Interview Universcience TV de Robert Barouki, 2011
Le 3 mai 2011, l’assemblée nationale votait en première lecture un projet de loi visant à interdire l’utilisation des phtalates et des parabènes, perturbateurs endocriniens très répandus dans les produits de la vie quotidienne. Juin 2011, universcience.tv fasait le point avec Robert Barouki, toxicologue à l’Inserm.
Tall Girls, Short Boys, and the Medical Industry’s Quest to Manipulate Height
“Normal at Any Cost” is the story, told decade by decade, of medical attempts to tinker with one inherited characteristic: height. It reveals the way drug companies redefined normal in order to expand markets, and how the best motives and worst motives combined to result in widespread experimentation on children. We think the temptations to tamper with heredity are just beginning.
Susan Cohen‘s book tells the horrible story of drug use to adjust the height of adolescent boys and girls who were threatening to be short, or tall, adults. DES was prescribed to prevent girls from growing “too tall.”
Sources and book reviews
At What Height, Happiness? A Medical Tale, DES Action.
Normal at Any Cost: Tall Girls, Short Boys, and the Medical Industry’s Quest to Manipulate Height, N Engl J Med 2009.
In humans, like other vertebrates, there is a susceptibility for epigenomic alteration by the environment during intrauterine development
Environmental toxicants can alter epigenetic regulatory features such as DNA methylation and microRNA expression. As the sensitivity of epigenomic regulatory features may be greatest during the in utero period, when critical windows are narrow, and when epigenomic profiles are being set, this review will highlight research focused on that period. I will focus on work in human populations, where the impact of environmental toxicants in utero, including cigarette smoke and toxic trace metals such as arsenic, mercury and manganese, on genome-wide, gene-specific DNA methylation has been assessed. In particular, arsenic is highlighted, as this metalloid has been the focus of a number of studies and its detoxification mechanisms are well understood. Importantly, the tissues and cells being examined must be considered in context in order to interpret the findings of these studies. For example, by studying the placenta, it is possible to identify potential epigenetic adaptations of key genes and pathways that may alter the developmental course in line with the developmental origins of health and disease paradigm. Alternatively, studies of newborn cord blood can be used to examine how environmental exposure in utero can impact the composition of cells within the peripheral blood, leading to immunological effects of exposure. The results suggest that in humans, like other vertebrates, there is a susceptibility for epigenomic alteration by the environment during intrauterine development, and this may represent a mechanism of plasticity of the organism in response to its environment as well as a mechanism through which long-term health consequences can be shaped.
Sources and more information
Influence of environmental exposure on human epigenetic regulation, jeb.biologists, doi: 10.1242/jeb.106971 January 1, 2015.
A representative of one of Europe’s most influential cancer organisations, the association of European cancer leagues (ECL) recently told a meeting of MEPs against cancer that curbing exposure to endocrine disrupting chemicals should become a central part of cancer prevention strategy in Europe.
ECL, which focuses on the prevention and control of cancer, brings together national and regional cancer leagues with a staff of more than 6000 throughout Europe. Its director Wendy Tse Yared said that rapid rises in rates of breast and prostate cancer in recent decades could not be explained by improved diagnostics.
She noted that this upward trend coincided with an increase in chemicals and that sufficient evidence now exists that endocrine disrupting chemicals heighten cancer risk.
Effective regulation could contribute to reductions in hormonal cancers, including of the breast, which is the most commonly diagnosed cancer in women and of the prostate, the most commonly diagnosed cancer in men.
It may also help to bring down rates of testicular cancer, which is increasing among young men in Europe. A recent study by Nordic countries on male reproductive health problems associated with these chemicals suggested that endocrine disrupting chemicals might be responsible for up to 40 per cent of all cases of testicular cancer.
Dutch toxicologist Dr Majorie B.M. van Duursen told the meeting that numerous studies on breast cancer showed that exposure to endocrine disrupting chemicals, such as BPA, PBDE and pesticides, can adversely affect the normal development of the mammary gland, potentially making it more susceptible to cancers.
She stressed that one or two new studies were appearing each day on endocrine disrupting chemicals and chronic conditions, including hormonal cancers, infertility, obesity and diabetes.
A review by the world health organisation in 2012 recorded the considerable advances in the scientific evidence that had been made since 2002. No-one can say that we don’t know enough to justify reducing people’s exposure to these chemicals, said Dr Duursen.
The not-for-profit Health and Environment Alliance (HEAL), which brings together over 70 member organisations to address how environmental protection can improve health in the European Union has been advocating stronger action to reduce exposure to harmful chemicals for many years.
Genon K. Jensen, HEAL’s director told the meeting that her members, which include cancer groups, are convinced that exposure to EDCs is a likely explanation of why cancers that are hormone dependent have been rising.
She said that HEAL was part of a coalition of non-governmental organisations called ‘EDC-Free Europe‘ that was helping ordinary individuals to respond to the EU consultation on EDCs. An online platform launched five weeks ago has allowed more than 10,000 individuals to respond.
But despite the rapidly growing scientific evidence and the growing public concern, the delays in effective action continue. What is needed now is a proper identification of EDCs – one that ensures these harmful chemicals are found and ultimately eliminated.
My hope is that this MEPs against cancer meeting will help convince the commission that action now needs to happen. Not tomorrow, but today.
Perch and roach from British rivers can be toxic, say experts
A government-funded study suggested that many fish from rivers and canals are ending up on our dining tables are contaminated with toxic chemicals above safe limits.
Fish can bioaccumulate environmental contaminants and so can contribute a significant amount to dietary exposure to those chemicals.
Mike Berthet, director of fish and seafood at M&J Seafood, voiced his concerns at the growing tendency of angling for personal consumption. “The inland water in the UK is notoriously polluted,” he said. “Anyone not buying fish from registered companies or markets with requisite quality control is always going to be at risk.”
Sources and more information
Contamination of fish in UK fresh water systems: Risk assessment for human consumption, sciencedirect, 19 December 2014.
Chemicals in freshwater fish put health at risk, independent, 11 January 2015.
DES daughters haved 2-3 times the risk of being diagnosed with paraovarian cysts
DES Follow-up Study Summary
We investigated the association between prenatal Diethylstilbestrol DES exposure and benign gynecologic tumors among women participating in the DES collaborative follow-up study. A total of 85 cases of uterine fibroids and 168 cases of ovarian or paraovarian cysts were confirmed by medical records. After adjustment for age, no association was found between prenatal DES exposure and ovarian cysts or uterine fibroids. DES daughters had 2-3 times the risk of being diagnosed with paraovarian cysts, which are cysts that originate from remnants of the Mullerian ducts and are located near the ovary and fallopian tubes. Paraovarian cysts are not known to cause any health problems.
We recommend caution when interpreting the results for paraovarian cysts. First, the pathologist making the initial diagnosis was not blinded as to the patient’s exposure status. Therefore, the pathologist’s knowledge of a patient’s DES status may have influenced the recording of cysts, particularly those that have little clinical significance (e.g., paraovarian cysts), which in the absence of such exposure history were often not recorded. Second, the lining of the Mullerian duct derives from coelomic epithelium, as does the covering of the ovary from which epithelial cysts arise. It is unlikely that DES exposure would be associated with an increase in cysts of Mullerian origin (e.g., paraovarian), but not of ovarian epithelial origin (e.g., cystadenomas). Thus, greater incidental detection of paraovarian cysts among DES daughters, or more likely the absence of recording in non-exposed daughters, could have produced the positive association observed in our study.
2005 Study Abstract
To investigate the association between prenatal diethylstilbestrol (DES) exposure and risk of benign gynecologic tumors.
We conducted a collaborative follow-up study of women with and without documented intrauterine exposure to DES. We compared the incidence of self-reported ovarian cysts, paraovarian cysts, and uterine leiomyomata confirmed by medical record in DES-exposed and unexposed women.
A total of 85 cases of uterine leiomyomata and 168 cases of ovarian or paraovarian cysts were confirmed histologically. After adjustment for age, no association was found between prenatal DES exposure and ovarian cysts or uterine leiomyomata. Prenatal DES exposure was positively associated with paraovarian cysts.
The present results do not support the hypothesis that prenatal DES exposure increases risk of uterine leiomyomata or ovarian cysts. Prenatal DES exposure was associated with an increased risk of paraovarian cysts, but detection bias cannot be ruled out as an explanation of this finding.
Risk of benign gynecologic tumors in relation to prenatal diethylstilbestrol exposure,NCBI, PMID: 15625159, Obstet Gynecol. 2005 Jan;105(1):167-73.