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.

New generation flames retardants chemicals escaping into breathed air at alarming levels

Inhalation is an important route that should be taken into consideration in assessments of flame retardants

MemoryFoam-fast
Researchers report inhalation is an important exposure route for new generation of flame retardant chemicals. Memory foam.

As Washington state decides on stronger toxics law, residents are breathing flame retardants, by Brian Bienkowski, on Environmental Health News, January 25, 2016.

A new generation of chemicals added to furniture, building insulation and baby products like car seats to slow the spread of flames are escaping into air at higher levels than previously thought, according to a new study out of Washington state.

The findings come as Washington lawmakers decide on bolstering flame retardant bans. The state was one of the first to ban an earlier generation of retardants, known as PBDEs.

The new research found flame retardant chemicals used to replace polybrominated diphenyl ethers (PBDEs) also escape, are ubiquitous in indoor air and suggest inhalation is a major route of exposure for people.

The compounds, called chlorinated organophosphate flame retardants, found in the study have been linked to cancer and reproductive problems, and some can alter hormones essential for development.

“We’ve been underestimating what total exposure is”

said Erika Schreder, staff scientist at the Washington Toxics Coalition and lead author of the study published this month in the scientific journal Chemosphere.

Researchers gave 10 people from Washington state an air sampler that simulates breathing to wear during a normal day: office work, commuting, hanging out at home. They tested for a suite of the new generation of chlorinated flame retardants and found all 10 were breathing some amount of them throughout the day.

Exposure to one of the most prevalent compounds was up to 30 times greater than ingesting the chemicals via dust. The distinction is important: dust exposure occurs largely through the mouth, previously thought to be the major exposure route for banned PBDEs.

“With PBDEs, inhalation wasn’t considered as important,” Inhalation of PBDEs accounted for between 10 and 20 percent of exposure, “With the replacements, we see quite a different picture.”

said Amina Salamova, an environmental chemist and researcher at Indiana University Bloomington who studies toxic pollutants.

Chlorinated flame retardants are used mostly in polyurethane foam, often in building insulation and everyday products such as furniture, children’s car seats and baby strollers. The compounds are substitutes for PBDEs, which were widely used as flame retardants until scientists reported they were building up in people and wildlife and various bans took hold.

The American Chemistry Council, which represents chemical manufacturers, has long maintained flame retardant chemicals are necessary to prevent fires and protect people. In response to the recent study, Bryan Goodman, director of product communications for the council, said in an email that

exposure via ingestion and inhalation is “anticipated and regulators generally take this into account” when assessing the risk of chemicals.

However, Salamova, who was not involved in the recent study, said the inhalation concerns raised by Schreder’s study were especially alarming and novel because it was levels of really small particles that were quite high. She said:

“These really go all the way down your air tract and penetrate into the lung tissue,”

While chlorinated flame retardants have been around for decades, Salamova said scientists have recently started to understand them as, at first, it was thought they weren’t harmful or able to accumulate in people and wildlife. However there is evidence the replacement are following the same path as PBDEs: chlorinated flame retardants have been found in household dust, children’s products, drinking water, and mother-toddlers pairs.

Two chlorinated flame retardants have been flagged by the state of California as carcinogens, and animal research suggests they may hamper brain development as well.

Washington state legislators introduced bills in the state House and Senate to ban five flame retardants from furniture and children’s products, which would also set up a system to make sure new replacements are safe. The bill includes flame retardants found in the air in the recent study. The House bill will have a hearing this Wednesday.

Erika Schreder, study lead author, said:

The study doesn’t give us the final answer on exposure, but it does offer “a good indication of the range” that people are exposed to.

For questions or feedback about this piece, contact Brian Bienkowski.

Pesticide Exposure and Depression among Farmers and Farm Residents

Pesticide poisoning and depression in farm residents

Farm image
The studies support a positive association between pesticide exposure and depression, including associations with several specific pesticides.

Pesticide Exposure and Depression among Male Private Pesticide Applicators in the Agricultural Health Study

Background:
Pesticide exposure may be positively associated with depression. Few previous studies have considered the episodic nature of depression or examined individual pesticides.

Objective:
We evaluated associations between pesticide exposure and depression among male private pesticide applicators in the Agricultural Health Study.

Methods:
We analyzed data for 10 pesticide classes and 50 specific pesticides used by 21,208 applicators enrolled in 1993–1997 who completed a follow-up telephone interview in 2005–2010. We divided applicators who reported a physician diagnosis of depression (n = 1,702; 8%) into those who reported a previous diagnosis of depression at enrollment but not follow-up (n = 474; 28%), at both enrollment and follow-up (n = 540; 32%), and at follow-up but not enrollment (n = 688; 40%) and used polytomous logistic regression to estimate odds ratios (ORs) and 95% CIs. We used inverse probability weighting to adjust for potential confounders and to account for the exclusion of 3,315 applicators with missing covariate data and 24,619 who did not complete the follow-up interview.

Results:
After weighting for potential confounders, missing covariate data, and dropout, ever-use of two pesticide classes, fumigants and organochlorine insecticides, and seven individual pesticides—the fumigants aluminum phosphide and ethylene dibromide; the phenoxy herbicide (2,4,5-trichlorophenoxy)acetic acid (2,4,5-T); the organochlorine insecticide dieldrin; and the organophosphate insecticides diazinon, malathion, and parathion—were all positively associated with depression in each case group, with ORs between 1.1 and 1.9.

Conclusions:
Our study supports a positive association between pesticide exposure and depression, including associations with several specific pesticides.

Depression and pesticide exposures among private pesticide applicators enrolled in the Agricultural Health Study

Background:
We evaluated the relationship between diagnosed depression and pesticide exposure using information from private pesticide applicators enrolled in the Agricultural Health Study between 1993 and 1997 in Iowa and North Carolina.

Methods:
There were 534 cases who self-reported a physician-diagnosed depression and 17,051 controls who reported never having been diagnosed with depression and did not feel depressed more than once a week in the past year. Lifetime pesticide exposure was categorized in three mutually exclusive groups: low (< 226 days, the reference group), intermediate (226-752 days), and high (> 752 days). Two additional measures represented acute high-intensity pesticide exposures: an unusually high pesticide exposure event (HPEE) and physician-diagnosed pesticide poisoning. Logistic regression analyses were performed relating pesticide exposure to depression.

Results:
After adjusting for state, age, education, marital status, doctor visits, alcohol use, smoking, solvent exposure, not currently having crops or animals, and ever working a job off the farm, pesticide poisoning was more strongly associated with depression [odds ratio (OR) = 2.57; 95% confidence interval (CI), 1.74-3.79] than intermediate (OR = 1.07; 95% CI, 0.87-1.31) or high (OR = 1.11; 95% CI, 0.87-1.42) cumulative exposure or an HPEE (OR = 1.65; 95% CI, 1.33-2.05). In analysis of a subgroup without a history of acute poisoning, high cumulative exposure was significantly associated with depression (OR = 1.54; 95% CI, 1.16-2.04).

Conclusions:
These findings suggest that both acute high-intensity and cumulative pesticide exposure may contribute to depression in pesticide applicators. Our study is unique in reporting that depression is also associated with chronic pesticide exposure in the absence of a physician-diagnosed poisoning.

A cohort study of pesticide poisoning and depression in Colorado farm residents

Purpose:
Depressive symptoms have been associated with pesticide poisoning among farmers in cross-sectional studies, but no longitudinal studies have assessed the long-term influence of poisoning on depressive symptoms. The purpose of this study was to describe the associations between pesticide poisoning and depressive symptoms in a cohort of farm residents.

Methods:
Farm operators and their spouses were recruited in 1993 from farm truck registrations using stratified probability sampling. The Center for Epidemiologic Studies-Depression scale was used to evaluate depression in participants using generalized estimating equations. Baseline self-reported pesticide poisoning was the exposure of interest in longitudinal analyses.

Results:
Pesticide poisoning was significantly associated with depression in three years of follow-up after adjusting for age, gender, and marital status (odds ratio [OR] 2.59; 95% confidence interval [CI] 1.20-5.58). Depression remained elevated after adjusting for health, decreased income, and increased debt (OR 2.00; CI 0.91-4.39) and was primarily due to significant associations with the symptoms being bothered by things (OR 3.29; CI 1.95-5.55) and feeling everything was an effort (OR 1.93; CI 1.14-3.27).

Conclusions:
Feeling bothered and that everything was an effort were persistently associated with a history of pesticide poisoning, supportive of the hypothesis that prolonged irritability may result from pesticide poisoning.

Sources and more information
  • Pesticide Exposure and Depression among Male Private Pesticide Applicators in the Agricultural Health Study, ehp, 1 September 2014.
  • Depression and pesticide exposures among private pesticide applicators enrolled in the Agricultural Health Study, NCBI PMID: PubMed 19079725, 2008 Sept 9.
  • A cohort study of pesticide poisoning and depression in Colorado farm residents, NCBI PMID: PubMed 18693039, 2008 Aug 9.

Link between Air Pollution and ADHD in Children

Environmental factors may be contributing to attention problems in a significant way…

Could ADHD be triggered by mothers being exposed to air pollution while pregnant? New York City children exposed in the womb to high levels of pollutants in vehicle exhaust had a five times higher risk of attention problems at age 9, according to research by Columbia University scientists published in PLOS one:

Abstract

EHN logo image
Environmental factors may be contributing to attention problems in a significant way…

Importance:
Polycyclic aromatic hydrocarbons are widespread urban air pollutants from combustion of fossil fuel and other organic material shown previously to be neurotoxic.

Objective:
In a prospective cohort study, we evaluated the relationship between Attention Deficit Hyperactivity Disorder behavior problems and prenatal polycyclic aromatic hydrocarbon exposure, adjusting for postnatal exposure.

Materials and Methods:
Children of nonsmoking African-American and Dominican women in New York City were followed from in utero to 9 years. Prenatal polycyclic aromatic hydrocarbon exposure was estimated by levels of polycyclic aromatic hydrocarbon- DNA adducts in maternal and cord blood collected at delivery. Postnatal exposure was estimated by the concentration of urinary polycyclic aromatic hydrocarbon metabolites at ages 3 or 5. Attention Deficit Hyperactivity Disorder behavior problems were assessed using the Child Behavior Checklist and the Conners Parent Rating Scale- Revised.

Results:
High prenatal adduct exposure, measured by elevated maternal adducts was significantly associated with all Conners Parent Rating Scale-Revised subscales when the raw scores were analyzed continuously (N = 233). After dichotomizing at the threshold for moderately to markedly atypical symptoms, high maternal adducts were significantly associated with the Conners Parent Rating Scale-Revised DSM-IV Inattentive (OR = 5.06, 95% CI [1.43, 17.93]) and DSM-IV Total (OR = 3.37, 95% CI [1.10, 10.34]) subscales. High maternal adducts were positivity associated with the DSM-oriented Attention Deficit/Hyperactivity Problems scale on the Child Behavior Checklist, albeit not significant. In the smaller sample with cord adducts, the associations between outcomes and high cord adduct exposure were not statistically significant (N = 162).

Conclusion:
The results suggest that exposure to polycyclic aromatic hydrocarbons encountered in New York City air may play a role in childhood Attention Deficit Hyperactivity Disorder behavior problems.

Sources and more information:
  • Early-Life Exposure to Polycyclic Aromatic Hydrocarbons and ADHD Behavior Problems, PLOS one, DOI: 10.1371/journal.pone.0111670, November 05, 2014.
  • Air pollution linked to children’s attention problems, Environmental Health News, Nov. 5, 2014.
  • Could ADHD be triggered by mothers being exposed to air pollution while pregnant?, DailyMail, 7 November 2014.
  • Are pollution and attention problems related?,
    NHS Choices, 10 November 2014.

Prenatal DiNP Phthalate Exposure and Changes in Baby Boys’ Genitals

Study raises concern about DiNP, a phthalate being used in increased amounts in products that contain vinyl plastics, and the impact on the developing fetus

newborn
This study raises concern about DiNP, a phthalate being used in increased amounts in products that contain vinyl plastics, and the impact on the developing fetus.

Boys exposed in the womb to high levels of a chemical found in vinyl products are born with slightly altered genital development, according to research published today. The study of nearly 200 Swedish babies is the first to link the chemical di-isononyl phthalate (DiNP) to changes in the development of the human male reproductive tract.

Abstract:

Background:
Phthalates are used as plasticizers in soft polyvinyl chloride (PVC) and in a large number of consumer products. Due to reported health risks, di-isononyl phthalate (DiNP) has been introduced as a replacement for diethyl hexyl phthalate (DEHP) in soft PVC. This raises concerns since animal data suggest that DiNP may have anti-androgenic properties similar to DEHP. The anogenital distance (AGD) – the distance from the anus to the genitals – has been used to assess reproductive toxicity.

Objective:
The objective of this study was to examine the associations between prenatal phthalate exposure and AGD in Swedish infants.

Methods:
AGD was measured in 196 boys at age 21 months and first trimester urine was analyzed for ten phthalate metabolites of DEP, DBP, DEHP, BBzP as well as DiNP and creatinine. Data on covariates were collected by questionnaires.

Results:
The most significant associations were found between the shorter of two AGD measures (anoscrotal distance, AGDas) and DiNP metabolites and strongest for oh-MMeOP and oxo-MMeOP. However, the AGDas reduction was small (4%) in relation to more than an interquartile increase in DiNP exposure.

Conclusions:
These findings call into question the safety of substituting DiNP for DEHP in soft PVC, particularly since a shorter male AGD has been shown to relate to male genital birth defects in children and impaired reproductive function in adult males and the fact that human levels of DiNP are increasing globally.

Sources and more information:
  • Prenatal Phthalate Exposures and Anogenital Distance in Swedish Boys, EHP, DOI:10.1289/ehp.1408163, 29 October 2014.
    Full study PDF.
  • Plastics chemical linked to changes in baby boys’ genitals,
    EHN, Oct. 29, 2014.

U.S. Companies emitted about 26 Tons of BPA in the Air in 2013…

BPA is also contaminating the air near manufacturing plants…

BPA in the air, image via Barb Henry

As concerns mount over people’s exposure to the plasticizer bisphenol A in everyday products, it’s also contaminating the air near manufacturing plants: U.S. companies emitted about 26 tons of the hormone-disrupting compound in 2013.

Although research is sparse, experts warn that airborne BPA could be a potentially dangerous route of exposure for some people. Of the 72 factories reporting BPA emissions, the largest sources are in Ohio, Indiana and Texas, according to the Environmental Protection Agency’s Toxics Release Inventory. ”

… continue reading BPA in the air: Manufacturing plants in Ohio, Indiana, Texas are top emitters, on environmentalhealthnews, October 14, 2014.