General Toxicology

Intended learning objectives

Students will be expected to develop
competencies in the following areas:-
List different classes of common toxic
substances and environmental pollutants. Explain the
circumstances of intoxications, toxic doses, toxic kinetics,
clinical pictures, differential diagnosis of different drugs
and toxic substances. Describe the general principles of
analytical toxicology. Explain initial appropriate first aid
treatment and antidotal measures for different drugs and
toxic substances.
At the end of these lessons the student will be able
to:
1.Understand the history of toxicologys &
epidemiology of poisoning.
2. Define different terminologies used in
toxicology.
3. Understand the basic classification of toxicology.
4. Describe toxicokinetics & toxicodynamics.
5. Describe the potential causes of toxicity
6. Understand the environmental consideration of
toxicology.
7. Describe poison prevention & control strategies
 Poison prevention tips
Keep all household products & medicines locked
up out of sight & reach of children. Most
poisonings occur when the product is in use. If the
door or phone rings when you are using a
potentially harmful drug, take it with you or put it
out of the child’s reach. Don’t turn your back on a
child when a poisonous product is nearby. Never
use salt solutions as emetics. Never refer to
medicines or vitamins as candies. Use child-
resistant locks on cabinets & cupboards containing
medicines & household cleaners.
Keep the poison in its original container. Keep the
poison stored in a different cupboard from food
products. Many poisonous products look alike
and come in containers very similar to drinks or
food. An example of it is apple juice and specific
cleaner. Teach the children never to take
medications unless given by an adult they know
and trust. Discard old or outdated household &
chemical products. Communicate with other
household members when a medication is given
to a child in order to avoid unnecessary repeat
doses. Always turn the light on when taking or
giving medicine.
Always read the label or measure the dose of
medication to be given carefully. Avoid taking
medicine in front of children. Take time to teach
children about poisonous substances. Pesticides
can get through the skin and can be extremely
toxic. Keep children away from areas that have
recently been sprayed. Know the names of plants
in your home and in your yard. Label all of your
plants. If you are having difficulty identifying a
plant take a sample to nursery for identification.
Teach children not to eat mushrooms growing in
your yard for some of them can be poisonous.
Teach children not to eat leaves& berries in the
yard. Don’t assume a plant is safe to eat if you see
wild animals eating it. Have a list of poisonous and
non poisonous plants from your regional poison
control center. You must know the telephone
number of the poison control centre. New
recommendations from the American Academy of
Pediatrics advise that parents should not use
syrup of ipecac routinely as a poison treatment
intervention in the home.
 Toxicology

(From the Greek words

τοξικός - toxicos "poisonous" and logos). It is a
branch of biology, chemistry, and medicine
concerned with the study of the adverse effects
of chemicals on living organisms. It is the study
of symptoms, mechanisms, treatments and
detection of poisoning, especially the poisoning
of people. Poisoning is a very common clinical
problem.
 Toxicology is the science of poisons. It deals
with:-
1- Origin (source)
2- Properties (chemical and physical)
3- Physiological actions and symptoms
4- Lethal doses
5- Proper antidotes
6- Specific identification, quantitative
determination (which would first include
isolation and purification from body tissues and
fluids).
• 7- Evaluation and scientific interpretation of
those analytical results.
• What is a poison?
• A chemical or a physical agent which affects
health or causes death.
• Classifications of poisons:-
• No classification can possibly encompass the
multitudinous actions of so many poisons, and
only a broad outline of arrangements into
groups can be made.
• Nature:- solid, liquid, solution and gas.
• Site (action): Local, remote and local + remote.
• Target:- CNS (stimulants= Amphetamines,
depressants = anaesthetics, ethanol,
hypnotics).
• GIT:- ( Metals, corrosives, etc. ).
• Kidney:- ( Mercury, cadmium, etc.).
• Liver:- ( Paracetamol, Iron, Phosphorous).
• CVS:- (Digitalis, etc.).
• Lungs:- (Gases, fumes, vapours, etc. ).
• Many poisons have compound actions. For
instance:-
• Oxalates are GIT irritants & neuro-depressants.
• Mercuric chloride is irritant & nephro toxic.
• Phosphorous is both irritant & a liver toxic.
• Specific elections for tissues:-
• Strychnine affects the spinal cord.
• HCN affects the tissue oxidases.
• Arsine gas (AsH3) affects the red cells
• Almost every event in our life follows upon a
meal since we eat every 3-4 hours. Toxicology
is the study of the adverse effects of chemicals
on living organisms. It is the study of
symptoms, mechanisms, detection laboratory
(investigation), treatment & prevention.
Toxicology deals with source, kinetics & action,
diagnosis (clinical effects, lab. investigations &
D.D.), prevention & treatment.
• History
• (1552 B.C.) Egyptians’ Papyrus ebers.
Mathieu Orfila (Spain, 1813) father of modern
toxicology.
Orifila (1787-1853 AD),
Spanish physician who contributed to forensic
toxicology by devising means of detecting
poisonous substances. From then on toxicology
began in a more scientific manner & began to
include the study of the mechanism of action of
poisons.
• The renaissance is that time when a new
interest in learning arose in Europe, about
(1300 - 1500). It is new birth of anything.
Paracelsus ( 1493 – 1541) a Swiss physician
made his theory about poisons at that time.
• Paracelsus theory:-
• (All substances are poisons. There is non which
is not a poison. The right dose differentiates
between a poison and a remedy).
i.e. the amount of exposure to the substance.
 Tabulation of toxicity classes
Possible Single application Inhalation 4 hour vapour Single oral Commonly used Toxicity
lethal to skin of rabbits exposure mortality 2/6-4/6 dose, rats term rating
dose for LD50 rats (ppm). LD5Tabulation
man Routes of administration of toxicity
classes

A taste, a 5 mg or less / Kg 10 1 mg or less/ Kg Extremely toxic 1

drop, 1
grain
1 5-43 m g /Kg 10-100 1-50 mg /Kg Highly toxic 2
teaspoon
ful (4ml)
1 ounce 44-340 mg / Kg 100-1000 50-500 mg /Kg Moderately toxic 3
(30 gm)
1 pint 0.35-281 g /Kg 1000-10,000 0.5-5 g /Kg Slightly toxic 4
(250 gm)
1 quart 2.82-22.59 g / Kg 10,000-100,000 5-15 g /Kg Practically non- 5
or 1 litre toxic
> 1 quart 22.6 g or more / Kg 100,000 15 g / Kg and Relatively 6
or > 1 more harmless
litre
Oxygen toxicity
Like other agents oxygen may result in cellular toxicity
if given into a too high concentration over too long a
period of time. High concentrations of oxygen are
required to achieve a normal arterial oxygen tension.
But when pure oxygen is breathed for 5 hours at sea
level, for 3 hours at 3 atmospheres, 30 minutes at 4
atmospheres, or 5 minutes at 7 atmospheres, signs &
symptoms of toxicity will follow. These will include
nausea, dizziness, bronchial irritation, hypothermia,
increased depth of respiration, bradycardia,
pulmonary discomfort or injury ( congestion,
bronchitis, oedema pneumonia), peripheral
vasoconstriction, amblyopia or loss of vision, syncope,
epileptic seizures and death.
 Factors modifying toxic effects
1.Poison factors 2. Patient (host) factors 1-
Poison
Poison factors include:-
toxicokinetic &toxicodynamic factors
( quantity, quality, route of administration,
accumulation, chemical interaction). 2-
Patient
Patient (host) factors include:- Age,
GIT pH, health, amount and type of food,
tolerance, toxicogenetics (idiosyncrasy),
.hypersensitivity i.e. allergy
• The more poison taken , the more severe the
reaction to it. Increase the dose → increase
severity of signs and symptoms. All substances
known to man are poisons , only the dose
determines the effect.
• Gases are rapidly absorbed > liquids > solids
( powders > lumps).
• Poisons may enter the body through skin or
vagina, by i.m. injection, by stomach or
rectum, through the lungs, or by injection into
veins, and will become circulated with a
rapidity increasing in the order of entry stated.
• Grease on the skin or food in the stomach may
interfere with absorption. A fatty meal
increases absorption of fat- soluble poisons.
• Many poisons entering the body in small
quantities repeatedly are broken down or
excreted whilst exercising their effects and
chronic poisoning will be likely to occur only
where there is some accumulative action as
with arsenic and lead.
• Accumulation = Rate of intake > Rate of
elimination, e.g. digitalis.
• Chemical interaction of the poison:-
1- Addition:- (1+1=2) e.g. simple analgesics
Aspirin+ Paracetamol.
• 2- Synergism:- (1+1=3) e.g. Inhibition of
respiratory center, EtOH + Barbiturates.
• 3- Antagonism:- BAL + Pb.
• How drugs act at a cellular level?
Most drugs chemically resemble an
endogenous compound and bind to a specific
molecule which may be an enzyme or part of
the cell membrane (receptor).
• Drugs can be either:-
• (a) Agonists which activate the receptor or
• (b) Antagonists which prevent agonists
combining with the receptor.
• Form of poison:-
( Gaseous, solid, fluid). Gaseous and dissolved
or fluid poisons will naturally enter the
circulation with greater ease than a solid
poison.
• The speed of absorption of a poison:-
Prussic acid fumes (HCN), Carbon monoxide
(CO), sewer gases (H2S,etc) are rapidly
absorbed → ill effects. A mixture of corrosive
sublimate in alcohol is more rapid in action
than a solution in water. The poison being less
soluble in water. Some poisons have a surface
corrosive action, like Lysol or causing vomiting,
like aspirin may reduce their own absorption
thereby.
Dose response
This notion of dose is critical for understanding
toxic effects. Based on the model we are looking
at (threshold or hormesis), even some of the
most toxic chemicals known will cause either no
discernable effect or a positive effect on humans
at very low doses. On the other hand, at very
high doses, even essential substances like
oxygen and water will harm or kill. In between,
different quantities of toxic agents can induce
different degrees of harm.
A ‘dose-response’ relationship is the
quantitative relationship between the amount
of a toxic agent exposed to and the extent of
a specific effect that is induced. The units for
dose are mg/kg, which represents the
amount of toxic agent per amount of body
weight. The two main characteristics of dose
response, its patterns (linear, threshold,
hormesis) and range of effects (acute,
subchronic, chronic) can be explained by
how the toxic agent acts at the molecular
level and the body’s disposition mechanisms
for it.
 Patterns –
The dose-response relationship of a toxic agent
acting in an individual follows three different
patterns – linear, threshold and hormesis – based
on the strength of effect (either positive or
negative) produced at different doses.
Linear - In this pattern, toxic response is directly
proportional to dose and there are adverse
effects at all doses, even low ones. This can
happen when there are no defense mechanisms
in the body that can overcome the toxic effects
produced by an agent.
Traditionally, this model has been applied to
many mutagenic carcinogens in which damage
of genetic material is assumed to have no lower
limit—even one base pair deletion caused by a
very small amount of a carcinogen can produce
a mutation in a gene, which then spurs the
formation of a tumor. However, currently there is
substantial controversy over whether the linear
model is applicable to mutagenic carcinogens,
based on the finding that most of our
background radiation comes from radioactivity in
our own body
We have at least 9,000 radioactive disintegrations in our
body each second, and this number can significantly
vary depending on where an individual was born and
raised. The resulting radiation strikes billions of our cells
each hour. Thus, the idea that radiation to one cell can
initiate cancer may be viewed as illogical, as background
radiation is proof that the body has defense or repair
mechanisms against it. In terms of non-mutagenic
carcinogens (which bind to DNA, RNA or protein), the
linear model definitely does not apply, because there are
known mechanisms in the body that can overcome the
damage caused. Nonetheless it is standard for many
agencies to use the linear model for all carcinogens, so
as to be on the safe side and lower the risk of harmful
effects.
 Threshold - Toxic response is directly proportional to dose,
but unlike the linear model, there is a dose, called a
threshold, below which there are no apparent adverse
effects from exposure to the toxic agent. In this situation the
human body has defenses against the toxic agents that
follow this model. Some organs, especially the liver and
kidneys, can biotransform chemicals into non-toxic
substances that can be eliminated from the body. However,
if the dose is so large (over the threshold) that the body’s
defense mechanisms are exhausted, the body must absorb
the toxic insult. This model applies to many non-
carcinogenic toxic agents. For example, the threshold dose
for DDT is 10 mg/kg.
Hormesis - In this pattern, toxic substances may impart
beneficial or stimulatory effects at low doses, but adverse
effects at higher doses. The curve of a hormetic model is U-
shaped or J-shaped.
When a toxic agent challenges the body’s adaptive capacity, if the
dose of the toxic agent is small enough, the body is capable of
biotransforming and/or eliminating the toxic substance and then
returning to its normal balance point (homeostasis). In addition,
the body over-compensates for the initial disruption and damage,
leading to a stimulatory response such as growth, longevity,
reduction in cancer risk and birth defect incidence. However, at
any dose higher than the hormetic threshold, the toxic agent
overwhelms the body’s capacity to eliminate it and produces its
negative damaging effects. An example is Tylenol, whose active
ingredient is acetaminophen. Taken at the suggested low dose,
this chemical produces its therapeutic response, and then is
rapidly biotransformed, with the metabolites eliminated. However,
at a high dose, the normal level of biotransforming enzymes may
not be sufficient and the excess acetaminophen is sent to a
cytochrome P450 enzyme, which produces a reactive metabolite
that is toxic to the liver
 Some other examples of hormetic substances are
metals (e.g. trace amounts of arsenic can lower body
weight) and alcohol (controlled consumption can
decrease the risk of cardiovascular disease). Recently,
some studies have shown that radiation may follow the
hormetic model, which has caused much controversy.
Range of effects - The type of effect that occurs is
dependent on the dose of the toxic agent administered,
and its duration and frequency of exposure, as well as
the action of the toxic agent at the molecular level. The
effects can either have an immediate impact (acute) or
develop gradually over longer periods of time
(subchronic or chronic): · Acute - This type of effect
takes place immediately after a single episode or
incidence of a toxic agent that is very potent, or one that
is administered in a larger dose.
In either of these cases, when the toxic agent
enters the body, it can begin to induce damage right
at the site of exposure (GI tract, lungs, skin) or in
areas where it is easily absorbed (blood, brain),
because it produces cellular dysfunction or necrosis
in the first cells that it comes in contact with. For
example, acute skin exposure to many toxicants
such as mercury and formaldehyde can induce
contact dermatitis. An acute exposure to DDT
causes paraesthesia (tingling and numbness),
which occurs as a result of rapid migration of the
toxic agent into the CNS, where it reduces the
permeability of the neuronal membrane and makes
it extremely sensitive to even small stimuli.
In a few cases, acute exposure can also explain some
systemic effects. For example, an important acute
side effect of the drug ecstasy is unwanted muscle
contraction in the jaws, arms and legs caused by the
increased release of monoamine transmitters
(serotonin, noradrenalin, dopamine). For the
quantification of acute toxicity, the terms lethal dose,
effective dose and toxic dose are used. Sub chronic -
A sub chronic effect occurs as a result of repeated
exposure but of smaller doses over several weeks.
This type of effect represents diseases caused by the
cumulative damage of the toxic agent in specific organ
systems.
 A small dose of a toxic agent can be absorbed and distributed to
an organ where it is mostly biotransformed and/or eliminated. The
amount that is not detoxified or excreted may cause minimal,
inconsequential damage, and over a short period of time remains
unnoticeable. However, with repeated exposure, the effect may
become cumulative in the damaged organ. For example,
workplace exposure to lead over a period of several weeks can
result in anemia. Ingestion of Coumadin tablets (blood thinners)
for several weeks as a treatment for venous thrombosis (clumping
of platelets and fibrin in the veins) can cause internal bleeding.
Chronic2 - A chronic effect occurs as a result of repeated
exposure but of smaller doses over several months or years (as
opposed to weeks in subchronic). This can be explained by the
same reasoning for a subchronic effect, except that the extent of
damage is more pronounced. Chronic effects tend to involve
damage to organs where biotransformation and elimination
occur, as well as the development of various types of cancer.
Subchronic and chronic exposures can result in systemic effects
as well as long-term local effects. For example, over a period of
time, alcohol consumption can result in 2 The definitions of
subchronic and chronic exposure used here are standard
definitions. Often it is difficult to distinguish between the
subchronic and chronic exposure, given that the duration of
exposure is inferred from the toxic effects produced;
these can be very similar in the two situations.
development Genetics - Genetic variation in biotransforming
capability accounts for most of the large variation among
humans. In particular, acetylation, a type of phase II reaction
(see ‘Modification- Biotransformation’) is influenced by
genetic differences in humans, so that in people with slow
acetylation, the blood or tissue levels of certain drugs (or
Phase I metabolites) exceeds their toxic threshold. For
example, slow acetylation of isoniazid, an anti-tuberculosis
drug, can yield nerve and liver damage. Other genetic
variations can increase susceptibility to toxic agents as well.
For instance, in humans with defective monooxygenase (an
enzyme that catalyzes oxidation reactions), there is an
excessive fall in blood pressure due to hydralazine (anti-
hypertensive drug).
• Certain broad groups of poisons may be
defined by their common mode of action.
Roughly:-
• 1- Abortifacients e.g. ergot, quinine, hormone,
pituitary, mesoprestol,etc.
• 2-Corrosives e.g. strong acids (mineral,
organic), cresol, alkalis, etc.
• 3- Deliriants and convulsants e.g. cocaine,
strychnine, aconite, etc.
• 4- Hypnotic or narcotic e.g. barbiturates,
chloral, morphine.
• 5- Irrespirable poisonous gases or vapours
e.g. CO, H2S, HCN, tetrachlorethane, etc.
• 6- Irritants:- metallic e.g. (AS, Hg, Sb).
Vegetable e.g. (castor oil).
Gases e.g. (SO2, NH3,etc).
Non metallic e.g. phosphorus.
• 7- Paralytics and anti-cholinesterase:-
e.g. coniine, curare, nicotine etc.
• Organic poisons are gradually destroyed in
bodies undergoing putrefaction, but in the
early stages of decomposition such poisons
may be isolated, e.g. ethanol has been
recovered from peripheral blood seventy two
hours and longer after death.
• Inorganic metallic poisons can not be
destroyed by putrefaction and poisons such
as arsenic may be detected in residual
portions of putrefied tissues or skeletal
remains many years after burial.
Factors controlling the effects of poisons
a/ The state of the poison:- (quality)
Gases, liquids, solid (lumps & powders).Gas
forms are most rapid than solids. If an agent
is insoluble and not absorbed it may not be
toxic like red phosphorus and yellow arsenic.
b/ The routes of administration:-
Inhalation, i.v. i.m., s.c., intradermal, oral,
rectal, intact skin. But intact skin can absorb
rapidly some substances like phenols,
organophosphorus insecticides and tetra ethyl
lead.
c/ The dose:- (quantity)
It is widely held that every poison regularly kills at a
certain dose – the fatal dose so commonly referred
to in cases of criminal poisoning.Different patients
react differently to the same dose of a drug and that
the same patient may react differently to the same
dose of the same drug at different times. Any way
the larger the dose the more effective is the poison.
The factors influencing the response are age, sex,
nutrition, weight, etc. This variability in response is a
fundamental biological principle. The increase in
dose leads to increase in severity of symptoms.
 The age:-
d/

We can classify people in children, adults and

elders. The two extremes of age are more
susceptible to toxic agents generally. Infants,
due to their labile nervous and respiratory
systems, are intolerant to narcotics and
hypnotics and are resistant to the effects of
atropine. Children are still developing
physiological processes while elders have
debilitating diseases.
e/ Hypersensitivity:- Allergy= exaggerated
response to the drug. Antigen-Antibody
reaction.
Very small harmless doses of drugs may
produce severe symptoms and even
anaphylaxis in some hypersensitive
individuals e.g. ASA or penicillin.
Toxicogenetics (Idiosyncrasy).
Abnormal response to drugs. Hereditary basis e.g.
favism & sulphanomide in G6PD deficiency →
Haemolytic anaemia.
f/ The state of the stomach in orally administered
poisons:- Amount, types (of food)
The food in the stomach delays the action of poisons
due to dilution. Fatty food materials make a coat of
the gastric mucosa. Emptying is thus delayed due to
the liberation of more enterogastrin and hence a
slower motility. A fatty meal increases absorption of
fat soluble poisons. An empty stomach increases
toxicity. The pH of the stomach affects toxicity. If it is
more acidic it increases the toxicity of aspirin. If it is
less acidic it decreases CNH (cyanide) toxicity.
pH = potential power of hydrogen ion.
g/ Tolerance:-
The repeated intake of certain drugs produce a
state where the individuals can withstand big or
even toxic doses. It happens with dependence
drugs such as morphine, ethanol, etc. It is due to
the stimulation of antibody production beside
acquired better power of detoxification or excretion.
h / Accumulation:-
Here the rate of intake is greater than the rate of
elimination. After repeated small doses of certain drugs ,
which are not metabolized easily, the effect of a single
large dose is reached, e.g. digitalis.
i/ Health state:-
Diseases of the liver and kidney magnify the effects of
poisons due to decrease in the hepatic destruction
(detoxification ) of the poison and its renal excretion. A
depressed CNS is very susceptible to narcotics and
hypnotics, but in CNS excitation, as in convulsions and
mania, large doses of hypnotics can be safely
administered. A diseased heart is more susceptible to
digitalis toxicity than the normal heart. It impairs hepatic
and renal circulation in addition to impaired metabolism.
The best example is digitalis where the picture of
toxicity is the same whether a single toxic dose is
ingested or in the therapeutic use as in heart failure.
Accordingly the toxic level is reached by giving small
single doses. It is not a state of chronic poisoning but is
similar to acute poisoning.
j/ Drug interaction:-
Two drugs or more are administered at the same time.
There may be harmful or beneficial effects which
deserve careful consideration in prescribing and
treating by different compounds. Drugs interact by the
following mechanisms:-
1/ Synergism
2/ Antagonism
1/ Synergism:-
is the toxicological co-operation by:-
i/ Summation. 1+1=2 e.g. Aspirin + paracetamol
ii/ Potentiating. 1+1=3 e.g.
Summation is the simple additive effect of the similarly
acting drugs e.g. amyl nitrite and methylene blue to
form methaemoglobin in the treatment of cyanide
poisoning.
Potentiation means that the effect of the administered
similarly acting drugs is greater than simple algebraic
sum e.g. ethanol greatly potentiates the toxic effects of
barbiturates and tranquilizers i.e. 1+1=3.
2/ Antagonism
means the opposing effects of two drugs by:-
i/ Chemical means
ii/ Competitive means
iii/ Non competitive means
iv/ Physiological means
Chemical means include neutralization of an alkali by
weak acids.
In competitive antagonism the drugs compete for the
same receptor e.g. naloxone or nalorphine compete
with morphine for the respiratory centre. Ethanol
compete with methanol for their metabolic enzyme
alcohol dehydrogenase in the liver.
Non competitive antagonism occurs when the
antagonist acts at another site that differs
from that of the drug e.g. inhalation of short-
acting barbiturates for treating convulsions
produced by strychnine poisoning.
While physiological antagonism takes place
when the drugs have opposing physiological
actions e.g. atropine in treating the muscarinic
effects of poisoning by organophosphorus
insecticides.
Doctor's duties in cases of poisoning
(intended objectives): -
A knowledge of different classes of common
toxicants and environmental pollutants,
differential diagnosis of chemicals and clinical
picture, first aid treatment and antidotal
measures. A poison is any substance that can
produce harmful effects when administered.
That means any substance can become a
poison.
Classification of poisons: -
Poisons could be classified according to action,
alphabetically, manifestations and nature.
The incidences of poisoning are mainly: -
Accidental or intentional (suicidal, homicidal),
Exhibitional (for creating sympathy), Abortifacient
(induce abortion), Aphrodisiacal (to arouse sexual
desire), Pesticides, Insecticides, Rodenticides, Herbicides,
etc. (to kill animals, insects, mice, herbs etc.).
Epidemiology of Poisoning: -
It is the study of causative factors associated with
the occurrence and number of cases of diseases and
illnesses in a specific population.
The following toxicological data are derived from
American association of poison control center.
So it is mostly a description of the epidemiology of
unintentional poisoning. It is very difficult to find the
primary data of poisoning in our country because most
of the screening & confirmatory tests
are not done routinely in our set up. Additionally, we
don’t have well organized poison control center.
Today, poisoning (both accidental and intentional), is a
significant contributor to mortality and morbidity. It
has been estimated that 7% of all emergency room
visits are the result of toxic exposures. Household
cleaner, over-the-counter and prescription drugs,
cosmetics, and solvents comprise the most frequent
human toxic exposures. Young children and elderly are
most likely to be accidentally exposed to drugs or
household chemicals at home. During adolescence
and young adulthood the exposures are more likely to
be intentional, either through suicide attempts or
experimentation with drugs or alcohol.
More than 72.4% of all poison exposures occur in
children and adolescents less than 17 years of age.
Exposures are equally reported in males and females.
However, adult men have been reported to be more at
risk of occupational exposures than adult women. Route
of entry of exposures reported was by mouth in most
cases: 77% were the result of ingestion, 7.0% were
transdermal, 5.9% were ophthalmic; and 5.5% were by
inhalation. Site of exposure was a residence in 91.9% of
all, followed by the workplace, schools and health
facilities. Most poison exposures do not result in clinical
toxicity. In general, nearly everyone is at risk of acute
and chronic toxic exposures to hazardous substances in
the ambient environment.
Medical statistics from poison Information &
Control Centers in U.S.A.
There are at least 430 Poisoning Information &
Control Centers.
One year, they received 1.5 million calls.
91% exposure occurred at home.
60% children under five years of age.
89.9% of the cases constitutes accidental
poisoning.
8.2% constitutes intentional poisoning.
Exercise
1. Define toxicology & the terms used in toxicology.
2. Discuss the epidemiologic aspects of toxicology.
3. Discuss the basic classifications of toxicology.
4. Explain what toxicokinetics and toxicodynamics deals
with.
5. Write some of the important environmental
considerations in toxicology.
6. List some of the potential sources of toxicity.
7. Mention poisoning prevention & control strategies