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PCOL MIDTERMS > UNIT 5: INTRODUCTION TO TOXICOLOGY > Flashcards

UNIT 5: INTRODUCTION TO TOXICOLOGY Flashcards

1
Q

The branch of pharmacology that concerns the study, regulation, and treatment of adverse effects in humans resulting from exposure to chemicals encountered at work or in the general environment.

A

Toxicology

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2
Q

How do we get exposed to such chemicals?

A
  • Environment (air, water, soil, food)
  • Occupational
  • Most common chemicals (used in households, personal care, consumer products)
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3
Q

What variables affect the extent of the effect of the toxic chemicals?

A
  • Dose
  • Duration of exposure
  • Vulnerability of individuals
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4
Q

What are the most commonly affected system/organs of these chemicals?

A
  • Central nervous system
  • Liver (hepatotoxicity), kidneys (nephrotoxicity)
  • Reproductive system (teratogenic effects)
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5
Q

Deals with the effects of chemicals in the workplace.

A

Occupational Toxicology

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6
Q

The amount of exposure to a given agent that is deemed safe for a stated time period.

A

Threshold limit value

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7
Q

Deals with the deleterious impact of chemical pollutants in the environment, on living organisms, or to the ecosystem itself.

A

Ecotoxicology

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8
Q

Deals with the effects of agents found in the environment.

A

Environmental toxicology

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9
Q

The ability of a chemical agent to cause injury/disease in a given situation or setting.

A

Hazard

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10
Q

Expected frequency of the occurrence of an undesirable effect; the likelihood of harm taking place.

A

Risk

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11
Q

Hazard + exposure equates to?

A

Risk

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12
Q

What is the route of exposure in industrial settings?

A

Inhalational > Transdermal > Oral

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13
Q

What is the route of exposure for water & soil pollutants?

A

Inhalational > Ingestion > Transdermal

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14
Q

Exposure to a toxic substance that is absorbed by the target human or animal.

A

Dose

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15
Q

Single/multiple exposure over a brief period of time.

A

Acute exposure

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16
Q

Single/multiple exposure over a longer period of time

A

Chronic exposure

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17
Q

What is the Hierarchy of Controls?

A

In order: (Most to least effective)
Elimination
Substitution
Engineering Controls
Administrative Controls
PPEs

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18
Q

The increasing concentration of a substance in the environment that leads to accumulation in biologic tissues.

A

Bioaccumulation

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19
Q

The concentration of the contaminant is magnified hundreds or thousands of times as the contaminant passes up the food chain.

A

Biomagnification

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20
Q

An odorless, colorless, non-irritating gas which is a byproduct of incomplete combustion

Air Pollutants

A

Carbon monoxide

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21
Q

What is the mechanism of action of CO?

Air Pollutants

A

Combining tightly but reversibly on oxygen-binding sites of hemoglobin, forming carboxyhemoglobin.

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22
Q

True or False:
Oxygen has a higher affinity to hemoglobin than CO

Air Pollutants

A

False; CO has a higher affinity (220x higher affinity)

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23
Q

What is the primary clinical effect of carbon monoxide poisoning?

Air Pollutants

A

Tissue hypoxia

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24
Q

What clinical effect/s occurs when approximately 40% of hemoglobin has been converted to carboxyhemoglobin?

Air Pollutants

A

Collapse & syncope

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25
Q

Prolonged hypoxia due to carbon monoxide poisoning causes what?

Air Pollutants

A

Irreversible damage to the brain and myocardium?

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26
Q

**True or False: **
Carbon monoxide have potential teratogenic effects

Air Pollutants

A

True

Exposure at critical fetal developmental periods: fetal death/serious and irreversible but survivable birth defects

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27
Q

What is/are the recommended treatment options for carbon monoxide poisoning?

Air Pollutants

A

Supportive treatment and oxygenation

Supportive treatment - removal from source

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28
Q

__________ __________ accelerates the clearance of carbon monoxide

Air Pollutants

A

Hyperbaric oxygen

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29
Q

A colorless, irritant gas formed from the combustion of fossil fuels

Air Pollutants

A

Sulfur dioxide

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30
Q

What is the mechanism of action of sulfur dioxide?

Air Pollutants

A

Forms sulfurous acid on contact with moist mucous membranes

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31
Q

What is/are the primary sign of exposure for sulfur dioxide?

Air Pollutants

A

Conjunctival & bronchial irritation

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32
Q

What are the primary clinical effects of sulfur dioxide exposure?

Air Pollutants

A
  • eyes, nose, throat irritation
  • reflex bronchroconstriction
  • increased bronchial secretions
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33
Q

What are the primary treatment options for sulfur dioxide exposure?

Air Pollutants

A

Supportive, non-specific

Non-specfic treatment includes: oxygenation, bronchodilation, use of mucolytics

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34
Q

A brownish, irritant gas associated with fires and silage on farms

Air Pollutants

A

Nitrogen oxides

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35
Q

What is the mechanism of action for nitrogen oxide exposure?

Air Pollutants

A
  • acts as a deep lung irritant, affecting the alveoli,
  • damaging the lung infrastructure producing the surfactant
  • dissolving the surfactant itself
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36
Q

What is/are the primary clinical effect/s for nitrogen oxide exposure?

Air Pollutants

A

Deep lung irritiation and pulmonary edema

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37
Q

Other names for nitrogen oxide exposure

Air Pollutants

A
  • Silo-Filler’s Disease
  • Non-allergic Asthma
  • Twitchy-airway Disease
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38
Q

What is the chronic effect for nitrogen oxide exposure?

Air Pollutants

A

Emphysematous changes

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39
Q

What is the treatment for nitrogen oxide exposure?

Air Pollutants

A

Supportive, non-specifc

Measures to reduce inflammation and pulmonary edema are important

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40
Q

A bluish, irritant gas, found in air & water purification devices, eletrical fields and in the Earth’s atmosphere.

Air Pollutants

A

Ozone

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41
Q

What is the mechanism of action for ozone exposure?

Air Pollutants

A
  • Acts as an irritant of mucous memranes
  • Formation of reactive free radicals
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42
Q

What are the primary clinical effects of ozone exposure?

Air Pollutants

A
  • Irritation and dryness of mucous membranes
  • Decrease in pulmonary compliance
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43
Q

What are the acute clinical effects of ozone exposure?

Air Pollutants

A
  • Substernal pain
  • Acure respiratory distress (ARDS)
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44
Q

What are the treatment options for ozone exposure?

Air Pollutants

A

Supportive, non-specific

Measures to reduce inflammation and pulmonary edema are important

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45
Q

What are the two types of solvents encountered that may cause toxicity?

Solvents

A
  • Halogenated Aliphatic Hydrocarbons
  • Aromatic Hydrocarbons
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46
Q

True or False:
Do solvents contribute to air pollution?

Solvents

47
Q

Other name for halogenated aliphatic hydrocarbons

Solvents

A

Halohydrocarbons

48
Q

What are examples of halohydrocarbons?

Solvents

A
  • Carbon tetrachloride
  • Trichloroethylene
  • Tetrachloroethylene
  • 1,1,1-trichloroethane
  • Chloroform
49
Q

True or False:
Most halohydrocarbons are classified as known or probable human carcinogens

Solvents

50
Q

What is the primary clinical effect for halohydrocarbon poisoning?

Solvents

A

CNS depression

51
Q

What are the chronic clinical effects to halohydrocarbon poisoning?

Solvents

A

hepatic toxicity, nephrotoxicity

52
Q

What is the effect of long-term exposure to tetrachloroethylene/trichloroethane?

Solvents

A

Peripheral neuropathy

53
Q

What is the primary treatment options for halohydrocarbon poisoning?

Solvents

A

Supportive, non-specific

54
Q

What is the treatment option for peripheral neuropathy?

Solvents

A

Vitamin B12 intake

55
Q

What are examples of aromatic hydrocarbons?

Solvents

A
  • Benzene
  • Toluene
  • Xylene
56
Q

What is the primary acute effect for exposure to any of the aromatic hydrocarbons?

Solvents

A

CNS depression

57
Q

True or False:
Toluene and Xylene are carcinogenic and myelotoxic

Solvents

A

False

Only benzene is carcinogenic/myelotoxic

58
Q

True or False:
Benzene is not a clastogen

Solvents

59
Q

A colorless, sweet-smelling agent

Solvents

60
Q

What are the classifications of pesticides?

Pesticides

A
  • Organophosphates, Carbamates (Acetylcholinesterase Inhibitors)
  • Chlorinated Hydrocarbons (Organochlorates, DDT)
  • Botanical Agents (Nicotine, Rotenone, Pyrethrum Alkaloids)
61
Q

Chemicals in the environment that have estrogen-like/antiandrogenic activity or disrupt thyroid function.

A

Endocrine Disruptors

62
Q

These agents are persistent, poorly metabolized, lipophilic chemcicals that exhibit significant bioaccumulation.

Pesticides

A

Chlorinated Hydrocarbons

63
Q

Aryl, carbocylcic or herterocyclic compounds with chlorine substituents

Pesticides

A

Organochlorine Pesticides

64
Q

What is the mechanism of action for organochlorate exposure?

Pesticides

A

Interfere with inactivation of the sodium channels, causing rapid repetitive firing in most neurons

65
Q

What is the primary clinical effect for organochlorate exposure?

Pesticides

66
Q

Examples of organochlorates

Pesticides

A
  • Paraquat dichloride
  • DDT (dichlorodiphenyltrichloroethane)
  • Rotenone
  • Pyrethrine I
67
Q

What is the treatment option for organochlorate exposure?

Pesticides

A

No specific treatment available

68
Q

These are effective pesticides with short environmental half-lives, inexpensive, and are heavily used in agriculture.

Pesticides

A

Cholinesterase inhibitors

69
Q

What is the mechanism of action for cholinesterase inhibitors?

Pesticides

A
  • increase nicotine & muscarinic cholinergic activity
  • inhibition of acetylcholinesterase activity through phosphorylation of the esteratic state
70
Q

What is/are the primary clinical effect/s for organophosphate exposure?

Pesticides

A

M.U.D.D.L.E.S

miosis, urination, diarrhea, diaphoresis, lacrimation, excitation of the CNS, salivation

71
Q

What is the most common cause of death from exposure to cholinesterase inhibitors?

Pesticides

A

Respiratory failure

72
Q

What is the treatment option for organophosphate exposure?

Pesticides

A

Specific treatment: Pralidoxime & physostigmine

73
Q

What drug is used to control muscarinic excess?

Pesticides

A

Atropine

in large doses

74
Q

What does pralidoxime do?

Pesticides

A

Regenerate cholinesterase

75
Q

Enumerate

Botanical Pesticides (3)

A

Nicotine
Rotenone
Pyrethrum

76
Q

What is the mechanism of action for nicotine?

Pesticides

A

excitation, followed by paralysis of ganglionic, CNS and neuromuscular transmission.

77
Q

A plant alkaloid pesticide

Pesticides

78
Q

What are the clinical effects of rotenone?

Pesticides

A

Ingested: gastrointestinal distress
Direct contact: conjunctivitis and dermatitis

79
Q

A mixture of plant alkaloids that causes contact dermatitis as its common toxic effect.

Pesticides

80
Q

What are the most important members of chlorophenoxy acids?

Pesticides

A
  • 2,4-dichlorophenoxyacetic acid
  • 2,4,5-trichlorophenoxyacetic acid
81
Q

What are the clinical effects after long term exposure to chlorophenoxy acids?

Pesticides

A

muscle hypotonia and coma

82
Q

What is the principal ingredient of weed killers?

Pesticides

A

Glyphosate

83
Q

What is the target of glyphosate in plants?

Pesticides

A

5-enolpyruvylshikimate-3-phosphate synthase

84
Q

What is/are the primary clinical effects of glyphosate exposure?

Pesticides

A

Significant eye and skin irritation

kahit i-skip niyo pa to e’

85
Q

A bipyridyl herbicide

Pesticides

86
Q

What is/are the primary clinical effects of paraquat contact?

Pesticides

A

None

Paraquat is only toxic when ingested

87
Q

What is/are the primary clinical effects of paraquat ingestion?

Pesticides

A
  • Gastrointestinal irritation with hematemesis and bloody stools
  • Pulmonary impairment to pulmonary fibrosis, leading to death

Hematemesis - vomiting blood

88
Q

Chemical compounds that contribute to environmental pollution.

A

Environmental Pollutants

89
Q

Highly halogenated biphenyl compounds that are poorly metabolized, lipophilic, and is highly persistent in the environment.

Environmental Pollutants

A
  • Polychlorinated Biphenyls
  • Polybrominated Biphenyls
90
Q

What is the primary source of PCB/PBB for humans?

Environmental Pollutants

91
Q

What is the primary clinical effect of PCB/PBB toxicity?

Environmental Pollutants

A

Dermatoxicity

92
Q

What are the other clinical effects of PCB/PBB?

Environmental Pollutants

A
  • Potent endocrine disruptors
  • Severe reproductive and teratogenic effects
93
Q

These chemicals are used as:
- coolant material
- used as heat-, stain-, and stick-resistant coating

Environmental Pollutants

A

Perfluorinated Compounds

94
Q

A group of naturally occurring long, flexible mineral fibers most commonly contaning silicon; widely used in manufacturing and building

Environmental Pollutants

95
Q

True or False:
Asbestos is poorly metabolized, lipophilic, and highly persistent in the environment.

Environmental Pollutants

96
Q

What is/are the primary clinical effects of asbestos inhalation?

Environmental Pollutants

A
  • asbestosis
  • mesothelioma
  • lung cancer
97
Q

True or False:
Asbestos has no synergistic effect with cigarette smoking & exposure to radon daughters.

Environmental Pollutants

98
Q

What are examples of toxic metals used in the industry?

Metals

A

Beryllium and Cadmium

99
Q

A light alkaline metal that enters through inhalation

Metals

100
Q

A transitional metal that is either inhaled or ingested

Metals

101
Q

What is/are the primary clinical effect/s of beryllium poisoning?

Metals

A
  • Progressive pulmonary fibrosis
  • Acute & Chronic Beryllium Disease
102
Q

What is/are the primary clinical effect/s of cadmium poisoning?

Metals

A
  • Progressive pulmonary fibrosis
  • Renal failure
  • Cadmium Fume Fever
103
Q

What is the Carcinogen Classification of Cadmium & Beryllium

Metals

A

Class 1 (Known carcinogen to humans)

104
Q

Any material, natural or manufactured, bearing the size of at least 1 - 100 nm in size

Metals

A

Nanomaterials

105
Q

What is the route of exposure for nanomaterials?

Metals

A
  • Inhalation
  • Oral
  • Dermal
  • Parenteral
106
Q

True or False:
Nanomaterials cannot cross cellular membranes, penetrate nuclear material and genetic information

Metals

A

False

Due to their small size, it is possible for nanomaterials to cross cellular membranes and dependent on the nanomaterial, can affect genetic material.

107
Q

Identify

Aldicarb
Aminocarb
Carbaryl
Carbofuran
Dimetan
Dimetilan
Isolan
Methomyl
Pyramat
Pyrolan
Zectran

A

Carbamate Pesticides

108
Q

Enumerate

Herbicides (5)

A

Chlorophenoxy Acids
2,4-Dichlorophenoxyacetic Acid
2,4,5-Trichlorophenoxyacetic Acid
Glyphosate
Biphyridyl Pesticides (Paraquat)

109
Q

Enumerate

DDT and analogs

Organochlorine Pesticides

A

Dichlorodiphenyltrichloroethane (DDT)
Methoxychlor
Tetrachlorodiphenylethane (TDE)

110
Q

Enumerate

Benzene hexachlorides

Organochlorine Pesticides

A

Benzene hexachloride (BHC)
Lindane

111
Q

Enumerate

Cyclodienes

Organochlorine Pesticides

A

Aldrin
Chlordane
Dieldrin
Heptachlor

112
Q

Enumerate

Toxaphenes

Organochlorine Pesticides

A

Toxaphene (camphechlor)

lol

113
Q

Identify

Azinphos-methyl
Chlorfenvinphos
Diazinon
Dichlorvos
Fenitrothion
Malathion
Parathion
Parathion-methyl
Trichlorfon

A

Organophosphorous Pesticides

PCOL MIDTERMS (10 decks)

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