This alarmist article is based upon a study published in 2012. If you read what they did, you wonder how we get from point A to point B. 

> We conducted these assays in cultured cerebellar neurons from neonatal rats. Primary neonatal cerebellar neurons have been used as a suitable model to evaluate developmental neurotoxicity. The overall aim of this study was to determine whether these two neonicotinoids exert effects similar to those of nicotine on cerebellar neurons from neonatal rats.

EFSA took this and stated:

> What are EFSA’s main conclusions on whether acetamiprid and imidacloprid exhibit DNT effects? The PPR Panel concludes that both acetamiprid and imidacloprid show some indications of DNT potential. Acetamiprid and imidacloprid may adversely affect the development of neurons – the building blocks of the nervous system and the cells that carry messages from the brain to other parts of the body. Consequently, the PPR Panel concluded that exposure to the two neonicotinoids could have the potential to affect some brain functions such as learning and memory. As a result of its review, EFSA proposes the following changes: For aceptamiprid – the current ADI and AOEL of 0.07 mg/kg bw per day and the ARfD of 0.1 mg/kg bw should be lowered to 0.025 mg/kg bw (per day)

Based on no tests on either food nor humans, they basically say the current levels are too high and should be lowered. No mention is ever made as to what the levels usually are, how they correlate to application, etc. In other words, how much cabbage do I have to eat to reach the maximum safe level? And where is the evidence that effect on baby rat neurons grown in a petri dish even remotely relates to an effect in human beings?

Pete

             ***********************************************
The BEE-L mailing list is powered by L-Soft's renowned
LISTSERV(R) list management software.  For more information, go to:
http://www.lsoft.com/LISTSERV-powered.html