Category Archives: Forensic Toxicology

Marsh Test For Arsenic

James Marsh and the Marsh Test

An important test used in early toxicology was developed in 1836 by chemist James Marsh (1794–1846).

In 1832 John Bodle had been accused of poisoning his grandfather. It was said that Bodle mixed Arsenic in his grandfather’s Coffee. Marsh was asked by the prosecution to check the viscera of the victim.

Old Method

James Marsh used a hydrogen sulfide method and was able to produce a yellow solid consistent with the presence of arsenic. But, the solid degraded between the time it was prepared and when it was presented to a jury. Bodle was acquitted because of the degraded sample.

New Aim

Marsh went into his lab with one simple goal: develop a reliable and visually convincing method to detect arsenic in messy and complex samples like tissue and stomach contents.
First, he turned to Scheele’s procedure in which arsenic was converted to arsine gas. Marsh knew that under the proper conditions compounds containing arsenic, such as arsine, could be manipulated to form arsenic metal. Magnus had demonstrated that conversion centuries earlier.
Marsh realized that metallic arsenic is stable, and if he could capture the arsine gas, he could manipulate it so that metallic arsenic would form on a solid surface.

Marsh Test also known as Plating Out.

This process is sometimes called “plating out.” This simple idea took Marsh four years to perfect, and the method became known as the Marsh test. This famous procedure was the first reliable analytical test for arsenic. For his efforts Marsh received wide acclaim and a gold medal from the Royal Society of Arts.

Danbury Tremor

Question and Answer on Danbury Tremor

Question 1- What is Danbury tremor?
Answer- Danbury tremor or Danbury shakes is seen in the case of Mercury Poisoning.

Question 2- What is Mercury?
Answer- Mercury is a heavy metal with known toxicity. Mercury is sometimes called quicksilver. It is a heavy, silvery-white liquid metal.

chemical properties of Mercury (part of Periodic Table of the Elements imagemap)

Mercury is the only elemental metal that is liquid at room temperature.

Question 3- What is “Danbury” in Danbury tremor?
Answer- Danbury is a city in Fairfield County, Connecticut, United States, located approximately 50 miles northeast of New York City, making it part of the New York metropolitan area.

Question 4- What is the reason behind adding the name of city of Danbury in “Danbury tremor”?
Answer- Danbury is a city which was earlier popular for hat production. And due to tremendous production of hats, this city was started to name as “Hat City”. Although Danbury’s hat-making industry dated back to 1780, advances in the mechanization of manufacturing processes contributed to its rapid growth in the mid-19th century as did consumer demand for felted fur hats. During the lots of production of hats,(mercury was involved in processing) worker suffered from the tremor which was named as “hatter’s shakes”. which was known as Danbury Tremor afterwards. 

Question 5- Danbury tremor is seen in which type of poisoning?
Answer- Mercury poisoning.

Question 6- What are the other names of Danbury tremors?
Answer-
 Hatter’s shakes,
 Glass blower’s shakes,
 Intention tremors or
 Shaking palsy.

Question 7- What are other compounds or chemicals that can cause tremors?
Answer- Following Compounds can cause Tremors:

— Alcohol,

— Phosphorus Salts,

— Carbon Monoxide,

— Anti-depressants,

— Phenothiazines,

— Caffeine,

— and, Theophylline, etc.

Question 8- Danbury tremor is first seen in which body part?
Answer- Danbury shakes were first starting with hands then progresses to lips, tongue, arms, and legs.

Question 9- What is the most severe form of tremor in Mercury Poisoning?
Answer- Concussion Mercurilis.

Question 10- What are the other specific diseases related to mercury positioning?
Answer-
 Mercurialentis: Brown reflex of the anterior lens capsule of the eye which can be seen by Slit-lamp examination.
 Acrodynia or Pink disease: are mostly in children having pinkish acral rashes
 Minamata disease: caused by Organic Contamination like eating fish. It causes disturbances in hand coordination, gait, speech, etc.

 Question 11- What is the common drug treatment for mercury poisoning?
Answer- Treatment of mercury intoxication is with penicillamine or succimer.

N-acetyl penicillamine is the chelator agent along with DMPS may improve the neurological conditions. 

Worst Stinky Chemicals/Substances on the Earth

We smell many substances / chemicals in our daily lives. Some smell good but some do not. While not all compounds produce odors, several compounds do have recognizable odors, including: Cadaverine and putrescine smell like rotting flesh. Skatole has a strong feces odor. Indole has a mustier, mothball-like smell. Here is a list of similar chemicals that cause the most smell.

☠ World War Weapon-“Who Me?”:

During World War II, the Allied Forces created Who Me – one of the most nefarious chemical weapons. Its was produced to make the target smell like feces.

😷 Ethyl Mercaptan (ethanethiol):

Ethyl Mercaptan smells like leek. 1 part of Ethyl Mercaptan can be detected – without instrumentation – in 2.8 billion parts of air.

The Mirror reads: “The French stench: Gas leak from factory in France causes a stink 200 miles away in UK” and the subheadline reads: “The leak released a colourless gas called mercaptan – listed in the Guinness Book of Records as “the world’s smelliest substance”.

🤢 Butyl seleno-mercaptan (C4H9SeH):

Ethyl mercaptan (C2H5SH) and butyl seleno-mercaptan (C4H9SeH) have an odor reminiscent of a combination of rotting cabbage, garlic, onions, burnt toast and sewer gas. Ethyl mercaptan is added to odorless gas to act as a warning agent.

🤧 Cadaverine :

Cadaverine is decarboxylated lysine that may be isolated from cadavers or pretty much any decaying dead animal. As living flesh decays, amino acids interact and create Cadaverine.

🤯 Skatole:

Skatole or 3-methylindole is an organic compound belonging to the indole family. Occurring in high concentrations, it is the primary odor of feces. But, do you know small amounts of skatole is used to flavor vanilla ice cream. But when it’s not being blended into dairy products, skatole is known for giving human feces part of its odor.

🤮 Butyric Acid:

Butyric acid is a carboxylic acid found in rancid butter, parmesan cheese, and vomit, and has an unpleasant odor and acrid taste, with a sweetish aftertaste (similar to ether). Butyric acid is a fatty acid occurring in the form of esters in animal fats and plant oils.

😤 Dibutyl Telluride:

When you smell “garlic” after tellurium exposure, is (CH3)2Te, or dimethyl telluride. The body metabolizes tellurium the same way it does sulfur, one of the elements that makes garlic stinky.

👾 Pyridine:

It is a highly flammable, weakly alkaline, water-miscible liquid with a distinctive, unpleasant fish-like smell which will not go easily. Pyridine is colorless, but older or impure samples can appear yellow. Historically, pyridine was produced from coal tar.

🧟‍♀️ Putrescine:

Putrescine smells like rotting flesh. In fact, the compound at the heart of putrescine is the same as that created by actual rotting flesh.

🥚 Hydrogen selenide:

Hydrogen Selenide smells like rotten eggs mixed with rotten radishes, and poisons you as it “clings” to the insides of your nostrils. It is more toxic than Hydrogen Cyanide, and dulls your sense of smell, making it incredibly dangerous on top of being unpleasantly fragrant.

💨 Mustard Gas:

Mustard Gas (HN3) doesn’t smell like mustard. In reality, Mustard Gas induces fear and hysteria in those unlucky enough to encounter it. Having no antidote, Mustard Gas caused more deaths during World War I than any other chemical weapon despite being less toxic than nerve gas.

🐠 Trimethylamine oxide:

This chemical is found more commonly in ocean sea life and is the reason that cod starts smell faster than river caught catfish. This scent is caused by the breakdown in bacteria combined with the fish enzymes.

💦 Ammonia:

Ammonia is 1 part Nitrogen, 3 parts Hydrogen and all parts repugnant. Some of the more pleasant liquids with traces of ammonia include concentrated cleaning products, cat piss and human sweat.

🙊 Isovaleric Acid:

Isovaleric acid has an identity crisis. On the one hand, the acid gives off at athletic foot smell and makes the body stink of B.O. On the other hand, one of isovaleric acid’s compounds (esters) is used in perfumes due to its fragrant scent. Let’s just hope you catch it on one of its “up” days.

👃Any Thiol:

A thiol is an organic sulfur compound. A familiar example is the rotten egg smell of hydrogen sulfide. Compounds with the S-H group tend to be toxic as well as smelly.

🥡Formaldehyde:

While fly food and disinfected cultures stink, they won’t hurt you. If you can smell formaldehyde, on the other hand, you know you’re poisoning yourself. The chemical, often used as a preservative, has a distinctly unpleasant odor. The nausea and headache are from the toxicity, not just the scent. Paraformaldehyde, a related chemical also used as a fixative, possibly smells even worse.

🍾 n-Butanol:

Trace amounts of fusel alcohols give beer and wine distinctive odors. However, the pure chemical smells vile. n-Butanol is a primary alcohol produced during carbohydrate fermentation. While it’s a solvent in the lab, you’ll also find it as an artificial flavoring in many foods and as a natural chemical in beer, wine, and other fermented products.

🔴 Beta-Mercaptoethanol:

 Beta-mercaptoethanol (2-mercaptoethanol) is used to lower the volatility of chemical solutions and as an antioxidant. The odor is like a cross between rotten eggs and burnt rubber. In high doses, it’s deadly toxic.

Hair analysis

General characteristics of Human Hair

1Colour:White, blonde, light brown, gray brown, dark brown, gray, black, auburn, red.
2Reflectivity:Opaque, gray, translucent, transparent, auburn, clear.
3Length:Fragment, 1”, 1-3”, 3-5”, 5-8”, 8-12”, 12-18”, 18-30”, segment.
4Diameter:20-30 um, 30-40 um, 40-50 um, 50-60 um, 60-70 um, 70-80 um, 80-90 um, 90-100 um, 100-110 um.
5Spatial Configuration:Undulating, kinky, curly, wavy, curved, straight, sinuous
6Tip:Singed, uncut, tapered, rounded, sharp cut, cut at angle, frayed, split, crushed, broken.
7Base:Cut, damaged, pigmented, clear, enlarged, tapering, broken.
8Root:Stretched, absent, bulbous, sheathed, atrophied, follicular, wrenched.
9Cross-section:Polygonal, oval, round oval, undulating, round.
10Pigment:Absent, non-granular, granular, multicolour, chain, massive (clumped), dense, streaked, opaque.
11Medulla:Absent, sparse, scanty, fractional, broken, globular continuous, irregular, double, cellular.
12Cortical fusi:Absent, few, abundant, bunched, linear, central, periphery, roots.
13Cortical cells:Brittle, damaged, fibrous, cellular, invisible, fusiform, ovoid bodies.
14Cosmetic Treatment:Bleached, rinsed, natural, dyed, damaged.
15Cuticle:Ragged, serrated, looped, narrow, layered, wide, cracked, absent, clear, dyed.
16Scales:Flattened, smooth, level, arched, prominent, and serrated.

 Morphological Characteristics of Human Hair for Racial Determination

RaceDiameterCross-sectionPigmentationCuticleUndulation
Negroid60 – 90 umFlatDense & clumpedPrevalent
Caucasoid70 – 100 umOvalEvenly distributedMediumUncommon
Mongoloid90 – 120 umRoundDense AuburnThickNever

 General characteristics of Human Hair from Different Sites

ScalpHead hair, 100 – 1000 mm long, 25-125 um diameter, 0.4 mm/day growth; small root, tapered tip, little diameter variation, various medullation, often with cut tips, may artificially treated.
PubicPudental, 10 – 60 mm long, coarse diameter and prominent diameter, variation and buckling, broad medulla, follicular tags common, asymmetrical cross section twisted and constricted, may be straight, curved or spirally tufted.  
VulvarSecondary pubic hair, finer and shorter than pubic hair, may be abraided.  
ChestPectoral, moderate to considerable diameter variation, long fine arch-like tip, usually longer than pubic hair.
BeardFacial hair, very coarse, 50-300 mm long, large root, irregular structure, often triangular cross section, complex medullation, blunted or razor cut tips, grows 0.4 mm/day.  
AxillaryArm pit, 10-50 mm long, grows 0.3 mm/day, coarse, blunt tip, abraided or frayed, usually straighter than pubic hair, many cortical fusi, sometimes yellowed and bleached.
EyebrowSuperciliary, 1 cm long, 0.16 mm/day growth, curved, relatively coarse for length, smooth curve with punctate tip and large medulla.  
EyelashCiliary, less than 1 cm long, short curved pointed hair.  
LimbLeg and arm hair, 3-6 mm long, fine tips, irregularly medullated, often indistinctly, slightly pigmented.  
EarTragi, pinnae, down  
ButtocksAnal hair, short blunted and abraided hair.  
NoseSimilar to facial hair.  

General Differences between Human Hair and Animal Hair

FeatureHuman HairAnimal Hair
ColourRelatively consistent along shaftOften showing profound colour changes and banding
CortexOccupying most of the width of shaft greater than medullaUsually less than width of medulla
Distribution of pigmentEven, slightly more towards cuticleCentral or denser towards medulla
MedullaLess than one-third width of shaft. Amorphous, mostly not continuous when presentGreater than one-third width of shaft. Continuous, often varying in appearance along shaft, defined structure
ScalesImbricate, similar along shaft from root to tipOften showing variation in structure along shaft from root to tip

MCQs On Forensic Toxicology

1. Which of the following is NOT a side effect of Digoxin toxicity?

A. Bradycardia
B. Yellow vision changes
C. Scooping of the T segment on ECG
D. Hypokalemia

2. Which information can be obtained from an acute toxicity study?

A. Median toxic dose (TD50)
B. Median lethal dose (LD50)
C. No Observed Adverse Effect Level (NOEL)
D. Target organ
E. All of the above

3. A particular dose of a substance X is minimal toxic to animal. Substance Y is also minimal toxic to the animals at the same dose, but when both the substances are administered together they show the toxicity several orders of magnitude higher than compared with individual administrations. This is an example of:

A. Potentiation
B. Synergism
C. Additivity
D. Acute Toxicity
E. Agonism

4. Which of the following chelating agents is recommended for acute Lead poisoning with signs of encephalopathy?

A. Succimer
B. Penicillamine
C. Dimercaprol
D. Calcium EDTA
E. Dimercaprol + Calcium EDTA

5. Which of the following dermatologic findings and potential causes is INCORRECT?

A. Cyanosis- Methemoglobinemia
B. Erythroderma – Boric Acid
C. Pallor – Carbon Monoxide
D. Jaundice – Hypercarotinemia (excess carrot intake)

6. All of the following symptoms can occur with Ciguatera poisoning EXCEPT…

A. Myalgias
B. Flushing
C. Metallic taste
D. Reversal of temperature sensation

7. Which of the following is true with regard to Acetaminophen toxicity?

A. The Rumack-Matthew Normogram may be used for both acute and chronic ingestions.
B. The APAP level should ideally be checked within 1-4 hours of ingestion.
C. The Rumack-Matthew Normogram applies for ingestions up to 48 hours post-ingestion.
D. N-Acetylcysteine (NAC) should be started within 8 hours of ingestion if an APAP level cannot be obtained.

8. All of the following are treatment options for toxic alcohol poisoning, EXCEPT…

A. Fomepizole
B. Hydroxocobalamin
C. Thiamine
D. Folic Acid

9. Which one of the following are the main targets of lead toxicity?

A. Liver and kidneys
B. Nervous system and hematopoietic system
C. Heart and lung
D. Bones and muscles

10. ‘Itai-itai’ disease is caused by______

A. Cadmium
B. Mercury
C. Lead
D. Copper


Answers with Explanation:

1. Answer: D.

Despite the number of patients who come in taking Digoxin, it is important to remember that this medication comes with a large range of side effects. Bradycardia (along with any of the other SLUDGE Toxidrome symptoms) is a common effect due to the Parasympathetic activity of Digoxin. (Note: This is also the reason it works as a second-line agent for rate control of Atrial Fibrillation.) Yellow, halo-like vision changes (think Van Gogh’s ‘Starry Night’) are a more rare, but classic finding.

2. Answer: E.

In an acute toxicity study any end point parameter such as death, brain damage, liver damage etc. can be used to obtain information regarding a particular toxicant.


References:

Wright RO et al. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999 Nov;34(5):646-56.

Prescott LF, Illingworth RN, Critchley JA, et al. Intravenous N-acetylcysteine: the treatment of choice for paracetamol poisoning. BMJ. 1979 Nov 3;2(6198):1097-100.

Yeates PJ, Thomas SH. Effectiveness of delayed activated charcoal administration in simulated paracetamol (acetaminophen) overdose. Br J Clin Pharmacol. 2000 Jan;49(1):11-4.

Sivilotti ML, Burns MJ, McMartin KE, et al. Toxicokinetics of ethylene glycol during fomepizole therapy: implications for management. For the Methylpyrazole for Toxic Alcohols Study Group. Ann Emerg Med. 2000 Aug;36(2):114-25.

Brent J. Fomepizole for ethylene glycol and methanol poisoning. N Engl J Med. 2009 May 21;360(21):2216-23.

Lheureux P, Penaloza A, Gris M. Pyridoxine in clinical toxicology: a review. Eur J Emerg Med. 2005 Apr;12(2):78-85.