C H A P T E R

24
Toxicology in the workplace
Marie Fortin1,2 and Marie Capdevielle3
1
Early Development Department, Jazz Pharmaceuticals, Philadelphia, PA, United States
2
Rutgers University, Department of Pharmacology and Toxicology, Piscataway, NJ, United States
3
MCD Toxicology Consulting, LLC., Middletown, NJ, United States

24.1 Introduction hygienists, engineers, and regulators to help

24.1.1 Genesis of occupational
toxicology
Sir Percivall Pott is often considered the
founder of modern occupational medicine. In
1775 the surgeon, orthopedist, and scientist
recognized the existence of a relationship
between a specific occupation—chimney
sweep—and a rare type of cancer—scrotal
cancer. Since the beginning of industrializa-
tion, physicians have advocated for better
working conditions and this led to the identi-
fication of the classic chemical occupational
hazards: soot, lead, cadmium, coal, benzene,
and asbestos. In 1971 the Occupational Safety
and Health Administration (OSHA)1 was
founded to “assure safe and healthful work-
ing conditions for working men and women
by setting and enforcing standards and by
providing training, outreach, education and
assistance.” Occupational toxicologists have
since worked with physicians, industrial
protect workers.
24.1.2 Role of the toxicologist in the
workplace
Occupational toxicologists save lives and
prevent illnesses and injury. In many occupa-
tional environments, exposure to chemicals is
ubiquitous. While many of the chemicals han-
dled in the workplace may not be highly haz-
ardous, it is imperative to identify and
understand hazards, and properly manage
exposures to protect workers. By creating and
implementing programs to systematically
review chemicals prior to their use in the work-
place, toxicologists can provide guidance on
the adequate engineering controls and personal
protective equipment (PPE) to limit worker
exposure and mitigate risks. The role of the
occupational toxicologist is summarized in
Table 24.1.

An Introduction to Interdisciplinary Toxicology

DOI: https://doi.org/10.1016/B978-0-12-813602-7.00024-7 327 © 2020 Elsevier Inc. All rights reserved.
328 24. Toxicology in the workplace

TABLE 24.1 Potential roles of the occupational toxicologist.

• Assign occupational exposure bands
• Develop occupational exposure limits
• Contribute/manage hazard communication program
• Author safety data sheets according to global harmonized system of classification and labeling2

• Conduct reproductive safety assessments

• Subject matter expert when evaluating employee accidental overexposures
• Collaborate with industrial hygienists, process engineers, safety officers
• Contribute/manage occupational medical programs
• Understand chemistry, pharmacokinetics, toxicology, physiology
• Communicate with manufacturing plant operators and senior management

24.1.3 Fundamental concepts
A number of important concepts are funda-
mental to the practice of occupational toxicol-
ogy. These concepts impact the safety
evaluation of the chemicals, the potential realm
of adverse health effects, and dictate monitor-
ing and risk mitigation strategies. Specifically
the occupational toxicologist must consider
which types of health effects might occur such
as local versus systemic effects, and immediate
versus delayed effects. In addition, the revers-
ibility of the possible adverse health effect is
critical to the understanding and predicting the
potential consequences of an adverse exposure.
Because chronic and latent effects are often
harder to detect, anticipate, and prevent; they
are of chief concern to the occupational toxicol-
ogist. These necessary notions should be briefly
reviewed (Table 24.2) before the case studies.
24.2 Case studies
This chapter is not intended to provide the
full scope of potential effects observed in occu-
pational settings; it will rather highlight classi-
cal examples and important lessons learned in
the field. Toward the end of the chapter, the
main types of assessments performed by occu-
pational toxicologists will also be presented.
24.2.1 Case study 1: Margarita
photodermatitis
While most beach-side bars do not have
occupational toxicologists on staff, most bar-
tenders do wear PPE (gloves) when slicing
lime before a hot sunny day. Ever wondered
why? Lime oil contains a chemical that can
cause phytophotodermatitis (8-methoxypsora-
len).7 A number of other chemicals of industrial
or pharmaceutical relevance can cause photo-
toxicity; these include several essential oils (e.g.,
bergamot), tetracyclines, coal tar derivatives,
anthraquinones (e.g., dyes), salycilates and ben-
zophenones, and isotretinoin.8 10 Phototoxicity
can occur via two main mechanisms:
Photoirritation occurs when a chemical
absorbs energy from sunlight and changes
energy state in such a way that it becomes
more reactive or that it releases damaging free
radicals (and becomes more of an irritant than
without light exposure). Clinically this usually
presents as an exaggerated sunburn which
may include vesicles (blisters) and scaly skin.

V. Toxicology at home and the workplace

 24.2 Case studies
This type of reaction is immediate but can
worsen over a couple of days before the clinical
presentation ameliorate. The resolution can
take several days and scarring may remain
depending on severity.11,12
Photosensitization, on the other hand, occurs
when the energy of the sunlight turns a chemical
into a sensitizer. While photosensitizers require
photoactivation, most sensitizing chemicals actu-
ally do not need light exposure to cause sensiti-
zation. At the molecular and cellular level, the
sensitizer must have electrophilic properties and
will bind nucleophilic sites in skin proteins (e.g.,
cysteine and lysine residues primarily), the hap-
ten protein complex (or antigen) is recognized
329
as foreign by antigen-presenting skin dendritic
cells (Langerhans cells) that will migrate to the
lymph node to trigger T-cell differentiation and
proliferation as memory T-cells (induction
phase). Upon subsequent exposure (elicitation
phase), the memory T-cells will cause inflamma-
tion through the activation of mitogen-activated
protein kinase pathways and proinflammatory
cytokine release.13 It is noteworthy that for a
(photo)sensitization reaction to be elicited, there
must have been previous exposure to the perpe-
trating chemical or to one that is cross reactive.14
While irritation (reversible) or sometimes
corrosion (irreversible) usually occur due to
accidental dermal or ocular overexposure,

Progression of a photodermatitis due to lime juice.

V. Toxicology at home and the workplace

330 24. Toxicology in the workplace

TABLE 24.2 Fundamental concepts.

Concept Definition Example

Local effect Occur at the site of contact/exposure between the Upon inhalation, the very reactive chlorine gas reacts
body and the chemical. Usually, very little of the with the tissues of the respiratory tract, producing
chemical is absorbed in the bloodstream swelling and damage to the lungs3
Systemic Require absorption and distribution of the chemical Benzene may be inhaled, but the long-term effects
effect through the body and result in effects in one or more are manifested in the blood and bone marrow,
locations often distant from the original point of entry resulting in leukemia and other blood cancers4
Target The organ where a chemical manifests its first or For benzene, the bone marrow is said to be the
organ of most important toxicity. It may not be the port of “target organ of toxicity”
toxicity entry or the tissue which has the highest
concentration. The target organ generally displays an
increased vulnerability due to specific biological
pathways of its cells and tissues
Reversible The reversibility of the response is often dependent The liver is considered to be more resilient than
effects on the tissue affected and the concentration of the central nervous system. This is due to the capacity of
chemical at the site of action. Some tissues are more the hepatocytes to readily regenerate compared to
resilient and will more readily recover from a toxic the limited ability of the brain to undergo
exposure but all organs and tissues generally have a neoneurogenesis.5 Extreme liver damage can
“point of no return” however lead to liver failure which is irreversible

Irreversible Irreversible effects will persist well beyond the Compounds that leads to the formation of DNA
effects cessation of exposure and are therefore considered adducts formation and causes mutations might
chronic eventually lead to cancer, an irreversible condition
Acute Acute health effects typically result from accidental If several employees start complaining of eye
effects overexposure and are usually readily identifiable. In irritation, immediate action to prevent further
these types of adverse events, the cause is usually exposure would be taken, usually resulting in a
identifiable and traceable and can in most cases be reversal of the exposure and the effects
remediated entirely
Chronic Chronic exposure or sometimes a single overexposure Pulmonary fibrosis in workers chronically exposed to
effects which may not result in any identifiable acute effects, wood dust
can cause chronic effects. Chronic effects are those
that will either remain, or even progress, after
termination of the exposure
Delayed Delayed effects are those that manifest weeks to years Asbestosis is diagnosed years after exposure to
effects after the initial exposure. Delayed effects are often asbestos has begun6
chronic
Latency The time between the exposure and the manifestation Organophosphate-induced delayed polyneuropathy
period of an adverse effect, varies by chemical, endpoint, occurs 1 4 weeks after single or short-term
and exposure regimen overexposures and is characterized by the distal
degeneration of axons of the peripheral and central
nervous systems

sensitization and phototoxicity are more diffi- Nowadays in vitro tests have largely replaced
cult to prevent and control as there is often a in vivo tests to assess phototoxicity, irritation,
delay between the exposure and the reaction and sensitization.15 Specifically the following
which complicates the root cause analysis. Organization for Economic Cooperation and

V. Toxicology at home and the workplace

 24.2 Case studies
Development guidelines can be used for this
purpose: Test No. 432: In Vitro 3T3 NRU
Phototoxicity Test; Test No. 439: In Vitro Skin
Irritation: Reconstructed Human Epidermis
Test Method; and Test No. 442E: In Vitro Skin
Sensitisation.16 Overall many chemicals present
in the workplace can trigger irritation, sensiti-
zation, and phototoxic reactions. These effects
are likely those most frequently encountered
in the workplace. To mitigate these potential
adverse effects, it is critical to understand the
hazards of the chemicals present in the work-
place and to implement safe work practices
and adequate use of engineering controls and
PPE such as gloves, and safety googles. Next
time you’re making margaritas from scratch
on a sunny day . . . don’t forget to use gloves.
24.2.2 Case study 2: Lead neurotoxicity
Lead pipes used in ancient Rome’s aqueduct
systems have been said to have contributed to
the Empire’s decline,17 yet lead is still present
in solders and other components of aqueduct
systems, in many communities, such as Flint,
Michigan. Lead has had a number of other
industrial uses and workers, including jewe-
lers, miners, smelters, and painters, as well the
general public, are still overexposed to
lead.18,19
Although lead has been associated with a
host of adverse health effects ranging from
immunotoxicity to endocrine dysfunction and
epigenetic effects, its primary target organ is
the central nervous system. The pathophysiol-
ogy and severity of the adverse neurological
outcomes is life-stage dependent. Children,
who are more susceptible than adults, display
altered neurocognitive development and func-
tion following low-level lead exposure.20 In
fact lead is one of the few chemicals considered
to not have a threshold and for which all level
of exposure is associated with some form of
risk. In workers overexposed to lead, the
V. Toxicology at home and the workplace
331
clinical presentation can range from forgetful-
ness to the “wrist and foot drop” where motor
function is severely impaired. Severe cognitive
and motor impairment and even deaths have
been historically linked to lead exposure. There
is evidence of decreased cognitive performance
in adults with blood levels greater that 25 µg/
dL,21 but more subtle effects could occur at
lower levels.
The nature and magnitude of the neurologi-
cal impairments change according to the extent
of lead exposure and early effects are difficult
to detect (i.e., forgetfulness) which complicates
the toxicological evaluation. Given the ubiqui-
tous nature of lead, airborne monitoring is not
practical, nor sufficient, to protect workers.
While the workplace exposure can be similar
for two industrial painters, their specific work
practices, their home environment, and expo-
sure to other sources (e.g., going to a shooting
range or making jewelry as a hobby) will influ-
ence their internal lead burden. Even nutri-
tional status is known to modulate lead
absorption, with deficiencies in calcium and
iron increasing gastrointestinal absorption.
Another interesting aspect of lead toxicity is
that bone lead generally represents about 95%
of the total lead body burden.22 Lead substi-
tutes calcium in the bone matrix and its half-
life in bones is approximately 7 years, which is
considerably longer than the blood half-life of
approximately 28 days. Although bone storage
is thought to have a protective effect, bone
lead can eventually be released in the circula-
tion since the bone and blood are in
equilibrium.
Although the OSHA standard defines an air-
borne limit of 0.5 mg/m3 ; a program of biologi-
cal monitoring and medical surveillance is to
be made available to all employees exposed
to lead above the action level of 30 µg/m3
time-weighted average (TWA) for more than
30 days each year. This program consists of
periodic blood sampling and medical evalua-
tion to be performed regularly as dictated by
332 24. Toxicology in the workplace
previous laboratory results, worker complaints
or concerns, and the clinical assessment of the
examining physician. This approach allows a
more precise assessment to the internal expo-
sure to lead. Current United States regulation
states that employees must be notified of a
blood lead level of 40 µg/100 g and levels
greater than 50 µg/100 g might require removal
from the workplace.21
24.2.3 Case Study 3: Crystalline silica
Crystalline silica occurs extensively in
nature.23 It is one of the most abundant consti-
tuents of the earth’s crust. Silicon is the element
and it exists primarily in the form of its dioxide,
SiO2, silica. Silica is 59% of the earth’s crust and
is detected in many mined materials at varying
concentrations (i.e., talc, calcium carbonate,
cement).23 Examples of occupations with known
high-silica exposure include mining, sandblast-
ing, road construction, pottery making, tunnel-
ing operations, and stone masonry.
The Committee on Pneumoconiosis and the
Committee on Standards of the American
Public Health Association, at a joint meeting in
November 1932, adopted a definition of silico-
sis which included fibrotic changes and miliary
(innumerable) nodulation in lungs, with
decreased chest expansion, lessened capacity
for work and characterized by X-ray findings.
Susceptibility to tuberculosis was also identi-
fied in conjunction with silica exposure. Three
stages were defined in the progression.24
The development of silicosis is dependent on
the dosage of silica, the amount of dust in the
inspired air, the amount of silica in the dust,
and the extent of the exposure.24
Silicosis is caused by the inhalation of crystal-
line silica that triggers a fibrotic response in
lung parenchyma.25 The condition is irreversible
and continues even after exposure has
stopped.26 It presents as a diffuse interstitial dis-
ease and the clinical expression ranges from no
V. Toxicology at home and the workplace
symptoms to chronic respiratory failure. As
nodules may form in the lung prior to any iden-
tifiable effect on lung function, chest radiogra-
phy is used for diagnosis and monitoring
silicosis which is characterized as simple (multi-
ple small nodules) or complicated (progressive
massive fibrosis).26 Amorphous forms of silica
(noncrystalline) have very low fibrogenic poten-
tial.27 Additionally silicosis may be acute,
chronic, or accelerated.
The initiating event in silicosis is the ingestion
of silica particles by pulmonary alveolar macro-
phages. Iron complexed with silica promotes
reactive oxygen species production, contributing
to granuloma development.28,29 In addition, to
the fibrotic response, there is decreased anti-
body- and cell-mediated immune parameters,30
toxicity to macrophages, and polymorphorpho-
nucleocytes, and an increased susceptibility to
infectious pathogens. Silica is also a pulmonary
irritant;31 it decreases reticuloendothelial system
clearance, suppresses humoral immunity, and
cell-mediated response against allogeneic fibro-
blasts and may also inhibit phagocytosis of bac-
terial antigens.32
While silicosis mortality in developing coun-
tries is decreasing, reports of new occupations
with silica exposures continue to emerge. The
World Health Organization in conjunction with
the International Labor Organization established
the Global Program for the Elimination of
Silicosis in 1995. Development of new exposures
to crystalline silica underscores the need to have
high awareness of the sources (i.e., engineered
stone countertops, sandblasting denim, and
hydraulic fracturing) and prevention strate-
gies.33,34 In 1997 the International Agency for
Research on Cancer classified crystalline silica
from occupational exposure as a carcinogen to
humans (Group 1).35
What you may not know is that the full name
of silicosis is a 45-letter word and possibly the
longest word in the English language: pneumono
ultramicroscopicsilicovolcanoconiosis.34
 24.2 Case studies
24.2.4 Case Study 4: Popcorn lung
Diacetyl is used extensively in the flavoring
and food production industry, and occupa-
tional exposure to this substance has been asso-
ciated with a severe obstructive lung disease,
bronchiolitis obliterans, and a decrease in pul-
monary function. It has been associated with
degraded quality of life and increased mortal-
ity. The United States National Institute for
Occupational Safety and Health (NIOSH) has
suggested diacetyl, when used in artificial but-
ter flavoring (as used in many consumer
foods), may be hazardous when heated and
inhaled over a long period. The disease has
been called “popcorn worker’s lung” because it
was first seen in former workers of a micro-
wave popcorn factory in Missouri, but NIOSH
refers to it by the more general term “flavor-
ings-related lung disease.”36,37
In bronchiolitis obliterans, inflammation and
scarring occur in the smallest airways of the lung
and can lead to severe and disabling shortness of
breath. The disease causes airway epithelial dam-
age, with tracheal bronchial inflammation, where
the bronchioles are compressed and narrowed
by fibrosis. In 2008 Dan Morgan and colleagues
at NIEHS/NTP investigated the respiratory tox-
icity of diacetyl in C57BL/6 mice and demon-
strated that oropharyngeal aspiration of
occupationally relevant doses reaches the distal
airways and results in lesions of endobronchiolar
fibrohistiocytosis, suggestive of early stages of
bronchiolitis obliterans. In 2011 they demon-
strated severe airway epithelial injury, aberrant
repair, and bronchiolitis obliterans after diacetyl
instillation in rats, which replicated the features
of the human disease.38
The main respiratory symptoms experienced
by workers affected include cough (usually
without phlegm) and shortness of breath on
exertion. These symptoms continue when
workers go home for the day, and are gradual
in onset and progressive, but severe symptoms
can occur suddenly. After they are no longer
V. Toxicology at home and the workplace
333
exposed to flavoring vapors, the cough may
diminish, but shortness of breath on exertion
persists. Very severe disease may require lung
transplant. Using cross-sectional pulmonary
function data from diacetyl-exposed employ-
ees, NIOSH recommended occupational expo-
sure limits (OELs) for diacetyl, both a TWA
and a short-term exposure limit.36
Although the danger of inhalation and expo-
sure to diacetyl were determined in the 1980s,
the use of diacetyl as a flavoring component is
considered acceptable in the United States and
Europe. The main concerns are when the
chemical is heated and inhaled over a long
period of time. Interestingly the concerns with
diacetyl continue with recent concerns about
the use of diacetyl as a flavoring in vaping
fluids in e-cigarettes.39
24.2.5 Case Study 5: Chimney sweep
carcinoma
In 1775 Percivall Pott described the occur-
rence of scrotal cancer in chimney sweeps in
England. This was the first time a malignant
disease was connected with a specific occupa-
tion.40,41 There is an interesting history linked
to this occupational disease. After the Great
Fire in London in 1666, new building regula-
tions were implemented to prevent another
huge fire. Fireplaces had to be built with nar-
rower chimneys and had to be kept free of
obstruction. These new regulations prompted
the use of small children as chimney sweeps.
These boys would shimmy into the narrow
fireplace flues to knock the soot, loose dressed
only in trousers and shirts and occasionally
naked. They would be covered in soot, inhal-
ing it, and often sleeping on the bags used to
collect the soot or under them to keep warm.
When these boys reached adolescence, they
would often develop Chimney Sweep Cancer,
which was cancer of the scrotum, scrotal squa-
mous cell carcinoma.42 This practice continued
334 24. Toxicology in the workplace
until 1875 when a bill was passed in
Parliament that put an end to using children as
chimney sweeps.43 Interestingly the disease
was not an issue in Germany. In Germany
chimney sweeps wore tight fitting protective
clothing which prevented the soot from
accumulating on the lower surface of the
scrotum.40
Chimney soot is a fine black or dark brown
powder formed from the incomplete combus-
tion of wood or coal in a confined space. The
organic fraction consists mainly of polyaromatic
hydrocarbons (PAHs) and their derivatives. The
active carcinogen discovered in Chimney
Sweep Cancer was 3,4-benzopyrene (also called
benzo[a]pyrene, BaP). Polycyclic aromatic
hydrocarbons are recognized as skin carcino-
gens in humans and animals. They accumulate
in cell membranes, are hydroxylated by a num-
ber of cytochrome P450 isozymes (primarily
1A1 and 1B1) in epidermal cells, and are conju-
gated for excretion. The formation of reactive
metabolites is key in the toxicity of PAH. Diol
epoxides—PAH intermediate metabolites—are
mutagenic and affect normal cell replication
when they react with DNA to form adducts.
BaP diol epoxide covalently binds to the nucleo-
philic guanine bases in DNA.44 A mutation
occurs during cell replication if the aberration
remains unrepaired, potentially starting the pro-
cess that can lead to cancer. Cells affected most
significantly are those with rapid replicative
turnover, such as those in bone marrow, skin,
and lung tissue.42 There are indications that the
BaP diol epoxide targets the protective p53
gene, a transcription factor that regulates the
cell cycle and functions as a tumor suppressor,
inactivating this ability.45 Despite awareness of
the concerns caused by soot and other PAH-
containing materials, incidence of occupation-
ally related scrotal squamous cell carcinoma has
continued (i.e., car mechanics, car and airplane
manufacture, gas workers, engineers, steel man-
ufacture, and aluminum workers).46 48
V. Toxicology at home and the workplace
24.3 Managing exposures and protecting
workers
In 1960 the first birth control pill was
approved by the U.S. Food and Drug Agency.
Pharmaceutical production of sexual hormones
ramped up, but at the time, little consideration
was given to workplace exposures. Men work-
ing in the pharmaceutical manufacturing of
these hormones started experiencing a variety
of side effects, including breast development.
This is an example where a chemical can have
significant effects in both men and women, but
where effects are dramatically different, a phe-
nomenon described as sexual dimorphism. In
men exposed to the birth control pill, the chief
complaint was gynecomastia. Female workers
overexposed to sex hormones would likely
experience a decrease in fertility (which is the
intended pharmacological response). To reme-
diate this situation, OELs were introduced to
manage exposure and protect workers, both
male and female, and programs were put in
place to prevent such effects from occurring in
the future.
Occupational toxicologists assess chemicals
(or pharmaceuticals) before they are intro-
duced into the workplace to anticipate and mit-
igate risks to employees. One widely used
pragmatic strategy consists of placing chemi-
cals in an occupational exposure band (OEB)
based on their toxicity potential.49 This
approach initially emerged in the pharmaceuti-
cal industry and is currently under consider-
ation by NIOSH.50,51 To “band” a chemical, the
toxicologist reviews its properties (including,
but not limited to, acute and chronic adverse
health effects, genotoxicity and carcinogenicity,
reproductive toxicity and developmental
effects, respiratory and skin sensitization, skin
and eye irritation, and corrosion) and its
potency. This framework, similar to the bio-
safety levels, used by the Center for Disease
Control and Prevention for pathogens, enables
 24.3 Managing exposures and protecting workers 335
TABLE 24.3 Example of occupational exposure bands.
Band Chemical Toxicity Engineering Personal protective equipment

1 Maltodextrin Low Manual handling Overalls, nitrile gloves, dust mask, hair net
toxicity and scooping

6 Fentanyl High Completely Positive pressure suit, powered air purifying respirator, double gloves
toxicity enclosed system (with tape sealed cuffs), misting shower on exit

TABLE 24.4 Occupational exposure limits.

Chemical Occupational exposure limit Source

8-Methoxypsoralen Not available

Lead (metal) 50 µg/m3 (total dust) ACGIH, OSHA52,53

Crystalline silica 25 µg/m3 ACGIH, OSHA52,53
Diacetyl (2,3-pentanedione) 0.02 ppm (gas) (equivalent to 70 µg/m3) ACGIH52
Soot (coal tar) 200 µg/m3 (as soluble benzene fraction) ACGIH, OSHA52,53

toxicologists to make judgments, based on the
available data, which may range from essen-
tially no information to complete datasets.
Most systems have four to six bands or “buck-
ets” in which chemicals can be placed. Each
band represents a different toxicity potential
and correlates with different engineering con-
trols and use of PPE in the workplace. See
Table 24.3 for example; the engineering con-
trols and PPE required to handle both com-
pounds differ dramatically.
In circumstances where more robust datasets
are available and a specific product is made on a
regular basis, the occupational toxicologist might
derive an OEL (called permissible exposure limit
by OSHA) for the chemical. The OEL is defined
as the airborne concentration to which employ-
ees can be exposed 40 hours per week over their
working lifetime without experiencing any
health effects.52 The critical effect is generally the
biologically significant effect that would occur at
the lowest exposure. It is generally understood
that if you protect against the critical effect, you
will protect against all other effects. To identify
the critical effect, it is necessary to understand
the full spectrum of potential effects, the
dose response of these effects, and the toxico-
kinetics of the chemical of interest. For com-
modity chemicals in the United States, the
NIOSH and the American Conference of
Governmental Industrial Hygienists (ACGIH)
publish OELs on a regular basis, which are
adopted by many companies and countries.
OSHA is, however, responsible for setting
enforceable limits in the United States. Limits
established for the chemicals discussed in
the case studies are presented in Table 24.4.
When an OEL is available, industrial hygienists
can perform air monitoring to provide a quan-
titative evaluation of the performance of the
engineering controls. It is common practice
in the field to recommend the addition of
engineering controls to reduce the airborne
concentration to less than half of the OEL (this
value is generally called the “action level”).
In some cases, it is not practical to have an
airborne limit because other sources or routes
of exposure exist and biomarkers are then used
to monitor worker exposures and to assess
recovery.

V. Toxicology at home and the workplace

336 24. Toxicology in the workplace
24.4 Conclusion
A wide range of occupations can result in
occupational chemical exposures: from the lab-
oratory scientist doing western blots, to the
nurse administering oncology drugs, to the
fireman responding to a hazardous leak, and
the laborer working in a shipyard. It is the
responsibility of occupational toxicologists,
irrespective of whether they work in academia,
industry, government, or not-for-profit, to
ensure these workers get to go home as healthy
as they were when they came into work over
their entire lifetime. Occupational toxicologists
must operate and provide pragmatic solutions
under vastly different circumstances: no data
are available, the chemical is volatile and hard
to contain, unforeseen effects may occur
because the route of exposure differs from the
route employed in toxicology tests, and some-
times different subpopulations of individuals
respond differently to chemicals/exposures.
Many new chemicals have not been properly
investigated and do not have OEBs or limits, to
help manage risks via exposure containment
and mitigation. In the United States, OSHA and
industry need to work hand-in-hand to be pro-
active and prevent the occurrence of adverse
health effects like those discussed in the case
studies presented. With each era, new toxico-
logical hazards and concerns emerge, and occu-
pational toxicologists will continue to be at the
forefront of protecting the health of workers.
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