題　名：「The Poison Cause of Poliomyelitis And Obstructions To Its Investigation」（HTML）

著　者：Ralph R. Scobey

掲載年：1952年4月

PMID  ：14924801

掲載誌：Archives of Pediatrics(N.Y.)

• スコビー論文（1952）日本語

注）現在、オリジナルの論文はネット上で入手困難であり、ここではJim West氏に掲載しているテキストを使用した。

Statement prepared for the Select Committee to Investigate the Use of Chemicals in Food Products, United States House of Representatives, Washington, D.C.

The disease that we now know as poliomyelitis was not designated as such until about the middle of the 19th Century. Prior to that, it was designated by many different names at various times and in different localities[1,2]. The simple designations, paralysis, palsy and apoplexy, were some of the earliest names applied to what is now called poliomyelitis.

Paralysis, resulting from poisoning, has probably been known since the time of Hippocrates (460-437 B.C.), Boerhaave[3], Germany, (1765) stated: "We frequently find persons rendered paralytic by exposing themselves imprudently to quicksilver, dispersed into vapors by the fire, as gilders, chemists, miners, etc., and perhaps there are other poisons, which may produce the same disease, even externally applied." In 1824, Cooke[4], England, stated: "Among the exciting causes of the partial palsies we may reckon the poison of certain mineral substances, particularly of quick silver, arsenic, and lead. The fumes of these metals or the receptance of them in solution into the stomach, have often causes paralysis."

Colton[5] (1850) mentions the case of a patient who swallowed some arsenic accidentally and was admitted to the hospital. The primary effects of the poison had been successfully combated with proper remedies, but seven days afterward he became paralyzed. It is significant to note that there was a latent period of several days before the paralysis appeared since this delayed reaction is comparable to the incubation period in infectious diseases.

Vulpian[6] (1879) experimentally produced paralysis of the extensor muscles of a dog by lead poisoning. The lesions, consisting in colloid degeneration and cell atrophy of the anterior horn cells of the spinal cord were pronounced by Vulpian as poliomyelitis. Adamkiewitz[7] (1879) reported two parallel cases, one of poliomyelitis and one of lead poisoning.

In 1881, Popow[8] of St. Petersburg, published an essay upon the pathological anatomy of arsenical paralysis as produced artificially in animals. The work of Popow was carried out under the guidance of the distinguished neurologist and microscopist, Professor Mierzeyeski. Popow concluded that arsenic, even in a few hours after its ingestion, may cause acute central myelitis or acute poliomyelitis.

During an epidemic of poliomyelitis in Australia in 1897, Altman[9] pointed out that phosphorus had been widely used by farmers for fertilizing that year. This observation may be of significance since in recent years organic phosphorus insecticides, such as parathion, have been suspected as possible causes of poliomyelitis.

Onuff[10] (1900) reported a case of a painter with flaccid paralysis of both legs, in whom the autopsy showed lesions characteristic of poliomyelitis.

Obsrastoff[11] (1902) reported a case of acute poliomyelitis resulting from arsenic poisoning. Phillippe and Gauthard[12] (1903) reported a case of anterior poliomyelitis from lead poisoning.

Gossage[13] (1902), writing on infantile paralysis, says: "The nerve cells or fiber may be acutely disabled by the action of some poison circulating in the blood, and it is possible that such poison would only temporarily impair their functions or so seriously affect them that recovery would be impossible."

Dr. David E. Edsall[14] (1907), writing on the pathology of carbon monoxide poisoning in Osler's System of Medicine, states: "Peripheral neuritis had repeatedly been described and poliomyelitis and disseminated encephalitis have been seen."

Collins and Martland[15] (1908) reported a case of poliomyelitis in a man, 38 years of age, which resulted from the use of cyanide as a silver polish. The illness began with diarrhea, followed by headache and pain and stiffness in the back of the neck. About eight days after the onset of the illness, he became paralyzed. In discussing Collins and Martland's paper, Larkin stated that he had seen one instance of this disease following potassium cyanide poisoning.

In the spring of 1930, there occurred in Ohio, Kentucky, Alabama, Mississippi and other states an epidemic of paralysis[16,17]. The patients gave a history of drinking commercial extract of ginger. It is estimated that at the height of the epidemic there were 500 cases in Cincinnati district alone. The cause of the paralysis was subsequently shown to be triorthocresyl phosphate in a spurious Jamaica ginger. Death resulted not infrequently from respiratory paralysis similar to the bulbar paralysis deaths in poliomyelitis. On pathological examination, the anterior horn cells of the spinal cord in these cases showed lesions similar to those of poliomyelitis.

These incidents show that epidemics of poisoning occur and furthermore, that epidemic diseases do not always indicate that they are caused by infectious agents. Moreover, following the ingestion of the spurious Jamaica ginger, the symptoms appeared two to ten days later. In some cases a longer time elapsed. This latent period is comparable to the incubation period of infections diseases. As a matter of fact, the incubation period of poliomyelitis is commonly stated to be seven to 10 days on the average with considerable variation in either direction. The so-called incubation period in poliomyelitis and the latent period in these cases of poisoning, therefore, are strikingly similar in length.

Leenhardt et al.[18] (1951) described acrodynia in the course of three cases of acute poliomyelitis. Some authorities have considered acrodynia to be caused by a poison. Elmore[19] (1948) reported two cases of this disease following the ingestion of mercury and Warkany and Hubbard[20] (1951) found mercury in the urines of 38 (92.7 per cent) of 40 acrodynia patients. Meyerhofer[21] (1939) reported that infantile acrodynia may immediately follow certain forms at atypical poliomyelitis, especially encephalomyelitis. Mercury is used as an insecticide and a fungicide and the above clinical observations indicate that it might be a factor in producing some cases of poliomyelitis.

Gougerot[22] (1935) reported that during arsenical therapy for syphilis, poliomyelitis developed in two patients, and lethargic encephalitis followed by Parkinson's disease in one.

In 1936, during a campaign to eliminate yaws in Western Samoa by the injection of arsenicals, an epidemic of poliomyelitis appeared simultaneously.23 In one community all of the patients developed paralysis in the same lower limbs and buttocks in which they had received the injections and this pattern was repeated in 37 other villages, whereas there was no paralysis in uninoculated districts. The natives accused the injections as the cause of the epidemic of poliomyelitis. Most of the cases of paralysis occurred one to tow weeks after the injection of the arsenic.

n 1936, during a campaign to eliminate yaws in Western Samoa by the injection of arsenicals, an epidemic of poliomyelitis appeared simultaneously[23]. In one community all of the patients developed paralysis in the same lower limbs and buttocks in which they had received the injections and this pattern was repeated in 37 other villages, whereas there was no paralysis in uninoculated districts. The natives accused the injections as the cause of the epidemic of poliomyelitis. Most of the cases of paralysis occurred one to tow weeks after the injection of the arsenic.

Dr. Robert W. Lovett24 of the Massachusetts State Board of health (1908), describing the epidemic of poliomyelitis in Massachusetts in 1907, and after reviewing the medical literature on experimental poliomyelitis, states: "The injection experiments prove that certain metallic poisons, bacteria and toxins have a selective action on the motor cells of the anterior cornua when present in the general circulation; that the paralysis of this type may be largely unilateral; that the posterior limbs are always more affected than the anterior; and that the lesions in the cord in such cases do not differ from those in anterior poliomyelitis." It appears to be of great importance that various poisons, lead, arsenic, mercury, cyanide, etc., found capable of causing paralysis are employed in relation to articles of food that are used for human consumption.

The foregoing reports indicate that poisons can cause poliomyelitis. It would appear that not any one poison in particular would be responsible for all cases of poliomyelitis but the effect of any one of several could produce the same ultimate result. When a disease is known to be caused by a poison, it is obvious that a search for a germ or virus in relation to it would not be made. Conversely, if a so-called virus is believed to be associated with the disease, then the possibility of poisoning as the cause of the disease would not be considered. It will be shown, moreover, that some so-called virus diseases and virus inclusions can be caused by poisons

Dr. Robert W. Lovett[24] of the Massachusetts State Board of health (1908), describing the epidemic of poliomyelitis in Massachusetts in 1907, and after reviewing the medical literature on experimental poliomyelitis, states: "The injection experiments prove that certain metallic poisons, bacteria and toxins have a selective action on the motor cells of the anterior cornua when present in the general circulation; that the paralysis of this type may be largely unilateral; that the posterior limbs are always more affected than the anterior; and that the lesions in the cord in such cases do not differ from those in anterior poliomyelitis." It appears to be of great importance that various poisons, lead, arsenic, mercury, cyanide, etc., found capable of causing paralysis are employed in relation to articles of food that are used for human consumption.

There are two abnormal findings in cases of poliomyelitis that point strongly to poisoning as the cause of this disease. One consists in the appearance of increased amounts of porphyrin in the urine; the other is the presence of increased amounts of guanidine in the blood. It is a well-known fact that porphyria can follow poisoning by a number of chemicals. Guanidine has been found in increased amounts in the blood in arsenic, chloroform, and carbon tetrachloride poisonings.

The fact that ascorbic acid has been effective in the treatment of poliomyelitis appears justly to imply that this disease has a poison cause. Ascorbic acid has been used as a reducing agent in the treatment of poisoning resulting from a number of toxic agents, including coal tar antipyretics, nitro compounds, aniline, cyanide, benzene, lead, arsenic, etc[32-40]. Paralleling these modern scientific investigations is the observation over a century ago that lime juice and lemon juice were protective against the poisoning by fish which sometimes resulted in paralysis[41,42]. This early observation is perhaps the principle reason why lemon juice is customarily served today when fish are eaten.

The fact that methylene blue[43], another reducing agent, is effective in the treatment of poliomyelitis also points to the poison cause of this disease. Methylene blue has been used as an antidote in the treatment of nitrite, cyanide, carbon monoxide and other poisonings.

Another fact that strongly implies that human poliomyelitis is caused by a poison is found in the recent report (1951) by Dr. Irwin S. Eskwith[44] of Bridgeport, Conn., that BAL (dimercaprol) was effective in bringing about complete recovery in a moribund 4 1/2 year-old girl with bulbar poliomyelitis. BAL counteracts the effects of poisons; it has been shown not to be effective in infectious diseases.

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In 1907, Dr. H. C. Emerson[54], Massachusetts State Inspector of Health, District 14, investigating an epidemic of poliomyelitis in that state, made a careful inquiry regarding the diet. No infant who was fed exclusively on the breast developed poliomyelitis. He found in six cases that fruit and berries had been a large item of the diet. In the cases of two infants, bananas and berries had been given in the diet in addition to breast milk. In three cases of poliomyelitis, the illness was attributed to the eating of large amounts of blackberries and blueberries. In one case the illness was credited to eating heartily of English mulberries. In 39 instances it was stated that food supplied were bought from fruit and vegetable peddlers in their localities.

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Dingman[55] (1916) reported a milk-borne epidemic of poliomyelitis and several similar outbreaks have been reported since then that were traceable to milk.

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Chapman[58], raised the question of food poisoning to explain the epidemic of poliomyelitis in England in 1947, when he stated: "Is it not possible that the present prevalence of infantile paralysis may, in part at any rate, be due to some article in our restricted and modified dietary?"

（中略）

Toomey and August[59] (1932) pointed out that some authors thought that poliomyelitis is a disease of gastrointestinal origin which might follow the ingestion of foodstuffs. In 193360, they noted that the epidemic peak of poliomyelitis corresponds with the harvest peak of perishable fruits and vegetables. They called attention to the fact that the disease occurs only in those countries which raise the same type of agricultural products. Dr. C.W. Burhans[60], one of the colleagues of the authors, thought that green apples might be a factor in the etiology of poliomyelitis. Toomey et al[61]. (1943) points out that there is frequently a history of dietary indiscretions previous to an attack of poliomyelitis. They suspected that a virus could be found on or in unwashed fruit or in well water during epidemics of poliomyelitis. Every year for eight years, therefore, grapes, apples, peaches, and pears were collected from the vineyards and trees in Northern Ohio at the time of the ripening. In none of their studies was the so-called virus of poliomyelitis demonstrated when the washings of the fruit or the well water were injected into experimental animals. However, no chemical tests were made to determine whether or not a chemical substance on or within the fruit or in the well water, acting by oral ingestion to produce poliomyelitis, was present.

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Draper[62] (1935) recorded a series of cases of poliomyelitis which he postulated originated from a Greek fruiterer. All of the cases were in contact with the Greek as business associates, relatives or customers, and there was nothing in the evidence to point to infection being carried by the Greek himself other than the fruit he supplied.

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Barber[64] (1939) reported four cases of poliomyelitis that developed simultaneously on the same day from the eating of strawberries in a single house of a boarding school. He says that the simultaneous onset of these cases resembled food poisoning. The seasonal and climatic incidence of poliomyelitis, he points out, agree closely with the seasonal increase in the consumption of fresh garden production. He says that the epidemiological distribution of poliomyelitis resembles food poisoning.

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Chenault[65] (1941) noted that the history of poliomyelitis points to a "suggested parallelism between a number of epidemics and the appearance of fresh fruits and vegetables." [With regard to these numerous statements regarding fruit and milk, note the high production of pesticides in the form of lead and arsenic compounds during this pre-DDT period, graphed]

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Goldstein et al[66] (1946) reported an epidemic of polioencephalitis at a naval training school among the cadets. The epidemic was explosive in character and involved over 100 persons. Epidemiological evidence suggested that some food served in the mess hall was the cause of the disease.

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Gebhardt and McKay[68] (1946) found during an epidemic of poliomyelitis in Utah that of a total of 206 persons surveyed, 192 persons, or 93.2 per cent, had one to two weeks prior to the onset of the disease eaten fresh fruits. The authors found in Utah, New York and California, during 1943, that the cases of poliomyelitis paralleled the harvest peaks. Most of the multiple cases in families were found to have developed at the same time, suggesting means other than contact as the mode of spread. Among the fruits more commonly eaten were apples, peaches and pears; tomatoes headed the list of vegetables. The authors stated that the data appeared to fit into the jigsaw puzzle of epidemic poliomyelitis.

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Abbott[71] (1948), of Auckland, New Zealand, stated: "The public has always been fully convinced that they caught poliomyelitis from one another by direct infection. The 'germ' idea is indeed deeply ingrained in both the profession and the public. It will be many years before our prolific writers of medical textbooks attain the degree of sophistication that would enable them to understand how and why poliomyelitis would be more likely to be contacted from the flour-bag, or some homely article of food, rather than from their neighbors."

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Barondes[72] (1949) points out that a study of the epidemiology of poliomyelitis shows a definite correlation with the harvesting of fruit and vegetable crops and to changes in climate, weather and humidity. The harvesting of such fruits as cherries, grapes, berries, apricots, etc. and the edible vegetables, as lettuce, radish, cucumbers, etc. usually from June to September, corresponds with the period of poliomyelitis epidemics, Barondes points out.

Toomey et al[74] (1949) made some important experimental observations that appear to show a correlation of the poison and virus theories of poliomyelitis. They considered it possible that a food (fruit) which enters the gastrointestinal tract could in some way act as a precursor of catalytic enzyme on a normal constituent of the tract and accelerate the production of poliomyelitis. Various materials, together with fruit extracts, were tested.

When supernates of peach skin mash were injected intracerebrally into cotton rats, followed at intervals with intracerebral injections of the so-called poliomyelitis virus, accelerated production of paralysis occurred. Because of the presence of cyanophore glucosides in peach skins, a synthetic preparation, succinotrile, was injected intracerebrally into the experimental animals. This chemical accelerated the production of the disease similar to that produced with the peach supernates. Toomey et al. emphasize that the injections of fruit supernates were made in a manner that does not occur under natural circumstances.

Sabin[75] (1951), although insisting on the virus etiology of poliomyelitis, implicates food and drink as important factors in the cause of this disease. He points out that measures which are often advocated to combat poliomyelitis epidemics are not warranted, such as (a) avoidance of crowds, large gatherings or sports events, (b) exclusion of children under 16 years of age from movies, churches, or schools, and (c) exclusion of poliomyelitis patients and suspects from general hospital wards.

（中略）

The implications [of the foregoing] should be obvious that investigations of foods eaten by the poliomyelitis victim prior to his or her illness should be carefully considered.

The public, as well as many physicians, is under the impression that viruses are living organisms comparable to a germ that enters the human, animal or plant to cause the disease. The scientists, who are authorities on virus diseases, are in disagreement as to the nature of a virus.