Afecta negativamente el desarrollo del cerebro

Tiempo de lectura: 8 minutos

En Brasil, el estado de Pernambuco ya era un gran productor de caña de azúcar cuando su gobierno decidió impulsar esa producción rebajándole a la mitad los impuestos a las empresas que producen alcohol a partir de caña (1). El cultivo de caña de azúcar en Pernambuco y otros estados del nordeste brasileño se beneficia del uso de glifosato (2). Según las autoridades de la salud (3), Pernambuco está sufriendo una ”epidemia” de nacimientos de niños con cerebro demasiado pequeño (”microcefalia”).

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En Estados Unidos, el estado de Washington es un gran productor agrícola y el Departamento de Agricultura del Estado de Washington permite que sus agricultores utilicen una gran cantidad de glifosato a lo largo de sus cursos de agua (4). El Departamento de Salud del mismo estado ha detectado que en algunas zonas de Washington la cantidad de niños nacidos sin cerebro, o con cerebro muy pequeño, está muy por arriba del promedio nacional (5)

La influencia negativa del glifosato sobre el desarrollo del cerebro cuenta con aval científico y se sabe por ejemplo que el glifosato puede causar uso microcefalía (6).

Aún así, no sabemos si la contaminación ambiental causada por el uso masivo de glifosato en Washington y Pernambuco es parte de los problemas de salud mencionados arriba. Quizás el glifosato no es el único responsable de la epidemia de microcefalia. Quizás actúa en combinación con otros agrotóxicos y otros factores, distintos en cada caso. El virus Zika podría ser uno de esos factores en Brasil pero no en Washington, porque allí  este virus no existía cuando las autoridades comenzaron a detectar el problema de los nacimientos de niños con cerebro malformado. En todo caso, no lo sabemos, porque casi no hay estudios científicos y esta falta se debe, entre otras cosas, a que los gobiernos que promueven el desarrollo de una agricultura basada en el uso masivo de glifosato no han promovido también el estudio de las consecuencias que esto podría tener para el ambiente y la salud humana.

La Dra. Allison Ashley-Koch, investigadora de la universidad de Duke experta en estas anomalías del cerebro, se ofreció para estudiar la posible conexión entre los bebés nacidos sin cerebro, o con cerebro muy chico, y la contaminación ambiental. Las autoridades le respondieron ”Thank you, but not thank you” (Gracias pero no, gracias, 7).

La prensa del estado de Washington, por su parte, hace de cuenta de que el glifosato no existe. Una búsqueda en cinco grandes periódicos y semanarios sobre notas publicadas durante 2015 que contuviesen la palabra ”glyphosate” sugiere que el tema es tabú.

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El Seattle Times, uno de los periódicos de mayor circulación en el estado de Washington tiene 357 notas con el término ”Donald Trump”; 65 con ”GMO” y 0 con ”glyphosate”. La tabla informa sobre el número de notas en las cuales aparece la palabra ”glifosato”, publicadas en 2015 por grandes periódicos y semanarios del estado de Washington.

También en Uruguay, como en Estados Unidos y Brasil, las autoridades se empecinan en seguir permitiendo el uso masivo de glifosato en la agricultura, concediendo incluso permisos a variedades transgénicas de soja y maíz que necesariamente implican un aumento muy grande del uso de glifosato, pero sin promover el estudio científico de las posibles consecuencias. Por el contrario, para justificar estos permisos las autoridades se basan casi exclusivamente en informes escritos por personal de Monsanto, el vendedor del veneno o por científicos que financian sus estudios con dineros de Monsanto y otras empresas del ramo.

Sería interesante saber si las autoridades que concedieron los permisos para el uso masivo del glifosato en nuestro, al permitir la introducción de distintas variedades de soja y maíz transgénico (8), sabiendo que su cultivo forzosamente incluye uso masivo de glifosato, si además de considerar los folletos e informes de las empresas que se enriquecen con estos productos también tuvieron en cuenta los informes de científicos que no son financiados por estas empresas.

Por Rafael Cantera, marzo de 2016

La ONDA digital Nº 759 (Síganos en Twitter y facebook)

 

(1)Datos y noticias publicados por el gobierno de Pernambuco en su página oficial (http://www.pe.gov.br/secretarias/

(2) Azania et al., 2016. dn.intechopen.com/pdfs-wm/44988.pdf

(3) Ver la página web del Ministerio de Salud brasileño y la de la Organización Mundial de la Salud: http://portalsaude.saude.gov.br y http://www.who.int/csr/don/8-january-2016-brazil-microcephaly/es/.

(4)http://agr.wa.gov/plantsinsects/weeds/npdespermits/docs/IPMFreshwaterEmergentNoxiousQuarantineListedWeeds.pdf

(5)Página web oficial del Departamento de Salud del estado de Washington.

http://www.doh.wa.gov/YouandYourFamily/IllnessandDisease/BirthDefects/AnencephalyInvestigation

(6)Varios estudios científicos han establecido fírmemente un nexo entre el glifosato y el desarrollo del cerebro; ver por ejemplo Dallegrave et al. 2003; Rull et al., 2006; Paganelli et al., 2010; Roy et al., 2016; Coullery et al., 2016.

(7)Yakima Herald, Diciembre 12, 2015.

(8)Desde el 2008 hasta recientemente esta autoridad era el Gabinete Nacional de Bioseguridad.

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Scientific papers linking exposure to glyphosate with brain development disorders:

Toxicol Lett. 2003 Apr 30;142(1-2):45-52.

The teratogenic potential of the herbicide glyphosate-Roundup in Wistar rats.

Dallegrave E1, Mantese FD, Coelho RS, Pereira JD, Dalsenter PR, Langeloh A.

The aim of this study was to assess the teratogenicity of the herbicide glyphosate-Roundup (as commercialized in Brazil) to Wistar rats. Dams were treated orally with water or 500, 750 or 1000 mg/kg glyphosate from day 6 to 15 of pregnancy. Cesarean sections were performed on day 21 of pregnancy, and number of corpora lutea, implantation sites, living and dead fetuses, and resorptions were recorded. Weight and gender of the fetuses were determined, and fetuses were examined for external malformations and skeletal alterations. The organs of the dams were removed and weighed. 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.

Am J Epidemiol. 2006 Apr 15;163(8):743-53.

Neural tube defects and maternal residential proximity to agricultural pesticide applications.

Rull RP1, Ritz B, Shaw GM.

Residential proximity to applications of agricultural pesticides may be an important source of exposure to agents that have been classified as developmental toxins. Data on two case-control study populations of infants with neural tube defects (NTDs) and nonmalformed controls delivered in California between 1987 and 1991 were pooled to investigate whether maternal residential proximity to applications of specific pesticides or physicochemical groups of pesticides during early gestation increases the risk of these malformations. Maternal residential proximity within 1,000 m of pesticide applications was ascertained by linking mothers’ addresses with agricultural pesticide use reports and crop maps. Odds ratios were computed by using conventional single- and multiple-pesticide and hierarchical multiple-pesticide logistic regression. In single-pesticide models, several pesticides were associated with NTDs after adjustment for study population, maternal ethnicity, educational level, cigarette smoking, and vitamin use. In a hierarchical multiple-pesticide model, effect estimates for only benomyl and methomyl suggested a possible association. Elevated risks of NTDs and anencephaly or spina bifida subtypes were also associated with exposures to chemicals classified as amide, benzimidazole, methyl carbamate, or organophosphorus pesticides and with increasing numbers of pesticides. These results suggest that ambient exposure to certain categories of agricultural pesticides may increase the risk of NTDs.

Chem Res Toxicol. 2010 Oct 18;23(10):1586-95. doi: 10.1021/tx1001749.

Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling.

Paganelli A1, Gnazzo V, Acosta H, López SL, Carrasco AE.

Abstract

The broad spectrum herbicide glyphosate is widely used in agriculture worldwide. There has been ongoing controversy regarding the possible adverse effects of glyphosate on the environment and on human health. Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH) are used led us to undertake an embryological approach to explore the effects of low doses of glyphosate in development. Xenopus laevis embryos were incubated with 1/5000 dilutions of a commercial GBH. The treated embryos were highly abnormal with marked alterations in cephalic and neural crest development and shortening of the anterior-posterior (A-P) axis. Alterations on neural crest markers were later correlated with deformities in the cranial cartilages at tadpole stages. Embryos injected with pure glyphosate showed very similar phenotypes. Moreover, GBH produced similar effects in chicken embryos, showing a gradual loss of rhombomere domains, reduction of the optic vesicles, and microcephaly. This suggests that glyphosate itself was responsible for the phenotypes observed, rather than a surfactant or other component of the commercial formulation. A reporter gene assay revealed that GBH treatment increased endogenous retinoic acid (RA) activity in Xenopus embryos and cotreatment with a RA antagonist rescued the teratogenic effects of the GBH. Therefore, we conclude that the phenotypes produced by GBH are mainly a consequence of the increase of endogenous retinoid activity. This is consistent with the decrease of Sonic hedgehog (Shh) signaling from the embryonic dorsal midline, with the inhibition of otx2 expression and with the disruption of cephalic neural crest development. The direct effect of glyphosate on early mechanisms of morphogenesis in vertebrate embryos opens concerns about the clinical findings from human offspring in populations exposed to GBH in agricultural fields.

Environ Toxicol Pharmacol. 2016 Jan 4;42:45-54. doi: 10.1016/j.etap.2016.01.003.

Glyphosate induces neurotoxicity in zebrafish.

Roy NM1, Carneiro B2, Ochs J2.

Abstract

Glyphosate based herbicides (GBH) like Roundup® are used extensively in agriculture as well as in urban and rural settings as a broad spectrum herbicide. Its mechanism of action was thought to be specific only to plants and thus considered safe and non-toxic. However, mounting evidence suggests that GBHs may not be as safe as once thought as initial studies in frogs suggest that GBHs may be teratogenic. Here we utilize the zebrafish vertebrate model system to study early effects of glyphosate exposure using technical grade glyphosate and the Roundup® Classic formulation. We find morphological abnormalities including cephalic and eye reductions and a loss of delineated brain ventricles. Concomitant with structural changes in the developing brain, using in situ hybridization analysis, we detect decreases in genes expressed in the eye, fore and midbrain regions of the brain including pax2, pax6, otx2 and ephA4. However, we do not detect changes in hindbrain expression domains of ephA4 nor exclusive hindbrain markers krox-20 and hoxb1a. Additionally, using a Retinoic Acid (RA) mediated reporter transgenic, we detect no alterations in the RA expression domains in the hindbrain and spinal cord, but do detect a loss of expression in the retina. We conclude that glyphosate and the Roundup® formulation is developmentally toxic to the forebrain and midbrain but does not affect the hindbrain after 24h exposure.

Neurotoxicology. 2016 Jan;52:150-61. doi: 10.1016/j.neuro.2015.12.004.

Neuronal development and axon growth are altered by glyphosate through a WNT non-canonical signaling pathway.

Coullery RP1, Ferrari ME1, Rosso SB2.

Abstract

The growth and morphological differentiation of neurons are critical events in the establishment of proper neuronal connectivity and functioning. The developing nervous system is highly susceptible to damage caused by exposure to environmental contaminants. Glyphosate-containing herbicides are the most used agrochemicals in the world, particularly on genetically modified plants. Previous studies have demonstrated that glyphosate induces neurotoxicity in mammals. Therefore, its action mechanism on the nervous system needs to be determined. In this study, we report about impaired neuronal development caused by glyphosate exposure. Particularly, we observed that the initial axonal differentiation and growth of cultured neurons is affected by glyphosate since most treated cells remained undifferentiated after 1 day in culture. Although they polarized at 2 days in vitro, they elicited shorter and unbranched axons and they also developed less complex dendritic arbors compared to controls. To go further, we attempted to identify the cellular mechanism by which glyphosate affected neuronal morphology. Biochemical approaches revealed that glyphosate led to a decrease in Wnt5a level, a key factor for the initial neurite development and maturation, as well as inducing a down-regulation of CaMKII activity. This data suggests that the morphological defects would likely be a consequence of the decrease in both Wnt5a expression and CaMKII activity induced by glyphosate. Additionally, these changes might be reflected in a subsequent neuronal dysfunction. Therefore, our findings highlight the importance of establishing rigorous control on the use of glyphosate-based herbicides in order to protect mammals’ health.

 

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