Images Of Poliomyelitis
During The Epidemic
"Some foods contain enough
pesticides that, if prepared for
children, they can contain a nearly toxic dose."
ATSDR, U.S. Public Health Service, "Healthy Children--Toxic Environments", 4/28/97
DDT: Dosage Studies
"Publication of my findings drew some sharp criticism. They were characterized as 'totally without foundation,' 'highly uncontrolled,' 'hysterical' and so on. The only evidence provided in refutation was the alleged lack of toxic effect from the military and public health users of DDT... The animal work could hardly be cited because virtually all of it shows DDT to be extremely dangerous." (Biskind, 12/12/1950)
Species Sex Comment Author Toxicity of a one dose (LD50) 113 Mouse M [mg/kg is equal to "ppm" in terms of weight] Gaines (1960) Susceptibility 25 Rat M largest dosage without clinical effect Garret (1947); Hsieh (1954); Neal et al (1946); Velbinger (1947; Hayes (1959) 6 Human smallest dosage with clinical effect Ibid 16 Human smallest dosage with serious effect (convulsions) Ibid 285 Human largest nonfatal dosage (partly vomited) Ibid 50 Rat M smallest dosage with serious effect Gaines (1960, 1969) 175 Rat M largest, nonfatal dosage Ibid 50 Rat M smallest, fatal dosage Ibid 200 Rat M uniformly fatal dosage Ibid Susceptibility to repeated dosage 0.5 for >600 days Human (age not mentioned but probably adult) increased storage, no clinical effect Hayes et al (1956) 0.24 for 161 days Rat M/F histopathological changes of the liver Laug et al (1950) Penetration of through the gastrointestinal tract 2% in 30 minutes Rat application site was the intestine, solvent was bile, method was intestinal loop [this represents the lowest GI absorbtion environment] Turner and Shanks (1980) 55%
in 1 hour
Mouse application site was oral, solvent was Emulfor, method was GI content [Emulfor is closer to the solvent efficiency of fat or milk lipids] Ahdaya et al (1981) Dermal penetration 34%
in 1 hour
Mouse application site was dermal, solvent was acetone, method was patch Shah et al (1981) 15%
in 1 hour
Roach application site was dermal, solvent was acetone, method was patch Shah et al (1983) 5%
in 1 hour
Hornworm application site was dermal, solvent was acetone, method was patch Shah et al (1983) 22%
in 1 hour
Quail application site was dermal, solvent was acetone, method was patch Shah et al (1983) 13%
in 1 hour
Frog application site was dermal, solvent was acetone, method was patch Shah et al (1983)
Also, DDT and its metabolites have been found in numerous animal studies to be tumorigenic at very low sustained dosages, as low as 0.4 ppm.tumorigenic
Warfarin can be mixed with DDT for potentiation.
Study mg/kg Species Sex Comment Author Susceptibility to repeated dosage 0.14 indefinitely Human maintenance, therapeutic dose. Friedman (1959) 0.29-1.45 for 15 days Human hemorage in 12 people (40-70 yr) followed by recovery. Lang and Terveer (1954) 1.7 for 6 days Human hemorage in a 22 year-old man, followed by recovery. Lange and terveer (1954) 0.83-2.06 for 15 days Human Fatal to 19 year-old male and a 3 year-old girl. Holmes and Love (1952) 0.08 for 40 days Rat M/F Fatal to 5 of 10 rats Hayes and Gaines (1959) 0.39 for 15 days Rat M/F Fatal to 10 of 10 rats Hayes and Gaines (1959)
13.8 ppm DDT in Milk
Just one year before polio incidence peaked, in 1951, doubts about the safety of DDT became prominent enough for U.S. government and industry to hold hearings and investigations (the Delaney Committee) . These investigations allowed the number 13.8 ppm to surface regarding the highest concentration of DDT found in dairy milk. This number and other numbers found in literature are utilized in the tables below. I found 13.8ppm in Thomas R. Dunlap's, DDT: Scientists, Citizens, and Public Policy, Princeton University Press (1981), p69.
In the first and second tables, 13.8ppm is used to determine how much DDT was reaching human infants and this is compared with the amount of DDT needed to cause human infant illness and death. Infants were the primary victims of polio.
The third table uses 13.8ppm to determine how much DDT was being applied to fodder crops for dairy cattle. This calculation is of more general interest and serves as an exercise to verify the previous calculations and the context of the number 13.8ppm.
Since application recommendations are never followed perfectly, due to human imperfection, error probability, and the multiple coincidence of these, it seems that ppm in milk could easily exceed the amount required in LD50 studies, thus causing illness, paralysis, and death in infants.
In the following charts, bolded numbers are official "givens". Regular fonts portray calculations from the given numbers.
Lethal Dosage For Infant Human
Human DDT concentration, for severe illness 6 mg/kg http://grove.ucsd.edu/cruise_chem/pesteffects.html Human DDT concentration, for death (LD50) 150 mg/kg Dresden, Physiological Investigations into the Action of DDT (1949) Infant hypersensitivity factor 12 x See discussion below Infant Weight 6.4 kg Assume 14 lbs, near age of highest incidence (6 to 10 months) Infant Illness: minimum DDT dose 4.8 mg Calculated from above numbers. Illness could manifest as headache, nausea, fever, porphyria, vomiting, diarrhea, tremors, and spasms. Infant Death: minimum DDT dose 119 mg Calculated from above numbers. Death could arrive via fever, cough, porphyria, vomiting, diarrhea, spasms, nerve damage, paralysis, and suffocation due to paralysis.
Infant Hypersusceptibility: This is a powerful factor, often neglected in presentations of DDT toxicity. Infants generally have much greater susceptibility to neurotoxins because their nervous system is in a state of rapid growth up until about the 7th year. At birth, much of an infant's nerve system is not protected with a myelin sheath and the sheathing process continues up to the 7th year.
Because of the (understandable) lack of available studies regarding human infant hypersusceptibility to DDT, this factor has been estimated, as follows: In animal studies it is known that DDT can be passed via milk through two nursing female hosts to kill the infant offspring of the second host. Because the excretion of DDT is 1/4 of the ingested DDT in a nursing female, the infant factor for hypersusceptibility is at least 16.
In other words, at least 1/16th (i.e., 1/4 x 1/4) of the DDT ingested by the first nursing female does reach the infant offspring of the second female host and this relatively small amount is enough to kill the infants via nerve damage and paralysis, while leaving the adult female hosts apparently unharmed, giving us a minimum hypersusceptibility factor of 16.
The fraction 1/4 is from Modern Toxicology (1997), p114, and refers to experiments with dairy cows. The study of two female hosts is from Daniel Dresden's Physiological Investigations into the Action of DDT (1949) and refers to the first host as a nursing female goat and the second host as a nursing female rat.
A likely criticism of this approach could be that in this consideration there is a variety of carrier media (food types): the dairy cow eats mostly grass and beans, the female rat drinks goat milk, and the rat's infant offspring drink rat milk. Thus there is a variability of DDT absorption into the host. A defense is that the variability is negligible because dairy fodder, whole grass and beans, contains fats and proteins, as does milk, and that these are efficient carriers of DDT, and that dairy cows have a powerful digestive system, they thoroughly digest through mastication, regurgitation and re-mastication, giving ample opportunity for DDT to be integrated into the fatty component of the nutrients, building a DDT carrier approximating the efficiency of milk. It is likely that 1/4 would apply also to the female goat since its diet and digestive system are similar enough to the dairy cow. To give critics the benefit, larger fractions than 1/4, such as 1/3 to 1/2 are applied herein to the female rat (which drinks the goat's milk), assuming that milk is a more efficient DDT carrier than grass. Therefore, the range of susceptibility would range from 8 to 12 (inversions of 1/4 x 1/2 to 1/4 x 1/3). Since 8 and 12 are minimums, we should assume them to be closer to 12 to 18 and the average of these is 15.
General studies of chemical susceptibility in infants vs adults has arrived at hypersusceptibility numbers as high as 750 for some chemicals. Hayes and Laws uncritically report as factual, that infant rats are less sensitive to DDT than infants. However, the "two adult hosts" phenomena above, and numerous statements throughout toxicology literature clearly contradict Hayes and Laws' defense of DDT. The considerations above arrive reasonably at a minimum infant hypersusceptibility factor of 12, which is used herein.
Pesticides News (Issue No. 40, June 1998) states:
In 1994, one fatal poisoning was reported in the US involving a child who ingested one ounce (28g) of a 5% DDT and kerosene solution. (http://www.gn.apc.org/pesticidestrust/aifacts/ddt.htm)
The above fatal dosage works out to 12 to 80 mg/kg for a child (variance due to child's weight, not provided in reference). Studies cannot easily be done in this area on humans, however, in this incident the level of child susceptibility translates to 2 to 15 times higher than for an adult LD50. Since the LD50 is the number where 50% of a group dies at a given dosage, with some dying at less dosages and some at higher dosages, 2 to 15 represents only the middle range of lethal susceptibility. Therefore, susceptibility could be much higher than even 15.
Infant Dosage Of DDT In 1953
DDT In milk (official high number) 13.8 ppm Dunlap (op. cit.) Milk ingested by infant per day 700 grams Handbook of Pesticide Toxicity, p306 DDT ingested by 14 lb infant per day 9.7 mg
9.6 mg DDT per infant per day falls into the range of the first table for infant illness. Thus the potential for illness due to DDT dosage clearly existed in the U.S. in the 1950s, using 13.8ppm. Since this does not account for accumulative dosage, and DDT does accumulate in the body, with it and its metabolites having a half-life of almost one year, a real danger exists for polio-like diseases due to pesticide exposure in milk. This data, in addition to the direct correlation of DDT production with polio incidence, and the similarity of the physiologies of DDT toxicity and polio give ample reason to suspect DDT causality for poliomyelitis, other CNS diseases.
The following tables show the relationships between DDT application, DDT residue on grass, cow ingestion of DDT and how these numbers show a coherent relation to 13.8 ppm. This gives a wider perspective and acts as a partial cross check for the tables above. Authorities must have been aware of this numerical context as they arrived at the number 13.8 ppm.
DDT, Pasture Grass, and Milk Per Cow
DDT retained on pasture grass 10 percent Van Nostrand Enc. of Science and Technology (1995), p1725 DDT ingested by cow and excreted in cow's milk 25 percent Modern Toxicology (1997), p114 Milk per cow per year 2,769 kg Encyclopedia Britannica (1906) Pasture required for one cow 3.5 acres Encyclopedia Britannica (1906)
DDT ppm, Recommended Usage
The above numbers are used to generate this table:
DDT in milk (official high number) 13.8 ppm Dunlap (op. cit.) DDT excreted in milk per cow per year 0.038 kg DDT retained on pasture grass, eaten by cow .15 kg DDT applied to pasture grass per cow 1.53 kg DDT applied to pasture grass per acre .44 kg i.e., 1 pound/acre, the generally recommended application for DDT, Toxic Terror: The Truth Behind The Cancer Scares (1992)
The official given numbers in the above two tables are pat, i.e., they fit together too well. Were officials pondering such a table before they came up with 13.8ppm? It is interesting to see that the recommended application amount of 1 lb per acre works out to 13.8ppm of DDT in cow's milk. If there is a relation between the recommended application concentration and DDT ppm then it appears that "a high average ppm for recent years" was reported as "the highest ppm". If we accept these figures what would be the probability that they could be exceeded due to combinations of error, ignorance, aggressive purpose in application, or deliberate sabotage?
Biskind states that the Dept. of Agriculture study found a range of DDT in dairy milk of from 0.5ppm to 25ppm (Biskind, "Clinical Intoxication From DDT", Journal of Insurance Medicine, May 1951, p9).
DDT In Human Milk
Hayes and Laws state that the first studies regarding DDT in human milk were by Laug in 1951, even though Biskind reported human milk studies in April, 1949 where a concentration of 116ppm is found in the milk of a woman who had been under study for neuropsychiatric disorders, whereby, suspecting a toxic cause, her milk was analyzed for DDT levels immediately after she gave birth. The results were: 116ppm, 18ppm, 2ppm, 5ppm, 5ppm. Apparently such extreme numbers are only found when tests include the colostrum (milk excreted just after birth). Milk excretion is known to be a form of toxin catharsis for adult females, at the expense of their offspring.
The Laug study on human milk came out a year after Biskind's report, so perhaps Laug's study, based in Washington, D.C., was in response to Biskind's progress. Laug utilized Negro women (only) for his studies of DDT in human fat tissue and human milk. The milk studies utilized "32 samples from 32 different Negro women outpatients from a District of Columbia Hospital...". It is interesting to note that during the first major worldwide polio epidemic in 1916, Negros were considered immune to polio. It is possible that this "immunity" was conferred for dietary reasons, as it is commonly known that the high consumption of dairy products is primarily a European habit, often not shared by those of African descent.
Hayes and Laws report 0.13ppm as the concentration given for DDT in human milk according to studies by Laug et al (1951). Hayes and Laws do not mention that this is an average. If we look at the original Laug publication we find that 0.13ppm is a mean average and that the high was 0.77ppm.
If the first human milk at birth (mentioned by Biskind and not measured by Laug) can contain as high as 116ppm DDT, then the DDT in commercial dairy milk must have reached much higher ppm since animal standards are much lower regarding pesticide exposure. Cows may have eaten fodder that was treated with pesticides. Cows were often treated with 5% DDT solutions during feeding (Zimmerman, O.T., Ph.D., Lavine, Irvin, Ph.D., DDT - Killer of Killers, Industrial Research Service, Dover, New Hampshire (1946)). DDT can also be absorbed through the skin of dairy animals and concentrate in their milk.
Officially, DDT levels were 106 times higher in dairy milk compared to human milk (13.8ppm vs .13ppm) who probably preferred a diet low in dairy products. Infants fed exclusively on human milk do not get polio, according to an investigation into the diet of polio victims by a Massachusetts State Health Inspector, during an epidemic in 1908. Albert (not Carl) Sabin wrote in May, 1950 that human milk and "certain" cow's milk conferred protection from polio. In 1949, it was reported that Eskimo polio epidemics did not affect breastfed Eskimo infants.
The NYC epidemic of 1916 rarely affected infants under the age of 6 months. This information is reflected in the following graph of Haven Emerson's data on age and polio incidence:
Scobey reported that, "In 1908, [during] an epidemic of poliomyelitis... no infant who was fed exclusively on the breast developed poliomyelitis."
It is interesting to tentatively view the vertical axis as "Dairy Milk As Percent Of Diet", as in 1916, such a graph would likely have the same shape.
In 1946, when the Great Polio Epidemic was exploding, Zimmerman and Lavine advocated that farmers spray 5% DDT solutions upon dairy animals during feeding, in the air, upon their bodies and bedding.
In the early 1950s, when the average dietary level for the U.S. population in the early 1950s was reported to be 5ppm, rat studies showed that liver damage was being caused at dietary levels of DDT at 5ppm (generally, high dosages of pesticides are recognized soon because of nerve damage, and repeated low dosages over a longer period of time cause cell and membrane damage, first apparent in the liver.)
Biskind (1953) wrote:
In 1950, a year in which more than 200 million pounds of insecticides were used in agriculture alone in this country, investigators of the Federal Food and Drug Administration announced:
"The finding of hepatic [liver] cell alteration at dietary levels as low as 5 p.p.m. of DDT, and the considerable storage of the chemical at levels that might well occur in some human diets, makes it extremely likely that the potential hazard of DTT has been underestimated."
In 1951, the United States Public Health Service pointed out:
"DDT is a delayed-action poison. Due to the fact that it accumulates in the body tissues, especially in females, the repeated inhalation or ingestion of DDT constitutes a distinct health hazard. The deleterious effects are manifested principally in the liver, spleen, kidneys and spinal cord.
"DDT is excreted in the milk of cows and of nursing mothers after exposure to DDT sprays and after consuming food contaminated with this poison. Children and infants especially are much more susceptible to poisoning than adults."
In spite of Biskind's warnings and the evidence, by 1956 the National Research Council stated in "Safe Uses of Pesticides In Food Production", regarding pesticide law before 1954, that:
...the old procedures had protected the public, as shown by the absence of authenticated association of pesticide residues with human illness...
A mouse study in 1973 found DDT to be tumorigenic at dosages of .25 mg/kg (Terracini et al). Another mouse study found DDT tumorigenic at 2 mg/kg (Tomatis et al). In 1969 a mouse study found a DDT metabolite to be tumorigenic at the range of 0.4 to 0.7 mg/kg (Innes et al). Yet, DDT's relation to cancer is still said to be questionable.
Biskind wrote that he was attacked via the citing of false data, such as, the purported safety of DDT among army personnel, although Albert B. Sabin had found that U.S. army personnel in the Phillipines (treated heavily with DDT) suffered more than 10 times the poliomyelitis as the army personnel in the U.S. Additionally, Sabin wrote that polio was the leading cause of death next to battle casualties and that soldiers in DDT-treated areas suffered a great variety of severe illnesses, as opposed to soldiers in untreated areas who were "without ailments of any sort" according to interviews of soldiers by Biskind.
The points made herein can be summarized in two graphs. Various dosages and hypersusceptibility factors are presented below. Assumed is a 14 lb infant, drinking 700 grams of milk per day, and the resulting vertical axis is "Days To Accumulate Illness Dosage" in the first table and "Days To Accumulate Death Dosage" in the second. These graphs demonstrate that between the two extremes (illness and death) exists an impressive array of possibilities for DDT causality.
[Original graphic not found]
[Original graphic not found]
Criticism of this approach could be that:
1) "Days To Accumulate DDT Dosage" does not consider that DDT is converted to metabolites of more or less toxicity after ingestion. 2) DDT is stored after ingestion in "safer" areas of the body such as in fatty tissue.
The rebutt of such criticism is that:
1) DDT does not readily metabolize to significantly less toxic or non-toxic forms. 2) Repeated dosages at the levels found in human diets over a 2 to 60 day period are known to cause neurological disease. 3) Once any susceptibility factors are included, the criticism exponentially becomes invalid. 4) At dosages of 25ppm or 116ppm, criticism clearly becomes invalid. 5) During periods of fasting, fat storage is metabolized and pesticides can be released at potentially dangerous levels. 6) Fatty tissue includes the myelin, which is the nerve sheath. Thus DDT accumulatives in the nerve sheath and has obvious opportunities to cause nerve damage.
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