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  • Volume 27 Number 2 ( July - December 2026) | Anil Aggrawal's Forensic Ecosystem

    < Back To Main Page. LinkedIn X (Twitter) Facebook Copy link Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Volume 27 Number 2 ( July - December 2026) Contents Papers Domestic Violence Leading to Pediatric Burns: A Clinical Forensic Case From East Java, Indonesia Ibnu Chaldun ¹ , Ahmad Yudianto ² , Putu Bagus Dharma Permana ³ Forensic Medicine and Medicolegal Specialist Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia Postgraduate Forensic Science Study Program, Faculty of Medicine, Universitas Airlangga, Surabaya Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia DOI: 10.5281/zenodo.15743408 Read

  • Forensic Science Fiction | Anil Aggrawal's Forensic Ecosystem

    Forensic Science Fiction The Freak I was surprised. Extremely surprised. Never before had a patient come to me with such a complaint. I asked him again. "Are you sure, you keep moving back and forth in time? Just how do you know?" Rajiv coughed nervously. "All of a sudden sometimes, I feel dizzy. Then I feel as if I am falling in ordinary three dimensions. In an abyss. Rapidly. But it's not the height I loose. I find I have gone back in time. I see all sorts of things. Mughal splendor. Coming of the English people. Freedom struggle. Everything." "Are you sure you are not hallucinating? I am asking this because people of your species can control movement in time you see." "Yes, we four-dimensionals are not like you. Sure enough we can control movements in time just as you can in space. But I just don't know what's the trouble with me. I just can't control it. Look at this ancient coin. I brought it yesterday, when I tipped back in time." I looked carefully at the coin. A rare gold circlet from the reign of Akbar. There was no mistake about it. This four-dimensional sure enough meant business. He wasn't joking. In the last twenty years of my practice, I must have treated thousands of people - both three dimensionals as well as four-dimensionals. But never before had I seen such a patient. There wasn't much of a difference in the anatomy and physiology of the two major human species currently living on earth. Just a little difference here and a little there - so that the four dimensionals could adapt to their special needs and requirements. Four dimensionals were so called mainly because they had a special ability to move back and forth in time at will. We three dimensionals could do so only in three ordinary dimensions. How the four-dimensionals had come to live on earth is a long story. Centuries before, a space ship went from earth in search of intelligent life. After some years of departure, the radio contact between the space ship and the earth broke down and despite best efforts could not be re-established. God knows what happened to those humans, but when they came back some years ago, inhabitants on earth found they had acquired a new ability - to move back and forth in time at will. They couldn't tell anything as they didn't seem to know much. Exobiologists surmised that their forefathers- the ones that left the earth- must have been captured by a super intelligent race and they must have used them as guinea pigs for their genetic experiments. Most probably the ability to move back and forth in time had come as a result of massive genetic alteration by those super-intelligent beings. Anyway the fact was that their genetic makeup had been substantially altered - so much so that they couldn't interbreed with ordinary three-dimensionals. In spite of my best efforts, I couldn't treat Rajiv. He kept falling back and forth in time. The best I could do was to administer antihistaminics like Avomine so he wouldn't feel dizzy. But that wasn't much help as everybody would agree. Then one day I received the sad news that Rajiv had expired. I was shocked. Worst of all, I had to conduct a post-mortem examination and find the cause of death. I opened the body and as expected found petechial hemorrhages in all internal organs-liver, spleen, heart, brain, everywhere. Hemorrhages of the shape of pin-point. The cause of death was clear. He had been falling continuously over long periods. Small Hemorrhages kept on accumulating everywhere and their effect on the brain was devastating. Tried hard as I did, I couldn't locate any other abnormality. I started closing the body when suddenly I was gripped with a strange curiosity. Could I find the cause of his uncontrollable movements in time? I had more working space now. I had his entire dead body. I could examine all his organs in detail. I might hit upon some curious finding. Besieged with this strange curiosity, I ripped open the stitches and took out all the organs once again. Then I donned my researcher's hat and got down to work. Till late night I had made sections of all his major body organs and examined them under the microscope in great detail. I could find nothing. Tired, I decided to call it a day. I asked my assistant to wrap up the body in formalin and keep it in the cold room. I would have a last go tomorrow. And then I went to sleep. At 4 am I woke up with a start. My subconscious mind must have been working at the problem. That's why I had this ridiculous dream. I thought I had found out the cause of his strange abnormality. I couldn't contain my anxiety, and wanted to test the hypothesis right away. I took out my car and headed for the mortuary in the darkness. The roads, drowned in darkness at that time of the night appeared unusually spooky. At the mortuary, as expected, I found everything closed. The assistant had locked up the main gate, mortuary doors, cold rooms, everything- and had gone away to his house. I took out my duplicate set of keys and opened the mortuary. In the cold room, I opened catacomb number 13, the one where Rajiv was resting. Needless to say, my hands were trembling; perhaps both from fear and from the anxiety of making an unknown discovery. I took out the body myself and laid it out neatly at the table. The skull cap and brain matter were already removed. I looked at the base of skull- at the petrous part of the temporal bone. The one that forms the roof of the middle and inner ear. The mystery could be lying there, I told myself. Gradually and neatly I started chiselling away the temporal bone, so that none of the inner ear structures would be damaged. And then with great precision I took out the inner ear contents. The cochlea, the utricle, the saccule and the semicircular canals, along with vestibular nerves. I kept the whole complex under a simple hand lens and examined it - especially the semicircular canals. Suddenly I found myself trembling in excitement. My conjecture was correct. There were only three semicircular canals in his body, while actually there should have been four. The three semicircular canals are at right angles to each other, each representing a single dimension of space. Whenever someone tips in one or the other dimension, the otoliths inside the appropriate semicircular canal would start moving and activate the vestibular nerve which would send the information to the brain immediately. The brain would then send orders to proper muscles and joints to correct the body position. Those who had a disease of semicircular canals would not be able to stand erect properly. Since each semicircular canal represented one dimension, four dimensionals must have four canals, all perpendicular to each other. Three dimensionals like us, of course had only three canals. My reasoning was this. If Rajiv tipped slightly in the fourth dimension and didn't have the fourth semicircular canal representing the fourth dimension of time, the brain wouldn't get the necessary information and he would keep on falling in that dimension. Of course when he started seeing ancient scenario, he realized he was falling and could thus consciously control the fall. But by that time he would have gone quite far back in time and had to come forward in time on his own. This was the reason for his constant trippings in time. One last thing. How could one have four canals perpendicular to one another in ordinary three dimensions? One may wonder, where exactly I expected to see the fourth canal. Well, a four dimensional cube can be projected in three dimensions as a tesseract. What I expected to see was a tesseract of the semicircular canals, but there was none. There were just three semicircular canals. The finding has since been confirmed by dissection of other four-dimensionals. They all show their semicircular canals as a tesseract. They have four mutually perpendicular canals alright, but they show up as a tesseract, in ordinary three dimensions. This unexpected discovery gave me much satisfaction in itself. But the thing that surprised me most was to find my name in the Padma Shree winners of next year. *** This story was Published in July 1988 issue of 2001 (Science Today) on centerfold page under the title Time and Again

  • SCIENCE IN CRIME DETECTION-24 | Anil Aggrawal's Forensic Ecosystem

    SCIENCE IN CRIME DETECTION-24 CLUES FROM PUTREFACTION I had a tremendous response for my article on abrasions, published in the Feb,1995 issue of Crime & Detective. However I keep receiving stray requests from interested readers to publish stories of their interest in our forthcoming issues. One of the most interesting letters I received this month is from Ashok Rawat of Sector-J, Rail Nagar, Lucknow, who has sent me an interesting clipping from the Times of India of Feb.13, 1995. I will narrate the story briefly for the benefit of our readers. One Ms Meera Juneja, a 47 year old single woman was living alone in Sector 11, Noida. She was the daughter of a former UN official. In December 1994, she reportedly told her parents that she was going to Kanpur to take her LLB examinations. Her father visited her Noida house on January 8,1995, but the door was locked and a milk packet was lying outside the door. Perhaps her father thought that she had left for Kanpur, so he returned. However when he visited Kanpur in February and checked up with his relatives, he found that she had not reached Kanpur. This worried him and he lodged a complaint with the police on February 6,1995. The police went to her house on February 10 and broke open the door. Inside, they found a highly decomposed body of Ms Juneja. The post mortem report said that she had been dead for more than one month. This eased the investigations of the police very much. Mr. Rawat now wants to know how the doctor could say that she had been dead for more than a month. This is an interesting topic and it reminded me of an interesting case I was involved in about 3 years back. I thought that in this instalment I must share that experience with my readers. After reading this true story, much of the mystery surrounding Ms Juneja's death will also become clear. But before I dwell on this story, I must thank my readers for sending me such interesting stories and clippings. And thanks Rawat very much, for sending this interesting clipping. Please keep sending me such clippings for the benefit of all our readers. On 29 July, 1992, the dead body of 67 year old Bankelal was found in a secluded spot outside the city. It was quite decomposed and putrefied. He was a millionaire but did not have any child. He used to live in his palatial house along with his 64 year old wife Ramadevi. She was healthy and not suffering from any disease. On 15th July, Bankelal left his city for Madras to finalize an important business deal. He had to return to his house on 28 July. He did not leave any forwarding address, as it was not of any use. Going away from his house was normal for him and his wife had become used to it. Some interesting events occurred after he left the house. On 22nd July, his wife Ramadevi suffered a massive heart attack and expired. So when Bankelal did not return on 28th there was no one to worry about him. His body was accidentally found the next day by some passers-by. When the police brought the body to me for post-mortem, the first and foremost thing they wanted to know from me was the time of his death. This is normally necessary in all cases of murder, but in this particular case this question assumed a highly significant role. I will explain that in a moment. But before I say anything I would like to add that this case is highly similar to the case of Ms. Juneja referred to earlier. In both cases the time of death was calculated using the putrefactive changes found in the dead body. Ramadevi had a greedy brother Bihari, who lived alone. He had had a tiff with his wife long back, and was now living separately from her. Bankelal also had two brothers. They were married and were living a decent life with their respective families. Since Bankelal had no child, and he had died intestate (without a will), the property which amounted to millions of Rupees should have gone to Banke's brothers. But Ramadevi's brother Bihari contacted the best lawyers and came up with an interesting legal point. If a person dies intestate, the first right of inheritance is of his wife and children. If the wife is already dead, and their are no children,(as was the case with Banke), then the right passes on to the next legal heirs which are the brothers and sisters of the deceased. In Banke's case, his wife Ramadevi was alive till 22nd July. Now if Banke had died before 22nd July, the property automatically passes to Ramadevi, even if she is unaware of his death. Banke's brothers are automatically cut off from his property. Now if Ramadevi dies, the property passes the her legal heirs, which is only Bihari. But the situation changes dramatically if Banke had died after 22nd. On 22nd Ramadevi died. Now suppose Banke died on 25th. What is the legal situation. On 25th the only living heirs of Banke are his two brothers. And thus the property should pass on to them. In this situation, Bihari does not get anything. Bihari's lawyers told him that he could cash in on this confusion. So Bihari gave an application in the court saying that the property be passed to him, because Banke had died before 22nd July. Of course there was no reason to assume that he had died before 22nd, but Bihari said it because this situation suited him. The police now wanted to know from me if I could solve this case. In this case I took the help of putrefactive changes which I found on Banke's body. Let me tell you briefly what putrefactive changes are. When a person dies, his body can no longer defend itself against the bacteria - both inside and outside his body. Our environment is full of millions of bacteria although we can not see them. If they could have their way, they would invade our body immediately. But the defence mechanisms of our body keep them at bay. After death they attack the body both from outside and within and cause it to deteriorate. By their actions on the body tissues they form a gas called hydrogen sulphide. When eggs get rotten, same gas is liberated. The peculiar smell of rotten eggs is due the hydrogen sulphide only. This gas interacts with the haemoglobin present within the red blood cells, and forms a greenish coloured compound sulphmethaemoglobin. This compound is greenish black in colour. Because of this the body assumes a greenish colour. The first part of body to become green is the right lower side of abdomen. This colour appears 12 to 24 hours after death. Thus if we see the greenish discolouration of the right lower side of the abdomen in a dead body, we can say that the person must have been dead for at least 12-24 hours. In the next 24 hours i.e. after 36 to 48 hours after death, the whole body turns greenish-black. Around the same time another peculiar change appears in the dead body. It is called marbling. In this change several parts of the body such as legs, arms, shoulders and chest show long tortuous greenish coloured streaks (reproduce fig 2.7 on page 60 here). These streaks are nothing but veins, which are stained by the sulpmethaemoglobin produced within the body. After death, the red blood cells break down, and haemoglobin from them is released. This haemoglobin combines with hydrogen sulphide gas and forms sulphmethaemoglobin as already explained. This compound then stains the vessels of the skin, in much the same way ink stains your hands. Thus the veins, which are normally invisible become visible as green streaks. Marbling begins in about 24 hours and is well pronounced in 36-48 hours. When I see pronounced marbling in a dead body, I can say that the person must have been dead for almost 36 to 48 hours! Another putrefactive change is the appearance of gases. When bacteria feed on body tissues, they release foul smelling gases. These gases collect beneath the tissues, and bloat the features of the dead person. The tongue may begin to protrude. The features may become so distorted that even close relatives find it hard to identify the dead body (reproduce fig. 2.8 on page 60 here). After about 36 hours, flies lay eggs around the natural orifices of the body such as nose, mouth, eyes, ears, anus and vagina. These places provide a safe nidus for the young ones of insects and they choose these places quite instinctively. In the next 24 hours, maggots come out of these eggs. These maggots look very much like miniature earthworms. Each maggot is of the size of a rice grain, and is seen wriggling leisurely. Thousands of such worms may be found wriggling all over the body. This is not a very pleasant sight, and most persons will begin to retch at such a sight. Only a forensic pathologist is well trained to stand such a ghastly sight. These maggots become pupa in the next 4-5 days, and in another 4-5 days, the pupa becomes the adult fly and flies away from the dead body. Thus we can roughly calculate the time of death from the appearance of these maggots. The following table will make the things a little bit clearer. 1. If we find eggs on the body the death could have been 36 hours before. 2. If we find maggots on the body, we add 24 hours (because maggots appear 24 hours after the eggs have been laid). Thus the time since death becomes 36+24=60 hours. This is about 22 d ays. In actual practice, we can never be so sure, so we take the time of death in such cases to be between 2 to 3 days. 3.If we find pupa (which looks like a grain of wheat), the death should have been about 6 days back. This is because maggots appear about 2 days after death, and become pupa in another 4 days. 4. If we find only the empty pupa shells, it means that pupa became the adult fly which escaped from the shell. This means that the death must have occurred about 10 days before. Three more changes help us determine the time since death. In about 3 days after death, the nails become loose. In 4 days teeth become loose in their sockets and in 5 days the brain matter becomes totally liquefied. Normally the brain matter is much like a jelly. In about 12 to 14 days, so much gases collect within the body, that the body cavities like abdomen burst open. This is called colliquative putrefaction. If the body has been thrown in river or sea where there are predators, they will feed upon the body. After sometime much of the body tissues disappear from the body. It is rather tricky to opine on the time of death in such cases but nevertheless, with experience, we can give a rough estimate of the time since death. In the photograph shown here, the person had been thrown in the sea for about 3 months (reproduce fig. 2.9 on page 61 here). As one can see, most of the body tissues have been devoured by the marine predators. Coming to our case. There was no colliquative putrefaction, so I could say with certainty that at least Banke had not been dead for 12 or more days. Since I did the post mortem on 30th July, I subtracted 12 days from that. This meant that Banke must have died after 18th July. Further, I found that many maggots were crawling around the anus of Bankelal. Thus clearly he had died more than 2 days before. Thus by noting just these two changes, I could say that Banke must have died between 18 and 28 July. There was no pupa on the body. Had I found a pupa on the body, I would have concluded that Banke had died about 6-7 days previously i.e. around 23-24 July. Thus clearly Banke had died after 23 July and Bihari's claim was wrong. Actually to refute Bihari's claim, only this much examination was necessary. But I could do better than that. Banke's teeth were loose, but his brain matter had not liquefied. Thus I could say that Banke had died 4-5 days before or between 25th and 26 July. This was a victory of Forensic medicine. The doctors in Ms Meera Juneja's case found out the time of death using these types of techniques only.

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

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

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE NOVEMBER 1999 ISSUE THE POISON SLEUTHS DEATH BY CICUTOXIN -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this man is Radhey and he is about 54 years old. He was a carpenter by profession and had been in good health till yesterday. Yesterday morning he went to catch some fish in a nearby lake, along with his friend Shyam. Both of them were very friendly. While they were fishing, a person by the name of Lal came there and offered some sweet potatoes to them. Sweet potatoes as you perhaps know are known as ShakkarKandi in Hindustani. Both of them ate some of it. Shyam however spat out after one bite, because he thought it was not tasting how it should be. Radhey took some lusty bites from it, because he was hungry, and he liked its taste too. Half an hour after eating the plant, Radhey felt nauseated and dizzy and had stomach pains. Following this, he suddenly stiffened, fell on the ground unconscious, and made gross, irregular movements of his arms and legs. Shyam was alright by this time.” “Oh, from the story it appears to me, that Lal had given Radhey some poison mixed in sweet potatoes.” “Yeah, it sure does. The police has investigated into the background of Lal, and they have found that Lal held some grudge against Radhey. He wanted to settle an old score with him. So it does appear that Lal had a motive to give him some poison. The question is whether we can prove he gave him some poison or not. According to the only eye witness available - Shyam - the only thing Lal gave to Radhey was sweet potatoes. And sweet potatoes are not poisonous. So the police is going to have a tough time in the court proving anything against Lal. Sure enough they are banking heavily on my investigation.” “So what have you found doctor?” “Let me complete my story first. About one and a half hour after eating the sweet potatoes, Radhey was admitted to a hospital emergency room. On the way to the hospital, he was reported to have had four convulsions. I have asked the doctors who treated Radhey, about his condition when they first saw him. They tell me that when he was brought to them - at about 10 am yesterday - he was comatosed, and was bluish all over. This bluishness is known as cyanosis in medical terminology.” “Oh, that is terrible!” “Yes. He was not responding to any painful stimuli, which means he was really in a deep coma. His blood pressure was normal, but his pulse was more than twice the normal- about 150 per minute. The normal rate as you know is about 72 per minute. His breathing was stertorous. He was perspiring extensively, drooling saliva from his mouth, and his parotid glands were markedly swollen. He alternately clenched and ground his teeth and made chewing movements. His tongue was bleeding from a left sided laceration. His arms and legs showed intermittent, coarse, uncoordinated, and restless movements. He had extreme but intermittent muscle spasms, in particular of the muscles of shoulder and neck, causing throwing back of the neck. The pupils of his eyes were markedly constricted. In fact so constricted were they, that the doctors told me they were like pin points. You know that normally the pupils have a diameter of about 4mm. In this case, they were smaller than half a mm. His eyes were red. The eyeballs protruded somewhat.” “Oh, Radhey must surely have died dreadfully. What did the doctors diagnose?” “They couldn’t know what had befallen Radhey. They gave some conservative treatment, but Radhey’s condition worsened and he expired yesterday night at about 10 pm, about 14 hours after having ingested those mysterious ‘sweet potatoes’.” “Doctor, how do you think Radhey must have died? I think Lal injected some poison in those sweet potatoes.” “He probably could have done that. But by listening to the history of this case, and after talking to the doctors, I can only think of one poison.” “What is that poison doctor. Please tell me. I am getting curious.” “Tarun, the symptoms are so peculiar that there could only have been one poison- Water hemlock.” “What? Water hemlock? Never heard of it as a poison. Could you tell me more about it please?” “Tarun, Water Hemlock is a member of the genus Cicuta, of the Umbelliferae family of plants. There are nine subspecies of Cicuta, and all are very poisonous. Cicuta virosa is the common European water hemlock, and Cicuta maculata and Cicuta douglasii are the varieties found in North America. These varieties are found in India also. Common eponyms for Cicuta are cowbane, five-finger root, snake weed, wild carrot, dead man’s fingers, poison parsnip, wild parsnip, beaver poison, muskrat weed, spotted hemlock, spotted cowbane, musquash root, false parsley, fever root, mockeel root, wild dill, spotted parsley and carotte à moreau. They are found in marshy sloughs and meadows and on the banks of streams. Cicuta plants are difficult plants to identify, which may explain why Radhey mistook them for sweet potatoes. In fact, they have been mistaken for many diverse edible plants such as artichokes, celery, sweet potatoes, sweet anise, and wild parsnip. Cicuta plants are difficult to identify in the early spring, when only the fleshy swollen roots, particularly toxic at this time, are present. Later in the year, the roots are less poisonous, but the leaves and stem then contain sufficient poison to prove fatal if ingested.” “Oh, I see. What is the poisonous substance present in these plants doctor?” “Cicutoxin. Chemically, it is a highly unsaturated higher alcohol. Its formula -if you care- is: HOCH₂ (CH₂)₂ (C≡C)₂ (CH=CH)₃ CH(OH)CH₂CH₂CH₃ There is another poison in these plants, and that is Oenanthotoxin. This is found in Cicuta virosa, and is actually an isomer of cicutoxin. It was first isolated by a scientist Boehm in 1876 and was crystallized by Clarke in 1949.” “Doctor, how do these poisons actually kill the person?” “Tarun, Cicutoxin belongs to a category of poisons known as cholinergic poisons. This name comes from a natural substance found in the nerve endings, acetylcholine. You may be surprised to know that although acetylcholine is normally found in nerve endings - in fact it is essential for muscle contraction - an excess of this substance can prove dangerous to human body. Many insecticides such as organophosphorus compounds also show cholinergic effects and prove poisonous because of that.” “Oh, I see. Please tell me more about these poisons doctor.” “Cholinergic poisons exhibit two main groups of symptoms. One are called muscarinic effects, because they resemble the symptoms caused by eating a poisonous mushroom Amanita muscaria. These symptoms include salivation, perspiration and constriction of pupils. In fact, the moment I heard these symptoms from the doctor, coupled with the information that Radhey had been given “sweet potatoes” by a potential foe, I came to the conclusion that he had been given the root of some plant of the Cicuta species. The second group of symptoms is called the nicotinic effects, because they include symptoms caused by nicotine, a very poisonous alkaloid found in tobacco. Main among these symptoms are muscle twitchings and convulsions.” “Doctor, we have all the circumstantial evidence that Lal gave some poisonous roots to Radhey, but how are you conclusively going to prove in the court that Lal indeed gave him this substance?” “Tarun, I have taken the stomach contents of Radhey and have done a chemical test on that. They have proved positive for Cicutoxin and Oenanthotoxin. This surely means he has been given Cicuta roots by Lal. I did not stop at that. I specifically asked the police to raid Lal’s house. They raided and found many more such roots. Here they are, and any botanist can tell to the court that they are roots of Cicuta plants. Do we need any more proof than that?” "Surely not doctor. That was very clever of you doctor. Without your clever deduction - especially your noticing the peculiar symptoms of Radhey at the time of his death, and your sound knowledge of botany- 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- Brodifacoum."

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MARCH 1998 ISSUE THE POISON SLEUTHS DEATH BY COMMON SALT -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a very young female infant today. What happened to her? Please tell me." "Good morning Tarun. The name of this 6 month old tiny girl is Babli. When she was born, her mother died due to some obstetric complication. Her father Ramdev soon remarried a nubile young girl Rekha. Before marriage she had promised that she would look after Babli well, but after marriage she often showed frank animosity towards this girl. She would not look after her well and would often not even feed her properly.." "Oh, so she probably starved her to death?" "Don't jump to conclusions Tarun. Look at her body. She doesn't look starved. An infant who dies of starvation looks just like a bag of bones. There is no fat in his or her body. But this girl is looking fairly well fed. What I was going to tell you is that Babli's grandmother Shanti Devi, i.e. Ramdev's mother, is still alive. She was not in favor of Ramdev getting married to Rekha in the first place. She probably knew that Rekha was not of good nature. Rekha was undoubtedly not feeding her well, but Shanti would always make up for her, giving her feeds in time. In fact that is why starvation was never a problem for Babli." "Then how did Babli die?" "Babli died of some respiratory disorder. At least that is what her physician told me just now. I will tell you what happened yesterday. Till yesterday morning, Babli was fine. Ramdev left for work in the morning at 8. As usual Rekha started seeing TV just after that, completely ignoring Babli. Seeing that it was her feeding time, Shanti prepared her feed, and filled her milk bottle with that. Just then a neighbor came to meet her, and she went to the drawing room to attend her, leaving the bottle in the kitchen. For half an hour they discussed about some religious programme they were going to attend that evening. After the guest left, Shanti went back to the kitchen, picked up the bottle and gave the feed to Babli. About half an hour later, Babli, who had consumed only about half the bottle by that time, started showing some strange symptoms. She started crying. It appeared as if she was irritable. She vomited twice. Shanti tells me that she had convulsions and muscular twitchings, fluttering of eyelids and of facial muscles. She displayed avid thirst. Shanti knows this because when she gave her water, she would feel a little relaxed, but after some time she would start crying again. But what was most prominent was that she was not breathing well. She had extreme difficulty in respiration. Shanti called Rekha for help, but she kept on seeing TV. Then Shanti phoned her son Ramdev, who immediately got in touch with their family doctor on phone. Dr. Saxena, the family doctor, arrived within 15 minutes, and found that the child was in real bad shape. Ramdev also reached home soon after. Dr. Saxena injected some medicines for respiratory distress, but although the injections seemed to help initially, they weren't of any lasting help. The doctor couldn't really understand what had happened to her. He thought that probably it was an attack of asthma. But what was most confusing was that Babli never displayed this symptom before. They were preparing to shift her to some big hospital for diagnosis and treatment, but before arrangements could be made, Babli died." "Oh, I see. So Babli's body has been brought to you to let them know how she really died?" "Yes, that's right. Actually Dr. Saxena was quite prepared to give the cause of death as asthma, but Shanti Devi immediately raised doubts. She has alleged that while her guest came to meet her, Rekha went to kitchen and mixed some poison in her feed. That is why Babli started having those strange symptoms immediately after having that feed. Rekha, of course, vehemently denied this, and Ramdev too refused to believe her mother, but she wouldn't listen to anyone. She phoned police immediately and called them to their house. The police ransacked the whole house and even searched all Rekha's belongings, but they couldn't find any poison anywhere in the house. That is what is lending weight to Dr. Saxena's theory that Babli indeed died of asthma. Every one including the police is thinking that Shanti Devi is making all this fuss, because she didn't like Rekha in the first place." "Yeah, that looks likely to me as well. So what are you going to do now?" "Tarun, since the matter has reached the police, Dr. Saxena preferred not to give cause of death and leave that to me. The body has been brought to me for post-mortem so that I could comment upon the cause of death." "How do you think Babli died?" "Tarun, the symptoms that Babli displayed surely point towards some respiratory trouble. But the symptoms also point towards a very unusual poison, a poison no one can ever think of. And that is why I have to be extra careful. You have got to remember, that I have a reputation as a poison sleuth, and so I can not afford to leave out even a remote possibility as far as administration of poison is concerned. "Come on doctor. No poison was ever found in the possession of Rekha. Not even that, there was no poison in the whole house. How could anyone administer any poison to Babli?" "Yeah, that sounds very convincing to the police, and that's why they think Shanti Devi is a nut. But I don't think so. I know of a poison which produces exactly the same symptoms as displayed by Babli..." "Please don't talk in riddles doctor. Explain everything to me in clear terms." "Yeah sure. To test my theory, I took some of the stomach contents of Babli and subjected them to chemical analysis. Not to my great surprise, they have shown very high concentrations of salt. Then I took Babli's blood and examined it chemically too. And again it showed very high levels of sodium. I am inclined to think that Babli has been killed with ...." "With what?" "With common salt!" "Common salt? You must be joking doctor. How can anyone be killed with common salt. This is what all of us take daily in our food. Well my father is so fond of common salt he always puts an extra teaspoonful of common salt in his dal." "Yeah, this is what is not known to most people. Common salt is a deadly poison. The only difference between this and other commonly known poisons is that one has to administer rather large quantities to kill with it. One or two teaspoonfuls of salt would not kill an adult but can easily kill a 6 month old baby. Come to think of it, even an adult can be killed with common salt. Only he would have to be fed larger quantities. About 40 teaspoons of common salt would kill an adult human being too." "Well the information is getting interesting. Why don't we begin from the beginning doctor?" "Tarun, before you start visualizing it as a villain, I must hasten to add that there is no doubt that common salt or sodium chloride (NaCl) is indeed essential to all life. It is the basic milieu of mammals. It occurs as colorless cubic crystals or as white crystalline powder. When salt is administered in larger quantities than required, it can cause death too. One teaspoonful of salt weighs about 5 gms. Normal uptake by adults is about 5 to 15 g daily or about 1-3 teaspoonfuls. Children consume less. Salt is even necessary for normal growth in children. The sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, which decreases to 0.1 mEq/kg at 6 months. The average content of sodium in human milk is 7 mEq/L and that in cow milk is 21 mEq/L ..." "Doctor, you started your answer telling me weights in grams, but suddely you have switched to milliEquivalents. I don't really understand the concept of milliEquivalent so well. And why should we talk in milliEquivalents, when we can talk equally well in grams?" "Tarun, in ordinary day-to-day life, it is useful and convenient to talk in grams and kilograms, but chemists and biochemists often find it easier to talk in terms of equivalent weights because of several reasons. You would surely agree that chemists are mainly interested in chemical combinations, and Equivalent weights are actually measures of the characteristic proportions in which given elements combine. For this reason, this term is also often known as Combining weight. Equivalent weights can be used for elements as well as for compounds. In plain and simple words, they are the measure of the combining capacity of a substance with other chemical substances. Well, even if after this, you are feeling inconvenient with equivalent weights, let me add that 1 mEq of sodium equals 23 mg and that of salt equals 58.5 mg. I would also like to tell you that 1 milliequivalent would be equal to 1/1000 Equivalent weight. Now when I say that the sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, I simply mean that for every kg of baby's weight, 0.5 mEq of sodium is needed. Thus if the infant weighed, say, 4 kg, he would need 4x0.5 or about 2 mEq of sodium. Since 1 mEq of sodium is 23 mg, it would mean that the infant would need about 46 mg of sodium daily. This much sodium would be available from about 117 mg of salt. Thus in effect, a baby from birth to 3 months needs about 117 mg of salt. Similarly you can convert other values which I told you earlier in grams. I told you the sodium contents of human milk, because this is the only food available to young babies." "Oh, I see. Doctor, you were saying that 40 teaspoons of salt would kill even an adult?" "Yes Tarun. The toxic oral dose of salt is 0.5 to 1.0 gm/kg. For a 70 kg man this amounts to about 35-70 gm. That means that if an adult consumes about 70 g of salt (or about 14 teaspoons), he would be severely poisoned. The estimated fatal amount, i.e. one that would kill is about 1 to 3 gm/kg. This amounts to about 70-210 gm (or about 40 teaspoonfuls) of salt for a 70 kg man." "Oh, that is interesting. Has salt been used to kill people before?" "Tarun, interestingly the Chinese used saturated salt solution for suicide. Salt intoxication and death have occurred when it is used to induce vomiting." "Why would one want to vomit anyway?" "When somebody has consumed some poison, it is imperative to remove as much poison from his stomach as possible. One of the best ways to do this is to make the person vomit. It has been known from ancient times, that a strong solution of common salt induces vomiting, and that is why for centuries, it was a favorite method of doctors to induce vomiting in poisoned patients. But it is known now that saturated solution of salt itself can cause salt poisoning, so it is rarely used these days." "Oh, I see. So you are suggesting that Rekha mixed salt in Babli's feed when Shanti was talking to her neighbor in the drawing room." "Babli's stomach contents, and her blood analysis definitely tells me that salt has been administered to her. I have examined her brain tissue under the microscope too, and I have found that the capillaries of her brain are damaged. They are full of blood, and there are innumerable bleeding points - technically known as hemorrhages- in her brain. There is bleeding underneath one of the coverings of the brain. We call it subarachnoid bleeding, because it occurs underneath the covering known as arachnoid mater. Many venous channels of her brain - technically known as dural sinuses- are blocked. All these findings are strongly in favor of salt poisoning. I have no doubt that someone had indeed mixed salt in her feed. To tell you the truth now, I surreptitiously picked up the milk bottle from Ramdev's house and have analyzed it for salt. It showed as much as 11 g of salt and it was only half full. It means that the full bottle must have contained about 22 g of salt. In other words, Rekha must have put about 4 teaspoonfuls of salt in Babli's bottle when Shanti was talking to her neighbor. There was no other person in the house at that time, and no one except Rekha could have done that." "Rekha indeed is a wicked woman. It is surprising she knew that salt can kill." "I have enquired about Rekha's background. She studied biochemistry in college, although she dropped out of college later. Surely when she was studying biochemistry she must have learnt that salt is a poison and can be used to kill infants. It is indeed a rather safe poison, because you don't need to buy anything. It is available right at everyone's home. And the police won't suspect you either, because they won't find any poison....any traditional poison, I mean. Come let us tell the police that Babli didn't die of asthma. It is Rekha who has added salt to Babli's feed to kill her." "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- iodine"

  • SCIENCE IN CRIME DETECTION-4 | Anil Aggrawal's Forensic Ecosystem

    SCIENCE IN CRIME DETECTION-4 WAS SHE ACTUALLY RAPED ? Sexual crimes are on the increase these days. Many times we are asked to examine girls and young women- both alive and dead- who have been sexually molested. The questions which the police wants to ask us are many. One of the questions which is invariably asked is whether the woman has been raped or not. It might seem surprising to many here, why the police wants to ask this question. After all, if a woman is asserting that she has been raped then she must have been. Unfortunately this is not true in all cases. Many times women falsely accuse innocent men of having raped them. In such cases it becomes very important for medical personnel to thoroughly examine the victims and tell the police whether she has been raped or not. To determine the answer to this question, the doctor relies very heavily on examination of female genitalia and it would be pertinent to have a quick review of the structures present there. Fig 1 shows the genitalia of a female who has recently had a sexual intercourse. On the top one can see the pubic hair and at the bottom is anus. In between are structures which are collectively known as vulva. Two main openings can be seen. The upper one is urethra through which urine come out. The lower one is the vaginal opening. Intercourse takes place through this opening. Menstrual blood comes out of this opening too. Both these openings are covered by two very thick fleshy lips called labium majus . Clitoris, a very sensitive, pea sized organ lies at the top, between the folds of the labium majus. The vaginal opening is covered in the virgins by a thin delicate membrane- the hymen. It is very thin and delicate and ruptures on sexual intercourse. The first thing that we do is to look whether the hymen is intact or not. If the hymen is intact, the presumption is that the female is telling a lie and trying to implicate the person falsely. In the diagram 1, the hymen is showing a tear at 5 O' clock position. By referring to figure 2, you can know why this tear is called to be at 5 O' clock position. Forcible intercourse also causes injuries to vestibule, an area lying between urethra and vagina (see fig 1) . Injuries may also occur to fourchette and perineum. These are very strong indications that the woman has been raped. Even married women, who are used to sexual intercourse by their husbands don't show rupture of fourchette, perineum or vestibule. Sometimes the walls of the vagina may be so severely torn that they may reach the anus. This is a very severe injury and may even cause death. This is a certain sign of forcible rape (fig 3) . Most people who commit rape are of low socio-economic status and suffer from multifarious venereal diseases. During intercourse they transmit these diseases to their victims. A careful examination of the victim for the signs of disease is also very helpful in estimating whether rape has been done or not. This is a very valuable pointer to us. Interestingly, this can happen the other way round too. An infected woman may give the disease to her attacker, and can thus punish him in more ways than one! She not only gives him a nasty disease, but if the same disease is found in the accused, as that in the woman, it may be a strong indication that he really assaulted the female. We also introduce a cotton swab deep in the vagina (fig 4) and take out the semen from the vagina. In an unmarried female the presence of semen in the vagina is a very strong indication that rape has taken place. We can identify the semen by making a smear of the semen on a glass slide and looking under the microscope. If the material picked up by the swab is indeed the semen, then we see thousands of little snake like sperms (fig 5). Thus the presence of sperms almost confirms that we are dealing with a case of rape. But what about rape on married women? Married women may have sperms in their vagina as a result of intercourse with their husbands. For this we have a slightly more complicated technique. These days there is a special technique called DNA fingerprinting which can differentiate between sperms of any two or more given individuals. We apply this technique and know whether the sperms belonged to the victim's husband or not. Other injuries that we look for are injuries on the thighs, buttocks and abdomen. During a forcible rape, the person tries to force the thighs apart while the women wants to keep them together, to avoid rape. In this scuffle, injuries appear almost invariably on the inner side of abdomen (fig 6). During passionate love storm, the assailant may attack victim's breasts, producing multifarious injuries to the breasts. He may tug at the breasts, squeeze and scratch them, suck them or even bite the nipple off. This might produce several injuries to the breasts including teeth bite marks (fig 7) . These injuries strongly suggest that forcible intercourse may have taken place. Most of the times, the victim scratches at the assailant and thus small tags of skin can be found underneath her nails. These tags of skin obviously belong to the assailant. We can take these tags of skin out and can estimate the blood group of the individual. This can help us greatly in nabbing the criminal. We can even do DNA fingerprinting with these skin tags. This can pick out the culprit from among millions. When the accused is apprehended, he might deny that he had sexual intercourse with the victim. Forensic experts again come to the rescue of police here. If his body shows multiple scratches, abrasions and bruises, it is a clear indication that he has had a scuffle with someone. But he case is clinched by another very ingenious technique. If the accused has had a sexual intercourse with the victim, there could be vaginal cells over his penis. These vaginal cells can not be seen with the naked eye, but can be detected by a test. These cells turn brown when exposed to the vapors of a chemical (Lugol's iodine). We wipe the skin of the penis with a filter paper moistened with salt solution and then expose it to vapors of Lugol's iodine. It the filter paper turns brown, we can tell the police that he has indeed had sexual intercourse with the victim. Thus we can see that by a clever battery of tests, not only can we say that the woman is raped or not, we can also say who raped her. This medical evidence goes a long way in sending the accused to jail.

  • Forensic Science Fiction by Dr. Anil Aggrawal | Anil Aggarwal's Forensic Ecosystem

    Explore a unique collection of forensic science fiction curated by Dr. Anil Aggrawal. Blending medical accuracy with thrilling narratives, these stories captivate students, professionals, and lovers of scientific mysteries alike. Anil Aggrawal's Forensic Science Fiction Page Hi, I am Professor Anil Aggrawal from India. I teach forensic medicine and toxicology at the Maulana Azad Medical College, New Delhi. I love reading and writing science fiction, especially that related to forensic medicine. My favorite SF author is....yes, you guessed it right- Isaac Asimov! Unfortunately he was not a forensic man, and so not many stories related to forensic medicine exist in current SF literature. Although I am no Asimov, I have made a humble attempt and tried to fill up this gap by writing SF stories related to forensic medicine. Some of these stories have been hosted on the net by science fiction enthusiasts. Anyone wishing to exchange ideas with me on forensic medicine, science, and science fiction is welcome. Many of my Science Fiction stories have been published in Spandan, the inhouse magazine published by the students association of Maulana Azad Medical College. You may want to go to this site for some other very interesting articles. Anil Aggrawal's Forensic science fiction stories ~ ( click on title below to access ) The mysterious old man The Freak A tale of detection The New Antibiotic The mystery of the drowned man The mystery of the burnt bride The mystery of the electrocuted man The mystery of the slain General The mystery of the dead infant The mystery of the assassinated prince Anil Aggrawal's other science fiction stories Why dinosaurs became extinct ? The Weird House. (click on title above to access) My favorite science fiction pages Isaac Asimov Check Website DO YOU HAVE AN INTERESTING TALE TO TELL? E-MAIL ME, AND I WILL PUT YOUR STORY ON THE WEB WITH CREDIT TO YOU. YOU WILL FIND NEW STORIES ON THIS PAGE VERY OFTEN. BOOKMARK THESE PAGES. YOU MAY WANT TO COME TO THESE PAGES AGAIN! Contact

  • SCIENCE IN CRIME DETECTION-7 | Anil Aggrawal's Forensic Ecosystem

    SCIENCE IN CRIME DETECTION-7 WHEN THE BODY TURNS BLUE ! The police found the hanging body of Basesar at 7.15 am. on February 26, 1983. The body was naked except for a dhoti ( dhoti is a piece of cloth wrapped over the loins. It is a popular piece of garment in warm countries like India) over his loins. The head was tilted to one side. The body was hanging from the branch of a thick fat banyan tree at the outskirts of his village. From a preliminary look one could say that he had been hanging for several hours. His wife had been looking for him since the previous day. He usually came back from work at 5.00 p.m., but on the evening of February 25, he did not turn up. His anxious wife waited for him till 8.00 p.m., then made inquires from relatives. When everybody answered in the negative, she made a complaint at the police station at about 9.00 p.m. To be sure, Basesar was facing several difficulties. Last year he had taken a loan of over one lakh rupees ( Lakh is an Indian measure, meaning one hundred thousand. Rupees is Indian currency) from the local moneylender against the security of his house and fields. He had married off his two daughters with that amount and had done some long-pending repair work in his house. He was sure that he would he able to repay his loan, but this year’s crop was destroyed in the rain and he did not have enough money to run even his own house. The moneylender had been demanding his money from Basesar for the last several days. Last week he had even sent two goons to him to terrify him into paying back the money. The moneylender had set his eyes on Basesar’s property, which he could acquire at very cheap rates. It was not hard to imagine that under such desperate circumstances, the aging Basesar had taken the extreme step of committing suicide. When Basesar’s wife saw his dead body, she started crying and wailing. The police took off the body from the tree and then called for me to make a preliminary examination of the dead body and of the place, where the dead body was hanging. They thought that they could get some lead from my examination. When I reached the spot, the body had been lying on the ground for some half hour. I looked at the feet and then turned over the body. The back was bluish purple. I pressed the back with my thumb for about half a minute, then removed my thumb and looked at the back again. Then I turned to the Investigating officer, Gajendra Singh, and said, “It’s a case of murder and not suicide”. Gajendra Singh was obviously taken by surprise. I had hardly examined the body in any detail. I had not even conducted a postmortem examination. Then how on earth could I say it was a case of murder? Let us start the story from the beginning. When a person dies, his heart stops beating and the blood comes to a standstill. Gradually this blood starts gravitating to the lower portion of the body. If you moisten a sponge thoroughly and keep it on a table for 3-4 hours, you will find that its top portion has dried while the bottom portion has become even more moist. What actually happens is that the water within the fibers of the sponge starts gravitating to the bottom portion of the sponge. After 3-4 hours practically all water has seeped to the bottom of the sponge. This makes the top portion dry and bottom portion moist after some time. Practically the same thing happens in a dead body. All the blood starts seeping to the bottom portion of the body. After death, generally a body lies on its back, so all the blood collects on the back. This collection of blood gives a characteristic bluish purple color to the portion of the body where it collects. This coloration is known as postmortem staining or hypostasis (Figure 1). Those portion of the body which are in firm contact with the ground remain pressed and no blood collects there. So these areas remain pale. In Figure 1, one can see that the hips and shoulder blades which remain in firm contact with the ground are pale, but rest of the body has turned bluish purple. Post-mortem staining or hypostasis can tell us many important points regarding a crime. Post-mortem staining (or p.m. staining, for short) starts to appear by about 2-1 hour after death and in 4 hours, it is quite well established. If at this time, one presses the area of p.m. staining for about 2 minute, the blood collected blood starts to clot. So after 6 hours of death, if one presses the area for 2 minute or even more, the area will not blanch. The p.m. staining is now said to be fixed. The fixation of p.m. staining appears after 6 hours. So, by seeing the p.m. staining and if it is fixed or not, we can say how long a person has been dead. P.M. staining tells us another vital aspect about death - the position of the body after death. The blood will gravitate to the lowest portion of the body and stain it. Thus if the body was lying on its back, the back portion will get stained as shown in Figure 1. But if the body were lying prone, i.e. on its stomach, then chest and stomach will get stained. If the body were hanging as in the case of Basesar, then feet will get stained (Figure 3 ). On the other hand, if somebody tied the body by legs and hanged it upside down, the face and hands will get stained (Figure 4 ). It all depends on which portion of the body was lowest. If the body was lying on its back for say 3 hours, then the p.m. staining would develop on the back , but it swill not be fixed (as we have already seen). If at this time somebody turned the body, so that it came to lie on its stomach, the blood collected at the back would start moving to the chest and stomach, because in the new position these are the portions which are lying lowest. This causes the staining to disappear from the back and reappear on chest and stomach. This is called shifting of the p.m. staining. Continuing will our old analogy of sponge, if after keeping the wet sponge for 3-4 hours, you invert it, the previously dry portion will become wet and the wet portion dry, because the water will start moving to the new low position. However when the p.m. staining has become fixed, then the turning of the body does not cause shifting of the post-mortem staining. It is because fixation involves clotting of blood and the clotted blood does not move. Thus if a body has been lying on its back for say 8 hours the p.m. staining would become fixed on the back. Turning the body over on its stomach now would not cause shifting of p.m. staining to a new area. Now I must tell you what I found in Basesar’s body. When I examined Basesar’s legs, I did not find any p.m. staining there, which puzzled me somewhat, as Basesar had been found hanging. Then I turned over the body and looked at the back. The back showed p.m. staining. This meant that the body had been lying on its back for a minimum period of 6 hours, after which someone hanged the body to give the appearance of suicide. Since the p.m. staining has already become fixed on the back, it did not shift to the legs later on when the body was hanged. From this examination, I could deduce the whole crime scenario in great detail. Basesar was murdered at least 6-8 hours before, perhaps 10 hours before. Then for some reason his body was kept lying on its back for 6-8 hours. Then someone hanged his body to give the appearance of suicide. The police swung into action now. The local moneylender Dhanprasad denied any hand in the murder. Under sustained interrogation however, he did admit having sent his two goons, Kallu and Lalla to Basesar. But he reiterated that they had been instructed merely to terrify him into paying. Murder was never his aim. Kallu and Lalla, when interrogated, denied all knowledge of murder. They said that on Dhanprasad’s instructions they did go to Basesar at about 5 p.m. on February 25, but had merely enquired from him about the repayment of loan. They said that they had departed after half an hour when Basesar had assured them to do something regarding the loan soon. However the police knew the blueprint of the story now, so they pressed them further. Under sustained interrogation, they broke down and told the whole story which was an eye opener. On the evening of February 25, when Kallu and Lalla met Basesar at 5.00 p.m. he expressed his inability to repay the loan. Kallu and Lalla then took him to the outskirts of the village. The idea was to beat the hell out of him. However before they could start a beating, an altercation started and Kallu grabbed Basesar by the neck. In the heat of passion, he did not realize that Basesar by the neck. In the heat of passion, he did not realize that Basesar was an old and ailing man and the slightest pressure on his neck could prove dangerous. It was only after he felt Basesar going limp in his arms, did he realize that he had unwittingly murdered Basesar. Both of them now panicked. They did not know what to do. Lalla suggested that they should hang Basesar’s body from the branch of a banyan tree. Everybody would then think that Basesar had committed suicide. The idea appealed to Kallu. They did not have a rope however. It was decided that they would cover Basesar’s body with leaves, twigs and grass, go back to village and bring some rope. When they were leaving for the village, it was about 8.00 p.m. They saw a big marriage procession coming towards them and gathering towards some tents which had been pitched to receive those guests. Doing all the gymnastics of hoisting Basesar’s body up the banyan tree was no easy task, especially with so many people only a few hundred yards away. Anyone could wander towards the jungle and catch them in the act. It was decided that they would wait for the marriage procession to dispense away and then they would start their work. It was nearly 4.00 a.m. on February 26, when finally the marriage rites were completed and everybody went away. Now Kallu and Lalla returned to the jungle and hoisted Basesar’s body up. So Basesar’s body was lying on its back for almost 8-10 hours. This caused p.m. staining to appear on the back and become fixed there too. So when finally Basesar’s body was hanged, the p.m. staining did not shift to the legs. This little knowledge of p.m. staining could help me to unravel this seemingly impossible case in no time. There is hardly any doubt that without medical evidence, the case would have passed off as a suicide. The court admitted the medical evidence and awarded a sentence of 7 years’ rigorous imprisonment to both Kallu and Lalla.

  • Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem

    Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JULY 1998 ISSUE THE POISON SLEUTHS DEATH BY DNOC -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young girl today. What happened to her? Please tell me." "Good morning Tarun. The name of this young girl is Seema, and she died this morning in the hospital. Yesterday night she had some severe problem for which her neighbors had taken her to a hospital, but there she died soon after. Well, let me tell you everything from the beginning. She is 24 years old and used to live alone. She is originally from UP, where her parents and family is still residing. She was doing a job in Delhi as a typist, and so was living here for about 2 years. She apparently had a love-affair with one of her colleagues Ramesh. They had a good relation for quite some time, and there were rumours that they were even going to marry." "Oh, I see. But how did she die?" "About a month back, Ramesh's parents fixed his marriage somewhere else, to which Ramesh also did not object much, which in effect meant, that he had tacitly consented for the marriage. When Seema came to know about it, she became mad, and there was a verbal duel between the two. Quite coincidentally, this happened in their office, and everyone saw them fighting them in this manner. That's how we know about this incident." "What was she saying during the verbal duel?" "The colleagues who were present there told the police, that the verbal duel suddenly started and went on for about 15 minutes, till their colleagues intervened. She was saying that Ramesh had shown utter meanness and had deserted her because of her looks. As you can see, she is quite fat. I have measured her height and weight. She is 157 cm in height and her weight is 76 Kg, which as you can see is quite much for her height. Apparently there were sexual relations between the two also, and she was heard saying that Ramesh used their friendship for his advantage, and is now deserting her. He never intended to marry her in the first place." "Is this accusation correct?" "Well, nobody knows for sure. But from what I hear from the office colleagues, Seema was not a very attractive girl, and no male was much interested in her, except for official relations. If Ramesh started nurturing relations with her, it's quite possible, that he was looking for some free fun. Once he had his fun, he decided to marry elsewhere." "Are you hinting that he killed Seema?" "No. Not me. I do not say anything before I have scientifically confirmed my facts. The sequence of events was this. Ramesh had visited her flat last night. Apparently the meeting was aimed at reconciliation. Ramesh wanted to explain Seema the circumstances under which he was marrying elsewhere. The fact of his visit last night is confirmed by Seema's neighbors. Even Ramesh himself has agreed to this fact. Apparently, he stayed there for about 15 minutes and then left. Sometime after he left, Seema knocked at a neighbor's door and told her she was not feeling well. She was sweating profusely, had very high fever, complained of intense thirst, and was in great distress. The neighbors immediately realized that something was terribly wrong with her. They took her to the nearby hospital. Before the doctors could ask her anything, she fell into a coma, from which she never recovered. She died after 6 hours." "Oh, I see. So how did she die? "I will tell you about that a little later, when I tell you about my scientific deductions. But before that, it would be very necessary for you to know, why this case has been brought to me. Her parents were immediately informed by the neighbors and they have arrived this morning. After hearing everything, they have put a very damning allegation on Ramesh. They say that last night during his visit, Ramesh must have given her something to eat because of which these symptoms started. The fact that the symptoms started just after Ramesh left has given credence to this allegation. The police also believes this theory. They think that Ramesh wanted to get rid of Seema, otherwise she could have made life hard for him. She could even have kept troubling him after marriage, and could even infuse all kinds of doubts in the mind of his future wife, so the best course for Ramesh was to put an end to her life." "What does Ramesh have to say in this regard?" "The police has enquired Ramesh, and he says that he did visit Seema to explain her his position. The marriage was being held at the instance of his parents, and he could not interfere in that. But Seema was not ready to listen to him. She was very depressed. After about 15 minutes of unsuccessful attempts at reconciliation, he left." "What do the doctors at the hospital say about the cause of her death?" "The doctors did not have much time to examine her. I have talked to the doctors there. They feel it could be a case of salicylate poisoning or perhaps even thyrotoxicosis." "I don't really understand these two terms. Please explain them to me." "Tarun, acetylsalicylic acid is used in modern medicine for the relief of pain. Ordinary dispirin, which is available in the market for pain relief contains 350 mg of acetylsalicylic acid. If too many tablets are ingested, one can get salicylate poisoning. The toxic dose of acetylsalicylic acid is about 200-300 mg/kg. Thus you can plainly see that for Seema who was 76 kg, the toxic dose is about 65 tablets. People may ingest pain killers for committing suicide. This practice although very common in foreign countries, is not so common in our country, mainly because people are not aware of this fact. But Seema was an educated girl, and she might be well aware of this fact. She was depressed because of recent developments and she might have ingested these tablets after Ramesh left. Ramesh obviously could not give her so many tablets to eat, and even if he had given her, she would not have eaten them. So if this case does turn out to be that of salicylate poisoning, it is quite probable that Ramesh is indeed speaking the truth, and had nothing to do with her death." "Why did the doctors at the hospital think in the first place that she was having salicylate poisoning?" "Because of her symptoms. The symptoms of high fever, thirst and profuse sweating are seen in salicylate poisoning. It might surprise you to know, that although acetylsalicylic acid is normally used for the control of high temperature, during overdose, it produces high fever itself. The doctors also noted difficulty in respiration and very rapid heart rate. Before she went into coma, she also had convulsions. These features are quite typical of salicylate poisoning. The same features are also seen in thyrotoxicosis, a disorder of the thyroid gland, in which the thyroid starts secreting excessive amounts of thyroxine. That is why the doctors gave this as the second diagnosis." "Oh, so now we have all the views. Now tell me what your investigation reveals." "Tarun, we can straightaway rule out thyrotoxicosis. In this disorder, the person is excessively lean and as you can see, Seema is very much overweight. Acetylsalicylic acid poisoning seems a more likely choice. But when I examined her hands, I found some yellow stains on them. This, and certain other findings, which I shall explain shortly, immediately alerted me in the direction of another poison- a very rare one, but one which causes exactly the symptoms exhibited by Seema" "What is that poison doctor? Please tell me. I am getting curious." "Tarun it is known as DiNitroOrthoCresol or DNOC for short." "DNOC? Never heard of this poison. Please tell me something more about this poison." "Tarun, DNOC belongs to a family of compounds known as dinitrophenols (DNP). These compounds are highly toxic and can rapidly produce death. Toxic effects often appear at blood concentrations greater than 30 mg/l while concentrations greater than 60 mg/l are associated with severe toxicity. Dinitrophenols are mainly used as pesticides. Dinitro-ortho-cresol (DNOC) and Dinitrophenol are the two main phenolic pesticides. These substances are used in agriculture chiefly as selective weed killers for cereal crops and for the destruction of potato haulm. In dilute solution they may be used as an insecticidal winter wash for fruit trees. The principal risk of poisoning is in the agricultural use of concentrated solutions for spraying crops. Absorption occurs by inhalation and ingestion and also through the skin; excretion is extremely slow so the poison tends to accumulate in the body. The risk of absorption is much greater during hot weather. Those exposed to these chemicals (such as farmers when spraying these chemicals) are generally recommended to wear respirators to avoid inhaling them. They are also subjected to periodical examination to determine the concentration of these compounds in the blood, which should not exceed 20 micrograms per gram. Dinitrophenolic compounds, especially DNOC stimulate the human metabolism very strongly. In fact DNOC can increase the tissue metabolism by 1200%! The effects of dinitrophenol in stimulating metabolism have been known since 1885, and at one time DNOC was even used in the treatment of obesity and misused for "slimming". "I couldn't understand that last point very well doctor." "Tarun, any compound which stimulates metabolism that greatly basically burns up your energy stores in the body. The main energy store in the body is the fat. If it is burnt, the person will get slim. All exercises are aimed at this only- to burn as much fat as possible. But exercise is time consuming, boring and exerting, so people are on the lookout for easy way out such as chemicals and drugs which can either reduce appetite or enhance metabolism, i.e. help burn up excessive fat. For the former effect, drugs known as amphetamines were once very popular, but they have lost favour as their side effects are too many and too serious. DNOC stimulates metabolism by as much as 1200%, i.e. it burns fats 12 times faster than in a normal man. Obviously this will form a good candidate for weight reduction." "Then why don't doctors prescribe it for weight reduction?" "Because it is a very toxic drug. But early in the century several people did take it for the reduction of weight. When fatalities started occurring, the doctors came to know about its serious toxic nature, and they advised the people against taking this drug. But it was commonly available, as it was a herbicide, so people purchased it with impunity and many overweight girls are known to have consumed it in an attempt to become slim overnight. But in fact nothing of that sort happened. They died instead. Following the deaths of several girls in this way, the availability of this drug was restricted to certain people only. But still many people can get hold of this drug and may consume it. You may be surprised to know that today DNP and DNOC can be illegally bought over the internet too! Many gullible youngsters who fall prey to these internet advisers are paying with their lives. These internet advisers are quacks who encash upon the gullibility of such youngsters. They claim that their concoction would cause a quick weight reduction, but it doesn't. It kills them instead. DNOC is about 5 times as potent as dinitrophenol. The characteristic effect of these two drugs is the uncoupling of the oxidative phosphorylation, causing a great increase in tissue metabolism......" "Sorry to interrupt you doctor. You just talked about uncoupling of oxidative phosphorylation. I don't understand this term quite well. Can you explain me please?" "Tarun, this is a technical term the details of which I may not be able to explain in such a short discussion. But I will tell you certain basics. When glucose is burnt in the body to carbon dioxide and water, it passes through 3 stages. The last stage is technically known as oxidative phosphorylation. During each stage some energy is liberated, which is stored in the form of ATP (Adenosine TriPhosphate) molecules. DNOC and other dinitrophenolic compounds inhibit the formation of ATP molecules, without inhibiting the process of oxidative phosphorylation. This means that although body is burning glucose continually, it is not getting any energy in the form of ATP molecules. This situation when energy is being produced, but is not available for the formation of ATP molecules is technically known as uncoupling of oxidative phosphorylation. This excess energy has to be dissipated in the form of heat. That is why patients poisoned by this poison show high body temperature and sweating. Since body is not getting adequate amounts of energy, it tries to burn more and more glucose in a futile attempt to get energy. Even fat stores are mobilized, but all the energy produced is dissipated as heat. This is the basis of increase of metabolic rate by these compounds." "Oh, I see. But the symptoms are also seen in salicylate poisoning. How did you know she had taken DNOC?" "By the yellow stains on her hands. This yellow staining is very typical of dinitrophenolic compounds. When these compounds come in contact with skin, they form trinitrophenol or picric acid, which is yellow in color. By the yellow stains on her hands, I immediately realized that she must have handled dinitrophenol compounds. I believe she was quite concerned about her weight, and was taking this compound reqularly in small doses. I do not know where she procured this compound from, but probably she must have contacted one of those quick weight reducing quacks, who must have given her this compound. When she was taking small doses, nothing dangerous happened. But due to recent developments, she was quite convinced that she had lost Ramesh because of her weight problem. In a bid to overcome her weight problem overnight, she must have tried to get at it in one go, and may have consumed a great amount of drug immediately after Ramesh left. That is how the symptoms appeared." "But how are you sure, Ramesh did not administer her this drug?" "Because of this drug's peculiar color, odor and taste. No one can administer this drug to another by deceit, without the other immediately coming to know about it. I have exmained her blood and have found high amount of DNOC in her blood. The levels are about 100 mg/l, which is surley a fatal level. Subsequent to this, I asked the police to search her house and look for all medication bottles there. Normally the police would never have even peeped there. But following this discovery, they looked at her almirah and did indeed find a medicine chest. They brought her entired medicine chest. I noticed 3 suspect looking bottles and put their contents to examination, and in one of these, not very surprisingly, I did find high amounts of DNOC. The police have noted the name and address of the doctor from the label of that bottle, and a party has been despatched to UP to arrest that doctor. It appears that the quack who prescribed this medicine to her is based in UP, and during one of her visits to her parents, Seema must have picked this medicine." "Oh, how very clever of you doctor. Without your clever deduction, poor Ramesh would have unnecessarily been arrested and implicated. 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- Cadmium."

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