Special Drug Groups - routledge.com · Lidocaine 0.01–15 0.01–5.9 0.8 0.9–2.9 12–204 6.6–135 9–13 20 Mepivacaine 51–59 51–83 51 51 Table 2.3 Pharmacokinetic Parameters

3

2Special Drug Groups Acetylcholinesterase Inhibitors

While acetylcholinesterase inhibitors were historically used as pesticides and herbicides, in recent years they have been used to develop medica-tions to treat Alzheimer’s disease and myasthenia gravis. Commonly, their toxicity is measured by the percentage of acetylcholinesterase (ACh) activ-ity with toxicity beginning 20% below the level of normal activity (or 80% activity level) and becoming pronounced by 50% activity level. Severe tox-icity and death occur at 90% suppression (measured activity level = 10%). Postmortem testing should utilize the red blood cell (RBC), ACh as it better reflects neural ACh activity.

Table 2.1 is a non-comprehensive list of common drugs, nerve agents, and insecticide/pesticides that are acetylcholinesterase inhibitors.

Copyright Material – Provided by Taylor & Francis

4 Handbook of Forensic Toxicology for Medical Examiners

Tab

le 2

.1

Ace

tylc

holi

nest

eras

e In

hib

itor

s

Dru

gs—

Alzh

eim

er’s

dise

ase

Don

epez

il (A

ricep

t)G

alan

tam

ine

(Raz

adyn

e, Re

min

yl,

Niv

alin

)H

uper

zine

ALa

dost

igil

Met

rifon

ate

Riva

stig

min

e (E

xelo

n)Ta

crin

e (C

ogne

x)

Dru

gs—

mya

sthen

ia gr

avis

Am

beno

nium

(Myt

elas

e)Ed

roph

oniu

m (T

ensil

on, E

nlon

, Re

vers

ol)

Neo

stig

min

e (P

rost

igm

in)

Phys

ostig

min

e (A

ntili

rium

)Py

ridos

tigm

ine

(Mes

tinon

, Re

gono

l)

Dru

gs—

glau

com

a

Dem

ecar

ium

(Hum

orso

l)Ec

hoth

ioph

ate

(Pho

spho

line

iodi

de)

Poiso

ns—

nerv

e age

nts

Cyc

losa

rinSa

rinSo

man

Tabu

nV

XV

EV

GV

M

Inse

ctic

ides

or p

estic

ides

Ace

phat

e (O

rthe

ne)

Ald

icar

b (T

emik

)A

zinp

hos-

met

hyl (

Gut

hion

)Be

ndio

carb

(Fic

am)

Bufe

ncar

bC

arba

ryl (

Sevi

n)C

arbo

fura

n (F

urad

an)

Car

boph

enot

hion

(Trit

hion

)C

hlor

fenv

inph

os (B

irlan

e)C

hlor

pyrif

os (D

ursb

an, L

orsb

an)

Cou

map

hos (

Co-

Ral)

Cro

toxy

phos

(Cio

drin

, Cio

vap)

Cru

fom

ate

(Rue

lene

)D

emet

on (S

ysto

x)D

iazi

non

(Spe

ctra

cide

)

Dic

hlor

vos (

DD

VP,

Vap

ona)

Dic

roto

phos

(Bid

rin)

Diis

opro

pyl fl

uoro

phos

phat

e (D

yflos

)D

imet

hoat

e (C

ygon

, De-

Fend

)D

ioxa

thio

n (D

elna

v)D

isulfo

ton

(Di-S

ysto

n)EP

NEt

hiof

enca

rbEt

hion

Etho

prop

(Moc

ap)

Fam

phur

Fena

mip

hos (

Nem

acur

)Fe

nitr

othi

on (S

umith

ion)

Fens

ulfo

thio

n (D

asan

it)

Form

etan

ate

(Car

zol)

Fent

hion

(Bay

tex,

Tig

uvon

, Ent

ex)

Fono

fos (

Dyf

onat

e)Is

ofen

phos

(Ofta

nol,

Am

aze)

Mal

athi

on (C

ythi

on)

Met

ham

idop

hos (

Mon

itor)

Met

hida

thio

n (S

upra

cide

)M

ethi

ocar

b (M

esur

ol)

Met

hom

yl (L

anna

te, N

udrin

)M

ethy

l par

athi

on (P

ennc

ap-M

)M

evin

phos

(Pho

sdrin

)M

onoc

roto

phos

Nal

ed (D

ibro

m)

Oxa

myl

(Vyd

ate)

Oxy

dem

eton

-met

hyl (

Met

a sy

stox

-R)

Para

thio

n (N

iran,

Pho

skil)

Phor

ate

(Thim

et)

Phos

alon

e (Z

olon

c)Ph

osm

et (I

mid

an, P

rola

te)

Phos

pham

idon

(Dim

ecro

n)Pi

rimic

arb

(Piri

mor

)Pr

opox

ur (B

aygo

n)Te

mep

hos (

Aba

te)

TEPP

Terb

ufos

(Cou

nter

)Te

trac

hlor

vinp

hos (

Rabo

n,

Gar

dona

)Tr

ichl

orfo

n (D

ylox

, Neg

uvon

)


5Special Drug Groups

Anesthetic Agents

General Anesthetics

General anesthetic agents are commonly used in the clinical setting to induce or maintain anesthesia. When used for this purpose, in a monitored clinical setting and in ventilated patients, the risk of death due to overdose is minimal. Some anesthetic agents are associated with other toxic effects, such as malignant hyperthermia, liver toxicities, and prolonged QT, but a discussion of these effects is beyond the scope of this book. However, when such agents are abused outside of the monitored clinical setting, even therapeutic concentrations can be lethal. Table 2.2 summarizes lethal concentrations of these medications, which have been reported in the literature.

Ketamine and propofol deserve special mention and are described in more detail below.

• Ketamine• In addition to being a widely used anesthetic agent, ketamine

has become a drug of abuse known as Jet, Special K, Vitamin K, and Special K lube when combined with ethanol and gamma hydroxybutyric acid (GHB).

• As ketamine is also used as a recreational drug, its presence alone may not indicate a lethal intoxication. The following nontoxic concentrations have been reported:

Blood (mg/L)

Liver (mg/kg)

Kidney (mg/kg)

Brain (mg/kg)

Cardiac Muscle (mg/kg)

Skeletal Muscle (mg/kg)

0.5–9 0.8 0.6 4 3.5 1.2

Table 2.2 Lethal Concentrations of General Anesthetic Agents

Anesthetic Agent

Blood (mg/L)

Vitreous (mg/L)

Liver(mg/kg)

Kidney (mg/kg)

Brain (mg/kg)

Lung (mg/kg)

Muscle (mg/kg)

Etomidate 0.4 0.3Halothane 3.4–720 1.7–880 12–14 104–1560 500Isoflurane 1.8–48 31–1000 27–53 29–307 9–34 9 (skeletal)Ketamine 1.5–38 4.9–6.6 3.2–3.6 3.2–4.3 2.4

(cardiac)Nitrous oxide 11–2030 47–2200 370–2420Propofol 0.03–5.5 1.4–27 1.8–5.5 2.9–17 222

(skeletal)Sevoflurane 8–26 87 31–269 13–29



• Propofol• With high volume of distribution and lipophilicity, it can be found

several days following a surgical procedure at low tissue and blood concentrations and may not indicate an acute intoxication.

• Can cause propofol infusion syndrome—characterized by metabolic acidosis, bradyarrhythmias, rhabdomyolysis, hypo-tension, and cardiac failure.

• Therapeutic/nontoxic concentrations of propofol have been reported from 0.4 to 6.8 mg/L in blood.

Local Anesthetics

Local anesthetics usually result in toxicity and death by central nervous sys-tem excitation and seizure activity. They can also be cardiotoxic, resulting in arrhythmias and ventricular fibrillation.

Tables 2.3 and 2.4 summarize the pharmacokinetic properties and non-lethal and lethal concentrations of several local anesthetic agents.

Table 2.4 Additional Tissue Concentrations for Lidocaine and Mepivacaine

Anesthetic Agent

Nontoxic Concentrations Lethal Concentrations

Kidney (mg/kg)

Brain (mg/kg)



Kidney (mg/kg)

Brain (mg/kg)



Lidocaine 0.01–15 0.01–5.9 0.8 0.9–2.9 12–204 6.6–135 9–13 20Mepivacaine 51–59 51–83 51 51

Table 2.3 Pharmacokinetic Parameters and Toxic and Lethal Concentrations of Local Anesthetic Agents

Anesthetic Agent ʎ (h) Vd (L/kg)

Nontoxic Blood (mg/L)

Nontoxic Liver

(mg/kg)

Toxic Blood (mg/L)

Lethal Blood (mg/L)

Lethal Liver

(mg/kg)Benzocaine Unknown Unknown 0.05–0.5 1.0–5.2a 3.5a

Bupivacaine 1–3 0.4–1 0.2–3.5 0.3–20 3.8Lidocaine 0.7–5 1–4 0.3–5 0.01–4 8–12 12–44 10–96Mepivacaine 1.5–2 0.5–4 0.1–5 4–9 16b–50 75Prilocaine 0.5–2.5 0.7–4 0.9–5 0.3–2.8 13–15 14a–49Procaine 7–8 min 0.3–1 4–43 18–96Ropivacaine 2–4 0.5–1 0.4–3 1.5–6 2 4.4a Children.b Mixed with lidocaine 4.9 mg/L.



Lidocaine, benzocaine, and prilocaine deserve special mention and are described in additional detail below.

• Benzocaine and prilocaine toxicity can result in methemoglobinemia.• Lidocaine is metabolized by CYP 1A2 and 3A4 to the active metab-

olite, monoethylglycinexylidide (MEGX) and has been used as an adulterant in illicit drugs.

Neuromuscular Blocking Agents

Neuromuscular blocking agents block neuromuscular transmission at the neuromuscular junction, resulting in paralysis. These are most often used in anesthesia to assist in intubation. The use of these agents in the clinical setting, while the patient is being artificially ventilated, should not result in death. The presence of these agents outside of a clinical setting, in a non- ventilated patient, can result in death at any concentration.

Common neuromuscular blocking agents include: atracurium, cisatra-curium, doxacurium, gallamine, mivacurium, pancuronium, pipecuronium, rapacurium, rocuronium, succinylcholine, tubocurarine, and vecuronium.

Succinylcholine deserves an additional note, because it

• Can be difficult to find in postmortem cases due to short half-life.• Absorbs onto glassware during storage.• Is rapidly hydrolyzed to succinylmonocholine, choline, and succinic

acid, all of which are found endogenously.



Metals and Metalloids

Humans are exposed to metals and elements through the environment, food and water, smoking, and certain occupations or hobbies. Some metals have also been used not only medicinally but also as poisons, including being components of insecticides or pesticides. The concentrations of metals seen in blood and tissues are often extremely variable due to diet, environment, and occupation, making interpretation of postmortem metal concentrations extremely difficult; it is rec-ommended that such interpretation be done with great skepticism and reflection.

Metals tend to be eliminated by and accumulate in the kidneys, so renal tissue is often the preferred tissue when testing for an acute overdose. Chronic exposure can often be delineated by testing of the hair and/or fingernails. Tables 2.5 and 2.6 outline reported metal concentrations.

Numerous procedures can be utilized to test for metals, including inductively coupled plasma mass spectrophotometry (ICP), atomic absorption spectros-copy (AAS), atomic emission spectrophotometry (AES), and x-ray defraction. Be certain to contact the testing laboratory for any specific requirements.

The following metals deserve special consideration:

Aluminum• Classic exposure was through dialysis; no longer common.• Blocks incorporation of calcium into bone.• Associated with elevated calcium concentrations.

Arsenic• Is a metalloid. Used medicinally for years.• A known carcinogen.• Elemental arsenic (Aso) is not toxic; can be found in shellfish and

seafood.• Arsenate (As+5), arsenite (As+3), and arsine gas (AsH3) are toxic—

As+5 < As+3 < AsH3.• Can cause white lines across the nails, known as Mees lines or leuk-

onychia striata.

Barium• Often used in medical procedures as 40%–80% suspension (e.g.,

Entero-H and Barotrast).• Overdose can cause hypokalemia.

Cadmium• Most common exposure is from smoking and fish consumption.• Inhalation of cadmium fumes can cause fatal pneumonitis.



Tab

le 2

.5

Non

toxi

c C

once

ntra

tion

s of

Com

mon

Met

als

Met

alλ

Bloo

d (m

g/L)

Live

r (m

g/kg

)K

idne

y (m

g/kg

)Br

ain

(mg/

kg)

Car

diac

Mus

cle

(mg/

kg)

Skel

etal

Mus

cle

(mg/

kg)

Lung

(m

g/kg

)O

ther

(m

g/kg

)

Alu

min

um8

h–8

yr0.

004–

0.4

0.6–

20.

07–0

.40.

2–0.

90.

07–0

.9Bo

ne 1

–12

Ant

imon

yU

nkno

wn

0.00

2–0.

060.

01–0

.07

0.01

–0.1

0.01

–0.1

0.01

–0.1

0.01

–0.1

0.03

–0.2

Hai

r 0.1

–2N

ail 0

.2–2

Ars

enic

10–3

0 h

0.00

3–0.

30.

02–0

.09

0.02

–0.1

0.02

–0.1

0.02

–0.0

60.

04–0

.10.

05–0

.1Bo

ne 0

.05–

0.2

Nai

l 0.9

Hai

r 0.0

2–8

Bariu

m10

–80

h0.

001–

0.1

0.00

30.

01–0

.09

0.00

40.

009

0.16

Bism

uth

5–11

d0.

003–

0.5

0.01

–73

0.6

0.9

Cad

miu

m10

–30

yr0.

001–

0.1

0.7–

231–

166

0.02

–0.2

0.06

–0.3

0.07

–10.

2–2

Bone

0.0

2–0.

1H

air 5

27–9

67C

oppe

r15

–25

d0.

7–1.

82–

231–

132–

82–

120.

4–3

0.8–

2Sp

leen

4Bo

ne 3

Iron

3–6

h0.

3–1.

529

–479

7–16

08–

966–

7311

–59

112–

280

Sple

en 5

7–60

0Le

adBl

ood

1–2

mo

Bone

>20

yr

0.00

3–0.

50.

2–4

0.1–

20.

02–0

.80.

01–1

0.02

–0.5

0.05

–2Bo

ne 0

.2–4

Hai

r 0.1

–20

Nai

l 0.0

6–1.

5Li

thiu

mSe

e pa

ge 1

24M

ercu

ry14

–50

d0.

002–

0.2

0.00

2–1

0.2–

30.

04–0

.20.

001–

0.1

0.02

–0.2

0.02

–0.3

Bone

0.0

5–0.

07H

air 1

–15

Nai

l 0.0

6–0.

8Th

alliu

m3–

30 d

0.00

2–0.

080.

1–0.

90.

001–

0.08

0.00

1–0.

02H

air 0

.005

–0.0

1



Tab

le 2

.6

Tox

ic a

nd L

eth

al C

once

ntra

tion

s of

Com

mon

Met

als

Met

alTo

xic B

lood

(m

g/L)

Bloo

d (m

g/L)

Live

r (m

g/kg

)K

idne

y (m

g/kg

)Br

ain

(mg/

kg)

Sple

en

(mg/

kg)

Lung

(m

g/kg

)H

air

(mg/

kg)

Oth

er

(m

g/kg

)

Alu

min

um0.

02–0

.20.

4–24

5–90

3–32

1–5

Bone

1–3

0A

ntim

ony

0.05

–210

4.6

4532

66

6C

ardi

ac m

uscl

e 4

Ars

enic

0.02

–30.

1–10

2–40

00.

2–10

00.

2–20

0.5–

200

10–2

00N

ail 5

0–67

Skel

etal

mus

cle

12Ba

rium

0.3–

270.

2–23

2–14

17–

162

0.4–

3123

–26

15–2

4V

itreo

us 2

6–50

Car

diac

mus

cle

17–2

2Bi

smut

h0.

05–2

1–10

03–

25C

adm

ium

0.01

–0.0

50.

1–1

11–2

0070

–598

00.

5–3

1–4

Hea

rt 8

–12

Cop

per

1–13

2–74

8–14

109–

611–

11Ir

on3–

262–

50a

1504

982

483

Lead

0.1–

61–

58–

348–

247–

74Bo

ne 2

–268

0Li

thiu

mSe

e pa

ge 1

24M

ercu

ry0.

05–6

0.2–

121–

217

2–28

41–

351–

100

3–23

400–

1600

Car

diac

mus

cle

1–17

Thal

lium

0.05

–80.

2–11

1–54

1–37

2–55

0.5–

110

–14

Skel

etal

mus

cle

6–13

Car

diac

mus

cle

2–13

a Se

rum

conc

entr

atio

ns.



Lead• Associated with blood smear basophilic stippling.• Can cause Burton’s lines (thin blue lines along the gums at the dental

margin).• Causes hypochromic microcytic anemia.

Mercury• Previously used medicinally and as dental amalgam fillings.• Component of cinnabar pigment.• In fish, may be found in elevated concentrations.• Associated with acrodynia.• Is found in three forms: elemental, inorganic, and organic. Inorganic

forms of mercury are the most toxic.

Thallium• May also cause Mees line and alopecia.• Toxicity may be misdiagnosed as Guillain Barre syndrome.



Novel Psychoactive Substances

A novel psychoactive substance is a new term used to describe a large group of drugs that are meant to mimic the effects of more commonly known drugs such as amphtemaines, cocaine, opiates, or delta-9-tetrahydrocannabinol (THC). With many new identifications appearing monthly, the number of these drugs has grown significantly in recent years. Therapeutic, toxic, and/or lethal concentrations overlap, and drug interactions are not well known. Caution should be used when interpreting their potential role in deaths, taking into account the circumstances surrounding death.

Novel psychoactive substances can be sedating, stimulating, or halluci-nogenic compounds. The main classes of these drugs can be separated into synthetic cannabinoids, synthetic stimulants and hallucinogens, and syn-thetic opioids.

Synthetic Cannabinoids

Synthetic cannabinoids are a class of drugs manufactured to mimic the effects of delta-9-tetrahydrocannabinol, the active ingredient in marijuana. Similar to THC, synthetic cannabinoids bind to cannabinoid receptors. However, it is important to note that THC is a weak partial agonist at these receptors, while synthetic cannabinoids are full agonists. In addition, their affinity for the receptors is greatly increased allowing them to have increased adverse effects. Some adverse effects can include seizures, agitation, irritation, anxi-ety, confusion, paranoia, tachycardia, hypertension, chest pain, hypokale-mia, hallucinations, tremors, delusions, nausea, and vomiting.

In vitro stability of some synthetic cannabinoids has been shown to be short; therefore, it is best to keep samples frozen and test as soon as possible. There are hundreds of synthetic cannabinoids, and new drugs are developed regularly. Table 2.7 is a non-comprehensive list of some common synthetic cannabinoids that have been implicated in causing toxicities.

Synthetic Opioids

Synthetic opioids are a class of drugs that bind to opioid receptors, much like opiates (codeine, morphine) and semi-synthetic opioids (hydrocodone, oxyco-done) and as such, they cause pain relief and anesthesia. In addition to pain relief and anesthesia, much like other opiates and opioids, these drugs can cause sedation, respiratory depression, and drowsiness, which can lead to coma and death.

Table 2.8 is a non-comprehensive list of synthetic opioids that have been implicated in causing toxicities.



Table 2.8 Synthetic Opioids Implicated in Causing Toxicities

3-Methylfentanyl4-ANPP4-Fluorobutyrfentanyl4-Methoxy-butyryl fentanyl4-Methylphenethyl acetylfentanylα-ME fentanylAcetylfentanylAcrylfentanylAcryloylfentanylAH7921AlfentanylAlpha-methylfentanylBeta-hydroxythiofentanylButyrylfentanylCarfentanilCyclopropylfentanylDespropionyl fentanylFIBF (Para-Fluoro-Isobutyryl Fentanyl)

p-Fluorobutyrylfentanylp-FluorofentanylFuranylfentanylIsobutyryl fentanylMethoxyacetyl fentanylMT 45 (1-cyclohexyl-4-(1,2-diphenylethyl)piperazine)OcfentanylOrtho-fluorofentanylPara-fluorofentanylSufentanilTetrahydrofuranyl fentanylThiafentanilU-47700 (3,4-dichloro-N-[2-(dimethylamino)cyclohexyl]-N-methylbenzamide)

U-48800U-49900 (trans-3,4-dichloro-N-[2-(diethylamino)cyclohexyl]-N-methyl-benzamide)

U-50488 (rel-3,4-dichloro-N-methyl-N-[(1R,2R)-2- (1-pyrrolidinyl)cyclohexyl]-benzeneacetamide)

Valerylfentanyl

Table 2.7 Synthetic Cannabinoids Implicated in Causing Toxicities

5F-AB-0015F-ADB5F-ADBICA5F-ADB-PINACA5F-AMB5F-APICA5F-APINACA5F-MN-A85F-PB-22A-796260AB-CHMINACAABDICAAB-FUBINACAAB-PINACAADB-CHMINACA

ADB-FUBINACA

ADBICAADB-PINACAAF-AMBAM-1248AM-2201AM-2233AM-679AM-694AMBAMB-FUBINACA

APICAAPINACAAPP-CHMINACA

BB-22CP 47-,497CP-55,940

CUMYL-THPINACA

EG-2201FUB-144FUB-AKB-48FUB-AMBFUBIMINAFUB-JWH-018FUB-PB-22HU-210JWH-015JWH-018JWH-018-5-Chloropentyl

JWH-019JWH-022JWH-073JWH-081

JWH-122JWH-133JWH-200JWH-210JWH-250JWH-251JWH-260MAB-CHMINACA

MDMB-CHMCZCA

MDMB-CHMINACA

MDMB-FUBINACA

MDMB-CHMICA

MMB-CHMICA

MMB-CHMINACA

MN-18MN-25

MO-CHMINACANM-2201NNE1PB-22PX1/PX-1PX2/PX-2RCS-4RCS-4-C4RCS-8THJ-018THJ-2201UR-144WIN 55-212XLR-11



Synthetic Stimulants and Hallucinogens

Synthetic stimulants and hallucinogens mimic other more commonly known stimulants and hallucinogens such as methamphetamine, cocaine, and lyser-gic acid diethylamide (LSD). Similarly, they act on monoamines by inhibit-ing their transport and/or inducing their release. Synthetic stimulants are generally amphetamines, cathinones, tryptamines, phenethylamines, piper-azines, piperidines, or related substances. Some adverse effects can include tachycardia, restlessness, anxiety, agitation, hypertension, nausea, vomiting, and diarrhea among others.

In vitro stability of some synthetic drugs has been shown to be short, therefore, it is best to keep samples frozen and test as soon as possible. Table 2.9 includes non-comprehensive lists of some common synthetic stimulants and hallucinogens that have been implicated in causing toxicities.

Volatiles

Volatiles as a class of drugs are considered forensically when they are inten-tionally inhaled with the intent of obtaining psychoactive effects; they are also referred to as inhalants. Volatiles are commonly constituents of fuel gases, propellants, solvents, anesthetics, automotive fuels, refrigerants, paint thinner, glues, and dry-cleaning agents. These compounds most commonly include aromatic and halogenated hydrocarbons and fluorocarbons. They are known to be cardiotoxic and are associated with lethal arrhythmias; they can also cause death by oxygen exclusion.

Common volatile compounds include benzene, butane, carbon tetrachlo-ride, chloroform, diethyl ether, enflurane, ether, ethyl ether, fluothane, freon, gasoline, helium, isoflurane, methyl ether, nitrous oxide, oxybismethane, perchloroethylene, propane, tetrachloroethene, tetrafluoroethane, toluene, trichloroethylene, trichloroethane, trichloromethane, trifluoroethane, and xylene.

Volatiles are highly lipophilic, so in addition to blood, the brain is often a good secondary source. In fact, 1,1-difluoroethane has been detected in cerebral material approximately 50 hours after exposure and prolonged hospitalization.

Diagnosis of volatile or inhalant toxicity usually depends upon the circumstances of death and the presence of such a substance in the blood or tissue samples, regardless of concentration of the substance. However, concentrations in fatal cases have been reported and are described in Table 2.10.



Tab

le 2

.9

Synt

heti

c St

imu

lant

s an

d H

allu

cino

gen

s Im

plic

ated

in

Cau

sin

g T

oxic

itie

s

2 A

I (2-

Am

inoi

ndan

e)2

DPM

P (2

-Dip

heny

lmet

hylp

iper

idin

e)2

MA

PB (1

-(be

nzof

uran

-2-y

l)-N

-met

hylp

ropa

n-2-

amin

e)2

Met

hoxy

diph

enid

ine

2 M

ethy

l PPP

(2-m

ethy

l-alp

ha-p

yrro

lidin

opro

piop

heno

ne)

2 M

MC

(2-M

ethy

lmet

hcat

hino

ne)

25 B

NBO

Me

25 C

NBO

Me

25 H

NBO

Me

25 I

NBO

Me

2C B

(4-B

rom

o-2,

5-di

met

hoxy

phen

ethy

lam

ine)

2C B

FLY

(8-B

rom

o-2,

3,6,

7-te

trah

ydro

benz

o[1,

2-b:

4,5-

b′]d

ifura

n-4-

etha

nam

ine)

2C C

(2,5

-Dim

etho

xy-4

-chl

orop

hene

thyl

amin

e)2C

E (2

,5-D

imet

hoxy

-4-io

doph

enet

hyla

min

e)2C

H (2

,5-D

imet

hoxy

phen

ethy

lam

ine)

2C I

(2,5

-Dim

etho

xy-4

-iodo

phen

ethy

lam

ine)

2C N

(2,5

-Dim

etho

xy-4

-nitr

ophe

neth

ylam

ine)

2C P

(2,5

-Dim

etho

xy-4

-pro

pylp

hene

thyl

amin

e)2C

T (2

,5-D

imet

hoxy

-4-m

ethy

lthio

phen

ethy

lam

ine)

2C T

2 (2

,5-D

imet

hoxy

-4-e

thyl

thio

phen

ethy

lam

ine)

2C T

4 (2

,5-D

imet

hoxy

-4-is

opro

pylth

ioph

enet

hyla

min

e)2C

T7

(2,5

-Dim

etho

xy-4

-pro

pylth

ioph

enet

hyla

min

e)3

FMC

(3 F

luor

omet

hcat

hino

ne)

3 M

eO P

CP

(3-M

etho

xy-p

henc

yclid

ine)

3 M

MC

(3 M

ethy

lmet

hcat

hino

ne)

3,4

DM

MC

(3,4

Dim

ethy

lmet

hcat

hino

ne)

3,4

MD

PBP

(3,4

Met

hyle

nedi

oxy-

alph

a-py

rrol

idin

obut

ioph

enon

e)3,

4 M

DPV

(3,4

-Met

hyle

nedi

oxyp

yrov

aler

one)

4 C

AB

(4-C

hlor

ophe

nylis

obut

ylam

ine)

4 Fl

uoro

amph

etam

ine

4 M

BC (4

-Met

hylb

enzy

liden

e ca

mph

or)

4 M

EC (4

-Met

hyle

thca

thin

one)

4 M

eO P

CP

(4-M

etho

xyph

ency

clid

ine)

4 M

ethy

lam

phet

amin

e4

Met

hylth

ioam

phet

amin

e4

MPB

P (4

-Met

hyl-2

-pyr

rolid

inob

uryr

ophe

none

)4

MTA

(4-M

ethy

lthio

amph

eatm

ine)

4 O

H D

ET (4

-Hyd

roxy

die

thyl

tryp

tam

ine)

5 A

PDI (

5-(2

-Am

inop

ropy

l)-2,

3-di

hydr

o-1H

-inde

ne5

APB

(5-(

2-A

min

opro

pyl)b

enzo

fura

n)5

APD

B (5

-(2-

Am

inop

ropy

l)-2,

3-di

hydr

oben

zofu

ran)

5 IA

I (5-

Iodo

-2-a

min

oind

ane)

5 IT

(5-(

2-A

min

opro

pyl)i

ndol

e)5

MA

PB (5

-(2-

Met

hyla

min

opro

pyl)b

enzo

fura

n)5

MeO

AM

T (5

-Met

hoxy

-alp

ha-m

ethy

ltryp

tam

ine)

5 M

eO D

ALT

(N,N

-Dia

llyl-5

-Met

hoxy

tryp

tam

ine)

5 M

eO D

iPT

(5-M

etho

xy-N

,N-d

iisop

ropy

ltryp

tam

ine)

5 M

eO D

MT

(5-M

etho

xy-N

,N-d

imet

hyltr

ipta

min

e)5

MeO

MiP

T (5

-Met

hoxy

-N-m

ethy

l-N-is

opro

pyltr

ypta

min

e)6

APB

(6-(

2-A

min

opro

pyl)b

enzo

fura

n)6

IT (6

-(2-

Am

inop

ropy

l)ind

ole)

(Con

tinue

d)



Alp

ha P

BP (a

lpha

-Pyr

rolid

inob

utio

phen

one)

Alp

ha P

HP

(2-(

1-py

rrol

idin

yl)-

hexa

noph

enon

e)A

lpha

-PH

PP (a

lpha

-Pyr

rolid

inop

entio

phen

one)

Alp

ha P

PP (a

lpha

-pyr

rolid

inop

ropi

ophe

none

)A

lpha

PV

P (a

lpha

Pyr

rolo

dino

pent

ioph

enon

e)A

lpha

PV

T (a

lpha

-pyr

rolid

inop

entio

thio

phen

one)

AM

T (a

lpha

met

hyltr

ypta

min

e)BC

P (B

enoc

yclid

ine)

BDB

(Ben

zodi

oxol

e-5-

buta

nam

ine)

Brep

hedr

one

Brol

amfe

tam

ine

Brom

o dr

agon

FLY

Buph

edro

neBu

tylo

neBZ

P (B

enzy

lpip

eraz

ine)

Cat

hino

neD

2PM

(Dip

heny

l-2-p

yrro

lidin

emet

hano

l)D

BZP

(1,4

-Dib

enzy

lpip

eraz

ine)

DET

(N,N

-Die

thyl

tryp

tam

ine)

Dib

utyl

one

Dim

ethy

lcath

inon

eD

imet

hylo

neD

iPT

(N, N

-diis

opro

pyltr

ypta

min

e)

DM

A (2

,5 D

imet

hoxy

amph

etam

ine)

DM

AA

(Met

hylh

exan

amin

e)D

MT

(N, N

-Dim

ethy

ltryp

tam

ine)

DO

B (4

Bro

mo

2,5

dim

etho

xyam

phet

amin

e)D

OC

(4 C

hlor

o 2,

5 di

met

hoxy

amph

etam

ine)

DO

ET (2

,5 D

imet

hoxy

4 et

hylam

phet

amin

e)D

OI (

4 Io

do 2

,5-d

imet

hoxy

amph

etam

ine)

DO

M (2

,5 D

imet

hoxy

4 m

ethy

lamph

etam

ine)

DPT

(Dip

ropy

ltryp

tam

ine)

EEC

(Eth

ylet

hcat

hino

ne)

Esca

line

Ethc

athi

none

Ethy

lamph

etam

ine

Ethy

lcath

inon

eEt

hylet

hcat

hino

neEt

hylo

neEt

hylp

heni

date

Euty

lone

Fene

thyl

line

Flep

hedo

neFl

uoro

met

ham

phet

amin

eFM

C (F

luor

omet

hcat

hino

ne)

Tab

le 2

.9 (C

onti

nu

ed)

Synt

heti

c St

imu

lant

s an

d H

allu

cino

gen

s Im

plic

ated

in

Cau

sin

g T

oxic

itie

s

(Con

tinue

d)



MBD

B (N

-Met

hyl-1

,3-B

enzo

diox

olyl

buta

nam

ine)

MBZ

P (M

ethy

lben

zylp

iper

azin

e)m

CPP

(1-(

3-Ch

loro

phen

yl)p

iper

azin

e)M

DA

I (5,

6-M

ethy

lened

ioxy

2-am

inoi

ndan

e)M

DEA

(Met

hylen

edio

xyet

hylam

phet

amin

e)M

DPP

P (M

ethy

lened

ioxy

-alp

ha-p

yrro

lidin

opro

piop

heno

ne)

MeO

PP (1

-(4-

Met

hoxy

phen

yl)p

iper

azin

e)M

eOPP

P (4

-Met

hoxy

-alp

ha-p

yrro

lidin

opro

piop

heno

ne)

Mep

hedr

one

Mep

hent

erm

ine

Met

hcat

hino

neM

ethc

opro

pam

ine

Met

hedr

one

Met

hiop

ropa

min

eM

etho

xeta

min

eM

etho

xyam

phet

amin

eM

etho

xym

etha

mph

etam

ine

Met

hylo

neM

MC

(Met

hylm

ethc

athi

none

)M

PHP

(Met

hyl-a

lpha

-pyr

rolid

inoh

exan

ophe

none

)M

XE (M

etho

xeta

min

e)M

XP (M

etho

xphe

nidi

ne)

N-E

thyl

pent

ylon

eN

aphy

rone

NEB

(N-E

thyl

buph

edon

e)Pe

nted

rone

Pent

ylon

ePM

A (P

horb

ol 1

2-m

yrist

ate 1

3-ac

etat

e) P

MM

A

(par

a-M

etho

xym

etha

mph

etam

ine)

Pyro

valer

one

TFM

PP (1

-(m

-Trifl

uoro

met

hylp

heny

l)pip

eraz

ine)

TMA

(Trim

etho

xyam

phet

amin

e)W

IN 3

5428

(bet

a-C

arbo

met

hoxy

-3-b

eta-

(4-fl

uoro

phen

yl)tr

opan

e)

Tab

le 2

.9 (C

onti

nu

ed)

Synt

heti

c St

imu

lant

s an

d H

allu

cino

gen

s Im

plic

ated

in

Cau

sin

g T

oxic

itie

s



Tab

le 2

.10

Let

hal

Con

cent

rati

ons

of S

elec

ted

Vol

atil

e Su

bsta

nces

Vola

tile

Bloo

d (m

g/L)

Vitr

eous

(m

g/L)

Live

r (m

g/kg

)K

idne

y (m

g/kg

)Br

ain

(mg/

kg)

Lung

(m

g/kg

)A

dipo

se T

issue

(m

g/kg

)Sk

elet

al M

uscl

e (m

g/kg

)C

ardi

ac M

uscl

e (m

g/kg

)

Benz

ene

0.9–

120

2.6–

379

5.5–

7514

–179

2222

–120

Buta

ne0.

05–1

290.

5–14

70.

4–78

0.4–

288

0.03

–128

1.8–

234

5.4–

112

Car

bon

tetr

achl

orid

e57

–260

170

59–1

4215

017

5–24

339

–127

7178

–188

Chl

orof

orm

29–8

3426

–298

38–1

2421

–133

14–9

279

–128

Difl

uoro

etha

ne(F

reon

152

a)3.

2–38

02.

6–20

088

118

6023

6

Tric

hlor

o-flu

orom

etha

ne

(Fre

on 1

1)0.

6–63

45–7

450

61–1

0932

–149

407

Chl

orod

ifluo

ro-m

etha

ne

(Fre

on 2

2)26

–560

0.7–

14.

4–38

133

–75

2.8–

414

1.6–

80

Tric

hlor

o-tr

ifluo

roet

hane

(F

reon

113

)0.

4–32

2.9–

8147

60.

5–13

700.

05–3

.55.

48.

8

Prop

ane

0.2–

690.

3–33

0.2–

751–

128

0.2–

550.

9–12

760.

3–21

31.

7–34

Tolu

ene

(met

hyl-b

enze

ne)

1–11

43.

6–43

339

19–7

406.

6–10

012

63Tr

ichl

oro-

etha

ne0.

1–72

04.

9–22

02.

6–12

03.

2–12

301.

8–22

2.6–

49Tr

ichl

oro-

ethy

lene

1.1–

210

2.5–

747

12–7

832

–809

9.3–

21Xy

lene

(dim

ethy

l-ben

zene

)4.

9–11

03.

6–29

6.1–

197.

112



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B. Levine (Ed.), American Association for Clinical Chemistry, Washington, DC, pp. 345–353.

Dart RC (Ed). (2004). Section 10 Metals in Medical Toxicology (3rd ed.), Lippincott Williams & Wilkins, Philadelphia, PA, pp. 1387–1474.

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Documents

Special Drug Groups - routledge.com · Lidocaine 0.01–15 0.01–5.9 0.8 0.9–2.9 12–204 6.6–135 9–13 20 Mepivacaine 51–59 51–83 51 51 Table 2.3 Pharmacokinetic Parameters