What does independent research tell us about Roundup & Glyphosate?

DSC_0001 (2)No test for Roundup held by the EPA, WHO/FAO or EU’s EFSA actually tests Roundup!

…..When setting the ADI for glyphosate and for assessing reproductive and developmental toxicity – whether Roundup is safe for the pregnant mother and foetus (and also the mother trying to get pregnant).

All the tests only use the pure formulation of glyphosate – not the stronger formulation that includes adjuvants (the agent/chemical added to increase the effect of the active chemical)!

Please can the main assessment bodies for the safety of glyphosate and Roundup include these independent (financially disinterested) studies?

Open Source‘s well researched document: “Roundup & Birth Defects: Is the public being kept in the dark” has the clearest explanations of these complex studies, but from a European angle.  Please note the strongest science showing danger at lower levels and for the full Roundup formulation does come from Europe and Brazil because that is where funding for independent public-interest research science seems to be more available.

The Open Source document is essential reading for any European who 1. Eats food and/or either 2. Wants healthy children or 3.Wants healthy grandchildren. 4. Buys feed for livestock (I think that covers it….).

The following studies includes extracts (& page no’s) from this document:


Dallegrave 2003: Found that sublethal oral doses of Roundup cause craniofacial ossification defects, loss of caudal vertebrae, and misshapen atlas and other cervical and thoracic vertebrae in rats. The author did not use the word “craniofacial” but described the nature of the malformations, which included the craniofacial type: “incomplete skull ossification and enlarged fontanel”. The effects were statistically significant and dose-dependent, strengthening the conclusion that they were caused by the glyphosate formulations [1]. Page 25

Dallegrave 2003 says: Results showed a 50% mortality rate for dams treated with 1000 mg/kg glyphosate. Skeletal alterations were observed in 15.4, 33.1, 42.0 and 57.3% of fetuses from the control, 500, 750 and 1000 mg/kg glyphosate groups, respectively. We may conclude that glyphosate-Roundup† is toxic to the dams and induces developmental retardation of the fetal skeleton.

Dallegrave 2007: examined the reproductive effects of Roundup on male and female offspring of Wistar rats treated with 50, 150 or 450 mg/kg of Roundup during pregnancy and lactation. The study found that these doses of Roundup did not induce maternal toxicity but did induce adverse reproductive effects on male offspring. Findings include a decrease in sperm number and daily sperm production during adulthood, an increase in the percentage of abnormal sperms, a dose-related decrease in the serum testosterone level at puberty, and signs of sperm cell degeneration during both periods. The study showed that Roundup is a reproductive toxin at non-maternally toxic doses [2].   Page 12

Carrasco et al, 2010: showed that the best-selling herbicide Roundup causes malformations in frog and chicken embryos at doses much lower than those used in agricultural spraying. The malformations found were mostly of the craniofacial and neural crest type, which affect the skull, face, midline, and developing brain and spinal cord [3].

The maximum residue limit (MRL) allowed for glyphosate in food and feed products in the EU is 20 mg/kg.  Soybeans have been found to contain glyphosate residues at levels up to 17mg/kg.  Carrasco found malformations in frog and chicken embryos injected with 2.03 mg/kg glyphosate – ten times lower than the MRL. While an injected dose is not the same as eating food containing glyphosate residues, no attempt has been made to properly investigate how much glyphosate people and animals are ingesting.   Page 6

(SafeSaysWho note: The MRL for cereal grains (rye, barley, sorghum and wheat) for the WHO and USA EPA is 30mg/kg).

Carrasco built on the findings of Dallegrave in that he identified the mechanism for the teratogenic activity of Roundup/glyphosate. Such malformations in humans and animals are known to be linked with an excess of retinoic acid (RA), an oxidized form of vitamin A.   [Refs below: 4 5 6 7 8 9 10 11] The link between RA and malformations is the reason why pregnant women are advised not to take vitamin A supplements. Carrasco found that glyphosate increased RA activity in frog embryos and that this was the mechanism through which the malformations occurred. Page 25

Paumgartten 2010: says that in cases of maternal toxicity, it is not possible to know whether an effect on the embryo is only due to maternal poisoning or due to a direct action of the chemical at doses that also adversely affect the mother. In the latter case, the chemical would be a developmental toxin [12].  Page 11

A study on rats showed that a Roundup formulation was a potent endocrine disruptor and caused disturbances in reproductive development when the exposure was performed during the puberty period. Adverse effects, including delayed puberty and reduced testosterone production, were found at all dose levels, including the LOAEL of 5 mg/kg. The dose-response relationship was clear [13].  One of the critical failures of regulatory toxicity tests is to ignore important developmental windows such as puberty. This study helps to fill that knowledge gap.  Page 18

A 75-day study on rats showed that GlyphosateBiocarb (a Brazilian formulation) caused damage to liver cells in a dose-response manner, including at the LOAEL of 4.87 mg/kg. According to the authors, the findings suggest that the damage to liver cells was “irreversible” [14].   Page 18

No dose below these two LOAELs was tested in these studies, so the true NOAEL is lower – by how much, no one knows. But the NOAEL could reasonably be assumed to be 2.5 mg/kg bw/d. Applying the usual 100-fold safety margin results in a scientifically defensible ADI of 0.025 mg/kg bw/d. This is over ten times lower than the Germany’s ADI, which is currently in force. The MRL (safe level in food) should be correspondingly revised downward.

Of course, all assumptions need to be tested, and not even independent science has explored the full picture of Roundup and glyphosate’s toxicity.  Page 18

Studies should be carried out immediately to determine the true NOAEL and ADI for glyphosate and Roundup, using the most comprehensive, up to-date scientific knowledge. These studies would involve:

● testing for more effects

● using lower, more realistic doses that will allow accurate determination of the NOAEL

● using larger numbers of animals to ensure sufficient statistical power to reliably detect effects from realistic doses

● dosing during vulnerable developmental windows

● extending study time-frames to allow mid- and long-term effects to show up, instead of killing the test animals before disease has a chance to develop. Industry test animals are killed at the human equivalent of about 60 years old, so many effects of the chemical tested are missed.

End of Extract.

SAFE SAYS WHO? NOTE: The excellent Open Source document, written by scientists is the most comprehensive and clearly understandable document discussing glyphosate and its potential to create malformations in animals and humans.  It is written for the Europeans to help them understand complex decisions who and how regulators are (mysteriously) delaying a glyphosate reassessment in 2012 and also attempting (mysteriously) to get glyphosate reassessed using the old regulation directive (91/414) standard and ignoring a new pesticides regulation (1107/2009) that requires glyphosate to be assessed taking into account the full range of independent literature.

I have said this before and I repeat it again:  not one study for reproductive or developmental toxicity for the EPA, FAO/WHO or the European Union covers glyphosate or glyphosate formulation dosing leading up to pregnancy and in the first week of pregnancy.

There is no requirement for testing of the glyphosate formulations, only pure glyphosate.

Risk assessment to permit pesticide use should ensure a pesticide cannot be approved if it is carcinogenic, mutagenic, a reproductive toxin, persistent in the environment, bio-accumulative, or an endocrine disruptor (apart from specific uses, such as in closed systems).   Risk assessment must be based on the lowest NOAEL.

This blog ONLY attempts to cover maternal/reproductive/mutagenic aspects of glyphosate because the entire field of risk assessment is so confusing and difficult to understand, I have wanted to illustrate clearly the issues we are facing for the most vulnerable members of our human and animal populations – the pregnant mother and the unborn child – across the three major world pesticide assessment regulatory authorities.

Risk assessment to permit pesticide use must require submission of peer-reviewed independent scientific studies.  Existing accepted studies must be released for public scrutiny.

Everyday, independent scientists are lobbying to get these studies included, but scientists need people behind them, public pressure to persuade the major organisations of the EPA, FAO/WHO and the EU (EFSA/DG SANCO) to stop hiding behind walls of scientific corporate protectionism and to create safe, independent regulatory structures for evaluation of plant protection products.




[1] Dallegrave, E., Mantese, F. D. et al. 2003. The teratogenic potential of the herbicide glyphosate-Roundup in Wistar rats. Toxicol Lett 142(1-2): 48.

[2] Dallegrave, E., Mantese, F. D. et al. 2007. Pre- and postnatal toxicity of the commercial glyphosate formulation in Wistar rats. Arch Toxicol 81: 665–673

[3] Paganelli, A., Gnazzo, V., Acosta, H., López, S.L., Carrasco, A.E. 2010. Glyphosate-based herbicides produce terato-genic effects on vertebrates by impairing retinoic acid signaling. Chem. Res. Toxicol., 23(10):1586-1596.

[4] Lammer, E. J., Chen, D. T. et al. 1985. Retinoic acid embryopathy. N Engl J Med 313: 837–841. 170.

[5] Sulik, K. K., Cook, C. S. et al. 1988. Teratogens and craniofacial malformations: relationships to cell death. Development 103 Suppl: 213-231.

[6] Durston, A. J., Timmermans, J. P. et al. 1989. Retinoic acid causes an anteroposterior transformation in the developing central nervous system. Nature 340(6229): 140-144.

[7] Lopez, S. L., Carrasco, A. E. 1992. Retinoic acid induces changes in the localization of homeobox proteins in the anteroposterior axis of Xenopus laevis embryos. Mech Dev 36(3): 153–164.

[8] Lopez, S. L., Dono, R. et al. 1995. Differential effects of retinoic acid and a retinoid antagonist on the spatial distribution of the homeoprotein Hoxb-7 in vertebrate embryos. Dev Dyn 204(4): 457–471.

[9] Clotman, F., Van Maele-Fabry, G. et al. 1998. Structural and gene expression abnormalities induced by retinoic acid in the forebrain. Reprod Toxicol 12(2): 169–176.

[10] Clotman, F., Van Maele-Fabry, G. et al. 1997. Retinoic acid induces a tissue-specific deletion in the expression domain of Otx2. Neurotoxicol Teratol 19(3): 163–169.

[11] Padmanabhan, R. 1998. Retinoic acid-induced caudal regression syndrome in the mouse foetus. Reprod Toxicol 12(2): 139–151.

[12] Paumgartten, F. J. 2010. Influence of maternal toxicity on the outcome of developmental toxicity studies. J Toxicol Environ Health A 73(13-14): 944-951.

[13] Romano, R. M., Romano, M. A. et al. 2010. Prepubertal exposure to commercial formulation of the herbicide Glyphosate alters testosterone levels and testicular morphology. Archives of Toxicology 84(4): 309–317.

[14]  Benedetti, A. L., Vituri, C. d. L. et al. 2004. The effects of sub-chronic exposure of Wistar rats to the herbicide GlyphosateBiocarb. Toxicol Lett 153(2): 227–232.

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