Review of the earth open source (eos) report " roundup and birth defects: is the public being kept in the dark?"



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2.5 Neurotoxicity of glyphosate / glyphosate-based herbicides


The EOS article describes glyphosate as an organophosphate, and asserts that it has shown a range of neurotoxic effects. These include neurobehavioural disorders in the children of pesticide applicators (Garry et al, 2002), Parkinson’s disease in a man who accidently sprayed himself (Barbosa et al, 2001), biochemical abnormalities in rat brain cells including depletion of the neurotransmitters serotonin and dopamine (Anadon et al, 2008) and loss of mitochondrial trans-membrane potential (Astiz et al, 2009), and synergistic toxicity with diazinon towards neuroblastoma (nerve cancer) cells in vitro (Axelrad et al, 2003).

APVMA comment

Glyphosate is an organic chemical containing a phosphorus atom, but does not exhibit the same biological activity as organophosphate insecticides. In fact, there is a substantial body of evidence from laboratory animal studies that glyphosate does not affect cholinesterase (ChE) activity in the brain or blood, or cause acute, delayed or chronic toxicity to the nervous system.

In an acute neurotoxicity study with glyphosate trimesium in rats gavaged at 645, 968 and 1290 mg/kg bw, the mid and high doses caused behavioural depression, hypothermia and deaths but no inhibition of brain or RBC ChE activity. Glyphosate trimesium did not depress ChE activity in a two-year dietary study in rats at up to 42 (males) / 56 (females) mg/kg bw/d (Stauffer Chemical Co, 1984), in a two-generation rat reproduction study at dietary doses up to ca 100 mg/kg bw/d (Stauffer Chemical Company, 1983) or in dogs gavaged at up to 50 mg/kg bw/d for 12 months (Stauffer Chemical Co, 1987b) (DoHA, 1991).

The JMPR (2004b) review of glyphosate included BVL evaluations of acute (single oral dose) and 13–week (dietary administration) neurotoxicity studies in rats, performed according to OECD Test Guideline 424 (Horner, 1996a,b). Despite the occurrence of general toxicity, there was no behavioural or histological evidence of toxicity to the central or peripheral nervous systems at the respective highest doses of 2000 mg/kg bw and 1547 mg/kg bw/d. Similarly, glyphosate displayed no acute delayed neurotoxicity when tested in chickens by OECD Test Guideline 418 at an oral dose of 2000 mg/kg bw (Johnson, 1996). There was no treatment-related depression in brain acetylcholinesterase (AChE) activity or neuropathy target esterase activity in the brain or spinal cord.

The EU review of glyphosate included BVL assessments of two 21-day oral repeat-dose neurotoxicity studies in chickens, performed with glyphosate at up to 1000 mg/kg bw/d (Bhide, 1987) and Glycel 41 SL at doses up to an equivalent of 1600 mg glyphosate/kg bw/d (Bhide, 1988d). Both studies investigated behaviour, spinal cord and sciatic nerve histology, plasma ChE activity, haematology and clinical chemistry. Slight ataxia (loss of touch sensation) occurred in 1/3 high dose hens on day 18 of Bhide (1987), but otherwise there was no behavioural or histological evidence of neurotoxicity, and no depression in ChE activity. The EU concluded there was no primary neurotoxic effect. The Australian DoHA (1992) assessment of Bhide (1987) agreed that there was no neurotoxicity or neurological change in the spinal cord or peripheral nerves.

The case report of Parkinson’s disease in a man following exposure to glyphosate (Barbosa et al, 2001) is inconsistent with previous findings in animals and humans, and insufficient to prove a causal relationship (JMPR, 2004b). In a review of published epidemiological studies, Mink et al (2011) cite a case-control study (Weschler et al, 1991) reporting an unadjusted OR of 4.04 for Parkinson’s disease and use of Roundup at home, based on 19 cases (14 exposed) and 22 controls (9 exposed). However, the strength of the association is questionable due to the small sample size and variability in the data (the 95% CI of 0.91–19.3 was very wide and included 1.0). Furthermore, there was no association between glyphosate exposure and Parkinson’s disease in a much larger cohort study of pesticide applicators and their spouses (Kamel et al, 2007), either at enrolment (relative risk of 1.1 in 79 640 subjects) or follow—up (RR of 1.0 in 56 009 subjects).

Garry et al (2002) conducted a cross-sectional analysis of pesticide applicators and their families. Parent-reported ADD / ADHD in children was associated positively and significantly with use of glyphosate, with 6/14 affected children having parents who had exposure to glyphosate or Roundup (OR = 3.6; 95% CI = 1.35–9.65). ADD / ADHD diagnosis was not confirmed by a clinician, however (Mink et al, 2011). The biological significance of findings by Anadon et al (2008), Astiz et al (2009) and Axelrad et al (2003) is unknown, and it is uncertain whether these studies are indicative of any hazard to humans.

The APVMA will monitor the scientific literature for future developments in this area, ensure that relevant research reports are reviewed, and take action if required.


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