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毒 物 与 吸 毒 Poisons and drug abuse Department of Forenxic Toxicology SHIZHONG BIAN. Intentional Poisoning* Advantages Gender Silent Male 46% Precise targeting Female 39% Depersonalized Unknown 16% Safe for attacker Profile Background Caucasian Public 71%

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slide1

毒 物 与 吸 毒

Poisons and drug abuse

Department of Forenxic Toxicology

SHIZHONG BIAN

slide2

Intentional Poisoning*

AdvantagesGender

Silent Male 46%

Precise targeting Female 39%

Depersonalized Unknown 16%

Safe for attacker

ProfileBackground

Caucasian Public 71%

Male Physician 8%

Average or above intelligence Political 4%

Underachiever Nurse 4%

Personality defect Other 5%

Cowardly, nonconfrontational Unknown 9%

Nonathletic

Neat and orderly, meticulous

Careful planner *Source: Criminal Poisoning (2000)

Loner J. H. Trestrail, Humana Press

slide3

Properties of Ideal Poison

Undetectable by senses

Soluble

Delayed effect

Easily obtained

Not traceable

Symptoms mimic actual disease

Chemically stable (?)

Undetectable by instrumentation

Potent

slide4

“The dose makes the poison”

Potencies of Poisons

Agent Lethal dose

Botulinum toxin 0.05 mg

Ricin 0.5 mg

Strychnine 100 mg

Sodium arsenite 200 mg

Sodium cyanide 250 mg

Thallium 1000 mg

NB: A dime is 2300 mg

slide5

Sources of Poisons

Commercial

Laboratories

Underground catalogs

Antique drug collections

Hobbies/natural sources (e.g., plants)

slide6

Pesticide Poisons of Note

Synthetic – Organophosphates

Carbamates

Paraquat

Fluroacetate (1080 bait)

Plant-derived – Oleander

Poison hemlock

Mushroom

Ricin

Atropine/belladonna

Nicotine

Strychnine

Cyanogenic glycosides

slide7
毒物与中毒的概念:某种物质进入机体后,通过化学或物理化学作用,使组织细胞结构发生改变、代谢或功能遭受损害,从而引起健康障碍、疾病或死亡者,称为中毒。凡在一定剂量时能引起中毒的各种物质,就称为毒物。毒物与中毒的概念:某种物质进入机体后,通过化学或物理化学作用,使组织细胞结构发生改变、代谢或功能遭受损害,从而引起健康障碍、疾病或死亡者,称为中毒。凡在一定剂量时能引起中毒的各种物质,就称为毒物。
  • 毒物与药物不能机械地划分。
  • 毒物广泛分布于人的周围环境中。
  • 毒物的概念只是相对的,没有在任何条件下都可产生毒性作用的毒物。食盐一次服用15~60克即有碍于健康,一次用至200~250克,可因其吸水作用和所致的离子平衡障碍引起死亡。
slide8
毒物的分类:毒物的种类繁多,目前尚无一个完善的分类法。为了法医学鉴定中毒的需要,在分析中毒症状病理变化时,宜采用按毒理作用分类;在作法医化学分析时则采用按毒物的化学性质分类;为追溯毒物来源,则可采用按毒物用途、来源和作用混合分类。毒物的分类:毒物的种类繁多,目前尚无一个完善的分类法。为了法医学鉴定中毒的需要,在分析中毒症状病理变化时,宜采用按毒理作用分类;在作法医化学分析时则采用按毒物的化学性质分类;为追溯毒物来源,则可采用按毒物用途、来源和作用混合分类。
slide9
按毒物的化学性质分类

1.挥发性毒物 氰化物、醇、有机磷农药

2.非挥发性毒物 巴比妥类催眠药、吗啡

3.金属毒物 砷、汞、钡、铬、锌

4.阴离子毒物 强酸、强碱、亚硝酸盐

5.其他毒物 煎毒碱、CO、硫化氢

slide10
按毒理作用分类

1、腐蚀毒 强酸、强碱、酚类

2、实质毒 砷、汞

3、酶系毒 有机磷、氰化物

4、血液毒 CO、亚硝酸盐及某些蛇毒等

5、神经毒 醇类、麻醉药、催眠药、士的宁、烟碱等抑制或兴奋中枢神经的药物。

slide11
混合分类法

1、腐蚀性毒物

2、毁坏性毒物(即实质毒)

3、障碍功能的毒物

4、农药

5、杀鼠剂 敌鼠钠、安妥等

6、有毒植物 乌头、钩吻等

7、有毒动物 蛇毒、河豚、斑蝥等

slide12
中毒发生的条件

1、毒物的量。中毒量;致死量(g/kg体重)

2、毒物的性状。气态;液态;固态。

3、毒物进入机体的途径。心脏或血管内注射>呼吸道吸入>腹腔注射>肌肉注射>皮下注射>口服>直肠灌注。

4、毒物的协同作用与拮抗作用。

5、机体状态。体重;年龄;性别;健康状态;习惯性或成瘾性;过敏性;体内蓄积。

6、其他。

slide13
毒物的转运、转化及其法医学意义

1、吸收。消化道;呼吸道;皮肤吸收;注射吸收。

2、分布。毒物在体内的分布并非均匀。

3、代谢。氧化;还原;水解;结合。

4、排泄。肾;胆道;其他(上皮、皮脂腺、唾液腺、乳腺、消化液)。

slide14
中毒的法医学鉴定
  • 案情调查
  • 症状分析
  • 现场勘验
  • 尸体检查
  • 检材采取
  • 毒物分析结果的评价
  • 中毒尸体挖掘取材的价值
slide15

Poison plants readily available from

nurseries, arboreta, backyards, wild areas

Foxglove Datura Oleander Autumn Poison Lantana Ricinus communis

purpurea crocus hemlock (Castor bean)

digitalis atropine cardiaccolchicine coniine lantadene ricin

glycosides

Not visible: Lupine (lupanine)

slide16

Top 5 Homicidal Poisons

Agent Frequency Target

Arsenic 31% Energy generation

Cyanide 9% “

Strychnine 6% Nervous system

Morphine 3% “

Chloroform 2% “

slide17

Analysis

Evidence in vicinity of victim

Pill bottle, drug paraphernalia

Food, beverage leftovers

Symptoms

Acute

Chronic

Sampling

Organs, fluids

Accessory material

Detection

Analytical instrumentation

HPLC, GC, Mass Spec

Motivation

Love, money, power

Disguised as random

slide18

Poison Symptoms

Constricted/dilated pupils (opioids, organophosphates)

Breath odor (arsenic – garlic)

Hair loss (thallium)

Convulsions (strychnine)

Paralysis (botulism)

Coma (depressants, hypnotics)

Skin color (CO – cherry red; nitrites – blue)

Skin appearance (arsenic – hyperkeratosis, warts)

(dioxin – chloracne)

slide20

TCDD (dioxin) – Chloracne

Poisoning of Victor Yushchenko just before Ukraine presidential election

slide21

Dioxin (TCDD) Sensitivities

Species LD50(µg/kg)

Guinea pig 2

Rat 40

Monkey 50

Human ?

Mouse 130

Rabbit 200

Hamster 4000

slide22

Autopsy samples

Organs (brain, liver, kidney, muscle)

Blood (heart, peripheral)

Vitreous humor

Bile (insoluble metabolites)

Urine (soluble)

Gastric contents (alkaloids)

Hair

Bone

Maggots

slide23

Environmental/Accidental Contamination

Differential diagnosis

Accidental death or homicide?

Compensable injury or carelessness?

Background that could confound interpretation

Verify authenticity/natural source or show adulteration

How did the mass poisoning occur?

Substitution of inferior/contaminated component?

Track source of environmental contamination

Environmental justice for underserved?

Safeguards not enforced

Children often victims

Which companies are breaking the law?

slide24

Marine Toxins in Food

Pufferfish

Delicacy in Japanese restaurants

Gives tingling of lips when properly prepared

Tetrodotoxin concentrated in liver and ovary (removed)

Blocks sodium channel in nerves

Fatal in excess (lethal dose 1 mg)

Shellfish Tainted by Red Tide (3 examples)

Saxitoxin – Paralytic shellfish poison (blocks sodium channel), potentially fatal

Domoic acid – Amnesic shellfish poison (glutamate neurotransmitter analog)

Disorientation, loss of short term memory at moderate doses

Fatal excitotoxin activity at higher doses

Okadaic acid – Diarrhetic shellfish poison (phosphatase inhibitor), nonfatal

Harmful Algal Blooms

Thought increasing due to coastal pollution, ocean warming

Of 4,400 known algal species, >1% produce toxins

Known causes of wildlife epidemics

Marine mammal mortality off California coast from domoic acid

slide25

Accidental Food Contamination

Iraq 1972:5-6,000 people hospitalized, 10% died.

Seed grain donated with methyl mercury antifungal agent.

Distributed 100,000 tons to farmers, improperly identified.

Grain (wheat, barley) mistakenly used to make bread.

Michigan 1973:Nearly 2 million livestock destroyed.

Several hundred pounds PBBs mixed with dairy feed.

Coverup by company and state officials compounded problem.

Spain 1981: 11,000 people hospitalized, >500 died.

Industrial rapeseed oil from France containing aniline refined.

Refining process produced toxic components.

Resold fraudulently as cooking oil (59 tons) after mixing olive oil.

Adulturation of vegetable oils (soybean/canola in olive) frequent.

Biochemical components becoming available for detection.

slide26

Commercial Activity - Mercury

A woman holds a victim of

"Minamata Disease", or mercury

poisoning, in Minamata, Japan,

in 1973. The girl has a malformed

hand, like many victims of the

disease who suffer from physical

deformities and mental retardation.

Chisso Corporation, a Japanese

fertilizer, petrochemical and

plastics company, dumped an

estimated 27 tons of mercury

compounds into Minamata Bay

between 1932 and 1968. Up to

10,000 people were affected by

eating seafood from the bay.

Many sources of mercury exist, either natural (fish) or associated with

human activity (chloralkali plants, gold mines, effluent from power plants).

Elemental form is methylated by micro-organisms in the environment.

slide27

Commercial Activity - Lead

Targets: Blood cells (anemia), kidney (gout), sperm (infertility)

Nervous system most sensitive target

Adults: Occupational exposures

Lead smelters, battery factories, lead additives

Painters got peripheral neuropathy (wrist drop)

Children: Colic (acute) and mental retardation (chronic)

Legacy of leaded paint and gasoline

• Eating peeling paint (many inner cities)

• Playing in contaminated yards (e.g., Oakland)

slide28

Commercial activity – Acrylamide

Sweden 1997: Hallandsas tunnel construction halted.

Acrylamide used in grouting to prevent water seepage.

20 workers experienced neurological symptoms (reversible).

Several cows grazing nearby showed severe neural effects.

Dead fish found in hatchery supplied by water from tunnel.

Acrylamide found in ground water near tunnel.

Sensitive methods developed to detect acrylamide showed

high background levels in humans.

Surprisingly high levels found in fried foods (potato chips).

Potential exposures in typical labs using acrylamide gels

(including DNA identification labs).

slide29

Intracellular Targets of Neurotoxins

Ion channels – Signal conduction

Sodium

Potassium

Calcium

Chloride

Synaptic region – Neurotransmitter processing

Release

Reuptake of excess

Receptor response (stimulate, block)

Channels and receptors - multigene families

Located in different parts of the nervous system

Responsible for differential effects

slide30

Uses of Amphetamines and Derivatives

Treatment for narcolepsy - 1930’s

Maintaining military alertness - 1940’s

Occupational alertness (students, truckers) – 1950’s

Appetite suppressant

Suppress childhood attention deficit disorder

Dietary supplement (ephedrine) as “natural energizer”

opioid analgesics
Opioid Analgesics
  • Background
  • Pharmacokinetics
  • Pharmacodynamics
  • Tolerance and Dependence
  • Side Effects and Toxicity
  • Pharmacotherapy
opioids background
Opioids:Background
  • Poppy (Papaver somniferum)
  • Morphine isolated in 1803 (“Morpheus”)
    • German chemist, Serturner
  • Codeine isolated by accident in 1830s
    • French chemist, Robiquet
opioids background1
Opioids:Background
  • Heroin
    • made from morphine, 1898, Bayer Co.
    • advertised as having all benefits, none of liabilities of morphine and codeine
opioids background2
Opioids:Background
  • Harrison Narcotics Act of 1914
  • 1924, Heroin added
  • Current Use levels: illicit
morphine heroin pharmacokinetics
Morphine/Heroin:Pharmacokinetics
  • Absorption
    • routes of administration
    • physical properties: base; poor lipid solubility (except heroin)
    • peak absorption rapid via IV and inhalation
morphine heroin pharmacokinetics1
Morphine/Heroin:Pharmacokinetics
  • Distribution
    • lungs, liver, spleen
    • blood protein binding
    • pass placental barrier
    • difficulty passing blood/brain barrier
    • active system pumps opiates out of brain
    • Heroin is very lipid soluable--exception
morphine heroin pharmacokinetics2
Morphine/Heroin:Pharmacokinetics
  • Inactivation
    • Metabolism
      • Heroin metabolized to monoacetylmorphine, then to morphine in brain
      • Morphine metabolized by conjugation; P450 enzymes in liver
      • Morphine 1/2 life is 2 hours
    • Elimination
      • 4 hours 1/2 life
morphine heroin pharmacodynamics
Morphine/Heroin:Pharmacodynamics
  • Cellular sites and mechanism(s) of action
    • 1973, opioid receptors discovered
    • Mu, Epsilon, Delta, Kappa
    • Mu receptors are metabotropic:
      • activation enhances flow of K+ out of cell and/or decreases activity of voltage-sensitive Ca++
morphine heroin pharmacodynamics1
Morphine/Heroin:Pharmacodynamics
  • Brain sites of action
    • Medulla
    • Basal ganglia
    • Hippocampus
    • Amygdala
    • hypothalamus
morphine heroin pharmacodynamics2
Morphine/Heroin:Pharmacodynamics
  • Brain sites of action (cont.)
    • Periaqueductal grey
    • locus coeruleus
    • Frontal cortex
    • Inhibitory interneurons in VTA (GABAr)
morphine heroin tolerance and dependence
Morphine/Heroin: Tolerance and Dependence
  • Tolerance
    • Fastest to euphoric and analgesic effects
      • 40-50x non-tolerant dose
    • Cellular/Pharmacodynamic (not metabolic)
      • decreased receptor sensitivity
morphine heroin tolerance and dependence1
Morphine/Heroin: Tolerance and Dependence
  • Dependence
    • Withdrawal peaks at 2-3 days
    • Naloxone test for dependence
    • Seldom life-threatening, “flu-like”
    • Methadone treatment of withdrawal
morphine heroin side effects and toxicity
Morphine/Heroin: Side Effects and Toxicity
  • Lethality
    • lowers seizure threshold
    • tolerance to desired v. lethal effects
    • life style v. direct effect of drug
morphine heroin pharmacological treatment
Morphine/Heroin: Pharmacological Treatment
  • Methadone maintenance
  • Naltrexone/Naloxone
  • Buprenorphine
  • Rapid detoxification