Occupational asthma

Occupational asthma

Occupational asthma is an occupational condition 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]

Asthma is defined as a respiratory disease caused by narrowing of the air passages[citation needed]. It is synonymous with difficulty in breathing, tightness of 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] (and this is true of other developed countries too) and has increased fourfold in the last 20 years. Various reasons can be identified for this increase - Of course better diagnosis and facilities along with a greater awareness regarding the disease have played 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 adults affected by the disease report an aggravation of their symptoms while at work and an improvement when away, which implies that they may be suffering from Occupational Asthma. 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.[3] At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties.[4] 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,[5] whereas in Canada the principal cause is wood dust, followed by isocyanates.

Hypersensitivity pneumonitis is a related condition, with many occupational examples (e.g. "Farmer's Lung", "Malt Worker's Lung" and "Humidifier Lung" etc.). 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[6] rather than type I hypersensitivity[7][8] of asthma. Unlike asthma, hypersensitivity pneumonitis targets lung alveoli rather than bronchi.[9]

Contents

Signs and symptoms

Less than five years of exposure to an occupational agent can be enough for the appearance of the first OA symptoms. This depends on whether the reason for the OA 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:

  1. Are any of the above symptoms recurrent/chronic?
  2. Are they present at work?
  3. Do they worsen towards the end of the work day and/or end of the week?
  4. 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 OA. 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.

Diagnosis

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”.[10]

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.[11] 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).[12]

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.[13]

IgE-specific tests

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]

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.[15]

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).[16]

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.

Prevention and 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[11]:

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

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.

  • Preventers

Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can be used depending on the severity of the case.

History

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.[17] Thus, it was 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, for his contribution to research on asthma in the workplace, Dr Jack Pepys is considered as the Father of Occupational Asthma.[18] His work on the role of Aspergillus species in pulmonary diseases as also on the cause of farmer’s lung have heavily influenced the emergence of OA as an occupational disease. And, thanks to his work on Specific Inhalation Challenge, the compensatible aspect of the disease was recognized.

Society and culture

Compensation

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.[19][20] 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.[21]

Occupations at risk

The following tables show occupations that are known to be at risk for occupational asthma, and main substances involved.[22]

Yet, the riskiest occupations for asthma 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)[23]

Grains, flours, plants and gums

Occupation [22]

Agent [22]

Bakers, millers

Wheat

Chemists, coffee bean baggers and handlers, gardeners, millers, oil industry workers, farmers

Castor beans

Cigarette factory workers

Tobacco dust

Drug manufacturers, mold makers in sweet factories, printers

Gum acacia

Farmers, grain handlers

Grain dust

Gum manufacturers, sweet makers

Gum tragacanth

Strawberry growers

Strawberry pollen

Tea sifters and packers

Tea dust

Tobacco farmers

Tobacco leaf

Woollen industry workers

Wool

Animals, insects and fungi

Occupation [22]

Agent [22]

Bird fanciers

Avian proteins

Cosmetic manufacturers

Carmine

Entomologists

Moths, butterflies

Feather pluckers

Feathers

Field contact workers

Crickets

Fish bait breeders

Bee moths

Flour mill workers, bakers, farm workers, grain handlers

Grain storage mites, alternaria, aspergillus

Laboratory workers

Locusts, cockroaches, grain weevils, rats, mice, guinea pigs, rabbits

Mushroom cultivators

Mushroom spores

Oyster farmers

Sea pineapples (Hoya)

Pea sorters

Mexican bean weevils

Pigeon breeders

Pigeons

Poultry workers

Chickens

Prawn processors

Prawns

Silkworm sericulturers

Silkworms

Zoological museum curators

Beetles

Chemicals/Materials

Occupation [22]

Agent [22]

Aircraft fitters

Triethyltetramine

Aluminum cable solderers

Aminoethylethanolamine

Aluminum pot room workers

Fluorine

Autobody workers

Acrylates (resins, glues, sealants, adhesives)

Brewery workers

Chloramine-T

Chemical plant workers, pulp mill workers

Chlorine

Dye weighers

Levafix brilliant yellow, drimarene brilliant yellow and blue, cibachrome brilliant scarlet

Electronics workers

Colophony

Epoxy resin manufacturers

Tetrachlorophthalic anhydride

Foundry mold makers

Furan-based resin binder systems

Fur dyers

Para-phenylenediamine

Hairdressers

Persulphate salts

Health care workers

Glutaraldehyde, latex

Laboratory workers, nurses, phenolic resin molders

Formaldehyde

Meat wrappers

Polyvinyl chloride vapour

Paint manufacturers, plastic molders, tool setters

Phthalic anhydride

Paint sprayers

Dimethylethanolamine

Photographic workers, shellac manufacturers

Ethylenediamine

Refrigeration industry workers

CFCs

Solderers

Polyether alcohol, polypropylene glycol

Isocyanates and metals

Occupation [22]

Agent [22]

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

TDI

Boiler cleaners, gas turbine cleaners

Vanadium

Car sprayers

Hexamethylene diisocyanate

Cement workers

Potassium dichromate

Chrome platers, chrome polishers

Sodium bichromate, chromic acid, potassium chromate

Nickel platers

Nickel sulphate

Platinum chemists

Chloroplatinic acid

Platinum refiners

Platinum salts

Polyurethane foam manufacturers, printers, laminators

Diphenylmethane diisocyanate

Rubber workers

Naphthalene diisocyanate

Tungsten carbide grinders

Cobalt

Welders

Stainless steel fumes

Drugs and enzymes

Occupation [22]

Agent [22]

Ampicillin manufacturers

Phenylglycine acid chloride

Detergent manufacturers

Bacillus subtilis

Enzyme manufacturers

Fungal alpha-amylase

Food technologists, laboratory workers

Papain

Pharmacists

Gentian powder, flaviastase

Pharmaceutical workers

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

Poultry workers

Amprolium hydrochloride

Process workers, plastic polymer production workers

Trypsin, bromelin

Woods

Occupation [22]

Agent [22]

Carpenters, timber millers, woodworkers

Western red cedar, cedar of Lebanon, iroko, California redwood, ramin, African zebrawood

Sawmill workers, pattern makers

Mansonia, oak, mahogany, abiruana

Wood finishers

Cocabolla

Wood machinists

Kejaat

See also

References

  1. ^ Chan-Yeung M, Malo JL, Tarlo SM, et al. (February 2003). "Proceedings of the first Jack Pepys Occupational Asthma Symposium". Am. J. Respir. Crit. Care Med. 167 (3): 450–71. doi:10.1164/rccm.167.3.450. PMID 12554630. http://ajrccm.atsjournals.org/cgi/content/full/167/3/450/. 
  2. ^ C-Health: Asthma in Canada(2007)
  3. ^ Work-related is the most common occupational lung disease {REF}
  4. ^ (T78) Occupational Asthma : Table of agents, products and substances which can cause asthma
  5. ^ Ameille J, Pauli G, Calastreng-Crinquand A, et al. (February 2003). "Reported incidence of occupational asthma in France, 1996–99: the ONAP programme". Occup Environ Med 60 (2): 136–41. doi:10.1136/oem.60.2.136. PMC 1740458. PMID 12554842. http://oem.bmj.com/cgi/pmidlookup?view=long&pmid=12554842. 
  6. ^ Mohr LC (September 2004). "Hypersensitivity pneumonitis". Curr Opin Pulm Med 10 (5): 401–11. doi:10.1097/01.mcp.0000135675.95674.29. PMID 15316440. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=1070-5287&volume=10&issue=5&spage=401. 
  7. ^ "Lecture 14: Hypersensitivity". http://www-immuno.path.cam.ac.uk/~immuno/part1/lec13/lec13_97.html. Retrieved 2008-09-18. 
  8. ^ "Allergy & Asthma Disease Management Center: Ask the Expert". http://www.aaaai.org/aadmc/ate/category.asp?cat=1008. Retrieved 2008-09-18. 
  9. ^ Page 503 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson (2007). Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.
  10. ^ Diagnosis of Occupational Asthma Tarlo S.
  11. ^ a b 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
  12. ^ Milton DK, Solomon GM, Rosiello RA, Herrick RF (January 1998). "Risk and incidence of asthma attributable to occupational exposure among HMO members". Am. J. Ind. Med. 33 (1): 1–10. doi:10.1002/(SICI)1097-0274(199801)33:1<1::AID-AJIM1>3.0.CO;2-2. PMID 9408523. 
  13. ^ Kroczyńska-Bednarek J, Grzelewska-Rzymowska I, Tymińska K (March 1997). "[Nonspecific bronchial hyperreactivity in patients with seasonal bronchial asthma observed through two consecutive years]" (in Polish). Pol. Arch. Med. Wewn. 97 (3): 216–23. PMID 9333767. 
  14. ^ Allergy Society of South Africa. The Skin Prick Test. Toerien A,Potter P C, Buys C
  15. ^ Specific Test Key To Determine Whether Or Not Allergy Symptoms Are Really Allergy-Related
  16. ^ Measurement of Ventilatory Function
  17. ^ Major R.H. (April 1970). "The father of occupational medicine". Chest 57 (4): 332. doi:10.1378/chest.57.4.332-a. http://chestjournal.chestpubs.org/content/57/4/332.1.full.pdf.  C.C. Thomas Springfield 1954
  18. ^ Occupational Asthma: The Past 50 years. Chan-Yeung M.
  19. ^ MedlinePlus Medical Encyclopedia: Peak expiratory flow rate
  20. ^ Dewitte JD, Chan-Yeung M, Malo JL (May 1994). "Medicolegal and compensation aspects of occupational asthma". Eur. Respir. J. 7 (5): 969–80. PMID 8050556. http://erj.ersjournals.com/cgi/pmidlookup?view=long&pmid=8050556. 
  21. ^ Leigh JP, Romano PS, Schenker MB, Kreiss K (January 2002). "Costs of occupational COPD and asthma". Chest 121 (1): 264–72. doi:10.1378/chest.121.1.264. PMID 11796461. http://chestjournal.chestpubs.org/content/121/1/264.long. 
  22. ^ a b c d e f g h i j k l m 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
  23. ^ MayoClinic --> Occupational asthma May 23, 2009

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