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- Dr. Anil Aggrawal's Forensic Medicine Hub – Journals, Books, Careers, Programming & More | Anil Aggarwal's Forensic Ecosystem
Explore Dr. Anil Aggrawal’s comprehensive forensic medicine ecosystem—featuring peer-reviewed journals, forensic books, career guidance, programming tutorials, expert quotes, book reviews, and more. A one-stop resource for students, professionals, and researchers in forensic science and toxicology. Anil Aggrawal's Forensic Ecosystem The World's First Online-only Journal dedicated to Forensic Medicine & Toxicology Dedicated to the advancement and dissemination of forensic science and medicine, the platform integrates rigorous scholarship, practical insights, and comprehensive educational resources. It strives to support and connect the global forensic community by fostering academic excellence, profesional development. and , multidisciplinary collaboration, serving as an essential resource for students, educators, and practiconers alike. Fully Open Access Journal International Authorship Publishing Since 2000 Access the journal Anil Aggrawal's Forensic Ecosystem Forensic Medicine & Toxicology Internet Journal Forensic Science Fiction Forensic Quotes & Aphorisms Forensic Programming Forensic Jokes, Puns and Tidbits Forensic Toxicology Science in Crime Detection Forensic Career Explore Books. 2nd Edition Textbook Of Forensic Medicine And Toxicology Price ₹2,510.00 Clinical and Forensic Toxicology Regular Price ₹6,000.00 Sale Price ₹5,789.00 Necrophilia: Forensic and Medico-legal Aspects Regular Price ₹14,727.00 Sale Price ₹12,274.00 Forensic Medicine and Toxicology for MBBS Price ₹1,090.00 Essentials of Forensic Medicine and Toxicology Price ₹1,155.00 Forensic Medicine and Toxicology for Ayurveda Price ₹984.00 Forensic Medicine and Toxicology for Homeopathy Out of stock Basic Sciences As Applied to Forensic Medicine And Toxicology Regular Price ₹1,350.00 Sale Price ₹1,310.00 FORENSIC AND MEDICO LEGAL ASPECTS OF SEXUAL CRIMES AND UNUSUAL SEXUAL PRACTICES Price ₹8,164.00 Injuries Forensic and Medicolegal Aspects Regular Price ₹4,500.00 Sale Price ₹3,999.00 Self Assessment and Review of Forensic Medicine: Volume 1 Regular Price ₹650.00 Sale Price ₹595.00 Narcotic Drugs Price ₹240.00 Modern Diagnostics Out of stock SOME COMMON AILMENTS Price ₹125.00 Textbook of Forensic Medicine and Toxicology (1st Edition) Out of stock
- Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology | Peer-Reviewed Global Resource | Anil Aggrawal's Forensic Ecosystem
Explore a leading peer-reviewed journal in forensic medicine and toxicology. Access original research, case reports, dissertations, and expert insights—freely available to forensic professionals worldwide. ISSN: 0972-8066 (CD version) ISSN: 0972-8074 (Online version) NLM Unique ID: 100960452 Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology ( Peer-reviewed electronic journal for Forensic professionals ) (Published biannually on the 1st January and 1st July every year) [Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology is Indexed / Listed with EMBASE / the Exerpta Medica database, NCJRS (National Criminal Justice Reference Service), Chemical Abstracts Service (A division of the American Chemical Society), Ulrich's Periodicals Directory, MedWebPlus (A service of Flexis, Inc., California), Genamics JournalSeek, getCITED, National Library of Medicine's LocatorPlus, Scopus™ (A service of Elsevier B.V., Amsterdam), Leids Universitair Medisch Centrum, Electronic Journal Miner, EBSCO, Budapest Open Access Initiative (BOAI), Electronic Journals Library (maintained by the University Library of Regensburg), Index Copernicus, Galter Health Sciences Library, Chicago, Directory of Open Access Journals (DOAJ), HINARI and Clarivate Analytics' Emerging Sources Citation Index.] Mentioned in the British Medical Journal [BMJ Volume 324 9 February 2002, page 372 Column - Netlines by Harry Brown, general practitioner, Leeds DrHarry@dial.pipex.com 1st entry in the column mentions this journal A t that time, the journal was hosted at a different URL, which is mentioned in the column. That URL still accesses the journal.] Read this Article (on BMJ) In Association With NCJRS (National Criminal Justice Reference Service), USA Major sources indexing this journal are given below. [For a complete listing, please refer to above paragraph]: Combined index of all Issues Current Issue Volume 27, Number 1, January - June 2026 View Archives Issue Volume-1 Volume-2 Volume-3 Volume-4 Volume-5 Volume-6 Volume-7 Volume-8 Volume-9 Volume-10 Volume-11 Volume-12 Volume-13 Volume-14 Volume-15 Volume-16 Volume-17 Volume-18 Volume-19 Volume-20 Volume-21 Volume-22 Volume-23 Volume-24 Volume-25 Volume-26 Number 1 January - June 2000 January - June 2001 January - June 2002 January - June 2003 January - June 2004 January - June 2005 January - June 2006 January - June 2007 January - June 2008 January - June 2009 January - June 2010 January - June 2011 January - June 2012 January - June 2013 January - June 2014 January - June 2015 January - June 2016 January - June 2017 January - June 2018 January - June 2019 January - June 2020 January - June 2021 January - June 2022 January - June 2023 January - June 2024 January - June 2025 Number 2 July - December 2000 July - December 2001 July - December 2002 July - December 2003 July - December 2004 July - December 2005 July - December 2006 July - December 2007 July - December 2008 July - December 2009 July - December 2010 July - December 2011 July - December 2012 July - December 2013 July - December 2014 July - December 2015 July - December 2016 July - December 2017 July - December 2018 July - December 2019 July - December 2020 July - December 2021 July - December 2022 July - December 2023 July - December 2024 July - December 2025 (Archived issues can be accessed by clicking on them) IMPORTANT NOTE: THE READERS OF THIS JOURNAL HAVE THE RIGHT TO READ, DOWNLOAD, COPY, DISTRIBUTE, PRINT, SEARCH, OR LINK TO THE FULL TEXTS OF ALL ARTICLES AND OTHER MATERIALS APPEARING IN THIS JOURNAL. HOWEVER THE ARTICLES AND OTHER MATERIALS MAY NOT BE REPOSTED ON THE NET OR REPRINTED FOR COMMERCIAL GAIN WITHOUT THE PERMISSION OF THE EDITORIAL BOARD. Scope of the Journal Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology is published online twice a year. It is the world's first online journal of forensic medicine and toxicology. Started by Professor Anil Aggrawal of Maulana Azad Medical College, New Delhi, on 25 February 2000, it publishes original on forensic medicine, toxicology, medical law, science and the law and allied subjects such as criminology, police science, deviant behavior, forensic psychiatry and psychology. Any subject that has a forensic interest e.g., forensic astronomy, forensic economics, forensic geoscience, forensic gemology, forensic herpetology, forensic hypnosis, forensic limnology, forensic linguistics, forensic mathematics and statistics, forensic metallurgy, forensic microbiology, forensic microscopy, forensic nursing, forensic palynology, forensic pharmacy, forensic phonetics, forensic social work, jurimetrics, nanoforensics, teleforensics, veterinary forensics, wildlife forensics etc., as well as papers related to medicolegal aspects of various medical disciplines, such as pediatrics, surgery, ENT, ophthalmology etc. are also published. The journal has regular undergraduate and postgraduate sections, book reviews, interviews with famous forensic professionals, poster sessions, announcements of conferences etc. All back issues are archived for easy access and are available to all. The journal has an impressive editorial board comprising of at least one specialist from every single continent of the world. About 10,000 visitors visit and read the journal daily from all parts of the world. The journal is indexed/listed with several major abstracting services such as Chemical Abstracts Service, EMBASE, Index Copernicus, SCOPUS, and Web of Science [Clarivate (formerly Thomson Reuters)]. For more information, please visit following link (Wikipedia). Submit Here Call for Reviewers Interested in becoming a reviewer for this journal? Check Details Anil Aggrawal's Internet Journal Of Forensic Medicine & Toxicology (Access the pages by clicking on them.) Main Page (current Issues & Archives) Paper/Thesis Submission Guidelines Call for Reviewers Aims & Objectives Frequently Asked Questions (FAQs) Undergraduate Section Postgraduate Section History of the Journal Contributing Partners Be our Sponsor Editorial Board Journal CD Awards Credits Cumulative Index (Sorted by Publishers) of Reviews of Forensic gadgets/toys/other tidbits Models related to Forensics/Toxicology Electronic books related to Forensics/Toxicology Calenders related to Forensics/Toxicology Software/Multimedia/Videotape Reviews Books on CD/Audio books, CDs and tapes Cumulative Index of Editorials Theses/Dissertations Online Courses Reviews with Quizzes Animated Book Reviews Featured Reviews Interviews with Prominent Writers/Authors/Forensic Professionals/ Toxicologists Cumulative index of Book Reviews Sorted by Publishers Subjects (General) Subjects (Technical) The Punjab Corneal Grafting Act, 1963 Leading papers Aggrawal A., Busuttil A. Age Estimation in the living. The Police Surgeon (Journal of The Association of Police Surgeons). No. 38, Jan 1991, Pp 33-36. Aggrawal A. References to the paraphilias and sexual crimes in the Bible. J Forensic Leg Med. 2009 Apr;16(3):109-14. [Pubmed ] Aggrawal A. Estimation of age in the living: in matters civil and criminal. J Anat. 2009 May 11. [Pubmed ] Aggrawal A. A new classification of necrophilia. J Forensic Leg Med. 2009 Aug;16(6):316-20. [Pubmed ] Aggrawal A. A new classification of zoophilia. J Forensic Leg Med. 2011 Feb;18(2):73-8. [Pubmed] Some selected chapters in books and encyclopedias Aggrawal A. (2003) Age Estimation in the Living. In: Payne-James JJ, Busuttil A, Smock W (Eds.) Forensic Medicine: Clinical and Pathological Aspects, Pp. 391-408. Greenwich Medical Media, San Francisco & London Aggrawal A. (2005) Allergies. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 1, Pp. 58-68. Elsevier Academic Press, London Aggrawal A. (2005) Drug Induced Injury, Accidental and Iatrogenic. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 2, Pp. 230-238. Elsevier Academic Press, London Aggrawal A. (2005) Drug Prescribed: Product Liability. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 2, Pp. 243-252. Elsevier Academic Press, London Aggrawal A. (2005) History of Toxicology. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 2, Pp. 525-538. Elsevier Academic Press, London Aggrawal A. (2005) Internet: Toxicology. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 3, Pp. 171-181. Elsevier Academic Press, London Aggrawal A. (2005) Mass Murder. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 3, Pp. 216-223. Elsevier Academic Press, London Aggrawal A. (2005) Mass Poisonings. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 3, Pp. 223-229. Elsevier Academic Press, London Aggrawal A. (2005) Refugee Medicine. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 3, Pp. 514-525. Elsevier Academic Press, London Aggrawal A. (2005) Terrorism: Medicolegal Aspects. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 4, Pp. 269-276. Elsevier Academic Press, London Aggrawal A. (2005) Terrorism: Nuclear and Biological. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 4, Pp. 277-289. Elsevier Academic Press, London Aggrawal A. Tsokos M (2005) Terrorism: Suicide Bombing, Investigation. In: Payne-James JJ, Byard RW, Corey TS, Henderson C (Eds.) Encyclopedia of Forensic and Legal Medicine, Vol. 4, Pp. 289-296. Elsevier Academic Press, London Aggrawal A. (2006) Agrochemical poisoning. In: Tsokos M (Ed.) Forensic pathology reviews vol 4. Humana Press, New Jersey, chapter 10, Pp 261-327. Aggrawal A. (2007) Bride Capture. In: David S. Clark (Ed.) Encyclopedia Of Law And Society: American And Global Perspectives. SAGE Publications, Thousand Oaks, London. Pp. 134-35 (vol. 1). Aggrawal A. (2007) Discrimination, Sociology of. In: David S. Clark (Ed.) Encyclopedia Of Law And Society: American And Global Perspectives. SAGE Publications, Thousand Oaks, London. Pp. 418-20 (vol. 1). Aggrawal A. (2007) Dowry Customs. In: David S. Clark (Ed.) Encyclopedia Of Law And Society: American And Global Perspectives. SAGE Publications, Thousand Oaks, London. Pp. 435-7 (vol. 1). Aggrawal A. (2007) Homicide. In: David S. Clark (Ed.) Encyclopedia Of Law And Society: American And Global Perspectives. SAGE Publications, Thousand Oaks, London. Pp. 709-11 (vol. 2). Aggrawal A. (2007) Incest. In: David S. Clark (Ed.) Encyclopedia Of Law And Society: American And Global Perspectives. SAGE Publications, Thousand Oaks, London. Pp. 730-2 (vol. 2). Aggrawal A. (2011) Sexual Deviant Behavior and Crimes. In: Lynch, VA, Duval, JB (Eds.) Forensic Nursing Science, 2nd ed, ch 41,Pp. 512-20. Elsevier Mosby, Missouri. Aggrawal A., Sardana K (2014) Medicolegal aspects of Lasers in Dermatological practice. In: Sardana K, Garg VK (Eds.) LASERS in Dermatological practice, ch 16,Pp. 441-54. Jaypee, New Delhi. "I play 90 hours a week. Many people call it work."
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE AUGUST 1999 ISSUE THE POISON SLEUTHS DEATH BY DIGITALIS -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. What happened to him? Please tell me." "Good morning Tarun. The name of this young man is Surendra, and he died early this morning in the hospital. He was a business partner of Lokesh. They were in the business of assembling computers and distributing them to the customers. Lokesh has done an assorted medley of jobs before coming to this business, not the least significant of which was his brief stint as a pharmacist. He in fact is a qualified pharmacist and had tried his hand at that job in the beginning. But when he couldn't succeed in that job, he changed to other professions, changing them frequently, until finally he settled in the business of computers about a year back. It is said that his company Goodwin Computers Ltd was doing a business of several lakhs." "Do all these facts have a bearing on Surendra's death?" "I am coming to that. Lately Goodwin Computers Ltd was running in a loss. Surendra found out that Lokesh was illegally siphoning off a major chunk of money to his own personal company Lokesh Computers Ltd, which he had floated simultaneously only about a couple of months back. Surendra realized that very soon, he would siphon off all the money from their joint company to his own personal company. So he was clamouring for a dissolution of their joint company and to give him his due share. It is estimated that Goodwin Computers Ltd was worth about 50 to 60 Lakhs, so obviously Surendra's share was about 30 Lakhs. Lokesh always denied that he was illegally siphoning off money as alleged by Surendra. Ultimately to sign the deal, Lokesh agreed to come over to Surendra's house yesterday evening. After the initial pleasantries, Surendra offered Lokesh drinks which he readily agreed to. They were sitting in the drawing room. After the first drink, Surendra went inside to the bedroom to phone a nearby restaurant for some food. When he returned he found that Lokesh had prepared the second drink for both of them. They were to have dinner after that, after which Surendra and Lokesh would sign the deal to dissolve the company and share the proceeds. Surendra was himself trained in law, and had already prepared the deal. After Surendra finished his second drink, Lokesh got a call on his mobile and he expressed his desire to go to his home for some little work. He said that he would be back within 15 minutes. Just after Lokesh left, Surendra felt a nauseating feeling; in fact he vomited once or twice. But he thought that it was probably because of alcohol. But soon he complained of diarrhoea, fatigue and marked muscular weakness. He knew something was wrong with him, so he phoned his doctor. His doctor advised him immediate hospitalization. In the hospital, he became drowsy and restless. He complained of several strange visual symptoms. He had blurred vision and complained of seeing big dark circles. He also said that things were appearing yellowish to him. The symptoms rather confused the doctors. They were still investigating his case, when today morning Surendra suddenly expired. Surendra's parents have alleged that he has been poisoned and that is why the police has handed over his body to me for post-mortem. My job of course is to find out if indeed he has been poisoned." "What do you make out of this case doctor? Is it really a case of poisoning?" "Tarun, I have made a detailed study of Surendra's symptoms. And again and again my mind is coming back to one poison only - Digitalis. Indeed his characteristic visual symptoms are leading me to that. Of course I will have to do the detailed autopsy to find out if indeed it was digitalis which killed him." "Digitalis! Never heard of it being used as a poison. What is it anyway?" "Tarun, Digitalis is a drug which is given usually to heart patients. And regarding its use as a poison, it has been used several times before for killing people. The effects of this drug are best known to doctors. Indeed one of the first murderers to use digitalis to eliminate his victims was a doctor." "Oh, looks like we are again on to one of your exciting stories. Please tell me about digitalis from the beginning doctor." "Tarun, Digitalis comes from a plant called Foxglove. Its botanical name is Digitalis purpurea, and it has beautiful bell-shaped purple flowers. Figure 1: Foxglove plant from which comes the drug digitalis. Note the characteristic bell shaped flowers hanging like bells In fact the species name purpurea is derived from the purple color of its flowers. The term foxglove actually is a corruption of "folks-glove", which means "fairies glove". The name comes from the finger like appearance of its flowers. Because of the same appearance, it is called fingerhut in German, which literally means "finger hat" or "thimble". The botanical name digitalis is also derived in a similar fashion. In Latin digitus actually means a finger or toe. You may be interested to know that since early man counted on his "fingers", even the numerals 0-9 came to be known as digits, and from this comes our modern word "digital calculator". Isn't it interesting that as widely different terms as digitalis and digital calculator have similar origins?" "It surely is. Since when is this plant known to mankind?" "Tarun, the plant foxglove has been known to man since antiquity and has been used by herb doctors and wise old women (The proverbial "Dadi Ma")(Note to Non-Hindi Readers: Dadi Ma is a word of affection used widely in India for wise, loving grandmother) in multifarious concoctions. But it was used systematically for the first time by a young English doctor William Withering (1741-1799) in 1776. Figure 2: William Withering (1741-1799) seated in his chair. Note the Foxglove plant with the characteristic bell shaped flowers in his hand He received his M.D. Degree from the University of Edinburgh in 1766, and in 1775 came to practice in Birmingham General Hospital. In those days, physicians usually picked their own drugs from the plants, and thus botany was a subject included in medical curriculum. Oddly in his studies at Edinburgh the one subject Withering loathed was botany! But one of his first patients, Miss Helena Cooke, a talented flower painter, changed his loathing into love. She encouraged the young doctor to collect plants for her. Later their love grew, and Withering married Miss Cooke! After marriage he moved to Birmingham to take up his job at Birmingham General Hospital. It may interest you to know that Erasmus Darwin, grandfather of the great biologist, Charles Darwin had actually recommended Withering for this position. His friends included such great luminaries as Joseph Priestley, the chemist and James Watt." "That's interesting. How did Withering come to know of foxglove?" "At Birmingham, one of Withering's Hospital associates named John Ash informed Withering that one Dr. Cawley, principal of Brasenose College of Oxford University, was cured of a heart disease with a secret formula used by an old woman of Shropshire. She was a lady called Mrs. Hutton, and used a decoction containing some 20 herbs. One of these 20 herbs was foxglove, and Withering quickly realized that out of all the 20 herbs, it was the foxglove which was doing the trick. Figure 3: William Withering paying Mrs. Hutton with Gold coins for the secret of Foxglove. Note the Foxglove plants with the characteristic bell shaped flowers in the background Legend has it that Withering paid Mrs. Hutton with several Gold coins for the secret of foxglove which Mrs. Hutton gave him." "Oh, this is most interesting. So how does digitalis help the patient in the heart disease. And how come, a drug which is so useful in heart disease can act as a poison?" "Tarun, all medicines are potentially poisons. Indeed the great Swiss physician and Chemist, Paracelsus (1495-1541) said that all substances are poisons. There is none, which is not. He said that the right dose differentiates a poison and a remedy. You have already seen in my earlier discussions how innocuous looking substances as chilli powder (see Science Reporter November 1997) and common salt (see Science Reporter March 1998) have been used to kill people. You asked how digitalis helps the patient in heart disease. Well, it increases the force of contraction of the heart. In technical language we say that digitalis has a positive inotropic effect on the heart. But in large doses digitalis can be fatal." "Doctor, how much digitalis is fatal?" "Tarun, first of all, I must tell you that digitalis is the name given to the dried leaf of the plant Digitalis purpurea. It contains two principal drugs digoxin and digitoxin. Digitoxin is more toxic than digoxin. While the fatal dose of digoxin varies from 5 to 25 mg, the fatal dose of digitoxin is just 3-5 mg. For this reason, digitoxin is not used by doctors in the treatment of heart disease, because if they used this drug, there would be more fatal accidents, than with digoxin. I must tell you that digoxin is commonly available in the market under the names of Cardioxin, Digitran-250, Digox, Digoxin and Lanoxin. Different drug companies market the same chemical compound, i.e. digoxin under different commercial names. This tablet is available as 0.25 mg tablets. So about 20-100 tablets would be fatal. A patient of heart disease would require about 3-6 tablets daily." "How are you going to determine whether Surendra indeed died of digoxin poisoning?" "Tarun, normally there should be no digoxin in the blood. But even if we presume, Surendra was taking digitalis for some heart ailment, his blood should show very low quantities of digoxin. These low levels are called the therapeutic levels. The therapeutic levels of digoxin in the blood of a patient taking digoxin as a remedy should be around 0.5 to 2.5 nanograms per ml (one nanogram is 10-9 of a gram). Toxic levels are about 3.0 ng/ml. And levels of 10-30 ng/ml are associated with severe poisoning. I have estimated the levels of digoxin in the blood of Surendra, and I have found levels of 35.6 ng/ml. There is indeed no doubt that Surendra had been given digitalis by Lokesh. Lokesh definitely wanted to eliminate Surendra, so he could not ask for his due share in their joint business. In fact, when Surendra went inside to order for food on phone, Lokesh quickly prepared his drink, and laced it with about 30 to 35 tablets of digoxin, which he had already brought with him. Surendra was already a little tipsy because of the first peg of alcohol which he had taken, so he couldn't notice the slight change in taste that must have been induced by the addition of these tablets. I am almost sure this is how Lokesh has killed Surendra. In fact, I have already instructed the police to search Lokesh's house thoroughly. Oh, here comes a policeman with something in his hand which he has found from Lokesh's house. Lo and behold, these are the strips of digoxin tablets. Lokesh would have tough time explaining to the police and the court what these digoxin tablets were doing in his home, especially when he is not suffering from any heart disease." "That was very clever of you doctor. Without your clever deduction - especially your noticing the peculiar visual symptoms of Surendra at the time of his death- everybody would have thought Surendra died of some mysterious natural disease. This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Yellow Kaner. "
- SCIENCE IN CRIME DETECTION-8 | Anil Aggrawal's Forensic Ecosystem
SCIENCE IN CRIME DETECTION-8 WHEN THE BODY TURNS INTO WAX ! Saroj, 16, and Mahendra, 12 were brother and sister. On June 8, 1987, they went to play as usual in the garden, but they never returned. Saroj was a beautiful girl and her parents were always quite reserved in allowing her out alone. On that day however, she was able to cajole her parents into allowing her to go out with her brother. A complaint with the police did not result in any benefit either. The police asked various questions, including about the people the parents suspected. But the family had no enemies whatsoever. As time passed, it became clear that Saroj and Mahendra were kidnapped by some gang, presumably with the purpose of having intercourse with Saroj. There was a gang in town which had once kidnapped a young 19 year old girl, kept her in detention for as many as three months, during which she was forced into intercourse day and night. When the gang members were tired of sex, they would all sit together in a circle and ask her to perform naked dances in the center. After meting out this inhuman treatment to her for three months, they finally did away with her. Her body was found three and a half months later, quite putrefied in a forest. Only one member of the gang could be arrested and from him, the whole story was revealed. The body bore several stab marks, which showed that the modus operandi of the gang was to kill by stabbing. Lakhiram and Revati, the parents of Saroj and Mahendra shivered at this thought. They kept searching for their children, but without any success. On January 15, 1988, one highly putrefied body was found in a forest about 50 miles away from the village of Lakhiram and Revati. Most of the body had been eaten away by animals and maggots were crawling on what remained of the corpse. It was impossible to identify the dead person from the remains. I was called by the police inspector at the place. I made some preliminary examination of the bone and told the police that the bones belonged to a male between 11 and 13 years of age. Moreover, the person, whoever he was, had suffered osteomyelitis (an infection of the bone) in his right leg, about two year before. This description fitted Mahendra exactly. Lakhiram and Revati were immediately contacted and they admitted that Mahendra had suffered from a terrible weeping sore about two and a half years back and also that the sore had healed with great difficulty after about six months of treatment. This, of course, is not the main part of the story. This only established that the victim was Mahendra. But I could not say who had killed him or how had he been killed. This was vital for the police to know. One thing however became clear. If Mahendra had been killed, it was quite possible that his sister Saroj had also been killed and was disposed off in a nearby area itself. A police party launched a massive search for the body of Saroj. They were expecting her body, too, to be in the same state of deterioration; so everyone's stomach was turning topsy-turvy. But lo and behold! Two days later a constable of the search party accidentally stumbled upon a quite well-preserved body of a teenaged girl on the shores of a nearby pond. The body was naked and so well preserved that everybody could at once recognize it was Saroj. When the search party touched the body, it felt as it was like soft wax. Everyone was nonplussed. What had happened to Saroj? I was called immediately. When I arrived there and looked at the body, I realized at once that I was dealing with an adipocere. I rubbed some of the body's material between my thumb and index finger. It gave me a cheesy feeling. I smelt the material. The smell was somewhat similar to that of old cheese. Here then was the body of Saroj, turned into adipocere and intuitively I knew that now I could tell a lot of things to the police regarding the crime. Let us introduce a red herring into the story and first see what an adipocere is. The word adipocere comes from two Latin words, adeps meaning fat and sera meaning wax. It is also known by several other names such as Grave Wax, Mortuary Fat , or Saponified Tissue . This is a situation when the body fat turns into wax under certain special conditions. When a person is killed and thrown away in a forest, his body will normally putrefy. But if there is water in the vicinity or the ground on which the body is thrown is wet and the temperature is quite high then the conditions are just right for the body fats to turn into wax. A very complex chemical reaction takes place for this to happen. For the more scientifically-minded readers, the unsaturated body fats are first saturated to firmer fats and this firmer fat is then split into fatty acids and glycerol. Glycerol usually drains away. The remaining fatty acids (mainly saturated fatty acids such as palmatic acid, stearic acid, hydroxystearic acid and oleic acid) may then combine with body calcium to form soaps and waxes. Adipocere is thus essentially composed of saturated fatty acids such as palmatic acid, stearic acid, hydroxystearic acid, oleic acid and their calcium salts. Adipocere forms mainly at those parts of the body where there is a lot of accumulation of body fat. Such areas are cheeks, buttocks, breasts and thighs. Since Saroj's body had been thrown near a pond, the conditions were just right for her body to be turned into adipocere. Once a body turns into adipocere, it does not undergo normal decomposition, and remains as such. It gives the forensic expert a lot of benefits. For one thing, the features of the person remain discernible. Secondly, since the body is more or less preserved, one can say how the person died. Adipocere is a yellowish white, greasy, wax like substance with a rancid smell. It is lighter than water. If we cut out some adipocere from the body of such a person, and put it in water, we find that it will float. It cuts easily and burns with a faint yellow flame giving offensive odor. Fresh adipocere is soft and moist, but old samples are dry and brittle. Adipocere takes about 3 months to form, so we can form a idea when the person was done to death. The body of Saroj was found on January 15, 1988. So, at a rough guess, she must have been killed on or around October 15, 1987. She had been kidnapped on June 8, 1987. So it appeared that she had been kept in captivity for about 4 months. This pointed to her having been used for sexual purposes. Since her body was well preserved, I could examine her genitals, which too had been converted into adipocere. Her hymen, the soft membrane which cover the vagina, was completely mutilated indicating that she had indeed been used for sexual intercourse. Her left breast and both buttocks showed very clear stab wounds. These stab wounds would normally have been obliterated if normal putrefaction had set in. But since her body had been converted into the wax-like adipocere, the stab marks were clearly visible. Her kidnapping and confinement, her use as an object of sexual intercourse and the method of her killing, all pointed to the dreaded Devi gang which had earlier done the same deed. Devi gang had big political connections and until and unless the police had solid clues to back them, they could not dare to touch the gang. But now since I had provided them with all vital clues, they went fully armed to nab the Devi Gang and made tough inquires. Sure enough, very soon, the gang cracked up and confessed to the abduction, sexual molestation and killing of Saroj. They had to finally kill Saroj because she had become pregnant. When the case went to court, the court admitted my medical evidence and had no difficulty in convicting the members of Devi gang. In this particular case, my knowledge of science helped me to unravel crime. A non-specialist would have been quite nonplussed to see the waxy body of Saroj, but I knew it was adipocere. To summarize, this adipocere formation helped me to (i) establish her identity (ii) establish the cause of her death and (iii) indicate the time of her death. These facts together enabled me to weave a coherent story which ultimately helped in catching the culprits.
- Cookie Policy | Anil Aggrawal's Forensic Ecosystem
Cookie Policy Anil Aggrawal’s Forensic Ecosystem Including Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology Last Updated: [June 20, 2025] 1. Introduction This Cookie Policy outlines how cookies and similar technologies are used on the website operated under Anil Aggrawal’s Forensic Ecosystem , which includes Anil Aggrawal’s Internet Journal of Forensic Medicine and Toxicology . By continuing to use this site, you acknowledge your understanding of this policy. 2. What Are Cookies? Cookies are small text files stored on your device when you visit a website. They are widely used to ensure websites function efficiently and to provide usage analytics for improving content and user experience. 3. Types of Cookies We Use We use only essential and functional cookies , which are required for: Website security and stability Page load performance Session management (e.g., login and logout functionality) Spam prevention in submissions and forms These cookies do not collect personal information and are not used for advertising or tracking across sites . 4. Analytics and Anonymous Tracking We use Wix Analytics , a built-in service provided by our website platform, to collect limited, anonymized statistical data , including: Country of origin Visitor counts and session duration Pages viewed This information helps us understand overall site performance and user engagement. The data is aggregated and cannot identify you personally , unless you are logged in. This service is built into the Wix platform and cannot be disabled individually by us. If you wish to prevent any tracking, you may disable cookies directly through your browser settings. 5. Personal Data Collection via Forms We collect personal data through specific forms on the website for legitimate academic and functional purposes, such as: Paper submissions Store checkouts Guestbook comments Collected data may include: Full name Email address Phone number Submission content (e.g., academic papers) Use of Personal Data: Email addresses of authors may be published alongside accepted papers for academic contact purposes. Phone numbers are collected for internal verification only and are never published or shared externally . Submitted papers are shared only with authorized editorial or peer-review personnel and not disclosed to third parties . Users are informed of any data usage at the point of collection (i.e., on the form itself), in line with the principle of transparency under applicable privacy laws. 6. Login and Session Data Some sections of the website, such as the submission portal, comment areas, and store checkout, may require login. When you log in: Session information is stored for site functionality We may associate activity (such as page visits) with your session No behavioral tracking or profiling is conducted You may log out manually or clear your browser history and cookies to end your session. No data is sold, shared, or used for marketing. 7. Data Sharing and Third Parties We do not sell, rent, or share your personal data with advertisers, analytics firms, or other third parties.We do not display ads or embed third-party trackers. All analytics and session functionality are managed within the secure environment of the Wix platform. 8. Managing Cookies As we use only essential cookies and platform-level analytics, no opt-out functionality is provided within the site. However, you can manage cookies and tracking through your browser: Block all cookies Clear stored cookies Enable private browsing modes Please note that disabling cookies may impact the functionality of features such as login, submission, or checkout. 9. Contact Information For any questions or concerns regarding this Cookie Policy or your data, please contact us via the official email listed on our [ Contact Page ] or within the journal section of the website. We remain committed to protecting your privacy and providing a safe and secure academic environment.
- SCIENCE IN CRIME DETECTION-14 | Anil Aggrawal's Forensic Ecosystem
SCIENCE IN CRIME DETECTION-14 CONTUSIONS - THE VITAL EVIDENCE A remarkable case came to me in the summer of 1992. Bali Ram, a nine‑year‑old stepchild of Hari Ram and Bhairon Devi had fallen down the stairs and had fallen down the stairs and had died. Actually, when he fell down the stairs, there was a big hue and cry in the neighborhood. Some neighbors came to the spot immediately and brought the child to LNJP casualty. The child was declared dead on arrival and sent to me for post mortem examination. A few facts about the family may be said her, before we go on further. HariRam had lost his first wife Kasturi about 5 years back. She had died of tuberculosis. Bali Ram was Kasturi's son. After Kasturi's death, Hari Ram became a recluse for almost two years, but gradually the shock of his wife's death faded and Hari Ram married for the second time. From the beginning, it was apparent that Bhairon Devi, the new bride hated Bali Ram intensely. In the beginning, she would merely ignore him but gradually she started handing him more severe punishment. She would often beat him and deny him food. I got this history from the neighbor. The moment I got this history, I became very cautious and decided to look for clues that might give me the correct story. The boy had died from head injury which he had sustained during the fall from stairs. There were several fractures on his skull, and the brain inside showed blood clots. This was ample proof that he had indeed fallen down the stairs. However, the clues that could give me some 'behind‑the scene' story still eluded me. Finally I turned over the body and looked for injuries more closely. There were several contusions on the back. these are also known as bruises. In common parlance, in Hindi, we know these as " Neel ". These are commonly caused by blunt force application. I had looked at these contusions before starting the post‑mortem, but at that time I thought that they were produced by fall from stairs. Contusions can indeed be produced by a fall from the stairs. However, when I looked at them closely, I found them to have some pattern. These contusions are known as patterned contusions and are quite helpful in the forensic work. They tell us the shape of the object which was used to hit the deceased. If the hitting object was a lathi or an iron rod, the contusions would be linear in shape. If a hockey stick was used to beat the deceased, the contusions would take the shape of hockey stick and so on. Look at the figure A and you would realize that the contusions indeed have a pattern. I tried to decipher what the object could be, but the exact object eluded me. Then suddenly, like a flash of lightning, the object came to my mind. It had to be a coat‑hanger. The contusions looked exactly like that. I told this fact to the police officer Tejpal. I thought that Bali Ram was first mercilessly beaten by Bhairon Devi and then pushed down from the stairs. If this point of view could be proved, it would change the whole scenario from an accident to murder! The case was beginning to take a serious turn. Bhairon Devi was summoned by Tejpal, the investigating officer, and questioned. She reaffirmed that Bali Ram had indeed fallen down the stairs and she hadn't beaten him. She asserted that she loved Bali Ram like her own child. How ever her neighbors refused to confirm her assertion that she loved Bali Ram like her own child. They asserted that she often beat Bali Ram. Finally Tejpal decided to search her house. The specific thing he was looking for, was the hanger with which Baliram was supposed to have been beaten. Finally he indeed found the hanger and brought it to me. When I matched the shape of the hanger with that of the contusions, the shapes corresponded completely. (See figure B). This testified that the boy was indeed beaten. This evidence broke Bhairon Devi and she confessed the whole crime. She was duly prosecuted by the court on my evidence and sentenced to life imprisonment. This case amply illustrates, how a seemingly trivial clue can turn a case entirely.
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE AUGUST 2000 ISSUE THE POISON SLEUTHS DEATH BY ETHYLENE GLYCOL -Dr. Anil Aggrawal “Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this young man is Ramlal and he died this morning. Yesterday night his friend Shyam visited his house with a bottle of liquor as he was reportedly getting married next month, and wanted to enjoy with his friend. Many neighbors saw them enjoying together. He left at around 10 pm. Around 2 am in the night, Ramlal began vomiting severely. Quite alarmingly there was blood in his vomit. At that time only his sister was there at the house. She took him to the hospital, where he died this morning. The doctors were unable to find out what disease he was suffering from. So the police has handed over his body to me, so I can tell them, how he died” “Doctor, are you suspecting some foul play?” “The police certainly is. Ramlal and Shyam are childhood friends. About a year back Ramlal had a severe tiff with Shyam as he had caught him in a compromising position with his sister. Shyam was having an affair with Ramlal’s sister and he (Ramlal) did not like that. At one time in the past, Ramlal had severe fight with Shyam too in this regard. Later Shyam compromised with Ramlal, and swore that he would never meet his sister. Following this Ramlal relented and the two met sometimes, although not as often as they used to be in the past.” “Do you think Shyam give him some poison mixed with alcohol?” “The police thinks so. I have met the doctors and asked them in great detail the symptoms he exhibited at the time of admission. The doctors told me that he was quite inebriated, which was quite natural as till ten p.m. the previous day, he was taking alcohol. But what interested me were the symptoms like coma, seizures, nystagmus, paralysis of muscles of eye and gait, depressed reflexes and tetany. Coma is a technical term for unconsciousness. Nystagmus is also a technical term which describes oscillatory movements of the black circular portion of the eyes (cornea). Tetany refers to spasms of the muscles. Depressed reflexes refers to depression of reflexes like the knee jerk. You may recall that if a person is sitting in a relaxed state, and if his knee is hit gently, at a particular point with a rubber hammer, the lower leg suddenly gives a jerk. This is known in medical parlance as the “knee jerk”. In many diseases, it can not be elicited, i.e. it disappears while in many others it is accentuated. Accentuation of the knee-jerk means that the lower leg would give a more energetic jerk than normal. Knee jerk is a very useful sign for doctors for diagnosing diseases. Neurologists -doctors who diagnose and treat disease of the nervous system - make good use of this jerk for diagnosing diseases. Toxicologists also make use of this knee jerk for diagnosis poisonings, as many poisonings can cause depression of the knee jerk. One of the poisons that cause this is ethylene glycol.” “So you think Ramlal died because of ethylene glycol. Never heard of this being used as a poison. Anyway how can you be so sure that he died of ethylene glycol poison, as you yourself say that many poisons can cause depression of knee jerk?” “That’s right. But look at the cluster of symptoms that he had. They are very typical of ethylene glycol poisoning. Anyway, I would confirm my suspicions by various typical findings after the autopsy is completed..” “Doctor, although I have heard about ethylene glycol in my chemistry class, yet I do not know enough about it to follow your conversation. Kindly tell me something about this poison.’ “Tarun, Ethylene glycol is also called 1,2-ethanediol. Its molecular formula is (CH2)2(OH)2. It is a colourless, odorless, water soluble, viscous, oily liquid possessing a sweet taste and mild odour. It is produced commercially from ethylene oxide, which is obtained from ethylene. Ethylene glycol is widely used as antifreeze in automobile cooling systems..” “Excuse me doctor, what is an antifreeze? Kindly tell me.” “Tarun, antifreeze is a compound which is used in cars to prevent the water in its radiators from freezing. In cold weather, freezing water can cause a burst in the radiator of a car which has been left standing. This freezing can be avoided by adding ethylene glycol to lower its freezing point. Good-quality solutions sold as antifreeze have a sodium-based inhibitor added, to prevent corrosion. Generally a 25% content of antifreeze in the radiator water will give protection against freezing, but some manufacturers prefer 33.33% solution. Antifreeze gives protection against corrosion too, so it is left in the radiator all the year round. An interesting fact is that manufacturers add a fluorescent dye called fluorescein to ethylene glycol. This dye fluoresces in ultraviolet light. This “trick” allows mechanics to detect radiator leaks by using an ultraviolet light. But this very fact can be made use of by doctors in detecting poisoning of patients by this compound. They direct Wood’s lamp on the patient’s urine. If the urine fluoresces, it is a sure sign of ethylene glycol poisoning.” “Doctor, you have used another term with which I am not familiar - the Wood’s lamp. What is it? Is it some kind of lamp made of wood?” “No, no. Wood is actually the name of a physicist who devised this lamp. He was a Baltimore physicist and his name was Robert William Wood (b. 1868). In this lamp, there is a special glass called Wood’s glass, which transmits only the ultraviolet radiation (with some red in the visible region). The radiation thus passed is known as “Wood’s rays”, and have a wave length of about 360 nm. This glass contains nickel oxide. One use of this lamp is for the detection of small spore ringworm of the scalp. I have taken some urine from the urinary bladder of Ramlal and have shone Wood’s light over it. Come on, you can also see it.” “Oh, doctor, I can clearly see the urine fluorescing. This is remarkable. This is enough proof that Ramlal died of ethylene glycol.” “I will do better than that, and come up with some more proofs. So I was telling you that ethylene glycol is used as an antifreeze. It was even used as a coolant in the Lunar Module! It is also used in the manufacture of man-made fibres, low-freezing explosives, and brake fluid. I may tell you that it was discovered as a substitute for glycerine (used in enemas). It has also been used in commercial products such as detergents, paints, lacquers, pharmaceuticals, polishes and cosmetics. It’s other uses are as a preservative in juices and as a deicer. Since the compound is easily available, has a warm sweet taste and produces a state of inebriation much like that of ethyl alcohol, it has been used by poor people in place of alcohol. For the same reasons, it has also been used by people for committing suicide. One can easily mix it in alcohol and give it to his adversary for killing him. Only about 100 ml are sufficient to kill an adult human being. I must tell you that Ethylene Glycol poisoning is one of the most serious and dramatic intoxications encountered in clinical toxicology. Just like methanol and isopropanol, it is used as a second-rate substitute for ethyl alcohol by poor people, because it is cheaper. However, while methanol poisoning occurs in epidemics, ethylene glycol poisoning is sporadic. There was a time when it was used in pharmaceutical preparations (as a solvent), but now it is banned. Yet many cases of poisoning still occur. In May 1998, over 20 children died in Gurgaon after consuming medicines, which were thought to be adulterated with ethylene glycol” “Oh, that’s terrible. How does ethylene glycol kill doctor?” “Toxicity due to ethylene glycol is not as much because of the compound itself, as because of its breakdown produces. Ethylene glycol itself causes some CNS depression, and a state of inebriation quite like that produced by ethyl alcohol. After ingestion, peak blood levels occur at 1 to 4 hours. Half-life of ethylene glycol is 3 hours, which means that half of the quantity ingested would get metabolized in 3 hours. Principally four breakdown products cause damage, namely aldehydes, glycolate, lactate and oxalate. The first three are responsible for severe acidosis. This means that the pH of the blood becomes less alkaline. The damage because of oxalate is because it gets deposited in tissues and causes widespread tissue destruction. Kidney damage is particularly likely. The compound itself is mildly toxic. Acute inflammation of the eye has been reported following accidental eye contact. Contact with skin can cause mild skin irritation. Inhalation can cause toxicity too. Factory workers who are exposed to vapors of ethylene glycol can suffer from chronic poisoning. The symptoms are nystagmus and recurrent attacks of unconsciousness. Toxicity occurs due to two main reasons. Tissue destruction due to deposition of calcium oxalate crystals (mainly in kidneys, but also in brain, blood vessels, liver and pericardium. Because of chelation of calcium, hypocalcemia occurs, and production of severe acidosis due to aldehyde, glycolate and lactate production.” “What symptoms does the victim of poisoning experience doctor?” “Tarun, the symptoms appear in three fairly well-defined phases. The first phase occurs within 30 minutes to 12 hours after ingestion. The patient appears drunk, but there is no characteristic alcoholic odour from his breath. Nausea, vomiting and hematemesis may be seen. CNS effects include coma, seizures, nystagmus, paralysis of muscles of eye and gait, depressed reflexes and tetany is seen as was seen in the case of Ramlal. The tetany is due to fall in calcium levels in the blood. This occurs because ethylene glycol produces oxalic acid in the body and it combines with calcium in the blood to form calcium oxalate crystals. The second phase begins 12-14 hours after the onset of first phase. By this time there is widespread deposition of oxalate crystals in the tissues. This results in tachycardia (increase in heart beat), mild hypertension (raised blood pressure), pulmonary edema (water logging of lungs) and congestive cardiac failure (heart becoming unable to pump blood out to the body). The third phase occurs 24-72 hours after ingestion. There is flank pain, with tenderness in the chest and evidence of kidney disease usually manifested by stoppage of urine. This is technically known as oliguria. Proteinuria (protein appearing in the urine) and microscopic hematuria (blood appearing in the urine) may occur. Urine with a low specific gravity may be observed.” “Doctor what is its fatal dose and fatal period?” “The Fatal dose is about 2 ml/kg weight, or about 120 g for a 60 kg man. About 90% patients die within 24 hours due to CNS damage. Rest die in about 8-12 days from renal failure.” “Doctor, I was reading somewhere that in 1937, more than 100 people died in USA because of ethylene glycol. Is this information correct?” “ Oh, you are talking about the famous Elixir of Sulfanilamide-Massengill disaster of 1937, which occurred during the months of September and October 1937. No, the incriminating compound was NOT ethylene glycol, but DIETHYLENE GLYCOL - sometimes also known as ETHYLENE DIGLYCOL. There is a difference between ethylene glycol and diethylene glycol. While the formula of ethylene glycol is (CH2)2(OH)2 or C2H6O2, as I told you earlier; that of diethylene glycol is HO[CH2CH2O]2H, or C4H10O3. In fact, the formula of Polyethylene Glycols (PEGs) is HO[~CH2CH2O~]nH. You can go on substituting n for 1,2,3 etc to get higher ethylene glycols. Substitute n for 1, and you get the so-called (mono)ethylene glycol - or simply ethylene glycol - about which we have been taking. Substitute n=2, and you get diethylene glycol, the one responsible for the tragedy you are talking about. Substitue n=3 and you get triethylene glycol. I do not know of any interesting disaster connected with this or any of the higher ethylene glycols. But Polyethylene glycols are toxic no doubt. Polyethylene glycols with molecular weights between 200 and 600 Daltons are clear viscouse liquids, while those with molecular weights between 1000-6000 are rather wax like or waxiform. These are known as Carbowaxes. Their solubility in water is - very roughly - inversely proportional to their molecular mass.” “Good. So what was the "Elixir of Sulfanilamide-Massengill" disaster all about?” “Tarun, Let me first give you some background, so you could appreciate the full significance of this disaster. Scientists had long been hunting for some kind of a magic bullet which could kill disease causing bacteria. The first antibiotic - as we all know - was penicillin. Although it had been described by Alexander Fleming as early as 1928, a usable form was not developed till 1941. So before this time, the world was practically devoid of antibiotics." “Sorry to interrupt you doctor, but what exactly do we mean by the term "antibiotic"?” “Tarun, the term antibiotic - as we all understand and use it - refers to a chemical substance produced by a LIVING ORGANISM, generally a microorganism, that is detrimental to other microorganisms. If the chemical is NOT produced a LIVING ORGANISM, we would NOT call it an antibiotic, even if it killed or were detrimental to microorganisms. Therapy by such a chemical would be known as "chemotherapy", as against "antibiotic therapy", if it were to be done by antibiotics." “Oh, I see.” Prontosil soluble Sulphanilamide Note the -SO ₂ NH ₂ moiety in both. “Coming back to our story. Before 1941, some of these other chemicals (i.e. those not produced by living organisms) were known. The first one to be described was a red dye PRONTOSIL RUBRUM - or "prontosil red" as some would call it - which cured certain bacterial infections in mice. It was described by a German chemotherapist Gerhard Domagk (1895-1964), in 1932. Domagk was awarded the 1939 Nobel Prize for Medicine for this remarkable discovery. Drugs against bacteria were very much sought after during this period, and virtually anyone who could discover an effective medication could get the Nobel Prize. Alexander Fleming, who discovered Penicillin, the first antibiotic got the Nobel Prize for Medicine 6 years later - in 1945. Thankfully his discovery penicillin had come in handy for wounded soldiers during World War II, which had started in 1939." “It must have been a proud moment for Domagk to receive the award.” “No, he never received it, because he was not allowed to." “Why so? That is preposterous.” “Tarun, Domagk lived in the era of Hitler's Germany. Right from the days of Ossietzky, Hitler had adopted a policy never to allow any German to receive the Nobel Prize." “Doctor, I know I am deviating, but who was Ossietzky.” “Tarun, Carl von Ossietzky (1889-1938) - sometimes spelled as Ossietsky- was a German journalist and pacifist who was against the war, and wrote a lot against the Nazis. He was declared the winner of the Nobel Prize for Peace for 1935. Hitler was enraged because the award had been received for writing against him. At least he perceived the situation like that. So he didn't allow Ossietzky to receive the award. In fact a policy was developed never to let any German accept the award. Domagk became a victim to this policy. It was only two years after the war ended - in 1947 - that he could travel to Stockholm to receive the award, but unfortunately by that time the award money had been reverted to the Nobel Foundation, so he did not receive any money. He did however receive the gold medal and the citation (the diploma)." “Doctor, you know so many stories. I am amazed. This must have been a great setback for Domagk.” “Sure it was. However I think that for Domagk, the greatest reward would have been when his own daughter Hildegarde was saved by his drug "Prontosil Rubrum". In February 1935, she pricked her finger with a needle and developed a severe bacterial infection - called septicaemia. Domagk's new drug "Prontosil Rubrum" was given to her and her life was saved. While on the subject of "Prontosil Rubrum", I may tell you that a related compound "Prontosil soluble" also became available during this period. It soon became clear that these compounds themselves were not responsible for the killing action. Instead, a chemical moiety - known as sulphonamide group - broke off from these compounds within the body. It was this chemical moiety which was responsible for the antibacterial activity of Prontosil. The chemical formula of this moiety is -SO2NH2. Scientists derived a number of drugs from this chemical moiety. All these drugs became famous as Sulpha drugs, and they heralded the era of modern chemotherapy against bacterial infections. By 1935, many of these sulpha drugs had become very popular and were marketed as tablets and capsules. One such drug was Sulphanilamide, which was successfully marketed by The Massengill Company of the US. In September and October of 1937, the executives of this company decided to market the same product for children too. But since small children can not take tablets or capsules, it was decided to sell the formulation in the form of an elixir. Technically speaking an elixir meant the solution of a drug in ethyl alcohol and NOT in any other solvent. But the company decided to make a solution of Sulfanilamide in diethylene glycol. Their Elixir was essentially a solution of 10% Sulphanilamide in 72% percent diethylene glycol, with some flavouring and coloring agents. In those times, it was not legally required for a company to test a new drug on animals before marketing it. So The Massengill Company floated the new elixir without any tests. Since diethylene glycol is a dangerous poison, about 76 people died as a result of taking this elixir. The cause was severe liver and kidney damage caused by diethylene glycol. These 76 were the confirmed deaths, but there are unconfirmed reports asserting that more than 100 people died as a result of this disaster.” “That is amazing. The Massengill Company must definitely have been sued by the relatives of all these people?” “No. How could anyone? The Massengill Company was well within its legal rights to sell anything to the consumers. You may laugh at it, but the company could only be prosecuted for mislabelling its product as an elixir, which applies only to an alcoholic solution and not to a solution in diethylene glycol. That is a very small offence though. The fact is that at that time all drug manufacturing and distribution companies were being guided by a very old and archaic law - The Pure Food and Drugs Act of 1906. Althouth it had been amended by the Sherley Amendment of 1912, it still allowed lot of freedom to drug manufacturers. It was only this tragedy, that the much more modern law - The Food, Drug and Cosmetic Act of 1938 was passed. In our country too, a similar Act was passed two years later. It was initially known as The Drugs Act of 1940. In 1962, by an amendment, cosmetics were also included within the purview of this Act and it became known as The Drugs and Cosmetics Act. It is unfortunately true, that it usually takes a great disaster for the government to change an archaic Act.” “Oh, come on. You can't say that just because of one incident, can you?” “Perhaps you are right. But interestingly yet another disaster occurred in late 50s and early 60s which caused further changes in similar Acts around the world. It was the much feared Thalidomide disaster, but if I were to tell you about this, we would be deviating from our initial topic - ethylene glycol.” “Doctor, either you should have not brought about this new topic at all, or you should explain it fully. Since you have mentioned it, my curiosity is aroused. Please let me know about this disaster. I don't mind being late at home.” Thalidomide Glutethimide Glutethimide is still sometimes used as a sedative. Note the structural similarity of both. “Alright, as you wish. But let me tell you an additional fact about Diethylene Glycol. Its story did not end with the Massengill company. This compound keeps raising its head again and again. As recently as in July 1985, Diethylene Glycol was again in the news - this time because it was discovered that Austrian wines were contaminated with this substance. Stocks of all Austrian wines were promptly withdrawn throughout the UK. About Thalidomide? Well it is chemically written as C13H10O4N2. This drug was marketed in more than 40 countries - mainly in West Germany and the UK in the late 50s and early 60s. In Germany, it was manufactured by Chemie Grünenthal and marketed by it as Contergan since 1956, and enjoyed good sales. In Britain it was licensed by Chemie Grünenthal to the Distillers Company. It became available in Great Britain from the beginning of 1958 as Distaval. In Sweden the license was given to a local company Astra. It was being used by pregnant women to counter nausea, which is usually seen in early pregnancy. It also acted as a sedative. Developed in West Germany in the mid-1950s, Thalidomide was touted as one of the safest sedative-hypnotics, just as Titanic was hailed as the unsinkable! Ironically both suffered the same fate. Titanic sank on its maiden voyage, and Thalidomide sank too - in a figurative sense. It caused birth defects in children known as peromelia. An estimated 5,000-10,000 children suffered from this terrible deformity. This ultimately caused its downfall.” “What is peromelia doctor? I have never heard this term.” “Tarun, peromelia is the collective name given to a number of deformities, where there is a congenital absence or malformation of the extremities. It is caused by errors in the formation and development of the limb bud, which normally occurs from about the fourth to the eighth week of intrauterine life. As I told you peromelia has several forms. One of the worst and most horrible is amelia in which there is a complete absence of all limbs. There is just head and the trunk of the baby - absolutely nothing else. Since all the essential organs of the body - brain, heart, lungs, kidneys, liver etc reside in head and trunk, such an infant, if cared for properly would not die. But imagine the quality of life of such an infant. He is just like a plant - with an essential difference. He can see, feel and sense his absolute helplessness. Fortunately this condition was very rarely seen in thalidomide disaster. The second form is Ectromelia, in which there is the absence of one or more extremities. There was also an interesting condition known as phocomelia or “seal extremities", because the extremities resembled like those of a seal. In this condition, the upper part of the limb was extremely underdeveloped or missing, and the lower part was attached directly to the trunk, resembling the flipper of a seal. It was as if the palms and feet were directly stuck to the trunk. Its counterpart was Hemimelia in which the upper part of the limb was well formed but the lower part was rudimentary or absent. Finally there was a condition known as Sirenomelia, in which the newborn resembled a mermaid or siren. The term literally means “mermaid extremity”. This was also a very severe abnormality in which the legs were fused to a greater or lesser degree and contained malformed bones; the anal and urinary orifices were absent, and the genitals and parts of the intestinal and urinary tracts were malformed. As limb buds form during fourth to the eighth week of intrauterine life, this condition was very common in women who took thalidomide during this period. Exposure during the later periods of pregnancy did not cause any abnormalities. Interestingly in the US, the rights had been given by Chemie Grünenthal to a local company W.S.Merrell Co., but they could not market it, because of the earlier Act passed by the Govt, about which I have already told you. The Food and Drug Administration (FDA) was simply not convinced of its safety. In Canada, a license to market it was granted by the Canadian Food and Drug Directorate. In our country too the drug failed to gain entry because of usual bureaucratic hurdles. Thus US and India were the two big countries which were saved of this disaster!” “Chemie Grünenthal must have been prosecuted for their wanton act?” “Tarun, it has traditionally been very difficult to prosecute big giants. Nine senior members of Chemie Grünenthal were tried in a criminal court in Aachen, but they disputed the very fact that the limb deformities had been caused by thalidomide, although there was very strong statistical evidence in favour of the fact that thalidomide did cause this disaster." “What was this evidence doctor?” “Phocomelia is such a rare disease that no case was reported in Germany in ten years between 1949 and 1959. But in just a single year in 1961, there had been 477 cases! Moreover after this drug was taken off in 1961, the cases stopped once again. Yet the defendants challenged the causation. Finally trials had to be conducted on rabbits to convince the court that it was indeed the thalidomide which had caused these deformities. Yet the case dragged on for about two years and was finally abandoned. The representatives of the deformed children however settled the issue with Chemie Grünenthal for just about 114 million Deutschmarks! In Britain, a good thing that happened was that The Medicines Act was passed in 1968, which forbade any company to market drugs like this. As I told you earlier, it is an unfortunate truism that it often takes a great disaster for governments to "wake up" from their slumber. This was yet another case of a disaster paving the way for the passing of a law. In our country too, this disaster had its echoes. The Drugs and Cosmetics Act of 1940, which had become archaic, was amended in 1964, mainly because of this disaster. Many other indigenous drugs were brought into its purview, which includes Ayurvedic and Unani drugs. As an aside I may tell you that Thalidomide comes in two enantiomers. While the right-handed molecules had the desirable property of sedation, it were the left-handed molecules which caused the deformities. So if somehow, only the right handed molecules had been used for sedation, there would have been no adverse effects at all!” “Now you are introducing new things. Please tell me what are enantiomers?” “Tarun, certain chemical compounds are mirror images of each other. So although their chemical and even structural formula is same, they are not exactly the same molecules. They are in fact mirror-images of each other. These compounds are called enantiomers. Your right and left palms are good examples of enantiomers. Although they are similar looking, you can't superimpose your one palm over the other. If you look at your right palm in the mirror, it will look like a left palm and vice-versa. If a chemical compound exists in its two enantiomeric forms, they would roughly be equal in number. When the scientists of Chemie Grünenthal manufactured thalidomide in their factories, roughly equal number of both enantiomers were produced. Only the right handed molecules - the so called D forms - were beneficial. The left handed molecules - the so called L forms - caused the defects.” “How very sad! Had they known about this, they would only have manufactured the D forms.” “It appears doubtful to me, because technology to do so did not exist at this time. Although once formed, they could have perhaps separated the two. I may tell you that there are several other drugs, which show the same dilemma. One of the best known is Dihyroxyphenylalanine (DOPA) which is used for a Central Nervous System disorder Parkinsonism. In this disorder, the person trembles and has a staggering gait. This disorder can be treated by DOPA. This too comes in two enantiomers - a D form and an L form. I may tell you here that these forms can be differentiated by a very shrewd test. It you pass a beam of polarized light through them, the D form would shift it to the right and the L to the left. In fact the D form and L form get their names from this property. D stands for Dextrorotatory (or turning to the right) and L stands for Laevorotatory (turning to the left). In the case of DOPA, the L form of the molecules are effective. D forms are not effective, but fortunately they do not cause any deformity too. It still makes far better sense to give just L-Dopa or Levodopa (as some call it) than just plain DOPA, which would contain both forms of the drug, of which the D form would be totally useless. You may be interested to know that in 2001, three scientists received Nobel Prize in chemistry for developing the first ever chiral catalysts [N.B. by the author: The original article appeared in AUGUST 2000 - at a time when these Nobel Prizes had not been awarded, so one would not find this information in the original article. It has been added subsequently]. These are the Japanese Noyori Ryoji (1938 - ) and the American scientists K. Barry Sharpless (1941 - ) and William S. Knowles (1917 - ). It was as late as in 1968, that Knowles produced the first ever chiral catalyst. This was seven years after thalidomide had been banned from everywhere. So as I said earlier, even if scientists would have known about the L forms of thalidomide causing problems, they probably would not have been able to synthesize it preferentially." “Doctor you have talked about chiral catalysts. What exactly are these?” “Tarun, chiral means "handedness". Remember that the art of palmistry - studying hands - is also known as Chiromancy, or Chirosophy! Chiral catalysts can favour a chemical reaction in the direction of a particular enantiomer - literally a left handed or a right handed molecule. Thus if one were to manufacture L-dopa without the help of these chiral catalysts, one would get both D and L forms in roughly equal quantities. But if these chiral catalysts were used, one could manufacture only the useful L-form. These catalysts are thus very helpful in the drug industry.” “Doctor you are amazing. Coming back to our initial topic. How do doctors diagnose ethylene glycol poisoning?” “One of the best points in favour of ethylene glycol poisoning is that the person appears inebriated without accompanying smell of alcohol. Calcium oxalate crystals in the urine are present. I have examined the urine of Ramlal and have found calcium oxalate crystals. The White Blood Count (WBC Count) may rise to 10,000-40,000 per cubic mm, while normally the maximum limit is just about 11,000 per cubic mm. On autopsy, there is extensive destruction of the renal substance. On microscopic examination of kidneys, birefringent crystals of oxalate are seen. I have found all these changes in Ramlal’s body after autopsy. I can now guess what happened yesterday at Ramlal’s house. Shyam was stung at Ramlal’s behavior and wanted to get even with him. He arrived at his house with a bottle of liquor and a can of coolant. This was probably hidden somewhere in his clothes. Shyam was preparing the pegs. After two or three pegs, when Ramlal was sufficiently inebriated, Shyam furtively mixed some quantity of coolant in his alcohol. Ethylene glycol is tasteless, so Ramlal did not know that something had been mixed in his drink. Moreover he was already drunk and was not paying very much attention to him. After giving him two or three more pegs like this, he left for his house. He was quite pleased with himself, as he had thought he had planned a perfect murder. Lo! Here comes the policeman from Shyam’s house and he has recovered the left over bottle of coolant from his house. Shyam does not have a car and would have tough time explaining to the court what this bottle was doing in this house.” “That is very clever of you doctor. Without your clever deduction it would have been impossible to say how Ramlal died and Shyam may have gone scot-free. What are you going to tell me next time?” “Tarun, next time, I would tell you about a very interesting poison - Botulinum Toxin.”
- Author Submission | Anil Aggrawal's Forensic Ecosystem
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- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE AUGUST 1997 ISSUE THE POISON SLEUTHS POISONING BY METHYL BROMIDE -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? Oh well, today you are examining the dead body of a young infant. What happened to him? Please tell me." "Good morning Tarun. The name of this 3 month old girl is Varsha. She is the daughter of RadheyShyam and Sita who were living in the ground floor of Mahajan's house as tenants. RadheyShyam and Sita are a young couple in their late twenties. Mahajan was living with his family on the first floor. He had been asking RadheyShyam and Sita to vacate his house for quite sometime but they refused to vacate the house. Many times Mahajan had threatened them with dire consequences, but nobody took it seriously..." "So obviously he killed Varsha to teach them a lesson?" "Don't jump to conclusions Tarun, I haven't finished yet. Yesterday, i.e. on 20 August, RadheyShyam, Sita and their daughter Varsha had gone to attend a marriage party from where they returned late in the night. On entering their house, both RadheyShyam and Sita experienced a foul smell. However, as they had experienced smell from the sewage during previous days, they took little notice of the smell. These sewage problems had resulted in maintenance work on the sewage pipes in their street just after noon on the very same day. They nourished the infant and went to bed in their room at about 10.30 pm., keeping the door open to the infant's next door room. Two hours later at 1.30 am and about 3 hours before expected, Varsha started to cry vigorously. The mother took care of the child, who vomited and had severe diarrhoea. At the same time the parents were alarmed by a "burning" sense in their eyes, throat and mouth, and they also started to vomit. They contacted a local doctor on phone but he didn't turn up. Without knowing what was happening in the house, they realized that something very wrong was going on, especially as Mahajan was threatening them with dire consequences for quite some time. They came out of their house immediately along with their child, called a Taxi and went to Sita's parents' house to spend the rest of the night. Subsequently Varsha became drowsy and unable to drink water or milk. At noon on 21st August, Sita's parents and all the other adults went to the city's hospital arriving there at about 1 pm. But unfortunately she was declared dead on arrival." "Oh, that's indeed very sad and depressing. So what do you think was going on in the house?" "Tarun, the whole scenario and symptoms of the three persons involved point very strongly in favor of one poison- methyl bromide." "What? Methyl Bromide? Doesn't sound like a common poison to me. Please tell me more about it." "Sure Tarun. Methyl Bromide surely is not commonly known, but it is indeed a very interesting poison. Methyl Bromide (CH3Br) is also known as bromomethane, monobromomethane, Embafume or iscobrome. Pure methyl bromide is a colorless gas that is heavier than air. Thus it is one of those rare poisons which occur as gases. Odorless and tasteless in low concentrations, it has a musty, acrid smell in high concentrations. That's why RadheyShyam and Sita noticed that strange smell on coming back from the marriage party." "Doctor, who in the world uses methyl bromide, and why?" "Tarun, Methyl Bromide is in relatively widespread industrial use as a fumigant and insecticide because of its effective penetrating power and absence of fire or explosion hazard. Occupational exposure to it also occurs frequently. Nobody knows about Indian figures, but it is estimated that about 75,000 American workers are occupationally exposed to this gas annually. Its toxicity is severe and despite safeguards, cases of acute and chronic intoxication occur, chiefly in fruit and tobacco industries, because of its use in these industries as a fumigant and an insecticide. It has also been used as a refrigerant, solvent, methylating agent, and in dyes and fire extinguishers." "Quite interesting. How can poisoning occur due to this gas?" "Tarun, toxic exposure to this gas can occur by inhalation as in the case of Varsha or by skin absorption. Body tries to excrete this poison out of the system. Excretion takes place mainly through the lungs. The remainder is metabolized in the body, and inorganic bromine is excreted in the urine. In European countries cases of accidental poisoning due to fumigation of houses are quite well-known." "But at the time of fumigation, the houses are vacated. How can one possibly get poisoned?" "Yes, you are right Tarun, yet poisoning has occurred in sinister ways. In many European countries, the houses are made up of wood, and the European house-bores (Hylotrunes bajulus) occasionally invade old wooden houses. To kill these house-bores methyl bromide is often used for fumigation, and as you rightly say, the houses are indeed vacated for fumigation. But cases are known in which the gas has entered the sewage pipes of the fumigated house (which of course had been vacated) and from there it travelled to the main sewage pipe. From there it gained access to the adjacent houses or even to houses at quite some distance. Of course, it can occur only if the houses in question don't have the water-locks that are now obligatory in all sewage pipes. Now you must be able to understand why you have water-locks in the sewer pipes of the places where you relieve yourself. If these water-locks were not made obligatory, gases from the adjacent houses, or even from the main sewer could easily enter one's house." "Quite interesting. Have people died in such a way?" "Yes, I am personally aware of persons dying in such exotic manner. These cases are frequently reported in learned journals too." "Doctor, how does methyl bromide kill a person? Since bromine itself is a poison, I would tend to believe that the bromide ion in the methyl bromide molecule does the damage." "Tarun, it would indeed appear so, but it is not true. I will give you certain figures which will make things very clear in your mind. Normal bromide levels in adults are about 0.3-0.4 mg/dL and come primarily from bromide residues in fumigated foodstuffs. If one ingests an inorganic bromide, such as sodium or potassium bromide then he does die of bromine toxicity. Technically we know it as bromism. In the case of a fatality due to inorganic bromide ingestion, the blood levels of bromine are quite high- almost 300 mg/dl, which as you can see are almost 1000 times the normal level. Levels lower than this produce serious toxicity but not death. For instance levels of 100 mg/dl produce toxic symptoms and level of 200 mg/dL produce serious toxicity. But in the case of methyl bromide intoxication, which is an organic bromide, death may occur when the bromine levels of the blood are as low as 8-9 mg/dL. This clearly means that bromide ion is not responsible for the death in the case of methyl bromide intoxication." "Then what is the cause of death in these cases?" "Tarun many important enzymes in our body contain important entities called Sulfhydryl groups. These groups can chemically be represented as "-SH". Methyl bromide releases methyl ions in the body, which combine with these sulfhydryl groups and make the enzymes ineffective. This is technically known as methylation of the sulfhydryl groups. Enzymes in the central nervous system seem particularly prone to this destruction. That is why a patient suffering from methyl bromide poisoning displays neurological symptoms quite prominently. Major manifestations are vomiting, headache, vertigo, gait disturbances, double vision, delirium and seizures. All the three persons in question have displayed several of these symptoms. Since methyl bromide affects the brain in a major way, in cases of death, the main changes are observed in the brain. The brain is water-logged and swollen, which we term as edema of the brain. The coverings of the brain, or the meninges are red and there may be hemorrhages under them. Loss of neurons have also been seen at times." "Did you see these changes in the body of Varsha?" "Yes, Indeed I did. But the most interesting finding was the bromine levels in her blood which are almost 17 mg/dL. As you know this is much above the normal limit and does indicate that she was exposed to methyl bromide." "Then surely Mahajan has done the trick. But how did he introduce the gas in RadheyShyam's house?" "Mahajan was asking RadheyShyam and his family to vacate his house for quite some time, but they were not doing so, so he decided to finish them off in a very clever and sinister manner. I must admit that I have never heard of such an exotic method to kill an entire family. In fact, he would have easily got away with the murders, had the police not decided to contact me..." "Doctor, I am getting curious. How did he do it?" "He contacted an insecticide company and bought a cylinder of Methyl Bromide gas on the pretext that he wanted to fumigate his crops. From the cylinder he connected a pipe and inserted the other end of the pipe into the chimney which leads to the kitchen on the ground floor. Since the top of the chimney is on the barsati above the first floor, where Mahajan was living, it was accessible to him. After making this elaborate arrangement, he opened the valve of the cylinder releasing the gas in the chimney. The gas being heavier than air, quickly "dropped down" into the kitchen and from there it seeped into the entire ground floor. When RadheyShyam and his family entered their house after attending their party, Mahajan had literally converted their place into a gas chamber! RadheyShyam showed presence of mind and left the house quickly with his family, otherwise even he and his wife would have died. I have asked the police personnel to look specifically for a gas cylinder in Mahajan's house. Oh here comes the police inspector... What! you did find the methyl bromide cylinder in his house. Look Tarun, I was right. My investigation has indeed worked. The police can now successfully prosecute Mahajan." "Fantastic! And many thanks for letting me know about such an interesting poison. You indeed are a great poison sleuth. What are you going to tell me next time?" "Tarun, next time I shall tell you about ratti seeds, which as you shall see is another important poison. This is a vegetable poison, as you shall see. "
- This is a Title 02 | Anil Aggrawal's Forensic Ecosystem
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- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE SEPTEMBER 1999 ISSUE THE POISON SLEUTHS DEATH BY YELLOW KANER -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a very young girl today. What happened to her? Please tell me.” “Good morning Tarun. The name of this six year old girl is Radha. Her father is a Secretary to the Government of India, and fairly well-to-do person. He had only one child. Yesterday she was playing along with her friends under a tree in a park near her house. The time was around 4 pm. There were about 5-6 other boys and girls with her. They were apparently fine when they were playing. Suddenly Radha started vomiting. She had diarrhoea too. She was rushed to the hospital, where the doctors thought she was having gastro-enteritis, and she was being treated along those lines. The doctors also noted some additional symptoms. I have talked to the doctors who treated her. And they say that they noted clamminess of skin, coldness in extremities, dilation of pupils, sunken eyes and delirium. The pulse was slow and feeble in the beginning, but later it became fast and irregular. After a few hours she had convulsions, then paralysis, and finally death. She died at about 8 am in the morning today." "Oh, that is most terrible doctor? Why do you think she died? Did she die of any natural disease? Or did she die of infections such as gastro-enteritis?" "Tarun, it doesn't look like natural death to me. The symptoms are pointing towards a poison which affected her heart. So probably we are talking about some heart poison here. I have gone to the place where she was playing, and I was surprised to see that there were lot of Yellow Kaner plants in the garden where she was playing. These plants are known to botanists as Cerbera thevetia or Thevetia peruviana. In normal everyday parlance, they are known as Pila kaner or be-still tree. I am inclined to believe that either she took the seeds of that plant by mistake, or somebody gave it to her on purpose.” “That’s most preposterous. I have seen Kaner plants growing along the roads, but I never believed it was such a dangerous poison” “Oh, sure they are poisonous. The yellow oleander or be-still tree is a native of tropical America and is now widely cultivated as an ornamental shrub in tropical and subtropical regions of the world, including India. It is a small shrub with milky sap. Leaves are evergreen, alternate, ribbon like, about 6 inches long, 3/16 to 3/8 inch wide, dark and glossy above and pale beneath. Flowers are more or less fragrant, funnel form, yellow or peach-colored, rarely white, 2 to 3 inches long and to 2 inches wide, the five lobes spirally twisted and not spreading. Fruit is somewhat diamond-shaped -distinctly so in cross section. It is about one and half inches wide and 5/8 inch thick. It turns from green to yellow; then the thin layer of flesh becomes completely dehydrated, the skin becomes black and wrinkled and disintegrates, exposing the bony, light brown, attractive stone, which contains two to four flat gray seeds. The sap of the plant may cause skin inflammation in sensitive individuals. Chewing the bark or seed kernel causes a slight numbing sensation and a feeling of heat in the mouth, and purging. Ingestion of a toxic dose causes burning in the mouth, tingling of the tongue, dryness of the throat, headache, vomiting, purging, excitement followed by drowsiness.” “Sounds like a very dangerous plant to me. Are all parts of the plant poisonous? Also please tell me, which poisons are found in this plant?” “Except for the thin layer of flesh covering the stone, all parts of the plant are poisonous, especially the seeds, which contain 3.6 to 4 per cent of the cardiac glycoside thevetin. This toxin is one eighth as potent as ouabain and very similar to digitalis in activity, about which we have talked last time. Also present are thevetoxin (C30H46O10), similar to but less toxic than thevetin; neriifolin (C33H61O30) more potent than thevetin in action on cat heart; peruvoside (C30H44010); and also ruvoside (C30H46010). There has also been reported a bitter principle that acts on the central nervous system and produces tetanoid convulsions.” “Doctor, how much portion of the plant can cause death in a human being?” “Nothing is positively known about the fatal dose in human beings, although experiments have been done on animals. Fifteen to twenty grams of dry leaves are fatal to the horse; lesser amounts are fatal to cattle. Since such fatal experiments can not be conducted on human beings, our knowledge of the fatal dose of Cerbera thevetia depends upon actual cases of death which have occurred following its ingestion. A single seed has caused death in a child; 8 to 10 seeds in an adult. About 5-10 leaves of the plant are also said to be fatal. The root is very poisonous.” “Oh, I see.” “Tarun, this plant is a very popular ornamental in warm regions of both hemispheres, especially in dry coastal areas because of its resistance to drought and salinity and because it is not eaten by goats and cattle. It is often planted in numbers as a hedge. Grazing animals instinctively avoid this plant, and that is why this is a very popular plant as a hedge in India. Besides India, it is also found in other parts of the world. It is occasionally seen in the southern half of Florida and California, is very common in the West Indies, Latin America, Africa, and the Orient. In the Hawaiian Islands it has been declining in popularity with the realization that it is the most frequent local cause of human poisoning. The fruit flesh is eagerly consumed by chickens and is casually eaten by humans in Ghana and Queensland. The handsome stones, after polishing, are worn as pendants, tied together as rattles, or strung with other seeds in necklaces. Many myths and legends are associated with this plant. In the West Indies, the stone is carried in the pocket in the belief that it will ward off hemorrhoids. In East Africa, it is put in the hand of an infant at birth as a good luck token. Quantities of the seeds have been exported from Hawaii to the mainland of the United States for extraction of thevetin as a substitute for digitalis, but 40 per cent of the patients receiving this drug have suffered gastrointestinal disturbances. Indian scientists believe the more recently discovered peruvoside holds greater promise in cardiac therapy. In Africa, the seed kernels are occasionally chewed to cause purging. In the Philippines, half of one leaf is given as an emetic and purgative. The sap and bark have been utilized in small amounts to treat malarial fever as well as to induce vomiting and purging, but overdoses have caused paralysis and death. The sap has been applied to sores and ulcers, also to tooth cavities and decayed teeth to relieve toothache. It is said to cause the teeth to disintegrate. In Brazil, the seed is taken as an abortifacient. In Indonesia, immigrants from India have been seen to dry and smoke the leaves. The toxicity of the plant has been generally known since the sixteenth century. Its Sanskrit name "Ashwamarak" is translated as "horse killer. Early European explorers in tropical America reported that the Indians used the seed for homicidal purposes. In India, the seeds are commonly employed for suicide and homicide, and in Bombay they are used for killing cattle. They have poisoned pigs in Queensland.” “Looks like a very interesting plant to me. Have there been cases of poisoning with this plant before?” “Several cases of Yellow Kaner poisoning have been recorded in India. In 1900, a woman in India took two seeds in a suicide attempt. The following day, she experienced vomiting, purging, pain in the throat, headache, and fainting spells alternating with drowsiness. Her pupils were normal; heart action was weak and pulse slow. She recovered after three days of treatment. In November 1962, a four-year-old boy in Poona, India, swallowed a seed at 6 P.M., vomited 15 to 20 times, was hospitalized, was found very restless, with sunken eyes but normal pupils, dry tongue, and cold extremities. An electrocardiogram showed severe abnormalities. The following morning diarrhea occurred; on the second day the pulse became irregular, and it remained so for 36 hours. Treatment was continued for eight days; then the child was discharged with normal pulse and heart action. Some interesting cases have come from Queensland, Australia. In one case, a 3-year-old girl played "tea parties" under a yellow oleander tree in her backyard. She later developed persistent vomiting, sweating and bradycardia. Cardiac arrest occurred during her transfer to hospital and she could not be resuscitated. Another young girl was "dared" by her brother to eat the fruit of the yellow oleander. She did, and later developed severe vomiting and a variety of cardiac arrhythmias which persisted for three days before she recovered. In southwest Africa, two European children were poisoned by eating the seeds, and one died in six hours. In Southern Rhodesia, a death occurred two hours after ingestion of one seed." "Looks like this plant has really caused deaths! In this case doctor, how are you going to prove to the court of law that this child died of Cerbera thevetia poisoning?" "Tarun, I have examined her stomach, and have found remains of some leaves which look very much like Cerbera thevetia leaves. This is a very strong indication that she was given the leaves of Yellow Oleander to eat. I did not stop at that. I examined the extracts of her heart muscle and it demonstrated the presence of poisons found in Thevetia leaves or fruit. This is ample proof for any court of law to assume that Radha died of Yellow oleander poisoning. Actually when I saw Kaner plants growing in the garden nearby, I got suspicious. I thought that there might be some foul play involved in this. I found out that the father of this girl, one Mr. Sharma, had sacked one of his juniors Katkar about a year before, and since then Katkar held a grudge against Mr. Sharma. I may tell you that Katkar was a fairly intelligent man, and in his college, he had studied botany and chemistry with keen interest. Apparently he was aware of the poisonous nature of the Cerbera thevetia plant. He wanted to get even with Mr. Sharma very keenly. He had observed that there were Cerbera thevetia plants in the nearby garden, and that Mr. Sharma's only child Radha used to play there. On that fateful day, he came to the child and somehow coaxed her to chew those leaves. I really don't know what he told to the child, but her friends who were playing at a short distance away are saying that they did see Katkar talking to Radha, and Radha subsequently chewing the leaves of Kaner plant. You might think that it is very silly for a child to listen to such strangers, but you must keep in mind that a six year child does not have much judgement of her own. She apparently chewed some leaves on Katkar's insistence and that was the cause of her death. Come, let us tell the police to catch Katkar, because it is he who is responsible for her death. "That was very clever of you doctor. Without your clever deduction everybody would have thought Radha died of some mysterious natural disease. This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. You would normally think it to be a vitamin, essential for growth, but it is a very dangerous poison too. I will talk about Vitamin A next time."
- SCIENCE IN CRIME DETECTION-11 | Anil Aggrawal's Forensic Ecosystem
SCIENCE IN CRIME DETECTION-11 WHAT DO THE BONES TELL US ? Two years back, I was called to a village near Alwar to solve a very bizarre case. While some digging was going on for a construction purpose, a laborer unearthed several bones. He immediately ran to his contractor and showed him the bones. The contractor contacted the police and the police in turn contacted me. That is how I came into the picture. While I was going through the police records of the area, I realized that about 2 years back a 22‑year‑old boy was reported missing from that village. His name was Suresh. There was a widely held rumor that Suresh had run away from his house in search of a proper job. It was common view that he was quite dissatisfied with his parents and wanted to live away in an independent manner. So, when, one day Suresh was not found in his home, everyone in the village assumed that he had run away from home. Suresh's parents however were not ready to admit that he had run away. They constantly maintained that he had fallen in the hands of some criminal who had killed him and had buried him somewhere. The real story was deeper than this. Actually, before Suresh's disappearance, nobody could even think about it. Suresh was in love with a local belle Geeta. She was the daughter of a rich money‑lender of the village, Karan Singh. Karan Singh had repeatedly warned Suresh not to meet Geeta but, since his own daughter was secretly in love with Suresh, he couldn't stop their meetings. Once he had openly sworn to kill them both, if they met again. About a month after Suresh's disappearance, Geeta was found missing from her house too. The story took a new turn now. Was Geeta secretly kidnapped by Suresh? Were Suresh and Geeta separately kidnapped and murdered by Karan Singh's goons? Or, was their disappearance totally unrelated to each other? Nobody knew what indeed had happened. To be sure, Geeta was extremely beautiful and she could very well have fallen in the hands of a rapist and murderer. But, how to know what had really happened. Nobody even was sure that Suresh and Geeta had been killed. When I examined the bones preliminary, I found two skulls among the bones, so it was sure that I was dealing with a least two dead people. But, I had to prove that out of them one skull was a male and the other, a female. Only then, could we prove that Karan Singh had indeed got Suresh and Geeta murdered. Not only that I had to prove that out of other bones too, half belonged to a male and half to a female. This was challenging task, but I decided to undertake it. How do we find out sex of the victim from the bones? Many times I have been asked this question by the police officers and public. In this case, I am going to provide you with my well kept secrets. Many sexual differences are found in the skull. Look at fig.1, carefully, which shows two skulls‑ one of a male and the other a female one. The upper one is male skull, while the lower one is a female. There are several ways in which we can say that a given skull is male or a female. One is to look at the bone just beneath the eyebrows. This is technically known as SUPRA ORBITAL RIDGE . It is much more prominent in a male skull than in a female skull (shown in the figure by arrows). Further when you see the angulation between the forehead and the nose, you find that in a male skull, this angulation is very prominent. The bone behind the ear is known as MASTOID PROCESS . This is larger, round and blunt in a male skull and smaller, smoother and pointed in a female skull. This point is also shown in the figure by arrows. There are several other differences in the skulls, but these three are very prominent in the given diagram and I generally infer the sex from these 3 points. Let us now come to the jaw technically known as MANDIBLE. The jaw bone above is of male, while the jaw bone below is of female. The jaw bone is squarer in the males while it is much more rounded in the females Fig 2. Hip bone shows the maximum differences between the two sexes. There are two hip bones in each individual. If you stand with your arms akimbo, your palms are over the hip bones. These hip bones unite with the back bone(SACRUM) and from a circular jug like structure known technically as PELVIS. Nature has made pelvis much wider in women because , women have to bear children. The babies, while they are within the bomb, remain enclosed by pelvis. If nature had made pelvis narrower in females, babies would find it very difficult to come out of womb at the time of delivery. It is the wide pelvis, which gives the females their characteristic waddling gait. We make use of this fact in determining, whether a given hip bone is of a male or of a female. Look at Fig.3, it shows 2 hip bones. The upper one is a male hip bone, while the lower one is a female. The angulation of the bone is more in male as shown in the diagram. There is a notch in the hip bone which is known as GREATER SCIATIC NOTCH . This notch is shown in Fig 4. This notch is more acute in the male and much wider in the female(as shown). The backbone or sacrum is shown in Fig 5. Sacrum is narrower in the male. You can guess that the sacrum on the left is a male one. Feeling like a detective already? Well, let's go on. There are differences in arm bones and thigh bones. The rounded projection, which you are seeing fits into the shoulder. This rounded projection is noticeably larger in the male. Yes, you are right; the bone on the left is a male one. Finally look at fig 7, it shows the thigh bones. The lower position fits into the knee joint. If we stand, the thigh bone erect on the table, then the male thigh bone known technically as FEMUR , makes a greater angulation than the female thigh bone. In the given figure, the bone on the left shows an angle of 80 0 and the bone on the right shows an angle of 76 0 , so obviously the left bone belongs to a male. Using these criteria, I could prove that there were in fact two sets of bones‑ one belonging to a male and the other to female. Armed with this knowledge, police raided the house of Karan Singh and took him into custody for interrogation, In the beginning he denied of knowing anything, but later broke under pressure. He admitted to having killed both of them when he realized that Geeta had becomes pregnant. The court gave him rigorous imprisonment for life. By reading this account you must yourself be feeling like a detective already. If you like, you may preserve these issues of 'Crime & Detective'. Who knows, one day you might turn out to be a great detective and help the police.
