In 1986, decades after the Minamata disaster, workers still discarded mercury-tainted fish from the bay.
The Asahi Shimbun/Getty Images
The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong.
No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory’s wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. But methylmercury is not the culprit, says Ingrid Pickering, an x-ray spectroscopist at the University of Saskatchewan. “Our work is indicating that it’s something else”: an unusual mercury compound that may say little about the broader threat of mercury pollution.
Minamata has long been a vivid case study of mercury’s dangers. The metal is toxic on its own, but it becomes far more dangerous when bacteria in natural environments convert it into methylmercury, an organic compound, readily absorbed by living tissues, that can be concentrated and passed up food chains. Since the 1990s, scientists have argued that the Chisso chemical factory in Minamata produced methylmercury and dumped it directly into the bay.
The dead cat now challenging that picture dates to 1959, when the then-mysterious neurological disease was sweeping through the city. A doctor working for the Chisso factory mixed wastewater with cat food and fed it to cats, which started to convulse and were paralyzed before dying. He autopsied two of them, known only as 400 and 717. Their behavior and lesions in their brains suggested the same disease as the one raging outside. Factory supervisors hushed up the finding.
The Chisso cats were lost until 2001, when Komyo Eto, a pathologist at the National Institute for Minamata Disease, studied samples of the cats and the wastewater that had been found in storage at nearby Kumamoto University—along with lab notebooks lent by the factory doctor’s wife. His measurements showed that less than half of the mercury in the cats’ brain samples occurred as methylmercury; the rest was inorganic. Only a minuscule fraction of the wastewater’s mercury was methylmercury, but Eto thought that was probably because the compound had broken down over the 4 decades since the samples were taken.
Now, Pickering and her colleagues have reanalyzed samples of cat 717’s cerebellum at the Stanford Synchrotron Radiation Lightsource, blasting them with x-rays and analyzing the resulting spectrum for the fingerprints of specific molecules. The molecules that best fit the spectrum don’t contain any methylmercury at all, they found. Instead, three-quarters of the sample’s mercury appears to be an obscure organic compound called alpha-mercuri-acetaldehyde that likely came straight from the wastewater, they argue. The rest was inorganic mercury.
The finding suggests the Minamata disaster—and methylmercury poisoning more generally—is due for a rethink, the researchers argue in their study, published in Environmental Science & Technology in January. Methylmercury played no significant role in the poisoning, says Graham George, Pickering’s husband and co-leader of the experiment, who is also at the University of Saskatchewan. Because previous studies used less sensitive techniques, they missed the major form of mercury in Minamata samples, he argues. “Were there other more prevalent forms of mercury present that were not detected? Yes, we think so.”
But to other researchers, the team may be overstating its conclusions in the service of a larger agenda. Many of the authors have downplayed the toxicity of methylmercury for years, says Philippe Grandjean, an environmental toxicologist at Harvard University. The work doesn’t do anything more than identify an unusual chemical in one preserved cat brain, he says. “They did an admirable piece of chemistry, but it should not be interpreted beyond what it really shows.”
Charles Driscoll, an environmental scientist at Syracuse University, says the new mercury compound might be a product of the cat’s metabolism or an artifact of the sample’s long preservation. And even if it did spew directly from the factory, the residents of Minamata were exposed to mercury from seafood they ate, not from factory wastewater, he says. “Quite a few things in [the study] give me pause,” he says. “I was, frankly, surprised it would get published.”
The dispute reflects a schism dating to the 1980s, when dueling research teams looked at the neurological consequences of methylmercury from seafood. One team, at the University of Rochester, studied the brain development of children in the Seychelles islands, where the diet is heavy in fish that can acquire methylmercury in the open ocean from natural and human sources of mercury. “We have not been able to confirm any adverse effects of methylmercury from fish,” said Gary Myers, a University of Rochester neurologist who also participated in the study on cat 717. But a competing study by Grandjean and others in the Faroe Islands concluded methylmercury from seafood was harming children.
In 2000, when the U.S. Environmental Protection Agency (EPA) defined the maximum daily amount of mercury thought to be safe to ingest, the agency found the Faroe Islands evidence more convincing and set a low limit. In 2019, EPA began to reassess this limit; Grandjean fears the new study could be used to support relaxing the standard. At the same time, the Trump administration is working to weaken a separate rule called the Mercury and Air Toxics Standards, which limits mercury emissions from power plants.
Last year, Grandjean, Driscoll, and other mercury researchers submitted a comment to EPA as part of the agency’s reassessment. They pointed out that Minamata is not the only example of methylmercury toxicity; the compound caused another industrial poisoning in Iraq in 1971, and studies of babies and children around the world have found that even low-level exposure can harm brain development, Grandjean says. Compared with past decades, “We know better now.”
Eto, who loaned the samples and was credited as a study co-author, said in an email that he still believes methylmercury was the most important cause of the tragedy. But Pickering and George plan to move beyond a single cat sample to bolster their controversial claim. They have already borrowed preserved samples from human victims from the National Institute for Minamata Disease, and plan to test for the same obscure compound.