Chlorine dioxide

Sensitisation data (human)

Administrative data

Endpoint:

sensitisation data (humans)

Type of information:

experimental study

Adequacy of study:

other information

Study period:

No data

Reliability:

other: Not applicable

Cross-reference

Cross-reference 1

Reason / purpose for cross-reference:

reference to same study

Cross-reference 2

Reason / purpose for cross-reference:

reference to other study

Data source

Reference

Reference Type:

publication

Title:

Nasal pathology and ultrastructure in patients with chronic airway inflammation (RADS and RUDS) following an irritant exposure

Author:

Meggs, W.J.; Elsheik, T.; Metzger, W.J.; Albernaz, M. and Bloch, R.M.

Year:

1996

Bibliographic source:

Clinical Toxicology, 34(4):383–396

Materials and methods

Type of sensitisation studied:

respiratory

Study type:

case report

Test guideline

Qualifier:

no guideline followed

Principles of method if other than guideline:

Biopsies were taken of the nasal mucosa in patients with reactive upper airway dysfunction syndrome and in some cases reactive airways syndrome developing in temporal association with a chlorine dioxide exposure, to see if a histological basis for the persistent rhinitis and sensitivity to chemical irritants could be determined.

GLP compliance:

not specified

Test material

Test material information

Constituent 1

Reference substance name:

Chlorine dioxide

EC Number:

233-162-8

EC Name:

Chlorine dioxide

Cas Number:

10049-04-4

Molecular formula:

ClO2

IUPAC Name:

Chlorine Dioxide

Details on test material:

No data

Method

Type of population:

occupational

Subjects:

The clinical evaluation was performed on the patients 5 years after a documented occupational exposure to chlorine dioxide associated with a leak in a pipe of a water purification system.

- Number of subjects exposed: 12 female, 1 male plus control subjects for biopsies
- Age: Mean age 48 years, range 30 to 61
- Known diseases: Healthy

Clinical history:

No data

Controls:

No data

Route of administration:

inhalation

Details on study design:

Examinations: Nasal biopsies were performed by otolaryngologists under local anaesthesia. A biopsy forcep was used to remove tissue from the inferior aspect of the right middle nasal turbinate. Specimens were fixed and stained using haematoxylin and eosin, Giemsa stain or periodic acid Schiff stain. Immunohistochemical studies were performed on paraffin fixed tissue by the use of Avidin-Biotin complex technique. Stains for S-100 protein, substance P VIP, L-26 (a marker for B-lymphocytes) and MT-1 (a marker for T-lymphocytes) were performed. Some biopsies were stained for neutral endopeptidase (NEP).

Results and discussion

Results of examinations:

Clinical signs: Nasal examination was abnormal in all patients and included injection, telangectasia, paleness, cobblestoning, edema and thick mucous. Depression, fatigue and dyspnea were reported.

Examinations: Nasal biopsies obtained from symptomatic subjects showed a spectrum of changes ranging from congestion and edema and mild inflammation to severe inflammation. In the majority of cases there was chronic inflammation with lymphocytes and plasma cells present within the lamina propria. Occasionally lymphocytes infiltrated the overlying mucosa. Reactive epithelial changes were seen in the overlying mucosa and submucosal glands. T-lmphocytes comprised the predominant lymphoid cell population. Nonspecific nuclear staining of mucosal and acinar epithelial cells. Nerve fibres were present mainly in the lamina proparia, mostly concentrated around blood vessels. Fibrosis was seen in two patients with mild inflammation.

Any other information on results incl. tables

No data

Applicant's summary and conclusion

Conclusions:

Inflammation ratings of exposed individuals were higher than for the non-exposed individuals. The study suggests a mechanism by which ongoing low level exposures perpetuate airway inflammation after inducing toxic inhalation.

Executive summary:

In a poisonning accident study, 12 female patients and one male were exposed unintentionally by inhalation to Chlorine dioxide.

The clinical evaluation was performed on the patients 5 years after a documented occupational exposure to chlorine dioxide associated with a leak in a pipe of a water purification system.
Biopsies were taken of the nasal mucosa in patients with reactive upper airway dysfunction syndrome and in some cases reactive airways syndrome developing in temporal association with a chlorine dioxide exposure, to see if a histological basis for the persistent rhinitis and sensitivity to chemical irritants could be determined. Biopsies were also taken from control patients.

Nasal examination was abnormal in all patients and included injection, telangectasia, paleness, cobblestoning, edema and thick mucous. Depression, fatigue and dyspnea were reported.

Nasal biopsies obtained from symptomatic subjects showed a spectrum of changes ranging from congestion and edema and mild inflammation to severe inflammation. In the majority of cases there was chronic inlflammation with lymphocytes and plasma cells present within the lamina propria. Reactive epithelial changes were seen in the overlying mucosa and submucosal glands. Nerve fibres were present mainly in the lamina proparia, mostly concentrated around blood vessels.

Inflammation ratings of exposed individuals were higher than for the non-exposed individuals. The study suggests a mechanism by which ongoing low level exposures perpetuate airway inflammation after inducing toxic inhalation.