Ethylenediamine

Sensitisation data (human)

Administrative data

Endpoint:

sensitisation data (humans)

Type of information:

experimental study

Adequacy of study:

supporting study

Study period:

1982 or before

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

other: Well reported study

Data source

Reference

Reference Type:

publication

Title:

Piperazine-Induced Occupational Asthma

Author:

Hagmar L, Bellander T, Bergoo B, Simonsson BG

Year:

1982

Bibliographic source:

J. Occup. Med. 24(3): 193-197

Materials and methods

Type of sensitisation studied:

respiratory

Study type:

survey

Test guideline

Qualifier:

no guideline followed

Principles of method if other than guideline:

Survey of workers in a chemical factory

GLP compliance:

no

Test material

Test material information

Constituent 1

Reference substance name:

Ethylenediamine

EC Number:

203-468-6

EC Name:

Ethylenediamine

Cas Number:

107-15-3

Molecular formula:

C2H8N2

IUPAC Name:

ethane-1,2-diamine

Constituent 2

Reference substance name:

Piperazine

EC Number:

203-808-3

EC Name:

Piperazine

Cas Number:

110-85-0

Molecular formula:

C4H10N2

IUPAC Name:

piperazine

Method

Type of population:

occupational

Ethical approval:

not specified

Subjects:

- Number of subjects employed in direct production: 131 (Sex: 130 male, 1 female); 38 thought to have asthma were examined
- Number of former employees identified as probably having had asthma: 69 (58 were interviewed)

Route of administration:

inhalation

Results and discussion

Results of examinations:

Of the 131 workers, 15 had experienced asthma, in 7 of these confirmed by medical records. None had a history of asthma or were atopic. Inducing agents were stated (no further information provided) to be piperazine in 13 cases and EDA in 2 cases.
Of the previous 58 workers interviewed, inducing agents were stated to be piperazine in 16 cases, EDA in 1 case, and 2-methyl-3,5-dinitrobenzamide in 1 case. From 13 persons medical records supported the diagnosis.
One subject exposed to EDA showed aspecific bronchial hyperreactivity (metacholine); one subject exposed to EDA (not known whether this was the same person) had increased level of serum IgE.
18% of the non-asthmatics and 45% of the workers with asthma had chronic bronchitis.
83% of the non-asthmatics and 91% of the asthmatic were smokers or ex-smokers.
Bronchial provocation tests were carried out with piperazine, not with EDA.

Applicant's summary and conclusion

Conclusions:

In this study current workers and former workers were assessed on occupational asthma. Of the 33 asthmatic workers, 29 were assigned to piperazine exposure, 3 to EDA, and one to another chemical. However, it was not clear on what basis these 3 cases had been assigned to EDA exposure, and no spceific bronchial hyperreactivity with EDA was performed.

Executive summary:

Asthmatic reactions were studied among 131 factory workers who currently handled amines and other chemicals; 58 former employees (identified as probably having had asthma) were interviewed by phone. Among present employees, 15 cases of asthma were found associated with occupational exposure to chemicals, 13 were assigned to piperazine exposure, and 2 to EDA. Among former employees there were 18 cases noted; 16 assigned to piperazine, 1 to EDA, and 1 to another chemical. No information was provided on what basis the inducing agent was judged to be piperazine or EDA. The asthma in EDA was of the late type (present worker) or dual type (the other present worker and one former worker); immediate reactions alone were not seen.