Bibliography Tag: science team publication

Haas et al., 2015

Haas, D. M., Parker, C. B., Wing, D. A., Parry, S., Grobman, W. A., Mercer, B. M., Simhan, H. N., Hoffman, M. K., Silver, R. M., Wadhwa, P., Iams, J. D., Koch, M. A., Caritis, S. N., Wapner, R. J., Esplin, M. S., Elovitz, M. A., Foroud, T., Peaceman, A. M., Saade, G. R., Willinger, M., Reddy, U. M., & NuMo, M. b study; “A description of the methods of the Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be (nuMoM2b);” American Journal of Obstetrics & Gynecology, 2015, 212(4), 539 e531-539 e524; DOI: 10.1016/j.ajog.2015.01.019.


OBJECTIVE: The primary aim of the “Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be” is to determine maternal characteristics, which include genetic, physiologic response to pregnancy, and environmental factors that predict adverse pregnancy outcomes.

STUDY DESIGN: Nulliparous women in the first trimester of pregnancy were recruited into an observational cohort study. Participants were seen at 3 study visits during pregnancy and again at delivery. We collected data from in-clinic interviews, take-home surveys, clinical measurements, ultrasound studies, and chart abstractions. Maternal biospecimens (serum, plasma, urine, cervicovaginal fluid) at antepartum study visits and delivery specimens (placenta, umbilical cord, cord blood) were collected, processed, and stored. The primary outcome of the study was defined as pregnancy ending at <37+0 weeks’ gestation. Key study hypotheses involve adverse pregnancy outcomes of spontaneous preterm birth, preeclampsia, and fetal growth restriction.

RESULTS: We recruited 10,037 women to the study. Basic characteristics of the cohort at screening are reported.

CONCLUSION: The “Nulliparous Pregnancy Outcomes Study: monitoring mothers-to-be” cohort study methods and procedures can help investigators when they plan future projects.


Perry et al., 2019

Perry, M. J., Mandrioli, D., Belpoggi, F., Manservisi, F., Panzacchi, S., & Irwin, C.; “Historical evidence of glyphosate exposure from a US agricultural cohort;” Environmental Health, 2019, 18(1), 42; DOI: 10.1186/s12940-019-0474-6.


In response to the recent review by Gillezeau et al., The evidence of human exposure to glyphosate: A review, Environmental Health 1/19/19, here we report additional glyphosate biomonitoring data from a repository of urine samples collected from United States farmers in 1997-98. To determine if glyphosate exposure could be identified historically, we examined urine samples from a biorepository of specimens collected from US dairy farmers between 1997 and 98. We compared samples from farmers who self-reported glyphosate application in the 8 h prior to sample collection to samples from farm applicators who did not report using glyphosate. Of 18 applicator samples tested, 39% showed detectable levels of glyphosate (mean concentration 4.04 mug/kg; range:1.3-12) compared to 0% detections among 17 non glyphosate applicator samples (p-value < 0.01). One of the applicator samples that tested positive for glyphosate also tested positive for AMPA. Concentrations of glyphosate were consistent with levels reported in the prior occupational biomonitoring studies reviewed by Gillezeau et al.Accurately detecting both glyphosate and AMPA in this small sample of Wisconsin farmers demonstrates a) glyphosate exposures among farmers were occurring 20 years ago, which was prior to the widespread planting of genetically engineered glyphosate tolerant crops first approved in 1996; and b) liquid chromatography tandem mass spectrometry (LC-MS/MS) can be used for sensitive characterization in cryopreserved urine samples. These data offer an important historical benchmark to which urinary levels from current and future biomonitoring studies can be compared. FULL TEXT

Perro, 2019

Perro, Michelle, “Childhood Leukemia, the Microbiome, and Glyphosate: A Doctor’s Perspective,”, January 15, 2019.


  • Childhood leukemia is on the rise
  • Exposure to pesticides is known to increase the risk of childhood leukemia, as well as other types of cancer
  • New research links an impoverished gut microbiome (bacterial community) and chronic inflammation with increased risk of childhood leukemia
  • Diet-related ways are being sought to improve the microbiome and prevent the inflammation that triggers childhood leukemia
  • Glyphosate herbicides are used on around 90% of GM crops; glyphosate has been classified as a probable carcinogen by the World Health Organization’s cancer agency IARC
  • Exposure to glyphosate-based and other pesticides has been shown to disrupt the gut microbiome in laboratory animals
  • People who eat organic food have been found to have a 25% reduced risk of cancer
  • Clinical experience shows that switching to an organic and non-GMO diet improves people’s health
  • Controlled studies are needed to verify how switching to an organic and non-GMO diet affects the microbiome and certain disease conditions.


Perro and Adams, 2017

Perro, Michelle and Adams, Vincanne, “What’s Making Our Children Sick? How Industrial Food Is Causing an Epidemic of Chronic Illness, and What Parents (and Doctors) Can Do About It,” Chelsea Green Publishing, 2017.


With chronic disorders among American children reaching epidemic levels, hundreds of thousands of parents are desperately seeking solutions to their children’s declining health, often with little medical guidance from the experts. What’s Making Our Children Sick? convincingly explains how agrochemical industrial production and genetic modification of foods is a culprit in this epidemic. Is it the only culprit? No. Most chronic health disorders have multiple causes and require careful disentanglement and complex treatments. But what if toxicants in our foods are a major culprit, one that, if corrected, could lead to tangible results and increased health? Using patient accounts of their clinical experiences and new medical insights about pathogenesis of chronic pediatric disorders—taking us into gut dysfunction and the microbiome, as well as the politics of food science—this book connects the dots to explain our kids’ ailing health.

What’s Making Our Children Sick? explores the frightening links between our efforts to create higher-yield, cost-efficient foods and an explosion of childhood morbidity, but it also offers hope and a path to effecting change. The predicament we now face is simple. Agroindustrial “innovation” in a previous era hoped to prevent the ecosystem disaster of DDT predicted in Rachel Carson’s seminal book in 1962, Silent Spring. However, this industrial agriculture movement has created a worse disaster: a toxic environment and, consequently, a toxic food supply. Pesticide use is at an all-time high, despite the fact that biotechnologies aimed to reduce the need for them in the first place. Today these chemicals find their way into our livestock and food crop industries and ultimately onto our plates. Many of these pesticides are the modern day equivalent of DDT. However, scant research exists on the chemical soup of poisons that our children consume on a daily basis. As our food supply environment reels under the pressures of industrialization via agrochemicals, our kids have become the walking evidence of this failed experiment. What’s Making Our Children Sick? exposes our current predicament and offers insight on the medical responses that are available, both to heal our kids and to reverse the compromised health of our food supply.

Mesnage et al., 2019

Mesnage, R., Benbrook, C., & Antoniou, M. N.; “Insight into the confusion over surfactant co-formulants in glyphosate-based herbicides;” Food and Chemical Toxicology, 2019, 128, 137-145; DOI: 10.1016/j.fct.2019.03.053.


Glyphosate is the active ingredient in glyphosate-based herbicides (GBHs). Other chemicals in GBHs are presumed as inert by regulatory authorities and are largely ignored in pesticide safety evaluations. We identified the surfactants in a cross-section of GBH formulations and compared their acute toxic effects. The first generation of polyethoxylated amine (POEA) surfactants (POE-tallowamine) in Roundup are markedly more toxic than glyphosate and heightened concerns of risks to human health, especially among heavily-exposed applicators. Beginning in the mid-1990s, first-generation POEAs were progressively replaced by other POEA surfactants, ethoxylated etheramines, which exhibited lower non-target toxic effects. Lingering concern over surfactant toxicity was mitigated at least in part within the European Union by the introduction of propoxylated quaternary ammonium surfactants. This class of POEA surfactants are approximately 100 times less toxic to aquatic ecosystems and human cells than previous GBH-POEA surfactants. As GBH composition is legally classified as confidential commercial information, confusion concerning the identity and concentrations of co-formulants is common and descriptions of test substances in published studies are often erroneous or incomplete. In order to resolve this confusion, laws requiring disclosure of the chemical composition of pesticide products could be enacted. Research to understand health implications from ingesting these substances is required. FULL TEXT

Landrigan and Goldman, 2011

Landrigan, Philip J, & Goldman, Lynn R; “Children’s vulnerability to toxic chemicals: a challenge and opportunity to strengthen health and environmental policy;” Health Affairs, 2011, 30(5), 842-850; DOI: 10.1377/hlthaff.2011.0151.


A key policy breakthrough occurred nearly twenty years ago with the discovery that children are far more sensitive than adults to toxic chemicals in the environment. This finding led to the recognition that chemical exposures early in life are significant and preventable causes of disease in children and adults. We review this knowledge and recommend a new policy to regulate industrial and consumer chemicals that will protect the health of children and all Americans, prevent disease, and reduce health care costs. The linchpins of a new US chemical policy will be: first, a legally mandated requirement to test the toxicity of chemicals already in commerce, prioritizing chemicals in the widest use, and incorporating new assessment technologies; second, a tiered approach to premarket evaluation of new chemicals; and third, epidemiologic monitoring and focused health studies of exposed populations.  FULL TEXT

Winchester et al., 2019

Winchester, Paul, Reiter, Jill L., Proctor, Cathy, Gerona, Roy R., Avery, Kayleigh D., Bromm, Jennifer R., Elsahy, Deena A, Hadley, Emily A., McGraw, Sara N., & Jones, Dana D., “Glyphosate in 1st Trimester of Pregnancy: Herbicides in the Womb,” 2019, Presented at the Pediatric Academic Societies (PAS) Meeting 2019, 4/24-5/1/2019, Baltimore, MD.


BACKGROUND: Our previous study demonstrated that >90% of pregnant Midwest women had detectable glyphosate (GLY) in their urine. Most glyphosate exposure occurs through food & certain beverages but not through drinking water. Shorter pregnancies, rural address and caffeinated beverages were associated with higher GLY levels. The cohort was small and predominantly Caucasian. The current study was needed to confirm high rates of GLY detection in a racially more diverse high risk population.
OBJECTIVE: Will GLY be detected in a majority of pregnancies regardless of race/ethnicity? Are GLY levels associated with adverse pregnancy outcomes? Do GLY levels vary by season of collection in pregnancy?
DESIGN/METHODS: Prospective observation study. Discarded urine from 1st trimester pregnancies were collected prospectively from a high risk University obstetrical clinic. All pregnancy outcomes and neonatal outcomes were abstracted. Urines were frozen, shipped to analytical lab (USCF, RG) for analysis. Urine GLY (Glyphosate (N(phosphomethyl) glycine) was analyzed via liquid chromatography-tandem mass spectrometry (LC-MS/MS), limit of quantification of 0.1 ng/mL. GLY measured as independent variable was compared to multiple variables using bivariate analysis.
RESULTS: GLY was detected in 99% (186 of 187) pregnancies. Levels varied from 1.004 to 10.31ng/mL with geometric mean 3.264ng/mL. Mean maternal age was 30, with 69% white, 4.2% Hispanic, 12% Black, 3.7% Asian and one “other”. GLY levels did not differ significantly by racial/ethnic group. GLY levels were not significantly difference between preterm and term outcomes, multiple/singleton or between fetal loss and live births. GLY levels were higher with increasing gestation at enrollment with 4-8 weeks GLY 2.73 vs 9-13 weeks 3.51(p=.0098). Significantly higher GLY levels were found in April-July pregnancies vs other months(3.64 vs 3.07 p=.03). NICU admission rates were 85% for preterm and 35% for term. Birth defect rate was12% and 37% had intrauterine drug exposure or NAS. Preterm birth rate was 31%. CONCLUSIONS: Glyphosate was found in virtually all of these high risk pregnancies in the first trimester regardless of race/ethnicity, plurality, fetal loss or gestation at birth. GLY levels rose with increasing gestation in the first trimester suggesting that gestation at measurement impacts GLY levels. Dietary sources contribute to GLY but we did find April-July are associated with higher GLY levels than other months. The fetal epigenetic consequences of 1st trimester GLY exposure remains unknown. 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.


• 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

Benbrook, 2019

Benbrook, Charles M., “How did the US EPA and IARC reach diametrically opposed conclusions on the genotoxicity of glyphosate-based herbicides?,” Environmental Sciences Europe, 2019, 31(1), DOI:10.1186/s12302-018-0184-7.


BACKGROUND: The US EPA considers glyphosate as “not likely to be carcinogenic to humans.” The International Agency for Research on Cancer (IARC) has classified glyphosate as “probably carcinogenic to humans (Group 2A).” EPA asserts that there is no convincing evidence that “glyphosate induces mutations in vivo via the oral route.” IARC concludes there is “strong evidence” that exposure to glyphosate is genotoxic through at least two mechanisms known to be associated with human carcinogens (DNA damage, oxidative stress). Why and how did EPA and IARC reach such different conclusions?

RESULTS: A total of 52 genotoxicity assays done by registrants were cited by the EPA in its 2016 evaluation of technical glyphosate, and another 52 assays appeared in the public literature. Of these, one regulatory assay (2%) and 35 published assays (67%) reported positive evidence of a genotoxic response. In the case of formulated, glyphosatebased herbicides (GBHs), 43 regulatory assays were cited by EPA, plus 65 assays published in peer-reviewed journals. Of these, none of the regulatory, and 49 published assays (75%) reported evidence of a genotoxic response following exposure to a GBH. IARC considered a total of 118 genotoxicity assays in six core tables on glyphosate technical, GBHs, and aminomethylphosphonic acid (AMPA), glyphosate’s primary metabolite. EPA’s analysis encompassed 51 of these 118 assays (43%). In addition, IARC analyzed another 81 assays exploring other possible genotoxic mechanisms (mostly related to sex hormones and oxidative stress), of which 62 (77%) reported positive results. IARC placed considerable weight on three positive GBH studies in exposed human populations, whereas EPA placed little or no weight on them.

CONCLUSIONS: EPA and IARC reached diametrically opposed conclusions on glyphosate genotoxicity for three primary reasons: (1) in the core tables compiled by EPA and IARC, the EPA relied mostly on registrant-commissioned, unpublished regulatory studies, 99% of which were negative, while IARC relied mostly on peer-reviewed studies of which 70% were positive (83 of 118); (2) EPA’s evaluation was largely based on data from studies on technical glyphosate, whereas IARC’s review placed heavy weight on the results of formulated GBH and AMPA assays; (3) EPA’s evaluation was focused on typical, general population dietary exposures assuming legal, food-crop uses, and did not take into account, nor address generally higher occupational exposures and risks. IARC’s assessment encompassed data from typical dietary, occupational, and elevated exposure scenarios. More research is needed on real-world exposures to the chemicals within formulated GBHs and the biological fate and consequences of such exposures. FULL TEXT

Benbrook, 2018

Benbrook, Charles, “Why Regulators Lost Track and Control of Pesticide Risks: Lessons From the Case of Glyphosate-Based Herbicides and Genetically Engineered-Crop Technology,” Current Environmental Health Reports, 5:3, 387-395, 2018, DOI:10.1007/s40572-018-0207-y.


PURPOSE OF REVIEW: The approval of genetically engineered (GE) crops in the late 1990s triggered dramatic changes in corn, soybean, and cotton pest management systems, as well as complex, novel regulatory challenges. Lessons learned are reviewed and solutions described.

RECENT FINDINGS: Government-imposed resistance management provisions can work and adapt to changing circumstances, but within the private sector, pressures to gain and hold market share have thus far trumped the widely recognized need for resistance management. Risks arising from the use of formulated pesticides often exceed by a wide margin those in regulatory risk assessments based on data derived from studies on nearly 100% pure active ingredients.

SUMMARY: Innovative policy changes are needed in four problem areas: excessive faith in the accuracy of pre-market risk assessments and regulatory thresholds; post-approval monitoring of actual impacts; risk arising from formulated pesticides, rather than just pure active ingredient; challenges inherent in assessing and mitigating the combined impacts of all GE traits and associated pesticides on agroecosystems, as opposed to each trait or pesticide alone; and, tools to deal with failing pest management systems. FULL TEXT