Chemical Agents that
eases), as well as occupational cancers.
Cause Occupational
Diseases
JOHN WAH LIM
SSH School of Public Health, National University
of Singapore
DAVID KOH
SSH School of Public Health, National University
of Singapore
Chemicals are used extensively both in
industry and in our daily lives. Many useful
products are derived from chemicals, such as
plastics, paints, pharmaceuticals, detergents,
and so on. Some chemicals may appear harm-
less, but can result in injury upon contact.
Some adverse health effects develop only after
prolonged exposure and after a latent period.
Occupational disease (OD) refers to any dis-
ease contracted as a result of exposure to factors
arising from work activity (ILO 2011). Diagnosis
of OD requires establishment of the causal rela-
tionship between exposure in a specific working
environment or work activity and a specific dis-
ease; and the disease occurs among exposed
persons with a frequency above the average
morbidity of the rest of the population. The list
of ODs prepared by the International Labour
Organization (ILO) has four main groups: ODs
caused by exposure to agents arising from work
activities (such as chemical, physical, and bio-
logical agents); ODs by target organ systems;
occupational cancer; and other diseases.
Chemical agents account for 41 of the ODs
that are caused by exposure to agents from
work activities; they are the commonest
occupational hazard that can result in OD. In
addition, chemical agents are also the main
contributors to ODs classified by target organ
The Wiley Blackwell Encyclopedia of Health, Illness, Behavior, and Society, First Edition.
Edited by William C. Cockerham, Robert Dingwall, and Stella R. Quah.
© 2014 John Wiley & Sons, Ltd. Published 2014 by John Wiley & Sons, Ltd.
systems (especially respiratory and skin dis-
This entry describes the toxicity of chemi-
cals, their route of exposure, and different
health effects caused by chemical agents, with
a focus on ODs and cancer caused by chemi-
cals. Principles of preventive measures in the
workplace will also be discussed.
TOXICITY OF CHEMICAL AGENTS
Toxicology is the study of poisons and how
they affect the body. Toxicity is an inherent
property of a chemical that causes bodily
injury or disease to a living organism as a
result of physiochemical interaction with liv-
ing tissue. All substances, including chemi-
cals, are potentially poisons. However, all
chemicals can be used safely if exposure is
kept to below tolerable limits. There are vari-
ous factors that influence the toxicity and the
health effects of a chemical agent. These
include its physical state, dose or concentra-
tion, aerodynamic diameter or size, route of
absorption, duration of exposure, and pres-
ence of other chemicals. Personal factors also
determine the susceptibility of a worker to
the adverse effects of a chemical. These
include genetic factors, age, gender, health
status, hypersensitivity, personal habits and
hygiene, and pregnancy and lactation.
HAZARD CLASSIFICATION OF
CHEMICALS
A hazard is anything with the potential to
cause bodily injury, and includes any physical,
chemical, biological, mechanical, electrical, or
2
ergonomic hazard. The Globally Harmonized
System (GHS) divides hazardous chemicals in
the workplace into different categories: physical
hazards, health hazards, and environmental
hazards (see Table 1) (GHS 2007).
Table 1 Globally Harmonized System hazard
classes
Hazard types Hazard categories
Physical hazard Explosives
Flammable gases
Flammable aerosols
Oxidizing gases
Gases under pressure
Flammable liquids
Flammable solids
Self-reactive substances
Pyrophoric liquids
Pyrophoric solids
Self-heating substances
Substances which, on contact
with water, emit
flammable gases
Oxidizing liquids
Oxidizing solids
Organic peroxides
Corrosive to metals
Health hazard Acute toxicity (oral, dermal,
and inhalation)
Skin corrosion/irritation
Serious eye damage/eye
irritation
Respiratory sensitizer
Skin sensitizer
Mutagenicity
Carcinogenicity
Toxic to reproduction
Specific Target organ toxicity
following single exposure
Specific Target organ toxicity
following repeat exposure
Aspiration hazard
Environmental Acute hazards to the aquatic
hazard environment
Chronic hazards to the
aquatic environment
ROUTES OF EXPOSURE
Chemicals can enter the human body via
inhalation, ingestion, or dermal contact.
Inhalational and dermal exposure represent
the main pathways of exposure to hazardous
substances at work.
Inhalation of airborne chemical agents that
exist in physical form, such as gases, vapors,
and particulate matters (including dust,
smoke, fumes, aerosols, and mists), results in
rapid absorption, especially if the chemical is
inhaled into the lungs. It can then be absorbed
into the general circulation system before
reaching distant target organs.
The rate of absorption through skin is usu-
ally slower compared to inhalation or inges-
tion. However, dermal absorption can occur
rapidly if there is a cut or wound on the skin.
Many chemical compounds, especially fat
soluble chemicals, can be absorbed through
the intact skin. Dermal exposure to hazard-
ous chemical agents can also result in occupa-
tional skin diseases.
Absorption of chemicals through the skin
can occur without being noticed by the
worker. Some commonly used chemicals in
the workplace (e.g., pesticides, organic sol-
vents) could potentially result in systemic
toxicity if they penetrate the skin and enter
the systemic circulation to cause health
effects away from the site of entry. Sometimes,
workers have erroneous beliefs about the
route of entry of a chemical, based on its
chemical properties. In the case of pesticides
that have a strong smell, some workers think
that the main route of entry is via inhalation.
They mistakenly believe that wearing a mask
would protect them from its absorption.
However, pesticides which are fat soluble are
mainly absorbed through the skin and
mucous membranes. For such forms of
exposure, workers are required to wear pro-
tective clothing for the skin, including gloves
and eye protection.

Toxic chemical compounds can be absorbed
from the digestive system into general circula-
tion. Ingestion of chemicals in the workplace
can happen unknowingly by workers.
One  instance is when workers, because of
sociocultural norms, eat or drink using their
contaminated bare hands. Another example is
smoking in the workplace, with contaminated
hands handling the cigarettes, resulting in
inadvertent ingestion of the chemical.
HEALTH EFFECTS
Toxic chemicals can cause either local or more
generalized systemic health effects. Local
effects occur at the site of bodily contact, such
as skin or eye irritation. Systemic effects occur
at a site distant from the route of entry of the
chemicals, such as liver or kidney damage.
The onset of health effects can be
either acute or chronic. Acute effects are usu-
ally immediate, resulting from short-term
and often high-level exposure. Chronic
effects are delayed onset health effects follow-
ing cumulative exposure to chemicals.
Health effects from exposure to chemicals
can be reversible or irreversible. Reversible
health effects are often temporary and will
disappear when exposure to that chemical
ceases. One example is dermatitis due to
exposure to mild irritants. Irreversible effects
are permanent health changes that cannot be
repaired. Examples of irreversible ODs
caused by chemicals include cancer, silicosis,
and asbestosis.
MECHANISMS OF TOXIC EFFECTS
There are various ways in which chemicals
can cause harm or disease in humans.
Irritants (e.g., isopropyl alcohol, acetone)
produce reversible inflammatory changes
3
of the skin, eyes, or mucous membranes of
the respiratory tract. The substance is
corrosive if the damage is irreversible.
Sensitizers are chemicals capable of producing
an allergic response. The body produces lit-
tle or no immune response at the initial
exposure. However, with repeated exposure,
the immune system can be sensitized and
subsequently evoke an allergic response to
the allergen. Respiratory tract sensitizers,
such as isocyanates, natural rubber latex
proteins, or ethylene diamine, can cause
asthma. Skin sensitizers, such as nickel,
fragrances, chromates in cement, formalde-
hyde, and glutaraldehyde, can cause allergic
contact dermatitis.
Genotoxicity is a specific type of toxicity.
Genotoxic chemicals can damage and
alter genetic materials within the cells,
which may cause carcinogenicity or birth
defects.
Carcinogens are chemicals capable of causing
cancers in humans. A list of carcinogens
has been prepared by the International
Agency for Research on Cancer (IARC) of
the World Health Organization (WHO).
Mutagens are chemicals that can cause
changes in the DNA of cells (mutations),
which may result in various diseases or
abnormalities in future generations.
Mutagens such as chloroform and ethylene
oxide can affect cells of the reproductive
system (sperms and ova). Other mutagens,
including benzene, lead, and vinyl chlo-
ride, can affect cells that are not part of the
reproductive organs (e.g., liver, kidney, or
blood cells).
Teratogens are chemicals that cause birth
defects, abnormalities, developmental
delays, or fetal death, but cause no dam-
age to the mother. Methyl mercury,
lead, and xylene are some examples of
chemical teratogens. The developing
fetus at the two- to eight-week stage is at
highest risk.
4
Reproductive toxins are chemicals that
can  affect the ability of both men and
women to produce offspring. The adverse
effects of  reproductive toxins include
sterility, reduced fertility, and spontaneous
abortion.
COMMON OCCUPATIONAL DISEASES
CAUSED BY CHEMICAL AGENTS
Occupational cancers
The International Agency for Research on
Cancer (IARC) classifies agents into various
groups. These are Group 1: carcinogenic to
humans (109 agents); Group 2A: probably
carcinogenic to humans (65 agents); Group
2B: possibly carcinogenic to humans (275
agents); Group 3: not classifiable in terms of
its carcinogenicity to humans (503 agents);
and Group 4: probably not carcinogenic to
humans (IARC 2012). Some proven occupa-
tional carcinogens and their target organs are
shown in Table 2.
Many of these agents are encountered in
occupational settings. Occupational carcinogens
are an important cause of death and disability
Table 2 Proven occupational carcinogens
Agent
Asbestos
Metalliferous carcinogens
• Arsenic
• Beryllium
• Cadmium
• Chromium
• Nickel
Aromatic amine carcinogens
• 4-aminibiphenyl and its nitro derivatives
• Β-Naphthylamine
Benzene in petroleum associated industries
Ethylene oxide
Formaldehyde
Polycyclic aromatic hydrocarbons and aromatic amines
worldwide, with an estimated 152,000 deaths
annually due to exposure to occupational car-
cinogens (Driscoll et al. 2005a). Cancers due
to occupation are largely preventable, and the
estimated burden of occupational carcino-
gens can be diminished by improving work-
ing conditions.
Occupational cancers develop after a long
latent period. The time between first expo-
sure to the carcinogen and presentation of
cancer is usually more than 10–15 years. It
can be even longer – as in the case of asbes-
tos-related mesothelioma, which can take
40–50 years to develop. Susceptibility to
occupational carcinogens is higher when the
exposure happens at a younger age, or if there
are combined exposures such as smoking and
asbestos.
Occupational skin diseases
Occupational skin diseases can be caused by
chemical agents, mechanical trauma, physical
agents, and biological agents. Chemical
agents are the main cause of occupational
skin disease and can act as either irritants or
sensitizers.
Target organ(s)
Lung, larynx, ovary
Lung, skin
Lung, prostate
Lung
Lung
Lung, nasal sinuses
Urinary tract (especially bladder)
Hemopoetic (blood forming organ)
Lung, bladder, skin
Nasal, paranasal sinuses
Lung, bladder, skin
 5

Contact dermatitis is the most common
type of occupational skin disease. It refers to
an inflammation of the skin due to exposure
to a hazardous agent. There are two main
subtypes” irritant contact dermatitis (ICD)
and allergic contact dermatitis (ACD).
ICD is a non-immunologic reaction of
skin  inflammation caused by direct damage
to the skin following exposure to an irritant.
The reaction is typically localized to the site
of contact. It may be caused by acute expo-
sure to highly irritating agents (e.g., acids,
bases, oxiding/reducing agents), or chronic
cumulative exposure to mild and weak irri-
tants (e.g., water, detergents, weak cleaning
agents). It is much more common than ACD.
ACD is a delayed hypersensitivity reaction
triggered by dermal contact to a skin sensitizer
(allergen). A worker must first be sensitized
to the allergen. Subsequent exposure of the
skin to the same allergen elicits an immuno-
logic reaction resulting in inflammation of
the skin. The reaction is not confined to the
site of contact and may result in systemic
responses and skin rashes elsewhere on the
body. Common allergens at the workplace
that can cause ACD include industrial com-
pounds (e.g., metals, epoxy, and acrylic res-
ins), agrochemicals (e.g., pesticides and
fertilizers), and latex.
A less common type of occupational skin
disease is contact urticaria. This is an imme-
diate wheal and flare reaction to a contact
urticant. The symptoms develop within 30
minutes of contact. Common causes of con-
tact urticaria are latex proteins in rubber
latex gloves and raw proteinaceous food
materials handled by food preparation
workers.
Occupational respiratory diseases
According to the global burden of occupa-
tional diseases study, the annual number of
deaths attributed to occupational respiratory
diseases is estimated at 318,000 for chronic
obstructive pulmonary diseases, 38,000 for
asthma, and 30,000 for pneumoconiosis
(Driscoll et al. 2005b). Table 3 shows both the
acute common and the chronic occupational
respiratory diseases that are a result of expo-
sure to toxic chemical agents (Lee, Takahashi,
and Tan 2011).
Occupational asthma is a disease charac-
terized by variable airflow limitation and
airway hyperresponsiveness due to specific
agents inhaled in the workplace. A large pro-
portion of adult-onset asthma is attributable
to occupational exposure. Occupational
asthma can be immune or non-immune
mediated. Immunologic asthma develops
after a latent period of exposure to sensitiz-
ers. Common agents that can cause immu-
nologic occupational asthma are isocyanates,
wood dust, soldering, and welding fumes.
Non-immunologic asthma, also known as
reactive airway disease, can develop rapidly
without a period of latency. It is usually
associated with exposure to high concentra-
tion of chemical irritants. Accidental inhala-
tion of irritant gas (e.g., chlorine), fumes,
and vapors can lead to reactive airway dis-
ease. The symptoms of airway irritability
Table 3 Common acute and chronic occupational
respiratory diseases
Acute occupational Chronic occupational
respiratory diseases respiratory diseases
Occupational asthma Silicosis
Acute respiratory Coal workers’
reactions to irritant pneumoconiosis
gases Asbestosis and other
Acute systemic asbestos-related
reactions to metal diseases (including
fumes, polymer cancers)
fumes, and organic Hard metal lung disease
dusts Beryllium disease
Hypersensitivity Chronic obstructive lung
pneumonitis disease
6
usually resolve spontaneously, but can persist
indefinitely.
Pneumoconiosis is the diffuse fibrotic
reaction of the lung tissues that occurs after
prolonged inhalation of mineral dust. The
commonest type of pneumoconiosis world-
wide is silicosis. This is caused by inhalation
of dust containing crystalline silicon dioxide.
High-risk occupations are mining, quarrying,
sandblasting, stone cutting, and polishing.
PRINCIPLES OF PREVENTION OF
OCCUPATIONAL DISEASES DUE TO
CHEMICAL AGENTS
Many of the ODs that are the result of specific
chemical agents are preventable. Three levels
of prevention can be implemented (see
Table 4).
Primary prevention aims to prevent the
occurrence of a disease by eliminating the
causal agent or preventing it from causing
bodily damage. Secondary prevention aims to
detect disease in its early stages and to  halt
the progression of the disease before it mani-
fests as clinical symptoms and signs. Tertiary
prevention is applicable to people with estab-
lished disease, who require treatment and
rehabilitation to minimize complications and
disabilities or to improve quality of life if the
disease is incurable.
Table 4 Prevention of occupational diseases due to chemical agents
Primary prevention
Hierarchy of controls:
• Elimination
• Substitution
• Engineering controls to minimize exposure
• Administrative controls
• Personal protective equipment
Environmental and biological monitoring
Pre-placement medical examinations to identify
vulnerable workers
Once an OD due to chemical exposure is
diagnosed, management of the disorder
should go beyond prescribing medication to
cure the condition. The following measures
may be needed: suspension of the worker
from further exposure; investigating and con-
trolling the source of exposure; notification
to relevant authorities; educating the patient
and employer; identifying other workers who
could also be exposed; rehabilitation; assess-
ment of permanent disability; and compensa-
tion for affected workers.
CONCLUSION
Chemicals can be beneficial or harmful to us
depending on how they are used. As with any
other occupational disease, illness due to
exposure to chemical hazards can be prevent-
able. Control measures, especially primary
preventive measures, should be implemented
to protect the health and safety of workers
and prevent unwanted effects from exposure
to the chemicals.
SEE ALSO: Cancer; Cancer Prevention;
Cancer Prevention Services, Utilization of;
Occupational Health and Safety; Risk;
Screening; Screening for Disease: Challenges;
Surveillance
Secondary prevention Tertiary prevention
Screening: early detection of Medical treatment
exposures and effects Rehabilitation
Periodic medical examinations Compensation

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