In an article published on August 15, 2017 by news provider U.S. News, writer Elaine K. Howley discusses whether exposure to endocrine disrupting chemicals (EDCs) can elevate the risk of developing breast cancer. She starts out by noting that “breast cancer is considered a disease of aging;” however, “exposure to certain compounds in the environment while we’re still developing in the womb could flip the switch that turns mutated cells into breast cancer later in life.” She further explains that EDCs can block or mimic hormones in the body and thus disrupt the body’s hormonal balance. According to Ana Soto, professor of integrative physiology and pathobiology at Tufts University Medical School in Boston, U.S., this imbalance could result in the development of cancer later in life, because “chemicals that affect mammary gland development may also increase the propensity to develop breast cancer.” As examples of EDCs, Howley highlights the synthetic estrogens diethylstilbestrol (DES, CAS 56-53-1), dichlorodiphenyltrichloroethane (DDT, CAS 50-29-3), and bisphenol A (BPA, CAS 80-05-7). BPA is used in rigid plastics (e.g. polycarbonate (PC)) and in food can coatings, Howley informs. Therefore, “eating fewer canned foods, selecting products labeled ‘BPA-free’ and using a glass, steel or ceramic water bottle rather than single-use plastic water bottles may also help you reduce your exposure to these chemicals,” she suggests. In addition to trying to avoid exposure, Ana Soto recommends contacting governments and regulators to demand action against the continued use of EDCs.

Read more

Elaine K. Howley (August 15, 2017). “Can endocrine disruptors elevate risk of breast cancer?” U.S. News

In an article published on July 24, 2017 in the peer-reviewed journal Toxicology Letters, Ashley Bolden and colleagues from The Endocrine Disruption Exchange (TEDX) and University of Colorado, both U.S., reported on the results of a scoping review performed to identify potential human health impacts of exposure to melamine (CAS 108-78-1), focusing on the effects other than the well-known renal toxicity of this substance (see FPF dossier on melamine).

A scoping review uses a “systematic methodology to map a research area and identify the available evidence in order to pinpoint potential research questions for systematic review.” While this exercise may generate evidence-based research questions for a subsequent systematic review, by itself it does not yet generate answers to these questions, the authors note.

The literature search performed by the authors identified 2,849 articles in PubMed and 9,362 articles in Web of Science. Of these, 43 studies were identified, based on the title and abstract, to be relevant for inclusion in the present scoping review. All 43 studies were published after 2010. In vivo studies were performed in mice (11 studies), rats (17 studies), fish and chickens (two studies each), and humans (one study). In addition, 15 studies reported on in vitro experiments performed in neuronal, prostate, ovarian, and other cell lines.

Three broad endpoint categories that were identified by this scoping review as candidates for a potential systematic review included neurophysiological effects (i.e. neurological and behavioral), as well as reproductive and anthropometric effects.

Neurophysiological studies, especially those that assessed learning and memory effects of melamine (FPF reported), were concluded to constitute “a strong candidate for systematic review,” because similar endpoints were evaluated across several studies, and the mechanistic data appear to be highly relevant to the observed effects in animals. However, although the authors recommended that “a systematic review of learning and memory be conducted to determine if melamine is a hazard to human health,” they also emphasized that “human epidemiological studies on melamine exposure and neurodevelopment (especially learning and memory), as well as more mechanistic studies would be extremely useful for clarifying the [neurophysiological] effects [of melamine] on human health.”

The studies on potential reproductive effects of melamine concerned both female and male reproduction. Of these, some studies showed effects on female fertility, particularly by influencing the oocyte competence, but others did not. More studies (especially human and mechanistic) would be beneficial to resolve the question posed by the mixed evidence, the authors suggested. Endocrine disruption research initiated by several published studies on endocrine activity of melamine could help find a mechanistic explanation for the observed reproductive effects of melamine.

Among the anthropometric studies looking at body weight, body length, and fetal growth following melamine exposure at several life stages, the first parameter was identified as the most suitable endpoint for a systematic review. However, while both animal and human evidence streams are available, any relevant mechanistic data are currently lacking.

Several endpoints identified as “not well-studied with respect to melamine exposure” included “immune, mutagenic/DNA damage, and hematological endpoints.” Furthermore, no endpoints related to “cardiovascular health, respiratory health, and metabolic diseases” have been examined so far in relation to melamine exposure. When deciding which of these less-studied endpoints to pursue further, “it is important to keep in mind that research and resources should be carefully allotted for the maximum protection of human and environmental health,” the authors noted.

Melamine is frequently used in food packaging and food utensils, including tableware, as well as in a variety of other consumer products, but also in agricultural pesticide formulations. Melamine-containing food contact items are made from the polycondensation of melamine and formaldehyde (CAS 50-00-0). Both of these chemicals were shown to migrate out of melamine-ware, with migration rates increasing after microwave heating (FPF reported) and ageing (FPF reported).

Read more

Chemical Watch (August 24, 2017). “NGO calls for more research on melamine’s neurology effects.”

Reference

Bolden, A., et al. (2017). “Melamine, beyond the kidney: A ubiquitous endocrine disruptor and neurotoxicant?” Toxicology Letters (published July 24, 2017).

On August 19, 2017, a review study entitled “Food contact materials and gut health: Implications for toxicity assessment and relevance of high molecular migrants” was published in the peer-reviewed journal Food and Chemical Toxicology. Ksenia Groh and colleagues from the Food Packaging Forum (FPF), Zurich, Switzerland, reviewed the scientific literature regarding the influence of food contact chemicals on gut health.

The review shows that some chemicals migrating from food contact materials (FCMs) may negatively impact gut health. These chemicals include, for example, surfactants, N-ring containing substances, some polymers, endocrine disrupting chemicals (EDCs) such as bisphenol A (BPA, CAS 80-05-7), nanoparticles, and antimicrobials.  Therefore, the authors argue, gut toxicity appears to be an underappreciated endpoint in the chemical risk assessment of compounds migrating from FCMs. A better understanding of this endpoint may contribute to prevention of gut-related chronic diseases.

Further, several subpopulations may have increased intestinal permeability due to a variety of physiological, pathological, chemical, and lifestyle factors, and may therefore be exposed to higher levels of both low (<1000 Da) and high (>1000 Da) molecular weight compounds. As a consequence, the commonly held assumption that the intestinal uptake of high molecular weight compounds is generally negligible may be scientifically unjustified.

Even small amounts of high molecular weight compounds and/or nanoparticles may trigger potentially adverse immune responses in the immune system of the gut, leading for example to inflammation. Low-grade inflammation in the gut and other organs is commonly observed to accompany several chronic disease states. Therefore, the intestinal uptake and potential immune system effects of high molecular weight compounds migrating from FCMs may require further investigation to better understand their risk for human health.

Both the permeability of the gut epithelial barrier and the composition of the gut microbiota contribute to the regulation of immune homeostasis in the gut. The proper functioning of this interconnected system is crucial for gut health and the well-being of an organism as a whole. Indeed, scientific studies have shown that disruption of gut health may be involved in the etiology of several non-communicable diseases, including intestinal, autoimmune, and metabolic disorders, and highlighted the possible contribution of chemical exposures.

Read more

Chemical Watch (October 5, 2017). “FCM assessments should include gut health, says foundation.”

Reference

Groh K., et al. (2017). “Food contact materials and gut health: Implications for toxicity assessment and relevance of high molecular weight migrants.” Food and Chemical Toxicology (published August 19, 2017).

In an article published on September 6, 2017 by the U.S. magazine Undark, journalist Ramin Skibba reported on the use of the chemical bisphenol A (BPA, CAS 80-05-7) and its common substitutes such as bisphenol S (BPS, CAS 80-09-1) and bisphenol F (BPF, CAS 620-92-8). Skibba outlined the concerns about the safety of BPA due to its endocrine disrupting properties and the U.S. Food and Drug Administration’s (FDA) subsequent ban of the substance in baby food contact materials (FCMs). Further, Skibba illustrated the emergence of ‘BPA-free’ products using substitute chemicals such as BPS and BPF. These chemicals are structurally similar to BPA and thus “likely to have analogous effects on health,” meaning “that a ‘BPA-free’ label might be of little consequence to a consumer concerned about the potential impacts of exposure,” Skibba explained.

Read more

Ramin Skibba (September 6, 2017). “The pros and cons of ‘BPA-free.’” Undark

On September 20, 2017, Danish retailer Coop Denmark launched a campaign addressing the ‘cocktail effect’ of hazardous chemicals in everyday consumer products. In particular, the campaign focuses on per- and polyfluoroalkyl substances (PFASs) and bisphenols. Both substance groups comprise endocrine disrupting chemicals (EDCs) and are linked to health effects such as cancer, obesity, diabetes, heart disease, impaired brain development and learning ability, anxiety and depression, impaired fertility, miscarriage, and weakened immune system. Prominent examples of PFASs and bisphenols include perfluorooctanoic acid (PFOA, CAS 335-67-1), perfluorooctane sulfonate (PFOS, CAS 1763-23-1), bisphenol A (CAS 80-05-7), and bisphenol S (BPS, CAS 80-09-1), all of which occur in consumer products such as food contact materials (FCMs).

Coop Denmark prepared a draft regulation proposing to ban all PFASs and bisphenols in FCMs and certain other consumer products. The retailer is asking the Danish population to endorse the draft regulation by emailing it to the country’s politicians. On its YouTube channel, Coop Denmark published a campaign video.

Read more

Coop Denmark (September 20, 2017). “Coop vil have folketinget med i kampen mod farlig kemi.” (in Danish)

Coop TV Denmark (September 19, 2017). “Lad os stramme kemikalie-lovgivningen | Nykemilov.nu.” YouTube (in Danish)

ChemSec (September 20, 2017). “Coop Denmark calls on Danish authorities to ban bisphenols and fluorinated substances.”

Chemical Watch (September 21, 2017). “Danish retailer urges ban on bisphenols and fluorinated substances in FCMs.“

In an article published on September 27, 2017, the non-government organization Health and Environmental Alliance (HEAL) informed about the new report released by the World Health Organization (WHO) in September 2017.

The WHO’s report, titled “Preventing noncommunicable diseases (NCDs) by reducing environmental risk factors,” presents the contribution of environmental factors to the NCDs burden, and highlights “the special relevance of environmental risks for NCDs.” According to the WHO’s estimation, “23% of all global deaths are linked to the environment,” and among these “nearly two thirds” can be attributed to NCDs. Environmental factors potentially contributing to NCDs, as named by the WHO, include “ambient (outdoor) and household air pollution,” as well as “second-hand tobacco smoke, exposure to chemicals, radiation and noise, and occupational risks.” Further, WHO emphasized that “early life exposure to environmental risks, such as chemicals and air pollutants, might increase NCD risk throughout the life course.”

Given the evidence presented in the WHO’s report, HEAL’s executive director Génon Jensen emphasized that NCDs “could be prevented through disease prevention strategies focusing on healthier air, energy, transport and nontoxic environments,” and called on the EU to “prioritize WHO’s evidence and step up its action to promote health.”

Read more

HEAL (September 27, 2017). “New WHO report on non-communicable diseases (NCDs) shows 23% of deaths globally can be prevented through healthier environments.”

Reference

WHO (2017). “Preventing noncommunicable diseases (NCDs) by reducing environmental risk factors.” (pdf)

In an article published on October 11, 2017 by news provider Reuters, journalist Stephanie Nebehay informed about a new study by the World Health Organization (WHO) on worldwide trends in body weight. The study was conducted by the Risk Factor Collaboration on non-communicable diseases (NCD-RisC) and published in the peer-reviewed journal The Lancet on October 10, 2017. According to the WHO report, the number of obese children and adolescents has increased tenfold over the past 40 years: About 8% of boys and 6% of girls worldwide were obese in 2016, in contrast to less than 1% for both boys and girls in 1975. Obesity rates are accelerating in low- and middle-income countries, particularly in Asia. In rich countries, obesity rates have stabilized, but remain “unacceptably high.” The U.S. had the highest obesity rates (19.5% for girls and 23.3% for boys) among high-income countries. The study further projects that, if current trends persist, there will be more obese than underweight children and teens worldwide by 2022. According to the study’s lead author Majid Ezzati of the Imperial College London, UK, “changing environments, food, behaviors, portions, consumption patterns” contribute to the global obesity epidemic. Also, “highly processed food is more available, more marketed and it’s cheaper,” Ezzati noted.

In a blog post published on October 11, 2017 by the non-profit organization Green Science Policy Institute (GSP), author Robin Blades highlighted environmental toxins as a contributing factor to obesity. Chemicals known as metabolic disruptors (or obesogens) are “mimicking hormones that regulate fat storage,” Blades explained. Examples include phthalates, bisphenol A (BPA, CAS 80-05-7), flame retardants, and per- and polyfluoroalkyl substances (PFASs); all are used or can be found in food contact materials (FCMs) and many other consumer products.

Read more

Stephanie Nebehay (October 11, 2017). “Child and teen obesity soars tenfold worldwide in 40 years: WHO report.” Reuters

Robin Blades (October 11, 2017). “The obesity epidemic: What’s to blame?” GSP

IFT (October 11, 2017). “Child, teen obesity soars tenfold worldwide in 40 years.”

Foodwatch (October 11, 2017). “Kinder weltweit von Fettleibigkeit bedroht.” (in German)

Reference

NCD-RisC (2017). “Worldwide trends in body-mass index, underweight, overweight, and obesity from 1975 to 2016: A pooled analysis of 2,416 population-based measurement studies in 128.9 million children, adolescents, and adults.” The Lancet (published online October 10, 2017).

On October 19, 2017 “The Lancet Commission on pollution and health” published an extensive analysis of the contribution of environmental pollution to the global burden of disease. The authors report that “diseases caused by pollution were responsible for an estimated 9 million premature deaths in 2015—16% of all deaths worldwide.” Pollution mainly causes non-communicable diseases (e.g. asthma, cancer, neurodevelopmental disorders, birth defects, heart disease, stroke, chronic obstructive pulmonary disease) with the majority of pollution-linked deaths occurring in low-income and middle-income countries, they explain. Pollution is caused by e.g. industrial emissions, vehicular exhaust, and toxic chemicals, and is increasing globally, most significantly in rapidly developing and industrializing countries. The analysis further outlines the economic burden of pollution-linked diseases and the economic benefit of pollution prevention and remediation. The authors make six key recommendations, including making pollution prevention a national and international priority, monitoring pollution and its health effects, and carrying out research to understand and control pollution.

Read more

Susan Brink (October 19, 2017). “Report: Pollution kills 3 times more than AIDS, TB and malaria combined.” NPR

Ananya Roy (October 20, 2017). “Pollution is responsible for 9 million deaths globally: Two-thirds are due to air pollution.” EDF Health

Sam Morgan (October 20, 2017). “Pollution racks up 9 million deaths a year worldwide.” Euractiv

Reference

Landrigan, P.J. et al. (2017). “The Lancet Commission on pollution and health.” The Lancet (published online October 19, 2017).

In an article published on November 16, 2017 by regulatory news provider Chemical Watch, Julie A. Miller reported that the Californian Office of Environmental Health Hazard Assessment (OEHHA) has added perfluorooctanoic acid (PFOA, CAS 335-67-1) and perfluorooctane sulfonate (PFOS, CAS 1763-23-1) as developmental toxicants to the list of chemicals known to the U.S. state to cause cancer or reproductive toxicity (“Proposition 65 List”). OEHHA based its decision on findings by the U.S. Environmental Protection Agency (EPA) that both chemicals cause adverse developmental effects. Industry groups, such as the American Chemistry Council (ACC), protested against the listing of PFOA and PFOS because EPA has only published non-regulatory guidance and not formally classified the chemicals as reproductive toxicants. Proposition 65 requires “businesses to inform Californians about exposures” to the listed chemicals. Miller explained that PFOA and PFOS have been widely used in various consumer products such as carpets, textiles, leather, non-stick cookware, and food packaging.

In October 2017, OEHHA also listed the flame retardant tetrabromobisphenol A (TBBPA, CAS 79-94-7) as a carcinogen under Proposition 65, as reported by Miller in an article published on November 7, 2017. TBBPA is included in the FACET inventory of food contact materials (FCMs), as well as in the SIN List of substances of very high concern.

Read more

Julie A. Miller (November 16, 2017). “California lists PFOA and PFOS as reproductive toxicants under Prop 65.” Chemical Watch

Julie A. Miller (November 7, 2017). “California lists TBBPA as carcinogen under Prop 65.” Chemical Watch

Kelly Franklin (September 19, 2016). “California proposes listing PFOA, PFOS under Prop 65.” Chemical Watch

In an article published on December 5, 2017, the non-profit organization Health and Environment Alliance (HEAL) reported on a new scientific study calculating the economic health costs associated with exposure to environmental chemicals. The study was published on the same day in the peer-reviewed journal Environmental Health and conducted by Philippe Grandjean from the Harvard T.H. Chan School of Public Health, U.S., and the University of Southern Denmark, together with Martine Bellanger from the EHESP School of Public Health, France. In their calculation, the authors considered exposures to neurotoxicants, air pollution, and endocrine disrupting chemicals (EDCs), and made cost estimates for the U.S., the EU, OECD countries, and industrializing countries. Their results suggest that environmental chemical exposures contribute to health costs that may exceed 10% of the global gross domestic product (GDP). HEAL stated that “the new findings are yet another reason to bring health to the top of the policy agenda and focus more on prevention strategies against non-communicable diseases, in Europe and beyond.”

Read more

HEAL (December 5, 2017). “Human exposure to preventable environmental chemicals is resulting in health costs of 10% of global GDP.”

Reference

Grandjean, P. and Bellanger, M. (2017). “Calculation of the disease burden associated with environmental chemical exposures: Application of toxicological information in health economic estimation.” Environmental Health 16:123 (published online December 5, 2017).

In an article published on December 19, 2017 by news provider Environmental Health News, journalist Brian Bienkowski reported on a new scientific review addressing the toxicity of chemicals and the applicability of safe levels. The review was published on the same day in the peer-reviewed journal PLOS Biology and conducted by Bruce P. Lanphear from the Faculty of Health Sciences, Simon Fraser University, Canada. Lanphear reviewed studies on some of the most common and extensively tested chemicals and pollutants, including radon, lead, airborne particles, asbestos, tobacco, and benzene. He highlighted that “scientists have found that the amount of toxic chemical linked with the development of a disease or death . . . is proportionately greater at the lowest dose or levels of exposure.” This is contrary to the principle “the dose makes the poison” commonly applied by regulatory agencies in risk assessing chemicals and determining safe levels. “We have underestimated the impact of toxic chemicals on death and disease,” Lanphear stated. “If widely disseminated chemicals and pollutants . . . do not exhibit a threshold and are proportionately more toxic at the lowest levels of exposure, we will need to achieve near-zero exposures to protect public health,” he suggested.

Read more

Brian Bienkowski (December 19, 2017). “It’s time to rethink chemical exposures —‘safe’ levels are doing damage: Study.”

Reference

Lanphear, B.P. (2017). “Low-level toxicity of chemicals: No acceptable levels?” PLOS Biology (published online December 19, 2017).

On December 18, 2017, the peer-reviewed journal PLOS Biology launched a special collection of articles entitled “Challenges in environmental health: Closing the gap between evidence and regulations.” The articles highlight “key advances in the science of environmental health as well as barriers to incorporating these advances into public health policy,” Liza Gross from the Public Library of Science, San Francisco, U.S., explained in a PLOS Blogs post.

The collection includes an editorial by Liza Gross and Linda S. Birnbaum, affiliated with the U.S. National Institutes of Health (NIH), on the regulation of toxic chemicals to protect public and environmental health. An article by Sheldon Krimsky from Tufts University, U.S., explores the factors hindering “a comprehensive and rational policy for regulating toxic chemicals” under the U.S. chemicals’ law Toxic Substances Control Act (TSCA). Bruce P. Lanphear reviewed scientific research on toxic substances and highlights that some chemicals are “proportionately more toxic at the lowest levels of exposure” (FPF reported). An article by Joseph M. Braun and Kimberly Gray from Brown University, U.S., and the U.S. National Institutes of Environmental Health Sciences (NIEHS), respectively, discusses the challenges in studying the effects of early life exposures to environmental chemicals. Gloria B. Post , Jessie A. Gleason, and Keith R. Cooper, affiliated with the U.S. state of New Jersey Department of Environmental Protection, the New Jersey Department of Health, and Rutgers University, U.S., respectively, focus on exposure to perfluoroalkyl acids (PFAAs) and drinking water guidelines. Maricel V. Maffini, an independent consultant based in the U.S., Thomas G. Neltner, and Sarah Vogel, both from the U.S. non-profit organization Environmental Defense Fund (EDF), address hazardous chemicals in the U.S. food system and outline the specific case of perchlorate as an example (FPF reported).

Read more

Liza Gross (December 18, 2017). “PLOS Biology explores gaps between environmental health science and policy.” PLOS Blogs

Julian Cribb (December 21, 2017). “Major journal sounds alarm over global mass poisoning.” Cosmos

References

Gross, L., and Birnbaum, L.S. (2017). “Regulating toxic chemicals for public and environmental health.” PLOS Biology (published online December 18, 2017).

Krimsky, S. (2017). “The unsteady state and inertia of chemical regulation under the U.S. Toxic Substances Control Act.” PLOS Biology (published online December 18, 2017).

Lanphear, B.P. (2017). “Low-level toxicity of chemicals: No acceptable levels?” PLOS Biology (published online December 19, 2017).

Braun, J.M., and Gray, K. (2017). “Challenges to studying the health effects of early life environmental chemical exposures on children’s health.” PLOS Biology (published online December 19, 2017).

Post, G.B., et al. (2017). “Key scientific issues in developing drinking water guidelines for perfluoroalkyl acids: Contaminants of emerging concern.” PLOS Biology (published online December 20, 2017).

Maffini, M.V. et al. (2017). “We are what we eat: Regulatory gaps in the United States that put our health at risk.” PLOS Biology (published online December 20, 2017).

In a perspective article published on December 20, 2017 in the peer-reviewed journal PLoS Biology, Maricel Maffini, independent consultant, and colleagues working at the non-governmental organization Environmental Defense Fund (EDF) argued that the U.S. Food and Drug Administration (FDA) is not able “to effectively manage the safety of hundreds of chemicals,” falling “short of fully enforcing its mandates [to ensure the safety of chemicals in food],” and that this failure “is putting our children’s health at risk.”

The authors summarized that “thousands of chemicals,” with chronic effects “woefully understudied” and health risks “inadequately assessed,” have entered the food system since 1958, when FDA was given its current authority to assess and regulate chemicals used in or contaminating food. The two areas of particular concern are the effects of chemicals “at low levels and during susceptible developmental stages.” A recent example used by the authors to illustrate the current regulatory gaps in managing chemical contamination in food in the U.S. is the case of thyroid disruptor perchlorate (FPF reported).

In a blog article published on December 20, 2017 by EDF Health, Maffini’s co-author Sarah Vogel emphasized that “protecting the most vulnerable from hazardous chemicals is a common goal that we should all be striving towards to build a safer and healthier future.”

Read more

Sarah Vogel (December 20, 2017). “We are what we eat: New paper outlines how the regulatory gaps in the US threaten our health.” EDF Health

Reference

Maffini, M., et al. (2017). “We are what we eat: Regulatory gaps in the United States that put our health at risk.” PLoS Biology (published December 20, 2017).

On January 11, 2018, the European Parliament Committee on the Environment, Public Health and Food Safety (ENVI) discussed and voted on a draft proposal by the European Commission (EC) to regulate bisphenol A (BPA, CAS 80-05-7) in some food contact materials (FCMs). The EC’s draft foresees to lower the specific migration limit (SML) for BPA in plastics from 0.6 mg/kg to 0.05 mg/kg. The new SML would also apply to varnishes and coatings. Further, migration of BPA shall be banned for all FCMs intended for infants and toddlers (FPF reported). The ENVI Committee adopted the EC’s draft regulation and rejected a separate motion objecting the EC’s proposal and asking for a complete ban on BPA in all FCMs.

The non-profit organization Health and Environment Alliance (HEAL) regrets the ENVI Committee’s decision, stating that the EC’s proposal “fails to protect citizens’ health and will mainly benefit the chemical industry.” HEAL demands a “full ban [on BPA], because exposure to even very low doses can have serious long-term health impacts.” BPA is listed as a substance of very high concern (SVHC) under REACH due to its reprotoxic and endocrine disrupting properties with effects on human health, HEAL reminds (FPF reported).

Read more

HEAL (January 11, 2018). “Europeans will remain exposed to BPA in food packaging.”

Clelia Oziel (January 10, 2018). “MEPs to vote on proposal to restrict BPA in food packaging.” Chemical Watch

On February 1, 2018, Philip J. Landrigan, professor of pediatrics, environmental medicine and public health, and Dean for Global Health at Icahn School of Medicine at Mount Sinai, U.S., and Mary M. Landrigan, a public health educator, published a book entitled “Children and environmental toxins: What everyone needs to know®.”

“Environmental toxics cause disease, and children are exquisitely sensitive to disease caused by chemicals,” the authors write in a commentary published on February 2, 2018 by news provider Environmental Health News (EHN). Prenatal exposures to chemicals such as organophosphate insecticides, pesticides, benzene, brominated flame retardants, polychlorinated biphenyls (PCBs), phthalates, and bisphenol A (BPA, CAS 80-05-7) can cause non-communicable “disorders of neurobehavioral development such as dyslexia, mental retardation, attention deficit/hyperactivity disorder [(ADHD)] and autism,” “birth defects in the reproductive organs of baby boys,” as well as “cancer, especially leukemia and brain cancer,” the authors further explain.

The book contains “practical, actionable advice for mitigating the threat of chemical toxins in one’s home and environment.”

Read more

Philip J. Landrigan and Mary M. Landrigan (February 2, 2018). “Commentary: It’s up to us to keep children safe from toxics.” EHN

Nneka Leiba (February 5, 2018). “Every parent concerned about their kids’ health should read this book.” EcoWatch

Reference

Landrigan, P.J., and Landrigan, M.M. (February 1, 2018). “Children and environmental toxins: What everyone needs to know®.” Oxford University Press, ISBN: 9780190662639.

In an article published on January 9, 2018 in the peer-reviewed journal Biological Psychiatry, Angelique Quartier and colleagues from the University of Strasbourg, France, presented in vitro evidence suggesting that prenatal exposure to androgens may disrupt brain development, leaving males more susceptible “to develop neurodevelopmental disorders such as autism spectrum disorder (ASD) and intellectual disability.”

The researchers studied gene expression in human neural stem cells to investigate gene targets of androgens. They identified a set of ASD-related genes which were “reproducibly regulated by different androgens in different genetic backgrounds,” and demonstrated the involvement of the androgen receptor in the regulation of these genes. Further, androgens were found to “increase human neural stem cell proliferation and survival in nutrient-deprived culture conditions.”

The authors suggested that their findings could help explain the known predisposition of males to autism. Currently, about four times more males than females are being diagnosed with this disease. Prenatal exposure to the male hormone testosterone (an androgen) may result in prolonged survival of neuronal progenitor cells. This in turn could be the reason for the excessive brain growth known to occur in people with ASD during childhood. In addition, androgens regulated the expression of the key genes related to ASD. Due to these actions of androgens, the brain of boys could become more susceptible to developing ASD, making it more sensitive to the influence of other accompanying factors, such as genetic predisposition or environmental exposure.

Some synthetic chemicals contaminating food, including some food contact chemicals, have also been shown to interact with androgen receptor. Most commonly, an antiandrogenic activity is observed  (FPF reported). However, several extracts of paper/board food contact materials have also been observed to activate the androgen receptor (FPF reported).

Read more

Science Direct (February 7, 2018). “Male susceptibility to autism linked to male hormones in early-stage brain development.”

Reference

Quartier, A., et al. (2018). “Genes and pathways regulated by androgens in human neural cells, potential candidates for the male excess in autism spectrum disorder.” Biological Psychiatry (published January 9, 2018).

On October 5, 2017, the Food Packaging Forum (FPF) held its fifth annual workshop in Zurich, Switzerland, focusing on “Scientific challenges in the risk assessment of food contact materials.”

Dr. Jean-Pierre Cravedi, Director of Research at the French National Institute for Agricultural Research (INRA), Toulouse, France, reported on the contamination of food with mineral oil saturated hydrocarbons (MOSH) (FPF reported). In a short interview, he highlighted that MOSH mainly accumulate in the liver and and can cause liver damage. Watch his speaker spotlight on YouTube or on the 2017 FPF Workshop website.

Dr. Cravedi’s entire presentation at the 2017 FPF Workshop can be found here.

In an article published on February 13, 2018 by The Guardian, editor Ian Sample reported on a new scientific study linking exposure to per- and polyfluoroalkyl substances (PFASs) with increased weight gain. The study was published on the same day in the peer-reviewed journal PLOS Medicine and conducted by Gang Liu and colleagues from Harvard T.H. Chan School of Public Health, Louisiana State University, and Tulane University, all U.S.. The researchers analyzed data for 621 overweight and obese people who had participated in a two-year clinical dieting trial in the mid-2000s. Liu and colleagues found that participants with the highest blood concentrations of PFASs gained the most weight back after the dieting phase. This link was most pronounced among women. Also, higher PFASs blood levels were significantly associated with lower resting metabolic rates.

“Our findings have revealed a novel pathway through which PFASs might interfere with human body weight regulation and thus contribute to the obesity epidemic,” stated Qi Sun, senior author of the study. PFASs are used in various consumer products such as stain-resistant carpets, waterproof textiles, non-stick cookware, and food packaging.

Read more

Ian Sample (February 13, 2018). “Chemicals in packaging, carpets and non-stick pans ‘may contribute to obesity.’” The Guardian

Science Daily (February 13, 2018). “PFASs, chemicals commonly found in environment, may interfere with body weight regulation.” Science Daily

Brian Bienkowski (February 14, 2018). “Another potential PFAS problem: Weight gain.” Environmental Health News

Lorraine Chow (February 14, 2018). “Non-stick chemicals used in pans, food wrappers linked to weight gain.” EcoWatch

Reference

Liu, G., et al. (2018). “Perfluoroalkyl substances and changes in body weight and resting metabolic rate in response to weight-loss diets: A prospective study.“ PLOS Medicine (published online February 13, 2018).

In an article published on February 2, 2018 in the peer-reviewed journal The Journal of Steroid Biochemistry and Molecular Biology, Valentina Pomatto and colleagues from the University of Turin, Italy, reported on adipogenic effects of several plasticizers increasingly used in food contact materials (FCM) as “safer alternatives” to several phthalates restricted as substances of very high concern (SVHC) under REACH. These plasticizers are diisononyl phthalate (DiNP, CAS 28553-12-0), diisodecyl phthalate (DiDP, CAS 26761-40-0), diethylene glycol dibenzoate (DEGDB, CAS 120-55-8), and tri-m-cresyl phosphate (TMCP, CAS 563-04-2). Bisphenol A (BPA, CAS 80-05-7) and rosiglitazone (CAS 122320-73-4) were used as reference compounds. Rosiglitazone is a well-known pro-adipogenic agonist of peroxisome proliferator activated receptor gamma (PPARγ). The researchers used 3T3-L1 cells to test the above compounds at a wide range of concentrations.

All four tested plasticizers enhanced lipid accumulation and were shown to bind to PPARγ in silico, with TMCP having the greatest potency in both assays. BPA also enhanced lipid accumulation, but likely through other pathways not involving PPARγ. The tested plasticizers were also found to modulate the expression of several adipogenesis-related genes.

The authors conclude that their results “suggest that exposure to low, environmentally relevant doses [(low nanomolar concentrations)] of the plasticizers DiNP, DiDP, DEGDB and TMCP increase lipid accumulation in 3T3-L1 adipocytes, an effect likely mediated through activation of PPARγ.” This shows that “these four plasticizers may not be harmless substitute[s] of currently restricted compounds.” The scientists further point out that, although individual chemicals showed a “moderate” effect on lipid accumulation, their global effect “could be significantly higher in mixtures.” Importantly, FCMs are known to often contain multiple plasticizers. This calls for further studies evaluating the effects of mixtures of these plasticizers.

Reference

Pomatto, V., et al. (2018). “Plasticizers used in food-contact materials affect adipogenesis in 3T3-L1 cells.” The Journal of Steroid Biochemistry and Molecular Biology (published February 2, 2018).

In an article published on February 19, 2018 by The Guardian, journalist David Cox addressed the question “Can exposure to plastics harm your health?” which is currently being much debated. Special focus was on the chemical bisphenol A (BPA, CAS 80-05-7). BPA is used in the manufacture of epoxy coatings found in most food and beverage cans as well as in polycarbonate (PC) plastics that are used in, e.g., refillable water bottles. Migration of BPA from the packaging into food and drink and subsequent dietary intake is one of the main routes of consumer exposure.

Cox referred to a recent scientific study finding that the majority of UK teenagers have BPA in their bodies and that exposure is hard to avoid (FPF reported). Cox further informed that exposure to BPA has been linked to, e.g., male infertility, type 2 diabetes and insulin resistance, coronary artery disease, and breast cancer. However, it is difficult “to get concrete proof that BPA is definitively involved in many of these diseases,” he explained.

“Because you can’t establish a direct causal link, it’s hard to make strong conclusions, and that’s what causes the controversy,” stated Tamara Galloway, professor of ecotoxicology at the University of Exeter, UK, who led the dietary intervention study with teenagers. Despite precautionary measures set out in government regulations, it is not easy “to avoid coming into contact with BPA as it’s simply everywhere, from plastic drinks bottles to the epoxy resins that line the cans of tinned food,” Cox noted. Nevertheless, Galloway recommended taking certain steps to limit exposure to BPA, such as breastfeeding children or using BPA-free baby bottles, buying unpackaged fruit and vegetables, avoiding heavily processed and packaged food, and refraining from microwaving food in PC containers.

Read more

David Cox (February 19, 2018). “Are we poisoning our children with plastic?” The Guardian

Monica Amarelo and Samara Geller (February 11, 2018). “5 ways to reduce your exposure to toxic BPA.” EcoWatch