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Asthma Essay With Conclusions
Info: 2061 words (8 pages) Nursing Essay Published: 11th Feb 2020
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Work‐related asthma: A position paper from the Thoracic Society of Australia and New Zealand and the National Asthma Council Australia
1 Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne VIC, Australia
2 Allergy, Asthma and Clinical Immunology, The Alfred Hospital, Melbourne VIC, Australia
Jonathan Burdon
3 National Asthma Council, Melbourne VIC, Australia
4 School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle NSW, Australia
Susan Miles
5 Department of Medicine, Calvary Mater Newcastle, Newcastle NSW, Australia
Jennifer L Perret
6 Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, The University of Melbourne, Melbourne VIC, Australia
Shivonne Prasad
Naghmeh radhakrishna, janet rimmer.
7 Woolcock Institute of Medical Research, University of Sydney, Sydney NSW, Australia
Malcolm R Sim
Deborah yates.
8 Department of Thoracic Medicine, St Vincent's Hospital, Sydney NSW, Australia
Graeme Zosky
9 Menzies Institute for Medical Research, Tasmanian School of Medicine, University of Tasmania, Hobart TAS, Australia
Work‐related asthma (WRA) is one of the most common occupational respiratory conditions, and includes asthma specifically caused by occupational exposures (OA) and asthma that is worsened by conditions at work (WEA). WRA should be considered in all adults with asthma, but especially those with new‐onset or difficult to control asthma. Improvement in asthma symptoms when away from work is suggestive of WRA. Clinical history alone is insufficient to diagnose WRA; therefore, objective investigations are required to confirm the presence of asthma and the association of asthma with work activities. Management of WRA requires pharmacotherapy similar to that of non‐WRA, however, also needs to take into account control of the causative workplace exposure. Ongoing exposure will likely lead to decline in lung function and worsening asthma control. WRA is a preventable condition but this does rely on increased awareness of WRA and thorough identification and control of all potential occupational respiratory hazards.
Introduction
Definitions
Epidemiology
Clinical features
Investigations
Compensation and impairment assessment
Abbreviations
Introduction.
Asthma affects approximately 2.7 million Australians, and remains a significant cause of death, with more than 400 people dying of asthma in Australia in 2017. More than one‐third of people with asthma report that this significantly affects their daily living, and the economic and social costs of asthma remain high despite improvements in treatment. Work‐related causes of asthma are often forgotten about by patients and healthcare professionals, yet remain an important preventable cause of morbidity and disablement.
Work‐related asthma (WRA) is a general term which includes both asthma caused by an inciting exposure in the workplace (occupational asthma, OA) and asthma that is worsened by workplace conditions (work‐exacerbated asthma, WEA) (Fig. (Fig.1 1 ). 1 WRA is a common occupational lung disease in developed, low‐ and middle‐income countries and is generally preventable. 2 It is estimated that 25% of adults with asthma have WRA. 1 , 3 Although WRA is likely to be encountered frequently in clinical practice, it remains under‐recognized and under‐reported. 4 Failure to identify and manage WRA may lead to worsening asthma control. Conversely, inaccurate diagnosis may lead to unnecessary absence from work and potential economic hardship. 5
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Relationship of asthma to the workplace (Reproduced from Tarlo et al ., 1 with permission).
The purpose of the position paper is to increase awareness of the association between work and asthma, and provide a structure for diagnosis and management. The paper is intended to provide general advice and does not represent guidelines. The target audience is all healthcare professionals who manage patients with asthma. The clinical relevance of the paper will be reviewed 5 years after the date of publication.
In accordance with the Thoracic Society of Australia and New Zealand (TSANZ) policy, a call for expressions of interest was sent to all members of the Society. Following review of provided curriculum vitae, the position paper writing group was established with 10 respiratory physicians and 1 occupational physician. Based on their areas of expertise, members were assigned specific sections to undertake a comprehensive literature review and develop draft recommendations. Inclusion of articles was determined by the assigning author and they were not systematically reviewed. All drafted sections were reviewed by the entire group for the opportunity to provide further contributions. Three authors (R.H., J.R. and J.B.) then compiled and edited the manuscript. All authors reviewed and approved the final manuscript.
DEFINITIONS
OA is new‐onset asthma, or the recurrence of previously quiescent asthma, induced by an occupational exposure. The timely diagnosis of OA is important as ongoing exposure to the causative agent may result in rapid and often irreversible decline in lung function. 6 , 7 OA can be characterized as sensitiser‐induced or irritant‐induced occupational asthma.
Sensitiser‐induced OA is the most common form of OA (approximately 90%) and may be caused by high‐ or low‐molecular weight (HMW and LMW) agents. 1 Sensitiser‐induced OA is characterized by development of asthma after a latency period ranging between days and years after initial occupational exposure. HMW agents (>10 kDa) act as antigens and induce production of antigen‐specific IgE. 8 Although some LMW agents also induce specific IgE by acting as haptens, most LMW chemicals induce asthma via cellular immune‐mediated pathways. Sensitisation to more than one occupational agent may occur, and more than one mechanism can be involved in any individual. The phenotypes of HMW and LMW OA appear to differ. An international multicentre study noted that HMW OA was more associated with work‐related rhinitis, early asthmatic reactions and airflow limitation, and LMW OA more with work‐related chest tightness, late reactions and severe exacerbations. 9
Over 300 workplace agents have been described to cause OA (Table (Table1 1 ). 10 Australian prevalence data from 2014 showed that occupational exposure to one or more agent is common (47% men, 40% women). 11 Among men, common exposures include bioaerosols (29%), metals (27%), arthropods/mites (25%) and latex (22%), and among women: latex (25%), industrial cleaning and sterilizing agents (20%), bioaerosols (18%) and arthropods/mites (16%).
Summary of workplace agents causing sensitiser‐induced occupational asthma 4 , 10 , 11 , 12 , 13
Agent | At‐risk occupations | |
---|---|---|
) | ||
Plant allergens | Grains, cereals (e.g. rye, soya, malt and wheat flour) | Farmers, bakers, millers, combine harvester drivers |
Dust (tea, tobacco, coffee beans) | Packers, cafe workers | |
Flowers, pollen | Florists, gardeners | |
Vegetable gums | Pharmaceutical industry, carpet factory workers | |
Cotton | Textile industry workers | |
Hay | Farmers | |
Psyllium | Healthcare workers | |
Latex | Healthcare workers, toy and medical equipment manufacturers | |
Animal allergens | Dander, excreta | Laboratory workers, veterinary workers, farmers, breeders, animal handlers, groomers |
Insects | Laboratory workers, entomologists | |
Bird products, egg protein | Process workers, breeders, poultry and hatchery workers | |
Crustaceans, seafood | Process workers, cooks, fishermen | |
Enzymes | Protease, amylase, lipase, cellulase | Detergent manufacturers, warehouse workers, bakers, cleaners, hospital staff |
Fungi | Moulds, yeasts | Food processors, bakers, farmers |
) | ||
Chemicals | Isocyanates | Spray painters, adhesive workers, polyurethane foam manufacturers, insulation workers, automotive industry |
Formaldehyde | Embalmers, healthcare workers, cosmetic industry | |
Glutaraldehyde | Laboratory workers, tanners, plastic industry workers, endoscopists | |
Dyes and bleaches | Fabric and fur dyers, hairdressers | |
Alkaline persulphates | Hair dressers, plastic and synthetic rubber manufacturers | |
Complex amines | Agrichemical and pharmaceutical manufacturers | |
Fungicides | Gardeners | |
Glues and resins (epoxy, acrylates, acid anhydrides) | Flooring installers, tilers, plastic manufacturers, polyurethane foam manufacturers, dental technicians | |
Metal salts, dusts or fumes | Platinum salts, nickel, cobalt, chromium, iron, tin, zinc oxide, titanium, stainless steel, tungsten | Metal platers and galvanizers, electronic industry workers, photographers, dentists, chemists |
Aluminium pot room emission | Aluminium fluoride, chlorine, sulphur dioxide, hydrofluoric acid | Aluminium smelter workers |
Pharmaceuticals | Penicillins, tetracycline, cephalosporins, opiates, colistin | Chemists, healthcare professionals |
Solder flux | Colophony | Metallurgists, jewellery makers, artists, electronics workers, welders |
Wood dusts | Western red cedar (plicatic acid), oak, redwood, chicory, exotic woods | Carpenters, saw mill workers, arborists, sanders |
The primary risk factor for the development of sensitiser‐induced OA is the level or dose of workplace exposure to the inciting agent, but the duration of exposure is also important. 14 A history of atopy also confers a higher risk of developing sensitiser‐induced OA when exposed to HMW antigens. A history of smoking is a risk factor for the development of OA for most antigens, but this has not been demonstrated for all.
Where uncertainty exists regarding exposure to potential agents, there are useful web‐based lists of agents with search tools which can help in deciding whether an agent is a likely cause of OA (e.g. www.occupationalasthma.com and www.aoecdata.org ).
In 1985, Brooks described reactive airway dysfunction syndrome (RADS) as sudden‐onset asthma occurring within a few hours of a single high‐level exposure to an irritant substance. 15 Subsequently, the term irritant‐induced (occupational) asthma (IIA) has been utilized more widely. IIA includes the RADS clinical phenotype, but also development of asthma in workers with multiple irritant exposures and asthma with a delayed onset after chronic exposure to moderate levels of irritants 1 , 4 , 15 , 16 , 17 (Table (Table2). 2 ). The association between IIA and frequent low‐level exposures to respiratory irritants is not entirely clear, but has been described in case reports and small case series involving cleaners (domestic and industrial), nurses, textile workers, poultry workers and aluminium pot room workers. 4 , 20 There has been increasing recognition of the association between cleaning agents and disinfectants and asthma, in particular formaldehyde, glutaraldehyde, hypochlorite bleach, hydrogen peroxide and enzymatic cleaners. 21 There is evidence that irritant mechanism is more common in association with these agents; however, an immunological mechanism has been noted in case reports. 22
Common workplace exposures associated with work‐exacerbated asthma and irritant‐induced asthma 16 , 18 , 19
Work‐exacerbated asthma | Irritant‐induced asthma |
---|---|
Respiratory irritants (dusts, fumes, sprays, gas, aerosols, liquids) | Acetic, hydrochloric, sulphuric and other acids |
Aeroallergens (dust mite, pollens, animal dander) | Bleaching, cleaning, sealing agents, diesel exhaust |
Thermal stress | Sulphur dioxide |
Emotional stress | Ammonia |
Physical exertion | Chlorine, chlorofluorocarbons |
Although the definitive pathogenic mechanism remains unclear, IIA is likely due to bronchial epithelial cell damage resulting in pro‐inflammatory responses, neurogenic inflammation due to exposed nerve endings, increased lung permeability and remodelling of the airway epithelium. 18
WEA describes the exacerbation of pre‐existing or coincident (new‐onset, non‐occupational) asthma because of workplace conditions. 16 WEA may present with increased symptom frequency, medication use or acute exacerbations. Conditions at workplaces that can exacerbate asthma are common and varied (Table (Table2 2 ). 16 WEA is common, with a median prevalence of 21.5% among adults with asthma. 16
EPIDEMIOLOGY
To date, epidemiological estimates of WRA have been wide‐ranging. Surveillance‐based systems suggest that the incidence of OA is approximately 4–17/100 000 workers per year, 23 , 24 although data from a prospective multi‐national survey, which included Australia, suggest that the incidence may be as high as 25–30/100 000 people per year. 25 The no longer operational voluntary reporting scheme SABRE (Surveillance of Australian workplace Respiratory Based Events) recorded an incidence of OA of 0.5/100 000 workers per year in NSW and 3/100 000 in Victoria. 26 These rates are far lower than similar countries overseas, likely to be due to under‐reporting to this scheme. 26 Finland has one of the most comprehensive data sets regarding work‐related disease due to compulsory physician reporting of all known or suspected occupational diseases. 23 The Finnish Registry of Occupational Disease (FROD) reported a mean OA annual incidence rate of 17.4 cases/100 000 employed workers. 23 Cases caused by animal allergens, or flours, grains and fodders accounted for 60% of the total.
The population burden of asthma attributable to occupational exposures has been estimated to be between 15% and potentially as high as 20%, 27 although studies using strict definitions of OA suggest attributable fraction closer to 4.7%. 24 In Australia, estimates of new cases of asthma caused by work range from approximately 1000 to 3000 per year. 28 There are limited data on the contribution of irritants to OA incidence. Survey data from New South Wales estimated a population attributable risk to new‐onset asthma due to work of 9.5% overall and 0.2% for irritant exposures. 29 However, early data from Canada noted that IIA was relatively common among a sample of workers diagnosed with OA at a specialist occupational lung disease clinic (10/59). 17
WEA has been noted to be a common condition. 30 An American Thoracic Society (ATS) consensus statement reviewed 12 general population or primary healthcare studies noting an average prevalence of 21.5% (range: 13–58%) of WEA among working asthmatic patients. 16 Other studies using more objective measures of asthma control (interviews, serial peak expiratory flow (PEF) measures and medication usage) identified WEA prevalence of 13–22% among all those with asthma. 31
CLINICAL FEATURES
A relationship between asthma and exposures in the work setting should be considered in all people of working age with asthma, particularly if asthma develops during adult life or has been difficult to control.
A detailed history of clinical symptoms is required to determine if symptoms are consistent with asthma or an alternative diagnosis (Table (Table3). 3 ). An OA screening questionnaire has been developed (OASQ‐11) and has moderate discrimination for OA when used in a clinical setting. 36 Typical asthma symptoms include episodic breathlessness, wheeze, cough or chest tightness. 37 The presence of work‐related dysphonia and cough has been noted to be more common with work‐associated irritable larynx syndrome than asthma, especially when associated with sensory irritants including odours, perfumes, exhaust fumes and cleaning products. 35 Symptoms of occupational allergic rhinitis (nasal itch, rhinorrhoea and congestion) often precede symptoms of asthma especially related to HMW agents. 38 Asthma present before occupational exposure, but associated with worsening at the start of a new occupational exposure, suggests the presence of WEA.
Differential diagnosis of work‐associated respiratory symptoms and diagnostic evaluation
Condition | Diagnostic evaluation |
---|---|
WRA | Refer to Table 4 |
WILS (also known as vocal cord dysfunction) | Clinical history and laryngoscopy |
COPD | Pulmonary function testing and high‐resolution CT chest |
Bronchiectasis and other obstructive lung disorders | Pulmonary function testing and high‐resolution CT chest |
Upper respiratory tract irritation | Clinical history |
Hypersensitivity pneumonitis | Pulmonary function testing and high‐resolution CT chest, specific serum IgG antibodies, when available |
Rhinosinusitis | Clinical history, CT sinuses, specific IgE antibodies |
Eosinophilic bronchitis | FeNO, induce sputum cytology |
Non‐WRA | Pulmonary function testing |
Odour or irritant‐induced hyperventilation | Clinical history |
Psychogenic factors | Clinical history |
COPD, chronic obstructive pulmonary disease; CT, computed tomography; FeNO, fractional exhaled nitric oxide; WILS, Work‐associated Irritable Larynx Syndrome; WRA, work‐related asthma.
Irritant‐induced OA symptoms commence at the time of inducing workplace exposure. However, sensitiser‐induced OA is characterized by a period of latency between first exposure to the occupational agent and development of asthma symptoms. This period may range from days to years. Subsequently, symptoms typically improve during times away from work, such as weekends and holidays, and worsen at work. This temporal association of symptoms lessens when asthma becomes more prolonged or severe.
A detailed work exposure history should be obtained to identify likely exposure(s) known to cause WRA (Tables (Tables1, 1 , ,2). 2 ). The patient should be asked to provide a detailed description of his/her work schedule, tasks and exposures, and of possible exposures related to other activities in the environment. Details of control strategies including respiratory protection and ventilation should be obtained. The patient should request that their employer provide safety data sheets (SDS) relevant for their work environment. SDS are documents that provide critical information about hazardous chemicals. However, these sheets may be incomplete and not identify the potential of the agent to cause asthma.
INVESTIGATIONS
Clinical history alone is insufficient to accurately diagnose WRA. 39 Objective investigations are required to:
- Confirm the presence of asthma (symptoms, variable airflow obstruction and/or non‐specific bronchial hyperresponsiveness (NSBH)).
- Evaluate the association between asthma and the workplace.
- Demonstrate sensitisation to, or identify in other ways, the specific causal agent (wherever possible).
Investigations should be commenced as soon as WRA is suspected and should be performed when the worker is still in the role suspected to be associated with asthma. Relocation during the process of investigating WRA is only necessary if asthma is severe.
Given the individual limitations of investigations, an approach which includes clinical history and a combination of testing will increase diagnostic accuracy 1 , 4 (Table (Table4 4 ).
Diagnostic criteria for forms of work‐related asthma
OA | Work‐exacerbated asthma | ||
---|---|---|---|
Sensitiser‐induced | Irritant‐induced | Required criteria | |
Required criteria (need all for a definite diagnosis) | Supportive criteria | Required criteria | |
New‐onset asthma or recurrence of previously quiescent asthma , Diagnosis of asthma made on the basis of BOTH: , ,
Onset of asthma symptoms after a period of latency following initial exposure to a sensitiser in the work environment , Asthma symptoms occurring in association with work and exhibiting remission or improvement during periods off work , , ,
Objective association between asthma and the workplace. , The following criteria should be sought in all patients and at least ONE should be present for a diagnosis , ,
| History of work in an at‐risk occupation Suggestive signs and symptoms (see section Clinical features) Evidence of work‐related airway inflammation, such as FeNO measurements , , | History of new‐onset or recurrence of previously quiescent asthma while working , Symptom onset following one or more high‐level exposures , Symptoms can begin ≤24 h and up to several days after exposure Occupational exposure to gas, fume, spray or dust with known irritant properties , Symptoms persisting for ≥3 months , Physiological testing showing EITHER variable airflow obstruction OR NSBH , | Pre‐existing asthma based on symptoms, medical history, variable airflow obstruction or NSBH on lung function testing or medication usage prior to occupational exposure , , Presence of conditions at work that can exacerbate asthma (Table 2) , Demonstration of worsening of asthma after start of employment, change in work process or environment through at least ONE of the following , :
OA is unlikely. An exacerbation of OA due to the initial causative agent is considered an exacerbation of OA |
FeNO, fractional exhaled nitric oxide; NSBH, non‐specific bronchial hyperresponsiveness; OA, occupational asthma; PEF, peak expiratory flow.
The following are suggested:
- Confirm the presence of asthma
Spirometry with bronchodilator reversibility assessment should be performed in every worker with suspected WRA in accordance with best practice guidelines to identify variable airflow limitation . 37 , 40 The presence of expiratory airflow limitation (forced expiratory volume 1 s/forced vital capacity (FEV 1 /FVC) < lower limit of normal for age) and FEV 1 increase ≥200 mL and ≥12% from baseline in response to a β2‐agonist is consistent with the diagnosis of asthma in this context. 37 However, normal spirometry at the time of initial assessment does not rule out the diagnosis of asthma. The quality of spirometry is important and may give clues to the possibility of other diagnoses.
If spirometry does not identify variable airflow limitation, then bronchial provocation testing should be considered to identify the presence of NSBH.
Bronchial provocation testing in the setting of OA has a high sensitivity (84%) and a high negative predictive value (75%), 41 such that a negative test or a lack of NSBH in a symptomatic individual, especially if performed within 24 h of work exposure, can generally be used to rule out active asthma. 1 , 42 Assessment for NSBH should be carried out when the patient is still exposed to the suspected offending agent, as airway hyperreactivity can return to normal rapidly once exposure ceases. 42 A negative bronchial provocation test is helpful in excluding active asthma, but due to low specificity and low positive predictive value, a single positive test should be interpreted in combination with other investigations and clinical aspects. 43
Bronchial provocation testing can be done using either direct agents (methacholine or histamine) or indirect agents (mannitol). The latter is now commonly used in Australian laboratories and has been shown in a small study to be positive in patients with more active disease, 44 but there are more data on methacholine.
- Evaluation of association between asthma and work exposure
Serial NSBH
Comparison of bronchial hyperreactivity at work and after a 10‐ to 14‐day period away from the work exposure has shown moderate sensitivity and specificity for diagnosing WRA. A 2‐ to 3‐fold change in the dose of methacholine or histamine needed for a positive test is considered significant. 1 There is only a slightly greater sensitivity with reduced specificity compared to using PEF measurements alone.
The use of recording PEF during periods at and off work is helpful and can be evaluated visually by experienced respiratory and occupational physicians, although this method has been shown to have moderate between‐ and within‐expert agreement. 45 If there are expert disagreements, computer evaluations using quantitative analysis of changes in mean PEF values can be used (OASYS‐2; OASYS Research Group, Midland Thoracic Society, Birmingham, UK, http://www.occupationalasthma.com/occupational_asthma_pageview.aspx?id=4443 ). 43 Computer‐based analysis has an equivalent sensitivity to visual inspection technique but greater specificity (91% vs 69%) and would be useful in confirming OA. 43
PEF measurements should be recorded four times per day (on awakening, noon, at the end of working day and before bedtime) for a total of 4 weeks, including 2 weeks away from work. 1 Cross‐shift PEF or FEV 1 seems to be less reliable than serial PEF testing. The cross‐shift method has a high specificity (91%) but a low sensitivity (50–60%). 46
Specific inhalation challenge
Specific inhalation challenge (SIC) involves exposing workers who are suspected of having sensitiser‐induced OA to the presumed causative agent in a safe and controlled manner within an enclosed challenge room. 1 , 47 However, SIC testing requires a high level of expertise and is only performed in a few centres around the world. International guidelines recommend a 3‐ to 4‐day protocol of testing and admission to hospital for the duration of the challenge test due to the risk of late phase excessive reactions. 47 At this time, SIC testing is not routinely available in Australia or New Zealand.
- Demonstrate sensitisation to, or identify, the specific causal agent (where possible)
Only a few of the 300 known asthma‐causing agents are commercially available for testing. Skin prick tests (SPT) and assessment of serum allergen‐specific IgE (sIgE) antibodies are useful to demonstrate IgE‐mediated sensitisation to many HMW and some LMW agents. Other than latex, cat and bee venom extracts, there is a worldwide relative lack of standardization and validation for other occupational agents. SPT with LMW agents should be performed with caution as allergenic extracts are not standardised and most of these agents are potentially irritant to the skin and may produce false‐positive results with lower specificity.
Combination testing
Combining the presence of NSBH with a positive SPT or sIgE test markedly increased the specificity of NSBH assessment alone, while sensitivity was not consistently improved. 43 , 48 Assessment of indices of eosinophilic airway inflammation (fractional exhaled nitric oxide (FeNO) ≥ 25 ppb or a sputum eosinophil count ≥ 1%) has also recently been demonstrated to increase the sensitivity of evaluation when performed in combination with NSBH assessment. 33
WRA should be suspected in all adults with asthma, but in particular those with new‐onset or difficult to control asthma. Asking if asthma symptoms differ during times away from work such as weekends or holidays can be a useful initial screening question. 1 Those who answer yes will require more detailed evaluation for possible WRA. Due to the potential for the diagnosis to impact employment, it is important to utilize objective testing to confirm a diagnosis, as outlined in Table Table4 4 .
The pharmacological treatment of WRA is the same as that for non‐WRA. 1 , 37 A stepwise approach, using anti‐inflammatory and bronchodilator therapy, should be used to achieve symptom control with subsequent dosage adjustment to achieve good symptomatic control at the lowest effective dose, as per existing guidelines. 37 , 49 For patients with difficult to control asthma symptoms, there should be consideration of referral to a specialist severe asthma clinic. Evaluation may include assessment of eligibility for access to monoclonal antibody therapy.
There is insufficient evidence that pharmacological management of sensitiser‐induced OA with inhaled corticosteroids and long‐acting β2‐agonists is able to prevent the long‐term deterioration of asthma in subjects who remain exposed to the agent causing OA. 50 One study showed that early treatment with oral corticosteroids may improve outcomes for patients with IIA; however, until confirmed this cannot be recommended. 51 Every opportunity should be taken to assist smoking cessation if relevant. The ATS has published a position paper on WRA, 16 and specific standards of care were developed by the British Thoracic Society and updated in 2012. 52 These contain very similar recommendations, and can be applied worldwide. The Australian Asthma Handbook ( http://www.asthmahandbook.org.au ) also has useful information.
Sensitiser‐induced OA
Continued exposure will most likely lead to worsening symptoms, airflow limitation and airway hyperresponsiveness. 53 , 54 Conversely, complete avoidance will almost certainly result in improvement in asthma control, although symptoms may remain in two‐third of cases. 55
Optimal management of sensitiser‐induced OA involves accurate identification of the sensitiser and early and complete avoidance of ongoing exposure. 50 , 56 The latter may involve:
- Control of exposure at the workplace, including substitution with an alternative.
- Effective engineering controls.
- Other means to reduce air levels, such as extraction ventilation or wetting the process for dusts.
- Redeployment to a job or work area with absence or reduction of the exposure. 5
- Use of protective clothing, masks or independent air supplies, although low‐level exposure may induce symptoms in established sensitiser‐induced asthma despite protective equipment. 50
- Communication with the employer (with patient consent) regarding recommendations to eliminate or reduce exposure.
- Seeking alternative employment.
Patients with confirmed or suspected sensitiser‐induced OA who continue to have potential exposure to the sensitiser should be monitored closely by a specialist. A recommendation has been made for 3 monthly reviews for 1 year and then 6 monthly afterwards. 52 Workers need to be counselled regarding the risk of deteriorating asthma control and airflow obstruction posed by persistent occupational exposure.
If a worker leaves a workplace due to OA, even if based on medical recommendation, there is likely to be a significant negative socio‐economic impact for that worker. 57 The diagnosis should therefore be objectively confirmed by a specialist with experience in investigating WRA, prior to making this decision. Workers who have left the workplace may have slow symptomatic and lung function improvement and should be monitored for a minimum of 3 years. 52
Irritant‐induced OA
Workers should be able to continue their job unless repetitive exposure to respiratory irritants is likely to occur. Employers should ensure control measures are in place to minimize the risk of exposure to respiratory irritants for all workers as far as practicable. For those with IIA, symptom control may be possible, whilst continuing their job, provided an effective reduction in trigger exposure can be achieved in the workplace. 18
Work‐exacerbated asthma
The literature regarding the natural history and optimal management of WEA is limited. 1 , 16 Identification of exacerbating triggers and reducing potential harmful exposures can minimize the risk of ongoing problems. Workers should be able to stay in the same job if control of exposure can be achieved, with close monitoring of their asthma control.
COMPENSATION AND IMPAIRMENT ASSESSMENT
Most jurisdictions in Australia, as part of their workers' compensation system, have produced lists of deemed diseases. These are conditions that are considered to be work related and the assumption is made that an exposed worker with WRA is deemed to have a work‐related condition unless there is strong evidence to the contrary. 58 Therefore, it is important that the diagnosis of WRA is accurately confirmed by a specialist.
Persons suffering from WRA will commonly require periods of time away from the workplace. Most will consequently incur both social and financial costs, including loss of income, medical fees and costs of therapies. For these reasons, compensation will usually be sought and is appropriate.
Early referral to the employer's workers' compensation insurer is recommended to allow timely assessment of liability and institution of measures to address the worker's health. This may also expedite the process of reducing exposure for other workers.
In cases with ongoing respiratory impairment, lump sum compensation payments may be payable. An assessment of permanent impairment should be delayed until asthma symptoms have been stable for at least 12 months. In all states of Australia, the assessment of respiratory impairment is based on the American Medical Association Guides to the Evaluation of Permanent Impairment . In general, the fourth (third printing) and fifth editions are used and measured spirometric indices are applied to the relevant tables published in the guides. Requirements vary in the different editions but all require:
- Measurements of pre‐ and post‐bronchodilator spirometry; predicted values as published in the guides.
- Determination that the lung function is stable (not expected to vary by more than 3% in the future).
- A record of medication requirements 59 including inhaled glucocorticoids.
In Victoria, the Impairment Assessment in Workers with OA is used as an extension of table 10 of the AMA 4th Edition guides and also takes into account clinical symptomatology and exercise capacity. 60
All occurrences of WRA are potentially preventable. Because a new diagnosis of OA is a sentinel event, the managing clinician has an ethical responsibility to communicate with the workplace and facilitate measures that protect co‐workers. These may involve the accurate identification of the causative exposure, a review of workplace control measures, the introduction or modification of a health surveillance programme to screen other co‐workers as well as optimizing case management. 61 Involvement of an occupational physician to address some of these issues may be warranted. Ideally, a positive workplace culture will facilitate workers to report safety concerns and potential early symptoms of asthma. 52
Elimination, substitution and enclosure
Elimination of the agent is strongly recommended as the primary preventive method. 62 An example has been the substitution of powdered latex gloves by latex‐free gloves and powder‐free, protein‐poor natural rubber latex (NRL) gloves minimizing occupational allergy and asthma in health care. 63
Exposure reduction
This is the next favoured approach if elimination is not possible. Exposure levels are kept as low as feasible through partial substitution, partial segregation and/or optimization of ventilation by engineering controls and/or automation of some work practices. 64
Respiratory protective equipment as a preventive measure is ranked lowest in the hierachy of controls. 61 , 62 If used, it must be appropriately selected for the exposure (such as isocyanate‐containing spray paints), 65 and adequate training of the workers must be provided. Respiratory protection must be regularly fit tested and well maintained. Powered or air supplied respirators may be required to ensure a suitable degree of protection is obtained.
Health surveillance
Although exposure reduction may lessen the progression of subclinical asthma and sensitisation, this strategy also requires careful monitoring of workers for the potential emergence of disease. Workplace surveillance using questionnaires, followed by the investigation of suggestive symptoms by a specialist clinician, is recommended. 62 Serial spirometry, serological testing and/or SPT as part of a more comprehensive medical surveillance programme differ between industries and/or individual workers and jobs within an industry. Specific IgE (or SPT) surveillance is strongly recommended for ongoing potential exposure to HMW agents such as animal care workers, bakers dust, enzyme and latex exposures. 66 It is also used for occasional LMW allergens such as complex platinum salts. 1 Although the evidence to support surveillance programmes is considerable, 61 optimal monitoring frequency and efficacy of individual components have not yet been established.
Pre‐placement assessment
Testing of workers for specific sensitisation to HMW allergens before employment is strongly recommended for high‐risk industries. 62 Workers should be made aware of the common sensitisers, existing control measures and typical symptoms of occupational rhinitis and asthma that suggest a need for further evaluation following commencement of work. For prospective employees with pre‐existing asthma and/or atopy, results from screening investigations (such as spirometry and/or assessment of allergen‐specific IgE) may be used as a starting point for surveillance and health education. 66 While such applicants might consider avoiding ‘at‐risk’ employment, employer selection based on these common predisposing conditions is not useful as many workers will never develop WRA. 14 , 66
The development of asthma from an occupational exposure is an important, preventable factor which has substantial negative health and socio‐economic implications for an individual. The worsening of asthma control due to workplace conditions is also common and requires careful management. Diagnosis of WRA can be challenging and requires a thorough approach with objective measures of respiratory function. The influence of work on asthma should be considered as part of routine asthma care, and if WRA is suspected, early referral to a specialist for further evaluation and management is usually required. Diagnosis of WRA should also lead to evaluation of a workplace's prevention measures to minimize the risk to other exposed workers. 3
Disclosure statement
The authors do not have any competing interests to disclose.
Acknowledgements
The authors would like to acknowledge the support of the National Asthma Council and the Thoracic Society of Australia and New Zealand for their assistance with planning and development of the position paper.
Hoy R, Burdon J, Chen L, et al. Work‐related asthma: A position paper from the Thoracic Society of Australia and New Zealand and the National Asthma Council Australia . Respirology . 2020; 25 :1183–1192. 10.1111/resp.13951 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
This study is endorsed by the Thoracic Society of Australia and New Zealand.
Received 14 June 2020; invited to revise 11 August 2020; revised 24 August 2020; accepted 31 August 2020.
Associate Editor: Giorgio Piacentini; Senior Editors: Philip Bardin and Paul Reynolds
Contributor Information
Ryan Hoy, Email: [email protected] .
Malcolm R Sim, Email: [email protected] .
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Occupational Asthma
Asthma and your occupation.
Approximately 10 to 25 percent of adults with asthma experience occupational asthma. Occupational asthma is a type of asthma caused by exposure to inhaled irritants in the workplace. Occupational asthma is often a reversible condition, which means the symptoms may disappear when the irritants that caused the asthma are avoided. However, permanent damage can result if the person experiences prolonged exposure. Examples of workplace irritants include:
What are the symptoms of occupational asthma?
Occupational asthma symptoms are the same as any asthma exacerbation, such as wheezing, shortness of breath, runny nose, nasal congestion, eye irritation, and chest tightness. These symptoms may get worse during exposure to the irritant(s) at work. The cause can be allergic or nonallergic in nature. Symptoms may get better when the person is not at work. Sometimes, occupational asthma symptoms do not appear until several hours after the exposure, even while at home after work. At the onset of the disease, symptoms may subside during weekends and vacations, but exposure to an occupational irritant can cause asthma within 24 hours. However, during later stages of occupational asthma, asthma symptoms may become a problem during exposure to other, more common asthma triggers, such as smoke, dust, and temperature changes.
What substances cause occupational asthma?
Although new substances are developed every day that may cause occupational asthma, some known airborne irritants in the workplace include:
|
|
|
---|---|---|
| Isocyanates, trimellitic anhydride, phthalic anhydride | Manufacturers of foam mattresses and upholstery, insulation, packaging materials, plasticizers, and polyurethane paint |
| Bacterial dusts, dander, hair, mites, protein dusts, small insects | Farmers, animal handlers, kennel workers, jockeys, and veterinarians |
| Cereals, coffee, flour, grains, tea | Millers, bakers, and other food processors |
| Dusts from cotton and textile industry | Cotton and textile workers |
| Chromium, nickel sulfate, platinum, soldering fumes | Manufacturers of metals and refineries |
![occupational asthma essay Man wearing a face mask while sanding a wood floor.](https://www.hopkinsmedicine.org/-/media/images/health/1_-conditions/asthma/getimage-(7).png?h=250&iar=0&mh=360&mw=520&w=187&hash=87CE315E14B785D2E086D815B6F4F635)
How can occupational asthma be prevented?
Avoidance of triggers is the best prevention against asthma. If occupational asthma symptoms do occur, you may need to change jobs to avoid exposure. However, certain steps taken in the workplace can help reduce the risk of occupational asthma:
Change the work process to better handle irritant exposure
Use industrial hygiene techniques that are appropriate for the type of irritant you are exposed to and that will keep exposure levels to a minimum
Have regular medical checkups to identify possible damage that may be occurring to the lungs or other medical conditions specifically related to the irritant exposure
Be aware of any personal and/or family medical history of asthma which may put you at greater risk for occupational asthma in certain industries
The degree to which cigarette smoking contributes to occupational asthma is not known, but smokers are more likely than nonsmokers to develop lung problems in general.
How is occupational asthma diagnosed?
Diagnosis of occupational asthma usually includes a detailed medical history and a medical examination to establish the relationship of the symptoms to exposure at work. Other diagnostic procedures may include pulmonary function tests before and after work to detect narrowing of the airways, blood and sputum lab tests, and a chest X-ray to rule out other lung diseases.
Treatment for occupational asthma
Treatment for occupational asthma usually includes avoiding the substance that triggers the asthma attack or symptoms. Persons with occupational asthma should also avoid inhaling gases, such as chlorine, or nitrogen dioxide, and sulfur dioxide, as these substances can make asthma symptoms more severe. Other treatment may include medications to control the asthma. If the occupational asthma is advanced, treatment may also include:
Medications
Physical therapy
Breathing aids
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Asthma: environmental and occupational factors
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Paul Cullinan, Anthony Newman Taylor, Asthma: environmental and occupational factors, British Medical Bulletin , Volume 68, Issue 1, December 2003, Pages 227–242, https://doi.org/10.1093/bmb/ldg021
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Asthma is in several ways a difficult disease to study. Generally arising in childhood, its pattern is often one of remission and relapse; at any point there are difficulties in translating its characteristic, clinical features into an operational definition. Geographical and temporal patterns in its distribution – whereby the disease appears to have increased in frequency in more ‘westernised’ countries –suggest strong environmental determinants in its causation although there are, too, undoubted and important genetic influences on both its incidence and presentation. Recent aetiological research has concentrated on the function of allergen exposure or on the role of early-life microbial contact that may regulate the development of a range of childhood allergies, including asthma. To date the ‘hygiene hypothesis’ offers the most efficient explanation for the distribution of the disease in time and place although convincing evidence for it remains elusive.
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- Preventing Work-related Asthma
- Information for Clinicians
- Work-related Asthma Exposures
- Diagnosing Work-related Asthma
- Treating Work-related Asthma
About Work-related Asthma
- Asthma is a disease that affects your lungs.
- Work-related asthma is triggered or develops from exposures at work.
- Workplace irritants, allergens, and physical conditions are triggers.
- Work-related asthma symptoms are the same as non-work related asthma.
![occupational asthma essay Worker using inhaler working on his laptop.](https://www.cdc.gov/niosh/media/images/asthmaticintheworkplace.png)
Work-related asthma is asthma triggered by exposures at work. Asthma affects the lungs and causes the airways to become narrow and inflamed. To control it, avoid triggers that cause asthma symptoms and take prescribed medicine.
Many triggers can be in the workplace. Over 300 known substances in the workplace can cause or worsen asthma. Avoiding triggers can prevent asthma from getting worse.
Worsening asthma or new onset asthma in a worker should raise questions about workplace causes. Asthma symptoms can develop shortly after exposure. However, they can also develop months or years after repeated exposures to harmful substances.
Signs and symptoms
![occupational asthma essay A female worker coughing.](https://www.cdc.gov/niosh/media/images/coughing.jpg)
Symptoms of work-related asthma are the same as symptoms for non-work-related asthma. They include:
- Chest tightness
- Shortness of breath
Asthma symptoms can come and go, and some workers might not have all of the symptoms. Workers can get work-related asthma even when using personal protective equipment such as respirators or face masks. Sometimes breathing problems start at work and continue after leaving work when exposure has stopped.
How do I know if I have work-related asthma?
Symptoms for work-related asthma tend to get better on weekends, vacations, or other times when away from work. However, in some cases, symptoms do not improve until extended time away from exposures or triggers.
Your doctor can diagnose work-related asthma. Tell your doctor about work exposures and possible triggers including your job, tasks, and materials you use.
Also consider recording when and where your symptoms occur to help determine any patterns. Your doctor will ask questions about your symptoms and will conduct a physical examination. The doctor might also order one or more tests, such as:
- Breathing tests (e.g., peak flow readings, spirometry, methacholine challenge)
- Allergy tests such as skin or blood tests
If your doctor is concerned about a condition other than asthma, he/she might order other tests such as x-rays or other imaging tests.
![occupational asthma essay Water-damaged wall with mold.](https://www.cdc.gov/niosh/media/images/molddamagewallwithladder.png)
Work-related asthma is associated with exposure to worksite triggers (irritants, allergens, and physical conditions). Examples of asthma triggers are:
- Animal dander, insects, and dust mites
- Chlorine-based cleaning products
- Cigarette smoke
- Materials from cockroaches
- Dust from wood, grain, flour, or green coffee beans
- Gases such as ozone
Other possible triggers include:
- Irritant chemicals
- Physical exertion
- Pollen and plants
- Strong fumes
- Vapors from chemicals (e.g., ammonia, isocyanates, and solvents)
Symptom management
![occupational asthma essay Close up of an inhaler.](https://www.cdc.gov/niosh/media/images/blueinhaler.png)
The most important step of managing asthma is stopping or reducing exposure to triggers causing symptoms. Work with your doctor to develop a personal asthma control plan. Medical professionals often treat asthma with two general types of medicine:
- Quick -relief rescue inhalers (e.g., albuterol, levalbuterol) to open the airways. People use these medicines to treat asthma attacks or flare-ups. Quick relief medications are often used in combination with long-term control medicines such inhaled corticosteroids.
- Lo ng-term control medicines to reduce inflammation in the airways. People use these medicines to help keep asthma symptoms from occurring. When these medicines are working well, quick relief medicine is not used as much.
National Institute for Occupational Safety and Health (NIOSH)
The Occupational Safety and Health Act of 1970 established NIOSH as a research agency focused on the study of worker safety and health, and empowering employers and workers to create safe and healthy workplaces.
Work-related Asthma
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Consequences of occupational asthma
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- Peer review
- Julie Cannon , clinical nurse specialist a ,
- Paul Cullinan , lecturer a ,
- Anthony Newman Taylor , professor a
- a aDepartment of Occupational and Environmental Medicine, National Heart and Lung Institute, London SW3 6LR
- Correspondence to: Ms Cannon.
- Accepted 26 June 1995
Some 500 new cases of occupational asthma are reported annually in the United Kingdom, a figure considered to underestimate the true incidence by at least threefold 1 ; most patients are young and economically active. Previous studies of the socioeconomic outcomes of occupational asthma have not distinguished the consequences of developing asthma from those specific to occupational asthma. 2 3
Patients, methods, and results
We surveyed all patients referred to a specialist clinic between 1987 and 1992 who had been given a final diagnosis of asthma. All had been referred for investigation of a possible occupational cause; most had subsequently been discharged. Using the clinician's final diagnosis, patients were divided into three categories: those with occupationally induced asthma, those with pre-existing or coexisting asthma exacerbated by work, and those with asthma unrelated to work. Diagnoses were made by a combination of clinical history, measurement of specific antibodies, serial peak flow recordings, and specific inhalation testing. A postal questionnaire inquired into job changes made because of asthma, consequences on income, difficulties in acquiring new work, and current treatment. Socioeconomic group was recorded by using a standard classification. 4
We surveyed 225 subjects: 113 (50%) had occupational asthma, 37 (16%) had asthma exacerbated by work, and 75 (33%) has asthma unrelated to work. These proportions did not change over the five years, allowing a similar length of follow up for each category. The response rate was 89% after exclusion of 24 who did not receive a questionnaire. Responders did not differ significantly from non-responders in age, sex, diagnosis, or socioeconomic group.
Asthma: effects on income and employment. Values are numbers (percentages)
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The mean age in each category was about 40 years. Thirty one per cent of those with occupational asthma were women (35); 33% (37) were in socioeconomic groups I and II, accounted for by the high proportion of research scientists and technicians. The other categories had twice as many men as women and had higher proportions in lower socioeconomic groups.
The effects on income and employment were similar in patients with occupational and work exacerbated asthma but differed significantly in patients with asthma unrelated to work (table). Proportions of those currently employed were similar in all categories, but those with occupational and work exacerbated asthma reported greater difficulty in finding new work and higher proportions had changed or suffered disruption to their jobs. There were no consistent differences between men and women. Those in manual socioeconomic groups reported greater difficulty in finding new work, greater loss of income, and were less likely to be currently employed.
Earnings were adversely affected in all categories, more in those with occupational or work exacerbated asthma, of whom 30% reported losing more than 40% of income (χ 2 =7.43, df=1, P=0.006) compared with those whose asthma was unrelated to work. This loss was not offset by industrial injuries disablement benefit, which was more commonly received by patients referred before 1990.
In addition to the respiratory disability caused by asthma, patients with work related asthma, whether initiated or provoked by agents inhaled at work, suffer adverse economic and employment consequences. For most outcomes there was little difference between those with occupational or work exacerbated asthma. For many patients, continuing a chosen career, often after many years' training, was not possible. Those in higher socioeconomic groups found it easier to diversify into related careers; skilled manual workers had less opportunity to transfer into equally skilled work and often obtained unskilled work or became unemployed. Those with work related asthma who had made no change (10%) may have decided that their livelihood was as important as their health. The low proportion receiving disablement benefit has been a consistent finding in similar studies. Some patients did not claim benefit because they believed it would stigmatise them in the job market. Patients clearly need appropriate advice about their entitlements.
These findings highlight the importance of correctly identifying any relation between asthma and work and also the dangers of false attribution.
Funding Department of Health.
Conflict of interest None.
- Robertson A ,
- Sherwood Burge P
- Venables K ,
- Davison A ,
- Newman Taylor A
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- Occupational asthma
![occupational asthma essay Woman using spirometer, assisted by technician](https://www.mayoclinic.org/-/media/kcms/gbs/patient-consumer/images/2013/11/15/17/38/ds00957_-as00003_-ds00591_-ds00296_-ds00251_-ds00031_-ds00916_-ds00592_-ds00962_-ds00482_-my00413_-ds01040_im01608_as7_spiromthu_jpg.jpg)
A spirometer measures how much air your lungs can hold and how quickly you can breathe out.
Diagnosing occupational asthma is similar to diagnosing other types of asthma. However, your healthcare professional also will try to identify whether a workplace substance is causing your symptoms and what substance is causing problems.
An asthma diagnosis needs to be confirmed with a test called a lung function test. This test shows how well your lungs work. An allergy skin prick test can show if you have allergic reactions to some allergy-causing substances. Blood tests, X-rays or other tests may be necessary to rule out a cause other than occupational asthma.
Testing your lung function
Lung function tests include:
Spirometry. During this 10- to 15-minute test, you take deep breaths and forcefully exhale into a hose connected to a machine called a spirometer. A spirometer measures how much air your lungs can hold and how quickly you can breathe out. This is the preferred test for diagnosing asthma.
You will repeat the test after inhaling asthma medicine that helps open airways. Improved lung function after using the medicine supports a diagnosis of asthma.
Peak flow measurement. You may be asked to carry a small hand-held device called a peak flow meter. This device measures how quickly you can force air out of your lungs. The slower you exhale, the worse your condition.
You'll likely be asked to use your peak flow meter at certain times during working and nonworking hours. If your breathing improves significantly when you're away from work, you may have occupational asthma.
Tests for causes of occupational asthma
You may need tests to see whether you have a reaction to specific substances. These include:
- Allergy skin tests. During a skin test, small amounts of common allergy-causing substances are scratched into your skin. Then the area is observed for about 15 minutes. Swelling or a change in skin color indicates an allergy to the substance. These tests can show an allergy to animals, mold, dust mites, plants and latex. They can't be used to measure a reaction to chemicals.
- Challenge test. You inhale a mist containing a small amount of a suspected chemical to see if it triggers a reaction. Your lung function will be tested before and after the test is given to see if the chemical affects your ability to breathe.
- Chest X-ray. Occupational asthma is one kind of occupational lung disease. You might need a chest X-ray to diagnose other kinds of job-related breathing problems.
The goal of treatment is to prevent symptoms and stop an asthma attack in progress.
Avoiding the workplace substance that causes your symptoms is important. Once you become sensitive to a substance, tiny amounts may trigger asthma symptoms, even if you wear a mask or respirator.
You may need medicines for successful treatment. The same medicines are used to treat both occupational and nonoccupational asthma.
The right medicine for you depends on many things. These include your age, symptoms, asthma triggers and what seems to work best to keep your asthma under control.
Long-term control medicines
- Inhaled corticosteroids. Inhaled corticosteroids reduce inflammation and have a relatively low risk of side effects.
- Leukotriene modifiers. These medicines are alternatives to corticosteroids. Sometimes, they're taken with corticosteroids.
- Long-acting beta agonists (LABAs). LABAs open the airways and reduce inflammation. For asthma, LABAs generally should only be taken in combination with an inhaled corticosteroid.
- Combination inhalers. These medicines contain a LABA and a corticosteroid.
Quick-relief, short-term medications
- Short-acting beta agonists. These medicines ease symptoms during an asthma attack.
- Oral and intravenous corticosteroids. These relieve airway inflammation for severe asthma. These are taken by mouth or given as a shot. Over the long term, they cause serious side effects.
If you need to use a quick-relief inhaler more often than recommended, you may need to adjust your long-term control medicine.
Also, if allergies trigger or worsen your asthma, you may benefit from allergy treatments. These treatments include medicines taken by mouth or with a nasal spray. Antihistamines help block some immune system activity that causes allergy symptoms. Decongestants help relieve a stuffy nose.
Alternative medicine
Many people claim alternative remedies reduce asthma symptoms. But in most cases, more research is needed to see if they work and if they have possible side effects. Alternative remedies that need further study include:
- Breathing techniques. These include structured breathing programs such as the Buteyko method, the Papworth method, lung-muscle training and yoga breathing exercises. While these techniques may help improve quality of life, they have not proved to improve asthma symptoms.
- Acupuncture. This technique has roots in traditional Chinese medicine. It involves placing very thin needles at strategic points on the body. Acupuncture is safe and generally painless, but there is not enough evidence to show it treats asthma.
Preparing for your appointment
You're likely to start by seeing your primary healthcare professional. Or you may start by seeing a doctor who specializes in asthma, such as an allergist-immunologist or a pulmonologist.
Here's some information to help you prepare for your appointment.
What you can do
- Be aware of any pre-appointment restrictions. When you make the appointment, ask if there's anything you need to do in advance. You may need to stop taking antihistamines if you're likely to have an allergy skin test.
- Write down any symptoms you're experiencing, including any that do not seem related to problems with breathing.
- Note the timing of your asthma symptoms — for example, note if your symptoms are worse at work and get better when you're away from work.
- Make a list of all possible workplace lung irritants and anything else that seems to trigger your symptoms. You may want to take a look at the material safety data sheet (MSDS) for your work area, if there is one. This sheet lists toxic substances and irritants used on your job site. Keep in mind, not all occupational asthma triggers are listed in the MSDS .
- Write down key personal information, including major stresses or recent life changes and changes in your job or workplace.
- Bring a list of all medicines, vitamins or supplements you take.
- Bring a family member or friend along, if possible. Someone who accompanies you may remember information you missed or forgot.
- Write down questions to ask your care healthcare professional.
For occupational asthma, some basic questions to ask include:
- Is a workplace irritant a likely cause of my breathing problems or asthma attacks?
- What are other possible causes for my symptoms or condition?
- What tests do I need? Do these tests require any special preparation?
- Is my condition likely temporary or chronic?
- How do I treat occupational asthma? Do I have to quit my job?
- What are the alternatives to the treatment you're suggesting?
- I have other health conditions. How can I best manage these conditions together?
- Are there restrictions that I need to follow?
- Should I see a specialist?
- Is there a generic alternative to the medicine you're prescribing?
- Are there brochures or other printed material I can take with me? What websites do you recommend?
Don't hesitate to ask other questions.
What to expect from your doctor
Your healthcare professional is likely to ask you several questions, such as:
- When did you first notice your symptoms?
- If you already use asthma medicine, how often do you use a quick-relief inhaler?
- Do you have breathing problems when you're away from work or only when you're on the job?
- Have your symptoms been continuous, or do they come and go?
- Have you been diagnosed with allergies or asthma?
- Are you exposed to fumes, gases, smoke, irritants, chemicals, or plant or animal substances at work? If so, how often and for how long?
- Do you work in unusual environmental conditions, such as extreme heat, cold or dryness?
- What, if anything, seems to improve your symptoms?
- What, if anything, appears to worsen your symptoms?
- Do other members of your family have allergies or asthma?
- Burks AW, et al. Occupational allergy and asthma. In: Middleton's Allergy: Principles and Practice. 9th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Feb. 3, 2022.
- Broaddus VC, et al., eds. Asthma in the workplace. In: Murray and Nadel's Textbook of Respiratory Medicine. 7th ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Feb. 3, 2022.
- Bernstein DI, et al. Occupational asthma: Definitions, epidemiology, causes, and risk factors. https://www.uptodate.com/contents/search. Accessed Jan. 17, 2024.
- Work-related asthma. The National Institute for Occupational Safety and Health (NIOSH). https://www.cdc.gov/niosh/topics/asthma/default.html. Jan. 17, 2024.
- Asthma. National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/asthma. Accessed Jan. 17, 2024.
- Occupational asthma. American Academy of Allergy, Asthma & Immunology. https://www.aaaai.org/tools-for-the-public/conditions-library/asthma/occupational-asthma. Accessed Jan. 17, 2024.
- Lemière C, et al. Occupational asthma: Management, prognosis and prevention. https://www.uptodate.com/contents/search. Accessed Jan. 17, 2024.
- Ferri FF. Occupational allergy and asthma. In: Ferri's Clinical Advisor 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Feb. 15, 2022.
- Hazard communication standard: Safety data sheets. Occupational Safety and Health Administration. https://www.osha.gov/occupational-asthma/standards. Accessed Jan. 17, 2024.
- Asthma and complimentary health approaches: What the science says. National Center for Complementary and Integrative Health. https://www.nccih.nih.gov/health/providers/digest/asthma-and-complementary-health-approaches-science#acupuncture. Accessed Jan. 8, 2024.
- Li JTC (expert opinion). Mayo Clinic. Feb. 21, 2022.
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Epidemiology
Prevalence:, prevention:, conclusion:, references:.
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- Global Strategy for Asthma Management and Prevention 2010 (update)
- Pauwels, R. A., Buist, A. S., Calverley, P. M., Jenkins, C. R., & Hurd, S. S. (2001). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. American journal of respiratory and critical care medicine, 163(5), 1256-1276.
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- Malo, J.L. and Chan-Yeung, M., 2009. Agents causing occupational asthma. Journal of Allergy and Clinical Immunology, 123(3), pp.545-550.
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- Gautrin D, Newman-Taylor AJ, Norman H, Malo J. Controversies in the epidemiology of occupational asthma. Eur Respir J 203; 22: 551-559
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- Meredith SK, Taylor VM, McDonald JC. Occupational respiratory disease in the United Kingdom 1989: a report of the British Thoracic Society and the Society of Occupational Medicine by the SWORD project group. Br J Ind Med. 1991; 48:2928
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- Vandenplas, O. and Malo, J.L., 2003. Definitions and types of work-related asthma: a nosological approach. European Respiratory Journal, 21(4), pp.706-712.
- Mehuys, E., Van Bortel, L., Annemans, L., Remon, J.P., Van Tongelen, I., Van Ganse, E., Laforest, L., Chamba, G. and Brusselle, G., 2006. Medication use and disease control of asthmatic patients in Flanders: a cross-sectional community pharmacy study. Respiratory medicine, 100(8), pp.1407-1414.
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- Rabell-Santacana, V., Panadès-Valls, R., Vila-Right, R., Hernandez-Huet, E., Sivecas-Maristany, J., Blanché-Prat, X., Prieto, G., Muñoz, L. and Torán, P., 2015. Prevalence of Work-Related Asthma in Primary Health Care: Study Rationale and Design. The open respiratory medicine journal, 9, p.127.
- Cowl, C.T., 2011. Occupational asthma: a review of assessment, treatment, and compensation. Chest, 139(3), pp.674-681.
- Descatha, A., Leproust, H., Choudat, D., Garnier, R., Pairon, J.C. and Ameille, J., 2007. Factors associated with severity of occupational asthma with a latency period at diagnosis. Allergy, 62(7), pp.795-801.
- Sherwood B. Recent developments in occupational asthma. SWISS MED WKLY 2010; 14 0 (9 – 10): 12 8 – 13 2.
- Moore, V.C., Jaakkola, M.S. and Burge, P.S., 2009. A systematic review of serial peak expiratory flow measurements in the diagnosis of occupational asthma. The Annals of Respiratory Medicine, 1(1), p.1.
- Fishwick, D., Barber, C.M., Bradshaw, L.M., Harris-Roberts, J., Francis, M., Naylor, S., Ayres, J., Burge, P.S., Corne, J.M., Cullinan, P. and Frank, T.L., 2008. Standards of care for occupational asthma. Thorax, 63(3), pp.240-250.
- Vilozni, D., Livnat, G., Dabbah, H., Elias, N., Hakim, F. and Bentur, L., 2009. The potential use of spirometry during methacholine challenge test in young children with respiratory symptoms. Pediatric pulmonology, 44(7), pp.720-727.
- Pendharkar, S. and Mehta, S., 2008. The clinical significance of exhaled nitric oxide in asthma. Canadian respiratory journal, 15(2), pp.99-106.
- De Groene, G.J., Pal, T.M., Beach, J., Tarlo, S.M., Spreeuwers, D., Frings‐Dresen, M.H., Mattioli, S. and Verbeek, J.H., 2011. Workplace interventions for the treatment of occupational asthma. Cochrane Database of Systematic Reviews, (5).
- Cote J, Kennedy S, Chan-Yeung M. Outcome of patients with cedar asthma with continuous exposure. Am Rev Respir Dis 1990; 141:373
- Pisati G, Baruffini A, Zedda S. Toluene diisocyanate induced asthma: outcome according to persistence or cessation of exposure. Br J Ind Med 1993; 50:60.
- Ortega HG, Kreiss K, Schill DP, Weissman DN. Fatal asthma from powdering shark cartilage and review of fatal occupational asthma literature. Am J Ind Med 2002; 42:50
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- Collins, J.J., Anteau, S., Conner, P.R., Cassidy, L.D., Doney, B., Wang, M.L., Kurth, L., Carson, M., Molenaar, D., Redlich, C.A. and Storey, E., 2017. Incidence of Occupational Asthma and Exposure to Toluene Diisocyanate in the United States Toluene Diisocyanate Production Industry. Journal of occupational and environmental medicine, 59(Suppl 12), pp.S22-S27.
- Banks DE, Rando RJ, Barkman HW Jr. Persistence of toluene diisocyanate induced asthma despite negligible workplace exposures. Chest 1990;97: 121-5
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Asthma - An Introduction
What is asthma.
Asthma is a common condition which affects the small airways or tubes in the lungs. It often develops in childhood and may be caused by allergy to house dust mite, pollen, and /or pet dander. Often there is a family history of asthma. It is easy to recognise allergic asthma caused by pollen because symptoms appear and disappear with the seasons. The body produces antibodies which react with the allergic agent to trigger cells in the body to produce chemicals such as histamine. These chemicals cause intermittent spasm of the muscles around the small airways causes the airways to narrow leading to episodes or bouts of symptoms of chest tightness, difficulty breathing, wheezing and coughing. Inflammation of the airways may also be accompanied by the production of sputum or phlegm. Most people who suffer from asthma have periodic attacks of symptoms separated by symptom-free periods. Symptoms can be aggravated by cold air and cigarette smoke and are often worse at night or early in the morning. Symptoms often improve or disappear as children approach adulthood. However, in some children asthma can persist into adulthood; and sometimes asthma can present for the first time in adulthood – usually without any associated allergies.
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Asthma Essay With Conclusions. Info: 2061 words (8 pages) Nursing Essay Published: 11th Feb 2020. Reference this ... infections and occupational factors such as dust and chemicals can be considered asthma's risk factors, and healthcare professionals need to provide client education in order to prevent and minimize asthma attacks. Chronic ...
According to Vandenplas et al. (2017), occupational asthma symptoms are similar to those of non-professional bronchial asthma. It is characterized by wheezing, coughing, chest compression, and shortness of breath. We will write a custom essay on your topic. 809 writers online.
A systematic analysis of population attributable risk showed that an estimated 16.3% of all cases of adult-onset asthma are caused by occupational exposure. 38 There is a discrepancy between the ...
Overview. Occupational asthma is a type of asthma caused by breathing in fumes, gases, dust or other substances while on the job. These substances can trigger an immune system response that changes how the lungs work. Occupational asthma also is called work-related asthma. In asthma, the airways narrow and swell. They also may make extra mucus.
Work‐related asthma (WRA) is a general term which includes both asthma caused by an inciting exposure in the workplace (occupational asthma, OA) and asthma that is worsened by workplace conditions (work‐exacerbated asthma, WEA) (Fig. (Fig.1 1). 1 WRA is a common occupational lung disease in developed, low‐ and middle‐income countries ...
Occupational asthma symptoms are the same as any asthma exacerbation, such as wheezing, shortness of breath, runny nose, nasal congestion, eye irritation, and chest tightness. These symptoms may get worse during exposure to the irritant (s) at work. The cause can be allergic or nonallergic in nature. Symptoms may get better when the person is ...
In contrast with the previous research that focused on the industry that is not known as a typical source of occupational asthma, the research by Baldi et al. (2014) investigated the risk of respiratory conditions in agricultural specialisations - a field with a high rate of occupational asthma prevalence.
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Occupational asthma is caused by an immune reaction to specific agents that are inhaled in the workplace. It differs from asthma that is aggravated at work by non-specific factors—for example, exposure to dusts or fumes, cold air, physical exertion, and even shift patterns. Offer all adults with suspected occupational asthma referral to an ...
Most regulatory bodies and all legislatures consider occupational asthma to be more important in terms of prevention and compensation. However it has been argued that this focus is too narrow 62. Community surveys of asthma and occupation suggest that approximately 10% of all adult asthma can be attributed to work 63.
Overview. Work-related asthma is asthma triggered by exposures at work. Asthma affects the lungs and causes the airways to become narrow and inflamed. To control it, avoid triggers that cause asthma symptoms and take prescribed medicine. Many triggers can be in the workplace. Over 300 known substances in the workplace can cause or worsen asthma.
A postal questionnaire inquired into job changes made because of asthma, consequences on income, difficulties in acquiring new work, and current treatment. Socioeconomic group was recorded by using a standard classification. 4. We surveyed 225 subjects: 113 (50%) had occupational asthma, 37 (16%) had asthma exacerbated by work, and 75 (33%) has ...
This case study, "Occupational Asthma: Michelle's Case" is published exclusively on IvyPanda's free essay examples database. You can use it for research and reference purposes to write your own paper.
Occupational Asthma Essay. Satisfactory Essays. 67 Words; 1 Page; Open Document. Occupational asthma is defined as asthma caused by exposure to airborne dust, vapors or fumes to individuals in the working environment without previous exposure to asthma, the term work-related asthma comprises of occupational asthma.
Diagnosis. Diagnosing occupational asthma is similar to diagnosing other types of asthma. However, your healthcare professional also will try to identify whether a workplace substance is causing your symptoms and what substance is causing problems. An asthma diagnosis needs to be confirmed with a test called a lung function test.
Asthma is the most prevalent work-related lung disease according to the American Lung Association, (ALA 2008) and NIOSH estimates that more than 2 million people may have work-related asthma (NIOSH 2012). Work-related asthma includes asthma caused by work, termed occupational asthma, and asthma aggravated by work, termed work-exacerbated asthma.
Occupational asthma can lead to serious health consequences, loss of employment and financial losses for employers. Early diagnosis is important for the removal of the precipitating agent during the first year of the onset of symptoms and can lead to a better prognosis (26). ... Essay on Environmental and Occupational Health: Analysis of ...
Asthma is a common condition which affects the small airways or tubes in the lungs. It often develops in childhood and may be caused by allergy to house dust mite, pollen, and /or pet dander. Often there is a family history of asthma. It is easy to recognise allergic asthma caused by pollen because symptoms appear and disappear with the seasons.
This study will describe asthma as a chronic condition, including its symptoms and signs, incidences, surveillance, reporting, epidemiological analysis, screening, prevention, and prevalence by state and national statistics. Get a custom essay on Asthma: Epidemiological Analysis and Care Plan. 184 writers online.
Occupational Asthma References and Papers. Welcome to the references section of this website. Over 5000 occupational asthma references are presented, over 2,500 with abstracts and some with links to the full text. We are adding these all the time but it is a slow process. Any references that were studied as part of the BOHRF occupational asthma ...
This website contains information on Occupational Asthma and a free multi award winning computer program called OASYS, which is used to help diagnose Occupational Asthma from serial peak flow records. Oasys shows further information and downloads for the Oasys program. References is a searchable database of more than 5000 published papers in ...
To the Editor: Re "Why Medical Students Are Shunning Pediatrics," by Aaron E. Carroll (Opinion guest essay, July 7): The dwindling number of physicians choosing to pursue pediatrics is a grave ...
Inflammation's Role in Asthma Development. This work is written in order to study the role of inflammation plays in the development of asthma on the basis of research papers. The Use of Tezspire: The Management of Asthma. The brochure describes the use of Tezspire, which is a drug used for the management of asthma.