The Autism Puzzle: Connecting the Dots Between Environmental Toxins and Rising Autism Rates

Uncounted NumbersUrban Exposures, Chemical Concentrations, and the Question of Race Thanks to years of public health campaigns and plenty of media cover­age, many people are aware that certain types of fish are contaminated by mercury. Mercury released through emissions from coal-burning power plants and municipal and medical waste incinerators takes to the air and is carried along, sometimes for miles, before settling in soil or water. The inorganic mercury is absorbed into microorganisms in the water and converted to an organic substance, methylmercury, which is then consumed by fish. Big fish like shark, swordfish, king mackerel, and tilefish eat small, contaminated fish and accumulate high concen­trations of toxic methylmercury. Both white (albacore) and canned light tuna contain mercury, too, with a January 2011 investigation from Consumer Reports finding that “children and women of childbearing age can easily consume more mercury than the Environmental Protec­tion Agency considers advisable simply by eating one serving [about 2.5 ounces] of canned white tuna or two servings of light tuna per week. Women who eat large quantities of such fish, both during and after pregnancy, can readily pass that mercury on to infants through umbilical cord blood and through their breast milk. Pregnant women exposed to methylmercury from fish—particularly canned fish—have shown a greater likelihood for giving birth prematurely, and a child born with low birth weight (4.4 pounds or less), such as happens when babies are born premature, is five times as likely to be diagnosed with autism as a child born at normal weight. Recognizing that mercury from seafood “may harm an unborn baby or young child’s developing nervous sys­tem,” the Food and Drug Administration (FDA) has advised women to limit their consumption of certain fish while pregnant.Knowing of these dangers, many women choose not to eat fish high in mercury during pregnancy. But most populations exposed to toxic chemicals are not made aware that their food, water, or air could be poi­sonous. The likelihood of chemical exposure is deeply intertwined with a community’s socioeconomic status; factories that spew pollution are often allowed to operate with impunity alongside poor communities whose residents aren’t given the choice to opt out by simply avoiding contaminated items. An early example of what can occur when factories pollute unchecked happened in Minamata, Japan, a small village of rice farmers and fisher­men who depended on fish and shellfish from the Minamata Bay and the Shiranui Sea. In 1907 the Chisso Corporation opened a carbide plant on the shores of the bay. The townspeople initially welcomed the factory with the hope that it would bring economic prosperity. In 1930 the Chisso factory turned its attentions to the production of materi­als that could be used for Japan’s growing military needs—specifically acetaldehyde, or ethanol, a needed energy source for a country without its own oil supplies, and polyvinyl chloride (PVC), which was used for airplane parts. As the factory rapidly expanded its production, it dumped increasing amounts of untreated waste into local water sup­plies, contaminating the bay and the sea with methylmercury from 1932 to 1968. As the chemical bioaccumulated in the local fish and shellfish, widespread mercury poisoning—Minamata disease, as it came to be called—seeped into the village. It was the cats they noticed first—acting crazy, falling into the sea, as if they were committing suicide. The first official case of Minamata dis­ease was recorded in 1956, when two sisters, ages five and two, exhibited symptoms that included convulsions, muscle contractions, twisting and repetitive movements of the hands and feet, and sudden scream­ing fits. They were determined to have an unknown disease of the central nervous system. Soon researchers from Kumamoto University discovered that many residents living around Minamata Bay showed an inability to grasp small objects and difficulty with hearing, seeing, walking, running, and swallowing. Once the symptoms began, they could progress within weeks to massive convulsions, insanity, coma, and death. A black-and-white image of a mother and child known as “La Pieta de Minamata” has come to symbolize the heartbreak. The mother’s head is wrapped in a scarf, her shoulders bare, her face lit ethereally, as she cradles and bathes her profoundly disabled child. The child looks, in fact, to be a young man, his neck muscles strained, legs and arms shortened and deformed, hands shriveled and bent. The National Institute for Minamata Disease reports that as of 2001 there have been nearly 3,000 certified patients with the disease—some 1,784 of whom have died—and more than 10,000 with “applicable conditions such as sensory disorders or a high consumption of marine products.” Not until April 2006, nearly fifty years from the first report of the disease, did sufferers and their caregivers receive a formal apology from Prime Minister Junichiro Koizumi for the Japanese government’s failure to stop the pollution. Many victims are still fighting legal battles for compensation. The Minamata tragedy was clearly linked to the Chisso factory, but it is often difficult to pin symptoms and diseases on exposure to chemicals from one particular source. People living in highly polluted urban areas are subject to a host of environmental contaminants that can lead to preterm birth. Pregnant mothers are more likely to give birth prema­turely, or give birth to babies who are small for their gestational age, when they live near highways and are exposed to the associated air pol­lution, including carbon monoxide, nitrogen dioxide, sulfur dioxide and particulate matter.