The Iraqi mercury poisonings were among the worst in a series of poisonings resulting from agricultural products treated with mercury. After the Iraqi epidemic, the U.S. Environmental Protection Agency announced that all pesticide uses of mercury should cease.
The clinical symptoms of mercury poisoning were diagnosed and described as early as 1533. It was known that mercury could be absorbed through the skin and lungs and that it could be ingested; the mercury then traveled through the body and accumulated in the tissues of the brain and other vital organs. Although its toxic nature was recognized, mercury was used therapeutically to combat illnesses such as syphilis. Inorganic mercury poisoning became an increasing problem once humans entered the industrial age, when it began to be used routinely in the processing of many materials. The use of organic mercury compounds increased dramatically in the second half of the twentieth century in both industry and agriculture.
Conservationists in Sweden were the first to raise the alarm and report that birds exposed to agricultural materials treated with mercury were dying in large numbers. In Minamata, Japan, eleven people were killed or severely disabled between 1953 and 1960 from the effects of mercury poisoning; in 1965, five more people died. (These statistics did not reflect teratogenic effects, colloquially called birth defects.) Both Japan and Sweden ensured the removal of mercury from agricultural products in their countries and monitored the release of inorganic and organic mercuries from industry. Between 1964 and 1969, the mercury used in Sweden as seed treatment and for other agricultural uses declined by 70 percent.
From the 1950’s to the 1970’s, alkyl mercury fungicides were used routinely to treat seeds for the prevention of crop disease. When Iraqi peasants consumed, rather than planted, treated seed grain exported to Iraq that had been ordered by the Iraqi government, many were poisoned; in 1956 and 1960, there were estimates of 350 poisoned and 36 dead. These incidents did not prevent a similar, even more serious epidemic in early 1971.
Identification of the problem in Iraq was complicated by the fact that there was often a considerable time lapse between government distribution of the grain and its consumption in the form of bread. Moreover, because mercury accumulates in the body, weeks or months may elapse before symptoms appear. Many farmers had tested the grain initially on chickens, sheep, or goats and concluded that the grain was safe when they saw no immediate adverse effects.
In 1967, the World Health Organization indicated that studies of mercury in human consumables and human tissue were urgently needed, as it was impossible to set meaningful limits for dietary intake of mercury without appropriate data. It had been documented, however, that mercury poisoning was essentially irreversible. After being exposed to or ingesting mercury, humans and other animals have no symptoms while the deadly compound gradually accumulates. The first symptoms may be minor emotional disorders such as depression and excitability, as well as headaches, fatigue, decreased physical coordination, and loss of memory. Eventually, mercury poisoning causes brain and nerve damage and may lead to blindness, loss of muscle control, advanced senility, and even death. Mercury can also produce extreme teratogenic effects, as it readily crosses the placenta; it may even be passed to infants in the mother’s breast milk. Mercury has also been documented to have serious consequences for aquatic, bird, and rodent populations.
In the United States, courts had suspended interstate shipment of treated seed grain, but manufacturers were permitted to dispose of warehouse stocks by export or by intrastate sales. In 1970, the Iraqi government negotiated a trade agreement with one of the international subsidiaries of Cargill Incorporated of Minneapolis, Minnesota, for a shipment of 73,201 metric tons of treated seed wheat and 22,262 metric tons of treated seed barley. It was later documented that the barley originated in the United States; the exact source of the wheat—whether from the United States, Canada, or Mexico—was disputed. The treated grain was dyed red as a warning and labeled in either English or Spanish with the word “poison” as well as with the emblem of a skull and crossbones.
The conditions that led to the tragedy in Iraq included the fact that most of the people involved—the peasants of Iraq—were completely illiterate; most of them were sharecroppers who struggled with the burdens of low crop yields, primitive agricultural methods, abused soils, and chronic debt to the landowner. These people lived in extreme poverty, with very little knowledge of the outside world and with little or no access to medical facilities. Winter barley and wheat were the major crops for these people. The Iraqi government had arranged to have grains shipped from the United States because a prolonged drought in the country had caused severe famine. The effects of the drought were all the more severe as three-fifths of the country was not suited to agriculture to begin with.
The imported grain began to arrive in Iraq in October, 1971, but was not fully distributed until January, 1972. After distributing the grain, the Iraqi government broadcast radio warnings to people not to consume the grain; these warnings were either ignored or not received. Birds that ate grain lying on the ground died in large numbers. The peasants nevertheless fed the grain to their animals and ate it themselves. The animals, most of which were fed the barley, soon began to die, and because their meat was contaminated with mercury, sales from rural slaughterhouses were banned. When the Iraqi government established the death penalty for anyone convicted of selling the contaminated seed, some frightened peasants dumped seed in the Tigris River, which resulted in a ban on sales of local fish. Only about five thousand tons of the mercury-treated grain were ever recalled.
The treated grain contained approximately 6.7 parts per million of alkyl mercury fungicide. Each loaf of bread made from the grain contained an estimated 1.2 milligrams of mercury. With the average Iraqi consuming three loaves of bread daily, each individual accumulated mercury at a rate of 3.6 milligrams per day. Swedish and Japanese scientific literature indicated that the first symptoms of poisoning appear once the body has accumulated 30 milligrams of mercury. Other studies indicated that it would require as much as 100 milligrams before symptoms appeared. In Iraq, the ingestion of large amounts of bread occurred over a six-month period because supplies of other foods were generally lacking. A thousand tons of wheat contained enough alkyl mercury to poison 60,000 people.
By December 27, 1971, 50 cases of mercury poisoning had been recognized in Iraq. By January, 1972, the Iraqi Ministry of Health reported 400 hospital admissions each day. Following the beginning of the epidemic, the Iraqi government imposed a news blackout. Tourists in Iraq reported thousands of people with brain damage, blindness, and paralysis. Unofficial estimates reported that as many as 60,000 peasants could have consumed enough of the treated grain to have suffered damage. Official tolls eventually reported that a total of 6,530 victims were hospitalized and that 459 died, of whom 34 percent were under the age of ten. All the reported cases were in rural areas; in urban areas the baking of bread was under government control.
After the poisoning epidemic, T. W. Clarkson, chair of the Department of Environmental Medicine at the University of Rochester in New York, was invited to conduct research in Iraq with a polystyrene sulfhydryl resin (17-B) that was thought to bind ingested mercury and increase the rate of its excretion. The resin was never intended to be a cure, but it was hoped that it would help pregnant women flush the mercury out of their systems before it could be transmitted to developing fetuses. Clarkson initially arrived with only enough resin to treat two people, but Dow Chemical eventually donated an additional one hundred pounds, and the Food and Drug Administration granted a permit to administer experimental doses. Some progress was made in the treatment and rehabilitation of surviving patients, but most of the resin arrived after the alkyl mercury damage had been done.
In the United States, the toxic effects of mercury were well recognized by the 1960’s and resulted in a legislative initiative to remove alkyl mercurials as seed treatments and to restrict the agricultural use of mercury. The use of mercury in the United States declined by 10 percent in 1968, by 22 percent in 1969, and by 33 percent in 1970. The agricultural use of mercury in Canada declined from 18 percent of the total mercury consumed worldwide in 1964 to approximately 3 percent in 1970. On March 9, 1970, the Pesticides Regulation Division of the U.S. Department of Agriculture (USDA) issued PR Notice 70-7, which suspended registration for all alkyl mercury compounds used in seed treatment. The notice specifically stated that mercury compounds cause irreversible injury to the nervous system. Materials already produced, however, were not recalled, nor did the proclamation cover exports. Sweden also continued to export alkyl mercury fungicides and grain treated with these materials even after it had banned their use within the country in 1966. Shipments to Iraq in 1971 were clearly made by persons aware of the toxic potential of the seed treatments.
Even before the Iraqi epidemic, there had been many incidents worldwide of severe poisonings from mercury compounds used in agricultural products. In 1967, more than 144 persons were poisoned and twenty died from eating mercury-contaminated corn in Ghana. In Guatemala in 1965, forty-five people became ill and twenty died from ingesting mercury-coated seed. In West Pakistan in 1961, one hundred people were poisoned. Fatalities among farmers using alkyl mercury-treated seeds in Sweden occurred in 1929, 1932, 1949, and 1954. Concerned citizens and scientists had recorded dramatic effects of mercury on birds, including bird deaths, refusal to nest, abandonment of nests before the eggs hatched, rotten eggs, and declines in common species of birds.
In 1969, three children in a New Mexico family were permanently injured by ingesting pork fed with mercury-treated corn. The corn, although dyed red and labeled poisonous with a skull and crossbones, had been fed to hogs belonging to the family. The story was released on television by the National Broadcasting Company on February 17, 1970. One day later, the USDA suspended the mercury fungicide registration of the manufacturer of the seed. Although mercury use in the United States declined by one-third from 1969 to 1970, exports increased in that year. Experts warned that countries with large, illiterate peasant populations would have difficulties with warnings such as labels and dyes. If animals fed the treated grain did not die, peasants often washed off the dye, assuming they were thus removing the danger. Some suggested that a different dye be added to the grain to give it an unpleasant taste and render it inedible. Others advised that the warnings be written in the language of the country to which the grain was shipped.
After the Iraqi epidemic, on March 22, 1972, the U.S. Environmental Protection Agency
The fact that the poisoning incident occurred in a foreign country reflected the prevalent U.S. attitude toward the manufacture, control, and distribution of dangerous pesticides. The Nelson-Hart Amendment to the Pesticide Act of 1971 required that foreign governments be notified of the potential toxic effects of pesticides being shipped to them. If those governments elected to have pesticide-treated products or pesticides shipped to their countries, they were required to sign waivers. Notification of the shipments would be made to the United Nations and other international organizations.
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Broehl, Wayne G., Jr. Cargill: Going Global. Hanover, N.H.: Dartmouth College Press, 1998. Second volume of a “biography” of the Minnesota-based grain company, from 1960 to the end of the twentieth century. -
Friberg, Lars, and Jaroslav J. Vostal. Mercury in the Environment: An Epidemiological and Toxicological Approach. Cleveland: CRC Press, 1972. Provides extremely technical data and statistics useful for documenting the presence and effects of mercury in the environment. Intended for readers with some background in chemistry. -
Harmer, Ruth M. Unfit for Human Consumption. New York: Prentice Hall, 1971. Factual and scientific presentation of modern neglect of human health and welfare. Discusses how such events have been handled in the political and academic arenas and how they have affected scientific research and regulatory actions taken by the government. -
Harris, George L. Iraq. New Haven, Conn.: Hraf Press, 1958. Interesting discussion of the civilization and culture of Iraq and its people prior to the country’s economic, political, and social modifications. -
Montague, Peter, and Katherine Montague. “Mercury.” Saturday Review 5 (February 6, 1971), 50-55. Excellent factual report on the poisoning epidemic in Iraq while it was in progress. -
U.S. Congress. Senate. Subcommittee of Commerce. Amendment to the Pesticide Act of 1971. 92d Congress, 1972. Contains transcripts of the activities in the U.S. Senate after the poisoning epidemic in Iraq led Senator Gaylord Nelson to fight for amendments to the Pesticide Act to regulate exports of dangerous pesticides to other countries.
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