Acute Irritant-induced Asthma Research Articles

Occupations and exposure events in acute and subacute irritant-induced asthma

BackgroundExposures leading to irritant-induced asthma (IIA) are poorly documented.MethodsWe retrospectively screened the medical records of patients with IIA diagnosed in an occupational medicine clinic during 2000–2018. We classified the cases...

Environmental Causes of Asthma.

Environmental factors which cause asthma are those that induce airway inflammation with eosinophils (more common) or neutrophils along with airway hyperresponsiveness (AHR). The most common of these (indeed the most common cause of asthma) are IgE-mediated inhalant allergen exposures. Allergen-induced AHR and inflammation are both associated with the allergen-induced late asthmatic response (LAR). Although allergens were previously recognized only as causes of symptoms and bronchoconstriction in asthmatics, we now appreciate them as causes of the fundamental pathophysiologic features of asthma. Low-molecular-weight chemical sensitizers, causes of occupational asthma, also cause asthma in a manner analogous to allergen. Acute irritant-induced asthma (reactive airways dysfunction syndrome) following a very heavy irritant exposure and chronic irritant-induced asthma following repeated high exposures can also induce persistent or permanent changes (inflammation and AHR) consistent with asthma. Textile dust exposure produces a different form of airway disease (byssinosis) which is less frequently observed currently. Environmental exposure to tobacco smoke facilitates the development of asthma in children. Personal smoking and environmental air pollution have an inconsistent and likely generally small effect in causing asthma.

Irritants, Irritancy and Irritant Induced Asthma

An irritant represents a non-corrosive chemical that causes a reversible non-immunologic inflammatory reaction after direct contact with the skin, eyes, nose and/or respiratory system. There are numerous reactions to irritants including change in spirometry, elevated exhaled breath levels of nitric oxide, enhancement of the response to allergen provocation and alteration of antioxidant defenses. Irritancy prompts an “inflammatory soup” of signaling molecules leading to tissue changes characterized by infiltration of mononuclear inflammatory cells, vascular congestion, augmented blood flow, contiguous edema with leaking of plasma, glandular hyper secretion and nervous hyperresponsiveness. Acute irritant-induced asthma, also referred to as Reactive Airways Dysfunction Syndrome (RADS), is a non-allergic type of asthma presenting without a prior time-period of latency. The manifestations of RADS begin within 24 h following a single massive exposure to an irritating gas, vapor or fume resulting in continuing airway inflammation, changed airway remodeling, persistent structural changes, neural disturbances and unrelenting airway hyperresponsiveness. Recommendation is that RADS or any serious inhalation exposure be handled in a hospital setting. Serial bronchoscopic assessments assist management decisions. Management requires astute judgment and skill for a rapidly changing clinical scenario. The influence of odors and emotion in the pathogenesis irritant-induced inhalational responses is significant.

Do chronic workplace irritant exposures cause asthma?

The present review summarizes the recent literature on the relation between chronic workplace irritant exposures and asthma, focusing on exposures of low to moderate levels. We discuss results from epidemiological surveys, potential biological mechanisms, and needs for further research. These aspects are largely illustrated by studies on exposure to cleaning products. Recent results from nine population-based and workplace-based epidemiological studies, mostly cross-sectional, found an increased risk of both new-onset and work-exacerbated asthma among participants exposed to moderate level of irritants and/or cleaning products. Evidence of a causal effect of chronic workplace irritant exposure in new-onset asthma remains limited, mainly because of a lack of longitudinal studies and the difficulty to evaluate irritant exposures. However, recent epidemiological studies strengthen the evidence of an effect of chronic exposure to irritants in work-related asthma. The underlying mechanism remains unknown but may be related to oxidative stress, neurogenic inflammation and dual irritant and adjuvant effects. However, disentangling chronic irritant effects from either acute irritant-induced asthma or immunological low molecular weight agent-induced asthma is difficult for some agents. Further research is needed to improve assessment of irritant exposures and identify biomarkers.

Long-Term Outcomes of Acute Irritant-induced Asthma and World Trade Center–related Lower Airway Disease

Long-Term Outcomes of Acute Irritant-induced Asthma and World Trade Center–related Lower Airway Disease

Long-term pathologic consequences of acute irritant-induced asthma

Acute irritant-induced asthma (IrIa) or reactive airways dysfunction syndrome is caused by exposure to a high concentration of an agent. The long-term pathologic consequences of IrIa remain thus far unknown. The aim of our study was to investigate the chronic airway inflammation and remodeling that occur in association with IrIa. Ten subjects with a history of IrIa (mean interval of 10.9 years, minimum of 4 years, since the inhalational accident) underwent bronchoscopy followed by bronchoalveolar lavage and bronchial biopsies. Immunologic and morphologic data from patients with IrIa were compared with those of patients with mild to moderate asthma as well as healthy controls. Bronchoalveolar lavage fluid analysis showed increased eosinophil and neutrophil counts in 30% and 60% of subjects with IrIa, respectively. In the supernatant of bronchoalveolar lavage, we found a significant increase in the majority of mediators compared with healthy subjects and a significant increase in eosinophilic cationic protein, IL-8, basic fibroblast growth factor, and matrix metalloproteinase 1 compared with control patients with asthma. Evaluation of basement membrane thickness (subepithelial fibrosis) demonstrated a significant increase in patients with IrIa compared with healthy subjects and subjects with asthma. Basement membrane thickness also significantly correlated with the PC(20) value. The epithelial cell detachment showed an elevated although not significant trend compared with subjects with asthma and control subjects. Immunocytochemical analysis demonstrated increases in the number of eosinophil cationic protein and TGF-beta1-positive cells compared with healthy controls. This study provides evidence of a significant eosinophilic and neutrophilic inflammation as well as remodeling in IrIa many years after an inhalational accident.

Diesel exhaust causing low-dose irritant asthma with latency?

Diesel exhaust exposure may cause acute irritant-induced asthma and potentiate allergen-induced asthma. There are no previous reports of occupational asthma due to diesel exhaust. To describe occupational asthma with latency in workers exposed to diesel exhaust in bus garages. The Shield database of occupational asthma notifications in the West Midlands, UK, was searched between 1990 and 2006 for workers where diesel exhaust exposure was thought to be the cause of the occupational asthma. Those without other confounding exposures whose occupational asthma was validated by serial peak expiratory flow (PEF) analysis using Oasys software were included. Fifteen workers were identified with occupational asthma attributed to diesel exhaust. Three had validated new-onset asthma with latency. All worked in bus garages where diesel exhaust exposure was the only likely cause of their occupational asthma. Occupational asthma was confirmed by measures of non-specific reactivity and serial measurements of PEF with Oasys scores of 2.9, 3.73 and 4 (positive score > 2.5). The known non-specific irritant effects of diesel exhaust suggest that this is an example of low-dose irritant-induced asthma and that exposures to diesel exhaust in at least some bus garages are at a sufficient level to cause this.

Long-Term Outcomes of Acute Irritant-induced Asthma

The long-term outcomes of acute irritant-induced asthma (IIA) are mostly unknown. To study the long-term outcomes of IIA. We reassessed 35 subjects who experienced IIA at a mean interval of 13.6 +/- 5.2 years. The causal agent was chlorine in 20 cases (57%). At diagnosis, the mean +/- SD FEV(1) was 74.5 +/- 19.5% predicted, and all subjects showed bronchial hyperresponsiveness. At reassessment, all subjects reported respiratory symptoms, and 24 (68%) were on inhaled steroids. There were no significant improvements in FEV(1) and FEV(1)/FVC values. Twenty-three subjects had a methacholine test, and only six subjects had normal levels of responsiveness. Of the remaining 12 subjects, six had improvement in FEV(1) after bronchodilator >or=10%. In samples of induced sputum obtained from 27 subjects, six had eosinophils >or=2%. Levels of inflammatory and remodeling mediators were higher than in control subjects but were no different from subjects with occupational asthma due to sensitization. Quality of life score was 4.4 +/- 1.5 on a 0 (worst) to 7 (best) scale. Twelve subjects had an abnormal depression score. This study provides the first evidence of significant long-term impact of acute IIA on various outcomes.

Defining and investigating occupational asthma: a consensus approach

Background: At present there is no internationally agreed definition of occupational asthma and there is a lack of guidance regarding the resources that should be readily available to physicians running...

Prolonged respiratory symptoms caused by thermal degradation products of freons.

The chlorofluorocarbons (CFC) used in refrigeration systems decompose on heating and produce substances that are highly irritating to the airways (eg, chlorine, carbonyl fluoride, and hydrogen fluoride). This study examined persistent respiratory symptoms among several workers exposed to thermal decomposition products of CFC. Seven patients with respiratory symptoms caused by inadvertent exposure to thermal decomposition products of CFC in a restaurant kitchen or during refrigerator repair were studied with the use of spirometry, peak flow follow-up, and histamine challenge tests. Three patients also underwent bronchoscopy and bronchoalveolar lavage. In five of the cases, cough or dyspnea lasted longer than 1 month; for three of the five, the symptoms lasted more than 4 years. Three cases showed increased bronchial hyperreactivity, and two of the three had increased diurnal peak flow variation. Three patients fulfilled the criteria for acute irritant-induced asthma or reactive airway dysfunction syndrome. One case exhibited bronchiolitis while, for the other six, the clinical picture was consistent with bronchitis. The studied cases indicate that the thermal decomposition products of CFC used in refrigerators may cause irritant-induced airway diseases of long duration.