What are you putting on your baby? Or on your genitals?

Sanitary pads and diapers contain higher phthalate contents than those in common commercial plastic products

2019 Study Highlights

  • Three VOCs and 4 phthalates were measured in commercial sanitary pads and diapers.
  • Air in the packages of sanitary pads and diapers contained as high as 5.9 ppb of VOCs.
  • Sanitary pads and diapers contained as high as 8,014.9 ppb of phthalates.
  • VOCs and phthalates contained in the commercial products considerably vary among the brands.

Abstract

Sanitary pads and diapers are made of synthetic plastic materials that can potentially be released while being used. This study measured the amounts of volatile organic compounds (VOCs) (methylene chloride, toluene, and xylene) and phthalates (DBP, DEHP, DEP, and BBP) contained in sanitary pads and diapers. In sanitary pads, 5,900- and 130-fold differences of VOC and phthalate concentrations were seen among the brands. In the diapers, 3- and 63-fold differences of VOC and phthalate concentrations were detected among the brands. VOC concentrations from the sanitary pads and diapers were similar to that of the residential air. However, phthalate concentrations of sanitary pads and diapers were significantly higher than those found in common commercial plastic products. As sanitary pads and diapers are in direct contact with external genitalia for an extended period, there is a probability that a considerable amount of VOCs or phthalates could be absorbed into the reproductive system.

 

Fracking chemicals entering the food chain

Accumulation of Marcellus Formation Oil and Gas Wastewater Metals in Freshwater Mussel Shells

Radioactive fracking chemicals dumped in the Allegheny River a decade ago are still showing up in mussels, Environmental Health News
reports. Chemicals from fracking wastewater dumped into Pennsylvania’s Allegheny River before 2011 are still accumulating in the bodies of freshwater mussels downstream, according to a new study.

Abstract

For several decades, high-salinity water brought to the surface during oil and gas (O&G) production has been treated and discharged to waterways under National Pollutant Discharge Elimination System (NPDES) permits.

In Pennsylvania, USA, a portion of the treated O&G wastewater discharged to streams from 2008 to 2011 originated from unconventional (Marcellus) wells.

We collected freshwater mussels, Elliptio dilatata and Elliptio complanata, both upstream and downstream of a NPDES-permitted facility, and for comparison, we also collected mussels from the Juniata and Delaware Rivers that have no reported O&G discharge.

We observed changes in both the Sr/Cashell and 87Sr/86Srshell in shell samples collected downstream of the facility that corresponded to the time period of greatest Marcellus wastewater disposal (2009–2011). Importantly, the changes in Sr/Cashell and 87Sr/86Srshell shifted toward values characteristic of O&G wastewater produced from the Marcellus Formation. Conversely, shells collected upstream of the discharge and from waterways without treatment facilities showed lower variability and no trend in either Sr/Cashell or 87Sr/86Srshell with time (2008–2015).

These findings suggest that

  1. freshwater mussels may be used to monitor changes in water chemistry through time and help identify specific pollutant sources
  2. and O&G contaminants likely bioaccumulated in areas of surface water disposal.

How (living) close to a fracking site is too close (to residents for safety) ?

Setback distances for unconventional oil and gas development: Delphi study results

Regulations on how close fracking facilities can be to buildings and homes in Pennsylvania are too lax to adequately protect public health, according to a new study.

To protect public health, a panel of experts recommends more than doubling the required distance between frack wells and homes, Environmental Health News reports, Aug 23, 2018.

Abstract

Emerging evidence indicates that proximity to unconventional oil and gas development (UOGD) is associated with health outcomes. There is intense debate about “How close is too close?” for maintaining public health and safety.

The goal of this Delphi study was to elicit expert consensus on appropriate setback distances for UOGD from human activity.

Three rounds were used to identify and seek consensus on recommended setback distances. The 18 panelists were health care providers, public health practitioners, environmental advocates, and researchers/scientists. Consensus was defined as agreement of ≥70% of panelists.

  1. Content analysis of responses to Round 1 questions revealed four categories:
    1. recommend setback distances;
    2. do not recommend setback distances;
    3. recommend additional setback distances for vulnerable populations;
    4. do not recommend additional setback distances for vulnerable populations.
  2. In Round 2, panelists indicated their level of agreement with the statements in each category using a five-point Likert scale.
  3. Based on emerging consensus, statements within each category were collapsed into seven statements for Round 3:
    • recommend set back distances of <¼ mile;
    • ¼—½ mile;
    • 1–1 ¼ mile;
    • and ≥ 2 mile;
    • not feasible to recommend setback distances;
    • recommend additional setbacks for vulnerable groups;
    • not feasible to recommend additional setbacks for vulnerable groups.

The panel reached consensus that setbacks of < ¼ mile should not be recommended and additional setbacks for vulnerable populations should be recommended. The panel did not reach consensus on recommendations for setbacks between ¼ and 2 miles.

The results suggest that if setbacks are used the distances should be greater than ¼ of a mile from human activity, and that additional setbacks should be used for settings where vulnerable groups are found, including schools, daycare centers, and hospitals. The lack of consensus on setback distances between 1/4 and 2 miles reflects the limited health and exposure studies and need to better define exposures and track health.

Stress and depression higher among people living near fracking sites

Associations of unconventional natural gas development with depression symptoms and disordered sleep in Pennsylvania

People who live near unconventional natural gas operations such as fracking are more likely to experience depression, Environmental Health News reports.
Featured image credit frackfreeryedale.org.

Abstract

Environmental and community factors may influence the development or course of depression and sleep problems.

In this study, we evaluated the association of unconventional natural gas development (UNGD) with depression symptoms and disordered sleep diagnoses using the Patient Health Questionnaire-8 and electronic health record data among Geisinger adult primary care patients in Pennsylvania.
Participants received a retrospective metric for UNGD at their residence (very low, low, medium, and high) that incorporated dates and durations of well development, distance from patient homes to wells, and well characteristics.

Analyses included 4,762 participants with no (62%), mild (23%), moderate (10%), and moderately severe or severe (5%) depression symptoms in 2014–2015 and 3,868 disordered sleep diagnoses between 2009–2015. We observed associations between living closer to more and bigger wells and depression symptoms, but not disordered sleep diagnoses in models weighted to account for sampling design and participation.

High UNGD (vs. very low) was associated with depression symptoms in an adjusted negative binomial model (exponentiated coefficient = 1.18, 95% confidence interval [CI]: 1.04–1.34). High and low UNGD (vs. very low) were associated with depression symptoms (vs. none) in an adjusted multinomial logistic model.

Our findings suggest that UNGD may be associated with adverse mental health in Pennsylvania.

Link between fracking chemicals and immune system problems

Developmental Exposure to a Mixture of 23 Chemicals Associated With Unconventional Oil and Gas Operations Alters the Immune System of Mice

Chemicals commonly found in groundwater near fracked oil and gas wells appear to impair the proper functioning of the immune system, Environmental Health News reports.

The new study suggests that baby girls born to mothers near fracking wells may not fight diseases later in life as well as they could have with a pollution-free pregnancy.

2018 Study Abstract

Chemicals used in unconventional oil and gas (UOG) operations have the potential to cause adverse biological effects, but this has not been thoroughly evaluated. A notable knowledge gap is their impact on development and function of the immune system.

Herein, we report an investigation of whether developmental exposure to a mixture of chemicals associated with UOG operations affects the development and function of the immune system. We used a previously characterized mixture of 23 chemicals associated with UOG, and which was demonstrated to affect reproductive and developmental endpoints in mice. C57Bl/6 mice were maintained throughout pregnancy and during lactation on water containing two concentrations of this 23-chemical mixture, and the immune system of male and female adult offspring was assessed. We comprehensively examined the cellularity of primary and secondary immune organs, and used three different disease models to probe potential immune effects: house dust mite-induced allergic airway disease, influenza A virus infection, and experimental autoimmune encephalomyelitis (EAE). In all three disease models, developmental exposure altered frequencies of certain T cell sub-populations in female, but not male, offspring. Additionally, in the EAE model disease onset occurred earlier and was more severe in females.

Our findings indicate that developmental exposure to this mixture had persistent immunological effects that differed by sex, and exacerbated responses in an experimental model of autoimmune encephalitis. These observations suggest that developmental exposure to complex mixtures of water contaminants, such as those derived from UOG operations, could contribute to immune dysregulation and disease later in life.

Serious health hazards for infants and children living near fracking sites

Neurodevelopmental and neurological effects of chemicals associated with unconventional oil and natural gas operations and their potential effects on infants and children

Multiple pollutants found in the air and water near fracked oil and gas sites are linked to brain problems in children.

2017 Study Abstract

Heavy metals (arsenic and manganese), particulate matter (PM), benzene, toluene, ethylbenzene, xylenes (BTEX), polycyclic aromatic hydrocarbons (PAHs) and endocrine disrupting chemicals (EDCs) have been linked to significant neurodevelopmental health problems in infants, children and young adults.

These substances are widely used in, or become byproducts of unconventional oil and natural gas (UOG) development and operations. Every stage of the UOG lifecycle, from well construction to extraction, operations, transportation and distribution can lead to air and water contamination. Residents near UOG operations can suffer from increased exposure to elevated concentrations of air and water pollutants.

Here we focus on five air and water pollutants that have been associated with potentially permanent learning and neuropsychological deficits, neurodevelopmental disorders and neurological birth defects. Given the profound sensitivity of the developing brain and central nervous system, it is reasonable to conclude that young children who experience frequent exposure to these pollutants are at particularly high risk for chronic neurological diseases.

More research is needed to understand the extent of these concerns in the context of UOG, but since UOG development has expanded rapidly in recent years, the need for public health prevention techniques, well-designed studies and stronger state and national regulatory standards is becoming increasingly apparent.

More Information

  • Full study (free access) Neurodevelopmental and neurological effects of chemicals associated with unconventional oil and natural gas operations and their potential effects on infants and children, Reviews on Environmental Health, doi.org/10.1515/reveh-2017-0008, 2017-10-25.
  • Fracking chemicals and kids’ brains don’t mix: Study, Environmental Health News, 2017-10-25.
  • Featured image credit WildEarth Guardians and @EnvirHealthNews.

Efficient technology to remove BPA and similar chemicals from water

A multidisciplinary investigation of the technical and environmental performances of TAML/peroxide elimination of Bisphenol A compounds from water

As water treatment plants struggle to keep up with the chemical cocktail heading into our pipes, researchers say they’ve come up with a solution to remove one of the most ubiquitous contaminants—BPA.

There now exists economically viable, efficient technology to remove bisphenol A (BPA) and a host of similar chemicals from water.

2017 Study Conclusion

In developing Green Chemistry, it is important that chemists come to understand the scope of the challenges posed by everyday-everywhere endocrine disruptors (EDs) to the sustainability of both the chemical enterprise and our complex global civilization. The most troubling such EDs, like BPA, invariably hold their protected positions in the economy because of seductive technical and cost performances that enable large, diverse, profitable markets. For sustainable chemicals, the health, environmental and fairness performances also have to be integral components of the value proposition. Understanding the negative performances of unsustainable chemicals helps in mapping the properties sustainable chemicals should not have. Key aspects of this understanding include the knowledge of which chemicals are and are not EDs and are and are not capable of eliciting low dose adverse effects by non-endocrine processes, the extent and routes by which the environment and people are exposed to commercial EDs, the environmental and human health consequences of ED exposures, the methods of assessment of endocrine activity including the TiPED, the mechanisms of the low dose adverse effects, the design approaches to attaining new and replacement chemicals free of such effects, and the stewardship methodologies that are currently deployed or might be deployed to better protect health and the environment from commercial EDs. This BPA case study traverses the appropriate multidisciplinary landscape with emphasis on the integration of chemistry and environmental health science in the development of endocrine disruption-free processes to aid the chemical enterprise and society in reducing BPA exposures. Importantly, the litany of unfortunate facts presented about BPA exposures and health and environmental performances is relieved to some extent by the possibility of reduced releases arising from the TAML/H2O2 technology mapped out in the empirical section.

This experimental component demonstrates that TAML/H2O2 provides simple, effective water treatment methodologies, which depending on the pH, either decompose BPA or isolate it in low solubility oligomers. Both processes require only very low concentrations of TAML activator and H2O2 in further reflection of the remarkable efficiencies of the peroxidase enzymes that are faithfully mimicked by TAML activator and in marked contrast with the much higher relative iron- and peroxide-requiring Fenton processes. It remains to be established whether the current laboratory studies project to real world scenarios. These may include treatment of BPA-contaminated landfill leachates and paper plant processing solutions where the concentrations are similar to those employed in this study. In such scenarios, TAML/H2O2 would present an enzyme-mimicking method which in the case of TAML activator is comprised exclusively of biochemically common elements and has passed multiple TiPED assays that, in contrast with existing real world processes, avoids generation of BPA-contaminated sludges and associated subsequent releases to soil, that does not generate a contaminated adsorbent which must be replaced or regenerated at elevated temperature, that does not generate chlorinated forms of BPA, that does not generate a concentrated retentate, and that is remarkably simple to deploy using very low and cheap chemical inputs with all the positive potential consequences thereof for capital and operating expenses.

Finally, in order to avoid the habit or perception of greenwashing, a realistic perspective is essential to the integrity of green chemistry. We view the sustainability challenges posed by BPA as enormous—the experimental work presented could evolve into a solution for some of these problems but is, by no means, a general quick fix. BPA markets large and small are expanding rapidly, especially as the industry has learned how to produce even more effective replacements for glass and metal products. Huge new markets are developing such as those of plastic glass houses, and even houses, and automobile body parts that are comprised primarily of BPA. In this build-up, BPA’s unfortunate health and environmental performances continue to be given short shrift. Continuation of the present BPA expansion trends without limits, technical corrections and more aggressive stewardship advances of multiple kinds will menace society with an ever increasing oestrogenization of the entire ecosphere.

Sources and More Information
  • BPA breakthrough: New treatment takes controversial chemical out of water, EHN, August 2, 2017.
  • Science: Pay attention to two other messages in the breakthrough BPA water treatment paper, EHN, August 8, 2017.
  • A multidisciplinary investigation of the technical and environmental performances of TAML/peroxide elimination of Bisphenol A compounds from water, pubs, 19th July 2017.
  • Feature image credit Leland Francisco.

The Florence Statement on Triclosan and Triclocarban

More than 200 scientists outline a broad range of concerns for triclosan and triclocarban and call for reduced use worldwide

Two ingredients used in thousands of products to kill bacteria, fungi and viruses linger in the environment and pose a risk to human health, according to a statement released today by more than 200 scientists and health professionals.

The scientists say the possible benefits in most uses of triclosan and triclocarban – used in some soaps, toothpastes, detergents, paints, carpets – are not worth the risk.

SUMMARY

“Triclosan and triclocarban have been permitted for years without definitive proof they’re providing benefits.”

Avery Lindeman, Green Policy Institute

The Florence Statement on Triclosan and Triclocarban documents a consensus of more than 200 scientists and medical professionals on the hazards of and lack of demonstrated benefit from common uses of triclosan and triclocarban.

These chemicals may be used in thousands of personal care and consumer products as well as in building materials. Based on extensive peer-reviewed research, this statement concludes that triclosan and triclocarban are environmentally persistent endocrine disruptors that bioaccumulate in and are toxic to aquatic and other organisms. Evidence of other hazards to humans and ecosystems from triclosan and triclocarban is presented along with recommendations intended to prevent future harm from triclosan, triclocarban, and antimicrobial substances with similar properties and effects.

Because antimicrobials can have unintended adverse health and environmental impacts, they should only be used when they provide an evidence-based health benefit. Greater transparency is needed in product formulations, and before an antimicrobial is incorporated into a product, the long-term health and ecological impacts should be evaluated.

Sources, Studies, Press Releases

  • The Florence Statement on Triclosan and Triclocarban, Environ Health Perspect; DOI:10.1289/EHP1788, JUNE 2017.
  • Patterns, Variability, and Predictors of Urinary Triclosan Concentrations during Pregnancy and Childhood, Environ. Sci. Technol., DOI: 10.1021/acs.est.7b00325, May 18, 2017
  • Hundreds of scientists call for caution on anti-microbial chemical use, EHN, June 20, 2017.
  • Hygiene leaves kids with loads of triclosan, EHN, June 1, 2017.
  • Image credit Mike Mozart.

Will experts prove a cover-up of the toxicity and dangers of the herbicide glyphosate ?

Of mice, Monsanto and a mysterious tumor

By Carey Gillam, for Environmental Health News, June 8, 2017.
Glyphosate spraying image via Chafer Machinery.

Call it the case of the mysterious mouse tumor.

It’s been 34 years since Monsanto Co. presented U.S. regulators with a seemingly routine study analyzing the effects the company’s best-selling herbicide might have on rodents. Now, that study is once again under the microscope, emerging as a potentially pivotal piece of evidence in litigation brought by hundreds of people who claim Monsanto’s weed killer gave them cancer.

This week tissue slides from long-dead mice in that long-ago research study are being scrutinized by fresh eyes as an expert pathologist employed by lawyers for cancer victims looks for evidence the lawyers hope will help prove a cover-up of the dangers of the weed killer called glyphosate.

Glyphosate, which is the active ingredient in Monsanto’s branded Roundup products, is the most widely used herbicide in the world, and is applied broadly in the production of more than 100 food crops, including wheat, corn and soy, as well as on residential lawns, golf courses and school yards.

Residues have been detected in food and human urine, and many scientists around the world have warned that exposure through diet as well as through application can potentially lead to health problems. The World Health Organization’s International Agency for Research on Cancer (IARC) declared glyphosate a probable human carcinogen in 2015 based on a review of scientific literature, triggering the wave of lawsuits against Monsanto, and pushing California regulators to announce they would add glyphosate to a list of known carcinogens.

What the expert finds, or doesn’t find, is expected to be key evidence in hearings slated for the week of Dec. 11 in dozens of consolidated cases being overseen by a federal judge in San Francisco.

Rewind to 1983

Monsanto, as well as many other scientists and regulatory bodies, have defended glyphosate’s safety. They say research showing a cancer connection is flawed and hundreds of studies support its safety.

And yet—rewind to July 1983 and a study titled “A Chronic Feeding Study of Glyphosate (Roundup Technical) in Mice.” Following the document trail that surrounds the study offers an illuminating look into how science is not always clear-cut, and the lengths Monsanto has had to go to in order to convince regulators to accept scientific interpretations that support the company’s products.

The two-year study ran from 1980-1982 and involved 400 mice divided into groups of 50 males and 50 females that were administered three different doses of the weed killer or received no glyphosate at all for observation as a control group. The study was conducted for Monsanto to submit to regulators. But unfortunately for Monsanto, some mice exposed to glyphosate developed tumors at statistically significant rates, with no tumors at all in non-dosed mice.

February 1984 memo from Environmental Protection Agency toxicologist William Dykstra stated the findings definitively: “Review of the mouse oncogenicity study indicates that glyphosate is oncogenic, producing renal tubule adenomas, a rare tumor, in a dose-related manner.” Researchers found these increased incidences of the kidney tumors in mice exposed to glyphosate worrisome because while adenomas are generally benign, they have the potential to become malignant, and even in noncancerous stages they have the potential to be harmful to other organs. Monsanto discounted the findings, arguing that the tumors were “unrelated to treatment” and showing false positives, and the company provided additional data to try to convince the EPA to discount the tumors.

“Glyphosate is suspect. Monsanto’s argument is unacceptable.”

Herbert Lacayo, EPA, wrote in response to Monsanto’s 1985 defense of the weedkiller

But EPA toxicology experts were unconvinced. EPA statistician and toxicology branch member Herbert Lacayo authored a February 1985 memo outlining disagreement with Monsanto’s position. A “prudent person would reject the Monsanto assumption that Glyphosate dosing has no effect on kidney tumor production,” Lacayo wrote. ”Glyphosate is suspect. Monsanto’s argument is unacceptable.”

Eight members of the EPA’s toxicology branch, including Lacayo and Dykstra, were worried enough by the kidney tumors in mice that they signed a consensus review of glyphosate in March 1985 stating they were classifying glyphosate as a Category C oncogen, a substance “possibly carcinogenic to humans.

Research rebuttal

That finding did not sit well with Monsanto, and the company worked to reverse the kidney tumor concerns. On April 3, 1985, George Levinskas, Monsanto’s manager for environmental assessment and toxicology, noted in an internal memorandum to another company scientist that the company had arranged for Dr. Marvin Kuschner, a noted pathologist and founding dean of the medical school at the State University of New York at Stony Brook, to review the kidney tissue slides.

Kushner had not yet even accessed the slides but Levinskas implied in his memo that a favorable outcome was assured:

“Kuschner will review kidney sections and present his evaluation of them to EPA in an effort to persuade the agency that the observed tumors are not related to glyphosate,”

Levinskas wrote. Notably, Levinskas, who died in 2005, was also involved in efforts in the 1970s to downplay damaging findings from a study that found rats exposed to Monsanto’s PCBs developed tumors, documents filed in PCB litigation revealed.

Kuschner’s subsequent re-examination did —as Monsanto stated it would—determine the tumors were not due to glyphosate. Looking over slides of the mouse tissue from the 1983 study, Kuschner identified a small kidney tumor in the control group of the mice – those that had not received glyphosate. No one had noted such a tumor in the original report. The finding was highly significant because it provided a scientific basis for a conclusion that the tumors seen in the mice exposed to glyphosate were not noteworthy after all.

Additionally, Monsanto provided the EPA with an October 1985 report from a “pathology working group” that also rebutted the finding of the connection between glyphosate and the kidney tumors seen in the 1983 study. The pathology working group said “spontaneous chronic renal disease” was “commonly seen in aged mice.” Monsanto provided the report to the EPA stamped as a “trade secret” to be kept from the prying eyes of the public.

The EPA’s own scientists still did not agree, however. An EPA pathologist wrote in a December 1985 memo that additional examination of the tissue slides did not “definitively” reveal a tumor in the control group. Still, the reports by the outside pathologists brought into the debate by Monsanto helped push the EPA to launch a reexamination of the research.

And by February 1986 an EPA scientific advisory panel had dubbed the tumor findings equivocal; saying that given the tumor identified in the control group by some pathologists, the overall incidences of tumors in the animals given glyphosate were not statistically significant enough to warrant the cancer linkage.

The panel did say there may be reason for concern and noted that the tumor incidences seen in the mice given glyphosate were “unusual.”

The advisory panel told the EPA the studies should be repeated in hopes of more definitive findings, and that glyphosate be classified into what the agency at that time called Group D—“not classifiable as to human carcinogenicity.” The EPA asked Monsanto for a repeat of the mouse oncogenicity study but Monsanto refused to do so.

The company argued “there is no relevant scientific or regulatory justification for repeating the glyphosate mouse oncogenicity study.” Instead, the company provided EPA officials with historical control data that it argued supported its attempt to further downplay the tumor incidences seen in the worrisome 1983 study.

“There is no relevant scientific or regulatory justification for repeating the glyphosate mouse oncogenicity study.”

– Monsanto, in response to EPA requests to replicate the mouse study

The company said the tumors in mice appear “with some regularity” and were probably attributable to “genetic or environmental” factors. “It is the judgement of Monsanto scientists that the weight-of-evidence strongly supports a conclusion that glyphosate is not oncogenic in the mouse.” Monsanto said repeating the mouse study would “require the expenditure of significant resources… and tie-up valuable laboratory space.”

Feds fold

The discussions between Monsanto and the EPA dragged on until the two sides met in November 1988 to discuss the agency’s request for a second mouse study and Monsanto’s reluctance to do so. Members of the EPA’s toxicology branch continued to express doubts about the validity of Monsanto’s data, but by June of 1989, EPA officials conceded, stating that they would drop the requirement for a repeated mouse study.

By the time an EPA review committee met on June 26, 1991, to again discuss and evaluate glyphosate research, the mouse study was so discounted that the group decided that there was a lack of convincing carcinogenicity evidence in relevant animal studies. The group concluded that the herbicide should be classified far more lightly than the initial 1985 classification or even the 1986 classification proposed by the advisory panel. This time, the EPA scientists dubbed the herbicide a Group E chemical, a classification that meant “evidence of non-carcinogenicity for humans.” At least two members of the EPA committee refused to sign the report, stating that they did not concur with the findings. In a memo explaining the decision, agency officials offered a caveat. They wrote that the classification “should not be interpreted as a definitive conclusion that the agent will not be a carcinogen under any circumstances.”

Despite the EPA’s ultimate conclusion, the mouse study was among those cited by IARC for classifying glyphosate as a probable human carcinogen. Indeed, many other animal studies have similarly had questionable results, including a 1981 rat study that showed an increase in incidences of tumors in the testes of male rats and possible thyroid carcinomas in female rats exposed to glyphosate and a 1990 study that showed pancreatic tumors in exposed rats. But none have swayed the EPA from its backing of glyphosate safety.

Christopher Portier, who was an invited specialist to the IARC review of glyphosate and is former director of the National Center for Environmental Health and Agency for Toxic Substances and Disease Registry at the U.S. Centers for Disease Control and Prevention, believes the evaluations applied to glyphosate data by regulators are scientifically flawedand putting public health at risk.

“The data in these studies strongly supports the ability of glyphosate to cause cancer in humans and animals; there is no reason to believe that all of these positive studies arose simply by chance,”

Portier said.

Monsanto fought the plaintiffs’ request to view the mouse tissue slides, calling it a “fishing expedition,” but was overruled by U.S. District Judge Vince Chhabria who is overseeing the roughly 60 combined lawsuits under his purvey. Monsanto has confirmed that roughly 900 additional plaintiffs have cases pending in other jurisdictions. All make similar claims – that Monsanto manipulated the science, regulators and the public in ways that hid or minimized the danger posed by its herbicide.

“The importance of the original kidney slides and the re-cut kidney slides is immense to the question of general causation and played a critical role in the EPA’s decision to re-categorize glyphosate…”

the plaintiffs’ attorneys stated in a court filing.

Plaintiffs’ attorney Aimee Wagstaff reiterated that in a recent court hearing, telling Judge Chhabria that the events surrounding the 1983 mouse study “sort of dominoed,” and potentially are “extremely relevant” to the cancer litigation.

Carey Gillam,
Research Director at U.S. Right to Know and veteran journalist who specializes in coverage of food, agriculture and environmental issues.

High doses of pesticides can potentially impact DNA, triggering cancers later in life

Researchers find pesticide spills, accidents may alter farmworkers’ DNA

Farmworkers who have a high pesticide exposure event—such as a spill—are more likely to experience molecular changes on DNA that may lead to certain cancers, according to a large U.S. study of pesticide applicators in Iowa and North Carolina.

The research, part of the ongoing Agricultural Health Study that is monitoring the health of more than 57,000 private and commercial pesticide applicators in Iowa and North Carolina, adds to growing evidence that high exposure to certain pesticides may spur prostate and other cancers in people handling the chemicals.

2017 Study Abstract

High pesticide exposure events and DNA methylation among pesticide applicators in the agricultural health study, Environmental and molecular mutagenesis, NCBI PubMed PMID: 27996157, 2017 Jan.

Researchers find pesticide spills, accidents may alter farmworkers’ DNA, Environmental Health News , February 16, 2017.

Image credit Brad Covington.

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.