APHA’s Oldest and Most Prestigious Award, the Sedgwick Medal.” APHA News (Dec 11, 2005). This newsletter is no longer online, but the Wikipedia entry for the Sedgwick medal shows Levy as the 2005 recipient. Sedgwick Medal, in WIKIPEDIA, available at https://en.wikipedia.org/wiki/Sedgwick_Memorial_Medal.

[7] See Schachtman, Silica Litigation: Screening, Scheming & Suing; Washington Legal Foundation Critical Legal Issues Working Paper Series No. 135 (Dec. 2005) (exploring the ethical and legal implications of the entrepreneurial litigation in which Levy and others were involved). See also Lofgren v. Motorola, Inc., 1998 WL 299925, No. CV 93-05521 (Ariz. Super. Ct., Maricopa Cty. June 1, 1998); Harman v. Lipari, N.J. L. Div. GLO-L-1375-95, Order of Nov. 3, 2000 (Tomasello, J.) (barring the opinions of B.S. Levy in a class action for medical monitoring damages); Castellow v. Chevron USA, 97 F. Supp. 2d 780, 793-95 (S.D. Tex. 2000); Knight v. Kirby Inland Marine Inc., 482 F.3d 347 (5th Cir. 2007); Watts v. Radiator Specialty Co., 990 So. 2d 143 (Miss. 2008); Aurand v. Norfolk So. Ry., 802 F. Supp.2d 950 (2011); Mallozzi v. Ecosmart Technologies, Inc., 2013 WL 2415677, No. 11-CV-2884 (SJF) (ARL) (E.D.N.Y. May 31, 2013).

[8] .  In re Silica Products Liability Litigation, 398 F. Supp. 2d 563, 611-16, 622 & n.100 (S.D. Texas 2005) (expressing particular disappointment with Dr. Barry Levy, who although not the worst offender of a bad lot of physicians, betrayed his “sterling credentials” in a questionable enterprise to manufacture diagnoses of silicosis for litigation).

[9] See Ultraprocessed Food Section, AM. J. PUB. HEALTH online, available at https://ajph.aphapublications.org/ultraprocessedfoodssection.

[10] See Jennifer L. Pomeranz & Kelly D. Brownell, Litigation as a Necessary Tool to Challenge Food Industry’s Toxic Practices, AM. J. PUB. HEALTH, published online on June 3, 2026, at https://ajph.aphapublications.org/doi/10.2105/AJPH.2026.308539.

IARC & the Reference Manual on Scientific Evidence

May 12th, 2026

Given the outsized role that IARC can sometimes take in litigation and regulation, lawyers and judges should pay some attention to, and give some critical thought about, how the Reference Manual on Scientific Evidence addresses IARC’s classifications and evaluations of putative carcinogens.

The Reference Manual is published by the Federal Judicial Center and the National Academies of Science, Engineering and Medicine to remedy the gaps and defects in the knowledge base of judges who must conduct trials and gatekeep expert witness opinion testimony on scientific issues. The third edition of the Reference Manual on Scientific Evidence was published in 2011; a fourth edition was released in the still of the night on the last day of the last month of 2025. Given the imprimatur of its publishers, the Reference Manual can be influential. Whether its influence is deserved or warranted is very much a matter of debate.

Without any citation support or analysis, the third edition of the Reference Manual accorded IARC undeserved honorifics and accolades. Various chapters of the third edition referred to IARC as “well-respected and prestigious,” “well regarded,” and “reputable.”[1]

The late Professor Margaret Berger, in her opening chapter of the third edition, misleadingly characterized IARC’s review processes as “not review[ing] each scientific study individually for whether it reliably supports the causal claim being advocated or opposed.”[2] Berger’s chapter was published after her death, and it cited cases that were decided after her death. The error noted above cannot be fully attributed to her; as with the posthumous case references, other parts of her chapter may have been introduced gratuitously by an overzealous editor. The gist of the mistaken representation of IARC’s process, made without any reference to the Preamble, is, however, consistent with Professor Berger’s lifetime publications.

Berger’s peculiar, erroneous take on the IARC process appears to accord with her personal belief that courts should not look at the validity of individual studies. According to the Preamble, however, IARC’s working groups are very much supposed to review individual epidemiologic studies for whether they reliably report an association, or animal studies for whether they support a causal interpretation (for the animals in the study).[3]

The new, fourth edition of the Reference Manual[4] continues the tradition of giving IARC a higher regard than the evidence would warrant. The new edition’s chapter on toxicology, for instance, carries forward the characterization of IARC as “respected.”[5] Readers will have a difficult time of what to make of the chapter’s approbation, when the same toxicology chapter references IARC in connection with its discussion of risk assessments, even though IARC most decidedly does not conduct risk assessments.[6] Readers of the Manual may ask whether the authors of the Manual have any idea of what they are saying.

The toxicology chapter engages in some special pleading for animal evidence to remain within the scope of evidence for human health effects. In the context of cancer causation, this chapter points to IARC as a source for justifying the use of animal evidence, and even high-exposure, maximum-tolerated dose, rodent studies as evidence for human carcinogenicity.[7] Not surprisingly, the chapter glibly avoids addressing difficult questions about extrapolating from non-primate studies to conclusions of human carcinogenicity.

What is perhaps more unsettling is that the toxicology chapter epistemically trespasses upon the epidemiology chapter in order to settle a grievance of one of the toxicology chapter’s authors.[8] One of the toxicology chapter’s authors, Bernard Goldstein, fellow of the Collegium Ramazzini, was an expert witnesses for plaintiffs in a case that went up to the highest court in New York State, Parker v. Mobil Oil,[9] which affirmed the exclusion of Goldstein’s testimony. Footnote 37 in the toxicology chapter attempts to offer a defense of Goldstein’s litigation opinions in a way that hardly does justice to the decision of the New York Court of Appeals. More disturbing is that the chapter never discloses that Goldstein, one of the chapter’s authors, was a partisan expert witness in the Parker case. At the time Parker was decided, gasoline was an IARC 2B (“possible”) human carcinogen. Within a few years, in what may have been the result of advocacy groups, IARC reconsidered gasoline and bumped it up two categories to group 1, speaking through a working group that appeared to lack balance and credibility.[10]

Turning to the Manual’s epidemiology chapter,[11] we find again an uncritical and unscholarly description of IARC monographs as “well regarded,” and an assertion that courts “generally recognize” IARC monographs as “authoritative.”[12] The authors offer no support for the former claim. In support of their latter assertion, the chapter cites to a rather dubious appellate decision, which affirmed a trial court’s ruling that an expert witness was permitted to reference the IARC 2A classification of glyphosate in his testimony.[13] The case cited by the Manual never held that the IARC monograph at issue was “authoritative”; indeed, the court never used the word authoritative at all. The two law professor authors of the epidemiology chapter know, or should know, that “authoritative” is a term of art in the law of evidence. Federal Rule of Evidence 803(18), for instance, makes statements made in a so-called learned treatise admissible in evidence if “established as a reliable authority.” The glyphosate case cited by the Manual never suggested that there had been a determination that the glyphosate IARC monograph, or the IARC classification of glyphosate, was a reliable authority. There is a fair amount of learned opinion that IARC badly bungled its evaluation of glyphosate.

IARC did, in fact, controversially, classify glyphosate as 2A, or “probably carcinogenic” to humans.  “Probably,” as used and defined in the key IARC document, the Preamble,[14] has no quantitative meaning according to IARC.  A more accurate translation into common parlance would have us say that IARC classified glyphosate as “very possibly” carcinogenic to humans. The Manual’s chapter on epidemiology failed to cite the actual Preamble. Instead, the authors cited to a poster that fails to give the relevant definitions.[15] This abridgement distorted the presentation of IARC ideas, such as they are, and thwarted critical scrutiny of the IARC process.

The epidemiology chapter affirmatively misrepresents the work of IARC working groups and their classifications by describing IARC as convening working groups and asking them to reach “consensus” on carcinogenicity. In fact, the working group, and its subgroups, treat a bare majority as sufficient.[16] The Manual also describes IARC as employing a “weight-of-the-evidence” approach, a descriptor so subjective and vague as to be unfalsifiable.

There are many reasons that IARC monographs and classifications should not be well regarded. For a fuller discussion of those reasons, see the recent paper published by the Washington Legal Foundation, on IARC’s Precautionary Science: How the WHO Cancer Research Agency Misinforms Regulation and Litigation.[17]


[1] National Academies of Science, Engineering & Medicine and Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE at 20, 564 n.46, 646 (3d ed. 2011).

[2] Margaret A. Berger, The Admissibility of Expert Testimony, in REFERENCE MANUAL, id.

[3] IARC MONOGRAPHS ON THE IDENTIFICATION OF CARCINOGENIC HAZARDS TO HUMANS – PREAMBLE (2019) [cited herein as Preamble], https://perma.cc/LJE4-K7HH

[4] National Academies of Sciences, Engineering, and Medicine & Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE (4th ed. 2025) (cited as RMSE 4th ed.).

[5] David L. Eaton, Bernard D. Goldstein, & Mary Sue Henifin, Reference Guide on Toxicology, 1027, 1045, in RMSE 4th ed.

[6] Id. at 1036 (citing Hardeman v. Monsanto Co., 997 F.3d 941 (9th Cir. 2021) for its affirmance of a lower court’s allowing an expert opinion to rely upon and discuss at trial the IARC classification, not its risk assessment, of glyphosate as a “probable carcinogen”).

[7] Id. at 1044.

[8] Id. at 1044 n. 37.

[9] Parker v. Mobil Oil Corp., 7 N.Y.3d 434, 857 N.E.2d 1114 (2006).

[10] Craig DillardJohn Kalas, “IARC Classifies Gasoline As a Human Carcinogen – Litigation May Follow,” Nelson Mullins (April 15, 2025).

[11] Steve C. Gold, Michael D. Green, Jonathan Chevrier, & Brenda Eskenazi, Reference Guide on Epidemiology 897, in RMSE 4th ed.

[12] Id. at 919 n. 68.

[13] Hardeman v. Monsanto Co., 997 F.3d 941, 967 (9th Cir. 2021), cert. denied, 142 S. Ct. 2834 (2022).

[14] Preamble, https://perma.cc/LJE4-K7HH

[15] Reference Guide on Epidemiology, RMSE 4th ed. at 919 n. 68 (incorrectly citing the Preamble to a URL, https://perma.cc/XXY4-7DKF, which is a one page abridgement of the actual Preamble, devoid of definitions and qualifications.

[16] Reference Guide on Epidemiology, RMSE 4th ed. at 974.

[17] Schachtman, IARC’s Precautionary Science: How the WHO Cancer Research Agency Misinforms Regulation and Litigation, Washington Legal Foundation Monograph (May 2026), available at https://www.wlf.org/wp-content/uploads/2026/05/05-26Schachtman-Monograph.pdf

Reference Manual’s Chapter on Expert Witness Testimony Admissibility – Part 5

March 7th, 2026

By ignoring Milward’s expert witnesses’ omissions from, and abridgements of, WOE and IBE, the appellate court blinded itself to these witnesses’ distortions of scientific method. The need for judgment, which the Milward court was keen to honor, does not mean that there are not aberrant or deviant judgments, or deviations from the standard of scientific care that are disqualifying. The need for judgment must also allow for equipoise and uncertainty that stands in the way of an inculpatory or exonerative verdict. And then there is the business of questionable research practices that subvert causal judgment. The district court had followed and acknowledged the showing of questionable research practices that pervaded Martyn Smith’s for-litigation opinions. The cheerleaders for Milward seem eager to obscure these practices by their insistence that causation is, after all, only a judgment.

The Milward decision, in its embrace of some truly aberrant methodology and judgment, and some absence of methodology, made some of its own whoopers. Martyn Smith’s incompetent analyses of the epidemiologic evidence had been thoroughly debunked in the district court, but the circuit court glibly adopted Smith’s characterizations. The appellate court failed to understand and come to grips with Smith’s rejiggering of data, and his inconsistently redefining exposures and outcomes in epidemiologic studies to make up new, fanciful results that favored his WOE-ful opinion. The appellate court also failed to understand that scientific judgment is not some vague, amorphous, unstructured decision that turns on whatever looks to be “explanatory.” Even the International Agency for Research on Cancer, which issues hazard classifications that are distorted by non-scientific precautionary principle reasoning, insists that three streams of evidence (epidemiologic, toxicologic, mechanistic) be considered separately, in accordance with criteria, with attention to the validity of each study, and synthesized into a judgment of causality following a carefully structured analysis.[1]

The appellate court in Milward took the demonstration of Smith’s failure to calculate odds ratios correctly to be something that merely went to the weight, not the admissibility, on the theory that a jury, which does not have access to the Reference Manual or to the actual studies as published, could sort it all out. And yet, when the court improvidently set out a definition of what an odds ratio is, it bungled the definition beyond understanding:

“An odds ratio represents the difference in the incidence of a disease between a population that has been exposed to benzene and one that has not.”[2]

The court’s definition is not even wrong. The difference between incidence of a disease in an exposed group and a non-exposed group is the risk difference. It is not an odds ratio. Perhaps the court might have realized what most third graders know, that there is a difference between a ratio (division) and a difference (subtraction). And of course, the odds of exposure is not the same as the incidence of a disease. The relevant odds ratio represents the odds of exposure in cases with APML diagnoses divided by the odds of exposure in study subjects without APML. The odds ratio does involve measurements of incidence although in some cases the odds ratio will approximate a risk ratio, which does involve a ratio of incidences. This is not some hyper-technicality; it is a vivid display that Chief Judge Lynch, writing for a panel of three judges of the First Circuit, had no idea of what she was reviewing or writing.

Richter and Capra devote two pages to a discussion of the Milward case and its embrace of WOE and IBE. There is not, in this discussion, a single adjective of approval or of disapproval. The attention to this one intermediate appellate court opinion far exceeds any other case decided at a level below the Supreme Court, and an engaged reader must ask why the authors of the first chapter of the new Reference Manual wrote about this case at all, especially given the 2023 amendments to Rule 702, which would suggest that Milward was bad law when decided in 2011, and clearly and emphatically bad law in December 2025, when the new Manual was published.

The chapter provides one not-so-subtle clue of the authors’ intent. At the conclusion of their extended, uncritical, and incomplete exposition of Milward,[3] Richter and Capra refer the reader to a law review symposium,[4] “[f]or a detailed analysis of the Milward decision and the weight of the evidence approach to scientific reasoning.” Like Richter and Capra’s coverage of Milward, the cited symposium was hardly an objective analysis; rather, it was more like a drunken celebration at a family reunion.

There have been many law review articles that have discussed the Milward case, but Richter and Capra chose to cite to one particular symposium, which was sponsored by two corporations, the Center for Progressive Reform (CPR) and the Robert A. Habush Foundation. The Center for Progressive Reform (CPR) is a not-for-profit corporation. Its website describes the CPR as a “research and advocacy organization that works in the service of responsive government; climate justice, mitigation, and adaptation; and protecting against environmental harm.”[5] CPR describes one of its key activities as defending science from corporate interference. Presumably its own corporate activities and those of the lawsuit industry are acceptable, but those of corporate manufacturing industry are not. From reviewing CPR’s website, it is not clear that the CPR believes manufacturing corporations should even be allowed to defend against lawsuits. Milward’s retained expert witness Carl Cranor is a “member scholar” at CPR, which makes CPR’s sponsorship of the symposium rather incestuous.[6]

CPR is also apparently comfortable with one highly politicized “corporation,” namely the American Association for Justice (AAJ), which is the trade group for the American lawsuit industry.[7] The AAJ describes itself as a corporation, or a “collective,” that supports plaintiff trial lawyers as their “collective voice … on Capitol Hill and in courthouses across the nation … .” The Robert A. Habush Foundation is endowed by the AAJ, and serves its “educational” mission.  Through the Habush Foundation, the AAJ funds educational programs, “think tanks,” and writing projects designed to influence judges, law professors, lawyers, and the public, on issues of importance to the AAJ:  “the civil justice system and individual rights” for bigger, better, and more profitable litigation outcomes. The AAJ may be a “not-for-profit” corporation, but it represents the interests of one of the most powerful, wealthiest, interest groups in American society — the plaintiffs’ bar.

The Milward symposium agenda and papers from its participants were published at the website for the Wake Forest Journal of Law and Public Policy, but now are marked as “currently private. If you would like to request access, we’ll send your username to the site owner for approval.”

The symposium cited by Richter and Capra for “analysis,” was very much a family affair. The choice of venue, at the Wake Forest Law School, was connected to the web of interests involved. CPR board member, Sid Shapiro, is a law professor at Wake Forest. Shapiro presented at the symposium, along with the Wake Forest professor Michael Green. Cranor, Shapiro’s CPR colleague, and party expert witness for plaintiff, presented.[8] There was only one practicing lawyer who presented at the symposium, Steven Baughman Jensen, who was a past chair of the AAJ’s Section on Toxic, Environmental, and Pharmaceutical Torts. Jensen represented Milward, and hired Cranor as one of the plaintiff’s expert witnesses. Attorney Jensen’s contribution to the symposium has been published along with Cranor’s as well, in the proceedings of the Milward symposium were published volume 3, no. 1 of the Wake Forest Journal of Law and Public Policy,[9] which is now also marked private. Jensen also published an abbreviated paean to Milward in in the AAJ’s trade journal.[10] No defense counsel or defense expert witness participated at the symposium, referenced by Richter and Capra.

Consistent with the financial, advocacy, and political interests of the symposium sponsors, the articles are almost all partisan high-fives for the Milward decision. Writing for the Federal Judicial Center and the National Academies, the authors of a chapter on the law of expert witnesses, a legal issue, for the Reference Manual, should have been aware of the partisan nature of the CPR-AAJ sponsored symposium. They should have flagged the advocacy nature of the symposium, and identified the funding sources and the conflicts created. Furthermore, Richter and Capra should have cited papers that criticized the Milward case, from various perspectives, including its failure to adhere to the law of Rule 702.[11] Their failure to do so is a significant failure of this chapter.


[1] IARC MONOGRAPHS ON THE IDENTIFICATION OF CARCINOGENIC HAZARDS TO HUMANS – PREAMBLE (2019).

[2] Milward, 639 F.3d at 23.

[3] Richter & Capra at 33n.96 (“For a detailed analysis of the Milward decision and the weight of the evidence approach to scientific reasoning…”).

[4] Symposium: Toxic Tort Litigation: After Milward v. Acuity Products, 3 WAKE FOREST JOURNAL OF LAW & POLICY 1 (2013).

[5] The Center for Progressive Reform, at https://progressivereform.org/, last visited on Feb. 24, 2026

[6] Carl Cranor Biography, Center for Progressive Reform, Member Scholars, at https://progressivereform.org/member-scholars/

[7] The AAJ was previously known by the more revealing name, Association of Trial Lawyers of America (ATLA®). 

[8] Carl F. Cranor, Milward v. Acuity Specialty Products: Advances in General Causation Testimony in Toxic Tort Litigation, 3 WAKE FOREST JOURNAL OF LAW & POLICY 105 (2013).

[9] Steve Baughman Jensen, Sometimes Doubt Doesn’t Sell: A Plaintiffs’ Lawyer’s Perspective on Milward v. Acuity Products, 3 WAKE FOREST JOURNAL OF LAW & POLICY 177 (2013).

[10] Steve Baughman Jensen, Reframing the Daubert Issue in Toxic Tort Cases, 49 TRIAL 46 (Feb. 2013).

[11] See Eric Lasker, Manning the Daubert Gate: A Defense Primer in Response to Milward v. Acuity Specialty Products, 79 DEF. COUNS. J. 128, 128 (2012);

David E. Bernstein, The Misbegotten Judicial Resistance to the Daubert Revolution, 89 NOTRE DAME L. REV. 27, 29, 53-58 (2013); David E. Bernstein & Eric G. Lasker, Defending Daubert: It’s Time to Amend Federal Rule of Evidence 702, 57 WM. & MARY L. REV. 1, 33 (2015); Richard Collin Mangrum, Comment on the Proposed Revision of Federal Rule 702: “Clarifying” the Court’s Gatekeeping Responsibility over Expert Testimony, 56 CREIGHTON LAW REVIEW 97, 106 & n.45 (2022); Thomas D. Schroeder, Toward a More Apparent Approach to Considering the Admission of Expert Testimony, 95 NOTRE DAME L. REV. 2039, 2045 (2020); Lawrence A. Kogan, Weight of the Evidence: A Lower Expert Evidence Standard Metastasizes in Federal Court, Washington Legal Foundation Critical Legal Issues WORKING PAPER Series no. 215 (Mar. 2020); Note, Judicial Conference Amends Rule 702. — Federal Rule of Evidence 702, 138 HARV. L. REV. 899, 903 (2025); Nathan A. Schachtman, Desultory Thoughts on Milward v. Acuity Specialty Products, DOI: 10.13140/RG.2.1.5011.5285 (Oct. 2015), available at https://www.researchgate.net/publication/282816421_Desultory_Thoughts_on_Milward_v_Acuity_Specialty_Products .

Reference Manual’s Chapter on Expert Witness Testimony Admissibility – Part 4

March 5th, 2026

In the district court, Judge George O’Toole conducted a pre-trial hearing over four days, and heard testimony from Smith and Cranor, as well as from defense expert witnesses. Judge O’Toole’s published opinion carefully and accurately stated the facts, the applicable law, and presented a well-reasoned judgment as to why Smith’s opinion was not admissible under Rule 702. Without admissible opinions on general causation to support Milward’s case, Judge O’Toole granted summary judgment to the defendants.

Milward appealed the judgment. A panel of judges in the First Circuit heard argument, and reversed in an opinion that is riddled with serious errors.[1] In reviewing the district court’s application of Rule 702, the panel, in an opinion written by Chief Judge Lynch, credulously accepted most of Smith’s and Cranor’s arguments that an ill-defined WOE approach is acceptable method of guiding scientific judgment. Cranor equated WOE, as used by Smith, to the approach that Sir Austin Bradford Hill described, in 1965, for identifying causal associations from epidemiologic data.[2] Chief Judge Lynch’s opinion tracked accurately Cranor’s and Milward’s lawyers’ misrepresentations about Sir Austin’s paper:

“Dr. Smith’s opinion was based on a ‘‘weight of the evidence’’ methodology in which he followed the guidelines articulated by world-renowned epidemiologist Sir Arthur [sic] Bradford Hill in his seminal methodological article on inferences of causality. See Arthur [sic] Bradford Hill, The Environment and Disease: Association or Causation?, 58 Proc. Royal Soc’y Med. 295 (1965).

Hill’s article explains that one should not conclude that an observed association between a disease and a feature of the environment (e.g., a chemical) is causal without first considering a variety of ‘viewpoints’ on the issue.”[3]

The quoted language from the First Circuit opinion, which twice refers to “Arthur Bradford Hill,” rather than Austin Bradford Hill, may suggest that neither Chief Judge Lynch nor his judicial colleagues and their law clerks read the classic paper. An even stronger indicator that the appellate court did not actually read this paper is evidenced in the court’s equating WOE to Bradford Hill viewpoints, without consideration of the necessary predicate for those nine viewpoints. In his short paper, Sir Austin clearly spelled out that there was a foundation needed before parsing the nine viewpoints:

“Disregarding then any such problem in semantics we have this situation. Our observations reveal an association between two variables, perfectly clear-cut and beyond what we would care to attribute to the play of chance. What aspects of that association should we especially consider before deciding that the most likely interpretation of it is causation?”[4]

Whatever Sir Arthur had to say about the matter, Sir Austin defined the starting point of causal analysis as an association free of invalidating bias and random error. The Milward decision ignored this all important predicate for assessing the various considerations that might allow for a valid association to be considered a causal association.[5] The resulting abridgement was a failure of scientific due process that distorted the Bradford Hill paper.

The First Circuit amplified its error when it asserted that from the nine considerations “no one type of evidence must be present before causality may be inferred.”[6] Although Sir Austin said something similar, one of the considerations he noted was “temporality,” in which the putative cause must come before the effect.  Most scientists would consider this consideration to be essential, unless they were observing events that were moving faster than the speed of light. The other eight considerations are more dependent upon context of the exposures and outcomes of interest, but surely strength and consistency of the clear-cut association across multiple studies is an extremely important consideration.

The First Circuit proceeds from misreading Sir Austin’s paper to misunderstanding another paper invoked by Cranor and by Milward’s lawyers. Carelessly tracking Cranor, the appellate court suggested that there was no “hierarchy of evidence”:

“For example, when a group from the National Cancer Institute was asked to rank the different types of evidence, it concluded that ‘‘[t]here should be no such hierarchy.’’ Michele Carbon [sic] et al., Modern Criteria to Establish Human Cancer Etiology, 64 Cancer Res. 5518, 5522 (2004); see also Sheldon Krimsky, The Weight of Scientific Evidence in Policy and Law, 95 Am. J. Pub. Health S129, S130 (2005).”[7]

This quoted language from the Milward opinion shows how slavishly and credulously the court adopted and regurgitated plaintiff’s argument. Sheldon Krimky was actively involved with SKAPP, and his article was presented at the SKAPP-funded Coronado Conference, discussed earlier in this series. Krimsky actually acknowledged that although “the term [WOE] is applied quite liberally in the regulatory literature, the methodology behind it is rarely explicated.”

As for the article by Carbon [sic], this publication never rejected a hierarchy of evidence. The court’s language, quoted above, follows immediately after the court’s discussion of Sir Austin’s nine types of corroborating evidence that would support the causal interpretation of an association. As such, the court seems to imply, incorrectly, that there was no hierarchy of these considerations.[8]

The court’s language also suggests that the quoted language came from the National Cancer Institute (NCI), but its provenance is quite different. The cited article’s lead author, Michele Carbone (not Carbon), was reporting on a workshop hosted by the NCI at an NCI building; it was not an official NCI event or publication. The NCI did not sponsor or conduct the meeting, and Carbone’s paper was not an official statement of the NCI. Carbone’s paper was styled “Meeting Report,” and published as a paid advertisement in Cancer Research, not in the Journal of the National Cancer Institute as a scholarly article.

The discipline of epidemiology was not strongly represented at the meeting; most of the chairpersons and scientists in attendance were pathologists, cell biologists, virologists, and toxicologists. The authors of the meeting report reflect the interests and focus of the scientists in attendance. The lead author, Michele Carbone, a pathologist at the University of Hawaii, was an enthusiastic proponent of Simian Virus 40 as a cause of mesothelioma, a hypothesis that has not fared terribly well in the crucible of epidemiologic science.

The cited article did report some suggestions for modifying Bradford Hill’s criteria in the light of modern molecular biology, as well as a sense of the group that there was no “hierarchy” in which epidemiology was at the top of disciplines.  The group definitely did not address the established concept that some types of epidemiologic studies are analytically more powerful to support inferences of causality than others — the hierarchy of epidemiologic evidence. The group also did not address or reject a ranking of importance of Bradford Hill’s nine viewpoints. There was nothing remarkable about the tumor biologists’ statement that in some cases causality can be determined by careful identification of genetic inheritance or molecular biological pathways. There was no evidence of this sort in the Milward case, and the citation by Cranor and Milward’s lawyers was nothing more than hand waving.

Carbone’s meeting report summarizes informal discussion sessions at the 2003 meeting.  Those in attendance broke out into two groups, one chaired by Brook Mossman, a pathologist, and the other group chaired by Dr. Harald zur Hausen, a virologist. The meeting report included a narrative of how the two groups responded to twelve questions. Drawing from plaintiff’s (and Cranor’s) argument, the court’s citation to this meeting report is based upon one sentence in Carbone’s report, about one of twelve questions:

6. What is the hierarchy of state-of-the-art approaches needed for confirmation criteria, and which bioassays are critical for decisions: epidemiology, animal testing, cell culture, genomics, and so forth?

There should be no such hierarchy. Epidemiology, animal, tissue culture and molecular pathology should be seen as integrating evidences in the determination of human carcinogenicity.”[9]

Considering the fuller context of the meeting, there is nothing particularly surprising about this statement.  The full question and answer in the meeting report does not even remotely support the weight given to it by the court. There was quite a bit of disagreement among meeting participants over criteria for different kinds of carcinogens, as seen the report on another question:

“2. Should the criteria be the same for different agents (viruses, chemicals, physical agents, promoting agents versus initiating DNA-damaging agents)?

There were different opinions. Group 1 debated this issue and concluded that the current listing of criteria should remain the same because we lack sufficient evidence to develop a separate classification. Group 2 strongly supported the view that it is useful to separate the biological or infectious agents from chemical and physical carcinogens due to their frequently entirely different mode of action.”[10]

Carbone and the other authors of the meeting report noted the importance to epidemiology for general causation, while acknowledging its limitations for determining specific causation:

“Concerning the respective roles of epidemiology and molecular pathology, it was noted that epidemiology allows the determination of the overall effect of a given carcinogen in the human population (e.g., hepatitis B virus and hepatocellular carcinoma) but cannot prove causality in the individual tumor patient.”[11]

Clearly, the report was not disavowing the necessity for epidemiology to confirm carcinogenicity in humans. Specific causation of Mr. Milward’s APML was irrelevant to his first appeal to the First Circuit. Carbone’s report emphasized the need to integrate epidemiologic findings with molecular biology; it did not suggest that epidemiology was not necessary or urge that epidemiology be ignored or disregarded:

“A general consensus was often reached on several topics such as the need to integrate molecular pathology and epidemiology for a more accurate and rapid identification of human carcinogens.”[12]

                 * * * * *

“Ideally, before labeling an agent as a human carcinogen, it is important to have epidemiological, experimental animals, and mechanistic evidence (molecular pathology).”[13]

The court’s implication that there was “no hierarchy of evidence” is unsupported by the meeting report. The suggestion that WOE allows some loosey-goosey, ad hoc, unstructured assessment of diverse lines of evidence is rejected in the meeting report with a careful admonition about the lack of validity of some animal models and mechanistic research:

“Moreover, carcinogens and anticarcinogens can have different effects in different situations. As shown by the example of addition of β-carotene in the diet, β- carotene has chemopreventive effects in many experimental systems, yet it appears to have increased the incidence of lung cancer in heavy smokers. Animal experiments can be very useful in predicting the carcinogenicity of a given chemical. However, there are significant differences in susceptibility among species and within organs in the same species, and differences in the metabolic pathway of a given chemical among human and animals could lead to error.”[14]

Inference to the Best Explanation

The First Circuit asserted that “no serious argument can be made that the weight of the evidence approach is inherently unreliable.”[15] As discussed above, this assertion is demonstrably false. In his testimony at the Rule 702 pre-trial hearing, Cranor classified WOE as based upon “inference to the best explanation,” and the First Circuit obsequiously accepted this claim. In articulating and accepting Cranor’s reduction of scientific method to IBE, the appellate court seemed unaware that IBE as an epistemic theory has been roundly criticized. In a very general sense, IBE draws on Charles Pierce’s description of abduction as a mode of reasoning, although many writers have been eager to distinguish abduction from IBE. Bas van Fraassen criticized IBE as lacking merit as a mode of argument in a way germane to Cranor’s presentation of the notion, and the First Circuit’s uncritical acceptance:

“As long as the pattern of Inference to the Best Explanation—henceforth, IBE—is left vague, it seems to fit much rational activity. But when we scrutinize its credentials, we find it seriously wanting.”[16]

The IBE approach raises thorny problems of knowing how to discern the best explanation, or how to tell whether an explanation is simply the best of a bad lot. Other philosophers of science have questioned why explanatoriness should matter as opposed to predictive ability and resistance to falsification upon severe or robust testing.

In the hands of Smith and Cranor, these philosophical quandries become largely beside the point. For Smith and Cranor IBE becomes telling just so stories, which transform “but for” causation into “could be” causation. Drawing directly from Cranor, the Circuit Court explained that an inference to the best explanation involves six general steps for scientists:

“(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.”[17]

Of course assessing causation requires judgment, but Cranor and Smith radically abridge the process of judging by eliminating:

  • the robust testing of, and attempts to falsify, hypotheses,
  • the weighting of study designs,
  • the pre-specification of kinds of studies to be included or excluded, the assignment of weights to different kinds and qualities of studies, and
  • the pre-specification of criteria of study validity, experimental design, consistency, and exposure-response.

The vague, contentless IBE and WOE, in the hands of Smith, operates just as van Fraassen anticipated. With Cranor’s “philosophizing,” IBE creates a permission structure to reach any desired conclusion. Indeed, Cranor’s approach makes no allowance for when careful scientists withhold judgment because the evidence is inadequate to the task. Furthermore, Cranor’s approach and the Milward decision would cheerily approve cherry picking of studies and data within studies, post hoc weighing of evidence, and even fabricating and rejiggering of evidence, all of which was on display in Smith’s for-litigation opinion.

The First Circuit uttered its mantra of approval of Smith’s scientific delicts in language that became the target of the revision of Rule 702 in 2023:

“the alleged flaws identified by the [district] court go to the weight of Dr. Smith’s opinion, not its admissibility. There is an important difference between what is unreliable support and what a trier of fact may conclude is insufficient support for an expert’s conclusion.”[18]

Earlier in its opinion, the appellate court quoted from the version of Rule 702 in effect when it heard the appeal:

“if (1) the testimony is based upon sufficient facts or data, (2) the testimony is the product of reliable principles and methods, and (3) the witness has applied the principles and methods reliably to the facts of the case.”[19]

Sufficiency, reliability, and validity were all preliminary questions to be decided by the court as part of its gatekeeping responsibility.  The appellate court simply ignored the law in its decision to green light Smith’s testimony.

                    (to be continued)


[1] Milward v. Acuity Specialty Products Group, Inc., 639 F.3d 11 (1st Cir. 2011), cert. denied sub nom., U.S. Steel Corp. v. Milward, 565 U.S. 1111 (2012).

[2] Austin Bradford Hill, The Environment and Disease: Association or Causation?, 58 PROC. ROYAL SOC’Y MED. 295 (1965).

[3] Milward, 639 F.3d at 17.

[4] Id. at 295.

[5] See Frank C. Woodside, III & Allison G. Davis, The Bradford Hill Criteria: The Forgotten Predicate, 35 THOMAS JEFFERSON L. REV. 103 (2013).

[6] Milward, 639 F.3d at 17.

[7] Id. (internal citations omitted).

[8] The Reference Manual chapter on medical testimony carefully discusses the hierarchy of evidence as it factors into the assessment of medical causation. John B. Wong, Lawrence O. Gostin & Oscar A. Cabrera, Reference Guide on Medical Testimony, in National Academies of Sciences, Engineering and Medicine & Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 687, 723 -24 (2011); John B. Wong, Lawrence O. Gostin, & Oscar A. Cabrera, Reference Guide on Medical Testimony, in National Academies of Sciences, Engineering and Medicine & Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 1105, 1150-52 (4th ed. 2025). Interestingly, the chapter on epidemiology in the third edition of the Reference Manual cited to the Carbone workshop with apparent approval, but the same chapter in the fourth edition has dropped the reference. Compare Michael D. Green, D. Michal Freedman & Leon Gordis, Reference Guide on Epidemiology, in National Academies of Sciences, Engineering and Medicine & Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 549, 564 n.48 (3rd ed. 2011) with Steve C. Gold, Michael D. Green, Jonathan Chevrier, & Brenda Eskenazi, Reference Guide on Epidemiology, in National Academies of Sciences, Engineering and Medicine & Federal Judicial Center, REFERENCE MANUAL ON SCIENTIFIC EVIDENCE 897 (4th ed. 2025).

[9] Carbone at 5522.

[10] Carbone at 5521.

[11] Carbone at 5518 (emphasis added).

[12] Carbone at 5518.

[13] Carbone at 5519.

[14] Carbone at 5521.

[15] Milward, 639 F.3d at 18-19.

[16] Bas van Fraassen, LAWS AND SYMMETRY 131 (1989).

[17] Milward, 639 F.3d at 18.

[18] Milward, 639 F.3d at 22.

[19] Milward, 639 F.3d at 14.

The First Daubert Motion

February 20th, 2026

As every school child knows, or at least every law student in the United States knows, Daubert was a Bendectin case. The plaintiff claimed that his mother’s use of Bendectin, a prescription anti-nausea medication, during pregnancy caused him to be born with a major limb reduction defect.

Filed in 1984, the Daubert case was pending, in summer 1989, before Judge Earl Ben Gilliam, in the Southern District of California. A trial date was approaching, and a deadline for motions for summary judgment. The first Daubert motion was filed in August 1989, in Daubert v. Merrell Dow Pharmaceuticals, Inc.[1] It was a motion for summary judgment, not a motion specifically to exclude plaintiffs’ expert witness’s proffered testimony.

By the time of the first Daubert motion, the plaintiff was relying upon the anticipated testimony of John Davis Palmer, M.D. For the time, John Davis Palmer was not an unlikely expert witness. Although Palmer practiced internal medicine, he had a doctorate in pharmacology. Palmer, however, had no experience studying Bendectin, and no real expertise in epidemiology. He had never designed or published an epidemiologic study, and he had never done any kind of research on Bendectin. The standard for qualifying an expert witness, even in federal court, has always been very low, and thus not an effective way to police the quality of scientific evidence.

Palmer was a rather late substitute for expert witnesses previously listed by the plaintiff. Alan Kimball Done, a pediatrician, had been the main warhorse of the Bendectin plaintiffs, but he was withdrawn by plaintiff’s counsel after he was found to have committed perjury about his academic credentials in another Bendectin case.[2]

Plaintiff also needed to drop another expert witness, William Griffith McBride, who had been a star in plaintiff’s counsel’s stable. McBride helped show the teratogenicity of thalidomide in the early 1960s,[3] and his work in the Bendectin litigation gave these dodgy cases some patina of respectability. In 1988, however, McBride was accused of fraud, for which he would eventually lose his medical license.[4] McBride also chose, rather improvidently, to sue journalists, journals, and Merrell Dow executives, for reporting his rather extensive fees, only to lose that litigation.[5] When plaintiff’s counsel withdrew McBride, plaintiff was left with only Dr. Palmer to serve as plaintiff’s sole expert witness on both general and specific causation.

At the time that the first Daubert motion was filed, manufacturer Merrell Dow had voluntarily withdrawn Bendectin from the market, without any suggestion from the FDA that this action was necessary or in the public interest. The manufacturer had also enjoyed considerable success in court. The company had tried a case that consolidated the general causation claims of over 800 plaintiffs, to a defense jury verdict, in 1985, before Chief Judge Carl Rubin, of the Southern District of Ohio.[6] Despite some isolated trial losses, the company was vindicated in three federal circuits at the time its lawyers filed the “Daubert” motion.[7] The First, Fifth, and District of Columbia Circuits of the United States Court of Appeals, had all held that the plaintiffs’ case was legally insufficient to sustain a verdict against the defendant, or that the expert testimony involved was inadmissible.

In the Daubert case, Merrell Dow Pharmaceuticals was represented by the law firm Dickson, Carlson & Campillo. The important task of drafting the motion for summary judgment landed on the desk of a first year associate, Pamela Yates, who is now a partner at Arnold & Porter. Given that Merrell Dow had succeeded in other appellate courts, the task may have seemed straight forward, but the legal theories were actually all over the map.

The first Daubert motion was not styled as a motion to exclude expert witness opinion testimony, but rather as a motion for summary judgment, pursuant to Federal Rule of Civil Procedure 56, on the issue of causation. Merrell Dow’s supporting brief did not clearly invoke the distinction between general and specific causation, which distinction was not widely drawn until later in the 1990s. The supporting brief implicitly addressed both general and specific causation.

At the time that the first Daubert motion was made, there was no clear consensus of precedent that identified the source of support for a trial court’s ruling peremptorily on a weak evidentiary display on the causation issue. The evidence supporting the defense expert witnesses’ opinion that Bendectin had not been shown to cause birth defects generally and limb reduction defects specifically was strong. For all major congenital defects, there had been no change in overall incidence for the years in which Bendectin was marketed. Such an ecological argument usually has no validity, but in the case of Bendectin, for several years, roughly half of all pregnant women used the medication. When the medication was abruptly withdrawn,[8] not because of the science but because of the cost of the litigation, the rate of birth defects remained unaffected. The great majority of birth defects have no known cause, and there was no scientific consensus that Bendectin caused birth defects; indeed by 1989, the nearly universal consensus was that Bendectin did not cause birth defects.[9]

There were also many analytical epidemiologic studies, which both individually or in combination failed to support a conclusion of causation.

In the face of the defense’s affirmative evidence, the plaintiff relied upon a potpourri of evidence:

1) chemical structure activity analysis;

2) in vitro (test tube) studies;

3 ) in vivo studies (animal teratology) studies; and

4) reanalysis of epidemiology studies.

Plaintiff’s lead counsel Barry Nace[10] had concocted this potpourri approach, which he called “mosaic theory,” and which might more aptly be called the tsemish or the shmegegge theory.[11] Whatever Nace called it, he fed it to his expert witness to argue that:

“Like the pieces of a mosaic, the individual studies showed little or nothing when viewed separately from one another, but they combined to produce a whole that was greater than the sum of its parts: a foundation for Dr. Done’s opinion that Bendectin caused appellant’s birth defects.”[12]

Although philosopher Harry Frankfurt had not yet written his seminal treatise on the subject, most courts saw that this was bullshit, which tends to result “whenever a person’s obligations or opportunities to speak about some topic exceed his knowledge of the facts that are relevant to that topic.”[13]

In addition to favorable opinions from the First, Fifth, and District of Columbia Circuits, Merrell Dow had a favorable Zeitgeist working in its favor. The plaintiff-friendly influential judge, Judge Jack Weinstein, had rolled up his sleeves and taken a hard look at the plaintiffs’ scientific evidence in the Agent Orange litigation. Judge Weinstein found that evidence wanting in an important opinion in 1985.[14] Although the alleged causal agent in Agent Orange was not Bendectin, Judge Weinstein recognized that epidemiological studies were, in a similar medico-legal context, “the only useful studies having any bearing on causation.[15] Judge Weinstein relied heavily upon Federal Rule of Evidence Rule 703, which governed what inadmissible studies expert witnesses could rely upon, to whittle down the reliance list of plaintiffs’ expert witnesses before declaring their opinions too fragile to support a reasonable jury’s verdict in favor of plaintiffs.

More generally, discerning members of the legal system were reaching the end of their tolerance for the common law laissez-faire approach to expert witness evidence. In 1986, the Department of Justice issued a report that explicitly called for meaningful judicial gatekeeping of expert witnesses.[16] And in that same year, 1986, Judge Patrick Higginbotham wrote an influential opinion, in which he warned that expert witness opinion testimony was out of control, with expert witnesses becoming mouth pieces for the lawyers and advocates of policy beyond their proper role. Judge Higginbotham observed that trial judges (with support from appellate court judges) had a duty to address the problem by policing the soundness of opinions proffered in litigation, and to reject the system’s reliance upon expert witnesses simply because they “say[] it is so:”[17]

“we recognize the temptation to answer objections to receipt of expert testimony with the short hand remark that the jury will give it ‘the weight it deserves’. This nigh reflective explanation may be sound in some cases, but in others it can mask a failure by the trial judge to come to grips with an important trial decision. Trial judges must be sensitive to the qualifications of persons claiming to be experts … . Our message to our able trial colleagues: It is time to take hold of expert testimony in federal trials.”[18]

Although Merrell Dow had a substantial tailwind behind its motion for summary judgment, there was no one clear theory upon which it could rely. Some of the Bendectin appellate court opinions were based upon the insufficiency of the plaintiffs’ expert witness evidence, on the basis of the entire record after trial. The evidence in Daubert was virtually the same if not more restricted than what was of record in some of those appellate court cases. The ecological evidence was clear.

Some of the judgments relied upon by Merrell Dow were based upon the Frye test, and some were based upon Rule 703, which addresses what kinds of otherwise inadmissible evidence expert witnesses may rely upon in formulating their opinions. Finally, some courts, such as Fifth Circuit in In Re Air Crash Disaster at New Orleans, were beginning to see Rule 702 as the source of their authority to control wayward expert witness opinion testimony.

Merrell Dow advanced multiple lines of analyses to show that plaintiffs cannot establish causation based upon the then current scientific record. The first Daubert motion had no clear line of authority, and so, understandably, it cast a wide net on all available potential legal rules and doctrines to oppose the plantiff’s potpourri Bendectin causation theory. The motion harnessed precedents based upon sufficiency of the plaintiffs’ proffered expert witness, Federal Rules 702 and 703, as well as the 1923 Frye case.[19]

The cases that invoked Frye doctrine presented several interpretative problems. Frye was a criminal case that prohibited expert witnesses from testifying about their interpretations of the output of a mechanical device. The Frye case’s insistence upon general acceptance, when imported into a causation dispute in a tort case, was ambiguous as to what exactly had to be generally accepted: the specific causal claim, or the method used to reach the causal claim, or the method used as applied to the facts of the case. Furthermore, Frye’s requirement of general acceptance was not explicitly incorporated into either Rule 702 or 703, when promulgated in 1975.[20]

Merrell Dow had ample evidence that there was no general acceptance of the plaintiff’s causal claim, but its counsel also showed that by applying generally accepted methodology, scientists could not reach the plaintiff’s causal conclusion, and no scientist outside of the litigation had done so. In particular, there was general acceptance of the propositions that non-human in vivo and in vitro teratology experiments have little if any predictive ability for human outcomes. Because randomized controlled trials were never an option for testing human teratogenicity, observational epidemiology was required, and the available studies were largely exonerative. Only by post-publication data dredging and manipulation was plaintiffs’ expert witness Palmer (following what Shann Swan had done in previous cases) able to raise questions about possible associations. Plaintiff’s expert witness Palmer could not show that these manipulations were a generally accepted method for interpreting or re-analyzing published studies.

In its last point, the first Daubert motion also maintained that the standard for medical causation required that the relevant relative risk exceed two.[21] As noted, the brief did not distinguish general from specific causation, a distinction that had not entered the legal lexicon fully in 1989. The brief’s citation to swine-flu cases, however, clarifies the nature of Merrell Dow’s argument. In the swine-flu litigation, the United States government assumed liability for adverse effects of a vaccine for swine flu. The government recognized that within a certain time window after vaccination, patients had more than a doubled risk of Guillain-Barré syndrome (GBS), an autoimmune neurological condition. The government refused compensation for claimants outside that window. Merrell Dow relied heavily upon one swine flu case, Cook v. United States, which articulated and applied the principle:

“Wherever the relative risk to vaccinated persons is greater than two times the risk to unvaccinated persons, there is a greater than 50% chance that a given GBS case among vaccinees of that latency period is attributable to vaccination, thus sustaining plaintiff’s burden of proof on causation.”[22]

In other words, the government had conceded that the swine-flu vaccine could cause GBS in some temporal situations, but not others. The magnitude of the causal association had been quantified in relative risk terms by epidemiologic studies. Only for those claimants vaccinated in time windows with relative risks greater than two could courts conclude that GBS was, more likely than not, caused by vaccination.

Unlike the federal government in the swine-flu GBS litigation, Merrell Dow was not, however, conceding general causation for any exposure scenarios. The first Daubert motion can only be read to deny general causation, but to explain further that even if the court were to assume, arguendo, that Bendectin causes limb reduction deficits based upon Palmer’s schmegegge and Swan’s re-jiggered risk ratios, that there would still be no proper inference that Bendectin more likely than not caused Jason Daubert’s birth defects.

In response to these arguments, the plaintiff’s counsel argued their mosaic, potpourri, schmegegge theories. Although plaintiffs were down to Dr. Palmer, they filed transcripts and affidavits from a host of other expert witnesses, from previous Bendectin cases.

As for the legal rules of decision, Barry Nace, on behalf of plaintiffs, argued that Rule 703 had “absorbed” the Frye rule. Having been shown to be qualified under the minimal standard of Rule 702, these expert witnesses then satisfied Rule 703 by relying upon “scientific evidence” of the sort that experts in their field rely upon, even if other scientists would not rely upon such evidence in support of a conclusion. Otherwise those expert witnesses were unrestrained by the law, and they were free to assess their relied upon facts and data as sufficient to show that Bendectin probably causes birth defects and that Bendectin caused Jason Daubert’s birth defects. Nace argued that as long as expert witnesses, properly qualified, offered relevant opinions, based upon “things of science,” they could opine that the earth was flat, and it was for the jury to sort out whether to believe them.

Judge Earl Gilliam found Nace’s position untenable, and granted summary judgment later in 1989.[23] Interestingly Judge Gilliam’s opinion in the district court never cited Federal Rule of Evidence 702. Instead, the opinion pointed to Rule 703, as restricting evidence, even if “science,” unless the proponent showed that the underlying principle had gained general acceptance in the relevant field.[24] Opinions not based upon facts or data “of a type reasonably relied upon by experts in the particular field” would be confusing, misleading, and unhelpful, and thus inadmissible. The reference to helpfulness might perhaps be taken as an implicit invocation of Rule 702.

Judge Gilliam had the benefit of the Circuit decisions in Brock, Richardson, and Lynch, with their various holdings of insufficiency or inadmissibility of plaintiffs’ expert witness evidence. In particular, Judge Gilliam cited Brock for the proposition that trial courts must “critically evaluate the reasoning process by which the experts connect data to their conclusions in order for courts to consistently and rationally resolve the disputes before them.”[25] Following Judge Weinstein on Agent Orange, and the previous federal decisions on Bendectin, Judge Gilliam observed that causation in the Bendectin cases could be established, under the circumstances of plaintiffs’ evidentiary display, only through reliance upon epidemiologic evidence. Dr. Done’s schmeggege, concocted as it was by Barry Nace, would not get plaintiffs to a jury.

Judge Gilliam went further to point out that some of plaintiffs’ proffer did not even purport to claim causation. Shanna Swan’s prior testimony asserted that Bendectin was “associated” with limb reduction. Jay Glasser, a specialist in biostatistics, epidemiology and biometry had opined that “Bendectin is within a reasonable degree of epidemiological certainty associated with congenital disorders, including limb defects.” Dr. Johannes Thiersch, a specialist in pathology and pharmacology, proclaimed that “structure analysis” was “of great interest.”[26] In other words, there was a good deal of true, true, but immaterial opinion in what Mr. Nace had thrown over the transom, in opposition to the motion for summary judgment.

Nace appealed, and the Daubert case was argued to the Ninth Circuit in 1991. In a short opinion by Judge Kozinski, the appellate court affirmed the judgment below.[27] The affirmance did not mention Rule 702; rather it relied upon the decisions of other Circuits, in which the plaintiffs’ evidentiary display had been found insufficient to sustain a reasonable jury verdict.

Judge Kozinski’s opinion tilted towards Rule 703 and the Frye standard in citing to cases that stated, based upon Frye, that expert witnesses must use generally accepted techniques from the scientific community. As a legal determination, the determination of general acceptance vel non was a legal determination reviewable de novo. For its de novo decision on general acceptance, the Ninth Circuit relied upon the cases coming from the First, Fifth, and District of Columbia Circuits,[28] and of course, the record below.

By 1991, another Circuit, the Third, had weighed in on the same evidentiary display, when it reversed summary judgment for Merrell Dow, and remanded for reconsideration under the Third Circuit’s approach to Rule 702. Judge Kozinski declared that the Third Circuit’s approach was not followed in the Ninth Circuit, and proceeded to ignore the DeLuca case.[29]

Judge Kozinski treated the insufficiency and the invalidity of the Nace/Done schmeggege theory as legal precedent, and thus the court’s opinion gave very little attention by way of expository description or explanation of the problems with the four factors (in vitro, in vivo, structure analysis, and re-analysis of epidemiologic studies). As Judge Kozinski put the matter:

 “For the convincing reasons articulated by our sister circuits, we agree with the district court that the available animal and chemical studies, together with plaintiffs’ expert reanalysis of epidemiological studies, provide insufficient foundation to allow admission of expert testimony to the effect that Bendectin caused plaintiffs’ injuries.”[30]

And thus, summary judgment was proper in Daubert. Judge Kozinksi, like Judge Gilliam in the district court, never reached the specific causation argument that involved risk ratios less than two.

Some of the Circuit court cases relied upon by Judge Kozinski delved into the invalidity of these methods for determining the causes of human birth defects. The Lynch decision explored in some detail the Shanna Swan made-for-litigation rejiggering of a study based upon data from the Metropolitan Atlanta Congenital Defects Program, which included a challenge to whether it could be reasonably relied upon (Rule 703), as well as its pretense to support a scientific conclusion (Rule 702).[31] Later commentators would skirt the validity issue by asserting that re-analysis, in the abstract, is not impermissible or invalid, without addressing the specific issues discussed in the reported decisions. Other commentators have misrepresented Swan’s re-analysis as a meta-analysis, which it was not.

Some commentators have complained that the defense in Daubert made too much of the lack of statistical significance. Their complaint, in the abstract, might have some salience. In some contexts, an isolated and elevated risk ratio greater or less than one may well have important information, even if the p-value is a bit above 0.05. The lack of statistical significance at the conventional five percent, however, conveys important information about the finding’s imprecision, especially when there was a large dataset to evaluate. In 1994, a meta-analysis was published that found a summary estimate of all birth defects in the available epidemiologic studies to be an odds ratio of 0.95 (95% C.I., 0.88-1.04), and the summary estimate for limb reduction defects to be an odds ratio 1.12 (95% C.I., 0.83-1.48).[32]


[1] Defendant’s Memorandum of Points and Authorities in Support of Its Motion for Summary Judgment on the Issue of Causation, Daubert v. Merrell Dow Pharms., Inc., Case No. 84-2013-G(I) (S.D. Cal. Aug. 2, 1989). The motion was made in a companion case before Judge Gilliam as well, Schuller v. Merrell Dow Pharms., Inc., Case No. 84-2929-G(I). The first Daubert motion may not have been the first one drafted. The linked brief is the first one as filed.

[2] See Oxendine v. Merrell Dow Pharms., Inc., 563 A.2d 330 (D.C. Ct. App. 1989).

[3] William Griffith McBride, Thalidomide and Congenital Abnormalities, 278 LANCET 1358 (1961).

[4] William Griffith McBride, McBride criticizes inquiry, 336 NATURE 614 (1988); Norman Swan, Disciplinary tribunal for McBride, 299 BRIT. MED. J. 1360 (1989); G. F. Humphrey, Scientific fraud: the McBride case, 32 MED. SCI. LAW 199 (1992); Mark Lawson, McBride found guilty of fraud, 361 NATURE 673 (1993); Leigh Dayton, Thalidomide hero found guilty of scientific fraud, NEW SCI. (Feb.27, 1993); William McBride: alerted the world to the dangers of thalidomide in fetal development, 362 BRIT. MED. J. k3415 (2018).

[5] McBride v. Merrell Dow & Pharms., Inc., 800 F.2d 1208 (D.C. Ct. App. 1986). McBride ultimately failed against all his litigation targets.

[6] See In Re Richardson-Merrell. Inc. Bendectin Prods. Liab. Litig., 624 F.Supp. 1212 (S.D. Ohio 1985); aff’d sub nom. In re Bendectin Litig., 857 F.2d 290 (6th Cir. 1988); cert. denied, 488 US 1006 (1989).

[7] Brock v. Merrell Dow Pharmaceuticals Inc., 874 F.2d 307 (5th Cir. 1989); Richardson y. Richardson-Merrell, 857 F.2d 823 (D.C. Cir. 1988); Lynch v. Merrell-National Labs., 830 F.2d 1190 (1st Cir. 1987) (affirming grant of summary judgment).

[8] US Food & Drug Admin., Determination That Bendectin Was Not Withdrawn from Sale for Reasons of Safety or Effectiveness, 64 FED. REG. 43190–1 (1999).

[9] Brief at 3-4.

[10] Barry Nace was one of the lead plaintiffs’ counsel in the Bendectin litigation, and he represented the Daubert family. Nace was also formerly President of the lawsuit industry’s principal lobbying organization, the American Trial Lawyers Association (now the AAJ). See also In re Barry J. Nace, A Member of the Bar of the District of Columbia Court of Appeals (Bar Registration No. 130724), No. 13–BG–1439, Slip op. (Sept. 4, 2014), available at <https://www.dccourts.gov/sites/default/files/pdf-opinions/13-BG-1439.pdf>, last visited on Feb. 8, 2026.

[11] See Michael D. Green, Pessimism about Milward, 3 WAKE FOREST J. L & POL’Y 41, 63 (2013) (paraphrasing Nace as describing the mosaic theory as “[d]amn brilliant, and I was the one who thought of it and fed it to Alan [Done].”).

[12] Id. at 61 (2013) (citing Oxendine v. Merrell Dow Pharm., Inc., 506 A.2d 1100, 1110 (D.C. 1986).

[13] Harry Frankfurt, ON BULLSHIT 63 (2005).

[14] In re “Agent Orange” Prod. Liab. Litig., 611 F. Supp. 1223 (E.D.N.Y. 1985), aff’d, 818 F.2d 187 (2d Cir. 1987), cert. denied, 487 U.S. 1234 (1988).

[15] Id. at p. 1231.

[16] United States Dep’t of Justice, Tort Policy Working Group, Report of the Tort Policy Working Group on the causes, extent and policy implications of the current crisis in insurance availability and affordability at 35 (Report No. 027-000-01251-5) (Wash. DC 1986), available at https://archive.org/details/micro_IA41152903_0369.

[17] In Re Air Crash Disaster at New Orleans, 795 F.2d 1230, 1233-34 (5th Cir. 1986).

[18] Id. at 1233-34.

[19] The Brief, at 2, cited United States v. Kilgus, 571 F.2d 508, 510 (9th Cir. 1987) (citing Frye).

[20] An Act to Establish Rules of Evidence for Certain Courts and Proceedings. Pub. L. 93–595, 88 Stat. 1926 (1975).

[21] Brief at 17.

[22] 545 F.Supp. 306, 308 (N.D. Cal. 1982). See generally Richard E. Neustadt & Harvey V. Fineberg, THE SWINE FLU AFFAIR: DECISION-MAKING ON A SLIPPERY DISEASE (Nat’l Acad. Sci. 1978).

[23] Daubert v. Merrell Dow Pharms., Inc., 727 F.Supp. 570 (S.D. Cal. 1989).

[24] Id. at 571, citing United States v. Kilgus, 571 F.2d 508, 510 (9th Cir.1978).

[25] Id. at 572 (citing Brock, 874 F.2d at 310).

[26] Id. at 574. The use of “association” was at best ambiguous, because it begged the question whether it as an association that was “clear cut” (reasonably free from bias and confounding), and beyond that which we would care to attribute to chance.

[27] Daubert v. Merrell Dow Pharms., Inc., 951 F.2d 1128 (9th Cir. 1991).

[28] Brock v. Merrell Dow Pharms., Inc., 874 F.2d 307, modified, 884 F.2d 166 (5th Cir.1989), cert. denied, 494 U.S. 1046 (1990); Richardson v. Richardson–Merrell, Inc., 857 F.2d 823 (D.C.Cir.1988), cert. denied, 493 U.S. 882 (1989); Lynch v. Merrell–National Labs., 830 F.2d 1190 (1st Cir.1987).

[29] DeLuca v. Merrell Dow Pharmaceuticals, Inc., 131 F.R.D. 71 (D.N.J.) (granting summary judgment), rev’d and remanded, 911 F.2d 941 (3d Cir.1990). On remand, the district court entered summary judgment on the alternative reasoning of Rule 702, as interpreted by the Third Circuit. DeLuca v. Merrell Dow Pharms., Inc., 791 F.Supp. 1042, 1048 (D.N.J. 1992) (re-entering summary judgment after considering Rule 702), aff’d, 6 F.3d 778 (3d Cir.1993) (per curiam), cert. denied, 510 U.S. 1044 (1994).

[30] Daubert v. Merrell Dow Pharms., Inc., 951 F.2d 1128, 1131 (9th Cir. 1991).

[31] Lynch v. Merrell–National Labs., 830 F.2d 1190, 1194-95 (1st Cir.1987).

[32] Paul M. McKeigue, Steven H. Lamm, Shai Linn & Jeffrey S. Kutcher, Bendectin and Birth Defects: I. A Meta-Analysis of the Epidemiologic Studies, 50 TERATOLOGY 27 (1994). This meta-analysis made no correction for multiple comparisons in examining many different types of birth defects.

Prada – Fashionable, But Unreliable Review on Acetaminophen and Autism

September 30th, 2025

Back in the first week of this month, I posted about a paper (Prada 2025),[1]  which featured a so-called navigation-guide systematic review of the scientific evidence on the issue whether pregnant women’s ingestion of acetaminophen causes their children to develop autism.[2] The focus of my post was on some dodgy aspects of the Prada review, such as its anemic disclosures of interest, and its squirrely claim to have been “NIH funded.”

Since posting, the Prada review has been very much in the news. Last week, President Trump held a news conference, where we learned that he cannot pronounce acetaminophen and that he has a strongly held opinion that acetaminophen causes autism.[3] Trump was surrounded by officials in his administration, including plaintiffs’ lawyer Robert Kennedy, Jr., and three physicians, Drs. Oz, Makary, and Bhattacharya, who looked on in apparent approval. Once upon a time, a risk communication such as this one about acetaminophen, would have come out from a non-political FDA employee, such as Janet Woodcock, who was head of Drug Safety, and for many years the Director of Center for Drug Evaluation and Research. Over her tenure, Dr. Woodcock weighed in on many pharmaceutical safety issues. Those of us who have been involved in litigation of those safety issues remember that Dr. Woodcock chose her language very carefully. She did not just give opinions; she marshalled facts.

Admittedly, Trump’s autism press conference was not as deranged as his 2020 press conference at which he suggested that injecting sodium hypochlorite (bleach) into patients would cure Covid-19 infections. Still, most of the world was left with the impression that Trump was replacing (DOGE-ing) scientific research and replacing it with irrational speculation. Trump’s press conference on acetaminophen and vaccines was widely met with skepticism and disbelief. Medical ethicist Dr. Arthur Caplan, who is not given to hyperbole, called the conference “the saddest display of a lack of evidence, rumors, recycling old myths, lousy advice, outright lies, and dangerous advice I have ever witnessed by anyone in authority.”[4]

When the administration physicians communicated with the public, they said something very different from Trump’s presentation. In her press release, Press Secretary Karoline Leavitt used the meaningless locution, “suggested link,” and cited the Prada review, which eschewed causal conclusions:[5]

“Andrea Baccarelli, M.D., Ph.D., Dean of the Faculty, Harvard T.H. Chan School of Public Health: “Colleagues and I recently conducted a rigorous review, funded by a grant from the National Institutes of Health (NIH), of the potential risks of acetaminophen use during pregnancy… We found evidence of an association between exposure to acetaminophen during pregnancy and increased incidence of neurodevelopmental disorders in children.

Harvard University: Using acetaminophen during pregnancy may increase children’s autism and ADHD risk.”

Of course, saying that something “may increase risk” is not even close to saying that something causes the outcome in question. And Baccarelli’s description of his paper, Prada review, as funded by the National Institutes of Health is misleading at best.[6]

Leavitt went on to declare that “[t]he Trump Administration does not believe popping more pills is always the answer for better health.” Unless of course, it is Propecia for Mr. Trump, testosterone for Mr. Kennedy, or ketamine for Mr. Musk.

FDA Commissioner Martin A. Makary issued a Notice, the same day, in which he declared:

“In recent years, evidence has accumulated suggesting that the use of acetaminophen by pregnant women may be associated with an increased risk of neurological conditions such as autism and ADHD in children.

* * *

To be clear, while an association between acetaminophen and autism has been described in many studies, a causal relationship has not been established and there are contrary studies in the scientific literature.”[7]

So the FDA is clearly not declaring that acetaminophen causes autism.

Dr. Mehmet Oz, former surgeon and television talking head, who stood mute by Trump’s side at the infamous press conference, found his voice later in the week, when he acknowledged that pregnant women of course should take acetaminophen when physicians direct them to do so.

In Europe, where pharmaceutical regulation is typically more precautionary than in the United States, both the European Medicines Agency and the U.K.’s Medicines and Healthcare Products Regulatory Agency announced that using acetaminophen during pregnancy was safe with no showing that it causes autism in offspring.[8] Steffen Thirstrup, the EMA’s Chief Medical Officer, announced a day after the Trump bungle, that:

“Paracetamol [acetaminophen] remains an important option to treat pain or fever in pregnant women. Our advice is based on a rigorous assessment of the available scientific data and we have found no evidence that taking paracetamol during pregnancy causes autism in children.”

Most medical organizations were appalled at the administration’s sloppy messaging. The day after the press conference, the American College of Medical Toxicology (ACMT) issued a statement in response, to affirm the safety of acetaminophen in pregnancy.[9] The ACMT noted that its position was in agreement with the American College of Obstetrics and Gynecologists, the Society for Maternal-Fetal Medicine, the American Academy of Pediatrics, and the Society for Developmental and Behavioral Pediatrics.

The acetaminophen kerfuffle seems always to come back to the Prada “navigation guide” systematic review and its authors, including the Harvard Dean, Andrea Baccarelli, who was the well-paid member of the plaintiffs’ expert witness team in acetaminophen litigation.[10] Why did Dr. Andrea Baccarelli in the Prada review use this curious, arcane, and infrequently used method of review? Why did Baccarelli and his co-authors publish this review in Environmental Health, which is dedicated to publishing “manuscripts on important aspects of environmental and occupational medicine,” which places maternal ingestion of a licensed pharmaceutical outside its stated competence? Why did Baccarelli offer a litigation opinion that acetaminophen causes autism, but retreat to “association” when writing for the scientific community? And why did Baccarelli and his co-authors not disclose that Baccarelli had submitted essentially the same navigation guide systematic review as his proffered expert witness testimony, and that a federal court had rejected his opinion as not “the product of reliable principles and methods,” and not “a reliable application of the principles and methods to the facts of the case”[11]? Perhaps the answers are obvious to most observers, but candid disclosures certainly would have provided important context, and saved some people the embarrassment of relying upon the Prada review.

In digging deeper into the history of the navigation guide method itself, the earliest citation I could find to such systematic reviews was in 2009, in a conference paper that discussed this approach as a proposal.[12] The authors that made up the Navigating the Scientific Evidence to Improve Prevention Workshop Organizing Committee were not particularly well known or distinguished in the field of research synthesis. Still, there must be other reasons that “navigation guide” reviews are not more prevalent if the Organizing Committee had been truly on to something important.

The Committee never identified a rationale for a new systematic review approach. When the Organizing Committee outlined its approach in 2009, there were well over three decades of experience with systematic reviews,[13] with well-regarded full-length textbook treatment by experts in the field.[14]

In addition to the lack of experience among its authors and the preemption of the subject by comprehensive treatments elsewhere, there were three additional curious take aways from a cursory reading of the Organizing Committee’s 2009 manuscript. First, Committee emphasized the alleged need for a review methodology for environmental exposures. This emphasis was never accompanied by a showing that well-described methodologies long in use were somehow inadequate or inappropriate for environmental exposures.

Second, the authors urged the need for precautionary assessments, which might make their method fine where syntheses for precautionary pronouncements were called for. In the United States, regulatory assessments vary depending up the governing statutes that create the regulatory mandate.  In personal injury litigation, the precautionary principle is nothing less than an end run around the burden of proof on the party claiming harm and suing in tort. The designated subject matter of environmental exposures for the proposed systematic review technique offers an insight into why these authors believed that they had to propose a new fangled systematic review methodology. Previously described methods interfered with authors’ ability to elevate “iffy” associations into conclusions of causality in the name of the precautionary principle.

The third curiosity in the 2009 manuscript is that the authors never described the need for a pre-specified protocol. Later articles on this proposed methodology similarly failed to describe the need for such a protocol,[15] although by 2014, authors from the original Organizing Committee reversed course to add a pre-specified protocol to the requirements for a navigation guide systematic review.[16]

A recent article defines a systematic review essentially in terms of a protocol:

“Systematic review (SR) is a rigorous, protocol-driven approach designed to minimise error and bias when summarising the body of research evidence relevant to a specific scientific question.”[17]

The purpose of a protocol may be obvious to anyone who has been paying attention to the replication crisis in biomedical literature, but the same article offers a helpful description of its rationale:

“The purposes of the protocol are to discourage ad-hoc changes to methodology during the review process which may introduce bias, to allow any justifiable methodological changes to be tracked, and also to allow peer-review of the work that it is proposed, to help ensure the utility and validity of its objectives and methods.”[18]

Systematic reviews vary widely in quality, methodological rigor, and validity, but one of the key determinants of their validity is whether they were preceded by pre-specified protocol. Although systematic reviews are often described the “gold standard” for evidence synthesis, their methodological rigor vary widely. Reviews that lack a pre-specified protocol are decidedly less rigorous than those reviews that employ a protocol.[19] The absence of a protocol is thus an important tell that a systematic review may be untrustworthy.

The Prada paper put together by Baccarelli’s team has no protocol. It may satisfy the Trump administration’s Fool’s Gold Standard for Science, but that is far short of the requirements of Federal Rule of Evidence 702. Given Baccarelli’s abridgement of scientific method, we should not be overly surprised by Judge Cote’s judgment of the failures of Baccarelli’s and the other plaintiffs’ expert witnesses’ proffered opinions in the acetaminophen litigation:

“their analyses have not served to enlighten but to obfuscate the weakness of the evidence on which they purport to rely and the contradictions in the research. As performed by the plaintiffs’ experts, their transdiagnostic analysis has obscured instead of informing the inquiry on causation.”[20]

Judge Cote carefully reviewed Baccarelli’s proffered testimony and found it replete with cursory analyses, cherry-picked data, and result-driven assessments of studies.[21] Her Honor’s findings would seem to apply with equal measure to the Prada review.


[1] Diddier Prada, Beate Ritz, Ann Z. Bauer and Andrea A. Baccarelli, “Evaluation of the evidence on acetaminophen use and neurodevelopmental disorders using the Navigation Guide methodology,” 24 Envt’l Health 56 (2025).

[2] See Schachtman, “Acetaminophen & Autism – Prada Review Misleadingly Claims to Be NIH Funded,” Tortini (Sept. 9, 2025).

[3] Jeff Mason, Ahmed Aboulenein, and Julie Steenhuysen, “Trump Links Autism to Tylenol and Vaccines, Claims Not Backed by Science,” Reuters (Sept. 22, 2025); Brianna Abbott & Andrea Petersen, “The Trump administration said acetaminophen could cause autism. Doctors maintain it is safe during pregnancy,” Wall St. J. (Sept. 22, 2025) (“Studies looking at a link [sic] between acetaminophen and autism are inconclusive.”); Will Weissert, “Dr. Trump? The president reprises his COVID era, this time sharing unproven medical advice on autism,” Wash. Post (Sept. 23, 2025).

[4] Ali Swenson & Lauran Neergaard, “Trump makes unfounded claims about Tylenol and repeats discredited link between vaccines and autism,” Assoc. Press (Sept. 23, 2025).

[5] Leavitt, “FACT: Evidence Suggests Link Between Acetaminophen, Autism,” The White House (Sept. 22, 2025).

[6] See Schachtman, “Acetaminophen & Autism – Prada Review Misleadingly Claims to Be NIH Funded,” Tortini (Sept. 9, 2025). The referenced grants had nothing to do with acetaminophen and autism, or even autism generally. The NIEHS granted Dr. Baccarelli money to study air pollution and brain aging. The exposure of interest was not acetaminophen, and the outcome of interest was not autism. By claiming that his research was “NIH funded,” Baccarelli was attempting to boost the prestige of the research even though his acetaminophen review was done for litigation, not for the federal government. Apparently the NIEHS acquiesces in this charade because it suggests to the uninitiated that its research grants result in more published papers, even though the topics of those papers are unrelated to the funded research proposal, and the unrelated topics never receiving committee peer review.

[7] Martin A. Makary, “Notice to Physicians on the Use of Acetaminophen During Pregnancy,” (Sept. 22, 2025).

[8] E.M.A., “Use of paracetamol during pregnancy unchanged in the EU,” (Sept. 23, 2025).

[9] ACMT Supports the Safe Use of Acetaminophen in Pregnancy (Sept. 23, 2025).

[10] Rebecca Robbins & Azeen Ghorayshi, “Harvard Dean Was Paid $150,000 as an Expert Witness in Tylenol Lawsuits,” N.Y. Times (Sept. 23, 2025).

[11] Fed. R. Evid. 702.

[12] Patrice Sutton, Heather Sarantis, Julia Quint, Mark Miller, Michele Ondeck, Rivka Gordon, and Tracey Woodruff, “Navigating the Scientific Evidence to Improve Prevention: A Proposal to Develop A Transparent and Systematic Methodology to Sort the Scientific Evidence Linking Environmental Exposures to Reproductive Health Outcomes,”  (July 29, 2009).

[13] See Quan Nha Hong & Pierre Pluye, “Systematic reviews: A brief historical overview,” 34 Education for Information 261, 261 (2018) (describing the evolution of systematic reviews as made up of a “foundation period 1970-1989,” an “institutionalization period 1990-2000, and a “diversification period” from 2001 forward.)

[14] Matthias Egger, Julian P. T. Higgins, and George Davey Smith, Systematic Reviews in Health Research: Meta-Analysis in Context (3rd ed. 2022). The first edition of this text was published in 1995.

[15] Tracey J. Woodruff, Patrice Sutton, and The Navigation Guide Work Group, “An Evidence-Based Medicine Methodology To Bridge The Gap Between Clinical And Environmental Health Sciences,” 30 Health Affairs 931 (2011); Julia R. Barrett, “The Navigation Guide Systematic Review for the Environmental Health Sciences,” 122 Envt’l Health Persp. A283 (2014).

[16] Tracey J. Woodruff & Patrice Sutton, “The Navigation Guide Systematic Review Methodology: A Rigorous and Transparent Method for Translating Environmental Health Science into Better Health Outcomes,” 122 Environ Health Perspect. 1007 (2014).

[17] Paul Whaley, Crispin Halsall, Marlene Ågerstrand, Elisa Aiassa, Diane Benford, Gary Bilotta, David Coggon, Chris Collins, Ciara Dempsey, Raquel Duarte-Davidson, Rex Fitzgerald, Malyka Galay-Burgos, David Gee, Sebastian Hoffmann, Juleen Lam, Toby Lasserson, Len Levy, Steven Lipworth, Sarah Mackenzie Ross, Olwenn Martin, Catherine Meads, Monika Meyer-Baron, James Miller, Camilla Pease, Andrew Rooney, Alison Sapiets, Gavin Stewart, and David Taylor, “Implementing systematic review techniques in chemical risk assessment: Challenges, opportunities and recommendations,” 92-93 Env’t Internat’l 556 (2016).

[18] Id. at 560.

[19] Julia Menon, Fréderique Struijs & Paul Whaley, “The methodological rigour of systematic reviews in environmental health,” 52 Critical Rev Toxicol. 167 (2022).

[20] In re Acetaminophen ASD-ADHD Prods. Liab. Litig., 707 F. Supp. 3d 309, 334, 2023 WL 8711617 (S.D.N.Y. 2023) (Cote, J.).

[21] Id. at 354-56.