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

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

41
TI
Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models.
AU
White CW, Martin JG
SO
Proc Am Thorac Soc. 2010;7(4):257.
 
Humans can come into contact with chlorine gas during short-term, high-level exposures due to traffic or rail accidents, spills, or other disasters. By contrast, workplace and public (swimming pools, etc.) exposures are more frequently long-term, low-level exposures, occasionally punctuated by unintentional transient increases. Acute exposures can result in symptoms of acute airway obstruction including wheezing, cough, chest tightness, and/or dyspnea. These findings are fairly nonspecific, and might be present after exposures to a number of inhaled chemical irritants. Clinical signs, including hypoxemia, wheezes, rales, and/or abnormal chest radiographs may be present. More severely affected individuals may suffer acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). Up to 1% of exposed individuals die. Humidified oxygen and inhaled beta-adrenergic agents are appropriate therapies for victims with respiratory symptoms while assessments are underway. Inhaled bicarbonate and systemic or inhaled glucocorticoids also have been reported anecdotally to be beneficial. Chronic sequelae may include increased airways reactivity, which tends to diminish over time. Airways hyperreactivity may be more of a problem among those survivors that are older, have smoked, and/or have pre-existing chronic lung disease. Individuals suffering from irritant-induced asthma (IIA) due to workplace exposures to chlorine also tend to have similar characteristics, such as airways hyperresponsiveness to methacholine, and to be older and to have smoked. Other workplace studies, however, have indicated that workers exposed to chlorine dioxide/sulfur dioxide have tended to have increased risk for chronic bronchitis and/or recurrent wheezing attacks (one or more episodes) but not asthma, while those exposed to ozone have a greater incidence of asthma. Specific biomarkers for acute and chronic exposures to chlorine gas are currently lacking. Animal models for chlorine gas inhalation have demonstrated evidence of oxidative injury and inflammation. Early epithelial injury, airways hyperresponsiveness, and airway remodeling, likely diminishing over time, have been shown. As in humans, ALI/ARDS can occur, becoming more likely when the upper airways are bypassed. Inhalation models of chlorine toxicity provide unique opportunities for testing potential pharmacologic rescue agents.
AD
Pediatrics, National Jewish Health, 1400 Jackson St., Denver, CO 80206, USA. whitec@njc.org
PMID
43
TI
Long-term respiratory symptoms in World Trade Center responders.
AU
Mauer MP, Cummings KR, Hoen R
SO
Occup Med (Lond). 2010;60(2):145.
 
BACKGROUND: New York State (NYS) employees who responded to the World Trade Center (WTC) disaster on or after 11 September 2001 potentially experienced exposures that might have caused persistent respiratory effects. NYS responders represent a more moderately exposed population than typical first responders.
AIMS: To assess whether NYS employees who were WTC responders were more likely than controls to report lower respiratory symptoms (LRS) or a diagnosis of asthma 5 years post-9/11. Persistence and severity of symptoms were also evaluated.
METHODS: Participants were initially mailed self-administered questionnaires (initial, Year 1, Year 2) and then completed a telephone interview in Year 3. Data were analysed using Poisson's regression models.
RESULTS: WTC exposure was associated with LRS, including cough symptoms suggestive of chronic bronchitis, 5 years post-9/11. When exposure was characterized using an exposure assessment method, the magnitude of effect was greater in those withexposure scores above the mean. WTC exposure was associated with persistence of LRS over the 3 year study period. Results also suggest that participants with the highest exposures were more likely to experience increased severity of their asthma condition and/or LRS.
CONCLUSIONS: Our findings suggest that even in a moderately exposed responder population, lower respiratory effects were a persistent problem 5 years post-9/11, indicating that some WTC responders require ongoing monitoring.
AD
Bureau of Occupational Health, Center for Environmental Health, New York State Department of Health, Troy, NY 12180, USA. mpm08@health.state.ny.us
PMID
44
TI
Chronic rhinitis in workers at risk of reactive airways dysfunction syndrome due to exposure to chlorine.
AU
Leroyer C, Malo JL, Girard D, Dufour JG, Gautrin D
SO
Occup Environ Med. 1999;56(5):334.
 
BACKGROUND: To assess the frequency of chronic upper airways symptoms and to relate the presence of these symptoms to accidental exposure to chlorine and changes in lower airways symptoms, airway function, and bronchial responsiveness in a cohort of workers at risk of sporadic occupational exposure to high concentrations of chlorine.
METHODS: Data were collected on symptom assessment, spirometry, and methacholine challenge tests from 211 workers seen twice at a 2 year interval (1992-4).
RESULTS: The proportion of workers reporting chronic rhinitis was 46.9% in 1992 and 42.2% in 1994. Chronic rhinitis reported in 1994 was significantly associated with acute exposure to chlorine (self reports, p = 0.02; first aid reports, p = 0.001). In a multivariate logistic regression analysis the presence of reported accidents at the first aid unit (one accident, odds ratio (OR) 3.1, 95% confidence interval (95% CI) 1.3 to 7.5; two or more accidents, OR 6.2, 1.1 to 35.8) and of personal atopy (OR 5.5, 2.2 to 10.8) were significant predictors of chronic rhinitis in 1994. Chronic lower airways symptoms were more frequent in 1994 among workers reporting chronic rhinitis on both assessments than in others (p = 0.03) and changes in bronchial responsiveness were more pronounced in those with persistent rhinitis (p = 0.09).
CONCLUSIONS: These results suggest that persistent nasal symptoms in workers at risk of reactive airways dysfunction syndrome could be a useful marker of lower respiratory tract abnormalities.
AD
Department of Chest Medicine, Hôpital du Sacré-Coeur, Montreal, Canada.
PMID
57
 
 
Global Strategy for Asthma Management and Prevention, Global Initiative for Asthma (GINA) 2012. Full text is available online at: http://www.ginasthma.com (Accessed on March 12, 2013).
 
no abstract available
58
TI
Bronchial hyperresponsiveness can improve while spirometry plateaus two to three years after repeated exposure to chlorine causing respiratory symptoms.
AU
Malo JL, Cartier A, Boulet LP, L'Archeveque J, Saint-Denis F, Bherer L, Courteau JP
SO
Am J Respir Crit Care Med. 1994;150(4):1142.
 
Repeated exposure to chlorine in pulp mills and paper can induce persistent asthma-like symptoms such as bronchial hyperresponsiveness and variable changes in airway caliber. The long-term time course of bronchial hyperresponsiveness has not been examined. We studied 20 of 29 subjects (69% participation rate) who demonstrated bronchial hyperresponsiveness to methacholine when they were first assessed, 18 to 24 mo after repeatedly inhaling "puffs" of high concentrations of chlorine in a paper mill over a 3-mo period. Each subject answered a respiratory questionnaire and underwent spirometry and a methacholine inhalation test 12 mo after the initial survey, 30 to 36 mo after the chlorine inhalations. Three subjects required inhaled steroids at the time of the initial survey and three at the time of the second, including two who carried on using these preparations. Only one subject changed smoking habits. There were no significant overall changes in FEV1 on the two occasions, nine subjects having a FEV1<80% on the first occasion and eight on the second. Six of the 18 subjects (33%) who underwent a methacholine inhalation test on both occasions had significantly improved PC20 results, including five for whom the PC20 value was within the normal range. All six subjects had normal FEV1 values on both assessments. Although changes in spirometry induced by repeated exposure to chlorine seem to persist, bronchial hyperresponsiveness can improve significantly in those with normal airway caliber. This suggests that less pronounced bronchial alterations induced by repeated exposures to chlorine may be reversible.
AD
Department of Chest Medicine, Hôpital du Sacré-Coeur, Montreal, Hôpital Laval, Quebec City, Canada.
PMID
59
TI
Lung function after acute chlorine exposure.
AU
Jones RN, Hughes JM, Glindmeyer H, Weill H
SO
Am Rev Respir Dis. 1986;134(6):1190.
 
Chlorine gas, spreading from a train derailment, caused the deaths of 8 persons and the hospitalization of 23 with sublethal respiratory injuries. Twenty-five others had at least one sign of lower respiratory abnormality but were not hospitalized. One hundred thirteen who were examined for gas effects in the forty-eight hours after exposure, including 20 of 23 of those hospitalized and 21 of 25 of those not hospitalized but with respiratory abnormality, participated in follow-up studies. Probability of admission to hospital was related to distance from the spill, but by 3 wk after exposure there was no detectable difference in lung function relating to distance or apparent severity of injury. In 60 adults tested multiple times over the following 6 yr, longitudinal change in lung function showed expected differences related to smoking but none related to distance or severity of injury. The average annual change in FEV was -34 ml/yr in current smokers and -18 ml/yr in ex and never-smokers. The lack of a discernible chlorine effect in this cohort accords with the findings in most previous studies. Without pre-exposure measurements, a single, lasting reduction in lung function cannot be excluded, but there is no evidence for a persisting abnormal rate of decline.
AD
PMID
60
TI
The diversity of the effects of sulfur mustard gas inhalation on respiratory system 10 years after a single, heavy exposure: analysis of 197 cases.
AU
Emad A, Rezaian GR
SO
Chest. 1997;112(3):734.
 
OBJECTIVE: To find out the late pulmonary sequelae of sulfur mustard gas inhalation in 197 veterans, 10 years after their exposure.
DESIGN: Cross-sectional clinical study.
SETTING: University hospital.
PATIENTS: One hundred ninety-seven veterans with a single, heavy exposure to sulfur mustard gas in 1986 and 86 nonexposed veterans as their control group.
INTERVENTIONS: Pulmonary function tests, carbon monoxide diffusion capacity, bronchoscopy, and high-resolution CT of the chest were performed in all patients. Transbronchial lung biopsy was done in 24 suspected cases of pulmonary fibrosis.
RESULTS: Asthma was diagnosed in 21 (10.65%), chronic bronchitis in 116 (58.88%), bronchiectasis in 17 (8.62%), airway narrowing due tosearing or granulation tissue in 19 (9.64%), and pulmonary fibrosis in 24 (12.18%) cases. None of these were found among the control group except for a single case of chronic bronchitis.
CONCLUSION: Although the respiratory symptoms of an acute sulfur mustard gas inhalation are usually transient and nonspecific, it can lead to the development of a series of chronic destructive pulmonary sequelae in such cases.
AD
Department of Internal Medicine, Shiraz University of Medical Sciences, Iran.
PMID