Persistent Asthma After Inhalation of a Mixture of Sodium Hypochlorite and Hydrochloric Acid

Deschamps, D.; Stolzmann, Paul; Rosenberg, Nicole; Baud, Frédéric J.; Gervais, Pierre

doi:10.1378/chest.105.6.1895

Cited by 96 publications

(63 citation statements)

References 8 publications

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“…BROOKS et al [1] first described RADS and reported the presence of bronchial wall inflammation (mostly lymphocytes and plasma cells with no eosinophils), desquamation of respiratory epithelium in one biopsy and goblet cell hyperplasia in another. DESCHAMPS et al [9,20] performed biopsies several months after exposure to sodium hypochlorite and hydrochloric acid. They reported similar findings: epithelial destruction associated with a mild inflammatory reaction (predominantly lymphocytes with no eosinophils) and subepithelial fibrosis without thickening of the basement membrane.…”

Section: Discussionmentioning

confidence: 99%

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Demnati¹,

Fraser²,

Ghezzo³

et al. 1998

Eur Respir J

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Reactive airways dysfunction syndrome (RADS) is an asthma-like condition that follows exposure to very high concentrations of an irritant material. We assessed the time-course of pathophysiological alterations in a model of RADS. Sprague-Dawley rats were exposed to 1,500 parts per million (ppm) of chlorine for 5 min. Lung resistance (RL), responsiveness to inhaled methacholine (MCh), the airway epithelium and bronchoalveolar lavage (BAL) were assessed over a 3 month period after exposure. RL increased significantly up to 3 days after exposure, reaching a maximal change of 110+/-16% from baseline. There was a significant decrease in the concentration of MCh required to increase RL by 0.20 cmH2O x mL(-1) x s from days 1-7 after exposure. In some rats, MCh hyperresponsiveness and RL changes persisted after exposure for as long as 1 and 3 months, respectively. Histological evaluation with morphometric evaluation revealed epithelial flattening, necrosis, increase in smooth muscle mass and evidence of epithelial regeneration. BAL showed an increased number of neutrophils. The timing of maximal abnormality in the appearance of the epithelium (days 1-3) corresponded to that of the maximal functional changes. Acute high chlorine exposure results in functional and pathological abnormalities that resolve in the majority of animals after a variable period; however, these changes can persist in some animals. Functional abnormalities in the initial stages may be related to airway epithelial damage.

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Section: Discussionmentioning

confidence: 99%

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Demnati¹,

Fraser²,

Ghezzo³

et al. 1998

Eur Respir J

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“…Exposure of the general population may occur through inappropriate mixing of household cleaning agents, such as hypochlorite (bleach) and acids (cleaners) [4]. Following acute Cl 2 inhalation, pulmonary oedema may manifest itself clinically by the presence of blood-tinged frothy fluid in the airways.…”

mentioning

confidence: 99%

Chlorine gas induced acute lung injury in isolated rabbit lung

Ménaouar¹,

Anglade²,

Baussand³

et al. 1997

Eur Respir J

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This study was designed to investigate the pathogenesis of chlorine gas (Cl 2 ) induced acute lung injury and oedema.Isolated blood-perfused rabbit lungs were ventilated either with air (n=7) or air plus 500 parts per million (ppm) of Cl 2 (n=7) for 10 min.Capillary pressure, measured by analysing the pressure/time transients of pulmonary arterial, venous and double (both arterial and venous) occlusions, was unchanged in both groups. In Cl 2 -exposed lungs, the fluid filtration rate increased from -0.228±0.25 to 1.823±1.23 mL·min -1 ·100 g -1 (p<0.001) and the filtration coefficient increased from 0.091±0.01 to 0.259±0.07 mL·min -1 ·cmH 2 O -1 ·100 g -1 (p<0.001). No changes were observed in the control lungs. The extravascular lung water/blood-free dry weight ratio was 8.6±1.6 in the Cl 2 group and 4.0±0.5 in the control group (p<0.001), confirming that the increase in lung weight was related to accumulation of extravascular fluid.Although the alveolar flooding by oedema is explained, in part, by the Cl 2 -induced epithelial injury, our results suggest that Cl 2 exposure induces acute lung injury and oedema due to an increased microvascular permeability.

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“…There are earlier case reports of RADS having been caused by exposure to hydrofluoric acid and thermal degradation of fluorocarbons [9][10][11] , as well as hydrobromic acid 12) . In addition, several cases of RADS have been attributed to chlorine or chlorine-containing chemicals 13,14) . However, there are no previous reports of RADS caused by reaction products of iodine.…”

Section: Discussionmentioning

confidence: 99%

Reactive Airway Dysfunction Syndrome (RADS) in a Chemistry Teacher Induced by Fumes of Mixed Iodine Compounds

Hannu

Riihimäki²,

Piirilä

2009

Ind Health

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Persistent Asthma After Inhalation of a Mixture of Sodium Hypochlorite and Hydrochloric Acid

Cited by 96 publications

References 8 publications

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Time-course of functional and pathological changes after a single high acute inhalation of chlorine in rats

Chlorine gas induced acute lung injury in isolated rabbit lung

Reactive Airway Dysfunction Syndrome (RADS) in a Chemistry Teacher Induced by Fumes of Mixed Iodine Compounds

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