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The Age of Autism: Connecting new dots

By DAN OLMSTED, UPI Senior Editor   |   Oct. 17, 2005 at 6:08 PM

Until now, the debate over a possible link between ethyl mercury and autism has focused on its use in vaccines beginning in the 1930s, when the first children diagnosed with the disorder were born.

But medicines were not the only commercial products to harness this highly toxic form of mercury. Starting about the same time, ethyl-mercury-based fungicides appeared on the market.

In fungicides as well as vaccines, ethyl mercury did the same job -- it killed micro-organisms including fungi and bacteria. Fungicides, in fact, appear to have been a much more common application of ethyl mercury than vaccinations in their first decades of use.

Now Mark Blaxill, whose group SafeMinds opposes the use of mercury in medicines, is putting forward a new hypothesis: Fungicide exposure might help connect the dots in the very first reported cases of autism. His theory sprang from a discussion with Age of Autism about the natural history of the disorder, the focus of this ongoing series.

Many experts -- including child psychiatrist Leo Kanner, who first diagnosed autism as a separate disorder in 1943 -- have puzzled over the demographic of the first families of autistic children: The parents were notably well-educated and accomplished. Many had advanced degrees and were doctors, lawyers, engineers, scientists, professors.

That common bond led some researchers to conclude brainy, "geeky" parents might be prone to having autistic children. Others believe that such families -- affluent, medically sophisticated and well-educated -- were the likeliest to vaccinate their children at a time when that was not routine.

Just about everyone thinks it's a clue, and Blaxill's hypothesis is a new way of interpreting that clue. But is there anything to suggest an association between exposure to fungicide and those early autism cases? Consider two of the first 11 cases described by child psychiatrist Kanner in his landmark 1943 paper:

-- Case 2, Frederick W., born in 1936, was the son of "a university graduate and a plant pathologist" who "traveled a great deal in connection with his work," Kanner wrote.

"A plant pathologist is a professional who specializes in plant health much as a physician specializes in human health," according to the American Phytopathological Society. "Keeping plants healthy requires an understanding of the organisms and agents that cause disease as well as an understanding of how plants grow and are affected by disease. ... Plant diseases are caused by a variety of living organisms (called pathogens) such as fungi ... "

-- Case 3, Richard M., born in 1937, was the son of "a professor of forestry in a southern university. He is very much immersed in his work, almost entirely to the exclusion of social contacts."

Playing out this scenario, it might be pertinent that Richard's father worked in the south; fungus is a big problem in that hot, humid climate.

Another child -- Case 1, Donald T. -- was also from the south, making that the only geographic link cited in Kanner's original study.

Donald's Mississippi home -- at age 72, he still lives in the small town he grew up in -- is surrounded by land that was clear-cut before the Depression. By the early 1930s the area was being planted with thousands of seedlings by workers from the Civilian Conservation Corps. Donald was born there in 1933.

Possibly relevant: The father of Case 8, Alfred L., was a chemist-lawyer at the U.S. Patent Office, perhaps involved with new chemical compounds. Another -- the father of Paul G., Case 4 -- was a mining engineer, which could have exposed him to toxins including heavy metals like mercury.

This approach puts the focus not on the advanced education of the fathers of the first autistic children, but on what they did with that education. It fits with a view this column expressed earlier this year: "What really connects these first families is more precise and less bizarre than an 'intellect' effect: It is a college education, defining the parents of these early autistic children by what they did (go to college) instead of who they were (brainiacs)."

But we noted this "raises an unpleasant prospect: Some outside factor, unique to that remarkably homogeneous group at that time, could have triggered autism in their children -- and then spread."

There is no question that commercial use of ethyl mercury began spreading widely in the 1930s -- in vaccines as the preservative thimerosal, allowing for multi-dose vials and mass vaccination; and in fungicides as the active ingredient, protecting nascent plants, crops and trees.

-- "A History of Plant Pathology in Virginia" quotes from a 1937 edition of the magazine Southern Planter. An ethyl-mercury fungicide "was recommended for cabbage, peas, and watermelon ... (and) cotton seed treatment ... for control of damping-off and seed rot."

-- The Northwest Monthly of the University of Minnesota Agriculture School reported in 1936 that seed wheat should be treated with a "new improved" ethyl-mercury-based fungicide "at the rate of 1/2 oz. per bushel of seed. At present this treatment is recommended since it controls covered smut and other seedborne diseases and may increase the emergence of seedlings considerably."

In the 1920s the same scientist who invented thimerosal also patented the technique for making ethyl-mercury-based fungicides. He appeared to be working on both applications simultaneously, and he succeeded by solving the same problem: Making ethyl mercury water-soluble, harnessing it for commercial use.

"Ethyl mercury does something unexpected," SafeMinds' Blaxill said in explaining how environmental exposure might trigger autism. "It delivers the toxic form of mercury to an infant brain more efficiently than any other common mercury compound."

Once there, he said, it is turned into inorganic mercury that "has no way back out of the brain and into the body." And inorganic mercury, Blaxill said, is the pathway by which "sub-clinical exposures have damaging effects on brain tissue."

We'll pursue this possible pathway from environment to infant in upcoming columns.

--

This ongoing series on the roots and rise of autism welcomes reader response. E-mail: dolmsted@upi.com

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