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Bibliography Tag: cancer

Landrigan and Benbrook, 2015

Phillip Landrigan and Charles Benbrook, “GMOs, Herbicides, and Public Health,” Commentary in New England Journal of Medicine, 2015, 373:8, DOI: 10.1056/NEJMp1505660.

ABSTRACT:

Not Available

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Guyton et al., 2015

Kathryn Z Guyton, Dana Loomis, Yann Grosse, Fatiha El Ghissassi, Lamia Benbrahim-Tallaa, Neela Guha, Chiara Scoccianti, Heidi Mattock, Kurt Straif, on behalf of the International Agency for Research on Cancer Monograph Working Group, “Carcinogenicity of tetrachlorvinphos, parathion, malathion, diazinon, and glyphosate,” The Lancet, 2015, 16, DOI: 10.1016/S1470-2045(15)70134-8.

ABSTRACT:

Not Avaialble

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IARC, 2017

International Agency for Research on Cancer. “IARC monographs on the evaluation of carcinogenic risks to humans, volume 112. Glyphosate,” IARC; 2017.

ABSTRACT:

The IARC Monographs identify environmental factors that can increase the risk of human cancer. These include chemicals, complex mixtures, occupational exposures, physical agents, biological agents, and lifestyle factors. National health agencies can use this information as scientific support for their actions to prevent exposure to potential carcinogens.  FULL TEXT

De Roos et al., 2005

Anneclaire J. De Roos, Aaron Blair, Jennifer A. Rusiecki, Jane A. Hoppin, Megan Svec, Mustafa Dosemeci, Dale P. Sandler, and Michael C. Alavanja, “Cancer Incidence among Glyphosate-Exposed Pesticide Applicators in the Agricultural Health Study,” Environmental Health Perspectives, 2005, 113, DOI: 10.1289/EHP.7340.

ABSTRACT:

Glyphosate is a broad-spectrum herbicide that is one of the most frequently applied pesticides in the world. Although there has been little consistent evidence of genotoxicity or carcinogenicity from in vitro and animal studies, a few epidemiologic reports have indicated potential health effects of glyphosate. We evaluated associations between glyphosate exposure and cancer incidence in the Agricultural Health Study (AHS), a prospective cohort study of 57,311 licensed pesticide applicators in Iowa and North Carolina. Detailed information on pesticide use and other factors was obtained from a self-administered questionnaire completed at time of enrollment (1993–1997). Among private and commercial applicators, 75.5% reported having ever used glyphosate, of which > 97% were men. In this analysis, glyphosate exposure was defined as a) ever personally mixed or applied products containing glyphosate; b) cumulative lifetime days of use, or “cumulative exposure days” (years of use × days/year); and c) intensity-weighted cumulative exposure days (years of use × days/year × estimated intensity level). Poisson regression was used to estimate exposure–response relations between glyphosate and incidence of all cancers combined and 12 relatively common cancer subtypes. Glyphosate exposure was not associated with cancer incidence overall or with most of the cancer subtypes we studied. There was a suggested association with multiple myeloma incidence that should be followed up as more cases occur in the AHS. Given the widespread use of glyphosate, future analyses of the AHS will allow further examination of long-term health effects, including less common cancers. FULL TEXT

Vogt et al., 2012

Vogt R, Cassady D, Frost J, Bennett DH, Hertz-Picciotto I, “An assessment of exposures to toxins through diet among California residents,”  Environmental Health, 2012;11:83.

ABSTRACT:

BACKGROUND:  In the absence of current cumulative dietary exposure assessments, this analysis was conducted to estimate exposure to multiple dietary contaminants for children, who are more vulnerable to toxic exposure than adults.

METHODS: We estimated exposure to multiple food contaminants based on dietary data from preschool-age children (2-4 years, n=207), schoolage children (5-7 years, n=157), parents of young children (n=446), and older adults (n=149). We compared exposure estimates for eleven toxic compounds (acrylamide, arsenic, lead, mercury, chlorpyrifos, permethrin, endosulfan, dieldrin, chlordane, DDE, and dioxin) based on selfreported food frequency data by age group. To determine if cancer and non-cancer benchmark levels were exceeded, chemical levels in food were derived from publicly available databases including the Total Diet Study.

RESULTS: Cancer benchmark levels were exceeded by all children (100%) for arsenic, dieldrin, DDE, and dioxins. Non-cancer benchmarks were exceeded by >95% of preschool-age children for acrylamide and by 10% of preschool-age children for mercury. Preschool-age children had significantly higher estimated intakes of 6 of 11 compounds compared to school-age children (p<0.0001 to p=0.02). Based on self-reported dietary data, the greatest exposure to pesticides from foods included in this analysis were tomatoes, peaches, apples, peppers, grapes, lettuce, broccoli, strawberries, spinach, dairy, pears, green beans, and celery.

CONCLUSIONS: Dietary strategies to reduce exposure to toxic compounds for which cancer and non-cancer benchmarks are exceeded by children vary by compound. These strategies include consuming organically produced dairy and selected fruits and vegetables to reduce pesticide intake, consuming less animal foods (meat, dairy, and fish) to reduce intake of persistent organic pollutants and metals, and consuming lower quantities of chips, cereal, crackers, and other processed carbohydrate foods to reduce acrylamide intake.

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Benbrook, 2016c

John Peterson Myers, Michael N. Antoniou, Bruce Blumberg, Lynn Carroll, Theo Colborn, Lorne G. Everett, Michael Hansen, Philip J. Landrigan, Bruce P. Lanphear, Robin Mesnage, Laura N. Vandenberg, Frederick S. vom Saal, Wade V. Welshons and Charles M. Benbrook. “Concerns over use of glyphosate-based herbicides and risks associated with exposures: a consensus statement,” Environmental Health, 2016, 15:19, DOI: 10.1186/s12940-016-0117-0.

ABSTRACT:

The broad-spectrum herbicide glyphosate (common trade name “Roundup”) was first sold to farmers in 1974. Since the late 1970s, the volume of glyphosate-based herbicides (GBHs) applied has increased approximately 100-fold. Further increases in the volume applied are likely due to more and higher rates of application in response to the widespread emergence of glyphosate-resistant weeds and new, pre-harvest, dessicant use patterns. GBHs were developed to replace or reduce reliance on herbicides causing well-documented problems associated with drift and crop damage, slipping efficacy, and human health risks. Initial industry toxicity testing suggested that GBHs posed relatively low risks to non-target species, including mammals, leading regulatory authorities worldwide to set high acceptable exposure limits. To accommodate changes in GBH use patterns associated with genetically engineered, herbicide-tolerant crops, regulators have dramatically increased tolerance levels in maize, oilseed (soybeans and canola), and alfalfa crops and related livestock feeds. Animal and epidemiology studies published in the last decade, however, point to the need for a fresh look at glyphosate toxicity. Furthermore, the World Health Organization’s International Agency for Research on Cancer recently concluded that glyphosate is “probably carcinogenic to humans.” In response to changing GBH use patterns and advances in scientific understanding of their potential hazards, we have produced a Statement of Concern drawing on emerging science relevant to the safety of GBHs. Our Statement of Concern considers current published literature describing GBH uses, mechanisms of action, toxicity in laboratory animals, and epidemiological studies. It also examines the derivation of current human safety standards. We conclude that: (1) GBHs are the most heavily applied herbicide in the world and usage continues to rise; (2) Worldwide, GBHs often contaminate drinking water sources, precipitation, and air, especially in agricultural regions; (3) The half-life of glyphosate in water and soil is longer than previously recognized; (4) Glyphosate and its metabolites are widely present in the global soybean supply; (5) Human exposures to GBHs are rising; (6) Glyphosate is now authoritatively classified as a probable human carcinogen; (7) Regulatory estimates of tolerable daily intakes for glyphosate in the United States and European Union are based on outdated science. We offer a series of recommendations related to the need for new investments in epidemiological studies, biomonitoring, and toxicology studies that draw on the principles of endocrinology to determine whether the effects of GBHs are due to endocrine disrupting activities. We suggest that common commercial formulations of GBHs should be prioritized for inclusion in government-led toxicology testing programs such as the U.S. National Toxicology Program, as well as for biomonitoring as conducted by the U.S. Centers for Disease Control and Prevention.  FULL TEXT

Portier et al., 2016

Christopher J Portier, Bruce K Armstrong, Bruce C Baguley, Xaver Baur, Igor Belyaev, Robert Bellé, Fiorella Belpoggi, Annibale Biggeri, Maarten C Bosland, Paolo Bruzzi, Lygia Therese Budnik, Merete D Bugge, Kathleen Burns, Gloria M Calaf, David O Carpenter, Hillary M Carpenter, Lizbeth López-Carrillo, Richard Clapp, Pierluigi Cocco, Dario Consonni, Pietro Comba, Elena Craft, Mohamed Aqiel Dalvie, Devra Davis, Paul A Demers, Anneclaire J De Roos, Jamie DeWitt, Francesco Forastiere, Jonathan H Freedman, Lin Fritschi, Caroline Gaus, Julia M Gohlke, Marcel Goldberg, Eberhard Greiser, Johnni Hansen, Lennart Hardell, Michael Hauptmann, Wei Huang, James Huff, Margaret O James, C W Jameson, Andreas Kortenkamp, Annette Kopp-Schneider, Hans Kromhout, Marcelo L Larramendy, Philip J Landrigan, Lawrence H Lash, Dariusz Leszczynski, Charles F Lynch, Corrado Magnani, Daniele Mandrioli, Francis L Martin, Enzo Merler, Paola Michelozzi, Lucia Miligi, Anthony B Miller, Dario Mirabelli, Franklin E Mirer, Saloshni Naidoo, Melissa J Perry, Maria Grazia Petronio, Roberta Pirastu, Ralph J Portier, Kenneth S Ramos, Larry W Robertson, Theresa Rodriguez, Martin Röösli, Matt K Ross, Deodutta Roy, Ivan Rusyn, Paulo Saldiva, Jennifer Sass, Kai Savolainen, Paul T J Scheepers, Consolato Sergi, Ellen K Silbergeld, Martyn T Smith, Bernard W Stewart, Patrice Sutton, Fabio Tateo, Benedetto Terracini, Heinz W Thielmann, David B Thomas, Harri Vainio, John E Vena, Paolo Vineis, Elisabete Weiderpass, Dennis D Weisenburger, Tracey J Woodruff, Takashi Yorifuji, Il Je Yu, Paola Zambon, Hajo Zeeb,Shu-Feng Zhou, “Differences in the carcinogenic evaluation of glyphosate between the International Agency for Research on Cancer (IARC) and the European Food Safety Authority (EFSA),” Journal of Epidemiology and Community Health, 2016, 0:0, DOI: 10.1136/JECH-2015-207005.

ABSTRACT:

Not Available

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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

Rusiecki et al., 2017

Rusiecki JA, Beane Freeman LE, Bonner MR, Alexander M, Chen L, Andreotti G, Barry KH, Moore LE, Byun HM, Kamel F, Alavanja M, Hoppin JA, Baccarelli A,”High pesticide exposure events and DNA methylation among pesticide applicators in the agricultural health study,” Environmental and Molecular Mutagenesis, 2017, 58:1, DOI: 10.1002/em.22067.

ABSTRACT: Pesticide exposure has been associated with acute and chronic adverse health effects. DNA methylation (DNAm) may mediate these effects. We evaluated the association between experiencing unusually high pesticide exposure events (HPEEs) and DNAm among pesticide applicators in the Agricultural Health Study (AHS), a prospective study of applicators from Iowa and North Carolina. DNA was extracted from whole blood from male AHS pesticide applicators (n = 695). Questionnaire data were used to ascertain the occurrence of HPEEs over the participant’s lifetime. Pyrosequencing was used to quantify DNAm in CDH1, GSTp1, and MGMT promoters, and in the repetitive element, LINE-1. Linear and robust regression analyses evaluated adjusted associations between HPEE and DNAm. Ever having an HPEE (n = 142; 24%) was associated with elevated DNAm in the GSTp1 promoter at CpG7 (chr11:67,351,134; P < 0.01) and for the mean across the CpGs measured in the GSTp1 promoter (P < 0.01). In stratified analyses, elevated GSTP1 promoter DNAm associated with HPEE was more pronounced among applicators >59 years and those with plasma folate levels ≤16.56 ng/mL (p-interaction <0.01); HPEE was associated with reduced MGMT promoter DNAm at CpG2 (chr10:131,265,803; P = 0.03), CpG3 (chr10:131,265,810; P = 0.05), and the mean across CpGs measured in the MGMT promoter (P = 0.03) among applicators >59 years and reduced LINE-1 DNAm (P = 0.05) among applicators with ≤16.56 ng/mL plasma folate. Non-specific HPEEs may contribute to increased DNAm in GSTp1, and in some groups, reduced DNAm in MGMT and LINE-1. The impacts of these alterations on disease development are unclear, but elevated GSTp1 promoter DNAm and subsequent gene inactivation has been consistently associated with prostate cancer.

Roberts and Karr, 2012

Roberts JR, Karr CJ,  “Pesticide exposure in children,” 2012, Pediatrics,  130:6.

ABSTRACT: This statement presents the position of the American Academy of Pediatrics on pesticides. Pesticides are a collective term for chemicals intended to kill unwanted insects, plants, molds, and rodents. Children encounter pesticides daily and have unique susceptibilities to their potential toxicity. Acute poisoning risks are clear, and understanding of chronic health implications from both acute and chronic exposure are emerging. Epidemiologic evidence demonstrates associations between early life exposure to pesticides and pediatric cancers, decreased cognitive function, and behavioral problems. Related animal toxicology studies provide supportive biological plausibility for these findings. Recognizing and reducing problematic exposures will require attention to current inadequacies in medical training, public health tracking, and regulatory action on pesticides. Ongoing research describing toxicologic vulnerabilities and exposure factors across the life span are needed to inform regulatory needs and appropriate interventions. Policies that promote integrated pest management, comprehensive pesticide labeling, and marketing practices that incorporate child health considerations will enhance safe use.  FULL TEXT

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