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Occupational module
Gianna Moscato
Department of Public Health, Experimental and Forensic Medicine University of Pavia, Italy
Investigating allergic effects of environmental exposures
2 - 5 July 2014 Brindisi, Italy
Allergy School
• Occupational exposures play an important role in allergic respiratory diseases.
• The work-related diseases of major interest in allergy are: – Work-related asthma and variants – Work-related rhinitis
• Others conditions are – Hypersensitivity pneumonitis – Allergic Bronchopulmonary Aspergillosis (ABPA) – Respiratory symptoms variously related to work:
work-related cough, other aspecific symptoms and signs
– Irritable larynx syndrome
Work-related asthma
• Occupational exposures account for 10-25% of adult asthma in the general population (Kogevinas, 2007).
• Occupational exposure can cause or exacerbate asthma (work-related asthma, WRA), and can also be associated with asthma variants (eosinophilic bronchitis, aluminium potroom asthma) or to symptoms that mimic asthma (e.g. the irritable larynx syndrome).
• WRA has health, social and economic costs
– USA, 1996: PAR 15% 1.6 billion dollars (Leigh, Chest 2002),
– Europe € 1.2 billion (Jinhai, 2010),
– UK £ 135 million (Ayres 2011)
• It is a burden for the society
Bernstein,2013
Allergic OA
• The most frequent form of OA (almost 80% of cases)
• Characterized by a latency period between the beginning of exposure and onset of symptoms
• Caused by workplaces sensitizers: i) Most high-molecular weight (HMW) agents (e.g.
flours) and some low-molecular weight (LMW) (e.g. Platinum salts) agents for which an IgE-mediated mechanism similar to non-WRA has been proven, and
ii) Some specific LMW-agents in which the allergic mechanisms responsible have not yet been fully characterized (e.g. Isocyanates)
Irritant-induced OA • Less frequent form of OA
• The most definite form of IIOA is the “Reactive Airways Dysfunction Syndrome” (RADS), which occurs as an acute onset of asthma after a single exposure to high concentrations of an irritating gas, vapour, fume or smoke.
• A less definite form, due to the paucity of reports and case studies, is non-acute irritant-induced OA where the onset of asthma is delayed and follows multiple, less massive exposures to irritants. It has been recently re-classified (Vandenplas et al, EAACI Pos Paper, Accepted Allergy)
No latency period
Close temporal
relationship
between exposure
and onset of
asthma
“Acute-onset IIA”,
“RADS”
Latency period
Epidemiological
evidence of an
excess incidence
of asthma in high-
risk occupations/
or jobs
“Low-dose IIA”,
“Not-so-sudden
IIA”, “IIA with
latency”
Latency period
Documentation of
repeated
symptomatic
exposures
“Sub-acute IIA”
Acute Delayed/insidious
IRRITANT-INDUCED ASTHMA?
Single, high-level Multiple, high-level Chronic, moderate
Delayed/insidious
* **
DEFINITE IIA PROBABLE IIA POSSIBLE IIA
ONSET OF ASTHMA
MODE OF
EXPOSURE
CLINICAL
CHARACTERISTICS
DIAGNOSTIC
LIKELIHOOD
Vandenplas et al, EAACI Pos Paper, Allergy, “Accepted Article”; doi: 10.1111/all.12448
Bernstein,2013
9
• Work-exacerbated asthma (WEA) is defined as preexisting or concurrent asthma that is worsened by workplace conditions.
• Recognizing and preventing asthma exacerbations is important, since the occurrence of severe asthma exacerbations is associated with an accelerated decline of respiratory function
• In non-work related asthma environmental exposure
factors appear to have a lesser role than host factors
when compared with OA.
• Occupational factors that potentially increase the risk of
asthma include
– high-risk jobs
– exposure to sensitizing agents
– exposure to low-level irritants in the workplace
– the mode and route of exposure
– the level of exposure
– concomitant exposures to pollutants at the workplace.
Curr Opin Allergy Clin Immunol 2014, 14:84–94
Hairdressers
Chest 2005;128;3590-3598
2010; 65: 784
AM J Ind Med 2011 Jul;54(7):565-8.
•Need for preventive strategies •Possible preventive measures encompass the substitution of cleaning sprays, bleach and ammonia, avoidance of mixing products, the use of respiratory protective devices, workers’ education and medical surveillance
Irritant-induced OA
CLEANERS Identified as a population at high risk for both non-
WRA and WRA in developed countries
offices, industrial plants, kitchens and hospitals
home
High-molecular weight agents
Occupation Agent
Baking, milling, pastry making Flour(s), -amylase, other enzymes, egg
white
Laboratory animal researchers and
technicians
Rat, mouse, guinea pig, ferret, etc. proteins,
egg
Health care workers Latex
Detergent enzyme manufactures Detergent protease, amylase, lipase, cellulase
Tea packers, coffee processors Herbal teas, green coffee bean
Sea food processors Prawn, crab, other (shell) fish proteins
Other food processors Garlic, egg, enzymes
Flower and vegetable farmers Pollens, moulds
Moscato et al. EAACI Position Paper on WRA diagnosis, Allergy 2012
ALLERGIC OA Sensitizers and occupations at risk
Low-molecular weight agents
Occupation Agent
Spray painters, French polishers Di-isocyanates
Electronic solderers Colophony fume
Health care workers Glutaraldehyde,methyl/butyl
methacrylate
Plastic and foam manufacturers Diisocyanates, acid anhydrides, epoxy
resins
Woodworkers, lumberjack Red cedar, iroko, other tropical sawdusts
Textile workers Reactive dyes
Hairdressers Persulphates
Pharmaceutical manufacturers Penicillins, morphine, cimetidine
Moscato et al. EAACI Position Paper on WRA diagnosis, Allergy 2012
ALLERGIC OA Sensitizers and occupations at risk
MODE AND ROUTE OF EXPOSURE
•Inhalation is by far the main route for many agents that cause occupational asthma.
•Despite the industry efforts to reduce exposure to chemicals through the inhalation route, occupational asthma continues to occur, suggesting skin exposure causing sensitization
nasopharyngeal region
trachea
primary bronchi
secondary bronchi
terminal bronchioles
respiratory bronchioles
alveoli
Entry and interaction of particles with the respiratory tract
tho
raci
c (4
-10
µm
)
inh
alab
le (
<10
0 µ
m)
resp
irab
le (
<4 µ
m)
Does particle size influence sensitization?
Exposure by inhalation
• The evidence supporting a dose-response relationship between the exposure level to occupational agents and the development of IgE-mediated sensitization and work-related respiratory symptoms for agents acting through an IgE-mediated mechanism is strong (Nicholson 2010; Vandenplas 2011).
• For sensitizers there is no exposure level
which entirely eliminates the risk (Heederik, 2012)
Level of exposure
Work-related asthmaWork-related asthma Work-related rhinitis
Asthma
caused
by work
=
Occupational
Asthma
(OA)
Asthma
exacerbated
by work
=
Work-
Exacerbated
Asthma (WEA)
Rhinitis
caused
by work
=
Occupational
Rhinitis
(OR)
Rhinitis
exacerbated
by work
=
Work-
Exacerbated
Rhinitis (WER)
Allergic OA (with latency period):
IgE-mediated
Non-IgE-mediated
Non-allergic OA (without latency):
Single exposure: RADS*
Multiple exposures: Irritant-
induced OA
Allergic OR (with latency period):
IgE-mediated
Non-IgE-mediated
Non-allergic OR (without latency):
Single exposure: RUDS**
Multiple exposures: Irritant-
induced OR
Corrosive rhinitis* RADS = Reactive Airways Dysfunction Syndrome
** RUDS = Reactive Upper airways Dysfunction Syndrome
Classification of work-related rhinitis and asthma
2008
EAACI POSITION PAPER OCCUPATIONAL RHINITIS
Moscato G et al, Allergy 2008
2008: 969-980
Relationships between OA and occupational rhinitis
• Rhinitis symptoms may be present in up to 92% cases of occupational asthma
• OA and OR share the same etiologic agents and mechanisms
• Rhinitis may precede of 6 - 24 months the onset of OA Occupational rhinitis may be a marker of the likelihood of developing occupational asthma
Moscato, Curr Opin Allergy Clin Immunol 2014; Siracusa, EAACI Pos Paper, submitted to Allergy
OCCUPATIONAL ANAPHYLAXIS
CONCLUSIONS • Work-related diseases are a typical example of the
influence of environment on human health
• Work-related respiratory diseases are the most frequent, however also occupational anaphylaxis may be found
• A recent review has shown that in non-work related asthma environmental exposure factors appear to have a lesser role than host factors when compared with occupational asthma.
• Occupational and non-occupational asthma have common features and OA is an excellent model for studying asthma