Formaldehyde

Additional toxicological data

Administrative data

Endpoint:

additional toxicological information

Type of information:

experimental study

Adequacy of study:

supporting study

Reliability:

2 (reliable with restrictions)

Rationale for reliability incl. deficiencies:

study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference

Reference Type:

review article or handbook

Title:

Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol

Author:

IARC

Year:

2006

Bibliographic source:

Lyon, International Agency for Research on Cancer, IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man, Vol. 88, pp 39-325

Materials and methods

Test material

Test material information

Constituent 1

Reference substance name:

Formaldehyde

EC Number:

200-001-8

EC Name:

Formaldehyde

Cas Number:

50-00-0

Molecular formula:

CH2O

IUPAC Name:

formaldehyde

Details on test material:

- Name of test material (as cited in study report): formaldehyde

Applicant's summary and conclusion

Conclusions:

Genotoxicty and cytoxicity play important roles in the carcinogenesis of the test substance in nasal tissues.

Executive summary:

The following summary and evaluation of the mode of action is given in IARC (2006), page 279 -280:

"The current data indicate that both genotoxicty and cytoxicity play important roles in the carcinogenesis of formaldehyde in nasal tissues. DNA–protein cross-links provide a potentially useful marker of genotoxicity. The concentration–response curve for the formation of DNA–protein cross-links is bi-phasic, and the slope increases at formaldehyde concentrations of about 2–3 ppm [2.4–3.7 mg/m3] in Fischer 344 rats. Similar results are found in rhesus monkeys, although the dose–response curve is less well defined in this species. Cell proliferation, which appears to amplify greatly the genotoxic effects of formaldehyde, is increased considerably at concentrations of formaldehyde of about 6 ppm [7.4 mg/m3], and results in a marked increase in the occurrence of malignant lesions in the nasal passages of rats at concentrations above this level. Several possible mechanisms were considered for the induction of human leukaemia, such as clastogenic damage to circulatory stem cells. The Working Group was not aware of any good rodent models that simulate the occurrence of acute myeloid leukaemia in humans. Therefore, on the basis of the data available at this time, it was not possible to identify a mechanism for the induction of myeloid leukaemia in humans."