SCIENCE IN CRIME DETECTION-34 DEATH BY COCAINE On 23 December 1992, a very interesting case was brought to me. A 23 year old youth was found dead in a park. The youth was identified as one Geeta who studied in a local college. The police found several wounds on her body (Please reproduce figures XX-16,17,18 on page 543 here). It was suspected that Geeta had been killed by someone. Their main reason for thinking this was the multiplicity of the so-called wounds on her body. When the police made enquiries they found that Geeta belonged to a rich trader family. Her father had a flourishing export business. Geeta used to get a good amount of pocket money. Lately she was demanding her parents to increase her pocket money to Rs 10,000 per month. Previously she was getting only about Rs 5,000. It was found that lately she was going steady with a boy Harish, who also studied in the same college. Geeta was previously in love with another boy Ganesh, who was somewhat of a dada of his college. When Geeta switched favors, Ganesh held Harish responsible for this and told him to keep off his girl friend. He also told Geeta not to meet Harish. But neither Geeta nor Harish paid any attention to him. Once while sitting in canteen Ganesh bragged among his goons that if Geeta did not mend her ways he would finish her off. The police immediately summoned Ganesh and held him responsible for the murder. Ganesh seemed horrified to know that Geeta had actually been killed. He admitted that he did brag about killing her, but actually he had done nothing to her. But the police wouldn't listen to him, and took him to their "torture chamber" to get the truth out of him. It was at this stage that the case was brought to me. When I had a careful look at the body, I found that she had a strange key like thing dangling from her neck, which the police had completely ignored thinking it was an ordinary medallion usually worn by girls (reproduce fig XX-24 on page 551 here). This was not the ordinary medallion. It gave me some inkling as to the cause of her death. Then I looked closely at the hair of her nose, and as I had suspected, I found some white particles sticking there. I plucked some of those hairs with tweezers, and sent them for chemical analysis. I wanted to find out the chemical composition of those particles. Her nasal septum, the cartilage that divides the nose into two nostrils, showed a perforation. I immediately realized how she must have died. I called the investigating officer, and told him that Ganesh hadn't killed Geeta. I told him that I knew how she had died, and asked him not to torture Ganesh any more and release him at once. 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 Ganesh has nothing to do with this death? How can you tell the cause of death in this case?" "Well, experience my boy, experience!", I said in smug confidence, and then wrote out a cause of death, on a rough sheet of paper, and asked him to keep it in his pocket. Of course the subsequent autopsy conducted by me proved that I was right. The cause of death given by me after conducting an autopsy was the same as I had given the police officer on the rough sheet of paper immediately after seeing the body. The readers may be surprised as to what magic I had done to find out the cause of death so quickly. Well, before going any further, let me tell you a little bit about a dangerous narcotic drug cocaine . The youth of today is in the grips of narcotic drugs. Many narcotic drugs are in use, main among them being heroin, LSD, amphetamines, barbiturates, cocaine and several others. Heroin is the narcotic drug of choice today, but now many users are shifting to cocaine, especially in America. Its use in India is also increasing. The use of cocaine has permeated into the powerful and socially prominent circles. It is used by the youth of rich families. Of all the drugs cocaine is considered the largest producer of illicit income in the United States today. Cocaine is a white, crystalline powder derived from the leaves of coca plant (known botanically as Erythroxylon coca ). The coca plant is native to South America, particularly the countries of Peru, Bolivia, Brazil, Chile and Colombia, and must not be confused with the similar‑sounding coca plant from which chocolate is made. The scientific name of the plant is derived from the Greek word erythros meaning `red', and xylon meaning `wood'. The name is based on the flesh‑red colour of the inner layers of the bark. The wood itself is tinged with red or yellow. Although the coca plant is natural to South America, it has been successfully cultivated in Java, West Indies, Australia and India . It's not that cocaine use has become popular in modern times only. It has been in use for a long time. Recent archaeological findings in Ecuador indicate that the use of cocaine dates back to at least 5,000 years. Small bags of coca leaves have been found in the graves of the Incas, mysterious South American people, who lived in the Cuzco Valley of the Andes mountains on the west coast of South America. This area roughly constitutes the modern‑day Peru. Cocaine which is used these days is usually available in adulterated form only. During its "journey" from the clandestine lab where it is prepared to the addict, it is adulterated a number of times, a practice often known as cutting . Every dealer who gets hold of the cocaine powder mixes some adulterant powder in it. The cutting or diluting agents can be any soluble powder that is not disruptive to the body such as baking soda, powdered sugar, powdered milk, starch, etc. Since pure cocaine is also a white crystalline powder, these agents can not easily be detected and serve as good dilutants. Other agents which are usually employed to cut cocaine are lactose, dextrose, Epsom salts (magnesium sulphate), quinine or powdered vitamins. A dangerous narcotic, methamphetamine, known as speed , is also sometimes used. Cocaine use is a very expensive habit and because of the expense, cocaine habit is often referred to as the king's habit . Cocaine has traditionally been popular with pimps, prostitutes, musicians, jet‑setters and the wealthy. It can be taken by the addict in a number of ways, but the most commonly employed method is by inhalation (known as snorting or horning ). In snorting cocaine, the immediate euphoric effect (known as the rush ) takes place within about thirty minutes. The usual time period for euphoric effects are generally in the same range when cocaine is injected directly into a vein. When cocaine is taken by mouth, the effects begin after five minutes and the rush is not as great as when cocaine is injected or snorted . That is why oral intake of cocaine, or cocaine eating , as it is often known, is not a preferred method among the addicts. There is a little compensation however. The euphoric effect after an oral intake lasts about fifteen to thirty minutes longer. The rush is most intense when cocaine is injected. Snorting produces a slightly lesser effect, yet the effect is not so minor as to make injection a preferred method. In snorting cocaine, the user brings the powdered cocaine up to one nostril, holding the other nostril closed and sniff the cocaine into the nose. The user may use any nostril but usually holds the other nostril closed for better suction. The immediate effect of snorting cocaine is a burning or freezing of the nostril area, depending on the purity of the cocaine and the substance the cocaine has been adulterated with . If it has been "cut" with procaine, there will be more of a freezing. The user may snort anywhere from one‑tenth of a gramme to half of a gramme at one time. Sometimes little particles of cocaine can get lodged in hair of the nose, and if they remain there for any length of time, they tend to irritate the membrane and cause sores and bleeding. Because of this irritation, chronic cocaine addicts usually have a perforated nasal septum. This is what I found in Geeta's dead body, and that is why I took no time in concluding that she had died of cocaine poisoning. Geeta was actually a cocaine addict . She had to buy cocaine regularly from the underworld of drug dealers. This was the reason she was pestering her parents for increasing her allowance. Usually for snorting, the users simply put the cocaine powder on a paper or a knife blade, hold it up to the nose, close one nostril and snort. Some users, however, adopt a very elaborate ritual. For instance they use a coke spoon, purchased from head shops (illegal shops selling drugs and drug paraphernalia), which is a highly ornamental tiny spoon, to hold about 50 mg of cocaine powder. The spoon, containing the cocaine, is brought up to the nostril and then the cocaine snorted. One can often identify a cocaine addict by seeing this spoon, which is often attached to a chain and worn round the neck. Some coke spoons have two small bowls so that the cocaine can be snorted into both nostrils at the same time. This was the key like thing which I found around Geeta's body, and which had been ignored by the police as an ordinary medallion. It was actually the spoon used by her for snorting. In fact, this spoon is so characteristic of cocaine users, that just its presence was enough for me to say that Geeta was a cocaine addict. Some addicts inject the cocaine directly into the veins or just beneath the skin. Injecting cocaine beneath the skin is commonly known as skin popping . It can cause ulcers, which often look like maps of various countries. Because of their fancied resemblance to maps, these ulcers are also known as geographical ulcers . I found these ulcers also on Geeta's dead body. Obviously Geeta was not only snorting cocaine, but injecting it too. Because of this practice, there were ulcers all over her body. These were the so-called wounds which the police was suspecting as indicative of homicide. She was probably going to the park to have her regular dose of cocaine. On the day of her death, she went to the park, and chose a lonely corner for her regular dose. First of all she snorted cocaine for some time. This was responsible for the white cocaine particles sticking to her nasal hair. Then she perhaps decided that she should inject cocaine for more intense feeling. During the procedure, she accidentally injected an overdose of cocaine. That is how she had died. It was an accidental death due to overdose of cocaine. No one had murdered her. Chemical analysis of her body organs revealed lethal doses of cocaine. Analysis of the white powder particles sticking to her nasal hair also turned out to be cocaine! When the police told Geeta's already depressed parents that she was a cocaine addict, they couldn't believe their ears. They realized that they should not have been giving such a heavy pocket money to her. Well, this is a warning to all parents to see what their children have been doing with their pocket money. It is not surprising if the large pocket money they are demanding is for the purposes of narcotism only. When the police released Ganesh, he came and fell on my legs. He said that his life had been saved because of me only. The poor boy 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 )

Forensic Science Fiction A tale of detection The man had been dead for five days! At least that is what the forensic pathologist Dr. Chandra would have everyone believe. The body was in an advanced state of putrefaction and there were maggots over the body. Every pathologist knows that flies lay eggs in and around natural orifices of the dead body a little after about 3 days and maggots hatch in another two days. So if a body is found full of maggots, it must be dead five days before. All evidence pointed towards Papi Singh as the killer. He and Bachan Singh, the dead man had been sworn enemies. They both ran rival gambling dens and when two months back Bachan Singh spat over Papi Singh after a drunken brawl, Papi Singh had sworn to get even with him. Everybody knew about that. The body of Bachan Singh was found of the night of 27th May. That put the time of death round about the night of 22nd May. Throughout the proceedings Papi Singh kept asserting he hadn't killed Bachan Singh. Some of his cronies swore they had seen Bachan Singh roaming around on the night of 23rd May with a lady of ill repute but nobody believed them. In fact nobody could think of suspecting Dr. Chandra's judgement. But the defence lawyer Basu was a shrewd man. He was a man of multiple interests and had his fingers in several pies. He studied the autopsy report in great detail and found that the main reason for Dr Chandra's judgement was the presence of maggots on the body. All the putrefactive changes plus the maggots put the time of death as five days, but the same changes minus the maggots put the time of death as merely three days and put the date of death as the night of 24th May. That suited his client Papi Singh, as he had left for Chandigarh on 24th morning by train making his alibi watertight. Everybody knew about it, and furthermore he had the train tickets to prove that. Papi Singh even had some minor scuffle with the guard of the train, and the guard remembered it. Even he could be called as a witness to say that Papi Singh had indeed made the journey to Chandigarh on the morning of 24th May. This was as good an alibi as could possibly be. In essence, Papi Singh could be saved from the gallows, if it could somehow be proved that Bachan Singh had died just 3 days before and not 5 days before as Dr. Chandra had indicated in his post-mortem report. But from where did the maggots emerge? That was the sixty-four thousand dollar question. The answer began emerging in Basu's mind a few days later. While reading the latest issue of the American Journal of Ornithology he read with interest the report of an Indian ornithologist who had reported finding a new species in India called Passeriformes peculiaris. The females of the species ate small seeds while the males ate eggs of insects. This in itself was not a very startling or amazing finding as the same situation is prevalent in many known species. Male anopheles for instance sucks flower juice while the female anopheles sucks blood. The real amazing find was that if by mistake the female bird swallowed the insect eggs which look very much like the seeds it ate, it would not be able to digest them. It would be able to keep the eggs in its gizzard as long as they did not hatch. But once the maggots hatched, they would start irritating the gizzard, and the bird would be forced to disgorge the maggots immediately. Still more surprisingly, the bird would search for decaying flesh, so that it could get nauseated strong enough and be able to evacuate its gizzard as completely as possible. The female of the species seemed to have a kind of aversion for these maggots, so to say. What Basu decided was this. Bachan Singh was killed on 24th night by someone else, and his body thrown away in the open. As the species Passeriformes peculiaris was rather abundant in the region where the body was found, some birds, which had earlier ingested the insect eggs accidentally, disgorged some of the maggots on the decaying flesh. In other words flies never laid eggs on the corpse. Quite simply, the body had not been dead long enough for that to happen. Maggots were directly disgorged upon it by the female Passeriformes peculiaris, and that put the time of death as just 3 days. Maggots were in fact only artifacts. But in the court everybody laughed at this outlandish conjecture. New reports had to be taken with a pinch of salt, they said. However the defence kept harping on the authenticity and reputation of the journal. Finally the judge appointed a committee of ornithologists, entomologists and forensic experts to look into the issue and give its report. The main task of course was to look into whether such a bird really disgorges maggots on decaying flesh or not. And when finally the report came after a month, it acquitted Papi Singh. It said laconically, "The girly bird retches the worm!" *** This story was published in Published in Spandan (Maulana Azad Medical College's Magazine) 1990-91 on Page 8

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 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 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 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!"

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE FEBRUARY 2000 ISSUE THE POISON SLEUTHS DEATH BY GOLD -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of an old lady today. She appears to have a gray pigmentation all over her body. What happened to her? Please tell me.” “Good morning Tarun. The name of this 58 old lady is Rita, and she belongs to a very rich family. She married a relatively young, smart and ambitious doctor about a year back, after the death of her first husband. She was a chronic patient of rheumatoid arthritis - a disease mainly affecting women, in which there is intense pain in the joints- and was constantly taking medications for it. For some days however, she was complaining of vague symptoms, like stomach upsets, sore throat and tongue, a general lassitude and so on. Her own husband -the second one - was a doctor. He was treating her by his own medicines, but when things went out of his hands, he took her to the hospital. The senior doctors at the hospital also couldn't diagnose anything specific, and were treating her along general lines. Today morning her husband reported to the hospital that Rita was dead, and could they please issue a death certificate. That is how the case came to me." "But you only deal with police cases doctor, and this doesn't seem like a police case to me at all. After all, she was an old lady and was suffering from a disease for which she was taking medications too. The doctors should have issued her a death certificate and that would have been an end of it. Why at all has she been brought to you for a post-mortem examination?" "Tarun, this lady is worth about 65 crores of Rupees, and her husband Satyanand stands to inherit all that money. Some cousin of Rita has alleged that Rita has not died a natural death as is alleged by Satyanand, but in fact he has killed her by some poison. He has approached the police too, and lodged an FIR to this effect also. That is why her body has come to me. Naturally, like every other time, I have to tell the police, if she died of a natural death, or if some poison was used to finish her off." "Oh, I see. So what do you think of this case doctor?" "Tarun, I have taken a detailed history from that cousin of her, from the neighbors and from the doctors at the hospital who treated her. Two or three things have been bothering me quite a lot. Firstly the grayish pigmentation over her body, about which even you commented when you entered this post-mortem room. Secondly that almost all mucus membranes of her body are inflamed. She has an inflammation of her food pipe, wind pipe, her tongue, and even her vagina is inflamed. At her age, I wouldn't expect her vagina to be so inflamed. Moreover she appears to have a strange skin disease. I have examined her skin closely under the microscope and found that she is suffering from a special skin disease known as Lichen planus." "What does this all point to doctor?" "Tarun, to me, it seems to be a case of one and only one poison. A very unlikely one for you - one which would undoubtedly baffle you - gold!" "What? Gold? You must be joking doctor. Never heard of gold being used a poison." "Death by gold is surely a very very unlikely phenomenon. Nevertheless, it is possible. We must not forget that Rita was suffering from Rheumatoid arthritis, and one of the medications for it is gold. So gold salts were available in her house, and they could jolly well be used to kill her. We must also not forget that her husband was a young and ambitious doctor, and he surely knew that gold salts can be toxic in high doses.' "Doctor, I feel, we are again on the trails of one of your great poison cases. Can we start the tale of gold from the beginning please? Please tell me about gold in some detail, so I could follow your conversation better." "First, a few basic facts about gold. Known since antiquity, gold is a soft, malleable, lustrous yellow metal that steadfastly resists corrosion. Its atomic weight is 197 and it is a member of Group 1B in the periodic table of elements. Metallic gold is one of the least active metals chemically. It does not oxidise or burn in air even when heated and it is inert to strong alkalis and virtually all acids, except to selenic acid and to aqua regia, which as you know is a mixture of Concentrated nitric and hydrochloric acid." "Doctor you were telling me, that Rita was taking gold salts for her ailment. So that means that gold is useful as a medicine too?" "Sure. Gold, in elemental form, has been employed for centuries to relieve the itching palm. The real interest in gold as a medicine started when in 1890 the great bacteriologist Robert Koch told an international congress in Berlin that gold-cyanide complexes were most effective of all known antiseptics against tuberculosis bacteria, at least when tested in the test tube at high dilution. Unfortunately animals having tuberculosis could not be treated with these complexes. This dampened everybody's interest in gold compounds. In 1924, a Danish veterinarian demonstrated that gold sodium thiosulphate (known as Sanochrysine when sold in the form of a drug) had a beneficial effect in tuberculosis of the cow. Physicians tried the same compound in humans, but no success could be achieved. In those times, arthritis (pain in the joints) was wrongly thought by some to be a tuberculous manifestation. Under this impression Lande in Germany administered aurothioglucose (Solganal, a gold compound prepared by the Schering Corporation), to thirty-nine patients suffering from a variety of complaints. Many of these patients had joint pains due to rheumatic fever, and most of these patients reported relief of joint pain. Lande concluded that a full-fledged trial of the drug in arthritis would be worthwhile. Four years later in 1929, Jacques Forestier in Paris began to use another gold compound, gold-thiopropanol sodium sulphonate (Allochrysine) in rheumatoid arthritis. His observations were favorable, and it were mainly these observations which were largely responsible for the popularity of use of gold compounds in medicine. Therapy with gold compounds now even has a name; it is called chrysotherapy. Gradually the use of gold preparations in arthritic conditions began to spread, but it was not until 1944 that the results of a properly controlled clinical trial were first published by Fraser in Glasgow. He reported that clinical improvement occurred in 82% of 57 rheumatic patients who received intramuscular injections of sodium aurothiomalate (Myochrysin). Sodium aurothiomalate had been investigated in 1939, but only after the Glasgow trial was its value in therapeutics generally accepted. At present Gold is employed mainly in the treatment of rheumatoid arthritis. Its use is usually reserved for those patients with rapidly progressive disease who do not obtain satisfactory relief from therapy with aspirin-like drugs. Gold has however also been used in the treatment of several other diseases, but by and large, its use in other diseases is not very beneficial. Gold has also been used as a prosthetic. Because of its malleability and its anti-corrosive characteristics, gold has been employed as a prosthetic in dentistry and has been used widely as the predominant component of dental alloys containing silver, copper and small amounts of platinum and lead. These alloys can be heat treated to develop strengths as great as 150,000 psi (per square inch). Ophthalmologists have successfully implanted carefully balanced metallic gold weights into eyelids, as a surgical correction for patients who suffer from lagophthalmos. Before proceeding further, I may tell you that lagophthalmos is the technical name for the inability to voluntarily close an eyelid; the name comes from Greek lagos, meaning hare, because many people feel that in this disease, the eyes become rather like those of a hare! Gold has been recently used for delivery of genes inside the cells by genetic engineers. It has been seen that DNA can be absorbed to the surface of minute metallic gold particles and efficiently delivered by a controlled helium pulse to cells of the inferior epidermis. This is a painless maneuver, and results in notably efficient gene expression." "Oh, I see. It seems, gold is really a useful metal for doctors. Can you tell me which compounds of gold are most commonly used as medications?" "Sure Tarun. Mainly three compounds of gold are in clinical use. These are aurothioglucose, gold sodium thiomalate and auranofin. Aurothioglucose (SOLGANAL) and Gold sodium thiomalate (MYOCHRYSINE), both contain approximately 50% of gold by weight (For instance, gold sodium thiomalate is C4H3O4Na2SAu. Thus the molecular weight of the molecule comes to 390 of which 197 is gold, making it almost 50% by weight). Solganal is sold as a sterile suspension in a suitable fixed oil. Commercial preparations contain 50 mg/ml. Myochrysine is available as a sterile aqueous solution for injection. The usual dose is 10 mg of either of these compounds in the first week as a test dose, followed by 25 mg in the second and third weeks. Thereafter about 50 mg is administered at weekly intervals until the cumulative dose reaches 1 g (i.e. for about 20 weeks). A favorable response is generally not evident till after a few months. If neither significant toxicity, nor clinical response is visible, the dose is increased, but never more than 100 mg a week. Auranofin is available in India as GOLDAR, and RIDAURA. Both are available as 3 mg tablets, one tablet costing about Rs 12. The oral dose is 6 mg daily (i.e. about 42 mg a week) or one tablet two times a day, for a minimum of 3-6 months. As you can see in the accompanying formulae of these compounds, you will find that all significant medicinal preparations of gold are those in which the atom of gold is attached to an atom of sulphur. Nobody knows how gold salts work as medicines. But two facts are known about gold; one that monovalent gold has a strong affinity for sulphur and two that they have inhibitory effects on various enzymes of the body. This has led theoreticians to speculate that the therapeutic effects of gold salts might derive from inhibition of sulfhydryl systems which are present in the body. I may tell you that sulphydryl enzymes of the body have sulphur as their main component. However, other sulfhydryl inhibitors do not appear to have therapeutic actions in common with gold." "Doctor, is gold a component of normal human body also?" "Very little. An average human being has just about 2.45 mg of gold in his body. This however leads us to an interesting fact. Considering that the total population of the earth is about 6 billion at present, it follows, that the total gold contained in all human bodies is about 20 metric tons!" "Oh, that is really an amazing fact. Doctor, when a patient takes gold salts for his ailment, where does it go? Does it go to joints?" "Tarun, gold does go to the affected joints where its concentration is about ten times that in muscle, bone or fat. When one takes 50 mg of gold, about half of it disappears from the body in about 7 days. Technically doctors like to put this fact by saying that the half-life of gold is about 7 days for a 50-mg dose. You must however not confuse this half life with that used in radioactivity. But when a patient goes on taking successive doses, the half life lengthens, and values of weeks and months may be observed after prolonged therapy. After a cumulative dose of 1 g of gold, about 60% of the amount administered is retained in the body. In normal adults, minute amounts of gold can be detected in the hair, nails and skin. Using Neutron Activation Analysis (NAA), values ranging from 0-1.1 micrograms per gram of dry tissue weight, with a mean of 0.35 micrograms per gram (i.e. 0.35 ppm) have been reported. Following a course of gold therapy for 12 months, an increase of about 2-5 fold in these values occurs. After termination of treatment, urinary excretion of gold can be detected for as long as a year, even though concentrations in blood fall to the normal trace amounts in about 40 to 80 days. Substantial quantities of gold have been found in the liver and skin of patients many years after the cessation of therapy. Large amounts of gold salts, or their metabolic by products are commonly contained within phagolysosomes called aurosomes. The excretion of gold is 60 to 90% renal and 10 to 40% fecal, the latter mostly by biliary secretion. "Doctor, now I feel, I know enough about gold compounds used as medications. Now tell me what are their adverse effects, and how can they be used as poisons." "Tarun, with gold therapy, skin and mucus membranes are affected most, and occur in about 15% of all patients. Skin reactions may vary from simple redness to severe inflammation. The minimum cumulative dose of gold salts that has been associated with skin reactions is 250 mg. Dermatitis is so common that, out of all reported adverse reactions to gold therapy, almost 66% constitute diverse forms of dermatitis. Lesions of mucus membranes include stomatitis, pharyngitis, tracheitis, gastritis, colitis, glossitis and vaginitis, as we have seen in Rita's case. As with silver, a gray-to-blue pigmentation (Chrysiasis) may occur in skin and mucus membranes, especially in areas exposed to light. This pigmentation is due to the excessive collection of aurosomes in the skin cells. We have seen this too in her case. In 5-8% of patients, the kidneys may be affected to some extent. Kidneys may begin to pass proteins and even blood in about 1-3% of cases. Gold may also cause severe blood disorders, inflammation of the brain and peripheral neuritis, and of the liver. The usual fatal dose of gold is 50-500 mg/kg of the body weight. This means that for a person weighing 50 kg, which was Rita's weight, a dose of gold, as little as 2500 mg is sufficient to kill. We have seen that the Commercial preparations of Aurothioglucose (SOLGANAL) contain 50 mg/ml. This means that an injection of about 50 ml of this drug was sufficient to kill her. Before proceeding further, I must tell you the contraindications of gold therapy. Contraindications of a therapy means those conditions, in which that particular therapy should not be performed, otherwise it could prove dangerous. Gold therapy is contraindicated in patients with kidney, liver and blood diseases. Patients who have recently received radiation (as those suffering from cancers) should also not receive gold. Gold is also poorly tolerated by aged individuals, and should thus be given to them with care. I have examined Rita's body, and have found that she was suffering from kidney ailments. Thus gold should not have been administered to her in the first place. Obviously this fact was known to Satyanand. She was an old patient too, in which case too, gold should not have been given to her. Now I think I know what happened. Satyanand was administering gold to her unsuspecting wife for quite some time, under the pretext that he was giving her medicines. Rita had no reason of suspecting him. Even if she had consulted some other doctor, he would have told her that he was giving her the right drug. That was precisely his plan. He knew that nobody would suspect him of administering her a poison, as gold is commonly used as a drug in rheumatoid arthritis, which was exactly what Rita was suffering from. But he was administering gold to her in very high quantities. Rita did get some symptoms of gold poisoning, and to show to everyone, that he was really concerned about her, he took her to various hospitals fully convinced that the doctors wouldn't be able to diagnose gold poisoning in her case, because it is so rare. And he was right! Then yesterday night, or probably early in the morning today, he gave her a heavy dose of gold by injection - may be about 40-50 ml-, thus giving a final blow to her. I have examined her liver, spleen and lymph nodes chemically and have found heavy doses of gold in those organs. Satyanand would have tough time explaining how such large doses of gold reached her organs. I also examined Rita's hip area where Satyanand gave her the last injection, and the muscle beneath is loaded with gold. This also is a point against him. Satyanand had probably used gold in the belief that nobody would ever be able to catch him, as this is a poison, so rarely used. But the typical hue of Rita's body, and her other body findings gave him away. Come, let us tell the police that Rita did not die a natural death. It was Satyanand, who administered her gold to kill her." "Unbelievable! 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 - Radon."

Forensic Science Fiction

Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JUNE 1997 ISSUE THE POISON SLEUTHS POISONING BY SILVER -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? Oh well, today you are examining an old man. What happened to him? His body appears to be grayish blue all over. Please explain" "Good morning Tarun. The name of this person is Pyarelal, and he is 65 years old. He can not do much work now, and is mainly dependent on his son and daughter-in-law for his day-to-day needs. He however has a good bank balance which represents his life long savings. During his life time he had worked in relatively respectable positions." "So why is he with you today?" "Tarun, this makes an interesting story. He was quite unwanted by his son and daughter-in-law. His son is working in a private firm as an executive and his daughter-in-law is a chemist. For a few days he has discovered a grayish blue discoloration of his body, especially over the exposed parts of his body, and he contacted a local physician for this. He also complained of some tiredness, but besides this, he was alright. The local physician could not make much of his problem, so referred him to a specialist, and in turn this specialist referred this case to me." "But you are a forensic medicine man. As far as I know, you deal with criminal cases only. How can you be helpful in this case?" "You are right Tarun. I am a specialist in forensic medicine, and these specialists look at cases-live or dead- which are involved legally in some way. Well it goes like this. This specialist friend of mine thought that somebody might be trying to poison him slowly, and he consulted me on phone. When I had a look at this man, I thought he may be right. I enquired about his family life from Pyarelal and after talking to him for sometime, I became all the more convinced that it could indeed be a case of poisoning....." "Do you mean to say that a man who develops bluish gray discoloration of his skin is getting slowly poisoned?" "Not necessarily. There are other causes for this too, but my specialist friend had exhausted all those causes by various tests. Now only one possibility remained; slow poisoning by silver, a condition technically known as argyria, and that's why he referred this case to me. As you know, all cases of poisonings have some legality involved, so they are dealt with by forensic specialists. Before you start feeling uncomfortable with the word argyria, I must tell you that it comes from the Latin word for silver argentum. The chemical symbol Ag for silver has also come from the same Latin word. This condition was first described in 1816 by Johann Abraham Albers." "So you decided Pyarelal was being poisoned. But by whom? and how?" "Probably by his son or his daughter-in-law on whom he was a burden. They had an eye over his money too. Probably some silver salt was being mixed in his food. This rare and exotic poison was probably chosen because it is a relatively unknown poison, and it was probably thought by the culprits that doctors would find it impossible to detect it. But as you can see in a moment they had underestimated the capabilities of modern poison sleuths, who have an impressive array of facilities at their disposal. I asked him not to consume one day's food given to him by his daughter-in-law and instead submit it to me. He has done that today and I have submitted it to the lab for chemical analysis. While the test reports are awaited, let me tell you something about this rare but interesting poison." "Oh, sure I would love to know about it. In fact I didn't even know silver was a poison" "Well, in metallic form, it indeed is not. It is the chemical salts which are poisonous. Compounds of silver important from a toxicological standpoint are silver nitrate, silver lactate, silver picrate, silver acetate and the silver halides. Silver nitrate is a poisonous salt, also known as Lunar Caustic. Silver was likened to the moon by the ancient chemists on account of the latter's silvery color, hence the word Lunar. You would probably recall that Latin luna means moon. This term appears in the term "lunar month" which refers to the period during which the moon waxes and wanes completely once. This period as you know is equal to 28 days. This term also appears quite surprisingly in the word "lunatic". It is because ancient people thought that madness results from the effects of full moon. Even today, an excessively sentimental, dazed or a lunatic person is sometimes referred to as moonstruck." "Interesting! And what is the origin of the term caustic?" "The term caustic refers to the salt's caustic properties both as crystals and in aqueous solution. Silver has both medicinal and non-medicinal uses. Among the main non-medicinal uses are in jewelry, coins, silverware, tableware, and in manufacturing of mirrors and electrical wiring. You will probably recall that pure silver has the highest thermal and electrical conductivity of all metals. That is the basis for its use in electrical wiring." "Yes, I do. And what are its main medicinal uses?" "Tarun, silver and its salts have been used as medicines for various ailments throughout history. During the nineteenth century it was prescribed for the treatment of digestive disorders, including stomach ulcer. Later small sticks of compressed crystals of silver nitrate began to be used for cauterization, notably of throat lesions, because of its astringent properties...." "Excuse me doctor. You have used certain terms which I don't quite understand. What is cauterization and what is meant by the term astringent?" "Tarun, an astringent is a drug which precipitates proteins and causes contraction of tissues. The term comes from Latin astringere which means "to draw tight". Astringents have so little penetrability that only surface of cells is affected. Application of astringent often arrests secretions or discharge, so it is often applied to lesions which are discharging secretions. Precipitation of proteins also kills the cells. The idea of applying these drugs was also that it would kill any infective microorganisms lurking in the lesions, by precipitating proteins in their cells. The most popular astringents are salts of zinc and aluminum. Zinc sulfate (0.25%) is often recommended as an eye medication. Another common astringent is tannic acid. Cauterization is the destruction of tissues by the application of an astringent. Of course cauterization can be done by heat too. Warts can be cauterized by heat or by some astringent substance. There was a time when silver salts were popularly used for cauterization of warts." "Oh, I see. Are these salts still used today for cauterization?" "Not usually. This procedure carried a substantial risk of the silver nitrate stick getting broken and the patient swallowing -or worse- inhaling the detached fragment. Certain quacks in India still keep these sticks for such purposes. These sticks have been known to be used for the cauterization of infected umbilical stumps and in the treatment of nosebleeds too. They have been used in the treatment of warts as I told you earlier. Ayurvedic doctors are known to use Bhasmas (roughly equivalent to ashes) which contain various noble metals, of which silver may be one. Indian sweetmeat manufacturers often decorate sweetmeats with a paper thin sheet of silver, and consumers are known to consume sweetmeats along with it, but I am not aware of silver poisoning occurring by this means. Several other typical Indian preparations such as paan are also decorated in this way." "Does silver nitrate have other medicinal uses too?" "It is used as prophylaxis for ophthalmia neonatorum, which is an infective condition of the eyes in the newborn because of the gonorrhoea bacterium. Infants suffer from this condition when their mothers are known to be suffering from gonorrhoea. Silver nitrate is used in this condition, because of its known antiseptic effect against gonorrhoea bacteria. Dressings soaked in 0.5% silver nitrate have been extensively used in the treatment of burns. Topical use of silver nitrate in this way can produce poisoning although it is not common. Poisoning due to silver iodide nose drops has been reported. Silver is also used in dentistry for dental fillings. Silver salts, because of their germicidal properties, are also used as drinking water disinfectants. Such treated water may contain upto 50 mg/L of silver. Drinking water not treated with silver, usually contains extremely low concentrations of silver -up to 5 mg/L only." "So silver is used for disinfecting water too. I didn't know that. I thought only chlorine is used for disinfecting water." "Oh yes, silver indeed is used for disinfecting water. These days some companies are even marketing gadgets called "mobile electronic water purifiers" which work by generating silver ions. These are shaped like pens. The device is to be opened and dipped in water. In fact it has two silver electrodes and while in water, it is supposed to generate silver ions which in turn are supposed to kill microorganisms lurking in water. But as you know now, such disinfected water has more than the normal quantity of silver in it." "Can one ingest silver accidentally too" "Tarun, silver can be ingested accidentally in a most unexpected manner. To understand how it is possible, first of all I must tell you that sea water is known to contain silver in concentrations of 0.055-1.5 mg/L. Much higher concentrations have been reported in waste water effluents. For instance effluents entering southern California coastal basins have been known to contain silver in concentrations as high as 0.03 mg/L! Note that I am talking of milligrams here, not micrograms. Silver has been accumulated in concentrations of 14-20 mg/kg in bottom sediments in these areas. Molluscs ingesting this water accumulate seawater in their bodies. Molluscs collected from coastal areas of the North Sea have been reported to contain silver concentrations of up to 2.0 mg/kg. Ingestion of these molluscs as well as other marine food can thus lead to chronic silver poisoning!" "Oh, that certainly is most unusual!" "Exposure to silver can occur in other unusual ways too. For instance it can also occur from small amounts released from dental fillings and from eating out of utensils made of silver. Human activity has been known to increase silver concentration in the air. You perhaps know that a silver salt -silver iodide- is sometimes used to seed clouds precipitate rain artificially. The emission of silver iodide crystals during cloud seeding has been estimated to result in silver concentration in air of about 0.1 ng/m3. Silver concentrations in rainwater as a result of this process have been estimated to be between 0.04 pg/ml and 5 ng/ml. I must tell you that ng stands for nanogram and pg for picograms. 1 nanogram (ng) is equal to 10-9 g and 1 picogram (pg) is equal to 10-12 g. There is some amount of silver in tobacco too, but this is generally too low. Because of its high boiling point, most of the silver in cigarettes is not inhaled." "This is quite interesting information about silver. But what happens to silver once it enters inside the body? I know this is not a normal constituent of the body, nor can the body make any use of it. Then how does it handle silver?" "That's a good question Tarun. In humans, more than 50% of the body burden of silver goes in the liver. Elimination is mainly via faeces. The concentrations of silver in kidneys, liver and spleen of normal people have been reported to be about 0.4, 0.7 and 2.7 mg/kg respectively on a dry weight basis. This means that if these organs were dried into powder and then silver estimation done, one would get these figures. Normal concentrations in skin are 0.009 mg/g. This latter figure is on wet weight basis, i.e. estimation is done on the skin as such, without first converting it into dry powder. Daily excretion in urine is 0.006-0.015 mg/day and 0.02-0.11 in feces." "Doctor, how much silver is needed to kill a person?" "Tarun, fifty mg or more of collargol which is a silver salt has been reported to be lethal after intravenous injection for therapeutic purposes. Autopsy findings in such cases have included watery lungs, and destruction of bone marrow, liver and kidney. Silver nitrate has been used by quacks to induce criminal abortions. These are abortions done in a clandestine manner by quacks on girls who do not want a baby. Most of these girls are unmarried girls who contact these quack abortionists to get rid of unwanted pregnancies. They use all sorts of weird chemical compounds to get rid of these pregnancies. In a case which has been reported in medical literature, intrauterine administration of approximately 25 g of silver nitrate caused rapid death of the mother." "And what is argyria?" "The cases which I have mentioned above are cases of acute poisoning- cases in which silver is administered in one single big shot. Poisoning can occur in a chronic fashion, in which small doses of poison are administered slowly. In my earlier stories I told you about acute and chronic poisonings. Argyria is a chronic poisoning with silver. It is an interesting condition, which once seen is never forgotten. The patient- as in the case of Pyarelal- acquires a blue-grey color of the skin, especially over exposed areas. Silver bound to body proteins, is deposited widely in the body tissues. Internal body viscera may get discolored too. Pigmentation results partly from stimulation of melanin deposition but mainly from photoactivated reduction to metallic silver in the dermis- hence the distribution over areas exposed to light. It is like exposure of a photographic plate. The whole body -which has absorbed silver- becomes a kind of photographic plate which blackens on exposure to the sun." "Can you prove this in the case of Pyarelal?" "Yes certainly. In cases of argyrosis, microscopically detectable silver containing granules are found in the skin cells and particularly around the hair follicles and in the sebaceous and sweat glands. I have taken a skin sample from his neck area and have done electron microscopy on it. The dermis of this area showed irregular silver granules both inside as well as outside the skin cells. I also did a special investigation - neutron activation analysis. This technique can tell the exact amount of a chemical in a given sample. This technique showed that the silver concentration in his skin was 72 mg/g, far exceeding the normal 0.009 mg/g. You can plainly see that it represents an accumulation 8000 times normal. His total body content of silver is almost 8 g which is really quite high. In addition he shows a black colored line near the teeth, which is because of the deposition of silver there. It is called the silver line. I must tell you that although silver shines as a metal, in a colloidal state it appears black. That's the reason a photographic negative receiving more light becomes black. It is at these regions that silver halides are converted to colloidal silver by sunlight." "That certainly is quite interesting. If silver is administered slowly to a person, how much silver needs to be introduced before the person suffers from argyria?" "Tarun, it has been estimated that a total dose of about 1-8 g of silver is required by inhalation for argyrosis to occur. The dosage by ingestion seems a little higher; between 1 to 30 g of a soluble silver salt. Blond people are considered more susceptible than others. The reason for this is unknown. Argyrosis seemed to have become only of historical interest, but it has recently reappeared, especially in the West. Respaton an anti-smoking lozenge, available in the West from retail chemists since 1974, contains silver acetate and ammonium chloride. Another similar anti-smoking lozenge is Tabmint. Manufacturers of these lozenges claim that regular sucking of these lozenges can reduce one's desire to smoke. They recommend a maximum of 6 lozenges per day. Chronic use of these lozenges has caused argyria in several cases. The patient remains discolored for life and ironically the smoking habit for which he took all the trouble remains!" "That is certainly most interesting. Can argyria occur in other ways too?" "Tarun, repeated occupational handling of silver objects, especially if repeated minor injury is involved, may give rise to so called local argyria, which is bluish-gray discoloration of the skin at the exposed site. This condition is however considered harmless apart from aesthetic considerations." "So it is now almost certain that Pyarelal was being given some silver salt in low concentrations by his son and daughter-in-law." "Yes it is. Here comes the chemical analysis report of the food and milk submitted by Pyarelal. Oh it shows a rather high concentration of silver nitrate. So my worst fears have proved correct. His daughter-in-law was taking advantage of her position as a chemist and was regularly giving him silver nitrate in his milk and food- probably just a drop or two in his milk. But over the years this has caused silver poisoning in this poor fellow. We have all the evidence now. Let us go to the police and tell them the whole story." "Sure we should. And thank you doctor for telling me about such an interesting poison. What are you going to tell me next time?" "Tarun, next time I shall tell you about vanadium which as you shall see is a very important poison. "

Cookie Policy Anil Aggrawal’s Forensic Ecosystem Including Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology Last Updated: [June 20, 2025] 1. Introduction This Cookie Policy outlines how cookies and similar technologies are used on the website operated under Anil Aggrawal’s Forensic Ecosystem , which includes Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology . By continuing to use this site, you acknowledge your understanding of this policy. 2. What Are Cookies? Cookies are small text files stored on your device when you visit a website. They are widely used to ensure websites function efficiently and to provide usage analytics for improving content and user experience. 3. Types of Cookies We Use We use only essential and functional cookies , which are required for: Website security and stability Page load performance Session management (e.g., login and logout functionality) Spam prevention in submissions and forms These cookies do not collect personal information and are not used for advertising or tracking across sites . 4. Analytics and Anonymous Tracking We use Wix Analytics , a built-in service provided by our website platform, to collect limited, anonymized statistical data , including: Country of origin Visitor counts and session duration Pages viewed This information helps us understand overall site performance and user engagement. The data is aggregated and cannot identify you personally , unless you are logged in. This service is built into the Wix platform and cannot be disabled individually by us. If you wish to prevent any tracking, you may disable cookies directly through your browser settings. 5. Personal Data Collection via Forms We collect personal data through specific forms on the website for legitimate academic and functional purposes, such as: Paper submissions Store checkouts Guestbook comments Collected data may include: Full name Email address Phone number Submission content (e.g., academic papers) Use of Personal Data: Email addresses of authors may be published alongside accepted papers for academic contact purposes. Phone numbers are collected for internal verification only and are never published or shared externally . Submitted papers are shared only with authorized editorial or peer-review personnel and not disclosed to third parties . Users are informed of any data usage at the point of collection (i.e., on the form itself), in line with the principle of transparency under applicable privacy laws. 6. Login and Session Data Some sections of the website, such as the submission portal, comment areas, and store checkout, may require login. When you log in: Session information is stored for site functionality We may associate activity (such as page visits) with your session No behavioral tracking or profiling is conducted You may log out manually or clear your browser history and cookies to end your session. No data is sold, shared, or used for marketing. 7. Data Sharing and Third Parties We do not sell, rent, or share your personal data with advertisers, analytics firms, or other third parties.We do not display ads or embed third-party trackers. All analytics and session functionality are managed within the secure environment of the Wix platform. 8. Managing Cookies As we use only essential cookies and platform-level analytics, no opt-out functionality is provided within the site. However, you can manage cookies and tracking through your browser: Block all cookies Clear stored cookies Enable private browsing modes Please note that disabling cookies may impact the functionality of features such as login, submission, or checkout. 9. Contact Information For any questions or concerns regarding this Cookie Policy or your data, please contact us via the official email listed on our [ Contact Page ] or within the journal section of the website. We remain committed to protecting your privacy and providing a safe and secure academic environment.

Forensic Science Fiction The mystery of the assassinated prince When I got a telephone call from the Indian High Commission in Timbuktoo, I was relaxing in my bed with a cup of coffee and the morning newspaper. My wife was sitting besides me, and we were gossiping. Nothing irritates me more at such times than a telephone call. With some measure of irritation, I picked up the receiver. “Is it Dr. Aggrawal, Professor of Forensic Medicine at the Maulana Azad Medical College?”, a faint voice asked from the other side. “That’s right”, I replied. “Dr. Aggrawal, I am Abhinav Sinha, High Commissioner of the Indian High Commission in Timbuktoo. We are in a great problem. We have a doctor here, who is being falsely framed in a medical negligence case. I am convinced he is innocent. Could you please come and help us?” and without waiting for my reply, added, “Your tickets are being sent to your house, along with some money to take care of your travel expenses. All the hospitality here will be taken care of by us.” “Look.. .”, I protested, “I don’t know what your problem is, and I am really not sure I can help you in this case. Moreover I can’t possibly leave my college for any great length of time.” “Everything has been taken care of sir. Your trip is official. You will be treated as on duty. All expenses paid. Please come as soon as possible”, and he hung up. I was quite nonplussed, and I was almost sure, it was some practical joker trying to play a fast one on me. But within five minutes, I received a phone call from the Ministry repeating the same thing almost verbatim. Within half an hour, a government official came to my house with some travelers cheques and a club class return air ticket to Timbuktoo. There was an accompanying letter from someone higher up in the Ministry asking me to proceed to Timbuktoo immediately. It also said that I would be treated as on duty. There was no option now. The flight was at 9 pm. I looked at my watch. It was still 8 am. I had about 13 hours for preparations. I requested my wife to start packing. For those, who are not aware of Timbuktoo, it is a very tiny principality somewhere in the Middle of Africa - quite near Lake Victoria. It is a hereditary monarchy. Elections have never taken place here. Kings have been ruling this principality since time immemorial from the same family clan. Mostly the eldest son gets the chance to rule, but sometimes court intrigues result in murders, and the younger brother gets the throne. There have been cases, when a still younger brother has in turn killed his second brother and got the throne! In short, the history of this principality is rife with murders, court intrigues, treachery, debauchery and so on. Our country had no diplomatic relations with this country till sometime back, but recently in the wake on the so-called Non Aligned Movement, we had developed diplomatic relations with them. A small mission had been opened there, which was staffed by just six people. One of them was a young Indian doctor, whose main job was to look after the Indian officials and their families, as the medical fraternity in that principality was really in a very nascent stage. After a relatively comfortable nine hour flight, I landed at the King Hassan Airport in Timbuktoo. The High Commissioner of the mission was there personally to take me to my hotel. Along with him was the young doctor posted in the Mission. His name was Dr. Harish. While I was being driven to my hotel, I looked out of my window, and was amazed at the clean air and greenery all around in that tiny nation. Coming from New Delhi, it was certainly a very welcome change. The hotel was comfortable and clean. After I took bath and changed, the duo narrated their story to me, and it was something like this: Ndubuisi Eke was the king of this nation since about three years. He had a younger brother called Mombutu Eke, who wanted to usurp his throne. On 18 February 2001 - a Sunday - when Ndubuisi was taking his morning stroll, one unidentified man came from somewhere and stabbed him in the neck. The attack was so sudden that Ndubuisi’s two bodyguards couldn’t do anything. However there were rumors that they had been “bought” and did not try to stop the attacker on purpose. There was an immediate commotion all around, and in the mêlée that ensued, the attacker managed to slip away. Again people who had an ear to the ground said that this was also stage managed. The killer was someone hired by Ndubuisi’s younger brother Mombutu, who wanted to usurp his throne. As luck would have it, Ndubuisi did not die immediately thereafter. He did however receive a nasty gash in the neck. As the whole of Timbuktoo did not have a reasonably smart surgeon, he was brought to Dr. Harish in the Indian Embassy. To be sure, he too was young and rather inexperienced, but better than the best Timbuktooan doctor. Dr. Harish tried his best to save Ndubuisi, but he died immediately after arriving at the hospital. No autopsy was ever conducted on the body, and the body was cremated in haste. Mombutu Eke ascended the throne immediately thereafter. However the public - who loved Ndubuisi no end - was restless. In Mombutu, they saw a killer and usurper. There were hushed voices all around. And perhaps to silence his critics - and perhaps to clear him as well - Mombutu ordered an enquiry against Dr. Harish. It certainly was against diplomatic norms. But as far as Mombutu was concerned, it didn’t matter as his throne was in jeopardy. He wanted to show that the wound received by Ndubuisi was not fatal, and the death occurred instead because of Dr. Harish’s negligence. It was where I came into picture. I was to prove that Dr. Harish had tried his best. There was no negligence on his part and the death occurred prima facie because of the wound. But how could I do that? Had Ndubuisi’s body been with us, it would have been a relatively simple matter for me. All that I needed to do in that case was to conduct a thorough autopsy on his body to find out the correct cause of death. But the body had already been cremated in haste. Now all I had in my possession were some reports prepared by Dr. Harish, when Ndubuisi first arrived at the hospital. I interviewed Dr. Harish in great detail. He was young and inexperienced, but certainly a very bright doctor. Obviously he was terrified. He was being prosecuted in an alien land, and if found guilty, they could send him behind bars for a lengthy period of time. Something had to be done very fast. Fortunately Dr. Harish had prepared a very detailed injury report. I read the injury report over and over again, and found that the most significant part was that his left sternocleidomastoid had received a gash 6x2x4.5 cm in size. It was that wound which appeared fatal to me. But the volume of blood that Ndubuisi lost was not very much. Dr. Harish had immediately sutured the wound. At a rough guess, he had lost about 500 cc of blood. Now that is not sufficient to cause death by shock. One would require at least 2000 cc for that. Obviously Ndubuisi had died because of some other reason. But what? That was the million dollar question. I could not sleep that night. I kept thinking the whole night. And I do not know when I fell asleep. But soon I started dreaming. I saw Ndubuisi going down and down in deep water. He was struggling to stay at the surface. But something was taking him down and down. Bubbles of air were streaming through his nostrils. Bubbles of air.. .. I woke up with a start. It came to my mind in a flash. It had to be air embolism! Perhaps I was thinking about air embolism subconsciously. That is why I dreamed of those air bubbles, perhaps. For recapitulation, let me state what air embolism is. It was Rudolf Virchow, the famous 19th Century German pathologist who introduced the term embolus and embolism into modern medicine. In 1856 he applied the term embolus to a loose clot in the blood stream. These words are of Greek origin and come from the Greek word “emballe” meaning to throw in, or to lay in or to put in as a stopper, peg or bolt. A loose blood clot in the circulation indeed acts as a stopper or a peg. As long as it travels in vessels bigger than its size, it is alright, but as soon as it encounters a vessel smaller than its own size, it gets stuck there, acting as a stopper or a peg. Many of you would be surprised to know that embolism is used in a general sense too, meaning the adding or “throwing in” of an extra day to the year. In relation to medicine, we usually speak of embolism in relation to blood clots which travel from leg veins upwards and get lodged in pulmonary arteries. This is a serious condition causing almost instantaneous death. Under certain conditions - as when veins are cut - air can get sucked inside the veins. It forms a bubble inside and this bubble travels towards the heart along with the blood stream, and gets lodged in the pulmonary arteries just as a blood clot does. A bubble of air is incompressible, and there is no way the blood stream can negotiate this bubble. Inside the vein this bubble acts just like a blood clot. That is, it blocks the circulation just as effectively as does ordinary blood clots, causing immediate death. It is almost as if someone had put an arterial clamp over that place! Detecting ordinary blood clots in pulmonary arteries, or for that matter anywhere else in the body, is relatively easy, but detecting air embolism is a different game altogether. It remains one of the most challenging tasks faced by a forensic pathologist. The reason is that the moment you open pulmonary arteries, the bubble is going to disappear in the air. For this reason, forensic pathologists usually dissect the heart under water in suspected cases of air embolism, but believe me it is a very difficult and challenging procedure. Nobody loves it. There is a silver lining though. If you are suspecting air embolism in a case, before you start the autopsy, one of the best things you can do is to X-ray the body. If an air bubble is present in the heart or pulmonary arteries, it will show up in the X-rays. So you conduct this difficult procedure only in the cases in which you see the bubble in the X-rays, and leave out the rest. In fact, the X-ray plate itself is proof that the person died of air embolism and many forensic pathologists don’t take the trouble to dissect the heart under water after that. But we all know, no post mortem was ever conducted on Ndubuisi. Even if it had been conducted, I am doubtful, if anyone would have been able to detect the cause of death as air embolism, as there was no forensic pathologist in the whole of Timbuktoo. I was now in a very unenvious position. I did not have the dead body of Ndubuisi, and I had to prove that he had died of air embolism. That was the only way to save Dr. Harish. Only then we could prove conclusively that it was the initial stab wound which caused the death (by air embolism), and not negligence on the part of Dr. Harish. But how could I do it? That was the million dollar question. In the evening, I was sitting by the lakeside looking at the beautiful lake and the birds leisurely floating in it. I was recalling my younger days, when we had to send almost all bodies for X-rays, in which we suspected air embolism. Then for many months, our X-ray unit was out of order, and we had to start the autopsy without the benefit of the initial X-ray plates. This meant that effectively we had to open all hearts under water and nobody liked that. You have to make a sac in the pericardial cavity by making appropriate cuts in the pericardium; then you fill that pericardial sac up with water with an assistant holding up both the flaps of pericardium with forceps; and then finally you inserted the blade in the pulmonary artery and under various heart cavities, twisting and turning it expecting a bubble to rise through water. Not many forensic pathologists love this. And many complained. To solve the problem, I came up with an interesting formula. I had for long observed that more people tend to die of embolism if the cut was longer and deeper. Similarly if the muscle involved was more voluminous, chances of air embolism were higher than if the muscle were less voluminous. Thus if someone got a 5 cm cut in gluteus maximus, he would stand much greater chances of getting air embolism than if he got a cut of the same size in, say, temporalis muscle. It was because temporalis muscle is less massive than gluteus maximus. Could I turn this observation into a strict mathematical formula, I had asked myself at that time. And quite interestingly I did come up with an interesting formula. It was: E=mc² Now if you think you are already familiar with the formula, probably you are wrong. E in our formula stands for Embolism (rate of), m for muscle mass (in grams) and c was a somewhat complicated parameter, which I called the “Cut factor”. I had observed that air embolism tended to depend both on the length and the depth of the cut, but depth had a greater effect on producing air embolism than the length. Thus if the length of the cut was twice, the chances of air embolism in a person would be doubled, but if the depth was twice, the chances would be four times. To take this observation into account, I put the Cut factor equal to [(cut depth)2 x (cut length)]. The interesting thing about this formula was that this stands true across all animal species. Once this formula was in place, we applied it in some experimental animals too, namely rats, guinea pigs, hamsters and pigs. To my satisfaction the formula proved true in all cases. Now as you can see, this formula actually gives the rate of embolism. To put it in other words, it would give you the probability that the person might have suffered air embolism. What we did with this formula was to look at the muscle which was cut and the size of the cut, and put the numbers in the formula (we had to put the decimal back by four digits, i.e. we had to effectively divide the figure by 10,000 to arrive at the correct rate of probability). If we got a figure, say, 50, it effectively meant that the person had a 50% chance of getting air embolism. If we got a figure of, say, just 2, there was just a two percent chance of getting air embolism and the forensic pathologist could perhaps look the other way and forget about dissecting the heart under water. Gradually all forensic pathologists in our institution got round to opening the heart under water if the figure was greater than 50. This made sense too, because if the probability of getting an air embolism is greater than 50%, you must take enough trouble to find it out. For those, who are able to follow me only vaguely, I would illustrate with an example. Gluteus maximus’ weight on the average is 493 g. Now if it sustains a cut which is 5 cm long and 3 cm deep, what are the chances that the person would die of air embolism? We would calculate it as follows: The cut is 5 cm long and 3cm deep. Since the cut factor is equal to [(cut depth)² x (cut length)], simple mathematics would show that it would be 45. Now putting this figure in our earlier formula E=mc² We get 493 x 452 or 998325 We put four decimals behind and we get 99.8325. This means that a person getting a 5 cm long and a 3 cm deep cut would stand a 99.8325% chances of getting an air embolism. This is well near hundred percent, and I would certainly like to take all trouble to dissect the heart under water. Over the years this formula had gained International acceptance, and almost every forensic pathologist was using it in his day-to-day practice. Could I use this formula in Ndubuisi’s case? Then suddenly I remembered that Dr. Harish had been careful enough to record the dimensions of the cut quite accurately. I jumped and ran back to my hotel room. Once inside the hotel room I phoned Dr. Harish immediately and in a most excited voice asked him to give me the dimensions of the cut. He was a little surprised at my strange request but gave the figures to me. The dimensions were 6x2x4.5 cm. Now my only problem was to find out the weight of the sternocleidomastoid muscle. I am no anatomist and did not know its weight at all. But fortunately I have many good anatomists as friends. One of them is Dr. R.K.Suri, Professor of Anatomy at our own medical college. I immediately made an overseas call, forgetting the time difference completely. It was 2 am in India, and he picked up the phone with some measure of irritation. “Dr. Suri, what is the weight of Sternocleidomastoid muscle?” “Is it Dr. Aggrawal?” he asked in great irritation. “Never mind. The weight?” I insisted. “Why! it is 153 grams. But why do you ask this question in the thick of the night?” He was obviously quite nonplussed. “Thanks” I said, ignoring his question completely, banged the receiver back and got back to crunching numbers. The cut factor in this case would be 121.5 as the length of the wound was 6 cm and its depth 4.5 cm. Now putting all the figures in our good old formula E=mc², we get: 153x(121.5)2 =153 x 14762.25 or 2258624.25 Putting the decimal back by four points, we arrive at the figure 225.862425 I jumped on my feet in glee. The probability of getting air embolism was even greater than 100! To a mathematician it may look silly, but we had encountered such figures before. It meant that the person was sure to get air embolism. Everything was clear now. With such a deep cut on his Sternocleidomastoid muscle, Ndubuisi stood a 225% chance of getting air embolism. In other words, he died of air embolism. That was for sure. We immediately filed our answer in the Law Ministry of Timbuktoo. I am given to believe that the Ministry was going to dismiss that answer too, but before doing that they took the advice of some international forensic experts, and all of them advised that my reasoning was watertight and there was no scope of rebutting it. In fact if they did it, they would go down in the eyes of the International Community as an utterly unjust nation, and would stand the risk of getting completely isolated. Mombutu obviously did not want to take this risk. Dr. Harish was immediately cleared of all charges. I returned back to India, and the very next day went to Dr. Suri and thanked him for the help he rendered us. He was still very very angry with me, especially because I had banged the phone on him, but when he heard the great service he had rendered for our nation, he forgot all anger and is once again a very great friend of mine.

Anil Aggrawal's Internet Journal of Book Reviews Aims and Objectives This journal has been started by Dr Anil Aggrawal, Professor of Forensic Medicine at the Maulana Azad Medical College, New Delhi - 110002. Dr. Aggrawal is quite keen to interact with people who are interested in books. Dr. Aggrawal adores books and literally thrives on them. Though being a medical doctor specializing in forensic medicine, he loves books on all subjects encompassing such diverse ranges from astronomy and zoology to paleontology, history, occult science, philosophy, mathematics, and classical literature, et al. His penchant for books was conceived quite early in life. Even as a three year old he always pined for books instead of toys-as his siblings did. There is a legend about the Greek mathematician and engineer Archimedes (ca. 287 B.C. - ca. 212 B.C.). When Roman armies sacked Syracuse in 212 B.C. he was busy studying a geometrical figure made in sand. When a Roman soldier commanded him to come along, he motioned to him imperiously, "Don't disturb my circles". The soldier felt so insulted that he killed Archimedes on the spot! In a similar situation Dr. Aggrawal would probably say, "Don't disturb my books!" Writers and thinkers have always been his idols. Some of the people who have inspired him are (i)Lord Buddha (he remains first on his list) (ii)Albert Einstein (iii)Robert James Fischer (The only American who has been an official World Chess Champion) and (iv)Isaac Asimov (he wrote close to 500 books, and is reputed to be the only author to have published books in all ten categories of the Dewey Decimal System! Oh, well, we all know it's not true, but he has really written so widely, it seems cruel to challenge this statement.) Aggrawal is no Asimov, but like him, he loves writing books. He has written nine books so far (till 2006 end). Four of them are quiz books, which reflect his morbid passion for quizzes. The books, in order they were published are (i) 1000 Crime Quiz (published 30 March 1992) (ii)1000 Love & Sex Quiz (published 13 August 1992) (iii) Some Common Ailments (Published 27 January 1993)(iv)The Book of Medicine (Published 5 February 1994) (v)Narcotic Drugs (Published on 2 May 1995) (vi) 1000 Biology Quiz (Published on 29 August 1995) (vii)Modern Diagnostics (Published on 8 March 2001) (viii) Health Quiz Book (Published on 5 August 2002) (ix) Self Assessment and review of Forensic Medicine and Toxicology (the first book related to his profession). And since we all love statistics, here is a detailed statistics of these books. Here they are: Book Statistics Book 1000 Crime Quiz 1000 Love & Sex Quiz Some common Ailments The Book Of Medicine Narcotic Drugs 1000 Biology Quiz Modern diagnostics Health Quiz Book Self assessment and review of Forensic Medicine & Toxicology Started On 1.2.91 1.6.91 1.6.91 Nov 92 1.1.93 6.1.92 1995 Feb 2002 2005 Completed On 31.5.91 5.1.92 28.11.91 Jan 93 9.5.94 17..3.93 1995 July 2002 2006 Submitted On 31.5.91 7.1.92 28.11.91 15.1.93 9.5.94 19.3.93 1996 July 2002 April 2006 Published March 1992 Aug 1992 Jan 1993 Frb 1994 May 1995 Aug 1995 March 2001 Aug 2002 May 2006 Publisher Rupa Rupa NBT Rupa NBT Rupa NBT Ocean Books PeePee Cost 30 30 25 30 46 80 80 200 295 (Books published till 2007 end) N.B. 1. NBT stands for National Book Trust, India. 2. Dates mentioned are in this format: day/month/year. 3. The cost is in Indian Rupees. 4. Some Common Ailments has been translated in Assamiya, Bangla, Hindi, Kannada, Konkani, Marathi, Nepalese, Oriya, Punjabi, Telugu and Urdu (Total 12 languages). 5. Narcotic Drugs has been translated in Assamiya, Bangla, Hindi, Punjabi and Urdu (Total 6 languages). 6. Health Quiz Book has been translated in Hindi (Total 2 languages). Why is Dr. Aggrawal interested in writing book reviews? Whenever he reads a book he tries to discover its strong points. There is a subconscious effort on his part perhaps, to incorporate those points in his own writings. He then wants to share his findings with everyone. In the year 2000, he started an Internet Journal of Forensic Medicine and Toxicology, and out of his sheer interest in books, he included a book review section to it. The unprecedented popularity of the review section took him by complete surprise. He received books from authors and publishers in thousands. And they belonged to all subjects-not only forensic medicine and toxicology, which he had intended at the inception of the above journal. With time he and his group realized that they must conjure another journal devoted solely to Book Reviews for books of all genre. In this all-new journal they would accommodate all kinds of books, and hence the present Anil Aggrawal's Internet Journal of Book Reviews. Dr. Aggrawal fondly cites the examples of many regular journals (not devoted to book reviews), which have come out with issues especially devoted to book reviews. One pertinent example is Archives of Sexual Behavior, which came out with an issue (Volume 28, Number 5 / October, 1999, pages 377-467) especially devoted to book reviews in 1999. -Puneet Setia Journal Associate