Developmental and Reproductive Outcomes in Humans and Animals After Glyphosate Exposure: A Critical Analysis

Abstract

Glyphosate is the active ingredient of several widely used herbicide formulations. Glyphosate targets the shikimate metabolic pathway, which is found in plants but not in animals. Despite the relative safety of glyphosate, various adverse developmental and reproductive problems have been alleged as a result of exposure in humans and animals. To assess the developmental and reproductive safety of glyphosate, an analysis of the available literature was conducted. Epidemiological and animal reports, as well as studies on mechanisms of action related to possible developmental and reproductive effects of glyphosate, were reviewed. An evaluation of this database found no consistent effects of glyphosate exposure on reproductive health or the developing offspring. Furthermore, no plausible mechanisms of action for such effects were elucidated. Although toxicity was observed in studies that used glyphosate-based formulations, the data strongly suggest that such effects were due to surfactants present in the formulations and not the direct result of glyphosate exposure. To estimate potential human exposure concentrations to glyphosate as a result of working directly with the herbicide, available biomonitoring data were examined. These data demonstrated extremely low human exposures as a result of normal application practices. Furthermore, the estimated exposure concentrations in humans are >500-fold less than the oral reference dose for glyphosate of 2 mg/kg/d set by the U.S. Environmental Protection Agency (U.S. EPA 1993). In conclusion, the available literature shows no solid evidence linking glyphosate exposure to adverse developmental or reproductive effects at environmentally realistic exposure concentrations.

Potential toxic effects of glyphosate and its commercial formulations below regulatory limits

“…They can be toxic by themselves or facilitate a better uptake of environmental pollutants, and hence increase the body burden of the exposed organism. This is also underlined in reviews sponsored by pesticide manufacturers (Williams et al, 2012). The toxicity of adjuvants appears as a general feature of pesticide toxicology, specifically shown in this major model of the main herbicide worldwide, GlyBH, but also described for other pesticides (Eddleston et al, 2012).…”

“…Inhibition of EPSPS by glyphosate causes protein shortage, and consequently plant death. Since this biochemical pathway does not exist in vertebrates, it is generally assumed that glyphosate is safe for mammals, including humans (Williams et al, 2012). As a consequence, glyphosate jumped to a leading position among commercial pesticides from the 1970s.…”

Glyphosate and aminomethylphosphonic acid are not detectable in human milk

“…Because these amino acids are not synthesized by humans, glyphosate would not be expected to have a physiological effect. Indeed, the human genome does not encode for 5-enolpyruvylshikimate-3-phosphate synthase, and a large body of epidemiologic and experimental literature supports the safety of glyphosate in mammals (5,6). In addition, neither glyphosate nor its metabolite aminomethylphosphonic acid (AMPA) 8 seem to bioaccumulate in animal tissues (7)(8)(9).…”

Are Ready for Market Genetically Modified, Conventional and Organic Soybeans Substantially Equivalent as Food and Feed?

“…Other studies claim that glyphosate is not linked to developmental or reproductive effects in animals and humans, but that surfactants may cause some toxic effects (Williams et al 2012;Williams et al 2000). This controversy has been reviewed in depth by (Antoniou et al 2012), reaching the conclusion that the weight of evidence indicates that glyphosate itself is a teratogen and that adjuvants commonly used in conjunction with glyphosate amplify this effect.…”