11/15. Diesel asthma. Reactive airways disease following overexposure to locomotive exhaust.While some of the gaseous and particulate components of diesel exhaust can cause pulmonary irritation and bronchial hyperreactivity, diesel exhaust exposure has not been shown to cause asthma. Three railroad workers developed asthma following excessive exposure to locomotive emissions while riding immediately behind the lead engines of caboose-less trains. asthma diagnosis was based on symptoms, pulmonary function tests, and measurement of airways hyperreactivity to methacholine or exercise. One individual's peak expiratory flow rates fell in a work-related pattern when riding immediately behind the lead diesel engine. None had a previous history of asthma or other respiratory disease and none were current smokers. All three developed persistent asthma. In two cases, physiologic abnormalities suggesting reversible restriction were observed. This is the first report implicating diesel exhaust as a cause of reactive airways disease.- - - - - - - - - - ranking = 1keywords = work (Clic here for more details about this article) |
12/15. Reactive airways dysfunction syndrome (RADS) following exposure to toxic gases of a swine confinement building.We describe the case of a 58 year old male, who developed a reactive airways dysfunction syndrome (RADS) after exposure to a high level of toxic gases in a swine confinement building. This previously healthy, nonatopic man developed moderate, partially reversible, airway obstruction and increased responsiveness within a month after the toxic exposure. The circumstances of the incident and the concomitant death of two sows make it likely that hydrogen sulphide was the causative agent. To our knowledge, this is the first case of reactive airways dysfunction syndrome reported from swine confinement buildings and, therefore, should raise awareness of this potential risk in that work environment.- - - - - - - - - - ranking = 0.5keywords = work (Clic here for more details about this article) |
13/15. hypersensitivity pneumonitis-like reaction and occupational asthma associated with 1,3-bis(isocyanatomethyl) cyclohexane pre-polymer.Twenty-three of 34 workers who had worked in the injection molding operation making polyurethane foam parts at an automobile parts manufacturing plant developed respiratory symptoms and/or systemic symptoms over a 2-month period following the full production use of a new diisocyanate paint that contained 1,3-bis(isocyanatomethyl)cyclohexane pre-polymer (BIC)(CAS #75138-76-0, 38661-72-2). At 3 months, all subjects underwent an interview, physical examination, pre- and post-shift pulmonary function tests, and either methacholine challenge test or bronchodilator challenge at an occupational health clinic. The most frequently cited symptoms were dyspnea (65%), cough (61%), chest tightness (57%), chills (57%), wheezing (30%), and myalgias, arthralgias, and nausea (26%). Thirteen subjects had either a positive methacholine challenge test or a positive response to bronchodilator challenge, making the overall prevalence of airway hyperresponsiveness 38%. The overall prevalence of hypersensitivity pneumonitis-like reactions among line operators in the injection molding process was 27%. This disease outbreak suggests that 1,3-bis(isocyanatomethyl)cyclohexane pre-polymer may cause asthma and hypersensitivity pneumonitis-like reactions. The use of BIC was discontinued 6 months after the first workers developed symptoms.- - - - - - - - - - ranking = 1.5keywords = work (Clic here for more details about this article) |
14/15. Reactive airways dysfunction syndrome due to chlorine: sequential bronchial biopsies and functional assessment.Very little information is available on the acute histopathological bronchial alterations caused by reactive airways dysfunction syndrome (RADS). We had 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 exposure), and also to assess spirometry and bronchial responsiveness to methacholine. A 36 year old worker in a water-filtration plant (nonsmoker) abruptly inhaled high concentrations of chlorine on September 12, 1994. He experienced immediate nasal and throat burning, retrosternal burning and wheezing, and these symptoms persisted during and after the workshift. Two days later, he complained of retrosternal burning, dyspnoea and wheezing. Inspiratory wheezing was documented. His forced expiratory volume in one second (FEV1) was 66% of predicted and the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) was slightly abnormal (2.5 mg.mL-1). On the following day, the patient underwent bronchial biopsies, which showed almost complete replacement of the epithelium by a fibrinohaemorhagic exsudate. The subject was prescribed inhaled steroids. Fifteen days after the accident, the PC20 was improved to 6 mg.mL-1. Bronchial biopsies showed considerable epithelial desquamation with an inflammatory exudate and swelling of the subepithelial space. Five weeks after the accident, the PC20 was normal (57 mg.mL-1). Inhaled steroids were stopped. Two months after the accident, the PC20 deteriorated to 4 mg.mL-1. Biopsies then showed regeneration of the epithelium by basal cells and there was still a pronounced inflammatory infiltrate. Inhaled steroids were restarted. Three and five months later, the PC20 was normal (24 mg.mL-1). Bronchial biopsies showed a greatly improved epithelium and 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.- - - - - - - - - - ranking = 1keywords = work (Clic here for more details about this article) |
15/15. Occupational asthma due to chromium.We describe a 28-year-old subject employed as a roofer in a construction company since the age of 19, who developed work-related symptoms of a cough, shortness of breath, wheezing, rhinitis and headaches. A description of a usual day at work suggested that the symptoms worsened while he was sawing corrugated fiber cement. Baseline spirometry was normal, and there was a mild bronchial hyperresponsiveness to carbachol. A skin patch test to chromium was negative. A specific inhalation challenge showed a boderline fall in forced expiratory volume in 1 s (FEV1) after exposure to fiber cement dust. Exposure to nebulization of potassium dichromate (K2Cr2O7), at 0.1 mg.ml-1 for 30 min, was followed by an immediate fall by 20% FEV1. Simultaneously, a significant increase in bronchial hyperresponsiveness was demonstrated.- - - - - - - - - - ranking = 1keywords = work (Clic here for more details about this article) |
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