When the population is exposed to a chemical agent known to produce in animals lesions in the spinal cord resembling those in human polio, and thereafter the latter disease increases sharply in incidence and maintains its epidemic character year after year, is it unreasonable to suspect an etiologic relationship?

Particularly relevant to recent aspects of this problem are neglected studies by Lillie and his collaborators of the National Institutes of Health, published in 1944 and 1947 respectively, which showed that DDT may produce degeneration of the anterior horn cells of the spinal cord in animals. These changes do not occur regularly in exposed animals any more than they do in human beings, but they do appear often enough to be significant.

Before finding Biskinds work, I had spent months engaged in a nearly futile search for the physiology of acute DDT poisoning. I began to sense that American DDT literature as a whole intends to convey that DDT is not dangerous except with regard to its general environmental effects due to persistent bioaccumulation, and that the physiology of acute DDT poisoning is therefore trivial. DDT literature uniformly jumps from descriptions of symptoms, over physiology, to the biochemistry of DDT-caused dysfunction in nerve tissue.

It was as though detectives had come upon a mass-murder scene and immediately became obsessed with the biochemistry of dying cells around bullet holes, while ignoring the bullet holes.

Eventually , I did find one study (in Germany) of the physiology of acute DDT poisoning by Daniel Dresden (Physiological Investigations Into The Action Of DDT, G.W. Van Der Wiel & Co., Arnhem (1949)) . This study confirms that DDT poisoning often causes polio-like physiology:

Conspicuous histological degeneration was, however, often found in the central nervous system. The most striking ones were found in the cerebellum, mainly in the nucleus dentatus and the cortex cells. Among other things an increase of the neuroglia and a necrotic degeneration and resorption of ganglionic cells was found. The Purkinje cells were less seriously affected than the other neurons. Also in the spinal cord abnormalities of a degenerative nature were found. ...such changes were not found invariably... there is neither an obvious relation between the size and spreading of the lesion and the quantity of DDT applied... information of adequate precision about the nature of the anomalies is lacking. So we find that especially the cerebellum and the spinal cord are histologically affected by DDT.

And more recently, in the works of Ralph Scobey, MD,5 I found that from ancient times to the early 20th century, the symptoms and physiology of paralytic poliomyelitis were often described as the results of poisoning. It wasnt until the mid-19th century that the word poliomyelitis became the designation for the paralytic effects of both severe poisoning and polio-like diseases assumed to be germ-caused.

Today, various other forms of the word polio are still used to describe the effects of neurotoxins, although usually with regard to paralysis in animals. A search of Medline ("polio" and "poison") finds about 45 contemporary articles where poison causation is attributed to polio. The terminology found: "polioencephalomalacia", "poliomyelomalacia", "polyradiculoneuritis", "neurological picture similar to that of poliomyelitis", "polioencephalomyelomalacia", "lumbal poliomyelomalacia", "cerebrocortical necrosis (polioencephalomalacia)", "Lead poisoning in grey-headed fruit bats (Pteropus poliocephalus)", "multifocal-poliomyelomalacia", "spinal poliomalacia", "Polio and high-sulfate diets", "Atypical porcine enterovirus encephalomyelitis: possible interaction between enteroviruses and arsenicals", "Polioencephalomalacia and photosensitization associated with Kochia scoparia consumption in range cattle", "bovine polioencephalomalacia".

In contemporary Britain, a farmer turned scientist, Mark Purdey, has found substantial evidence that mad cow disease, a form of polio-like encephalitis, was caused by a government mandated cattle treatment consisting of organophosphate pesticide and a compound similar to thalidomide.6 Unlike most scientists, Mark Purdey became legally embroiled with the government during his research, and  . . . was shot at, blockaded in his home to prevent him giving a lecture, and saw a new farmhouse go up in flames the day he was due to move in. (http://www.whaleto.freeserve.co.uk)

Morton S. Biskind had the courage to write about humans. His views fell into disfavor after the introduction of the polio vaccines, which was a grand act that proved in most peoples minds that polio was caused by a virus. By October, 1955, Biskind, whose works had been published in established medical journals and who testified before the Senate on the dangers of pesticides, was forced to self-publish his writings, one of which I found while browsing through an old card catalog. A scan of MEDLINE finds no other works by him except for a very tame article in 1972, warning that diseases incurred during a patients stay in a hospital are not necessarily due to microbes. He died not long thereafter, in his late 60s. I don't have the precise date of death, though his birth was in 1906.

A Contemporary Study

Below are three graphs that confirm Biskind, utilizing data that spans far beyond his observations. Due to the paucity of data regarding pesticide exposure and locale, these findings of production data are presented as an indication of exposure, keeping in mind the great changes in public awareness and legislation beginning circa 1950, which also served to reduce DDT exposure. Pesticide production data comes from Hayes and Laws.

DDT vs Polio (1940-1970)

In this graph I did not include DDT data for the period of 1954 onward because DDT distribution was then being shifted out of the U.S. and into developing nations, while its U.S. production skyrocketed.

Governmental hearings, including those with Biskind, Scobey and others, brought about greater awareness of DDT dangers, as well as better labeling and handling methods.8 Due to public governmental debate in 1949-51 and numerous policy and legislative changes afterward,8,9,10,11 DDT production figures after these dates do not correlate with US usage or exposure to DDT.

DDT Before 1950

Before 1950, DDT was hailed as a miracle of progress that was virtually non-toxic to humans, in spite of FDA's warnings and attempts to keep it off the market. This photo on the left is one of several similar photos from Zimmerman, et al, DDT: Killer of Killers (1946). The advertisement on the right is from an unknown source, though it appears to be circa 1954.

Zimmerman, et al (1946) Phrase is 1947 Time Magazine cover

Ad is found in 1954 Time Magazine

Other photos in Zimmerman show and advocate 5% DDT solution sprayed directly on dairy cows (body, feed, and water):

This promotion of highly questionable products is reflected in post-2000 genetically engineered food campaigns.

DDT after 1950

Governmental hearings, including Biskind and Scobey, et al, brought about greater awareness of the dangers, better labeling and handling methods.

DDT after 1954

This period is given special consideration for DDT.

After 1954, DDT production increased tremendously , but mainly as an export product. Due to public governmental debate in 1950-51 and numerous policy and legislative changes afterward, its production figures thereon do not at all correlate with U.S. usage or exposure to DDT.

As many studies demonstrate, DDT exposure after 1954 declined sharply, and this decline is represented in the following graph, along with supporting data. DDT production is not shown, post-1954.

Historical context: DDT was incriminated from 1950 until its registration cancellation in 1968 and ban in 1972. Thus, 1950-1951 represent a point of increased public awareness, changes in legislation and policy, voluntary phase-out, and labeling requirements. It is significant for this comparison of DDT against infantile paralysis, that before the period of increased awareness, DDT was mandated on dairies, yet afterward, ruled out of dairies. Much of the domestic usage was shifted to forestry applications, placing less DDT directly into the food chain.

The visual impact of all the persistent pesticide graphs rests upon the assumption that production correlated with human exposure. Given the lack of regulation and the extreme media hype surrounding DDT before 1953, this is not an unrealistic assumption.

It is clear that post-1954 DDT production did not correlate with human exposure. Yet, it is possible to estimate relative values for exposure post-1954. This can be accomplished by reviewing DDT levels in adipose tissue (National Adipose Tissue Survey, and other studies)12, considering DDT in imported food, and considering the daily amounts of ingested DDT.

The early trend of National Adipose Tissue Survey's can be interpolated back to 1944, six years from 1950, the first Survey year, because it is safe to assume that DDT tissue levels were zero in 1944, since DDT was introduced for domestic usage in 1945. The estimate of DDT exposure is a reasonable because DDT has a half-life of about one year. To achieve any downward trend in the DDT/adipose line, DDT exposure had to have decreased sharply.

Note that no scale or factor is provided for "relative DDT exposure". The Survey values are presented without distortion, linearly, with the starting point at 1954, and values for DDT exposure are estimates based on the the Survey and DDT ingestion data.

Error is limited by two boundaries, for the estimated values of DDT exposure. 1) Exposure's downward slope must be much greater than the Survey line's downard slope, because of DDT's half-life. 2) Exposure values must continue at least through 1968.

Hayes and Laws also used a secondary evaluation, DDT intake per day, to explain that from 1954 to 1964-67, DDT ingestion decreased by an approximate factor of five. Significantly, the Salk vaccine program began in 1954.

"The observed decrease in the concentration of DDT in food (Walker et al., 1954; Durham et al., 1965a;

Duggan, 1968) offers an adequate reason for the decrease in storage in people. The average intake of

p,p-DDT and of total DDT-derived material was 0.178 and 0.280 mg/human/day, respectively, in 1954,

but only 0.028 and 0.063 mg/human/day, respectively, during the period 1964-1967."

- Hayes and Laws, page 303.

BHC vs Polio (1940-1970)

BHC (benzene hexachloride), a persistent, organochlorine pesticide, is several times more lethal than DDT, in terms of LD50, i.e., the lethal dosage required to kill 50 percent of a test population.

"Unlike the situation with DDT, in which there have been few recorded fatalities, there have been a number of fatalities following poisoning by the cyclodiene and hexachlorocyclohexane-type insecticides. The chlorinated cyclodiene insecticides are among the most toxic and environmentally persistent pesticides known."

- Hayes & Laws