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Medline ® Abstracts for References 41,43,44,57-60

of 'Reactive airways dysfunction syndrome and irritant-induced asthma'

41
TI
Increased rates of asthma among World Trade Center disaster responders.
AU
Kim H, Herbert R, Landrigan P, Markowitz SB, Moline JM, Savitz DA, Todd AC, Udasin IG, Wisnivesky JP
SO
Am J Ind Med. 2012 Jan;55(1):44-53. Epub 2011 Nov 8.
 
BACKGROUND: Studies have documented high rates of asthma symptoms among responders to the World Trade Center (WTC) disaster. However, whether there are increased rates of asthma among responders compared to the general population is unknown.
METHODS: The study population consisted of a prospective cohort of 20,834 responders participating in the WTC Medical Monitoring and Treatment Program between July 2002 and December 2007. We calculated prevalence and standardized morbidity ratios (SMRs) of lifetime asthma and 12-month asthma (defined as≥1 attacks in the prior 12 months) among WTC responders. The comparison population consisted of>200,000 adults who completed the National Health Interview Survey in 2000 (for pre-9/11 comparisons) and between 2002 and 2007 (for post-9/11 comparisons).
RESULTS: WTC responders were on average 43±9 years old, 86% male, 59% white, and 42% had an occupation in protective services. The lifetime prevalence of asthma in the general population was relatively constant at about 10% from 2000 to 2007. However, among WTC responders, lifetime prevalence increased from 3% in 2000, to 13% in 2002, and 19% in 2007. The age-adjusted overall SMR for lifetime asthma among WTC responders was 1.8 (95% CI: 1.8-1.9) for men and 2.0 (95% CI: 1.9-2.1) for women. Twelve-month asthma was also more frequent among WTC responders compared to the general population (SMR 2.4, 95% CI: 2.2-2.5) for men and 2.2 (95% CI: 2.0-2.5) for women.
CONCLUSIONS: WTC responders are at an increased risk of asthma as measured by lifetime prevalence or active disease.
AD
Department of Population Health, Hofstra North Shore-LIJ School of Medicine, New York, New York, USA.
PMID
43
TI
Reactive airways dysfunction syndrome induced by exposure to a mixture containing isocyanate: functional and histopathologic behaviour.
AU
Lemière C, Malo JL, Boulet LP, Boutet M
SO
Allergy. 1996;51(4):262.
 
A 31-year-old machinist experienced acute symptoms of rhinoconjunctivitis, coughing, shortness of breath, and wheezing after sudden exposure to fumes containing isocyanates and solvents. Lung function tests carried out 11 days after the event showed reduced flow rates. Forty days after the acute inhalational injury, expiratory flows improved, and the PC20 was 0.8 mg/ml, showing moderate bronchial hyperresponsiveness. Six days later, the subject underwent bronchoscopy. Bronchial biopsies showed a marked loss of epithelial cells, severe subepithelial oedema, and inflammatory cells infiltrate (mainly lymphocytes). The subject was given inhaled steroids. The PC20 was back to normal 42 days later. Bronchial biopsies then showed incomplete regeneration of the epithelial layer with few ciliated cells and persistence of inflammation (lymphocyte infiltrate) in epithelia and connective tissue. We conclude that irritant exposure to a mixture of isocyanates and solvents can cause occupational asthma without a latency period, i.e., reactive airways dysfunction syndrome.
AD
Sacré-Coeur Hospital, Quebec City, Canada.
PMID
44
TI
Reactive airways dysfunction syndrome due to chlorine: sequential bronchial biopsies and functional assessment.
AU
Lemière C, Malo JL, Boutet M
SO
Eur Respir J. 1997;10(1):241.
 
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.
AD
Sacré-Coeur Hospital, Montreal, Québec, Canada.
PMID
57
TI
Survey of construction workers repeatedly exposed to chlorine over a three to six month period in a pulpmill: I. Exposure and symptomatology.
AU
Courteau JP, Cushman R, Bouchard F, Quévillon M, Chartrand A, Bhérer L
SO
Occup Environ Med. 1994;51(4):219.
 
OBJECTIVE: The admission to hospital of three construction workers with acute respiratory distress caused by inhalation of chlorine gas prompted the inspection of a building site located in a kraft pulpmill. The accidental emissions had taken place in the bleach plant and the construction workers assigned there were surveyed to uncover possible large scale health effects.
DESIGN AND PARTICIPANTS: A questionnaire was presented to 281 workers (participation rate = 97%); 257 workers reported an average of 24 exposure episodes to chlorine and derivatives over a three to six month period. The air monitoring data available from the pulpmill's industrial hygienist were not useful in linking specific events reported by the workers to environmental conditions in the bleach plant.
RESULTS: Over 60% of the workers described a characteristic flu like syndrome that lasted for an average of 11 days and was exacerbated by new bouts of exposure. Irritation of the throat (78%) and eyes (77%), cough (67%), and headache (63%) were the most often reported symptoms. Shortness of breath was reported by 54% of the participants and was not associated with age, smoking state, or history of asthma or chronic bronchitis. First aid self referral was associated with significantly greater reporting of most symptoms, including dyspnoea and cough. A significantly greater proportion of workers in the dyspnoea group had gone at least once for first aid care after a gassing incident (64% as opposed to 48%, p = 0.008). Throat irritation and cough persisted for mean intervals of eight and 11 days respectively. A flu like syndrome lasted for an average of 20 days. Seventy one subjects were considered to be a moderate to high risk of having persisting respiratory symptoms.
CONCLUSION: Throat and eye irritation as well as cough and flu like symptoms are frequent occurrences after repeated accidental inhalation of chlorine. Subjects who consulted first aid care stations after a gassing incident are more likely to have persisting dyspnoea.
AD
Outaouais Community Health Department (DSC), Hull, Quebec, Canada.
PMID
58
TI
Persistent asthma following accidental exposure to formaldehyde.
AU
Vandenplas O, Fievez P, Delwiche JP, Boulanger J, Thimpont J
SO
Allergy. 2004;59(1):115.
 
AD
Service de Pneumologie Cliniques universitaires UCL de Mont-Godinne, B-5530 Yvoir, Belgium. olivier.vandenplas@pneu.ucl.ac.be
PMID
59
TI
Effects of accidental chlorine inhalation on pulmonary function.
AU
Charan NB, Lakshminarayan S, Myers GC, Smith DD
SO
West J Med. 1985;143(3):333.
 
In an industrial accident, 19 previously healthy workers were briefly exposed to high concentrations of chlorine gas. Pulmonary function tests were done at intervals for about two years but complete follow-up data were available in only 11 subjects. Immediately following the exposure, airway obstruction was detected in 10 of 19 patients; 700 days later this was found in only 3 of 11 patients. Two of these three patients had a history of smoking, however. The mean residual volume was 141% +/- 97 (mean +/- standard error of the mean) on day 1. In subsequent follow-up studies, the residual volume progressively fell in all patients, and 700 days later the mean residual volume was 90% +/- 5. In 5 of the 19 subjects, all pulmonary function test results were within normal limits on day 1. Apparently in some subjects acute exposure to chlorine gas may cause immediate changes in the lung functions, but these changes gradually resolve. Because of the small number of patients in our series, however, the long-term effects of chlorine are less apparent.
AD
PMID
60
 
 
Global Strategy for Asthma Management and Prevention, Global Initiative for Asthma (GINA) 2015. www.ginasthma.org (Accessed on January 26, 2016).
 
no abstract available