Increasing impact of estrogen pollution in waters and endocrine disruption in fish

The presence of both male and female characteristics within the same fish (intersex) is increasingly being observed

Endocrine-disrupting compounds can enter the aquatic environment via a number of different pathways and in particular via certain urban wastewater discharges, atmospheric deposition, etc. There, they can persist for years and bioaccumulate up the food chain. Exposure to these chemicals can disrupt several bodily systems, leading to changes in a number of wildlife species.

For example, the presence of both male and female characteristics within the same fish (intersex) is increasingly being observed, causing serious reproductive dysfunction. In humans, too, there is evidence that endocrine disruptors can have adverse effects on health. A number of concerning links have been made between endocrine-disrupting compounds and human health, including declining sperm counts, increased incidences of certain cancers and congenital malformations in children.

Increasing impact of oestrogen pollution through climate change and population growth, Science for Environment Policy News Alert, 27 May 2016.

This study focused on their effects on fish in rivers in England and Wales, where the main chemicals responsible for intersex in male fish are three steroid oestrogens: oestrone, oestradiol (natural hormones) and ethinyl oestradiol (a synthetic hormone used in oral contraceptive pills). The European Commission proposed annual average environmental quality standards for the latter two in 20121 , but instead they were placed on a watch list of substances to gather monitoring data to facilitate the determination of appropriate measures to address the risk posed by them.

Impact of climate change and population growth on a risk assessment for endocrine disruption in fish due to steroid estrogens in England and Wales, ScienceDirect, doi:10.1016/j.envpol.2014.11.017, February 2015.

In order to accurately regulate these substances, it is important to identify where and to what extent they pose risks, both under current and future circumstances. In the coming years, climate change will alter river flows and temperature, and is likely to affect the risk posed by steroid oestrogens by affecting their dilution and degradation in the aquatic environment. Increases in human populations will also increase the emission of steroid oestrogens.

This study tested the hypothesis that climate change and population changes will increase the risk of endocrine disruption in fish due to steroid oestrogens in England and Wales by 2050.

The researchers reproduced a risk assessment made in their previous study, in which risk was determined by comparing predicted environmental concentrations with threshold levels based on endpoints likely to cause a population response in fish (e.g 100% feminisation for oestradiol and reduced fertilisation effects for ethinyl oestradiol). The researchers incorporated changes in river flows, water temperatures and populations in order to assess future risk.

A model was used to predict the environmental concentrations of oestrogens in each river in England and Wales, and a combined toxic equivalent concentration was used to assess their collective biological effects. The risk of fish endocrine disruption in each river was classified as ‘no risk’, ‘at risk’ or ‘at high risk’.

To determine the potential impact of climate change, the researchers used three different scenarios based on the UK Met Office’s 2009 UK Climate Projections: average, wet and dry. These scenarios differ in average annual rainfall and river flows. The authors also accounted for differences in river temperature, which affects the rate of decay of chemical substances.

The researchers analysed the effects of human population increases using figures based on population projections for England and Wales in 2050 generated by the UK Office for National Statistics. They also accounted for ageing of the population, which for a given number of inhabitants will reduce excretion of ethinyl oestradiol due to the increase in menopausal women, and, therefore, fewer women taking the contraceptive pill.

The results suggest that risk will increase in the future, because the percentage of high risk sites increased across all three climate change scenarios. The combined percentage of river reaches at risk or at high risk was predicted to increase from 39% under the current conditions to 48%, 50% and 50%, for the wet, average and dry future scenarios, respectively.

However, climate change was not the primary driver of increased risk. The findings suggest that an increase in temperature would increase biodegradation within streams, and thus reduce concentrations of harmful compounds, and only a small fraction of the changes could be attributed to changes in river flow. By far the main driver of the increased risk was population growth.

These findings represent a warning to policymakers that current risk assessments may look much different in the future, largely driven by the increasing — and ageing — population. The pollution of the aquatic environment by oestrogens is not specifically regulated at the level of the Urban Waste Water Treatment Directive (91/271/EEC), which is essentially targeted at the removal of organic pollution in general from wastewater. However, additional treatment may be necessary to remove specific substances that could impact upon aquatic flora or fauna. This need for treatment should be determined in each Member State on a case-by-case basis in order to fulfil the requirements of other Directives such as the Water Framework Directive.

In utero exposure to phthalates and epigenetic regulation of neurodevelopmental genes response

Higher prenatal phthalate levels have been associated with offspring adverse neurodevelopment

Abstract

Epigenetic regulation of neurodevelopmental genes in response to in utero exposure to phthalate plastic chemicals: how can we delineate causal effects?, ScienceDirect, doi:10.1016/j.neuro.2016.05.011, 18 May 2016.

Accumulating evidence, from animal models and human observational studies, implicates the in utero (and early postnatal) environment in the ‘programming’ of risk for a variety of adverse outcomes and health trajectories.

The modern environment is replete with man-made compounds such as plastic product chemicals (PPC), including phenols and phthalates. Evidence from several human cohorts implicates exposure to these chemicals in adverse offspring neurodevelopment, though a direct causal relationship has not been firmly established.

In this review we consider a potential causal pathway that encompasses epigenetic human variation, and how we might test this mechanistic hypothesis in human studies. In the first part of this report we outline how PPCs induce epigenetic change, focusing on the brain derived neurotrophic factor (BDNF) gene, a key regulator of neurodevelopment. Further, we discuss the role of the epigenetics of BDNF and other genes in neurodevelopment and the emerging human evidence of an association between phthalate exposure and adverse offspring neurodevelopment. We discuss aspects of epidemiological and molecular study design and analysis that could be employed to strengthen the level of human evidence to infer causality. We undertake this using an exemplar recent research example: maternal prenatal smoking, linked to methylation change at the aryl hydrocarbon receptor repressor (AHRR) gene at birth, now shown to mediate some of the effects of maternal smoking on birth weight.

Characterizing the relationship between the modern environment and the human molecular pathways underpinning its impact on early development is paramount to understanding the public health significance of modern day chemical exposures.

Help us Fund Research to Treat and Cure TPP1 Deficiency

Atypical TPP1 Deficiency, CLN2, and Maya : Three Years later

Maya is very much a typical pre-teen who loves Meghan Trainor and Taylor Swift. However, in May of 2014, Maya was diagnosed with a rare disease called Atypical TPP1 Deficiency (aka SCAR7).  Atypical TPP1 Deficiency is a subset of Late Infantile Neuronal Ceroid Lipofuscinosis 2 (CLN2), a form of Batten Disease.  At the time of her diagnosis, Maya was one of eight reported cases in the world. Since her diagnosis, we have learned of ten other people with this disorder.

Atypical TPP1 Deficiency and CLN2 are caused by mutations in the TPP1/CLN2 gene resulting in deficient activity of the enzyme tripeptidyl peptidase 1 (TPP1). In the absence of TPP1, lysosomal storage materials, normally metabolized by this enzyme, accumulate in many organs, particularly in the brain. Buildup of these storage materials in the cells of the nervous system contribute to progressive and relentless neurodegeneration which manifests as loss of cognitive, motor, and other functions.  Patients typically present initially with language delay followed by movement disorders, motor deterioration, dementia, and early death. During the later stages of the diseases, feeding and tending to everyday needs become very difficult.  Currently, there is no cure for TPP1 Deficiency or CLN2.

In May of 2016, the Jan and Dan Duncan Neurological Research Institute (NRI) at Texas Children’s Hospital in Houston, Texas announced the commencement of a new research project to explore treatments for Atypical TPP1 Deficiency.  This project is dependent upon Maya’s friends and family for funding.

Get Involved

  • To help fund the research project and to raise awareness about Atypical TPP1 Deficiency we ask that you make a donation directly to Texas Children’s Hospital.  You can do so by giving directly to Texas Children’s. If you donate from this page, funds go directly to the research project for Atypical TPP1 Deficiency/SCAR7.
  • We also ask that you order a #FightingForMaya T-Shirt.  You can do so by going to Booster.com. Once you receive your shirt, we ask that every Friday you show that you are #fightingformaya, by:
    • Wearing your shirt
    • Taking a Selfie
    • Adding the hashtag #fightingformaya
    • and sharing your pic with the world.

    Go crazy, be creative and have fun!!!

“The most beautiful thing about her is her smile. It’s infectious…”

Image via RareDaily.

Thank you for helping to show Maya and others that you stand with them in the fight to find a treatment and cure for Atypical TPP1 Deficiency.

Beau James
bjames358.blogspot.co.uk

Can a Drug manipulate Gender Identity?

Certain doctors and researchers and those in the community believe the DES drug can make a person transgender

Video published on 24 May 2016 by DES Daugther Network channel via Dion Lim 5/6/11pm weeknight anchor/reporter at WTSP/CBS .

It was a pill meant to prevent miscarriages…

Can a drug manipulate gender identity asks Dion Lim?
Well, I know many DES sons who can confirm that yes, it did happen.

More DES DiEthylStilbestrol Resources

Will 2016 bring full transparency for drug company payments to doctors in the UK?

Will the ABPI central database go far enough?

Pharmaceutical firms currently pay about £40m every year to healthcare professionals, including doctors and pharmacists. These payments could be for anything from expert advice to sponsoring a healthcare professional’s medical education. Now, the Association of the British Pharmaceutical Industry (ABPI) has created a central database, going live in June, on which its member companies, and others that have signed up to comply with the ABPI code of practice, will disclose who these payments are made to, and for what. At the same time, Jeremy Hunt’s “sunshine rule” will make it mandatory for NHS staff to declare gifts received from drug companies.

Read: How much should patients know about pharma payments to doctors?, the guardian, 18 May 2016.

How will this new transparency affect the complex matrix of relationships between health professionals, pharmaceutical firms, the NHS and, most importantly, patients?

Put Down that Chicken Sandwich!

Animal Cruelty or the Price of Dinner?

If you’re reading this post while munching on a chicken strip or chicken sandwich, a word of advice: put the chicken down. Now.
Nicholas D. Kristof‘s column is about what actually goes on in the chicken barns and the way the industry is bad for chickens, for the farmers and for consumers.

When even chicken farmers say that the system has failed, it’s time for consumers to use their buying power to push for food that causes less harm to everyone.

Read Animal Cruelty or the Price of Dinner?, nytimes, APRIL 16, 2016!

Related posts

Ovarian failure caused by Gardasil HPV vaccine ?

2012-2014 studies on the association between human papillomavirus vaccine and adolescent primary ovarian failure

Adolescent Premature Ovarian Insufficiency Following Human Papillomavirus Vaccination

2014 Study Abstract

Adolescent Premature Ovarian Insufficiency Following Human Papillomavirus Vaccination, National Institutes of Health, NCBI pmc/articles/PMC4528880/, 2014 Oct-Dec.

Three young women who developed premature ovarian insufficiency following quadrivalent human papillomavirus (HPV) vaccination presented to a general practitioner in rural New South Wales, Australia. The unrelated girls were aged 16, 16, and 18 years at diagnosis. Each had received HPV vaccinations prior to the onset of ovarian decline. Vaccinations had been administered in different regions of the state of New South Wales and the 3 girls lived in different towns in that state. Each had been prescribed the oral contraceptive pill to treat menstrual cycle abnormalities prior to investigation and diagnosis. Vaccine research does not present an ovary histology report of tested rats but does present a testicular histology report. Enduring ovarian capacity and duration of function following vaccination is unresearched in preclinical studies, clinical and postlicensure studies. Postmarketing surveillance does not accurately represent diagnoses in adverse event notifications and can neither represent unnotified cases nor compare incident statistics with vaccine course administration rates. The potential significance of a case series of adolescents with idiopathic premature ovarian insufficiency following HPV vaccination presenting to a general practice warrants further research. Preservation of reproductive health is a primary concern in the recipient target group. Since this group includes all prepubertal and pubertal young women, demonstration of ongoing, uncompromised safety for the ovary is urgently required. This matter needs to be resolved for the purposes of population health and public vaccine confidence.

Human papilloma virus vaccine and primary ovarian failure: another facet of the autoimmune/inflammatory syndrome induced by adjuvants

2013 Study Abstract

Human papilloma virus vaccine and primary ovarian failure: another facet of the autoimmune/inflammatory syndrome induced by adjuvants, American journal of reproductive immunology New York, NCBI pubmed/23902317, 2013 Jul 31.

PROBLEM:
Post-vaccination autoimmune phenomena are a major facet of the autoimmune/inflammatory syndrome induced by adjuvants (ASIA) and different vaccines, including HPV, have been identified as possible causes.

METHOD OF STUDY:
The medical history of three young women who presented with secondary amenorrhea following HPV vaccination was collected. Data regarding type of vaccine, number of vaccination, personal, clinical and serological features, as well as response to treatments were analyzed.

RESULTS:
All three patients developed secondary amenorrhea following HPV vaccinations, which did not resolve upon treatment with hormone replacement therapies. In all three cases sexual development was normal and genetic screen revealed no pertinent abnormalities (i.e., Turner’s syndrome, Fragile X test were all negative). Serological evaluations showed low levels of estradiol and increased FSH and LH and in two cases, specific auto-antibodies were detected (antiovarian and anti thyroid), suggesting that the HPV vaccine triggered an autoimmune response. Pelvic ultrasound did not reveal any abnormalities in any of the three cases. All three patients experienced a range of common non-specific post-vaccine symptoms including nausea, headache, sleep disturbances, arthralgia and a range of cognitive and psychiatric disturbances. According to these clinical features, a diagnosis of primary ovarian failure (POF) was determined which also fulfilled the required criteria for the ASIA syndrome.

CONCLUSION:
We documented here the evidence of the potential of the HPV vaccine to trigger a life-disabling autoimmune condition. The increasing number of similar reports of post HPV vaccine-linked autoimmunity and the uncertainty of long-term clinical benefits of HPV vaccination are a matter of public health that warrants further rigorous inquiry.

Premature ovarian failure 3 years after menarche in a 16-year-old girl following human papillomavirus vaccination

2012 Study Abstract

Premature ovarian failure 3 years after menarche in a 16-year-old girl following human papillomavirus vaccination, BMJ Case Report, NCBI pmc/articles/PMC4543769, 2012 Sep 30.

Premature ovarian failure in a well adolescent is a rare event. Its occurrence raises important questions about causation, which may signal other systemic concerns. This patient presented with amenorrhoea after identifying a change from her regular cycle to irregular and scant periods following vaccinations against human papillomavirus. She declined the oral contraceptives initially prescribed for amenorrhoea. The diagnostic tasks were to determine the reason for her secondary amenorrhoea and then to investigate for possible causes of the premature ovarian failure identified. Although the cause is unknown in 90% of cases, the remaining chief identifiable causes of this condition were excluded. Premature ovarian failure was then notified as a possible adverse event following this vaccination. The young woman was counselled regarding preservation of bone density, reproductive implications and relevant follow-up. This event could hold potential implications for population health and prompts further inquiry.

2017 Update

Premature Ovarian Insufficiency – an update on recent advances in understanding and management

2017 Study Abstract

Premature ovarian insufficiency is a complex and relatively poorly understood entity with a myriad of etiologies and multisystem sequelae that stem from premature deprivation of ovarian sex hormones. Timely diagnosis with a clear understanding of the various comorbidities that can arise from estrogen deficiency is vital to appropriately counsel and treat these patients. Prompt initiation of hormone therapy is critical to control the unsolicited menopausal symptoms that many women experience and to prevent long-term health complications. Despite ongoing efforts at improving our understanding of the mechanisms involved, any advancement in the field in recent decades has been modest at best and researchers remain thwarted by the complexity and heterogeneity of the underpinnings of this entity. In contrast, the practice of clinical medicine has made meaningful strides in providing assurance to the women with premature ovarian insufficiency that their quality of life as well as long-term health can be optimized through timely intervention. Ongoing research is clearly needed to allow pre-emptive identification of the at-risk population and to identify mechanisms that if addressed in a timely manner, can prolong ovarian function and physiology.

Read the full study (free access) on the NCI PubMed, PMCID: PMC5710309.

Endocrine disruptors: the secret history of a scandal

What’s more secret than the TTIP text in the EU? It’s EDCs!

This is one of the best kept secrets in Europe. It is locked up somewhere in the maze of corridors in the European Commission, in a guarded room that only about 40 accredited officials have the right to enter. And then only with paper and pen. Smartphones are not allowed. This is a stricter safety protocol than even for transatlantic free trade agreement (or TTIP) between the European Union and the United States: If Members of the European Parliament want to access TTIP documents they can enter the reading room without anyone checking the contents of their pockets.

This is a translation of an article in Le Monde by Stéphane Horel entitled ’Perturbateurs endocriniens : l’histoire secrète d’un scandale’,
translated by the Health and Environment Alliance on May 20 2016.

The secret is a report of about 250 pages. Its title, in the jargon of the Commission, is “Impact Assessment“. It assesses the “socio-economic” impact of regulations related to a group of chemical pollutants. Known as endocrine disruptors, these chemicals are capable of interfering with the hormones of animal species, including humans, and are believed to be the cause of many serious diseases (hormone-dependent cancers, infertility, obesity, diabetes, neuro-behavioral disorders …). They are found in a multitude of consumer items, cosmetics, pesticides and plastics (such as Bisphenol-A – BPA). Whole sectors of industry will be affected by regulation of these chemicals in the medium term. Billions of Euros are at stake.

Defining criteria

The prospect of restrictions, perhaps even bans, raises serious worries among manufacturers. The pesticide industry has never hidden its hostility to the European Regulation on “plant protection products“, from which originates a decision-making process with twists and turns worthy of a TV series. Adopted by the European Parliament in 2009, the text provided for special treatment of pesticides: those recognised as endocrine disruptors would not be allowed on the market. But they must be able to be recognised.

The Commission was therefore obliged to find a way to distinguish endocrine disrupters from other chemicals. In concrete terms, its job was to lay down criteria to identify these substances. Without the criteria, the law cannot be implemented. National health authorities, industry and NGOs are thus in suspended animation awaiting a decision on these criteria for identification – a regulatory tool which will then enable restricting or, more radically, prohibiting the use of certain endocrine disrupters. Today, seven years later, these criteria still do not exist.

It is this impact assessment, with its highly confidential conclusions (as secret as the location of the fountain of youth), which is largely responsible for this delay. It was not originally part of the plan but industry called for it as a way to weaken the Regulation and then achieved its desire in early summer of 2013 after a lobbying blitzkrieg by pesticide and chemical industries working in tandem. Activities were coordinated mainly through their Brussels lobbying organizations: European Crop Protection Association (ECPA) and European Chemical Industry Council (CEFIC).

A hypersensitive file

The giants of agrochemicals were also on the battlefield: both the two German heavyweights, BASF and Bayer and the Swiss multinational, Syngenta. The Commission’s Secretary General Catherine Day finally yielded to their request for an impact assessment on the basis of “divergent opinions” in the scientific community and the “potential impacts on sectors of the chemical industry and international trade” – a direct reference to TTIP, on which negotiations were then just beginning. In an internal memo dated 2 July 2013, Ms Day, the then highest European Union official, described the criteria for endocrine disruptors as a “sensitive subject“. Sensitive, it stayed. And hypersensitive, it became.

The European Parliament had given a deadline for the Commission to write these infamous criteria: December 2013. Not seeing anything coming, Sweden had decided to take the Commission to court. This move was supported by France, Denmark, Finland and the Netherlands and also by the Parliament and the Council – a rare configuration.

The Court of Justice of the European Union did not delay in its response. Just before Christmas 2015, it found that the Commission, which is after all the guardian of the treaties, had “violated the law of the Union“. The judgement swept away the “alleged need for an impact assessment of the scientific criteria” that the Commission had placed at the heart of its defence. But the same day, the spokesperson of the European Commissioner for Health, the Lithuanian Vytenis Andriukaitis announced bluntly that the impact study would still be carried through. Already hypersensitive, the file became inflammable.

What cost of illness?

The European parliamentarians are furious. Some of them have already sent several letters to the President of the Commission. These had no effect. On 13 January, the President of the Parliament wrote to Jean-Claude Juncker. The Commission’s delay was “unacceptable“, underlined Martin Schulz. Equally, continuing the impact assessment was “in defiance of the judgment” of the highest court of the EU, to which he asked the Commission to “comply without delay“. The message was repeated in a second letter on 10 March. Sweden, for its part, continues to keep up the pressure. In a document dated 13 May that Le Monde has obtained, Sweden curtly reminds the Commission services that the Court “prohibits the use of economic considerations to define criteria”.

So what is the nature of the “economic considerations” contained in the pages of the impact study under lock and key? In addition to the impact on the industry, will they take into account the cost of diseases related to exposure to endocrine disruptors in Europe, which was estimated by independent studies to be at between 157 billion and 288 billion euros per year (University of Utrecht, 2016)? The suspense will end on 15 June. According to our sources, the final proposal on the criteria for the identification of endocrine disrupters will be presented in a meeting of the college of European Commissioners that day.

Stéphane Horel
Journalist for Le Monde, originally posted on 20 May 2016.

MORE INFORMATION

An Investigation
  1. The Manufacture of a Lie.
  2. A Denial of the State of the Science.
  3. The Interference of the United States.
Endocrine Disruptors

Adverse health effects in children of women exposed in utero to diethylstilbestrol

2016 study results confirmed a transgenerational transmission of defects in male genital tract

Abstract

OBJECTIVE
Exposure to diethylstilbestrol (DES) in utero is associated with adverse health effects, including genital anomalies in women and men, and cancers in women. Animal studies showed birth defects and tumors in the offspring of DES exposed mice, revealing transgenerational transmission of DES effects. In humans, birth defects, such as hypospadias were observed in children of prenatally exposed women. The aim of this research was to further assess the health effects in children of prenatally exposed women.

Adverse health effects in children of women exposed in utero to diethylstilbestrol (DES), US National Library of Medicine, NCBI pubmed/27203157, 2016 Feb 5.

Russian doll beauty and the beast, rawdonfox.

METHODS
In a retrospective cohort study, the reports of women exposed to DES in utero on their 4409 children were compared with those of unexposed women on their 6203 children. Comparisons used odd ratios (OR) between children of exposed and unexposed women and standardized incidence rate (SIR) with the general population. These cohorts were recruited on a voluntary basis to answer questionnaires.

RESULTS
There was a global increase of defects in children born to exposed women when compared with those born to unexposed (OR 2.29, 95% CI: 1.80-2.79, P<0.001) and with the general population (SIR 2.39, 95% CI: 2.11-2.68). Increased defects were observed in male genital tract, esophagus, lip or palate, musculoskeletal and circulatory systems. For female genital tract anomalies, there was no significant increase. However, this cohort being relatively young, further follow-up is needed. An increase of cerebral palsy was revealed. The incidence of cancers was not increased, in particular for breast, uterus and ovary.

CONCLUSION
Our results confirmed a transgenerational transmission of defects in male genital tract. With caution due to possible bias associated with this method, our data suggest an increase of defects for esophagus, lip or palate, musculoskeletal and circulatory system in children of exposed women.

More DES DiEthylStilbestrol Resources

DiEthylStilbestrol for veterinary use

DES Injection manufactured by RIDLEY LIFE SCIENCE PVT. LTD, Delhi, India

Diethylstilbestrol Injection box image
Diethylstilbestrol Injection manufactured by RIDLEY LIFE SCIENCE PVT. LTD, Delhi, India.

DES was sold under many names including Distilbène®, Stilbetin®, Stilboestrol-Borne®, Benzestrol®, Chlorotrianisene®, Estrobene® and Estrosyn® to name just a few.

Many different companies manufactured and marketed this drug under more than 200 different brand names.

This Diethylstilbestrol Injection is sold online via an Indian website.

DES Drugs Pictures
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