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EMF Studies

27 January 2013

International Workshop on Environmental Carcinogenesis: A Focus on Epigenetics, Royal Academy of Medicine, Brussels, 26 October 2012

On 26 October 2012, the European Cancer and Environment Research Institute (ECERI) held its first International Workshop at the Royal Academy of Medicine of Belgium, entitled "Environmental carcinogenesis: a focus on epigenetics”. 

The newly created ECERI (headquartered in Brussels, chaired by Prof. D. Belpomme, oncologist in Paris) is an association of several European research centers aimed at advancing research environment links to cancer and the resulting need for primary prevention methods. Professors Janos Fruhling and Luc Montagnier co-chair the Scientific Council of ECERI, which includes internationally recognized scientific personalities. Although ECERI is focused primarily on cancer, it does not ignore other chronic diseases such as obesity, type 2 diabetes, autism and Alzheimer's disease (the latter has recently shown a link with the environment--pointed out by Prof. Belpomme in his introductory lecture at the Workshop.

Prof. Belpomme was one of the first to promote the concept of environmental carcinogenesis. In the vast majority of countries, the incidence of cancer has increased in recent decades. The traditional cancer risk factors of aging populations and/or lifestyle, such as smoking, alcoholism, dietary imbalances, sedentary lifestyle, etc. do not alone account for that increase. So physical, chemical and biological degradation of our environment - in particular the presence of many carcinogenic, mutagenic and / or toxic for reproduction pollutants must be considered. Professor Belpomme along with Professor Montagnier had already delivered such a message in 2005, at the Begium Royal Academy of Medicine.  Since then, progress in molecular biology--particularly epigenetics--enables us to understand the role of the environment in carcinogenensis (and other diseases),

Following are summaries of two presentations at the workshop and concluding remarks. See here for the workshop’s summary document in full.

What is environmental carcinogenesis
Dominique BELPOMME, M.D. MSC
Paris Descartes University, ARTAC Research Center , ECERI

The growing incidence of a variety of cancers since the Second World War confronts scientists with the question of their genesis. In economically developed countries, expansion and ageing of the population and new/improved diagnostic and screening tests to detect previously hidden developing tumors/cancers do not fully account for the observed growing incidence of cancer. Our hypothesis is that in addition to oncogenic viruses and radiation, exposure to synthetic chemicals plays a more important role in cancer genesis than it is usually agreed:

(1) Over the last 2-3 decades, alcohol consumption and tobacco smoking in men have significantly decreased.

(2) Obesity is increasing in many countries and adipose tissue has been shown to be enhanced by environmental chemicals and to be a reservoir for carcinogenic lipophilic environmental pollutants.

(3) Our environment has changed over the same time scale as the recent rise in cancer incidence (including the accumulation of many new carcinogenic chemicals in the biosphere).

(4) Endogenous carcinogenesis susceptibility factors, such as an individual's genetic polymorphism, cannot so change over one generation and some may favour the role of exogenous carcinogens/procarcinogens, via gene-environment interaction.

(5) Population aging does not explain the rising incidence as most time series adjust for population aging and the increase is seen across all age categories, including children.

(6) The foetus is specifically vulnerable to exogenous carcinogenic agents. Chemical exposure during prenatal and early postnatal life could alter gene expression by genetic and epigenetic changes, causing biochemical functional changes in specific organs and tissues that may cause cancer occurrence during adult life, and increase cancer susceptibility in successive generations. This seems particularly the case for the increases in breast and prostate cancers, which have been shown in rodent models to result from the perinatal administration of endocrine disruptors.

A fetal exposure during a critical window period may explain why current epidemiological studies fail to find a link between cancer and environment in adults. Moreover carcinogenesis is being revealed to be a far more complex process than initially thought: It should be considered not only direct mutagenesis via the classical somatic mutation theory; but also epigenomic processes leading to metabolic dysfunction and indirect mutagenesis through environment-related epigenenomic alterations.

We therefore propose that the involuntary exposure to many carcinogens in the environment may contribute to the recent rising trend in cancer incidence; that the risk attributable to environmental carcinogens may be far higher than it is usually proposed; and that cancer should be considered to be a model of multifactorial environmental disease.

Obesity, Diabetes and Cancer: is mitochondrial dysfunction a common key target ? 
Philippe IRIGARAY, Ph.D.
ARTAC Research Center, ECERI Scientific Coordinator

Obesity, type 2 diabetes and cancer are recent epidemic plagues that concern mostly but not exclusively the developed world. Among classical lifestyle-related risk factors are a combination of excess dietary calories and a lack of physical activity. In addition to genetic predisposition, environmental risk factors, including endocrine disruptors, has been proposed as possible underlying mechanisms to explain these incidence increases.

Accumulating evidence suggests indeed that exposure to common man-made environmental CMR (carcinogenic, mutagenic and reprotoxic) chemicals increase the individual’s risk of not only of cancer but also of obesity and type 2 diabetes.

In humans, persistent organic pollutants (POPs) are stored primarily in adipose tissue. And it was recently observed that POPs levels in adipose tissue and serum correlate with biological markers of obesity-related dysfunctions. I have previously discovered a novel molecular mechanism of toxicity for one environmental pollutantbenzo[a]pyrene (B[a]P) and introduced the concept that chronic exposure to B[a]P and possibly to other polycyclic aromatic hydrocarbons (PAH) could be not only carcinogenic but also obesogen [foreign chemical compounds that disrupt normal development and balance of lipid metabolism, which in some cases, can lead to obesity]. Moreover at the foetal stage endocrine disruptors can not only induce hormone-dependent adulthood cancers, such as testis, breast and prostate cancer but also increase the number of pre-adipocytes, thus furthering obesity.

The obesity-related diabetes and insulin resistance (IR), increasing in incidence, may also be increased by chemicals - e.g. arsenic and polychlorinated biphenyls (PCBs).

IR can be a common key mechanism of diseases such as obesity, diabetes and cancer. Our hypothesis is that in addition to specific factors, mitochondrial dysfunction might be a key common target accounting for these disorders. IR may originate in the womb as the result of a mitochondrial dysfunction.

Moreover mitochondria not only have the essential role in powering cells, by generating ATP, but are also the major source of intracellular reactive oxidative species (ROS), which can be genotoxic and epigenotoxic and so far have a regulatory role in cell death and cell proliferation. Dysregulation of mitochondrial metabolism has been frequently observed in metabolic diseases and in human tumors, as have mutations in mitochondrial DNA, a finding that strongly reinforces our hypothesis.


This Workshop aimed at understanding the underlying biological mechanisms that promote and cause environmental carcinogenesis.

As introduced by Zdenko Herceg from IARC, recent advances in epigenetics and epigenomics have a tremendous impact on our understanding of the genesis of complex diseases such as cancer, to which environmental factors contribute, or cause outright (indeed it is important to clearly distinguish lifestyle risk factors from exogenous disease agents). In this new approach, the epigenome is considered to be an interface between the genome and the environment, allowing environmental factors to alter the control of the genome, causing disease occurrence. Hence the concept of epimutagens and epimutations.

Examples involving alterations of DNA methylation of cancer genes and silencing of tumor suppressor genes associated with DNA methylation and histone modifications were provided.

Moreover, it is now accepted that the initiation of chronic diseases such as cancer happens in utero or peri-natally. In fact, epigenetic disregulation in the foetus can be imprinted onto the genome and thus be passed on to future generations.

However disease genesis is probably even more multi-factorial than this, even more than is currently conceived. For example, environmental factors modify macrobiota such as the gut microflora and cause mitochondria dysfunction, leading cells to produce an excess of free radicals, the ultimate cause of secondary epigenetic alterations.

Finally, a very important animal experiment revealed that due to epigenetic mechanisms, the behavorial impact of psychological stress could be imprinted and passed on to future generations.

This international workshop was organised and supported by ECERI, an independent network of European and international scientific experts and researchers specialized in the fields of carcinogenesis, epigenetics, gene-environment interactions and environmental diseases.

ECERI's objectives are :

- boosting European research in the field of environmental carcinogenesis,
- spreading its research to all European countries by developing international scientific collaboration,
- creating pan-Europe data bases,
- providing scientific expertise to European institutions,
- making health recommendations to the public.

This workshop is the first step towards future scientific developments currently involving more than fifteen European research institutions.


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