Registration Dossier

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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Exposure related observations in humans: other data

Administrative data

exposure-related observations in humans: other data
Adequacy of study:
other information

Data source

Reference Type:
Bone marrow injury in lithographers exposed to glycol ethers and organic solvents.
Cullen, M.R. et al.
Bibliographic source:
Arch. Environ. Health 38, 347-354.

Materials and methods

Type of study / information:
Type of experience: Human

Test material

Constituent 1
Chemical structure
Reference substance name:
EC Number:
EC Name:
Cas Number:
Molecular formula:

Results and discussion

Applicant's summary and conclusion

Executive summary:

Three out of 7 lithographers using DPGME, ethylene glycol monoethyl ether, and a range of aliphatic, aromatic and halogenated hydrocarbons for offset and ultraviolet-cured multicoloured printing, showed normal peripheral blood parameters; however, bone marrow specimens showed stromal injury. It is unlikely that DPGME caused the observed effects. DPGME was present along with substituted benzenes, chlorinated solvents, n-propanol, and EGEE in workplace solutions. Suspicion of DPGME as a causal agent came from personal, area air samples and wipe samples. The most intense exposure to DPGME was from an ultraviolet curing wash and air sampling revealed 0.6 to 6.43 ppm air concentrations.
The authors of this article provide limited and inconclusive data that DPGME may be the cause of bone marrow injury in a small group of exposed lithographers. Because of the small group studied, it is difficult to causally link occupational exposure with the marrow lesions. This is further confounded by a lack of published data regarding the prevalence of such marrow injury parameters in workers or the general population. Besides the hypothesis that DPGME may play a role in the observed injury, the authors also suggest that it is plausible that marrow changes represent the result of ubiquitous insults from infectious agents, drugs, alcohol, or other environmental agents or unknown factors.
The most convincing evidence that DPGME is not responsible for such effects comes from a lack of recorded marrow effects in other subchronically and chronically tested PGE's (PGME, PGtBE). This is in contrast to EGME. DPGME itself when applied dermally up to 10 g/kg for 90 days produced no hematologicaleffects even though mortality was high at the 10 g/kg level.