Occupational asthma
|
Asthma Microchapters |
|
Diagnosis |
|---|
|
Other Diagnostic Studies |
|
Treatment |
|
Case Studies |
|
Occupational asthma On the Web |
|
American Roentgen Ray Society Images of Occupational asthma |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Lakshmi Gopalakrishnan, M.B.B.S. [2]
Overview
Asthma is defined as a respiratory disease caused by narrowing of the air passages that is synonymous with difficulty in breathing, tightness of chest, nasal irritation, coughing and wheezing.
Occupational asthma is defined as:
"a disease characterized by variable airflow limitation and/or airway hyper-responsiveness due to causes and conditions attributable to a particular occupational environment and not stimuli encountered outside the workplace".[1][2]
Historical Perspective
The first person to use it in reference to a medical condition was Hippocrates in 450 BC, 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.
In 1700, Bernardino Ramazzini, Doctor of Philosophy and Medicine from parma, Italy published the book De Morbis Artificum Diatriba (A Treatise on the Diseases of Workers). Although researchers like Olaus Magus had done work on diseases due to occupational causes as early as 1555, this was the first comprehensive work on work-related diseases. This volume described in detail the diseases of workers in 52 different occupations.[3] Thus, this formed the basis for the emergence of occupational medicine and even today, it is an important reference. Due to his important contribution to this field, Dr. Ramazzini is considered the father of occupational medicine.
Similarly, Dr. Jack Pepys, for his contribution to research on asthma in the workplace, is also considered as the father of occupational asthma[4]. His work on the role of aspergillus species in pulmonary diseases as an important pathogenic factor for farmer’s lung has been heavily influenced the emergence of occupational asthma as an occupational disease. And, thanks to his work on Specific Inhalation Challenge, the compensatible aspect of the disease was recognized.
Pathophysiology
- Occupational asthma is characterized by variable airflow limitation and/or airway hyper-responsiveness due to causes and conditions attributable to a particular occupational environment and not stimuli encountered outside the workplace.[1][2]
- Occupational asthma is the result of multiple genetic, environmental, and behavioral influences.
- The three main types of occupational asthma are:[5]
- Immunologically mediated with the involvement of specific IgE,
- Immunologically mediated without the evidence of IgE involvement, and
- Non-immunologic, irritant mediated such as in reactive airways dysfunction syndrome
- Glutathione S-transferase (GSTP1 and GSTM1) and N-acetyltransferase (NAT1) genes that are involved in airway remodeling, have shown to play are role in the pathogenesis of occupational asthma.[6][7]
- Skin exposure and inhalation of aero-allergens are the common modes of exposure in patients suffering from occupation asthma.[8]
- Certain high and low molecular weight occupational allergens such as animal proteins and platinum salts respectively, act as antigens and induce a antigen-specific IgE response that contributes to the immunologic pathogenesis.
- Non-immunologic mechanisms that play a role in the pathogenesis include the direct inhibition of β2 agonist or elaboration of substance P by injured sensory nerves.
Epidemiology and Demographics
Asthma affects as much as 15% of the Canadian population[9] (and this is true of other developed countries too) and has increased four fold in the last 20 years. Various reasons can be identified for this increase that includes better diagnostic facilities along with a greater awareness regarding the disease have shown to play a major role. But, one cannot deny the part of increased environmental pollution. Researchers have been working on the relation between the environment and human health since long and the air we breathe is the primary cause for lung diseases like asthma, rhinitis, COPDs, etc. that affect us today.
Approximately, 10 to 15% of the adult-onset asthma is affected by an aggravation of symptoms while at work and an improvement when away, which implies that they may be suffering from occupational asthma.[10][5] Thus, when an individual’s Asthma is caused, not aggravated, by workplace materials, it is defined as Occupational Asthma. In the USA, OA is considered the most common occupational lung disease[11]. At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties[12]. Their existence and magnitude vary from region to region and the type of industry and can be as varied as wood dust (cedar, ebony, etc.), persulfates (Hairsprays), zinc or even seafood like prawns. For example, in France the industries most affected in order of importance are Bakeries and cake-shops, automobile industry and hairdressers[13], whereas in Canada the principle cause is wood dust, followed by isocyanates.
Diagnosis
History and Symptoms
- Less than five years of exposure to an occupational agent can be enough for the appearance of the first occupational asthma symptoms. This depends on whether the reason for the occupational asthma to occur was exposure to the causative agent over a period of time (with a latency period) or a single exposure to an irritant but at a very high concentration (without latency period). Both eventually result in OA.
- Coughing, wheezing, nasal irritation, difficulty in breathing, tightness of chest are the most common symptoms and can be recognized more easily by asking oneself the following questions:
- Are any of the above symptoms recurrent/chronic?
- Are they present at work?
- Do they worsen towards the end of the work day and/or end of the week?
- Does the employee/worker feel an improvement in his condition when away from work, on vacation or on weekends?
- If these symptoms persist, the person is most likely suffering from occupational asthma. However, one must be aware that this could also be because the person is already suffering from asthma and his condition was simply aggravated by workplace irritants (Work-aggravated asthma). In this case, although he will suffer similar consequences as someone who is suffering from OA (loss of work, medical expenses, etc.), his disease cannot be considered as having an occupational origin.
- Like for any other disease correct diagnosis is important. According to Dr. Susan Tarlo:
“It is important to recognize, since if due to a workplace sensitizer and, if undetected and if the patient continues to work with even small exposure to the relevant sensitizing agent, the prognosis is worse”. She also concluded that, “the chance of eventual improvement in Asthma severity after stopping exposure decreases with the duration of exposure after the onset of the symptoms. The best chance of asthma clearing or significantly improving is associated with early diagnosis and early removal from ongoing exposure”[14].
- However, the biggest challenge is the first step – family doctors and patients alike do not have sufficient knowledge about occupational asthma - only 15% of the asthmatic patients are asked by their doctor if their symptoms are related to work[15]. And often, patients do not mention this possibility due to the fear of losing their jobs or simply because they are not aware of the association between their work and asthma. What they do not realize is that if they continue working under such circumstances, not only are they sure to lose their job in the long run but their asthma will also reach an irreversible stage. Clearly, an incorrect diagnosis will have considerable medical, social and financial consequences.
- Diagnosis of OA is a process and has to be done over a period of time. First, the patient’s occupational and clinical history is taken and his symptoms are charted (Charting is usually done at the end of a typical work week and within 24 hours of the occurrence of symptoms in order to get objective information). Once this has been established, the following diagnostic methods are used:
Non-specific bronchial hyperreactivity
A non-specific bronchial hyperreactivity test 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. Other non specific tests could even require the patient to run in open air or on a treadmill for a few minutes at a continuous pace. In this case, the individual’s Peak Expiratory Flow Rate (PEFR) is measured. (The peak expiratory flow rate measures how fast a person can exhale) [16].
Skin prick tests
Although called skin prick test, it does not involve drawing blood, in fact, the skin is not even scratched. It is usually performed on the inner aspect of the forearm where grid is marked (using a simple marker) and a drop of the allergen that is to be tested is placed on the arm at the end of each line. All the allergens that need to be tested can be similarly placed on 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. [17]
IgE-specific tests
Immunoglobulin E is an antibody found in our 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[18].
Spirometric tests
Conventionally, a spirometer can be defined as a device used to measure timed expired and inspired volumes. These volumes then enable us to measure how quickly the lungs can be emptied and filled and whether it is effective. These measurements need to be stated at body temperature, and the pressure will have to be saturated with water vapor to get the correct values. This is because, if the spirometer is dry the recorded volume of air displaced is lower than that actually displaced by the lungs[19].
Peak Expiratory Flow at work
This test uses the PEFR method. The only difference is that it measures the functioning of the patient's airways at his place of work and not necessarily in a controlled environment. The patient breathes into a Peak Expiratory Flow monitor (a hand-held device that has a mouth piece at one end and a scale with an indicator on the other).[20]
Specific inhalation challenge
- Realistic method “The Realistic 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.
- Closed-circuit method This 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 being minute and extremely stable minimize the risk of exaggerated responses.
Of the above methods of doing a diagnosis, procedures such as monitoring of spirometry or peak expiratory flow at work and Specific Inhalation Challenges (SIC) have been proved as the most objective and reliable methods.
Treatment
According to the Canadian Centre for Occupational Health and Safety (CCOHS) better education of workers, management, unions and medical professionals is the key to the prevention of OA. This will enable them to identify the risk factors and put in place preventive measures like masks or exposure limits, etc.
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[15]:
1) Reducing exposure
This method is most effective for those affected by irritant-induced OA. Thus, by reducing their exposure duration and level to the causative agent, the probability of suffering another reaction is lowered. But exposure can be reduced in other ways like making use of face masks or providing better ventilation. Now, more and more di-isocyanate free spray paints are available. Similarly, most hospitals and healthcare companies have exchanged latex gloves for other materials. Thus, reducing exposure to known asthmagens can also be used as a preventive measure.
2) Removal from exposure
Persons affected by OA that occurred after a latency period, whether a few months or years, must be immediately removed from exposure to the causative agent. This is their only chance of recovery. However, this entails severe socio-economic consequences for the worker as well as the employer due to loss of job, unemployment, compensation issues, quasi-permanent medical expenditures, hiring and re-training of new personnel, etc. Also, according to recent research the probability that those who suffer from OA remain unemployed longer than those who suffer from non-occupational asthma is higher. One solution to this problem is relocating the employee in the same company away from the causative agents.
3) Medical and pharmacological treatment
Anyone diagnosed with Asthma will have to undergo medical treatment. This is complementary to either removing or reducing the patient’s exposure to the causal agents. Two types of medication can be used:
- Relievers or bronchodilators
- Preventers Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can be used depending on the severity of the case.
Short-acting beta-agonists like salbutamol or terbutaline or long-acting beta-agonists like salmeterol and formoterol or anticholinergic, etc. 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.
Compensation issues
As mentioned earlier, when a person is diagnosed as having occupational asthma, it results in serious socio-economic consequences not only for the workers but also for the employer and the healthcare system. The employee has to be taken off job immediately to prevent any further damage to his health. And, the probability of being re-employed is lower for those suffering from OA as compared to those suffering from 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. [21][22]
Related Chapters
References
- ↑ 1.0 1.1 American Journal of Respiratory and Critical Care Medicine. Vol 167. pp. 450-471, (2003). Proceedings of the First Jack Pepys Occupational Asthma Symposium.
- ↑ 2.0 2.1 Tarlo SM, Balmes J, Balkissoon R, Beach J, Beckett W, Bernstein D et al. (2008) Diagnosis and management of work-related asthma: American College Of Chest Physicians Consensus Statement. Chest 134 (3 Suppl):1S-41S. DOI:10.1378/chest.08-0201 PMID: 18779187
- ↑ Major R H: A History of Medicine. CHEST, VOL. 57, NO. 4, APRIL 1970. C.C. Thomas Springfield 1954
- ↑ Occupational Asthma: The Past 50 years. Chan-Yeung M.
- ↑ 5.0 5.1 Maestrelli P, Boschetto P, Fabbri LM, Mapp CE (2009) Mechanisms of occupational asthma. J Allergy Clin Immunol 123 (3):531-42; quiz 543-4. DOI:10.1016/j.jaci.2009.01.057 PMID: 19281901
- ↑ Piirilä P, Wikman H, Luukkonen R, Kääriä K, Rosenberg C, Nordman H et al. (2001) Glutathione S-transferase genotypes and allergic responses to diisocyanate exposure. Pharmacogenetics 11 (5):437-45. PMID: 11470996
- ↑ Mapp CE, Fryer AA, De Marzo N, Pozzato V, Padoan M, Boschetto P et al. (2002) Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates. J Allergy Clin Immunol 109 (5):867-72. PMID: 11994713
- ↑ Redlich CA, Herrick CA (2008) Lung/skin connections in occupational lung disease. Curr Opin Allergy Clin Immunol 8 (2):115-9. DOI:10.1097/ACI.0b013e3282f85a31 PMID: 18317018
- ↑ C-Health: Asthma in Canada(2007)
- ↑ Dykewicz MS (2009) Occupational asthma: current concepts in pathogenesis, diagnosis, and management. J Allergy Clin Immunol 123 (3):519-28; quiz 529-30. DOI:10.1016/j.jaci.2009.01.061 PMID: 19281900
- ↑ http://www.lni.wa.gov/Safety/Research/files/AsthmaCme.pdf
- ↑ http://www.asmanet.com/asmapro/agents.htm
- ↑ Reported incidence of occupational asthma in France, 1996–99: the ONAP programme. J Ameille, G Pauli, A Calastreng-Crinquand, D Vervloët, Y Iwatsubo, E Popin, M C Bayeux-Dunglas and M C Kopferschmitt-Kubler2 and the corresponding members of the ONAP
- ↑ Diagnosis of Occupational Asthma Tarlo S.
- ↑ 15.0 15.1 Diagnosis and Management of Work-Related Asthma. Evidence Report/Technology Assessment number 129. Beach J, Rowe B, Blitz S, Crumley E, Hooton N, Russell K, Spooner C
- ↑ Risk and incidence of asthma attributable to occupational exposure among HMO members. Milton DK, Solomon GM, Rosiello RA, Herrick RF. Am J Ind Med 1998;33:1–10.
- ↑ http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9333767 Kroczyńska-Bednarek J, Grzelewska-Rzymowska I, Tymińska K.
- ↑ Allergy Society of South Africa. The Skin Prick Test. Toerien A,Potter P C, Buys C
- ↑ http://researchnews.osu.edu/archive/hayfcare.htm
- ↑ http://www.nationalasthma.org.au/html/management/spiro_book/sp_bk002.asp
- ↑ http://www.nlm.nih.gov/medlineplus/ency/article/003443.htm
- ↑ Medicolegal and compensation aspects of occupational asthma. Dewitte JD, Chan-Yeung M, Malo J-L.