Introduction to Toxicology: Occupational and Environmental Flashcards by JULIA CASSANDRA RECCION

Basic principles of toxicology

Mechanism of exposure
Toxicological effects
a. Recognition
b. Prevention
c. Treatment

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Exposure to chemicals maybe through the environment (air, water, soil, food) and/or occupational.

Occupational & Environmental Toxicology

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T/F: Most common chemicals are those used in households, personal care and consumer products; those used in agriculture and industry

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What systems are affected by Occupational & Environmental Toxicology?

CNS, liver & kidney, Reproductive system

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Signs and symptoms for chronic chemical poisoning of chemicals may be non-specific and may manifest as
headaches, nauseas, vomiting, dizziness, irritation of the skin, eyes and mucous membranes

F; acute chemical poisoning

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Effects of Occupational & Environmental Toxicology

Depending on dose, duration of exposure, vulnerability of individuals

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This area of toxicology deals with chemicals found in the
workplace

Occupational Toxicology

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Handles cases involving Occupational & Environmental Toxicology

Occupational Medicine Specialists and Toxicologists

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T/F: Treatment is available for Occupational & Environmental Toxicology.

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Occupational toxicology identifies?

Agents of concern
Acute & chronic diseases
Conditions for safe use
Preventive measures
Treatment
Surveillance

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Who established RA 11058 or the Labor Code of the PH?

Occupational Safety and Health Standards (OSHS)

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Standards for specific materials of particularly
serious toxicity

Permissible Exposure Limits (PELs): ppm

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Only serves as a guide
or reference points in the evaluation of potential
workplace exposures in the absence of OSHA requirements; it is still not implemented

Threshold limit values (TLVs)

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Deals with the deleterious impact of chemical pollutants in the environment, on living organisms

Environmental toxicology / Ecotoxicology

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Toxic effects of chemical and physical agent on
populations and communities of living
organisms within defined ecosystems

Environmental toxicology / Ecotoxicology

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Transfer pathways of those agents and interactions with the environment

Environmental toxicology / Ecotoxicology

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● Concerned with the impact on populations of living
organisms or on ecosystems
● Includes air, soil or water

Environmental toxicology / Ecotoxicology

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Environmental toxicology / Ecotoxicology is a product of?

Industrialization
Technologic development
Urbanization

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Ability of chemical agent to cause injury / disease in a
given situation or setting

Hazard

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Something that can potentially cause harm

Hazard

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Likelihood that a hazard will cause harm

Risk

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Potential to cause harm

Hazard

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Expected frequency of the occurrence of an undesirable effect arising from exposure to a chemical
or physical agent

Risk

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Inhalation and dermal

Atmospheric pollutants

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Hazard + exposure

Risk

Routes of Exposure in Industrial

Inhalational > Transdermal Route > Oral

Water and soil pollutants are absorbed through

○ Inhalation ○ Ingestion ○ Transdermal

Inhalation, ingestion, dermal

Water and soil pollutants

● Single or multiple exposure over a brief period of time ● (Ex.) accidental discharge

Acute exposure

● Single or multiple exposure over a longer period of time ● (Ex.) repetitive handling of chemical (done by laboratory technicians)

Chronic exposure

↑ dose = _ effect

↑

Physically remove the hazard

Elimination

replace the hazard

Substitution

isolate people from the hazard

engineering controls

Protect the worker with Personal Protective Equipment

PPE

Most effective in Hierarchy of Controls

Elimination

change the way people work

Administrative controls (Policies)

Least effective in Hierarchy of Controls

PPE

Polychlorinated biphenyls

Persistent organic pollutants (POPs)

Furans

Persistent organic pollutants (POPs)

Dioxins

Persistent organic pollutants (POPs)

Methyl mercury discharges causes __________.

neurotoxicity

T/F: Poorly degraded chemicals (by abiotic or biotic pathways) exhibit environmental persistence and can accumulate

Environmental considerations

Degradability, bioaccumulation, transport and biomagnification

Organochlorine pesticides bioaccumulate in body fat causes endocrine disruption, neurological disorders, and carcinogenesis

Lipophilic substances

T/F: Biodegradable are biotic

F; abiotic

↓ degraded = _ capacity to accumulate in the environment

↑

causative agent Minamata disease

Methylmercury

0ccurs when the metabolism of a chemical is low, thus preventing it from being excreted out since it cannot be turned into water soluble or excretable form

Bioaccumulation

Pollutants having the widest environmental impact are poorly degradable

Bioaccumulation

Relatively mobile in air, water, and soil

Bioaccumulation

Concentrates the chemical in organisms higher on the food chain

Biomagnification

n entails several organisms

Biomagnification

Colorless, tasteless, odorless and non-irritating gas

Carbon monoxide / CO

Byproduct of incomplete combustion

Carbon monoxide / CO

Sources of Carbon monoxide / CO

→ Unvented kerosene and gas space heaters → Leaking chimneys and furnaces → Back-drafting from furnaces → Gas water heaters → Wood stoves and Fireplaces → Gas stoves → Generators and other gasoline powered equipment → Automobile exhaust and attached garages → Tobacco Smoke

most famous source of carbon monoxide (CO)

Automobile exhaust and attached garages

● Easily absorbed through the lungs ● Exposure may be acute or chronic ● Has teratogenic potential

Carbon monoxide / CO

T/F: Carbon Monoxide combines tightly but reversibly with oxygen-binding site of Hemoglobin (Hb)

Sources of Carbon Monoxide in a home

→ Car left running in attached garage → Clogged chimney → Corroded or Disconnected Water Heater Vent Pipe → Gas or Wood-burning Fireplace → Cracked or Loose Furnace Exchanger → Improperly installed Kitchen Range or Vent → Operating a Grill indoors or in a Garage → Portable Kerosene or Gas Heaters

CO + oxygen-binding site of hemoglobin (Hb) = ?

Carboxyhemoglobin

cannot transport oxygen

Carboxyhemoglobin

CO has affinity of about ___ times that of oxygen

220

Interferes with the dissociation of oxygen from the remaining oxyhemoglobin as a result of the Bohr effect.

Carboxyhemoglobin

T/F: The presence of carboxyhemoglobin increases oxygen transfer to the tissues

F; decreases

What organs with the highest oxygen demand are most seriously affected?

1. Brain 2. Heart 3. Kidneys

carries oxygen and carbon dioxide

hemoglobin

T/F: Presence of carbon monoxide causes oxygen to not be carried in and out of the body

Complete combustion

Carbon dioxide (CO2)

Incomplete combustion

Carbon monoxide (CO)

Symptoms of Hypoxia

● Psychomotor impairment ● Headache and tightness in the temporal area ● Confusion and loss of visual acuity ● Tachycardia, tachypnea, syncope, and coma ● Deep coma, convulsions, shock, and respiratory failure

Hypoxia is aggravated by

● Heavy labor ● High altitude and ambient temperature ● Smoking exposure ● Cardiorespiratory diseases

Principle sign of carbon monoxide

Hypoxia

1st step of treatment when carbon monoxide is inhaled

Colorless irritant gas generated primarily by the combustion of sulfur-containing fossil fuels

Sulfur Dioxide

Treatment for Hypoxia

Remove from source of CO Give high conc of O2 Hypothermic therapy

Principal source of urban SO2

Burning of coal, both for domestic heating and in coal-fired power plants

Site of principal effect for sulfur dioxide

upper respiratory tract

Clinical effect if sulfur dioxide is INHALED

* Causes bronchial constriction * Produces profuse bronchorrhea * Parasympathetic reflexes and altered smooth muscle tone

Clinical outcome of Sulfur Dioxide

acute irritant asthma

Signs and symptoms of SO2 intoxication

* Irritation of the eyes, nose, and throat * Reflex bronchoconstriction * Increased bronchial secretions

Exposure to 5 ppm SO2 for 10 minutes

Increased resistance to airflow

Exposures of 5-10 ppm SO2

Cause severe bronchospasm

Severe exposure of SO2

Delayed-onset pulmonary edema

Cumulative effects from chronic low-level exposure of SO2

Aggravation of chronic cardiopulmonary disease

Treatment for SO2

Depends on therapeutic maneuvers used to treat irritation of the respiratory tract and asthma

NO2 is found in

Fresh silage Diesel equipment Automobile and truck traffic emissions

Brownish irritant gas sometimes associated with fires Relatively insoluble deep lung irritant

Nitrogen Oxides NO2

Most common source of human exposure to oxides of nitrogen

Automobile and truck traffic emissions

Capable of producing pulmonary edema and acute adult respiratory distress syndrome (ARDS)

Nitrogen Oxides

Inhalation damages the lung infrastructure that produces the surfactant necessary to allow smooth and low-effort lung alveolar expansion

Nitrogen Oxides

This cell appears to be the cells chiefly affected by acute low to moderate inhalation exposure of Nitrogen oxide

Type 1 cells of the alveoli

Intoxication of NO2 is associated with

○ Silo-Filler’s Disease ○ Non-allergic Asthma ○ “Twitchy Airway Disease”

Acute intoxication of NO2 symptoms

○ Irritation of eyes and nose, cough ○ Mucoid or frothy sputum production ○ Dyspnea and chest pain ○ Pulmonary edema ○ Fibrotic destruction of terminal bronchioles

Chronic exposure of NO2

emphysematous changes

Bluish irritant gas naturally found in the earth’s atmosphere

Ozone (O3) and other oxides

Ozone (O3) and other oxides are found in

○ Burning of fossil fuel ○ Emission from power plants, motor vehicles and other sources of high heat compounds ○ High-voltage electrical equipment and air and water purification systems ○ Agriculture

Sources of Ozone

● Area sources ● Oil and gas ● Biogenic sources ● Off-road engines ● On-road vehicles ● Non-road engines ● Point sources

Clinical effects of Ozone

Shallow, rapid breathing and decrease in pulmonary compliance

Clinical effects of Acute Ozone Exposure

○ Irritation and dryness to throat ○ Changes to visual acuity ○ Substernal pain and dyspnea ○ Acute Respiratory Distress Syndrome (ARDS)

Clinical effects of Chronic Ozone Exposure

○ Chronic bronchitis ○ Bronchiolitis ○ Emphysema

Treatment for Ozone exposure

No specific treatment for acute O3 intoxication