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Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE NOVEMBER 1998 ISSUE THE POISON SLEUTHS DEATH BY ARGEMONE MEXICANA -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. His whole body is swollen, especially his legs. What happened to him? Please tell me." "Good morning Tarun. The name of this young man is Ghanshyam, and he was found dead in his hospital bed today morning. He is about 32 years old, and belongs to a low socio-economic status family. He was a champion of the cause of downtrodden, and was their leader for quite sometime now. For some days he had been complaining of marked swelling of the whole body especially of his legs. He had some gastrointestinal symptoms also such as vomiting and diarrhea, but the doctors were not very much worried about these symptoms. The main cause of worry was his swelling which could be an indication of some heart or kidney trouble. He had been admitted to the hospital and investigations were being carried out, but today morning he was found dead. Doctors were initially quite at ease giving his cause of death as kidney failure, but there was some organization of Jhuggi-Jhompri settlements, which raised the doubt that the death could have been as a result of deliberate poisoning by someone. Obviously they seem to have some political clout too. Just after a delegation met the local MLA with this doubt, an inquiry was ordered, and hence the police has brought his dead body to me. My job is to find out how he actually died." "But why would a person want to kill Ghanshyam? He does not seem to have a fight with anyone, does he?" "We do not know yet. I may remind you, that Ghanshyam was a leader of the downtrodden, and he may have had some enemies. It is not uncommon for leaders to have enemies who can go to any extent to have the leader removed from their way. It is possible that Ghanshyam had some enemies, who might have done away with him with some poison. Once his body is cremated, and then if someone raises a doubt that he had been poisoned, we would not be in a position to do anything about it. But right now, we have his body in our possession. So it is indeed very prudent to find out the right cause of death right now. Especially since this has now become such a hot political issue." "So what are you going to do now?" "I went through the hospital records, and found out what symptoms he was suffering from. I also had a detailed discussion with the doctors who were treating him. I already told you that he was having diarrhea, vomiting and marked swelling of his body, especially his legs. On inquiring from the doctors, I found out some other symptoms too. He had loss of appetite, and his liver was enlarged and tender. He complained of tingling sensations in the skin, and tenderness of the calf muscles. But what really interested me was that he was also having increased intraocular pressure.." "Sorry to interrupt you doctor, but what is meant by intraocular pressure?" "Tarun, the word intraocular is a Latin word meaning inside the eye. It is the pressure exerted by the fluid inside the eye. Normal intraocular pressure or tension is about 15 mm of Mercury, which simply means that normally the pressure inside the eye is so much as to support a column of about 15 mm of mercury. If you compare this figure with certain other commonly known figures, you would be better able to appreciate this pressure. The normal systolic blood pressure is about 120 mm of mercury, which means that the pressure generated by heart during contraction is roughly 8 times the pressure inside the eye. The normal atmospheric pressure at sea level is 760 mm of mercury, which means that it is about 50 times higher than that found inside the eye. In raised intraocular tension, the pressure rises more than 25 mm of mercury. Increase in intraocular tension is technically known as glaucoma. Rise in intraocular tension occurs in very few poisonings. Coupled with other symptoms, I at once made a certain guess about the possible poison that he might have ingested.." "What is that poison? Please tell me doctor. I am getting curious." "Tarun, it comes from a plant called Satyanashi in vernacular. Botanically it is known as Argemone mexicana." "Oh, I have heard about Satyanashi. It is a common weed found in our country, isn’t it?" "Yes, you are right Tarun. Its seeds are very much similar to that of dark variety of mustard seeds. I must tell you mustard (which is edible) has two varieties of seeds, a dark variety (Brassica nigra) and a light variety (Brassica compestris). The light variety is yellowish and quite distinctive. The seeds of Argemone mexicana give out a very poisonous oil, known as Argemone oil or katkar oil. This oil also looks very much similar to mustard oil. So katkar oil is very much used to adulterate mustard oil. It appears Ghanshyam got adulterated mustard oil from somewhere and consumed it. That is why he got these symptoms." "Just one thing doctor before we go ahead. Could you tell me, why this plant is called Argemone mexicana?" "Yeah sure Tarun. The name Argemone comes from the Greek argema, meaning "a cataract in the eye". Interestingly, the juice of this plant was once very popular in the treatment of cataract and hence the name. Of course, now it is known that it is not only useless for treating cataract, but can in fact be dangerous to the eye. The name mexicana, simply refers to its native place Mexico. I may tell you that this is originally an American herbaceous annual belonging to the family Papaveraceae, but has now become a pantropical weed throughout tropical and subtropical parts of the world. It has come to India through activities of man and occurs as a local weed in cold season, exclusively in low rainfall regions at elevation from sea level to 2,500 m. It grows wild all over the country in wastelands and along roadsides. It is called Sialkanta in Bengal and North India, Satyanashi in Gujrat and Bharamdandi or Pila-Dhatura in Maharashtra. It is known by several other names such as Ujarkanta and Phirangi Dhatura. It is a robust prickly herbaceous annual, 1-4 ft high, with spreading branches. The flowers are 1-3 inch across and are colored yellow. Seeds are blackish brown, round and netted, and as I told you earlier, resemble those of mustard (Brassica nigra). The extract of the whole plant (latex) contains two alkaloids Berberine and Protopine. Seeds yield 22-36% of a pale yellow, nauseous, bitter, non-edible oil, which as I told you earlier is known as katkar oil or simply Argemone oil. This oil is rich in two other alkaloids Sanguinarine and Dihydrosanguinarine, the former being more toxic than the latter. These latter two alkaloids are mainly responsible for the poisonous symptoms produced by ingestion of Argemone oil. It is said that if katkar oil is heated to 2400 C for 15 minutes, it loses its toxic properties. Other alkaloids of lesser importance are cheletrythrine and coptisine." "Doctor, you told me that the seeds of the dark variety of mustard look very similar to those of Argemone mexicana. Is there some test, by which the two can be differentiated?" "Oh yes. Certainly. The light variety of mustard seeds (Brassica compestris) can easily be differentiated from Argemone by simple visual inspection. The tricky part is to differentiate the dark variety of mustard seeds (Brassica nigra) with those of Argemone. This is done by placing the seeds in normal saline. Mustard seeds will sink, while Argemone seeds will float. If you have trouble remembering this fact, remember the mnemonic 'False will Float'. Remember Argemone seeds are 'false' seeds." "Oh, that is truly marvelous. Is there a scientific way to detect adulterated mustard oil too?" "Oh, yes, there certainly is. There are at least three interesting color tests to detect adulterated mustard oil. The first is the Nitric acid test. We take 5 ml of adulterated oil and mix it with an equal volume of Nitric acid. The test tube is shaken and then allowed to stand. After some time the acid layer turns yellow, orange or crimson, depending on the amount of argemone oil in the adulterated sample. This is a simple test but has the great drawback of lack of specificity. This means that there are a number of false positives. The second is Ferric Chloride test. In this test, we use three reagents, namely Hydrochloric acid, ethanol and of course ferric chloride. The test is carried out in three steps. In step 1, two ml of adulterated oil is mixed with an equal amount of Hydrochloric acid and heated in a water bath at 35 degrees Celsius for two minutes. After this 8 ml of ethanol is added and heating continued for one more minute (Step 2). Finally in the third step we add 2 ml of ferric chloride, and the mixture is heated for a further ten minutes. If an orange-red precipitate forms, it indicates adulteration with Argemone oil. Finally there is the Cupric acid test, where 5 ml. of adulterated oil in taken in a test tube. One ml. glacial acetic acid and 2 mg. of cupric acetate solution are added to it. Development of green colour confirms the presence of argemone oil in the sample. Besides these color tests, the adulterated oil can also be detected by Paper chromatography and Thin Layer Chromatography (TLC). These are slightly complicated techniques, but I will tell you the basics of these tests. In paper chromatography, the mixture (of mustard and argemone oils) is allowed to run on a paper which is much like a blotting paper. The speeds with which each oil travels on this paper is different, with the result that after some time the two oils separate. These oils can be made visible by adding suitable reagents. This is the basis of paper chromatography. TLC is also quite similar. Paper chromatography is a very sensitive technique and can detect down to 0.0001% adulteration with argemone oil." "Doctor, you earlier told me that Katkar oil is used to adulterate mustard oil. So does this mean it is cheaper than mustard oil?" "Yeah sure. But an additional factor often held responsible for adulteration is the maturation periods of the two plants, which is almost similar. Those defending intentional adulteration (mainly merchants and retailers of mustard oil) often point to the fact that the two plants often grow together and ripe at the same time, so during harvesting, there is an inadvertent mixing of the two seeds. But this argument appears fallacious for several reasons. Argemone grows mostly on fallow land and mustard has a canopy that does not let anything grow under it. Mustard ripens in March and Argemone in May. By May mustard has already been harvested, so adulteration can only be intentional." "Oh, I see. Does this mean Katkar oil has no use at all? It is only misused for adulteration." "No Tarun. Katkar oil has several legitimate uses. It is used medicinally in several countries in the treatment of dropsy (swelling of the body), jaundice and skin diseases. It is often given as an aperient (laxative). It is also used for lighting lamps, as it is very cheap. I might tell you that although the seeds of Argemone look very much like those of mustard seeds, there are some important differences between the two. If the seeds are placed between two fingers and rubbed, the Argemone seeds are found to have spiny edges. Mustard seeds do not have such spiny edges. Furthermore the seeds of mustard are heavier having a specific gravity of 1.3 as compared to 1.08 of Argemone. This helps in easy differentiation. The seeds of mustard will drown in saline water of appropriate specific gravity (say 1.2), while those of Argemone will keep on floating. Always remember the mnemonic I told you earlier - 'False will Float" "Oh, that is certainly interesting. Could you tell me the name of the disease one suffers from, when he consumes Katkar oil?" "Tarun, the name of the disease is epidemic dropsy. Dropsy means swelling of the body, and the name epidemic is self-explanatory. This disease usually occurs in epidemic form. The reason is that when adulterated oil comes in the market, several people consume it and fall ill at the same time. That is why the name epidemic dropsy is quite apt, although modern textbooks of medicine rarely use this term now. I told you that the chief symptom of Argemone oil poisoning is marked swelling over the legs. The cause of this swelling (technically known as edema or dropsy) is the increased porosity of the blood vessels, which is caused by Sanguinarine. Because of the increased porosity, water leaves the blood vessels and comes to lie in the tissues. This is mainly responsible for the swelling. Sometime so much water oozes out of the blood that it accumulates in the cavities around the heart and lungs. Look here at Ghanshyam’s body. I have dissected the body for you. Can you see the fluid accumulated around his lungs and heart?" "Oh, sure doctor. There is lot of fluid around his lungs and heart. And of course his legs are very much swollen. It is becoming clear to me now that he died of Argemone oil poisoning. I was just curious to know how old this disease is." "Tarun, the first case of poisoning in the country was reported in Bombay in 1877. In 1926, a doctor in Bengal discovered its link with consumption of cooking oil adulterated with Argemone oil. In 1935, the scourge killed 1,500 people in Bengal, and in 1966 an outbreak incapacitated hundreds of people in Bombay. In 1983, dropsy created havoc in Delhi, and again in 1998 during the months of August and September. During 1998 epidemic in Delhi, a total of 2552 cases were reported officially of which as many as 65 died. I may tell you, that although katkar oil is poisonous to animals, they do not show classical symptoms of epidemic dropsy. Experiments have shown that monkeys and cats develop sleepiness and diarrhea culminating in death. Guinea pigs and mice lost weight and died without showing any symptoms. Since epidemic dropsy can not be produced in animals, most studies on the Argemone oil have been done on human volunteers." "Doctor, have the outbreaks of Argemone poisoning occurred in other countries too, or is it just a peculiarity of our country?" "Tarun, Argemone poisoning has occurred in several other countries too, namely Fiji islands, South Africa and the 3 Ms - Madagascar, Myanmar and Mauritius. In our own country, it seems to occur more commonly in Northern India. South India has rarely suffered from this condition perhaps because mustard oil is not very popular there. Another interesting fact is that while almost all outbreaks of poisoning have occurred due to contamination with argemone oil, in South Africa an epidemic occurred due to adulteration of wheat flour with argemone seeds." "Oh, I see. So how do we arrive at the final diagnosis that Ghanshyam indeed has died due to Argemone oil poisoning?" "Tarun, I looked at his eyes, and dissected the retina. His intraocular tension is high. In addition, I also saw retinal hemorrhages, which is another thing that occurs in Argemone oil poisoning. Look here at the retina, which I have dissected out. Can you see retinal hemorrhages here?" "Oh sure doctor, they are very obvious. What else?" "Tarun, I told you that Sanguinarine causes dilation of blood vessels. Owing to dilation of peripheral blood vessels, a bluish mottling appears on the skin. Here you can see those bluish mottlings all over his skin. You can also see some small, fleshy, dark red, warty growths or nodules in the mucous membranes of cheek, gums, tongue and nose. This is quite characteristic of Argemone oil poisoning. Another characteristic thing is enlargement of liver. In this case too, it is enlarged. So we are almost sure that Ghanshyam died of Argemone oil poisoning. I have enquired the place from where Ghanshyam used to buy his mustard oil. It is from a local retailer Kauwa Ram. Come let us tell the police to seize all oil from his possession. It is quite obvious that he has adulterated the mustard oil with Argemone oil, and is selling it to gullible public for his own profit." "Oh yeah, this was a most interesting discussion doctor. Because of your sterling sleuthing, this dishonest trader will be caught and the public will be saved of this unnecessary agony. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Sodium chlorate." "

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE FEBRUARY 1998 ISSUE THE POISON SLEUTHS DEATH BY SMFA -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young woman today. What happened to her? Please tell me." "Good morning Tarun. The name of this 22 year old female is Kabuli. She had got married to Radhey only a year back. Radhey works in a chemical factory involved in manufacturing various chemicals. Since the marriage day itself, there was a dispute among the couple regarding the insufficient dowry which Kabuli brought from her home. Radhey as well as his parents used to belittle her on every little matter. For about last one week, Radhey suddenly started a soft posture towards Kabuli, as if he had buried all differences with his wife. Last evening he became very sweet to her, and even made a cup of tea for her. She was a bit surprised, but thought that may be Radhey had changed his ways. She took tea, but soon after had vomiting, and seizures. After about 3-4 hours she died. A local doctor was called, who certified the cause of death as heart attack. But the relatives of Kabuli lodged a complaint with the police that Kabuli had actually been poisoned to death by Radhey. Subsequently the police went to Radhey's house and seized the remaining portion of the tea, as well as some other stuff from his almirah. The body of Kabuli was also seized and given to me for post-mortem. Now I have to conduct a post-mortem on the case and tell the police if Kabuli was really poisoned or not." "Just a minute doc. You said that a local doctor has already certified that the cause of death was heart disease. Then what more do you expect to find?" "Tarun, the relatives of Kabuli have already lodged a complaint with the police that she has been done to death by Radhey. Kabuli had got married only a year back. Under the Indian law, any death of a married female occurring within 7 years of marriage is termed as dowry death and is taken seriously. Had there been no complaint from Kabuli's relatives side, then everything would have been fine. But since a complaint has already been lodged, the police naturally want to be doubly sure that Kabuli really died of heart disease or not." "You mean that the local doctor gave a wrong cause of death? Do you?" "Well, the doctor had not seen Kabuli during life. The doctor could genuinely be mistaken. Sometimes, a doctor may give a cause of death just to avoid harassment to the relatives. If the doctor knows the family personally and is convinced that the death was natural, he would generally oblige the relatives by giving a cause of death, even if he had not seen the patient during life. He does so in order to save unnecessary harassment to the relatives at the hands of the police. Last but not the least, a doctor can actually be bought by unscrupulous relatives, to give a wrong and misleading cause of death." "Oh, I see. So you are doing the postmortem in order to find out how Kabuli died actually?" "Exactly. If my findings indicate that Radhey had indeed given poison to Kabuli, he could be prosecuted under section 304B of the Indian Penal Code, which is popularly known as Dowry Death. If the court finds Radhey guilty of murdering his wife, he would get no less than 7 years in jail. This is the punishment prescribed in section 304B of the Indian Penal Code." "Oh, I see. So what have you found out?" "Tarun, the most interesting thing is that while Kabuli was drinking tea, she did not complain of any bad odor or taste. This means that the poison, if indeed it was given to her, was tasteless and odorless. The tea also had its normal color, which means that the poison was colorless too. Such poisons, which are colorless, odorless and tasteless are generally very successful homicidal poisons, because the victim can not make out the poison while taking his food. I also took into account that Radhey was working in a chemical factory which was making rodenticides. Rodenticides are very strong poisons and can kill a person within a short time. It was quite possible for Radhey to steal a little quantity of rodenticide from his factory and give it to Kabuli for homicidal purposes. The only rodenticide, which is colorless, odorless and tasteless is a chemical compound known as Sodium Monofluoroacetate which is also known by its acronym SMFA. Its chemical formula is C2H2FNaO2 and it is also known as Compound 1080. Its other names are Sodium fluoroacetic Acid and Sodium fluoroacetate." "Compound 1080? That's rather a strange name. Why has it been given this mathematical name?" "That's an interesting question Taurn. But let me tell you about another compound which has been given a mathematical name too. It is arsphenamine, which is known as Compound 606. This has an interesting history too.." "Doctor, I am a sucker for interesting scientific histories. Please tell me the history of compound 606, and then of course we can go to the history of compound 1080" "Alright as you say. Well, you must surely be knowing about the German Scientist Paul Ehrlich (1854-1915). He is often known as the father of antibiotic therapy. In late 1800s and early 1900s - the era during which Ehrlich lived - one of the biggest problems faced by doctors was to create a drug which could kill bacterial cells but NOT human cells. If such a drug could be discovered, it could be given with impunity to humans in order to cure their infections, say syphilis (which as you surely must be knowing is caused by a bacterium known as Treponema pallidum). The drug would then selectively target bacterial cells killing them, while sparing the human cells. Such a drug could be called - as Ehrlich liked calling it during his entire life - a "magic bullet" ; a bullet magical enough to kill bacterial cells while leaving human cells alone. Since human and bacterial cells are so similar in nature biologically, it was difficult to find a chemical which could destroy one type of cell, leaving out the other. But of course there are differences too, and the answer lay in finding those differences and exploiting them. In the late 1800's, Elrich, was noting with interest that there existed some stains which could stain bacteria but not human cells and vice versa. A cell, as you know, gets stained only when it "takes up" that dye. If bacterial cells and human cells could take up different stains, surely there existed more chemicals which could be differentially absorbed by bacterial and human cells. And surely some could be toxic to them too. Ehrich started from this conjecture and started with one such dye. His aim was of course to find a chemical which could - instead of staining the bacterial cell - KILL it. There was absolutely no luck in the beginning and so he began to chemically alter it little by little, testing each new drug. When he reached 606th compound, he discovered, to his delight, that he had finally synthesized a chemical (it had changed so much by now, that it was no more a stain), which could kill bacteria, especially the bacteria causing syphilis. In the beginning he simply called it Compound 606, because it was the 606th compound synthesized by him. Of course later it became known as arsphenamine and was marketed as Salvarsan." "That's great. Doctor, you know so many stories. And now, what about the story of Compound 1080? So I take it when Ehrlich reached at 1080th compound, he gave it that name, and that compound was SMFA, right?" "No, not at all. In fact Ehrlich stopped at 606. To be sure, he did not live much after introducing that compound. Compound 606 was synthesized sometime in 1909 and the first tests on bacteria were announced in the spring of 1910. Ehrlich suffered a stroke in December 1914, and succumbed to a second stroke in August of the following year (1915). No, compound 1080 was not synthesized by him. There was a company, which was synthesizing chemicals for possible pesticide use, and SMFA was the 1080th compound tested by them. You might be interested to know that there is a compound known as Compound 1081 too. It is Fluoroacetamide. This also acts as a rodenticide and insecticide. This was of course the next compound made by the same company." "Fine. So you concluded that Radhey had given SMFA to Kabuli. Well I haven't heard much about SMFA. Please tell me something about it in detail." "Tarun, I must tell you that I have not concluded anything yet. I am simply trying to analyze the circumstances, and come to the most logical conclusion. That is what scientific thinking is all about. To tell you more about Sodium Monofluoroacetate, I must tell you that it is a highly toxic rodenticide. It contains fluorine, but its toxicity is not related to its fluoride content, but rather to its interference with the Kreb's cycle..." "What is Kreb's cycle doctor? This term is rather new to me." "Tarun before going any further, I must tell you that Kreb's cycle is named after a German-British Biochemist, Sir Hans Adolf Krebs who was born in Germany in 1900. He found out for the first time how lactic acid in the body gets broken down to release energy. Well, to begin from the beginning, glycogen in the liver is first converted to lactic acid, but this step gives only very little energy. Major energy comes from the further breakdown of lactic acid into simpler compounds such as carbon dioxide and water. The exact sequence of breakdown of lactic acid into simpler compounds was first worked out in great detail by Sir Hans Krebs, and hence these steps are known by the name Kreb's cycle. It is also known as tricarboxylic acid cycle. This however is a less fancied name. If any chemical interferes with Kreb's cycle, it would cause death because Kreb's Cycle is the main energy source of the body. Sodium Monofluoroacetate is one such chemical." "Oh, I see. Since how long do we know about this compound? Looks like it was developed fairly recently." "Tarun, SMFA was developed during World War II as an alternative to imported natural rodenticides. Because it is so highly toxic, its use is mostly limited to commercial exterminators. It is derived from some plants such as Palicourea (South America), Acacia (Australia), and a few other plants. As I told you earlier, SMFA is a white, odorless, tasteless, water-soluble salt. It looks like flour or baking soda. Unlike thallium about which we talked in one of our earlier meetings (see Science Reporter October 1997, pages 42-46), SMFA can not be absorbed through unbroken skin. However it is readily absorbed through the gastrointestinal and respiratory tracts, mucus membranes and broken skin. It is thus highly toxic when ingested, inhaled in dusts, or absorbed through open wounds." "Oh, I see. You said that Kabuli had vomiting after taking tea, and also that she had seizures. Are these the symptoms of SMFA poisoning?" "Well, almost. The toxic effects of SMFA are usually delayed for one to several hours and result from the conversion of the nontoxic fluoroacetate ions to toxic fluorocitric acid, which in turn blocks the Kreb's cycle. I have already told you that this cycle is essential to energy production. I must tell you that this cycle is important in mammalian cells only. Vomiting is commonly seen soon after ingestion. Toxic effects primarily involve the Central Nervous System and the heart. They include nausea and apprehension followed by disturbances of the heart beat, respiratory depression, seizures and coma. Apprehension, auditory hallucinations, and facial paresthesias often precede convulsions. By facial paresthesia, I mean that there are sensory disturbances in the facial area. There may be tingling sensations in the face, or there may be feeling of pins and needles." "How does death occur in SMFA poisoning doctor?" "Tarun, death results either from ventricular tachycardia which is a scientific term meaning that the ventricles of the heart start beating too rapidly. You might imagine that this is good for the body, but this is not so. When the ventricles of the heart beat rapidly, they just beat without really pumping any blood. So this in effect is actually a tremendous waste of effort on the heart's part. Death may also occur from the fibrillation of the heart, which is another condition, in which the heart starts beating very rapidly, without pumping adequate amount of blood. It may also occur from respiratory failure which may occur because of pulmonary edema. Pulmonary edema may sound a formidable term to you, but in effect it is nothing but filling up of lungs with water." "Oh, I see. How much SMFA would actually kill a person?" "Tarun, SMFA is a dangerous homicidal poison, not only because it is colorless, odorless and tasteless, but also because it kills in very small quantities. In humans, does of 0.5-2 mg/kg of the body weight are highly dangerous. This means that if a man weighing 60 kg ingests about 120 mg (60x2mg), he would be quite serious. Lethal dose is 5 mg/kg. Thus for the same man, the lethal dose should be around 300 mg, which as you can see is really small. Small doses make it that much easier for the poisoner to administer the poison, in his victim's food." "Oh, I see. Doctor is there any antidote for SMFA, which could have been given to Kabuli to save her life?" "Unfortunately there is no known antidote for SMFA, which makes it still more dangerous as a homicidal poison." "So did you find any tell-tale signs of SMFA poisoning in Kabuli's dead body?" "Tarun, SMFA, does not leave any tell-tale signs in the victim's dead body, which is yet another reason why SMFA is such a good homicidal poison. There are no specific post-mortem findings. However animals who die of SMFA poisoning develop stiffness of limbs rapidly and are found with their extremities in hyperextension. This in plain and simple terms means that the extremities are stretched fully at the joints. I have taken samples of tea taken by Kabuli from her stomach and have run chemical tests on it. And as expected I have found SMFA in it. Not only that, I have also examined chemically the tea remaining in Kabuli's cup, and have found SMFA in that cup too. In Radhey's almirah, the police found a small white packet in which some white salt was present. On chemical analysis, that salt has turned out to be SMFA as well. So there seems little doubt that Radhey had indeed given Kabuli the poison. He had probably stolen some of the rodenticide from his factory, and had mixed it in Kabuli's tea. That was also probably the reason, why he was going so soft towards her for the last one week or so. He wanted to gain, Kabuli's confidence, so she could accept anything from him, without doubting his intentions. Come on, let us tell the police, that Radhey indeed is the killer." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- common salt. You may believe that common salt is not a poison, but interestingly it can be, and has been, used to kill humans!"

Explore Dr. Anil Aggrawal’s comprehensive forensic medicine ecosystem—featuring peer-reviewed journals, forensic books, career guidance, programming tutorials, expert quotes, book reviews, and more. A one-stop resource for students, professionals, and researchers in forensic science and toxicology. Anil Aggrawal's Forensic Ecosystem The World's First Online-only Journal dedicated to Forensic Medicine & Toxicology Dedicated to the advancement and dissemination of forensic science and medicine, the platform integrates rigorous scholarship, practical insights, and comprehensive educational resources. It strives to support and connect the global forensic community by fostering academic excellence, profesional development. and , multidisciplinary collaboration, serving as an essential resource for students, educators, and practiconers alike. Fully Open Access Journal International Authorship Publishing Since 2000 Access the journal Anil Aggrawal's Forensic Ecosystem Forensic Medicine & Toxicology Internet Journal Forensic Science Fiction Forensic Quotes & Aphorisms Forensic Career Forensic Programming Forensic Jokes, Puns and Tidbits Forensic Toxicology Explore Books. 2nd Edition Textbook Of Forensic Medicine And Toxicology Price ₹2,510.00 Clinical and Forensic Toxicology Regular Price ₹6,000.00 Sale Price ₹5,789.00 Necrophilia: Forensic and Medico-legal Aspects Regular Price ₹14,727.00 Sale Price ₹12,274.00 Forensic Medicine and Toxicology for MBBS Price ₹1,090.00 Essentials of Forensic Medicine and Toxicology Price ₹1,155.00 Forensic Medicine and Toxicology for Ayurveda Price ₹984.00 Forensic Medicine and Toxicology for Homeopathy Out of stock Basic Sciences As Applied to Forensic Medicine And Toxicology Regular Price ₹1,350.00 Sale Price ₹1,310.00 FORENSIC AND MEDICO LEGAL ASPECTS OF SEXUAL CRIMES AND UNUSUAL SEXUAL PRACTICES Price ₹8,164.00 Injuries Forensic and Medicolegal Aspects Regular Price ₹4,500.00 Sale Price ₹3,999.00 Self Assessment and Review of Forensic Medicine: Volume 1 Regular Price ₹650.00 Sale Price ₹595.00 Narcotic Drugs Price ₹240.00 Modern Diagnostics Out of stock SOME COMMON AILMENTS Price ₹125.00 Textbook of Forensic Medicine and Toxicology (1st Edition) Out of stock

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Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE NOVEMBER 1997 ISSUE THE POISON SLEUTHS POISONING BY CAPSAICIN -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today. You seem to be doing the post-mortem on a very young infant. What happened to her? Please tell me." "Good morning Tarun. The name of this young 5 month old girl is Neeta. She was born to Pyarelal and his first wife Seema. Just after her birth, Seema expired because of some complication. Pyarelal soon remarried another woman Anita, apparently because he wanted someone to look after his young daughter. But from her behavior it did not appear that Anita had any great liking for Neeta. She would often keep her hungry and would torture her in several other ways. There were rumors that Anita even wanted to do away with Neeta for good. In fact she wanted that her own children - as and when they were born- get due importance in the family....." "So you think that Anita has killed this young child?" "No, I didn't say that. But certainly all facts have to be kept in mind while investigating suspicious deaths." "What do the parents of the girl say?" "The father Pyarelal was in the office when the girl died. The girl's stepmother Anita says that she had given milk to the child at 10 am in the morning, soon after Pyarelal left home for office. After that Anita put her to sleep and got busy in her household chores. At 2 pm when she wanted to give her the second feed, she found that the child was lying listless in the cot. She panicked and immediately phoned Pyarelal. He came home at once. A doctor was called, but when he found that the child was dead, he suspected some foul play, and informed the police. The police conducted some preliminary investigations, and then handed over the body to me, to find the cause of death." "So what have you found out?" "Tarun, you won't believe it but I have found a very strange cause of death in this case. She was poisoned by a very exotic poison.." "What is that poison doctor? Please tell me, I am getting curious." "Tarun, the poison in this case is a chemical known as Capsaicin. It might sound a very alien name to you, but it is found in a very common household item- chilies. In other words, Neeta was done to death with chilies!" "What? I don't believe that. How can anyone kill with chilies?" "Tarun, Chilies contain an exceedingly acrid, volatile poisonous substance Capsaicin. It is because of this substance that capsicum has a pungent smell and taste. In India, capsicum fruits are powdered and universally employed as a condiment known as red pepper or lal mirch. You may be surprised but chilies are used in India for a lot of criminal activities. They are used by the police for the purpose of torture for instance...." "Really? Well, I am beginning to believe that Capsaicin indeed is an interesting poison. Why don't we begin from the beginning doctor?" "Oh sure Tarun. There are so many interesting tales to tell about capsicum and its active principle capsaicin. While capsaicin in small quantities may tickle our palates, in large quantities, it may act as a poison. The fatal dose of capsaicin has been estimated to be about 150 mg/kg in mice and rats. Taking the same figure to be true for a human being, it would take almost 9 g of capsaicin to kill an adult human being weighing 60 Kg. This is rather a large amount as far as homicidal poisons go, but small children can be killed with far lesser doses. Experimental rats and mice die within 4 to 26 min after the fatal dose, so it appears to be rather a quick poison..." "Doctor, how does a person die of capsaicin?" "Tarun, as I told earlier death by chilies is unusual except in very small children. Death by capsaicin is due to fall in blood pressure and stoppage of respiration. At autopsy, the stomach lining is found to intense red due to irritation and there may be erosions and even ulcers." "Doctor, you said there are so many interesting tales about chilies and capsaicin. Please let me know some of them." "Sure. Tarun, chili plant belongs to the family Solanaceae. History of this plant is most interesting. Archaeological findings show that capsicum was eaten in Mexico already in prehistorical ages back to 7000 B.C. It was one of the first plants domesticated in the Americas. Beautiful pictures of Capsicum fruits are seen on pottery of the Nazca Culture in the Southern part of Peru; the fruits are linked to the forelegs of the "Mottled Cat" which was a fructiferous symbol. It is said that when Columbus arrived in 1492 in San Salvador, Cuba and Haiti, it was not only the first step into the New World, but also the entrance right into the center of the "Capsicum Countries". In his first letter to the Spanish Catholic Majesties Ferdinand and Isabella, he already mentioned the habit of the people to eat meat with very hot spices. On his second voyage he was accompanied by the physician Dr. Diego Alvarez Chanca from Sevilla. He gave the first detailed report about the hot spice called Agi, which was nothing but modern day chili. Fernandez de Ovieto described the plant in detail and mentioned already its common use by the Spaniards. Cortez regarded in a letter in 1526 Agi as one of the most valuable products of Mexico, saying clearly that he enjoyed the hot taste of this spice. Quite soon an exchange of seeds and plants between the Old and the New World took place: oranges, lemons, melons and grapes were brought to the West, capsicum, tobacco and maize to the East. It is remarkable that the ancient name Agi or Aji remain in use until present days in the territory formerly governed by the Inca. Tschudi, a Swiss traveller, who gave a detailed description of life in Peru around 1840, mentioned the meal "Piccante" being served for lunch every day. It contained so much Agi that after a few spoons the mouth started to burn like glowing coal. He mentioned that one soon got adapted and acquired a preference for the condiment; even the ingestion of large amounts of these hot fruits was devoid of any adverse effects on the gastro-intestinal tract. I may tell you here that an acetic acid extract of only two capsicum fruits, when applied to the skin, produces severe pain and reddening, followed by the formation of a blister." "Oh, so chilies were very common in South America, even in prehistoric ages. Were they used for killing in those times too?" "If they were, no records exist of such killings. Capsicum however captured the imagination of people as a condiment. Within a few decades after Columbus, Capsicum had been distributed world-wide. Its distribution in Europe started with the cultivation and use as a spice in the Iberian peninsula. It is however unknown whether Capsicum came from there to other parts of Europe. It seems more likely that Portuguese trade connections to Ormuz in Persia in 1513 and Diu in India in 1538 opened the way for Capsicum to Ottoman Turks. Capsicum probably reached Central Europe concomitantly with their invasion of the Balkan peninsula and of Hungary which was occupied by them for about 150 years. The collection of Herbal woodcuts, published by Leonhard Fuchs in 1545 in Basle, contained already three plates of Capsicum under the name of Indian and Calicut pepper. Capsicum was cultivated in monastery gardens of that time, as documented e.g. in Brünn (Brno) in Moravia in 1566. It seems that Capsicum was highly welcomed as spice in Europe to substitute for black pepper. From Greek and Roman times on, aromatic spices and frankincense came from the Orient to Europe via secret trade connections. These links between the Lands of Spices and Europe were for centuries the monopoly of Arabs and Venetian merchants, resulting in an exorbitant price for pepper. So costly was pepper that only very rich traders could expect to trade in it. It may interest you to know that in Germany even today, rich traders are called "Pfeffersäcke" which means pepper sacks! Black pepper, the spice most sought after, was so costly in old days that it was counted out peppercorn by peppercorn!" "Doctor, earlier you mentioned about the name Aji for chilies. I usually eat pepperoni pizza which contains lot of chilies. Now after talking to you, I realize the word "pepperoni" contains the word "pepper" too." "Yes, that's a good observation. Chili is known by a number of names around the world. In the West Indies and South America the ancient name "Aji" is still in use. In Mexico the Nahuatl word "Chili" was used when the Spaniards arrived; the name remained in use not only in Mexico but also in Northern America as chili or chili. The name of the long black pepper of India, Piper longum, was soon also used for Capsicum and remained in use as "pepper" in most English-speaking countries. Pepperoni is actually the name of a fairly hot variety of capsicum which is eaten in Italy. In Europe, Capsicum found its main domicile in Hungary. The Hungarian name paprika stems from the Slavic name peperke used in Balkan countries for pepper. Another version, although not based on linguistic sources, seems to be more charming: The Hungarian diminutive form for Ilona is Ilonka, and Mary is Marika. On the same lines it has been suggested that paprika was the definition for a small pepper!" "Doctor, how many varieties of capsicum exist in the world?" "Tarun, there are about 1600 to 1700 varieties of Capsicum in the world, but only around 200 of them are commercially available. The Mombasa variety, the black chili from Africa, is too hot to be eaten; it would blister the mouth! Other varieties are as mild as green peas and do not contain capsaicin." "That's interesting. Doctor, tell me why do people eat peppers, chili or paprika at all? Doesn't it appear more or less like a paradox to you? Chilies are so hot; by no stretch of imagination can they be called pleasant, yet people seem to enjoy the hot taste of chills. Why?" "Tarun, you must remember that highly spiced meals, flavored with chili, chili-containing curry, black or green pepper or ginger are preferentially consumed in countries with hot climates such as India. The common experience during such a fairly hot meal is sweating beginning in the face. This occurs only in hot climates or in a warm restaurant, but not in a cold environment. It is called gustatory sweating because it differs from sweating following physical exercise, protecting against hot environment or expressing emotional stress. The effect of gustatory sweating is explained by the action of capsaicin on thermoregulation. It stimulates heat sensitive fibers in the periphery and the temperature regulation center. This results in sweating, which is basically a heat loss reaction. This effect is observed not only in man but also in rats. This also counteracts the heat production by a heavy meal and facilitates food intake in hot climates. All these facts explain the enormous fascination of people with chilies. So high is the consumption of chilies in the world, especially in hot climates that the world-wide production of Capsicum is estimated to be in the range of 6 million metric tons each year. There is even an International Chili Society which arranges Local and World Championship Chili Cookoffs, thus connecting peppers with entertainment! Capsicum plays a very interesting cosmetic role in chickens too which has nothing to do with the action of pungent capsaicin..." "What is that?" "Tarun, when chickens have access to green food in springtime their feet become bright yellow and the yolk of their eggs almost orange red. This is based on the rising intake of carotenoils. Thus bright yellow color of chicken's feet and orange red color of egg yolks is indicative of the fact that chickens have had a lot of green food. In fact this is often touted as a "healthy color" to the customers. Quite strangely poultry owners can produce a similar color in their chickens without giving them green food." "How?" "Tarun, besides capsaicin, chilies also contain Capsanthin which is the red pigment of ripe paprika pods and accounts for about one third of their colorants. The red color of chilies is because of this pigment. When this red pigment is included in the food of chickens, a similar change in color in chicken's legs and in their egg yolks appears because Capsanthin accumulates there. The interpretation that the "healthy color" of legs or egg yolk is linked to life of chickens in open air is therefore suggested to the customer!" "That is certainly highly interesting doctor. You said earlier, that chilies are used for a lot of criminal activities in India. Can you tell me about some?" "Oh, sure. To begin with, I must tell you that homicide by pepper although a rarity, is a distinct possibility. The first report of a case of homicide by pepper in world's literature was published in 1964. Homicidal asphyxia by pepper has also been reported. In such cases, the pepper is forcibly introduced in the nostrils and mouth of very young children who get asphyxiated. Another reported criminal use of pepper is by robbers. They often throw chili dust in the eyes of their victims to "blind" them temporarily to facilitate robbery. This act can in fact be done by anyone to temporarily inactivate his enemy or opponent. Chili powder is often used by police in our country- and in fact in several third-world countries- to extract confession from criminals. It may be introduced in the mouth, nose, anus, urethra or vagina to torture a suspect and extract confession from him. It is said that during emergency in India in 1976, chilies were used as a means of torture by introducing them in rectum! This process was known as Hyderabadi Goli. In India, superstitious people use chili fumes to "scare away" ghosts and spirits. These fumes are very irritating to the eyes and the nasal passages and can cause severe inflammation. Such practices can cause severe breathing problems in children, if they are around. Finally, in our country, chili powder is often introduced in the vagina as a punishment for infidelity." "Doctor, what symptoms does the victim experience when chili powder is given to him?" "Tarun, capsaicin is mainly an irritant poison. Applied to skin, it causes irritation and vesication. When ingested in sufficient quantities, it acts as an irritant poison, with the usual symptoms of vomiting and diarrhoea and a burning sensation in the mouth, throat and stomach. Burning sensation also occurs during defecation. When thrown in the eyes, it can cause severe burning pain, watering of the eyes, intense spasm of the eyelids and photophobia, which is another term for sensitiveness to intense light. It is for this reason, that robbers and thugs use chili powder on their victims to rob them. Capsaicin is volatile and because of this, fumes arising from burning capsicum are highly irritant. Major toxic symptoms in experimental rats and mice are salivation, erythema of skin, staggering gait, slowing of respiration often leading to difficult and labored breathing, blueness of skin, tremor, convulsions." "Doctor, I feel now I know fair enough about capsaicin. I am now ready to see the autopsy of this young child. What important findings are present in this child?" "Tarun, when this child was brought to my dissection table, I noticed some pepper, or lal mirch as you would call it, sticking to her clothes. This immediately alerted me of some foul play, especially as I knew that pepper can be used to liquidate unwanted children. I asked about the relationship of the mother with the child in detail and the history made me still more suspicious. Then I looked at her mouth, and I was stunned to see lot of red pepper in her mouth. On opening her food pipe and stomach, I found still larger quantities of red pepper there too, which almost solved my case. Not only that, there were large quantities of red pepper in her windpipe and bronchi too. I can now imagine what must have happened. When Pyarelal left for office, Anita waited for some time. Then she brought a fistful of red pepper from her kitchen and forcibly introduced it in the child's mouth. The poor child could not resist. Whatever resistance she did make only helped to introduce chilies in her nose too. Needless to say, with so much of pepper in her stomach and windpipe, the child soon died. Anita then smoothed out everything, removed the traces of chili powder from her face and from the cot, and phoned her husband at 2 pm. She hoped that she could pass the death off as a natural death. She however forgot to clean Neeta's clothes completely, and I could find traces of chili powder in her clothes which immediately alerted me. Well, even if she had assiduously cleaned her clothes, I would still have found out the cause of death by looking at her stomach and windpipe. Come, let us tell the police that Neeta did not die a natural death; Anita is her killer." "Oh, how very clever of you doctor. This was a most interesting discussion. I never could imagine that chilies could be put to such a draconian use. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very deadly poisonous gas- Lysol "

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Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JANUARY 2000 ISSUE THE POISON SLEUTHS DEATH BY SUCCINYLCHOLINE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young boy today. What happened to him? Please tell me.” “Good morning Tarun. The name of this 26 year old young boy is Subodh, and he was a post-graduate medical student in a leading medical college of this city. For the last few months, he was in love with a fellow medical student Rita. Recently she had ditched him and had got married to someone else. This had hurt him very much. Actually a few days before her marriage, he had got a hint that she was going to ditch him. So he had gone to her to plead his case. At that time she was reportedly sitting with his fiancée Suresh, who literally pushed him out. There was a minor scuffle too, and Suresh had threatened to kill him, if he ever troubled Rita again. Today morning Subodh did not report at the O.P.D. his fellow doctors got suspicious, and went to his hostel room. There they found his dead body.” “Oh, that is indeed very unfortunate. So do you think that Suresh has carried out his threat?” “Let us get all the facts straight, before we can say anything. The body of Subodh was lying on his charpoy (a charpoy is a popular hand woven bed used in India mostly by villagers). A syringe was inserted in his leg vein. And there were two empty vials of Anectine lying on the floor beside him.” “What is Anectine doctor?” “Tarun, Anectine is the trade name of a very useful drug in medical practice. Its chemical name is succinylcholine, and it is a very useful drug for surgical operations.” “Oh, so obviously Subodh has not died of Succinylcholine. How has he actually died doctor? And do you think he has committed suicide?” “Why can’t he die of succinylcholine Tarun?” “How can a useful drug kill a person doctor? He must have died of something else.” “This is a mistake Tarun. All drugs are poisons in large doses, and many poisons may act as useful drugs in extremely small doses. Some time back I told you the story of a death by Digitalis (See Science Reporter Death By Digitalis (August 1999, Pages 22-24). Now Digitalis as you know is a very useful drug in several heart ailments, and yet it killed when given in more than the required dose. So it is incorrect for you to think that a useful drug can not kill. Now to your other questions. No one knows how he has actually died, and that is indeed why the police has handed over his dead body to me. As far as your conjecture concerning suicide is concerned, he might indeed have committed suicide. The scene certainly appears as if he has committed suicide. Had the room been locked from inside, and a suicide note found, we would have very strongly thought that he has committed a suicide. But neither was the room locked from inside, nor was any suicide note found. The police knows that Suresh had threatened to kill him some days back. Suresh - like Subodh - is a medical student and knows about drugs like succinylcholine. So it is quite clear that Suresh is the prime suspect with police. In fact, Subodh’s parents have lodged an FIR with the police, naming Suresh as the possible killer.” “Doctor, is succinylcholine very commonly used as a homicidal poison?” “No, not at all. In fact, I am aware of only one instance, when a person has been convicted of murder by succinylcholine. In 1983, a Texas-licensed vocational nurse Genene Jones was tried on a single charge of murder, even though those who had worked with her believed she had been responsible for the deaths of more than a dozen children under her care. In her first 31 days of work for a child specialist, nine incidents of respiratory failure involving eight patients occurred before Jones was finally arrested. She was finally sentenced to 99 years for the murder of one patient and 60 years for the attempted murder of a second. So succinylcholine can definitely be used for homicide, although its use is very rare. But before we come to any conclusions, we have to first prove that Subodh indeed died of succinylcholine poisoning.” “How are you going to prove that doctor?” “Tarun, to do that you must know a little bit about succinylcholine and how it actually kills. Succinylcholine actually mimics a natural chemical within the body, acetylcholine. The function of acetylcholine is to make a muscle contract. Whenever we make any muscular movement- be it walking, running, climbing, even laughing and crying - some muscle has to contract, and in most of the cases, it is the acetylcholine, which makes the muscle contract. First of all, a nerve impulse goes from the brain to the required muscle. Then a tiny amount of acetylcholine is liberated at neuro-muscular junction..” “Doctor, what is neuro-muscular junction?” “Tarun, it is technical name of the junction of that nerve with the muscle. It is also known as the myoneural junction. So I was telling you about acetylcholine, being released at the neuro-muscular junction. This small amount of acetylcholine starts a train of physical and chemical events at that junction, which ultimately leads to contraction of that muscle. Whole of this procedure takes a fraction of a second only. Of course, once acetylcholine has succeeded in making the muscle contract, it must be removed from the junction. For if it is not removed, the muscle would remain in a contracted position. And this can be very disastrous indeed. For instance, when the heart contracts, it is due to acetylcholine making the heart muscle contract. But if this acetylcholine could not be removed, the heart muscle would remain in a contracted state, and no useful purpose would be served. In fact, the person would die within minutes.” “Oh, I see. How does the body remove this acetylcholine then doctor?” “There is another chemical at the junction- acetyl cholinesterase. It destroys the acetylcholine, after it has done its work. Succinylcholine may be regarded as a sister chemical to acetylcholine. Earlier I was telling you that succinylcholine is widely used in surgery. Now you can understand why. In most abdominal operations, the doctors want that the abdominal muscles remain in a relaxed state. If the muscle is relaxed, doctors can make incisions easily, and make several manipulations in the abdomen easily. Succinylcholine is used to relax the abdominal muscles….” “Just a minute doctor. You said that acetylcholine makes the muscles contract, and also that succinylcholine is a sister chemical to acetylcholine. Doesn’t it mean that succinylcholine should also contract the abdominal muscles?” “That is an interesting question, Tarun. Actually succinylcholine belongs to a class of muscle relaxants, known as depolarizers. Let me first tell you the meaning of this new term. Earlier I told you that acetylcholine starts a train of physical and chemical events at the neuro-muscular junction, which ultimately leads to contraction of muscle. One of these events is the reversal of the electric charge normally found on the muscle fibres. In other words, the muscle is depolarized. Since succinylcholine depolarizes the muscle, it is known as a depolarizer or a depolarizing agent. There are several other depolarizing agents. One of these is decamethonium. It also acts very much like succinylcholine. All depolarizing agents, including succinylcholine, initially do act much like acetylcholine, i.e. they cause the muscle to contract. But since doctors give succinylcholine continuously in an intravenous drip, it keeps contracting the muscles. Finally a stage comes, when the muscle is exhausted, i.e. it can no more work. In other words it gets paralyzed. That is why despite acting very much like acetylcholine, succinylcholine paralyses the muscles, while acetylcholine makes the muscles contract. When an animal is injected with succinylcholine, the animal indeed shows repeated contractual movements of the muscles. These repetitive muscular movements have been given the name fasciculations. After a few minutes of fasciculations, the muscles get tired, and paralysis sets in.” “Doctor, is succinylcholine easily available in the market?” “Oh, yes. Succinylcholine is available as injections of Anectine. It is marketed also as a sterile powder. Injections are available in three different concentrations- 20 mg/ml, 50 mg/ml and 100 mg/ml. Now that you have understood some basic facts about succinylcholine, I can tell you, how this drug kills. It repeatedly stimulates and finally paralyses, respiratory muscles. This causes respiratory failure and death. The usual dose in surgical operations is 20 mg, but more can be given too. It is interesting to note that this succinylcholine not only relaxes abdominal muscles, but also respiratory muscles, so the anesthetists maintain the respiration of the patient artificially throughout the operation. If however the same dose is injected by a person for suicidal purposes, or by someone with homicidal intentions, it would easily kill, because there is no one to support the respiration artificially. In other words, the same dose helps a surgeon in operation, and the very same dose would kill a person, if it were given with homicidal intentions.” “Doctor how are we going to prove that Subodh indeed died of succinylcholine poisoning?” “Tarun, in the body, succinylcholine is broken down by enzymes in human plasma, especially by one known as pseudocholinesterase, into succinic acid and nitrogen containing choline. Both of these are normal components of human tissues. That is why it is indeed difficult to say by chemical examination of Subodh’s viscera alone that he died of succinylcholine poisoning. However, I have found the lungs to be swollen and loaded with water. In technical terms we say that the lungs are oedematous. This is a sign that Subodh’s respiration was compromised just before his death. If we couple this finding with other findings at the scene of his death, it becomes very plain and simple that Subodh has died of succinylcholine poisoning. Regarding the manner of death, I do not think, Suresh has injected this drug into Subodh’s body. Subodh would simply not allowed him to do that. It appears that Subodh has committed suicide because of failure in love.” “Doctor, had someone caught him during the act, or just after it, could he have been saved? In other words, what is the antidote of succinylcholine?” “Tarun, unfortunately there is no antidote to succinylcholine. The only thing one could have done is to give artificial respiration as the respiration is compromised in succinylcholine poisoning.” "This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison - Gold."

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Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE OCTOBER 1998 ISSUE THE POISON SLEUTHS DEATH BY ALUMINIUM PHOSPHIDE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young lady today. What happened to her? Please tell me." "Good morning Tarun. The name of this young lady is Sushila, and she was found dead in her bed today morning. It is suspected that her husband gave her something in her food, which took her life. I will tell you some details, which will put the whole crime in perspective for you. She was married to a young boy Suresh only 2 months back. Suresh is a petty clerk in a bank, and it appears that there was a dowry demand in the house, which was not properly catered to, by the bride's side. Because of this there was a lot of tension in the house, and Sushila had complained several times to her parents about it. Now suddenly she is found dead in her bed. It is suspected by Sushila's parents, as well as by the police that Sushila has been given some poison by Suresh and his parents to do away with her." "What makes them think that? Do they have any proof against them?" "Well, the main thing is that there is a very strong motive for Suresh's parents to kill Sushila- dowry. They could get their son married again for better dowry. It seems a reasonable motive. Moreover brides don’t usually die so mysteriously just after 2 months of their marriage, until and unless there is some serious trouble with the marriage." "But it is quite possible that she committed suicide. What makes the police think that it is a case of murder?" "Well it could be. But Suresh and his parents are going one step further. They are alleging that she may have died of some natural disease. In fact Suresh has alleged that she had some gynecological problem about which she once discussed with him." "Really? Did you find any evidence of a fatal disease in her body? And by the way, have you found something in her stomach?" "Tarun, I didn’t find any fatal disease in her body. If she had any of it, like leukemia, or other cancers, or some gynecological trouble, I would surely have found out. I have indeed analyzed the contents of Sushila's stomach and I have found out lot of Aluminum hydroxide in her stomach." "Aluminum hydroxide? Doesn't seem like a poison to me. It is a very weak alkali though. Can it kill someone?" "You are right. Aluminum hydroxide generally doesn't kill a person. But just by it's presence, I have come to know of the poison, which might have been administered to her." "And what that poison is doctor? Please tell me. I am getting curious." "Tarun, it is Aluminium Phosphide, a very dangerous poison. It is available in the market at tablets of Celphos, Quickphos or Fumigant. The last trade name is perhaps quite apt. These tablets are used for killing insects in the grains such as wheat and rice. Generally people buy these tablets and mix them with stored wheat. Insects which would otherwise appear in these grains after some time, generally don’t appear if you preserve the grains along with these tablets." "Oh, I see. I have heard about such tablets. But how do they prevent insects from breeding inside the grains." "Tarun, when Aluminium Phosphide comes in contact with water, or moisture in the air, it liberates a very dangerous gas phosphine. This gas is actually dangerous for the insects, and they can't breed inside the grains. Since you are so good in chemistry, I will give you the exact chemical equation of this chemical reaction. The chemical equation for the liberation of phosphine is: 2 AlP + 6 H2O = 2 Al(OH)3 + 2 PH3 I hope it is quite clear to you. The gas phosphine is liberated and aluminum hydroxide is left behind." "Yeah it indeed is clear to me. Tell me why such a dangerous poison is freely available in the market. I agree that it is such a good fumigant, but keeping in mind its poisonous nature, can't the scientists find some better alternative?" "That's a good point of discussion Tarun. In fact there has been much debate and discussion on this already. But I don’t want to go into that. For the time being I will tell you why they are finding it so hard to abandon it. Aluminum phosphide is commonly used as insecticide, rodenticide and fumigant all over India and even in developed countries. To be sure, there are several other fumigants available, such as ethylene dichloride, ethylene dibromide, carbon tetrachloride mixture and methyl bromide. But only aluminum phosphide is considered as an ideal fumigant over all other fumigants. It has almost all the properties of an ideal fumigant…." "Really? What are those? Please let me know." "Tarun, Aluminum Phosphide is highly toxic to almost all stages of insects with remarkable penetration power. It dissolves well in water, oils and fats. It is considered an ideal seed fumigant since the seeds' viability is not affected and is practically free from residual toxic hazards- provided the seeds contain less than 20% water. It is minimally absorbed and easily desorbed from the treated commodity such as wheat grains. It is non flammable at the prescribed dosage and devoid of tainting on fumigated stock. It has a distinct odor, which has been described as a fishy odor. Because of this and also because of delays in evolving phosphine provide considerable safety in handling this fumigant. Since the tablet generates the predetermined weight of gas, it is very convenient to administer the exact dose. Cost of fumigation is low and its effects on the fumigated stock last longer. It is easy to transport and handle. Treatment is more or less known, so in case accidental poisoning occurs in humans, they can be taken care of. But unfortunately no specific antidote is known. These are all very desirable properties in any fumigant, and all of these are available in aluminum phosphide." "Doctor how can you detect phosphine in the environment?" "Tarun, Phosphine is a colorless and odorless gas, but when it is generated from aluminum phosphide tablets available in the market, generally there are some impurities along with it. Because of this, the gas has a typical garlic odor. Besides the smell, the presence of phosphine can be detected by a simple test. When a filter paper soaked with silver nitrate solution comes in contact with the gas, it turns from brown to black. The usual fatal concentration of phosphine is 200 ppm. After the reaction with moisture, less than 25% of the original tablet weight is left behind from which the amount of aluminum phosphide consumed can be detected." "Doctor, tell me something more about these tablets. I need to know more about them, so next time I see them, I recognize them at once." "Tarun, the tablets are dark brown or grayish in color, 3 g in weight and measure 20 mm in diameter and 5 mm in thickness. They come in an aluminum container containing ten tablets. Aluminum phosphide is also available as 0.6 g pellets. The tablets are composed of pure aluminum phosphide (the active ingredient) and ammonium carbamate/carbonate (the inert ingredient). The ratio of the active and inert ingredient is generally about 56:44. On contact with moisture each 3 g tablet evolves about 1 g of phosphine along with carbon dioxide and ammonia, which prevents self ignition of phosphine gas. This is why it is also called "Protective gas". Carbon dioxide and ammonia are liberated by combination of water with other inert ingredients in the tablets. In fact the main function of the inert ingredients is to produce these gases, so phosphine may not ignite easily. The phosphine gas thus liberated spreads quickly and kills insects and rodents almost in all stages of development. After complete decomposition of the tablet, aluminum hydroxide is left behind as a harmless and non toxic grayish white residue." "And this is what you have found out in Sushila's stomach. So it is almost clear that she died of Aluminum Phosphide poisoning. But how can you prove whether it is a homicidal or suicidal poisoning?" "Tarun, Celphos poisoning is generally suicidal in nature. As I told you earlier, the tablet emits a strange fishy smell. So it is rather difficult to administer it homicidally. It is almost certain, that Sushila took it with suicidal intention. I will give my report to the police accordingly. Of course the police can still register the case as murder under Section 304B of Indian Penal Code. This section defines Dowry death. And this stipulates that the husband and his relatives are responsible for her death if the bride dies from any cause within seven years of marriage, and it is shown that she was harassed for dowry before her death. Of course, to bring Sushila's death under this section, the police would have to work hard, and prove positively beyond doubt that she was harassed for dowry, so I guess, it makes their task that much difficult." "Oh yeah, I am sure, they will be able to do that. This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Argemone mexicana. " Additional notes by readers On April 5, 2001, Sergio Salazar from Nicaragua wrote: In Nicaragua the aluminum phosphide is named "pastilla del amor" -tablets of love- because the suicides ingest these products. I'm a chemist and my job is analytical toxicology in the Instituto de Medicina Legal in Nicaragua. But when there are suicide by phosphine I don't know of any analytical procedure for the detection of phosphine residues. Would you suggest me any methodology? kind regards Sergio Salazar sergio1953@yahoo.com

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE AUGUST 2000 ISSUE THE POISON SLEUTHS DEATH BY ETHYLENE GLYCOL -Dr. Anil Aggrawal “Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this young man is Ramlal and he died this morning. Yesterday night his friend Shyam visited his house with a bottle of liquor as he was reportedly getting married next month, and wanted to enjoy with his friend. Many neighbors saw them enjoying together. He left at around 10 pm. Around 2 am in the night, Ramlal began vomiting severely. Quite alarmingly there was blood in his vomit. At that time only his sister was there at the house. She took him to the hospital, where he died this morning. The doctors were unable to find out what disease he was suffering from. So the police has handed over his body to me, so I can tell them, how he died” “Doctor, are you suspecting some foul play?” “The police certainly is. Ramlal and Shyam are childhood friends. About a year back Ramlal had a severe tiff with Shyam as he had caught him in a compromising position with his sister. Shyam was having an affair with Ramlal’s sister and he (Ramlal) did not like that. At one time in the past, Ramlal had severe fight with Shyam too in this regard. Later Shyam compromised with Ramlal, and swore that he would never meet his sister. Following this Ramlal relented and the two met sometimes, although not as often as they used to be in the past.” “Do you think Shyam give him some poison mixed with alcohol?” “The police thinks so. I have met the doctors and asked them in great detail the symptoms he exhibited at the time of admission. The doctors told me that he was quite inebriated, which was quite natural as till ten p.m. the previous day, he was taking alcohol. But what interested me were the symptoms like coma, seizures, nystagmus, paralysis of muscles of eye and gait, depressed reflexes and tetany. Coma is a technical term for unconsciousness. Nystagmus is also a technical term which describes oscillatory movements of the black circular portion of the eyes (cornea). Tetany refers to spasms of the muscles. Depressed reflexes refers to depression of reflexes like the knee jerk. You may recall that if a person is sitting in a relaxed state, and if his knee is hit gently, at a particular point with a rubber hammer, the lower leg suddenly gives a jerk. This is known in medical parlance as the “knee jerk”. In many diseases, it can not be elicited, i.e. it disappears while in many others it is accentuated. Accentuation of the knee-jerk means that the lower leg would give a more energetic jerk than normal. Knee jerk is a very useful sign for doctors for diagnosing diseases. Neurologists -doctors who diagnose and treat disease of the nervous system - make good use of this jerk for diagnosing diseases. Toxicologists also make use of this knee jerk for diagnosis poisonings, as many poisonings can cause depression of the knee jerk. One of the poisons that cause this is ethylene glycol.” “So you think Ramlal died because of ethylene glycol. Never heard of this being used as a poison. Anyway how can you be so sure that he died of ethylene glycol poison, as you yourself say that many poisons can cause depression of knee jerk?” “That’s right. But look at the cluster of symptoms that he had. They are very typical of ethylene glycol poisoning. Anyway, I would confirm my suspicions by various typical findings after the autopsy is completed..” “Doctor, although I have heard about ethylene glycol in my chemistry class, yet I do not know enough about it to follow your conversation. Kindly tell me something about this poison.’ “Tarun, Ethylene glycol is also called 1,2-ethanediol. Its molecular formula is (CH2)2(OH)2. It is a colourless, odorless, water soluble, viscous, oily liquid possessing a sweet taste and mild odour. It is produced commercially from ethylene oxide, which is obtained from ethylene. Ethylene glycol is widely used as antifreeze in automobile cooling systems..” “Excuse me doctor, what is an antifreeze? Kindly tell me.” “Tarun, antifreeze is a compound which is used in cars to prevent the water in its radiators from freezing. In cold weather, freezing water can cause a burst in the radiator of a car which has been left standing. This freezing can be avoided by adding ethylene glycol to lower its freezing point. Good-quality solutions sold as antifreeze have a sodium-based inhibitor added, to prevent corrosion. Generally a 25% content of antifreeze in the radiator water will give protection against freezing, but some manufacturers prefer 33.33% solution. Antifreeze gives protection against corrosion too, so it is left in the radiator all the year round. An interesting fact is that manufacturers add a fluorescent dye called fluorescein to ethylene glycol. This dye fluoresces in ultraviolet light. This “trick” allows mechanics to detect radiator leaks by using an ultraviolet light. But this very fact can be made use of by doctors in detecting poisoning of patients by this compound. They direct Wood’s lamp on the patient’s urine. If the urine fluoresces, it is a sure sign of ethylene glycol poisoning.” “Doctor, you have used another term with which I am not familiar - the Wood’s lamp. What is it? Is it some kind of lamp made of wood?” “No, no. Wood is actually the name of a physicist who devised this lamp. He was a Baltimore physicist and his name was Robert William Wood (b. 1868). In this lamp, there is a special glass called Wood’s glass, which transmits only the ultraviolet radiation (with some red in the visible region). The radiation thus passed is known as “Wood’s rays”, and have a wave length of about 360 nm. This glass contains nickel oxide. One use of this lamp is for the detection of small spore ringworm of the scalp. I have taken some urine from the urinary bladder of Ramlal and have shone Wood’s light over it. Come on, you can also see it.” “Oh, doctor, I can clearly see the urine fluorescing. This is remarkable. This is enough proof that Ramlal died of ethylene glycol.” “I will do better than that, and come up with some more proofs. So I was telling you that ethylene glycol is used as an antifreeze. It was even used as a coolant in the Lunar Module! It is also used in the manufacture of man-made fibres, low-freezing explosives, and brake fluid. I may tell you that it was discovered as a substitute for glycerine (used in enemas). It has also been used in commercial products such as detergents, paints, lacquers, pharmaceuticals, polishes and cosmetics. It’s other uses are as a preservative in juices and as a deicer. Since the compound is easily available, has a warm sweet taste and produces a state of inebriation much like that of ethyl alcohol, it has been used by poor people in place of alcohol. For the same reasons, it has also been used by people for committing suicide. One can easily mix it in alcohol and give it to his adversary for killing him. Only about 100 ml are sufficient to kill an adult human being. I must tell you that Ethylene Glycol poisoning is one of the most serious and dramatic intoxications encountered in clinical toxicology. Just like methanol and isopropanol, it is used as a second-rate substitute for ethyl alcohol by poor people, because it is cheaper. However, while methanol poisoning occurs in epidemics, ethylene glycol poisoning is sporadic. There was a time when it was used in pharmaceutical preparations (as a solvent), but now it is banned. Yet many cases of poisoning still occur. In May 1998, over 20 children died in Gurgaon after consuming medicines, which were thought to be adulterated with ethylene glycol” “Oh, that’s terrible. How does ethylene glycol kill doctor?” “Toxicity due to ethylene glycol is not as much because of the compound itself, as because of its breakdown produces. Ethylene glycol itself causes some CNS depression, and a state of inebriation quite like that produced by ethyl alcohol. After ingestion, peak blood levels occur at 1 to 4 hours. Half-life of ethylene glycol is 3 hours, which means that half of the quantity ingested would get metabolized in 3 hours. Principally four breakdown products cause damage, namely aldehydes, glycolate, lactate and oxalate. The first three are responsible for severe acidosis. This means that the pH of the blood becomes less alkaline. The damage because of oxalate is because it gets deposited in tissues and causes widespread tissue destruction. Kidney damage is particularly likely. The compound itself is mildly toxic. Acute inflammation of the eye has been reported following accidental eye contact. Contact with skin can cause mild skin irritation. Inhalation can cause toxicity too. Factory workers who are exposed to vapors of ethylene glycol can suffer from chronic poisoning. The symptoms are nystagmus and recurrent attacks of unconsciousness. Toxicity occurs due to two main reasons. Tissue destruction due to deposition of calcium oxalate crystals (mainly in kidneys, but also in brain, blood vessels, liver and pericardium. Because of chelation of calcium, hypocalcemia occurs, and production of severe acidosis due to aldehyde, glycolate and lactate production.” “What symptoms does the victim of poisoning experience doctor?” “Tarun, the symptoms appear in three fairly well-defined phases. The first phase occurs within 30 minutes to 12 hours after ingestion. The patient appears drunk, but there is no characteristic alcoholic odour from his breath. Nausea, vomiting and hematemesis may be seen. CNS effects include coma, seizures, nystagmus, paralysis of muscles of eye and gait, depressed reflexes and tetany is seen as was seen in the case of Ramlal. The tetany is due to fall in calcium levels in the blood. This occurs because ethylene glycol produces oxalic acid in the body and it combines with calcium in the blood to form calcium oxalate crystals. The second phase begins 12-14 hours after the onset of first phase. By this time there is widespread deposition of oxalate crystals in the tissues. This results in tachycardia (increase in heart beat), mild hypertension (raised blood pressure), pulmonary edema (water logging of lungs) and congestive cardiac failure (heart becoming unable to pump blood out to the body). The third phase occurs 24-72 hours after ingestion. There is flank pain, with tenderness in the chest and evidence of kidney disease usually manifested by stoppage of urine. This is technically known as oliguria. Proteinuria (protein appearing in the urine) and microscopic hematuria (blood appearing in the urine) may occur. Urine with a low specific gravity may be observed.” “Doctor what is its fatal dose and fatal period?” “The Fatal dose is about 2 ml/kg weight, or about 120 g for a 60 kg man. About 90% patients die within 24 hours due to CNS damage. Rest die in about 8-12 days from renal failure.” “Doctor, I was reading somewhere that in 1937, more than 100 people died in USA because of ethylene glycol. Is this information correct?” “ Oh, you are talking about the famous Elixir of Sulfanilamide-Massengill disaster of 1937, which occurred during the months of September and October 1937. No, the incriminating compound was NOT ethylene glycol, but DIETHYLENE GLYCOL - sometimes also known as ETHYLENE DIGLYCOL. There is a difference between ethylene glycol and diethylene glycol. While the formula of ethylene glycol is (CH2)2(OH)2 or C2H6O2, as I told you earlier; that of diethylene glycol is HO[CH2CH2O]2H, or C4H10O3. In fact, the formula of Polyethylene Glycols (PEGs) is HO[~CH2CH2O~]nH. You can go on substituting n for 1,2,3 etc to get higher ethylene glycols. Substitute n for 1, and you get the so-called (mono)ethylene glycol - or simply ethylene glycol - about which we have been taking. Substitute n=2, and you get diethylene glycol, the one responsible for the tragedy you are talking about. Substitue n=3 and you get triethylene glycol. I do not know of any interesting disaster connected with this or any of the higher ethylene glycols. But Polyethylene glycols are toxic no doubt. Polyethylene glycols with molecular weights between 200 and 600 Daltons are clear viscouse liquids, while those with molecular weights between 1000-6000 are rather wax like or waxiform. These are known as Carbowaxes. Their solubility in water is - very roughly - inversely proportional to their molecular mass.” “Good. So what was the "Elixir of Sulfanilamide-Massengill" disaster all about?” “Tarun, Let me first give you some background, so you could appreciate the full significance of this disaster. Scientists had long been hunting for some kind of a magic bullet which could kill disease causing bacteria. The first antibiotic - as we all know - was penicillin. Although it had been described by Alexander Fleming as early as 1928, a usable form was not developed till 1941. So before this time, the world was practically devoid of antibiotics." “Sorry to interrupt you doctor, but what exactly do we mean by the term "antibiotic"?” “Tarun, the term antibiotic - as we all understand and use it - refers to a chemical substance produced by a LIVING ORGANISM, generally a microorganism, that is detrimental to other microorganisms. If the chemical is NOT produced a LIVING ORGANISM, we would NOT call it an antibiotic, even if it killed or were detrimental to microorganisms. Therapy by such a chemical would be known as "chemotherapy", as against "antibiotic therapy", if it were to be done by antibiotics." “Oh, I see.” Prontosil soluble Sulphanilamide Note the -SO ₂ NH ₂ moiety in both. “Coming back to our story. Before 1941, some of these other chemicals (i.e. those not produced by living organisms) were known. The first one to be described was a red dye PRONTOSIL RUBRUM - or "prontosil red" as some would call it - which cured certain bacterial infections in mice. It was described by a German chemotherapist Gerhard Domagk (1895-1964), in 1932. Domagk was awarded the 1939 Nobel Prize for Medicine for this remarkable discovery. Drugs against bacteria were very much sought after during this period, and virtually anyone who could discover an effective medication could get the Nobel Prize. Alexander Fleming, who discovered Penicillin, the first antibiotic got the Nobel Prize for Medicine 6 years later - in 1945. Thankfully his discovery penicillin had come in handy for wounded soldiers during World War II, which had started in 1939." “It must have been a proud moment for Domagk to receive the award.” “No, he never received it, because he was not allowed to." “Why so? That is preposterous.” “Tarun, Domagk lived in the era of Hitler's Germany. Right from the days of Ossietzky, Hitler had adopted a policy never to allow any German to receive the Nobel Prize." “Doctor, I know I am deviating, but who was Ossietzky.” “Tarun, Carl von Ossietzky (1889-1938) - sometimes spelled as Ossietsky- was a German journalist and pacifist who was against the war, and wrote a lot against the Nazis. He was declared the winner of the Nobel Prize for Peace for 1935. Hitler was enraged because the award had been received for writing against him. At least he perceived the situation like that. So he didn't allow Ossietzky to receive the award. In fact a policy was developed never to let any German accept the award. Domagk became a victim to this policy. It was only two years after the war ended - in 1947 - that he could travel to Stockholm to receive the award, but unfortunately by that time the award money had been reverted to the Nobel Foundation, so he did not receive any money. He did however receive the gold medal and the citation (the diploma)." “Doctor, you know so many stories. I am amazed. This must have been a great setback for Domagk.” “Sure it was. However I think that for Domagk, the greatest reward would have been when his own daughter Hildegarde was saved by his drug "Prontosil Rubrum". In February 1935, she pricked her finger with a needle and developed a severe bacterial infection - called septicaemia. Domagk's new drug "Prontosil Rubrum" was given to her and her life was saved. While on the subject of "Prontosil Rubrum", I may tell you that a related compound "Prontosil soluble" also became available during this period. It soon became clear that these compounds themselves were not responsible for the killing action. Instead, a chemical moiety - known as sulphonamide group - broke off from these compounds within the body. It was this chemical moiety which was responsible for the antibacterial activity of Prontosil. The chemical formula of this moiety is -SO2NH2. Scientists derived a number of drugs from this chemical moiety. All these drugs became famous as Sulpha drugs, and they heralded the era of modern chemotherapy against bacterial infections. By 1935, many of these sulpha drugs had become very popular and were marketed as tablets and capsules. One such drug was Sulphanilamide, which was successfully marketed by The Massengill Company of the US. In September and October of 1937, the executives of this company decided to market the same product for children too. But since small children can not take tablets or capsules, it was decided to sell the formulation in the form of an elixir. Technically speaking an elixir meant the solution of a drug in ethyl alcohol and NOT in any other solvent. But the company decided to make a solution of Sulfanilamide in diethylene glycol. Their Elixir was essentially a solution of 10% Sulphanilamide in 72% percent diethylene glycol, with some flavouring and coloring agents. In those times, it was not legally required for a company to test a new drug on animals before marketing it. So The Massengill Company floated the new elixir without any tests. Since diethylene glycol is a dangerous poison, about 76 people died as a result of taking this elixir. The cause was severe liver and kidney damage caused by diethylene glycol. These 76 were the confirmed deaths, but there are unconfirmed reports asserting that more than 100 people died as a result of this disaster.” “That is amazing. The Massengill Company must definitely have been sued by the relatives of all these people?” “No. How could anyone? The Massengill Company was well within its legal rights to sell anything to the consumers. You may laugh at it, but the company could only be prosecuted for mislabelling its product as an elixir, which applies only to an alcoholic solution and not to a solution in diethylene glycol. That is a very small offence though. The fact is that at that time all drug manufacturing and distribution companies were being guided by a very old and archaic law - The Pure Food and Drugs Act of 1906. Althouth it had been amended by the Sherley Amendment of 1912, it still allowed lot of freedom to drug manufacturers. It was only this tragedy, that the much more modern law - The Food, Drug and Cosmetic Act of 1938 was passed. In our country too, a similar Act was passed two years later. It was initially known as The Drugs Act of 1940. In 1962, by an amendment, cosmetics were also included within the purview of this Act and it became known as The Drugs and Cosmetics Act. It is unfortunately true, that it usually takes a great disaster for the government to change an archaic Act.” “Oh, come on. You can't say that just because of one incident, can you?” “Perhaps you are right. But interestingly yet another disaster occurred in late 50s and early 60s which caused further changes in similar Acts around the world. It was the much feared Thalidomide disaster, but if I were to tell you about this, we would be deviating from our initial topic - ethylene glycol.” “Doctor, either you should have not brought about this new topic at all, or you should explain it fully. Since you have mentioned it, my curiosity is aroused. Please let me know about this disaster. I don't mind being late at home.” Thalidomide Glutethimide Glutethimide is still sometimes used as a sedative. Note the structural similarity of both. “Alright, as you wish. But let me tell you an additional fact about Diethylene Glycol. Its story did not end with the Massengill company. This compound keeps raising its head again and again. As recently as in July 1985, Diethylene Glycol was again in the news - this time because it was discovered that Austrian wines were contaminated with this substance. Stocks of all Austrian wines were promptly withdrawn throughout the UK. About Thalidomide? Well it is chemically written as C13H10O4N2. This drug was marketed in more than 40 countries - mainly in West Germany and the UK in the late 50s and early 60s. In Germany, it was manufactured by Chemie Grünenthal and marketed by it as Contergan since 1956, and enjoyed good sales. In Britain it was licensed by Chemie Grünenthal to the Distillers Company. It became available in Great Britain from the beginning of 1958 as Distaval. In Sweden the license was given to a local company Astra. It was being used by pregnant women to counter nausea, which is usually seen in early pregnancy. It also acted as a sedative. Developed in West Germany in the mid-1950s, Thalidomide was touted as one of the safest sedative-hypnotics, just as Titanic was hailed as the unsinkable! Ironically both suffered the same fate. Titanic sank on its maiden voyage, and Thalidomide sank too - in a figurative sense. It caused birth defects in children known as peromelia. An estimated 5,000-10,000 children suffered from this terrible deformity. This ultimately caused its downfall.” “What is peromelia doctor? I have never heard this term.” “Tarun, peromelia is the collective name given to a number of deformities, where there is a congenital absence or malformation of the extremities. It is caused by errors in the formation and development of the limb bud, which normally occurs from about the fourth to the eighth week of intrauterine life. As I told you peromelia has several forms. One of the worst and most horrible is amelia in which there is a complete absence of all limbs. There is just head and the trunk of the baby - absolutely nothing else. Since all the essential organs of the body - brain, heart, lungs, kidneys, liver etc reside in head and trunk, such an infant, if cared for properly would not die. But imagine the quality of life of such an infant. He is just like a plant - with an essential difference. He can see, feel and sense his absolute helplessness. Fortunately this condition was very rarely seen in thalidomide disaster. The second form is Ectromelia, in which there is the absence of one or more extremities. There was also an interesting condition known as phocomelia or “seal extremities", because the extremities resembled like those of a seal. In this condition, the upper part of the limb was extremely underdeveloped or missing, and the lower part was attached directly to the trunk, resembling the flipper of a seal. It was as if the palms and feet were directly stuck to the trunk. Its counterpart was Hemimelia in which the upper part of the limb was well formed but the lower part was rudimentary or absent. Finally there was a condition known as Sirenomelia, in which the newborn resembled a mermaid or siren. The term literally means “mermaid extremity”. This was also a very severe abnormality in which the legs were fused to a greater or lesser degree and contained malformed bones; the anal and urinary orifices were absent, and the genitals and parts of the intestinal and urinary tracts were malformed. As limb buds form during fourth to the eighth week of intrauterine life, this condition was very common in women who took thalidomide during this period. Exposure during the later periods of pregnancy did not cause any abnormalities. Interestingly in the US, the rights had been given by Chemie Grünenthal to a local company W.S.Merrell Co., but they could not market it, because of the earlier Act passed by the Govt, about which I have already told you. The Food and Drug Administration (FDA) was simply not convinced of its safety. In Canada, a license to market it was granted by the Canadian Food and Drug Directorate. In our country too the drug failed to gain entry because of usual bureaucratic hurdles. Thus US and India were the two big countries which were saved of this disaster!” “Chemie Grünenthal must have been prosecuted for their wanton act?” “Tarun, it has traditionally been very difficult to prosecute big giants. Nine senior members of Chemie Grünenthal were tried in a criminal court in Aachen, but they disputed the very fact that the limb deformities had been caused by thalidomide, although there was very strong statistical evidence in favour of the fact that thalidomide did cause this disaster." “What was this evidence doctor?” “Phocomelia is such a rare disease that no case was reported in Germany in ten years between 1949 and 1959. But in just a single year in 1961, there had been 477 cases! Moreover after this drug was taken off in 1961, the cases stopped once again. Yet the defendants challenged the causation. Finally trials had to be conducted on rabbits to convince the court that it was indeed the thalidomide which had caused these deformities. Yet the case dragged on for about two years and was finally abandoned. The representatives of the deformed children however settled the issue with Chemie Grünenthal for just about 114 million Deutschmarks! In Britain, a good thing that happened was that The Medicines Act was passed in 1968, which forbade any company to market drugs like this. As I told you earlier, it is an unfortunate truism that it often takes a great disaster for governments to "wake up" from their slumber. This was yet another case of a disaster paving the way for the passing of a law. In our country too, this disaster had its echoes. The Drugs and Cosmetics Act of 1940, which had become archaic, was amended in 1964, mainly because of this disaster. Many other indigenous drugs were brought into its purview, which includes Ayurvedic and Unani drugs. As an aside I may tell you that Thalidomide comes in two enantiomers. While the right-handed molecules had the desirable property of sedation, it were the left-handed molecules which caused the deformities. So if somehow, only the right handed molecules had been used for sedation, there would have been no adverse effects at all!” “Now you are introducing new things. Please tell me what are enantiomers?” “Tarun, certain chemical compounds are mirror images of each other. So although their chemical and even structural formula is same, they are not exactly the same molecules. They are in fact mirror-images of each other. These compounds are called enantiomers. Your right and left palms are good examples of enantiomers. Although they are similar looking, you can't superimpose your one palm over the other. If you look at your right palm in the mirror, it will look like a left palm and vice-versa. If a chemical compound exists in its two enantiomeric forms, they would roughly be equal in number. When the scientists of Chemie Grünenthal manufactured thalidomide in their factories, roughly equal number of both enantiomers were produced. Only the right handed molecules - the so called D forms - were beneficial. The left handed molecules - the so called L forms - caused the defects.” “How very sad! Had they known about this, they would only have manufactured the D forms.” “It appears doubtful to me, because technology to do so did not exist at this time. Although once formed, they could have perhaps separated the two. I may tell you that there are several other drugs, which show the same dilemma. One of the best known is Dihyroxyphenylalanine (DOPA) which is used for a Central Nervous System disorder Parkinsonism. In this disorder, the person trembles and has a staggering gait. This disorder can be treated by DOPA. This too comes in two enantiomers - a D form and an L form. I may tell you here that these forms can be differentiated by a very shrewd test. It you pass a beam of polarized light through them, the D form would shift it to the right and the L to the left. In fact the D form and L form get their names from this property. D stands for Dextrorotatory (or turning to the right) and L stands for Laevorotatory (turning to the left). In the case of DOPA, the L form of the molecules are effective. D forms are not effective, but fortunately they do not cause any deformity too. It still makes far better sense to give just L-Dopa or Levodopa (as some call it) than just plain DOPA, which would contain both forms of the drug, of which the D form would be totally useless. You may be interested to know that in 2001, three scientists received Nobel Prize in chemistry for developing the first ever chiral catalysts [N.B. by the author: The original article appeared in AUGUST 2000 - at a time when these Nobel Prizes had not been awarded, so one would not find this information in the original article. It has been added subsequently]. These are the Japanese Noyori Ryoji (1938 - ) and the American scientists K. Barry Sharpless (1941 - ) and William S. Knowles (1917 - ). It was as late as in 1968, that Knowles produced the first ever chiral catalyst. This was seven years after thalidomide had been banned from everywhere. So as I said earlier, even if scientists would have known about the L forms of thalidomide causing problems, they probably would not have been able to synthesize it preferentially." “Doctor you have talked about chiral catalysts. What exactly are these?” “Tarun, chiral means "handedness". Remember that the art of palmistry - studying hands - is also known as Chiromancy, or Chirosophy! Chiral catalysts can favour a chemical reaction in the direction of a particular enantiomer - literally a left handed or a right handed molecule. Thus if one were to manufacture L-dopa without the help of these chiral catalysts, one would get both D and L forms in roughly equal quantities. But if these chiral catalysts were used, one could manufacture only the useful L-form. These catalysts are thus very helpful in the drug industry.” “Doctor you are amazing. Coming back to our initial topic. How do doctors diagnose ethylene glycol poisoning?” “One of the best points in favour of ethylene glycol poisoning is that the person appears inebriated without accompanying smell of alcohol. Calcium oxalate crystals in the urine are present. I have examined the urine of Ramlal and have found calcium oxalate crystals. The White Blood Count (WBC Count) may rise to 10,000-40,000 per cubic mm, while normally the maximum limit is just about 11,000 per cubic mm. On autopsy, there is extensive destruction of the renal substance. On microscopic examination of kidneys, birefringent crystals of oxalate are seen. I have found all these changes in Ramlal’s body after autopsy. I can now guess what happened yesterday at Ramlal’s house. Shyam was stung at Ramlal’s behavior and wanted to get even with him. He arrived at his house with a bottle of liquor and a can of coolant. This was probably hidden somewhere in his clothes. Shyam was preparing the pegs. After two or three pegs, when Ramlal was sufficiently inebriated, Shyam furtively mixed some quantity of coolant in his alcohol. Ethylene glycol is tasteless, so Ramlal did not know that something had been mixed in his drink. Moreover he was already drunk and was not paying very much attention to him. After giving him two or three more pegs like this, he left for his house. He was quite pleased with himself, as he had thought he had planned a perfect murder. Lo! Here comes the policeman from Shyam’s house and he has recovered the left over bottle of coolant from his house. Shyam does not have a car and would have tough time explaining to the court what this bottle was doing in this house.” “That is very clever of you doctor. Without your clever deduction it would have been impossible to say how Ramlal died and Shyam may have gone scot-free. What are you going to tell me next time?” “Tarun, next time, I would tell you about a very interesting poison - Botulinum Toxin.”