This is actually the second time we have written on a decision from a case involving banana plantations.  The first involved violence against Colombian banana plantation workers by the paramilitary/terrorist group known by the initials of its Spanish name, AUC.  This one involves claims of various health effects from the application of a particular pesticide on various plantations in Central and South America.  Heavy stuff, so we will deflect by mentioning the beloved Caribbean ditty “Day-O,” also known as “The Banana Boat Song.”  If it were to start playing, you would probably be able to sing along with the familiar lyrics.  In one, it is said that “a beautiful bunch of ripe bananas . . . hides the deadly black tarantula.”  In fact, the only species of tarantula endemic to any Caribbean islands is neither black nor deadly to humans.  One of the recurring lyrics recounts stacking bunches of bananas so that the “tally man” can “tally [the] bananas.”  This references how the plantation worker would get the appropriate credit for the bananas he or she gathered.  Fun song that we have known since we were kids, but so what, you mumble.  Well, Patrickson v. Dow Chem. Co., No. SCWC-22-0000687, 2026 Haw. LEXIS 266 (Haw. Sept. 21, 2026), is about the standards for evaluation causation in toxic tort cases and the court made some elementary mistakes.

The Patrickson litigation has been going on for a long time.  The Blog previously included a 2015 Hawai’i Supreme Court decision in a post on cross-jurisdictional class action tolling.  That came more than a decade after the U.S. Supreme Court issued a 2003 decision in the litigation on the application of the Foreign Sovereign Immunities Act.  For a case this old, it is surprising that the standards for causation had not come up before.  How a Hawai’i state court would have jurisdiction over these claims and how they could possibly be timely—the plaintiff at issue on appeal sustained alleged injuries between 1971 and 1983 and literature was out by 1980 describing some association between the pesticide and reproductive harms—are perhaps even bigger mysteries.  We are also not sure the plaintiff (or his estate, because he died after filing) is the right one to sue for the alleged injuries, that they are compensable, or that the claims should have survived his death.  Setting all that aside, the pertinent facts are that the decedent worked for a subsidiary of one of the defendants in Costa Rica between 1971 and 1973, where he was allegedly exposed to a pesticide made by another defendant.  His job did not involve applying or distributing the pesticide and he never saw it applied, but he might have been around “sacks” of it in a warehouse if he sought shelter there during heavy rain.  His claimed injuries were “infertility” and other reproductive impacts based on 1) his wife having only four new pregnancies in the years following the relatively short employment at issue and 2) three of those new pregnancies ending in a miscarriage or spontaneous abortion.  (Plaintiff’s wife also had a child who was born and died of “an illness” in the year he started work, and they also adopted another child.)  After the case eventually proceeded to discovery, defendants won summary judgment on the lack of proof of exposure and excluded plaintiff’s causation expert, largely because he assumed there had been sufficient exposure to cause the claimed reproductive injuries.

The intermediate appellate court reversed, and an appeal to the Supreme Court of Hawai’i followed.  The Patrickson decision quickly went off the rails.  It took two separate dives into the court’s prior endorsement of the alternate market share theory of liability on a certified question from the Ninth Circuit in Smith v. Cutter Biological, Inc., 823 P.2d 717 (Haw. 1991).  2026 Haw. LEXIS 266, *2-4 & 16-23.  Smith may be noteworthy because it is the only high court decision we know that applied this silly theory in the context of a prescription medical product other than DES, but even Patrickson said up front that the theory was “inapposite” to the plaintiff’s claims because the identity of the manufacturer of the pesticide that plaintiff’s employer used was known.  Id. at *3.  Market share theories have nothing to do with single manufacturer cases or cases where plaintiffs have proof of exposure to a specific defendant’s product, which plaintiff claimed to have in Patrickson.  They are for cases where plaintiffs cannot satisfy basic product identification requirements applicable to all product liability cases.  So, what was the point of talking about Smith so much?  Patrickson’s circuitous reasoning was that Smith showed Hawai’i could make up new causation standards to help “innocent plaintiffs” recover against someone with money.  Id. at *3, 18 & 21.  But the plaintiff in Patrickson had identified defendants and did not need some new causation theory any more than the typical plaintiff who sues a prescription drug company over an injury alleged sustained from taking its drug.  Hawai’i already has causation standard for such a product liability case.  It also has its own version of Daubert and a Rule 702 that is patterned after an older version of Federal Rule of Evidence 702.  Id. at *28-30.  Using a prescription medical product case as the core reason why the court had to devise a “causation standard in toxic tort cases” or “how causation should be addressed in mass toxic tort cases” seems like poor justification.  Id. at *12 & 22.  If plaintiff cannot make out product liability claims because of lack of proof, then the solution should not be to relax those standards for an ill-defined subset of product liability cases.

Still, some of the discussion of what a plaintiff has to prove was really basic.  After looking at various cases and Restatement provisions, Patrickson declared that each toxic tort plaintiff has to prove exposure, general causation, and specific causation.  Id. at *23-24.  Everyone knows those are requirements in all but the simplest product liability cases (e.g., the injury is claimed from a blunt force trauma).  The only places where that is not clear in cases involving the ingestion of drugs, the implantation of a medical device, or exposure to an allegedly harmful chemical are where courts get confused about there being two kinds of causation.  Good for Patrickson to recognize the obvious.  Also, Patrickson noted that “expert testimony should be required to establish causation in toxic tort cases, just as in medical negligence cases, given the special difficulty these cases present in proving a connection between a toxic substance and the development of a specific disease with a potentially significant latency period.”  Id. at *25.  Again, this is the law everywhere for drug, device, and chemical exposure cases, but it is good to reinforce.  (Also, plaintiff did not claim any “significant latency” period in the alleged impact on his reproduction, so we do not know why latency was raised.)  Then things got, well, bananas as Patrickson essentially undercut the basic principles it had reaffirmed.

The court stated that it “declined” to require a plaintiff “to provide expert testimony quantifying the exposure level or dosage to meet their burden of production.”  Id. at *26 (emphasis in original)  Instead, after a discussion that strayed into unrelated issues, the court held “that a plaintiff should offer some evidence ‘that he or she was exposed to the toxin at issue, including the estimated amount and duration of exposure.’”  Id. at *28 (quoting Lowery v. Enbridge Energy Ltd. P’ship, 898 N.W.2d 906, 914-15 (Mich. 2017) (concurrence, Markman, C.J.)). First, those are not actually different standards.  Second, what the concurrence in Lowery actually described was the importance of the quantification of exposure in the causation analysis:  “Accordingly, a plaintiff’s evidence of general causation should be tailored to the estimated amount and duration of exposure at issue to enable the fact-finder to reasonably conclude that exposure to the defendant’s toxin in the amount and duration alleged is capable of causing the alleged injury.”  898 N.W.2d at 914 (emphasis in original).  In that case, the concurrence wrote, the “plaintiff’s general-causation evidence falls short because it fails to show what level and duration of exposure to VOCs can cause the severity and duration of coughing and vomiting that is necessary to cause a gastric artery to avulse.”  Id. at 919 (emphasis in original).  In other words, if the general causation evidence is going to tie to the specific causation evidence, then the quantification of the plaintiff’s exposure must be relevant to what the studies show.  When it comes to expert evidence, there is a word for that concept:  fit.  The plaintiff’s experts’ opinions on causation must fit the case, or “reflect[] a reliable application of the principles and methods to the facts of the case” in the language of current Fed. R. Evid. 702(d).

Several of the authorities cited in Patrickson as the court tried to justify lowering the bar on causation make it clear that fit on the level of exposure or dose is important.  For instance, In re Hanford Nuclear Rsrv. Litig., 292 F.3d 1124 (9th Cir. 2002), which Patrickson cited as supporting the proposition that both general and specific causation could be established without quantifying the level of exposure, actually concluded with, “On remand, the district court should assess the plaintiffs’ proffered expert testimony as it relates to the generic causation inquiry, i.e., whether the radiation released from Hanford has the capacity to cause the illnesses alleged by plaintiffs.”  That requires quantification and fit.  If you go to the Federal Judicial Manual on Scientific Evidence, which is widely cited in the cases that Patrickson cited, includes extensive discussions about how the plaintiff’s general and specific causation evidence has to match on the dose or exposure.  Just going off of subject headings, within the section on “Specific Causal Association Between an Individual’s Exposure and Onset of Disease” are subsections on “Was the Plaintiff Exposed to the Substance, and If So, Did the Exposure Occur in a Manner That Can Result in Absorption into the Body?” and “When Exposure to the Substance Is Associated with the Disease, Is There a Benchmark Dose or No Observed Adverse Effect Level, and If So, Was the Individual Exposed Above This Level?”  Pretty obvious.  We could go on.  We could also say more about how the issues of whether epidemiologic studies are required to prove general causation, whether they must show a greater than 2.0 relative risk, and what differential diagnosis has to do with causation do not have much if anything to do with what plaintiff has to who about the “estimated amount and duration of exposure” to the substance that allegedly harmed her.  2026 Haw. LEXIS 266, *26-28.  The result was a fuzzy standard disconnected from the authorities discussed and basic principles of science.

The application to the evidence in Patrickson that the circuit court had considered in granting summary judgment made things worse. 

The circuit court was requiring a certain level of exposure when it [excluded the causation expert and granted summary judgment]. But we conclude that DiBartolomeis’s expert testimony met the touchstone of relevance and reliability, and that the ICA correctly held that the circuit court abused its discretion by excluding that evidence.

Id. at *29.  The basis for the expert’s assumption of exposure was the plaintiff’s deposition testimony about mere possibilities of some uncertain level of exposure and a study that raised a mere possibility of a relationship to spontaneous abortions in agricultural workers with documented exposure.  According to Patrickson, these “do provide circumstantial proof to facilitate a reasonable inference as to exposure and specific causation.”  Id. at *31.  It further noted that it could be sufficient for an expert’s opinion about causation to say “that a toxic substance ‘might’ be or ‘probably’ was the cause of the injury.”  Id. at *33.  There are a bunch of things wrong with these two statements.  Somewhat ironically, the court quotes the same passage from the referenced study twice, but does so inconsistently:  “[I]t is plausible that DBCP is causing an increased rate of spontaneous abortion in the exposed population through its effect on spermatogenesis” and “[I]t is possible that DBCP is causing an increased rate of spontaneous abortion in the exposed population through its effect on spermatogenesis.”  Id. at *8 & 27 n.7.  Just as “plausible” and “possible” mean different things, opinions on merely possible (“might be”) causation and likely (“probably was”) causation are different.  The former is inadmissible and the latter might be admissible if it is otherwise reliable and relevant.  In addition, a study on agricultural workers in Israel cannot be proof of past exposure for a plaintiff who once was an agricultural worker in Costa Rica.  The study could be part of a reliable opinion on general causation, but it would not support specific causation unless the “the estimated amount and duration of exposure” shown in the plaintiff—which Patrickson said it required—was relevant to what the study showed increased the risk of the same alleged injury.  Allowing expert testimony on disconnected possibilities does not fulfill the court’s role as a gatekeeper, which Patrickson also emphasized:  “[T]rial courts should exercise their gatekeeping function to ascertain whether proposed expert testimony meets the touchstones of relevance and reliability.”  Id. at *28-29.  With all these inconsistencies, it is hard to say that the Patrickson court articulated a standard at all.

This brings us back to our lyrical detour.  You need proof of exposure and general causation evidence that matches up with the specific causation issues in the case.  If the allegation is that the plaintiff died from a black tarantula bite while on a Caribbean island, then there would need to be proof of a bite and there would need to be expert evidence that the bite was capable of producing death.  There are no black tarantulas native there and the pink ones do not have venom that can kill a human, apparently,  Exposure needs to be quantified so you can see how it fits with the general causation evidence.  You need to tally up your bananas in whatever measure is used for banana counting for purposes of payment.  Or you need to count your tarantula venom exposure by whatever measure of tarantula venom (or its neurotoxin components) is used in the studies.  There are surely less circuitous analogies to what should be included in a causation analysis in a case where an injury is claimed from exposure to a substance.  The disjointed analysis in Patrickson, however, just makes us want to go home.