Bibliography Tag: full text available

Bibliography Index

Hmielowski, 2019

Hmielowski, Tracy, “Glyphosate and Phosphate Interactions in soils,” CSA News, 2019, 64(1), DOI: 10.2134/csa2019.64.0103.

SUMMARY:

• Phosphate and glyphosate interact “competitively” when both are present in the soil.

• The application of inorganic P fertilizers after glyphosate has been applied was shown to mobilize glyphosate.

• Management strategies should consider the potential for glyphosate mobilization to reduce impacts on crops and glyphosate runoff to nearby water sources.

With both phosphorus and glyphosate being applied to agricultural fields across the globe, the chemicals are commonly present together. Phosphorus is applied as inorganic forms of P (PO₄³¯) and taken up through the plant roots. Glyphosate is absorbed through foliage, and while it readily adsorbs to soil, it has been found to degrade rapidly. The two chemicals have a competitive interaction, given the similarity between the PO₄³¯and the phosphonomethyl function group of glyphosate. This means that inorganic P fertilizers can potentially displace glyphosate, and vice versa, on the surface of soil particles. FULL TEXT

 

Hertz-Picciotto et al., 2018

Hertz-Picciotto, Irva, Sass, Jennifer B., Engel, Stephanie, Bennett, Deborah H., Bradman, Asa, Eskenazi, Brenda, Lanphear, Bruce, & Whyatt, Robin, “Organophosphate exposures during pregnancy and child neurodevelopment: Recommendations for essential policy reforms,” PLOS Medicine, 2018, 15(10). DOI: 10.1371/journal.pmed.1002671.

SUMMARY POINTS:

• Widespread use of organophosphate (OP) pesticides to control insects has resulted in ubiquitous human exposures.
• High exposures to OP pesticides are responsible for poisonings and deaths, particularly in developing countries.
• Compelling evidence indicates that prenatal exposure at low levels is putting children at risk for cognitive and behavioral deficits and for neurodevelopmental disorders.
To protect children worldwide, we recommend the following:
• Governments phase out chlorpyrifos and other OP pesticides, monitor watersheds and other sources of human exposures, promote use of integrated pest management (IPM) through incentives and training in agroecology, and implement mandatory surveillance of pesticide-related illness.
• Health professions implement curricula on the hazards from OP pesticides in nursing and medical schools and in continuing medical education courses and educate their patients and the public about these hazards.
• Agricultural entities accelerate the development of nontoxic approaches to pest control through IPM and ensure the safety of workers through training and provision of protective equipment when toxic chemicals are to be used. FULL TEXT

Guerrero Schimpf et al., 2018

Guerrero Schimpf, M., Milesi, M. M., Luque, E. H., & Varayoud, J.m “Glyphosate-based herbicide enhances the uterine sensitivity to estradiol in rats,” Journal of Endocrinology, 2018, 239(2), 197-213. DOI: 10.1530/JOE-18-0207.

ABSTRACT:

In a previous work, we detected that postnatal exposure to a glyphosate-based herbicide (GBH) alters uterine development in prepubertal rats causing endometrial hyperplasia and increasing cell proliferation. Our goal was to determine whether exposure to low-dose of a GBH during postnatal development might enhance the sensitivity of the uterus to an estrogenic treatment. Female Wistar pups were subcutaneously injected with saline solution (control) or GBH using the reference dose (2 mg/kg/day, EPA) on postnatal days (PND) 1, 3, 5, and 7. At weaning (PND21), female rats were bilaterally ovariectomized and treated with silastic capsules containing 17beta-estradiol (E2, 1mg/ml) until they were two months of age. On PND60, uterine samples were removed and processed for histology, immunohistochemistry and mRNA extraction to evaluate: i) uterine morphology, ii) uterine cell proliferation by the detection of Ki67, iii) the expression of the estrogen receptors alpha (ESR1) and beta (ESR2), and iv) the expression of WNT7A and beta-catenin. GBH-exposed animals showed increased luminal epithelial height and stromal nuclei density. The luminal and glandular epithelium were markedly hyperplastic in 43% of GBH-exposed animals. GBH exposure caused an increase in E2-induced cell proliferation in association with an induction of both ESR1 and ESR2. GBH treatment decreased membranous and cytoplasmic expression of beta-catenin in luminal and glandular epithelial cells and increased WNT7A expression in the luminal epithelium. These results suggest that early postnatal exposure to a GBH enhances the sensitivity of the rat uterus to estradiol, and induces histomorphological and molecular changes associated with uterine hyperplasia. FULL TEXT

Green, 2018

Green, J. M., “The rise and future of glyphosate and glyphosate-resistant crops,” Pest Management Science, 2018, 74(5), 1035-1039. DOI: 10.1002/ps.4462.

ABSTRACT:

Glyphosate and glyphosate-resistant crops had a revolutionary impact on weed management practices, but the epidemic of glyphosate-resistant (GR) weeds is rapidly decreasing the value of these technologies. In areas that fully adopted glyphosate and GR crops, GR weeds evolved and glyphosate and glyphosate traits now must be combined with other technologies. The chemical company solution is to combine glyphosate with other chemicals, and the seed company solution is to combine glyphosate resistance with other traits. Unfortunately, companies have not discovered a new commercial herbicide mode-of-action for over 30 years and have already developed or are developing traits for all existing herbicide types with high utility. Glyphosate mixtures and glyphosate trait combinations will be the mainstays of weed management for many growers, but are not going to be enough to keep up with the capacity of weeds to evolve resistance. Glufosinate, auxin, HPPD-inhibiting and other herbicide traits, even when combined with glyphosate resistance, are incremental and temporary solutions. Herbicide and seed businesses are not going to be able to support what critics call the chemical and transgenic treadmills for much longer. The long time without the discovery of a new herbicide mode-of-action and the epidemic of resistant weeds is forcing many growers to spend much more to manage weeds and creating a worst of times, best of times predicament for the crop protection and seed industry. (c) 2016 Society of Chemical Industry.  FULL TEXT

Gillezeau et al., 2019

Gillezeau, Christina, van Gerwen, Maaike, Shaffer, Rachel M, Rana, Iemaan, Zhang, Luoping, Sheppard, Lianne, & Taioli, Emanuela, “The evidence of human exposure to glyphosate: a review,” Environmental Health, 2019, 18(1), 2. DOI: 10.1186/s12940-018-0435-5.

ABSTRACT:

BACKGROUND: Despite the growing and widespread use of glyphosate, a broad-spectrum herbicide and desiccant, very few studies have evaluated the extent and amount of human exposure.

OBJECTIVE: We review documented levels of human exposure among workers in occupational settings and the general population.

METHODS: We conducted a review of scientific publications on glyphosate levels in humans; 19 studies were identified, of which five investigated occupational exposure to glyphosate, 11 documented the exposure in general populations, and three reported on both.

RESULTS: Eight studies reported urinary levels in 423 occupationally and para-occupationally exposed subjects; 14 studies reported glyphosate levels in various biofluids on 3298 subjects from the general population. Average urinary levels in occupationally exposed subjects varied from 0.26 to 73.5 mug/L; environmental exposure urinary levels ranged from 0.16 to 7.6 mug/L. Only two studies measured temporal trends in exposure, both of which show increasing proportions of individuals with detectable levels of glyphosate in their urine over time.

CONCLUSIONS: The current review highlights the paucity of data on glyphosate levels among individuals exposed occupationally, para-occupationally, or environmentally to the herbicide. As such, it is challenging to fully understand the extent of exposure overall and in vulnerable populations such as children. We recommend further work to evaluate exposure across populations and geographic regions, apportion the exposure sources (e.g., occupational, household use, food residues), and understand temporal trends. FULL TEXT

Feat-Vetel et al., 2018

Feat-Vetel, Justyne, Larrigaldie, Vanessa, Meyer-Dilhet, Geraldine, Herzine, Ameziane, Mougin, Camille, Laugeray, Anthony, Gefflaut, Thierry, Richard, Olivier, Quesniaux, Valerie, Montecot-Dubourg, Celine, & Mortaud, Stephane, “Multiple effects of the herbicide glufosinate-ammonium and its main metabolite on neural stem cells from the subventricular zone of newborn mice,” NeuroToxicology, 2018, 69, 152-163. DOI: 10.1016/j.neuro.2018.10.001.

ABSTRACT:

The globally used herbicide glufosinate-ammonium (GLA) is structurally analogous to the excitatory neurotransmitter glutamate, and is known to interfere with cellular mechanisms involved in the glutamatergic system. In this report, we used an in vitro model of murine primary neural stem cell culture to investigate the neurotoxicity of GLA and its main metabolite, 4-methylphosphinico-2-oxobutanoic acid (PPO). We demonstrated that GLA and PPO disturb ependymal wall integrity in the ventricular-subventricular zone (V-SVZ) and alter the neuro-glial differentiation of neural stem cells. GLA and PPO impaired the formation of cilia, with reduced Celsr2 expression after PPO exposure. GLA promoted the differentiation of neuronal and oligodendroglial cells while PPO increased B1 cell population and impaired neuronal fate of neural stem cells. These results confirm our previous in vivo report that developmental exposure to GLA alters neurogenesis in the SVZ, and neuroblast migration along the rostral migratory stream. They also highlight the importance of investigating the toxicity of pesticide degradation products. Indeed, not only GLA, but also its metabolite PPO disrupts V-SVZ homeostasis and provides a novel cellular mechanism underlying GLA-induced neurodevelopmental toxicity. Furthermore, we were able to demonstrate a neurotoxic activity of a metabolite of GLA different from that of GLA active substance for the very first time. FULL TEXT

EPA, 2018

Environmental Protection Agency, “Occupational Pesticide Handler Unit Exposure Surrogate Reference Table,” Office of Pesticide Programs, 2018, Available at: https://www.epa.gov/pesticide-science-and-assessing-pesticide-risks/exposure-surrogate-reference-table-pesticide-risk.

SUMMARY:

The Exposure Surrogate Reference Table provides pesticide exposure information for risk assessment based on exposure scenarios, exposure routes and applicable personal protective equipment. FULL TEXT

DeVito, 2017

DeVito, Michael, “Update on NTP Studies of Glyphosate,” Presented at the National Toxicology Program (NTP) Board of Scientific Counselors Meeting, December 7-8, 2017.

SUMMARY:

Not available.  FULL TEXT

Dellaferrera et al., 2018

Dellaferrera, Ignacio, Cortés, Eduardo, Panigo, Elisa, De Prado, Rafael, Christoffoleti, Pedro, & Perreta, Mariel, “First Report of Amaranthus hybridus with Multiple Resistance to 2,4-D, Dicamba, and Glyphosate,” Agronomy, 2018, 8(8). DOI: 10.3390/agronomy8080140.

ABSTRACT:

In many countries, Amaranthus hybridus is a widespread weed in agricultural systems. The high prolificacy and invasive capacity as well as the resistance of some biotypes to herbicides are among the complications of handling this weed. This paper reports on the first A. hybridus biotypes with resistance to auxinic herbicides and multiple resistance to auxinic herbicides and the EPSPs inhibitor, glyphosate. Several dose response assays were carried out to determine and compare sensitivity of six population of A. hybridus to glyphosate, 2,4-D, and dicamba. In addition, shikimic acid accumulation and piperonil butoxide effects on 2,4-D and dicamba metabolism were tested in the same populations. The results showed four populations were resistant to dicamba and three of these were also resistant to 2,4-D, while only one population was resistant to glyphosate. The glyphosate-resistant population also showed multiple resistance to auxinic herbicides. Pretreatment with piperonil butoxide (PBO) followed by 2,4-D or dicamba resulted in the death of all individual weeds independent of herbicide or population. FULL TEXT

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