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Semester II
Forensic Chemistry and Toxicology
Dr. Suchita Rawat
(MSc. MPhil PhD)
Unit 1: Introduction to Forensic Chemistry (co faculty) 10 hours
Arson: Definition and introduction; Chemistry of fire; Cause and origin of fire; Fire scene patterns; Recognition of type of
fire; Role of a forensic investigator; Examination of crime scene; Collection, preservation and analysis of clue materials in:
arson, accidental and vehicular fire; Analytical techniques in arson investigation: Pyrolysis Gas chromatography,
Headspace Gas chromatography; Post-flashover burning.
Definition, history, scope and branches of toxicology; Role of a forensic toxicologist; Poison: definition, dosage,
classification based on origin, mode of action, chemical nature; Mode of administration; Factors affecting the action of
poisons; Antidotes: Definition and types; Types of exhibits encountered; Collection and preservation of different
specimens in fatal and survival cases: choice of preservations, containers, labelling, sealing and storage.
Analysis of adulteration in: cement, oils, fats, cosmetics, paints, gold, silver, tobacco, tea, sugars and salts; Analysis of
adulterants like pesticides, metals and their alloys in water, cold drinks, milk and food materials
Unit 5: Introduction to Toxicology 14 hours
Unit 3: Arson Analysis 12 hours
https://z-lib.org/
History Toxicology
Famous cases
Unit 4: Introduction to Toxicology
Anthony Addington (1713–90)
first known chemical test ever for
arsenic detection
Mary Blandy. The daughter of Francis Blandy,
England, Capt. William Henry Cranstoun
James Marsh (1789–1846)
reliable arsenic detection and quantification
method
hydrochloric acid + zinc = arsine (led through a
heated glass tube) -----a brown deposit of
arsenic metal.
The arsenic is distinguished from antimony
(which gives a similar result) by the fact that
antimony does not dissolve in sodium
chlorate(I) (hypochlorite).
Mateo Jose´ Bonaventura Orfila
(1787–1853)
Famous textbook on systematic
approach to toxicity and detection of
poisons
Lafarge trial 1839
Toxicology on trial: Mathieu
Orfila and the Lafarge murder
case
Carl Remigius Fresenius (1818–97)
a separation scheme for inorganic cations
using H2S
Screening method for mineral poisons in a
biological material
✓ Hugo Emil Reinsch in 1841
✓ Carl Remigius Fresenius in 1845
✓ Lambert Heinrich von Babo in 1845
Jean-Servais Stas (1813–91)
isolation of alkaloids, notably
nicotine, from biological
specimens by solvent extraction
using diethyl ether after
deproteination with ethanol.
Robert Bunsen (1811–99)
Gustaf Kirchhoff (1824–87)
Flame EMMISION
SPECTROSCOPY
Friedrich Julius Otto (1809–70)
posed a modification of Stas’
method for the extraction of
nonvolatile acidic and basic
compounds
Ferdinand Ludwig
Winckler (1801–68
)
precipitation test for
alkaloids
Francesco Selmi (1817–81)
Fritz Feigl important
textbook on spot tests.
physiological tests (18th century)
✓ Strychnine
✓ Atropine
✓ Aconitine
✓ Morphine
✓ Digitalis
Louis Lewin (1850–
1929)
father of
psychopharmacology
Molecular Pharmacology (1920s)
Jean Delay (1907–87)
Pierre Deniker
(1917–98)
a new useful pharmacological classification of psychotropic drug
https://truecrimedaily.com/2015/09/23/10-infamous-poisoning-cases-solved-and-unsolved/
2013 1978 1986
2003 1999 1890
Daniel Bondeson
Koodathayi mass murder
References
● Wennig, R. (2013). Toxicology: History. Encyclopedia of Forensic Sciences, 205–
209. doi:10.1016/b978-0-12-382165-2.00308-1 (Research article)
● https://truecrimedaily.com/2015/09/23/10-infamous-poisoning-cases-solved-and-unsolved/
Unit 3 Forensic Toxicology and Pharmacology
Forensic Toxicology keyconcepts
Toxicology
● It is the study of poisons, including
their physical and chemical
properties, detection and
identification, biological effects,
treatment, and prevention of disease
conditions produced by them
SUB-DISCIPLINES OF TOXICOLOGY
CROSSWORD
Regulatory
Food
Environmental
Descriptive
Occupational
Clinical
forensic
Analytical
Mechanistics
➢ Toxicology
➢ Forensic toxicology (detection of
drugs or poisons in samples and
giving this evidence, if necessary,
in a court of law)
➢ Forensic toxicologist vs.
Analytical toxicologist (concerned
with the detection of substances,
and may not understand the specific
medicolegal requirements required in
forensic case)
Source: Lappas and Lappas, 2015
Source: Lappas and Lappas, 2015
Analytical Samples used for
toxicological analysis
Drummer, O. H. (2016).
Drummer, O. H. (2016).
Latin potus, a
drink that could
harm or kill. It is
any substance
that when taken
inwardly in a very
small dose or
applied in any
kind of manner to
a living body
depraves the
health or entirely
destroys life
Poison
phytotoxins,
mycotoxins,
zootoxins , and
bacteriotoxins
Systemic
Toxicant, Organ
Toxicant
Toxicant synthesized in a
specialized gland
and ejected by
the process of
biting or stinging
Venom
Acute Toxicity (24
hours)
Subacute Toxicity (1
month)
Subchronic Toxicity
(1-3months)
Chronic Toxicity
(greater than 3
months)
FREQUENCY
AND
DURATION
OF
EXPOSURE
Transient or
Reversible or
Temporary Toxicity
(eg, narcosis-produced
organic solvents).
Persistent or
Permanent or
Irreversible Toxicity
(eg, scarring of skin
produced by
corrosives).
Immediate Toxicity
(eg, cyanide
poisoning).
Delayed Toxicity
(peripheral neuropathy
produced by some
organophosphorus
insecticides).
Cumulative Toxicity
(eg, liver fibrosis
produced by ethanol).
TIME OF DEVELOPMENT
AND DURATION OF
INDUCED EFFECTS
References
● Drummer, O. H. (2016). Toxicology: overview. In Encyclopedia of Forensic and Legal Medicine (pp.
615-621). Academic Press. (Research article)
● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic
Press. (Book)
● Lappas, N.T. and Lappas, C.M., 2015. Forensic toxicology: Principles and concepts. Academic
press. (Book)
CLASSIFICATION OF POISONING
Accidental poisoning
Homicidal Poisoning
Suicidal Poisoning
Miscellaneous Poisoning
(crime facilitation)
CLASSIFICATION OF POISONS
• Strong Acids/Strong Alkaline
Corrosive
Poisons
(Caustics)
• Inorganic/organic/mechanical
Irritant Poisons
• Central Nervous System
(Neurotoxins)/Cardiovascular/Lun
gs (Asphyxiants)
Systemic
Poisons
• Domestic poisons/Therapeutic
substance/Food
poisons/Drugs of dependence
Miscellaneous
Poisons
Gupta, P.K., 2016
Gupta, P.K., 2016
Gupta, P.K., 2016
Gupta, P.K., 2016
Gupta, P.K., 2016
ACTION OF POISON
Both Locally and
Remotely Acting
(eg, carbolic
acid, etc.)
Locally Acting :
act only at the site
of application,
such as skin/
mucosa (eg,
corrosive
poisons).
Remotely Acting
:These act only
after being
absorbed into the
circulatory system
(eg, narcotic
poisons, cardiac
poisons, etc.).
FACTORS AFFECTING TOXICITY
Host factors
Factors related to
toxicant or
associated with
xenobiotics
Environmental
conditions
•Size
•Age
•Sex
•Pathological condition
•Idiosyncratic reaction/toxicity
•Physical state and chemical properties
of the toxicant
•Routes and rate of administration
•Previous or coincident exposure to
other chemicals (drug /drug
Interactions)
•Tolerance
•Temperature /Humidity (A warm, humid
environment is known to enhance
dermal absorption as well as affect
toxicity in certain inhalation toxicity
studies disintegration of formulations of
chemicals)
References
● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic
Press. (Book)
CORROSIVE POISONS
INORGANIC
& ORGANIC
ACIDS
• Hydrochloric Acid/Nitric Acid/Sulphuric
Acid/Carbolic Acid (Phenol)/Oxalic Acid
CAUSTIC
ALKALIS
• Ammonia/Sodium hydroxide/Potassium
permanganate
Hydrochloric Acid
Geber (800AD)
Salient
features
Colorless (yellow in
presence of Fe
impurities , fuming,
pungent liquid
Fatal
dose/Fatal
period
15-20 mL. / 12-24
hours.
Forensic
Relevance
Suicide/Accident
/Abortifacient
Signs and symptoms
Acute poisoning via Dermal contact and
ingestion/Inhalation/Contact with eyes
Chronic poisoning via chronic exposure to
fumes
((1) Eyes – (i) Conjunctivitis (ii) Corneal ulcers
(2) Nose - Coryza [inflammation of nasal mucous
membranes]
(3) Oral cavity - (i) Inflammation of gums (ii)
Loosening of teeth
(4) GIT – Pharyngitis
(5) Resp system - Bronchitis.
Nitric Acid
Salient
features
clear, colorless,
fuming, heavy liquid
having a peculiar
choking odor
Fatal
dose/Fatal
period
10-15 mLL. / 12-24
hours.
Forensic
Relevance Suicide
Signs and symptoms
a. Dermal contact and ingestion
(1) More eructation, greater abdominal distention
owing to gas formation
(3) Yellow discoloration - of tissues with which it comes
in contact [crowns of teeth, gums, lips, tongue,
esophagus, stomach wall].
b. Inhalation
(1) Resp system -(i) Coughing and dyspnea (ii)
Sneezing (iii) Intense irritation of throat and lungs
(iv) Suffocation
(2) General - cyanosis.
c. Contact with eyes
Eyes - (i) Lachrymation (ii) Photophobia.
Sulphuric Acid
Salient
features
It is a colorless,
odorless
and viscous liquid that
is miscible with water
at all concentrations
Fatal
dose/Fatal
period
10-15 mL. / 12-24
hours.
Forensic
Relevance
Vitriolage/Accidental
poisoning/Suicide/Disp
osal of dead
bodies/Occupational
hazard/Abortifacient/
Self defense
Signs and symptoms
a. Ingestion Immediate – (a) Burning pain in the
mouth, (b) dysphagia, (c) epigastric pain (d)
odynophagia e) pharyngeal pain [most common
presenting symptom] (f) salivation, (g) stridor
Intense thirst, eructations, nausea, vomiting
Findings in face - (a) Eyes – sunken (b) Pupils – dilated (c)
Lips – Swollen, excoriated (d) Angles of mouth – Brown or
black streaks (e) Mucus membranes of mouth, throat and
esophagus – corroded (f) Teeth – chalky white (g) Tongue –
black, sodden, swollen
b. Contact with skin. (1) Intense burning pain, (2) Immediate
corrosion, (3) destruction of skin.
Carbolic Acid (Phenol, C6H5OH)
Salient
features
i) Pure acid (short, colorless,
prismatic, needle like
crystals)/(ii) Commercial
(brownish liquid). Taste -
burning sweetish. Solubility
– Sparingly soluble in water
and Freely soluble in alcohol,
benzene, ether and glycerine
Fatal
dose/Fatal
period
10-15 g.. / 3-4 hours.
Forensic
Relevance
Suicide/
Accidental/
Criminal abortion
Signs and symptoms
i. Local (1) Skin -(i) Numbness(ii) burn (2)
Digestive tract –(i) Nausea, vomiting – in about
20% cases. ii) Hot burning pain – Extends from
mouth to stomach(iii) Lips, mouth, tongue –
corroded. Soon harden and become white
4. Chronic poisoning (phenol marasmus) (1)
General - (i) Anorexia (ii) Headache (iii) Vertigo
(iv) Wt loss (2) Urine – dark (3) Pigmentation –
(i) Yellowish (ocher-like) discoloration of
cartilage, sclera and skin [ochronosis]
Oxalic Acid
Salient
features
occurs in two forms –and
dihydrate(common).
Colorless, transparent
prismatic crystals,
Efflorescent. Solubility –
1 in 12 in H2O
Fatal
dose/Fatal
period
600 mg/kg. For a 60 kg
human 36 g./1-2 hours..
Forensic
Relevance
Accidental
poisoning/Abortifa
cient
Signs and symptoms
a. Contact
(1) Skin - rarely damaged. May just be discolored
(2) Mucosa – of eye, mouth etc may be greatly
damaged and “scalded”.
b. Ingestion
i. Immediate (1) Burning, sour or bitter taste in the
mouth which goes up to the stomach (2) Sense of
constriction around the throat (3) Intense thirst(4)
Mouth – may appear “scalded” or sometimes black
(5) Severe pain – Begins in the epigastrium, but
soon radiates all over the abdomen (6) Persistent
vomiting, eructations and diarrhea. Vomitus
contains altered blood [“coffee-ground” appearance]
and mucus. (8) Signs and symptoms due to
hypocalcemia -(i) Tetany (ii) Numbness and tingling
of fingertips and legs (iii) Chvostek sign +ve.
CAUSTIC ALKALIS - Ammonia
Salient
features
At room temperature,
ammonia (NH3) is a highly
water-soluble, colorless,
irritant gas with a unique
pungent choking odor.
Fatal
dose
15-20 mL.
Signs and symptoms
- Inhalation - (a) Head, ears, eyes, nose, throat
(HEENT) - Facial and oral burns and ulcerations
(b) Respiratory system – cough, decreased air
entry, oxygen desaturation, rhonchi, salivation,
stridor, Tachypnea, wheezing
(c) CNS - Loss of consciousness [if exposure is
massive].
Liquid Lye (NaOH, Caustic soda)
Salient
features
found in many
industrial solvents and
cleaners, and many
household products
Forensic
Relevance
vehicular
accidents
Signs and symptoms
Burns, Irritation, Necrosis of the skin
and underlying tissues
Potassium Permanganate [KMnO4]
Signs and symptoms
a. Ingestion
(1) Intense thirst, nausea, vomiting and diarrhea. Vomitus is
purple brown in color. Stools are black due to manganese
sulfide.(2) Burning pain - from mouth to stomach (3)
Dysarthria, dysphagi (4) Purple brown discoloration - of skin
and mucus membranes, with which it comes in contact. Lips,
gums, teeth, tongue, tonsils and pharynx. ( few minutes later
color changes to brown, dark brown and finally coal black due
to conversion to manganese dioxide. (5) Systemic -
Methemoglobinemia, because of oxidizing nature of KMnO4.
b. Local application
Locally applied as an abortifacient. (1) Vaginal
and cervical burns, erosions and ulcerations,
resulting in severe scarring. (2) Extensive
bleeding
Salient
features
dark purple slender
crystals, having a sweet
astringent taste. it is a
strong oxidizing agent
and is used as a
disinfectant
Fatal
dose/Fatal
period
5-10 g../Few hours..
Forensic
Relevance
Suicide/Accidental/ab
ortifacient/Production
of fictitious injuries
References
● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
INORGANIC POISONS (Irritants)
• Arsenic
• Mercury
• Copper
• Lead
• Thallium
• Barium
Inorganic
Metallic poison • Phosphorus
Inorganic Non Metallic
poison
ARSENIC
Toxic salts
Metallic arsenic not poisonous,
Toxic salts includes powder or porcelain
type Arsenious oxide [Arsenic trioxide,
As2O3], (a) White in color, tasteless and
odorless, Sparingly soluble in water
Arsenic acid [H3AsO4]
Arsenic trichloride (AsCl3)- Butter of
arsenic. Colorless poisonous oil
Arsenic trisulfide (As2S3) comes as the
mineral orpiment [hartal in India]
Copper acetoarsenite [Paris Green,
Emerald Green, Schweinfurt Green] Once
used as a pigment and insecticide
Copper arsenite [Scheele’s Green,
CuHAsO3]. (green pigment)
(7) Tetraarsenic tetrasulfide (As4S4)
Fatal dose/Fatal
period
(1) As2O3 - 200-300 mg/(2) Arsine
gas – 25-30 ppm is lethal in 30
min./ 1-2 days.
Forensic
Relevance
Homicidal
poison/Arsenophagists/Hydro
arsenicism/Arsenic in drugs of
addiction/Seafood
SIGN & SYMPTOMS / TOXICITY
a. Ingestion (1) GIT: (i) Odor – Garlicky (ii) Taste – sweetish metallic (iii)
Intense thirst,Ptyalism (iv) Nausea, Vomiting (v) Throat – feeling of
constriction, dysphagia (vi) Burning and colicky pain – in esophagus, stomach
and bowels (vii) Abdominal pain (viii) Diarrhea– (I) expelled frequently and
involuntarily (II) Color and odor - dark colored, stinking, bloody (c) May mimic
bacterial food poisoning or cholera.(2) Ocular: (i)Conjunctivitis (ii)
Lacrimation (3) Respiratory - Irritation of upper airways (4) Liver - Fatty
degeneration (5) Renal: (i) Pain - during micturition (ii) Oliguria (iii) Uremia
(iv) Urine –contains albumen, casts and RBCs (6) Muscular – Tenderness of
muscles (7) CNS: (i) Convulsions and tremors (ii) Formication (iii) Giddiness
(iv) Headache (v) Vertigo (vi) General paralysis (vii) Delirium (viii) Coma (8)
CVS: (i) Cardiac arrhythmias [ST-T wave changes, prolonged QT interval],
ventricular fibrillation (ii) Hypotension (iii) Ventricular tachycardia (9) Skin –
loss of hair [in case of survival], skin eruptions (10) General – hyperthermia
[Hyperpyrexia].
b. Inhalation [Arsine gas] (1) Hemolysis (2) hemoglobinuria (3) renal failure (4)
death is almost instantaneous.
MERCURY (QUICKSILVER)
Toxic
Salts of
Mercury
1. Organic salts ((1) methyl
mercury and (2)dimethyl
mercury.
2. Inorganic salts ((1) Mercuric
Chloride [HgCl2, Corrosive
sublimate](2) Mercurous
Chloride [Hg2Cl2](3) Mercuric
ammonium chloride(4) Mercuric
cyanide – [Hg(CN)2]-5) Mercuric
iodide - (HgI2, Protiodide)(6)
Mercuric nitrite (7) Mercuric
oxide (HgO)(8) Mercuric sulfate
(HgSO4)- odorless white
crystalline powder (9) Mercury
sulphide(10) Mercury
thiocyanate [Hg(SCN)2]
Fatal
dose/Fatal
period
1-4 g of HgCl2/3-5 days.
Forensic
Relevance
Criminal
abortion/Accidental/Quacks/
SIGN & SYMPTOMS / TOXICITY
Acute Poisoning: a. Elemental mercury
i. Inhalation (1) General – Headache, blurring of vision, Fever,
chills,Erythematous pruritic papular rash, conjunctivitis, salivation(2) Pulmonary –
chest pain, cough, dyspnea, interstitial pneumonitis, necrotizing bronchiolitis,
pulmonary edema, pulmonary failure(3) GIT – Metallic taste, deep red oral
mucosa, gingivitis, stomatitis, strawberry tongue, swelling of salivary glands, teeth
ii.Ingestion:Absorption is minimal [<0.01% is absorbed]. iii. Injection (1) S/c or IM
- Abscess formation, ulceration [exuding tiny droplets of Hg].
MERCURY (QUICKSILVER)
SIGN & SYMPTOMS / TOXICITY
b. Inorganic mercury (2 phase manifestation)
I. First phase
(1) Immediately after ingestion of corrosive mercury salts – Hot burning pain, sense of
constriction, ashen discoloration of the mucous membrane in mouth and throat. Burning
pain extends down to stomach and abdomen.
(2) Within a few minutes - Intense epigastric pain, followed by diffuse abdominal pain.
Nausea, retching and almost continuous vomiting of mucoid material, which frequently
contains blood and shreds of mucous membrane.Hoarse voice.(3) Mouth, tongue and
fauces – are corroded, swollen and show a grayish white coating.(4) Acrid metallic taste,
excessive salivation and thirst.(5) Severe purging, with liquid, bloody feces and
considerable tenesmus.(6) Rapid, weak pulse; breathing shallow and difficult; Pallor;
Prostration,circulatory collapse, and death
. ii. Second phase (If begins in 1-3 days ) in untreated cases(1) Oral - Marked salivation,
mercurial stomatitis, glossitis and ulcerative gingivitis within 24-36 hr. Loosening of teeth,
necrosis of the jaw. (2) Severe infections (3) Renal - PCT Necrosis in 2-3 days, transient
polyuria, albuminuria,cylindruria, hematuria, anuria, azotemia and renal acidosis. Recovery
may occur within 10-14 days, but death may also occur in some cases. (4) Late - After
many days after the original exposure (especially in untreated cases), a membranous
colitis may appear; dysentery, tenesmus, ulceration of the colonic mucosa, and
hemorrhage. Liver necrosis sometimes develops.
BARIUM
Toxic
salts
Soluble salts are
highly poisonous
(chlorides are most
poisonous).Barium
ions are also highly
poisonous.
Fatal
dose/Fatal
period
1g./12 hours.
Forensic
Relevance
accidental.
SIGN & SYMPTOMS / TOXICITY
. (1) Severe GIT irritation – (a) Nausea, Abdominal pain, vomiting, diarrhea
occur within 1 hour of ingestion. (b) Esophagitis (c) hemorrhagic gastritis (2)
Signs and symptoms associated with hypokalemia - (a) ventricular
dysrhythmia (b) hypertension (c) profound flaccid muscle weakness (d)
respiratory failure (e) lactic acidosis, (f) hypophosphatemia (g) rhabdomyolysis
(3) Secondary to tissue ischemia - (a) Altered level of consciousness (b)
seizures
COPPER
Toxic
Salts of
Copper
(1) Copper acetoarsenite(2)
Copper arsenite (3) Copper
subacetateused by Greek
artists as a green pigment
in their paintings (4)
Copper sulphate [blue
vitriol].
Fatal
dose/Fatal
period
0.15-0.3 g/kg (CuSO4), i.e.
about 20 g or a 70 kg
man/1-3 days.
Forensic
Relevance
Abortifacient / Cattle
poison/Accident/suicide
SIGN & SYMPTOMS / TOXICITY
Acute Poisoning ( Symptoms appear within 15-30 minutes). In mild cases there
is (i) a metallic taste in mouth (ii) -salivation (ptyalism) (iii) thirst (iv) nausea,
vomiting, eructations and diarrhoea (v) burning pain in the stomach with colicky
abdominal pain (vi) Vomited matter is bluish-green. In severe cases (i)
Hepatotoxicity – Acute hepatic necrosis and jaundice (ii) Hemolysis (iii)
hematemesis, melena – Due to ulceration in the GIT (iv)methemoglobinemia,
methemoglobinuria (v) Renal and pulmonary toxicity (vi) Hypotension and
cardiovascular collapse (vii) Neurological – lethargy, seizures, coma.
Chronic Poisoning:(1) Anemia (2) Green line on gums (3) Colic(4) Peripheral
neuritis(5) Degeneration and atrophy of muscles (6) Vineyard’s sprayer’s lung (7)
Chalcosis lentis(8) Greenish discoloration of hair
LEAD
Toxic
Salts of
Lead
(1) Lead carbonate
(PbCO3, safeda)(2) Lead
chromate (PbCrO4) ( bright
yellow color)(3) Lead
diacetate (sweet taste)(4)
Lead monoxide (PbO) (5)
Lead sulfide (PbS,
Galena)(6) Lead
tetraacetate [Pb(C2H3O2)4]
(7) Lead tetroxide (Pb3O4
or 2PbO·PbO2)-Also
known as red lead,
sindoor,vermilion. (8)
Tetraethyl lead
[CH3CH2)4Pb; TEL]
Fatal
dose/Fatal
period
(1) Lead acetate – 20 g;(2)
Lead carbonate – 40 g;(3)
Tetraethyl lead – 100
mg/kg/1-2 days.
Forensic
Relevance
Abortion/Cattle
poison/Drug
abusers/occupational
poisoning
SIGN & SYMPTOMS / TOXICITY
Acute poisoning :(1) an astringent and metallic taste, (2)headache, (3) dry throat,
(4) nausea and vomiting [occasionally diarrhea], (5)thirst, (6) peripheral circulatory
collapse [due to loss of water from GIT], (7)neurological signs [(i) paresthesias (ii)
rarely encephalitis (iii) cerebellar ataxiais common in children]. (8) Hemolysis
causes anemia and presence of hemoglobin in the urine, (9) decreased urine
output (damage to kidneys). (10)Death in severe cases.
Chronic Poisoning : a. Facial pallor, b. Anemia, c. Lead line d. Colic and
constipation d.Lead palsy (Weakness of muscles due to lead) f. Encephalopathy
g. Cardiorenal manifestations (1) Hypertension (2) Nephritis:(3) Saturnine gout
[syn, lead gout]- h.Reproductive system (1) Sterility and impotence (2) Menstrual
disorder(3) In pregnant females (i) Abortion – ii) Premature labor (iii) Intrauterine
growth retardation. h. Reproductive system . i. Eye (retinal stippling.) j. Other
systems (1) Anorexia (2) Drowsiness (3) Dyspepsia (4) Emaciation (5)
Exhaustion
THALLIUM
Fatal
dose/Fatal
period
6-40 mg/kg of Tl
salts/24-36 h.
Forensic
Relevance
Homicide
SIGN & SYMPTOMS / TOXICITY
Acute Poisoning:(1) GIT:(i) Abdominal pain [most common]. Accompanied by (ii)
Vomiting and either (iii) Diarrhea or Constipation (iv) Severe symptoms, eg
hematemesis and bloody diarrhea are more rare.(2) Chest – Tightness and
pain(3) CVS:(i) Tachycardia and (ii) Hypertension (ii) ECG abnormalities (4) Skin –
Maculo-papular skin eruption having butterfly distribution on face [very
characteristic] (5) Coma – Occurs with large exposures
B. Chronic Poisoning: (1)Most characteristic lesions, alopecia (begins in 10 days
total loss 30 days) and neurologic[appears after 2-5 days] symptoms [Thallium
triad].(2) Skin: (i) acne, (ii) palmar erythema, (iii) anhidrosis and (iv) dry scaly
skin(3) Nails - Mees lines appear within 2-4 weeks after exposure.
Phosphorus
Salient
feature
Four allotropes ((1) White
(2) Red [heating white
phosphorus to 250°C in
vacuum],(3) Violet
[dissolving white
phosphorus in molten lead
at 500°C, and then cooling
it slowly] and (4) Black
[heating white phosphorus
at 12,000 atm]. White
Fatal
dose/Fatal
period
1 mg/kg [60 mg for a 60 kg
person]./½ day to 8 days
Forensic
relevance
Suicide/Accident
SIGN & SYMPTOMS / TOXICITY
a. Local application (Causes both thermal and chemical burns. 2nd
and 3rd degree (Dupuytren) burns
b. Ingestion i. Acute fulminant poisoning: Vomiting, diarrhea, peripheral vascular
collapse. Death occurs within 12 hours.
ii. Subacute poisoning ((a) First stage [2 days] (1) Severe burning pain in the
mouth. Abdominal pain, vomiting, diarrhea (2) Garlicky odor (3) Luminous vomit
and stools(4) Fumes emanate from the stools (Smoking or smoky stool syndrome).
(b) Second stage [4 days] Patient is symptom free. (c) Third stage [2 days] (1)
Hepatic toxicity (i) Mousy odor of the breath (ii) Flapping tremor of hands [asterixis]
(iii) Hepatomegaly, jaundice, bleeding tendencies(iv) Finally hepatic
encephalopathy and death.
This Photo by
Unknown Author is
References
● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
SYSTEMIC POISONS
Central Nervous System (Neurotoxins) i.e. CNS
Depressants (1) Alcohols (2) Opium and its
derivatives (3) Sedative-hypnotics i.e Barbiturates/
Deliriant Poisons eg. Datura, Cannabis, Cocaine
Central Nervous System (SPINAL POISONS
eg, Strychnos Nux Vomica)
Cardiac Poisons eg. Aconite, Digitalis
Purpurea, Nerium Oleander
Asphyxiants and Toxics eg. Gase eg. Carbon
Monoxide (Co), Hydrocyanic Acid (Hcn), Hydrogen
Sulfide (H2s)
SPINAL POISONS: Strychnos Nux Vomica
Salient
feature
colorless, odorless
rhombic prisms, and
has intensely bitter
taste.
Active
Principles
whole tree, including
the seeds/strychnine
and brucine
Fatal
dose/Fatal
period
(1) One crushed seed
(2) Strychnine -
30mg/kg./ 1-2 hours.
Forensic
relevance
Homicide./cattle
poison/arow
poison/adulterant of
street
drugs/accidental
poisoning
SIGN & SYMPTOMS / TOXICITY
Dermal exposure - Tingling sensation locally. Other
symptoms as in ingestion.
Ingestion - (1) Bitter taste in mouth, a sense of
restlessness and uneasiness, anxiety, fear and a
feeling of suffocation (2) difficulty in swallowing (3)
Prodromal symptoms (4) Convulsions (5) Face - is
cyanosed
Cardiac Poisons: ACONITE
Salient
feature
igenus of flowering
plant belonging to the
buttercup family
(Ranunculaceae).
Active
Principles
(i) aconitine, (ii)
mesaconitine, (iii)
hypaconitine, (iv)
jesaconitine, (v)
Yunaconitine.
Fatal
dose/Fatal
period
(1) Root – 1-2 g (2) ild
plant – 1 g. (3)
Aconitine – 2 mg. (4)
Extract – 250 mg (5)
Tincture – 5 mL. /2-6
hours.
Forensic
relevance
Homicide./cattle
poison/arow
poison/suicide/accide
ntal poisoning
SIGN & SYMPTOMS / TOXICITY
Eyes exposed to Pollen " pain and swelling
/Touching – Leaves or roots handled for a long time or
rubbed on the skin "numbness, tingling/ Inhalation –
Root inhaled for a long time has a narcotic effect.
Ingestion:(1) GIT -(i) Burning sensation from the mouth
to stomach(ii) Numbness, tingling in the mouth tongue
and pharynx(iii) Salivation, nausea, vomiting, diarrhea
(iv) Later – Mouth is dry, thirst, dysphagia.(2) CVS –(i)
ECG and heart rhythm changes (ii)Pulse – slow, feeble,
irregular. (3) Respiratory –(i) Feeling of constriction in
the chest (ii) Respirations slow, labored and shallow. (4)
CNS –(i) Consciousness clear. Sometimes there may
be hallucinations (ii) Headache and giddiness (iii)
Numbness and tingling over entire body (iv)
Restlessness (v) Vertigo. (5) Muscular –(i) Marked
weakness of muscles with spasms and
twitchings,Cramps and convulsions. (6) Skin – (i) Pallor
(ii) profuse sweating (iii) cold and clammy skin..
CARDIAC POISONS: DIGITALIS PURPUREA
Salient
feature
The word digitalis
comes from the finger
shaped flowers
[L,digitus, a finger]
Active
Principles
(1) Leaves - (i)
Digitoxin, (ii)
Gitoxin/(2) Seeds - (i)
Digitalin.
Fatal
dose/Fatal
period
Digitalin – 15-30 mg
Digoxin [present in D.
lanata] – 10 mg
Digitoxin – 4mg/Leaves
1-2 (2g)/24 hrs
Forensic
relevance
accidental
poisoning/Iatrogenic
poisoning
SIGN & SYMPTOMS / TOXICITY
Cardiac – Almost every type of dysrhythmia is
produced.
Extracardiac – GIT – Nausea, vomiting, Abdominal
pain ,CNS –anxiety confusion delirium depression
disorientation drowsiness Fatigue, mental confusion,
restlessness, hallucinations,headache muscle
weakness.
Skin – Urticaria
Visual disturbances - transient amblyopia, blurring of
vision,chromatopsia (aberrations of color vision),
,photophobia, photopsia (perceived flashes of light),
scotoma and Xanthopsia(yellow halos).
CARDIAC POISONS: NERIUM OLEANDER
Salient
feature
belong to the Dogbane
family, Apocynaceae.
Poisonous parts - (i)
All plants of the plant
including (seeds and
roots contain the
highest percentage
toxins).
Active
Principles
(i) Adynerin, (ii)
Digitoxigenin, (iii)
Folineriin,
(iv)Nerioside [Nerin]
(v) Oleandrin (OD). (vi)
Oleandrigenin
Fatal
dose/Fatal
period
(1) Root: 15-20 g,(2)
Leaves: 5-15 in
number/24-36 h.
Forensic
relevance
Suicide/Abortifacient/
Cattle poison
SIGN & SYMPTOMS / TOXICITY
(1) Contact – Dermatitis
(2) Inhalation – of emanations from flower causes nausea,
headache, dizziness and respiratory difficulty.
(3) Ingestion –(1) GIT - (i) Profuse frothy salivation (ii)Vomiting
and Diarrhea (iii) Difficulty in swallowing and articulation
(iv)Abdominal pain (2) Neuromuscular - (i) Muscular twitchings
(ii) Tetanic spasms (iii) Lock-jaw (iv) Drowsiness (v) Coma. Later
respiratory paralysis. (3) Heart - Atrial and ventricular fibrillation,
AV block. In severely poisoned patients, ECG abnormalities
Asphyxiants and Toxic Gases:CARBON MONOXIDE (CO)
Salient feature
colorless, odorless, tasteless
and nonirritant gas
which is lighter than air and
insoluble in water. It burns
with a blue flame
Fatal
dose/Fatal
period
COHb conc.>60%
Forensic
relevance
Accidental CO poisoning
SIGN & SYMPTOMS / TOXICITY
Acute poisoning:(1) Symptoms due to tissue hypoxia -
headache, nausea, vomiting, dizziness,lethargy and a feeling of
weakness. (2)Skin - There may be a cherry red discoloration
of skin. (3) CVS – Chest pain, palpitations, -Heart rate. (4)CNS -
Neurological signs include poor concentration, confusion,
disorientation, visual disturbance, syncope and seizures. (5)
Respiratory – Shortness of breath. (6) Ophthalmoscopic
examination - Retinal hemorrhages may be seen.
2.Chronic poisoning:(1) Persistent headaches,
lightheadedness, depression, confusion, memory loss. (2) CVS
patients – symptoms may worsen (chronic hypoxia to heart). (3)
Permanent neurological damage (chronic hypoxia to brain). (4)
Visual disturbances (5) Elevated RBC count.
Asphyxiants and Toxic Gases: Hydrogen Cyanide
Salient feature
The name cyanide (Gk
Kyaneos, dark blue) is
derived from the colorful
Prussian blue from which
HCN [syn, prussic acid] was
first synthesized. Boiling
point is 26°C.
Fatal
dose/Fatal
period
a. Ingestion
(1) HCN - 50 to 60 mg (2) NaCN, KCN –
200 to 300 mg. b. Inhalation Air
concentration of HCN: (i) 1:50,000 is
fatal in few hours (ii) 1:10,000 within
few minutes (iii) 1:2,000 almost
immediately/HCN - 2-10 minutes, KCN
or NaCN - 30 min
Forensic
relevance
Accidental poisoning.
Suicidal poisoning/Arson
cases/chemical terrorism
SIGN & SYMPTOMS / TOXICITY
Acute Poisoning: Inhalation:. (1) Sense of constriction about
the throat and chest (2) Dizziness, vertigo (3) Insensibility (4)
Death from respiratory failure. b. Ingestion: (less doses):(1)
Nausea (2) Giddiness (3) Headache (4) Confusion (5) Loss of
muscular power ii. Massive [larger than fatal] doses (1)
Sudden loss of consciousness.(2) No voluntary act can be
performed after ingestion.(3) Prompt death from respiratory
arrest.
Chronic Poisoning (Produced by continued inhalation of low
conc of CN over long periods) (i) Leber hereditary neuropathy.
(ii) Tobacco amblyopia [progressive loss of visual function](iii)
Thyroid disorders development of hypothyroidism
Asphyxiants and Toxic Gases: HYDROGEN SULFIDE (H2S)
Salient feature
Hydrogen sulfide is a
colorless, flammable, gas
with the characteristic foul
odor of rotten eggs.
Fatal
dose/Fatal
period
(1) 20ppm - Maximum
allowable conc (2) 400-
700ppm - dangerous after an
exposure of half to 1 h. (3)
>1000 ppm - instantly fatal./
Few minutes to few hours.
Forensic
relevance
Accidental poisoning
SIGN & SYMPTOMS / TOXICITY
Acute poisoning : Exposure to high conc [750-1000 ppm] (1)
General - Weakness, malaise, sweating, abrupt physical collapse
[knockdown] (2) CVS – cardiac arrhythmias, conduction
defects(3) CNS – amnesia, confusion, delirium, hallucinations,
convulsions,Nystagmus, Somnolence 4.Respiratory paralysis,
asphyxial seizures,death.
2. Chronic exposure May occur in industrial workers. (1)
General – Headache, Weakness, Nausea, Weight loss (2) Gas
eye is common. Associated with reversible chromatic distortion
and visual changes. (3)ataxia, dystonia, choreoathetosis] (4)
Spontaneous abortions in female.
References
● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
DIAGNOSIS OF POISONING
Symptoms Poison commonly involved
Vomiting Irritant poisons like arsenic acids
Cramps Metallic poisons like arsenic, lead, antimony,mercury etc.
Convulsions Strychnine, cyanides, carbon monoxide,
Paralysis lead, arsenic, aconite,
snake venom etc.
Coma Carbon dioxide
DIAGNOSIS OF POISONING
Clinical Findings Poison commonly involved
(Skin colour) Cherry Pink Carbon monoxide
(Skin colour) Flushed pink skin cyanide
(Skin colour)Cutaneous bullae carbon monoxide
(Appearance of Blood) Red venous blood cyanide or carbon monoxide poisoning
Rhabdomyolysis carbon monoxide and strychnine
DIAGNOSIS OF POISONING
Pattern Poison commonly involved
Malaise, restlessness, nausea, weakness Carbon monoxide, lead, mercury,arsenic
Restlessness, hypertonia,hyperreflexia, pyrexia strychnine
Burns in mouth, disphagia, abdominal pain, distension. Corrosive
Renal failure mercurial compound, arsine, lead
Jaundice, hepatic failure Phosphorous, lead
REFERENCES
● Laboratory Procedure Manual- Forensic Toxicology Directorate of Forensic
Science, MHA, Govt. of India
DOSE AND RELATED TERMS
• Lethal Dose (LD)
• Lethal Dose 50 (LD50)
• Lethal Concentration (LC) (milligrams of
compound per kilogram of feed (or water)
• Lethal Concentration-50 (LC50)
Dose
Dose: The total or absolute
quantity or amount of a
substance applied or
administered at one time to an
individual to achieve the desired
pharmacological or toxicological
response
TIME ACTION CURVES: time –effect relationship of toxicant
Phase I: Time of
onset of action (Ta)
Phase II: Time to
peak effect (Tb)
Phase III: Duration
of action (Tc)
Phase IV: Residual
effects (Td)
SOURCE:
VARIABLES OF
DOSERESPONSE CURVE
• Efficacy: maximal effect
• Potency: diff dose same effect
• Slope: slope of dose-effect
• Biological variations
Transfer of Molecules Across Biological Membranes
ABSORPTION (Factors that influence absorption)
The solubility of
the chemicals
The
concentration of
chemicals
The circulation
The site of
absorption
The area of
absorbing
surface
The route of
administration
(GI tract, skin,
and lungs)
Absorption is defined as the
process of movement of an
unchanged compound from its site
of administration or exposure to the
blood stream.
GASTROINTESTINAL ABSORPTION
Transfer of molecules
(non ionic diffusion /
active processes)
Factors affecting
absorption (chemicals
properties i.e weak
acids / presence Food)
SKIN ABSORPTION
Chemicals absorbed through skin
(carbon tetrachloride/ . Pesticides
(parathion, malathion), nicotine
insecticides/Chlorovinylarsine
dichloride (Lewisite), a mustard
gas
Factors affecting
absorption (skin
layer i.e. SC or
chemical breakage
i.e acids, alkalis,
Dimethylsulfoxide)
Epidermis : 0.2 mm thick
LUNG ABSORPTION
Chemicals absorbed
through lungs i.e.
asphyxiants and irritants
or particulate material
Factors affecting
absorption (partition
coefficients i.e. lipid/
water partition
coefficients high / particle
size small)
PARENTERAL ADMINISTRATION
Types of administration (IM, SC, IV, IP,
Intraperitoneal injection )
Factors affecting absorption I.E. NON
IRRITATING via SM , irritating via SC
PARENTERAL ADMINISTRATION
DISTRIBUTION
SOURCE: Gupta, P.K., 2016
absorption into the
blood stream
penetrate in the
various
fluid compartments:
(1) plasma; (2)
interstitial fluid; (3)
transcellular fluid
(4) cellular fluids
*Bone and adipose tissue
Factors that
determine a
compound’s
rate and
extent of
distribution
1. Molecular size (ie, physicochemical properties of compound)
2. Lipophilicity
3. Plasma protein and tissue binding
4. Blood flow and organ size
5. Special compartmental and barriers (eg, bloodbrain barrier ,blood cerebrospinal
barrier, placental barrier, and other barriers)
6. Availability of special transport system
7. The ability to interact with transmembrane transporter proteins
TISSUE PERMEABILITY BARRIERS
Blood organs barrier
Blood urine
barrier
Blood
testes
barrier
Blood bile
barriers
Blood Brain
Barrier
FACTORS AFFECTING
DISTRIBUTION AND
TISSUE RETENTION
• Binding to Plasma Proteins
(albumin/globulin: longer duration of action)
• Storage in Body Fat i.e. organochlorinated
pesticides such as DDT
• Storage in the Brain Tissues i.e. CNS Drugs
(barbiturates) and psychotropic drugs
(chlordiazepoxide and chlorpromazine)
• Storage in Erythrocytes i.e. pharmacological
agents, such as p-nitro-aniline/ inorganic
ions lead, cadmium
• Other Tissues as a Storage Depot (skeleton
i.e tetracycline /kidney and liver i.e.
cadmium/blood i.e. CO/lungs i.e.
paraquat/thyroid i.e. percholrate)
EXCRETION
RENAL EXCRETION i.e. penicillin-G,
N-methyl-nicotinamide
BILIARY EXCRETION i.e
benzomethamine GASTROINTESTINAL TRACT
EXPIRED AIR i.e.
fluorobenzene, carbon
monoxide
SWEAT ie. diethyl di-thiol-iso-
phthalate
SALIVA
I.E sulfonamides, pentobarbitone
MILK i.e. s DDT, thiouracil,
tetracycline, and erythromycin,
References
● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic
Press.
Management of poising cases
Objectives of Treatment
❑ Removal of unabsorbed poison
❑ Administration of Antidote
❑ Elimination of absorbed poison
❑ Symptomatic Treatment
❑ Maintenance of patient general
condition
Removal of unabsorbed poison
For inhaled poison: AR
mixture of 95% of
oxygen and 5% of
carbon dioxide
For injecting poison: chemical antidotes, cold packing and vasoconstrictors
Contact Poisons: specific antidote
Removal of unabsorbed poison
For ingested poison:
Emetic agents
✓ lukewarm water/15 gm of mustard powder in
200 ml of water/About 30 gms of common salt
in 200 ml of water
✓ Zinc sulphate:1-2 gms in 200 ml of water
✓ Apomorphine: 6 mg by sub-cutaneous injection
by levallorphan 1-2 mg/ naloxone hydrochloride
5-10 mg intramuscular or intravenous
Removal of unabsorbed poison
For ingested poison:
Gastric aspiration and lavage
https://www.youtube.com/watch?v=5vWRAqWEkuk
Use of Antidotes
This Photo by Unknown Author is licensed
under CC BY-NC-ND
Mechanical or physical
Chemical
Physiological or
Pharmacological
Universal Antidotes
Antidotes are remedies to
counteract the effects of
poison
According to their
mode of action,
antidote types:
Mechanical or Physical:
impede absorption
Corrosive/irritant glass
Demulcents and Bulky Foods
10: 1 ratio, 4-8g , small dose of poison, 4-6 hours,
aspiration into lungs
Chemical : non toxic insoluble substances or oxidizes to non
toxic substances
POISON/TOXIC SUBSTANCES CHEMICAL ANTIDOTE
Corrosive alkalis dilute acetic acid
Corrosive acids Magnesium oxide or calcium oxide
oxalic acid Calcium oxide
carbolic acid magnesium sulphate
phosphorus copper sulphate
lead sulphates of alkalis
arsenic. freshly precipitated iron oxide
Tannin ( polyphenolic biomolecules) alkaloids glucosides and metals
1:1000 aq. potassium permanganate alkaloids, barbiturates, phosphorus,
cyanides etc.
Physiological or Pharmacological: produce opposite effects to that of the
poison (physiological antagonists)
Agent poison Effect
Nalorphin Morphine physiological
antagonists
caffeine Morphine physiological
antagonists
atropine and oximes organophosphorous
compounds
physiological
antagonists
chloroform strychnine physiological
antagonists
BAL (Dimercaprol),
EDTA (Ethylene
diamine tetra
acetate),
Heavy metals chelating agents
Universal Antidotes
ELIMINATION OF ABSORBED POISONS
Cathartic
hot packs
Forced
Diuresis
Peritoneal
Dialysis
Haemodialysis
Exchange
transfusion
TREATMENT OF GENERAL SYMPTOMS
Strong
analgesic
Artificial
respiration
Antibiotic
Cardiac
stimulants
Anaesthetic Saline infusion
Administration
of glucose
MAINTENANCE OF THE PATIENT’S GENERAL CONDITION
REFERENCES
● Laboratory Procedure Manual- Forensic Toxicology Directorate of Forensic
Science, MHA, Govt. of India
This Photo by Unknown Author is licensed under CC BY-SA

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MSCII_ FCT UNIT 5 TOXICOLOGY.pdf

  • 1. Semester II Forensic Chemistry and Toxicology Dr. Suchita Rawat (MSc. MPhil PhD)
  • 2. Unit 1: Introduction to Forensic Chemistry (co faculty) 10 hours Arson: Definition and introduction; Chemistry of fire; Cause and origin of fire; Fire scene patterns; Recognition of type of fire; Role of a forensic investigator; Examination of crime scene; Collection, preservation and analysis of clue materials in: arson, accidental and vehicular fire; Analytical techniques in arson investigation: Pyrolysis Gas chromatography, Headspace Gas chromatography; Post-flashover burning. Definition, history, scope and branches of toxicology; Role of a forensic toxicologist; Poison: definition, dosage, classification based on origin, mode of action, chemical nature; Mode of administration; Factors affecting the action of poisons; Antidotes: Definition and types; Types of exhibits encountered; Collection and preservation of different specimens in fatal and survival cases: choice of preservations, containers, labelling, sealing and storage. Analysis of adulteration in: cement, oils, fats, cosmetics, paints, gold, silver, tobacco, tea, sugars and salts; Analysis of adulterants like pesticides, metals and their alloys in water, cold drinks, milk and food materials Unit 5: Introduction to Toxicology 14 hours Unit 3: Arson Analysis 12 hours
  • 4. History Toxicology Famous cases Unit 4: Introduction to Toxicology
  • 5. Anthony Addington (1713–90) first known chemical test ever for arsenic detection Mary Blandy. The daughter of Francis Blandy, England, Capt. William Henry Cranstoun James Marsh (1789–1846) reliable arsenic detection and quantification method hydrochloric acid + zinc = arsine (led through a heated glass tube) -----a brown deposit of arsenic metal. The arsenic is distinguished from antimony (which gives a similar result) by the fact that antimony does not dissolve in sodium chlorate(I) (hypochlorite). Mateo Jose´ Bonaventura Orfila (1787–1853) Famous textbook on systematic approach to toxicity and detection of poisons
  • 6. Lafarge trial 1839 Toxicology on trial: Mathieu Orfila and the Lafarge murder case Carl Remigius Fresenius (1818–97) a separation scheme for inorganic cations using H2S Screening method for mineral poisons in a biological material ✓ Hugo Emil Reinsch in 1841 ✓ Carl Remigius Fresenius in 1845 ✓ Lambert Heinrich von Babo in 1845
  • 7. Jean-Servais Stas (1813–91) isolation of alkaloids, notably nicotine, from biological specimens by solvent extraction using diethyl ether after deproteination with ethanol. Robert Bunsen (1811–99) Gustaf Kirchhoff (1824–87) Flame EMMISION SPECTROSCOPY Friedrich Julius Otto (1809–70) posed a modification of Stas’ method for the extraction of nonvolatile acidic and basic compounds
  • 8. Ferdinand Ludwig Winckler (1801–68 ) precipitation test for alkaloids Francesco Selmi (1817–81) Fritz Feigl important textbook on spot tests. physiological tests (18th century) ✓ Strychnine ✓ Atropine ✓ Aconitine ✓ Morphine ✓ Digitalis
  • 9. Louis Lewin (1850– 1929) father of psychopharmacology Molecular Pharmacology (1920s) Jean Delay (1907–87) Pierre Deniker (1917–98) a new useful pharmacological classification of psychotropic drug
  • 11.
  • 12.
  • 14. References ● Wennig, R. (2013). Toxicology: History. Encyclopedia of Forensic Sciences, 205– 209. doi:10.1016/b978-0-12-382165-2.00308-1 (Research article) ● https://truecrimedaily.com/2015/09/23/10-infamous-poisoning-cases-solved-and-unsolved/
  • 15. Unit 3 Forensic Toxicology and Pharmacology Forensic Toxicology keyconcepts
  • 16. Toxicology ● It is the study of poisons, including their physical and chemical properties, detection and identification, biological effects, treatment, and prevention of disease conditions produced by them
  • 18. ➢ Toxicology ➢ Forensic toxicology (detection of drugs or poisons in samples and giving this evidence, if necessary, in a court of law) ➢ Forensic toxicologist vs. Analytical toxicologist (concerned with the detection of substances, and may not understand the specific medicolegal requirements required in forensic case)
  • 19. Source: Lappas and Lappas, 2015 Source: Lappas and Lappas, 2015
  • 20. Analytical Samples used for toxicological analysis
  • 21. Drummer, O. H. (2016).
  • 22. Drummer, O. H. (2016).
  • 23. Latin potus, a drink that could harm or kill. It is any substance that when taken inwardly in a very small dose or applied in any kind of manner to a living body depraves the health or entirely destroys life Poison phytotoxins, mycotoxins, zootoxins , and bacteriotoxins Systemic Toxicant, Organ Toxicant Toxicant synthesized in a specialized gland and ejected by the process of biting or stinging Venom
  • 24. Acute Toxicity (24 hours) Subacute Toxicity (1 month) Subchronic Toxicity (1-3months) Chronic Toxicity (greater than 3 months) FREQUENCY AND DURATION OF EXPOSURE Transient or Reversible or Temporary Toxicity (eg, narcosis-produced organic solvents). Persistent or Permanent or Irreversible Toxicity (eg, scarring of skin produced by corrosives). Immediate Toxicity (eg, cyanide poisoning). Delayed Toxicity (peripheral neuropathy produced by some organophosphorus insecticides). Cumulative Toxicity (eg, liver fibrosis produced by ethanol). TIME OF DEVELOPMENT AND DURATION OF INDUCED EFFECTS
  • 25. References ● Drummer, O. H. (2016). Toxicology: overview. In Encyclopedia of Forensic and Legal Medicine (pp. 615-621). Academic Press. (Research article) ● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic Press. (Book) ● Lappas, N.T. and Lappas, C.M., 2015. Forensic toxicology: Principles and concepts. Academic press. (Book)
  • 26. CLASSIFICATION OF POISONING Accidental poisoning Homicidal Poisoning Suicidal Poisoning Miscellaneous Poisoning (crime facilitation)
  • 27. CLASSIFICATION OF POISONS • Strong Acids/Strong Alkaline Corrosive Poisons (Caustics) • Inorganic/organic/mechanical Irritant Poisons • Central Nervous System (Neurotoxins)/Cardiovascular/Lun gs (Asphyxiants) Systemic Poisons • Domestic poisons/Therapeutic substance/Food poisons/Drugs of dependence Miscellaneous Poisons
  • 32. ACTION OF POISON Both Locally and Remotely Acting (eg, carbolic acid, etc.) Locally Acting : act only at the site of application, such as skin/ mucosa (eg, corrosive poisons). Remotely Acting :These act only after being absorbed into the circulatory system (eg, narcotic poisons, cardiac poisons, etc.).
  • 33. FACTORS AFFECTING TOXICITY Host factors Factors related to toxicant or associated with xenobiotics Environmental conditions •Size •Age •Sex •Pathological condition •Idiosyncratic reaction/toxicity •Physical state and chemical properties of the toxicant •Routes and rate of administration •Previous or coincident exposure to other chemicals (drug /drug Interactions) •Tolerance •Temperature /Humidity (A warm, humid environment is known to enhance dermal absorption as well as affect toxicity in certain inhalation toxicity studies disintegration of formulations of chemicals)
  • 34. References ● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic Press. (Book)
  • 35. CORROSIVE POISONS INORGANIC & ORGANIC ACIDS • Hydrochloric Acid/Nitric Acid/Sulphuric Acid/Carbolic Acid (Phenol)/Oxalic Acid CAUSTIC ALKALIS • Ammonia/Sodium hydroxide/Potassium permanganate
  • 36. Hydrochloric Acid Geber (800AD) Salient features Colorless (yellow in presence of Fe impurities , fuming, pungent liquid Fatal dose/Fatal period 15-20 mL. / 12-24 hours. Forensic Relevance Suicide/Accident /Abortifacient Signs and symptoms Acute poisoning via Dermal contact and ingestion/Inhalation/Contact with eyes Chronic poisoning via chronic exposure to fumes ((1) Eyes – (i) Conjunctivitis (ii) Corneal ulcers (2) Nose - Coryza [inflammation of nasal mucous membranes] (3) Oral cavity - (i) Inflammation of gums (ii) Loosening of teeth (4) GIT – Pharyngitis (5) Resp system - Bronchitis.
  • 37. Nitric Acid Salient features clear, colorless, fuming, heavy liquid having a peculiar choking odor Fatal dose/Fatal period 10-15 mLL. / 12-24 hours. Forensic Relevance Suicide Signs and symptoms a. Dermal contact and ingestion (1) More eructation, greater abdominal distention owing to gas formation (3) Yellow discoloration - of tissues with which it comes in contact [crowns of teeth, gums, lips, tongue, esophagus, stomach wall]. b. Inhalation (1) Resp system -(i) Coughing and dyspnea (ii) Sneezing (iii) Intense irritation of throat and lungs (iv) Suffocation (2) General - cyanosis. c. Contact with eyes Eyes - (i) Lachrymation (ii) Photophobia.
  • 38. Sulphuric Acid Salient features It is a colorless, odorless and viscous liquid that is miscible with water at all concentrations Fatal dose/Fatal period 10-15 mL. / 12-24 hours. Forensic Relevance Vitriolage/Accidental poisoning/Suicide/Disp osal of dead bodies/Occupational hazard/Abortifacient/ Self defense Signs and symptoms a. Ingestion Immediate – (a) Burning pain in the mouth, (b) dysphagia, (c) epigastric pain (d) odynophagia e) pharyngeal pain [most common presenting symptom] (f) salivation, (g) stridor Intense thirst, eructations, nausea, vomiting Findings in face - (a) Eyes – sunken (b) Pupils – dilated (c) Lips – Swollen, excoriated (d) Angles of mouth – Brown or black streaks (e) Mucus membranes of mouth, throat and esophagus – corroded (f) Teeth – chalky white (g) Tongue – black, sodden, swollen b. Contact with skin. (1) Intense burning pain, (2) Immediate corrosion, (3) destruction of skin.
  • 39. Carbolic Acid (Phenol, C6H5OH) Salient features i) Pure acid (short, colorless, prismatic, needle like crystals)/(ii) Commercial (brownish liquid). Taste - burning sweetish. Solubility – Sparingly soluble in water and Freely soluble in alcohol, benzene, ether and glycerine Fatal dose/Fatal period 10-15 g.. / 3-4 hours. Forensic Relevance Suicide/ Accidental/ Criminal abortion Signs and symptoms i. Local (1) Skin -(i) Numbness(ii) burn (2) Digestive tract –(i) Nausea, vomiting – in about 20% cases. ii) Hot burning pain – Extends from mouth to stomach(iii) Lips, mouth, tongue – corroded. Soon harden and become white 4. Chronic poisoning (phenol marasmus) (1) General - (i) Anorexia (ii) Headache (iii) Vertigo (iv) Wt loss (2) Urine – dark (3) Pigmentation – (i) Yellowish (ocher-like) discoloration of cartilage, sclera and skin [ochronosis]
  • 40. Oxalic Acid Salient features occurs in two forms –and dihydrate(common). Colorless, transparent prismatic crystals, Efflorescent. Solubility – 1 in 12 in H2O Fatal dose/Fatal period 600 mg/kg. For a 60 kg human 36 g./1-2 hours.. Forensic Relevance Accidental poisoning/Abortifa cient Signs and symptoms a. Contact (1) Skin - rarely damaged. May just be discolored (2) Mucosa – of eye, mouth etc may be greatly damaged and “scalded”. b. Ingestion i. Immediate (1) Burning, sour or bitter taste in the mouth which goes up to the stomach (2) Sense of constriction around the throat (3) Intense thirst(4) Mouth – may appear “scalded” or sometimes black (5) Severe pain – Begins in the epigastrium, but soon radiates all over the abdomen (6) Persistent vomiting, eructations and diarrhea. Vomitus contains altered blood [“coffee-ground” appearance] and mucus. (8) Signs and symptoms due to hypocalcemia -(i) Tetany (ii) Numbness and tingling of fingertips and legs (iii) Chvostek sign +ve.
  • 41. CAUSTIC ALKALIS - Ammonia Salient features At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent choking odor. Fatal dose 15-20 mL. Signs and symptoms - Inhalation - (a) Head, ears, eyes, nose, throat (HEENT) - Facial and oral burns and ulcerations (b) Respiratory system – cough, decreased air entry, oxygen desaturation, rhonchi, salivation, stridor, Tachypnea, wheezing (c) CNS - Loss of consciousness [if exposure is massive].
  • 42. Liquid Lye (NaOH, Caustic soda) Salient features found in many industrial solvents and cleaners, and many household products Forensic Relevance vehicular accidents Signs and symptoms Burns, Irritation, Necrosis of the skin and underlying tissues
  • 43. Potassium Permanganate [KMnO4] Signs and symptoms a. Ingestion (1) Intense thirst, nausea, vomiting and diarrhea. Vomitus is purple brown in color. Stools are black due to manganese sulfide.(2) Burning pain - from mouth to stomach (3) Dysarthria, dysphagi (4) Purple brown discoloration - of skin and mucus membranes, with which it comes in contact. Lips, gums, teeth, tongue, tonsils and pharynx. ( few minutes later color changes to brown, dark brown and finally coal black due to conversion to manganese dioxide. (5) Systemic - Methemoglobinemia, because of oxidizing nature of KMnO4. b. Local application Locally applied as an abortifacient. (1) Vaginal and cervical burns, erosions and ulcerations, resulting in severe scarring. (2) Extensive bleeding Salient features dark purple slender crystals, having a sweet astringent taste. it is a strong oxidizing agent and is used as a disinfectant Fatal dose/Fatal period 5-10 g../Few hours.. Forensic Relevance Suicide/Accidental/ab ortifacient/Production of fictitious injuries
  • 44. References ● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
  • 45. INORGANIC POISONS (Irritants) • Arsenic • Mercury • Copper • Lead • Thallium • Barium Inorganic Metallic poison • Phosphorus Inorganic Non Metallic poison
  • 46. ARSENIC Toxic salts Metallic arsenic not poisonous, Toxic salts includes powder or porcelain type Arsenious oxide [Arsenic trioxide, As2O3], (a) White in color, tasteless and odorless, Sparingly soluble in water Arsenic acid [H3AsO4] Arsenic trichloride (AsCl3)- Butter of arsenic. Colorless poisonous oil Arsenic trisulfide (As2S3) comes as the mineral orpiment [hartal in India] Copper acetoarsenite [Paris Green, Emerald Green, Schweinfurt Green] Once used as a pigment and insecticide Copper arsenite [Scheele’s Green, CuHAsO3]. (green pigment) (7) Tetraarsenic tetrasulfide (As4S4) Fatal dose/Fatal period (1) As2O3 - 200-300 mg/(2) Arsine gas – 25-30 ppm is lethal in 30 min./ 1-2 days. Forensic Relevance Homicidal poison/Arsenophagists/Hydro arsenicism/Arsenic in drugs of addiction/Seafood SIGN & SYMPTOMS / TOXICITY a. Ingestion (1) GIT: (i) Odor – Garlicky (ii) Taste – sweetish metallic (iii) Intense thirst,Ptyalism (iv) Nausea, Vomiting (v) Throat – feeling of constriction, dysphagia (vi) Burning and colicky pain – in esophagus, stomach and bowels (vii) Abdominal pain (viii) Diarrhea– (I) expelled frequently and involuntarily (II) Color and odor - dark colored, stinking, bloody (c) May mimic bacterial food poisoning or cholera.(2) Ocular: (i)Conjunctivitis (ii) Lacrimation (3) Respiratory - Irritation of upper airways (4) Liver - Fatty degeneration (5) Renal: (i) Pain - during micturition (ii) Oliguria (iii) Uremia (iv) Urine –contains albumen, casts and RBCs (6) Muscular – Tenderness of muscles (7) CNS: (i) Convulsions and tremors (ii) Formication (iii) Giddiness (iv) Headache (v) Vertigo (vi) General paralysis (vii) Delirium (viii) Coma (8) CVS: (i) Cardiac arrhythmias [ST-T wave changes, prolonged QT interval], ventricular fibrillation (ii) Hypotension (iii) Ventricular tachycardia (9) Skin – loss of hair [in case of survival], skin eruptions (10) General – hyperthermia [Hyperpyrexia]. b. Inhalation [Arsine gas] (1) Hemolysis (2) hemoglobinuria (3) renal failure (4) death is almost instantaneous.
  • 47. MERCURY (QUICKSILVER) Toxic Salts of Mercury 1. Organic salts ((1) methyl mercury and (2)dimethyl mercury. 2. Inorganic salts ((1) Mercuric Chloride [HgCl2, Corrosive sublimate](2) Mercurous Chloride [Hg2Cl2](3) Mercuric ammonium chloride(4) Mercuric cyanide – [Hg(CN)2]-5) Mercuric iodide - (HgI2, Protiodide)(6) Mercuric nitrite (7) Mercuric oxide (HgO)(8) Mercuric sulfate (HgSO4)- odorless white crystalline powder (9) Mercury sulphide(10) Mercury thiocyanate [Hg(SCN)2] Fatal dose/Fatal period 1-4 g of HgCl2/3-5 days. Forensic Relevance Criminal abortion/Accidental/Quacks/ SIGN & SYMPTOMS / TOXICITY Acute Poisoning: a. Elemental mercury i. Inhalation (1) General – Headache, blurring of vision, Fever, chills,Erythematous pruritic papular rash, conjunctivitis, salivation(2) Pulmonary – chest pain, cough, dyspnea, interstitial pneumonitis, necrotizing bronchiolitis, pulmonary edema, pulmonary failure(3) GIT – Metallic taste, deep red oral mucosa, gingivitis, stomatitis, strawberry tongue, swelling of salivary glands, teeth ii.Ingestion:Absorption is minimal [<0.01% is absorbed]. iii. Injection (1) S/c or IM - Abscess formation, ulceration [exuding tiny droplets of Hg].
  • 48. MERCURY (QUICKSILVER) SIGN & SYMPTOMS / TOXICITY b. Inorganic mercury (2 phase manifestation) I. First phase (1) Immediately after ingestion of corrosive mercury salts – Hot burning pain, sense of constriction, ashen discoloration of the mucous membrane in mouth and throat. Burning pain extends down to stomach and abdomen. (2) Within a few minutes - Intense epigastric pain, followed by diffuse abdominal pain. Nausea, retching and almost continuous vomiting of mucoid material, which frequently contains blood and shreds of mucous membrane.Hoarse voice.(3) Mouth, tongue and fauces – are corroded, swollen and show a grayish white coating.(4) Acrid metallic taste, excessive salivation and thirst.(5) Severe purging, with liquid, bloody feces and considerable tenesmus.(6) Rapid, weak pulse; breathing shallow and difficult; Pallor; Prostration,circulatory collapse, and death . ii. Second phase (If begins in 1-3 days ) in untreated cases(1) Oral - Marked salivation, mercurial stomatitis, glossitis and ulcerative gingivitis within 24-36 hr. Loosening of teeth, necrosis of the jaw. (2) Severe infections (3) Renal - PCT Necrosis in 2-3 days, transient polyuria, albuminuria,cylindruria, hematuria, anuria, azotemia and renal acidosis. Recovery may occur within 10-14 days, but death may also occur in some cases. (4) Late - After many days after the original exposure (especially in untreated cases), a membranous colitis may appear; dysentery, tenesmus, ulceration of the colonic mucosa, and hemorrhage. Liver necrosis sometimes develops.
  • 49. BARIUM Toxic salts Soluble salts are highly poisonous (chlorides are most poisonous).Barium ions are also highly poisonous. Fatal dose/Fatal period 1g./12 hours. Forensic Relevance accidental. SIGN & SYMPTOMS / TOXICITY . (1) Severe GIT irritation – (a) Nausea, Abdominal pain, vomiting, diarrhea occur within 1 hour of ingestion. (b) Esophagitis (c) hemorrhagic gastritis (2) Signs and symptoms associated with hypokalemia - (a) ventricular dysrhythmia (b) hypertension (c) profound flaccid muscle weakness (d) respiratory failure (e) lactic acidosis, (f) hypophosphatemia (g) rhabdomyolysis (3) Secondary to tissue ischemia - (a) Altered level of consciousness (b) seizures
  • 50. COPPER Toxic Salts of Copper (1) Copper acetoarsenite(2) Copper arsenite (3) Copper subacetateused by Greek artists as a green pigment in their paintings (4) Copper sulphate [blue vitriol]. Fatal dose/Fatal period 0.15-0.3 g/kg (CuSO4), i.e. about 20 g or a 70 kg man/1-3 days. Forensic Relevance Abortifacient / Cattle poison/Accident/suicide SIGN & SYMPTOMS / TOXICITY Acute Poisoning ( Symptoms appear within 15-30 minutes). In mild cases there is (i) a metallic taste in mouth (ii) -salivation (ptyalism) (iii) thirst (iv) nausea, vomiting, eructations and diarrhoea (v) burning pain in the stomach with colicky abdominal pain (vi) Vomited matter is bluish-green. In severe cases (i) Hepatotoxicity – Acute hepatic necrosis and jaundice (ii) Hemolysis (iii) hematemesis, melena – Due to ulceration in the GIT (iv)methemoglobinemia, methemoglobinuria (v) Renal and pulmonary toxicity (vi) Hypotension and cardiovascular collapse (vii) Neurological – lethargy, seizures, coma. Chronic Poisoning:(1) Anemia (2) Green line on gums (3) Colic(4) Peripheral neuritis(5) Degeneration and atrophy of muscles (6) Vineyard’s sprayer’s lung (7) Chalcosis lentis(8) Greenish discoloration of hair
  • 51. LEAD Toxic Salts of Lead (1) Lead carbonate (PbCO3, safeda)(2) Lead chromate (PbCrO4) ( bright yellow color)(3) Lead diacetate (sweet taste)(4) Lead monoxide (PbO) (5) Lead sulfide (PbS, Galena)(6) Lead tetraacetate [Pb(C2H3O2)4] (7) Lead tetroxide (Pb3O4 or 2PbO·PbO2)-Also known as red lead, sindoor,vermilion. (8) Tetraethyl lead [CH3CH2)4Pb; TEL] Fatal dose/Fatal period (1) Lead acetate – 20 g;(2) Lead carbonate – 40 g;(3) Tetraethyl lead – 100 mg/kg/1-2 days. Forensic Relevance Abortion/Cattle poison/Drug abusers/occupational poisoning SIGN & SYMPTOMS / TOXICITY Acute poisoning :(1) an astringent and metallic taste, (2)headache, (3) dry throat, (4) nausea and vomiting [occasionally diarrhea], (5)thirst, (6) peripheral circulatory collapse [due to loss of water from GIT], (7)neurological signs [(i) paresthesias (ii) rarely encephalitis (iii) cerebellar ataxiais common in children]. (8) Hemolysis causes anemia and presence of hemoglobin in the urine, (9) decreased urine output (damage to kidneys). (10)Death in severe cases. Chronic Poisoning : a. Facial pallor, b. Anemia, c. Lead line d. Colic and constipation d.Lead palsy (Weakness of muscles due to lead) f. Encephalopathy g. Cardiorenal manifestations (1) Hypertension (2) Nephritis:(3) Saturnine gout [syn, lead gout]- h.Reproductive system (1) Sterility and impotence (2) Menstrual disorder(3) In pregnant females (i) Abortion – ii) Premature labor (iii) Intrauterine growth retardation. h. Reproductive system . i. Eye (retinal stippling.) j. Other systems (1) Anorexia (2) Drowsiness (3) Dyspepsia (4) Emaciation (5) Exhaustion
  • 52. THALLIUM Fatal dose/Fatal period 6-40 mg/kg of Tl salts/24-36 h. Forensic Relevance Homicide SIGN & SYMPTOMS / TOXICITY Acute Poisoning:(1) GIT:(i) Abdominal pain [most common]. Accompanied by (ii) Vomiting and either (iii) Diarrhea or Constipation (iv) Severe symptoms, eg hematemesis and bloody diarrhea are more rare.(2) Chest – Tightness and pain(3) CVS:(i) Tachycardia and (ii) Hypertension (ii) ECG abnormalities (4) Skin – Maculo-papular skin eruption having butterfly distribution on face [very characteristic] (5) Coma – Occurs with large exposures B. Chronic Poisoning: (1)Most characteristic lesions, alopecia (begins in 10 days total loss 30 days) and neurologic[appears after 2-5 days] symptoms [Thallium triad].(2) Skin: (i) acne, (ii) palmar erythema, (iii) anhidrosis and (iv) dry scaly skin(3) Nails - Mees lines appear within 2-4 weeks after exposure.
  • 53. Phosphorus Salient feature Four allotropes ((1) White (2) Red [heating white phosphorus to 250°C in vacuum],(3) Violet [dissolving white phosphorus in molten lead at 500°C, and then cooling it slowly] and (4) Black [heating white phosphorus at 12,000 atm]. White Fatal dose/Fatal period 1 mg/kg [60 mg for a 60 kg person]./½ day to 8 days Forensic relevance Suicide/Accident SIGN & SYMPTOMS / TOXICITY a. Local application (Causes both thermal and chemical burns. 2nd and 3rd degree (Dupuytren) burns b. Ingestion i. Acute fulminant poisoning: Vomiting, diarrhea, peripheral vascular collapse. Death occurs within 12 hours. ii. Subacute poisoning ((a) First stage [2 days] (1) Severe burning pain in the mouth. Abdominal pain, vomiting, diarrhea (2) Garlicky odor (3) Luminous vomit and stools(4) Fumes emanate from the stools (Smoking or smoky stool syndrome). (b) Second stage [4 days] Patient is symptom free. (c) Third stage [2 days] (1) Hepatic toxicity (i) Mousy odor of the breath (ii) Flapping tremor of hands [asterixis] (iii) Hepatomegaly, jaundice, bleeding tendencies(iv) Finally hepatic encephalopathy and death. This Photo by Unknown Author is
  • 54. References ● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
  • 55. SYSTEMIC POISONS Central Nervous System (Neurotoxins) i.e. CNS Depressants (1) Alcohols (2) Opium and its derivatives (3) Sedative-hypnotics i.e Barbiturates/ Deliriant Poisons eg. Datura, Cannabis, Cocaine Central Nervous System (SPINAL POISONS eg, Strychnos Nux Vomica) Cardiac Poisons eg. Aconite, Digitalis Purpurea, Nerium Oleander Asphyxiants and Toxics eg. Gase eg. Carbon Monoxide (Co), Hydrocyanic Acid (Hcn), Hydrogen Sulfide (H2s)
  • 56. SPINAL POISONS: Strychnos Nux Vomica Salient feature colorless, odorless rhombic prisms, and has intensely bitter taste. Active Principles whole tree, including the seeds/strychnine and brucine Fatal dose/Fatal period (1) One crushed seed (2) Strychnine - 30mg/kg./ 1-2 hours. Forensic relevance Homicide./cattle poison/arow poison/adulterant of street drugs/accidental poisoning SIGN & SYMPTOMS / TOXICITY Dermal exposure - Tingling sensation locally. Other symptoms as in ingestion. Ingestion - (1) Bitter taste in mouth, a sense of restlessness and uneasiness, anxiety, fear and a feeling of suffocation (2) difficulty in swallowing (3) Prodromal symptoms (4) Convulsions (5) Face - is cyanosed
  • 57. Cardiac Poisons: ACONITE Salient feature igenus of flowering plant belonging to the buttercup family (Ranunculaceae). Active Principles (i) aconitine, (ii) mesaconitine, (iii) hypaconitine, (iv) jesaconitine, (v) Yunaconitine. Fatal dose/Fatal period (1) Root – 1-2 g (2) ild plant – 1 g. (3) Aconitine – 2 mg. (4) Extract – 250 mg (5) Tincture – 5 mL. /2-6 hours. Forensic relevance Homicide./cattle poison/arow poison/suicide/accide ntal poisoning SIGN & SYMPTOMS / TOXICITY Eyes exposed to Pollen " pain and swelling /Touching – Leaves or roots handled for a long time or rubbed on the skin "numbness, tingling/ Inhalation – Root inhaled for a long time has a narcotic effect. Ingestion:(1) GIT -(i) Burning sensation from the mouth to stomach(ii) Numbness, tingling in the mouth tongue and pharynx(iii) Salivation, nausea, vomiting, diarrhea (iv) Later – Mouth is dry, thirst, dysphagia.(2) CVS –(i) ECG and heart rhythm changes (ii)Pulse – slow, feeble, irregular. (3) Respiratory –(i) Feeling of constriction in the chest (ii) Respirations slow, labored and shallow. (4) CNS –(i) Consciousness clear. Sometimes there may be hallucinations (ii) Headache and giddiness (iii) Numbness and tingling over entire body (iv) Restlessness (v) Vertigo. (5) Muscular –(i) Marked weakness of muscles with spasms and twitchings,Cramps and convulsions. (6) Skin – (i) Pallor (ii) profuse sweating (iii) cold and clammy skin..
  • 58. CARDIAC POISONS: DIGITALIS PURPUREA Salient feature The word digitalis comes from the finger shaped flowers [L,digitus, a finger] Active Principles (1) Leaves - (i) Digitoxin, (ii) Gitoxin/(2) Seeds - (i) Digitalin. Fatal dose/Fatal period Digitalin – 15-30 mg Digoxin [present in D. lanata] – 10 mg Digitoxin – 4mg/Leaves 1-2 (2g)/24 hrs Forensic relevance accidental poisoning/Iatrogenic poisoning SIGN & SYMPTOMS / TOXICITY Cardiac – Almost every type of dysrhythmia is produced. Extracardiac – GIT – Nausea, vomiting, Abdominal pain ,CNS –anxiety confusion delirium depression disorientation drowsiness Fatigue, mental confusion, restlessness, hallucinations,headache muscle weakness. Skin – Urticaria Visual disturbances - transient amblyopia, blurring of vision,chromatopsia (aberrations of color vision), ,photophobia, photopsia (perceived flashes of light), scotoma and Xanthopsia(yellow halos).
  • 59. CARDIAC POISONS: NERIUM OLEANDER Salient feature belong to the Dogbane family, Apocynaceae. Poisonous parts - (i) All plants of the plant including (seeds and roots contain the highest percentage toxins). Active Principles (i) Adynerin, (ii) Digitoxigenin, (iii) Folineriin, (iv)Nerioside [Nerin] (v) Oleandrin (OD). (vi) Oleandrigenin Fatal dose/Fatal period (1) Root: 15-20 g,(2) Leaves: 5-15 in number/24-36 h. Forensic relevance Suicide/Abortifacient/ Cattle poison SIGN & SYMPTOMS / TOXICITY (1) Contact – Dermatitis (2) Inhalation – of emanations from flower causes nausea, headache, dizziness and respiratory difficulty. (3) Ingestion –(1) GIT - (i) Profuse frothy salivation (ii)Vomiting and Diarrhea (iii) Difficulty in swallowing and articulation (iv)Abdominal pain (2) Neuromuscular - (i) Muscular twitchings (ii) Tetanic spasms (iii) Lock-jaw (iv) Drowsiness (v) Coma. Later respiratory paralysis. (3) Heart - Atrial and ventricular fibrillation, AV block. In severely poisoned patients, ECG abnormalities
  • 60. Asphyxiants and Toxic Gases:CARBON MONOXIDE (CO) Salient feature colorless, odorless, tasteless and nonirritant gas which is lighter than air and insoluble in water. It burns with a blue flame Fatal dose/Fatal period COHb conc.>60% Forensic relevance Accidental CO poisoning SIGN & SYMPTOMS / TOXICITY Acute poisoning:(1) Symptoms due to tissue hypoxia - headache, nausea, vomiting, dizziness,lethargy and a feeling of weakness. (2)Skin - There may be a cherry red discoloration of skin. (3) CVS – Chest pain, palpitations, -Heart rate. (4)CNS - Neurological signs include poor concentration, confusion, disorientation, visual disturbance, syncope and seizures. (5) Respiratory – Shortness of breath. (6) Ophthalmoscopic examination - Retinal hemorrhages may be seen. 2.Chronic poisoning:(1) Persistent headaches, lightheadedness, depression, confusion, memory loss. (2) CVS patients – symptoms may worsen (chronic hypoxia to heart). (3) Permanent neurological damage (chronic hypoxia to brain). (4) Visual disturbances (5) Elevated RBC count.
  • 61. Asphyxiants and Toxic Gases: Hydrogen Cyanide Salient feature The name cyanide (Gk Kyaneos, dark blue) is derived from the colorful Prussian blue from which HCN [syn, prussic acid] was first synthesized. Boiling point is 26°C. Fatal dose/Fatal period a. Ingestion (1) HCN - 50 to 60 mg (2) NaCN, KCN – 200 to 300 mg. b. Inhalation Air concentration of HCN: (i) 1:50,000 is fatal in few hours (ii) 1:10,000 within few minutes (iii) 1:2,000 almost immediately/HCN - 2-10 minutes, KCN or NaCN - 30 min Forensic relevance Accidental poisoning. Suicidal poisoning/Arson cases/chemical terrorism SIGN & SYMPTOMS / TOXICITY Acute Poisoning: Inhalation:. (1) Sense of constriction about the throat and chest (2) Dizziness, vertigo (3) Insensibility (4) Death from respiratory failure. b. Ingestion: (less doses):(1) Nausea (2) Giddiness (3) Headache (4) Confusion (5) Loss of muscular power ii. Massive [larger than fatal] doses (1) Sudden loss of consciousness.(2) No voluntary act can be performed after ingestion.(3) Prompt death from respiratory arrest. Chronic Poisoning (Produced by continued inhalation of low conc of CN over long periods) (i) Leber hereditary neuropathy. (ii) Tobacco amblyopia [progressive loss of visual function](iii) Thyroid disorders development of hypothyroidism
  • 62. Asphyxiants and Toxic Gases: HYDROGEN SULFIDE (H2S) Salient feature Hydrogen sulfide is a colorless, flammable, gas with the characteristic foul odor of rotten eggs. Fatal dose/Fatal period (1) 20ppm - Maximum allowable conc (2) 400- 700ppm - dangerous after an exposure of half to 1 h. (3) >1000 ppm - instantly fatal./ Few minutes to few hours. Forensic relevance Accidental poisoning SIGN & SYMPTOMS / TOXICITY Acute poisoning : Exposure to high conc [750-1000 ppm] (1) General - Weakness, malaise, sweating, abrupt physical collapse [knockdown] (2) CVS – cardiac arrhythmias, conduction defects(3) CNS – amnesia, confusion, delirium, hallucinations, convulsions,Nystagmus, Somnolence 4.Respiratory paralysis, asphyxial seizures,death. 2. Chronic exposure May occur in industrial workers. (1) General – Headache, Weakness, Nausea, Weight loss (2) Gas eye is common. Associated with reversible chromatic distortion and visual changes. (3)ataxia, dystonia, choreoathetosis] (4) Spontaneous abortions in female.
  • 63. References ● Aggrawal, A., 2014. Forensic Medicine and Toxicology. Ed, 1, pp.299-310.
  • 64. DIAGNOSIS OF POISONING Symptoms Poison commonly involved Vomiting Irritant poisons like arsenic acids Cramps Metallic poisons like arsenic, lead, antimony,mercury etc. Convulsions Strychnine, cyanides, carbon monoxide, Paralysis lead, arsenic, aconite, snake venom etc. Coma Carbon dioxide
  • 65. DIAGNOSIS OF POISONING Clinical Findings Poison commonly involved (Skin colour) Cherry Pink Carbon monoxide (Skin colour) Flushed pink skin cyanide (Skin colour)Cutaneous bullae carbon monoxide (Appearance of Blood) Red venous blood cyanide or carbon monoxide poisoning Rhabdomyolysis carbon monoxide and strychnine
  • 66. DIAGNOSIS OF POISONING Pattern Poison commonly involved Malaise, restlessness, nausea, weakness Carbon monoxide, lead, mercury,arsenic Restlessness, hypertonia,hyperreflexia, pyrexia strychnine Burns in mouth, disphagia, abdominal pain, distension. Corrosive Renal failure mercurial compound, arsine, lead Jaundice, hepatic failure Phosphorous, lead
  • 67. REFERENCES ● Laboratory Procedure Manual- Forensic Toxicology Directorate of Forensic Science, MHA, Govt. of India
  • 68. DOSE AND RELATED TERMS • Lethal Dose (LD) • Lethal Dose 50 (LD50) • Lethal Concentration (LC) (milligrams of compound per kilogram of feed (or water) • Lethal Concentration-50 (LC50) Dose Dose: The total or absolute quantity or amount of a substance applied or administered at one time to an individual to achieve the desired pharmacological or toxicological response
  • 69. TIME ACTION CURVES: time –effect relationship of toxicant Phase I: Time of onset of action (Ta) Phase II: Time to peak effect (Tb) Phase III: Duration of action (Tc) Phase IV: Residual effects (Td) SOURCE: VARIABLES OF DOSERESPONSE CURVE • Efficacy: maximal effect • Potency: diff dose same effect • Slope: slope of dose-effect • Biological variations
  • 70. Transfer of Molecules Across Biological Membranes
  • 71. ABSORPTION (Factors that influence absorption) The solubility of the chemicals The concentration of chemicals The circulation The site of absorption The area of absorbing surface The route of administration (GI tract, skin, and lungs) Absorption is defined as the process of movement of an unchanged compound from its site of administration or exposure to the blood stream.
  • 72. GASTROINTESTINAL ABSORPTION Transfer of molecules (non ionic diffusion / active processes) Factors affecting absorption (chemicals properties i.e weak acids / presence Food)
  • 73. SKIN ABSORPTION Chemicals absorbed through skin (carbon tetrachloride/ . Pesticides (parathion, malathion), nicotine insecticides/Chlorovinylarsine dichloride (Lewisite), a mustard gas Factors affecting absorption (skin layer i.e. SC or chemical breakage i.e acids, alkalis, Dimethylsulfoxide) Epidermis : 0.2 mm thick
  • 74. LUNG ABSORPTION Chemicals absorbed through lungs i.e. asphyxiants and irritants or particulate material Factors affecting absorption (partition coefficients i.e. lipid/ water partition coefficients high / particle size small)
  • 76. Types of administration (IM, SC, IV, IP, Intraperitoneal injection ) Factors affecting absorption I.E. NON IRRITATING via SM , irritating via SC PARENTERAL ADMINISTRATION
  • 77. DISTRIBUTION SOURCE: Gupta, P.K., 2016 absorption into the blood stream penetrate in the various fluid compartments: (1) plasma; (2) interstitial fluid; (3) transcellular fluid (4) cellular fluids *Bone and adipose tissue
  • 78. Factors that determine a compound’s rate and extent of distribution 1. Molecular size (ie, physicochemical properties of compound) 2. Lipophilicity 3. Plasma protein and tissue binding 4. Blood flow and organ size 5. Special compartmental and barriers (eg, bloodbrain barrier ,blood cerebrospinal barrier, placental barrier, and other barriers) 6. Availability of special transport system 7. The ability to interact with transmembrane transporter proteins
  • 79. TISSUE PERMEABILITY BARRIERS Blood organs barrier Blood urine barrier Blood testes barrier Blood bile barriers Blood Brain Barrier FACTORS AFFECTING DISTRIBUTION AND TISSUE RETENTION • Binding to Plasma Proteins (albumin/globulin: longer duration of action) • Storage in Body Fat i.e. organochlorinated pesticides such as DDT • Storage in the Brain Tissues i.e. CNS Drugs (barbiturates) and psychotropic drugs (chlordiazepoxide and chlorpromazine) • Storage in Erythrocytes i.e. pharmacological agents, such as p-nitro-aniline/ inorganic ions lead, cadmium • Other Tissues as a Storage Depot (skeleton i.e tetracycline /kidney and liver i.e. cadmium/blood i.e. CO/lungs i.e. paraquat/thyroid i.e. percholrate)
  • 80. EXCRETION RENAL EXCRETION i.e. penicillin-G, N-methyl-nicotinamide BILIARY EXCRETION i.e benzomethamine GASTROINTESTINAL TRACT EXPIRED AIR i.e. fluorobenzene, carbon monoxide SWEAT ie. diethyl di-thiol-iso- phthalate SALIVA I.E sulfonamides, pentobarbitone MILK i.e. s DDT, thiouracil, tetracycline, and erythromycin,
  • 81. References ● Gupta, P.K., 2016. Fundamentals of toxicology: essential concepts and applications. Academic Press.
  • 82. Management of poising cases Objectives of Treatment ❑ Removal of unabsorbed poison ❑ Administration of Antidote ❑ Elimination of absorbed poison ❑ Symptomatic Treatment ❑ Maintenance of patient general condition
  • 83. Removal of unabsorbed poison For inhaled poison: AR mixture of 95% of oxygen and 5% of carbon dioxide For injecting poison: chemical antidotes, cold packing and vasoconstrictors Contact Poisons: specific antidote
  • 84. Removal of unabsorbed poison For ingested poison: Emetic agents ✓ lukewarm water/15 gm of mustard powder in 200 ml of water/About 30 gms of common salt in 200 ml of water ✓ Zinc sulphate:1-2 gms in 200 ml of water ✓ Apomorphine: 6 mg by sub-cutaneous injection by levallorphan 1-2 mg/ naloxone hydrochloride 5-10 mg intramuscular or intravenous
  • 85. Removal of unabsorbed poison For ingested poison: Gastric aspiration and lavage
  • 87. Use of Antidotes This Photo by Unknown Author is licensed under CC BY-NC-ND Mechanical or physical Chemical Physiological or Pharmacological Universal Antidotes Antidotes are remedies to counteract the effects of poison According to their mode of action, antidote types:
  • 88. Mechanical or Physical: impede absorption Corrosive/irritant glass Demulcents and Bulky Foods 10: 1 ratio, 4-8g , small dose of poison, 4-6 hours, aspiration into lungs
  • 89. Chemical : non toxic insoluble substances or oxidizes to non toxic substances POISON/TOXIC SUBSTANCES CHEMICAL ANTIDOTE Corrosive alkalis dilute acetic acid Corrosive acids Magnesium oxide or calcium oxide oxalic acid Calcium oxide carbolic acid magnesium sulphate phosphorus copper sulphate lead sulphates of alkalis arsenic. freshly precipitated iron oxide Tannin ( polyphenolic biomolecules) alkaloids glucosides and metals 1:1000 aq. potassium permanganate alkaloids, barbiturates, phosphorus, cyanides etc.
  • 90. Physiological or Pharmacological: produce opposite effects to that of the poison (physiological antagonists) Agent poison Effect Nalorphin Morphine physiological antagonists caffeine Morphine physiological antagonists atropine and oximes organophosphorous compounds physiological antagonists chloroform strychnine physiological antagonists BAL (Dimercaprol), EDTA (Ethylene diamine tetra acetate), Heavy metals chelating agents
  • 92. ELIMINATION OF ABSORBED POISONS Cathartic hot packs Forced Diuresis Peritoneal Dialysis Haemodialysis Exchange transfusion
  • 93. TREATMENT OF GENERAL SYMPTOMS Strong analgesic Artificial respiration Antibiotic Cardiac stimulants Anaesthetic Saline infusion Administration of glucose
  • 94. MAINTENANCE OF THE PATIENT’S GENERAL CONDITION
  • 95. REFERENCES ● Laboratory Procedure Manual- Forensic Toxicology Directorate of Forensic Science, MHA, Govt. of India
  • 96. This Photo by Unknown Author is licensed under CC BY-SA