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Tox 2 midter, > midterm > Flashcards

midterm Flashcards

1
Q

what are the most accessible tissues to measure exposure to metals?

A

Blood (recent, acute exposure)

Urine (recent, acute exposure)

Hair (not reliable – external contamination complicates analyses)

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2
Q

what are the best targets of metal toxicity ?

A

Metal binding proteins
namely enzymes

metals can also bind to non specific proteins

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3
Q

what are metallothioneins?

A

Many have no known enzymatic activity

May be involved in de-toxification of metals

Have high affinity for several essential and non-essential metals, such as Cd, Cu, Hg, Ag, and Zn

Transferrin: binds ferric iron in plasma

Ferritin: iron-storage protein in liver, spleen, and bone

Ceruloplasmin: converts plasma ferrous iron to ferric iron (to bind to transferrin)

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4
Q

what are two common types of transporters

A

Phosphate and sulfate transporters

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5
Q

what is chelation therapy

A

Chelation: metal ion binds to ligand with two donor atoms to form ring-structure

Metals may react with OH, COOH, SH, NH2, NH, and N

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6
Q

Metal plus ligand equals

A

complexation

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7
Q

what do chelating agents have to be ?

A

Characteristics of chelating agents

Water soluble

Resistant to biotransformation

Able to reach sites of metal storage

Capable of forming nontoxic complexes with toxic metals

Capable of being excreted

Have low affinity for essential metals

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8
Q

What is BAL

A

BAL (British Anti-Lewisite)
(2,3-dimercaptopropanol)

Developed during WWII as a specific antagonist to arsenical war gases

Based on observation that arsenic has affinity for sulfhydryl-containing substances

Also effective against mercury, cadmium, chromium, etc.

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9
Q

where is arsenic usually found

A

Commonly found in
Drinking water
Seafood
Pressure-treated wood
Cigarette smoke

Common exposure from
Pesticide and herbicide manufacturers
Smelting industries

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10
Q

where is arsenic released form and what is its mechanisms of toxicity?

A

Arsenic inhibits succinic dehydrogenase and uncouples oxidative phosphorylation
Leads to stimulation of mitochondrial ATPase activity

Arsenic inhibits the energy-linked functions of mitochondria in two ways

Competition with phosphate during oxidative phosphorylation

Inhibition of energy–linked reduction of NAD

Leads to decreased ATP production and increased H2O2

Leads to oxidative stress through ROS

Inorganic arsenic is released into the environment from
Copper, zinc, and lead smelters
Glass manufacturers
Chemical manufacturers

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11
Q

what are symptoms of arsenic

A

Neurotoxicity of PNS and CNS

Neurotoxicity begins with paresthesia and muscle tenderness

Neuropathy may affect sensory and motor neurons

Eventual demyelination of axon nerve fibers

Liver injury may also manifest as jaundice and may progress to cirrhosis

Reproductive and teratogenic effects
Malformation of fetus in animals
Effects have not been observed in humans with excessive occupational exposure

Carcinogenicity
Studies indicate cancer incidence in response to ingestion and inhalation

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12
Q

what is cadmium used for and what is the exposure like

A

Used in (as)
Electroplating, galvanizing, battery production
Non-corrosive
Pigment in paints and plastics

Exposure
Plants readily take up Cd from contaminated soil, water, and fertilizers

Enter food chain and can contaminate meats, fruit, and fish

Shellfish accumulate cadmium

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13
Q

what does acute and chronic cadmium toxicity look like?

A

Chronic toxicity
Chronic pulmonary disease (respiratory exposure)
Emphysema (respiratory exposure)
Renal tubular disease
Skeletal system problems (Cd may affect calcium metabolism)

Nephrotoxicity
Cd toxic to renal tubular cells and glomeruli (binds to sulfhydryl groups of critical proteins) and leads to proteinuria

Metallothioneins in kidney can bind cadmium – nontoxic
Toxicity may occur when systems become overwhelmed

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14
Q

Describe Lead and its exposure

A

Toxic metal detectable in practically all phases of the inert environment and all biological systems

Exposure
Food and drinking water
Lead-based indoor paint
Air (industrial emissions)

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15
Q

what are primary effects of lead in children?

A

Neurologic, neurobehavioral, and developmental effects in children

Vomiting
Lethargy
Ataxia
Encephalopathy
Coma
Death

Toxicity may manifest itself over time in children
Decreased attention span
Reading disabilities

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16
Q

what are common lead mechanisms of effect on the developing nervous system

A

Pb exposure results in modification of neuronal circuitry
-Alterations in noradrenaline, dopamine, and acetylcholine concentrations
-Impairs calcium homeostasis, calcium and NT concentrations play a role in frequency and sensitivity of nerve firing

Lead-induced peripheral neuropathy
Axonal degeneration
Schwann cell degeneration

Lead-induced hematologic effects
Lead-induced anemia
Pb affects heme synthesis

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17
Q

where does mercury exposure come from

A

Natural degassing of the earth’s crust (vapor) and pollution

this is how it gets into octane, the in gets methylated and accumulates in small fish, then get bio concentrated into larger fish, where we eat it

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18
Q

what are effects of mercury vapor toxicity?

A

Mercury vapor toxicity
Acute, corrosive bronchitis
CNS effects (tremors)
Memory loss
Gingivitis
Hg follow calcium pathways into saliva, reacts with bacteria resulting in a precipitate
Delirium
Hallucination

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19
Q

what are the effects of methylmercury toxicity ?

A

Major source of exposure is fish consumption

Symptoms include
Numbness
Ataxia (clumsy, stumbling gait)
Weakness
Vision/hearing loss
Tremors
Coma
Death
Disrupts protein synthesis, creates ROS

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20
Q

what is nickel

A

Ubiquitous in nature
Exposure may occur via inhalation, ingestion or through dermal contact
Exposure can also occur through food, jewelry, and cooking utensils

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21
Q

what does nickel toxicity look like?

A

Toxicity
Carcinogen (can cause cross-linking of DNA)
Allergen
Respiratory tract cancers in factory workers exposed to nickel sulfides and nickel oxides
Ni accounts for 4-9% of allergic dermatitis
Jewelry

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22
Q

Describe copper exposure and toxicity and what disease it can cause

A

Exposure
Drinking water
Food

Toxicity
Nausea
Hepatic necrosis
Death

wilsons disease
Accumulation of copper in liver, brain, kidneys
Due to inability to excrete copper (billiary)

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23
Q

what does iron do, and what are the effects of acute and chronic toxicity

A

Iron homeostasis very complex
Hemoglobin
Iron increases lipid peroxidation

Acute toxicity
Overdose
Vomiting
Liver damage
Coagulation defects
Renal failure

Chronic toxicity
Hereditary
Abnormal absorption from GIT
Excess Fe in diet

Effects
Liver dysfunction
Cardiovascular effects

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24
Q

what does zinc do and what can it cause

A

Approx. 200 enzymes require Zn as a cofactor
Zinc fingers (Zn + His) allow proteins to interact with DNA, hormone receptors and membranes
Excessive exposure to zinc is uncommon

Exposure
Seafood
Meat
Dairy Products
Legumes

Toxicity
GI distress

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25
Q

what is the function of a pesticide

A

The function of a pesticide is to kill or harm some form of life

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26
Q

Describe insecticides and the classes of insecticides?

A

All of the chemical insecticides in use today are neurotoxicants and they act by poisoning the nervous system of target (also non-target) organisms.

Classes of Insecticides:
Organochlorine Insecticides
Organophosphate/Carbamate Insecticides
Pyrethroid Insecticides

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27
Q

what are the 4 types of organochlorine insecticides

A

dichlorodiphenylethanes (e.g. DDT)
chlorinated cyclodienes (e.g. Endrin)
chlorinated cyclohexanes (e.g. lindane)
Chlordecone (e.g. kepone)

the organochlorineare chlorinated hydrocarbons

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28
Q

what are the properties of organochlorines that make them good insecticides

A

Properties which made them good insecticides:

low volatility
chemical stability
lipid solubility
slow rate of biotransformation and degradation

These properties also led to their demise because of their persistence in the environment, bioaccumulation, and biomagnification through the food chains.

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29
Q

what is kepone different thant DDT

A

Chronic exposure with kepone can cause impairment of spermatogenesis and epileptic convulsion, and skin rashes

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30
Q

what happens to the skin from organochlorine exposure

A

Patch test develops hyperpigmentation in 15-20% of subjects tested with dienochlor - resembles reaction to Balsam of Peru

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31
Q

what are DDT type pesticides mechanism

A

periodic sequences of persistent tremoring and/or convulsive seizures suggestive of repetitive discharges in neurons.

these tremors, seizures can be initiated by tactile and auditory stimuli, indicating that the sensory nervous system appears to be much more responsive to stimuli.

There is a characteristic prolongation of the falling phase of the action potential. The nerve membrane remains in a partially depolarized state and is extremely sensitive to complete depolarization again by very small stimuli.

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32
Q

why does DDT cause prolonged repolarization?

A

1) DDT affects the permeability of the nerve cell membrane to K+ ions reducing K+ transport across the membrane.

(2) DDT alters the Na+ channels, they open normally but are closed (inactivated) slowly.

(3) DDT inhibits neuronal ATPase activity particularly Na/K ATPase and Ca ATPase which play a role in repolarization of the neuron.

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33
Q

what is the function of chrloridinated cyclodine insecticide

A

These insecticides act in the CNS.
(1) Mimic the action of the chemical picrotoxin, a nerve excitant and antagonist of the neurotransmitter GABA found in the CNS.

GABA induces the uptake of chloride ions by neurons.

The blockage of this uptake results in only partial repolarization of the neuron and a state of uncontrolled excitation.

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34
Q

how is DDT broken down?

A

Very slow rate for DDT due to complex aromatic ring structure and chlorination. Half-life is 335 days in cattle.

DDT broken down to DDE both nonenzymatically and by cytochrome P450 reductive dechlorination. All metabolites are highly lipophilic.

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35
Q

what happens to aldrin and hepatchlor when metabolized

A

Aldrin and Heptachlor are converted by cytochrome P450 oxidation reactions to dieldrin and heptachlor epoxide without a change in lipid solubility or toxicity.

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36
Q

what can be given to control the convulsions ?

A

In addition to decontamination and supportive treatment, diazepam or phenobarbital may be administered to control the convulsions

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37
Q

what is the mechanism of action of organophosphate and carbamate insecticides

A

Both organophosphate and carbamate insecticides act by inhibiting the action of acetylcholinesterase (AchEase) at the synapse between two neurons or between a motor neuron and a muscle.

AChEase is the enzyme responsible for the breakdown of the neurotransmitter acetylcholine (ACh).

Organophosphate compounds are irreversible inhibitors of AChEase while carbamate compounds are reversible inhibitors of AChEase.

organophosphates cause damage that is irreversible

The reaction between an organophosphate and the active site on AChEase (a serine hydroxyl group) results in the formation of an intermediate that undergoes partial hydroylsis with the loss of the “Z” group, leaving a stable, phosphorylated, permanently inhibited enzyme.

Signs and symptoms are prolonged and persistent. Without intervention, the toxicity will persist until sufficient amounts of “new” AChEase are synthesized in 20 to 30 days

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38
Q

What are the ways to manage cholinesterase inhibitor poisoning ?

A

Collect serum, urine, & clothing samples

Hospitalize for severe symptoms

Specific treatment
Atropine
Pralidoxime (2-PAM)–OPs only

Workplace restrictions

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39
Q

What does Atropine do ?

A

Reverses SLUD, DUMBELS syndrome

Intravenous dose:
-Diagnostic
1 mg adult
0.01 mg/kg pediatric

-Therapeutic
1 mg - 4 mg adult
0.05 mg/kg pediatric
Repeat every 10-30 minutes

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40
Q

What does Pralidoxime do ?

A

(2Pam)

Enzyme aging occurs if not treated
Treatment effective within 48 hours
2-PAM reactivates cholinesterase
Cholinesterase levels rise

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41
Q

Both insecticides undergo what mechnaisms

A

phase 1 and phase 2

One reaction, oxidative desulphuration, results in a significant increase in toxicity. In parathion, methyl parathion and malathion, the presence of the P = S reduces the AChEase inhibiting properties of the compound.

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42
Q

what are the health effects of pyrethroid insecticides?

A

Low systemic toxicity

Respiratory sensitization
Asthma

Skin reactions
-Paresthesia
-Allergic dermatitis

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43
Q

what are pyrethroid insecticides used for ?

A

Examples of use
-Structural & agricultural
-Pet flea control
-Pediculicide

Vector control
-West Nile virus
-Aircraft “disinsection”

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44
Q

what is the pyrethrins mechanism of toxicity ?

A

Prolong inactivation of nerve membrane sodium channels

Pyrethroid structure
Type I (non-cyano)
Shorter inactivation

Type II (alpha-cyano)
Longer inactivation

Type I pyrethroids affect Na+ channels in nerve membranes (both sensory and motor) and gives long afterpotential similar to DDT.

Type II pyrethroids cause persistent depolarization and prolonged repetitive firing of sensory receptors and muscle fibers.

Both types also inhibit Ca/Mg ATPase resulting in increased intracellular Ca++ levels and increased neurotransmitter release

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45
Q

Treatment for pyrethrin and pyrethroid illness ?

A

Decontamination
Vitamin E cream
Symptomatic therapy
Remove from further exposure if needed

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46
Q

what are the health effects of glyphosate

A

Health effects
Case reports of eye, skin irritation
Death due to ingestion of large amounts
Experimental studies fail to show skin irritation

Mechanism of human toxicity unknown
Surfactant preservative?

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47
Q

what are the two chlorophenoxy herbicides ?

A

2,4,5-trichlorophenoxyacetic acid (2,4,5-T)
Derived from tetrachlorobenzene
Dioxin byproducts

2,4-dichlorophenoxyacetic acid (2,4-D)
Derived from phenol
Dioxin contaminants not present

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48
Q

what does acute and chronic toxicity look like for chlorophenoxy herbicides?

A

Acute
CNS depression
Skin, GI, mucous membrane irritation
Renal failure, myopathy

Chronic
Anemia, hepatic, renal effects
Tumor formation(?)

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49
Q

what are types of fumingants

A

Halogenated hydrocarbons
-Methyl bromide
-Ethylene dibromide, DBCP

Inorganic compounds
-Sulfuryl fluoride

Pro-fumigants
-Metam sodium

Metal phosphides
-Aluminum, Zinc, Magnesium

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50
Q

what are the characteristics of methyl bromide

A

High vapor pressure
Heavier than air
Odorless
-Chloropicrin (tear gas) added
Toxic mechanism
-Tissue methylation

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51
Q

what are the characteristics of methyl bromide acute toxicity

A

Vesicant
-Blistering dermatitis
Lower respiratory toxicant
-Delayed pulmonary edema
Central nervous system depressant
-Usual cause of death

CNS depression
Other CNS depressants

Pulmonary edema
Hepatic & renal disease
Acute severe asthma

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52
Q

what are chronic toxicity of methyl bromide

A

Central nervous system
-Cognitive, behavioral effects
-Polyneuropathy

Reproductive system
-Teratogen
-Genotoxic, mutagenic

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53
Q

what symptoms do the sulfuryl fluoride do ?

A

-Pulmonary
—Dyspnea, cough, delayed pulmonary edema, fatal hypoxia
-Renal
CNS
—Weakness, nausea, vomiting, restlessness, muscle twitching, seizures

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54
Q

what does metam sodium do ?

A

Hydrolyzes to mixture of irritants

health effects
-Irritant dermatitis
-Reactive airways dysfunction syndrome/asthma

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55
Q

what do phosphide compounds do and what are their characteristics ?

A

Metal phosphides hydrolyze
Aluminum, zinc, magnesium

Phosphine
Colorless, fish/garlic odor
Highly explosive, corrosive
Rapidly oxidizes to phosphoric acid

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56
Q

what are types of fungicides

A

Thiocarbamates
-Zineb, maneb, ziram, thiram

Pthalimide derivatives
-Captan, captafol,

Substituted aromatics
Chlorothalonil, hexachlorobenzene
Inorganic
Sulfur

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57
Q

what are health effects of fungicides

A

Acute
Irritant & allergic dermatitis

Chronic
Chronic dermatitis
Possible carcinogens

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58
Q

Thiocarbamates resemble what

A

Resemble rubber accelerator thiuram

Sensitization reported in exposed workers

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59
Q

what does chlorothalonil do

A

Fungicide- substituted aromatic
Blue-gray pigmentation in antecubital area
Positive skin reaction to chlorothalonil
Diagnosis: Ashy dermatitis
-Disruption of basal membrane of epidermis
Melanin deposits in dermis

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60
Q

Elemental sulfur

A

fungicide

Potent skin irritant
-Animal experiments equivocal

Airway irritant

61
Q

types of rodenticides

A

Botanicals
Red squill – effects heart
Strychnine – blocks glycine receptors in spinal cord - convulsions

Inorganics
Phosphorous – GI track
Thallium – hair loss, nervous system
Zinc phosphide – GI track

Anticoagulants
Warfarin – inhibits blood clotting
Vacor – newer blood clot inhibitors

62
Q

what is toxinology?

A

Specialized area of toxicology that deals specifically with animal, plant, and microbial toxins

The science of toxic substances produced by or accumulated in living organisms, their properties and their biological significance for the organisms involved

63
Q

what is a poison

A

Any agent capable of producing an adverse response in a biological system

64
Q

difference between poisonous animals vs venomous animals

A

Poisonous Animals
Animals whose tissues, either in part or in their entirety, are toxic
No mechanism or structure for delivery of their poisons

Venomous Animals
Animals that are capable of producing a poison in highly developed glands
Toxin can be delivered during a biting or stinging act

65
Q

venom contains

A

Proteins
Amines
Lipids
Steroids
Free amino acids
Histamine
Phospholipases
Etc.

66
Q

what are the problems with venom analysis

A

Venom must be “taken apart” to look at components
Quality of venom may be destroyed
Interplay between various components may be lost

67
Q

bioavailability of venoms is determined by

A

Determined by:
Composition
Molecular size
Amount or concentration gradient
Solubility
Degree of ionization
Rate of blood flow to exposed tissue
Site of exposure (or route of exposure!)
Is venom injected?

68
Q

what are the 4 ways venom absorption happens

A

Injection (possible IV injection!)
Active transport
Facilitated diffusion
Pinocytosis

69
Q

describe the action of venom

A

Tissue destruction

Receptor-mediated toxicity
-Receptors have highly variable degrees of sensitivity
-Complex venoms may affect many receptor types (or even sub-types)

70
Q

what are factors affecting distribution of venom

A

Protein binding
Variations in pH
Membrane permeability
Rate of blood flow to a particular site
Etc.

71
Q

what are arthropods

A

Insects, crustaceans, arachnids (scorpions, spiders), and myriapods (centipedes) that are characterized by a chitinous exoskeleton and a segmented body to which jointed appendages are articulated in pairs

More than one million species

All are not significantly venomous

Most don’t have fangs or stingers long or strong enough to penetrate human skin

72
Q

what are the signs and symptoms of scorpion envenomation?

A

Signs and symptoms of scorpion envenomation

Localized pain
Swelling
Mild paresthesia
Tachycardia and hypertension
Rare systemic reactions including fever and muscle fasciculations in adults
Systemic reactions in children more common; lead to motor weakness and respiratory paralysis
Symptoms often resolve in 12-36 hours

73
Q

What is spiders name scientific and what does the venom do

A

Latrodectus (Widow spiders)

Found worldwide in temperate and tropical climates
Only female has fangs large enough to penetrate human skin

Venom affects neurotransmitter release

74
Q

what does latrodectus venom contain

A

latrotoxins

Major latrotoxin is a presynaptic toxin which depolarizes neurons by increasing [Ca2+]i

Stimulates exocytosis of neurotransmitter at nerve terminals

75
Q

how do latrodectus bites look like

A

Clinical symptoms include numbing pain in affected extremity
Pain, cramping, and rigidity in large muscle masses
Local skin reactions rare
Muscle fasciculations
Rarely fatal

76
Q

Describe Loxosceles bites

A

Initial sting
Burning sensation at bite site
Swelling and redness in mild bites
Serious bite cases exhibit hemorrhage, blistering, pustule formation, necrosis
Systemic effects may include fever, nausea, hematuria
Rarely fatal

77
Q

What are ticks and what disease do they cause?

A

type of arachnida

Saliva is toxic

Microbacterial organisms transmitted by ticks

Rocky Mountain spotted fever, typhus, tick-borne encephalitis, Lyme disease

78
Q

what is lyme disease caused by, and what happens during lyme disease

A

Caused by bacterium Borrelia burgdorferi

The action of Borrelia toxin is to prevent, through its action as a proteolytic enzyme, the release of the neurotransmitter acetylcholine

Bite symptoms include fever, headache, fatigue, and a characteristic circular skin rash at bite site

If left untreated, infection can spread to joints, lymph nodes, the heart, and the nervous system

If caught early, antibiotic therapy is often successful

79
Q

what are chilopoda

A

Centipedes

Found worldwide
First pair of legs are modified poison jaws
Venom contains proteinases, esterases, histamine, etc.
Venom causes redness and swelling
Necrosis rare

80
Q

what is teh scientific name of caterpillars

A

lepidoptera

Most possess urticating hairs (setae) which are attached to unicellular poison glands at the base of each hair
In most cases, itching and redness subside shortly

81
Q

what are fire ants name and what do their venoms do

A

Formicidae (Ants)

Solenopsis (Fire ants) are clinically important
Native to S. America and Southern US

Venom contains formic acid, and alkaloids

Stings give rise to intense burning, swelling, pustule formation, and necrosis

Severe envenomations may result in respiratory difficulties and rarely death

82
Q

what are bees name and what do their venom contain

A

Apidae (Bees)
Venom contains phopholipase A, histamine, etc.

83
Q

what are true bugs and what do their venom contain

A

insecta

Heteroptera (True bugs)
Six legs, most have wings
Venom has protease function (digestive enzymes)
Some bugs have no mechanism to deliver their venom and are therefore poisonous!
Envenomation usually very mild

84
Q

what are poison arrow frogs

A

amphibians

they are classified and dendrobates and phyllobates

85
Q

Describe the arrow frogs poison

A

Batrachotoxin
Arguably the most toxic naturally produced poison

Steroidal alkaloid with high specificity for certain nerve structures in the peripheral nervous system

Sodium channel blocker
-Locks the channel in the open position

Results in constant stimulation and release of acetylcholine

-Muscles contract and are unable to relax

Death may result from respiratory paralysis

86
Q

what is a heloderma suspectum and what is the venom like

A

Gila monster

Venom contains phospholipases as well as proteolytic and hyaluronidase activities (increases tissue permeability)

Venom drawn up via capillary action along grooves in the teeth

87
Q

describe the 3 types of venoms from reptiles- snakes

A

Crotalid venoms: Rich in proteolytic activity and thrombin-like enzymes

Vipirid venoms: Moderate-rich in proteolytic activity and thrombin-like enzymes

Elapid venoms: Little or no proteolytic activity (although phospholipases may be strongly represented), few thrombin-like enzymes, neurotoxic activity! Venoms may cause death in as little as 5-10 minutes

88
Q

Describe what happens in terms of mortality from 3 venoms

A

Crotalid and viper envenomation
-Hypotension/shock from decrease in circulating blood volume secondary to capillary permeability

-Elapid envenomation
Respiratory arrest from neurotoxic activity

89
Q

what do antivenoms contain

A

Contain neutralizing antibodies
-Monovalent or polyvalent

Antibodies bind to venom components rendering them ineffective

90
Q

what is anaphylaxis and anaphylaxis shock

A

All venoms have the capability of inducing anaphylaxis

Anaphylaxis is an acute systemic (rapid, multi-system) and severe allergic reaction

Anaphylactic shock—will usually lead to death in minutes if left untreated

91
Q

what causes anaphylaxis

A

Symptoms of anaphylaxis are related to the action of IgE and other anaphlatoxins, which act to release histamine and other signaling substances

In addition to other effects, histamine induces vasodilation of arterioles and constriction of bronchioles in the lungs – also known as bronchospasm (constriction of the airways)

May occur in response to venom or antivenom!

92
Q

what is a solvent ?

A

A solvent is a liquid at room temperature used to dissolve other substances

examples like alcohol, glycols, aldehyde, ketones

93
Q

what are properties of solvents

A

Solubility

Non-flammability/
Flammability/
Explosivity

Volatility

Metabolism

Complex mixtures

94
Q

Routes of solvent exposure

A

Inhalation

Absorption
-skin
-mucous membranes

Ingestion

Injection

95
Q

General Toxicological Principles-1 is

A

Solvent exposure affected by airborne concentration, solubility, and exposure frequency.

Higher vapor concentrations for enclosed spaces with poor ventilation, and with solvents having a high vapor pressure.

When inhaled, lipid-soluble solvents will easily enter the blood

Solvents also can pass through the skin, although not usually a significant route of exposure.

Solvents often de-fat or irritate the skin.

96
Q

General Toxicological principles-2

A

-Toxic effects of solvents include:
depression of the central nervous system, and
irritation of membranes and tissues.

-CNS depression tends to increase as the length of the carbon chain increases.
–Molecules with more than 5 carbons generally are not volatile enough to cause hazardous exposures.

-CNS-depressant properties are increased with the addition of halogens and alcoholic functional groups:

alkanes <alkenes <alcohols <organic acids <esters <ethers <halogenated compounds

97
Q

General Toxicological Principles-3

A

All organic chemicals can cause tissue irritation.
-Solvents can extract lipids from cell membranes, casing irritation and cell damage.

As the molecular size increases, the potential for irritation increases

In general, irritation increases with the addition of functional groups

Unsaturated compounds are stronger irritants than their saturated counterparts

98
Q

Hepatic effects of solvents

A

Chemical hepatitis, with transaminases indicating hepatocellular injury

Steatosis (fatty liver), occasionally progressing to hepatic necrosis

Possible cirrhosis on recovery

Reduced metabolism of other xenobiotics

? Acetylcysteine

Mechanisms of hepatotoxicity
-free radical formation

-Halogenated hydrocarbons have greatest toxicity
carbon tetrachloride, chloroform&raquo_space;
1,1,1-trichloroethane, trichlorethylene&raquo_space;
non halogenated hydrocarbons

99
Q

Describe the renal toxicity of solvents

A

Acute tubular necrosis
-acute heavy exposure
-halogenated HCs, glycols, toluene, petroleum distillates

Glomerulonephritis
-chronic, long term exposure
-gasoline implicated

100
Q

Describe acute central neurotoxicity of solvents

A

General anesthesia-like activity or selective inhibition
narcosis
euphoria
agitation (disinhibition)
dyscoordination, ataxia, dysarthria

101
Q

What is TCE

A

It is a chlorinated hydrocarbons

TCE is a widely used solvent for metal degreasing

At high acute exposure TCE can cause respiratory depression and cardio toxicity

There is a weak association between TCE exposure and multiple myeloma, Hodgkin disease and cancers of the prostate, skin and cervis

The IARC concluded that TCE is “probably carcinogenic to humans” based on its assessment of sufficient evidence in animals and limited evidence in humans

102
Q

Describe relationship between TCE and the Air and drinking water

A

TCE contamination in ground water can release TCE vapors to the subsurface

At many sites these vapors may then enter buildings from below, similar to radon

Indoor air concerns may lead to cleanup of groundwater not considered a current or potential drinking water source (e.g., water table aquifers), and therefore not subject to drinking water regulations

There is no single regulatory standard set by rulemaking for TCE in air

103
Q

Describe the metabolism of TCE

A

With rare exceptions, the toxicities associated with TCE are thought to be mediated by metabolites rather that by the parent compound

The majority of TCE undergoes oxidation via cytochrome P450s, with a small proportion being conjugated with GSH via glutathione transferases

104
Q

TCE Human risk assessment describe it

A

The human relevance of TCE induced rodent tumor is an unresolved issue

For liver tumors: humans appear to be similar to rats than mice in the oxidative metabolism capacity

For kidney tumors evidence exists that the rat have a greater GSH metabolism capacity

With regards to lung cancer, the CYP450 content and the number of Clara Cells in the human lung are but a fraction of those in the mouse

Based on the above, it appears that direct extrapolation from rodent data would overstate human TCE cancer risk

105
Q

Describe carbon tetrachloride and chloroform chcl3

A

they are organic solvents
and halogenated hydrocarbons

Carbon tetrachloride, CCl4
–Strong CNS depressant
–Potent liver toxin
—–Acute exposure can cause death
——Chronic exposure can cause cirrhosis

Chloroform, CHCl3
–CNS depressant
–High exposure levels can cause liver and kidney damage and cardiac arrhythmias.

106
Q

Describe vinyl chloride

A

-Vinyl chloride , CH2CHCl
–Skin irritant with CNS depressant properties
–Much industrial hygiene concern over this chemical is due to its carcinogenic potential
—–Chronic exposure may result in liver cancer (angiosarcoma) and other cancers as well.

107
Q

Describe methylene chloride

A

Methvlene chloride, CH2Cl2

Not as toxic as the other chlorinated methanes
A suspected carcinogen
An excellent solvent
Widely used in industry

The 1997 OSHA methylene chloride standard should result in a reduction in the use of this chemical.

108
Q

what is beneze and what does it do

A

organic solvent
aromatic hydrocarbon

Benzene has been used for many industrial purposes, component of gasoline

High exposure levels can cause death by CNS depression or cardiac arrhythmias

Skin exposure causes dermatitis

Inhalation of high concentrations may result in bronchial irritation or pulmonary edema.

Chronic exposure causes blood disorders of aplastic anemia and leukemia.

Victims of chronic benzene poisoning usually have a red blood cell count that is only 50% of normal.

109
Q

what is an alkyl benzene

A

organic solvent
alkyl benzene

Alkyl benzenes include toluene, xylenes, etc.
More powerful narcotic effect than benzene
Not known to cause blood disorders

110
Q

what is ethanol

A

organic solvent
alcohol

Irritant and a depressant

The toxicology of this compound is well know through centuries of voluntary ingestion

It does not have the neurotoxic properties of methanol

111
Q

what is methanol

A

organic solvent
alcohol

Methanol, CH3OH (wood alcohol, methyl alcohol)
Common industrial solvent
Methanol poisoning may result in blindness, other neurological damage, or death.

-Methanol poisoning 8 - 36 hrs after ingestion

-Caused by compounds produced by methanol metabolism

-Inhibited by administering ethanol

112
Q

what is the mechanism of toxicity for methanol

A

Mechanism of toxicity

Methanol slowly metabolized to formaldehyde
Formaldehyde rapidly metabolized to formic acid
-Acidosis
-Ocular toxicity

113
Q

what is a methanol specific antidote

A

Fomepizole (4-methylpyrazole)

Inhibits alcohol dehydrogenase

Produces same end result as ethanol without causing intoxication

114
Q

What is ethylene glycol description

A

Antifreeze (95% ethylene glycol)
Tastes sweet
Kids, animals like taste/drink large quantities

115
Q

What is ethylene glycol mechanism

A

Mechanism of toxicity

Metabolized via alcohol dehydrogenase to glycoaldehyde then to glycolic , glyoxylic, and oxalic acids

Acids lead to anion gap metabolic acidosis

Oxalate binds with calcium
-Forms crystals causing tissue injury
-Produces hypocalcemia

116
Q

what does ethylene glycol overdose presentation look at 3 hours and 4-12 hours

A

Overdose Presentation (first 3-4 hours)
Patient may appear intoxicated
Gastritis, vomiting
Increase in osmolar gap
No initial acidosis

Overdose Presentation (after 4-12 hours)
Anion gap acidosis
Hyperventilation
Seizures, coma
Cardiac conduction disturbances, arrhythmias
Renal failure
Pulmonary, cerebral edema

117
Q

what is ethylene glycol management look like after overodse

A

Lavage if within 2 hours

Sodium bicarbonate

Fomepizole or ethanol

Folic acid, pyridoxine, thiamine (enhance metabolism of glyoxylic acid to nontoxic metabolites)

118
Q

Describe aldehydes

A

organic solvents

-Aldehydes are strongly irritating to mucous membranes

Can cause CNS depression, but their irritating nature usually prevents significant exposure.

-Formaldehyde is regulated by OSHA as a carcinogen.

-Can cause sensitization in about 4 - 8% of the population.

-Glutaraldehyde

–Commonly used in hospitals to sterilize endoscopes and other equipment
–Also causes sensitization.

119
Q

Describe ketones

A

organic solvents

CNS depressants

Irritating effects cause workers to avoid high exposures
-Toxic properties of ketones generally increase with increasing molecular weight.

Acetone, (2-propanone) is a relatively safe solvent, as its principle toxic effect is irritation.

120
Q

Describe ethers

A

Organic solvents

Anesthetic effect of ethers increases with the size of the molecule

Very flammable, and they can be easily oxidized to explosive peroxides.

Ethyl ether, CH3CH2OCH2CH3 (diethyl ether)
Had been widely used as an anesthetic

121
Q

Describe phenols

A

Phenols are extremely irritating, capable of causing severe burns from direct contact.

Phenol is cytotoxic to all cells and tissues, and is toxic by all routes of exposure

-Rapidly absorbed through the skin

-Fatalities have resulted within 10 minutes of skin exposure.

122
Q

what is delayed contact sensitivity

A

Delayed contact sensitivity
aka allergic contact dermatitis

standard chemistry for sensitizers
-low molecular weight (haptens)
-react with cutaneous proteins

poison ivy and poison oak

develops after one or more contacts
subsequent exposure elicits response dependent on dose

3-5 weeks to develop skin reactivity

123
Q

what is contact urticaria

A

nettles
-hollow, stinging hairs inject chemical into skin
-mixture of acetylcholine, histamine, and serotonin

causes local vasodilation, sweating and pain
recovery in 3-5 days

124
Q

what is phototoxicity

A

parsnips, caraway, dill, parsley and citrus
sensitize skin to long-wave UV light
contain furocoumarins
skin burns within 6-24 hours of contact
range from mild irritation to severe blistering
relieved with aspirin or corticosteroids

125
Q

What is primary chemical irritation in plant skin injury

A

spurges, buttercups and wild pepper

resembles contact with corrosive acid

affected by dose, exposure time, genetics, temperature and humidity

serious eye damage possible

keratoconjunctivitis with transient blindness

126
Q

Plant toxins- Gastrointestinal

A

Direct stomach irritation - Nausea, vomiting and diarrhea
California buckthorn (sacred bark), tung nut, horse chestnut (active is called esculin), pokeweed

Antimitotic (stops cell division) – Nausea, vomiting, confusion, delirium
Lily family, glory lily, crocus, may apple
Colchicine (gout treatment)

Lectin toxicity – nausea, diarrhea, headache, confusion, dehydration, death
Wisteria, castor bean (Ricinus communis)
Ricin – block protein synthesis very toxic 5 to 6 beans can kill a child

127
Q

Plant toxins that cause cardiovascular 1

A

Digitalis like glycosides – cardiac arrhythmias

Foxglove (Digitalis purpurea), squill, lily of the valley
Contain glycosides that are similar to digitalis

The toxic effects is identical to that of Digitalis toxicity: nausea, vomiting and cardiac arrhythmias

128
Q

What are vasoactive chemicals

A

Mistletoe (berries contain toxin)
Cardiovascular

Toxin is called phoratoxin (produces hypotension, bradychardia, negative ionotropic effects and vasoconstriction of the vessels of skin and skeletal muscle)

Claviceps purpurea (ergot) is a fungus parasitic on grains of rye- this has caused an outbreak in several European countries in the Middle ages known as “Saint Anthony’s fire”.

129
Q

what are plant toxin effects on heart nerves

A

Heart nerves – decreased heart rate and blood pressure, general weakness

Lily, hellebore, death camas, heath family, monkshood, rhododendron

Alkaloids, aconitum, grayanotoxin (concentrated in honey) (honey poisoning)

It consists of marked bradbradycardia, hypotension, weakness, GI upset and in severe cases respiratory depression

The toxins gets into the honey from the nectar collected by the bees from the flowers (Rhododendrom ponticum)

130
Q

what plants cause seizures

A

Water Hemlock, mint family

131
Q

what plant toxins induce stimulation of nervous system

A

Excitatory Amino Acids – headache, confusion, hallucinations

Red alga (produces Kainic acid), Green alga (produces domoic acid). In 1987 there was a serious outbreak in Canada in individual eating mussels containing domoic acid)

coffee bean, tea, cola nut, caffeine most widely consumed stimulant in the world

132
Q

what plant causes aberrant behavior

A

very excitable, muscle weakness, death

locoweed

133
Q

What plant causes neurotoxic death

A

Poison hemlock (Conium maculatum)

Coniine – neurotoxic alkaloid – Poison used by Socrates

134
Q

what plant causes paralysis?

A

demyelination of peripheral nerves is caused by

Buckthorn, coyotillo, tullidora (U.S., Mexico)

135
Q

what plant causes atropine like effects like

A

dry mouth, dilated pupils, confusion, hallucinations, memory lose

Solanaceae family – jimsonweed, henbane, deadly nightshade (Atropa belladonna), angles trumpet (atropine and scopolamine)

136
Q

what plants cause nueromuscular effects

A

mild stimulation to muscle paralysis, respiratory failure (curare), death Coffee bean, tea, cola nut

Tobacco – South American – Strychnos family (curare) Blue green alga (anatonin A)

137
Q

what plant toxins effect the liver

A

Hepatitis” and cirrhosis of liver - From contaminated grain

Ragwort or groundsel
Pyrrolizidine alkaloids – attack liver vessels – effects humans, cattle but some species resistant

Liver failure and death
Mushrooms – “Death cap” (Amanita phalloides)
Amatoxin and phalloidin effects RNA and protein synthesis

Liver cancer
Fungus that grows on peanuts, walnuts, , etc…plant
Alfaltoxins– produced by fungus in poorly stored grain

138
Q

what plant toxins effect reproduction

A

Teratogen – malformations in offspring (sheep)
Veratrum californicum – native to North America
Veratrum – blocks cholesterol synthesis – seen offspring of mountain sheep

Abortifacients
Legumes (Astrogalus)
Bitter melon seeds (Momordica)
Swainsonine toxin – stops cell division
Lectins - halt protein synthesis– used by humans

139
Q

what happens with the toxicity of alpah amintin

A

through interference with RNA polymerase II, prevents the transcription of DNA

140
Q

what do phalotoxins do

A

are rapid-acting and interrupt actin polymerization, impair cell membrane function, has limited absorption

141
Q

what do mushrooms containg Monomethylhydrazine contain in terms of toxicity

A

Toxicity is due to gyromitrin which is metabolized to monomethylhydrazine

This metabolite reacts with pyridoxine resulting in inhibition of pyridoxal phosphate-related enzymatic reactions

142
Q

symptoms of monomethylhydrazine mushrooms

A

Headache, nausea, vomiting, seizures, and hepatorenal failure
Symptoms occur 6-10 hours after ingestion
Toxin may be eliminated with cooking but inhalation of cooking fumes may cause poisoning

143
Q

the therapy for monomethyl mushrooms

A

Pyridoxine, in dose of 25 mg/kg

144
Q

C. Muscarine-Containing Mushrooms do what to the human body

A

no lethality,

Small amounts of muscarine are in Amanitia muscaria

Symptoms: SLUDGE within 0.5-2 hours
Salivation, Lacrimation, Urination, Diaphoresis, Gastrointestinal motility, Emesis

Therapy: Atropine

145
Q

Coprine-Containing Mushrooms mechanism symptoms and therapy

A

Rarely fatal

Coprine has a disulfiram like effect(Blocks acetaldehyde dehydrogenase)

Toxic if alcohol is consumed within 48-72 hours after mushroom

Symptoms: Flushing, headache, hypotension, histamine induced vasodilation

Therapy: Supportive, anti H1 and anti H2, prostaglandin inhibitors

146
Q

what is colchichine

A

Antiinflammatory effects mediated by ability to inhibit microtubule and PMN activity

May cross placenta + found in breast milk

147
Q

What is ricin

A

a potent cytotoxin (toxic at cellular level) concentrated in the castor bean also contains highly toxic glycoproteins that block the synthesis of other good proteins causing cell death

used as a lubricant, boiling makes it non- toxic

148
Q

what are routes and symptoms of ricin poisoning

A

Intravenous-Introduced into a puncture or cut.
Inhalation- Aerosolized liquid or powder inhaled directly into the lungs.
Ingestion- Ricin enters through contaminated food or water into the stomach.

Symptoms range from fever, cough, nausea, chest tightness, sweating, cyanosis, hypo tension (very low blood pressure), dyspnea (labored breathing). Circulatory and respiratory collapse occur within 36-72 hrs leading to death.

149
Q

what is ricin mechanism of action

A

Death from Castor beans is caused by two lectins in the beans: Ricin I and Ricin II (more toxic)

Ricin II consists of two chains of amino acids. The A chain inactivates the 60s ribosomal subunit of cells by depurination of a single adenosine residue within the 28s rRNA and blocks protein synthesis

Exposure to high or very warm temperatures and or high humidity will diminish the strength of the toxin (denaturing effect).

Tox 2 midter, (2 decks)

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