Search Results
107 results found with an empty search
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE AUGUST-SEPTEMBER 1998 ISSUE THE POISON SLEUTHS POISONING BY CADMIUM -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a young girl today. What happened to her? Please tell me." "Good morning Tarun. The name of this young girl is Kanta, and she died this morning in the hospital. She was a chemistry student and about 19 year old. Yesterday night she took part in a party thrown by Sohan who was her classmate. Three other students also participated in that party, two of whom were girls. So in all there were 2 boys and 3 girls, including Kanta and Sohan. All are chemistry students studying in a local college. At the party, Kanta took some food and some soft drinks. Soon after that she complained of a choking sensation around her throat and excessive salivation. She also had a feeling of nausea and vomited several times, and had diarrhoea too. She was rushed to a local hospital, where the doctors diagnosed that she was suffering from gastroenteritis, a kind of infection of the stomach and intestines which gives rise to these symptoms. It was thought that she had some form of food poisoning. But what was surprising was that the other four students did not have any problem whatsoever. Had they suffered the same symptoms, the death could have been passed off as a natural death due to gastroenteritis, but since all the others are well off, the police has suspected some foul play and has brought her dead body before me. Of course they have requested me to conduct a post-mortem on the dead body and tell them about the cause of death." "Oh, so how are you going to find out the cause? Do you think that there has been some foul play somewhere?" "Well, anything is possible in this world. I contacted the doctors in the local hospital where she was taken, and also went through her hospital case sheet. What caught my attention was that Kanta was suffering from severe aches and pains too. And these aches and pains started only after she drank the soft drinks, and ate the foodstuff at Sohan’s house. I do not know of any form of gastroenteritis where you also get generalized aches and pains...." "So what are you trying to arrive at?" "Tarun, I have made a detailed study of the symptoms which Kanta displayed, and a very unusual poison is coming to my mind as the possible cause of her death" "Doctor, what is that poison? Please tell me. I am getting curious." "Tarun it is a very unusual poison- cadmium chloride." "Cadmium Chloride? Never heard of its being used as a poison. Is it a poison really? "Yeah it is indeed a very deadly poison. If fact its very discovery is related to its toxicity..." "Really? How? Seems like we are in for another of your interesting historical stories." "Yeah, it does make an interesting story. The story starts in the early part of 19th century. Zinc oxide was then widely used for a number of ailments, and was freely available at chemists shops. To ensure that the medicines were not adulterated, the Government of Germany in those days employed district physicians. Their job was to go to chemists’ shops and find out if the medicines they sold were spurious or not. One such physician named Rolow – who was incharge of the province of Hannover - got the reports of toxicity from zinc oxide being sold at local chemists’ shops. From the reports of symptoms, he suspected arsenic poisoning (for details of arsenic poisoning, see Science Reporter February 1997 issue). So he went around from shop to shop, collected zinc oxide samples from the shops and put them to test. One of the standard methods in those times to test for various oxides was to treat them with hydrogen sulphide. This caused various metallic sulphides to form which could be detected from their color. When Rolow treated zinc oxide with hydrogen sulphide, he got a yellow precipitate strongly resembling the sulphide of arsenic. From this he concluded that the samples of zinc oxide were indeed impure- they contained arsenic oxide as well." "So did they really contain arsenic?" "Wait. The local supply of zinc oxide was made by one influential businessman- a man called Hermann. He was also a chemist by profession. He got his own samples tested for arsenic in his own way. He employed all chemical tests known for arsenic at that time and came to the conclusion that his samples did not contain arsenic at all. On the strength of his analysis, he applied to the local authorities, requesting them to restart his supply of zinc oxide to the local chemists’s shops." "So how was this controversy resolved?" "To resolve the controversy, the authorities of Hannover employed the services of a very reputed chemist of those times- Professor Friedrich Stromeyer (1776-1835), head of the department of chemistry at the Göttingen University. The added advantage was that he also held the post of Inspector General of all Hanover chemists’ shops. Hermann’s factory was situated in a place called Schönebek. Samples of zinc oxide were sent from Schönebek to Göttingen where Professor Stromeyer got to work. Quite intelligently first he investigated how zinc oxide was being produced. He found that chemists in Schönebek calcined zinc carbonate to obtain zinc oxide. So he started from zinc carbonate instead, and heated it strongly. To his surprise he got a yellow colored compound. He was expecting zinc oxide, which as we all know is a white colored compound. He asked both Hermann and Rolow to explain that." "Oh, so even the Great Stromeyer was confused, is it?" "Not in the least. On the contrary he gave enough opportunities to both sides to explain their stand before he got to work. Interestingly both sides gave wrong explanations. Hermann explained away the color by saying that the samples contained iron, although it is not known how that explained the yellow color. For him it was better to explain by resorting to something like iron which is a natural constituent of the body, and can do no harm to anyone. Well, to be sure, even iron can be poisonous, but for that it should be administered in very large quantities. Rolow, who was intent on getting Hermann’s factory closed, explained away the color by contending that the samples contained arsenic. After listening to both sides, Stromeyer got to work and discovered a hitherto unknown metal in the samples. It looked very much like zinc, but could easily be separated from it by means of hydrogen sulphide. So much did it look like zinc that Professor Stromeyer preferred to call it Cadmium- after cadmea, a word which in Greek means zinc ore." "Oh, very interesting indeed!" "In fact how the zinc ore came to be called cadmea is in itself an interesting story. Legend has it that a Phoenician Cadmus was the first to have found a zinc rock and to notice that it gave a golden tinge to copper during smelting. It is from his name that zinc ore finally came to be called Cadmea. You may be surprised to know that naming chemical elements was a big fashion in 19th century Europe, becuase new and new elements were discovered almost every year, and it became fashionable to name elements after various Gods, legends, scientists, countries, even rivers. Element Rhenium for instance is named after the German river Rhine! In 1818, when Professor Stromeyer published his paper on Cadmium, many people came forward with the suggestion that they had already discovered that element first and even suggested names for this new element. German chemist Kersten, for instance, suggested that the new element be called melinium (yellow) after the color of its sulphide. Two other scientists Gilbert and John proposed two more names. One of them suggested that it be called junonium (after the newly discovered asteriod Juno in 1804) and the other suggested that it be called klaprothium, after the German chemist Martin Heinrich Klaproth (1743-1817), but ultimately the name given by Stromeyer stuck." "Oh, this is most interesting. Tell me some other important facts about Cadmium." "Tarun, Cadmium is used in a wide range of industrial processes, which include electroplating to impart corrosive resistance to ironware. Cadmium compounds are used as pigments, as components of batteries and photographic materials and cadmium is also used as a plastic stabilizer. Cadmium sulphate in a 1% solution, is a constituent of a shampoo used in the treatment of seborrheic dermatitis and dandruff." "So we were talking about the Cadmium poisoning. How can it occur?" "Cadmium poisoning can occur accidentally in a variety of circumstances. In the 1940s, it was usual for people to have their kitchenware electroplated with cadmium, as this makes them corrosion resistant. In the very beginning, Cadmium coating was deposited by immersing the metallic ware in molten cadmium...." "Sorry to interrupt you doctor, but melting cadmium must be quite a task. That too for just coating metals. Wasn’t it a very costly process?" "No, not at all. Cadmium melts very easily. It’s melting point is only 3210 C. In fact, its such a low melting point makes it a very suitable candidate for making low melting alloys. Among them Wood’s alloy containing 12.5 percent of cadmium was developed as far back as 1860 by a British Engineer Wood. These low melting alloys are used as solders and as the material for delicate and intricate castings, as well as in automatic fire-warning systems. Okay so I was telling you about the cadmium coating on kitchen ware. Later on, the coating was done with the help of electroplating. Unfortunately organic acids, many of which are used in day-to-day cooking such as vinegar (acetic acid), imli (tartaric acid) and lemon (citric acid) can dissolve cadmium from the thin electroplated layer, and this caused several cases of poisoning. In one accident which involved three adults and five children, the source of poison was "lemonade" ices prepared with citric acid in metal trays of a reconditioned refrigerator. All were sick and four also had diarrhoea, but recovery was complete within 24 hours. The citric acid solution contained 279 ppm (parts per million) of cadmium and it was estimated that each ice contained about 3 mg of cadmium. The ill effects resemble those of zinc poisoning. It is thought that the salts formed by organic acids are converted into cadmium chloride by HCl in the stomach. When the cause of these poisonings was discovered, the practice of cadmium electroplating was abandoned. But by no means are the incidences of accidental poisoning by cadmium ceased altogether. As late as in 1981, a case of accidental cadmium was reported. In this case, the victims inhaled fumes from a plated shelf of a refrigerator, used as an improvised barbeque grill!" "Oh, that is certainly most extraordinary!" "Yeah, that is right Tarun. Accidental cases of cadmium poisoning can also occur from cadmium fumes and dust. Cases have been reported where the poisoning occurred in some women who were using a cadmium powder to clean silver. These cases occur especially if the cleaning was being done in small, ill-ventilated rooms. It is interesting to keep in mind that inhaled cadmium is about six times more dangerous than ingested cadmium. Thus poisoning from inhaled cadmium fumes is much more dangerous. We have seen that in earlier times, metals were frequently electroplated with cadmium. Interestingly this practice has given rise to some cases of "delayed" poisoning now. Scrap metal from those times – if cut, dismantled, or recycled today, especially if with the help of oxyacetylene torches – can give rise to dangerous levels of cadmium fumes. Cases of fatal poisoning in such circumstances have been reported. It is important to realize that since cadmium was once used to electroplate metals, and there may be several such metallic objects in an average house, a housefire can give rise to cadmium fumes, and firemen must wear protective masks. There was a time when carbon tetrachloride was used as a fire extinguisher. But when carbon tetrachloride came in contact with hot metal surfaces, it gave rise to the poisonous phosgene (see Science Reporter Jan 1998 "Death by Phosgene"). Cadmium fumes, if produced during these fires were often confused with phosgene gas, and this caused serious blunders in treatment of such poisoned victims. But now since the use of carbon tetrachloride in fire extinguishers has been banned, chances of such graves mistakes are very remote." "This is very interesting. Have cases of poisoning occurred in such circumstances?" "Oh yes. In one interesting incident which occurred in 1956 in a chemistry laboratory in Leeds (Great Britain), some cadmium propionate was being dried in an oven for experimental purposes. This is a safe procedure as long as the temperature does not rise above 1000 C; above this temperature fumes of cadmium oxide and propionic acid are produced. Because of an inadvertent mistake, although the temperature of the oven reached 1600 C, it was read only as 600 C. Because of this, an explosion occurred, followed by a fire, and thick red fumes were seen to be coming out of that room. Four of the firemen, who entered the room to put out the fire inhaled those fumes, and one died after 6 days. On postmortem examination, significant amounts of cadmium were found in his internal body organs." "Oh, I see. Is cadmium found in some of our day to day products too?" "Tarun, Cadmium is found in significant amounts in unfiltered cigarettes, and this can be a cause of poisoning. Twenty unfiltered cigarettes a day can yield 6 mg of cadmium, of which the smoker may retain upto 65%." "Doctor you said that Kanta was suffering from muscle aches and pains and from this you deduced that she might be suffering from Cadmium poisoning. Can you elaborate on that?" "Oh, sure. This symptom is so prominent in Cadmium poisoning that it has even given a name to a disease caused by Cadmium. Let me elaborate. An outbreak of food poisoning due to Cadmium occurred in Japan in 1945. The syndrome has been called itai-itai disease, which when translated in English means ouch-ouch disease. The syndrome has been so called because it caused severe pain in the back and legs (which forced the victims to cry "ouch-ouch" so to say!). In more serious cases, there was decalcification and fracture of bone. Dislocations were also found to occur. For some strange reason, the complete syndrome was restricted to post-menopausal women, who had had several pregnancies. On investigation it was found that a local mine – the Kamioke zinc-cadmium-lead mine – released its effluents (containing cadmium) in the local Jintzu river. The water from this river was used both for drinking as well as for irrigating the local paddy fields. Thus cadmium found its way in the rice grown there as well. Cadmium ingested through intake of water as well as rice caused chronic cadmium poisoning, which was responsible for this syndrome. For the osteomalacia, undernutrition (common in post-war Japan) was also thought to be a factor." "So now it is becoming clear that somebody mixed Cadmium salts in Kanta’s drinks. Tell me has Cadmium been used for murder before?" "Not many times, but I do remember a case which was even reported in The Yorkshire Post of July 23, 1981. In this case two youths aged 14 and 15 administered cadmium chloride mixed in an orange drink to eleven children. They suffered from sickness and blurred vision, but fortunately no one died. The younger boy had strong political views and intended to poison his opponents. They had stolen the chemical from the Humberside Education Authority." "Doctor, you have already told me the symptoms one experiences when one ingests the poison. What happens when one inhales Cadmium fumes?" "Tarun, the initial symptoms and signs are sensation of constriction around the throat, a nasty taste in the mouth, irritation of the upper respiratory tract manifested by troublesome cough and redenning of the eyes. After a latent period of about one to two hours grave respiratory symptoms develop rapidly. Signs of pulmonary oedema (a technical name of a condition in which lungs are water logged) are also seen. The prominent respiratory symptoms are difficulty in respiration, pain in the chest, malaise, shivering and profuse sweating." "Has Cadmium been administered in some other way also?" "Tarun, I know of an interesting case of poisoning by intravenous injection which occurred in Japan. The patient had to be given an injection of calcium bromide, but by a rare accident, an injection of cadmium chloride was given. I may tell you that when Cadmium is given as a poison, the person usually dies in 24 hours, although death may be delayed for 7 to 14 days. If death occurs within 24 hours, the cause of death is shock due to loss of fluids. If the death is delayed, the cause is likely to be acute kidney failure or cardiopulmonary depression (depression of heart and lungs)." "Doctor, you have certainly made most interesting conclusions. Now how are you going to conclusively prove that Kanta was given Cadmium?" "Tarun, I have taken out Kanta’s internal organs, and have tested them for Cadmium. They have all given positive tests for Cadmium. Since it is not a normal body constitutent, it is clear that Cadmium has been given to her by someone. Following this I told police the whole story, and they investigated the death further. But this time they had murder in their minds, so they investigated more deeply. They found out that Sohan had been spurned in love by Kanta, and he wanted to take revenge. He stole some Cadmium Chloride from the chemistry lab, and then invited Kanta to his house. Although Kanta had spurned his love offer, she did not say no to his party as she wanted to continue a clean friendship with him. Moreover he told her that some other friends were coming over too. So there was nothing to be afraid of. When she and other friends arrived at Sohan’s house, he offered them cold drinks, and in the cold drink of Kanta, he mixed Cadmium Chloride. He probably chose this poison as this is such an unusual poison, and he thought that he could get away with that. But he didn’t know that forensic science can catch even the most intelligent of criminals. So even all his knowledge of chemistry could not come to his rescue." "Oh, how very clever of you doctor. If you had not made such an intelligent and logical deduction, Sohan could be roaming in free world today. Criminals like him are very dangerous and should be put behind bars. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Aluminium Phosphide. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JULY 1999 ISSUE THE POISON SLEUTHS DEATH BY OXALIC ACID -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle age man today. He shows some strange marks around his mouth. How did he die? Please let me know." "Good morning Tarun. The name of this unfortunate man is RadheyShyam. He is about 45 years old. He is living in a slum cluster of Delhi for the last several years. Some years back he was a fairly well-to-do man, but then suddenly his fortunes took a turn and he became quite poor. His wife and children deserted him, and he came to live in a shady slum cluster. He used to pick up odd jobs for his livelihood. He was very much in debt too, for the last so many months." "Oh, so you think one of his creditors killed him?" "I didn't say that. Although the police is investigating along those lines. He had taken about Rs. 25,000 from one Kale over a period of last few months, and Kale was pressing him to give his money back. Radhey Shyam had no means to pay him back his money. Yesterday night Kale had visited him. Everybody in the slum cluster saw him coming to his house and then leave surreptitiously. Nobody thought that he would go to such an extent as to kill him. Radhey's dead body was found in his house today morning. For all intents and purposes, it appears that it is Kale who has killed him." "So he killed Radhey Shyam, when he realized he is not going to get his money back. Perhaps it was his way of telling his other debtors that they must pay up or face dire consequences?" "Again this is the line police is investigating on. The police has arrested Kale and are questioning him. But Kale is swearing he did not do anything to Radhey Shyam. He does admit that he went to Radhey's house, but he simply gave a threat and came back. But police does not agree with his version. As for me, I generally don't give my opinion till I have examined all the facts, and especially till I have done the post-mortem. I have seen some strange things in this case, which tells me that it is probably not a case of homicide, but of suicide." "What makes you think that?" "Tarun, look at the strange whitish streaks running downwards from his mouth. You yourself remarked about them, when you first came here. Do you know what they are? They are in fact corrosion lines generally found when a person drinks acid. And let me tell you, acid is so corrosive, it is almost impossible to give it homicidally. Acid can only be taken by a person who wants to commit suicide. For instance if Kale had wanted to give Radhey this acid, he couldn't have done so, even if he had brought it mixed in some foodstuff, say, milk. The reason is that Radhey would have immediately discarded the milk after just the first sip." "So you think Radhey drank this acid to kill himself. But why would he do that?" "Radhey was upto his neck in debts. So it doesn't seem entirely confounding that he committed suicide. The question is which acid did he drink. And if we can find the half empty bottle of that acid from his house, our work is done. Finding a bottle of corrosive in the house is another proof that Radhey did commit suicide. Had Kale by any chance given him the acid, he would not have committed the blunder of leaving the bottle behind." "Yeah that seems fairly plausible. Which acid did he drink doctor? I am sure that this is an important question for you to answer, because the police as well as the court would be very interested in knowing the answer to this question." "Tarun, I have examined the stomach and kidneys of Radhey. And I have come to the conclusion that Radhey has drunk Oxalic Acid." "What? Oxalic Acid? Doesn't sound like a very common suicidal poison to me. How in the world did he get hold of Oxalic acid in the first place?" "Tarun, Oxalic acid is a constituent of many household products. It is found in many disinfectants, household bleach, metal cleaning liquids, antirust products and furniture polish. Its chemical formula is (COOH)2. Oxalic acid is a crystalline, colourless substance which is efflorescent. This means that it tends to become powdery on account of loss of water of crystallization. Its solubility is 1 in 12 in water. It is called Oxalic acid, after Greek "oxalis", which means sorrel. It occurs in the sorrel plant, and because of this the French chemist Lavoisier, in 1787, named it Oxalic acid." "Oh, that is really very interesting. Does it occur in other plants too?" "Oh yes. It occurs in the leaves and young stalk of rhubarb (Rheum rhaponticum), spinach and even cabbage. I must tell you that sorrel is a succulent acid herb used in salads. Accidental poisoning has been known to occur after a hearty meal of rhubarb or sorrel. Food rich in oxalate can also lead to kidney stones, because kidney stones are generally made up of oxalates." "Oh, that is really very interesting information." "Tarun, crystals of oxalic acid are similar in appearance to those of magnesium sulphate - also known as Epsom salt- and zinc sulphate. Because of this similarity, cases of accidental poisoning have occurred. Magnesium sulphate in doses of 15 g is used as a laxative, and is non-toxic. Since oxalic acid - a dangerous poison - is so similar looking to Epsom salt - a commonly used drug - it is necessary to be able to differentiate between the two. If the doctor or the nurse fails to differentiate between the two, accidental poisonings may occur. You may be interested to know that two patients at a mental hospital in Scotland died in 1956 after receiving doses of oxalic acid administered in mistake for Epsom salts. Zinc sulphate is also a commonly used drug. It has been used in such skin diseases and infections as acne, ivy poisoning, lupus erythematosus, and impetigo. Don't worry about the confusing disease names. What I want to impress upon you is that even zinc sulphate is a commonly used drug, and whenever a commonly used drug looks very similar to a dangerous poison, it becomes very necessary to be able to differentiate between the two." "So how do doctors differentiate between the two?" "Well, if you taste a small amount of crystal of each, oxalic acid is sour in taste, magnesium sulphate is nauseatingly bitter and zinc sulphate is metallic bitter. But surely, this is not the best of the methods to find out a poison. The reaction of oxalic acid is strongly acidic, that of zinc sulphate is slightly acidic, and that of magnesium sulphate is neutral. On application of heat oxalic acid sublimes while the rest of the two salts remain fixed. When you react each salt with sodium carbonate, oxalic acid shows effervescence, but no precipitation, while the other two salts show no effervescence, but a white precipitate. But perhaps the easiest test is to see if stains of ink or iron moulds disappear by a solution of one of these salts. While a solution of oxalic acid makes the stains disappear, the other two salts can not do that. In fact, that is why oxalic acid is used in products like ink removers and furniture polishes. Oxalic acid, as I have already told you, is used in households as a bleach to remove stains or to clean metals, notably brass or leather, and also in calico-printing. It was widely used when the straw hat industry flourished, during 1880-1910. Potassium oxalate is also used to remove ink stains and to cleanse metals. Solutions of oxalic acid and oxalates should never be left unguarded, since the colourless, and odourless fluid may readily be mistaken for water. However the taste is sour as I have already told you, so an unsuspecting person may take it, but would be quick in discarding it." "Can oxalic acid be used for homicide?" "No Tarun, that is not possible. That is why I think Kale is innocent. Because of its sour taste, it has not been used for homicide very much. Oxalates have however been used to procure abortion by vaginal injection. This is done by quacks who are approached by unmarried girls who have conceived due to premarital relations. But I may tell you that now no girl needs to contact such quacks. Now the law allows even unmarried girls to approach a properly qualified doctor in a government hospital to have an abortion done." "Doctor, how does oxalic acid affect the human body?" "Tarun, oxalic acid has both a local, and a systemic action on the body. By local action, I mean the action of stomach and intestinal walls with which it comes in contact. By systemic effect, I mean remote effect on organs with which it does not really come in contact. Oxalic acid readily corrodes the mucous membrane of the digestive tract. Unlike corrosive mineral acids and alkalies - like hydrochloric acid, sulphuric acid and nitric acid, oxalates do not lose their poisonous properties when diluted. On the contrary, dilute solutions of oxalates, can cause grave systemic effects. Oxalic acid however rarely damages the skin." "So these are the local effects of oxalic acid. What are its systemic effects?" "Large doses of oxalic acid can cause death due to shock. Oxalates can readily combine with the calcium ion in the body tissues, causing a precipitous fall in the level of ionized calcium. This can cause muscle irritability, tetany and convulsions, and irregular action and slowing of the heart. I may remind you that all muscle cells in the body are very much dependent on calcium for their proper functioning, and it includes heart muscle too." "Yeah I do know about that. Doctor, what are the signs and symptoms of oxalic acid poisoning?" "The symptoms of oxalic acid poisoning are modified by the size and concentration of the dose. A large concentrated dose would kill within a couple of hours by shock or hypocalcaemia, i.e. lowering of calcium levels in the blood. A large dilute dose would cause kidney failure. Depending on the size and concentration of dose, the clinical picture may vary. Fulminant poisoning occurs when a large concentrated dose of about 15 gms or more is taken. This is actually the lethal dose of oxalic acid. The clinical picture is dominated by gastrointestinal symptoms. There is immediate sour or bitter taste, associated with a burning sensation in the mouth, throat and food pipe because of the corrosive action of oxalic acid. Agonizing pain in the epigastrium, which soon spreads all over the abdomen associated with tenderness is seen. There is eructation, distension of abdomen, thirst, nausea and vomiting. The vomitus has a "coffee ground" appearance, because oxalic acid badly corrodes the stomach walls. There may be bloody vomiting for the same reason. Finally shock supervenes and death occurs. Acute poisoning occurs when a moderately large dose is taken and in such cases, the survival is upto 48 hours. The clinical picture is dominated by symptoms due to hypocalcaemia rather than due to gastrointestinal upset. These are muscle irritability, tenderness, tetany, convulsions, numbness and tingling of the finger tips and legs, cardiac irregularity, slowing of the heart, ventricular fibrillation (irregular and fast beating of the ventricles of the heart). In some patients, oxalates may have a narcotic effect. Delayed poisoning may occur when a smaller dose is taken. The clinical picture is characterized by symptoms of renal failure and uraemia. Death occurs in 5-14 days. I may tell you that the fatal dose of oxalic acid is about 15-20 gms, and the fatal period is 1-2 hours." "Doctor, in the case of Radhey, how exactly did you make out that it was a case of oxalic acid poisoning?" "Tarun, my first lead was given by these strange streaks running downwards from the angles of the mouth. Burns of the skin are actually quite rare in oxalic acid poisoning. Corrosion of the mucous membrane of the GIT, starting from lips is common. There is whitening or yellow-white discoloration of the lips, lining of the mouth, and upper surface of the tongue. The mucous membrane of the mouth gives an appearance similar to scalding. This is exactly the picture that I saw in Radhey Shyam. Then I got curious and did the post-mortem. I was very much interested in seeing his stomach. The lining of the stomach in oxalic acid poisoning is blackened by the production of acid haematin. There may be superficial corrosion. The stomach may contain fresh or altered blood. Furthermore, crystals of calcium oxalate can be demonstrated in scrapings of the stomach mucosa. Radhey Shyam's stomach showed all these findings, and I even could chemically demonstrate oxalic acid crystals sticking to his stomach mucosa. The kidneys of a person dying of oxalic acid poisoning are congested and swollen with oedema. The tubules contain oxalate crystals. The renal tubules are necrosed, which in plain and simple terms means that they are dead. I could demonstrate oxalic acid crystals even in the renal tubules of Radhey. I am sure it is a case of Oxalic acid poisoning. Lo and behold, here comes the policeman with the half empty bottle of Oxalic acid from Radhey Shyam's house. I had earlier sent him to Radhey Shyam's house to look for oxalic acid bottle. Now it is clear that it is a case of suicidal poisoning by oxalic acid. The police will now not harass Kale and would release him from custody." "Oh yeah, I am sure, the police will do that. 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- Digitalis. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE FEBRUARY 1997 ISSUE THE POISON SLEUTHS ARSENIC - THE KING OF POISONS -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing with this dead body? He seems to have a terrible rash all over his body. Would you explain me what he died of?" "Good morning Tarun. This man is Radheyshyam who is a 56 year old man. His first wife died about 5 years back, and soon after he married again. He was complaining of loose motions and vomiting off an on for the last two years. The doctors suspected he was suffering from gastroenteritis, which as you know is an inflammation of the stomach and intestines. But what they could not find out was the cause of this inflammation. Consequently he was being given only the symptomatic treatment. Finally he succumbed yesterday to his illness." "Then why is he here? Why haven't his relatives taken him for cremation. You are a forensic pathologist, and if I understand it correctly, you only look after cases with legal implications. What possible legal implication could be involved in this case." "Y ou are right Tarun. I deal only with legal cases. But yesterday, the brother of this person, Harishyam has alleged that his brother's relations with his new wife Shanti were not good. He suspects some foul play in his death. Many times he saw her mixing some whitish powder in his food. When he enquired, she would say it was some medicine she had brought from the local doctor for his illness. Immediately after his brother's death he reported the matter to the police. In response to his complaint, the police has registered a case against Shanti, and has submitted the body to me for post-mortem. Now my job is to find out if he really died of gastroenteritis." "Doctor, it seems very confusing. Just now you said that he did die of gastroenteritis. His symptoms were that of gastroenteritis, and he was getting treatment for it. Then what else could he die of?" "On the face of it, it does appear that he died of gastroenteritis, but there could be foul play as well. You yourself remarked over the rash he has all over the body. Well, in gastroenteritis one does not get rash over the body." "Then he might be having some concomitant skin disease, isn't it?" "Could be. But a more likely explanation could be arsenic poisoning, especially as Harishyam repeatedly saw Shanti mixing some white powder in his brother's food." "You mean Shanti was giving him arsenic, because of which he developed gastro-enteritis like symptoms and also the rash?" "Yes, that's what I mean Tarun. But I must tell you that pure metallic arsenic is seldom poisonous. It is its white colored salt Arsenious oxide, known in the vernacular as Sankhya or Somalkhar which is poisonous. It is this salt which is often loosely referred to as arsenic. When a chemist talks of arsenic, it is the pure arsenic, but when a toxicologist or a pathologist like me talks of arsenic, he is probably referring to arsenious oxide. We sometimes refer to it as white arsenic also, because of its white color" "Arsenic certainly seems an interesting poison. Please tell me more about it doctor." "Tarun, arsenic is a metallic poison known since ancient times. An eighth century Arab alchemist Geber produced arsenious oxide, from realgar, a naturally occurring red colored ore of arsenic found in lead and iron mining, and thus made available to the humanity one of the most cruel, deadly and widely administered poisons. In Imperial Rome a form of arsenic was used as a poison to such an extent, that kings, queens, and other important court officials regularly employed official food-tasters! It has been a favorite with the poisoners because it fulfills many of the criteria of an ideal homicidal poison..." "I beg your pardon? Do you mean to say that there are things like ideal homicidal poisons? What in the world does this term mean? How can anything as sinister as poison be ideal?" "Tarun, there not only are ideal homicidal poisons, but ideal suicidal poisons too. You see, there are several poisons in this world, but not all can be used homicidally or for suicide. Only certain poisons are ideally suited for these purposes. Poisons which suit well for these purposes are known as ideal poisons." "It is still not very clear to me. Would you please explain with some examples?" "Sure. Let us talk about homicidal poisons first. A bitter poison, like strychnine, can obviously not be given with homicidal intent. The victim would immediately spit it out. Thus a homicidal poison must be tasteless. Similarly a poison which is colored can not be given. Copper sulphate is poisonous, but it is blue colored. If a killer mixes it in water or milk, it will render these liquids blue, and the victim would not drink it. Thus a homicidal poison should be colorless too. There are several other criteria which have to be fulfilled as well before a poison qualifies as an ideal homicidal poison. It should be easily available, fatal in only a small quantity and symptoms of both acute and chronic poisoning must mimic natural diseases..." "Why should this be so?" "Because then the public at large would think that the person died of that natural disease whose symptoms the poisoning mimics, and the killer would go scot free. Arsenic qualifies well in all the above criteria. Symptoms due to its poisoning mimic natural diseases. While acute arsenic poisoning resembles gastro-enteritis, chronic arsenic poisoning presents a combined picture of stomach upsets, peripheral neuritis and dermatitis..." "Sorry to interrupt you doctor. You have introduced some new terms which I don't understand. What in the world is meant by acute and chronic arsenic poisoning?" "Tarun when a large dose of a poison is given in one go, killing the victim within minutes, it is called acute poisoning. On the other hand when small doses of a poison are given over a long period of time, typically over years, it is called chronic poisoning. If a wife wants to kill her husband, it would be very easy for her to mix sublethal doses of a poison in his food over a long period of time. By sublethal dose, I mean a quantity of poison which is not enough to kill the victim in one dose. The hapless husband would die in the end after a few years. In this case he would be said to have died of chronic poisoning." "oh, I see. So you were telling me about the criteria of an ideal homicidal poison." "Yes, I was telling you that the effects of arsenic poisoning resemble natural diseases. Its effects are cumulative, so the poisoner does not have to rely on one large, fatal dose; he can give it little and often, thereby weakening his victim by stages before delivering the fatal dose. An ideal homicidal poison should be undetectable in the dead body. About one and a half century back, arsenic fulfilled this criteria as well, but no more now. Before 1836, it was impossible to detect it in the body organs. All these facts made it the poisoner's ideal choice. So commonly and successfully was it used for homicidal poisoning that once it was variously referred to as king of poisons or poison of poisons. Since many people used it to do away with rich old uncles and aunts, it became known in France as poudre de succession, or "inheritance powder". The history of crime is replete with cases of homicidal poisonings by arsenic. Arsenic was ostensibly bought for killing rats, but it was often used for homicidal purposes. Women purchased it to kill rats; the rat in most cases used to be the husband!" "Funny joke! What about ideal suicidal poisons?" "A person who is going to commit suicide with poison, probably wouldn't worry about its color or even taste. He wouldn't be bothered with taking large doses too. He would be more concerned about the pain the poison is likely to produce. He needs a poison which produces minimum discomfort, and produces death or at least sleep within minutes, so his agony is lessened. Sulfuric acid is a deadly poison, but it would kill rather slowly; in about 12-24 hours. Moreover it is a strong corrosive producing severe burning pain in the mouth and throat. A potential suicide may be interested in death, but he probably wants a quieter death. So Sulfuric acid is not an ideal suicidal poison. Barbiturates or sleeping pills on the other hand are ideal suicidal poisons, because they would put a person rapidly to sleep, and then to death. There are no unpleasant symptoms." "Oh I see. While talking about arsenic you mentioned the year 1836. What happened in that year?" "In that year a successful test for arsenic was developed for the first time. It was called the Marsh test and it ultimately brought about its downfall as an extremely successful homicidal poison. One quality of arsenic makes it a very poor candidate as a homicidal poison; it can be detected in the dead body, virtually years after the body has been buried. Thus the poisoner leaves a permanent record of his deed in the dead body... "But how can anyone detect the poison in the body, once it has been buried?" "There are laws in all countries which allow the law enforcement agencies to unearth or exhume the body, if strong suspicion develops against some person later on. There have been cases where the bodies have been exhumed as late as 3-4 years after death, and arsenic has been detected in their bones. An ideal homicidal poison should immediately disintegrate after doing its job. Before 1836, this peculiar property of arsenic did not cause any problems to the poisoners because there was no test for arsenic in the first place. With the development of Marsh test, this property assumed paramount importance and it rapidly fell into disfavor." "So before the development of Marsh test, all the cases of poisoning must be going undetected?" "Yes! Many celebrated cases are on record when the suspected poisoner went Scot Free merely because of the inability of the chemists of those times to detect it in a dead body. In fact tests weren't available for any poison. The only reliable test was to feed the remains of the poison to an animal and see if it died. So desperate was public that Henry Fielding (1707-1754), a celebrated English novelist clamored in despair for some way to make poison visible so that one could hang the poisoner. That was in the year 1740. This was in connection with a case in which a widow was accused by neighbors of having poisoned her husband. But no poison was found in the widow's house, nor could it be proved that she had ever purchased poison. The only thing left, therefore, was to show that the corpse had poison in it. When Fielding appealed to the doctors, they answered that there was no way to do this. The widow had to be acquitted" "And then came the Marsh test"? "Marsh test came much later. Many interesting things happened before that. One of the most celebrated cases of arsenic poisoning occurred in 1752, when a 31-year old spinster Mary Blandy murdered her father with arsenic. Her court appearance was the first trial for murder by poison at which medical evidence was called in regard to the cause of death. Dr. Anthony Addington did not possess the knowledge to analyze the victim's organs for poison, nor was he able to use chemical tests to prove that the powder Mary used was arsenic. Nevertheless, on the basis of simple comparison he convinced the court that the powder was arsenic, and Mary Blandy was convicted and sentenced to death." "How were those comparisons made?" "Mary Blandy mixed white arsenic in gruel and gave it to her father. She wanted to kill him, because he was not agreeing for her marriage with someone she loved. Two days after eating the gruel, Mr. Blandy fell seriously ill. Some of the gruel left over was eaten by the charwoman and she was violently sick too. A maid also ate some of it, and she also fell sick. Because of this peculiar chain of events, they became suspicious and examined the pan used to prepare the gruel and saw a white sediment at the bottom. They locked up the pan and next day handed it over to the doctor." "And he compared that sediment with a known sample of arsenious oxide, and found them to be similar?" "Exactly. In today's parlance they would be called physical tests. He believed the sediment on the pan to be white arsenic because it had a milky whiteness, it was gritty and almost insipid. When put in cold water, part of it swam on the surface, but the greater part sank to the bottom and remained there undissolved. Arsenious oxide behaves in exactly the same way. When thrown on red-hot iron it did not burn, but sublimated, i.e. it rose in thick white fumes. These fumes had the stench of garlic. To be sure he did perform some simple chemical tests but they were also comparative in nature. This means that he conducted some chemical tests both on the sediment and on a known sample of arsenious oxide, and both gave similar looking reactions. The court accepted these tests- the first time any court accepted a scientific evidence in a case of arsenic poisoning- and sentenced Mary Blandy to death." "That certainly is interesting! I mean science ultimately catching up with the poisoners." "Twenty-three years after Mary was hanged, in 1775, a Swedish chemist made an important discovery. Karl Wilhelm Scheele found that he could change arsenious oxide to arsenious acid by treating it with nitric acid. Arsenious acid in turn when treated with zinc produced arsine, a highly poisonous gas. This epoch making work had the germs from which a reasonably good test for arsenic could be developed. This work was actively pursued by scientists in Germany, but the break-through was provided by an English chemist James Marsh. In 1836, he published a method for converting arsenic in body tissues and fluids into arsine gas, which was quite similar to that of Scheele. But the interesting thing was that Marsh was able to convert arsine back to metallic arsenic which could be shown to the court. It is much easier for a non-technical person like a judge to convict a criminal when he can actually be shown the poison which killed the victim." "How did Marsh convert arsine to metallic arsenic?" "As the gas escaped, the gas was ignited, and Marsh held a cold porcelain bowl against the flame. The metallic arsenic precipitated on the porcelain in the form of a black deposit. The process was unbelievably sensitive, making it possible to detect as little as a fiftieth of a milligram of arsenic! The Marsh test revolutionized the investigation of poisoning, and it was quickly taken up by crime scientists." "After the development of the Marsh test it must have become a lot easier for crime scientists to prove the presence of arsenic in a dead body?" "Yes surely. In 1840, the Marsh test was used in the celebrated Lafarge poisoning case. In January of that year Charles Lafarge, a minor French industrialist, died of suspected poisoning at his home in Le Glandier. Arsenious acid was found in his stomach, and it became known that his wife, Marie, had bought arsenic as rat-poison. She was arrested and sent for trial. The application of new scientific methods proved futile at first. When the Marsh Test was applied to corroborate earlier findings of arsenic by traditional methods, the results proved negative. The defence was elated, but the elation was short-lived, as the experts declared that the test worked better on organs other than the stomach. Exhumation of Lafarge's body was carried out for the purpose of retrieving these other organs for testing. Famous French toxicologist Dr. Mathieu Orfila was summoned by the court. He applied the Marsh test correctly and found arsenic in Lafarge's body. This case stirred up so much controversy in France, that the entire country was divided into Pro-Marie and anti-Marie factions. The case ended up in Marie being delivered the sentence of life imprisonment. Marie served 10 years of sentence. She was released by Napoleon III in 1850, and she died the following year still declaring her innocence! "Every killer does assert he is innocent. So arsenic has really been responsible for many killings. Good that the scientists ultimately came up with a good test for arsenic. Tell me doctor, what are your conclusions regarding this man Radheshyam?" "When his body was brought to me, I immediately suspected chronic arsenic poisoning..." "Really? What made you think so?" "The fact that his relations were not good with his wife, and that he was complaining of loose motions and vomiting for the last two years. The doctors were not able to find out a cause for his gastroenteritis. This is a classic picture of chronic arsenic poisoning, when the wife is stealthily mixing it in her husband's food. To top it all, she was often seen mixing some white powder in his food. But what clinched the diagnosis was the examination of his dead body. I am now positive he died of chronic arsenic poisoning." "How did you arrive at this conclusion?" "One of the landmark symptoms of chronic arsenic poisoning are the skin changes. The most important skin changes are, first, pigmentation and second hyperkeratosis, which is nothing but a technical term for thickening of the skin. If arsenic is given continuously for some years, even skin cancer may develop. You yourself remarked on the rash this person has all over his body. This rash is nothing but pigmentation. As you can see, this is finely mottled, brown rash, presenting a picture as if colored rain drops splashed his body. In fact this rash is often called "raindrop rash". This rash resembles measles rash in many ways. You can also see that his palms and soles are thickened. This is the hyperkeratotic change, another classical sign of chronic arsenic poisoning. In fact, even if I hadn't been told anything, just this change would have brought arsenic poisoning to my mind. You can also see that he has an irregular thickening of nails which is another good sign of chronic arsenic poisoning. The final clinching fact was the chemical test. when I applied Marsh test to his internal organs like liver, spleen and kidneys, arsenic was found to be present in abnormally high amounts. It is certain that he died of chronic arsenic poisoning. Let us phone the police and tell them about it." "Yes, certainly we should. Thank you doctor for giving me such interesting information on arsenic. What are you going to tell me the next time?" "Tarun, next time I shall tell you about Spanish Fly, which as you shall see has acquired a very notorious reputation. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE NOVEMBER 1999 ISSUE THE POISON SLEUTHS DEATH BY CICUTOXIN -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. What happened to him? Please tell me.” “Good morning Tarun. The name of this man is Radhey and he is about 54 years old. He was a carpenter by profession and had been in good health till yesterday. Yesterday morning he went to catch some fish in a nearby lake, along with his friend Shyam. Both of them were very friendly. While they were fishing, a person by the name of Lal came there and offered some sweet potatoes to them. Sweet potatoes as you perhaps know are known as ShakkarKandi in Hindustani. Both of them ate some of it. Shyam however spat out after one bite, because he thought it was not tasting how it should be. Radhey took some lusty bites from it, because he was hungry, and he liked its taste too. Half an hour after eating the plant, Radhey felt nauseated and dizzy and had stomach pains. Following this, he suddenly stiffened, fell on the ground unconscious, and made gross, irregular movements of his arms and legs. Shyam was alright by this time.” “Oh, from the story it appears to me, that Lal had given Radhey some poison mixed in sweet potatoes.” “Yeah, it sure does. The police has investigated into the background of Lal, and they have found that Lal held some grudge against Radhey. He wanted to settle an old score with him. So it does appear that Lal had a motive to give him some poison. The question is whether we can prove he gave him some poison or not. According to the only eye witness available - Shyam - the only thing Lal gave to Radhey was sweet potatoes. And sweet potatoes are not poisonous. So the police is going to have a tough time in the court proving anything against Lal. Sure enough they are banking heavily on my investigation.” “So what have you found doctor?” “Let me complete my story first. About one and a half hour after eating the sweet potatoes, Radhey was admitted to a hospital emergency room. On the way to the hospital, he was reported to have had four convulsions. I have asked the doctors who treated Radhey, about his condition when they first saw him. They tell me that when he was brought to them - at about 10 am yesterday - he was comatosed, and was bluish all over. This bluishness is known as cyanosis in medical terminology.” “Oh, that is terrible!” “Yes. He was not responding to any painful stimuli, which means he was really in a deep coma. His blood pressure was normal, but his pulse was more than twice the normal- about 150 per minute. The normal rate as you know is about 72 per minute. His breathing was stertorous. He was perspiring extensively, drooling saliva from his mouth, and his parotid glands were markedly swollen. He alternately clenched and ground his teeth and made chewing movements. His tongue was bleeding from a left sided laceration. His arms and legs showed intermittent, coarse, uncoordinated, and restless movements. He had extreme but intermittent muscle spasms, in particular of the muscles of shoulder and neck, causing throwing back of the neck. The pupils of his eyes were markedly constricted. In fact so constricted were they, that the doctors told me they were like pin points. You know that normally the pupils have a diameter of about 4mm. In this case, they were smaller than half a mm. His eyes were red. The eyeballs protruded somewhat.” “Oh, Radhey must surely have died dreadfully. What did the doctors diagnose?” “They couldn’t know what had befallen Radhey. They gave some conservative treatment, but Radhey’s condition worsened and he expired yesterday night at about 10 pm, about 14 hours after having ingested those mysterious ‘sweet potatoes’.” “Doctor, how do you think Radhey must have died? I think Lal injected some poison in those sweet potatoes.” “He probably could have done that. But by listening to the history of this case, and after talking to the doctors, I can only think of one poison.” “What is that poison doctor. Please tell me. I am getting curious.” “Tarun, the symptoms are so peculiar that there could only have been one poison- Water hemlock.” “What? Water hemlock? Never heard of it as a poison. Could you tell me more about it please?” “Tarun, Water Hemlock is a member of the genus Cicuta, of the Umbelliferae family of plants. There are nine subspecies of Cicuta, and all are very poisonous. Cicuta virosa is the common European water hemlock, and Cicuta maculata and Cicuta douglasii are the varieties found in North America. These varieties are found in India also. Common eponyms for Cicuta are cowbane, five-finger root, snake weed, wild carrot, dead man’s fingers, poison parsnip, wild parsnip, beaver poison, muskrat weed, spotted hemlock, spotted cowbane, musquash root, false parsley, fever root, mockeel root, wild dill, spotted parsley and carotte à moreau. They are found in marshy sloughs and meadows and on the banks of streams. Cicuta plants are difficult plants to identify, which may explain why Radhey mistook them for sweet potatoes. In fact, they have been mistaken for many diverse edible plants such as artichokes, celery, sweet potatoes, sweet anise, and wild parsnip. Cicuta plants are difficult to identify in the early spring, when only the fleshy swollen roots, particularly toxic at this time, are present. Later in the year, the roots are less poisonous, but the leaves and stem then contain sufficient poison to prove fatal if ingested.” “Oh, I see. What is the poisonous substance present in these plants doctor?” “Cicutoxin. Chemically, it is a highly unsaturated higher alcohol. Its formula -if you care- is: HOCH₂ (CH₂)₂ (C≡C)₂ (CH=CH)₃ CH(OH)CH₂CH₂CH₃ There is another poison in these plants, and that is Oenanthotoxin. This is found in Cicuta virosa, and is actually an isomer of cicutoxin. It was first isolated by a scientist Boehm in 1876 and was crystallized by Clarke in 1949.” “Doctor, how do these poisons actually kill the person?” “Tarun, Cicutoxin belongs to a category of poisons known as cholinergic poisons. This name comes from a natural substance found in the nerve endings, acetylcholine. You may be surprised to know that although acetylcholine is normally found in nerve endings - in fact it is essential for muscle contraction - an excess of this substance can prove dangerous to human body. Many insecticides such as organophosphorus compounds also show cholinergic effects and prove poisonous because of that.” “Oh, I see. Please tell me more about these poisons doctor.” “Cholinergic poisons exhibit two main groups of symptoms. One are called muscarinic effects, because they resemble the symptoms caused by eating a poisonous mushroom Amanita muscaria. These symptoms include salivation, perspiration and constriction of pupils. In fact, the moment I heard these symptoms from the doctor, coupled with the information that Radhey had been given “sweet potatoes” by a potential foe, I came to the conclusion that he had been given the root of some plant of the Cicuta species. The second group of symptoms is called the nicotinic effects, because they include symptoms caused by nicotine, a very poisonous alkaloid found in tobacco. Main among these symptoms are muscle twitchings and convulsions.” “Doctor, we have all the circumstantial evidence that Lal gave some poisonous roots to Radhey, but how are you conclusively going to prove in the court that Lal indeed gave him this substance?” “Tarun, I have taken the stomach contents of Radhey and have done a chemical test on that. They have proved positive for Cicutoxin and Oenanthotoxin. This surely means he has been given Cicuta roots by Lal. I did not stop at that. I specifically asked the police to raid Lal’s house. They raided and found many more such roots. Here they are, and any botanist can tell to the court that they are roots of Cicuta plants. Do we need any more proof than that?” "Surely not doctor. That was very clever of you doctor. Without your clever deduction - especially your noticing the peculiar symptoms of Radhey at the time of his death, and your sound knowledge of botany- everybody would have thought he died of some mysterious natural disease. This was a most interesting discussion doctor. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- Brodifacoum."
- Forensic Jokes, Puns & Tidbits | Anil Aggrawal's Forensic Ecosystem
Forensic Jokes, Puns & Tidbits Forensic Poems The Toxic Avenger From the grave, if lips could speak the person who was, pleads – you must seek the individual who had my trust, and thru deceit and cunning into the grave did thrust this body once alive and well, now silenced by death, who can not tell my death was NOT what all thought then, for a poison brought my life to end! Avenge me now, for you alone can find the truth beneath the stone. Look close and the clues you will see that tell the tale of what killed me. For you must tell all others now, That this was MURDER – and tell them how! For if no one looks to find what’s here, An injustice was done to a life so dear. If now only you could hear, My muted pleadings to make wants clear. I’d speak as plain as it could be. Since I can’t – You must AVENGE ME! -Anonymous. From a promotional leaflet on the book “Criminal Poisoning” by John Harris Trestrail, III (Acknowledgement: This leaflet was sent to me by John Harris Trestrail, III of the Regional Poison Center, Grand Rapids, MI) Milton Helpern (1902-1977) What kind of man is he we honor here, A doctor who has served his science well? Why, yes, of course, but most of us could tell Of science or profession served. A peer Without a peer in his own field and sphere? Why, yes, that too, but more than this, his spell Is cast by greatness of the mind. We dwell On inner strengths of character so dear To all who know him, radiance that springs From hidden depths of manliness and truth. These are the constant hallmarks of the soul That draw us to the man, these are the things Of which we offer now as humble proof The heartfelt testimony of this scroll -Anonymous. From the book “Autopsy – The Memoirs of Milton Helpern, the World’s Greatest Medical Detective” by Milton Helpern, M.D. with Bernard Knight, M.D. (Acknowledgement: This book was kindly lent to me by Dr. R.K. Sharma of the DDU Hospital)
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE SEPTEMBER 2000 ISSUE THE POISON SLEUTHS DEATH BY BOTULINUM TOXIN -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 Badal and he died in the hospital today morning, i.e. on 16th September at about 9 am. The doctors could not find out the cause of his death. He is only 25 years old, and everybody is concerned why he died. That is why the police has brought his body to me. My job of course is to find out how he died.” “Please explain the circumstances of his death doctor.” “Badal and Shatru were friends and they both loved a 21 year old girl Sudha. Both wanted to marry her, but Shatru could go to any length to get her. It so happened that Sudha showed more interest in Badal. Many times Shatru had asked Badal to get out of his way, otherwise the consequences would not be good for him. But Badal ignored his threats taking them to be just friendly pranks. On the outside both of them remained as friends, although it appeared to many that Shatru held a grudge against Badal. Badal was working as a clerk in a local private company and was living alone on a rented flat. On 12th September Shatru came to his flat in the evening with a bottle of whiskey apparently to celebrate his birthday. They both had whiskey together, and had dinner together. On 13th Badal was fine. On 14th morning, Badal started having some strange symptoms. First he had nausea, vomiting, diarrhea, abdominal distension and abdominal pain. He thought he was having an ordinary bout of diarrhea and contacted a local doctor for this. He too thought that he was having an attack of gastroenteritis, and prescribed some standard medicines. But they could not prove beneficial. On 15th morning, Badal developed double vision, technically known as diplopia, difficulty in speaking (dysarthria and dysphonia) and difficulty in swallowing (dysphagia). He became alarmed, informed one of his neighbors who immediately took him to a nearby hospital, where the doctors started investigating his illness. At the hospital, he reported some additional symptoms. He had dizziness, very dry and sore throat, blurred vision and drooping of eyelids. But the most alarming symptom of all was a paralysis of the muscles of his face and neck, which gradually moved downwards. That means that after the development of paralysis of muscles of his face and neck, first his arm muscles became paralysed, and then his leg muscles. Quite remarkably there was no fever. I have talked to the doctors who were treating him, and I have been told that his pupils were dilated. The doctors tried their level best to save him, but he died today morning, i.e. after about 48 hours of having those strange symptoms. On hearing his death, Badal’s family members have arrived here from the capital. They are blaming Shatru for his death. They think that when Shatru came to Badal’s house on 12th, he probably gave him some poison mixed in whiskey. They say that Shatru could do anything to get him out of his way. They are obviously very well connected. There was tremendous pressure on police to catch Shatru, and they have caught him today. But Shatru says he is innocent, and that he has done nothing.” “Doesn’t look like Shatru killed him. After all, Badal started having those symptoms almost 36 hours after he had that meal with Shatru. I have been discussing poisons with you for quite some time now. I don’t know of any poison which starts its action so late after being administered. To me it looks like he had a terrible disease. What disease did he die of doctor? Tell me.” “Tarun, I can say anything definitely only after a thorough post-mortem examination, but from the symptoms which have been told to me by the police and by the treating doctors at the hospital, I am of the opinion that Badal died of Botulism.” “Botulism? As far as I know this is a disease connected with food poisoning. Then why have the police apprehended Shatru? They must immediately release him.” “Tarun, I have asked them to continue keeping him in custody. I learnt that Shatru had studied microbiology at M.Sc. level. So I don’t want to take chances. I want to exclude everything, before I can say anything with confidence. In one of my earlier discussions with you (See Science Reporter May 1998 issue), I told you that the symptoms of botulism may resemble that of barium poisoning . In fact, so similar may be the symptoms that according to most doctors, barium poisoning should always be considered as a possible diagnosis in all cases of food poisoning accompanied by neurological complications. So the first thing I did was to exclude barium poisoning in this case, by checking for barium levels in various organs of Badal. And I could safely exclude barium poisoning, as I did not find any barium there.” “But if it is not barium, how can it be botulism? I mean how could Shatru give him Botulism even if he wanted to?” “Tarun, do you know that Botulin toxin is now used as a medicine too? And that medicine is available in vials. A certain number of vials, if mixed in one’s food, can definitely kill a person.” “A toxin being used as a medicine? Never heard of that. Looks like we are on to one more of your fantastic poison stories. Well, why don’t we begin from the beginning?” “Tarun, Botulism is a disease caused by the gram positive bacterium Clostridium botulinum. Before proceeding further I may tell you that the term gram positive refers to certain bacteria which take up a violet stain when stained with a special staining technique called gram staining. Gram staining was developed in 1884 by a Danish physician Hans Christian Joachim Gram (1853-1938). Bacteria which take up a pink color by this staining method are referred to as gram negative bacteria. So much so about gram staining and its nomenclature. So I was telling you about the Clostridium botulinum bacterium. I may tell you that its name comes from Latin botulus, meaning sausage. Indeed consumption of contaminated sausage was one of the major causes of this condition, when it was first recognized. It can however be caused by contamination of any type of foodstuff - vegetarian and non vegetarian. This bacterium is present in soil and infected water. Improper canning of foods at home may cause some contamination of food with soil or infected water during the process of canning. When canning is complete, the contents inside are devoid of air, a condition which is very much loved by these bacteria. In fact in technical terms Clostridium botulinum is known as a strict anaerobe, which means that a lack of oxygen is necessary for its growth; it gets killed in the presence of oxygen. This might appear paradoxical to you, since we are so used to talking about organisms which need oxygen for growth, but this is a fact. In an environment, which lacks oxygen, i.e. the closed can, these organism keep on multiplying. They produce a toxin known as botulin, which is supposed to be the most toxic substance found in nature. When someone consumes this food, he unwittingly consumes the toxin, and immediately becomes sick. He is said to be suffering from botulism. And he depicts almost the same symptoms, which were shown by Badal before his death. To summarize, we can say that Botulism is caused when food contaminated with Clostridium botulinum is canned or otherwise stored for long periods in anaerobic conditions.” “Doctor, many bacteria have different strains. Are there different strains of these bacteria too?” “Yes, there are eight different types of botulinum toxins have been described, and all of them are released by different strains of bacteria. They are all Clostridium botulinum, but differ in very subtle ways, so they are known as different strains of Clostridium botulinum. These different toxins are designated as A, B, C1, C2, D, E, F, and G. All are neurotoxins (poisons affecting the nerves), except for C2, which is a cytotoxin (poison having a direct effect on cells). Its significance is not clear. All these toxins are proteinaceous in nature, and thus antibodies against them may be prepared. However antibodies against any one of these toxins is effective only against that particular toxin and not against any other. Human poisoning mostly occurs due to A, B, and E. Type E poisoning is frequently associated with fish products. Rarely F and G can also cause human poisoning. C1, C2, and D cause poisoning in some mammals and birds. The toxin is not destroyed by acid or proteolytic (protein splitting) enzymes, but is heat labile and is destroyed when heated to 800C for 30 minutes, or 1000C for 10 minutes as during routine home cooking. It is thus a good practice to heat the canned food properly before cooking. Botulinum Toxin A (also known as BTX-A) has been isolated as a pure crystalline protein and is the most potent toxin known to man. You may be surprised at the fatal dose of this toxin. It is just 1 pg (10-12 g)/kg of body weight. This means that just about 10-10 g of toxin is required to kill a 100 Kg man! Even lesser doses would be required for ordinary human beings weighing 60-70 kg. Another figure may give you some idea of its lethality. One g of BTX-A toxin would kill 30,000 million mice! About 3 million molecules injected in the abdomen of a mouse would kill it. That would sound like lot of molecules, but the very fact that its lethal dose can be described in terms of molecules rather than in milligrams or grams speaks volumes about its lethality! So less is the fatal dose of BTX-A that it is often measured in a special unit called a mouse unit. It is a very small quantity. One Mouse Unit of BTX-A is equal to just 3 x 107 molecules. Again because of its such high lethality, many nations have seriously thought about using it as a biological weapon. As a biowarfare or terrorist agent, exposure is likely to occur following inhalation of aerosolized toxin or ingestion of food contaminated with the preformed toxin or microbial spores. Recently, Iraq admitted to active research on the offensive use of botulinum toxins and that they weaponized and deployed over 100 munitions with botulinum toxin in 1995.” “Oh, that is really interesting. Doctor, does this bacterium forms spores too?” “Oh, yes. The bacteria does form spores, when it finds that the conditions have become difficult for it to live. These spores (in contrast to toxin) are highly heat resistant, requiring exposure to moist heat at 1200C for 30 minutes for inactivation, as in steam sterilizers or pressure cookers. The spores are ubiquitous. They are present in soil, sea water and even air. Earlier I was telling about the fatal dose of BTX-A. I must tell you that its fatal period is just about 24 hours. I may also tell you that the toxins formed by Clostridium botulinum are known as exotoxins. Very broadly speaking exotoxins are those toxins which are produced by bacteria while they are still alive. On the contrary, there are certain other bacteria which release toxins when they get killed. Their cell walls rupture and the toxins are released. Those toxins are known as endotoxins. Thus the correct term for Botulinum toxin type A is BTX-A exotoxin.” “That is a lot of information doctor. You told that these bacteria make toxins while remaining in the can. Then the food inside must get spoiled too. Then why at all does someone consume such food?” “Unfortunately that is not the case. The food may or may not appear spoiled, depending on what strain of bacteria attacked it. If it released proteolytic enzymes, (the enzymes which break down proteins) along with the toxin, the food would spoil, otherwise not. Food contaminated by type A and B bacteria often appear putrefied, because they release proteolytic enzymes too. In contrast food infected with type E bacteria may look and taste normal, as they do not produce proteolytic enzymes. There are however ways to prevent botulism. First of all, if you are buying cans of food from a supermarket, never buy cans which are leaking, spouting, dented or otherwise show any other sign of abnormality. This is because the bacteria may release gases during their activity. And this build up of gas pressure inside the can may cause all these effects. Secondly all canned items should be cooked thoroughly by boiling and stirring for 15 minutes. This destroys any toxin if it is present. Commercial canners usually heat food to at least 1200C to guarantee the destruction of both toxins and spores. If you don’t want to use the food cans immediately, the cans should be frozen or refrigerated at very low temperatures. This is because some strains, especially type E, can produce toxin at temperatures as low as 50C. So a temperature lower than this must be achieved. There are some precautions suggested for those who do canning of food at home. One is the use of phosphoric and citric acids during canning. This is because the optimum pH for the growth of these bacteria is between 4.6 to 7.0. pH above and below this range are not conducive to their growth. Acid environment obviously is not conducive to their growth, and the use of phosphoric and citric acids provide a sound acidic environment. This is also the reason why acidic fruits may generally be safely canned. Many other facts seem to prove that an acidic environment prevents the growth of C. botulinum. Infants below the age of one year seem to become victims of infant botulism for the reason that their gastro-intestinal tract (GIT) is deficient in bile acids and gastric acid, which normally prevent the growth of C. botulinum. For preventing botulism, it has also been suggested that if you are canning meat at home, it should be cured with sodium nitrite (3.5% to 6%). This is said to prevent botulism, as sodium nitrite has an antimicrobial, especially antibotulinal activity. There is however a controversy that when such cured meats are fried, the nitrites may get converted to nitrosamines, a known carcinogen. But this is a different controversy and we would not concentrate it here now.” “Doctor, how does Botulinum A Exotoxin work? “BTX-A is an enzyme. It produces its effects by preventing release of acetylcholine (ACh) from the nerve endings. This chemical is very necessary for the transmission of impulses across nerves. Thus in a way the connections between nerves become ‘dead’, and the activities of the whole organism come to a stand still. Do you remember how Badal had a paralysis of his arms and legs? This is typical of botulism. Actually it was this symptom, which partly alerted me and made me think in this direction. I may tell you that the symptoms of food borne botulism start within about 18-36 hours of ingestion of contaminated food. After having food with Shatru, Badal also developed his symptoms roughly in the same time period. This period has often been referred to as the incubation period, but it is a actually a misnomer. The illness may be very mild for which no medical advice may be sought, or it may be so fulminant as to cause death within 24 hours. Badal died within three and a half days.” “Doctor, you have just mentioned a term “food borne botulism”. Does this mean there are other forms of botulism too?” “Oh yes. In fact the Center for Disease Control in Atlanta, USA (often referred to as CDC) currently classifies four different types of botulism. The first is the food borne botulism, which occurs from ingestion of preformed toxins. This is the best known form, and I have been talking about this form till now. The second form is infant botulism, which occurs mostly in infants below 6 months of age (90% cases). Rest of the cases occur between the ages of 6 months to 1 year. It occurs not from the ingestion of preformed toxins, but from ingestion of spores, which germinate in the mildly alkaline environment of the intestines, and produce toxin in-vivo, which gets absorbed. In adults the bile acids and the gastric acid tend to restrict the growth of C. botulinum. But the gastrointestinal tract of infants lacks these acids, and this factor may be responsible for their growth. Since the toxin is formed within the intestine and is absorbed gradually, the symptoms and signs are less dramatic, compared to adult type food-borne botulism, where preformed toxin is ingested all at once. The first signs to toxicity in infant botulism are constipation, feeding difficulty, feeble crying, and a “floppy” baby with diffuse decreased muscle tone, particularly apparent in the limbs and neck. Infant botulism is the most common form of botulism. Certain infants are more susceptible to infant botulism, while others seem resistant. The reason for this strange phenomenon is not clear. It is believed that giving of honey to infants may be a source of infection, as it contains spores of C. botulinum. Giving of honey to young infants is thus not advised now. The third form is Wound botulism, which occurs due to contamination of wounds with spores of C. botulinum. This usually occurs when they get soiled with dirt and nothing is done about it. The condition is also seen in chronic drug abusers and after caesarian delivery. This entity was first noted in California in 1976. This has now become the most common form of botulism. The symptoms and signs are quite similar to those seen in food borne botulism, except for the fact that gastric symptoms like nausea and vomiting are absent in wound botulism. Finally there is the Indeterminate type, which occurs in patients over 1 year of age with no recognized source for disease. Some authorities suggest that a mechanism similar to infant botulism may be at work here. Their studies suggest that the adults may ingest spores of C. botulinum, which may germinate in the gut, much like they do in infants. Several factors such as achlorhydria in these people, i.e. lack of acid in the stomach may be responsible for their germination. You may recall that I told you strongly acidic environments restrict the growth of this bacteria.” “Yes, I do. Doctor, in the beginning you told that this toxin is also used as a medicine. How can this toxin - which you say is the most dangerous toxin in the world - be used as a medicine? To me this sounds like a paradox.” “Tarun, now it is known that wrinkles in old people are caused by sustained contraction of facial muscles. If somehow these muscles could be paralysed, these wrinkles would go away too. BTX-A does this remarkably well. This toxin in nanogram doses is used for removal of wrinkles. Injection of BTX-A directly in these muscles causes their paralysis, which are then allowed to weaken by atrophy over a 3-week period. Similarly the toxin has been used in the treatment of certain eye disorders such as blepharospasm (abnormal contraction of eye lids) and in squint surgery. Commercially BTX-A is available under two different trade names - BOTOX and Dysport (produced by Speywood, Maidenhead, United Kingdom). BOTOX is prepared by a multiple precipitation technique, whereas Dysport is produced by column-based methods. These are technical terms and you need not bother about them. Suffice it to say, that this difference in production methods produces a differential between the effects on humans and mice. In particular, the dose (in mouse units) of Dysport required to produce a given effect is 3 to 4 times greater than the dose of BOTOX. Now I will come to the most important point. Work in primates, in conjunction with estimates derived from accidental botulism, suggests a human fatal dose of approximately 40 U/Kg if the toxin is delivered systemically. The BOTOX vial contains 100 units; the Dysport vial, 500 units. Thus a few vials if mixed in someone’s whiskey would be enough to kill him. This is actually what Shatru had done. I suspected him the moment I came to know that he was a brilliant student of microbiology and also when I heard the typical symptoms of Badal. I have chemically examined the blood of Badal and it shows BTX-A. I did not stop at that. I also did bioassays which proved that the blood of Badal contained something which paralyses muscles.” “What is a bioassay doctor? “Bioassay is a term which refers to determining a chemical by biological means. I prepared an extract from Badal’s serum, and injected it in mice. By doing this, I could produce paralysis in mice, which was a positive indication that some abnormal substance was there in Badal’s blood. I have lab reports to show to the court that this abnormal substance was in fact BTX-A. Now I will tell you one more secret. I sent policemen to Shatru’s house and they have recovered some empty BOTOX vials from his house. These vials had no business being present in his house, which tells us that he is the one who mixed those vials surreptitiously in Badal’s whiskey. Come let us tell the police to put him under more sustained questioning, and he would surely spill the beans.” “That is very clever of you doctor. Without your clever deduction it would have been impossible to say how Badal died and Shatru 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 - Lithium.”
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE APRIL-MAY 1997 ISSUE THE POISON SLEUTHS POISONING BY BORON -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the body of a young woman here." "You are right Tarun. This woman lying here on my table is Lata. She is a 23 year old young unmarried girl. Her parents tell me that she was not feeling well for the last few days. She got frequent bouts of vomiting and in general was down and out. They insisted to take her to a doctor, but she said the symptoms were not troublesome and she would soon get well. She did not inform her parents but the police has found out during the investigations that about a week back she contacted a quack Dr. Harish for treatment, and allegedly he administered her some medication. Soon after she began to feel nauseated. She had severe diarrhea and vomiting. Her parents tell me that the color of both her feces and vomitus was somewhat bluish green. She was also reported to have severe pain in her stomach, severe convulsions and tremors. They did not know why the symptoms had become so severe and they again insisted to take her to a doctor, but again she declined. Since two days she was feeling extremely lethargic and was having headaches off and on. She again contacted Dr. Harish yesterday and he was reported to have administered something to her again. Within about 2 hours of this she died. Now the police has brought her body to me to tell them how she died." "Should be quite simple. Obviously Dr. Harish has administered some poison to her." "Yes, it appears so. But the question is why he would administer her the poison. The police has talked to Dr. Harish and he seems quite confident that he gave her the correct medicine. He asserts that Lata died of her original illness which she was complaining of." "So what are you going to do now?" "Well, I will have to conduct an autopsy on her dead body. Do you see her fingers and fingernails? Do they not seem abnormal to you?" "Why! they certainly do. They appear as if they have been painted red! Doctor I am getting curious. Please let me know what this is?" "And if you look at her buttocks you would find the same change. In medicine, we call it erythema. It is a kind of inflammation of the skin. The skin as you can see, is sloughing off at several places. Of course the most prominent finding as you have noticed is the marked redness of the skin. You may be surprised to know that in toxicology there is a special term for this change. This is known as "boiled lobster" syndrome. The skin appears like a boiled lobster, doesn't it?" "Now that you tell me, it certainly does. But tell me doctor, does it indicate any particular poison?" "Yes Tarun. It indicates one and only one poison- boron. It appears to me that Dr. Harish gave her one of boron compounds." "What? Boron? Doesn't sound like a poison to me. Poison to me means things like cyanide. Please tell me more about boron." "Tarun, admittedly boron is not a common poison, but it is certainly poisonous and can cause death. Boron in elemental form is not poisonous, but its salts are. Its most common salts are sodium borate, sodium biborate, sodium pyroborate and sodium tetraborate. Boric acid (H3BO3) is a colorless, odorless compound commercially available as granules, and white powder. A teaspoon of 100% boric acid crystals contains approximately 4 g of boric acid..." "Sorry to interrupt you doctor, but does it have any medical use?" "Tarun, it was introduced in 1702 by Homberg as a sedative, pain-killer, and antispasmodic. An antispasmodic relieves spasms, especially those of the stomach and is thus useful in stomach pains. At that time it was widely known as "Homberg's sedative salt". But by next century it had fallen in disfavor till Joseph Lister (1827-1912) revived its use once again employing it as an antiseptic in 1875. A little later- in about 1885- it was used as a food preservative, being frequently added to milk to keep it from rotting. But it was soon discovered that its use as a food preservative can cause serious poisoning. Since then its use as a food preservative has been abandoned, but it has been used in several other forms- as solutions, medicated powders, skin lotions, ointments, toothpastes, mouthwashes, water softeners, topical astringents and antiseptics. In the early part of this century, it was recommended for the treatment of ammoniacal dermatitis in children...." "What is ammoniacal dermatitis, doctor?" "Tarun, dermatitis means inflammation or redness of the skin. Ammoniacal dermatitis is an inflammation of the skin caused by ammonia. You might be surprised how children can get exposed to such an unusual gas as ammonia. Well, the gas is produced as a result of the chemical breakdown of urine by bacteria in the feces. Nappies of very young children can get soiled with both urine and feces. The bacteria in the feces produce ammonia from the urine. Ammonia has a burning effect on soft baby skin. It produces a rash in the surrounding area. Since the rash is in the area of the diaper it is commonly known as diaper or nappy rash. In fact, so commonly was boric acid prescribed for diaper rash, that at one time it was suggested that a history of diaper rash in any infant under the age of one year, who has died unexpectedly, should raise the suspicion of boric acid poisoning! This aphorism was true for two reasons. Not only was it often applied as a remedy for diaper rash but its poisoning in children often took the appearance of a diaper rash, even if did not have it in the first place! You have seen marked redness of the skin in Lata's case; in children the same happens in the diaper area, giving an appearance mimicking diaper rash. Boric acid was once famous for the treatment of burns too. In fact it was successfully used in the treatment of burns sustained in the Cocoanut Grove disaster..." "Sorry to interrupt you once again doctor, but what was the Cocoanut Grove disaster?" "Tarun, Cocoanut Grove was a Boston night club in USA, which caught fire on Nov 28, 1942. A corner of the Lounge had fallen into complete darkness as someone -probably a customer- had taken out a bulb. A 16 year old employee of the club was asked to replace the bulb. He lighted a match in order to illuminate the area and tried to screw the bulb in position, but the match started an artificial palm tree burning, and the fire spread quickly. As a result 491 men and women lost their lives. During the two hours following the onset of fire, 114 casualties were brought to the Massachusetts General Hospital. Many were dead on arrival and many died soon afterwards. Only 39 lived and were treated. In this disaster, the doctors successfully used boric acid to treat many cases of burns. Following this success, it began to be used widely in the treatment of burns as a sterile boracic ointment in place of tannic acid, which was being used earlier. But it was once again shown that poisonous amounts of boric acid can get absorbed from burn wounds and can cause serious symptoms..." "So it appears boric acid is no good as a medicine after all" "You can say that again. British Medical Association in 1966 published a statement in which practitioners were advised to refrain from prescribing boric acid and related salts in any form of treatment. The Pharmaceutical Society of Great Britain in the same year advised pharmacists not to sell boric acid as a dusting powder, nor to supply borax in any form. Boric acid solutions have been used as antiseptic irrigating solutions for cleaning wounds and abscesses and even internally for irrigating bladder, pleural cavity and lower bowel, but as I have already told you, it may produce toxicity. Other poisonous compounds of boron are the boron hydrides.." "Doctor please tell me something about boron hydrides." "Tarun, Boron Hydrides are a class of chemical compounds having the general formula BnHn+4. They have been investigated as possible propellant fuels as they have nearly double the energy content of standard hydrocarbon fuels. Examples include diborane (B2H6), a gas; pentaborane (B5H9) a liquid, and decaborane (B10H14), a solid under standard conditions. They oxidize vigorously to produce boric acid, water and much heat. Some of the hydrides are spontaneously pyrophoric, i.e. they have the capability of catching fire spontaneously in air, just like phosphorus. Boron hydrides are extremely poisonous compounds. It is believed that they are even more poisonous that cyanide! Levels in air as low as 0.005 parts per million may be toxic!" "Have poisonings occurred from boron hydrides as well?" "Yes surely. Boron hydrides are used in the industry for several purposes. You must be knowing that for making semiconductors, the wafer of silicon has to be "doped" with boron. This doping is done with boron hydrides. There are several other complicated uses of boron hydrides in the industry. Cases have occurred when pentaborane has accidentally released in industrial area and poisoned the workers. This can cause quick death. Another curious boron preparation is the Dobell's solution...." "What is Dobell's solution doctor?" "Tarun, Dobell's solution was first prepared by the London physician Horace Benge Dobell (b. 1828) in the last century. It consists of a solution of borax, sodium bicarbonate, phenol and glycerine in water and it was used as an antiseptic in the last century and in the early part of this century. Borax (Na2B4O7.10H2O), another poisonous boron compound has been known as a cleaning agent since the days of the Greek and Roman empires and has long been used as a food preservative in Europe and America. Today the principal compound of boron easily available to a common man is sodium perborate. It is an oxidizer which is normally present in tooth powders and toothpastes. It is available to the general public in powder or tablet form for the cleansing of dentures. The white tablets of sodium perborate look quite like sweets and may be taken by curious children! Contact lens solutions also contain salts of boron." "Doctor, how can one get poisoned from boric acid or other boron salts? Can it be administered homicidally? "Tarun, Boric acid- one of the most important toxic salts of boron- can certainly be administered homicidally especially as it is a colorless and odorless compound, and is quite commonly available. But no homicidal poisoning with boric acid has yet been reported perhaps because its lethal dose is rather high- about 20 g. As I told you in one of my earlier meetings, an ideal homicidal poison is one which is not only colorless, odorless and tasteless, but whose lethal dose is very small too. But this is not to say that homicidal cases may not have occurred. It is quite possible that cases of homicidal poisoning occurred, but because of poor investigation techniques, the poisoners remained scot free." "Has it been taken for suicidal purposes?" "Not to my knowledge, but certainly people have got poisoned when they mistook it for certain other salts. There are cases on record when boric acid crystals have been mistaken for other innocuous salts and ingested. It has frequently been mistaken for Epsom salt.... "Sorry to interrupt you doctor, but is Epsom salt the same as magnesium sulphate?" "You are right Tarun. Epsom is actually a place in England, very near London which is now famous for Derby- the world's best known horse race. Before the first Derby race here - in 1780- this place was better known as a spa. A spa as you know is a place where one goes to take bath in natural spring waters. Mineral springs were discovered here in 1618, which were quite rich in magnesium sulphate. This is how magnesium sulphate came to be known as Epsom salt. It has great medicinal value and is taken orally to treat constipation and heartburn. It is also prescribed as injection to prevent seizures, especially in preeclampsia, a dangerous condition seen in pregnant mothers." "Well, I think now I know a lot about boron. Coming to our own case, why do you think Dr. Harish administered Boron to Lata? Did he want to kill her with an exotic little known poison, so that no one could suspect him?" "It is a possibility but I do not think it must have happened, especially as Dr. Harish had no motive to kill Lata. Actually Borax has a reputation among quacks as an emmenagogue; it is supplied to induce criminal abortion...." "Well, you have introduced two new terms doctor. What are emmenagogues, and what is criminal abortion?" "Tarun, emmenagogue is a drug which increases the flow of menstrual blood. The term comes from the Greek roots emmena, menses, and agogein, to draw forth. Thus literally the term refers to any drug which "draws forth the menses". Interestingly the root agogein is seen in many other medical terms such as cholagogue, which refers to any drug which increases the secretion of bile (from Greek chole, bile). Many drugs have a reputation as emmenagogues, some of them being aloes, potassium permanganate, pennyroyal, caulophyllin and apiol. You would surely remember that last time we talked about cantharides in another context. Well, it is also an emmenagogue. Borax is also a strong emmenagogue. Criminal abortion is any abortion done against the law. The law requires that the doctor doing the abortion should have certain requisite qualifications and experience. Girls who become pregnant before marriage can not go to regular doctors for abortion for obvious fears of facing embarrassment and insult in society. So they chose an easy way out; they go to quacks who often do it in a hush-hush manner so that no one else may come to know about it. But they do not have the requisite qualifications, so abortions performed by them are obviously criminal in nature. If found out, they could be prosecuted by law. Since these doctors are not properly qualified, they do not know of standard and safe methods of abortion. They resort to centuries' old dangerous methods of abortion; methods which properly qualified doctors do not resort to. One of the methods employed by the quacks is to administer emmenagogues. The idea is that by promoting the flow of menstrual blood, they would somehow be able to "wash down" the young embryo lodged in the uterine wall. This method does work at times but is an extremely dangerous method. It is like trying to cut your nails by banging your fingers against a sharp knife." "I am getting the picture now. Lata was pregnant and she contacted Dr. Harish for a criminal abortion. Dr. Harish administered her borax as an emmenagogue. But it did not work; it caused her death instead." "You are very right Tarun. This is indeed what happened. The symptoms which Lata had were symptoms of pregnancy. Since she was unmarried, she did not want to make it known to her parents. She herself contacted Dr. Harish who was quite sure that he could do the job, but he killed her instead. Post-mortem findings in boron poisonings are not very specific. The mucosa or the lining of the stomach may be bright red and the blood may be cherry red in appearance. Characteristic rash as described earlier may be seen. I have seen all these findings in Lata's body. But I have not relied on autopsy findings alone. I have conducted blood tests on Lata's blood which are confirmatory. The levels of boron in her blood were important. Normally boron levels in the blood are minimal. A level of 50 mg/100 ml indicates poisoning, but I found boron levels exceeding 500 mg/100 mg, which surely is enough to cause death. The actual lethal dose of a boron salt is between 15-20 g for adults and from 3-5 g in infants. So I believe the second time Dr. Harish must have administered her a dose greater than about 20 g. He must have given her a lesser dose the first time, but when it did not do the trick, he administered a larger dose the next time, which killed her. Let us call the police and tell them how she died." "Oh sure we should. And thank you doctor for telling me about such an interesting poison. What are you going to tell me the next time?" "Tarun, next time I shall tell you about silver which as you shall see is a very important poison. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JUNE 1999 ISSUE THE POISON SLEUTHS DEATH BY NITRIC ACID -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a middle aged man today. He has these strange yellowish stains over his face and chest. What has happened to him? Please tell me." "Good morning Tarun. The name of this middle aged man is Radhey Shyam, and he was living alone in this house for the last five years. His dead body has been found today morning from his house. His wife and son died long ago, and since then he is living in a very depressed state of mind. He had become alcoholic and had taken to gambling too. He had taken lot of loans from various sources. It is said that from one person Munna, he took as much as one lakh of rupees. Munna was actually a professional money lender and he used to give money at a very exorbitant rate of interest..." "Oh, I see. But what has all this to do with his death?" "I am coming to that Tarun. Munna was pressing Radhey Shyam for his money for quite some time. Last week Munna had visited Radhey Shyam's house, along with some of his goons for his money, and when Radhey expressed his inability to return the money for about six more months, Munna had threatened him with grave consequences." "So Munna has killed Radhey for retaliation?" "This is what the police thinks. Actually Munna had visited Radhey's house yesterday night too, and had threatened him with grave consequences once again. Today morning they have found the dead body of Radhey. So it is very natural to assume that Munna and his goons have killed Radhey." "What does Munna say?" "The police has arrested him. He looks terrified. He is swearing that he has nothing to do with this killing. He does admit that he had visited Radhey yesterday night, and that he indeed was with two of his goons. He also admits that he had threatened Radhey with grave consequences, but he swears he gave those threats merely to terrify Radhey into returning his money as soon as possible. He never intended to kill Radhey. He has also come out with an interesting argument. He says that he would not have got his money anyway by killing Radhey. So killing Radhey was not in his interest anyway." "Sounds like a valid argument. What do you think doctor?" "Tarun, as you know, I deal every case from a scientific angle. Are you looking at the yellowish stains over his face and chest and over his clothes?" "Yeah, they are very prominent. In fact that is the first thing I noticed, when I came here." "I have looked at his teeth and tongue too. Even they are stained yellow. Come, you also have a look" "Yes, indeed. But what are you trying to arrive at?" "Tarun, it seems to me, that Radhey has died because of Nitric Acid" "Nitric Acid? Never heard of this poison being used to kill anyone." "Nitric acid is not a homicidal poison. It can not be given homicidally to anyone, because it has such a pungent taste. It is in fact a suicidal poison." "Looks like we are on to another of your rare and exotic poisons. Doctor please tell me about nitric acid from the beginning." "Tarun, Nitric acid is a colorless or yellow fuming liquid with an acrid odour. It is a powerful oxidizing agent and reacts with organic matter such as with proteins to produce trinitrophenol or picric acid with the liberation of nitrogen monoxide. This is known as xanthoproteic reaction. Organic matter is thus turned yellow. Stains of this acid on clothing are also yellow, which is a distinctive feature of poisoning by nitric acid. In fact this is how I first suspected that this could be nitric acid poisoning." "Oh, I see. Can you tell me, what are the symptoms a person experiences when he consumes nitric acid?" "Sure. The person gets eructations and abdominal distension. Actually this symptom is also seen with other acids such as sulphuric acid, but eructations and abdominal distension are more severe in nitric acid than with sulphuric acid, because with nitric acid more gas is formed. Then, as you know by now, there is yellowish staining of the teeth as well as of the skin around the mouth, cheeks, and neck, which is very characteristic. Yellow stains may also be found on hands, forearms, and the chest because of splashing. In severe cases, the stomach may perforate, but this is unusual." "Doctor, what is the usual fatal dose of nitric acid?" "It is around 10-15 ml. Actually one tablespoonful contains about 5 ml of liquid. So about two to three table spoonfuls of nitric acid are enough to kill a person." "And what is the usual fatal period?" "It is around 18-24 hours" "How can a person obtain nitric acid to kill himself?" "Tarun, nitric acid is widely used in the art and manufacturing industry. It is used for cleansing nickel ornaments and separating gold from other metals. It is also used in the preparation of gun cotton, nitroglycerin, picric acid, and colouring matters. Because of its wide use in industry, and even in domestic affairs, it is commonly available in the market. And because of its easy availability, suicidal and accidental poisoning is quite likely." "Can a person commit murder with nitric acid?" "Majority of cases of poisoning by nitric acid are either suicidal or accidental. Homicide with nitric acid is extremely difficult, and perhaps even impossible. Because of the corrosive nature of the acid, it can not be given to an unsuspecting individual, who would immediately discard it on tasting. However forcible administration of this acid in drunk patients has been reported. A forensic expert by the name of Christison describes a case where nitric acid was forcibly poured down the throat of a woman when she was drunk. Nitric acid has also been used in vitriolage, although the use of sulphuric acid is more common for this purpose." "Excuse me doctor, you have used a new word. I am not quite familiar with this. What is vitriolage?" "Tarun, vitriolage is intentional throwing of a corrosive substance over the face of an enemy. Often the corrosive substance such as sulphuric or nitric acid is filled up in an old used bulb, and this bulb is then thrown over the face of the victim. A person who commits vitriolage generally does not intend to kill his victim. He merely wants to disfigure him or her. When this bulb smashes on the victim's face, the corrosive substance is released and corrodes the face of the individual. This method is usually employed by disgruntled youths to disfigure the face of beautiful girls who have spurned their love offers." "Oh, that is really sad. Now in the current case of Radhey, how did you reach the conclusion that he had died of nitric acid poisoning?" "By his peculiar post-mortem findings. I have already talked to you about his yellowish stains. These yellowish stains have to be differentiated from those of the iodine stains, because they can cause similar stains. However if ammonia or some other alkali is applied to the stains, the ones due to nitric acid deepen in colour to become orange, whereas those by iodine are decolorized. I did this test in this case, and found that these stains were indeed caused by nitric acid only. In addition, I found that his stomach was perforated. This can only happen if the acid has corroded the stomach wall. But I did not stop at that. I took some material from his stomach and chemically tested it in my lab. I have confirmed chemically that the substance which Radhey ingested was indeed nitric acid. Subsequent to this, I asked the police to search his house and look for some suspicious looking half filled bottle. And sure enough they found a bottle of nitric acid in his almirah which was half filled. Now I will tell you what must have happened. Munna indeed visited Radhey's house yesterday along with his goons, and he also threatened Radhey. But he did not kill him. After Munna had left, Radhey got depressed. He anyway was living alone and no meaning to life was left to him. He wanted to commit suicide and the only thing available to him was nitric acid. He consumed this acid and died. Come let us tell the police that Munna has not killed Radhey. He has actually committed suicide." "Very clever indeed. This was a most interesting discussion doctor. Without your masterly deduction, police could have unnecessarily went on harassing Munna. Everyone might have thought, it was a case of killing by Radhey. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison. It is oxalic acid. "
- Forensic Jokes, Puns & Tidbits | Anil Aggrawal's Forensic Ecosystem
Forensic Jokes, Puns & Tidbits Forensic Puns 1. A tourist in Vienna is going through a graveyard and all of a sudden he hears some music. No one is around, so he starts searching for the source. He finally locates the origin and finds it is coming from a grave with a headstone that reads: Ludwig van Beethoven, 1770-1827. Then he realizes that the music is the Ninth Symphony and it is being played backward! Puzzled, he leaves the graveyard and persuades a friend to return with him. By the time they arrive back at the grave, the music has changed. This time it is the Seventh Symphony, but like the previous piece, it is being played backward. Curious, the men agree to consult a music scholar. When they return with the expert, the Fifth Symphony is playing, again backward. The expert notices that the symphonies are being played in the reverse order in which they were composed, the 9th, then the 7th, then the 5th. By the next day the word has spread and a throng has gathered around the grave. They are all listening to the Second Symphony being played backward. Just then, the graveyard's caretaker ambles up to the group. Someone in the group asks him if he has an explanation for the music. "Don't you get it?" the caretaker asks incredulously. [Guess now, before scrolling down] No cheating, make a guess before scrolling. Not even a wild guess before scrolling? He's decomposing.* 2. I was standing in line at an airport to check in for a flight. For 15 minutes, the queue hardly moved, and patience was wearing thin. Suddenly an irate voice from the back demanded to know what the holdup was. A voice from the front replied,"I'm afraid Riga mortis has set in." (Contributed by Chris Bane. Published in Readers' Digest December 1999 page 32) 3. Is it correct to say that all Forensic Personnel are in a grave situation?
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE JULY 1997 ISSUE THE POISON SLEUTHS POISONING BY VANADIUM -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? Oh well, today you are examining a middle aged man. What happened to him?" "Good morning Tarun. The name of this person is Ramashanker. For some days he is having some respiratory problem. He has difficulty in breathing, persistent cough, sneezing and sore throat. As you can see he is having red eyes too, which in medical parlance is known as conjunctivitis. He is also reporting some weakness, ringing in his ears and headache for a few days. His local doctor prescribed medicines for these ailments but apparently he didn't get any relief. He was then referred to a specialist, who conducted thorough tests on him and then came to the conclusion that he was perhaps exposed to some poison, and that's how this patient came to me." "And what are your conclusions doctor?" "Initially Ramashanker was thinking that he is suffering from some natural ailment, but when he heard about himself being possibly exposed to poison, he immediately named his employer as a possible suspect who might be trying to poison him. According to him, his employer was trying to fire him on several occasions but each time the Workers Union intervened and he could not be fired. But his employer was bent upon getting rid of him, and Ramashanker thought that he was probably trying to poison him as a last resort." "But how can he possibly poison him?" "The lunch of all the workers is distributed by the employer. It is part of the work conditions. Ramashanker thinks that somebody- most probably his employer- is mixing some poison in his food, perhaps through the help of some goons." "Do you think he is speaking the truth doctor?" "Frankly Tarun, I was not convinced by Ramashanker's assertion. But I wanted to examine him in some more detail before coming to any conclusion. When I saw his tongue, I found that it was greenish colored. This set my mind working and I asked where he was working. He answered as I had expected. He was working as a boiler cleaner in a power plant." "I do not understand what you are referring to. Please explain in some detail." "Tarun, I think no one is trying to poison him, yet he is suffering from poisoning- poisoning from a very exotic poison." "Doctor please stop speaking in riddles and tell me what poisoning is he suffering from." "Tarun, this person surely is suffering from Vanadium toxicity..." "Vanadium! That doesn't sound like a common poison to me. And how is he suffering from this poisoning when no one gave it to him?" "Tarun, Boiler cleaning is a highly hazardous profession in which workers are exposed to high levels of Vanadium. Before we proceed further, I think I should tell you a little about Vanadium." "Yes surely doctor. I would appreciate that. Although I am a good student of chemistry, I know very little about Vanadium, and I would like to know more about it before we discuss its toxicity." "Tarun, Vanadium is an element having an atomic weight 50.94 and atomic number 23. Its density is 6.11 at 18.10 C. Its melting point is about 18900 C and its boiling point is 33800 C. Elemental Vanadium is a corrosion resistant, hard, steel-grey solid. It was discovered in 1831 by the Swedish chemist Nils Sefstrom. The story of its discovery is very interesting. About 30 years before its actual discovery, in 1801, the Mexican chemist and mineralogist Andres Manuel del Rio was almost on the verge of discovering it, but he missed it by the breadth of thin hair, so to say. In that year he was studying the brown lead ores of Mexico. During his experiments he came across several colored compounds which he initially thought were the compounds of a hitherto unknown metal. He was right. These were the compounds of Vanadium, which are in fact so beautifully colored that today one of their major uses is in coloring pottery and porcelain. He even gave the new element a name "panchromium". "Pan" as you know is a Greek prefix meaning "all". Thus the element meant "all colors", which was quite an apt name because Vanadium compounds come almost in all colors. Later he changed the name to "erytronium" which means "red". But even after all this, del Rio could not proved his discovery scientifically, and thus couldn't get the credit for its discovery. Later the German chemist Friedrich Wohler also made a similar mistake." "Then how did sefstrom find the element?" "In 1830s, metallurgy was making its first steps in Sweden and plants were going up in different parts of the country. Quite curiously metallurgists found that iron smelted from some ores was brittle while that from some other ores had great plasticity, i.e. it was less brittle. On investigation it was found that the ores came from different deposits. It was quite obvious that there was some unknown substance, probably a new element, in some ores which was giving rise to this high plasticity of steel. Sefstrom was determined to isolate this new element and after strenuous efforts he was able to do just that. He and another Swedish chemist Jons Jakob Berzelius named this new element Vanadium, after a Swedish Goddess of love, Vanadis!" Interesting! But why this element should be named after a goddess of love?" "Berzelius was an established chemist and he was a very imaginative person. He described the story of Vanadium's discovery as an interesting allusion. He construed the earlier scientists such as del Rio and Wohler as prospective lovers who knocked at the door of a nubile young girl, but couldn't get her simply because they were not persistent enough and went away after knocking just once. Sefstrom was persistent enough to knock at the door of this girl continuously till the girl opened the door and thus was able to get that girl. Obviously the allusion of the girl was to this new metal, and of the knocking to the efforts made to extract that metal. Since Berzelius likened the new metal to a young nubile girl, he preferred to name it after the Swedish Goddess of love, Vanadis. It is said that after Sefstrom's success Wohler wrote to a friend,`I was a real ass to have overlooked the new element in the brown lead ore, and Berzelius was quite right when he laughed at me and described, not without irony, how I knocked at the door of Vanadis, so feebly, bashfully and haplessly!'" "Interesting indeed. How is Vanadium extracted from ores today?" "Tarun, Vanadium accounts for about 0.2% of earth's crust, which may not sound much but would sound significant when you consider that even this concentration is about 15 times more than that of lead and 2,000 times more than silver. But the world production of this metal is far less than these two metals. The world production of Vanadium was just 3 tons in 1907. It however increased to 18,000 tons in 1971 and 21,000 tons in 1975. The main producers are South Africa, US, erstwhile USSR and Finland. The reason why the production of this metal is far less than the other two metals is that it is fairly evenly spread in the crust unlike the other two metals which often occur in accumulations. Vanadium rarely occurs in accumulations, and ores containing just one percent of Vanadium are regarded as exceptionally rich. Even ores containing a mere 0.1% are taken for industrial processing. There are about 60 Vanadium minerals but mining is restricted to carnatite, which is a source of both uranium and Vanadium and vanadinite. Curiously, the meteorites that hit the earth contain two to three times more Vanadium than the earth's crust. Solar matter is also much richer in this element than our planet is. On earth, coal and oil have high quantities of Vanadium. Some coals may have up to 1% Vanadium, but the average is about 30 mg/kg, which is still quite high. Among the oils the highest concentrations of Vanadium are found in the Middle Eastern and Venezuelan oils which may contain up to 100-1400 mg/kg of Vanadium. Because of this, a significant source of Vanadium is the extraction from the furnace (boiler) ash of power plants which are fueled with residual oils. Because of this very same reason, persons engaged in boiler cleaning business are exposed to exceptionally high levels of Vanadium and they are quite prone to Vanadium toxicity. And this is probably the problem of Ramashanker" "Oh, I see. Before we go on to its toxicity, can you please tell me how such a toxic metal can possibly be used in any way?" "Tarun, despite Vanadium being toxic, it finds use in many industries. Its greatest use is in the production of special steels. You may be surprised to know that about 80% of the world production of Vanadium is used for this purpose. A small addition -just fraction of a percent- of Vanadium to steel makes it fine grained, very resilient, very strong and better fit to resist impact and bending. In fact, it has been described as a "vitamin" for steel. Interestingly both words begin with V. There is an interesting story regarding this use..." "Oh, I am a sucker for good scientific stories. Please tell me this story doctor." "The motor king Henry Ford is supposed to have said,`But for Vanadium, there would have been no automobile'. In 1905, he was present at a big motor racing event. Quite coincidentally a collision occurred. Ford went to up to the scene of the accident and picked up a fragment of one of the crashed cars. It was a French car and the fragment had belonged to its valve spindle. Ford was struck by its lightness and considerable hardness. Out of curiosity he sent it to a laboratory for analysis. The report came that this unusually steel contained Vanadium. Ford introduced this technology on a much larger scale in his own cars. And thus although this technology was known to the French before, it really came to be used on a mass scale only after Ford came to know about it. Today such important vehicle parts as the engine, valve springs, suspension springs, axles, shafts and gears are manufactured from steel laced with vanadium." Interesting. What are its other uses?" "As I said earlier, its salts are beautifully colored. The colors of these salts range from green, yellow, red and black to golden and hence they are used in porcelain and pottery industry to color them. Vanadium pentoxide and certain compounds of vanadium known as metavanadates are important catalysts in inorganic and organic chemical industries. They are used in sulfuric acid and plastic production. But only about 3% of all Vanadium is used as catalysts." "Does it have any medical use too?" "Vanadium does not appear to have any medical use. However dental caries incidence in children aged 7-11 years was reduced three times as compared to controls by local application of ammonium vanadate in glycerol. This is however an early Russian study and other workers have not been quite convinced by these results." "You said Vanadium is toxic. Can we ingest it through food too? And what about other sources of Vanadium?" "Wide variations occur in Vanadium levels in food. In the potato the reported concentrations range from about 1 mg/kg to 1.5 mg/kg. This could be due to differences in Vanadium concentrations in soil or to the bias of analytical methods or both. In cow's milk Vanadium was found at levels from about 0.2 mg/kg to 10 mg/kg. Meat concentrations are about 1 mg/kg. Vanadium is present in the air too. Its concentrations recorded in rural areas in the United Kingdom and Canada varied from 0.25 to 75 ng/m3. The concentrations in urban areas are higher- 60 to 300 ng/m3. There is marked seasonal variation, the mean for winter months being 6 times higher than for summer months. It has been estimated that about 1 mg of Vanadium could enter the respiratory tract per day if air concentrations are assumed to be about 50 ng/m3. The major sources of atmospheric emission are metallurgical works, followed by oil and coal burning. Fossil fuel combustion is the largest source of air pollution by Vanadium. You may recall that coal and oil are among the richest sources of Vanadium. The concentrations of Vanadium in water depend largely on geographical location and may range from about 0.2 to more than 100 mg/L. Levels of Vanadium in drinking water in India are not known but in the United States the average level has been found to be 4.3 mg/L. However typical values in drinking water appear to be about 1 mg/L. Concentrations in the soil range from about 5 to 140 mg/kg, and may reach high values when the soils are polluted by fly-ash. Then the values may shoot up to 400 mg/kg." "You said Ramashanker was suffering from Vanadium toxicity and you said that this occurred because he was working as a boiler cleaner. Are their other jobs too in which Vanadium can be absorbed?" "Tarun, industries where exposure to Vanadium may occur are Vanadium pentoxide production, Vanadium metal production, and production of Vanadium catalyzers. But as I said earlier, the most dangerous profession still is probably boiler cleaning. Very high levels in air may occur in boiler cleaning which may range from 17 to 60 mg/m3." "Doctor, what happens to Vanadium inside the body. Since it is not a normal constituent of the body, it should not have any use for it?" "Ingested Vanadium compounds are, in general, poorly absorbed. The absorption of soluble Vanadium compounds is just about 2%, i.e. if someone ingests 100 mg of a soluble Vanadium compound, only about 2 mg of it would be absorbed. Thus Vanadium salts, are very poor candidates for homicidal poison; they are simply not absorbed from the gastrointestinal tract. On the other hand Vanadium is a very important and interesting environmental poison because it is rapidly absorbed from the lungs! Skin is a minor route of absorption in man. Absorbed Vanadium accumulates in mainly in bone, and to some extent in the liver, muscle and kidney. The whole Vanadium content of a normal human weighing about 70 kg has been estimated to be between 17 and 43 mg. Interestingly although Vanadium is toxic, it is an essential element for chicks and rats, and its deficiency may result in their growth reduction and impairment of reproduction!" "You said that Ramashanker is suffering from Vanadium toxicity. How can you prove it in a court of law, if Ramashanker prefers to sue his employer for poisoning him intentionally?" "Tarun, his symptoms, especially his respiratory symptoms and his greenish tongue, coupled with the fact that he is working as a boiler cleaner are quite strong proofs in support of my contention. Yet there is an interesting test by which I can prove my theory. In Vanadium toxicity, the cystine content of fingernails is supposed to decrease. Cystine as you know is an amino acid. Thus determination of the cystine content of finger-nails is a useful diagnostic tool during a continuing exposure of Vanadium. I have already done that and I have indeed found the cystine levels in his fingernails to be reduced. Thus I shall have no difficulty in explaining to the court that Ramashanker is indeed suffering from Vanadium toxicity, and nobody is trying to poison him intentionally. Of course under the various industrial laws, he is entitled for compensation, should his toxicity make him an invalid. But I feel he should be shifted to some other work, so that his exposure to Vanadium is minimized and in time he would be alright. I would also be giving him a drug called BAL. It stands for British Anti Lewisite and is useful in the toxicity of several metals. I am sure that in time, he would be completely alright." "Thank you doctor for letting me know about such an interesting poison. What are you going to tell me next time?" "Tarun, next time I shall tell you about Methyl Bromide, which as you shall see is a very important poison. "
- Forensic Toxicology | Anil Aggrawal's Forensic Ecosystem
Forensic Toxicology THE FOLLOWING ARTICLE APPEARED IN THE MARCH 1998 ISSUE THE POISON SLEUTHS DEATH BY COMMON SALT -Dr. Anil Aggrawal "Good morning doctor. Oh, my God, what are you doing today? You have the dead body of a very young female infant today. What happened to her? Please tell me." "Good morning Tarun. The name of this 6 month old tiny girl is Babli. When she was born, her mother died due to some obstetric complication. Her father Ramdev soon remarried a nubile young girl Rekha. Before marriage she had promised that she would look after Babli well, but after marriage she often showed frank animosity towards this girl. She would not look after her well and would often not even feed her properly.." "Oh, so she probably starved her to death?" "Don't jump to conclusions Tarun. Look at her body. She doesn't look starved. An infant who dies of starvation looks just like a bag of bones. There is no fat in his or her body. But this girl is looking fairly well fed. What I was going to tell you is that Babli's grandmother Shanti Devi, i.e. Ramdev's mother, is still alive. She was not in favor of Ramdev getting married to Rekha in the first place. She probably knew that Rekha was not of good nature. Rekha was undoubtedly not feeding her well, but Shanti would always make up for her, giving her feeds in time. In fact that is why starvation was never a problem for Babli." "Then how did Babli die?" "Babli died of some respiratory disorder. At least that is what her physician told me just now. I will tell you what happened yesterday. Till yesterday morning, Babli was fine. Ramdev left for work in the morning at 8. As usual Rekha started seeing TV just after that, completely ignoring Babli. Seeing that it was her feeding time, Shanti prepared her feed, and filled her milk bottle with that. Just then a neighbor came to meet her, and she went to the drawing room to attend her, leaving the bottle in the kitchen. For half an hour they discussed about some religious programme they were going to attend that evening. After the guest left, Shanti went back to the kitchen, picked up the bottle and gave the feed to Babli. About half an hour later, Babli, who had consumed only about half the bottle by that time, started showing some strange symptoms. She started crying. It appeared as if she was irritable. She vomited twice. Shanti tells me that she had convulsions and muscular twitchings, fluttering of eyelids and of facial muscles. She displayed avid thirst. Shanti knows this because when she gave her water, she would feel a little relaxed, but after some time she would start crying again. But what was most prominent was that she was not breathing well. She had extreme difficulty in respiration. Shanti called Rekha for help, but she kept on seeing TV. Then Shanti phoned her son Ramdev, who immediately got in touch with their family doctor on phone. Dr. Saxena, the family doctor, arrived within 15 minutes, and found that the child was in real bad shape. Ramdev also reached home soon after. Dr. Saxena injected some medicines for respiratory distress, but although the injections seemed to help initially, they weren't of any lasting help. The doctor couldn't really understand what had happened to her. He thought that probably it was an attack of asthma. But what was most confusing was that Babli never displayed this symptom before. They were preparing to shift her to some big hospital for diagnosis and treatment, but before arrangements could be made, Babli died." "Oh, I see. So Babli's body has been brought to you to let them know how she really died?" "Yes, that's right. Actually Dr. Saxena was quite prepared to give the cause of death as asthma, but Shanti Devi immediately raised doubts. She has alleged that while her guest came to meet her, Rekha went to kitchen and mixed some poison in her feed. That is why Babli started having those strange symptoms immediately after having that feed. Rekha, of course, vehemently denied this, and Ramdev too refused to believe her mother, but she wouldn't listen to anyone. She phoned police immediately and called them to their house. The police ransacked the whole house and even searched all Rekha's belongings, but they couldn't find any poison anywhere in the house. That is what is lending weight to Dr. Saxena's theory that Babli indeed died of asthma. Every one including the police is thinking that Shanti Devi is making all this fuss, because she didn't like Rekha in the first place." "Yeah, that looks likely to me as well. So what are you going to do now?" "Tarun, since the matter has reached the police, Dr. Saxena preferred not to give cause of death and leave that to me. The body has been brought to me for post-mortem so that I could comment upon the cause of death." "How do you think Babli died?" "Tarun, the symptoms that Babli displayed surely point towards some respiratory trouble. But the symptoms also point towards a very unusual poison, a poison no one can ever think of. And that is why I have to be extra careful. You have got to remember, that I have a reputation as a poison sleuth, and so I can not afford to leave out even a remote possibility as far as administration of poison is concerned. "Come on doctor. No poison was ever found in the possession of Rekha. Not even that, there was no poison in the whole house. How could anyone administer any poison to Babli?" "Yeah, that sounds very convincing to the police, and that's why they think Shanti Devi is a nut. But I don't think so. I know of a poison which produces exactly the same symptoms as displayed by Babli..." "Please don't talk in riddles doctor. Explain everything to me in clear terms." "Yeah sure. To test my theory, I took some of the stomach contents of Babli and subjected them to chemical analysis. Not to my great surprise, they have shown very high concentrations of salt. Then I took Babli's blood and examined it chemically too. And again it showed very high levels of sodium. I am inclined to think that Babli has been killed with ...." "With what?" "With common salt!" "Common salt? You must be joking doctor. How can anyone be killed with common salt. This is what all of us take daily in our food. Well my father is so fond of common salt he always puts an extra teaspoonful of common salt in his dal." "Yeah, this is what is not known to most people. Common salt is a deadly poison. The only difference between this and other commonly known poisons is that one has to administer rather large quantities to kill with it. One or two teaspoonfuls of salt would not kill an adult but can easily kill a 6 month old baby. Come to think of it, even an adult can be killed with common salt. Only he would have to be fed larger quantities. About 40 teaspoons of common salt would kill an adult human being too." "Well the information is getting interesting. Why don't we begin from the beginning doctor?" "Tarun, before you start visualizing it as a villain, I must hasten to add that there is no doubt that common salt or sodium chloride (NaCl) is indeed essential to all life. It is the basic milieu of mammals. It occurs as colorless cubic crystals or as white crystalline powder. When salt is administered in larger quantities than required, it can cause death too. One teaspoonful of salt weighs about 5 gms. Normal uptake by adults is about 5 to 15 g daily or about 1-3 teaspoonfuls. Children consume less. Salt is even necessary for normal growth in children. The sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, which decreases to 0.1 mEq/kg at 6 months. The average content of sodium in human milk is 7 mEq/L and that in cow milk is 21 mEq/L ..." "Doctor, you started your answer telling me weights in grams, but suddely you have switched to milliEquivalents. I don't really understand the concept of milliEquivalent so well. And why should we talk in milliEquivalents, when we can talk equally well in grams?" "Tarun, in ordinary day-to-day life, it is useful and convenient to talk in grams and kilograms, but chemists and biochemists often find it easier to talk in terms of equivalent weights because of several reasons. You would surely agree that chemists are mainly interested in chemical combinations, and Equivalent weights are actually measures of the characteristic proportions in which given elements combine. For this reason, this term is also often known as Combining weight. Equivalent weights can be used for elements as well as for compounds. In plain and simple words, they are the measure of the combining capacity of a substance with other chemical substances. Well, even if after this, you are feeling inconvenient with equivalent weights, let me add that 1 mEq of sodium equals 23 mg and that of salt equals 58.5 mg. I would also like to tell you that 1 milliequivalent would be equal to 1/1000 Equivalent weight. Now when I say that the sodium needed for growth is 0.5 mEq/kg from birth to 3 months of age, I simply mean that for every kg of baby's weight, 0.5 mEq of sodium is needed. Thus if the infant weighed, say, 4 kg, he would need 4x0.5 or about 2 mEq of sodium. Since 1 mEq of sodium is 23 mg, it would mean that the infant would need about 46 mg of sodium daily. This much sodium would be available from about 117 mg of salt. Thus in effect, a baby from birth to 3 months needs about 117 mg of salt. Similarly you can convert other values which I told you earlier in grams. I told you the sodium contents of human milk, because this is the only food available to young babies." "Oh, I see. Doctor, you were saying that 40 teaspoons of salt would kill even an adult?" "Yes Tarun. The toxic oral dose of salt is 0.5 to 1.0 gm/kg. For a 70 kg man this amounts to about 35-70 gm. That means that if an adult consumes about 70 g of salt (or about 14 teaspoons), he would be severely poisoned. The estimated fatal amount, i.e. one that would kill is about 1 to 3 gm/kg. This amounts to about 70-210 gm (or about 40 teaspoonfuls) of salt for a 70 kg man." "Oh, that is interesting. Has salt been used to kill people before?" "Tarun, interestingly the Chinese used saturated salt solution for suicide. Salt intoxication and death have occurred when it is used to induce vomiting." "Why would one want to vomit anyway?" "When somebody has consumed some poison, it is imperative to remove as much poison from his stomach as possible. One of the best ways to do this is to make the person vomit. It has been known from ancient times, that a strong solution of common salt induces vomiting, and that is why for centuries, it was a favorite method of doctors to induce vomiting in poisoned patients. But it is known now that saturated solution of salt itself can cause salt poisoning, so it is rarely used these days." "Oh, I see. So you are suggesting that Rekha mixed salt in Babli's feed when Shanti was talking to her neighbor in the drawing room." "Babli's stomach contents, and her blood analysis definitely tells me that salt has been administered to her. I have examined her brain tissue under the microscope too, and I have found that the capillaries of her brain are damaged. They are full of blood, and there are innumerable bleeding points - technically known as hemorrhages- in her brain. There is bleeding underneath one of the coverings of the brain. We call it subarachnoid bleeding, because it occurs underneath the covering known as arachnoid mater. Many venous channels of her brain - technically known as dural sinuses- are blocked. All these findings are strongly in favor of salt poisoning. I have no doubt that someone had indeed mixed salt in her feed. To tell you the truth now, I surreptitiously picked up the milk bottle from Ramdev's house and have analyzed it for salt. It showed as much as 11 g of salt and it was only half full. It means that the full bottle must have contained about 22 g of salt. In other words, Rekha must have put about 4 teaspoonfuls of salt in Babli's bottle when Shanti was talking to her neighbor. There was no other person in the house at that time, and no one except Rekha could have done that." "Rekha indeed is a wicked woman. It is surprising she knew that salt can kill." "I have enquired about Rekha's background. She studied biochemistry in college, although she dropped out of college later. Surely when she was studying biochemistry she must have learnt that salt is a poison and can be used to kill infants. It is indeed a rather safe poison, because you don't need to buy anything. It is available right at everyone's home. And the police won't suspect you either, because they won't find any poison....any traditional poison, I mean. Come let us tell the police that Babli didn't die of asthma. It is Rekha who has added salt to Babli's feed to kill her." "Oh, how very clever of you doctor. This was a most interesting discussion. Tell me what are you going to tell me the next time?" "Tarun, next time, I would tell you about a very interesting poison- iodine"
- Anil Aggrawal's Forensic Ecosystem
| Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology Paper/Thesis/Dissertation Submission GUIDELINES A ll papers can be submitted electronically (by E-mail, floppy, magneto-optical disk, zip drive, tape drive or CD). If you are comfortable with sending just a typed manuscript, this is also acceptable (please include your E-mail ID in the covering letter). The submitted material must come along with the submission letter. This is a signed statement on official letterhead, which must state the following: SUBMISSION LETTER 1. "I/We hereby submit that the paper/dissertation entitled [please give name of the paper/dissertation here] has been written by me/us along with [please include number of photographs here (write 0 if no photograph accompanies the paper)] photographs, [please include number of audio files here (write 0 if if no audio file accompanies the paper)] audio files and [please include number of video files here (write 0 if no video file accompanies the paper)] video files. This paper/dissertation/audio and visual files are my/our original work and has neither been published anywhere else, electronically or in print, nor has been submitted elsewhere simultaneously for publication. The paper has not been rejected previously by any journal*. The views expressed in this paper/dissertation/ audio and video files are entirely my/our own. I have agreed for this paper/dissertation/audio and video files to be published in Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology". *[Declaration whether the manuscript has been rejected by another journal - If the paper has been rejected by another journal/s previously, please omit the sentence "The paper has not been rejected previously by any journal". Instead, please state here "The paper has been rejected previously by journal/s entitled 'XYZ'". Please also submit the reviews or editorial statements forwarded to you by the journal/s along with a copy of the rejection letter / copy of the email rejecting the paper.] 2. I/we vouchsafe that the authorship of this article will not be contested by anyone whose name(s) is/are not listed by me/us here. 3. I/we vouchsafe that I/we have gone through all papers cited by me/us in the references section. I/we also understand that if requested by the reviewers for cross-checking facts stated in the paper, I/we would be able to send a pdf/scan/photocopy of the paper. 4. The article contains no libellous or other unlawful statements and does not contain any materials that violate any personal or proprietary rights of any other person or entity. In case, any legal action is instituted because of any statement(s) made by me in the paper, I will be completely responsible for it, and the journal would carry absolutely no liability in that matter. 5. I/we hereby acknowledge Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology's conflict of interest policy requirement to scrupulously avoid direct and indirect conflicts of interest. Therefore I/we hereby agree to promptly inform the editor-in-chief of any business, commercial or other proprietary support, relationships, grants or research support or any other interests that I/we may have which relate directly or indirectly to the subject of the work. 6. I/we also agree to the authorship of the paper in the following sequence: Authors' Names in sequence Signatures of authors 1. 2. 3. 4. 7. Detailed contribution statements (i.e., if a manuscript has more than one author: who contributed what part?) - If the manuscript has more than one author, please be kind enough to specify here the specific part played by each author towards the preparation of the final paper. 8. I/we understand that my/our paper may be published in a future issue as “publication ahead of print” or “epubahead.” [As mentioned in the guidelines page, the paper will be available online and citable by other workers, right from the day/year of publication as “epubahead”]. 9. I/we transfer the copyright of the paper/all associated photographs, line diagrams and other associated material to "Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology." Signed (First/Main author) Current Position with complete mailing address Telephone number Email Submission letters through Email Submission letters can be submitted via Email, as a scanned copy. They must (1) Clearly show signatures of authors (2) Must be on institution or personal letterhead (3) Should have contact details of all authors [emails, phones etc]. In addition, authors must keep in mind the following rules. (A) All documents related to the paper must be submitted in one lot and not in parts. (B) Only one paper [plus all related documents] can be submitted per email. More papers may be submitted, but each paper [plus all related documents] must be sent in a separate email. Some sample letters are given below. Please click to enlarge. S ubmission letters can be on multiple pages as below. Please click to enlarge. Submitting Images/Pictures/Photographs Authors whose papers are accompanied with Images/Pictures/Photographs must submit pictures in accordance with the guidelines set by PubMedCentral. Please click here to view these guidelines and requirements. Please also refer to the "Image Quality Specifications" by clicking here . Any paper accompanied by pictures not adhering to these guidelines cannot be accepted. Pictures must be *.jpg format. Pictures embedded in word, powerpoint, or any other file format will not be accepted. Audio and Video files The journal accepts audio and video files for publication. Papers accompanied by audio and video files are given preference . For an example please click here . These are merely illustrative audiovisual files unaccompanied by any paper. Only audio files [eg paper read aloud, sounds perceptible on clinical examination, eg heart and respiratory sounds etc] and only video files [eg displaying Chvostek’s and Trousseau’s signs] can also be sent. For more sample audio and video files, please request by sending an Email to the editor. Authors' Photographs Authors must submit their pics along with papers, because all papers in this journal are published with authors' pics. The guidelines for authors' photographs are same as above [See under the heading "Submitting Images/Pictures/Photographs" above]. Papers not accompanied by authors' pics cannot be accepted . Ethical policy on patient confidentiality Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology expects that a statement of consent must accompany any paper/article/other contribution containing identifiable patient information. If there is any doubt about whether or not information is identifiable, the Editor-in-chief is happy to discuss this before the piece is submitted. Reviewers will also be asked to take careful account of issues relating to patient confidentiality when reviewing articles/papers. Please discuss in case of any doubt by clicking here . Quality control We at the Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology believe in publishing only high quality papers. Please read Clarivate's Journal citation reports 2023 . Please also read the 24 rigorous quality criteria applied by them on the evaluation of journals. We follow each of these strictly. Online submission Online submission of papers is possible. If you want to submit papers online, please click here . Submission letter can similarly be sent online (Please see above). The paper would be considered only after all required documents, including the submission letter have been received. Note - This journal DOES NOT ACCEPT PAPERS THROUGH ANY OTHER WEBSITE / LINKS, than the one mentioned here. Why should you publish with us? Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology is indexed with most leading indexing databases, thus ensuring maximum visibility among your peers. The content of the journal being freely accessible to all is another factor of great advantage. This greatly increases the chances of your paper getting cited in other journals /books of repute. For some examples, please click links below: National Library of Medicine, Bethesda, USA Please see visit this journal at National Library of Medicine, USA. References in Journals Aggression and Violent Behavior. 2003 Sep;10(3):153-7. [Please see reference on page 145, highlighted in yellow]. International Orthopaedics (SICOT) (2004) 28: 187–190 [Please see reference 7, highlighted in yellow]. Journal of Clinical and Forensic Medicine. 2003 Sep;10(3):153-7. [Please see reference 15, highlighted in yellow]. Journal of Trauma. 2004;57:125–129. [Please see reference 18, highlighted in yellow]. J Forensic Sci, Jan. 2005, Vol. 50, No. 1. [This is a book review. Please see mention of the journal highlighted in yellow]. Pediatr Nephrol (2005) 20:1610–1614. [Please see reference 20, highlighted in yellow]. Journal of Clinical and Forensic Medicine. 2005 Jun;12(3):149-52. [Please see reference 14, highlighted in yellow]. The American Journal of Forensic Medicine and Pathology : March 2006 - Volume 27 - Issue 1 - pp 75-78 [Please see reference 12, highlighted in yellow]. Traffic Injury Prevention, Volume 7, Issue 1 March 2006 , pages 70 - 75 [Please see reference to this journal highlighted in yellow]. The American Journal of Forensic Medicine and Pathology : March 2007 - Volume 28 - Issue 1 - pp 86-90 [Please see reference 28, highlighted in yellow]. The Spine Journal 8 (2008) 703–704 [Please see reference 4, highlighted in yellow]. Leg Med (Tokyo). 2009 May;11(3):107-10. [Please see reference 4, highlighted in yellow]. References in Books / Book chapters Essential Forensic Biology , by Alan Gunn, 2nd ed ( Wiley , 2009) [Please see the reference on page 397, highlighted in yellow]. Forensic Entomology - An Introduction , by Dorothy E. Gennard, 1st ed ( Wiley , 2007) [Please see the reference on page 17, highlighted in yellow]. Forensic Evidence Science And The Criminal Law , by Terrence F. Kiely, 2nd ed ( CRC Press , 2006) [Please see the 11th reference on page 328, highlighted in yellow]. Manejo de la evidencia física de posible fuente biológica [Spanish], by Mercedes Salcedo Cifuentes ( Universidad del Valle , 2007) [Please see reference 29 on page 52, circled in yellow]. You can also visit this book on google books by clicking here . Please go to page 52. Other Papers of Interest Growing Visibility of Indian Biomedicine and Life Sciences Journals in Global Alerting Services , by N.C. Jain. 30 May 2008. Sawant, S. The current scenario of open access journal initiatives in India. Collection Building . 2009; 28(4) :159–163 Vancouver Style All manuscripts should conform to the Uniform Requirements for Manuscripts Submitted to Biomedical Journals (Ann Intern Med 1997;126:36-47). References must be in accordance with Vancouver style. Please visit the following sites for guidance on Vancouver style. AMA Style Guide Bibliographic Services Division of the United States National Library of Medicine, National Institutes of Health BMA - Reference styles Citing your sources - Vancouver style Download reference styles Sample PubMed Central Citations Vancouver Style Vancouver Style Quick guide - How to use it The Columbia Guide to Online Style , second edition by Janice R. Walker and Todd Taylor We can provide help and support if needed: Guideline Support It is important that authors double-check the grammar and style used in the paper. Publication of papers with defective English may be inordinately delayed. Authors wanting to refine the use of English in their manuscripts might consider utilizing the services of SPi. Please click here to visit. Keywords Please choose your keywords in accordance with Medical Subject Headings prescribed by the United States Library of Medicine, National Institutes of Health. Please click here to visit their site. Please click here to visit their MeSh (Medical Subject Headings) browser. Download a complete list of recommended keywords by clicking here . Citing References Pubmed journals Authors should strictly check the accuracy of each reference cited in their papers. Please do provide either the PMID of the paper cited in your own paper. For example if you want to cite the paper below: Szulman AE. The histological distribution of blood group substances A and B in man. J Exp Med. 1960;111: 785-800 . then please cite its PMID which is as below: PMID: 13774694 [Note: PMID of all papers is available from pubmed site . For more help, please download this sample paper by clicking here .] The complete citation in your paper should be as follows: Szulman AE. The histological distribution of blood group substances A and B in man. J Exp Med . 1960;111: 785-800. PMID: 13774694 or Aggrawal A, Setia P. Vertebral artery dissection revisited. J Clin Pathol . 2006;59(9):1000-2. PMID: 16935980 Note: If you visit the pubmed site, then inserting the PMID in the "search box" should get you the relevant paper. Please note that the PMID provided by you will not appear as such in the published paper. It will ONLY be used to provide pubmed links to your citations. For one example of how pubmed links will be provided to your citations, please click the following link: https://anil.aggrawal.org/ij/vol_006_no_002/papers/paper006.html Go down to the References section, and check the Pubmed Links. [Note: For further help, please download this sample paper by clicking here . Please go to the references section, where we have highlighted the PMID in yellow. You must provide the PMID in similar fashion.] medIND journals Indian Medlars Center (medIND) provides free fulltext of several journals participating in its program. If your reference quotes a paper from these journals, please provide a medIND link. For example if you want to cite a paper below: Jha N, Srinivasa DK, Roy G, Jagdish S. Injury pattern among road traffic accident cases: A study from South India. Indian Journal of Community Medicine 2003; 28(2):85-90. then please cite its medIND URL also as below. This URL will be used by us to give a link to medIND medIND URL: http://medind.nic.in/iaj/t03/i2/iajt03i2p85o.pdf The complete citation in your paper should be as follows: Jha N, Srinivasa DK, Roy G, Jagdish S. Injury pattern among road traffic accident cases: A study from South India. Indian Journal of Community Medicine 2003; 28(2):85-90.medIND URL: http://medind.nic.in/iaj/t03/i2/iajt03i2p85o.pdf Please note that as with pubmed links, the medIND URL provided by you will not appear as such in the published paper. This URL will ONLY be used to provide medIND links to your citations. For one example of how medIND links will be provided to your citations, please click the following link: https://anil.aggrawal.org/ij/vol_006_no_002/papers/paper006.html Electronic journals For electronic papers, please provide citations like below: Friedlander, ER. Cryptogenic Organizing Pneumonia Masquerading as Coal-Worker's Pneumoconiosis. Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology [serial online] , 2007; Vol. 8, No. 2 (July - December 2007): [about 8 p]. Available from : https://anil.aggrawal.org/ij/vol_008_no_002/papers/paper002.html Published : July 1, 2007, (Accessed: June 23, 2025) What's new in your paper All papers must be accompanied by a separate sheet detailing these four columns: 1. What is already known on this topic? 2. What question did this study address? 3. What does this study add to our knowledge? 4. Suggestions for further development These columns will make it clear in the mind of readers, what exactly is the new message given in your paper. Furthermore, it would give them new ideas for further research in the area, which should be the aim of all good academic journals. For further guidance on the above matter, you may want to visit the paper by Edward R. Friedlander entitled "Cryptogenic Organizing Pneumonia Masquerading as Coal-Worker's Pneumoconiosis?" appearing in Vol. 8, No. 2 (July - December 2007). To visit the paper, please click here . For a good web link available on the net, please click here . [Note: For further help, please download this sample paper by clicking here .] Peer Review Policy All material published in this journal undergoes editorial screening and peer review. Please allow about one to two months from the date of submission of papers till publication. The hard printed copy of the paper/dissertation, the photographs and the signed statement must be sent at the following address. Professor Anil Aggrawal Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology S-299 Greater Kailash-1New Delhi-110048 India Electronically submit your paper simultaneously by clicking here Please send photographs, charts, diagrams etc in original at the journal address. Please discuss in case of any doubt by clicking here . What can you do for Quick Publication There are no publication charges . Queries regarding article processing charges/publication fee for publication/quick publication will not be answered. All papers are checked for piracy/plagiarism by authentic softwares [ iThenticate, Turnitin, Urkund ], which may take some time. Papers which are accompanied with an antiplagiarism check report, may be considered for quick publication. Procedure for selection of Thesis and Dissertations Essentially the procedure for selection of thesis and dissertations is the same as that for papers. The thesis may be submitted electronically first. If found suitable, you would be informed accordingly by E-mail. You would then be required to send the actual thesis along with all photographs, charts, diagrams etc. to the journal address, along with a signed declaration as above. The thesis would become the property of the journal. It would be hosted on the net about a month or so after its receipt. Electronically submit your dissertation by clicking here Cumulative index of theses/dissertations published in this journal Please send photographs, charts, diagrams etc in original at the journal address. Returning of manuscripts/photographs/CDs/DVDs Please be careful to keep a copy of all materials including manuscripts, submission letters, photographs, CDs, DVDs etc which you send to the journal with you. Please do not send self-addressed stamped envelop with the manuscript. The journal has no arrangement for returning the unaccepted manuscripts/photographs/CDs/DVDs/other material. Publication ahead of print [Epubahead] Sometimes because of space constraints, a paper may be published as Publication ahead of print [Epubahead] . This paper will however be available online and citable by other workers, right from the day/year of publication as “epubahead”. Example: Suppose the year when the paper is submitted and accepted is 2026. The paper may be published as epubahead in, say, the year 2032. The paper will however be available online and citable by other workers, right from 2026 [the day/year of publication] as “epubahead”. Only the print/CD versions, will appear in 2032. How these papers and dissertations will be quoted by your peers Electronic papers can be quoted as references just as print papers are. For details please refer to the Vancouver Style sites mentioned above. To see how the papers are quoted, you may want to visit some papers in the journal. Dissertations would be cited similarly. Visit theses and dissertations in this journal to see how they are being quoted. Some Examples currently on the web Examples of how papers published in this journal have been cited in other journals can be found by visiting http://scholar.google.com/ . Examples of how papers published in this journal have been cited in Books can be found by visiting http://print.google.com/ . Submit Your Paper Here To inquire about the status of your submission, please use the following form: [ Link ]