Reactive Airways Dysfunction Syndrome Research Articles

Reactive airway dysfunction syndrome caused by chlorine gas from the point of view of Persian Medicine: A review article

Introduction: Chlorine gas inhalation is a toxic respiratory irritant associated with high lung complications. Despite its wide industrial and domestic applications such as bleaching detergents, there is no specific treatment for chlorine gas poisoning yet and common standard treatments are mostly supportive. In this regard, this study aimed to find a new treatment for this pathogenesis from the perspective of Persian medicine (PM).
 Materials and methods: In this review study, at first, we searched the etiologies and clinical symptoms associated with chlorine gas poisoning in modern medicine and then compared them with similar etiologies and symptoms in valuable Persian medical manuscripts. Then we reviewed the proposed treatments for similar illnesses from the point of view of PM.
 Results: The pathology of lung damage caused by inhalation of chlorine gas is reactive airway dysfunction syndrome (RADS), which leads to dyspnea, hypoxemia, respiratory tract obstruction, pneumonia, pulmonary edema, and finally acute respiratory distress syndrome (ARDS). In a comparative study, it seems that this pathology has the closest similarity with the Persian term“Varme-e-harr riye”. The treatment strategy for this syndrome in PM is bloodletting at the first and then the application of cold-temperament foods and medications to improve the lungs.
 Conclusion: According to the compatibility of acute pulmonary edema caused by chlorine inhalation and “varam-e-harr riye” in PM, it seems that wet cupping can be considered as a suggested primary and emergency treatment for this pathology in future clinical studies.

Toxic inhalation of sodium metabisulphite by-products from a shipping container.

Logistics workers who handle cargo containers are at risk of toxic inhalation injuries, although prevalence and severities of these injuries are not well characterized. We report on a previously healthy 37-year-old supervisor who was acutely exposed to sodium metabisulphite and its thermal degradation by-products during a routine inspection of a shipping container. The employee developed chemical pneumonitis with acute non-cardiogenic pulmonary oedema and subsequent severe reactive airway dysfunction syndrome.

Exposição ao gás cloro e padrões evolutivos da síndrome da disfunção reativa das vias aéreas: uma revisão sistemática

Abstract Introduction: chlorine is the most irritant gas to which people are commonly exposed to daily. One of its toxic effects is reactive airway dysfunction syndrome (RADS). Objective: this study aims to summarize the evidence from the evolutive patterns of RADS. Methods: this systematic review study was conducted using the databases of the University of São Paulo repository, BVS/LILACS, PubMed/Medline, and SciELO. Studies from September 1985 to July 2021 with “chlorine” and “occupational asthma” as descriptors, associated with “reactive airway dysfunction syndrome” or “irritant-induced asthma,” were included. These articles were assessed by two independent reviewers. The study’s quality was assessed using the Joanna Briggs checklist. Results: a total of 22 studies were retrieved, including 11 case series, 8 case reports, and 3 cross-sectional studies. The selected studies covered 1.335 participants from 11 countries, and only 170 had a diagnosis of RADS with documented evolution. Of these, 115 (65%) were due to occupational exposure. The most frequent RADS evolutive pattern was the long-term persistence of symptoms, spirometric alterations, and/or bronchial hyperresponsiveness, mainly in the occupational setting. A lack of standardization of adequate information reporting was found. Conclusions: chronicity was the most frequent RADS evolutive pattern.

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Abstract. Bronchial asthma (��) is one of the most common conditions of the respiratory system that develops in the military and civilian population in war zones, which is caused by the combined exposure of a complex of factors that pollute the environment during the military missions deployment. For Ukraine, the issue of the respiratory system morbidity from exposure to chemical air pollutants in the territory of hostilities is a new challenge. Materials and methods. Analytical review of scientific publications was performed using abstract databases of scientific libraries PubMed, Medline and text databases of scientific publishing houses PubMed, Central, BMJ group and other VIP databases using system and content analysis. Results. A wide range of chemical factors has a combined effect on the respiratory system of the military and civilian population, leading to the development of BA. Among them are components of explosive gases, particulate matter, emissions of diesel fuel, burn pits products, biological factors, consequences of fires, geological dust. According to epidemiological studies, the prevalence of BA among military personnel in combat zones is 3-6 %. During the functional examination of the lungs, 15 % of the examined showed bronchial hyperreactivity, which is a pathogenetic link of such diseases as BA, hypersensitivity pneumonitis, Reactive Airway Dysfunction Syndrome, which are related to DRLD � Deployment Respiratory Lung Diseases. Conclusions. BA is one of the most documented diseases of the respiratory system caused by exposure to chemical pollutants in war zones. In Ukraine, the system of providing medical aid to the military and civilian population in the territory of hostilities needs to be improved, taking into account the experience of other countries. In particular, the issue of approving the presumptive list of conditions recognized to be related to military service during hostilities and including BA should be considered.

Chlorine gas exposure and evolutive patterns of reactive airways dysfunction syndrome: a systematic review

Resumo Introdução: o cloro é o gás irritante a que as pessoas estão comumente expostas no cotidiano. Um dos seus efeitos tóxicos é a síndrome da disfunção reativa das vias aéreas (SDRA). Objetivo: resumir as principais evidências dos padrões evolutivos da SDRA. Métodos: Revisão sistemática da literatura de artigos publicados entre setembro de 1985 e julho de 2021 no repositório da Universidade de São Paulo (USP) e nas bases BVS/LILACS, PubMed/Medline e SciELO. Foram utilizados os descritores “cloro” e “asma ocupacional” associados à “síndrome da disfunção reativa das vias aéreas” ou “asma induzida por irritantes”. Dois revisores independentes selecionaram e avaliaram a qualidade dos estudos, com apoio do checklist do Instituto Joanna Briggs. Resultados: selecionaram-se 22 estudos: 11 séries de casos, oito relatos de caso e três estudos transversais. Os estudos selecionados abrangeram 1.335 participantes de 11 países, e apenas 170 tiveram diagnóstico de SDRA com evolução documentada. Destes, 115 (65%) foram devido à exposição ocupacional. Os padrões evolutivos mais frequentes foram persistência prolongada dos sintomas, alterações espirométricas e/ou hiper-responsividade brônquica, principalmente no ambiente ocupacional. Observou-se falta de padronização no relato de informações adequadas. Conclusões: a cronicidade foi o padrão evolutivo da SDRA mais frequente. Houve falta de informação apropriada que impediu uma análise adequada dos resultados.

Acute Accidental Exposure to Chlorine Gas: Clinical Presentation, Pulmonary Functions and Outcomes

To study the clinical presentation, pulmonary functions and outcomes in subjects who were accidentally exposed to chlorine gas. Prospective observational study of 64 patients who sustained acute accidental exposure to chlorine gas during a leak in the chlorination system of the public bathing pool of a temple. The major presenting symptoms and signs included acute dyspnoea (100%), chest discomfort (100%), cough (97%), eye irritation (88%), giddiness (72%), vomiting (46%), and heaviness in the head (44%); tachycardia (100%), tachypnoea (96%) and polyphonic wheezing (28%). All patients were managed in the emergency room with humidified oxygen inhalation and beta-2 agonist nebulisation and 52 were discharged within six hours. Twelve patients were severely affected and required hospitalisation; three of them were admitted into the intensive care unit. Three patients developed pulmonary oedema six to eight hours following admission. Pulmonary function testing (n = 12) at presentation revealed obstructive defect in eight and mixed obstructive-cum-restrictive defect in four patients. The mean duration of hospital stay was 5.1 +/- 2.1 days. None of the patients died. Reactive airway dysfunction syndrome (RADS) was observed in three of the 12 hospitalised patients, who complained of manifested persistent cough that lasted for three months period following discharge. Serial pulmonary functions recovered to normal range by the end of the six months in all patients and remained so at one-year follow-up. Acute exposure to chlorine gas is an uncommon, but important public health hazard and can cause RADS, acute lung injury and pulmonary function abnormalities, which are reversible on prompt and appropriate management.

The Heat Shock Protein 90 Inhibitor, AT13387, Protects the Alveolo-Capillary Barrier and Prevents HCl-Induced Chronic Lung Injury and Pulmonary Fibrosis.

Hydrochloric acid (HCl) exposure causes asthma-like conditions, reactive airways dysfunction syndrome, and pulmonary fibrosis. Heat Shock Protein 90 (HSP90) is a molecular chaperone that regulates multiple cellular processes. HSP90 inhibitors are undergoing clinical trials for cancer and are also being studied in various pre-clinical settings for their anti-inflammatory and anti-fibrotic effects. Here we investigated the ability of the heat shock protein 90 (HSP90) inhibitor AT13387 to prevent chronic lung injury induced by exposure to HCl in vivo and its protective role in the endothelial barrier in vitro. We instilled C57Bl/6J mice with 0.1N HCl (2 µL/g body weight, intratracheally) and after 24 h began treatment with vehicle or AT13387 (10 or 15 mg/kg, SC), administered 3×/week; we analyzed histological, functional, and molecular markers 30 days after HCl. In addition, we monitored transendothelial electrical resistance (TER) and protein expression in a monolayer of human lung microvascular endothelial cells (HLMVEC) exposed to HCl (0.02 N) and treated with vehicle or AT13387 (2 µM). HCl provoked persistent alveolar inflammation; activation of profibrotic pathways (MAPK/ERK, HSP90); increased deposition of collagen, fibronectin and elastin; histological evidence of fibrosis; and a decline in lung function reflected in a downward shift in pressure–volume curves, increased respiratory system resistance (Rrs), elastance (Ers), tissue damping (G), and hyperresponsiveness to methacholine. Treatment with 15 mg/kg AT13387reduced alveolar inflammation, fibrosis, and NLRP3 staining; blocked activation of ERK and HSP90; and attenuated the deposition of collagen and the development of chronic lung injury and airway hyperreactivity. In vitro, AT13387 prevented HCl-induced loss of barrier function and AKT, ERK, and ROCK1 activation, and restored HSP70 and cofilin expression. The HSP90 inhibitor, AT13387, represents a promising drug candidate for chronic lung injury that can be administered subcutaneously in the field, and at low, non-toxic doses.

Health-Related Quality of Life (HRQoL) of Residents with Persistent Lower Respiratory Symptoms or Asthma Following a Sulphur Stockpile Fire Incident.

Background: This study evaluated health-related quality of life (HRQoL) in residents with persistent lower respiratory symptoms (PLRS) or asthma six years after exposure to sulphur dioxide vapours emanating from an ignited sulphur stockpile. Methods: A cross-sectional study was carried out, using interview data collected at three time points (prior to, one- and six-years post incident), medical history, respiratory symptoms and HRQOL using the Medical Outcomes Study Form 36 (SF-36). Results: A total of 246 records, 74 with and 172 without PLRS or asthma, were analysed. The mean age was 42 (SD:12) years in the symptomatic group and 41 (SD:13) years in the asymptomatic group. Mean SF-36 scores were significantly lower for the symptomatic group in the Physical Functioning (24 vs. 39), Role—Physical (33 vs. 48) and General Health (GH) domains (24 vs. 37). Symptomatic residents experienced a significant decline in their Role—Physical (OR = 1.97; CI 1.09, 3.55) and GH (OR = 3.50; CI 1.39, 8.79) at year 6 compared to asymptomatic participants. Residents with co-morbid reactive upper airways dysfunction syndrome demonstrated stronger associations for GH (OR = 7.04; CI 1.61, 30.7) at year 1 and at year 6 (OR = 8.58; CI 1.10, 65.02). Conclusions: This study highlights the long-term adverse impact on HRQoL among residents with PLRS or asthma following a sulphur stockpile fire disaster.

Reactive Airways Dysfunction Syndrome: A Review of a Less Known Yet Severe Occupational Disease

Reactive Airways Dysfunction Syndrome: A Review of a Less Known Yet Severe Occupational Disease

TOLUENE-INDUCED ACUTE LUNG INJURY: CASE REPORT

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Toluene is an aromatic hydrocarbon widely used as a solvent in industrial and commercial products including paints, adhesives, ink, and rubber. It is occasionally used as an inhalant drug for its intoxicating properties. While mostly known for producing neurologic effects, here we report a case of toluene induced acute lung injury. CASE PRESENTATION: A 61-year-old female with a medical history of alcohol abuse, depression, congestive heart failure with preserved ejection fraction presented with one week of weakness and shortness of breath. She had been seen twice in the week prior having tested negative for SARS-COV2. In the emergency department, O2 saturation was 70% with respiratory distress on room air requiring high flow nasal cannula support. Labs were notable for a potassium of 2.7 mmol/L, acute kidney injury, elevated transaminases, lactate of 2.8 mmol/L and leukocyte count of 9800/nL. CT showed diffuse bilateral ground glass opacities involving the lung parenchyma concerning for atypical including viral pneumonia. Upon admission to the ICU she developed worsening hypoxia and respiratory failure requiring intubation.A discussion with the patient's husband revealed she had a history of glue sniffing. She had recently been decreasing her alcohol intake and substituting this with an increased frequency of sniffing both permanent markers and modeling glue. This raised suspicion for chemical pneumonitis secondary to toluene induced acute lung injury. DISCUSSION: Toluene is a highly lipophilic molecule readily inhaled via the lungs and distributed widely throughout the body producing side effects like ethanol intoxication via interfering mainly with GABA receptors. Neurologic manifestations range from euphoria and hallucinations to cognitive dysfunction and ataxia with chronic use. It specifically causes renal tubular acidosis typically manifesting as a normal anion gap hyperchloremic acidosis with hypokalemia. It can also cause hepatic injury and cardiac automaticity and conduction abnormalities.Acute lung injury secondary to toluene has been described but less frequently reported. Toxicity can result in Reactive Airway Dysfunction Syndrome (RADS) from acute or chronic exposure to various chemical irritants. All hydrocarbons, including toluene, can cause chemical pneumonitis by direct contact with the pulmonary parenchyma and destroying alveolar and capillary membranes resulting in vascular permeability and edema. Symptoms may include cough, wheezing, respiratory distress, and hypoxia. Bilateral interstitial infiltrates may be delayed for several hours after the development of pneumonitis. There is no specific antidote for toluene toxicity. CONCLUSIONS: Treatment for toluene and many chemical induced pneumonitides consists of supportive care, supplemental oxygen, bronchodilators, inhaled and systemic glucocorticoids and may require intubation and admission to an ICU in severe cases. REFERENCE #1: Camara-Lemarroy CR, Rodríguez-Gutiérrez R, Monreal-Robles R, González-González JG. Acute toluene intoxication--clinical presentation, management and prognosis: a prospective observational study. BMC Emerg Med. 2015;15:19. Published 2015 Aug 18. doi:10.1186/s12873-015-0039-0 REFERENCE #2: Alberts WM, do Pico GA. Reactive airways dysfunction syndrome. Chest. 1996;109(6):1618-1626. doi:10.1378/chest.109.6.1618 REFERENCE #3: Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila). 2014;52(5):479-489. doi:10.3109/15563650.2014.923904 DISCLOSURES: No relevant relationships by Ryan Lee, source=Web Response No relevant relationships by Dominic Valentino, source=Web Response

Drug Repurposing Patent Applications April–June 2021

Drug Repurposing Patent Applications April–June 2021

Surveillance of work-related asthma including the emergence of a cannabis-associated case series in Washington State

Objective We conducted surveillance for work-related asthma (WRA) in Washington State to identify the industry sectors and asthma exposures most commonly affecting injured workers and in need of prevention activities. Methods Using workers’ compensation data as the primary data source, valid cases were classified as work-aggravated asthma (WAA) or new onset asthma that includes occupational asthma (OA) and reactive airways dysfunction syndrome (RADS). The source of exposure that caused the worker’s asthma, their industry and occupation were determined. Results There were 784 valid work-related asthma cases identified for the period 2009–2016, WAA (n = 529) was most common followed by occupational asthma (n = 127) and RADS (n = 12). The Health Care and Social Assistance industry had the highest number of cases (n = 170) with 82% classified as WAA. The highest overall proportions of new onset asthma are occurring in Agriculture, Forestry, Fishing and Hunting (33% of work related asthma cases), Manufacturing (31%) and Construction (30%). The leading substances associated with new onset asthma across all industries include hop plant dust, wood and cedar dust, mineral and inorganic dust, mold, and cleaning materials. We describe ten cases of cannabis-associated asthma including seven from workers in the legalized cannabis industry, four of whom had OA. Conclusion State-based work-related asthma surveillance is critical in identifying the workers and exposures associated with this occupational disease, including the detection of a case-series in the cannabis industry.

Research advances on the diagnosis and treatment of hydrofluoric acid inhalation injury

Hydrofluoric acid inhalation injury is difficult to treat, despite it has low incidence. It could cause mild symptoms such as cough and sore throat, or severe symptom that may develop into life-threatening acute respiratory distress syndrome, and even rare pulmonary diseases such as reactive airway dysfunction syndrome and pulmonary alveolar proteinosis. Currently, there is no specific standard for the diagnosis and treatment of hydrofluoric acid inhalation injury. Authors summarize the incidence, injury mechanism, clinical diagnosis and treatment of hydrofluoric acid inhalation injury by searching literature at home and abroad and propose that pulse contour cardiac output monitor and extracorporeal membrane oxygenation have great application prospects in treatment of severe cases, so as to provide references for peers.

Updated review of reported cases of reactive airways dysfunction syndrome.

A previous systematic review of the diagnosis of reactive airways dysfunction syndrome (RADS), undertaken from 1985 to 2004, found a lack of standardization of case reporting, thus misattribution of symptoms can occur. We aimed to update the systematic review, update the list of reported causes and see whether a more structured approach to reporting has been adopted. We undertook a systematic literature review, using the databases EMBASE and Ovid MEDLINE, with search terms 'reactive airways dysfunction syndrome' or 'asthma AND acute irritant', and reported according to PRISMA guidelines. We included papers and abstracts published from January 2005 to September 2019, and articles were grouped by the presence or absence of diagnostic features: 'definite' RADS (met Brooks' criteria) or 'possible' RADS (Brooks' criteria not met or insufficient data). We collected demographic and diagnostic data for cases, where given. Eleven papers and six conference abstracts met the inclusion criteria, 13 of which were case series or reports, and comprised 752 cases in total; seven articles met Brooks' criteria for RADS diagnosis. A variety of agents were implicated, with chlorine or chlorine-releasing molecules most frequently reported. A lack of standardized reporting of RADS remains. The majority of published articles and conference abstracts either do not meet, or contain insufficient data to judge against, Brooks' criteria, particularly in relation to onset of symptoms and bronchial hyper-reactivity or variability of airflow obstruction. Some novel agents are described, in keeping with recognized structural taxonomies.

Is There An Explanation for How An Irritant Causes A Nonallergic Asthmatic Disorder Such as Reactive Airways Dysfunction Syndrome (RADS)?

Is There An Explanation for How An Irritant Causes A Nonallergic Asthmatic Disorder Such as Reactive Airways Dysfunction Syndrome (RADS)?

Claudins, VEGF, Nrf2, Keap1, and Nonspecific Airway Hyper-Reactivity Are Increased in Mice Co-Exposed to Allergen and Acrolein.

Acrolein, an α/β-unsaturated aldehyde, is volatile at room temperature. It is a respiratory irritant found in environmental tobacco smoke, which can be generated during cooking or endogenously at sites of injury. An acute high concentration of uncontrolled irritant exposure can lead to an asthma-like syndrome known as reactive airways dysfunction syndrome (RADS). However, whether acrolein can induce RADS remains poorly understood. The aim of study is to develop a RADS model of acrolein inhalation in mice and to clarify the mechanism of RADS. Mice were treated with ovalbumin (OVA) and exposed to acrolein (5 ppm/10 min). Airway hyper-responsiveness (AHR) was measured on days 24 and 56, and samples were collected on days 25 and 57. Tight junction protein, antioxidant-associated protein, and vascular endothelial growth factor (VEGF) levels were estimated by Western blotting and immunohistochemical staining. Reactive oxygen species (ROS) was calculated using enzyme linked immunosorbent assays. Acrolein or OVA groups exhibited an increase in airway inflammatory cells and AHR compared to a sham group. These effects were further increased in mice in the OVA + acrolein exposure group than in the OVA exposure group and persisted in the acrolein exposure group for 8 weeks. CLDNs, carbonyls, VEGF, Nrf2, and Keap1 were observed in the lungs. Our data demonstrate that acrolein induces RADS and that ROS, angiogenesis, and tight junction proteins are involved in RADS in a mouse model.

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.

The Development of Long-Term Adverse Health Effects in Oil Spill Cleanup Workers of the Deepwater Horizon Offshore Drilling Rig Disaster.

The purpose of this study was to assess the long-term adverse health effects of the 2010 Deepwater Horizon Gulf oil spill exposure in workers who participated in its cleanup work. Medical charts of both the oil spill exposed and unexposed subjects were reviewed. The changes in the white blood cells, platelets, hemoglobin, hematocrit, blood urea nitrogen, creatinine, alkaline phosphatase (ALP), aspartate amino transferase (AST), alanine amino transferase (ALT) levels, as well as their pulmonary and cardiac functions were evaluated. Medical records from 88 subjects (oil spill cleanup workers, n = 44 and unexposed, n = 44) were reviewed during initial and 7 years follow up visits after the disaster occurred. Compared with the unexposed subjects, oil spill exposed subjects had significantly reduced platelet counts (×103/µL) at their initial (254.1 ± 46.7 versus 289.7 ± 63.7, P = 0.000) and follow-up (242.9 ± 55.6 versus 278.4 ± 67.6, P = 0.000) visits compared with the unexposed subjects (254.6 ± 51.9 versus 289.7 ± 63.7, P = 0.008). The hemoglobin and hematocrit levels were increased significantly both at their initial and follow-up visits in the oil spill exposed subjects compared to the unexposed subjects. Similarly, the oil spill exposed subjects had significantly increased ALP, AST, and ALT levels at their initial and follow-up visits compared with those of the unexposed subjects. Illness symptoms that were reported during their initial visit still persisted at their 7-year follow-up visit. Notably, at their 7-year follow-up visit, most of the oil spill exposed subjects had also developed chronic rhinosinusitis and reactive airway dysfunction syndrome as new symptoms that were not reported during their initial visit. Additionally, more abnormalities in pulmonary and cardiac functions were also seen in the oil spill exposed subjects. This long-term follow-up study demonstrates that those people involved in the oil spill cleanup operations experiences persistent alterations or worsening of their hematological, hepatic, pulmonary, and cardiac functions. In addition, these subjects experienced prolonged or worsening illness symptoms even 7 years after their exposure to the oil spill.

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.

The effect of exposure of SO2 in high concentrations on CD19+ cells in reactive airway dysfunction syndrome in rat

Reactive airway dysfunction syndrome (RADS) has a clinical manifestation similar to asthma, but some features are different between both the diseases. To probe the effect of CD19+ cells in RADS pathogenesis by inhalation of sulfur dioxide (SO2), rats were exposed to SO2 at 600 ppm for 2 h per day for 7 days and the CD19 expression in lung tissue was detected both at mRNA and protein levels by RT-PCR and western blot. The percentages of CD19+ and CD19+ CD23+ cells were measured by flow cytometry. IgG, IgA, and IgE in serum and bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Histological analysis was performed. The results showed that expression of CD19 in SO2 exposure group was lower than that in the control both at mRNA and protein levels ( P < 0.05). Flow cytometry analysis showed that the percentages of CD19+ and CD19+ CD23+ were significantly lower in the SO2 exposed group than that in the control ( P < 0.05). There was no difference between the control and SO2 exposed groups in both serum and BALF levels of IgG, IgA, and IgE. Pathological changes, such as chronic bronchitis, local alveolar hemorrhage, and lymphocytes infiltration were observed in SO2 exposed. RADS is a non-immunogenicity, chronic airway inflammatory disease caused by irritation of harmful factor and manifests as airway hyperresposiveness.