Medline ® Abstracts for References 20,45

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

20
TI
Survey of construction workers repeatedly exposed to chlorine over a three to six month period in a pulpmill: II. Follow up of affected workers by questionnaire, spirometry, and assessment of bronchial responsiveness 18 to 24 months after exposure ended.
AU
Bhérer L, Cushman R, Courteau JP, Quévillon M, CôtéG, Bourbeau J, L'Archevêque J, Cartier A, Malo JL
SO
Occup Environ Med. 1994;51(4):225.
 
OBJECTIVE: The aim was to determine the prevalence of persistent respiratory symptoms and bronchial hyper-responsiveness due to reactive airways dysfunction syndrome in a population of construction workers at moderate to high risk of developing the syndrome, at an interval of 18 to 24 months after multiple exposures to chlorine gas during renovations to a pulp and paper mill.
DESIGN AND PARTICIPANTS: 71 of 289 exposed workers (25%) were identified on the basis of an exposure and the onset of respiratory symptoms shortly after this event (moderate to high risk). A standardised respiratory questionnaire was first presented, followed by spirometry and a methacholine inhalation test on those whose questionnaire suggested the persistence of respiratory symptoms.
RESULTS: 64 of 71 (90%) subjects completed the respiratory questionnaire at the time of the follow up. The questionnaire suggested a persistence of respiratory symptomsin 58 of the 64 workers (91%). Of the 58 subjects, 51 underwent spirometry and assessment of bronchial responsiveness. All of them used bronchodilators as required (not regularly) and four required inhaled anti-inflammatory preparations. Sixteen had bronchial obstruction (forced expiratory volume in one second) (FEV1<80% predicted) and 29 showed significant bronchial hyper-responsiveness.
CONCLUSION: Of the subjects (n = 71) who were at moderate to high risk of developing reactive airways dysfunction syndrome after being exposed to chlorine and were seen 18 to 24 months after exposure ended, 58 (82%) still had respiratory symptoms, 16 (23%) had evidence of bronchial obstruction, and 29 (41%) had bronchial hyper-responsiveness.
AD
Outaouais Community Health Department (DSC), Hull, Quebec, Canada.
PMID
45
TI
RADS and RUDS--the toxic induction of asthma and rhinitis.
AU
Meggs WJ
SO
J Toxicol Clin Toxicol. 1994;32(5):487.
 
Inhalation exposures can produce asthma and rhinitis by several mechanisms. Sensitization with the production of IgE specific for a substance can lead to symptoms on reexposure via mast cell degranulation and the release of inflammatory mediators. Some substances, known as environmental adjuvants, enhance the immune response to concomitant exposures with the environmental adjuvant. Respiratory irritants can lead to asthma and rhinitis through interaction with chemical irritant receptors in the airway, leading to release of substance P from sensory nerves and neurogenic inflammation. The reactive airways dysfunction syndrome is a chronic asthma-like syndrome resulting from a single acute exposure to a respiratory irritant, while the reactive upper-airways dysfunction syndrome is chronic rhinitis stemming from an irritant exposure. The dysregulation of neurogenic inflammation by chemical exposures may be an important mechanism in the toxic induction of reactive airways dysfunction syndrome and reactive upper-airways dysfunction syndrome and may play a role in understanding the sick building syndrome and the multiple chemical sensitivity syndrome.
AD
East Carolina University School of Medicine, Greenville, North Carolina.
PMID