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Transcription, translation and subsequent protein modification represent the transfer of genetic information from the archival copy of DNA to the short-lived messenger RNA, usually with subsequent production of protein. Although all cells in an organism contain essentially the same DNA, cell types and functions differ because of qualitative and quantitative differences in their gene expression. Thus, control of gene expression is at the heart of differentiation and development. Epigenetic processes, including DNA methylation, histone modification and various RNA-mediated processes, are thought to influence gene expression chiefly at the level of transcription; however, other steps in the process (for example, translation) may also be regulated epigenetically. (Gibney ER and Nolan CM Epigenetics and gene expression, Heredity, 2010).

PSGR was established at around the same time the Human Genome Project (HGP) mapped the human genome. HGP data showed us that genetic heredity played a much smaller role in driving health and disease than previously presumed and that often dozens if not hundreds of genes might play a role in disease aetiology.

Genes are driven by a vast array of physiological drivers – epigenetic processes, which act to modify gene expression and phenotype (physiological characteristics), turning genes on and off - and influencing how they work. The DNA or gene sequence remains unchanged. Epigenetics loosely translated, means ‘above the gene.’

Humans have one genome, and hundreds of epigenomes (Ficz 2015). Epigenetics was first described by embryologist Conrad Waddington in 1942, Conrad Waddington as ‘the complex of developmental processes between the genotype and phenotype’ (Deichmann 2016).

‘epigenetics refers to both heritable changes in gene activity and expression (in the progeny of cells or of individuals) and also stable, long-term, alterations in the transcriptional potential of a cell that are not necessarily heritable’

While the genome is identical and stable in vertebrates, the epigenome differs from cell to cell and is plastic, changing with time and with exposure to the environment (Gibney & Nolan 2010). Epigenetics challenges us because epigenetic marks are not transmitted through cell division or the germ line, and the precise definition of epigenetics and gene expression remains contested (Deichmann 2016).

Almost daily, scientists are demonstrating that DNA as genetic instructions of cellular biology, are only the tip of the iceberg when discussing human (and environmental) biology, from evolution to disease development. It is now understood that a liver cell is initially the same as a fingernail cell. The development and function of all living things are not solely dependent on our genetic instructions, but on epigenetic influences that arise from environmental exposures.

(Paper 'When is a gene not DNA?' by Professor Jack Heineman)

Epigenetics has been referred to as the ‘missing link between genetics, the environment, and endocrine functions’ (Zhang 2011). When a tadpole changes into a frog, the tadpole produces a surge of thyroid hormone which, as Dr Barbara Demeneix explains, turns into a series of epigenetic switches.

‘The epigenetic changes do not alter any DNA sequence, but they turn off certain genes and turn on others’ (Demeneix 2017, p.120).

In the long debate of nature versus nurture, scientists considered that our phenotype – who we are as a result of our genes and environment, was predominantly due to the influence of genes - genetic inheritance (recognised as Darwinian natural selection or Mendelian inheritance). Yet the relatively new field of epigenetics is clearly challenging this, and evidence that epigenetic traits can be inherited (without changing the gene) further muddies the (gene) pool. It is complicated, for example genetic sequences can influence subsequent developmental epigenetic events (Ficz 2015).

With this relatively new field of science, humanity doesn’t just need to know what is happening within the cell, we also need to understand what is going on in and between cells – rather than cellular biology – it’s molecular biology. Instead of acting as a closed loop within a neat biological system, our bodies constantly respond and interact to both our internal biological environment and the external environment.

The vast majority of environmental factors and toxicants do not have the ability to alter DNA sequence or promote genetic mutations. In contrast, the environment can dramatically influence epigenetic processes to alter gene expression and development. Therefore, epigenetics provides a molecular mechanism for the environment to directly alter the biology of an organism (Skinner 2014).

Gene expression is at the heart of differentiation and development. Gibney and Nolan's Review, Epigenetics and Gene Expression (2010), succinctly lays out the core mechanisms: DNA methylation, histone modifications, and RNA‑mediated regulation.

DNA methylation: Leads to transcriptional upregulation, silencing via multiple mechanisms.

DNA methylation is an epigenetic mechanism where methyl groups are added to cytosine bases, usually at CpG sites. When this occurs in promoter regions, it typically represses transcription by blocking transcription factor binding or attracting silencing proteins. Methylation doesn't always block or silence. In gene bodies, it can correlate with active transcription, possibly by maintaining gene stability. At enhancers, methylation usually reduces activity, while demethylation can lead to upregulation of distant genes. Methylation patterns are essential for development, X-chromosome inactivation, and silencing repetitive elements. They are heritable through cell division but responsive to environment, ageing, and disease. DNA methylation helps fine-tune gene expression—either silencing or supporting it—depending on genomic context.

Promoter methylation occurs just upstream of the gene (where transcription starts). Most frequently silencing the gene and switching it off. Gene body methylation occurs inside the gene (after the transcription commencement site). Often correlated with active transcription (can suppress spurious internal start sites and help with transcriptional efficiency), and the gene is typically on and stable. Regulatory DNA is any segment of DNA that helps control when, where, and how much a gene is expressed. It doesn’t code for proteins itself, but it controls the genes that do. Regulatory DNA is a category, encompassing nearby promoters, (and potentially far away) enhancers, silencers, insulators and operators (in bacteria), while for example, enhancers are the most well-known regulatory DNA. However, silencers, insulators, and locus control regions can also regulate transcription at a distance by shaping the 3D structure of the genome. Enhancer methylation occurs at regulatory DNA far from the gene it controls - upstream, downstream including within unrelated genes using chromatin looping to contact promoters. Silencers which repress gene expression, can also act over long distances and use chromatin looping which inhibits promoter activity. Insulators define boundaries between regulatory domains and can potentially block enhancer-promoter interactions, and can help mediate chromatin architecture through the binding of certain proteins. Finally, locus control regions act as complex regulatory hubs that can coordinate multiple genes, also using looping to bring distant elements into the shared transcriptional environment. (Vermunt et al 2019, Splinter et al 2006, Kadauke and Blobel 2010).

Histone modifications: post-translational modification of histone proteins and remodelling of chromatin.

Histones are structural proteins, their job is to package (organise and compact) DNA into a structure, chromatin. DNA wraps around histones and this packaging impacts whether genes are accessible to the cellular machinery, that then makes proteins (RNA polymerase, which transcribes DNA into RNA). Therefore, histones indirectly control which proteins are made as they control access to the genes that encode them.

Histone modification is an epigenetic mechanism that alters how tightly DNA is packaged in the nucleus, influencing gene expression. These are known as post-translational modifications because they occur after the protein is built. DNA wraps around proteins called histones, forming a structure known as chromatin. The ends of these histones—called tails—stick out and can receive chemical tags after the protein is made. Histones themselves are produced when histone genes are transcribed into messenger RNA (mRNA), which is then translated by ribosomes into protein. Once made, these histone proteins can be chemically modified—most commonly by the addition of acetyl, methyl, or phosphate groups. Such changes affect how the DNA–histone complex behaves: for example, acetylation generally loosens chromatin to allow gene activation, while methylation can either activate or silence genes, depending on the site. Histone modifications are reversible and dynamic, allowing cells to respond to signals and regulate genes without altering the DNA sequence itself. (Liu et al 2020, Bannister and Kouzarides 2011, Cavalieri 2021)

RNA‑mediated regulation: RNA molecules can influence gene expression without altering the DNA sequence.

RNA-mediated epigenetic regulation refers to how certain RNA molecules influence gene expression without altering the DNA sequence. The most well-known are non-coding RNAs—including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)—which don’t code for proteins but help control which genes are active or silent. miRNAs bind to messenger RNA (mRNA) to block translation or trigger degradation, reducing protein production. lncRNAs can recruit proteins that modify histones or DNA methylation patterns, guiding these changes to specific genes. Some RNAs also help form RNA–protein complexes that alter chromatin structure, switching genes on or off. These processes are vital in development, stem cell differentiation, and disease, especially cancer. Because RNA molecules can act precisely and reversibly, they offer powerful tools for fine-tuning gene expression through epigenetic pathways.(Holoch and Moazed 2015, Joh et al 2014, Bure et al 2022).

Allis and Jenuwein's paper The Molecular Hallmarks of Epigenetic Control (2016) substantially added to understanding of epigenetic regulation, detailing the enzymatic machinery, combinatorial code, 3D genome architecture, and disease relevance of epigenetic regulation, and effectively setting a framework for future research.

Outlined the role of enzymes as writers, erasers, and readers, of histone marks—enzymes that add (e.g. KMTs, HATs), remove (HDACs, demethylases), and recognize post‑translational histone modifications to regulate chromatin structure and transcriptional states.
Outline the histone code hypothesis, which articulates that specific combinations and spatial context of histone modifications (e.g. H3K4me3 vs H3K27me3) generate distinct functional outcomes, influencing both activation and repression of genes via multivalent reader complexes
Clarified thinking about chromatin architecture by integrating histone modification research with higher-order genome structures, (such as Topologically Associated Domains (TADs) and pioneer transcription factors), to demonstrate how epigenetic marks cooperate within three-dimensional chromatin frameworks to stabilise gene expression programs.
Emphasised the transgenerational and germline dimensions of epigenetic control, referencing cases where histone modifications survive epigenetic reprogramming and may carry signals to subsequent generation.

New mechanisms of epigenetic modifications are likely to emerge, however the:

‘key mechanisms underlying epigenetic modifications include: chromatin remodeling, methylation of cytosinein CpG dinucleotides (often referred to as DNA methylation), histone tail N-terminal modification, and post-translational modification of genes regulation by non-coding/small RNA (ncRNA/sRNA). Collectively, these processes and the components upon which they act constitute the epigenome. Individually or in concert, they play a key role in turning gene expression on or off, thus facilitating or inhibiting the production of specific proteins'. (Norouzitallab et al 2019).

Examples of the emerging literature on man-made technologies interfering/disrupting epigenetic processes:

Radiofrequency field radiation - Studies reveal low-level, non-ionizing EMF exposure can lead to rapid epigenetic modifications:

Cantu et al 2023: DNA methylation patterns examined in human keratinocytes exposed to 900 MHz RF-EMFs for 1 h at a low dose rate. The low-dose exposure caused genome-wide DNA methylation changes in human skin cells. Six genes were identified which showed both methylation and expression alterations shortly after exposure—suggesting swift epigenetic signalling via RF exposure.

Ravaioloi et al 2023: Cell lines exposed to 900 MHz influenced DNA methylation in repetitive elements (LINE-1 -long interspersed nuclear elements-1) and ribosomal repeats in terms of both average profiles and organisation of methylated and unmethylated CpG sites, in different ways in each of the three cell lines studied. The authors observed epigenetic instability via shifts in methylation diversity, theorising that this was possibly driven by RF-induced reactive oxygen species (ROS).

Pesticide exposures:

Rohr et al 2024: This review showed that pesticides—including herbicides, insecticides, endocrine disruptors, and persistent organic pollutants— can alter DNA methylation, histone modifications, and miRNA expression in cell and animal models. Review highlighted that these changes often persist after exposure and mirror patterns seen in disease states.

Nilsson and Skinner 2014: Environmental insults can lead to epigenetic changes (abnormalities, or epimutations) that are in turn increase susceptibility to disease. These changes (epimutations) can be heritable and transmitted across generations, increasing disease risk in adult offspring.

Thorson et al 2020: Demonstrated that epigenome-wide association studies (EWAS) can assist in finding biomarkers that are associated with transgenerational disease susceptibility. The study exposed rodents to a pesticide combination and looked at F3 generation differential DNA methylation regions (DMRs) in diseased and non-diseased rodents. The DMRs were disease specific. The pesticide combination promoted transgenerational testis disease, prostate disease, kidney disease, and the presence of multiple disease in the subsequent F3 generation great-grand offspring.

The developmental origins of health and disease (DOAD)

Humans are exposed to an unprecedented array of exposures from conception. We have a far greater body-burden than our ancestors (apart from those for example, that historically worked in or lived near toxic industrial sites). The blood brain barrier often does not protect the brain from exposures, and the developing foetus often shares many of the same exposures as the mother. Pre-conception exposures can damage subsequent generations.

Specific periods (or windows) of vulnerability in developmental life stages where the foetus, and the developing child, but also teenagers, are more susceptible to toxic environmental exposures. (WHO 2008) In the first trimester of pregnancy, the foetus is most vulnerable (Demeneix 2017). The impact of environmental chemicals on fertility is also recognised (Trasande 2019).

The chemical body-burden of the mother is absorbed by the foetus. Infants and young children will frequently consume more than adults relative to their body-weight. As a result, they are exposed to higher doses (Grandjean et al 2007). Chemicals can also persist and bioaccumulate in the body (WHO UNEP 2013).

Poor nutrition or environmental stressors increase risk for disease or syndrome states via toxic exposures.

Despite the insight that was gained from the HGP - genetic and molecular research for medicine or for industrial or agricultural applications trumps research exploring the complex drivers of disease - in humans or in agriculture. Research exploring the environmental drivers of health and disease remains low priority, even as technologies that could shed light on environmental and genetic drivers of disease have advanced.

Risk from electromagnetic field (EMF) may more adversely harm the developing foetus, babies and children than adults, adversely altering growth and development. Increased brain risk may arise from babies and children having smaller skulls, thinner bone density in the skull and more embryonic stem cells. EMF exposure can decrease DNA repair, while increasing DNA damage and EMF exposure. The relationship between these effects and increased cell division in young children, suggest exposed children may be at heightened risk for cancer (Environmental Health Trust, European Parliamentary Research Service (2021)).

Prenatal and postnatal chemical exposures can alter the way genes are expressed and predispose the individual to disease in later life. The 2007 Faroes Statement stated:

‘These epigenetic changes can cause lasting functional changes in specific organs and tissues and increased susceptibility to disease that may even affect successive generations'.

One of the earliest demonstrations of epigenetic influence was where mice parents’ (dams) diets were supplemented with B12, folic acid, choline and betaine. The phenotype was altered as a result, and the obese, yellow parent gave birth to brown offspring (Waterland and Jirtle 2003).

Image: James, P; Silver, M; Prentice, A (2018) Epigenetics, Nutrition, and Infant Health. In: The Biology of the First 1,000 Days. CRC Press, Boca Raton, FL, USA, p.341. ISBN 9781498756792

Epigenetic processes impact all cellular functions; however many scientists are focussing on neurodevelopmental exposures which can result in neurological damage and IQ loss. Early life epigenetic changes can influence later gene expression in the brain (Roth 2012). Neurodevelopmental damage frequently arises via endocrinologic processes. Harm from endocrine disruption from environmental chemicals including delay and IQ loss, has been estimated at as much of 2% of global GDP. (Attina et al 2016)

The environmental aetiology of disease - how environmental stressors (see Figure 22.3) shape and contribute to disease is poorly understood, and research in this area, in contrast to studies funding for the genetic causes of disease, is poorly funded (Demeneix 2017).

‘The root causes of the present global pandemic of neurodevelopmental disorders are only partly understood. Although genetic factors have a role, they cannot explain recent increases in reported prevalence, and none of the genes discovered so far seem to be responsible for more than a small proportion of cases' (Grandjean and Landrigan 2014).

Intergenerational Effect

Science is very clear that a wide range of chemicals not only exert epigenetic influences on the generation exposed to the particular chemical, but that these epigenetic influences can be carried through, in a process described as transgenerational epigenetic inheritance, to subsequent generations. For example, exposing a parent rat to the endocrine disrupting fungicide vinclozolin resulted in higher disease incidence in the great and great-great grand offspring (F3 and F4 generation) who were never exposed to the chemical. The transgenerational inheritance was paternally transmitted via sperm, altering non-coding RNA (Schuster et al 2016) (Skinner 2014).

As such, with full awareness of the potential intergenerational consequences of harmful exposures, it is becoming rather critical to understand the ‘exposome’ - our cumulative environmental exposures over a lifetime. Epigenetic mechanisms don’t only push one way, many epigenetic modifications may be reversible.

Governments and regulators in the areas of toxicity and risk assessment are yet to address epigenetics and the potential for chemical mixtures in food and environment to adversely affect biological function.

Dedicated public funding is required to address the environmental drivers of disease, the toxic exposures and stressors (among other things) that directly influence not only the development of mutations to the DNA in our cells, but also the way chemical mixtures drive harm, damaging developmental and driving disease pathways.

This knowledge has the potential to change how civil society and governance approach non-communicable disease and how governments address health policy. It is already driving pharmaceutical enterprise, there is a burgeoning field of epigenetic medicine and therapy.

This new molecular spotlight naturally draws attention to the role nourishing food plays, complete with essential minerals and vitamins - which we can now observe acting epigenetically. However, this also explains the toll on bodies of a bad diet, stress, chemicals and toxins.

Complex chemical mixtures such as personal care products and pesticides consumed in daily lives undergo very little regulation. They are not assessed for potential to influence delicate molecular level epigenetic functioning, particularly in relation to the endocrine system (Kortencamp and Faust 2018).

Paper: When is the gene not DNA?
Professor Jack Heinemann
Lecturer in Genetics
University of Canterbury, New Zealand

When is the gene not DNA?

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References

Attina et al 2016. Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis. Lancet Diabetes Endocrinol 2016; 4: 996–1003

ERMA (2004) Transfer Notice. Hazardous Substances (pesticides) Transfer Notice 2004. Issue No. 72. P.1645-1718 https://www.epa.govt.nz/assets/Uploads/Documents/Hazardous-Substances/Policies/Hazardous-Substances-Pesticides-Transfer-Notice-2004.pdf

Ficz, G. (2015) New insights into mechanisms that regulate DNA methylation patterning. Journal of Experimental Biology 2015 218: 14-20; doi: 10.1242/jeb.107961

Grandjean et al 2008. The Faroes Statement: Human Health Effects of Developmental Exposure to Chemicals in Our Environment. Basic & Clinical Pharmacology & Toxicology. 102(2):73-5. doi: 10.1111/j.1742-7843.2007.00114.x.

Grandjean, P., Landrigan, P.J. (2014) Neurobehavioural effects of developmental toxicity. Lancet Neurol. 2014:13, 330–338.

Gross L, Birnbaum LS (2017) Regulating toxic chemicals for public and environmental health. PLoS Biol 15(12): e2004814. https://doi.org/10.1371/journal.pbio.2004814

Kortenkamp and Faust 2018 Regulate to reduce chemical mixture risk. Science. Vol 361 Issue 6399. p.224-226

Norouzitallab et al 2019. Can epigenetics translate environmental cues into phenotypes? Science of the Total Environment. 647:1281-1293

Roth TL. (2012) Epigenetics of neurobiology and behavior during development and adulthood. Dev Psychobiol 2012; 54: 590–97.

Schuster A., Skinner M., and Yan W. (2016) Ancestral vinclozolin exposure alters the epigenetic transgenerational inheritance of sperm small noncoding RNAs. Environmental Epigenetics. 2016; 2(1): dvw001.

Skinner. M. (2014) Endocrine Disruptor Induction of Epigenetic Transgenerational Inheritance of Disease. Mol Cell Endocrinol. 2014 Dec; 398(0): 4–12. 2014 Jul 31. doi: 10.1016/j.mce.2014.07.019 PMCID: PMC4262585

Trasande et al 2015. Estimating Burden and Disease Costs of Exposure to Endocrine-Disrupting Chemicals in the European Union. J Clin Endocrinol Metab, April 2015, 100(4):1245–1255doi: 10.1210/jc.2014-4324 http://press.endocrine.org/doi/pdf/10.1210/jc.2014-4324

Trasande et al 2016. Burden of disease and costs of exposure to endocrine disrupting chemicals in the European Union: an updated analysis. Andrology. 2016 Jul;4(4):565-72. doi: 10.1111/andr.12178. Epub 2016

Trasande L. 2019 Sicker, Fatter, Poorer: The Urgent Threat of Hormone-Disrupting Chemicals to Our Health and Future . . . and What We Can Do About It. Houghton Mifflin Harcourt.

Attina T, Hauser R., Sathyanarayana S., Hunt P., Bourguignon J.P., Myers J.P. , Digangi J., Zoeller R.T., Trasande L.. Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden and cost analysis. The Lancet Diabetes & Endocrinology, 2016 DOI: 10.1016/S2213-8587(16)30275-3

UN Human Rights Council. Report of the Special Rapporteur on the implications for human rights of the environmentally sound management and disposal of hazardous substances and wastes on his mission to Germany* 14 September 2016. A/HRC/33/41/Add.2

World Health Organization, United Nations Environment Programme, Inter-Organization Programme for the Sound Management of Chemicals, Bergman, Åke, Heindel, Jerrold J. et al. (‎2013)‎. State of the science of endocrine disrupting chemicals 2012. World Health Organization.

Waterland, R.A. and Jirtle R.L. (2003) Transposable Elements: Targets for Early Nutritional Effects on Epigenetic Gene Regulation. Molecular and Cellular Biology 2003; 23(15): 5293–5300.

WHO. Children are not little adults. Children's Health & the Environment, WHO Training Package for the Health Sector World Health Organization July 2008

Zhang, X., and Ho, S.M. (2011) Epigenetics meets endocrinology. Journal of Molecular Endocrinology. 46(1): R11–R32. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071959/pdf/nihms-601840.pdf

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PSGR (New Zealand) recognizes that all life support systems on our planet are interconnected and interdependent and that our actions today impact future generations. Human wellbeing is dependent on healthy ecosystems, and global responsibility requires that where there is uncertainty decision-makers proceed cautiously and transparently to protect the public interest and ensure ecological sustainability.

Global responsibility encompasses matters of lawful conduct of national and international (e.g. the United Nations) governments. Governments are required to give priority weight to the public interest and environment protection in the shaping of laws and in governance efforts to ensure compliance with those public law principles - particularly in matters of agriculture, trade, medicine, science and technology. Global responsibility is intricately connected to the creation of not just law, but also timely, effective and appropriate monitoring and regulation of modern technologies and polluting industries to protect human and ecosystem health to ensure obligations in law are fulfilled.

PSGR works to educate and inform so that decisions made today will protect and sustain the integrity of our original healthy genome; and protect and improve human and ecosystem health.
PSGR recognises that there is concrete evidence planetary boundaries are being exceeded, with multiple, complex, adverse anthropogenically created issues including climate change; bioaccumulating pollution; soil and water degradation; and increased chronic health conditions risking wellbeing and health.
PSGR acknowledges that there is a need for ‘Democratic Renewal’ - for an enhanced participatory process to ensure public information adequately represents risk to protect future generations.
PSGR recognises earth jurisprudence, which acknowledges and values interconnectedness of earth systems, considering humans part of the web of life, reflecting kaitiakitanga. The wellbeing of humans depends on how humans nurture, guard and protect the wellbeing of Earth.
PSGR recognises that scientists, academics and health professionals working in the public or private sector may have important information that will help inform New Zealand civil society.
PSGR has identified the need for a practical collaborative space to bring complex and challenging health and environmental concepts to the public arena.
Transparency is critical. PSGR recognises that many powerful non-government organisations (including charities) in the public arena do not declare funding (1) and that most funding to political parties in New Zealand is not declared. (2) PSGR declares all funding over $1000.
PSGR accepts that our economy is nested in our ecology. The market sits alongside the commons, the household and government. PSGR works to inform and educate so that the non-material (socio-cultural) value of environment and health is acknowledged in decision-making in order to best prevent unanticipated adverse events that may be extraordinarily difficult to amend.
Where there is uncertainty, and effects are potentially irreversible, PSGR advocates for a strong interpretation of the Precautionary Principle to protect future generations
PSGR seeks to support the statutory obligations of our government to protect the health of the New Zealand public; our environment and native ecosystems; and future generations
PSGR cautions that in the public interest, greater public knowledge regarding the significant risk to children, especially in the first trimester of pregnancy from bioaccumulating urban, agricultural and industrial chemicals. Effects can be severe and untreatable, and greater education is warranted in order to prevent harm, and instead protect biological, and especially neurological functioning and wellbeing.
PSGR takes particular effort to highlight evidence-based research produced by independent scientists and researchers in often controversial areas where a disproportionate amount of scientific evidence may be produced by companies and industry funded organisations which may skew the data in favour of the industry with the financial interest.

Notes:

(1) Public benefit not-for-profit entities report in accordance with Tier 2 Not for profit PBE Accounting Standards (with income of under $30 million) and take advantage of Reduced Disclosure Regime (RDR) disclosure concessions to not declare funding sources. (Ref: External Reporting Board)

(2) Flahive, B. Inside the secretive world of political donations. Oct 16 2018. Stuff. https://www.stuff.co.nz/national/politics/107885929/inside-the-secretive-world-of-political-donations

Public good research that might triangulate, affirm, or challenge industry claims regarding long- and short-term risks from chemicals, commercial products, and technologies is persistently underfunded at a global scale. Similarly, public good research focusing on nutrition, particularly nutrient mixtures for neurological health and disease prevention across the life course, remains seriously under-resourced.

A critical challenge affecting the public’s right to be independently informed arises from the growing difficulty of accessing and evaluating scientific information produced in the public interest. Research funded and produced by industry-related institutions now vastly exceeds public good research. A clear example is the recent declaration by the Stockholm Resilience Institute that the planetary boundary for novel entities, including man-made chemicals and biotechnologies, has been exceeded, largely because environmental releases now outpace monitoring and stewardship capacity.

This raises fundamental questions. How can scientific information be judged as credible and trustworthy when a substantial proportion of the peer-reviewed literature is funded by institutions with political or financial conflicts of interest? How should such information be weighted when the objective is long-term stewardship of health and ecosystems?

Risk is never black and white. The interface between technology, pollution, and biology is inherently complex and uncertain.

Navigation of uncertainty and complexity in the public interest will always be an inexact science, because biological vulnerability and the need for protective action (i.e. stewardship) to safeguard a biological system over time, whether a river catchment, a fish, animal, insect population, plant species, or a young child, necessarily requires human judgement in complex and uncertain informational environments. Intergenerational harms can severely degrade population health, yet because these harms are slow-moving or ‘chronic’, they are often difficult to detect and attribute.

Decisions about system vulnerability and intervention inevitably require human judgement under conditions of incomplete information. This obliges decision-makers to engage not only with technical data, but with ethical questions concerning acceptable risk, system fragility, and intergenerational harm, and political questions of who funded the science, and what does that science seek to address, or not address.

Biological tipping points rarely follow linear trajectories. Stressors can disrupt and dysregulate feedback systems designed to maintain homeostasis. These disruptions may be subtle, cumulative, and difficult to predict. It is impossible to specify in advance when endocrine disruptors will impair cognition, fertility, or behavioural regulation, or when assaults on microbiome diversity in soil, water, or the gut will result in irreversible dysregulation.

Granularity around risk therefore obliges decision-makers to engage with ethical and moral questions of system vulnerability, including recognition that immature or developing organisms are inherently less resilient. Such judgement should also incorporate an awareness of strategic influences that shape the informational landscape.

In the period 2020–2030 and beyond, it is not only health that must be stewarded, but the scientific systems themselves.

BARRIERS TO KNOWLEDGE: GLOBAL NETWORKS & POLITICAL & FINANCIAL CONFLICTS OF INTEREST.

Barriers to public-good information and knowledge not only include time and scientific (including techno-biological) complexity. They include paywalls, strategic communications, hidden conflicts of interest, and institutional opacity. The problem is amplified by the concentration of influence within multinational investment structures that span agriculture, biotechnology, pharmaceuticals, media, and digital infrastructure.

Barriers arise from the difficulty of navigating information, disinformation, and misinformation within highly contested, politically-fraught, knowledge environments.

Conflicts of interest can often be hidden by sophisticated public relations messaging. Websites and information platforms can be designed to appear independent, but which are instead funded by powerful actors with financial and/or political-conflicts of interest who benefit from creating policy-like content, and effectively launder policy and information through these presumed-to-be-independent vehicles. These conditions make it difficult to identify and evaluate bias, or to detect conflicts of interest that may compromise the integrity and trustworthiness of scientific and policy-relevant information.

These barriers to trustworthy information, increase with the sequestering of financial and political conflicts of interests inside lobbyist think tanks; private-public partnerships, trade and treaty agreements; political and media financing and regulatory processes. Much of this has arisen from off-shore webs of influence that eclipse New Zealand owner-operator models. Multi-national investment fund managers oversee portfolios of trillions of dollars of assets, and they can influence domestic policy, something that small and medium sized firms cannot do.

INSTITUTIONAL IGNORANCE - THE UNDERFUNDING OF NON-COMMERCIAL SCIENCE

Over the past three decades, policy and funding systems have increasingly prioritised research aligned with innovation and economic growth. However, over the same period, funding programmes for science, law and policy research that might traverse the complex issues that revolve around ethics, power, risk and public-good judgement, which do not fit the 'innovation' definition - have been deprioritised.

This funding asymmetry is structural. Public interest research often conflicts with the objectives of powerful institutions. Provision of unbiased, public interest information can conflict with the principles and priorities of powerful institutions. Interdisciplinary science, legal research and ethics-based work has become wickedly difficult to fund if such research lies outside, or potentially contradicts, the policy aims of the state. Scholars who pursue critical, risk-focused, or stewardship-oriented work face chronic funding insecurity. Careers may be threatened when research challenges dominant policy narratives or commercial interests.

Market-driven (neoliberal) trends in governance have directed resources towards commercially focussed, market-oriented science, law and deliberation, and away from public good research that might triangulate claims of safety and efficacy by institutions. These trends shape the focus of many of our public science institutions. Many public science institutions, including universities and New Zealand Crown Research Institutes, now depend on patent income, royalties, and industry partnerships.

When publicly funded science organisations must secure patents and royalties to grow their business, this creates institutional incentives to deregulate the technologies that might potentially generate revenue streams. Deregulation, where institutions do not have to declare research, the formulation toxicity of their retailed products, inflammatory and neurodevelopmental impacts and risks, certain gene edited organisms, - and more - potentially enable the institutions to expand their research capacity without consequence for the health and environmental impact.

THE BROADER SOCIAL, POLITICAL & HEALTH-BASED IMPACT

As these institutions are tasked in production of innovation, no equal weight is placed upon (often complex and interdisciplinary) stewardship issues, such as exploring pollution from their or other technologies or disease risk from exposures to toxins. These issues do not have immediately identifiable opportunities for the production of intellectual property (such as royalties and patents).

The incentives, to produce IP, steer research communities in a different direction, resulting in governance failures - remember, these are taxpayer funded, public sector institutions - to provide informational feedback loops into regulation and policy.

The result is a systemic governance failure.

Policy-makers, law-makers and regulatory agencies, are less likely to face publicly-funded expert pressure that would require them to engage with complex ethics and uncertain risk-based issues.
This funding distortion shrinks independent expert communities who could be available to contest industry claims and provide evidence-based feedback loops back into the policy, governance and regulatory 'sphere'. Expert groups aren't available to challenge outdated guideline approaches which fail to reflect newer and more nuanced knowledges of the risks of the technologies and their emissions.
Regulators are left reliant on industry-supplied data protected by commercial confidentiality. The health effects can then be effectively 'buried' when government agencies claim an absence of evidence, based on their legacy scientific guideline processes and the advice from industry representatives tasked with organisational responsibility for liaising with regulatory authorities.
The remaining independent expert communities capable of contesting industry claims are marginalised. In current funding environments, scientists are unlikely to publicly critique technologies or pollutants. Research that does address such issues is typically short-term, fragmented, and underpowered.
Lay public concerns are easily dismissed because independent science is absent or inaccessible and there are no experts to 'back up' their scientific claims.
It is then easier for regulators to dismiss public (lay) claims of harm - despite the fact that the science regulators habitually depend on, is unavailable, due to commercial in confidence clauses that privilege the industry provider.

When scientific and research communities lack autonomy to carry out such work - scholars, policy-makers, the judiciary, medical doctors and the general public are left on the back-foot when discussing complex socio-biological issues. The barriers to research promote systemic ignorance and the science remains undone. Independent voices can be rare, and careers may be threatened if they deviate from established norms.

NEW TECHNOLOGIES, RISK, AND MISSED OPPORTUNITIES

Market prices rarely reflect biological or ecological externalities. Persistent, bioaccumulative and toxic (PBT) exposures can generate systemic harms. Advances in biomarker technologies now demonstrate that environmental risk factors frequently outweigh genetic determinants in health outcomes. For example, epigenetic and endocrine disruption, inflammation, and oxidative stress are now recognised as key mechanisms linking exposure to disease. These stressors can impair fertility, cognition, development, and learning across species. Yet research commitments and guideline approaches by government agencies do not prioritise scientific research to understand how technologies and their emissions can harm human systems when these pathways are disrupted.

Large-scale national research programmes who actively investigate the mixture toxicity of industrial and agricultural chemicals, who undertake biomarker surveillance to understand system level risks, and who research preventive infrastructure (such as advanced water filtration) remain absent in New Zealand. Similarly, New Zealand lacks a dedicated institute examining nutrient insufficiency and optimum nutrition in relation to metabolic disease, mental illness, and educational performance. These omissions have long-term implications for population resilience and national security.

New, globally relevant technologies have enabled scientists to confirm that environmental risk factors outweigh genetic influences in risk to health and wellbeing. A substantial literature provides evidence that healthy genetic function arises when surrounding environments support optimal health (such as nutrition, beneficial feedback loops, and absence of persistent stressors). New technologies, such as biomarker assisted technologies, can assist researchers to understand the biological interactions following exposure to a technology.

The lack of long-term independent research results in blind, or captured environments are slow to integrate technologies and interventions which are critical to human resilience and, arguably, national security. For example, it is unlikely New Zealand scientists are testing drinking water for mixture toxicity effects, and conducting laboratory research to identify biomarkers from exposure synergies.

Examples demonstrate our lag. As a consequence, there is no research investment at scale looking at enhanced filtration technologies to strip hormone-level chemicals from drinking water, but also to prevent emission of waste stream chemicals into rivers. In parallel, New Zealand's nutritional research environment is poor, and there is no evident science institute engaged in evaluating the relationship of nutrient insufficiency, and the role of optimum nutrition, not only to more greatly appreciate the scientific underpinnings of metabolic disease, but the impact on psychiatric and brain-related disorders and educational performance. Increasing levels of disease and disorder in the human population, lowers productivity, alters intelligence and impairs the capacity to contest future threats. Such high-level work is not undertaken.

SCIENCE ADVICE FOR PUBLIC GOOD STEWARDSHIP

The public, scientists and physicians and even judges in New Zealand courts, have legitimate expectations that governments and their regulatory institutions will act to intervene to prevent market failure. This is stewardship, where governing bodies will take precautionary action to protect the public and future generations, from unintended, off-target or accumulating risks that arise from free market activities. But the freedom to do such politically controversial research is not available.

Shifts have occurred from local government, up to the global level, and feedback into local media and regulatory environments, embedding technical processes which make it impossible for decision-makers to reason and weigh uncertain issues against ‘the economy’.

We continue to observe that white papers, conferences and policy papers, and science advisors, downplay and avoid highlighting industry (often global in scale) interests. This results in often contradictory environments where officials and elected members fail to soundly articulate reasons for their decisions but claim the new laws or policies are required. Then we observe institutional patterns that persistently operate to deny, dismiss, divert (or decoy) and displace meaningful discussion relating to the evidence in the scientific literature and the stewardship of technologies and regulation of pollutants and environmental risks. However, the processes - as institutional failure to reason in the public interest - are not targeted for exploration and discussion by the legacy media. Officials can also, simply fail to engage in scrutiny of scientific information even when they have the power to do so. For example, the recently established Mental Health and Wellbeing Commission, which is tasked with protecting mental health, has no language for the problem of nutrient insufficiency, neurodevelopmental risk from inadequate nutrition or toxic medical exposures, and drug-drug risk, both short and long-term which can impair mental health and well-being. Scientists that have been the public face advocating for the deregulation of gene editing technologies, are funded by the agency that is pursuing that deregulatory process.

Such contradictory environments consequently inflame and encourage accusations of misinformation and disinformation in the public arena. At times, these intractable issues have been ethically corrupted at an early stage by early-stage policy-framing, and through secret confidentiality agreements that prohibit transparency and accountability relating to the provenance and quality of the scientific information.

As such it is important for the public, for scientists and physicians, to recognise the political shifts and influences that distort the political and regulatory landscape, if they are to critically assess claims made by powerful interests.

Governance and regulatory arenas are intensely political. Billions of dollars are dedicated to science used specifically to support regulatory decision-making and on political lobbying to media interests, officials, elected members and science advisors. Vested commercial interests habitually present scientific evidence to support sufficient safety to authorise release of a technology as certain. However, once deployed into the environment, once there is evidence of human or environmental harm, their energies turn to the production of scientific information that perpetuates uncertainty and doubt in order to avoid and delay regulation.

PSGRNZ's work continues to reflect our charity objectives which include the provision of information and critical analysis in the service of the public’s right to be independently informed on issues concerning genetics, including genetic engineering and biotechnology, and other relevant matters of science and technology.

Support for and encouragement of robust transparent and accountable knowledge-making, across lay-public, policy-makers, scientists and expert communities, in order to promote 'public-good' spaces of knowledge and information, is what we do.

GE/Biotech: Glossary

GE/Biotech: FAQs

LINKS - INTERNATIONAL ORGANISATIONS

Bioscience Resource Project – Independent science journalism and public interest science

Centre for Responsible Nanotechnology – SourceWatch - a US-based non-profit group reviewing the potential risks of nanotechnology.

CorpWatch - provide accurate, timely and easily accessible articles, reports and data on violations by multinational corporations to activists, media.

The Endocrine Disruptor Exchange (TEDx) - this site, one of the oldest independent science-focused sites online is closing due to lack of funding

Environmental Health News - Respected science site with a focus on toxics and endocrine disruption.

Environmental Health Perspectives. “Pharmaceuticals and personal care products in the environment: agents of subtle change?” C G Daughton

ETC Group reports- ETC Group works to address the socioeconomic and ecological issues surrounding new technologies that could have an impact on the world’s poorest and most vulnerable people. http://www.etcgroup.org/content/mission-etc-group

ENSSER · The European Network of Scientists for Social and Environmental Responsibility

European Non-GMO Industry Association

Geoengineering Monitor

GM Contamination Register - registers GM crops

GRAIN - support small farmers and social movements to achieve community-controlled and biodiversity-based food systems.

Greenpeace International working directly with communities on the frontlines as they protect the environments they call home. Greenpeace is comprised of 27 independent national / regional organisations in over 55 countries across Europe, the Americas, Africa, Asia and the Pacific, as well as a co-ordinating body, Greenpeace

GM Watch. Issue regular information updates.

GMO Science - voice for independent science that supports, curates, interprets, and augments findings in a communal sphere, presented in a comprehensible fashion for nonscientists and the lay public.

Institute for Responsible Technology. To protect the genetic integrity and nature’s biological evolution by preventing the outdoor release of genetically modified organisms, and to protect human and animal health by preventing the use of GMOs in the food and feed supply.

Soil Association UK - The UK's leading food and farming charity and organic certification body, working to save our soils and make good food the easy choice.

Synthetic Biology Project ensuring benefits of synthetic biology are realized through responsible development. Synthetic biology specific news, events, publications and more.

Test Biotech Institute for Independent Impact Assessment of Biotechnology.

EMF & 5G

NEW ZEALAND

Safer EMR Technology Aotearoa NZ (STANZ)

Waiheke Ethical Action Group & Safe Tech Auckland

Safe ICT New Zealand (Wellington)

Earth Waves NZ

GLOBAL

Paper: 5G Risk: The Scientific Perspective M.L. Pall PhD.

Oceania Scientific Radiofrequency Advisory Association

Physicians for Safe Technology

Physicians Health Initiative for Radiation and the Environment

The International EMF Scientist Appeal

The 5G Appeal

Environmental Health Trust - ehtrust.org

Power Watch UK - PowerWatch.org.uk

Electromagnetic Health

BioInitiative 2012 - A Rationale for Biologically-based Public Exposure Standards for Electromagnetic Fields

Dr Joel Moskowitz Electromagnetic Radiation Safety

Dr. Magda Havas, PhD.

Dr Pri Bandara

International Commission on the Biological Effects of Electromagnetic Fields

AGRICULTURE

ESSENTIAL READING

V. Shiva. Agroecology and Regenerative Agriculture. (2022)

Stephen R. Gliessman. Agroecology The Ecology of Sustainable Food Systems, Third Edition 2014.

Miguel A. Altieri. Agroecology: The Science Of Sustainable Agriculture, Second Edition 2nd Edition (1995)

REGENERATIVE/ SUSTAINABLE FARMING ORGANIZATIONS (NZ)

Bio Dynamic Farming and Gardening Association in New Zealand

Organic Dairy and Pastoral Group

Organic Winegrowers New Zealand (OWNZ)

The BHU Future Farming Centre

BHU Organic Training College

Permaculture NZ

ORGANIC CERTIFICATION OPTIONS

AsureQuality

BioGro NZ certifier for organic produce and products, providing organic certification and accredit for over 750 producers.

Demeter The Bio Dynamic Farming and Gardening Association certifier; registered as a certification trademark in 1984.

ORGANIC SEEDS

Ecoseeds Index a supplier of vegetables, flowers and herb seeds for organic growing. Online mail ordering from Wellington New Zealand.

Koanga Gardens / Koanga Institute - 100% organic, regenerative and NZ grown seeds, trees, perennials, and workshop.

Nelson Seed Library

OTHER PAPERS:

Waugh, D (2013) Public Health Investigation of Epidemiological data on Disease and Mortality in Ireland related to Water Fluoridation and Fluoride Exposure. Report for
The Government of Ireland, The European Commission and World Health Organisation. Prepared By Declan Waugh BSc. CEnv. MCIWEM. MIEMA. MCIWM

Download

Endocrine-disrupting chemicals (EDCs) are chemicals that mimic, block, or interfere with hormones in the body's endocrine system. More than a thousand chemicals have been identified as endocrine disruptors, and many of them are in common use.

Recent studies continue to confirm and solidify decades old research that pointed to the potential for endocrine disrupting chemicals to cause outside-harm at ultra-low doses - such as at parts per billion. An endocrine disruptor might not impact a system at a higher level - where it is not obviously toxic, but also not recognised by the body as hormonally relevant. But once the dose is lower, an outsize effect at this lower dose - a nonmonotonic dose–response curve (NMDRC), can occur.

The relationship contrasts with conventional toxicological perspectives, which accepts that as a dose increases, so does the toxicity. Endocrine disrupting substances, by contrast, can exert a non-linear relationship between dose and effect.

It's not unexpected that evidence that common chemicals cause harm at ultra-low doses - doses that have been accepted by regulators as safe - would be largely downplayed or ignored by regulatory agencies.

However, studies which were once dismissed as 'descriptive' now 'provide a firm basis on which to build a solid theoretical framework.'

As EDC pioneer researchers Ana Soto & Cass Sonnenschein recently stated

In the span of more than 3 decades since we and others pioneered the field of endocrine disruptors, overwhelming evidence has been gathered in animal models and epidemiological studies showing that exposure levels to certain endocrine disruptors, such as BPA, are above those that produce deleterious health effects in animals. It is now well established that humans are exposed to mixtures of numerous endocrine-disrupting chemicals and that these mixtures can produce adverse health effects.

Despite three decades of science, New Zealand lacks policy articulating the health risk of endocrine disrupting chemicals. As PSGR principal researcher Jodie Bruning discovered, New Zealand not only lacks such a policy, but the science policy and research system lacks pathways for scientists to research endocrine disrupting compounds.

Linda Birmbaum has described the endocrine system beautifully:

‘A delicately balanced system of glands and hormones that maintain homeostasis and regulate metabolism, growth, responses to stress, the function of the digestive, cardio‑vascular, renal and immune systems, sexual development and reproduction, and neurobehavioural processes including intelligence. In fact, it governs - virtually every organ and process in the body.’

Scientists are increasingly drawing attention to the ‘tremendous economic as well as human health costs of endocrine-disrupting chemicals’, as a proportion of GDP, (2.3 percent of the USA’s and 1.28% of Europe’s gross domestic product) that are impacting health budgets. (Trasande et al 2015) (Trasande et al 2016) (Attina et al 2016) The 2015 paper concluded that:

‘endocrine disrupting chemical exposures in the EU are likely to contribute substantially to disease and dysfunction across the life course with costs in the hundreds of billions of Euros per year.’[1](Trasande et al 2015)

The 2016 study by Teresa Attina and colleagues advised:

‘Annual healthcare costs and lost earnings in the United States from low-level but daily exposure to hazardous chemicals commonly found in plastic bottles, metal food cans, detergents, flame retardants, toys, cosmetics, and pesticides, exceeds $340 billion.’ (Attina et al 2016)

What is startling, is that scientists could see studies demonstrated many of these problems in epidemiological and laboratory studies over two decades ago - including the potential for transgenerational effects from parental (or grandparental) exposures. The problems extend from neurological risk to the nervous system, intelligence and behaviour; to immunological, reproductive and sexual differentiation and cancer risk. Of course, these problems are not separate.

In 1996 the book Our Stolen Future by Theo Colborn, Dianne Dumanoski and Pete Myers was written thirty years ago. This book remains essential reading for those interested in hormone function and human and environmental health. These issues were evident in 1996:

DDT was known to have estrogenic effects in 1950 - many pesticides since that time have been found to exert estrogenic like effects
Exposure to pesticides in the animal kingdom causes complex problems: thinning eggs, feminisation (lacking males, female birds try to raise eggs together), failure to
Breast milk (and other body fats) accumulates toxins - breast milk can contain levels of endocrine disrupting chemicals 10-40 times the levels greater for daily exposure to an adult
Prenatal exposure to elevated levels synthetic or natural estrogen reduced sperm counts, increased risk in undescended testicals, hypospadias, and possibly testicular tumours in offspring
Sperm count has dropped from 1940 levels (Scientist have known for decades that humans are inefficient breeders, rats much more efficient)
Endometriosis was known to be spontaneously develop in monkeys a decade after their exposure to dioxin (which affects the immune as well as the endocrine system).
Estrogen receptors are the same across the animal kingdom - the paper noted that 'scientists have marvelled over the lack of changeover millions of years of evolution.
The estrogen receptor has been known to be 'promiscuous' for decades in that it so easily consorts with synthetic estrogens
5% of breast cancers were known to be genetic. The single most important risk factor for breast cancer is total estrogen exposure.
The book theorised 20 years ago that an 'imprinting' process sensitised women to estrogen exposure - when men are exposed to excess estrogen they become sensitised and produce excess androgen receptors - making prostates hypersensitive to testosterone and vulnerable to enlargement.
Children exposed to high levels chemicals were found to have frequent ear infections, abnormal immune systems, their bodies wouldn't produce an antibody response when vaccinated.
A single 'hit' at a vulnerable development stage can create problems years later
Behavioural effects and stress response: Rats fed fish contaminated with PCBs were fine in pleasant environments but would 'hyper-react' to even mildly negative events.The effects reached across two generations.
'Every little stress will be magnified' (Helen Daly p.192) This was observed in children exposed to similarly contaminated fish. Babes whose mothers were expsosed showed a 'larger number of abnormal reflexes, a greater immaturity in a lower automatic response score and a poor abituation to repeated disturbances. p.194
Humans and rats both 'habituated poorly' - reacting much more negatively to unpleasant events. The startle response normally erodes as a baby becomes accustomed to a disturbance.
'Scientists understand far more about the role of hormones in development than they do about the biological events that give rise to cancer. Moreover, the evidence shows that humans and animals respond in generally the same way to hormone-disrupting chemicals. The available human data and the effects seen in lab animals show 'a perfect correlation.' Our Stolen Future, 1996, p.86

Example: The thyroid

What is not well understood by the general population, is that it is not just humans that are impacted by endocrine disruptors. All vertebrates can be similarly vulnerable to the health and intelligence impact from exposure to endocrine disruptors. For example, all vertebrates can be harmed by chemicals that impair thyroid function.

Developing babies require the right amount of thyroid hormone, at the right time. Iodine deficiency, which hampers thyroid function, is the world’s main source of mental retardation. The thyroid hormone is central to the metabolism of nearly all tissues, and central to the development of the central nervous system. It's well understood that:

Insufficient iodine during pregnancy and infancy results in neurological and psychological deficits in children.

If this is considered more broadly - the implications of not researching and not understanding chemical exposures to soil, water, air and food are immense. As Barbara Demeneix has written:

‘all vertebrates, from fish and frogs to humans, produce and use thyroid hormone, and that thyroid hormone in all these different species has exactly the same chemical structure.’

This is why, as discussed in Toxic Cocktail, tadpoles can be used to measure the effects of chemicals on thyroid hormone action. The amphibian model is relevant to humans, and importantly, relevant to brain development. Demeneix quotes Jaques Legrand who has said:

‘Without a minimum of thyroid hormone at the right time, a tadpole fails to become a frog and a human baby becomes a cretin’.

Policy & research steps to protect human & environmental health in Aotearoa New Zealand from EDCs:

Doing nothing – not researching human health effects, not monitoring, nor establishing controls where there is evidence that endocrine disrupting substances and mixtures are present, ensures that only the polluting industries are protected. There are policies, principles and research strategies that can ensure nations can move forward responsibly and iteratively to address the knowledge gaps, - including to act where there is evidence of harm, but uncertainty remains, and to regulate in favour of human and environmental health so that future generations are protected:

Confirm EDCs constitute a distinct class of health hazard, equivalent to carcinogens & mutagens.
Adopt legal protections requiring neonatal and paediatric exposure to EDCs are avoided.
Require that substances identified as known or presumed EDs should not be authorized (“no exposure” logic) in products with general population exposure (Demeneix & Slama, 2019, p. 98).
Institute data collection by Statistics New Zealand of synthetic organic compounds and active ingredients imported and produced in New Zealand. This will ensure top-down measuring to assess risk, that may then be bottom up monitored for environmental and human health exposures.
Data collection can identify high volume chemicals that currently evade regulatory controls. e.g. glyphosate.
Once degraded water regions are detected, commence national screening for diffuse levels of synthetic chemicals (agrichemicals, plastics, industrial chemicals, pharmaceuticals, heavy metals, and sewerage).
Precaution must operate at a meta-level. Caution must not be one factor that a decision-maker must take into account. A precautionary approach is more than just part of risk assessment. Precaution is meant to guard against the unknowns and unanticipated consequences’(Iorns, 2018, p. 47).
Fund predictive analytics (data modelling, machine learning) to predict mixture stress from endocrine disruptors, carcinogens and mutagens to biological systems (human and aquatic) (Soil & Health Association and PSGR, 2019).
Monitor oestrogenic, androgenic, thyroid, steroid loads in drinking water.
Institute public funding for environmental and public health expert taskforces (in endocrinology and toxicology) separate from chemical industry influence to:
- Research endocrine disruptors in the New Zealand environment and in human tissues;
- Research pathways EDC can harm health from a basic science ‘public interest’ perspective;
- Share knowledge & work with international public health agencies to develop guidance documents;
- Develop a public health mandate to accelerate test development and validation protocols.
Recognise that in the interests of public health, export markets and environmental integrity, supporting, liaising with and harmonising with best practice jurisdictions (e.g. European Commission) may be the most effective, up to date and transparent method for controlling EDCs in the New Zealand environment.

PSGR have developed a short PDF with these recommendations, much drawn from recommendations by Catherine Iorns, from a 2019 paper by submitted to the European Parliament by Barbara Demeneix and Remy Slama and from our 2019 Freshwater paper:

Download

References

Attina, T., Hauser, R., Sathyanarayana, S., Hunt, P., Bourguignon, J., Myers, J., . . . Trasande, L. (2016). Exposure to endocrine-disrupting chemicals in the USA: a population-based disease burden
and cost analysis. Lancet Diabetes Endocrinol 2016; 4: 996–1003. Lancet Diabetes and Endocrinology, 996-1003.

Colborn, T., Myers, J., & Dumanoski, D. (1997). Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival? A Scientific Detective Story. Plume.

Demeneix B., Toxic Cocktail. Oxford University Press, 2017. p.30.

Demeneix, B., & Slama, R. (2019). Endocrine Disruptors: from Scientific Evidence to Human Health Protection. requested by the European Parliament's Committee
on Petitions. PE 608.866 - March 2019. Brussels: Policy Department for Citizens' Rights and Constitutional Affairs.

Gore, A., Chappell, V., Fenton, S., Flaws, J., Nadal, A., Prins, G., . . . Zoeller, R. (2015). 2015. EDC-2: The Endocrine Society’s Second Scientific Statement on
Endocrine-Disrupting Chemicals. Endocr Rev, 36(6), E1-E150.

Iorns, C. (2018). Permitting Poison: Pesticide Regulation in Aotearoa New Zealand. EPLJ, 456-490.

Trasande, L. (2019). Sicker, Fatter, Poorer: The Urgent Threat of Hormone-Disrupting Chemicals to Our Health and Future . . . and What We Can Do About It. Houghton Mifflin Harcourt.

Subcategories

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For over 20 years the Physicians and Scientists for Global Responsibility New Zealand Charitable Trust (PSGR) has produced reports and submitted to government Bills and Inquiries.

We’ve been extraordinarily busy over the past 2 years with our work.

This Update aims to inform members and colleagues – and act as a go-to summary of our recent work.

2022 UPDATE - PDF

As well as our recent work All PSGR’s submissions are available to the public on our Submissions pages. In addition, we are now on LinkedIn, Twitter, Odysee & Instagram.

MEMBERSHIP

Please – without your support and membership PSGR cannot do this work. We’ve kept our fees deliberately low because your membership is important to us.

MOVING FORWARD 2022+

The PSGR recognise that the perspectives that have been expressed by the PSGR from 2020 onwards will not necessarily reflect the perspectives of all trustees and all members.

However, we sincerely hope that PSGR’s perspectives are more likely to reflect the perspectives of the majority of our membership and of collegial organisations – which represents a diverse quorum of inquiring minds.

We hope that we have demonstrated a consistency to our work, that reflects and upholds the principles reflected in 20 years of research, information communications and submissions to policy

Reports and Papers

Royal Commission

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The developmental origins of health and disease (DOAD)

Intergenerational Effect

Paper: When is the gene not DNA?
Professor Jack Heinemann
Lecturer in Genetics
University of Canterbury, New Zealand

References

Risk is never black and white. The interface between technology, pollution, and biology is inherently complex and uncertain.

BARRIERS TO KNOWLEDGE: GLOBAL NETWORKS & POLITICAL & FINANCIAL CONFLICTS OF INTEREST.

INSTITUTIONAL IGNORANCE - THE UNDERFUNDING OF NON-COMMERCIAL SCIENCE

THE BROADER SOCIAL, POLITICAL & HEALTH-BASED IMPACT

NEW TECHNOLOGIES, RISK, AND MISSED OPPORTUNITIES

SCIENCE ADVICE FOR PUBLIC GOOD STEWARDSHIP

LINKS - INTERNATIONAL ORGANISATIONS

EMF & 5G

AGRICULTURE

Example: The thyroid

Policy & research steps to protect human & environmental health in Aotearoa New Zealand from EDCs:

References

Subcategories

old LINK

2022 UPDATE - PDF

MEMBERSHIP

MOVING FORWARD 2022+

Reports and Papers

Royal Commission

Information

Providing scientific & medical information & analysis in the service of the public's right to be independently informed on issues relating to human & environmental health.

The developmental origins of health and disease (DOAD)

Intergenerational Effect

Paper: When is the gene not DNA?Professor Jack HeinemannLecturer in GeneticsUniversity of Canterbury, New Zealand

References

Risk is never black and white. The interface between technology, pollution, and biology is inherently complex and uncertain.

BARRIERS TO KNOWLEDGE: GLOBAL NETWORKS & POLITICAL & FINANCIAL CONFLICTS OF INTEREST.

INSTITUTIONAL IGNORANCE - THE UNDERFUNDING OF NON-COMMERCIAL SCIENCE

THE BROADER SOCIAL, POLITICAL & HEALTH-BASED IMPACT

NEW TECHNOLOGIES, RISK, AND MISSED OPPORTUNITIES

SCIENCE ADVICE FOR PUBLIC GOOD STEWARDSHIP

LINKS - INTERNATIONAL ORGANISATIONS

EMF & 5G

AGRICULTURE

Example: The thyroid

Policy & research steps to protect human & environmental health in Aotearoa New Zealand from EDCs:

References

old LINK

2022 UPDATE - PDF

MEMBERSHIP

MOVING FORWARD 2022+

Reports and Papers

Royal Commission

Information

Paper: When is the gene not DNA?
Professor Jack Heinemann
Lecturer in Genetics
University of Canterbury, New Zealand