Decortication is a surgical procedure that removes a restrictive layer of fibrous

tissue overlying the lung, chest wall, and diaphragm. The aim of decortication is
to remove this layer and allow the lung to reexpand. When the peel is removed,
compliance in the chest wall returns, the lung is able to expand and deflate, and
patient symptoms improve rapidly.[1]
In most people, the pleural space is less than 1 mm thick. When this space is
violated by any number of pathological disorders, the distribution of certain cells
and fluid can be altered, with serious medical consequences.[2] One common
pathological process that affects the pleural space is fibrothorax, which is an
abnormal accumulation of fibrous tissues over the lung or visceral pleura. The
fibrous tissues that deposit over the lung parenchyma can be so intense that the
underlying lung fails to expand. Over time, the lung becomes entrapped or
encased.[1]
Although decortication is an effective surgical procedure for this condition, its
success depends on careful selection of patients. As in all thoracic surgery
procedures, the preoperative workup should be thorough and the surgery should
be done at a particular timed interval. Moreover, the surgeon should also be
technically skilled at entering the chest and removing the peel. In some cases, the
intercostal space is fused and it is almost impossible to enter the chest cavity.
See the images below.

A 23-year-old man
with a stab to the right chest presented 1 week later with fever, chills, and

dyspnea. The radiograph shows an inflammatory process that did not drain via a
needle.

CT scan showing a
large collection in the right chest. The collection is surrounded by a thick peel that
is typical of empyema.

Indications
The primary indication for decortication in a patient with fibrothorax is presence
of symptoms due to lung restriction resulting from development of a thick
fibrinous peel.[3] The timing of surgery is vital for success. In many cases, the peel
may spontaneously resolve and the symptoms may subside.[4] Most surgeons will
perform a decortication for the following conditions:

The pleural peel has been present for more than 4-6 weeks

Lung symptoms are disabling

There is radiological evidence of a trapped lung

Decortication is frequently necessary when other minor interventions (eg, chest

tube) have not resulted in clearance of the infection or hemothorax. Tuberculous
empyema is usually first treated with drugs and decortication is only undertaken
after long-term drug therapy fails.

Contraindications
Other than the physiological fitness of the patient, there are no absolute
contraindications to decortication. In some patients who also have underlying lung
disease, removal of the peel may not help the lung expand and thus surgery would
be futile.

Other conditions that may make decortication futile include the presence of a
pleural space infection and large airway stenosis. In such cases, the lung will not
expand to fill the pleural space. A more extensive pleuropneumonectomy may be
the only option, but only if the patient has been worked up preoperatively.
Pleuropneumonectomy is a major undertaking with a very high mortality.
Decortication may not be possible in presence of uncontrolled lung infection or
contralateral lung disease, or for a chronically debilitated patient. Medical
optimization may be required prior to undertaking surgery in these patients.
Ideally, the patient's nutritional status should first be normalized (with nasogastric
feedings if necessary) and sepsis should be controlled with appropriate antibiotic
therapy.
Other relative contraindications include coagulopathy, severe chest wall infection,
and terminal disease.

Technical Considerations
Decortication gives the best results in patients who seek early treatment.
Fibrothorax is a time-dependent process and can be prevented. Depending on the
cause, insertion of a chest tube to remove an effusion or hemothorax may prevent
the development of fibrothorax.
Among patients with chest trauma who suffer a hemothorax, placement of a chest
tube and complete drainage usually prevents development of fibrothorax.
Numerous studies have shown that early and complete evacuation of clotted
hemothorax and parapneumonic effusions leads to decreased morbidity and
mortality.
Some of the reasons that may explain an incomplete return of lung volume
include elevation of the diaphragm, mediastinal shift, intercostal muscle fibrosis,
or decrease in size of the thoracic cavity. Some experts believe that the longer the
empyema is allowed to progress, the less the likelihood that lung function will
return back to normal. Although some authors report an association between
shorter course of disease and improved outcomes, this is not a universal finding
among all surgeons.
Even though no studies have been done to explain failure of the lung to expand
after so-called successful decortication, the most likely reason is either technical
difficulties or incomplete removal of the peel. In many cases, the plane of
dissection can be difficult. Too much persistence in removing the thin peel can
also injure the underlying lung parenchyma and result in massive air leaks.
Inability to define the plane of dissection between the peel and the visceral pleura
is an especially troublesome technical challenge that can adversely affect results.
If visceral pleurectomy is performed, air leakage and postoperative hemorrhage

may compromise pulmonary function. Care must be taken throughout the

operation to protect the phrenic nerve from injury; fortunately, this usually is not
an issue, because the mediastinal pleura is rarely involved in the inflammatory
process. Incomplete parietal pleurectomy or inability to free the diaphragm may
also compromise results.
If patients are appropriately selected, complete reexpansion of the lung after
decortication can usually be achieved. Occasionally, however, an issue related to
residual pleural space might arise after an otherwise technically satisfactory
decortication. If this space is not obliterated, failure is inevitable.

Outcomes
The results after decortication are often fruitful. The morbidity and mortality after
a decortication is dependent on the patient age, underlying comorbidities, and
development of complications from the surgery. Decortication in general has an
excellent outcome in young people.
In younger patients with benign causes of fibrothorax, the outcome is excellent
and quality of life is much improved.[5] Most patients begin to feel relief of
symptoms soon after surgery. In elderly patients with multiple comorbidities,
recovery is often slow but symptom relief is also better. The majority of patients
regain their previous exercise endurance and are able to return back to their
original work.
However, when the procedure is done in patients with compromised lung
function, the morbidity can be high. Besides surgery itself, the thoracic incision
and general anesthesia also carry a high morbidity in people with no lung reserve.
Old data suggest that the overall mortality in healthy people is less than 1% but
may run as high as 4-6% in individuals with underlying lung disease. However
with video-assisted thoracoscopic surgery (VATs), the current mortality rates are
slightly lower.[6, 7, 8]
To avoid complications, the surgeon has to pay attention to detail. The peel should
be removed with great care and injury to nearby organs should be avoided. If the
decortication is done adequately, lung function improvement is remarkable.
However, the ultimate return of lung function depends on preoperative lung
disease.
If the lung parenchyma was normal prior to surgery, then complete reexpansion of
the lung and obliteration of the pleural space is certainly possible. In most cases,
lung volumes improve after decortication, but it is rare to see return to
preoperative values.

Anatomic Considerations

The boundaries of the pleural space are the visceral pleura, which envelops the
lungs, and the parietal pleura, which is the inner lining of the thoracic cavity.[9]
The goal of decortication is to remove all the fibrinous peel and necrotic tissue,
and help the lung reexpand and equally important not to leave any residual air
spaces.[10]
The two most common problems encountered when performing decortication are
a pleural cavity infection and fibrosis.[11] It is difficult for the underlying lung to
expand when there is a thick peel overlying the parenchyma. Consequently, there
is a large residual space left in the chest cavity that almost always gets infected.
Therefore, for the surgeon to have good success with decortication, timing of
surgery is crucial.
If the disease has been chronic, the rib spaces are often fused and the chest cavity
is severely constricted. Entry into the chest can be very difficult. If the peel is very
thick and adherent, injury to the lung parenchyma can occur with moderate air
leak. If the lung has an inherent disorder, the possibility of reexpansion may not
occur. Finally, decortication is not a trivial procedure and can be very bloody;
thus, the patient must also be physiological fit to undergo the procedure. All these
factors must be considered when planning a decortication.[12]
Moreover, once inside the chest cavity, no lung may initially be visible because of
the thick fibrous peel. The peel can vary in thickness from a few millimeters to
few centimeters. One may also find necrotic debris and abscess along the chest
cavity. It is important to avoid dissection along the medial border of the lung
because the heart chambers are close by. The dissection should be started on
lateral aspects or near the fissures. In most cases, the lower lobe is fused with the
diaphragm and one can easily enter the abdominal cavity if the dissection is too
deep.
For safe decortication, the chest cavity is best entered at the 5th/6th intercostal
space and dissection should be started where the peel is the thinnest and easily
removed. It is important to reassess the anatomy every few minutes to prevent
injury to the organs. Blind digital peeling should be avoided, especially near the
apex of the lung. This area is best approached when the upper lobe can be
retracted inferiorly and the lung apex is visible. Severe bleeding from injury to the
subclavian vessels and pulmonary artery has been reported.
Because extensive decortication or radical pleurectomy can be associated with air
leaks, methods have been described to reconstruct the diaphragm to help lower the
incidence of postoperative complications.[13, 14, 8]
When performing a VATS procedure, one must be aware of the adjacent structures
to avoid injury. On the superior aspect, the subclavian vessels can be found lying
deep to the pleura but clearly visible. Along the medial border, one may come
across the thymus, trachea, heart, phrenic nerve, aorta (on right), vena cava (on

left), and the esophagus (posteriorly). In the posterolateral chest, one may come
across the sympathetic chain, azygous vein, and the diaphragm (inferiorly).[1, 9]
BRITTLE ASTHMA

Brittle asthma: Management

Patients with brittle asthma pose difficult and complex management problems. Jon
Ayres identifies possible management strategies for these patients.
Jon Ayres, BSc, MD, FRCP, is Professor of Respiratory Medicine (University
of Warwick) in the Department of Respiratory Medicine, Birmingham
Heartlands Hospital, Birmingham.
The term 'brittle asthma' was first used by Turner-Warwick (1977) to describe
patients with asthma whose peak expiratory flow (PEF) varied 'chaotically'; a
pattern which could lead to death from an acute severe, attack (Bateman and
Clarke, 1979; Westerman et al, 1979). Morbidity from brittle asthma is
considerable, and this review aims to identify possible causes and management
strategies for this group of patients.
Definitions
Since 1977, the term brittle asthma has been used in different ways by different
physicians, leading to some confusion over whether such a group is truly
separable from other patients at the severe end of the asthma spectrum. In order to
try and clarify this area we have suggested a classification of brittle asthma into
two types; a feature of both types being a susceptibility to repeated severe attacks
resulting in hospital admission.
Type 1
Patients who consistently demonstrate wide peak flow variation (greater than 40%
diurnal variation for at least 50% of days), despite maximal medical therapy
including at least 1500 g/day of inhaled beclomethasone or equivalent, are
classified as having type 1 brittle asthma.
It is crucial that peak flow readings are corrected for non-linearity (Miller et al,
1992) when calculating diurnal variation in type 1 brittle asthma. These patients
are typically female (4:1 in our clinic) and aged between 15 and 55 years.
Type 2
Patients with type 2 brittle asthma appear to be well controlled between attacks
which are often sudden in onset (occurring within minutes) and are associated
with loss of or disturbed consciousness on at least one occasion.
The patient may not have been mechanically ventilated as a result of the attack but
is very likely to exhibit a severe respiratory acidosis in an attack and, if ventilated,

needs support for relatively short time periods (Wasserfallen et al, 1990). Type 2
brittle asthma seems to be equally prevalent in men and women.
Morbidity
Type 1 brittle asthma is a cause of significant morbidity associated with frequent
accident and emergency attendances and hospital admissions and the resultant use
of considerable amounts of medication. Consequently, side effects of therapy,
particularly oral corticosteroids, are common, e.g. osteoporosis, weight gain and
oesophageal reflux (Miles et al, 1993). In addition, this can result in the
development of obstructive sleep apnoea which may remain unsuspected because
poor sleep quality tends to be attributed to asthma, even though the symptom
pattern is exactly the same in these patients compared to isolated sleep apnoea.
Within our clinic 12% of subjects suffer from sleep apnoea and are treated with
nasal continuous positive airway pressure.
Risk factors
Atopy
Over 90% of patients with type I brittle asthma are strongly atopic (Miles et al,
1995), despite which over two-thirds keep pets at home, so continuing exposure to
aeroallergens may be important in maintaining symptoms in this group, especially
as they spend more time at home and indoors.
Food intolerance
Over 60 % of type I patients report at least one food or drink which makes their
asthma worse. Double blind placebo-controlled food challenge (Baker et al, 1996)
has confirmed a prevalence of food allergy at over 50% in type I brittle asthma
with wheat and dairy products being the most important triggers (Table 1).
Table 1: Positive Food Challenges in Brittle Asthma
Food
Dairy Products
Wheat
Fish
Citrus
Egg
Potato
Soya
Peanut
Yeast

% Positive Response
50
50
37
34
34
26
23
16
13

Psychosocial factors
Psychosocial factors are important in type I brittle asthma (Garden and Ayres,

1993), with a high incidence of depression and frequent evidence of broken

relationships and physical and sexual abuse in our experience. Just as common are
abnormal coping strategies for managing deteriorating asthma, where panic
frequently supervenes (Miles et al, 1997). However, it is difficult to be certain
whether brittle asthma is associated primarily with personality disorder, or
whether the threat of severe asthma induces psychological instability.
Steroid responsiveness
Patients with type I brittle asthma are usually treated with high doses of
inhaled/oral steroids, yet their asthma often remains poorly controlled suggesting
that there may be a degree of resistance to the anti-inflammatory effects of
steroids (Barnes and Adcock. 1995).
Management: Type I brittle asthma
These patients are, by definition, extremely difficult to manage. Many of them
have fallen out with their doctor, who perhaps understandably. has run out of ideas
and, often, patience. Management should be holistic, trying to approach all areas
which impact on an individual's symptoms. This involves identifying causal
factors and dealing where possible with psychosocial factors, before attempting to
wrestle with polypharmacy. Trying to identify psychosocial factors and dealing
with them (including help with Disability Living Allowance, for instance) can
help significantly, and group therapy has been of some use in patients who are
able to meet on a regular basis, by providing an auto-support network.
Allergen exposure
Removal of animals and determined efforts to reduce house dust mite exposure
would seem logical but there is no evidence to suggest that such control measures
are effective in this group. Indeed, given their psychosocial problems, these
patients invariably believe that their animals are more reliable than people, and
suggesting that their animals should be removed is invariably greeted with blunt
refusal.
Where foods are identified as allergic triggers they should be avoided. In some
cases such avoidance can be remarkably effective while in others the benefit is
limited, but compliance with what is often a difficult diet may not always be good.
Good dietary advice and support is crucial as Baker and colleagues (1995) have
shown that the diets of these patients are very often deficient in minerals such as
selenium and magnesium and in the anti-oxidant vitamins A, C and B. This is
probably because their diet lacks food that they are avoiding because of
intolerance and a desperate need to lose weight with consequent reduction in
calorie intake.
Compliance
The most important factor to identify is compliance with treatment but it should
be remembered that these patients appear to have wide variations in peak flow and

symptoms before they opt not to take treatment as we would wish. Noncompliance is not a cause of the severe asthma itself. Where identified this should
be openly addressed with the patient and their carer.
Drug therapy
The BIS guidelines (British Thoracic Society et al, 1996) are of limited help in
these patients. They are already taking large doses of inhaled steroids leaving an
increase in, or resumption of oral steroids as the next therapeutic step when
symptoms deteriorate, which many resist because of side effects. Consequently,
many patients simply increase their beta-2 (1-2) agonist use (Miles et al, 1997) in
an attempt to avoid oral steroids and hospital admission. Whether alternative
immunomodulatory treatment, such as methotrexate or cyclosporin, will be
effective is not yet certain but is worth trying in individual cases.
Subcutaneous 2 agonists
Type I patients with brittle asthma can be treated with long-term continuous
subcutaneous infusion of 2 agonist, usually terbutaline (CSIT) (O'Driscoll et al,
1988; Ayres, 1992). Using this technique, around half of patients with type I brittle
asthma show marked improvements in symptoms, variation in PEF (Figure 1) and
use of other asthma medication, including oral steroid use. Around 25 % show
some improvement in symptoms but less improvement in PEF while the
remainder do not respond. Chronic steroid-dependent asthmatics without intrinsic
PEF variability do not respond to this form of therapy.
Figure 1: Peak flow readings (before and after bronchodilator) in a patient with
type 1 brittle asthma

Before Subcutaneous Terbutaline

Salbutamol Inh.x n
Prednisolone 5mg
Salbutamol SR 8mg b.d.
Uniphylline 800mg nocte
Pulmicort ii q.d.s
Intal 5 iii q.d.s

On Continuous Subcutaneous Terbutaline

Salbutamol ii p.m.
Pulmicort ii q.d.s
Intal 5 ii q.d.s

On Terbutaline subcutaneously in 4 daily divided doses.

Salbutamol ii p.m.
Pulmicort ii q.d.s
Intal 5 ii q.d.s
The infusions are given through a battery-powered syringe driver (such as the
Graseby MS26, Graseby Ltd, UK) which need to be provided in successful cases
on a long-term basis. If provision of a pump is not possible then the daily dose can
be delivered by divided doses, albeit with slightly less effective control (Figure 1).
The best tolerated subcutaneous needles are the Sof-Set and the Disetronics
needles (Applied Medical Technology, Cambridge, UK), which although more
expensive than the standard butterfly, last much longer; one needle often remains
in situ for a week or more compared to 48 hours or less for the butterfly needle.
The usual dose needed ranges between 6 and 15mg a day, mean blood levels of
terbutaline achieved by this technique are around 150 nmol/litre, the normal
therapeutic range for oral terbutaline treatment (7.5 mg twice daily) being 10-20
nmol/litre but despite this, significant changes in serum potassium or glucose
concentrations are rare as, surprisingly, is tremor which may suggest the
development of tolerance to the side effects of this form of treatment. Muscle

cramps are common and may sometimes be severe, with elevation of plasma
creatinine phosphokinase (Sykes et al, 1991) although levels of the myocardial
fraction are normal. Some patients complain of an effect on memory and ability to
concentrate and occasionally menorrhagia is seen but this is not usually severe.
The main problem is the development of subcutaneous inflammatory nodules.
When biopsied these show an eosinophilic infiltrate (Lewis et al, 1987). These
usually settle down once that area of skin is avoided, but often leave a fibrotic
nodule. More recently a more aggressive type of lesion has been demonstrated
which sometimes leads on to frank abscess formation, the pus from which is
usually sterile. The formulation of the drug has not changed nor have the
preservatives, so the reason for these reactions remains elusive. Although using
nebulizer solution rather than the injectable form of terbutaline may help, in some
the skin changes are so severe that administration has to be changed to continuous
intravenous infusion via an indwelling line such as a Portacath or Hickman line,
although in those patients who have had many hospital admissions, such vascular
access may also be needed because of lack of useable veins.
Long-acting inhaled 2 agonists
In our experience, salmeterol has proved to be disappointing in these patients for
reasons that are not clear. Whether formoterol, which is a full agonist may be
more useful than salmeterol, a partial agonist, remains to be determined.
Management: Type 2 brittle asthma
Management of type 2 patients is less difficult. In view of the rapid onset of
attacks each patient should be provided with a medic alert bracelet or equivalent.
Again identification of inhaled or ingested triggers, e.g. peanuts (Loza and
Brostoff, 1995), is crucial, but the mainstay of self treatment for these attacks is
adrenaline. Although these patients often appear to be relatively symptom free
between attacks in some cases significant peak flow variability is seen which is
not matched by perceived symptoms, which may explain the appearance of
sudden attacks occurring on the background of significant but undetected airway
narrowing.
Adrenaline
Adrenaline may have theoretical advantages over selective 132 agonists, because
of its action as an alpha adrenoceptor against reducing airway oedema as
discussed in the section on acute airway narrowing above. Preloaded syringes
(Epi-Pen, ALK, UK; Ana Pen, Allerayde, UK) should be provided for emergency
treatment. Inhaled adrenaline may be more effective than a selective 132 agonist
inhaler. Once adrenaline has been injected the patient should be encouraged to use
a dose of nebulized salbutamol or terbutaline and go to casualty. One problem
with these patients is that, once they arrive in casualty, their symptoms have often
improved such that they are told either that they do not have asthma or are just
hyperventilating'. Rapid onset attacks such as these are often equally quick to

resolve leading to the opportunity for inadequate assessment of severity in these

cases.
Conclusion
Patients with brittle asthma, whether type 1 or type 2, pose difficult and complex
management problems. Trying to classify these severe patients will help to
determine the differing factors involved and, while this classification will not
embrace all patients with severe asthma, it will provide a framework for
beginning to unravel aetiology and treatment of this high morbidity group. Once
identified, dealing with individual factors may in themselves have only a small
impact on their condition but these can be cumulative, and even if these result in
only modest improvements in control, the patient will believe that some
improvement can after all be achieved.
References
Ayres JG (1992)
Subcutaneous terbutaline in the managemeni of brittle asthma. Br J Hosp Med 47:
569-71
Baker JS, Tunnicliffe WS, Duncanson RC, Ayres JG (1995)
Reduced dietary intakes of magnesium, selenium and vitamins A, C and F in
patients with brittle asthma. Thorax 50: A75
Baker JC, Tunnicliffe WS, Duncanson RC, Ayres JG (1996)
Double blind placebo controlled food challenge in type I and type 2 brittle asthma.
Thorax 51: A2
Barnes PJ, Adcock IM (1995)
Steroid resistant asthma. Q J Med 88: 455-68
Bateman JRM, Clarke SW (1979)
Sudden death in asthma. Thorax 34: 40-3
British Thoracic Society, British Paediatric Association, Royal College of
Physicians of London et al (1996)
Guidelines on the management of asthma. Thorax 52 (Suppl): S1-24
Garden GMF, Ayres JG (1993)
The psychiatric and social aspects of brittle asthma. Thorax 48: 501-5
Lewis LD, O'Driscoll BRC, Hartley RB, Cochrane GM (1987)
An unusual local reaction to continuous subcutaneous infused terbutaline in
unstable asthmatics. Br J Dis Chest 81: 189-93

Loza C, Brostoff J (1995)

Peanut allergy. Clin Exp Allergy 25: 493-502
Miles JF, Noble K, Matthews BR, Cayson RM, Ayres JG (1993)
Gastro-oesophageal reflux in patients with brittle asthma. Thorax 48: 1055
Miles JF, Cayton RM, Tunnicliffe WS, Ayres JG (1995)
Increased atopic sensitization in brittle asthma. Clin Exp Allergy 25: 1074-82
Miles IF, Garden GM, Tunnicliffe W, Cayton RM, Ayres JG (1997)
Psychological morbidity and coping skills in patients with brittle and non-brittle
asthma: a case-control study. Clin Exp Allergy (in press)
Miller MR, Dickinson SA, Hitchings DJ (1992)
The accuracy of portable peak flow meters. Thorax 47: 904-9
O'Driscoll BRC, Ruffles SP, Ayres JG, Cochrane GM (1988)
Long-term treatment of severe asthma with subcutaneous terbutaline. Br J Dis
Chest 82: 360-5
Sykes AP, Lawson N, Finnegan JA, Ayres JG (1991)
Creatinine kinase activity in patients with brittle asthma treated with long term
subcutaneous terbutaline. Thorax 46: 580-3
Turner-Warwick M (1977)
On observing patterns of airflow obstruction in chronic asthma. Br J Dis Chest 71:
73-86
Wasserfallen JB, Schaller MD, Feihl F, Perret CH (1990)
Sudden asphyxic asthma: a distinct entity? Am Rev Respir Dis 142: 108-11
Westerman DE. Benatar SR. Porigieter PD. Ferguson AD (1979)
Identification of high risk asthmatic patients. Am J Med 66: 565-72
Key Points

Brittle asthma is relatively uncommon and consequently has been

characterized in clinical terms.

Two types at least can be identified, type 1 characterized by wide peak

flow variation despite maximal therapy and type 2 by very sudden attacks.

Type 1 brittle asthma is associated with the female sex, atopy, high
psychosocial disturbance and food intolerance. Treatment has to be
holistic.

Type 2 brittle asthma is best treated with self-injectable adrenaline and

avoidance of recognized triggers.

OCC ASTHMA

Occupational asthma
From Wikipedia, the free encyclopedia

Occupational asthma
Classification and external resources
MedlinePlus
Patient UK
MeSH

000110
Occupational asthma
D059366
[edit on Wikidata]

Occupational asthma is an occupational lung disease and a type of asthma. Like

other types of asthma, it is characterized by airway inflammation, reversible
airways obstruction, and bronchospasm, but it is caused by something in the
workplace environment.[1]
Symptoms include shortness of breath, tightness of the chest, nasal irritation,
coughing and wheezing. The first person to use it in reference to a medical
condition was Hippocrates, and he believed that tailors, anglers and metalworkers
were more likely to be affected by the disease. Although much research has been
done since, the inflammatory component of asthma was recognized only in the
1960s.
Today, asthma affects as much as 15% of the Canadian population,[2] a statistic
reflective of other developed countries, and has increased fourfold in the last 20
years. Various reasons can be identified for this increase, including increase
environmental pollution, better diagnostic ability, and greater awareness.
Approximately 21% of the adults affected by asthma report an aggravation of
their symptoms while at work and an improvement when away, which implies that
they may be suffering from occupational asthma. In the United States,
occupational asthma is the most common occupational lung disease.[3] At present,
over 400 workplace substances have been identified as having asthmagenic or
allergenic properties.[4] Their existence and magnitude vary by region and industry

and can include diisocyanates, acid anhydrides, plicatic acid, and platinum salts
(all low molecular weight agents), and animal protein, enzymes, wheat, and latex
(high-molecular weight agents).[3][1] For example, in France the industries most
affected are bakeries and cake-shops, automobile industry and hairdressers,[5]
whereas in Canada the principal cause is wood dust, followed by isocyanates.
Furthermore, the most common cause of occupational asthma in the workplace are
isocyanates.[6] Isocyanates are used in the production of motor vehicles.[7]
Hypersensitivity pneumonitis is a related condition, with many occupational
examples (e.g. flock worker's lung, farmer's lung, and indium lung). However,
although overlapping in many cases, hypersensitivity pneumonitis may be
distinguished from occupational asthma in that it isn't restricted to only
occupational exposure, and involves type III hypersensitivity and type IV
hypersensitivity[8] rather than the type I hypersensitivity[9][10] of asthma. Also,
unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than
bronchi.[11]

Contents

1 Signs and symptoms

2 Diagnosis

3 Prevention and treatment

3.1 Prevention

3.2 Treatment and Recovery

3.3 Medical and pharmacological treatment

4 Society and culture

o

4.1 Compensation

5 Occupations at risk

6 Epidemiology

7 See also

8 References

9 External links

Signs and symptoms

Less than five years of exposure or a single exposure to a high-concentration
agent can result in symptoms. Coughing, wheezing, nasal irritation, shortness of
breath, and chest tightness are the most common symptoms, all of which worsen
after work and improve during time away from work. Pre-existing asthma can be
exacerbated by similar agents.[citation needed]

Diagnosis
Diagnosis of occupational asthma uses several techniques.[3]
A non-specific bronchial hyperreactivity test can be used to help diagnose
occupational asthma. It involves testing with methacoline, after which the forced
expiratory volume in 1 second (FEV1) of the patient is measured. This test is often
used for measuring the intensity of a person's asthma and to confirm that the
person needs to be treated for asthma.[3]
Other non specific tests could require the patient to run for a few minutes at a
continuous pace. In this case, the individuals peak expiratory flow rate (PEFR) is
measured, showing how fast a person can exhale.[12][unreliable medical source?] PEFR can
also be measured at work to see if there is a difference from the PEFR in a
controlled environment. Measuring PEFR at work is a highly reliable test for
occupational asthma.
A skin prick test is usually performed on the inner forearm where a grid is marked
and a drop of the allergens to be tested are placed on the arm in the grid. Once this
has been done, the skin is pricked through the drop using a lancet. Reactions, if
any, occur within 10 to 15 minutes and these results can then be analyzed.[13]
[unreliable medical source?]

Immunoglobulin E is an antibody found in human blood and is effective against

toxins. Since it can also trigger allergic reactions to specific allergens like pollen,
the IgE test is performed to evaluate whether the subject is allergic to these
substances.[14][3]
A spirometer is a device used to measure timed expired and inspired volumes, and
can be used to help diagnose occupational asthma.[15][unreliable medical source?]
Specific inhalation challenges test for reactions to substances found in the
workplace. One method is a whole body sealed chamber where the patient is
exposed to articles that are present in their workplace. This method has the
advantage of being able to assess, albeit highly subjectively, ocular and nasal

symptoms as well as a reduction in FEV1. Another test requires the patient to

breathe aerosols of the suspected asthmagens through an oro-facial mask. These
asthmagens are aerosolized using closed circuit chambers, and the quantities and
concentrations administered are minute and extremely stable, to minimize the risk
of exaggerated responses.[citation needed]

Prevention and treatment

Prevention

Prevention of occupational asthma can be accomplished through better education

of workers, management, unions and medical professionals. This will enable them
to identify the risk factors and put in place preventive measures, including
respiratory protection and exposure limits.[3]
Treatment and Recovery

Recovery is directly dependent on the duration and level of exposure to the

causative agent. Depending on the severity of the case, the condition of the patient
can improve dramatically during the first year after removal from exposure.
Three basic types of procedures are used for treating the affected workers:
reducing a worker's exposure, removing a worker from the environment with the
asthma-causing agent, and treatment with asthma medications.[16][3] Completely
stopping exposure is more effective treatment than reducing exposure.[3] By
reducing exposure, the probability of suffering another reaction is lowered.
Methods of reducing exposure include transferring an affected worker to a
position without the relevant asthmagen, use of respiratory protection, and
engineering controls. In 1984 innovator David Cornell discovered and invented
effective control equipment in the UK for the removal of many harmful workplace
fumes. 'BOFA' extraction products are now found in over 100 countries
worldwide.[17]
People affected by occupational asthma that occurred after a latency period,
whether a few months or years, should be immediately removed from exposure to
the causative agent. However, this can entail severe socio-economic consequences
for the worker as well as the employer due to loss of job, unemployment,
compensation issues, quasi-permanent medical expenditures, and hiring and retraining of new personnel. This can be mitigated by transferring the worker within
a company.[3]
Medical and pharmacological treatment

Short-acting beta-agonists like salbutamol or terbutaline or long-acting betaagonists like salmeterol and formoterol dilate airways which relieve the symptoms
thus reducing the severity of the reaction. Some patients also use it just before
work to avoid a drop in the FEV1.
Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can
also be used depending on the severity of the case.

Society and culture

Compensation

When a person is diagnosed with occupational asthma, it can result in serious

socio-economic consequences not only for the workers but also for the employer
and the healthcare system because the worker must change positions.[3] The
probability of being re-employed is lower for those with occupational asthma
compared to those with normal asthma. The employer not only pays compensation
to the employee, but will also have to spend a considerable amount of time and
energy and funds for hiring and training new personnel.[18][19] In the United States,
it was estimated that the direct cost of occupational asthma in 1996 was $1.2
billion and the indirect cost $0.4 billion, for a total cost of $1.6 billion.[20]

Occupations at risk
The following tables show occupations that are known to be at risk for
occupational asthma, and main substances involved.[21]
The occupations most at risk are: adhesive handlers (e.g. acrylate), animal
handlers and veterinarians (animal proteins), bakers and millers (cereal grains),
carpet makers (gums), electronics workers (soldering resin), forest workers,
carpenters and cabinetmakers (wood dust), hairdressers (e.g. persulfate), health
care workers (latex and chemicals such as glutaraldehyde), janitors and cleaning
staff (e.g. chloramine-T), pharmaceutical workers (drugs, enzymes), seafood
processors, shellac handlers (e.g. amines), solderers and refiners (metals), spray
painters, insulation installers, plastics and foam industry workers (e.g.
diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g.
anhydrides)[22]
Grains, flours, plants and gums

Isocyanates and metals

Occupation [21]

Agent [21]

Occupation [21]

Agent [21]

Bakers, millers

Wheat

Boat builders, foam TDI

Chemists, coffee bean

baggers and handlers,
gardeners, millers, oil
industry workers, farmers

Castor
beans

Cigarette factory workers

Tobacco
dust

manufacturers, office
workers, plastics
factory workers,
refrigerator
manufacturers, TDI
manufacturers/users,
printers, laminators,
tinners, toy makers

Boiler cleaners, gas

Vanadium
Drug manufacturers, mold
turbine cleaners
makers in sweet factories, Gum acacia
printers
Hexamethylene
Car sprayers
diisocyanate
Farmers, grain handlers
Grain dust
Gum manufacturers, sweet Gum
makers
tragacanth

Cement workers

Potassium
dichromate

Strawberry
Chrome platers,
pollen
chrome polishers
Tea dust

Sodium
bichromate,
chromic acid,
potassium
chromate

Tobacco farmers

Tobacco
leaf

Nickel platers

Nickel sulphate

Woollen industry workers

Wool

Platinum chemists

Chloroplatinic
acid

Platinum refiners

Platinum salts

Polyurethane foam
manufacturers,
printers, laminators

Diphenylmethane
diisocyanate

Rubber workers

Naphthalene
diisocyanate
Cobalt
Stainless steel

Strawberry growers
Tea sifters and packers

Animals, insects and fungi

Occupation [21]

Agent [21]

Bird fanciers

Avian proteins

Cosmetic
manufacturers

Carmine

Entomologists

Moths, butterflies

Feather pluckers

Feathers

Tungsten carbide
grinders

Field contact

Crickets

Welders

workers

fumes

Fish bait breeders

Bee moths

Drugs and enzymes

Flour mill workers,

Occupation [21] Agent [21]
Grain storage mites,
bakers, farm
alternaria,
Ampicillin
Phenylglycine acid
workers, grain
aspergillus
manufacturers chloride
handlers
Detergent
Locusts,
Bacillus subtilis
cockroaches, grain manufacturers
Laboratory workers
weevils, rats, mice,
guinea pigs, rabbits Enzyme
Fungal alpha-amylase
manufacturers
Mushroom
cultivators

Mushroom spores

Oyster farmers

Sea pineapples
(Hoya)

Pea sorters

Food
technologists,
laboratory
workers

Papain

Mexican bean
weevils

Pharmacists

Gentian powder,
flaviastase

Pigeon breeders

Pigeons

Poultry workers

Chickens

Prawn processors

Prawns

Silkworm
sericulturers

Silkworms

Methyldopa,
salbutamol,
dichloramine,
piperazine
dihydrochloride,
Pharmaceutical
spiramycin, penicillins,
workers
sulphathiazole,
sulphonechloramides,
chloramine-T,
phosdrin, pancreatic
extracts

Zoological museum
Beetles
curators
Chemicals/Materials

Poultry workers
Occupation
[21]

Amprolium
hydrochloride

Agent [21]

Aircraft fitters Triethyltetramine

Process
Trypsin, bromelin
workers, plastic
polymer
production

Aluminum
workers
Aminoethylethanolamine
cable solderers
Woods
Aluminum pot
Fluorine
room workers
Autobody
workers
Brewery
workers

Occupation [21]

Acrylates (resins, glues,

Carpenters,
sealants, adhesives)
timber millers,
woodworkers
Chloramine-T

Chemical plant
workers, pulp Chlorine
mill workers

Agent [21]
Western red cedar,
cedar of Lebanon,
iroko, California
redwood, ramin,
African zebrawood

Sawmill workers, Mansonia, oak,

pattern makers mahogany, abiruana
Wood finishers

Cocabolla

Levafix brilliant yellow,

Wood machinists Kejaat
drimarene brilliant
Dye weighers yellow and blue,
cibachrome brilliant
scarlet
Electronics
workers

Colophony

Epoxy resin Tetrachlorophthalic

manufacturers anhydride
Foundry mold Furan-based resin binder
makers
systems
Fur dyers

Para-phenylenediamine

Hairdressers

Persulphate salts

Health care
workers

Glutaraldehyde, latex

Laboratory
Formaldehyde
workers,
nurses,
phenolic resin

molders
Meat wrappers

Polyvinyl chloride
vapour

Paint
manufacturers,
plastic
Phthalic anhydride
molders, tool
setters
Paint sprayers Dimethylethanolamine
Photographic
workers,
Ethylenediamine
shellac
manufacturers
Refrigeration
industry
CFCs
workers
Solderers

Polyether alcohol,
polypropylene glycol

Epidemiology
Occupational asthma is the most common occupational lung disease.[3]

See also

Asthma

Chronic obstructive pulmonary disease (COPD)

Specific inhalation challenge

References
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C-Health: Asthma in Canada(2007)

 de Groene, Gerda J.; Pal, Teake M.; Beach, Jeremy; Tarlo, Susan
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(T78) Occupational Asthma : Table of agents, products and
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Unless else specified in boxes, then reference is: Canadian
Centre for Occupational Health and Safety (CCOHS) (a federal
government site) > OSH Answers > Diseases, Disorders & Injuries >
Asthma Document last updated on February 8, 2005
MayoClinic --> Occupational asthma May 23, 2009