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Dill, 2005

Gerald M Dill, “Glyphosate-resistant crops: history, status and future,” Pest Management Science, 2005, 61, DOI: 10.1002/PS.1008.

ABSTRACT:

The commercial launch of glyphosate-resistant soybeans in 1996 signaled the beginning of a new era in weed management in row crops. Today, over 80% of the soybeans grown in the USA are glyphosate resistant. Since that time, many crops have been transformed that have allowed crop applications of many classes of herbicide chemistries. Crops currently under production include maize, soybean, cotton and canola. Transformation technology and selection methods have improved and the rate of development as well as the breadth of crops being considered as commercial targets has increased. On the basis of recent adoption rates by growers around the world, it appears that glyphosate-resistant crops will continue to grow in number and in hectares planted. However, global public acceptance of biotechnology-derived products will continue to impact the rate of adoption of this and other new innovations derived from transformation technology. FULL TEXT

Binimelis et al., 2009

Rosa Binimelis, Walter Pengue, Iliana Monterroso, ‘‘’Transgenic treadmill’: Responses to the emergence and spread of glyphosate-resistant johnsongrass in Argentina,” Geoforum, 2009, 40:4.

ABSTRACT:

The broad-spectrum herbicide glyphosate has become the largest-selling crop-protection product worldwide. The increased use of glyphosate is associated with the appearance of a growing number of tolerant or resistant weeds, with socio-environmental consequences apart from the loss of productivity. In 2002, a glyphosate-resistant biotype of johnsongrass (Sorghum halepense (L.)) appeared in Argentina and now covers at least 10,000 ha. This paper analyzes the driving forces behind the emergence and spread of this weed and also examines management responses and their implications.

Preventive strategies against glyphosate-resistant johnsongrass fail because of the institutional setting. Reactive measures, however, transfer the risks to the society and the environment through the introduction of novel genetically modified crops that allow the use of yet more herbicide. This in turn reinforces the emergence of herbicide-resistant weeds, constituting a new phenomenon of intensification, the “transgenic treadmill”. FULL TEXT

Mortensen et al., 2012

David A. Mortensen, J. Franklin Egan, Bruce D. Maxwell, Matthew R. Ryan, Richard G. Smith, “Navigating a Critical Juncture for Sustainable Weed Management,” BioScience, 2012, 62:1.

ABSTRACT:

Agricultural weed management has become entrenched in a single tactic—herbicide-resistant crops—and needs greater emphasis on integrated practices that are sustainable over the long term. In response to the outbreak of glyphosate-resistant weeds, the seed and agrichemical industries are developing crops that are genetically modified to have combined resistance to glyphosate and synthetic auxin herbicides. This technology will allow these herbicides to be used over vastly expanded areas and will likely create three interrelated challenges for sustainable weed management. First, crops with stacked herbicide resistance are likely to increase the severity of resistant weeds. Second, these crops will facilitate a significant increase in herbicide use, with potential negative consequences for environmental quality. Finally, the short-term fix provided by the new traits will encourage continued neglect of public research and extension in integrated weed management. Here, we discuss the risks to sustainable agriculture from the new resistant crops and present alternatives for research and policy. FULL TEXT

Winchester et al., 2009

Winchester PD, Huskins J, Ying J, “Agrichemicals in surface water and birth defects in the United States,” Acta Paediatrica, 2009, 98:4, DOI: 10.1111/j.1651-2227.2008.01207.

ABSTRACT:

OBJECTIVES: To investigate if live births conceived in months when surface water agrichemicals are highest are at greater risk for birth defects.

METHODS: Monthly concentrations during 1996-2002 of nitrates, atrazine and other pesticides were calculated using United States Geological Survey’s National Water Quality Assessment data. Monthly United States birth defect rates were calculated for live births from 1996 to 2002 using United States Centers for Disease Control and Prevention natality data sets. Birth defect rates by month of last menstrual period (LMP) were then compared to pesticide/nitrate means using logistical regression models.

RESULTS: Mean concentrations of agrichemicals were highest in April-July. Total birth defects, and eleven of 22 birth defect subcategories, were more likely to occur in live births with LMPs between April and July. A significant association was found between the season of elevated agrichemicals and birth defects.

CONCLUSION: Elevated concentrations of agrichemicals in surface water in April-July coincided with higher risk of birth defects in live births with LMPs April-July. While a causal link between agrichemicals and birth defects cannot be proven from this study an association might provide clues to common factors shared by both variables. FULL TEXT

Winchester et al., 2016

Winchester P, Proctor C, Ying J, “County-level pesticide use and risk of shortened gestation and preterm birth,” Acta Paediatrica, 2016, 105:3, DOI: 10.1111/apa.13288.

ABSTRACT:

AIM: This study assesses the association between pesticide exposure in pregnancy, preterm birth (PTB) and shortened gestation.

METHODS: Pregnancy information was abstracted from the Centers for Disease Control (CDC) Non-Public Use Natality Datasets 1990-2005. Pesticide use in maternal county of residence was calculated using California Pesticide Use Reporting (PUR) data 1990-2005. Counties were ranked by pesticide use, and birth months were sorted by peak (May-June) or nonpeak (other months) pesticide use. Multivariate logistical regression models were used.

RESULTS: Counties with higher pesticide use were associated with higher PTB (low 8.59 ± 0.11%, moderate 9.25 ± 0.07%, high 10.0 ± 0.06%, p’s < 0.001) and shorter gestations (low 39.197 ± 0.014 weeks, moderate 39.126 ± 0.011 weeks, high 39.049 ± 0.011 weeks, p’s < 0.001). Peak pesticide months were associated with higher PTB (10.01 ± 0.05% vs. 9.36 ± 0.05%, p < 0.001) and shorter gestations (39.069 ± 0.007 weeks vs. 39.122 ± 0.007 weeks, p < 0.001). The pesticide effect on shortened gestation and higher PTB was found in all racial groups. Pesticide use was highest for fungicides > insecticides > fumigants > herbicides > others. Each pesticide type was found to be associated with higher PTB and shorter gestation.

CONCLUSION: PTB and shortened gestation were significantly associated with pesticide use in maternal county of residence regardless of race, gestation at birth, and in most risk categories. FULL TEXT

Weselak et al., 2008

Weselak M, Arbuckle TE, Wigle DT, Walker MC, Krewski D, “Pre- and post-conception pesticide exposure and the risk of birth defects in an Ontario farm population.,” Reproductive Toxicology, 2008, 25:4, DOI: 10.1016/j.reprotox.2008.05.060.

ABSTRACT: The use of pesticides has enhanced the health and economies of nations around the world by improving crop production. However, pesticides may pose health risks, particularly to the fetus and young children. In a secondary analysis of the Ontario Farm Family Health Study, we explored the relationship between birth defects and parental pesticide exposure during the 3 months prior to conception and the first trimester of pregnancy. A total of 3412 pregnancies were included in the study. Logistic regression fit by maximum likelihood was used in the analysis. The results showed that pre-conception exposure to both cyanazine (odds ratio=4.99, 95% confidence interval: 1.63-15.27) and dicamba (OR=2.42, 95% CI: 1.06-5.53) were associated with increased risk of birth defects in male offspring. Nevertheless, given the self-reported nature of the exposure and outcomes in this study, the present findings should be considered primarily as hypothesis generating, requiring verification in subsequent investigations. FULL TEXT

Thongprakaisang et al., 2013

Thongprakaisang S, Thiantanawat A, Rangkadilok N, Suriyo T, Satayavivad J, “Glyphosate induces human breast cancer cells growth via estrogen receptors,” Food and Chemical Toxicology, 2013 59, DOI: 10.1016/j.fct.2013.05.057.

ABSTRACT: Glyphosate is an active ingredient of the most widely used herbicide and it is believed to be less toxic than other pesticides. However, several recent studies showed its potential adverse health effects to humans as it may be an endocrine disruptor. This study focuses on the effects of pure glyphosate on estrogen receptors (ERs) mediated transcriptional activity and their expressions. Glyphosate exerted proliferative effects only in human hormone-dependent breast cancer, T47D cells, but not in hormone-independent breast cancer, MDA-MB231 cells, at 10⁻¹² to 10⁻⁶M in estrogen withdrawal condition. The proliferative concentrations of glyphosate that induced the activation of estrogen response element (ERE) transcription activity were 5-13 fold of control in T47D-KBluc cells and this activation was inhibited by an estrogen antagonist, ICI 182780, indicating that the estrogenic activity of glyphosate was mediated via ERs. Furthermore, glyphosate also altered both ERα and β expression. These results indicated that low and environmentally relevant concentrations of glyphosate possessed estrogenic activity. Glyphosate-based herbicides are widely used for soybean cultivation, and our results also found that there was an additive estrogenic effect between glyphosate and genistein, a phytoestrogen in soybeans. However, these additive effects of glyphosate contamination in soybeans need further animal study. FULL TEXT

Swan et al., 2003

Swan SH, Kruse RL, Liu F, Barr DB, Drobnis EZ, Redmon JB, Wang C, Brazil C, Overstreet JW, “Semen quality in relation to biomarkers of pesticide exposure,” Environmental Health Perspectives, 2003, 111:12.

ABSTRACT: We previously reported reduced sperm concentration and motility in fertile men in a U.S. agrarian area (Columbia, MO) relative to men from U.S. urban centers (Minneapolis, MN; Los Angeles, CA; New York, NY). In the present study we address the hypothesis that pesticides currently used in agriculture in the Midwest contributed to these differences in semen quality. We selected men in whom all semen parameters (concentration, percentage sperm with normal morphology, and percentage motile sperm) were low (cases) and men in whom all semen parameters were within normal limits (controls) within Missouri and Minnesota (sample sizes of 50 and 36, respectively) and measured metabolites of eight current-use pesticides in urine samples provided at the time of semen collection. All pesticide analyses were conducted blind with respect to center and case-control status. Pesticide metabolite levels were elevated in Missouri cases, compared with controls, for the herbicides alachlor and atrazine and for the insecticide diazinon [2-isopropoxy-4-methyl-pyrimidinol (IMPY)]; for Wilcoxon rank test, p = 0.0007, 0.012, and 0.0004 for alachlor, atrazine, and IMPY, respectively. Men from Missouri with high levels of alachlor or IMPY were significantly more likely to be cases than were men with low levels [odds ratios (ORs) = 30.0 and 16.7 for alachlor and IMPY, respectively], as were men with atrazine levels higher than the limit of detection (OR = 11.3). The herbicides 2,4-D (2,4-dichlorophenoxyacetic acid) and metolachlor were also associated with poor semen quality in some analyses, whereas acetochlor levels were lower in cases than in controls (p = 0.04). No significant associations were seen for any pesticides within Minnesota, where levels of agricultural pesticides were low, or for the insect repellent DEET (N,N-diethyl-m-toluamide) or the malathion metabolite malathion dicarboxylic acid. These associations between current-use pesticides and reduced semen quality suggest that agricultural chemicals may have contributed to the reduction in semen quality in fertile men from mid-Missouri we reported previously. FULL TEXT

Skinner, 2007

Skinner MK1, “Endocrine disruptors and epigenetic transgenerational disease etiology,” Pediatric Research, 2007, 61:5 Pt 2.

ABSTRACT: Exposure to an environmental factor (e.g. endocrine disruptor) during embryonic gonadal sex determination appears to be epigenetically reprogram the male germ-line and subsequently promote transgenerational adult-onset disease. Disease phenotypes resulting from this epigenetic phenomenon include testis abnormalities, prostate disease, kidney disease, tumor development, and immune abnormalities. The epigenetic mechanism is hypothesized to involve the induction of new imprinted-like DNA sequences in the germ-line to transgenerationally transmit disease phenotypes. This epigenetic transgenerational disease mechanism provides a unique perspective from which to view adult onset disease and ultimately offers new insights into novel diagnostic and therapeutic strategies. FULL TEXT

Skinner et al., 2012

Skinner MK, Manikkam M, Haque MM, Zhang B, Savenkova MI, “Epigenetic transgenerational inheritance of somatic transcriptomes and epigenetic control regions,” Genome Biology, 2012, 13:10, DOI: 10.1186/gb-2012-13-10-r91.

ABSTRACT:

BACKGROUND: Environmentally induced epigenetic transgenerational inheritance of adult onset disease involves a variety of phenotypic changes, suggesting a general alteration in genome activity.

RESULTS: Investigation of different tissue transcriptomes in male and female F3 generation vinclozolin versus control lineage rats demonstrated all tissues examined had transgenerational transcriptomes. The microarrays from 11 different tissues were compared with a gene bionetwork analysis. Although each tissue transgenerational transcriptome was unique, common cellular pathways and processes were identified between the tissues. A cluster analysis identified gene modules with coordinated gene expression and each had unique gene networks regulating tissue-specific gene expression and function. A large number of statistically significant over-represented clusters of genes were identified in the genome for both males and females. These gene clusters ranged from 2-5 megabases in size, and a number of them corresponded to the epimutations previously identified in sperm that transmit the epigenetic transgenerational inheritance of disease phenotypes.

CONCLUSIONS: Combined observations demonstrate that all tissues derived from the epigenetically altered germ line develop transgenerational transcriptomes unique to the tissue, but common epigenetic control regions in the genome may coordinately regulate these tissue-specific transcriptomes. This systems biology approach provides insight into the molecular mechanisms involved in the epigenetic transgenerational inheritance of a variety of adult onset disease phenotypes. FULL TEXT

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