Thousands of Japanese people suddenly lost the use of their legs. Others became blind, without warning. For more than a decade, doctors searched for a virus, a bacteria, a curse. The answer had been in the medicine cabinet from the start.
- Between 1957 and 1970, more than 10,000 Japanese suffered from SMON, a disease causing leg paralysis and blindness, whose origin remained mysterious for years.
- The cause was identified in 1970 thanks to a green urine: it was clioquinol, a common antibacterial used against diarrhea, forming a toxic chelate with iron.
- The ban on clioquinol in September 1970 reduced new cases from about 150 per month to just one in October, without the need for any vaccine or treatment.
- An epidemic that looked like a curse
- The real culprit hid in pharmacies
- A ban was enough to stop the carnage
An Epidemic That Resembled a Curse
Between 1957 and 1970, Japan witnessed the emergence of a disease as brutal as it was baffling. More than 10,000 people fell victim during this period, a figure that would be staggering for any single country.
The pattern was consistently similar. It began with seemingly ordinary abdominal pains, almost trivial. Then the body literally failed the patient.
The legs would lose sensation, then mobility. Some patients could no longer walk without assistance. Others saw their visual field shrink, until complete blindness in the most severe cases.
The Japanese doctors eventually gave this elusive malady a name: SMON, for subacute myelo-optic neuropathy. A technical label that did not reveal its origin, which remained completely mysterious at the time.
The Real Culprit Hid in Pharmacies
The investigation took a decisive turn thanks to a clue as strange as it was valuable. In May 1970, Japanese doctors Akira Igata, Mitsuhiro Hasebe and Takeo Tsuji noticed that the urine of some patients had turned green.
This sort of signal, odd as it was, proved a boon for researchers short on leads. By June 1970, Masayuki Yoshioka and Zenzo Tamura managed to isolate the pigment responsible for this unusual coloration.
The results of their analyses were unequivocal: this green pigment is a chelate, a molecule formed by the bond between a metal and an organic compound. Here, ferric iron tied to a widely used drug, clioquinol.
This product, a derivative of quinoline, was far from a new suspect. Initially used as a topical antiseptic, it had over decades become a common oral antibiotic, notably against diarrhea, a symptom that ultimately opened the door to SMON.
Neurologist Tadao Tsubaki, along with colleagues Y. Honma and M. Hoshi, documented this discovery in a 1971 article in The Lancet. Their work described in detail the neurological syndrome associated with taking this medication, long regarded as perfectly harmless.
A Ban Was Sufficient to Stop the Carnage
Faced with these early epidemiological results, the Japanese government did not wait for absolute certainty to act. In September 1970, it ordered an immediate suspension of all medicines containing clioquinol.
The effect was almost instantaneous, and perhaps the most striking aspect of this affair. By July 1970, around 150 new SMON cases were still being recorded each month nationwide.
Three months later, in October 1970, only one case was reported. No miracle vaccine, no revolutionary treatment: removing the cause from the market was enough to let the epidemic collapse on its own.
An investigative committee led by researcher R. Kono confirmed this cause-and-effect link in March 1972, after twenty months of methodical investigations. The scientific verdict then found judicial resonance: on August 3, 1978, the Tokyo District Court officially recognized clioquinol as responsible for SMON.
The consequences for the victims, however, proved far more lasting than the outbreak itself. A clinical analysis conducted 32 years after the ban showed that 95.6% to 97.7% of patients still retained persistent sensory disorders.
The number of officially recorded SMON patients in Japan gradually declined to 1,748 by 2013, a figure that reflects both the retreat of the disease and the heavy toll it continued to weigh on thousands of lives.
It is worth noting, however, that a portion of the mystery persists among some researchers. Clioquinol had been used for about twenty years before the outbreak, and no comparable case has ever been reported in other countries, where per-capita consumption was higher than in Japan.
This case remains a fascinating example for anyone interested in the history of medical science. It reminds us that a drug used for decades, seemingly harmless, can conceal an unsuspected danger, and that a simple color change in urine can sometimes be enough to pierce one of the century’s most troubling medical mysteries.
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