In an article published on June 4, 2018, Erik Solheim, Head of the United Nations Environment Programme (UN Environment), addressed the global widespread use of plastics and the effects on human health. “The fact is that while we are acutely aware of the alarming rising tide of plastic waste, there is not a great deal known about the long-term health impacts of this pollution crisis,” he stated.

In recent years, knowledge and evidence has been acquired regarding food packaging and chemical migration from it into food, Solheim highlighted. “The chemicals causing the most disquiet have been bisphenol A (BPA) and phthalates,” he noted. “BPA may disrupt hormone and reproductive systems,” he explained, and “[t]here are also suspicions that it could contribute to diabetes, heart disease and even cancer.” Phthalates “are linked to fertility problems, pregnancy complications and other health issues,” he further described.

Less is known about the human health effects of microplastics, a topic “UN Environment and others have been raising red flags about . . . for a few years now,” Solheim reminded. Microplastics are “pieces of plastic under 5 millimeters in length” and they “come from many sources: larger pieces of plastic that break up; microbeads, which are added to health and beauty products like toothpastes and face scrubs; and synthetic fibers,” he explained. Microplastic particles “pass through water filtration systems and end up in the ocean, water bodies and our drinking water” (FPF reported). According to Sherri Mason, a microplastics researcher at the State University of New York at Fredonia, U.S., “[w]e have seen the impacts on aquatic species – from dehydration/starvation to the transmission of bioaccumulative toxic compounds – and we shouldn’t expect it to be any different for us.”

“We need to be clear that we’re not against plastics,” Solheim wrote. “The problem isn’t plastic, it’s what we do with it,” he clarified. “We’ve become over reliant on single-use or disposable plastic,” he declared, thus urging “governments, industry, communities and individuals to break up with single-use plastic.”

Read more

Erik Solheim (June 4, 2018). “The missing science: Could our addiction to plastic be poisoning us?” UN Environment

On June 7, 2018, the non-profit organization Health and Environment Alliance (HEAL) published a briefing entitled “How can Europe lead the way to a non-toxic environment?” which recommends twelve priority actions. “Under the 7^th Environment Action Programme, the European Commission is legally committed to release a Union’s strategy for a non-toxic environment by the end of 2018,” HEAL explained. Thus, the organization calls on the Commission “to finally draw its long promised strategy.”

To achieve the vision of a non-toxic environment, HEAL proposes to: 1) put vulnerable population groups (e.g., pregnant women, children, adolescents, the elderly) first, 2) reduce chemical exposure across sources, taking into account chemicals’ lifecycle and disposal, 3) tackle endocrine disrupting chemicals (EDCs) beyond pesticides and biocides (e.g., in toys, food contact materials, cosmetics), 4) take on flame retardants, 5) tackle per- and polyfluoroalkyl substances (PFASs), 6) address excessive use of pesticides, 7) accelerate identification of substances of very high concern (SVHCs), 8) translate identification of SVHCs across all other relevant legislations, 9) address exposure to chemical mixtures, 10) improve knowledge generation and communication, 11) involve the health community in the strategy for better disease prevention, and 12) implement consumers’ right to know.

Read more

HEAL (June 7, 2018). “HEAL’s vision for Europe leading the way towards a non-toxic environment.”

Chemical Watch (June 11, 2018). “NGO urges Commission to consider EU non-toxic strategy priorities.”

Reference

HEAL (June 7, 2018). “How can Europe lead the way to a non-toxic environment?” (pdf)

In an article published on March 20, 2018 in the peer-reviewed journal Toxicological Sciences, Melissa Van Bossuyt and colleagues from the Department of Food, Medicines and Consumer Safety, Scientific Institute of Public Health, Brussels, Belgium evaluated the performance of several in silico models for prediction of mutagenicity of chemicals found in food contact materials (FCM).

The authors built on the results of their previous studies, where chemicals that could be constituents of printed paper and board FCM (FPF reported) were screened using four in silico models for mutagenicity (FPF reported). These models were either rule-based (also called structure-activity relationship (SAR) models, represented by Toxtree and Derek Nexus) or statistics-based (also called quantitative SAR (QSAR) models, represented by VEGA Consensus and Sarah Nexus). In the present study, the scientists collected experimental data on the substances’ mutagenicity from several different sources. These data were then compared with in silico predictions to evaluate the models’ accuracy, sensitivity, specificity, and predictivity.

The four individual models showed varying prediction capacity for substances within their application domain. In particular, all models had high accuracy, ranging from 83% (Toxtree) up to 96% (Sarah Nexus), but varied widely in sensitivity (from 62% to 90%) and positive predictivity (from 49% to 87%). In general, QSAR models showed higher sensitivity, particularly for the substances inside their application domain. Among these, both the free VEGA Consensus and the commercial Sara Nexus performed similarly well. The performance could be further improved when the two QSAR models’ results were combined. However, higher sensitivity often coincided with lower specificity.

Much poorer model performance was observed for substances outside the models’ applicability domain, and in general for new compounds outside the training set. Commenting on the latter, the authors noted that, “[a]lthough combining the two models improves the prediction performance, it is important to note that still only one out of two mutagens is picked up.”

Reference

Van Bossuyt, M., et al. (2018). “Performance of in silico models for mutagenicity prediction of food contact materials.” Toxicological Sciences (published March 20, 2018).

A review article published on June 11, 2018 in the peer-reviewed journal Environmental Research, focused on the links between autism spectrum disorder (ASD) and exposure to toxic metals (especially lead, mercury, aluminum) or metalloids (in particular, arsenic).

Having reviewed the existing evidence, the team of international researchers led by Geir Bjørklund from the Council for Nutritional and Environmental Medicine, Mo i Rana, Norway, concludes that “a possible association exists between ASD and exposure to toxic metals.” These toxic agents may contribute to ASD etiology in particular through induction of neuroinflammation and oxidative stress.

Currently, both an increase in autism cases (FPF reported) and a “worldwide increase in toxic environmental pollution” are observed. Therefore, the authors emphasize, detailed studies “on the role of pollutants in neurodevelopmental disorders, including direct effects on the developing brain,” are needed to better understand the potential associations and to define efficient preventive strategies.

ASD is a neurodevelopmental disorder characterized by deficits in social interaction and communication. Food contact materials represent but one of the many diverse sources contributing to exposure to toxic metals and metalloids.

Reference

Bjørklund, G., et al. (2018). “Toxic metal(loid)-based pollutants and their possible role in autism spectrum disorder.” Environmental Research 166: 234-250.

A special issue in the volume 101 of the peer-reviewed journal Hormones and Behavior, published in May 2018, focuses on endocrine disrupting chemicals (EDCs) and behavior.

The accompanying editorial is written by Emily Barrett from the Rutgers University and Heather Patisaul from the North Carolina State University, both U.S.. Barrett and Patisaul emphasize that the special issue on EDCs and behavior “comes at a critical point when U.S. chemical regulatory policy is being reevaluated and important protections, like the Endocrine Disruptor Screening Program and the National Center for Environmental Research, risk loss of funding.” Importantly, the 14 peer-reviewed articles included in the special issue “make an eloquent case for why we must continue to study endocrine disruptors.” The featured research adopts various approaches “from studying the biochemical and molecular mechanisms underlying endocrine disruption, to synthesizing large bodies of epidemiological work.” Collectively, this work raises “concern about how many of the 90,000+ chemicals in use today may disrupt our most basic endocrine systems with significant consequences for neurodevelopment, neurophysiology, healthy brain aging, and behavior.”

The review by Gore and colleagues discusses “how EDCs affect the development and manifestation of sexual traits, reproductive competence, and sexual behavior.”

Moosa and colleagues summarize the evidence on the “controversial question of whether widespread exposure to EDCs is contributing to the much publicized rise in autism spectrum disorders.” They focus on EDCs’ roles in the etiology of neurodevelopmental diseases and conclude that “prenatal exposures to EDCs . . . may cause long-lasting, epigenetic changes that contribute to disease risk in future generations.”

The review by Walley and Roepke addresses behavioral aspects involved in obesogenic actions of EDCs. They critically assess the scarce literature looking at the EDCs’ impact on feeding behavior and the associated neural circuits and “make recommendations regarding how research should progress in this underserved area of EDC research.”

Meakin and colleagues examine “EDC impacts on stress hormones” and show that “environmental adversity impacts the methylation of genes critical for HPA [(hypothalamic-pituitary-adrenal)], but also placental, function, with potential long-lasting effects on children’s neurodevelopment.” Another review by Sobolewski and colleagues also focuses on the stress axis and examines “interactions between maternal stress and chemical exposures.” The point out that some neurotoxic metals can act as EDCs, “by altering HPA axis and central nervous system activity, thereby disrupting behavior.”

Several articles address bisphenol A (BPA, CAS 80-05-7). Nesan and colleagues focus on “how BPA impacts the developing brain.” MacKay and Abizaid “highlight BPA’s ability to interact with a wide variety of hormone receptors . . . and discuss what this means for interpreting a complex and often seemingly paradoxical literature.” Further, Harris and colleagues “examine the potential for behavioral and other effects [of BPA] to be inherited by subsequent generations.” For example, they show that “gestational exposure to BPA affects pup ultrasound vocalizations, a measure of social communication, and adult operant responding in mice.” In another study, published on June 18, 2018 in the peer-reviewed journal PLoS One, similar findings were also reported for California mice. This species is used as a special model for parental behaviors with high relevance to humans, because they are monogamous, with both parents caring for neonates. In this study, Johnson and colleagues found changes in the vocalization patterns of the mice pups whose parents were exposed to BPA prenatally (i.e., through exposure of grandparents). These changes in communication abilities could have impacts on the amount of parental care they receive.

Braun and colleagues demonstrate that exposure to triclosan (CAS 3380-34-5) can alter thyroid activity in early childhood. The implications of their research are “extensive given the essential role of thyroid hormones in maturation of the brain, and particularly the cerebral cortex, during early development.” Further, a study by Heerema and colleagues “identifies a novel role for thyroid hormones on olfaction-related behaviors in tadpoles” and shows that “exposure to a cocktail of . . . chemicals found in municipal wastewater can . . . [result] in compromised predator avoidance behavior.” Important, this study “is a prescient reminder that all species, not just humans, are exposed to EDCs and at risk for adverse neurodevelopmental outcomes that compromise fitness and, possibly, survival.”

Vuong and colleagues review epidemiological literature on behavioral effects of polybrominated diphenylethers (PBDEs), also known to disrupt thyroid system. They conclude that “prenatal (and in some cases, early postnatal) exposure is linked to hyperactivity, conduct problems, and impaired executive functions in childhood,” building “a clear case in which links between exposures, even at low doses, and neurodevelopmental effects in children is particularly strong.”

Høyer and colleagues address perfluoroalkyl substances (PFASs), and in particular the newer type of short-chain PFASs used to replace the long-chain PFASs that are being phased out. They discuss studies “finding that prenatal exposure to several of these replacement chemicals may be linked to hyperactivity and other problem behaviors in children.” This review highlights the “pervasive problem of ‘regrettable substitution’ when one problematic chemical, or class of chemicals, is replaced by another that also poses health concerns.” It further “signals a clear need to better understand how these chemicals impact hormone-sensitive systems and behavioral endpoints.”

Other studies included in the special issue address behavioral effects of voluntary taken pharmaceuticals, including birth control pills, and pain medications.

Read more

Science Daily (June 18, 2018). “BPA can induce multigenerational effects on ability to communicate.”

References

“Endocrine Disrupting Chemicals and Behavior.” Hormones and Behavior 101(Suppl C): 1-148.

Emily Barrett and Heather Patisaul (2018). “Introduction to the special issue on endocrine disrupting chemicals and behavior.” Hormones and Behavior 101:1-2.

Gore, A., et al. (2018). “Mate choice, sexual selection, and endocrine-disrupting chemicals.” Hormones and Behavior 101: 3-12.

Moosa, A., et al. (2018). “Are endocrine disrupting compounds environmental risk factors for autism spectrum disorder?” Hormones and Behavior 101: 13-21.

Sabrina Walley and Troy Roepke (2018). “Perinatal exposure to endocrine disrupting compounds and the control of feeding behavior—An overview.” Hormones and Behavior 101: 22-28.

Meakin, C., et al. (2018). “Placental CpG methylation of HPA-axis genes is associated with cognitive impairment at age 10 among children born extremely preterm.” Hormones and Behavior 101: 29-35.

Sobolewski, M., et al. (2018). “Endocrine active metals, prenatal stress and enhanced neurobehavioral disruption.” Hormones and Behavior 101: 36-49.

Nesan, D., et al. (2018). “Opening the black box of endocrine disruption of brain development: Lessons from the characterization of Bisphenol A.” Hormones and Behavior 101: 50-58.

Harry MacKay and Alfonso Abizaid (2018). “A plurality of molecular targets: The receptor ecosystem for bisphenol-A (BPA).” Hormones and Behavior 101: 59-67.

Harris, P., et al. (2018). “Effects of maternal or paternal bisphenol A exposure on offspring behavior.” Hormones and Behavior 101: 68-76.

Braun, J., et al. (2018). “Associations of early life urinary triclosan concentrations with maternal, neonatal, and child thyroid hormone levels.” Hormones and Behavior 101: 77-84.

Heerema, J., et al. (2018). “Behavioral and molecular analyses of olfaction-mediated avoidance responses of Rana (Lithobates) catesbeiana tadpoles: Sensitivity to thyroid hormones, estrogen, and treated municipal wastewater effluent.” Hormones and Behavior 101: 85-93.

Vuong, A., et al. (2018). “Exposure to polybrominated diphenyl ether (PBDEs) and child behavior: Current findings and future directions.” Hormones and Behavior 101: 94-104.

Høyer, B., et al. (2018). “Exposure to perfluoroalkyl substances during pregnancy and child behavior at 5 to 9 years of age.” Hormones and Behavior 101: 105-112.

Mary Catanese and Laura Vandenberg (2018). “Developmental estrogen exposures and disruptions to maternal behavior and brain: Effects of ethinyl estradiol, a common positive control.” Hormones and Behavior 101: 113-124.

Bauer, A., et al. (2018). “Prenatal paracetamol exposure and child neurodevelopment: A review.” Hormones and Behavior 101: 125-147.

Johnson, S., et al. (2018). “Multigenerational effects of bisphenol A or ethinyl estradiol exposure on F2 California mice (Peromyscus californicus) pup vocalizations.” PLoS ONE 13(6):e0199107.

In May 2018, peer-reviewed journal Environmental Health presented a collection of its articles investigating the effects of fetal and developmental exposures. This topic was the focus of the PPTOX VI Conference that took place end of May 2018 in Tórshavn, Faroe Islands. PPTOX stands for “Prenatal Programming and Toxicity.” PPTOX VI organizers emphasize that fetal and early postnatal development constitutes “the most vulnerable stage of human life” in regard to environmental hazards, and even “subtle effects during early development may . . . lead to functional deficits and increased disease risks later in life.” This mechanism is postulated by the “fetal programming” hypothesis that has gathered “much support from both experimental and epidemiological studies.”

This year’s PPTOX VI conference had a dense program featuring recent research on the topic. The overall aim of the conference was “to assess the weight of evidence and highlight new achievements on the effects of prenatal and early postnatal exposure to toxicants” and “to stimulate improved interaction between research strategies and needs for documentation that can inspire decision-making to protect against adverse effects from developmental exposures to environmental hazards.” Conference conclusions will be published later this year.

Read more

PPTOX VI Conference

“Selected articles in Fetal and Developmental Exposure for PPTOX 2018.” Environmental Health (May 2018).

An article published on June 6, 2018, in the peer-reviewed journal Experimental Biology and Medicine reports that exposure to bisphenol A (BPA, CAS 80-05-7) may be a risk factor for development and relapse of the inflammatory bowel disease (IBD). IBD is a collective name for several inflammatory gut disorders, including ulcerative colitis and Crohn’s disease.

Jennifer DeLuca and colleagues from the Department of Nutrition and Food Science, Texas A&M University, U.S., used ovariectomized mice to study the effects of 15-days-long BPA exposure on the development and progression of the acute dextran sulfate sodium-induced colitis. In this disease model, they observed that BPA exposure “increased mortality and worsened disease activity as well as inflammation.” Further, BPA resulted in a specific alteration of metabolite profiles in the gut microbiota, namely a reduction in the levels of several anti-inflammatory molecules, and this regardless of colitis-inducing chemical treatment.

The authors conclude that their study is the first “to show that [BPA] treatment alone can reduce microbiota metabolites . . . in the colon which may be associated with increased colonic inflammation and inflammatory bowel disease.”

Read more

Science Daily (July 5, 2018). “BPA risk factor for inflammatory bowel disease.”

Reference

DeLuca, J., et al. (2018). “Bisphenol-A alters microbiota metabolites derived from aromatic amino acids and worsens disease activity during colitis.” Experimental Biology and Medicine 243(10):864-875.

In an article published on July 16, 2018 in the peer-reviewed Journal of Neuroscience, Daniel Kougias and colleagues from the Neuroscience Program, University of Illinois, Champaign, U.S., reported on the phthalates’ effects on the developing brain and cognitive flexibility in rats.

Female rats were orally exposed “through pregnancy and for 10 days while lactating” to a mixture of six phthalates at two concentrations comparable to the U.S. population exposure levels. The phthalate mixture contained 35% diethyl phthalate (DEP, CAS 84-66-2), 21% bis(2-ethylhexyl) phthalate (DEHP, CAS 117-81-7), 15% dibutyl phthalate (DBP, CAS 84-74-2), 15% diisononyl phthalate (DiNP, CAS 28553-12-0), 8% diisobutyl phthalate (DiBP, CAS 84-69-5), and 5% benzyl butyl phthalate (BBP, CAS 85-68-7). The offspring of the exposed rats were then tested as adults in a setup which assesses cognitive flexibility, followed by a quantification of the number of neurons, glia, and synapses in their brains, specifically in the medial prefrontal cortex (mPFC). This region is “involv[ed] in executive functions and implic[ated] in the pathology of many neuropsychiatric disorders,” including autism.

Both male and female rats perinatally exposed to phthalate mixture were found to have “a deficit in cognitive flexibility,” accompanied by “a reduction in neuron number, synapse number, and size of the mPFC.” The scientists observed that “the number of synapses was correlated with cognitive flexibility, such that rats with fewer synapses were less cognitively flexible than those with more synapses.”

The authors conclude that their results “demonstrate that perinatal phthalate exposure can have long-term effects on the cortex and behavior of both male and female rats” and “may have serious implication for humans.”

Read more

EurekAlert (July 16, 2018). “Plastic chemical linked to smaller prefrontal cortex, reduced cognitive ability in rats.”

Reference

Kougias, D., et al. (2018). “Perinatal exposure to an environmentally relevant mixture of phthalates results in a lower number of neurons and synapses in the medial prefrontal cortex and decreased cognitive flexibility in adult male and female rats.” Journal of Neuroscience (published July 16, 2018)

In an article published on June 28, 2018 in the peer-reviewed journal Lancet Oncology, the International Agency for Research on Cancer (IARC) summarized its evaluation of the four acrylate chemicals, classifying them in the group 2B, i.e., possibly carcinogenic to humans.

The four substances are methyl acrylate (MA, CAS 96-33-3), ethyl acrylate (EA, CAS 140-88-5), 2-ethylhexyl acrylate (EHA, CAS 103-11-7), and trimethylopropane tricacrylate (TMPTA, CAS 15625-89-5). All four are included in the FACET inventory of food contact materials (FCMs), and all except TMPTA are listed in the Annex I of the Regulation (EU) No 10/2011 on plastic FCMs. TMPTA is known to be used as a curing agent for UV-cured food contact adhesives.

In a press release published on July 11, 2018, trade association American Chemistry Council (ACC) called the IARC’s decision to classify MA, EA, and EHA in the Group 2B “erroneous and misleading” and said that it is “based on poor science and a flawed, non-transparent process.” ACC has a long history of criticizing the IARC’s work and classifications issued (FPF reported).

Read more

ACC (July 11, 2018). “Monograph 122 findings further highlight need for Dr. Weiderpass to spearhead reform of program.”

Chemical Watch (July 18, 2018). “Four acrylates ‘possibly carcinogenic,’ IARC says.”

Reference

Kromhout, H., et al. (2018). “Carcinogenicity of isobutyl nitrite, beta-picoline, and some acrylates.” Lancet Oncology (published June 28, 2018).

On July 23, 2018, two articles on food additives and child health were published in the peer-reviewed journal Pediatrics of the American Academy of Pediatrics (AAP): (1) a policy statement and (2) a technical report. The articles are authored by Leonardo Trasande from NYU School of Medicine, New York University, Rachel Shaffer, School of Public Health, University of Washington, Sheela Sathyanarayana, Pediatrics, University of Washington, and the Council on Environmental Health.

The authors “review and highlight emerging child health concerns [(e.g. “endocrine disruption and other adverse health effects”)] related to the use of colorings, flavorings, and chemicals deliberately added to food during processing (direct food additives) as well as substances in food contact materials, including adhesives, dyes, coatings, paper, paperboard, plastic, and other polymers, which may contaminate food as part of packaging or manufacturing equipment (indirect food additives).” They also “make reasonable recommendations that the pediatrician might be able to adopt into the guidance provided during pediatric visits” and “propose urgently needed reforms to the current regulatory process at the U.S. Food and Drug Administration (FDA) for food additives.”

The authors explain that “regulation and oversight of many food additives is inadequate because of several key problems in the Federal Food, Drug, and Cosmetic Act (FFDCA).” The “critical weaknesses” include insufficient requirements to ensure the safety of Generally Recognized as Safe (GRAS) food additives, conflicts of interest surrounding GRAS determinations, and the fact that “the FDA does not have adequate authority to acquire data on chemicals on the market or reassess their safety for human health.”

Therefore, the authors call for “substantial improvements to the food additives regulatory system.” These should include “greatly strengthening or replacing the GRAS determination process; updating the scientific foundation of the FDA’s safety assessment program; retesting all previously approved chemicals; and labeling direct food additives with limited or no toxicity data.”

A detailed guidance for pediatric counseling on minimizing EDC exposures from consumer products has also been provided by Katelyn Wong and Timur Durrani in a review published in the peer-reviewed journal Current Problems in Pediatric and Adolescent Health Care in 2017.

Read more

AAP (July 23, 2018). “American Academy of Pediatrics says some common food additives may pose health risks to children.”

Carly Weeks (July 23, 2018). “Children are being harmed by food additives, U.S. pediatric association warns.” The Globe and Mail

Kelly Franklin (July 23, 2018). “American pediatrics group presses for FCM reforms.” Chemical Watch

References

Trasande, L., et al. (2018). “Food additives and child health. Policy statement.” Pediatrics (published online July 23, 2018).

Trasande, L., et al. (2018). “Food additives and child health. Technical report.” Pediatrics (published online July 23, 2018).

Katelyn Wong and Timur Durrani (2017). “Exposures to endocrine disrupting chemicals in consumer products—A guide for pediatricians.” Current Problems in Pediatric and Adolescent Health Care 47(5): 107-118.

On August 3, 2018, the German Federal Institute for Risk Assessment (BfR) published a statement regarding the occurrence of the childhood disease Molar Incisor Hypomineralization (MIH) and children’s exposure to bisphenol A (BPA, CAS 80-05-7). Recently, there have been media reports linking this dental deficiency to uptake of BPA, the BfR informed. The reports are based on scientific studies in rats conducted by Katia Jedeon and colleagues and published in different peer-reviewed journals in 2013, 2014, and 2016.

The BfR evaluated the 2013 Jedeon study and concluded that there is no significant link between the uptake of BPA and the development of MIH in children. According to more recent data from the Netherlands (FPF reported), children’s exposure to BPA is much lower than the dose used by Jedeon and colleagues. Therefore, and because of the toxicokinetic differences between rats and humans in the neonatal phase, the BfR deems a direct link between BPA and MIH in humans unlikely.

Read more

BfR (August 3, 2018). “Zusammenhang zwischen „Kreidezähnen“ bei Kindern (Molar-Incisor-Hypomineralisation, MIH) und der Aufnahme von Bisphenol A ist nach derzeitigem Stand des Wissens unwahrscheinlich.” (pdf; in German)

References

Jedeon, K. et al. (2013). “Enamel defects reflect perinatal exposure to bisphenol A.” American Journal of Pathology 183(1):108-118.

Jedeon, K. et al. (2014). “Estrogen and bisphenol A affect male rat enamel formation and promote ameloblast proliferation.” Endocrinology 155(9):3365-3375.

Jedeon, K. et al. (2016). “Impact of three endocrine disruptors, Bisphenol A, Genistein and Vinclozolin on female rat enamel.” Bulletin du Groupement international pour la recherche scientifique en stomatologie & odontologie 53(1):e28.

Jedeon, K. et al. (2016). “Androgen Receptor Involvement in Rat Amelogenesis: An Additional Way for Endocrine-Disrupting Chemicals to Affect Enamel Synthesis.” Endocrinology 157(11):4287-4296.

In an article published on August 4, 2018, by the newspaper The Washington Post, journalist Rachel Cernansky reported on the risks posed by exposure to chemicals during pregnancy. There is “evidence suggesting that ingredients in plastics, vehicle exhaust and cosmetics additives can have profound impacts on babies’ health,” Cernansky explained, citing the 2013 opinion by the American College of Obstetricians and Gynecologists (ACOG), the 2015 opinion by the International Federation of Gynecology and Obstetrics (FIGO), and the Project TENDR, all reporting on the effects of environmental chemicals on reproductive and developmental health and calling for a reduction in exposure. “[R]esearchers have found a variety of links, including between some pesticides and impaired fetal growth and neurodevelopment; between phthalates (used in many plastics) and increased risk of premature birth and impaired neurodevelopment; and between fine-particle air pollution and altered expression of genes that influence neurodevelopment,” she specified.

However, according to a recent U.S. survey, most obstetricians and gynecologists (OBGYNs) do not discuss exposure to chemicals with their pregnant patients, Cernansky informed. “[W]omen are told to avoid alcohol and cigarettes, to make sure they get enough folate and omega-3 fatty acids, and to get adequate sleep and exercise,” but “[m]ost are told little or nothing about reducing their exposure to chemicals,” she asserted. Further, Cernansky compiled a list of advice on how to avoid chemical exposures from Project TENDR, the “Toxic Matters” website by the University of California San Francisco, U.S., and different scientific experts.

Read more

Rachel Cernansky (August 4, 2018). “Environmental toxins are seen as posing risks during pregnancy.” The Washington Post

References

American College of Obstetricians and Gynecologists (2013). “Exposure to toxic environmental agents. Committee Opinion No. 575.” Obstetrics and Gynecology 2013;122:931–935.

Di Renzo, G.C. et al. (2015). “International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals.” International Journal of Gynecology and Obstetrics (published online September 30, 2015)

Bennett, D. et al. (2016). “Project TENDR: Targeting environmental neuro-developmental risks. The TENDR consensus statement.” Environmental Health Perspectives 124:A118-A122.

Grindler, N.M., et al. (2018). “OBGYN screening for environmental exposures: A call for action.” PLOS One (published online May 16, 2018)

In an article published on August 13, 2018, by news provider The Conversation, Bruce Blumberg, professor of developmental and cell biology at the University of California, Irvine, U.S., and Raquel Chamorro-Garcia, associate specialist at the same institution, discussed the role of chemical exposures in the worldwide obesity and type 2 diabetes epidemic.

“The most common explanation for obesity is overeating calorie-rich foods and sedentary lifestyle,” the authors write. However, “a subset of endocrine-disrupting chemicals (EDCs) called obesogens has been shown to cause obesity in animals and were associated with more fat mass in humans,” they explained. Such EDCs can be found in “plastics, preservatives, pesticides and flame retardants,” Blumberg and Chamorro-Garcia listed, and “may be important contributors to the growing number of metabolic disorders – including obesity,” they further described.

Blumberg and Chamorro-Garcia’s research on tributyltin (TBT, CAS 1461-22-9) and dibutyltin (DBT, CAS 683-18-1) showed that the substances can activate hormone receptors linked to fat development, alter glucose metabolism, and increase fat storage in mice. TBT is a preservative and biocide; DBT is used in the manufacture of polyvinyl chloride (PVC) plastics.

Read more

Bruce Blumberg and Raquel Chamorro-Garcia (August 13, 2018). “Obesity and diabetes: 2 reasons why we should be worried about the plastics that surround us.” The Conversation

Reference

Chamorro-Garcia, R., et al. (2018). “Effects of perinatal exposure to dibutyltin chloride on fat and glucose metabolism in mice, and molecular mechanisms, in vitro.” Environmental Health Perspectives (published online May 21, 2018).

On August 16, 2018, the industry association American Chemistry Council (ACC) published a response to the American Academy of Pediatrics (AAP) report on food additives and child health. The AAP published a technical report and a policy statement on the topic on July 23, 2018, in the peer-reviewed journal Pediatrics (FPF reported). The AAP authors addressed emerging child health concerns (e.g., endocrine disruption) relating to the use of chemicals in food contact materials (FCMs) and other substances used in food.

In response, the ACC stated: “Unfortunately, the [AAP] report has created the false idea that the U.S. Food and Drug Administration (FDA) is not doing enough to ensure the safety of the products Americans use and consume.” However, “[t]he fact is that all food packaging materials are regulated by FDA under the Federal Food, Drug, and Cosmetic Act (FD&C Act)” and “FDA regulations are comprehensive and science-based,” the ACC asserted.

The ACC further highlighted the “importance of modern food packaging,” explaining that it is “essential to the quality and integrity of food, extends shelf life and helps in the safe transport and storage of food.” Also, the ACC compiled a “myth and fact sheet,” addressing U.S. food packaging regulations, chemical migration, endocrine disruption, bisphenol A, phthalates, perfluoroalkyl chemicals (PFCs), plastics, and other topics, “to help provide facts about the issue.”

In September 2017, the Food Packaging Forum (FPF) published a commentary article in the peer-reviewed journal Environmental Health Perspectives providing an overview of the key scientific challenges in the risk assessment of FCMs (FPF reported).

Read more

ACC Blog (August 16, 2018). “Setting the record straight: Response to American Academy of Pediatrics report.”

Kelly Franklin (July 30, 2018). “Industry groups defend FCMs following U.S. pediatrics report.” Chemical Watch

References

Trasande, L., et al. (2018). “Food additives and child health. Policy statement.” Pediatrics (published online July 23, 2018).

Trasande, L., et al. (2018). “Food additives and child health. Technical report.” Pediatrics (published online July 23, 2018).

Muncke, J., et al. (2017). “Scientific challenges in the risk assessment of food contact materials.” Environmental Health Perspectives (published online September 11, 2017).

An article published on August 1, 2018, in the peer-reviewed journal Human and Ecological Risk Assessment, reported on the comparison between data required to be submitted under the European Regulation on the Registration, Authorisation and Restriction of Chemicals (REACH) and data needed to support classifications under the Classification, Labelling and Packaging (CLP) Regulation. Marjolijn Woutersen and colleagues from the National Instituut for Public Health and the Environment (RIVM), Centre for Safety of Substances and Products (VSP), Bilthoven, the Netherlands, compared REACH data requirements for mutagenicity and carcinogenicity with corresponding CLP classification criteria as well as “the studies used as key evidence by [the] Committee for Risk Assessment (RAC) in drafting its opinions on the appropriate classification.” The motivation behind this analysis was that “classification and labeling is essential in the communication of the hazardous properties of substances and mixtures and is amongst others an important first step in the identification of a substance as a Substance of Very High Concern (SVHC).”

The analysis “revealed that the REACH information requirements will not provide sufficient information to conclude a substance is a Cat 1B mutagen and/or carcinogen.” Furthermore, obtaining “such information via a substance evaluation under REACH requires a large investment from the Member States and takes years,” the authors explain. Therefore, they conclude that “REACH will hardly generate sufficient information for classification of substances as category 1B for mutagenicity and carcinogenicity,” possibly resulting in a situation where “indications of very severe hazards of substances are missed and health risks could occur.”

Woutersen and colleagues propose “various ways to deal with this problem,” but comment that “most of these require adaptation of regulations” and thus “will cost considerable time and political will.” Their study is “a first step to raise awareness for the problem and to start a discussion to search for a sustainable solution,” the authors emphasize.

Reference

Woutersen, M., et al. (2018). “Does REACH provide sufficient information to regulate mutagenic and carcinogenic substances?” Human and Ecological Risk Assessment: An International Journal (published August 1, 2018).

An article published on August 18, 2018, in the peer-reviewed journal Environmental Research, reports about the results of a systematic review focused on exposure to di-(2-ethylhexyl) phthalate (DEHP, CAS 117-81-7) and neurodevelopmental outcomes in children. Dong-Wook Lee and colleagues from the Department of Preventive Medicine, College of Medicine, Seoul National University, Seoul, Republic of Korea, performed a systematic review and meta-analysis of studies focusing on the association between DEHP exposure and child neurodevelopment, paying “particular attention to study design (longitudinal vs. cross-sectional).” Initially, 106 studies were located in public databases, from which “eight longitudinal studies and two cross-sectional studies were included in the meta-analysis.”

With regard to prenatal DEHP exposure, the scientists found “significant association between DEHP exposure measured in prenatal period [in mothers’ urine] and the psychomotor development outcomes measured later” in their children. Concerning postnatal exposure, cross-sectional studies showed “a statistically significant association between the concentrations of DEHP metabolites and the neurodevelopment outcomes of children,” such as intelligence quotients.

The authors discuss “methodological limitations due to measuring intervals, duration of longitudinal cohort studies, and quantitative and qualitative analysis on differences among tests for cognitive development.” In order to characterize “more accurate trajectories of neurotoxic effects of phthalates,” it would be necessary to perform “prospective cohort studies of large population with repeated measures of mental and psychomotor development with both urine and serum concentration of phthalates over longer periods of time, taking into account environmental and individual factors.” These studies “should consider better experimental design with appropriately controlled confounding factors, refined measurement methods of biological exposure indices, and timely assessment of neurodevelopment,” the authors suggest.

The authors conclude that “DEHP carries risks of disturbed neurodevelopment in children” and warn that “the severity of problem is not negligible since DEHP is still the most commonly used phthalate.” They emphasize that “precautionary policies . . . for health hazards of DEHP should be made to protect neurodevelopment of children.”

Reference

Lee, D.-W., et al. (2018). “Prenatal and postnatal exposure to di-(2-ethylhexyl) phthalate and neurodevelopmental outcomes: A systematic review and meta-analysis.” Environmental Research 167: 558-566.

In an article published on August 28, 2018, in the peer-reviewed journal Science of the Total Environment, Yuanxiang Jin and colleagues from the College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou, China, report on the gut-related effects of oral exposure to polystyrene (PS) microplastic in mice.

The scientists exposed 6-week-old mice to PS particles with an average size of 5 µm. The particles were delivered with drinking water at two different concentrations, 100 and 1000 µg/L, corresponding to 1,456,000 and 14,560,000 particles per liter, respectively. The exposure continued for 6 weeks.

Secretion of gut mucus decreased in both treatment groups compared to unexposed mice, accompanied by a downregulation of several genes involved in mucus secretion and ion transport. Microplastic exposure also decreased abundance and diversity of gut microbiota.

In the serum of exposed mice, increased levels of serum pyruvate and decreased levels of triglycerides and total cholesterol were measured in microplastic-exposed groups. Furthermore, several metabolites known to be “associated with the occurrence of metabolic diseases,” were also affected. The authors summarized that “amino acid metabolism, the tricarboxylic acid (TCA) cycle and the urea cycle were . . . influenced” by exposure to microplastic. In addition, exposure to the higher concentration of microplastic was found to increase total bile acids in the liver, but not in the serum. An increased expression of several genes involved in bile acid synthesis and transport was also observed in the liver of microplastic-exposed mice.

The authors conclude that exposure to microplastic “could induce gut microbiota dysbiosis, intestinal barrier dysfunction and metabolic disorders.”

Several studies measuring microplastics in drinkable water reported concentrations up to 35,436 particles per liter in bottled mineral water (FPF reported). Large (>5 µm) particles of microplastics have also been detected in tap water, beer, salt, fish. Currently, particles smaller than 1.5 µm are considered to be the most relevant toxicologically, because they are more likely to penetrate deeper into the body (see, e.g., European Food Safety Authority’s (EFSA) statement on microplastics in food). It is assumed that concentrations of smaller particles could be even higher than those measured for particles sized 5 µm and above (FPF reported). However, reliably measuring microplastic particles sized at and below 1 µm remains technically challenging to date (FPF reported).

Reference

Jin, Y., et al. (2018). “Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice.” Science of the Total Environment 649: 308-317.

In an article published on September 11, 2018, by news provider Vox, correspondent Julia Belluz and intern Radhika Viswanathan discuss the health concerns regarding plastic food containers and the chemicals, for example phthalates and bisphenol A (BPA, CAS 80-05-7), that migrate from them into food.

“[T]here’s mounting scientific evidence that these plastics are harming our health, from as early as our time in our mother’s womb,” the authors write. They go on to summarize findings from experimental animal and epidemiological human studies that provide evidence on adverse health effects resulting from exposure to chemicals found in plastic packaging.

“Right now, it’s up to consumers to manage their exposures to the chemicals in plastics because of a surprising lack of regulatory oversight over the plastic packaging industry,” Belluz and Viswanathan state, referring to the regulatory system in the U.S.. They explain how the GRAS (Generally Recognized as Safe) rule allows “potentially harmful chemicals . . . [to] be used in food packaging.”

Lastly, Belluz and Viswanathan present a list with recommendations on how to limit exposure to chemicals migrating from plastics into food. “But even if you do all these things, it’s impossible to totally avoid these common chemicals,” they highlight. “Still, any effort to reduce your exposure is probably worth it,” the authors conclude.

Read more

Julia Belluz and Radhika Viswanathan (September 11, 2018). “The problem with all the plastic that’s leaching into your food.” Vox

In an article published on September 11, 2018, by regulatory news provider Chemical Watch, editor Kelly Franklin informed about a hearing on the environmental and human health impacts of per- and polyfluoroalkyl substances (PFASs) that was held at the subcommittee on Environment of the U.S. House of Representatives’ Energy and Commerce committee on September 6, 2018. The hearing discussion focused on how to set “enforceable and sufficiently protective drinking water standards” and also considered “restricting the substances’ manufacture and use . . . as a potential method for controlling their presence in the environment,” Franklin reported.

Eric Olson of the U.S. non-profit organization Natural Resources Defense Council (NRDC) testified at the hearing, calling on the U.S. Environmental Protection Agency (EPA) to ban new uses of existing PFASs and to also ban all new PFASs. Exceptions to the ban should only be granted for national defense needs, emergencies, and other urgent needs if no alternatives exist. Further, Olson submitted a letter signed by 51 local, state, and national organizations urging to phase-out the use of PFASs.

The industry group American Chemistry Council (ACC) issued a statement regarding the hearing, asserting that the “PFAS currently manufactured have been well studied and undergone rigorous regulatory review.” The ACC further highlighted that “[t]hose chemistries play an essential role in many products we depend on in modern life” and pledged that “industry will continue to be a constructive partner to state and federal regulators and other stakeholders affected by this important issue.”

Meanwhile, due to lacking federal measures, U.S. states and cities have taken regulatory action to reduce PFASs contamination in the environment as well as? consumer exposure: Among others, the State of Washington and the City and County of San Francisco have adopted laws to ban PFASs in food packaging and single-use food service ware.

Read more

Kelly Franklin (September 11, 2018). “U.S. environmental groups lobby Congress for ban on new PFASs.” Chemical Watch

Liz Hitchcock (September 7, 2018). “Members of Congress from both sides of the aisle show concern about PFAS water contamination crisis at hearing.” Safer Chemicals, Healthy Families

In an article published on September 13, 2018, by the magazine The Scientist, editor Kerry Grens informed about a new study on the health effects of replacement chemicals for bisphenol A (BPA, CAS 80-05-7). The study was published on the same day in the peer-reviewed journal Current Biology and conducted by Tegan S. Horan and colleagues from Washington State University and the University of California, San Francisco, both U.S..

The researchers exposed pregnant mice to daily oral doses of 20 ng/g body weight of BPA, its common substitutes bisphenol S (BPS, CAS 80-09-1) and diphenyl sulfone (CAS 127-63-9), or a placebo. They found that exposure to BPA and BPS led to a significant increase in chromosomal abnormalities in the female fetuses. Horan and colleagues also exposed male baby mice to oral doses of 20 ng/g of BPA, BPS, diphenyl sulfone, two further common BPA replacements bisphenol F (BPF, CAS 620-92-8) and (BPAF, CAS 1478-61-1), or a placebo. All bisphenols lead to significant chromosomal abnormalities in the mice’s sperm that continued to persist in subsequent generations.

“Although ‘BPA free’ is a valuable marketing tool, and most consumers interpret this label as an indication of a safer product, our findings add to growing evidence . . . that replacement bisphenols have the potential to induce adverse effects similar to those reported for BPA,” the researchers concluded.

Read more

Kerry Grens (September 13, 2018). “BPA and its replacements have same effects on mice.” The Scientist

Robert F. Service (September 13, 2018). “BPA substitutes may be just as bad as the popular consumer plastic.” Science

Maya Wei-Haas (September 13, 2018). “Why ‘BPA free’ may not mean a plastic product is safe.” National Geographic

Reference

Horan, T. S., et al. (2018). “Replacement bisphenols adversely affect mouse gametogenesis with consequences for subsequent generations.” Current Biology (published online September 13, 2018).