Management Of Occupational Asthma Research Articles

Occupational Asthma: The Knowledge Needs for a Better Management

The management of occupational asthma (OA) may be influenced by several factors and removal from exposure is the main tertiary prevention approach, but it is not always feasible without personal and socioeconomic consequences. Reducing the delay between the onset of suggestive symptoms of OA and the diagnosis of OA is associated with a better prognosis. Workers’ education to increase awareness to trigger agents and a medical surveillance program directed especially at at-risk workers could be helpful in reducing this latency time. An early identification of workers who develop rhinitis and conjunctivitis which often precede the onset of asthma symptoms could be important for an early identification of OA. This is particularly important for cases of asthma caused by high-molecular-weight sensitizers and in the early years of employment. The availability of financial support and compensation measures for workers with OA may influence the latency time before diagnosis and, consequently, may influence the OA outcomes. In conclusion, there is a need for high-quality cohort studies that will increase knowledge about risk factor that may influence the timing of diagnosis of OA. This knowledge will be useful for implementation of future surveillance and screening programs in workplaces.

Assessment and Management of Occupational Asthma

Exposures at work can give rise to different phenotypes of "work-related asthma." The focus of this review is on the diagnosis and management of sensitizer-induced occupational asthma (OA) caused by either a high- or low-molecular-weight agent encountered in the workplace. The diagnosis of OA remains a challenge for the clinician because there is no simple test with a sufficiently high level of accuracy. Instead, the diagnostic process combines different procedures in a stepwise manner. These procedures include a detailed clinical history, immunologic testing, measurement of lung function parameters and airway inflammatory markers, as well as various methods that relate changes in these functional and inflammatory indices to workplace exposure. Their diagnostic performances, alone and in combination, are critically reviewed and summarized into evidence-based key messages. A working diagnostic algorithm is proposed that can be adapted to the suspected agent, purpose of diagnosis, and available resources. Current information on the management options of OA is summarized to provide pragmatic guidance to clinicians who have to advise their patients with OA.

Assessment and Management of Occupational Asthma

Assessment and Management of Occupational Asthma

Progress in Occupational Asthma.

Occupational asthma (OA) represents one of the major public health problems due to its high prevalence, important social and economic burden. The aim of this review is to summarize current data about clinical phenotypes, biomarkers, diagnosis and management of OA, a subtype of work-related asthma. Most studies have identified two phenotypes of OA. One is sensitizer-induced asthma, occuring after a latency period and caused by hypersensitivity to high- or low-molecular weight agents. The other is irritant-induced asthma, which can occur after one or more exposures to high concentrations of irritants without latency period. More than 400 agents causing OA have been identified and its list is growing fast. The best diagnostic approach for OA is a combination of clinical history and objective tests. An important tool is a specific inhalation challenge. Additional tests include assessments of bronchial hyperresponsiveness to methacholine/histamine in patients without airflow limitations, monitoring peak expiratory flow at- and off-work, sputum eosinophil count, exhaled nitric oxide measurement, skin prick tests with occupational allergens and serum specific IgE. Treatment of OA implies avoidance of exposure, pharmacotherapy and education. OA is a heterogeneous disease. Mechanisms of its different phenotypes, their diagnosis, role of new biomarkers and treatment require further investigation.

Occupational asthma.

Work-related asthma is highly prevalent and represents a significant societal and financial burden worldwide. This State of the Art series article explores the epidemiology, clinical features, diagnosis and management of occupational asthma (OA), which comprises sensitiser-induced asthma and irritant-induced asthma (IIA). Sensitiser-induced OA is the development of asthma through sensitisation to a substance in the workplace. OA is largely underdiagnosed, and its clinical manifestations are non-specific, which makes its diagnosis challenging. Early and accurate diagnosis of OA through comprehensive testing is primordial to avoid unwarranted removal from exposure and to allow early management of confirmed cases. Despite optimal management, up to 70% of patients with OA will have persistent asthma several years after diagnosis. IIA classically refers to the development of de novo asthma acutely following an intense exposure to an irritant agent. However, some cases of IIA following multiple high-level exposures or a chronic low-dose exposure have been reported.

Occupational asthma; the limited role of air-fed respiratory protective equipment

Evidence-based reviews have found that evidence for the efficacy of respiratory protective equipment (RPE) in the management of occupational asthma (OA) is lacking. To quantify the effectiveness of air-fed RPE in workers with sensitizer-induced OA exposed to metal-working fluid aerosols in a car engine and transmission manufacturing facility. All workers from an outbreak of metal-working fluid-induced OA who had continuing peak expiratory flow (PEF) evidence of sensitizer-induced OA after steam cleaning and replacement of all metal-working fluid were included. Workers kept 2-hourly PEF measurements at home and work, before and after a strictly enforced programme of RPE with air-fed respirators with charcoal filters. The area-between-curve (ABC) score from the Oasys plotter was used to assess the effectiveness of the RPE. Twenty workers met the inclusion criteria. Records were kept for a mean of 24.6 day shifts and rest days before and 24.7 after the institution of RPE. The ABC score improved from 26.6 (SD 16.2) to 17.7 (SD 25.4) l/min/h (P > 0.05) post-RPE; however, work-related decline was <15 l/min/h in only 12 of 20 workers, despite increased asthma treatment in 5 workers. Serial PEF measurements assessed with the ABC score from the Oasys system allowed quantification of the effect of RPE in sensitized workers. The RPE reduced falls in PEF associated with work exposure, but this was rarely complete. This study suggests that RPE use cannot be relied on to replace source control in workers with OA, and that monitoring post-RPE introduction is needed.

Update on the Management of Occupational Asthma and Work-Exacerbated Asthma.

Work-related asthma is the most common occupational lung disease encountered in clinical practice. In adult asthmatics, work-relatedness can account for 15%–33% of cases, but delays in diagnosis remain common and lead to worse outcomes. Accurate diagnosis of asthma is the first step to managing occupational asthma, which can be sensitizer-induced or irritant-induced asthma. While latency has traditionally been recognized as a hallmark of sensitizer-induced asthma and rapid-onset a defining feature of irritant-induced asthma (as in Reactive Airway Dysfunction Syndrome), there is epidemiological evidence for irritant-induced asthma with latency from chronic moderate exposure. Diagnostic testing while the patient is still in the workplace significantly improves sensitivity. While specific inhalational challenges remain the gold-standard for the diagnosis of occupational asthma, they are not available outside of specialized centers. Commonly available tests including bronchoprovocation challenges and peak flow monitoring are important tools for practicing clinicians. Management of sensitizer-induced occupational asthma is notable for the central importance of removal from the causative agent: ideally, removal of the culprit agent; but if not feasible, this may require changes in the work process or ultimately, removal of the worker from the workplace. While workers' compensation programs may reduce income loss, these are not universal and there can be significant socio-economic impact from work-related asthma. Primary prevention remains the preferred method of reducing the burden of occupational asthma, which may include modification to work processes, better worker education and substitution of sensitizing agents from the workplace with safer compounds.

Fractional Exhaled Nitric Oxide (FeNO) in the Screening and Diagnosis Work-Up of Occupational Asthma

FeNO is a simple non-invasive tool used as a surrogate marker of airway inflammation in the management of asthma. FeNO has been assessed in several populations of workers exposed to high- and low-molecular weight agents. However, there are many confounding factors to consider in the interpretation of FeNO. As such, its use in the investigation of occupational asthma (OA) has yielded inconsistent results. In screening studies of OA to high molecular weight (HMW) agents, an increase of FeNO over time has been associated with the development of bronchial hyperresponsiveness (BHR). When used in the investigation of OA, increases in FeNO show high positive predictive values for a positive specific inhalation challenge (SIC) to HMW agents. Subjects with high specific IgE to their workplace allergens seem to present higher increases in FeNO than subjects without specific IgE to causal agent. Changes in FeNO have less frequently been observed in studies of OA to low molecular weight (LMW) agents than OA to HMW agents, except for isocyanate-induced OA. Cluster analyses of patients exposed to various HMW and LMW agents have documented significant increases of FeNO in clusters of patients with OA to HMW agents, but not LMW. Recent studies have provided useful information for improving our understanding of the pathophysiology of exhaled NO in OA despite the previously reported conflicting results. Future studies are still required to clarify its role in the screening, investigation, and management of OA.

Occupational Asthma in the Food Industry

Inhalation of food-derived allergens during food processing at the workplace represents a risk for developing occupational asthma (OA) in exposed workers. Cereal flours and seafood are the causal agents most frequently involved. The management of food-derived OA includes timely pharmacologic therapy and environmental interventions aimed to avoid or reduce exposure to the offending agent to increase the probability of recovery. Cessation of exposure is the best option, but when the causative agent cannot be completely avoided reduction of exposure, through modification of food processing, improving ventilation, mechanization, etc. can be considered as an alternative. Quantification of real exposure levels is crucial, and new accurate immunologic and chemical assays able to detect low levels of aerosolized flour and seafood allergens have recently been developed. Recent papers have described intervention strategies effective in reducing airborne allergen exposure in flour and seafood industry, but the long-term health impact of this intervention has still to be defined. Specific allergen immunotherapy (SIT) might be another management option in individuals with IgE-mediated food-induced OA. Both a short- and a long-lasting beneficial effect of SIT with wheat flour in reducing symptoms whilst keeping the patient at work has been shown in bakers’ asthma, but at present, SIT is not for routine use for bakers’ asthma due to the lack of commercial standardized extracts. A better identification on a molecular basis of allergens involved in flour and in other IgE-mediated food-derived OA might help in preparing new extracts suitable for immunotherapy. In selected cases of bakers’ asthma, the monoclonal antibody omalizumab has been effective in reducing symptoms. SIT and omalizumab might represent further management options in IgE-mediated OA in food industry.

Assessment of work-related asthma prevalence, control and severity: protocol of a field study.

BackgroundThere are still uncertainties regarding the respective prevalence, diagnosis and management of occupational asthma (OA) and work-exacerbated asthma (WEA). There is as yet no standardized methodology to differentiate their diagnosis. A proper management of both OA and WEA requires tools for a good phenotyping in terms of control, severity and quality of life in order to propose case-specific therapeutical and preventive measures. Moreover, there is a lack of knowledge concerning their actual costs.MethodsThis project aims at comparing 3 groups of asthmatic subjects at work: subjects with OA, with WEA, and with non-work-related asthma (NWRA) in terms of control, severity and quality of life on the one hand, and estimating the prevalence of OA, WEA and NWRA in active workers and the economic costs of OA and WEA, on the other hand. Control will be assessed using the Asthma Control Test questionnaire and the daily Peak Exploratory Flow variability, severity from the treatment level, and quality of life using the Asthma Quality of Life Questionnaire. A first step will be to apply a standardized diagnosis procedure of WEA and OA. This study includes an epidemiological part in occupational health services by volunteering occupational physicians, and a clinical case-study based on potentially asthmatic subjects referred to ten participating University Hospital Occupational Diseases Departments (UHODD) because of a suspected WRA. The subjects’ characterization with respect to OA and WEA is organized in three steps. In Step 1 (epidemiological part), occupational physicians screen for potentially actively asthmatics through a questionnaire given to workers seen in mandatory medical visit. In step 2 (both parts), the subjects with a suspicion of work-related respiratory symptoms answer a detailed questionnaire and perform a two-week OASYS protocol enabling us, using a specifically developed algorithm, to classify them into probably NWRA, suspected OA, suspected WEA. The two latter groups are referred to UHODD for a final harmonized diagnosis (step 3). Finally, direct and indirect disease-related costs during the year preceding the diagnosis will be explored among WRA cases, as well as these costs and the intangible costs, during the year following the diagnosis.DiscussionThis project is an attempt to obtain a global picture of occupational asthma in France thanks to a multidisciplinary approach.Electronic supplementary materialThe online version of this article (doi:10.1186/s12889-016-3824-0) contains supplementary material, which is available to authorized users.

An official American Thoracic Society Workshop Report: presentations and discussion of the fifth Jack Pepys Workshop on Asthma in the Workplace. Comparisons between asthma in the workplace and non-work-related asthma.

The fifth Jack Pepys Workshop on Asthma in the Workplace focused on the similarities and differences of work-related asthma (WRA) and non-work-related asthma (non-WRA). WRA includes occupational asthma (OA) and work-exacerbated asthma (WEA). There are few biological differences in the mechanisms of sensitization to environmental and occupational allergens. Non-WRA and OA, when due to high-molecular-weight agents, are both IgE mediated; it is uncertain whether OA due to low-molecular-weight agents is also IgE mediated. Risk factors for OA include female sex, a history of upper airway symptoms, and a history of bronchial hyperresponsiveness. Atopy is a risk factor for OA due to high-molecular-weight agents, and exposure to cleaning agents is a risk factor for both OA and non-WRA. WEA is important among workers with preexisting asthma and may overlap with irritant-induced asthma, a type of OA. Induced sputum cytology can confirm airway inflammation, but specific inhalation challenge is the reference standard diagnostic test. Inhalation challenges are relatively safe, with the most severe reactions occurring with low-molecular-weight agents. Indirect health care costs account for about 50% of total asthma costs. Workers with poor asthma control (WRA or non-WRA) are less likely to be employed. Income loss is a major contributor to the indirect costs of WRA. Overall, asthma outcomes probably are worse for adult-onset than for childhood-onset asthma but better for OA than adult-onset non-WRA. Important aspects of management of OA are rapid and proper confirmation of the diagnosis and reduction of exposure to sensitizers or irritants at work and home.

Human mesenchymal stem cells resolve airway inflammation, hyperreactivity, and histopathology in a mouse model of occupational asthma.

Occupational asthma (OA) is characterized by allergic airway inflammation and hyperresponsiveness, leading to progressive airway remodeling and a concomitant decline in lung function. The management of OA remains suboptimal in clinical practice. Thus, establishing effective therapies might overcome the natural history of the disease. We evaluated the ability of human adipose-tissue-derived mesenchymal stem cells (hASCs), either unmodified or engineered to secrete the IL-33 decoy receptor sST2, to attenuate the inflammatory and respiratory symptoms in a previously validated mouse model of OA to ammonium persulfate (AP). Twenty-four hours after a dermal AP sensitization and intranasal challenge regimen, the animals received intravenously 1 × 10(6) cells (either hASCs or hASCs overexpressing sST2) or saline and were analyzed at 1, 3, and 6 days after treatment. The infused hASCs induced an anti-inflammatory and restorative program upon reaching the AP-injured, asthmatic lungs, leading to early reduction of neutrophilic inflammation and total IgE production, preserved alveolar architecture with nearly absent lymphoplasmacytic infiltrates, negligible smooth muscle hyperplasia/hypertrophy in the peribronchiolar areas, and baseline airway hyperreactivity (AHR) to methacholine. Local sST2 overexpression barely increased the substantial efficacy displayed by unmodified hASCs. Thus, hASCs may represent a viable multiaction therapeutic capable to adequately respond to the AP-injured lung environment by resolving inflammation, tissue remodeling, and bronchial hyperresponsiveness typical of OA.

Concise guidance: diagnosis, management and prevention of occupational asthma

This concise guidance, prepared for physicians, summarises the British Occupational Health Research Foundation guideline for the prevention, identification and management of occupational asthma. Approximately one in six people of working age who develop asthma have work-related asthma, where work has either caused or aggravated their disease. Physicians who assess working adults with asthma need to ask the patient about their job and the materials they work with, and be aware of those that carry particular risks; they should also ask whether symptoms improve regularly on days away from work. A diagnosis of occupational asthma (ie asthma caused by work) should not be made on the basis of history alone, but be supported by immunological and physiological investigations of proven diagnostic benefit. Following a validated diagnosis of occupational asthma, physicians should recommend early avoidance of further exposure, because this offers the best chance of complete recovery. If appropriate and timely interventions are not taken, the prognosis of occupational asthma is poor, with only approximately one-third of workers achieving full symptomatic recovery.

Occupational asthma in Japan

Research into occupational asthma (OA) in Japan has been led by the Japanese Society of Occupational and Environmental Allergy. The first report about allergic OA identified konjac asthma. After that, many kinds of OA have been reported. Cases of some types of OA, such as konjac asthma and sea squirt asthma, have been dramatically reduced by the efforts of medical personnel. Recently, with the development of new technologies, chemical antigen-induced asthma has increased in Japan. Due to advances in anti-asthma medication, control by medical treatment tends to be emphasized and the search for causative antigens seems to be neglected. Furthermore, we do not have a Japanese guideline for diagnosis and management of OA. This article discusses the current state of OA in Japan.

The persistence of allergen exposure favors pulmonary function decline in workers with allergic occupational asthma

In asthmatics, a rapid decline in pulmonary function is observed, likely as a consequence of airways remodeling. Persistence of allergen exposure in patients with occupational asthma (OA) maintains chronic bronchial inflammation, resulting in a more severe lung function decline. Few studies were performed on the effects of allergen exposure cessation. This study aims at evaluating the influence of allergen exposure cessation on respiratory decline in allergic asthmatic workers. Two groups of workers with allergic OA were selected. The first group (30 workers) changed job after the diagnosis and was no more exposed to sensitizing allergens, and the second group (28 subjects) did not and, as a consequence of preventive measures in the work place, was exposed to a lower level of allergens. All were treated with conventional therapy, according to GINA protocols. FEV1 changes during a 12-year period were evaluated. Despite pharmacological therapy, the pulmonary function decay slope was steeper in workers continuously exposed to the sensitizing agent (even at reduced level) than in those with a complete cessation of exposure: final FEV1 loss was 512.5 ± 180 ml versus 332.5 ± 108 ml, respectively. The difference became significant after 4 years from the cessation of the exposure. The study shows that the cessation of the exposure to allergen in the work place appears the most effective measure in limiting pulmonary function decline in asthmatic workers and underlines the importance of allergic risk assessment and control in the management of occupational asthma.

Reduction of exposure in the management of occupational asthma

The management of immunologically mediated occupational asthma may be difficult in clinical practice since complete avoidance of exposure to the sensitizing agent is associated with a substantial adverse socio-economic impact. The purpose of this review was to critically analyze the available information on the effectiveness of reducing exposure as an alternative to complete avoidance. Short-term exposure studies showed that respiratory protective devices can reduce bronchial responses to sensitizing agents in patients with occupational asthma, but do not provide complete protection. Recent systematic reviews of long-term follow-up studies of workers with occupational asthma indicated that reduction of exposure to the causal agent is associated with a lower likelihood of improvement in asthma symptoms and a higher risk of worsening of symptoms and nonspecific bronchial hyper-responsiveness. There are insufficient data to compare the socio-economic consequences related to both of these management options. Available data indicate that a reduction of exposure to the agents causing occupational asthma cannot be routinely recommended as an alternative to complete avoidance. However, due to the methodological weaknesses of the published studies, further investigations are required to determine the evidence-based cost-effectiveness of the occupational asthma management strategies.

Management of occupational asthma: cessation or reduction of exposure? A systematic review of available evidence

Reduction of exposure to sensitising agents causing occupational asthma has been proposed as an alternative to total avoidance in order to minimise the adverse socio-economic impact of the condition. The aim of this systematic review was to compare the effects of these two management options on asthma and socio-economic outcomes. A bibliographic search was conducted to identify studies examining the outcome of workers with occupational asthma after reduction or cessation of exposure to the causal agent. The changes in asthma symptoms and nonspecific bronchial hyperresponsiveness after reduction or cessation of exposure were described in nine and five studies, respectively. The meta-analysis of pooled data showed that a reduction of exposure was associated with a lower likelihood of improvement (OR 0.16, 95% CI 0.03-0.91) and recovery (OR 0.30, 95% CI 0.11-0.84) of asthma symptoms and a higher risk of worsening of the symptoms (OR 10.23, 95% CI 2.97-35.28) and nonspecific bronchial hyperresponsiveness (OR 5.65, 95% CI 1.11-28.82), compared with complete avoidance of exposure. This systematic review indicates that reduction of exposure cannot be routinely recommended as an alternative to cessation of exposure in the management of occupational asthma. However, further investigations are required before drawing evidence-based conclusions on the cost-effectiveness of this approach.

Environmental and occupational allergies

Airborne allergens are the major cause of allergic rhinitis and asthma. Daily exposure comes from indoor sources, chiefly at home but occasionally at schools or offices. Seasonal exposure to outdoor allergens, pollens, and molds is another important source. Exposure to unusual substances at work causes occupational asthma, accounting for about 5% of asthma in adults. Indoor and outdoor air pollutants trigger airway inflammation and increase the severity of asthma. Diesel exhaust particles increase the production of IgE antibodies. Identification and reduction of exposure to allergens is a very important part of the management of respiratory allergic diseases. The first section of this chapter discusses domestic allergens, arthropods (mites and cockroaches), molds, and mammals (pets and mice). Indoor humidity and water damage are important factors in the production of mite and mold allergens, and discarded human food items are important sources of proliferation of cockroaches and mice. Means of identifying and reducing exposure are presented. The second section discusses outdoor allergens: pollens and molds. The particular plants or molds and the amount of exposure to these allergens is determined by the local climate, and local pollen and mold counts are available to determine the time and amount of exposure. Climate change is already having an important effect on the distribution and amount of outdoor allergens. The third section discusses indoor and outdoor air pollution and methods that individuals can take to reduce indoor pollution in addition to eliminating cigarette smoking. The fourth section discusses the diagnosis and management of occupational asthma.

Recent advances in the management of occupational asthma

Occupational asthma (OA) is the most common occupational lung disease in industrialized countries. This respiratory disorder remains poorly diagnosed and managed, and inadequately compensated for worldwide. The most appropriate treatment for OA remains early removal from exposure to ensure that the worker has no further exposure to the causal agent with preservation of income. However, various studies demonstrate that many workers with OA continue to remain exposed to the causative agent or suffer prolonged work disruption and discrimination, and may face unemployment. Despite removal from exposure, OA frequently turns into a chronic condition and requires intensive medical management, including appropriate pharmacotherapy and patient education and counseling. There are very few studies on allergen immunotherapy in OA. Subcutaneous immunotherapy with latex extract in healthcare workers and with wheat-flour extract in subjects with baker’s asthma, at adequate doses, appears to be a useful treatment in reducing cutaneous and respiratory symptoms, but should be considered as a high-risk treatment due to the appearance of systemic reactions.

Approaches to the diagnosis and management of occupational asthma amongst UK respiratory physicians

This study aimed to assess the approach to the diagnosis and management of occupational asthma amongst general (non-specialist) respiratory consultants in the UK. A random sample of 100 UK general respiratory physicians were invited to participate, and asked to provide information on their diagnostic approach to a case scenario of a patient with possible occupational asthma relating to flour exposure. Participation rates were 42% for the main part of the study. Less than half of consultants specifically reported they would ask whether symptoms improved away from work, and just over a third mentioned examining the patient. All of those interviewed recommended a chest X-ray, and 98% simple spirometry. Eighty-six per cent suggested measurement of serial peak flows, recorded for between 2 and 8 weeks, with measurements taken half-twelve hourly. Less than half advocated a specific flour allergy test, and almost one-quarter (23%) would not perform any immunological test at all. Once a diagnosis of occupational asthma was confirmed, less than two-thirds of those interviewed commented they would recommend some form of exposure reduction, and only 28% specifically stated they would offer compensation advice. The diagnosis of occupational asthma by general respiratory physicians within the UK lacks standardisation, and in some cases falls short of evidence-based best practise.