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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Direct observations: clinical cases, poisoning incidents and other

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Administrative data

direct observations: clinical cases, poisoning incidents and other
Type of information:
migrated information: read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
other information
4 (not assignable)
Rationale for reliability incl. deficiencies:
other: published data, documentation insufficient for assessment

Data source

Referenceopen allclose all

Reference Type:
Acute MCPP intoxication: report of two cases
Meulenbelt J
Bibliographic source:
Human Toxicology 7, 289-292
Reference Type:
secondary source
No information
The Danish Environmental Protection Agency
Bibliographic source:
Mecoprop-P, EU Review Programme on active substances in Plant Protection Products, Scientific Evaluation and Assessment, Draft December 1998 (Volume 3, Annex B, ) and Addendum II July 2002; see also SANCO/3065/99-Final, 2003

Materials and methods

Results and discussion

Any other information on results incl. tables

Cited from Mecoprop-P, EU Review Programme on active substances in Plant Protection Products, Scientific Evaluation and Assessment, The Danish Environmental Protection Agency, Draft December 1998 (Volume 3, Annex B) and Addendum II July 2002:

"In one of the patients a plasma level of mecoprop of 298 mg/l was determined 3-4 hours after ingestion. The plasma level decreased with a t½ of about 17 h.

The major clinical finings were coma, muscle cramps, respiratory failure and arterial hypoxemia. Respiratory depression and hypoxemia were thought partly to be due to CNS depression and partly due to aspiration. Both patients developed serious renal failure, probably caused by rhabdomyolysis. Rhabdomyolysis (elevated serum myoglobin and serum aldose activity) was suggested to be secondary to muscle cramps. Both patients developed hyperkalemia as a result of a combination of renal failure, muscle cell damage and metabolic acidosis. (The hyperkalaemia and the acidosis were treated with infusions of glucose/insulin and sodium bicarbonate). Both patients exhibited serious decrease in arterial blood pressure and developed anaemia and thrombocytopenia (the latter resulting in multiple petechia in one of the patients). Caustic mucous lesions were not observed in any of the patients. Both patients survived."

Applicant's summary and conclusion