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- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE APRIL 1998 ISSUE THE POISON SLEUTHS DEATH BY IODINE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of an old man. He has some brownish-yellow stains too around his mouth. What happened to him? Please tell me." "Good morning Tarun. The name of this 57 year old man is Ramlal. He was living alone in this house. He had no children, and his wife expired some time back. From all the accounts of neighbors, it appears he was having some depression. There were other reasons for depression too. He was a gambler and had taken a lot of money as loan from his friends. Some of them were pressing him to return his amount, and some were even threatening him with dire consequences, if he did not return the amount soon. The main among these was a person known as Mahto. He was seen entering Ramlal's house yesterday evening. Nobody knows what happened after that. Today morning when the maid came to Ramlal's house and knocked at his door, nobody opened the door. She got suspicious and called the neighbors. The neighbors broke the door open and found Ramlal dead." "Oh, I see. So definitely Mahto must have killed Ramlal." "Don't jump to conclusions Tarun. How do you know he didn't die a natural death?" "Well.....I thought that was the most natural conclusion to make. But come to think of it, Ramlal could well have died a natural death too." "But surely he didn't die a natural death. The reason is that a bottle was found in the room containing some dark liquid. The bottle was marked "poison" and it was half empty. As you can see Ramlal's face, the angles of his mouth are stained. It does appear he had taken this liquid." "Oh, yes, now I see. The area around his mouth is stained brownish yellow. So do you think Mahto gave him this poison?" "Well, this is what police is thinking. They have come to a startling conclusion. According to them, Mahto went to Ramlal's house to ask for money, but when Ramlal couldn't give him the money, Mahto wanted to get even with him, and gave him this poison. They have called Mahto, but he is denying this allegation completely. He says, that he did go to Ramlal's house and demanded his money, but when Ramlal expressed his inability to pay up, he left after giving him another warning." "It is quite possible that the police would torture Mahto to arrive at the truth." "Well, the possibility can not be ruled out. But I have examined Ramlal's dead body, and it appears to me Mahto is indeed innocent." "Oh, my God. How can you say about Mahto's innocence by just looking at Ramlal's dead body?" "Tarun. I have examined the contents of the empty bottle. It containes a strong tincture of iodine. It is the medicine which one applies to abrasions and wounds. It is used as an antiseptic. Iodine has a strong odor and a very bad taste. This poison can not be given to anyone as a poison...." "Do you think Ramlal never ingested the contents of the bottle, and died by some other means?" "No, Tarun, Ramlal did ingest the contents of the bottle. In fact, I have found signs on his dead body, which point to death by iodine. Not only this I have recovered some iodine from his stomach too. But the iodine was not given to him with homicidal intention. He ingested it himself with suicidal intentions. He probably did it so, because he was very depressed. He was not able to pay up his debts. Yesterday night Mahto visited him and demanded his money again. It dawned upon Ramlal, that he would not be able to stall his creditors for long, so after Mahto left, he consumed iodine to kill himself." "So iodine is such a strong poison, that it can kill? Well, can you tell me a little bit about iodine, so that I understand better how you detected iodine in his body?" "Tarun, Iodine was discovered by the French Chemist Bernard Courtois (1777-1838) in 1811. It might interest you to know that he was not interested in discovering a new element at all. He was actually in the buisiness of manufacturing potassium nitrate which was needed for making gunpowder. He used to get potassium nitrate from potassium carbonate (potash), which in turn he got from seaweed. As one of the steps to get the potassium carbonate, he had to heat the seaweed in acid. One day in 1811, he added too much acid and, on heating, obtained a beautiful violet vapor. On condensing the vapor, he produced dark lustrous crystals. This was in fact iodine. Courtois had in fact unwittingly discovered a new element! The element was given its name 3 years later by Sir Humphry Davy from the Greek iodes (like the violet). The name clearly refers to its unique color. It was originally prepared from the ashes of kelp and other seaweeds, just as Courtois had done. However at the present time, the major sources of iodine are natural and oil field brines, from which they are separated by a special process known as ion exchange chromatography. Kelps are very rich in iodine. I may tell you that although iodine in large amounts is poisonous to our body, it does need iodine in very small quantities. It is needed by the thyroid gland to make the hormone thyroxine. If someone's diet is deficient in iodine, his thyroid gland may enlarge. This disease is known as goitre. Kelps are so rich in iodine, that people who consume kelps don't suffer from goitre at all." "Oh, I see. How much iodine is required by our body daily?" "Tarun, the daily requirement of iodine is about 150 micrograms/day in adults, of which the thyroid gland takes up about 70 micrograms. Rest of the iodine is used for some other essential purposes. Some commercial preparations containing iodine are povidone-iodine and tincture of iodine. These are basically used as antiseptics and disinfectants. Ramlal probably kept the tincture of iodine in his general medical chest, as most of us do. Povidone-iodine is primarily used as a vaginal disinfectant. Tincture of iodine is usually applied on cuts and abrasions, to prevent them from getting infected. Tincture of iodine consists of 2% iodine, 2.4% sodium iodide, 47% ethyl alcohol and rest is water. Then there is the strong iodine tincture, which was found in Ramlal's house. It consists of 7% iodine, 5% potassium iodide, 83% ethyl alcohol, and water. It might interest you to know that the word tincture comes from the Latin tinctura (dyeing), which in turn comes from tingere (to dye). This Latin word also gives us the common English word tint. It is interesting that the word tincture is applied only to alcoholic solutions. Medicine and dyeing may appear to have no connection at all, but in fact there is an interesting link. In pharmacy alcoholic solutions are commonly called tinctures because many dyes will dissolve in alcohol but not in water. Tincture of iodine is reddish brown in color. In addition to tincture iodine, another preparation, Lugol's iodine is also available which consists of 5% iodine and 10% potassium iodide and the rest is water." "Oh, the information is interesting indeed. Can you tell me what symptoms does one experience if he is given iodine?" "I would like to tell you, it is not easy for someone to give iodine to others for homicidal purposes, because it has a characteristic color, odor and taste. Iodine vapors too have a characteristic odor and taste and are intensely irritating to the eyes, mucous membranes, and skin. In several countries, such as the US, the maximum allowable concentration is 0.1 ppm (1 mg/m3). Ppm, as you know stands for Parts Per Million. Even at this concentration, i.e. 0.1 ppm, some people may experience eye irritation. Higher concentrations may lead to excessive tearing, tightness in the chest, sore throat, headaches, irritation of the respiratory tract, and water-logging in the lungs, similar to that seen with chlorine gas exposure. Iodine is a powerful irritant and vesicant, which means it can cause skin eruptions. Symptoms may occur through inhalation, skin or eye contact, or ingestion. Iodine vapor may cause brown staining of the cornea. A 7% solution of iodine, which as you know now is the strong iodine tincture, is corrosive to the eye and the skin. Owing to its strong oxidizing action, iodine acts as an acid corrosive, precipitating cell proteins. Symptoms of iodine ingestion include unpleasant metallic taste, brownish-colored vomit, diarrhea, weak pulse, and retention of urine. There may be corrosion of skin and and mucus membrane with brownish yellow stains. Finally there may be delirium, stupor, and collapse. Changes in the body involve staining of the walls of food pipe and of stomach walls and rapid development of pneumonia-like symptoms." "Doctor, how much iodine is sufficient to kill a person?" "Tarun, about 3-4 g of elemental iodine or 30-250 mL of strong ticture can kill a person. Death usually occurs in the first 48 hours. However death can occur as early as about ½ hour after ingestion to as late as 52 days." "Oh, I see. Well, in the current case how can you prove to the court that Ramlal did die of iodine poisoning?" "As I told you, I found Iodine in his stomach. Iodine can be detected in stomach by some deceptively simple tests. If the stomach contents contains iodine, it may be made to sublime, by taking the stomach contents in a beaker and warming it gently. The purplish iodine vapours may be made to condense on a watch glass placed on the top of the beaker. Another test involves adding 1 ml of starch solution to 10 ml of stomach contents. A blue-black colour will develop immediately due to the formation of starch iodide. If death has occurred after 2-3 hours, some iodine may have reached urine too. To detect iodine in the urine, we add 5 ml of chloroform and a few drops of nitric acid to 10 ml of urine and allow to stand for 3 minutes. A pinkish violet chloroform layer forms, which confirms the presence of iodine in the urine. I have done all these three tests on Ramlal's body and have found iodine in stomach contents as well as in the urine." "You said you found some signs on Ramlal's body also which pointed towards iodine poisoning. What are those signs?" "Tarun, the main sign is the brownish or yellowish stains of skin, which you can see on Ramlal's body. Furthermore all internal organs such as liver and spleen are found engorged with blood. Sometimes there is a characteristic odor too from the body, but this is very rarely perceptible. Now since we have proved that this is a case of death due to iodine, we can easily prove that Mahto couldn't have given this solution to Ramlal. Come, let us tell the police about it, so they can release Mahto." "Oh, how very clever of you doctor. This was a most interesting discussion. It is doubtful if Mahto could have been proved innocent without your excellent detective work. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Barium "
- Index- Forensic Programming | Anil Aggrawal's Forensic Ecosystem
Tarun and Anil Aggrawal's Forensic Programming Page MASTER INDEX OF LESSONS Hi. It is at this page, where I ultimately intend to put some preliminary lessons in computers, internet and computer languages. The instructions would mainly be meant for forensic professionals, but professionals from other specialties can use the information with almost equal ease. Hopefully, after these basics in computers and programming, forensic professionals would be able to put together their own web pages. They would also be able to produce their own programs to manipulate their data. They would, for instance, be able to write programs, which could tell them in a matter of seconds, how many homicides they dealt with in the previous year, how many of them were, say, gun shots, how many stab wounds and so on. These programs could be very useful in writing statistical papers. To be sure, a number of such "ready made" can be bought from the software market. But if you think like I do, you would prefer to make your own programs. Besides the satisfaction of having been able to write your own programs, it has a more practical value. You could devise a program to "suit" YOUR needs, and not be dependent on some other "ready-made" program written by someone else, who was never aware of your own special needs in the first place. Here are some languages which I intend to put on these pages. But I am afraid, you will have to bear with me for some time. I have about ten other websites to maintain, besides of course, perform post-mortems, take undergraduate and postgraduate lectures, conduct research work and so on. I will gradually - but surely - be there. Languages C++ (To appear soon) HTML (To appear soon) DHTML (To appear soon) Visual Basic (To appear soon) JavaScript (To appear soon)
- Volume 26 Number 2 ( July- December 2025) | 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 26 Number 2 ( July- December 2025) Contents Papers Ivan Tsranchev Forensic Interpretation and Importance of Pathologic Findings in an Unusual Case of Hanging By 1. Ivan Tsranchev 2. Pavel Timonov 3. Iliana Toneva 4. Antoaneta Fasova 5. Elizabet Dzhambazova 6. Petar Uchikov Medical University of Plovdiv, Republic of Bulgaria, Europe DOI: 10.5281/zenodo.15708563 Read > Mukesh R Death due to Clinically Undiagnosed Hematolymphoid Malignancy: An Autopsy Case Report and Review By: Mukesh R ¹ , Pampa Ch Toi ² , Vinod Ashok Chaudhari ³ , Karpora Sundara Pandyean ⁴ , Kumaran M ⁵ 1. Assistant Professor, Forensic Medicine & Toxicology, JIPMER, Pondicherry, India 2. Professor, Pathology, JIPMER, Pondicherry, India 3. Additional Professor, Forensic Medicine & Toxicology, JIPMER, Pondicherry, India 4. Junior Resident, Forensic Medicine & Toxicology, JIPMER, Pondicherry, India 5. Associate Professor, Forensic Medicine & Toxicology, JIPMER, Karaikal, India DOI: 10.5281/zenodo.15708004 Read > Jitendra Kumar Proposing a Single centre as a Drug and Toxicology Unit for Complete Care of Substance Abuse and Poisoning Patients at Tertiary Care Centers By: Jitendra Kumar ¹ , Irfan Ahmad Khan ² , Mohammed Reyazuddin ³ , Afzal Haroon ⁴ , Farhan Ahmad Khan ⁵ 1. Assistant Professor, Department of Forensic Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India 2. Assistant Professor, Department of Pharmacology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India 3. Associate Professor, Department of Psychiatry, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India 4. Professor, Department of Forensic Medicine, Jawaharlal Nehru Medical College, Aligarh Muslim University, India 5. Professor, Department of Pharmacology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India DOI: 10.5281/zenodo.15708358 Read > Pravati Dalua Reluctant to Give: Exploring Youth Attitudes Towards Organ Donation in Delhi By: Pravati Dalua ¹ , Chittaranjan Behera ² 1. Associate Professor, Department of Sociology, Kamala Nehru College, Delhi University, August Kranti Marg, Delhi, India 110049 2. Professor, Department of Forensic Medicine, AIIMS, New Delhi, India DOI: 10.5281/zenodo.15708613 Read > Book Review (Technical Section) Basic Sciences as applied to Forensic Medicine and Toxicology by Anil Aggrawal Publisher: Arya Publishing Company, India (1st edtion) Pages: XVIII + 301 Publication Date: 2025 ISBN: 9789360590864 Language: English DOI: 10.5281/zenodo.15708670 Read >
- SCIENCE IN CRIME DETECTION-9 | Anil Aggrawal's Forensic Ecosystem
SCIENCE IN CRIME DETECTION-9 TESTING FOR HOMOSEXUALITY Two years back, I was involved in a most bizarre case. A young boy of eight, Kalu was once coming home from school. The time was around 2.00 p.m. Two sturdy looking persons came to him and lured him away with a chocolate. They took him to his house and tried to have intercourse with him tried to have intercourse with him through anus. When the boy protested, they offered him a ten‑rupee not for this "little job". He was told that he would not be hurt. Kalu was a poor boy and a sum of Rs.10/‑ was big amount for him. He could purchase many toys with that amount, which he had always wanted to. Although he did not like the idea of someone introducing his 'organ' in to his anus, yet the lure of the money let him allow that. During the act, however, he suffered from great pain and even bled slightly. His gait became painful and wobbling after that. When his parents asked him why he was walking in a peculiar way, he replied cautiously that he had fallen down and hurt himself. The parents paid no further attention to him. However things did not stop there. The next week, the two youths met Kalu and suggested the same bargain. The boy hesitated a little, but then decided that he could do with another ten rupee note! From then on, this became quite regular. Those two youths would regularly have anal intercourse with Kalu‑almost twice every week‑and would each time give him ten rupees. The affair went on for quite a number of weeks. Then trouble started when the boy developed some ulcers around his anus. These ulcers were discharging pus. His parents thought that the boy had caught some infection and so brought him to me. When I examined him I found that he was suffering from syphilis‑a venereal disease. Such a young boy could catch syphilis in only one way‑through anal intercourse. I explained the situation to his parents and at the same time informed the police also, because it had become a medico‑legal case. Kalu's parents lost their temper and started beating Kalu. Kalu then revealed that Jagga and Kaka, two youths of his area had been using him in this way. Before we go on with our story further, a few words about homosexuality or 'coitus through anus' would be in order. Intercourse through anus is known as sodomy or buggery. An adult male can perform anal intercourse on an adult male, adult female or on a young child(of either sex), as in Kalu's case. When homosexuality is done on an adult male, the practice is known as homosexual sodomy. When a male commits anal intercourse on a female, it is known as heterosexual sodomy. When a child is used, the practice is known as paederasty. This child is usually known as a catamite. The person who performs the act is known as the active agent and the one on whom the act is performed is known as the passive agent. Sometimes two adult males act as active and passive agents alternately. More commonly however, a passive agent always remains a passive agent. n our country, many people regularly earn their livelihood by acting as passive agents and charging a fat fee from their customers. These are known as male prostitutes. Several hijrahs whom are all familiar with, mostly act a passive agents,. Several boys like Kalu agree to become passive agents for the sake of money only. In our country, anal intercourse is a crime. According to section 377 of I.P.C., if it can be proved in anal intercourse, he can be sent to jail for 10 years. So Jagga and Kaka had every reason to deny their involvement in anal intercourse with Kalu. It was not merely a matter of shame, but a criminal act. As we shall see later, they did deny their involvement and it remained for me to prove conclusively that they had indeed used Kalu as a passive agent. An interesting thing is that if a passive agent consents for anal intercourse, even then the he can be incriminated under Section 377 of I.P.C. In our case, Kalu had consented for the act, but since he was only eight years old, his consent was not valid and he could not be incriminated. According to our law, any child under 16 years of age can not understand the nature of such acts and thus his consent for such act is not legal. Another interesting thing is that if a person performs anal intercourse on his own wife, even then he is a culprit under section 377 I.P.C. If his wife consents for such an act, then even she is a culprit and both can be sent to jail for 10 years. A wife can refuse her husband who demands anal intercourse from her. Interestingly she can not legally refuse normal vaginal intercourse to her husband even if she is not in "mood", but she can and must refuse anal intercourse, because if she does not refuse anal intercourse, she also becomes a culprit. If a wife refuses normal vaginal intercourse with her husband and her husband forcibly commits such an intercourse with her, she can not bring him before thee law, but the same is not true of anal intercourse. Not only can she send him to jail for 10 years (if she wants to), but is also entitled to divorce him In fact if a male commits anal intercourse on any man, child or woman, the wife is entitled to divorce him. So much regarding some of the legal points regarding homosexuality. When Jagga and Kaka were interrogated by the police regarding their criminals act, they denied any such involvement. So the burden of proving their involvement fell on me. Whenever a passive agent is brought to us, we examine mainly his anus which tells us several tell tale signs. The person is examined in a knee‑elbow position(Fig.1). In this position the person rests on his knees and elbows. This position is chosen because it exposes the anus in a most prominent way. I first 'inserted a cotton swab (just like Johnson's buds; but with longer handle) into Kalu's anus. The idea was that if any seminal fluid was present in the anal canal, it would be absorbed by the cotton. It could then be tested for the presence of seminal fluid. the presence of seminal fluid in the anal canal confirms that buggery has been done on the passive agent. One of the most common preliminary tests to confirm semen is the Florence test. In this test, we prepare an extract of the suspected, seminal fluid from the anus and mix it with the Florence reagent. If the suspected fluid is semen, then dark brown needle‑shaped crystals are formed (see figure 3) Formation of these crystals confirms the presence of semen. We also try to look at the extract under the microscope. The presence of small tadpole‑like sperm cells confirms the presence of semen. We also see the underwear of the active and passive agents under a special light, the ultraviolet light. If seminal stains are present on the underwear, they begin to glow brightly. The examination of anus also tells several things. Figure 2 shows three main findings in and around the anus. For the purpose of clarify, anal opening is shown slightly enlarged. An important is tearing of the skin around the anus. this is known as fissure. these fissures appear because of the introduction of large‑sized male organ in relatively narrow anal canal. Second important thing is the laxity of the anal sphincter. Anal sphincter is a circular muscle which acts much like a highly elastic rubber band (Figure 3). It actually checks the faecal matter from coming out involuntarily. But when male organ is repeatedly introduced in the anal canal, as during buggery, this sphincter becomes lax and the anus starts gaping. The third important sign is the smoothness of the covering of the anal canal. If we dilate the anus of a normal person and look inside, we find that the covering inside is much like an orange peel, i.e., rugged and rough. But repeated acts of penis insertion smoothers out the ruggedness of the covering. These three signs were quite suggestive that the boy was being used as a catamite. Interestingly, when I subjected the swab taken from Kaka's rectum to Florence test, it came positive for seminal fluid. His anus also showed all the three classical signs. The lawyers of Jagga and Kaka could not refute this hardcore medical evidence in the court. The court admitted my evidence and sentenced both of them to ten years of rigorous imprisonment.
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MARCH 1999 ISSUE THE POISON SLEUTHS DEATH BY DIESEL FUMES -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a old man today. What has happened to him? Please tell me." "Good morning Tarun. The name of this old man is Shyam. He was a big industrialist and was about 83 years old. His dead body was found today morning at about 9 am in his Ford saloon car. This car was parked in his garage. I may tell you that this car was fitted with a diesel engine." "So how do you think he has died?" "That is what I have to find out. But police has a suspect with them, and they think that he has killed Shyam. Well, let me begin from the beginning. Shyam had a business associate Sohan Lal. Both Sohan and Shyam had been working together for quite some time. However lately they had fallen out over some monetary matter. Sohan is a relatively young man - only about 48 years old. The police has interrogated many persons who knew both of them, and all of them have told the police that Sohan did not have good relations with Shyam. The things had deteriorated to such an extent that on one occasion, Sohan had even threatened Shyam with dire consequences." "Oh, I see. It does appear that Sohan has a hand in Shyam's killing." "Shyam Lal lives alone in his big mansion. His wife died about two years back and his only son is settled in Netherlands. He comes to India only occasionally. Rarely a guest comes to his house to spend a night with him. So for all practical purposes Shyam Lal lives alone in his house. Shyam Lal used to remain quite depressed after his wife's death, and it appears he had lost all will to live, especially as his only son had also left him. Two days before, i.e. on Saturday evening Sohan invited Shyam Lal for dinner. He came to Shyam Lal's house in his own car, parked it at his house and from there both of them drove to a 5-star hotel in Shyam Lal's car. It was somewhat surprising to Shyam, but he thought that probably Sohan wanted to settle matters with him, and so accepted his invitation. They had their dinner and returned quite late - at about 12 midnight. We know these details because the police has made thorough inquiries from the hotel staff. Shyam Lal was not seen on whole of Sunday, and on Monday morning, i.e. today his dead body has been found in the garage in his car. So the presumption is that Shyam Lal died just after his return from the hotel. I have made some preliminary examination of the dead body, and from the various changes seen in the body, I am also of the view that Shyam Lal died somewhere around 1 am on Sunday morning, i.e. just about one hour after return from the hotel." "So what do you conclude from all this?" "Well, the police has come up with an interesting story. According to them, Sohan mixed some poison in his food surreptitiously when they were having dinner together. He came with Shyam Lal back to his house. There he left him, collected his own car from his residence, and drove away. Shyam Lal was already feeling weak from the effect of the poison Sohan had given him. He wanted to get some rest. But just as we was parking his car in his garage, he fainted and dropped dead within his car. His body was only discovered today." "So what are they waiting for? They must immediately arrest Sohan." "They have already done that. But Sohan is swearing he didn't mix any poison in Shyam's food. He says that he did want to patch up things with Shyam, and for this purpose he had invited him for dinner. But from the talks it appeared to him that Shyam was reluctant to his proposal. They had talks for about 2 hours after which Sohan came back to Shyam's house, bade him good bye and went to his own house. He does not know what happened to Shyam Lal after that. However the police are reluctant to believe his version. They are holding him, and interrogating him more severely, so he could come out with the truth." "What do you think doctor?" "Tarun, a forensic pathologist goes only by the evidence that he has with him. I am a forensic pathologist and I won't form any theories merely from the details of circumstances. From the circumstances, it does appear that Sohan has a hand in the death, but I would make my deductions only from the hard scientific facts that I have seen for myself. I went to Shyam's house and made some preliminary observations. The first thing that struck me when I was examining the car was that, a hose pipe was connected to the interior of the car from the exhaust..." "Sorry to interrupt you doctor, but how is this observation important?" "Tarun. It is a common method of committing suicide. Carbon monoxide is known to emit from all car exhausts. Many persons - especially in the western countries- close themselves in a garage along with their car, run the engine of the car and simply wait there till the level of carbon monoxide rises enough to kill them. The attraction of this method among suicides is that it is a very painless death, and all persons wanting to commit suicide want a painless death. A hosepipe going to the interior of the car from the exhaust means an arrangement had been made to let the carbon monoxide come inside the car." "But doctor, these days most cars are fitted with catalytic converters. I believe such an advanced car as the Ford saloon, in which Shyam Lal's body was found must definitely be fitted with a catalytic converter." "You are right Tarun. Catalytic converters convert carbon monoxide to relatively non-toxic carbon dioxide. This has not only enabled the carbon monoxide levels in the atmosphere to go down, but also reduced the risk of suicides substantially. Now anyone who makes this arrangement for the purpose of committing suicide is likely to fail. The reason is that carbon dioxide is not as deadly as carbon monoxide. In fact, if you read medical literature, you will find many instances of failed suicides because of these catalytic converters." "Oh, I see." "Tarun, with the coming of new vehicles on the Indian roads, there is now an apparent progressive increase in diesel-driven motor vehicles in all forms of road transportation. Diesel is a commonly used vehicle now and it is believed to be safer than petrol as diesel fumes contain substantially less carbon monoxide. However their emissions are still potentially toxic. Diesel engines emit more than twice the amount of sulphur dioxide than that contained in petrol emissions. They also emit 14 times the amount of black smoke, i.e. particulate materials, than of petrol engines. Diesel emissions also contain marginally more nitrogen dioxide than petrol. Petrol, as I told you earlier, however creates more carbon monoxide - 28 times to be exact- than diesel." "Oh, I see. So if someone wants to commit suicide in the manner you just described, probably he is better off with a petrol engine than with diesel engine?" "You are right Tarun. The reason is obvious. Petrol engines create substantially more carbon monoxide. Of course only those petrol engines would do so, which are not fitted with catalytic converters. I must however tell you that both fuels cause acute toxicity if substantial quantities of their emissions are inhaled. However the mode of toxicity would be different. Whereas petrol engines cause death by carbon-monoxide poisoning, diesel fumes cause death by blocking the air passages with soot and other material in the emissions. The absorption of toxic materials in the latter case is increased owing to the blockage of tiny lung alveoli by the soot particles. These soot particles effectively plug the alveoli, thus "holding back" the toxic fumes within the alveoli. This greatly enhances the absorption of toxic substances. Thus although diesel fumes do not contain much carbon monoxide, they can still be very harmful." "Doctor, have you found any evidence that Shyam Lal died of diesel fumes?" "Tarun when I examined Shyam's heart, I found that the coronary arteries - the arteries that supply the muscles of the heart - were blocked to a great extent. However the amount of blocking was not sufficient to cause death, so I looked at other organs for more clues. The interesting finding was that the windpipe (trachea) and the bronchi were thickly covered with soot. The lungs were very much congested, which meant that they had been exposed to some irritating substance like diesel fumes. But what clinched the diagnosis in favour of death by diesel fumes was the fact that there were thick beads of black oily sticky material in the smaller bronchi. When I cut the lungs and pressed the cut ends, these thick beads of oily materials could be expressed. These beads were nothing but toxic material -including some diesel fuel- in the lungs. To see if the blood had any carbon monoxide in it, I did a toxicological analysis of the blood too, and found that there was less than 5% saturation with carbon monoxide. This indicates that there wasn't a substantial amount of carbon monoxide in the fumes that Shyam Lal inhaled. It is almost sure that Shyam Lal died of diesel fumes." "Oh, that is interesting. So would you reconstruct the events for me doctor?" "Sure. On Saturday evening, the talks between Shyam Lal and Sohan failed and this sent Shyam Lal again into a bout of depression, which he was already suffering from. He came back to his house and probably decided to take his own life. He had already lived a full life, his wife was no more there and his son was living far away from him. On that day, probably he lost all will to live. He was an educated man. He had read about deaths by carbon monoxide. I personally feel that he intended death by carbon monoxide. But it was a diesel engine, which does not emit carbon monoxide. He ultimately died of diesel fumes. Come let us tell the police that Sohan is innocent and they should release him." "Very clever indeed. This was a most interesting discussion doctor. Without your masterly deduction, police could have unnecessarily went on harassing Sohan. People might have thought, it was a case of killing by Sohan. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about death by arsine gas. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE FEBRUARY 1998 ISSUE THE POISON SLEUTHS DEATH BY SMFA -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young woman today. What happened to her? Please tell me." "Good morning Tarun. The name of this 22 year old female is Kabuli. She had got married to Radhey only a year back. Radhey works in a chemical factory involved in manufacturing various chemicals. Since the marriage day itself, there was a dispute among the couple regarding the insufficient dowry which Kabuli brought from her home. Radhey as well as his parents used to belittle her on every little matter. For about last one week, Radhey suddenly started a soft posture towards Kabuli, as if he had buried all differences with his wife. Last evening he became very sweet to her, and even made a cup of tea for her. She was a bit surprised, but thought that may be Radhey had changed his ways. She took tea, but soon after had vomiting, and seizures. After about 3-4 hours she died. A local doctor was called, who certified the cause of death as heart attack. But the relatives of Kabuli lodged a complaint with the police that Kabuli had actually been poisoned to death by Radhey. Subsequently the police went to Radhey's house and seized the remaining portion of the tea, as well as some other stuff from his almirah. The body of Kabuli was also seized and given to me for post-mortem. Now I have to conduct a post-mortem on the case and tell the police if Kabuli was really poisoned or not." "Just a minute doc. You said that a local doctor has already certified that the cause of death was heart disease. Then what more do you expect to find?" "Tarun, the relatives of Kabuli have already lodged a complaint with the police that she has been done to death by Radhey. Kabuli had got married only a year back. Under the Indian law, any death of a married female occurring within 7 years of marriage is termed as dowry death and is taken seriously. Had there been no complaint from Kabuli's relatives side, then everything would have been fine. But since a complaint has already been lodged, the police naturally want to be doubly sure that Kabuli really died of heart disease or not." "You mean that the local doctor gave a wrong cause of death? Do you?" "Well, the doctor had not seen Kabuli during life. The doctor could genuinely be mistaken. Sometimes, a doctor may give a cause of death just to avoid harassment to the relatives. If the doctor knows the family personally and is convinced that the death was natural, he would generally oblige the relatives by giving a cause of death, even if he had not seen the patient during life. He does so in order to save unnecessary harassment to the relatives at the hands of the police. Last but not the least, a doctor can actually be bought by unscrupulous relatives, to give a wrong and misleading cause of death." "Oh, I see. So you are doing the postmortem in order to find out how Kabuli died actually?" "Exactly. If my findings indicate that Radhey had indeed given poison to Kabuli, he could be prosecuted under section 304B of the Indian Penal Code, which is popularly known as Dowry Death. If the court finds Radhey guilty of murdering his wife, he would get no less than 7 years in jail. This is the punishment prescribed in section 304B of the Indian Penal Code." "Oh, I see. So what have you found out?" "Tarun, the most interesting thing is that while Kabuli was drinking tea, she did not complain of any bad odor or taste. This means that the poison, if indeed it was given to her, was tasteless and odorless. The tea also had its normal color, which means that the poison was colorless too. Such poisons, which are colorless, odorless and tasteless are generally very successful homicidal poisons, because the victim can not make out the poison while taking his food. I also took into account that Radhey was working in a chemical factory which was making rodenticides. Rodenticides are very strong poisons and can kill a person within a short time. It was quite possible for Radhey to steal a little quantity of rodenticide from his factory and give it to Kabuli for homicidal purposes. The only rodenticide, which is colorless, odorless and tasteless is a chemical compound known as Sodium Monofluoroacetate which is also known by its acronym SMFA. Its chemical formula is C2H2FNaO2 and it is also known as Compound 1080. Its other names are Sodium fluoroacetic Acid and Sodium fluoroacetate." "Compound 1080? That's rather a strange name. Why has it been given this mathematical name?" "That's an interesting question Taurn. But let me tell you about another compound which has been given a mathematical name too. It is arsphenamine, which is known as Compound 606. This has an interesting history too.." "Doctor, I am a sucker for interesting scientific histories. Please tell me the history of compound 606, and then of course we can go to the history of compound 1080" "Alright as you say. Well, you must surely be knowing about the German Scientist Paul Ehrlich (1854-1915). He is often known as the father of antibiotic therapy. In late 1800s and early 1900s - the era during which Ehrlich lived - one of the biggest problems faced by doctors was to create a drug which could kill bacterial cells but NOT human cells. If such a drug could be discovered, it could be given with impunity to humans in order to cure their infections, say syphilis (which as you surely must be knowing is caused by a bacterium known as Treponema pallidum). The drug would then selectively target bacterial cells killing them, while sparing the human cells. Such a drug could be called - as Ehrlich liked calling it during his entire life - a "magic bullet" ; a bullet magical enough to kill bacterial cells while leaving human cells alone. Since human and bacterial cells are so similar in nature biologically, it was difficult to find a chemical which could destroy one type of cell, leaving out the other. But of course there are differences too, and the answer lay in finding those differences and exploiting them. In the late 1800's, Elrich, was noting with interest that there existed some stains which could stain bacteria but not human cells and vice versa. A cell, as you know, gets stained only when it "takes up" that dye. If bacterial cells and human cells could take up different stains, surely there existed more chemicals which could be differentially absorbed by bacterial and human cells. And surely some could be toxic to them too. Ehrich started from this conjecture and started with one such dye. His aim was of course to find a chemical which could - instead of staining the bacterial cell - KILL it. There was absolutely no luck in the beginning and so he began to chemically alter it little by little, testing each new drug. When he reached 606th compound, he discovered, to his delight, that he had finally synthesized a chemical (it had changed so much by now, that it was no more a stain), which could kill bacteria, especially the bacteria causing syphilis. In the beginning he simply called it Compound 606, because it was the 606th compound synthesized by him. Of course later it became known as arsphenamine and was marketed as Salvarsan." "That's great. Doctor, you know so many stories. And now, what about the story of Compound 1080? So I take it when Ehrlich reached at 1080th compound, he gave it that name, and that compound was SMFA, right?" "No, not at all. In fact Ehrlich stopped at 606. To be sure, he did not live much after introducing that compound. Compound 606 was synthesized sometime in 1909 and the first tests on bacteria were announced in the spring of 1910. Ehrlich suffered a stroke in December 1914, and succumbed to a second stroke in August of the following year (1915). No, compound 1080 was not synthesized by him. There was a company, which was synthesizing chemicals for possible pesticide use, and SMFA was the 1080th compound tested by them. You might be interested to know that there is a compound known as Compound 1081 too. It is Fluoroacetamide. This also acts as a rodenticide and insecticide. This was of course the next compound made by the same company." "Fine. So you concluded that Radhey had given SMFA to Kabuli. Well I haven't heard much about SMFA. Please tell me something about it in detail." "Tarun, I must tell you that I have not concluded anything yet. I am simply trying to analyze the circumstances, and come to the most logical conclusion. That is what scientific thinking is all about. To tell you more about Sodium Monofluoroacetate, I must tell you that it is a highly toxic rodenticide. It contains fluorine, but its toxicity is not related to its fluoride content, but rather to its interference with the Kreb's cycle..." "What is Kreb's cycle doctor? This term is rather new to me." "Tarun before going any further, I must tell you that Kreb's cycle is named after a German-British Biochemist, Sir Hans Adolf Krebs who was born in Germany in 1900. He found out for the first time how lactic acid in the body gets broken down to release energy. Well, to begin from the beginning, glycogen in the liver is first converted to lactic acid, but this step gives only very little energy. Major energy comes from the further breakdown of lactic acid into simpler compounds such as carbon dioxide and water. The exact sequence of breakdown of lactic acid into simpler compounds was first worked out in great detail by Sir Hans Krebs, and hence these steps are known by the name Kreb's cycle. It is also known as tricarboxylic acid cycle. This however is a less fancied name. If any chemical interferes with Kreb's cycle, it would cause death because Kreb's Cycle is the main energy source of the body. Sodium Monofluoroacetate is one such chemical." "Oh, I see. Since how long do we know about this compound? Looks like it was developed fairly recently." "Tarun, SMFA was developed during World War II as an alternative to imported natural rodenticides. Because it is so highly toxic, its use is mostly limited to commercial exterminators. It is derived from some plants such as Palicourea (South America), Acacia (Australia), and a few other plants. As I told you earlier, SMFA is a white, odorless, tasteless, water-soluble salt. It looks like flour or baking soda. Unlike thallium about which we talked in one of our earlier meetings (see Science Reporter October 1997, pages 42-46), SMFA can not be absorbed through unbroken skin. However it is readily absorbed through the gastrointestinal and respiratory tracts, mucus membranes and broken skin. It is thus highly toxic when ingested, inhaled in dusts, or absorbed through open wounds." "Oh, I see. You said that Kabuli had vomiting after taking tea, and also that she had seizures. Are these the symptoms of SMFA poisoning?" "Well, almost. The toxic effects of SMFA are usually delayed for one to several hours and result from the conversion of the nontoxic fluoroacetate ions to toxic fluorocitric acid, which in turn blocks the Kreb's cycle. I have already told you that this cycle is essential to energy production. I must tell you that this cycle is important in mammalian cells only. Vomiting is commonly seen soon after ingestion. Toxic effects primarily involve the Central Nervous System and the heart. They include nausea and apprehension followed by disturbances of the heart beat, respiratory depression, seizures and coma. Apprehension, auditory hallucinations, and facial paresthesias often precede convulsions. By facial paresthesia, I mean that there are sensory disturbances in the facial area. There may be tingling sensations in the face, or there may be feeling of pins and needles." "How does death occur in SMFA poisoning doctor?" "Tarun, death results either from ventricular tachycardia which is a scientific term meaning that the ventricles of the heart start beating too rapidly. You might imagine that this is good for the body, but this is not so. When the ventricles of the heart beat rapidly, they just beat without really pumping any blood. So this in effect is actually a tremendous waste of effort on the heart's part. Death may also occur from the fibrillation of the heart, which is another condition, in which the heart starts beating very rapidly, without pumping adequate amount of blood. It may also occur from respiratory failure which may occur because of pulmonary edema. Pulmonary edema may sound a formidable term to you, but in effect it is nothing but filling up of lungs with water." "Oh, I see. How much SMFA would actually kill a person?" "Tarun, SMFA is a dangerous homicidal poison, not only because it is colorless, odorless and tasteless, but also because it kills in very small quantities. In humans, does of 0.5-2 mg/kg of the body weight are highly dangerous. This means that if a man weighing 60 kg ingests about 120 mg (60x2mg), he would be quite serious. Lethal dose is 5 mg/kg. Thus for the same man, the lethal dose should be around 300 mg, which as you can see is really small. Small doses make it that much easier for the poisoner to administer the poison, in his victim's food." "Oh, I see. Doctor is there any antidote for SMFA, which could have been given to Kabuli to save her life?" "Unfortunately there is no known antidote for SMFA, which makes it still more dangerous as a homicidal poison." "So did you find any tell-tale signs of SMFA poisoning in Kabuli's dead body?" "Tarun, SMFA, does not leave any tell-tale signs in the victim's dead body, which is yet another reason why SMFA is such a good homicidal poison. There are no specific post-mortem findings. However animals who die of SMFA poisoning develop stiffness of limbs rapidly and are found with their extremities in hyperextension. This in plain and simple terms means that the extremities are stretched fully at the joints. I have taken samples of tea taken by Kabuli from her stomach and have run chemical tests on it. And as expected I have found SMFA in it. Not only that, I have also examined chemically the tea remaining in Kabuli's cup, and have found SMFA in that cup too. In Radhey's almirah, the police found a small white packet in which some white salt was present. On chemical analysis, that salt has turned out to be SMFA as well. So there seems little doubt that Radhey had indeed given Kabuli the poison. He had probably stolen some of the rodenticide from his factory, and had mixed it in Kabuli's tea. That was also probably the reason, why he was going so soft towards her for the last one week or so. He wanted to gain, Kabuli's confidence, so she could accept anything from him, without doubting his intentions. Come on, let us tell the police, that Radhey indeed is the killer." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- common salt. You may believe that common salt is not a poison, but interestingly it can be, and has been, used to kill humans!"
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JANUARY 1999 ISSUE THE POISON SLEUTHS DEATH BY SODIUM NITRITE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young woman today. Her whole body seems to have a chocolate brown color. I remember last time too, I had seen a dead body with chocolate brown color. Did this woman also die of the same poison? Please tell me." "Good morning Tarun. The name of this young woman is Radhika, and she is about 25 years old. She died in her flat at about 9 am today morning. She was a junior executive in a private firm here in Delhi, and was living alone in this flat. Her family members are living in Jaipur. She was living here solely for the purpose of this job. Her parents were looking out for a match for her marriage." "Oh, I see." "Yesterday night she was fine. In fact, she met one of her neighbors Shyamala -also a 25 year old girl- at about 9pm, and she tells us that she was perfectly in good spirits. That rules out suicide...." "Wait a minute doctor. If a person is in good spirits and cheerful a day before his or her death, does it rule out suicide? Is it not possible that she was trying to mislead the neighbors by being cheerful so that nobody gets to know her intentions?" "There are other indications too. There is no suicide note. Generally a person who commits a suicide, leaves a suicide note." "Oh, I see" "Well, the police interrogated Shyamala more about her as she was the only one, who knew Radhika very well. She told the police that she (Radhika) was in love with Chaman, a 26 year old colleague in her office. Recently she had become pregnant by him, and she was pressing him for marriage. However Chaman had lost interest in her, and was trying to avoid her. Only 2 days back she had threatened him to go to his parents if he did not agree for the marriage. Chaman's parents are very religious and God-fearing, and he knew if she approached them, they would force him to marry her. To settle matters he came yesterday to Radhika's flat at about 7 pm. Shyamala knows because when he came, Radhika called her as a mediator. Shyamala tells the police that Chaman was looking very tense and jittery. She thought it was because he had such a difficult matter to resolve. Anyway she just sat there for about an hour. When she saw that the matter is going to take more time, she left the house making an excuse. When she left, Radhika was just preparing to go inside the kitchen to make tea for everyone. She offered Shyamala to go after having tea, but she just left. She however saw Chaman leaving Radhika's house only about 15-20 minutes later. She was sitting idly at her window when she saw him. He looked to be in great hurry." "Oh, I see. So did you find anything in the post-mortem that corroborates what Shyamala is saying?" "Yes, I found a 4 month old male baby inside Radhika's uterus, which definitely tells us that she was pregnant. I have kept the tissues of this fetus for his DNA profiling, which will tell us definitely if Chaman was his father or not. More about that later. What interested me was the color of her body. I told you last time (See SR December 1998 issue) that there are certain poisons which can cause methemoglobin to form inside the body. It is this compound which imparts such color to the body. Well one of such poisons is sodium nitrite. I got a hint that she might have died of sodium nitrite poisoning when I went to her flat and saw that she had unfinished breakfast on her table. She was in the habit of having a full meal in the morning itself. She had prepared Dal and Roti and must be eating it. And it was lying there unfinished. Nearby I could see some dried vomitus on the floor. Obviously when she was eating the food, she must have got sick and must have vomited. I saw a salt cellar on her table which was open. I got quite curious, when I glanced underneath the dining table and found lot of white salt like powder spilled over there. As a poison sleuth, I don't want to take chances and intuition told me there was something either in the salt cellar or in the powder spilled over the floor that we were looking for. So I quietly kept the salt cellar in my pocket and also some of the powder spilled over the floor underneath the dining table. I examined both these substances in my lab. And do you know what I found?" "What? Please tell me doctor. I am getting curious." "Tarun, I had the most extraordinary finding in the salt cellar. It had a substance looking like salt but it was not sodium chloride. It was sodium nitrite. And the salt like powder which was spilled underneath the table was nothing but sodium chloride. Do you get the picture now?" "Well, not really. I don't understand how such a curious thing happened." "To me it is clear like glass. Obviously someone replaced the salt in the cellar with sodium nitrite. And before doing this he spilled the salt underneath the table to empty the cellar so he could fill it with the poison he had brought with him. The only commonly available poison which looks and tastes like salt is sodium nitrite" "Really? Doctor I am getting curious. Please tell me more about sodium nitrite." "Tarun, as I told you earlier, sodium nitrite causes methaemoglobinaemia; even small doses of sodium nitrite can kill within a few minutes. Even the nitrates can be dangerous. Organic nitrates in fact are reduced to nitrites in the intestine. Inorganic nitrates, bismuth subnitrate excepted, are not normally reduced to nitrites in the body, but this may occur when the upper digestive tract (stomach and upper part of small intestines) is infected with nitrate-reducing bacteria, e.g. Escherichia coli. Inorganic nitrates are irritants of the stomach and, in large doses, potassium nitrate is a diuretic. A diuretic is a chemical which increases the production of urine. Poisoning by nitrites is actually not very common. It can result from mistaking this salt for common salt or Epsom salts." "Doctor, under what circumstances can sodium nitrite poisoning occur?" "Tarun, poisoning can be homicidal, accidental or suicidal. With sodium nitrite, accidental poisoning is probably most common, although homicidal poisoning is also possible as we have seen in the case of Radhika. One of the earliest reports of sodium nitrite poisoning came from Middlesborough, UK in 1936. Two adults and their daughter aged five were suddenly taken ill after the midday meal. The adults died before a doctor could reach them and their daughter died shortly after her admission to hospital. It appears they had complained to neighbors of acute abdominal pain and vomiting. Their faces went blue. Investigation showed very similar results to what I found in Radhika's case. A basin of cooking salt and a salt cellar contained sodium nitrite; the upper layer in the latter was of 98% sodium nitrite and the lower layer 98.2% common salt. Unconsumed food contained sodium nitrite, e.g. cabbage 6.5% and Yorkshire pudding 4.5%. The gastric contents of the man contained 4.275 g and those of the woman contained 1.284g of sodium nitrite. Over a gram of the poison was present in the child's vomit. The vomit of the adults was not available for analysis, but presumably they had ingested considerably more than remained in their stomachs. The source of the poison was not determined, but the man had had access to sodium nitrite in the course of his employment. Nobody knows how the mix up happened. Probably someone filled up a half empty salt cellar either intentionally or mistakenly with sodium nitrite." "Oh, that is most extraordinary and bears an eerie resemblance to the case we have on our hands." "Yeah sure. Accidental deaths due to the ingestion of sodium nitrite used in error for common salt in the preparation of soup have also occurred. Several such accidental deaths have been reported. Death in these cases occurred within a few minutes following symptoms which included nausea, headache, vertigo, urgent vomiting, profuse diarrhoea and cyanosis (bluing of the skin). Stomach contents in most of these cases contained sodium nitrite ranging from 1.74 to 84.0 mg/kg of the gastric contents. There was a more consistent concentration in the organs, e.g. in the liver, where the concentration was between 3.0 and 4.35 mg/kg. A quarter of a litre of the soup in most of these cases contained l.5 g of sodium nitrite. I must tell you that the fatal dose of sodium nitrite is from 1 to 2 g. I have already explained you the concept of fatal dose (see "Poisoning by Thallium" SR, October 1997)." "Yes doctor, I do remember you having mentioned it." "In another case, eleven men were poisoned after eating oatmeal seasoned with sodium nitrite in mistake for common salt. The men added more salt from salt shakers later shown to contain sodium nitrite. Immediately after the meal they felt sick and vomited. There was dizziness and abdominal cramps. They went blue and five lost consciousness. Methaemoglobin was later demonstrated in their blood. One of these men, aged 82, died the next morning; his organs had a diffuse brown colour. The source of the poison was nitrite used to cure meat. Only eleven of 125 persons who ate of the oatmeal were affected and these eleven had used contaminated salt shakers of which one contained 0.137% of nitrite. It was estimated they had taken at least 163 mg. In yet another case, a boy aged two months suddenly went blue, 'almost black', after his 7.0 am feed. Sodium citrate had been prescribed for the relief of indigestion and two tablets had been added to the feed. When seen in hospital, about five hours later, the appearance of the child simulated those of congenital heart disease; he was neither distressed nor febrile. A diagnosis of toxic methaemoglobinaemia was made and the remaining tablets, fortunately available, were subjected to analysis. They proved to contain 65 mg of sodium nitrite each. The infant, therefore, had ingested 130mg, the maximum dose for an adult. There are a host of other such cases of which I am aware." "Doctor please tell me a few interesting ones out of these." "In one case, two children aged two and three months respectively took feeds to which from 35 to 40g of sodium nitrite had been added in error for sodium citrate. The elder infant died. Cyanosis and blackening of the mouth were outstanding features. In another case, a boy aged two years vomited while playing with his elder brother aged nine. After a second vomit he was given a glass of water to drink. Vomiting continued and he was taken to hospital. He was deeply cyanosed, collapsed and crying with spasms of pain. Poison was taken out from the stomach with the help of a tube and oxygen was administered, but the child died at about three hours after being poisoned. Sodium nitrite was detected by analysis of his stomach contents. There was methaemoglobin in the blood. It is probable that the boy had ingested and absorbed appreciably more of the poison. The source of the poison in this case was a bottle of sodium nitrite, now nearly empty, which the elder boy had brought for the purposes of a chemical experiment. The dead child had licked the bottle. I must tell you that sodium nitrite is highly soluble in water and its taste resembles that of common salt and that is what makes it such an attractive homicidal poison. Interestingly sodium nitrite is used in machine oil also as a corrosion inhibitor, and deaths have occurred when someone accidentally drank machine oil. There is a case of a girl on record who died in this way. She was eleven years old, and drank a mouthful of machine oil accidentally, some of which she immediately spat out...." "Just a minute doctor. I think sodium nitrite is an oxidizing agent, and if I remember my chemistry alright, corrosion is an oxidative process. Then how can nitrite be used as a corrosion inhibitor?" "Tarun, sometimes oxidizers are also reducing agents. Such is the case of nitrite, which can be further oxidized to nitrate. I must tell you that the tendency of nitrite to act as an oxidizer is increased in an acid environment such as that found in the stomach. At higher pH levels its oxidizing potential is greatly decreased. Corrosion can be inhibited by using a sacrificial reducing agent such as nitrite. Sodium nitrite is also commonly put into packaged foods like meat to keep oxidation from happening. So I was telling you about that little girl. Within an hour she was unconscious and deeply cyanosed. Fortunately she recovered after proper treatment. Analysis showed that the oil contained 36.5% sodium nitrite, 7.5% of an emulsifying agent and 56.0% water. Her stomach washings contained 7-8mg/ 100 ml of sodium nitrite." "Oh, that is certainly most extraordinary!" "Tarun, sodium nitrite poisoning has happened in other ways too. Poisoning by well water drawn from badly constructed wells near farmyards may contain an appreciable amount of nitrate which makes it unfit for drinking and a source of poisoning newborn infants. This illness is however rarely fatal. About 30 cases are on record and only one, it appears, was fatal. It is apparent that the risk is only to infants of under 90 days old, who live in rural communities..." "Doctor, can boiling the water make such water safe? I have heard that boiling the water makes it cleaner." "Yes boiling the water does make it free of infective micro-organisms, because they get killed by boiling, but when the water is contaminated with a chemical substance, it gives no protection whatsoever. On the contrary, it concentrates the nitrates, which can get concentrated upto 3 times on boiling the water! Older children are unaffected, probably because they can tolerate the amount of nitrate likely to be present in their normal fluid intake. It does appear that poisoning in these circumstances is not dependent only upon the amount of nitrate ingested· It has been suggested that poisoning by nitrate will only occur in those whose gastric juice exceeds pH 4.0 and when nitrate-reducing bacteria are present in the upper digestive tract." "Doctor, this is a most extraordinary fact that you have told me. Can you tell me what is the concentration of nitrites in such contaminated water coming from wells?" "The contaminated water, usually drawn from shallow wells, of not over 75 feet deep, usually contains over 20 ppm (parts per million) of NaN03. Methaemoglobinaemia (the existence of too much methemoglobin in the blood) does not normally occur unless the water contains 30 ppm. The upper limit of nitrate should not exceed 10 ppm because as I told you earlier, if boiled the water could be concentrated threefold and thus to a dangerous concentration. Even cows which feed on beet tops rich in nitrates develop methaemoglobinaemia. This is known as the condition of 'purple' cows and is well recognized. Purple is the color the cows get when there is lot of methemoglobin in their blood." "Oh, this is most extraordinary." "There are more interesting facts Tarun. Nitrite poisoning from spinach has also occurred. During 1959-65 in Germany there were 15 cases of nitrite poisoning in infants, aged two to ten months, who had eaten spinach. Nitrite and the remains of spinach were found in the stomach contents of one of the infants. Two factors were responsible. First, the excessive use of nitrate fertilizer, which should not, but often did, exceed 80 kg/hectare. Second, bacterial activity converted the nitrate in spinach into nitrite. Samples of spinach, fresh, frozen and tinned, showed a nitrate contamination of from 40 to 2100 mg/kg. The risk arose when the feed was prepared in advance and stored overlong at room temperature. Even after cooking, a sufficient number of bacteria remained to produce nitrite. The maximum nitrate content of spinach should not exceed 200mg/kg. It has even been recommended that during the first three months infants should not be given spinach." "Doctor, such an interesting poison must have caught the fancy of suicides also. Have there been cases of suicidal poisoning too with sodium nitrite?" "Yes, sure. Suicidal poisoning with sodium nitrite has also occurred. A medical practitioner, aged 51, committed suicide in 1942 by ingesting sodium nitrite. He had been mentally ill for some time. On the night of his death he awoke his son, a medical student, and told him that his mother had suddenly been taken ill during the night. A doctor was summoned and while he was attending to the woman a bump was heard in the passage. The deceased was then found lying on the floor; he died within five minutes of his fall. Poisoning was suspected, but a search revealed only a glass of brandy and another which appeared to contain water. Toxicological analysis demonstrated 2g of sodium nitrite in the gastric contents. The blood was 'dark'. Unfortunately no analysis was made of the brandy or water, otherwise I am sure they would have found nitrite in the brandy. The deceased had given his wife some of the brandy during the night and this may have been the vehicle of poison responsible both for her illness and his death. I feel he first gave brandy laced with nitrite to his wife and then consumed the poison himself, but of course it is only a guess. But sure enough, it is possible to kill someone by lacing his or her drink with as little as 2 grams of sodium nitrite. It was believed that the poison was taken within an hour prior to his death. It was suggested by the relatives that he had died of a heart attack, but the doctor said that he had died of nitrite poisoning." "Oh, doctor. We could go on and on with such interesting stories. Tell me how you can prove Radhika died of nitrite poisoning?" "Tarun, I told you I examined both the contents of the salt cellar as well as the powder spilled over the floor. Now I will tell you what happened. Chaman came to Radhika's house not for reconciliation, but for killing her. He was sure, killing her was his only way out. He got sodium nitrite from a chemistry lab. We have still to find out, how he got hold of it, and who gave it to him. He came fully armed with this poison in a packet. When Shyamala left and Radhika went inside the kitchen to make a cup of tea, he quickly picked up the salt cellar, spilled the salt in it on the floor underneath the table and refilled it with the powder that he had brought. He knew that sometime she would consume the contents of the salt cellar thinking it was salt and she would die. It was no doubt a very clever plan, but thankfully we could catch it. The color of Radhika's body at once told me we were looking for a poison which produces methemoglobinemia, and that was Chaman's undoing. I have found an appreciable quantity of Sodium nitrite from Radhika's stomach contents, and to top it all, the police has found some left over sodium nitrite from Chaman's house too. Initially he denied having any hand in Radhika's death, but when he was told of all the medical and circumstantial evidence against him, he broke down and admitted his guilt." "Very clever doctor. This was a most interesting discussion doctor. Without your masterly deduction, Chaman could never have been caught. People might have thought, it was an accidental death. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. You may not have even thought that it was a poison. I will tell you about death by Potassium Permanganate."
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MAY 1999 ISSUE THE POISON SLEUTHS DEATH BY AFLATOXINS -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. What has happened to him? Please tell me." "Good morning Tarun. The name of this young man is Suman Dubey. He is 25 years old and unmarried. He died this morning in his rented house. He was living alone in this house. He was basically a farmer, but had recently shifted from his village to live in a suburb of Delhi. He was doing some odd jobs for carrying out his livelihood. But he was also getting assistance from his family in his village. I mean, he used to get most of his food supplies from his village." "That's alright doctor. But how exactly did he die?" "Tarun, I am coming to that. For quite some time he was complaining of some vague symptoms. For instance, he was having pain in the abdomen and loss of appetite. He also noted some loss in weight, and a vague swelling of the abdomen. Since he was from a rural background, he did not believe in modern medicine. He was a staunch believer in traditional medicine only. He kept on ignoring his symptoms for quite some time. Last week he visited his village, where he consulted a local doctor. The doctor, after examination told him, that he was getting slow poisoning from some source. He believed that some of his foe was administering poison to him." "Oh, really? And who was he?" "We don't know yet. But the moment Dubey was told about it, he believed it. In fact, he told his family that his milkman wanted to poison him, and was probably poisoning him by giving him a daily supply of poisoned milk. He was daily taking one liter of milk from a milkman called Ramnath." "But why would Ramnath want to kill him?" "That is exactly the question, Dubey's parents asked him. We know this, because we have now interrogated Dubey's parents. Suman Dubey was unmarried as I have already told you. One day, Ramnath came to Dubey's house to deliver the milk along with his young and nubile sister Sita. Immediately Dubey fell in love with her. Once or twice, when she came alone to deliver the milk to Dubey, he even made attempts to make passes at her. Sita immediately complained about this matter to her brother, who came to his house to resolve the matter. There was a big fight between the two. The whole neighborhood knew about it. After this Ramnath stopped delivering milk to Dubey. This was quite expected. But then quite unexpectedly Ramnath again started delivering milk to Dubey. Dubey was initially quite surprised, but he agreed because in this way, at least he could be in touch with Sita." "Oh, I see" "But when the village doctor told Dubey that someone was trying to poison him, he immediately realized why Ramnath had started delivering the milk to him again. Probably Ramnath wanted to get even with him by killing him. He thought that the best way would be to kill Dubey was by giving him small quantities of poison through the daily supply of milk. So he resumed the milk supply to him." "Oh, it indeed appears to me that Ramnath killed him through slow poisoning. Is slow poisoning possible doctor?" "Oh yes. Arsenic is notorious for this. One could give this poison in very small amounts over a long period of time, and the victim would die of slow poisoning. There are several other poisons which could be used for slow poisoning. Dubey's parents have lodged a strong complaint against Ramnath, and the police has apprehended him. He however is asserting that he is innocent and that the police should release him immediately." "What is your opinion in this case doctor?" "Tarun, I am a scientist, and I believe in hard facts. I have done an autopsy on this man, and have come forward with some amazing findings..." "Like what?" "The thing that caught my attention immediately was that his liver was enlarged. I took some liver cells from there and looked them under the microscope. I was surprised to find that Suman Dubey was suffering from a form of liver cancer, known as hepatoma. This finding set me thinking and I did certain other tests. I measured his blood glucose, and I found that it was much less than what it should have been. In technical terms, he was suffering from hypoglycemia, which in plain and simple words means "low sugar in the blood". I also found a chemical known as alpha fetoprotein in his plasma..." "Doctor, these symptoms don't appear like that of a poison to me. It rather appears to me that he died of liver cancer. Where is the criminality involved?" "Tarun, he indeed died of liver cancer. But the problem with me is that a serious allegation has been made by Dubey's parents against Ramnath." "That's right. And now you can tell the police that Ramnath is not guilty. And you can tell them that he died of liver cancer." "Tarun, you may be surprised to know that hepatoma can be induced by a poison, especially if low quantities of it are administered to someone over a long period of time" "Really? That is most preposterous. I wouldn't believe it, if it were not coming from your mouth. Well, anyway what is that poison?" "Tarun that is a very rare poison. It is called Aflatoxin" "Aflatoxin? Never heard of that." "Really. In fact, it is one of the most talked about poisons today. Some people believe that this poison is being used by certain nations in biological warfare." "Come on doctor. It looks like we are again on to some interesting tales about poisons. Tell me about aflatoxins from the beginning" "Tarun, our story of Aflatoxin starts at the most unusual place- the church..." "The church? Come on doctor. How can the story of a poison start from such a holy place as a church?" "In churches, a device if often used for sprinkling holy water. It is swollen at one end, and this swollen end has several tiny holes in it, through which holy water can be sprinkled. This little device is called aspergillum, after the Latin word for sprinkling, which is aspergo." "I still can't make any head or tail of how this will lead us to such a deadly poison as Aflatoxin." "It so happens that there is a particular species of fungus, which under the microscope looks exactly like the aspergillum. Its strands have a tiny end and a swollen end. To many mycologists - scientists who study fungi - this appeared rather like the aspergillum used in churches, so they named it Aspergillus. Since this fungus was yellow in color, and the Latin word for yellow is flavus, they preferred to call this fungus Aspergillus flavus, which became its botanical name. In 1960, an epidemic of serious liver disease was traced to the eating of moldy peanuts. Incidentally it was nothing but Aspergillus flavus, which had affected the peanuts. It was later realized that this fungus released a poison which actually caused the serious liver disease. The toxicologists were looking for a name for this newly discovered poison, and they resorted to the botanical name of the fungus from which the poison was coming. They took the first letter from the name of the genus (i.e. "A") and the first three letters from the name of the species (i.e. "fla"). Together the four letters form the word "Afla". Since toxin is another name for poisons, they added this world to "Afla", and the name of the new poison became Aflatoxin." "Oh, that is most interesting. Doctor, you are incredible. You make things so interesting." "Tarun, Aflatoxins are powerful, tasteless, odorless and colorless mycotoxins that are chemical metabolites produced not only by Aspergillus flavus, but by certain other species of Aspergillus as well such as Aspergillus parasiticus. It is also produced by certain other fungi such as Penicillum and Rhizopus. These are all soil based fungi. Several varieties of aflatoxins are known, but the most dangerous is Aflatoxin B1, with Aflatoxin G1, coming a close second. In fact, Aflatoxin B1 is thought to be the most potent liver cancer producing chemical. Aflatoxins are mutagenic (i.e. they cause mutations), carcinogenic (i.e. they produce cancers), teratogenic (i.e. they cause deformities in the fetus, if pregnant mothers take them), and acutely toxic to most animals and humans. They can cause animals, including humans, to lose their appetites, decrease their feed efficiency and/or cause death. Aflatoxins inhibit the body's immune system and reduce the effects of vaccines. In the U.S., the aflatoxins are the only mycotoxins that are specifically regulated by the Food and Drug Administration or FDA." "Oh, I see" "Human exposure to aflatoxins may occur accidentally by the consumption of foods that have been contaminated by Aspergillus during growth, harvest or storage. Nearly all agricultural products are potentially subject to contamination with aflatoxins. Common sources include grains (e.g., corn, rice, sorghum), peanuts, oilseeds (e.g., cottonseed oil, copra), legumes (soybeans, other beans), and tree nuts (e.g., almonds, pecans, walnuts). The use of Aflatoxin-contaminated feed for domestic animals may result in secondary exposure to humans by the consumption of products such as meat, milk and cheese, and eggs that contain residues of the aflatoxins or their toxic metabolites. The FDA has established enforcement levels of 0.5 part per billion (ppb) in milk and 20 parts per billion for other food products. This means that in the United States, concentrations of up to 20 ppb are permitted in human foods and only upto 0.5 ppb in the milk. Levels of up to 200 ppb are permitted in animal feeds, although there is now a serious concern for secondary exposure to aflatoxins from the use of animal products. As I told you, Aflatoxin B1 is a potent hepatocarcinogen in experimental animals, but tumors may also occur in the colon and kidneys. In rats, tumors develop after the administration of 0.2 micrograms per day or a single dose of 0.5 mg of Aflatoxin B1; the tumor incidence is 50 per cent at 26 months after the latter treatment. There are marked differences in the susceptibility of various species to carcinogenesis by Aflatoxin B1; rats are much more susceptible than mice." "Oh, that is interesting." "Tarun, very high levels of aflatoxins occur in foods in certain regions of Africa and Asia, and people in these regions suffer a high incidence of liver cancer. Within Swaziland, Kenya, Uganda, and Thailand, where epidemiological studies have been conducted, in certain areas the climatic conditions (i.e., high temperatures and high humidity) are favorable for fungal growth; the food supply from these regions shows a relatively high Aflatoxin contamination, and the average Aflatoxin consumption exceeds 10 micrograms per kg of body weight per day. In other areas of the same countries where lower temperatures and lower humidity prevail, the food supply shows a relatively lower Aflatoxin contamination and the average human Aflatoxin consumption is less. In these areas, the incidence of liver cancer is also less. This is a fairly good evidence that aflatoxins are connected with liver cancers. Within each country, there is a direct relationship between the incidence of liver tumors (cases/100,000 people/year) and the average daily dietary intake of aflatoxins in contaminated agricultural products." "That is interesting. You were saying that aflatoxins are also used by certain nations for biological warfare" "Tarun, first of all you must know, what biological warfare is. It is the use of living organisms or their products by a nation for killing the people of its enemy nation. The earliest instance of biological warfare is provided by ancient Mayans, who used to throw deadly snakes in their enemy camps. Now the biological warfare is much more advanced and complicated. People are thinking of using aerosols of deadly bacteria and viruses to decimate their enemies. These aerosols can be released in the enemy territories in the same way that traditional bombs are dropped. On 17.10.96, Alan George of the London Observer reported some interesting facts about Iraq's weaponizing of Aflatoxin. According to him, in May 1988 Iraq began studies on Aflatoxin at its Al Salman facility where the toxin was produced by the growth of the fungus Aspergillus in 5.3-quart flasks. In 1989 Iraq moved its Aflatoxin production to a facility at Fudaliyah. In November, 1989, trials using Aflatoxin warheads (in 122 mm artillery rockets and R400 aerial bombs) were conducted. In 1990 between spring and December 1990, it produced 481 gallons of Aflatoxin in solution. Between May 1990 and August 1990, trials using Aflatoxin warheads were continued. In December 1990 large scale "weaponization" of biological agents started. In 1991 Iraq's Gulf War arsenal included sixteen R400 Aflatoxin bombs and two Aflatoxin warheads for enhanced Scud missiles. In total Iraq produced 572 gallons of concentrated Aflatoxin, of which 410.8 gallons were put into munitions. There is however no evidence that these Aflatoxin weapons were ever used. But under these circumstances, United Nations has continued its sanctions over Iraq." "That is most interesting. Coming to our original case, do you think, Ramnath was intelligent enough to mix aflatoxins in the milk, to cause liver cancer in Suman Dubey so he may die?" "I don't think so. Although there is a distinct possibility of someone doing so, if he were intelligent enough. Ramnath is an illiterate person, and I don't think, he even knows about aflatoxins. I think the rice that he was getting from his village was moldy, and he got his poisoning from that. In fact, I have examined the rice stores in Dubey's house and they are indeed moldy. I examined some of the rice grains under the microscope and I could indeed find Aspergillus in it. So that solves our case. Come, let us tell the police that Ramnath is innocent and that they should release him." "Very clever indeed. This was a most interesting discussion doctor. Without your masterly deduction, police could have unnecessarily went on harassing Ramnath. Suman Dubey's relatives and other people might have thought, it was a case of killing by Ramnath. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison, nitric acid. "
- SCIENCE IN CRIME DETECTION-3 | Anil Aggrawal's Forensic Ecosystem
SCIENCE IN CRIME DETECTION-3 DID THE COMMUNISTS KILL THE CZAR ? Every one knows about the famous Russian Revolution of 1917, when a group of peasants under the leadership of Lenin overthrew the Russian King traditionally called the Czar. These peasants formed the Communist Party which ultimately brought in an era of long suppression. This long era of Communist rule was recently brought to an end. What is not generally known is that the Russian King at that time-Czar Nicholas II- along with his family was brutally murdered by the communists. According to tenets of democracy, even a tyrant King can not be killed without a fair trial. This caused discontentment among the Russian masses but they preferred to keep quiet because of the tyrannical communist rule. Recently, when the winds of change swept Russia, its people have begun to explore what really happened to their King in 1917. For this they have taken recourse to a new forensic technique- the DNA fingerprinting- and have roped in experts from Great Britain. Czar Nicholas II of Russia belonged to the Romanov family. At the time of Russian Revolution, 11 people living in Czar's palace were removed and imprisoned in the gloomy town of Ekaterinburg (This town is now known as Sverdlovsk, named after Jacob Sverdlov, the chief architect of the Czar's assassination). These 11 people included the Czar himself, his wife, his young son Alexie (who was suffering from a dangerous disease hemophilia. In this disease, even a minor scratch can lead to severe bleeding. His four daughters, Tatiana, Olga, Marie and Anastasia, his family physician Dr. Eugene Botkin, the empress maid Demidova, the Czar's valet Tropp and the family cook Kharitonov. These 11 people were shot dead on the night of July 16, 1918. Their bodies were taken to a mine shaft, where 150 gallons of gasoline were poured upon them and then the bodies burnt. The remains were hacked and sawn to pieces, then shoved down the shaft, with clothes and jewellery, 400 pounds of sulfuric acid dumped over it, all to dissolve the evidence of assassination. The world came to know of this horrible crime in 1919, when the White Army took over Ekaterinburg. Since then many theories have emerged that the grand duchess Anastasia survived the massacre. Some theories suggest that Anastasia and Alexie survived while some others suggest that the entire family somehow managed to escape the mass assassination. However, conclusive proof has never been forthcoming. Many imposters have tried to pass themselves as survivors of that massacre. The stakes were high- the Czar's family wealth in cash alone standing at a staggering $800 million. As early as February 17, 1920, a teenage girl was dragged semi-conscious from a canal in Berlin, who claimed to be Anastasia. She had a remarkable similarly to Anastasia and knew the minutest details of the royal family. Her claim was however rejected by a Hamburg Court in May 1968 and in February 1970, by the German Supreme Court. Nevertheless, it was necessary to know whether the Czar's family was massacred or not in 1918 and if at all it was, how many people were actually killed. Recent overthrow of the Communism in Russia fuelled this desire. Coupled with this was the fact that in 1985 a remarkable new forensic technique was developed by a British Scientist Prof. Alec jeffreys. This new technique is known as "DNA fingerprinting" or "Genetic fingerprinting". This was basically developed to find out whether a particular child belonged to a particular mother or not. The actual event which led to the development of this technique is very interesting. A Ghanaian woman and her child were living in Britain as British citizens. Once she and her child went to Ghana to meet their relatives. When they returned to Britain, the boy was stopped by the immigration authorities at the airport itself. They contended that the boy was an imposter and not the real son of that lady. In other words, they were asserting that the boy had been "switched" in Ghana. Blood tests of both the mother and alleged son were conducted, but they were not conclusive. Finally Prof Alec Jeffreys of Leicester University conclusively proved by his new technique that the child was indeed the son of that lady. This technique has now been used in a variety of criminal cases too. For example, if a scientist is given a drop of blood or semen of a person, he can pick out the man from whom it came, from among thousands of men. Every individual contains in his body cells, a unique chemical called DNA (Deoxyribose Nucleic Acid). This DNA differs in different individuals. The DNA of any particular individual will not match the DNA of any other individual in the world. this is the basis of DNA fingerprinting. This may appear to be a very astounding fact, but it isn't. We know that the face of an individual does not resemble the face of any other individual. We can recognize an individual among thousands by looking at his face. Prof Jeffreys developed a novel technique whereby the DNA of any individual could be seen as "bands" on a photographic place (Fig 1A) and matched with the DNA of any other individual. This technique is used in crime detection as follows. Suppose a raped and murdered woman is found. The scientist takes out the semen from the woman's genitals and prepares a DNA fingerprint from there (see fig 1B). This is the column A. Now suppose there are 3 suspects X 1 , X 2 and X 3 . Blood is taken from all the three suspects and DNA fingerprints prepared again. It is seen that DNA fingerprint of X 2 matches exactly with that prepared from the semen (A). Thus X 2 is proved to be the criminal. In July 1991, the KGB exhumed nine skeletons from the Czar's presumed graves in Ekaterinburg. So one thing was certain. 11 people were not killed. Two people in fact escaped somehow. A joint Russian-British project was set up to apply the newly developed technique of DNA fingerprinting. The scientists involved were Dr. Pavel, 37, head of the forensic laboratory for gene fingerprinting (another name for DNA fingerprinting), in the Russian Bureau of Chief Medical Legal Examiner, Dr. Peter Gill, pioneer of forensic gene technology at the Molecular Genetic Laboratory, Aldermaston, Britain and Evin Sullivan, head of the British Forensic Science. First of all they established the sex of the individual skeletons. It was found that there were five female and four male skeletons. Then they tried to find the family group within these nine skeletons, because obviously all were not of Czar's family. They found five skeletons in family relationship and it was established that they were Czar, his wife (Czarina) and their three daughters. So obviously one son and one daughter (presumably Alexie and Anastasia) were missing, which confirmed several rumors that they had escaped. How could the doctors establish that the skeletons belonged to the Czar's family? By a very complicated procedure they first extracted DNA from all skeletons and prepared DNA fingerprints from them. Now if they had the real "known" blood of Czar and his family with them, the scientists could have prepared DNA fingerprints from that "known" blood and compared it with the fingerprints prepared from the boxes. If the fingerprints had matched, they could have positively said that the bones belonged to Czar's family. But this blood was not available. So scientists resorted to a different method which we can explain as below. Look at figure (2). It shows 3 DNA fingerprints. The one on the extreme left is all red. They are the "bands" in the DNA fingerprint of a mother. The one on the extreme right contains all the white bands. They are the bands of father. Actually the bands do not have any color. They just look black. But here they are shown in different colors merely for understanding. Now the important fact to understand is that the son inherits half of his bands from his mother and half of the bands from his father. Which bands will be transferred from the mother and which ones from the father to the son is entirely a matter of chance, but one thing is certain- he will inherit just half of the bands from each parent. This is exactly what is seen in the middle of fig (2). There are many living Romanovs now and some of their bands must match with that of Czar and Czarina. British Royal Family is related to Romanov's family. Queen Victoria was the maternal grand mother of Russian Czarina (Alexandra Fedorovna) and Prince Philip of Edinburgh who is alive, is related to Queen Victoria. A mathematical calculation tells scientists just how many bands of Prince Philip must match the bands of Czarina and his daughters. Prince Philip was approached and he generously agreed to give his blood samples. From his blood, his DNA fingerprints were prepared. Simultaneously DNA fingerprints of Czarina and her daughters were prepared from the suspected skeletons. If those suspected skeletons really belonged to Czarina and her daughters, then a certain fixed number of bands prepared by mathematical biologists must match. To their surprise, the scientists found that the bands matched perfectly. This proved once and for all, that the suspected skeletons belonged to Czarina and her daughters Tatiana, Olga, and Marie. Now the problem was to find whether the suspected skeleton of Czar belonged to him or not. Since the identity of Tatiana, Olga and Marie was proved, it meant that half of their bands must have come from the Czar. When the matching was done between the DNA fingerprints of these three girls and the suspected Czar, the required number of bands matched again. This proved the identity of the Czar too. The problem now is to prove the identity of four other skeletons. Their relatives are being traced and once they are traced, the identity of these skeletons will also be proved beyond doubt. The problem remains: where are the skeletons of Alexie and Anastasia? Perhaps they really escaped as many rumors tell us. But where they are, nobody knows.
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE OCTOBER 1997 ISSUE THE POISON SLEUTHS POISONING BY THALLIUM -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today. You seem to be doing the post-mortem on a rather old man. And he seems to have a most peculiar rash over his face. His hair have also come off his head. Please tell me what happened to him." "Good morning Tarun. This man is a 56-year old man Ramlal, who worked in a store in New Delhi. He suddenly fell ill on 27 August. He developed acute griping pain in the stomach for about 1 hour, and he also had vomiting and diarrhoea. He was well until four days later when he developed severe burning pain in the toes of both feet and tingling sensation in the tips of all the fingers. These symptoms increased over the next five days with some reduction in the power of hand grip. His company admitted him to a leading private nursing home in Delhi. Some leading medical experts examined him, but couldn't diagnose his illness. Ramlal's condition remained unchanged until 9 September when he suddenly developed more symptoms. He had difficulty opening the eyes in strong light, a symptom known in medical parlance as photophobia. There was some disturbance in his vision also. His condition worsened further over the next few days and by 11 September there was drooping of eyelids (known in medical parlance as ptosis) and weakness of face muscles. Swallowing became increasingly difficult. He had difficulty in breathing too, which became so severe that on 15 September, a surgical opening had to made in his neck to help him breathe. However his condition continued to worsen and he died on 19 September, 23 days after his first symptoms started." "Oh, he had a most terrible illness. What do you think he died of?" "Everybody thought he had died from some undiagnosed natural illness. But when the dead body was brought to me, I noticed this curious rash over his face. I also noticed- as you also did- that his hair were also falling off his scalp. This made me suspect that Ramlal was being poisoned- perhaps with thallium." "What! Thallium!! I never thought that it could be used as a homicidal poison" "Tarun, on the contrary, it is a very good homicidal poison. I will tell you in a short while, why this is so. But before proceeding any further, let me tell you a little bit about thallium, so that you can know something about this interesting poison. "Sure doctor, go ahead. I like listening to good scientific stories." " Tarun, Thallium was discovered in 1861 by the British physicist Sir William Crookes (1832-1919). He was working with selenium ores, and in 1861 he came upon a sample of such ore that when heated showed in its spectrum a bright green line characteristic of no known element. It indicated a new hitherto undiscovered element. When he ultimately found it, he named it thallium, from the Greek word thallos meaning "green twig" after the color of its line. The botanical word thallophyta comes from the same root." "That's very interesting. And when did murderers start using it as a homicidal poison?" "It is significant that it was not used as a poison in the first instance. Its earliest use - albeit unaccountably- was to check the "night sweats" in tuberculosis, and when it was noticed that loss of hair occurred with its use, a scientist named Sabouraud instituted its therapeutic use for tinea capitis or ringworm in 1898. The salt used was thallium acetate. It was supplied as a cream (Koremlou cream), containing 7.18% thallium acetate. This practice was finally abandoned half a century later, when it was realized that it was a potential poison. Quite interestingly Thallium has also been used a rodenticide (e.g. to kill rats and moles) and as cockroach poison, particularly in Germany. For this purpose it was available either as tablets or pellets of thallium sulphate or as pastes. Some time in the 1920s the firm of Bayer-Leverkusen in Germany marketed 30 g tubes of a paste known as Zelio paste, each of which contained 2.3%, or about 600-700 mg of thallium sulphate. It had a wide sale on the continent and in the United States, apparently without any restriction of sale or purchase. A French preparation, Virus Rouge contained thallium nitrate. In 1965, the US banned the use of thallium as a commercial rodenticide. However thallium salts as cockroach poison may still be available today in many countries. It is still used in homeopathic remedies!" "Doctor, why did anyone use thallium as a rodenticide at all, when it was so dangerous to human beings?" "Tarun, the earlier rodenticides contained phosphorus, but the value of thallium as a rodenticide lay in the fact that the usual phosphorus containing rat-killer was harmful to the pigs that ate the poisoned rats, whereas the pigs seemed unaffected by rats killed with thallium salts! The use of thallium rodenticides in Europe spread when the Germans conquered and occupied most of Europe during the 2nd World War." "Is thallium useful for other purposes too?" "Yes, Thallium is widely used in industry. Its addition confers a high refractive index on optical glass. For this reason it is used in imitation jewellery which sparkles rather like diamonds. It is also used as an alloy, a catalyst, and for making low-temperature thermometers. But unfortunately like arsenic (see Science Reporter February 1997) , thallium also accumulates slowly in tissues, and over a short period of time, has cumulative toxicity. This method of administration has been used in many criminal cases. I must tell you that the fatal dose of thallium is about 1 g." "Excuse me doctor, what do we mean by the fatal dose?" "When dealing with poisons, we often speak of their fatal dose and fatal period. You will perhaps remember that we first talked about the concept of fatal dose, while talking about arsenic and Spanish Fly (see Science Reporter February 1997 & March 1997). Fatal dose of a poison is the average dose which is enough to kill an adult human being, while fatal period is the average period taken by the poison to kill. A tube of Zelio paste would contain about 0.6 to 0.7 g of thallium which is considered somewhat less than the average dose to kill a human being. Death usually occurs in 11 to 16 days, which is called the fatal period of thallium. If the patient survives 4 to 5 weeks, he would probably live, but the damage to organ systems may be permanent." "Tell me doctor, can thallium be taken for suicidal purposes too?" "Tarun, cases of both accidental and suicidal poisoning occur with thallium, but probably most sinister is its use as a homicidal poison, as it possesses many of the qualities of an ideal homicidal poison. Its salts are colorless, odorless and tasteless, besides being freely soluble in water. Furthermore, in the body the salts are converted into a relatively insoluble salt thallium chloride. This is favorable to the criminal, as the insoluble salts take longer to act; the effects are rarely noticeable before 12 hours and may be delayed as long as 48 hours. This gives the criminal enough time to cover its tracks. Because of the wide gap between ingestion and the onset of symptoms, it is also that much more difficult to associate the symptoms with what the criminal gave to the victim. The initial symptoms of an ideal homicidal poison must mimic some natural disease, and that's exactly what happens with thallium salts too; its initial symptoms are those of a digestive upset of a non-specific character. More specific neurological symptoms occur only after about 2 to 5 days, but still they are very difficult to differentiate from some neurological diseases such as Guillain-Barré syndrome. That is probably why the doctors were at a loss to diagnose thallium poisoning in the case of Ramlal. One of the most characteristic signs of thallium poisoning- gross loss of hair- does not appear until almost a fortnight has passed." "Excuse me doctor, you introduced quite a frightening term Guillain-Barré syndrome. I know I may be deviating from the main topic, but please let me know something about it." "Tarun, the actual name of this condition is Landry-Guillain-Barré Syndrome or LGBS. It is the name given to the conditions previously known by two different names- Landry's ascending paralysis and Guillain-Barré Syndrome. Now the two conditions are known to be identical. It is an acute disease of the nerves, in which they lose their outer protective covering or myelin. This myelin coat is also important for the smooth functioning of the nerves. The result of this loss of myelin coat is that the nerves can not conduct messages properly. This disease occurs at a rate of one case per million population per month. At this rate about 950 new cases of LGBS must be occurring in India every month. The weight of evidence favors that the cause of the disease may be immune related. However in over two-thirds of the cases, a viral infection is associated. After the infection, demyelination- or loss of myelin coat- in spinal and peripheral nerves occur. The symptoms of thallium poisoning may mimic this disease very much. The good news about LGBS is that its prognosis is good, with about 85% of the patients making a complete recovery. The mortality rate is just 3-4%. You would probably want to know, how the name of the disease came about. Well, it comes from the names of three doctors who described this disease at different intervals. The earliest to describe it was the Paris physician Jean Baptiste Landry (b. 1826). Subsequently Paris neurologist Georges Guillain (b. 1876) and Strasbourg neurologist Jean Alexander Barré (b. 1880) also described it correctly." "Excellent. Coming back to thallium. You said thallium fulfills many of the properties of an ideal homicidal poison. It means killers have got an ideal weapon, isn't it?" "Not exactly. Fortunately nature has put some negative qualities in it too. Had it not been for these counterbalancing features, thallium would indeed have been a poisoner's delight." "Really? And what are these counterbalancing features?" "An ideal homicidal poison must not be readily detectable by analysis, but thallium salts can be readily detected. Furthermore, an ideal homicidal poison must disappear from the body after doing its job. Of course a substance can not magically disappear from the body, but what it effectively means is that the poison must at least be destroyed by putrefaction, so that with the onset of time, it becomes impossible to detect that poison. I must tell you that this does happen with most vegetable poisons. Thallium however remains in the body even after putrefaction. It is also not a product of putrefaction." "Wait a minute doctor. You just said that thallium is not a product of putrefaction. You imply that if a poison is a product of putrefaction, it would be an ideal homicidal poison. Please explain this point to me in some detail." "Tarun, first of all you must know what exactly is meant by putrefaction. It is the destruction of the body with the onset of time. You must have noticed that dead animals start to rot after some time. The same happens with human bodies, if they are not disposed of properly. This rotting is known as putrefaction in medical parlance. Now imagine a killer has killed his victim with some poison, and has hidden the body somewhere, say in some bushes or a nallah. With the onset of time, putrefaction would start and the body would start to smell. This would soon lead to its discovery. Now if the poison is such that it is destroyed by putrefaction, the doctor doing the autopsy at this time would not be able to find this poison, and thus the killer would remain untraced. Wouldn't it make an ideal homicidal poison?" "Yes, I do appreciate that. But how can a poison be an ideal homicidal poison, if it is a product of putrefaction? That is what I really want to know." "Tarun, putrefaction is a chemical process, in which many chemicals are destroyed and many new chemicals appear. For instance, the chemicals skatol and indole are produced during putrefaction which indeed are responsible for the offensive smell of the body. If a poison is a known product of putrefaction, it could reasonably be argued by the defence in a court of law, that the detected poison (in a putrefied body) was not administered during life but was produced as a result of putrefaction. Cyanide, alcohol and ptomaines are well-known poisons which are products of putrefaction. Arsenic and thallium, which otherwise fulfil several of the criteria of an ideal homicidal poison do not fulfil this criteria. Similarly another criteria of an ideal homicidal poison is that it should normally be present in the soil." "Well, what is the explanation for that?" "In some communities, instead of cremation, the dead bodies are buried. Poisoners - and in fact all murderers- don't feel easy with this method of disposal of the body, because the potential evidence of murder -the body- remains beneath the soil. Any time after the burial of the body, if suspicion gathers momentum against the murderer, the body can be exhumed, i.e. unearthed and sent for a post-mortem examination. Now if a poison is normally present in the soil, it can be -and has successfully been- argued by the defence that the detected amount of poison had leached in the body from the surrounding soil. Arsenic - a deadly poison- is normally present in the soil in fairly good concentration, and this argument has successfully been used by many murders. But thallium is not present in the soil in any great quantity, and thus the same argument would not hold, if the poisoner had used thallium to dispose of his victim." "Oh, I see. Doctor, can you tell me what symptoms does the victim experience when thallium is given to him?" "Yes sure. Thallium salts irritate the stomach and intestines. It is a gastro-intestinal irritant so to say and that's why symptoms like abdominal colic, nausea, vomiting, diarrhoea occur first. Vomiting and diarrhoea may contain blood. There may be sores in the mouth, a symptom known in the medical parlance as stomatitis. The interesting difference from those of other irritant poisons is that the symptoms start very late- after about 24 to 48 hours of ingestion. In fact it is one of the idiosyncrasies of this poison which makes it a good homicidal poison. Thallium appears to act on nerves too. The symptoms relating to nerves ensue one to five or more days after ingestion. An intense pain develops in the body which is worse at night and is readily provoked by mild stimuli. For instance, even the weight of the bedclothing is enough to induce bouts of pain. The soles of the feet are first involved. The pain gradually travels upwards; to the legs and to the trunk. Sometimes there is intense pain in the big toe, and this can simulate gout. In some cases this may be the first sign. Joint pains which move from joint to joint also occur. There is numbness, especially of the fingers and toes, with detectable loss of sensation to pin-prick and to touch. There is a feeling of tiredness in the legs. This is followed by weakness and finally paralysis. The arms are always less affected. An interesting symptom is the appearance of a "butterfly" rash on the face. In fact this is the first thing I noticed on Ramlal's face, and that had alerted me at once. Another interesting symptom is alopecia or loss of hair. In fact it is highly characteristic of thallium poisoning. Hair loss occurs about a fortnight after the ingestion. The hair is lost in large tufts and within three weeks, the whole of head is bare. The root of the hair -the part of hair that remains buried underneath the skin- shows dense black coloration. This may be seen on the actual hair too, if there has been repeated intake. In fact, if there has been a repeated but interrupted intake, several dark bands coinciding with the period of intake may be seen. Interestingly the same thing happens in arsenic poisoning. It is widely thought that the great Napoleon was killed by the British in this manner. His hair too showed arsenic in bands. The bands are seen only on growing hairs. Thallium finally arrests hair growth and the hair falls. Even you noticed both the rash and the loss of hair, as soon as you entered the post-mortem room. During the autopsy I pulled some of his remaining hair and saw them under the microscope. I was struck with the finding that the hair root was completely black, while normally it is not so. The excessive blackness is considered to be due to an excess of melanin laid down through catalytic action by thallium." "Oh, I see. Coming to think of hair, I find that Ramlal's eyebrows look a little bit curious. Am I right?" "Yes, you sure are right Tarun. Just like hair on the scalp, eyebrows are also involved in thallium poisoning, but for some curious reason, their inner third is spared- only the outer two-third falls off. It is such a characteristic sign of thallium poisoning that it has even been accorded a name; the sign is called signe de sourcil. This is a French term, which literally means "The eyebrow sign"! It has been suggested that the inner third is spared because it is phylogenetically much older than the rest of the eyebrow hair. The fingernails may bear horizontal white bands or white cross lines. This change appears quite late- several weeks after the exposure. That's why you can't see this change in Ramlal's body." "Oh, this is most interesting indeed. Especially the information on eyebrows." "Tarun, there are more interesting nuggets I can give you. You would perhaps be quite interested to know that the noted English crime writer Agatha Christie has given a graphic description of the effects of thallium poisoning in her novel The Pale Horse (Christie, 1952), and this has led a nurse to correctly diagnose a case of thallium poisoning, which had earlier been diagnosed as a case of encephalitis by "experts"." "Really? Please tell me the details of this case" "Tarun, this case occurred in the late 70s. A 19-month-old girl in Qatar was having undiagnosed and unexplained ataxia, which in plain and simple terms means that she was unable to walk. Her physician in Qatar telephonically contacted experts in Hammersmith Hospital, London for help. She had a most extraordinary illness. It apparently began some 10 days earlier with a major convulsion lasting about 5 minutes and associated with a high fever. Over the next 3 days she became increasingly clumsy and lethargic and developed slurring of her speech. By the seventh day of her illness she was unable to sit, stand or walk, and had difficulty with swallowing. The following day she had a further generalized convulsion lasting about 5 minutes. At this stage she was transferred to Hammersmith Hospital. Detailed investigations led experts to believe she was suffering from encephalitis -an infection of the brain- but a staff nurse, who was reading Christie's novel The Pale Horse, realized that her symptoms were remarkably similar to those of thallium poisoning mentioned in the novel! The girl had also started losing hair which normally occurs in about 10-15 days of ingestion- a fact which was also mentioned in the book. She expressed her doubt to the doctors and on subsequent examination, she was indeed found to be suffering from thallium poisoning. On detailed discussion with the child's parents it seemed that the most likely source of thallium was domestic poison used to eliminate cockroaches and rodents in the drains and septic tank of their home. This is a common practice in Middle East!" "Oh, how very interesting. Has Thallium been used for murder in modern times? "Oh yes, it has. One of the most famous cases of murder with Thallium in modern times is that committed by George Trepal - a 42-year-old computer programmer - in 1988. He was a man with a very high I.Q. In fact he was a member of the high I.Q. club Mensa and this case later became famous as the Mensa Murder case. Trepal lived in the small central Florida town of Alturas. He was quite fed up with his neighbor Peggy Carr, 41, and her family, because they always listened to loud music which disturbed him. Carrs' dogs also used to trouble Trepal's cats, which he did not like. In June 1988, he sent the Carr family a chilling typewritten note in the mail. It said, 'You and all your so-called family have two weeks to move out of Florida forever or else you will die. This is no joke.' Carr's family did not pay much attention to this note. Four months later - in October 1988 - Peggy Carr was hospitalized with mysterious symptoms her doctors couldn't explain. At the same time, her son and stepson developed similar symptoms. While they recovered, Peggy did not, and she died with her doctors still mystified as to what killed her. One of her sons was permanently disabled. Officials were completely baffled. Trepal had actually surreptitiously spiked eight-pack of Coca-Cola bottles with thallium nitrate, and secreted them into Carrs' kitchen. Peggy Carr and her family members unsuspectingly consumed the drink. Peggy lapsed into a three-month coma and died thereafter. Four other members of her family were poisoned, though not fatally, but one son, as we have already seen was permanently disabled due to effects of Thallium on his Central Nervous System. Interestingly, Trepal was so confident of his "perfect murder" that when the investigating officials came to him for enquiries, instead of keeping quiet, or expressing his ignorance in this matter, he speculated that someone might poison people to get them to move out of the neighborhood! This immediately allerted the officials, who at once started thinking in terms of poisoning. When Trepal's home was searched, a small vial of thallium nitrate - generally unavailable to the public - was found there. Other incriminating things found in his house were a detailed homemade notebook titled, "General Poisoning Guides," with several entries on thallium, and an extensive store of dangerous chemicals. He was found guilty by the court, and sentenced to die." "Amazing! It appears we have another Trepal on our hands now. It is now sure that poor Ramlal died due to Thallium poisoning?" "Yes, and I confirmed this by several other means too. First of all I analyzed for thallium in his urine, and it was present in high quantities. Furthermore there was a widespread destruction of nerve cells in the brain. Liver and kidneys were damaged as is usually seen in thallium poisoning." "So from an apparent natural death, you have suddenly discovered murder in it. Who could possibly have poisoned him?" "Tarun, before you came, I had already given my findings to police and the police has done a detailed investigation subsequent to my report. You are right that someone was indeed trying to poison him. on detailed investigations, it was found that a colleague Karim was mixing Thallous acetate in his tea daily for some days. He had an old axe to grind with Ramlal. Faced with the scientific evidence, the police questioned Karim and he admitted his guilt. Thus a poisoner who could have gone scot free was caught with the help of forensic science." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very deadly poison - Capsaicin. "
- Contributing Partners
| Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Contributing Partners Gyan Fernando Gyan Fernando, MB, BS, MD, FRCPath, DMJHome Office Pathologist Devon & Cornwall UK E-mail Dr. Fernando Dr. Gyan Fernando was born in Colombo, Sri Lanka (then Ceylon) in 1949. His early education was in a Catholic school and in 1968 he entered the Faculty of Medicine, University of Ceylon, Colombo. Extra curricular activities, notably editing the student "rag" was more important to him than studies. This led to failing Anatomy and Biochemistry. He never failed another examination. However, he considers the five years spent in medical school to have been the best years of his life. In 1973, to the relief of his parents, he qualified as a doctor. Soon afterwards he got married to Ranji, a fellow medical student. He is still married to her. Because of living well away from their parents, the marriage survived the first few crucial years and a son was born in 1976. After a short spell in general medical and obstetric jobs he opted for Forensic Medicine purely because no one wanted the forensic job in a remote but beautiful part of the country where he wanted to live. In 1978 he moved to Britain where he soon discovered that training in Forensic Medicine did not exist. Wisely he decided on Histopathology and in 1984 obtained Membership of the Royal College of Pathologist by examination. (Later, "having furthered the interests of the College" without getting into trouble, he was made a Fellow.) In 1985 he obtained the Diploma in Medical Jurisprudence and was appointed the Senior Forensic Pathologist to the University of Dundee and very soon took over as caretaker head of department. In 1989 he was appointed Senior Lecturer in Forensic Medicine, University of Edinburgh. At present he is the Home Office appointed Consultant Forensic Pathologist for Devon and Cornwall in which post he has been in since 1993. As a firm believer that "autopsy" means "seeing for oneself" and not gathering knowledge from books, he has always been a hands-on pathologist and has very little respect for academics. Another of his pet dislikes is bureaucracy. Over the years he has surrounded himself with books mostly of humorous and satirical writing, favourite authors being P.G.Woodhouse and James Thurber. He also has a fondness for cartoons. Since his school days he has been interested in railways and combines holiday travel with study of railways. Ramesh Kaul Ramesh Kaul, MD., MS., FCCP USA E-mail Dr. Kaul Dr. Ramesh Kaul was born and brought up in India, where he qualified in medicine and surgery from the prestigious All India Institute of Medical Sciences. Later he obtained his post-doctoral qualification in otorhinolaryngology from the same institute. A man of many interests and tastes, he is widely known among his peers as the modern Leonardo da Vinci. He is Board Certified in Pulmonary Medicine, and is currently working as a pulmonologist in the US. His several fields of interest include investigations into metabotropic receptors. He runs his own sites on lung cancer. Among his best known and widely respected sites are www.thorax.us and www.lungcancercare.com and www.rameshkaul.com . He lives in Pittsburgh and New Castle.
- FAQs | Anil Aggrawal's Forensic Ecosystem
Frequently asked questions General What is an electronic journal? An electronic journal is a scholarly publication made available exclusively in digital format, accessible via the Internet. Unlike traditional print journals, it leverages the flexibility and speed of the web, allowing for immediate global dissemination, interactive content, and multimedia integration. Why is your journal titled Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology? Wouldn’t a simpler title, such as Internet Journal of Forensic Medicine and Toxicology, be more appropriate? The journal bears my name to clearly identify the editorial leadership and maintain accountability for content quality. This practice ensures transparency and reflects the personal commitment behind the journal’s establishment and ongoing standards. It is a deliberate choice to build trust and credibility in an era of proliferating online publications. But isn't it somewhat unusual for a journal to be named after its editor? Indeed, it is unconventional. However, the name reflects the pioneering nature of this project—an initiative deeply driven by a single individual’s expertise and passion for forensic sciences. It symbolizes responsibility and personal stewardship over the journal’s integrity and quality. What is the frequency of publication of this journal? The journal publishes biannually, issuing two comprehensive editions per year, each presenting the latest advances and research in forensic medicine and toxicology. How many electronic journals currently exist on the internet? There are numerous electronic journals available online—approximately a dozen that I have personally accessed and linked on our homepage. However, Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology remains a pioneering publication as India’s first true electronic journal across all disciplines and the world’s inaugural electronic journal dedicated to forensic medicine . This landmark journal was launched on February 25, 2000. Are the papers published in this journal peer-reviewed? Who are the editors? Yes. All submissions undergo a rigorous peer-review process before publication. The journal is guided by an International Board of Editors , comprising at least two subject-matter experts from each continent. For a full list of editors and their affiliations, please refer to the International Board of Editors page on our website. Can I cite articles from this journal in my book or academic papers? If so, how? Absolutely. Citing electronic journal articles is now standard academic practice. You are encouraged to reference our papers in your scholarly work. Detailed citation guidelines are available on the Instructions for Authors page. Do electronic journals simply act as repositories for papers rejected by traditional print journals? Not at all. The academic landscape has evolved significantly. Electronic journals are now widely respected, and many researchers specifically choose to submit to them. All papers published in this journal have been written and submitted exclusively for consideration here. Moreover, our journal has a distinct editorial scope and mission that sets it apart from conventional print journals. As outlined on our Home page, we embrace the unique capabilities of digital publishing—such as multimedia integration and broader accessibility—making it a purposeful and independent platform, not a fallback option.
