BPA bad for children’s hearts, study suggests

Early BPA exposure may influence cardiac function, according to new study in neonatal rats

A new study paves the way for translational research examining cardiovascular disease risk factors associated with short-term BPA exposure in infancy. By examining neonatal rat heart cells, researchers find the immature heart may respond to BPA with a slowed heart rate, irregular heart rhythm and calcium instabilities. The significance of this research is that plastics revolutionized the way doctors treat young patients, especially patients with compromised immune or cardiac function.

2018 Study Abstract

Bisphenol chemicals are commonly used in the manufacturing of polycarbonate plastics, polyvinyl chloride plastics, resins, and thermal printing applications. Humans are inadvertently exposed to bisphenols through contact with consumer products and/or medical devices. Recent reports have shown a link between bisphenol-a (BPA) exposure and adverse cardiovascular outcomes; although these studies have been limited to adult subjects and models. Since cardiac physiology differs significantly between the developing and adult heart, we aimed to assess the impact of BPA exposure on cardiac function, using a neonatal cardiomyocyte model. Neonatal rat ventricular myocytes were monitored to assess cell viability, spontaneous beating rate, beat rate variability, and calcium-handling parameters in the presence of control or bisphenol-supplemented media. A range of doses were tested to mimic environmental exposure (10−9–10−8M), maximum clinical exposure (10−5M), and supraphysiological exposure levels (10−4M). Acute BPA exposure altered cardiomyocyte functionality, resulting in a slowed spontaneous beating rate and increased beat rate variability. BPA exposure also impaired intracellular calcium handling, resulting in diminished calcium transient amplitudes, prolonged calcium transient upstroke and duration time. Alterations in calcium handling also increased the propensity for alternans and skipped beats. Notably, the effect of BPA-treatment on calcium handling was partially reversible. Our data suggest that acute BPA exposure could precipitate secondary adverse effects on contractile performance and/or electrical alternans, both of which are dependent on intracellular calcium homeostasis.

More Information

  • Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a, nature, 09 May 2018.
  • Early BPA exposure may influence cardiac function, according to new study in neonatal rats, sciencedaily, May 14, 2018.
  • Image credit James Graham.

Exposure to low levels of BPA during pregnancy can lead to altered brain development

These findings suggest that gestational exposure to BPA can lead to lasting and permanent changes in the brain

Chicago, IL – New research in mice provides an explanation for how exposure to the widely used chemical bisphenol A (BPA) during pregnancy, even at levels lower than the regulated “safe” human exposure level, can lead to altered brain development and behavior later in life. The research was presented Monday, March 19 at ENDO 2018, the 100th annual meeting of the Endocrine Society in Chicago, Ill.

BPA is a chemical that is added to many commercial products, including water bottles, paper receipts, can liners and food storage containers. It is known as an endocrine-disrupting chemical—a chemical that interferes with the body’s hormones.

“Decades of research in over 1,000 animal and 100 human epidemiological studies have demonstrated a link between BPA exposure and adverse health outcomes,”

said lead researcher Deborah Kurrasch, Ph.D., Associate Professor at the University of Calgary in Calgary, Canada.

“This is especially true for the developing brain, which is particularly sensitive to the estrogen-promoting effects of BPA during gestation. Indeed, several human studies have now correlated early life BPA exposure with behavioral problems later in childhood, suggesting BPA permanently alters brain development that leads to lasting effects on neural functioning.”

she noted.

Governmental agencies around the world, including the U.S. Food and Drug Administration, Health Canada, and European Food Safety Authority, declare BPA to be safe.

“One reason for this disparity is the absence of a smoking gun: if BPA is so toxic to developing brains, then where is the evidence of defective brains?”  “Our study is the first to use environmentally relevant doses of BPA and show exposure to the chemical during brain development can affect the timing of the birth of nerve cells, or neurons.”

Kurrasch said.

The researchers studied three groups of pregnant mice. One group ate food without BPA; a second group at food with high doses of BPA; and a third ate low-dose BPA food. They found an increase in the number of neurons created during early development in mouse pups exposed to high and low doses of BPA during pregnancy, compared with those not exposed to BPA.

“This is important because specific neurons are known to be born at a very distinct time points, and if they are born early—as is the case here—then presumably these early neurons will migrate to the wrong place and form the wrong connections. These findings start to provide a rationale as to how BPA might affect developing brains,”

Kurrasch said.

Siblings to these pups were given behavioral tests to assess whether the early birth of neurons led to changes that affected brain function later in life. The researchers found mice that were exposed to BPA-high and BPA-low food during gestation exhibited some behaviors that match those observed in human children whose mothers had high levels of BPA during pregnancy.

“The public is becoming well educated on the debate surrounding BPA safety, as well as other chemicals.” “Although there is still work to be done to translate these rodent effects to human pregnancy, this research could provide expectant mothers with important information on what to avoid to best protect their babies.”

Kurrasch said.

Early exposure to BPA linked to increased hyperactivity

Prenatal exposure to bisphenol A and hyperactivity in children: a systematic review and meta-analysis

Bisphenol-A, widely used in plastics, receipt paper and canned food linings, is a culprit in some children developing hyperactivity : a July 2017 review, available online 7 March 2018, of more than 30 scientific studies, concludes early life exposure to the endocrine disrupting chemical BPA leaves children more susceptible to hyperactivity later in life.

Study Highlights

  • We used the OHAT systematic review framework to examine if early exposure to BPA has an effect on hyperactivity
  • We found that, in both rodents and humans, early exposure to BPA is linked to increased hyperactivity
  • Integration of animal and human evidence finds that BPA is a presumed hazard to human health
  • We suggest the development of clinical recommendations for avoiding BPA exposure, especially for pregnant women and children

2018 Study Abstract

Background
Attention-deficit hyperactivity disorder (ADHD) has increased in prevalence in the past decade. Studies attempting to identify a specific genetic component have not been able to account for much of the heritability of ADHD, indicating there may be gene-environment interactions underlying the disorder, including early exposure to environmental chemicals. Based on several relevant studies, we chose to examine bisphenol A (BPA) as a possible contributor to ADHD in humans. BPA is a widespread environmental chemical that has been shown to disrupt neurodevelopment in rodents and humans.

Objectives
Using the Office of Health Assessment and Translation (OHAT) framework, a systematic review and meta-analysis was designed to determine the relationship between early life exposure to BPA and hyperactivity, a key diagnostic criterion of ADHD.

Data sources
Searches of PubMed, Web of Science, and Toxline were completed for all literature to January 1, 2017.

Study eligibility criteria
For inclusion, the studies had to publish original data, be in the English language, include a measure of BPA exposure, and assess if BPA exposure affected hyperactive behaviors in mice, rats or humans. Exposure to BPA had to occur at <3 months of age for humans, up to postnatal day 35 for rats and up to postnatal day 40 for mice. Exposure could occur either gestationally (via maternal exposure) or directly to the offspring.

Study appraisal and synthesis methods
Studies were evaluated using the OHAT risk of bias tool. The effects in humans were assessed qualitatively. For rodents exposed to 20 μg/kg/day BPA, we evaluated the study findings in a random effects meta-analytical model.

Results
A review of the literature identified 29 rodent and 3 human studies. A random effects meta-analysis showed significantly increased hyperactivity in male rodents. In humans, early BPA exposure was associated with hyperactivity in boys and girls.

Limitations, conclusions, and implications of key findings
We concluded that early life BPA exposure is a presumed human hazard for the development of hyperactivity. Possible limitations of this systematic review include deficiencies in author reporting, exclusion of some literature based on language, and insufficient similarity between human studies. SRs that result in hazard-based conclusions are the first step in assessing and mitigating risks. Given the widespread exposure of BPA and increasing diagnoses of ADHD, we recommend immediate actions to complete such risk analyses and take next steps for the protection of human health. In the meantime, precautionary measures should be taken to reduce exposure in pregnant women, infants and children. The present analysis also discusses potential mechanisms by which BPA affects hyperactivity, and the most effective avenues for future research.

Sources and Press Releases

BPA detected in urine of 86% of teenagers in the UK

Exposure to Bisphenol A ‘hard to avoid’ in everyday life

86 per cent of UK students aged between 17 and 19 years have traces of Bisphenol A (BPA), a chemical compound used to make plastics, in their body, an Engaged Research public engagement project in collaboration with the University of Exeter has found. Manneken Pis image credit David Kenny.

2018 Research Abstract

Objective
Bisphenol A (BPA) has been associated with adverse human health outcomes and exposure to this compound is near-ubiquitous in the Western world. We aimed to examine whether self-moderation of BPA exposure is possible by altering diet in a real-world setting.

Design
An Engaged Research dietary intervention study designed, implemented and analysed by healthy teenagers from six schools and undertaken in their own homes.

Participants
A total of 94 students aged between 17 and 19 years from schools in the South West of the UK provided diet diaries and urine samples for analysis.

Intervention
Researcher participants designed a set of literature-informed guidelines for the reduction of dietary BPA to be followed for 7 days.

Main outcome measures
Creatinine-adjusted urinary BPA levels were taken before and after the intervention. Information on packaging and food/drink ingested was used to calculate a BPA risk score for anticipated exposure. A qualitative analysis was carried out to identify themes addressing long-term sustainability of the diet.

Results
BPA was detected in urine of 86% of participants at baseline at a median value of 1.22 ng/mL (IQR 1.99). No effect of the intervention diet on BPA levels was identified overall (P=0.25), but there was a positive association in those participants who showed a drop in urinary BPA concentration postintervention and their initial BPA level (P=0.003). Qualitative analysis identified themes around feelings of lifestyle restriction and the inadequacy of current labelling practices.

Conclusions
We found no evidence in this self-administered intervention study that it was possible to moderate BPA exposure by diet in a real-world setting. Furthermore, our study participants indicated that they would be unlikely to sustain such a diet long term, due to the difficulty in identifying BPA-free foods.

Discussion

Exposure to the EDC BPA is ubiquitous, with growing evidence that it may be associated with adverse health outcomes. Here, 94 researcher participants aged 17–19 years designed and undertook a quantitative and qualitative engaged research project designed to assess the potential for reduction of personal exposure to BPA through moderation of diet, which would have utility in a ‘real-world’ setting. We conclude that the ‘real-world’ diet designed to reduce BPA exposure had no effect on creatinine-adjusted urinary BPA concentrations in our cohort over a period of 7 days in our dataset.

Although concentrations of urinary BPA in our study cohort were slightly lower at the outset of the study than in others, measurable concentrations were present in the vast majority of our participants. Participants were unable to achieve a reduction in their urinary BPA over the 7-day trial period, despite good compliance to supplied guidelines. Avoidance of BPA was not easily achieved on an individual level in our study population, with qualitative analysis indicating that participants experienced feelings of restriction and difficulties in sourcing BPA-free food due to inadequate labelling of foods and food packaging. This suggests that the intervention would be difficult to sustain in the longer term.

This work represents the largest group of unrelated participants in a high exposure demographic to date, since previous work has focused on families and related individuals, who may share common sources of BPA. Although other population demographics such as young children may have higher concentrations of BPA than our chosen study population, it would not have been possible to do the sort of engaged research project that we envisaged in this group. Our intervention is a ‘real-world’ diet, designed to a set of guidelines (such as reduction in the usage of tinned foods or foods with high levels of processing), rather than the strict, prescribed diets that have been used in other studies, which suggested that it was possible for participants to reduce their urinary BPA excretion by approximately 60% in a period of just 3 days. In our self-designed, self-administered study this was unachievable. This may reflect the difficulty in identifying and sourcing foods free of BPA in the current commercial environment. Finally, the qualitative thematic analysis has given an indication that adherence to even a ‘real-world’ BPA reduction diet with fewer restrictions and more choice over the longer term was unlikely in our study population due to difficulties in identifying foodstuffs likely to contain less BPA.

BPA has a terminal half-life of 6 hours. Spot samples may therefore not be as accurate as continuous sampling strategies (24 hours urine collection). However, recent studies suggest that despite its short half-life, measurable BPA remains present for up to 43 hours postfasting, indicating non-food exposures or accumulation in body tissues such as fat. We identified no impact of time of sample collection on BPA concentrations in our sample set, in either creatinine-adjusted or unadjusted data, indicating that our measurements were not influenced by time since the last meal. Spot sampling as used here may therefore represent an acceptable compromise and remains a practical option in the community setting. The large variability in urinary BPA within an individual sampled at different times may also have reduced our ability to observe an effect. This could be facilitated by the use of multiple sampling or pools of multiple urines, but was not feasible within the confines of our study.

Calculating an accurate BPA risk score is challenging. Data were self-reported, and foodstuffs are not labelled for BPA content. It is difficult to generalise across food types and large variations in BPA concentrations occur between different products of the same food type or even different lots of the same product. Foods that were free of BPA-containing packaging (as far as it was possible to tell) may have been highly processed or contain food items from a variety of sources. Highly processed and ‘fast’ food has previously been demonstrated to be a source of BPA. A study of the temporal trends seen in composite food samples found no change in the overall BPA content of the food, despite large reduction in the BPA content of some individual food items, illustrating the difficulties in effectively excluding BPA from a varied diet. Participants may therefore have changed BPA-containing foods for other, perceived healthier choices, which may still contain BPA by virtue of processing.

BPA enters foodstuffs by leaching from polycarbonate or epoxy resin after manufacture, or by hydrolysis of the polymer itself. The migration rate of BPA increases with higher temperatures, and with time and use, for example, repeated use of polycarbonate water bottles. Exposure to BPA can also occur through routes other than food, including dust ingestion and dermal absorption and this was not taken into account in our study. A study of volunteers who purposefully handled thermal receipts showed an increase in urinary BPA excretion of up to 84%, and their BPA levels took longer to return to pre exposure levels, suggesting a difference in the bioavailability of BPA through skin and oral routes. It is also possible that some manufacturers may have voluntarily reduced the amount of BPA-containing food packaging compared with their previous usage, given the attention that EDCs have received in the media. However, measurable levels of BPA were still detected in the majority of participants in our study, which suggests that there may be other, non-dietary, sources of BPA, and that exposure to BPA remains an issue. We may also have been underpowered to detect subtle changes in urinary BPA, given the heterogeneity in food choice; detection of such effects may need thousands of participants. Finally, our study, like other studies of its type, does not take account of interindividual differences in the metabolism and excretion of BPA arising from differences in genetic background between people. BPA is metabolised primarily by uridine 5′-diphospho-glucuronosyltransferases, and altered activity polymorphisms of these enzymes have been reported.

Emerging evidence suggests that that BPA may be linked to several chronic human health conditions, suggesting that continued study of the human health effects of BPA exposure is justified. The opinion of the European Food Safety Authority (EFSA), is that while uncertainty over the human health effects of BPA exists, caution should be exercised in ingestion of BPA. Our data suggest that in our study population, it is unlikely that participants could moderate their own BPA exposure in the long term by self-directed modification of diet in a ‘real-world’ setting, and furthermore, participants would have been reluctant to adopt such a lifestyle change in the longer term due to the restrictions in dietary choice and the effects on day-to-day life. Most of these barriers appear to arise from the pervasiveness of BPA in our food chain, and inadequate labelling of foods packaged in BPA-containing substances. We propose that until a definitive assessment of the health risks of BPA is available, informed choice over whether or not to consume BPA and similar chemicals in foodstuffs should be facilitated by better labelling.

Europeans will remain exposed to Bisphenol A in food packaging

MEPs reject ban on BPA in food packaging, Brussels, 11th January 2018

A European Commission proposal to regulate bisphenol A in food contact materials was discussed today in the European Parliament Environment Committee (ENVI). The Health and Environment Alliance (HEAL) regrets that Members (MEPs) gave the green light to a piece of legislation that fails to protect citizens’ health and will mainly benefit the chemical industry.

The European Commission regulation foresees to simply lower the migration limit rather than ban bisphenol A in the coatings and varnishes used in food packaging. This contradicts the European Parliament’s own 2016 demand to fully ban bisphenol A from food contact materials [3].

Bisphenol A has been listed as a substance of very high concern (SVHC) by the European Chemicals Agency due to its endocrine disrupting properties , and it is also classified as toxic for reproduction. HEAL alongside numerous civil society groups have long demanded its full ban, because exposure to even very low doses can have serious long-term health impacts.

Commenting on the outcome of the vote, Natacha Cingotti, HEAL’s policy officer on health and chemicals, said:

“The adverse health effects of Bisphenol A, even at low doses, are so well documented that it should already have been banned from all consumer products a long time ago – citizens shouldn’t have to worry that their food wrapper or packing contains BPA and might seep into their food and harm their health.”

“European politicians are failing in their responsibility to protect people’s health and to act on their earlier commitments, although safer alternatives are available and some governments such as France and industry retailers are already on the path to substitution. It’s not only dangerous but also incoherent – we should be getting the toxics out of the economy if we want it to be truly circular.”

HEAL has repeatedly called on European decision-makers to take steps to fix the loopholes that currently exist in terms of the evaluation and regulation of chemicals in food packages, and will continue to promote more ambitious action to protect Europeans – in particular vulnerable groups – as a formal evaluation of the European legislation on food contact materials is about to start.

Perinatal BPA exposure induces chronic inflammation in offspring by modulating gut bacteria

Exposure to Bisphenol A During Pregnancy Induces Chronic Inflammation in Rabbit Offspring via Modulation of Gut Bacteria and Their Metabolites

A chemical called bisphenol A (BPA) used in plastic packaging and in the linings of food and beverage cans, may be passed from a mother to her offspring during pregnancy and cause changes in the gut bacteria of the offspring.

Emerging evidence from a research study in rabbits suggests that environmental toxicants may influence inflammation-promoted chronic disease susceptibility during early life. BPA exposure just before or after birth leads to reduced gut bacterial diversity, bacterial metabolites such as short-chain fatty acids (SCFA) and elevated gut permeability – three common early markers of inflammation-promoted chronic diseases.

The researchers observed that exposure to BPA during pregnancy caused chronic inflammation in the offspring’s intestines and liver. The researchers also noted signs of increased gut permeability – or leaky gut – and a decrease in the diversity of gut bacteria and anti-inflammatory bacterial metabolites, such as short-chain fatty acids.

2017 Study Abstract

Bisphenol A (BPA) accumulates in the maturing gut and liver in utero and is known to alter gut bacterial profiles in offspring. Gut bacterial dysbiosis may contribute to chronic colonic and systemic inflammation. We hypothesized that perinatal BPA exposure-induced intestinal (and liver) inflammation in offspring is due to alterations in the microbiome and colonic metabolome. The 16S rRNA amplicon sequencing analysis revealed differences in beta diversity with a significant reduction in the relative abundances of short-chain fatty acid (SCFA) producers such as Oscillospira and Ruminococcaceae due to BPA exposure. Furthermore, BPA exposure reduced fecal SCFA levels and increased systemic lipopolysaccharide (LPS) levels. BPA exposure-increased intestinal permeability was ameliorated by the addition of SCFA in vitro. Metabolic fingerprints revealed alterations in global metabolism and amino acid metabolism. Thus, our findings indicate that perinatal BPA exposure may cause gut bacterial dysbiosis and altered metabolite profiles, particularly SCFA profiles, leading to chronic colon and liver inflammation.

IMPORTANCE
Emerging evidence suggests that environmental toxicants may influence inflammation-promoted chronic disease susceptibility during early life. BPA, an environmental endocrine disruptor, can transfer across the placenta and accumulate in fetal gut and liver. However, underlying mechanisms for BPA-induced colonic and liver inflammation are not fully elucidated. In this report, we show how perinatal BPA exposure in rabbits alters gut microbiota and their metabolite profiles, which leads to colonic and liver inflammation as well as to increased gut permeability as measured by elevated serum lipopolysaccharide (LPS) levels in the offspring. Also, perinatal BPA exposure leads to reduced levels of gut bacterial diversity and bacterial metabolites (short-chain fatty acids [SCFA]) and elevated gut permeability-three common early biomarkers of inflammation-promoted chronic diseases. In addition, we showed that SCFA ameliorated BPA-induced intestinal permeability in vitro. Thus, our study results suggest that correcting environmental toxicant-induced bacterial dysbiosis early in life may reduce the risk of chronic diseases later in life.

Sources

  • Perinatal Bisphenol A Exposure Induces Chronic Inflammation in Rabbit Offspring via Modulation of Gut Bacteria and Their Metabolite, msystems asm, DOI: 10.1128/mSystems.00093-17, 2017 Oct.
  • Exposure to chemical during pregnancy may cause health problems for offspring, The Pennsylvania State University, story/491849, November 8, 2017.
  • Microbial responses to the perinatal bisphenol A (BPA) exposure in rabbit offspring featured image credit PMC5634791/figure/fig2, 2017 Oct 10.

Prenatal and postnatal bisphenol A exposure and social impairment in 4-year-old children

BPA linked to social deficits in offspring, particularly in girls

2017 Study Abstract

Background
Prenatal and postnatal exposure to bisphenol A (BPA) may affect early brain development. Rodent studies suggest that prenatal and postnatal neurodevelopmental toxicity from BPA exposure may manifest as social deficits in offspring. We investigated the association between prenatal and postnatal exposure to BPA and social impairments in a sample of 4-year-old children.

Methods
We recruited second-trimester pregnant women between 2008 and 2011, and measured their creatinine-adjusted prenatal urine BPA levels. In 2014-2015, a subset of 4-year-old children born to these women underwent neurobehavioral assessment and physical examination. We collected urine and blood from the children and assessed social impairments, including deficits in social interaction, social communication, and other behavior patterns using the Korean version of the Social Communication Questionnaire (K-SCQ) (n = 304). We examined social impairments associated with prenatal exposure at mid-term pregnancy and postnatal exposure to BPA at 4 years of age, using linear and piecewise linear regression models.

Results
The relationship between prenatal BPA exposure and social communication was non-linear and statistically significant at or above the flexion point for BPA levels of 3.0 μg/g creatinine in girls (58.4%, 95% confidence interval [CI], 6.5% to 135.8%). Each 2-fold increase in postnatal BPA exposure was significantly associated with an 11.8% (95% CI, 0.6% to 24.3%) increase in impairment in social communication in 4-year old girls, as indicated by the linear regression model.

Conclusion
Prenatal and postnatal BPA exposure is associated with social impairment at 4 years of age, particularly in girls.

The prospective cohort study design is a strength of this study investigating the relationships between prenatal and postnatal BPA concentrations and social impairments at 4 years of age. Although the study has several limitations, including parent-reported questionnaires to evaluate social impairments and no participants with severe social impairments, the study makes a significant contribution to research on endocrine disruptors’ impact on children health because the relationship between BPA exposure and neurodevelopmental effects has not been fully elucidated in humans, and our results elucidate BPA exposure effects related to social impairments. Specifically, prenatal BPA exposure was significantly associated with impairments at or above the flexion point of 3.0 μg/g creatinine, whereas there was a linear association for postnatal BPA exposure. Further studies to evaluate the health implications and underlying mechanisms of these findings are warranted.

4 years old girl featured image credit kiwi huang.

Perturbateurs endocriniens, liste des substances anthropiques

Office parlementaire d’évaluation des choix scientifiques et technologiques, Rapport 2011

En 2011, à l’occasion d’une proposition de loi visant à interdire le Bisphénol A dans les plastiques alimentaires, l’Office parlementaire d’évaluation des choix scientifiques et technologiques a été saisi pour réaliser une étude portant sur la question des perturbateurs endocriniens et l’état des recherches.

Les substances anthropiques représentent des milliers de produits et comprennent des produits de l’industrie chimique (phtalates, bisphénol A, métaux lourds, etc.) et les produits phytosanitaires utilisés en agriculture (herbicides, fongicides, insecticides, etc.).

PRINCIPALES SOURCES DES PERTURBATEURS ENDOCRINIENS CONFIRMÉS OU POTENTIELS

Produits pharmaceutiques

  • DES (Distilbène), éthynil-oestradiol (contraceptif), kétokonazole (traitement du pityriasis, pommade)…

Produits dentaires

  • Bisphénol A

Produits vétérinaires

  • DES, trenbolones (augmentent la masse musculaire)…

Produits de combustion

  • Dioxines, furanes, HAP (hydrocarbure aromatique polycyclique)…
  • Produits à usage industriel ou domestique
  • Phtalates, bisphénol A, styrène (polystyrène)…
  • Polybromodiphényl éthers (PBDE), polychlorobiphényls, organoétains…
  • Alkylphénols, parabens (conservateurs dans les produits de beauté)…
  • Arsenic, cadmium…

Produits phytosanitaires

  • Organochlorés (DDT, chlordécone…)
  • Vinchlozoline (retirée en avril 2007), linuron (herbicide)…

Phytooestrogènes

  • Isoflavones (soja, trèfle)…

Mycotoxines

  • Zéaralénone…

Perturbateurs endocriniens, le temps de la précaution

Le Distilbène DES, en savoir plus

Toxic Time Bombs

Decades of evidence point to the untoward health effects of endocrine disruptor exposures, yet little is being done to regulate the chemicals

Abstract

… “Although the U.S. has been slow to control endocrine disruptors, pressure is mounting for legislators to make significant regulatory changes in Europe, although the European Commission has also dragged its feet. In December 2015, the European Union’s Court of Justice decreed that the Commission had breached EU law by failing to adopt scientific criteria for identifying and regulating endocrine disruptors. The European Parliament met in February 2017 to consider a proposal defining those criteria, but member states decided to postpone a decision. France did not wait for the E.U. to take effective action. As of January 2015, new French legislation outlawed any contact between the known endocrine disruptor bisphenol A (BPA) and beverages or food.

The challenge to developing appropriate regulations for endocrine disruptors is that evidence from epidemiology for health effects is indirect and difficult to collect. Cancers abound in modern industrialized societies. Environmental factors are surely involved, yet hard to pinpoint. It took three decades to establish that DDT (dichloro-diphenyl-trichloroethane) and DES (diethylstilbestrol) impair health. Both are now strictly controlled, but their effects persist across generations.” …

  • Read Opinion: Toxic Time Bombs, by Robert Martin for The Scientist, September 25, 2017.
  • Featured image Portrait of Sir Edward Charles Dodds credit wikimedia.
More DES DiEthylStilbestrol Resources

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.