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  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE OCTOBER 1999 ISSUE THE POISON SLEUTHS DEATH BY VITAMIN A -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 24 year old man is Ramlal, and he died in the hospital today morning. He was admitted to the hospital about two days back, with complaints of throbbing headache, pain in the stomach, diarrhoea, vomiting, irritability, dizziness, muscular weakness and cramps. Some peculiar symptoms, which confused most doctors at the hospital was that his skin was peeling off from many parts of the body, his hair were falling and that he had an irresistible desire to sleep. Doctors were trying to figure out what his illness was, but in the meantime he expired.” “Seems like a most strange illness to me doctor. But since you have said that his hair were falling, I can surmise that he might be suffering from Thallium poisoning.” “Tarun, I do remember having told you that hair start falling in thallium poisoning, but look at his other symptoms too. All the symptoms taken together are pointing towards only one direction - I can think of nothing but one poison, with which Ramlal must have been poisoned. It remains to be seen who gave him this poison.” “Doctor please tell me which is that poison. I am getting curious.” “Tarun, somebody has given Ramlal a dangerously high dose of Vitamin A, and probably that is why he has died.” “Vitamin A! Come on doctor. You are being preposterous. We all know that Vitamin A is an essential vitamin, which must be regularly taken to stay healthy. How can such a nutrient prove toxic?” “This is the paradox. Vitamin A acts as a double edged sword. Before saying anything, let me clarify a few basic concepts about Vitamin A. The term “Vitamin A” covers two chemicals - a true pre-formed vitamin known as retinol, and a pro-vitamin beta-carotene. A pro-vitamin is a substance which gets converted into the proper vitamin in the body. In human beings, some beta-carotene gets converted into Vitamin A in the intestinal mucosa, while the most gets converted in the liver. Vitamin A is usually measured in International Units or I.U. One I.U. of Vitamin A is equal to about 0.3 micrograms of retinol, which as you now know is the true Vitamin A. I must also tell you that one microgram of beta-carotene (which is the pro-vitamin) gets converted to about 0.167 micrograms of true vitamin A or retinol. Another way of saying this is that the “retinol equivalent” of one microgram of beta-carotene is 0.167.” “Oh, yes, I am understanding it. What is the daily requirement of Vitamin A, and what is its toxic dose?” “Normal daily requirement of Vitamin A for an adult is about 3000 I.U. per day. In pregnancy and lactation, it increases to about 4000 I.U. per day. Vitamin A capsules available in the market provide a little more than this amount. For instance Adexolin, a commonly available capsule of Vitamin A contains about 5000 I.U. of vitamin A. You must remember that Vitamin A and D are not soluble in water so if someone takes more quantities of these vitamins than required, there is no way they can be excreted. They generally are stored in the liver. On the other hand Vitamins B and C are water soluble vitamins. If someone takes enormous quantities of Vitamin B and C, they would be excreted in urine.” “Oh, I see. So this means Vitamin A can act as a poison too?” “Oh yes. Certainly. This is a fact which most people do not know. The medical condition which results from an intake of excessive amounts of Vitamin A is known as Hypervitaminosis A. About one million I.U. of vitamin A are very toxic to human beings, and about 3 million I.U. may prove fatal, as they have in the case of Ramlal. To put it another way, about a year’s requirement of Vitamin A if taken as a single dose may prove toxic, and about three years’ requirement taken as a single dose may kill a human being. Well, we do say often that ‘too much of a good thing can be bad’. Nowhere does this maxim prove truer than in the case of Vitamin A.” “Doctor, you are repeatedly saying that Ramlal died of Vitamin A poisoning, but how could he have got poisoned. You tell me that an average capsule of Vitamin A available in the market provides about 5000 I.U. of vitamin A, and also that about 3 million I.U. are fatal. This means that someone with an intent to kill his enemy has to administer as many as 600 capsules of Vitamin A to his enemy. How is that possible?” “Tarun, I did not tell you a very interesting fact. Most polar animals such as polar bears have dangerously high levels of Vitamin A in their liver. In fact there have been cases, where polar explorers have died of Vitamin A poisoning, because they ate the livers of animals residing in those regions.” “Really? That’s an interesting fact. How does such dangerous amounts of Vitamin A reach their liver?” “Vitamin A originates in marine algae, and then passes up the food chain to reach the large carnivorous animals. Toxic levels of Vitamin A may accumulate in the livers of a wide range of creatures such as Polar bears, seals, porpoises, dolphins, sharks, whales, Arctic foxes and huskies. Even a small meal of southern Australian seal liver, say 80 g, may produce illness in man. I may tell you that several foods are recommended as good sources of Vitamin A. Most of them contain well below the toxic levels of vitamin A, but one - Halibut liver oil - contains dangerously high amounts of Vitamin A, as you can see from the accompanying table. Source of Vitamin A Vitamin A content in International Units (I.U.) per gram of food Ox liver 550 Cod liver oil 600 Halibut liver oil 30,000 Table 1: Vitamin A content of some commonly recommended foods rich in Vitamin A In contrast look at the vitamin A contents of the livers of some common animals living in the polar regions in the following table. For comparison, I have also given the vitamin A content of the human liver. As you can see, most animals, especially the polar bear have very high amounts of Vitamin A in their livers. Common Name Zoological Name Vitamin A content of the liver in International Units (I.U.) per gm of specimen Weddel Seal Leptonychotes weddelli 444 Man Homo sapiens 575 Southern Elephant Seal Mirounga leonina 1,160 Antarctic huskies Canis familaris 10,570 Arctic bearded seal Erignathus barbatus 12,000-14,000 Polar bear Thalaractos maritimus 24,000-35,000 Table 2: Vitamin A content of the livers of some common animals living in polar regions - compared with that in humans “Oh, these two tables are real eye openers. Doctor, you were telling me that some polar explorers have actually died of Vitamin A poisoning. Could you tell me that story in detail please? I am getting curious.” “Oh sure. The story starts in January 1912, when a three man party of explorers from the Australasian Antarctic Expedition started their expedition to explore Antarctica. The team was led by Douglas Mawson, and the other two members were Lt. B.E.S. Ninnis and Xavier Mertz, a Swiss scientist. Disaster struck on December 14, 1912, when Ninnis fell into a very deep pit and died. With him also went precious food supplies. With most of their food gone, Mawson and Mertz decided to return to their base at Commonwealth Bay, which is at the shores of Antarctica. From here they could take the ship back to their country. But Commonwealth Bay was about 315 miles from where they were stationed. Covering that distance in the inhospitable surroundings of Antarctica would have taken them weeks, and they had only 10 days’ food left with them. They had six huskies with them. Huskies, as you know are Eskimo dogs, used as ponies in Antarctic region. They knew that sooner or later they would have to eat those dogs to remain alive.” “Oh, it was really terrible. But the story is getting interesting. What happened then?” “They did kill the huskies and ate their flesh, but the flesh was stringy and they could not eat it. In contrast to flesh, they found the liver softer and easier to eat so they took generous quantities of liver. Mertz was a near vegetarian; he could not eat the stringy flesh, so he took more liver than Mawson. Little did he realize that he was taking fatal amounts of Vitamin A in this form. On New Year’s Eve, Mertz began to feel ill. Next day he complained of stomach pains. Few days later both men began displaying typical symptoms of Vitamin A poisoning, although Mawson was affected less. Their skin was falling off their bodies in strips and their hair was dropping out in handfuls. A week later, Mertz fell into a delirious sleep - a sleep from which he never woke. As far as we know, he was the first case of death due to overdose of Vitamin A. Mawson survived, and ultimately did return to Commonwealth Bay." Note by the Editor There are counterclaims insisting that the death of Xavier Mertz and the suffering of Douglas Mawson was not due to overdose of Vitamin A. For more on this, please click here “This is certainly a most interesting incident doctor.” “So I was telling you about the vitamin A content of polar animals. With the amounts I told you, you can see that really very little quantities of livers of these animals are required to kill a human being. For instance, it would require about 30 to 90 g of the liver of a polar bear, 80 to 240 g of the liver of bearded seal and 100 to 300 g of the liver of Antarctic Husky to kill a human being. You may think that the livers of these animals are not commonly available. That is true, but Halibut liver oil also contains almost the same amounts of Vitamin A as that of the liver of Polar Bear. About 30 to 90 g of Halibut liver oil could thus prove fatal to a human being, and this is commonly available with the chemists. It is not very difficult for someone to coax another to drink this amount, especially when Halibut Liver Oil is commonly considered to be a health food.” “So you think someone coaxed Ramlal into drinking this amount of Halibut liver oil?” “This is exactly what has happened. I have made inquiries, and found that Suresh a person working in the same factory as Ramlal held a grudge against him. Suresh was an educated person - he held a first division in chemistry in college- and yet Ramlal, probably due to his hard work, rose to a higher position than him in the factory. He held another grudge against him, that Rekha, a co-worker whom he loved and wanted to marry was attracted more towards Ramlal.” “Oh, I see. But how did he coax Ramlal to drink a fatal amount of Halibut liver oil?” “Ramlal thought that he was not strong enough, and before marriage he could do with some more nutritious foods. Suresh knew about health foods well, and one day he took his advice. Suresh saw his chance and advised him to contact him the next day. Next day he handed him a bottle of Halibut liver oil and asked him to drink copious amounts from there. He told him that it acted as a good aphrodisiac and would serve him well before marriage. Poor Ramlal believed him, and drank almost the whole bottle, which contained 100 g of oil in one go. This is how he died.” “This is all very well doctor, but how are you going to prove in a court of law that Ramlal died of Vitamin A poisoning?” “Tarun, I have examined the vitamin A content of Ramlal’s liver and it is more than 40,000 I.U. per g. As you know, a human being should have at the most about 600 I.U. of Vitamin A per g of liver. This proves beyond doubt that Ramlal had Vitamin A poisoning. Added to this is the hospital record which gives us the typical symptoms of vitamin A poisoning. I don’t think the court would have any hesitation awarding sentence to Suresh. Come, let us tell the police to arrest Suresh.” "That was very clever of you doctor. Without your clever deduction - especially your noticing the peculiar symptoms of Ramlal at the time of his death- everybody would have thought he died of some mysterious natural disease. 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- Cicutoxin."

  • Science Fiction | Anil Aggrawal's Forensic Ecosystem

    Science Fiction WHY DINOSAURS BECAME EXTINCT? -Dr. Anil Aggrawal I know you won't believe me, but I first wrote this scientific report about 16 years back and sent it to the editor of a prominent science magazine for publication. I thought I had invented a new discipline of science, bioastronomy, an inter-relationship between biology and astronomy. Bioastronomy could be used to make predictions related to one science based on the data gathered from the other. For instance, I devised ways to predict and extrapolate the time of origin of life on earth (and on any other planet for that matter), by counting the number of stars in a sphere of 100 light years around that planet, and putting that number in a complicated formula. Similarly, by looking at the cellular structure of the animals on any planet, I could make useful predictions about the space around that planet. I know you would think I am beating about the bush, and I wouldn't blame you. If I didn't invent the science myself, and you told me the same thing, I would go to the extent of thinking you were crazy. That's what the editor of the Science magazine thought 16 years back. Actually what I had sent him was a report of an actual science experiment on bioastronomy that I had conducted. But he thought it was a Science Fiction story and refused to publish it, stating that the events mentioned in my report were too unlikely and unnatural even to be included in an SF story. That made me aghast with disbelief, but I couldn't help it. After all, we all writers are at the mercy of editors. If they don't like something, the writer's piece can't see the light of the day, whatever its merit. Then why am I writing it again now, you might ask. Well, much light has flown through the galaxies meanwhile and certainly in the present circumstances my report would appear more trustworthy to you. The world has been gripped with the dinosaur mania during this period, and that is the single most important factor which makes my report look more realistic today. My report as you would shortly see deals with resurrecting the dinosaurs and certainly the events in the story would appear less unnatural to you now. They certainly appeared realistic to my present editor and that's why you are able to read this story. Well, to begin with I must tell you that I am interested in finding the reasons for the extinction of dinosaurs. Years ago, I developed an interesting theory about the extinction of dinosaurs, but needed a live dinosaur to prove it. We all know that if we can somehow get a single intact nucleus of the ancient dinosaurs, we could clone a whole dinosaur from the DNA contained in that nucleus. Michael Crichton in his now famous SF novel, surmises that such an intact dinosaur nucleus could be found in the gastrointestinal tract of mosquitoes who fed on the blood of dinosaurs and then got entrapped in sticky amber flowing down the trees. But in actual life such a finding is extremely unlikely. I found intact dinosaur cells in another way - in Himalayan peat bogs. Peat bogs were marshy, muddy places where some dinosaurs might have strayed and got accidentally buried there. The peat bogs were very much like quicksand. They have a remarkable quality to preserve tissue specimens. Later on, with the coming of ice age the whole peat bogs, along with buried dinosaurs within them got covered with snow, which further helped preservation. I cloned the dinosaur nucleus in the fertilized ova of the American alligator (Alligator mississipiensis). Of course I first destroyed its own nucleus and then transplanted the dinosaur nucleus in the fertilized ova. The American alligator is the closest living relative of the dinosaurs, and it was the best medium to transplant the dinosaur nucleus in. Sure enough when I cloned the dinosaur (Tyrannosaurus rex), and studied its cellular enzymes in great detail, I found a gross abnormality in the respiratory enzyme Cytochrome oxidase. This is an essential respiratory enzyme which is vital to the functioning of the cells. There are about 100 atoms in the molecule. Most of the atoms are of carbon, hydrogen and oxygen, but there are two peculiar atoms- iron and copper. Empirically, the altered molecule had the same number of atoms as the natural molecule, but structurally the relative positions of all the atoms including those of iron and copper atoms had been changed drastically. This caused the enzyme to become at least 6 times less effective. Sure enough, the dinosaurs died as a result of this fatal mutation. But what caused the mutation? Well, I had just invented the science of bioastronomy. This helped me come up with a remarkable explanation. The earth had been visited about 65 million years ago by some super-intelligent extraterrestrials. They were masters of genetic engineering. They didn't come to earth on purpose. There was hardly any intelligent life on earth then. They stepped on it only in passing. However during the rest period the spent here, they played a little game, in which they sought to represent the position of their star in relation to the earth's star (The Sun). They did this by genetically altering the 3-dimensional structure of the most important respiratory enzyme of the most conspicuous creatures on earth-the dinosaurs. They did it in such a way, that various atoms in the cytochrome oxidase molecule came to represent the relative positions of all the stars in the vicinity of the Sun. In other words, if all the atoms of the changed cytochrome molecule were enlarged on a galactic scale, each atom of the changed molecule would faithfully represent a star in the vicinity of the sun. There are only two particularly peculiar atoms - iron and copper- in the cytochrome oxidase molecule. Now if the iron atom was taken as the position of the sun, the other unusual atom- copper- would represent their star. Such drastic genetic engineering served their purpose alright but it decreased the efficiency of the enzyme vastly, which over the years caused the dinosaurs to get asphyxiated. I brought out a 3-dimensional star chart and extrapolated the position of copper atom. It represented the star Tau ceti. This clearly meant that the race had come from Tau ceti. You might think I am crazy, but how on earth (excuse the pun) could you otherwise explain the uncanny similarity of the 3-dimensional structure of a macroscopic and a microscopic thing. This was unmistakably the handiwork of a super-intelligent race. Those beings evidently changed the genetic makeup of all dinosaurs in the same way. Doing this is not difficult if you can "programme" gamma rays to do just that and then irradiate the planet with them. Dinosaurs were so important in Jurassic ecology that with their extinction, several other species dependent on them for their survival perished too. This explains the disappearance of many other species simultaneously. I am happy to tell you that some exobiologists in the USA believe my theory and only yesterday I learnt with satisfaction that a very strong electromagnetic wave carrying a friendly message has been sent to Tau ceti.

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE OCTOBER 1997 ISSUE THE POISON SLEUTHS POISONING BY THALLIUM -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today. You seem to be doing the post-mortem on a rather old man. And he seems to have a most peculiar rash over his face. His hair have also come off his head. Please tell me what happened to him." "Good morning Tarun. This man is a 56-year old man Ramlal, who worked in a store in New Delhi. He suddenly fell ill on 27 August. He developed acute griping pain in the stomach for about 1 hour, and he also had vomiting and diarrhoea. He was well until four days later when he developed severe burning pain in the toes of both feet and tingling sensation in the tips of all the fingers. These symptoms increased over the next five days with some reduction in the power of hand grip. His company admitted him to a leading private nursing home in Delhi. Some leading medical experts examined him, but couldn't diagnose his illness. Ramlal's condition remained unchanged until 9 September when he suddenly developed more symptoms. He had difficulty opening the eyes in strong light, a symptom known in medical parlance as photophobia. There was some disturbance in his vision also. His condition worsened further over the next few days and by 11 September there was drooping of eyelids (known in medical parlance as ptosis) and weakness of face muscles. Swallowing became increasingly difficult. He had difficulty in breathing too, which became so severe that on 15 September, a surgical opening had to made in his neck to help him breathe. However his condition continued to worsen and he died on 19 September, 23 days after his first symptoms started." "Oh, he had a most terrible illness. What do you think he died of?" "Everybody thought he had died from some undiagnosed natural illness. But when the dead body was brought to me, I noticed this curious rash over his face. I also noticed- as you also did- that his hair were also falling off his scalp. This made me suspect that Ramlal was being poisoned- perhaps with thallium." "What! Thallium!! I never thought that it could be used as a homicidal poison" "Tarun, on the contrary, it is a very good homicidal poison. I will tell you in a short while, why this is so. But before proceeding any further, let me tell you a little bit about thallium, so that you can know something about this interesting poison. "Sure doctor, go ahead. I like listening to good scientific stories." " Tarun, Thallium was discovered in 1861 by the British physicist Sir William Crookes (1832-1919). He was working with selenium ores, and in 1861 he came upon a sample of such ore that when heated showed in its spectrum a bright green line characteristic of no known element. It indicated a new hitherto undiscovered element. When he ultimately found it, he named it thallium, from the Greek word thallos meaning "green twig" after the color of its line. The botanical word thallophyta comes from the same root." "That's very interesting. And when did murderers start using it as a homicidal poison?" "It is significant that it was not used as a poison in the first instance. Its earliest use - albeit unaccountably- was to check the "night sweats" in tuberculosis, and when it was noticed that loss of hair occurred with its use, a scientist named Sabouraud instituted its therapeutic use for tinea capitis or ringworm in 1898. The salt used was thallium acetate. It was supplied as a cream (Koremlou cream), containing 7.18% thallium acetate. This practice was finally abandoned half a century later, when it was realized that it was a potential poison. Quite interestingly Thallium has also been used a rodenticide (e.g. to kill rats and moles) and as cockroach poison, particularly in Germany. For this purpose it was available either as tablets or pellets of thallium sulphate or as pastes. Some time in the 1920s the firm of Bayer-Leverkusen in Germany marketed 30 g tubes of a paste known as Zelio paste, each of which contained 2.3%, or about 600-700 mg of thallium sulphate. It had a wide sale on the continent and in the United States, apparently without any restriction of sale or purchase. A French preparation, Virus Rouge contained thallium nitrate. In 1965, the US banned the use of thallium as a commercial rodenticide. However thallium salts as cockroach poison may still be available today in many countries. It is still used in homeopathic remedies!" "Doctor, why did anyone use thallium as a rodenticide at all, when it was so dangerous to human beings?" "Tarun, the earlier rodenticides contained phosphorus, but the value of thallium as a rodenticide lay in the fact that the usual phosphorus containing rat-killer was harmful to the pigs that ate the poisoned rats, whereas the pigs seemed unaffected by rats killed with thallium salts! The use of thallium rodenticides in Europe spread when the Germans conquered and occupied most of Europe during the 2nd World War." "Is thallium useful for other purposes too?" "Yes, Thallium is widely used in industry. Its addition confers a high refractive index on optical glass. For this reason it is used in imitation jewellery which sparkles rather like diamonds. It is also used as an alloy, a catalyst, and for making low-temperature thermometers. But unfortunately like arsenic (see Science Reporter February 1997) , thallium also accumulates slowly in tissues, and over a short period of time, has cumulative toxicity. This method of administration has been used in many criminal cases. I must tell you that the fatal dose of thallium is about 1 g." "Excuse me doctor, what do we mean by the fatal dose?" "When dealing with poisons, we often speak of their fatal dose and fatal period. You will perhaps remember that we first talked about the concept of fatal dose, while talking about arsenic and Spanish Fly (see Science Reporter February 1997 & March 1997). Fatal dose of a poison is the average dose which is enough to kill an adult human being, while fatal period is the average period taken by the poison to kill. A tube of Zelio paste would contain about 0.6 to 0.7 g of thallium which is considered somewhat less than the average dose to kill a human being. Death usually occurs in 11 to 16 days, which is called the fatal period of thallium. If the patient survives 4 to 5 weeks, he would probably live, but the damage to organ systems may be permanent." "Tell me doctor, can thallium be taken for suicidal purposes too?" "Tarun, cases of both accidental and suicidal poisoning occur with thallium, but probably most sinister is its use as a homicidal poison, as it possesses many of the qualities of an ideal homicidal poison. Its salts are colorless, odorless and tasteless, besides being freely soluble in water. Furthermore, in the body the salts are converted into a relatively insoluble salt thallium chloride. This is favorable to the criminal, as the insoluble salts take longer to act; the effects are rarely noticeable before 12 hours and may be delayed as long as 48 hours. This gives the criminal enough time to cover its tracks. Because of the wide gap between ingestion and the onset of symptoms, it is also that much more difficult to associate the symptoms with what the criminal gave to the victim. The initial symptoms of an ideal homicidal poison must mimic some natural disease, and that's exactly what happens with thallium salts too; its initial symptoms are those of a digestive upset of a non-specific character. More specific neurological symptoms occur only after about 2 to 5 days, but still they are very difficult to differentiate from some neurological diseases such as Guillain-Barré syndrome. That is probably why the doctors were at a loss to diagnose thallium poisoning in the case of Ramlal. One of the most characteristic signs of thallium poisoning- gross loss of hair- does not appear until almost a fortnight has passed." "Excuse me doctor, you introduced quite a frightening term Guillain-Barré syndrome. I know I may be deviating from the main topic, but please let me know something about it." "Tarun, the actual name of this condition is Landry-Guillain-Barré Syndrome or LGBS. It is the name given to the conditions previously known by two different names- Landry's ascending paralysis and Guillain-Barré Syndrome. Now the two conditions are known to be identical. It is an acute disease of the nerves, in which they lose their outer protective covering or myelin. This myelin coat is also important for the smooth functioning of the nerves. The result of this loss of myelin coat is that the nerves can not conduct messages properly. This disease occurs at a rate of one case per million population per month. At this rate about 950 new cases of LGBS must be occurring in India every month. The weight of evidence favors that the cause of the disease may be immune related. However in over two-thirds of the cases, a viral infection is associated. After the infection, demyelination- or loss of myelin coat- in spinal and peripheral nerves occur. The symptoms of thallium poisoning may mimic this disease very much. The good news about LGBS is that its prognosis is good, with about 85% of the patients making a complete recovery. The mortality rate is just 3-4%. You would probably want to know, how the name of the disease came about. Well, it comes from the names of three doctors who described this disease at different intervals. The earliest to describe it was the Paris physician Jean Baptiste Landry (b. 1826). Subsequently Paris neurologist Georges Guillain (b. 1876) and Strasbourg neurologist Jean Alexander Barré (b. 1880) also described it correctly." "Excellent. Coming back to thallium. You said thallium fulfills many of the properties of an ideal homicidal poison. It means killers have got an ideal weapon, isn't it?" "Not exactly. Fortunately nature has put some negative qualities in it too. Had it not been for these counterbalancing features, thallium would indeed have been a poisoner's delight." "Really? And what are these counterbalancing features?" "An ideal homicidal poison must not be readily detectable by analysis, but thallium salts can be readily detected. Furthermore, an ideal homicidal poison must disappear from the body after doing its job. Of course a substance can not magically disappear from the body, but what it effectively means is that the poison must at least be destroyed by putrefaction, so that with the onset of time, it becomes impossible to detect that poison. I must tell you that this does happen with most vegetable poisons. Thallium however remains in the body even after putrefaction. It is also not a product of putrefaction." "Wait a minute doctor. You just said that thallium is not a product of putrefaction. You imply that if a poison is a product of putrefaction, it would be an ideal homicidal poison. Please explain this point to me in some detail." "Tarun, first of all you must know what exactly is meant by putrefaction. It is the destruction of the body with the onset of time. You must have noticed that dead animals start to rot after some time. The same happens with human bodies, if they are not disposed of properly. This rotting is known as putrefaction in medical parlance. Now imagine a killer has killed his victim with some poison, and has hidden the body somewhere, say in some bushes or a nallah. With the onset of time, putrefaction would start and the body would start to smell. This would soon lead to its discovery. Now if the poison is such that it is destroyed by putrefaction, the doctor doing the autopsy at this time would not be able to find this poison, and thus the killer would remain untraced. Wouldn't it make an ideal homicidal poison?" "Yes, I do appreciate that. But how can a poison be an ideal homicidal poison, if it is a product of putrefaction? That is what I really want to know." "Tarun, putrefaction is a chemical process, in which many chemicals are destroyed and many new chemicals appear. For instance, the chemicals skatol and indole are produced during putrefaction which indeed are responsible for the offensive smell of the body. If a poison is a known product of putrefaction, it could reasonably be argued by the defence in a court of law, that the detected poison (in a putrefied body) was not administered during life but was produced as a result of putrefaction. Cyanide, alcohol and ptomaines are well-known poisons which are products of putrefaction. Arsenic and thallium, which otherwise fulfil several of the criteria of an ideal homicidal poison do not fulfil this criteria. Similarly another criteria of an ideal homicidal poison is that it should normally be present in the soil." "Well, what is the explanation for that?" "In some communities, instead of cremation, the dead bodies are buried. Poisoners - and in fact all murderers- don't feel easy with this method of disposal of the body, because the potential evidence of murder -the body- remains beneath the soil. Any time after the burial of the body, if suspicion gathers momentum against the murderer, the body can be exhumed, i.e. unearthed and sent for a post-mortem examination. Now if a poison is normally present in the soil, it can be -and has successfully been- argued by the defence that the detected amount of poison had leached in the body from the surrounding soil. Arsenic - a deadly poison- is normally present in the soil in fairly good concentration, and this argument has successfully been used by many murders. But thallium is not present in the soil in any great quantity, and thus the same argument would not hold, if the poisoner had used thallium to dispose of his victim." "Oh, I see. Doctor, can you tell me what symptoms does the victim experience when thallium is given to him?" "Yes sure. Thallium salts irritate the stomach and intestines. It is a gastro-intestinal irritant so to say and that's why symptoms like abdominal colic, nausea, vomiting, diarrhoea occur first. Vomiting and diarrhoea may contain blood. There may be sores in the mouth, a symptom known in the medical parlance as stomatitis. The interesting difference from those of other irritant poisons is that the symptoms start very late- after about 24 to 48 hours of ingestion. In fact it is one of the idiosyncrasies of this poison which makes it a good homicidal poison. Thallium appears to act on nerves too. The symptoms relating to nerves ensue one to five or more days after ingestion. An intense pain develops in the body which is worse at night and is readily provoked by mild stimuli. For instance, even the weight of the bedclothing is enough to induce bouts of pain. The soles of the feet are first involved. The pain gradually travels upwards; to the legs and to the trunk. Sometimes there is intense pain in the big toe, and this can simulate gout. In some cases this may be the first sign. Joint pains which move from joint to joint also occur. There is numbness, especially of the fingers and toes, with detectable loss of sensation to pin-prick and to touch. There is a feeling of tiredness in the legs. This is followed by weakness and finally paralysis. The arms are always less affected. An interesting symptom is the appearance of a "butterfly" rash on the face. In fact this is the first thing I noticed on Ramlal's face, and that had alerted me at once. Another interesting symptom is alopecia or loss of hair. In fact it is highly characteristic of thallium poisoning. Hair loss occurs about a fortnight after the ingestion. The hair is lost in large tufts and within three weeks, the whole of head is bare. The root of the hair -the part of hair that remains buried underneath the skin- shows dense black coloration. This may be seen on the actual hair too, if there has been repeated intake. In fact, if there has been a repeated but interrupted intake, several dark bands coinciding with the period of intake may be seen. Interestingly the same thing happens in arsenic poisoning. It is widely thought that the great Napoleon was killed by the British in this manner. His hair too showed arsenic in bands. The bands are seen only on growing hairs. Thallium finally arrests hair growth and the hair falls. Even you noticed both the rash and the loss of hair, as soon as you entered the post-mortem room. During the autopsy I pulled some of his remaining hair and saw them under the microscope. I was struck with the finding that the hair root was completely black, while normally it is not so. The excessive blackness is considered to be due to an excess of melanin laid down through catalytic action by thallium." "Oh, I see. Coming to think of hair, I find that Ramlal's eyebrows look a little bit curious. Am I right?" "Yes, you sure are right Tarun. Just like hair on the scalp, eyebrows are also involved in thallium poisoning, but for some curious reason, their inner third is spared- only the outer two-third falls off. It is such a characteristic sign of thallium poisoning that it has even been accorded a name; the sign is called signe de sourcil. This is a French term, which literally means "The eyebrow sign"! It has been suggested that the inner third is spared because it is phylogenetically much older than the rest of the eyebrow hair. The fingernails may bear horizontal white bands or white cross lines. This change appears quite late- several weeks after the exposure. That's why you can't see this change in Ramlal's body." "Oh, this is most interesting indeed. Especially the information on eyebrows." "Tarun, there are more interesting nuggets I can give you. You would perhaps be quite interested to know that the noted English crime writer Agatha Christie has given a graphic description of the effects of thallium poisoning in her novel The Pale Horse (Christie, 1952), and this has led a nurse to correctly diagnose a case of thallium poisoning, which had earlier been diagnosed as a case of encephalitis by "experts"." "Really? Please tell me the details of this case" "Tarun, this case occurred in the late 70s. A 19-month-old girl in Qatar was having undiagnosed and unexplained ataxia, which in plain and simple terms means that she was unable to walk. Her physician in Qatar telephonically contacted experts in Hammersmith Hospital, London for help. She had a most extraordinary illness. It apparently began some 10 days earlier with a major convulsion lasting about 5 minutes and associated with a high fever. Over the next 3 days she became increasingly clumsy and lethargic and developed slurring of her speech. By the seventh day of her illness she was unable to sit, stand or walk, and had difficulty with swallowing. The following day she had a further generalized convulsion lasting about 5 minutes. At this stage she was transferred to Hammersmith Hospital. Detailed investigations led experts to believe she was suffering from encephalitis -an infection of the brain- but a staff nurse, who was reading Christie's novel The Pale Horse, realized that her symptoms were remarkably similar to those of thallium poisoning mentioned in the novel! The girl had also started losing hair which normally occurs in about 10-15 days of ingestion- a fact which was also mentioned in the book. She expressed her doubt to the doctors and on subsequent examination, she was indeed found to be suffering from thallium poisoning. On detailed discussion with the child's parents it seemed that the most likely source of thallium was domestic poison used to eliminate cockroaches and rodents in the drains and septic tank of their home. This is a common practice in Middle East!" "Oh, how very interesting. Has Thallium been used for murder in modern times? "Oh yes, it has. One of the most famous cases of murder with Thallium in modern times is that committed by George Trepal - a 42-year-old computer programmer - in 1988. He was a man with a very high I.Q. In fact he was a member of the high I.Q. club Mensa and this case later became famous as the Mensa Murder case. Trepal lived in the small central Florida town of Alturas. He was quite fed up with his neighbor Peggy Carr, 41, and her family, because they always listened to loud music which disturbed him. Carrs' dogs also used to trouble Trepal's cats, which he did not like. In June 1988, he sent the Carr family a chilling typewritten note in the mail. It said, 'You and all your so-called family have two weeks to move out of Florida forever or else you will die. This is no joke.' Carr's family did not pay much attention to this note. Four months later - in October 1988 - Peggy Carr was hospitalized with mysterious symptoms her doctors couldn't explain. At the same time, her son and stepson developed similar symptoms. While they recovered, Peggy did not, and she died with her doctors still mystified as to what killed her. One of her sons was permanently disabled. Officials were completely baffled. Trepal had actually surreptitiously spiked eight-pack of Coca-Cola bottles with thallium nitrate, and secreted them into Carrs' kitchen. Peggy Carr and her family members unsuspectingly consumed the drink. Peggy lapsed into a three-month coma and died thereafter. Four other members of her family were poisoned, though not fatally, but one son, as we have already seen was permanently disabled due to effects of Thallium on his Central Nervous System. Interestingly, Trepal was so confident of his "perfect murder" that when the investigating officials came to him for enquiries, instead of keeping quiet, or expressing his ignorance in this matter, he speculated that someone might poison people to get them to move out of the neighborhood! This immediately allerted the officials, who at once started thinking in terms of poisoning. When Trepal's home was searched, a small vial of thallium nitrate - generally unavailable to the public - was found there. Other incriminating things found in his house were a detailed homemade notebook titled, "General Poisoning Guides," with several entries on thallium, and an extensive store of dangerous chemicals. He was found guilty by the court, and sentenced to die." "Amazing! It appears we have another Trepal on our hands now. It is now sure that poor Ramlal died due to Thallium poisoning?" "Yes, and I confirmed this by several other means too. First of all I analyzed for thallium in his urine, and it was present in high quantities. Furthermore there was a widespread destruction of nerve cells in the brain. Liver and kidneys were damaged as is usually seen in thallium poisoning." "So from an apparent natural death, you have suddenly discovered murder in it. Who could possibly have poisoned him?" "Tarun, before you came, I had already given my findings to police and the police has done a detailed investigation subsequent to my report. You are right that someone was indeed trying to poison him. on detailed investigations, it was found that a colleague Karim was mixing Thallous acetate in his tea daily for some days. He had an old axe to grind with Ramlal. Faced with the scientific evidence, the police questioned Karim and he admitted his guilt. Thus a poisoner who could have gone scot free was caught with the help of forensic science." "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 deadly poison - Capsaicin. "

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    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!"

  • SCIENCE IN CRIME DETECTION-36 | Anil Aggrawal's Forensic Ecosystem

    SCIENCE IN CRIME DETECTION-36 DEATH FOLLOWING MARIJUANA INTAKE On 12 January 1991, a very interesting case was brought to me. A 33 year old man Kanti was returning home after a party in his car when his Maruti car collided with another car. Besides Kanti there was another person in the car, a 37 year old male Ravindra. Kanti and Ravindra were friends and had gone to a friend's party. Both Kanti and Ravindra died immediately after the collision. The police arrested the driver of the other car, a person called Bhushan, for causing the death of two persons by rash and negligent driving. Bhushan swore that he was driving the car very carefully. In fact it was the other car which was swerving from left to right. It appeared to him that the driver of the other car had been drunk. But the police did not believe him as there was no smell of alcohol from either Kanti or Ravindra's mouth. If, as Bhushan was asserting, the driver of the other car Kanti was drunk, why was there no smell of alcohol from his mouth. The net effect of their conclusion was that Bhushan found himself behind the bars. It was at this stage that the case was brought to me. When I searched the bodies of the two carefully, I found a strange looking contraption in the pockets of Kanti. Some other objects were also found in Kanti's and Ravindra's pockets. All the contents that were found in their pockets are revealed in figure 1 (please reproduce fig XX-27 on page 553 here). I immediately realized what must have happened. I called the investigating officer, and told him that Bhushan had been speaking the truth. The car must really be swerving from left to right as he had suggested. The police officer looked back at me in surprise and said,"But sir, you have hardly had a look at the body, let alone do an autopsy. How could you say that Bhushan is speaking the truth?" "Well, it is my experience with marijuana deaths, my boy!", I said in smug confidence. The readers may be surprised as to what strange objects I found in their pockets which let me make such quick and confident deductions. Well, before going any further, let me tell you a little bit about marijuana . You must all be aware of the terms bhang, charas, hashish and ganja ? These substances are not different. They all come from various different parts of the same plant, called the Indian hemp (Please reproduce fig XX-26 on page 552 here). Botanically its name is Cannabis sativa . More than 400 chemicals have been isolated from the cannabis plant. But the main chemical which is responsible for its pleasurable effects is called delta‑9‑tetrahydrocannabinol or THC . THC is found mainly in the leaves and the flowering tops of the plant. The cannabis plant gives rise to several products with many of which we are quite familiar. Bhang consists of dried leaves and shoots. It is also known by the name of siddhi, patti or sabji . Among the objects recovered from Kanti and Ravindra's pockets was bhang (see upper left of fig 1) . It may be used as such or as an infusion in the form of a beverage, which produces intoxication. The infusion is prepared by rubbing some dried cannabis leaves on a stone slab along with sugar and black pepper. It is than mixed with water and strained through a muslin cloth. This infusion is commonly known as thandai and is usually drunk in our country during the Holi festival. Majun is a sort of confection prepared from bhang by treating it with sugar, flour, milk and butter. In India one can find barfis fortified with bhang . These are rather green coloured instead of the normal white. Sweetmeats like these are called majun . Yet another product which comes from the cannabis plant is ganja . This has a rusty green colour and a characteristic odour. It comes from the flowering tops of female plants, which contains a very strong concentration of THC. While bhang contains only 1 to 2 per cent of THC, ganja may contain upto 5 per cent of THC. The same ganja is known as 'marijuana' or 'marihuana' in the West (both terms are acceptable and correct). While bhang is eaten or drunk, ganja is smoked. About 1 to 2 gm of ganja is rubbed with a little water in the palm till it becomes sticky. It is then mixed with a little tobacco and is smoked in a pipe or chilam . In India sadhus, fakirs and poor laborers often smoke ganja as a form of recreation. In modern society, ganja is being smoked at parties too, especially those arranged and attended by the youth. As my investigations later revealed, both Kanti and Ravindra were coming back from such a party. They both had in fact been smoking marijuana. Westerners smoke ganja (or marijuana as they know it) in cigarettes known as 'reefers' or 'joints'. A thin, special quality paper is taken and about 500 mg marijuana kept in it. It is then rolled in the form of a cigarette. The ends are twisted to avoid any fall out. Sometimes two papers may be used to strengthen the 'reefer'. Marijuana can also be eaten just like bhang , or brewed like tea, but taking it by mouth reduces its effect. While ingestion may take up to an hour to feel the effect, smoking may have an instantaneous effect. Marijuana is sometimes baked in biscuits too (known as 'cookies' or `brownies') and eaten. Smoking marijuana is referred to as 'turning on'. The `reefers' are often wetted with the tongue in order to slow the burning. This does not make the reefer very pleasing aesthetically, but it serves a practical purpose. Quite frequently the 'reefer' is grey, soggy, repulsive looking and unhygienic. Some people prefer a pipe or a 'bong' and the best pipes for this purpose have smaller bowls than ordinary pipes. 'Reefers' or pipes are frequently smoked in groups, the pipe being passed among the people sitting in a dark room in which candles and incense are kept burning. Smokers may either be members of a 'closed', or an 'open' circle. The difference lies in the amount of information that is exchanged about the stuff. In the 'closed' circle, for instance, marijuana is consumed but information like where it came from, is not disseminated. On the other hand, the 'open' circle has no restrictions about discussing the origin, amount, distribution and so forth about the drug. 'Open' circles are thus much more relaxed and intimate. A puff on a 'reefer' is called a toke , and the object is to inhale as deeply and hold it in the lungs as long as possible. Smoking a 'reefer' as if it were an ordinary cigarette would produce little effect. The smoker must hold the smoke deep in his lungs for at least twenty to thirty seconds until it penetrates the lung tissues and enters the blood. A typical 'reefer' contains about 500 mg of marijuana. It we take the THC content of marijuana as about 1 per cent, then the THC content of an average 'reefer' comes to around 5 mg. Many high quality `reefers' may contain up to 1 gm of very high quality marijuana (containing upto 10 to 15 per cent THC). Thus a high quality 'reefer' might easily contain 100 to 150 mg of THC and if sprinkled with hash oil, the potency might be doubled. THC delivery by smoking is 50 per cent efficient. Thus even a low quality 'reefer' delivers about 2.5 mg THC to the body. This is equivalent to 7.5 mg THC taken orally. Many heavy users consume numerous high quality `reefers' each day, thus incorporating almost 150 to 200 mg THC into their bodies. When such a large quantity is taken for two to three weeks and then abruptly discontinued, withdrawal symptoms occur. While the butt of an ordinary cigarette is thrown away, the end of a 'reefer', called the roach because it resembles one, is the most potent part because much of the THC collects there during smoking. It is at least one‑third and possibly half as powerful as the whole 'joint'. Various ways of consuming the roach have been devised, ranging from eating it to the more refined method of smoking it by holding it with a hairpin or some other special device to avoid burning the fingers. Among the objects recovered from Kanti and Ravindra's pockets were some roaches too (see upper right of fig 1). Marijuana is almost never injected intravenously (in stark contrast to heroin). However, some illicit intravenous use has been reported with subjects 'shooting' crude marijuana, but this remains an extremely unusual practice and is accompanied by severe medical complications. Another product from the cannabis plant is charas , also known as hashish in the Western world. Hashish contains 10 to 15 per cent THC and is much stronger than marijuana. Thus bhang, ganja , and charas represent three different varieties of the same drug, but in increasing concentrations. In the underworld of drugs, there is only one other drug which is available in so widely variable concentrations and this is alcohol (although it is more or less socially acceptable, unlike marijuana). A weaker brand of alcohol is beer (which may be compared to bhang ), a stronger is wine (comparable to marijuana) and a still stronger, whiskey (comparable to charas ). Charas or hashish is of a dark green or brown colour. It is the concentrated resin exuding from the leaves and stems of plants. It is very popular with the hippies. When I examined the contents recovered from Kanti and Ravindra's pockets, I became quite sure they were returning from a marijuana party. I have already mentioned that I recovered bhang and roaches from their pockets, but I recovered some other interesting items as well. At the bottom of the fig 1 you can see a strange looking pipe which is actually a marijuana pipe. So it appeared they were smoking marijuana too, besides eating Bhang . Eating and smoking cannabis products can lead to a drunken like state, and that may produce problems in driving. That is how I concluded that Bhushan must be speaking the truth. But I needed to gather more scientific proof-one which could stand the rigors of the cross-examination in a court of law. So I took chloroform swabs from the fingers and the inner aspects of the teeth. Taking chloroform swabs involves wetting a piece of cotton in some chloroform and rubbing it on the area from where you want to take a swab. In this case I rubbed it over the fingers and inner aspects of the teeth of the two deceased persons. If the two had been eating and smoking cannabis products, some cannabis components must be sticking to these areas. The chemical analysis report from the lab confirmed that the fingers and the teeth of the two deceased indeed contained THC, an important chemical found in Cannabis as we have already seen. This was a confirmatory proof that both of them were returning from a marijuana party. Since they had consumed too much Cannabis, they were unable to drive well. This had actually caused the accident and their death. This conclusion led to immediate release of Bhushan from police custody. When the police released Bhushan, he came and fell on my legs. He said that his life had been saved because of me only. The poor fellow did not know that it was not me, but forensic science which had saved him. I only used the science! ( To protect the identity of the individuals, their names, as well as the various dates of occurrence have been changed )

  • Vol 27 No 1 | Anil Aggrawal's Forensic Ecosystem

    < Back To Main Page. [Epub ahead] Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 27, Number 1, January - June 2026 Contents Papers Posttraumatic Ischemic Brain Stroke After Sharp Neck Injury: A Case Report Based on Autopsy By: Ivan Tsranchev ¹ , Pavel Timonov ² , Stela Yancheva ³ , Kristina Hadzhieva ⁴ , Teodora Gudelova ⁵ , Mirena Sotirova ⁶ , Antoaneta Fasova ⁷ , Elizabet Dzhambazova ⁸ , Petar Uchikov ⁹ Read Ivan Tsranchev

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JUNE 1999 ISSUE THE POISON SLEUTHS DEATH BY NITRIC ACID -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. He has these strange yellowish stains over his face and chest. What has happened to him? Please tell me." "Good morning Tarun. The name of this middle aged man is Radhey Shyam, and he was living alone in this house for the last five years. His dead body has been found today morning from his house. His wife and son died long ago, and since then he is living in a very depressed state of mind. He had become alcoholic and had taken to gambling too. He had taken lot of loans from various sources. It is said that from one person Munna, he took as much as one lakh of rupees. Munna was actually a professional money lender and he used to give money at a very exorbitant rate of interest..." "Oh, I see. But what has all this to do with his death?" "I am coming to that Tarun. Munna was pressing Radhey Shyam for his money for quite some time. Last week Munna had visited Radhey Shyam's house, along with some of his goons for his money, and when Radhey expressed his inability to return the money for about six more months, Munna had threatened him with grave consequences." "So Munna has killed Radhey for retaliation?" "This is what the police thinks. Actually Munna had visited Radhey's house yesterday night too, and had threatened him with grave consequences once again. Today morning they have found the dead body of Radhey. So it is very natural to assume that Munna and his goons have killed Radhey." "What does Munna say?" "The police has arrested him. He looks terrified. He is swearing that he has nothing to do with this killing. He does admit that he had visited Radhey yesterday night, and that he indeed was with two of his goons. He also admits that he had threatened Radhey with grave consequences, but he swears he gave those threats merely to terrify Radhey into returning his money as soon as possible. He never intended to kill Radhey. He has also come out with an interesting argument. He says that he would not have got his money anyway by killing Radhey. So killing Radhey was not in his interest anyway." "Sounds like a valid argument. What do you think doctor?" "Tarun, as you know, I deal every case from a scientific angle. Are you looking at the yellowish stains over his face and chest and over his clothes?" "Yeah, they are very prominent. In fact that is the first thing I noticed, when I came here." "I have looked at his teeth and tongue too. Even they are stained yellow. Come, you also have a look" "Yes, indeed. But what are you trying to arrive at?" "Tarun, it seems to me, that Radhey has died because of Nitric Acid" "Nitric Acid? Never heard of this poison being used to kill anyone." "Nitric acid is not a homicidal poison. It can not be given homicidally to anyone, because it has such a pungent taste. It is in fact a suicidal poison." "Looks like we are on to another of your rare and exotic poisons. Doctor please tell me about nitric acid from the beginning." "Tarun, Nitric acid is a colorless or yellow fuming liquid with an acrid odour. It is a powerful oxidizing agent and reacts with organic matter such as with proteins to produce trinitrophenol or picric acid with the liberation of nitrogen monoxide. This is known as xanthoproteic reaction. Organic matter is thus turned yellow. Stains of this acid on clothing are also yellow, which is a distinctive feature of poisoning by nitric acid. In fact this is how I first suspected that this could be nitric acid poisoning." "Oh, I see. Can you tell me, what are the symptoms a person experiences when he consumes nitric acid?" "Sure. The person gets eructations and abdominal distension. Actually this symptom is also seen with other acids such as sulphuric acid, but eructations and abdominal distension are more severe in nitric acid than with sulphuric acid, because with nitric acid more gas is formed. Then, as you know by now, there is yellowish staining of the teeth as well as of the skin around the mouth, cheeks, and neck, which is very characteristic. Yellow stains may also be found on hands, forearms, and the chest because of splashing. In severe cases, the stomach may perforate, but this is unusual." "Doctor, what is the usual fatal dose of nitric acid?" "It is around 10-15 ml. Actually one tablespoonful contains about 5 ml of liquid. So about two to three table spoonfuls of nitric acid are enough to kill a person." "And what is the usual fatal period?" "It is around 18-24 hours" "How can a person obtain nitric acid to kill himself?" "Tarun, nitric acid is widely used in the art and manufacturing industry. It is used for cleansing nickel ornaments and separating gold from other metals. It is also used in the preparation of gun cotton, nitroglycerin, picric acid, and colouring matters. Because of its wide use in industry, and even in domestic affairs, it is commonly available in the market. And because of its easy availability, suicidal and accidental poisoning is quite likely." "Can a person commit murder with nitric acid?" "Majority of cases of poisoning by nitric acid are either suicidal or accidental. Homicide with nitric acid is extremely difficult, and perhaps even impossible. Because of the corrosive nature of the acid, it can not be given to an unsuspecting individual, who would immediately discard it on tasting. However forcible administration of this acid in drunk patients has been reported. A forensic expert by the name of Christison describes a case where nitric acid was forcibly poured down the throat of a woman when she was drunk. Nitric acid has also been used in vitriolage, although the use of sulphuric acid is more common for this purpose." "Excuse me doctor, you have used a new word. I am not quite familiar with this. What is vitriolage?" "Tarun, vitriolage is intentional throwing of a corrosive substance over the face of an enemy. Often the corrosive substance such as sulphuric or nitric acid is filled up in an old used bulb, and this bulb is then thrown over the face of the victim. A person who commits vitriolage generally does not intend to kill his victim. He merely wants to disfigure him or her. When this bulb smashes on the victim's face, the corrosive substance is released and corrodes the face of the individual. This method is usually employed by disgruntled youths to disfigure the face of beautiful girls who have spurned their love offers." "Oh, that is really sad. Now in the current case of Radhey, how did you reach the conclusion that he had died of nitric acid poisoning?" "By his peculiar post-mortem findings. I have already talked to you about his yellowish stains. These yellowish stains have to be differentiated from those of the iodine stains, because they can cause similar stains. However if ammonia or some other alkali is applied to the stains, the ones due to nitric acid deepen in colour to become orange, whereas those by iodine are decolorized. I did this test in this case, and found that these stains were indeed caused by nitric acid only. In addition, I found that his stomach was perforated. This can only happen if the acid has corroded the stomach wall. But I did not stop at that. I took some material from his stomach and chemically tested it in my lab. I have confirmed chemically that the substance which Radhey ingested was indeed nitric acid. Subsequent to this, I asked the police to search his house and look for some suspicious looking half filled bottle. And sure enough they found a bottle of nitric acid in his almirah which was half filled. Now I will tell you what must have happened. Munna indeed visited Radhey's house yesterday along with his goons, and he also threatened Radhey. But he did not kill him. After Munna had left, Radhey got depressed. He anyway was living alone and no meaning to life was left to him. He wanted to commit suicide and the only thing available to him was nitric acid. He consumed this acid and died. Come let us tell the police that Munna has not killed Radhey. He has actually committed suicide." "Very clever indeed. This was a most interesting discussion doctor. Without your masterly deduction, police could have unnecessarily went on harassing Munna. Everyone might have thought, it was a case of killing by Radhey. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. It is oxalic acid. "

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MAY 1999 ISSUE THE POISON SLEUTHS DEATH BY AFLATOXINS -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 has happened to him? Please tell me." "Good morning Tarun. The name of this young man is Suman Dubey. He is 25 years old and unmarried. He died this morning in his rented house. He was living alone in this house. He was basically a farmer, but had recently shifted from his village to live in a suburb of Delhi. He was doing some odd jobs for carrying out his livelihood. But he was also getting assistance from his family in his village. I mean, he used to get most of his food supplies from his village." "That's alright doctor. But how exactly did he die?" "Tarun, I am coming to that. For quite some time he was complaining of some vague symptoms. For instance, he was having pain in the abdomen and loss of appetite. He also noted some loss in weight, and a vague swelling of the abdomen. Since he was from a rural background, he did not believe in modern medicine. He was a staunch believer in traditional medicine only. He kept on ignoring his symptoms for quite some time. Last week he visited his village, where he consulted a local doctor. The doctor, after examination told him, that he was getting slow poisoning from some source. He believed that some of his foe was administering poison to him." "Oh, really? And who was he?" "We don't know yet. But the moment Dubey was told about it, he believed it. In fact, he told his family that his milkman wanted to poison him, and was probably poisoning him by giving him a daily supply of poisoned milk. He was daily taking one liter of milk from a milkman called Ramnath." "But why would Ramnath want to kill him?" "That is exactly the question, Dubey's parents asked him. We know this, because we have now interrogated Dubey's parents. Suman Dubey was unmarried as I have already told you. One day, Ramnath came to Dubey's house to deliver the milk along with his young and nubile sister Sita. Immediately Dubey fell in love with her. Once or twice, when she came alone to deliver the milk to Dubey, he even made attempts to make passes at her. Sita immediately complained about this matter to her brother, who came to his house to resolve the matter. There was a big fight between the two. The whole neighborhood knew about it. After this Ramnath stopped delivering milk to Dubey. This was quite expected. But then quite unexpectedly Ramnath again started delivering milk to Dubey. Dubey was initially quite surprised, but he agreed because in this way, at least he could be in touch with Sita." "Oh, I see" "But when the village doctor told Dubey that someone was trying to poison him, he immediately realized why Ramnath had started delivering the milk to him again. Probably Ramnath wanted to get even with him by killing him. He thought that the best way would be to kill Dubey was by giving him small quantities of poison through the daily supply of milk. So he resumed the milk supply to him." "Oh, it indeed appears to me that Ramnath killed him through slow poisoning. Is slow poisoning possible doctor?" "Oh yes. Arsenic is notorious for this. One could give this poison in very small amounts over a long period of time, and the victim would die of slow poisoning. There are several other poisons which could be used for slow poisoning. Dubey's parents have lodged a strong complaint against Ramnath, and the police has apprehended him. He however is asserting that he is innocent and that the police should release him immediately." "What is your opinion in this case doctor?" "Tarun, I am a scientist, and I believe in hard facts. I have done an autopsy on this man, and have come forward with some amazing findings..." "Like what?" "The thing that caught my attention immediately was that his liver was enlarged. I took some liver cells from there and looked them under the microscope. I was surprised to find that Suman Dubey was suffering from a form of liver cancer, known as hepatoma. This finding set me thinking and I did certain other tests. I measured his blood glucose, and I found that it was much less than what it should have been. In technical terms, he was suffering from hypoglycemia, which in plain and simple words means "low sugar in the blood". I also found a chemical known as alpha fetoprotein in his plasma..." "Doctor, these symptoms don't appear like that of a poison to me. It rather appears to me that he died of liver cancer. Where is the criminality involved?" "Tarun, he indeed died of liver cancer. But the problem with me is that a serious allegation has been made by Dubey's parents against Ramnath." "That's right. And now you can tell the police that Ramnath is not guilty. And you can tell them that he died of liver cancer." "Tarun, you may be surprised to know that hepatoma can be induced by a poison, especially if low quantities of it are administered to someone over a long period of time" "Really? That is most preposterous. I wouldn't believe it, if it were not coming from your mouth. Well, anyway what is that poison?" "Tarun that is a very rare poison. It is called Aflatoxin" "Aflatoxin? Never heard of that." "Really. In fact, it is one of the most talked about poisons today. Some people believe that this poison is being used by certain nations in biological warfare." "Come on doctor. It looks like we are again on to some interesting tales about poisons. Tell me about aflatoxins from the beginning" "Tarun, our story of Aflatoxin starts at the most unusual place- the church..." "The church? Come on doctor. How can the story of a poison start from such a holy place as a church?" "In churches, a device if often used for sprinkling holy water. It is swollen at one end, and this swollen end has several tiny holes in it, through which holy water can be sprinkled. This little device is called aspergillum, after the Latin word for sprinkling, which is aspergo." "I still can't make any head or tail of how this will lead us to such a deadly poison as Aflatoxin." "It so happens that there is a particular species of fungus, which under the microscope looks exactly like the aspergillum. Its strands have a tiny end and a swollen end. To many mycologists - scientists who study fungi - this appeared rather like the aspergillum used in churches, so they named it Aspergillus. Since this fungus was yellow in color, and the Latin word for yellow is flavus, they preferred to call this fungus Aspergillus flavus, which became its botanical name. In 1960, an epidemic of serious liver disease was traced to the eating of moldy peanuts. Incidentally it was nothing but Aspergillus flavus, which had affected the peanuts. It was later realized that this fungus released a poison which actually caused the serious liver disease. The toxicologists were looking for a name for this newly discovered poison, and they resorted to the botanical name of the fungus from which the poison was coming. They took the first letter from the name of the genus (i.e. "A") and the first three letters from the name of the species (i.e. "fla"). Together the four letters form the word "Afla". Since toxin is another name for poisons, they added this world to "Afla", and the name of the new poison became Aflatoxin." "Oh, that is most interesting. Doctor, you are incredible. You make things so interesting." "Tarun, Aflatoxins are powerful, tasteless, odorless and colorless mycotoxins that are chemical metabolites produced not only by Aspergillus flavus, but by certain other species of Aspergillus as well such as Aspergillus parasiticus. It is also produced by certain other fungi such as Penicillum and Rhizopus. These are all soil based fungi. Several varieties of aflatoxins are known, but the most dangerous is Aflatoxin B1, with Aflatoxin G1, coming a close second. In fact, Aflatoxin B1 is thought to be the most potent liver cancer producing chemical. Aflatoxins are mutagenic (i.e. they cause mutations), carcinogenic (i.e. they produce cancers), teratogenic (i.e. they cause deformities in the fetus, if pregnant mothers take them), and acutely toxic to most animals and humans. They can cause animals, including humans, to lose their appetites, decrease their feed efficiency and/or cause death. Aflatoxins inhibit the body's immune system and reduce the effects of vaccines. In the U.S., the aflatoxins are the only mycotoxins that are specifically regulated by the Food and Drug Administration or FDA." "Oh, I see" "Human exposure to aflatoxins may occur accidentally by the consumption of foods that have been contaminated by Aspergillus during growth, harvest or storage. Nearly all agricultural products are potentially subject to contamination with aflatoxins. Common sources include grains (e.g., corn, rice, sorghum), peanuts, oilseeds (e.g., cottonseed oil, copra), legumes (soybeans, other beans), and tree nuts (e.g., almonds, pecans, walnuts). The use of Aflatoxin-contaminated feed for domestic animals may result in secondary exposure to humans by the consumption of products such as meat, milk and cheese, and eggs that contain residues of the aflatoxins or their toxic metabolites. The FDA has established enforcement levels of 0.5 part per billion (ppb) in milk and 20 parts per billion for other food products. This means that in the United States, concentrations of up to 20 ppb are permitted in human foods and only upto 0.5 ppb in the milk. Levels of up to 200 ppb are permitted in animal feeds, although there is now a serious concern for secondary exposure to aflatoxins from the use of animal products. As I told you, Aflatoxin B1 is a potent hepatocarcinogen in experimental animals, but tumors may also occur in the colon and kidneys. In rats, tumors develop after the administration of 0.2 micrograms per day or a single dose of 0.5 mg of Aflatoxin B1; the tumor incidence is 50 per cent at 26 months after the latter treatment. There are marked differences in the susceptibility of various species to carcinogenesis by Aflatoxin B1; rats are much more susceptible than mice." "Oh, that is interesting." "Tarun, very high levels of aflatoxins occur in foods in certain regions of Africa and Asia, and people in these regions suffer a high incidence of liver cancer. Within Swaziland, Kenya, Uganda, and Thailand, where epidemiological studies have been conducted, in certain areas the climatic conditions (i.e., high temperatures and high humidity) are favorable for fungal growth; the food supply from these regions shows a relatively high Aflatoxin contamination, and the average Aflatoxin consumption exceeds 10 micrograms per kg of body weight per day. In other areas of the same countries where lower temperatures and lower humidity prevail, the food supply shows a relatively lower Aflatoxin contamination and the average human Aflatoxin consumption is less. In these areas, the incidence of liver cancer is also less. This is a fairly good evidence that aflatoxins are connected with liver cancers. Within each country, there is a direct relationship between the incidence of liver tumors (cases/100,000 people/year) and the average daily dietary intake of aflatoxins in contaminated agricultural products." "That is interesting. You were saying that aflatoxins are also used by certain nations for biological warfare" "Tarun, first of all you must know, what biological warfare is. It is the use of living organisms or their products by a nation for killing the people of its enemy nation. The earliest instance of biological warfare is provided by ancient Mayans, who used to throw deadly snakes in their enemy camps. Now the biological warfare is much more advanced and complicated. People are thinking of using aerosols of deadly bacteria and viruses to decimate their enemies. These aerosols can be released in the enemy territories in the same way that traditional bombs are dropped. On 17.10.96, Alan George of the London Observer reported some interesting facts about Iraq's weaponizing of Aflatoxin. According to him, in May 1988 Iraq began studies on Aflatoxin at its Al Salman facility where the toxin was produced by the growth of the fungus Aspergillus in 5.3-quart flasks. In 1989 Iraq moved its Aflatoxin production to a facility at Fudaliyah. In November, 1989, trials using Aflatoxin warheads (in 122 mm artillery rockets and R400 aerial bombs) were conducted. In 1990 between spring and December 1990, it produced 481 gallons of Aflatoxin in solution. Between May 1990 and August 1990, trials using Aflatoxin warheads were continued. In December 1990 large scale "weaponization" of biological agents started. In 1991 Iraq's Gulf War arsenal included sixteen R400 Aflatoxin bombs and two Aflatoxin warheads for enhanced Scud missiles. In total Iraq produced 572 gallons of concentrated Aflatoxin, of which 410.8 gallons were put into munitions. There is however no evidence that these Aflatoxin weapons were ever used. But under these circumstances, United Nations has continued its sanctions over Iraq." "That is most interesting. Coming to our original case, do you think, Ramnath was intelligent enough to mix aflatoxins in the milk, to cause liver cancer in Suman Dubey so he may die?" "I don't think so. Although there is a distinct possibility of someone doing so, if he were intelligent enough. Ramnath is an illiterate person, and I don't think, he even knows about aflatoxins. I think the rice that he was getting from his village was moldy, and he got his poisoning from that. In fact, I have examined the rice stores in Dubey's house and they are indeed moldy. I examined some of the rice grains under the microscope and I could indeed find Aspergillus in it. So that solves our case. Come, let us tell the police that Ramnath is innocent and that they should release him." "Very clever indeed. This was a most interesting discussion doctor. Without your masterly deduction, police could have unnecessarily went on harassing Ramnath. Suman Dubey's relatives and other people might have thought, it was a case of killing by Ramnath. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison, nitric acid. "

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE DECEMBER 1998 ISSUE THE POISON SLEUTHS DEATH BY SODIUM CHLORATE -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 seems to have a chocolate brown color. Well, this is the most peculiar color I have ever seen in a dead body. What happened to him? Please tell me." "Good morning Tarun. The name of this young man is Radhey, and he died in Dr. Gupta's nursing home today morning. Yesterday he and his friend Shyam had a dinner at a 5-star hotel. While they were still having dinner, Shyam got a phone call and had to leave suddenly leaving the dinner unfinished. Radhey became sick immediately thereafter. He started vomiting. Seeing his condition, the hotel staff called the ambulance, and he was shifted to Dr. Gupta's nursing home. The doctors there started a battery of tests to arrive at a diagnosis, but before any diagnosis could be made, he died." "Oh, looks like he died of some natural disease. You said he had vomiting. May be he died of gastroenteritis." "Doesn't look like to me. Look at his body. It is so darkly colored. You yourself remarked on that as soon as you came here. One doesn't get that kind of color in gastroenteritis. There may be more to his death, than meets the eye." "Really? Well, let me know. I am all ears." "Tarun, I have asked the police investigating this case. It appears, Radhey and Shyam did not have good relations. They were business partners, but lately there had been lot of tussle between the two regarding the ownership of certain business properties, which ran into lakhs of rupees. Naturally each wanted the other out of way. In fact, yesterday's meeting at the 5-star hotel was meant just to sort out these problems...." "Oh, so you are hinting that probably Shyam killed Radhey. Did he administer some poison to him?" "Tarun, I have enquired in detail from the police about yesterday's events. They have taken the help of waiters and other staff to find out what exactly happened yesterday evening. Radhey and Shyam arrived in the dinner hall at about 7.30 pm yesterday night, and first of all they started having some drinks. After about two drinks, they called for soups. Just when the soups were brought, a phone call came for Radhey. We know this from the waiter who received the call. Well the waiter tells us that Radhey came back within a minute and started having soup. Soon after Shyam got a phone call and he had to leave. After this Radhey became sick. This peculiar story, coupled with the fact that the body of Radhey is showing this characteristic chocolate brown color, leads me to think that Radhey indeed has been poisoned..." "Really? With what poison doctor?" "Tarun, it is a very interesting poison. May be you never realized it is a poison. It is a very common salt available in all chemistry laboratories- sodium chlorate." "Sodium chlorate? Yeah indeed it is a very commonly available salt. But I never realized it is a poison also." "Yes, Tarun, it is a very deadly poison. In fact the brown color of Radhey's body led me to that. It causes browning of the body, because it forms a brownish colored compound in the body- methemoglobin." "Don't really know what methemoglobin is. Please tell me more about it doctor." "Tarun you know that all of us have hemoglobin in our bodies. It is the basic pigment which picks up oxygen from the lungs and delivers it to all tissues. It resides in the Red Blood Corpuscles or R.B.C.s. If anything were to go wrong with hemoglobin, oxygen transport to the tissues would be seriously hampered and the person may die. Hemoglobin molecule has four iron atoms in it, all of which are in the reduced or ferrous state. This is usually written by the chemical symbol Fe++. Methemoglobin is nothing but a molecule of hemoglobin, in which one or more of iron atoms - may be just one, or all four- are oxidized to Ferric state. Chemically we can represent these iron moieties as Fe+++. Once the hemoglobin molecule is modified in this way, it no more remains useful as an oxygen carrier. It becomes useless in other words, and the person may die for want of oxygen. Sodium chlorate is a strong oxidizing agent. It oxidizes the hemoglobin to methemoglobin and this may cause rapid death." "Just a minute doctor. You said that normally hemoglobin takes oxygen from the lungs and delivers it to all tissues. Doesn't that too oxidize the hemoglobin and render that useless?" "Oh, no Tarun. That is a very loose combination of hemoglobin with oxygen. In fact nature has devised it to be so loose that it readily delivers its oxygen to the tissues. In this combination, all iron atoms remain in the ferrous state. Only the whole molecule simply picks up the oxygen molecule, much as you would pick a hot coal with a tong. But Sodium chlorate really "oxidizes" the molecule rendering it useless. So although Hemoglobin normally carries oxygen around, it doesn't get oxidized in the true sense of the word. In fact, if it were to be oxidized by any means, it would immediately be rendered useless." "Oh, Sodium chlorate really appears to be an interesting poison doctor. Please tell me more about it." "Tarun. Two chlorates are very important from a toxicologist's standpoint- Sodium and Potassium chlorate. Chemically we can write them as KClO3 and NaClO3. At one time potassium chlorate was widely used in medicine and being obtainable without restriction, it was a popular household remedy, especially for sore throat. It has now been completely abandoned as a remedy and therefore it is a rare source of poisoning today. Sodium chlorate on the other hand, has a reputation as a safe and effective weedkiller, and is commonly available. Sodium Chlorate is also used as an explosive in many parts of the world. It is still commonly available in the market. Unfortunately many people think that it is non-poisonous, and this wrong belief has given rise to several poisonings." "Doctor, how can poisoning with sodium chlorate occur usually?" "Tarun, poisoning with sodium chlorate can occur accidentally, suicidally or even homicidally as seems to be the case I am handling today. Accidental poisoning is perhaps the most common. Sodium chlorate has been mistaken for common salt and Epsom salts..." "Sorry to interrupt you doctor, but what exactly is Epsom salt?" "Tarun, it is a bitter, white crystalline powder consisting of hydrated magnesium sulfate. It was once used in medicine as a cathartic and to reduce inflammation such as in sore throat. Its formula is MgSO4.7H2O. It is named after a place called Epsom, in Surrey, England, where it was originally prepared from the water of mineral springs. If magnesium sulfate is prescribed for some disorder, and the person inadvertently took sodium chlorate, which looks very much like it, he may be severely poisoned. In some cases poisoning has occurred when potassium chlorate was taken as a medicine, mainly to treat inflammation or septic spots. In many such cases, potassium chlorate was given for local application, but it was swallowed instead. In one such case, a person was having an ulcer in his mouth. He was given potassium chlorate to gargle his mouth with, but he swallowed it, and was severely poisoned. Illegible prescriptions have also given rise to some poisonings. In one such case, the intended drug to be given was potassium chloride. But on the prescription, only the words "potassium chl." were written. This was misinterpreted by the chemist as potassium chlorate. This drug was dispensed and the patient was severely poisoned!" "Very interesting indeed!" "Tarun, I know of several instances when potassium and sodium chlorates have caused inadvertent deaths. In one case, a 5 year old girl had scarlet fever. Inflammation of her throat was treated with repeated sponging with a 2% solution of potassium chlorate. On 7th day, the symptoms of poisoning appeared, and even though the treatment was stopped on that very day, the girl died on the tenth day. In another case, a 61 year old woman sucked daily on 20 tablets of potassium chlorate (324 mg each) for 6 to 10 weeks. She thought that a cancer was developing on her tongue and that she would be cured by this. She was severely poisoned. In one case, a chemist gave his wife several tablets of potassium chlorate for treating her tonsillitis. She died after five days. But probably the most interesting is the case of a 48 year old gardner who was severely poisoned in a curious way. He was using a concentrated solution of sodium chlorate in an atomizer, while a strong wind was blowing. In consequence, spray was blown on to his face and he inhaled and ingested some of the solution. Symptoms of poisoning started the same evening. He could be saved with some heroic effort on the part of the doctors, yet he could only return to full-time work at the end of about a year." "Doctor, what symptoms does one get on swallowing this poison?" "Tarun, immediately there is acute digestive upset. Vomiting is usual. It may persist for upto 48 hours. There may be severe pain behind the breast bone or in the abdomen. Red Blood Cells begin to break down and may reduce in number to half. Red cells may only be 2.5 x 1012/L in this poisoning, while normally they are 5 x 1012/L. Heinz bodies are seen in the red cells...." "What are Heinz bodies doctor?" "Tarun, Heinz bodies are nothing but denatured hemoglobin. I told you that sodium chlorate destroys hemoglobin. This destroyed or denatured hemoglobin, also known as methemoglobin precipitates in the RBCs as Heinz bodies. These bodies were first described by a German doctor Robert Heinz. Hence the name. Besides these symptoms, acute renal failure also occurs in sodium chlorate poisoning. This is in part due to direct action of chlorate on the kidney and in part due to mechanical obstruction of tubules of the kidney by hemoglobin set free from the red cells. Urine is scanty and dark brown. Total stoppage of urine may also occur." "Doctor, how much sodium chlorate is needed to kill an adult robust man?" "Tarun, about 20-35 grams would be required. And the person would die in about 4-5 days, although death can be quicker as in this case." "Oh, Doctor, now I know all about sodium chlorate. Tell me how you deduced that Radhey died of sodium chlorate poisoning?" "Tarun, the color of Radhey's body gave away the poison to me. You will agree the color is very peculiar. It is chocolate brown. This is the color of methemoglobin. So the moment I saw the chocolate color of Radhey, I knew I was looking for some poison, which converts hemoglobin to methemoglobin, and sodium chlorate is one such poison. Then I made a blood film of Radhey and saw it under the microscope. RBCs were broken, and they showed fragmentation which was expected in sodium chlorate poisoning. Numerous Heinz bodies were also seen in the RBCs. His kidneys as you can see are enlarged, as we would expect in sodium chlorate poisoning. I have made a microscopic examination of the kidneys too. And I have found that the tubules of the kidney are occluded with broken red cells and brown pigment granules. You surely know what the tubules of the kidney are. They are the microscopic tubes through which filtered blood - or urine- passes forwards. These tubules are dilated and many are completely blocked by debris. This is exactly the change that we would expect in sodium chlorate. There is no doubt that Shyam has given Sodium chlorate to Radhey." "But how could he do that? They were both having dinner together." "Tarun, Shyam was probably working with some accomplice, who was sitting outside the dinner hall probably with a mobile phone. Just when the soups were served, the accomplice phoned from his mobile to the reception desk of the dinner hall, asking for Radhey. When Radhey went to pick up the phone, Shyam quickly mixed the sodium chlorate which he already had in his possession. Radhey discovered that it was a blank call and returned to his table and started having his soup. The taste of sodium chlorate is somewhat similar to that of common salt, so one may not discover any change in taste, especially when he is already drunk as Radhey was. When he had finished his soup, Shyam and his accomplice knew it was not safe to remain there any more. So according to their pre-arranged plan, the accomplice phoned again- this time to Shyam. He took the call, came back to Radhey and told him that he had to leave as he had got some important call. The idea was to leave the scene immediately to remain out of trouble. You know the rest of the story." "Very clever indeed. But how do you know the story with such gory details?" "Tarun you will be surprised but Shyam has told us this story himself. Actually when I conducted the post-mortem, I immediately suspected I was looking for sodium chlorate. I told the police about it. They raided Shyam's house and recovered a small sachet, containing a white powder. When I examined it chemically, I discovered it was nothing but sodium chlorate. Faced with this fact, police renewed their interrogation of Shyam. Faced with all the scientific evidence against him, Shyam broke down and told these details to the police. The police are now looking for his accomplice, who is on the run." "Very clever doctor. This was a most interesting discussion doctor. Without your masterly deduction, Shyam could never have been caught. Every one would have thought that it was a case of death due to gastroenteritis. 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 nitrite. " "

  • Forensic Science Fiction | Anil Aggrawal's Forensic Ecosystem

    Forensic Science Fiction The mystery of the drowned man The man had been drowned for five days! At least that is what Dr. Khanna made me believe. Dr. Sunil Khanna as we all know is a leading forensic expert of our country and his opinion had to be respected. Well! before proceeding further, I shall explain what forensic experts are. They are doctors who, among other things, cut up dead bodies and try to find out the cause and manner of death. After we completed our graduation in medicine, we decided to devote our energies to the detection of crime, rather than to the routine, drab, utterly boring checking of festering sores, furred tongues, missed heart-beats, aberrant pulse rates and bizarre temperature patterns. Coming back to our case. The man was ultimately identified as one Ramlal. When the police made investigations, they came up with some rather dubious evidence that Ramlal had been killed by Jagga and then thrown in the Indian Ocean, off the coast of Gujrat. It is well-known that in our country, criminals often kill their victims and then do dispose of the body by throwing it in this manner in deep ocean, river, lake or pond or some such similar body of water where it would be difficult to retrieve the body for quite some time. But it so happened that I personally knew Jagga and was quite convinced that Jagga could not kill anybody. I talked to Jagga, and after talking to him, I became all the more convinced that Jagga was not the killer. When I talked to Jagga, he categorically denied his hand in Ramlal's killing. He requested me to save him from the clutches of the law. Well then, if Ramlal had not been killed by Jagga, how had he died. I surmised that Ramlal must have gone to the sea shore for a bath and then must have been carried away by the tidal waves. He thus drowned accidentally. But I was told that Ramlal was an accomplished swimmer. If this was true how could he drown accidentally? Well, even accomplished swimmers have been known to drown in sea water. The tidal waves are really very strong, and can carry the person deep inside the ocean in no time. Before the person has time to think, he finds himself deep inside in the sea. The waves are so forceful that they do not allow him to swim back to the shore. The person gets exhausted and ultimately drowns. This is what should have happened to Ramlal. But the law wants solid proof. The courts do not pay attention to mere conjectures. If I wanted to save Jagga, I had to produce some real good scientific evidence in favour of my theory of accidental drowning. The police was bent upon implicating Jagga. They had even requested the court and taken him in police remand for a period of 15 days. I had to do something fast. I consulted Dr. Khanna and he suggested me that our question basically boiled down to proving that Ramlal's drowning was a case of antemortem drowning. If the police version was correct, then Ramlal's drowning was a case of post-mortem drowning. Before proceeding further, I must tell you a little bit about ante-mortem drowning and post-mortem drowning, in case you are unaware of it. This is an age old question in forensic medicine and one for which no satisfactory answer has been found yet. Basically ante-mortem drowning means that the person drowned when he was still alive. Post-mortem drowning on the other hand, means that the person was first killed by someone and then thrown in water to conceal crime. While post-mortem drowning almost certainly points to homicide, ante-mortem drowning could be anything; accidental, suicidal or homicidal, roughly in that order. It is rather difficult for someone to drown a conscious adult person with homicidal intent, so on the face of it, a case of ante-mortem drowning goes against homicidal drowning. I had to do an autopsy on the dead body of Ramlal and find out the cause and manner of his death. Now if I could prove that it was a case of antemortem drowning, it would go in favour of my theory that Ramlal had died accidentally while taking a swim. If on the other hand the autopsy showed it to be a case of post-mortem drowning, it would be a very strong evidence in favour of the police theory that Jagga had done him to death and then thrown away the dead body in the ocean. Of course we forensic scientists know that one of the best ways to differentiate between ante-mortem and post-mortem drowning is to conduct the so-called diatom test. I won't bother you with details, but just give you the outline of the principle of this test so that you could follow the story better. In all bodies of water- in rivers, lakes, ponds, oceans, even in tap water- are present some minute microscopic unicellular organisms called diatoms. These are microscopic algae with hard and highly refractile silicon shells. They come in all kinds of shapes; in fact about 15,000 different species are known. Under the microscope they all appear very beautiful and symmetrical, presenting rather a kaleidoscopic picture. Diatoms are quite abundant. A mere c.c. of water would contain literally thousands of diatoms. Now if a man drowns while he is still alive, he would make violent efforts to respire. Water would enter his respiratory passages along with respiratory air, and would reach the alveoli, the fine balloon like terminals of the lungs. Sure enough diatoms would also reach the alveoli along with the water. Due to the violent respiratory efforts, some of the alveoli would get ruptured causing the water (and the diatoms along with it) to be sucked in the tiny blood vessels lining the alveoli. From here they would find their way to the left chamber of the heart and from there the aorta would pump this water (and the diatoms along with it) to all the conceivable organs of the body- liver, spleen, brain, bone marrow, everywhere. In case the person was thrown in the water when he was already dead, neither his lungs, nor his heart would be functioning. Thus in the first place almost no diatoms would enter the lungs. If due to sheer pressure of water, some diatoms did enter the lungs, they would not be able to penetrate the alveolar wall. Further, for the sake of argument if we assume that the water pressure was enough to break some of the alveoli, and some diatoms did enter the alveolar blood vessels, they couldn't be pumped to all the systemic organs for the simple reason that the heart would not be beating. Thus a simple test to prove a case of antemortem or postmortem drowning was simply to look for diatoms in some internal organ, say liver or spleen or brain. If you found diatoms there, it was a case of antemortem drowning; if you didn't find any, it was of course a case of postmortem drowning. When I conducted a post mortem on the body of Ramlal, I found all his internal body organs literally infested with diatoms. Diatoms were to be found everywhere- in his liver, spleen, brain, bone-marrow, everywhere. This naturally made me very jubilant, as this proved beyond doubt that my theory was correct and Ramlal had indeed died while he was alive. But when I contacted Dr. Khanna with these findings, he seemed doubtful. He reminded me that the diatom test was in fact challengeable. Well, I will digress for a moment and tell you why he said so. It so happens that the diatoms are rather ubiquitous; they are present in all bodies of water- even in the tap water as I have already said. Now imagine a situation when a person has been drinking tap water all his life. Suppose he has an ulcer in his stomach (or for that matter, even some minor abrasion anywhere in his gastrointestinal tract) the diatoms would be entering his circulation all his life and be pumped throughout his internal organs. The internal organs of such a person would show diatoms irrespective of the cause of his death. Such a person might die of, say, electrocution and yet his internal body organs would show diatoms. Dr. Khanna rightly told me that my findings could be challenged by a well-informed prosecution. I could see his point, especially as I knew the prosecution was taking the help of Dr. George Paul, another well-known medico-legal expert of our country. Certainly Dr. George Paul, when called to the court would rip my theory apart. What should I do then? This question gave me many restless moments. Then like a flash of lightning, a possible solution crossed my mind. I recalled that a few days back, there had been a big oil spill off the coast of Gujrat. A big oil tanker had been bringing crude petroleum somewhere from the Gulf, when just off the coast of Gujrat, a crack appeared on the bottom of the tanker and many thousand tonnes of crude oil leaked into the sea. This incident had been the talk of several environmentalists, especially as this was causing threat to marine life. Well, if there was crude oil in the sea water, and if Ramlal was breathing at the time of immersion (as I believed), then some petroleum must have seeped into his circulation, through the same route as the diatoms would normally take in a breathing man. This would result in traces of petroleum being present in his internal body organs. If I found traces of petroleum in, say, liver or spleen, I could prove my point beyond doubt. In that case, Dr. George Paul was definitely going to have a hard time explaining how it reached there, otherwise than what I was suggesting. We all know that petroleum is not a normal constituent of the body and no sane person drinks petroleum, so indeed there was no conceivable way for the petroleum to reach the internal body organs other than through ante-mortem drowning. This naturally made me very jubilant, and I used our newly acquired Gas-Liquid Chromatograph to determine petroleum in Ramlal's body organs. But contrary to my expectations, Ramlal's internal body organs failed to show any trace of petroleum. What had gone wrong? Well, Dr. Khanna suggested that may be I was wrong from the very beginning. Ramlal was indeed killed by Jagga first and then thrown in sea water. Otherwise why didn't I find petroleum in Ramlal's internal organs? Failure to find petroleum there meant only one thing- that Ramlal was not respiring at the time of his immersion in water. But I refused to believe Dr. Khanna. Something deep inside my heart told me that Jagga was innocent. But if he was innocent why was I not getting any traces of petroleum in Ramlal's internal body organs? That was the sixty-four thousand dollar question. Soon I forgot the question anyway. Meanwhile Dr. Khanna and I jointly started an ICMR project in which we intended to find out the etiology of solvent abuse or glue sniffing. It is a poorly understood phenomenon, in which the addict gets an inordinate pleasure in sniffing various hydrocarbons. Most commonly sniffed substances include various glues, paint thinners, gasoline, chloroform, carbon tetrachloride and so on. We were trying to find a biological cause for this phenomenon. It so happened that one day I was talking casually to Dr. S.K.Gupta, Professor of Biochemistry in our college. He was working on some new cellular enzymes, and his work was being internationally appreciated. While talking to him, suddenly a weird thought crossed my mind, and I ran back to my department, silently crying "Eureka", much in Archimedean fashion. Thank God I had my clothes on! I retrieved some of Ramlal's tissues I still had in bottles, and brought them back to Dr. Gupta. I asked him to look for a specific cellular enzyme, which had not been discovered till then. Dr. Gupta, as is his wont, told me I was a fool, but I let that pass, and asked him to look for that enzyme anyway. But after a few days, Dr. Gupta was quite surprised that I was right. He could indeed find the enzyme I had asked him to look for. In fact he reported that the cells were very rich in that enzyme. I know you are getting curious. What was that enzyme, you may ask. You will laugh at what I will tell you, but you can confirm it from Dr. Gupta who has lab reports to confirm my statement. In fact even he would not have believed me, had he not found the enzyme himself. This was an entirely new enzyme. An enzyme which metabolizes hydrocarbons! Dr. Gupta suggested that we should call it Petroleum dehydrogenase. Dr. Gupta found 50 microgrammes of Petroleum dehydrogenase per c.c. of tissue, which is quite high as you can understand. A minor mutation in Ramlal's body gave rise to that enzyme. He was a mutant in other words. Well, how does this fact fit in our story. I will tell you shortly. But first things first. While talking to Dr. Gupta, I was subconsciously working on my own multifarious problems and suddenly it occurred to me that the solution to my problems lay in the realm of biochemistry. Perhaps Ramlal had an enzyme in his tissues which metabolized any petroleum that had seeped in his body cells during drowning. Now we were indeed able to find that enzyme in Ramlal's body cells. This changed our investigation much in our favour. I will tell you what happened. Ramlal was indeed breathing at the time of immersion. Some petroleum did seep inside his circulation and got deposited in his internal organs as explained earlier. Molecular death, as we all know occurs a few hours after the somatic death. Somatic death is the time when a doctor pronounces a person dead. But we all know that molecular activity continues for a few hours after that. During the interval between the somatic and the molecular death, the enzyme Petroleum dehydrogenase metabolized any traces of petroleum that had seeped in Ramlal's body tissues. That was the reason why we did not find any traces of petroleum in Ramlal's body despite the fact that he died while still breathing. You might say this is spurious reasoning. It is quite possible that there was no petroleum in Ramlal's tissues in the first place. Merely the fact that the enzyme Petroleum dehydrogenase had been discovered in Ramlal's tissues does not necessarily mean that this was responsible for the absence of crude petroleum in his tissues. This was certainly one of the possibilities but the possibility of crude petroleum being absent in Ramlal's tissues from the very beginning could not be ruled out. I knew if confronted with my new findings, Dr. George Paul would certainly come up with this question. So I decided to play one up on him from the very beginning. I took out Ramlal's preserved tissues once again, and looked for the metabolites of Petroleum in them. I had worked out its metabolites in detail, and one of them was 2-Butyne. In my renewed analysis with my Gas-Liquid Chromatograph, I looked not for petroleum but for its metabolites, mainly 2-Butyne. You can perhaps imagine my joy when I found fairly rich quantities of 2-Butyne in Ramlal's tissues. Earlier when I was not specifically looking for it, I met with failure, but now I knew what I had to look for and sure enough I got it. All of us know that 2-Butyne is not a normal constituent of body cells. Thus the only way it could have accumulated in the tissues is through metabolism of crude petroleum by the enzyme Petroleum dehydrogenase. This was the final vindication of my theory. Of course if Ramlal had survived longer, even 2-Butyne would have got metabolized further to carbon dioxide and water. Petroleum dehydrogenase was capable of metabolizing all hydrocarbons down to their very basic elements. I knew I had killed two birds with one stone. I enquired from his family members and was quite satisfied to find out that Ramlal was a glue sniffer. In fact I was quite sure of this fact when I was submitting his tissues to Dr. Gupta. I will tell you now what happens in a glue sniffer. These glue sniffers are all mutants. They have the enzyme Petroleum dehydrogenase in their body cells. Petroleum dehydrogenase is able to metabolize not only petroleum products but all hydrocarbons, liberating a good amount of energy in the process. These glue sniffers sometime during the course of their life discover accidentally that sniffing hydrocarbons gives them a renewed sense of well-being. What actually happens is that they are able to metabolize the hydrocarbons quite effectively which gives them short bursts of energy, which they construe as a sense of rejuvenation or well-being. They ultimately get addicted to the hydrocarbons. So now Dr. Khanna and I had hit upon an entirely new and novel theory of glue-sniffing. Initially Dr. Khanna was quite hesitant about accepting it, but I am happy to tell you that since my fateful meeting with Dr. Gupta, I have submitted blood samples of more than 50 glue sniffers to Dr. Gupta and he has found Petroleum dehydrogenase in all of them, which is a good confirmation of my theory! Thanks to Ramlal's death mystery, we found out a solution to an age old forensic question. Oh, yes, I must also tell you that the court admitted my findings and released Jagga. But the thing that satisfied me most, was that when Dr. Khanna read our paper on glue sniffing at The International Conference on Drug Addiction at Tokyo next year, it was adjudged the best paper of the conference! *** This story was published in Spandan, 1995-96 on Pages 13-17

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