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Occupational Asthma
Abstract and Figures
Population-based studies suggest that one in 10 cases of new, recurrent, or deteriorating asthma in adulthood is related to the workplace environment. Nonspecific, irritant exposures at work can upset symptom control in pre-existing disease (work-exacerbated asthma); where disease arises de novo from the workplace (occupational asthma) it generally has an allergic basis, arising from airborne exposure to a sensitizing agent. Over 350 workplace substances have been identified as asthmagens; most are either proteins or highly reactive chemicals. The diagnosis of occupational asthma should be rapid but precise because definitive identification of the causative exposure provides the greatest opportunity for appropriate workplace adaptations and functional improvement. The majority of cases can be diagnosed through a combination of a careful history, appropriate immunology (where available), and the detection of work-related variability in measurements of lung function made serially at work and at home. Occupational asthma is a disease that is potentially preventable and often curable; positive outcomes are dependent more on changes in the workplace than on pharmacological therapy.
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... Another recent review again emphasized this point; the diagnosis of OA should be rapid and precise, given that the identification of causative exposures at work offers the best opportunity for appropriate workplace adaptations. 31 It is additionally evident, both in the UK and internationally, 32 that work-related asthma is under-recognized. 33 OA normally develops after a period of workplace exposure to an agent known to cause asthma (an allergen or asthmagen), and often leads to persisting asthma, even after the diagnosis is established and attempts have been made to reduce relevant exposures. ...
Background
The link between asthma and inhaled workplace exposures has been long appreciated, and yet aggravation of asthma symptoms by work conditions, known as work-aggravated asthma (WAA), remains relatively common.Sources of dataA review of the literature published over the last 3 years was carried out, and additional key articles were included from outside this timeframe.AgreementWAA is commonly reported by workers with asthma. One published assessment of 12 studies identified a median prevalence of 21.5% among workers with asthma. Commonly reported causes included a variety of inhaled dusts, smoke, vapours, fumes, gases and mists, common and workplace-specific aeroallergens, physical environmental factors including temperature and humidity and physical activity at work.ControversyRemains in relation to definition, and how to distinguish WAA from occupational asthma in which there is sensitization to an agent in the workplace. Both these areas, and the development of workplace interventions to reduce WAA, are timely topics for future research.
Mouse models are helpful in unveiling the mechanisms underlying sex disparities in asthma. In comparison to their female counterparts, male mice are hyperresponsive to inhaled methacholine, a cardinal feature of asthma that contributes to its symptoms. The physiological details and the structural underpinnings of this hyperresponsiveness in males are currently unknown. Herein, BALB/c mice were exposed intranasally to either saline or house dust mite once daily for 10 consecutive days to induce experimental asthma. Twenty‐four hours after the last exposure, respiratory mechanics were measured at baseline and after a single dose of inhaled methacholine that was adjusted to trigger the same degree of bronchoconstriction in both sexes (it was twice as high in females). Bronchoalveolar lavages were then collected, and the lungs were processed for histology. House dust mite increased the number of inflammatory cells in bronchoalveolar lavages to the same extent in both sexes (asthma, P = 0.0005; sex, P = 0.96). The methacholine response was also markedly increased by asthma in both sexes (e.g., P = 0.0002 for asthma on the methacholine‐induced bronchoconstriction). However, for a well‐matched bronchoconstriction between sexes, the increase in hysteresivity, an indicator of airway narrowing heterogeneity, was attenuated in males for both control and asthmatic mice (sex, P = 0.002). The content of airway smooth muscle was not affected by asthma but was greater in males (asthma, P = 0.31; sex, P < 0.0001). These results provide further insights regarding an important sex disparity in mouse models of asthma. The increased amount of airway smooth muscle in males might contribute functionally to their greater methacholine response and, possibly, to their decreased propensity for airway narrowing heterogeneity.
Purpose of review:
Bronchial asthma is a common disorder that affects about 300 million people worldwide. Its signs and symptoms however, can be present in other pulmonary and/or airway diseases and therefore a careful workup of patients with respiratory symptoms that might be due to asthma is required to a) keep a broad differential diagnosis, especially in cases that do not respond well to standard antiasthmatic therapy and b) attempt to subphenotype patients within the syndrome of asthma to diagnose e.g. precipitating factors, inflammatory subtypes and comorbidities.
Recent findings:
The syndrome of asthma contains a number of different phenotypes that offer the possibility of personalized medicine based on the respective asthma phenotype. There are attempts to combine asthma and COPD in newly postulated overlap syndromes which this review discourages to do but instead, based on new and old information concerning asthma phenotyping, suggests to rule in comorbidities and rule out a number of other diseases that can mimick asthma clinically.
Summary:
Bronchial asthma, although one of the most common respiratory diseases, can be mimicked by a number of other pulmonary and airway diseases, and especially patients with so called severe or treatment refractory asthma should receive a detailed diagnostic workup with a rather broad differential diagnosis.
Occupational asthma (OA) and work-exacerbated asthma (WEA), collectively known as work-related asthma (WRA), have been recognized as the most prevalent work-related lung diseases in the industrialized world. OA is asthma caused by workplace conditions, and is subdivided into sensitizer-induced (allergic) OA and irritant-induced (nonallergic) OA. WEA is asthma that is made worse, but was not initially caused, by workplace conditions. Although WRA is rarely fatal, patients with WRA frequently experience excessive time lost from work, workplace-specific severe disability, loss of income, job loss, and related psychosocial and financial problems. More than 400 workplace environmental agents have been reported to cause WRA, and are classified by molecular weight and allergenic and irritant properties. Diagnosis of WRA requires confirmation of a diagnosis of asthma plus evidence that the asthma was caused or worsened by workplace conditions. Accuracy of diagnosis is important because either overdiagnosis or missed diagnosis of WRA can be problematic for the patient. Self-reported clinical symptoms alone have only fair sensitivity and specificity for OA. If possible, diagnostic assessment should also include objective evidence with functional and immunologic testing. Treatment and prevention of onset or worsening of WRA can be highly effective and typically include both optimal medical management (generally the same as for non-WRA) and, importantly, avoidance of sensitizer or irritant exposures that caused or exacerbate the asthma. In most cases of OA, prognosis is better with cessation rather than reduction of exposure, and this may require substantial changes in the workplace environment or change of job or even profession.
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Occupational asthma (OA) is characterized by allergic airway inflammation and hyperresponsiveness (AHR), leading to progressive airway remodelling 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 x 10<sup>6</sup> 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 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 remodelling and bronchial hyperresponsiveness typical of OA.
Very little information is available on the ,acute histopathological bronchial alterations caused by reactive airways dysfunction syndrome ,(RADS). Wehad,the opportunity to carry ,out sequential bronchial biopsies in a ,subject with RADS due to chlorine (60 h, 15 days, 2 and 5 months after the acute expo- sure), and also to assess spirometry and bronchial responsiveness to methacholine. A36 year old worker in a water-filtration plant (nonsmoker) abruptly inhaled high concentrations of chlorine on September 12, 1994. He experienced immedi- ate nasal and throat burning, retrosternal burning and wheezing, and these symp- toms persisted during and after the workshift. Two days later, he complained of retrosternal burning, dyspnoea and wheezing. Inspiratory wheezing was docu- mented. His forced expiratory volume in one second (FEV1) was 66% of predict- edand,the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) was slightly abnormal (2.5 mg·mL,). Bronchial biopsies showed a greatly improved epitheli- umand,reduction of the inflammatory infiltrate. This case report shows that reactive airways dysfunction syndrome ,can cause acute, marked, though partially reversible, histological abnormalities. Inhaled steroids may,modulate changes in bronchial responsiveness in this condition. Eur Respir J., 1997; 10: 241‐244.
Rationale: The relationships between allergen exposures and allergy and asthma are complex. High exposure levels to cat allergen are associated with IgG- and IgG(4)-specific antibody responses without sensitization or risk of asthma, a process described as a "modified Th2 response." Attenuation of risk of allergy and asthma at high exposure levels has been reported in longitudinal studies of both childhood and occupational asthma. Objectives:To investigate, using an occupational model, the relationships among estimated exposure to aeroallergens, the production of specific IgE, IgG and IgG(4) antibodies, and the prevalence of associated symptoms. Methods: Cross-sectional survey of employees exposed to rats at work on six pharmaceutical sites across the United Kingdom. A total of 689 (89%) provided a blood sample and completed a questionnaire. Measurements and Main Results: At highest exposure to rats, there was an attenuation of the exposure response for sensitization and symptoms. In contrast, the frequency of individuals producing high quantities of specific IgG and IgG4 increased with exposure intensity. Ratios of IgG(4)/IgE were highest in those handling the greatest number of rats. Risk of developing work-related chest symptoms was lower for those who produced both specific IgE and IgG4 Compared to those with specific IgE only. Conclusions: High exposure to rats is associated with lower rates of specific IgE and symptoms but an increased frequency of high specific IgG and IgG(4) production. Specific IgG, produced together with specific IgE may reduce the risk of developing work-related chest symptoms compared with when specific IgE is produced alone.
Rationale Cleaning work and professional use of certain cleaning products have been associated with asthma, but respiratory effects of nonprofessional home cleaning have rarely been studied. Objectives: To investigate the risk of new-onset asthma in relation to the use of common household cleaners. Methods: Within the follow-up of the European Community Respiratory Health Survey in 10 countries, we identified 3,503 persons doing the cleaning in their homes and who were free of asthma at baseline. Frequency of use of 15 types of cleaning products was obtained in a face-to-face interview at follow-up. We studied the incidence of asthma defined as physician diagnosis and as symptoms or medication usage at follow-up. Associations between asthma and the use of cleaning products were evaluated using multivariable Cox proportional hazards or log-binomial regression analysis. Measurements and Main Results: The use of cleaning sprays at least weekly (42 70 of participants) was associated with the incidence of asthma symptoms or medication (relative risk [RR], 1.49; 95070 confidence interval [Cl], 1.12-1.99) and wheeze (RR, 1.39; 95 % Cl, 1.06-1.80). The incidence of physician-diagnosed asthma was higher among those using sprays at least 4 days per week (RR, 2.11; 95% Cl, 1.15-3.89). These associations were consistent for subgroups and not modified by atopy. Dose-response relationships (P < 0.05) were apparent for the frequency of use and the number of different sprays. Risks were predominantly found for the commonly used glass-cleaning, furniture, and air-refreshing sprays. Cleaning products not applied in spray form were not associated with asthma. Conclusions: Frequent use of common household cleaning sprays may be an important risk factor for adult asthma.
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 threefold1; 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
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 …
We report a survey of the number of persons handling laboratory animals in the UK in 1999–2000. This estimate has allowed us to calculate annual incidence rates of allergic asthma and rhinitis attributable to laboratory animals, insects, and birds using numerators derived from cases reported to a national surveillance scheme (SWORD). The number of exposed employees has almost halved since the early 1980s. From these data, the estimated annual incidence rate of occupational asthma among persons working with small mammals is 1.56/1000 employees. Although reported cases are rare, estimated incidence rates of asthma attributable to birds (23.9/1000/year) and insects (2.35/1000/year) are high.
Ten individuals developed an asthma-like illness after a single exposure to high levels of an irritating vapor, fume, or smoke. In most instances, the high level exposure was the result of an accident occurring in the workplace or a situation where there was poor ventilation and limited air exchange in the area. In all cases, symptoms developed within a few hours and often minutes after exposure. We have designated the illness as reactive airway dysfunction syndrome (RADS) because a consistent physiologic accompaniment was airways hyperreactivity. When tested, all subjects showed positive methacholine challenge tests. No documented preexisting respiratory illness was identified nor did subjects relate past respiratory complaints. In two subjects, atopy was documented, but in all others, no evidence of allergy was identified. In the majority of the cases, there was persistence of respiratory symptoms and continuation of airways hyperreactivity for more than one year and often several years after the incident. The incriminated etiologic agent varied, but all shared a common characteristic of being irritant in nature. In two cases, bronchial biopsy specimens were available, and an airways inflammatory response was noted. This investigation suggests acute high level, uncontrolled irritant exposures may cause an asthma-like syndrome in some individuals which is different from typical occupational asthma. It can lead to long-term sequelae and chronic airways disease. Nonimmunologic mechanisms seem operative in the pathogenesis of this syndrome.
The authors assessed the relations between occupation and risk of developing asthma in adulthood in a 1997– 2000 population-based incident case-control study of 521 cases and 932 controls in south Finland. The occupations were classified according to potential exposure to asthma-causing inhalants. Asthma risk was increased consistently for both men and women in the chemical (adjusted odds ratio (OR) = 5.69, 95% confidence interval (CI): 1.08, 29.8), rubber and plastic (OR = 2.61, 95% CI: 0.92, 7.42), and wood and paper (OR = 1.72, 95% CI: 0.71, 4.17) industries. Risk in relation to occupation was increased only for men—for bakers and food processors (OR = 8.62, 95% CI: 0.86, 86.5), textile workers (OR = 4.70, 95% CI: 0.29, 77.1), electrical and electronic production workers (OR = 2.83, 95% CI: 0.82, 6.93), laboratory technicians (OR = 1.66, 95% CI: 0.17, 16.6), and storage workers (OR = 1.57, 95% CI: 0.40, 6.19). Of the predominantly men’s occupations, metal (OR = 4.52, 95% CI: 2.35, 8.70) and forestry (OR = 6.00, 95% CI: 0.96, 37.5) work were the strongest determinants of asthma. For women, asthma risk increased for waiters (OR = 3.03, 95% CI: 1.10, 8.31), cleaners (OR = 1.42, 95% CI: 0.81, 2.48), and dental workers (OR = 4.74, 95% CI: 0.48, 46.5). Results suggest an increased asthma risk both in traditional industries and forestry and in several nonindustrial occupations.
Study objectives
To determine whether the use of respiratory protective equipment would reduce the incidence of occupational asthma due to exposure to hexahydrophthalic anhydride (HHPA).
Design
Prospective cohort study.
Setting
A facility that makes an epoxy resin product requiring HHPA for its manufacture.
Participants
Sixty-six individuals newly hired at a facility that makes an epoxy resin product requiring HHPA for its manufacture.
Intervention
Employees who wished to use respiratory protective equipment could choose from three types of masks: dust mask, half-face organic vapor respirator, or full-face organic vapor respirator.
Measurements
Workers were evaluated annually for development of positive antibody to HHPA and occupational, immunologic respiratory disease, including occupational asthma.
Results
With use of respiratory protective equipment, the rate of developing an occupational immunologic respiratory disease was reduced from approximately 10 to 2% per year. Occupational asthma developed in only three individuals, and they were all in the higher exposure category. Statistically, one respirator was not superior to the others.
Conclusion
Respiratory protective equipment can reduce the incidence of occupational immunologic respiratory disease, including occupational asthma, in employees exposed to HHPA.