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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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

Specific investigations: other studies

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Administrative data

Link to relevant study record(s)

Description of key information

Additional information

Endocrine disrupting properties

Following evaluation of each of the relevant studies individually and a subsequent weight of evidence evaluation, it can be concluded that the test substance cannot be considered an endocrine disrupter as defined by WHO/IPCS (2002) (Charlton A, 2015).

A publication by Rotroff et al (2014) provides a novel method for combining in vitro concentration response data from multiple assays and, when applied to a large set of oestrogen receptor signalling data, accurately predicted estrogenic responses and demonstrated its utility for chemical prioritization challenges. The test substance exerted no response in any assay, indicating no evidence of a direct effect on the endocrine system.

One important mode of action leading to toxicity is endocrine disruption, and the U.S. EPA’s Endocrine Disruptor Screening Program (EDSP) has been charged with screening pesticide chemicals and environmental contaminants for their potential to affect the endocrine systems of humans and wildlife. The test substance is not highlighted as an EDSP chemical (Reif, 2010).

A publication of Yéboué-Kouamé et al. (2010) describes the case study of a 37 year old farmer who had been exposed to a pesticide containing 106 g lambda-cyhalothrin and 141 g test substance presented with lesions indicative of Stevens-Johnson syndrome. It is not possible to exclude a link between this case of Stevens-Johnson syndrome and insecticide exposure.

Testis toxicity in the dog and rat

The test substance shows no evidence of direct interaction with the endocrine system or indirect interaction with the endocrine system through disruption of the HPT axis (Charlton A, 2016).