Occupational asthma

Last updated
Occupational asthma
Specialty Respiratory system

Occupational asthma is new onset asthma or the recurrence of previously quiescent asthma directly caused by exposure to an agent at workplace. It is an occupational lung disease and a type of work-related asthma. Agents that can induce occupational asthma can be grouped into sensitizers and irritants. [1]

Contents

Sensitizer-induced occupational asthma is an immunologic form of asthma which occurs due to inhalation of specific substances (i.e., high-molecular-weight proteins from plants and animal origins, or low-molecular-weight agents that include chemicals, metals and wood dusts) and occurs after a latency period of several weeks to years. [1]

Irritant-induced (occupational) asthma is a non-immunologic form of asthma that results from a single or multiple high dose exposure to irritant products. It is usually develops early after exposure; however, it can also develop insidiously over a few months after a massive exposure to a complex mixture of alkaline dust and combustion products, as shown in the World Trade Center disaster. Unlike those with sensitizer-induced occupational asthma, subjects with irritant-induced occupational asthma do not develop work-related asthma symptoms after re-exposure to low concentrations of the irritant that initiated the symptoms. [2] Reactive airways dysfunction syndrome (RADS) is a severe form of irritant induced asthma where respiratory symptoms usually develop in the minutes or hours after a single accidental inhalation of a high concentration of irritant gas, aerosol, vapor, or smoke. [3]

Another type of work-related asthma is work-exacerbated asthma (WEA) which is asthma worsened by workplace conditions but not caused by it. WEA is present in about a fifth of patients with asthma and a wide variety of conditions at work, including irritant chemicals, dusts, second-hand smoke, common allergens that may be present at work, as well as other "exposures" such as emotional stress, worksite temperature, and physical exertion can exacerbate asthma symptoms in these patients. [4] Both occupational asthma and work-exacerbated asthma can be present in an individual.

A number of diseases have symptoms that mimic occupational asthma, such as asthma due to nonoccupational causes, chronic obstructive pulmonary disease (COPD), irritable larynx syndrome, hyperventilation syndrome, hypersensitivity pneumonitis, and bronchiolitis obliterans.

Signs and symptoms

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. [5] Symptoms include shortness of breath, tightness of the chest, coughing, sputum production and wheezing. Some patients may also develop upper airway symptoms such as itchy eyes, tearing, sneezing, nasal congestion and rhinorrhea. [3]

Symptoms may develop over many years as in sensitizer-induced asthma or may occur after a single exposure to a high-concentration agent as in case of RADS.

Risk factors

At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties. [2] [6] [7] Agents such as flour, diisocyanates, latex, persulfate salts, aldehydes, animals, wood dusts, metals, enzymes usually account for the majority cases; however, the distribution of causal agents may vary widely across geographic areas, depending on the pattern of industrial activities. [2] [8] For example, in France the industries most affected are bakeries and cake-shops, automobile industry and hairdressers, [9] 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. [10] Isocyanates are used in the production of motor vehicles and in the application of orthopaedic polyurethane and fibreglass casts. [10]

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). [11]

The following tables show occupations that are known to be at risk for occupational asthma. The main reference is the Canadian Centre for Occupational Health and Safety. [12]

Diagnosis

To diagnose occupational asthma it is necessary to confirm the symptoms of asthma and establish the causal connection with the work environment. Various diagnostic tests can be used to aid in diagnoses of work-related asthma. [1] [3] [13] [14]

A spirometer is a device used to measure timed expired and inspired volumes, and can be used to help diagnose asthma.

A peak flow meter is a hand-held device which measures how fast a person can exhale – peak expiratory flow rate (PEFR) – and is a reliable test for occupational asthma. [15] Serial PEFR can be measured to see if there is a difference in ability to exhale at work compared to that in a controlled environment.

A non-specific bronchial hyperreactivity test can be used to support the diagnose occupational asthma. It involves measuring the forced expiratory volume in 1 second (FEV-1) of the patient before and after exposure to methacholine or mannitol. Presence of airway responsiveness, i.e. significant drop in FEV-1, can be seen in patients with occupational asthma. [1]

Specific inhalation challenges test consist of exposing the subjects to the suspected occupational agent in the laboratory and/or at the workplace and assessing for asthma symptoms as well as a reduction in FEV1. [3] [16]

Other tests such as the skin prick test, serum immunologic testing and measurement of sputum eosinophils can also be useful in establishing the diagnosis of occupational asthma. [13]

Prevention

Several forms of preventive measures have been suggested to prevent development of occupational asthma and also detect risk or disease early to allow intervention and improve outcomes. [17] These include: comprehensive programs, education and training, medical examinations, use of medications, reduction of exposures and elimination of exposures. [18] A review on the effectiveness of prevention measurements indicated that removal or reduction of exposure may improve asthma symptoms when compared to uninterrupted exposure. [19] Removal from exposure may improve lung function when compared to continued exposure. Removal from exposure may improve symptoms and lung function more than reduction of exposure among patients exposed to low molecular weight agents, such as isocyanates, diisocyanates, plicatic acid, metals and anhydrides. Two studies reported an increased of job loss associated with removal from exposure. Four studies reported a decrease in income of 20% to 50% after removal from exposure. The authors suggested that the benefit of a better improvement in air quality be weighed against the potential for a higher risk of job loss. [19]

A video on research on preventing asthma in health care

Asthma symptoms and airway hyperresponsiveness can persist for several years after removal from the offending environment. [13] Thus, early restriction from exposure to the trigger is advisable. Completely stopping exposure is more effective treatment than reducing exposure, but not always feasible. [8]

Management

Medication

Medications used for occupational asthma are similar to those used for other types of asthma such as short-acting beta-agonists like salbutamol or terbutaline, long-acting beta-agonists like salmeterol and formoterol and inhaled corticosteroids. Immunotherapy can also be used in some cases of sensitizer-induced occupational asthma. [14]

Epidemiology

Occupational asthma is one of the most common occupational lung disease. Approximately 17% of all adult-onset asthma cases are related to occupational exposures. [20] About one fourth of adults with asthma have work-exacerbated asthma. [4] Patients with work-related asthma are more likely to experience asthma attacks, emergency room visits, and worsening of their asthma symptoms compared with other adult asthma patients. [20]

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. [21] 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. [22] [23] 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. In most cases, the employer could have saved more money by adhering to safety standards rather than causing employees to become injured. [24]

However, this can entail severe socio-economic consequences for the worker as well as the employer due to loss of job, unemployment, compensation issues, medical expenditures, and hiring and re-training of new personnel. [21]

See also

Related Research Articles

<span class="mw-page-title-main">Asthma</span> Long-term inflammatory disease of the airways of the lungs

Asthma is a long-term inflammatory disease of the airways of the lungs. It is characterized by variable and recurring symptoms, reversible airflow obstruction, and easily triggered bronchospasms. Symptoms include episodes of wheezing, coughing, chest tightness, and shortness of breath. These may occur a few times a day or a few times per week. Depending on the person, asthma symptoms may become worse at night or with exercise.

<span class="mw-page-title-main">Isocyanate</span> Chemical group (–N=C=O)

In organic chemistry, isocyanate is the functional group with the formula R−N=C=O. Organic compounds that contain an isocyanate group are referred to as isocyanates. An organic compound with two isocyanate groups is known as a diisocyanate. Diisocyanates are manufactured for the production of polyurethanes, a class of polymers.

<span class="mw-page-title-main">Cough</span> Sudden expulsion of air from the lungs as a reflex to clear irritants

A cough is a sudden expulsion of air through the large breathing passages which can help clear them of fluids, irritants, foreign particles and microbes. As a protective reflex, coughing can be repetitive with the cough reflex following three phases: an inhalation, a forced exhalation against a closed glottis, and a violent release of air from the lungs following opening of the glottis, usually accompanied by a distinctive sound.

<span class="mw-page-title-main">Rhinitis</span> Irritation and inflammation of the mucous membrane inside the nose

Rhinitis, also known as coryza, is irritation and inflammation of the mucous membrane inside the nose. Common symptoms are a stuffy nose, runny nose, sneezing, and post-nasal drip.

<span class="mw-page-title-main">Hypersensitivity pneumonitis</span> Medical condition

Hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis (EAA) is a syndrome caused by the repetitive inhalation of antigens from the environment in susceptible or sensitized people. Common antigens include molds, bacteria, bird droppings, bird feathers, agricultural dusts, bioaerosols and chemicals from paints or plastics. People affected by this type of lung inflammation (pneumonitis) are commonly exposed to the antigens by their occupations, hobbies, the environment and animals. The inhaled antigens produce a hypersensitivity immune reaction causing inflammation of the airspaces (alveoli) and small airways (bronchioles) within the lung. Hypersensitivity pneumonitis may eventually lead to interstitial lung disease.

<span class="mw-page-title-main">Bronchoconstriction</span> Constriction of the terminal airways in the lungs

Bronchoconstriction is the constriction of the airways in the lungs due to the tightening of surrounding smooth muscle, with consequent coughing, wheezing, and shortness of breath.

<span class="mw-page-title-main">Byssinosis</span> Medical condition

Byssinosis is an occupational lung disease caused by inhalation of cotton or jute dust in inadequately ventilated working environments and can develop over time with repeated exposure. Byssinosis commonly occurs in textile workers who are employed in yarn and fabric manufacture industries. It is now thought that the cotton dust directly causes the disease and some believe that the causative agents are endotoxins that come from the cell walls of gram-negative bacteria that grow on the cotton. Although bacterial endotoxin is a likely cause, the absence of similar symptoms in workers in other industries exposed to endotoxins makes this uncertain. Current smokers are also at risk for developing byssinosis or having complications relating to byssinosis.

Exercise-induced bronchoconstriction (EIB) occurs when the airways narrow as a result of exercise. This condition has been referred to as exercise-induced asthma (EIA); however, this term is no longer preferred. While exercise does not cause asthma, it is frequently an asthma trigger.

Occupational lung diseases comprise a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases, infections, lung cancer and mesothelioma. These can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

Reactive airway disease (RAD) is an informal label that physicians apply to patients with symptoms similar to those of asthma. An exact definition of the condition does not exist. Individuals who are typically labeled as having RAD generally have a history of wheezing, coughing, dyspnea, and production of sputum that may or may not be caused by asthma. Symptoms may also include, but are not limited to, coughing, shortness of breath, excess mucus in the bronchial tube, swollen mucous membrane in the bronchial tube, and/or hypersensitive bronchial tubes. Physicians most commonly label patients with RAD when they are hesitant about formally diagnosing a patient with asthma, which is most prevalent in the pediatric setting. While some physicians may use RAD and asthma synonymously, there is controversy over this usage.

The use of podiatry drills, in the absence of engineering controls and personal protective equipment, is an occupational hazard to the healthcare provider. Nail dust collected during foot care procedures performed in office settings has been found to contain keratin, keratin hydrolysates, microbial debris, and viable fungal elements, including dermatophytes and saprotrophs. Exposure to nail dust and the associated risk will vary with the policies and practices in place, the type of podiatry drill used, therapy technique, frequency of procedures, personal protective equipment utilized and the use of ventilation systems.

The specific inhalation challenge (SIC) is a diagnosis tool to assess airway responsiveness to "sensitizing" substances as opposed to nonspecific stimuli such as pharmacological agents, cold air and exercise. Subjects are exposed to a suspected occupational agent in a controlled way under close supervision in a hospital laboratory. The specific inhalation challenges has been considered as the gold standard in confirming the diagnosis of occupational asthma.

<span class="mw-page-title-main">Obstructive lung disease</span> Category of respiratory disease characterized by airway obstruction

Obstructive lung disease is a category of respiratory disease characterized by airway obstruction. Many obstructive diseases of the lung result from narrowing (obstruction) of the smaller bronchi and larger bronchioles, often because of excessive contraction of the smooth muscle itself. It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling, and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD). Although COPD shares similar characteristics with all other obstructive lung diseases, such as the signs of coughing and wheezing, they are distinct conditions in terms of disease onset, frequency of symptoms, and reversibility of airway obstruction. Cystic fibrosis is also sometimes included in obstructive pulmonary disease.

Vocal cord dysfunction (VCD) is a pathology affecting the vocal folds characterized by full or partial vocal fold closure causing difficulty and distress during respiration, especially during inhalation.

<span class="mw-page-title-main">Exhaled nitric oxide</span> Breath test for respiratory inflammation

In medicine, exhaled nitric oxide (eNO) can be measured in a breath test for asthma and other respiratory conditions characterized by airway inflammation. Nitric oxide (NO) is a gaseous molecule produced by certain cell types in an inflammatory response. The fraction of exhaled NO (FENO) is a promising biomarker for the diagnosis, follow-up and as a guide to therapy in adults and children with asthma. The breath test has recently become available in many well-equipped hospitals in developed countries, although its exact role remains unclear.

<span class="mw-page-title-main">Pathophysiology of asthma</span> Medical condition

Asthma is a common pulmonary condition defined by chronic inflammation of respiratory tubes, tightening of respiratory smooth muscle, and episodes of bronchoconstriction. The Centers for Disease Control and Prevention estimate that 1 in 11 children and 1 in 12 adults have asthma in the United States of America. According to the World Health Organization, asthma affects 235 million people worldwide. There are two major categories of asthma: allergic and non-allergic. The focus of this article will be allergic asthma. In both cases, bronchoconstriction is prominent.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases. The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

<span class="mw-page-title-main">Flock worker's lung</span> Occupational disease

Flock worker's lung is an occupational lung disease caused by exposure to flock, small fibers that are glued to a backing in order to create a specific texture. People who work in flocking are at risk of inhaling small pieces of the flock fibers, which causes interstitial lung disease. The disease was initially described in 1998, when a group of workers at a flocking plant developed interstitial lung disease of unknown cause.

Chronic cough is long-term coughing, sometimes defined as more than several weeks or months. Generally a cough lasting for more than eight weeks for an adult would meet the clinical definition of a chronic cough; and for children this threshold is lower. The term can be used to describe the different causes related to coughing, the three main ones being upper airway cough syndrome, asthma and gastroesophageal reflux disease. It occurs in the upper airway of the respiratory system. Generally, a cough lasts around one to two weeks; however, chronic cough can persist for an extended period of time defined as six weeks or longer. People with chronic cough often experience more than one cause present. Due to the nature of the syndrome, the treatments used are similar; however, there are a subsequent number of treatments available, and the clinical management of the patients remains a challenge. Risk factors include exposure to cigarette smoke, and exposure to pollution, especially particulates.

<span class="mw-page-title-main">Asthma trigger</span> Factor that provokes symptoms of asthma

Asthma triggers are factors or stimuli that provoke the exacerbation of asthma symptoms or increase the degree of airflow disruption, which can lead to an asthma attack. An asthma attack is characterized by an obstruction of the airway, hypersecretion of mucus and bronchoconstriction due to the contraction of smooth muscles around the respiratory tract. Its symptoms include a wide range of manifestations such as breathlessness, coughing, a tight chest and wheezing.

References

  1. 1 2 3 4 Tarlo, Susan M.; Balmes, John; Balkissoon, Ronald; Beach, Jeremy; Beckett, William; Bernstein, David; Blanc, Paul D.; Brooks, Stuart M.; Cowl, Clayton T. (September 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. ISSN   0012-3692. PMID   18779187.
  2. 1 2 3 Murray & Nadel's Textbook of Respiratory Medicine. Elsevier. 2016. pp. 1295–1306. ISBN   9781455733835.
  3. 1 2 3 4 Tarlo, Susan M.; Lemiere, Catherine (2014-02-13). "Occupational asthma". The New England Journal of Medicine. 370 (7): 640–649. doi:10.1056/NEJMra1301758. ISSN   1533-4406. PMID   24521110.
  4. 1 2 Henneberger, Paul K.; Redlich, Carrie A.; Callahan, David B.; Harber, Philip; Lemière, Catherine; Martin, James; Tarlo, Susan M.; Vandenplas, Olivier; Torén, Kjell (2011-08-01). "An official american thoracic society statement: work-exacerbated asthma". American Journal of Respiratory and Critical Care Medicine. 184 (3): 368–378. doi:10.1164/rccm.812011ST. ISSN   1535-4970. PMID   21804122.
  5. ↑ "Asthma & Allergies". NIOSH. April 3, 2012.
  6. ↑ (T78) Occupational Asthma : Table of agents, products and substances which can cause asthma
  7. ↑ Baur, Xaver; Bakehe, Prudence (May 2014). "Allergens causing occupational asthma: an evidence-based evaluation of the literature". International Archives of Occupational and Environmental Health. 87 (4): 339–363. doi:10.1007/s00420-013-0866-9. ISSN   1432-1246. PMID   23595938. S2CID   38640302.
  8. 1 2 de Groene, Gerda J.; Pal, Teake M.; Beach, Jeremy; Tarlo, Susan M.; Spreeuwers, Dick; Frings-Dresen, Monique Hw; Mattioli, Stefano; Verbeek, Jos H. (2011). "Workplace interventions for treatment of occupational asthma". The Cochrane Database of Systematic Reviews (5): CD006308. doi:10.1002/14651858.CD006308.pub3. ISSN   1469-493X. PMID   21563151.
  9. ↑ 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.
  10. 1 2 Chan-Yeung, Moira; Malo, Jean-Luc (1995). "Occupational Asthma". New England Journal of Medicine. 333 (2): 107–112. doi:10.1056/NEJM199507133330207. ISSN   0028-4793. PMID   7777015.
  11. ↑ "Occupational asthma". Mayo Clinic. 23 May 2009.
  12. 1 2 3 4 5 6 7 8 9 10 11 12 13 "OSH Answers Asthma, Work-related". Canadian Centre for Occupational Health and Safety. December 16, 2013.
  13. 1 2 3 Baur, X.; Sigsgaard, T.; Aasen, T. B.; Burge, P. S.; Heederik, D.; Henneberger, P.; Maestrelli, P.; Rooyackers, J.; Schlünssen, V. (2012-03-01). "Guidelines for the management of work-related asthma". European Respiratory Journal. 39 (3): 529–545. doi: 10.1183/09031936.00096111 . ISSN   0903-1936. PMID   22379148.
  14. 1 2 "Occupational/Work-Related Asthma Medical Treatment Guideline" (PDF).
  15. ↑ Moscato, G.; Godnic-Cvar, J.; Maestrelli, P.; Malo, J. L.; Burge, P. S.; Coifman, R. (September 1995). "Statement on self-monitoring of peak expiratory flows in the investigation of occupational asthma. Subcommittee on Occupational Allergy of the European Academy of Allergology and Clinical Immunology. American Academy of Allergy and Clinical Immunology. European Respiratory Society. American College of Allergy, Asthma and Immunology". The European Respiratory Journal. 8 (9): 1605–1610. doi: 10.1183/09031936.95.08091605 . ISSN   0903-1936. PMID   8575590.
  16. ↑ Vandenplas, Olivier; Suojalehto, Hille; Aasen, Tor B.; Baur, Xaver; Burge, P. Sherwood; de Blay, Frederic; Fishwick, David; Hoyle, Jennifer; Maestrelli, Piero (June 2014). "Specific inhalation challenge in the diagnosis of occupational asthma: consensus statement". The European Respiratory Journal. 43 (6): 1573–1587. doi: 10.1183/09031936.00180313 . ISSN   1399-3003. PMID   24603815.
  17. ↑ Tarlo, Susan M.; Liss, Gary M. (July 2010). "Prevention of occupational asthma". Current Allergy and Asthma Reports. 10 (4): 278–286. doi:10.1007/s11882-010-0118-y. ISSN   1534-6315. PMID   20424999. S2CID   20166471.
  18. ↑ "NIOSH: Prevention of Work-related Asthma". 2018-11-23.
  19. 1 2 Henneberger, Paul K; Patel, Jenil R; de Groene, Gerda J; Beach, Jeremy; Tarlo, Susan M; Pal, Teake M; Curti, Stefania (2019-10-08). Cochrane Work Group (ed.). "Workplace interventions for treatment of occupational asthma". Cochrane Database of Systematic Reviews. 10 (10): CD006308. doi:10.1002/14651858.CD006308.pub4. PMC   6781842 . PMID   31593318.
  20. 1 2 "NIOSH: Work-related asthma". 2019-01-03.
  21. 1 2 Cowl, Clayton T. (2011). "Occupational Asthma". Chest. 139 (3): 674–681. doi:10.1378/chest.10-0079. PMID   21362654.
  22. ↑ "Occuptational Asthma". MedlinePlus Medical Encyclopedia.
  23. ↑ Dewitte JD, Chan-Yeung M, Malo JL (May 1994). "Medicolegal and compensation aspects of occupational asthma". Eur. Respir. J. 7 (5): 969–80. doi: 10.1183/09031936.94.07050969 . PMID   8050556. S2CID   41120422.
  24. ↑ Leigh JP, Romano PS, Schenker MB, Kreiss K (January 2002). "Costs of occupational COPD and asthma". Chest. 121 (1): 264–72. CiteSeerX   10.1.1.455.4942 . doi:10.1378/chest.121.1.264. PMID   11796461.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.