Scientists critical of EU chemical policy found to have industry ties
Alexis Sobel Fitts, Editor for CJR.org confirms Stéphane Horel and Brian Bienkowski deserve a laurel for their article investigating a group of scientists who authored a controversial editorial condemning a proposed regulatory policy for endocrine disruptors.
Indeed the two EHN reporters chronicled the scientists’ financial and political affiliations – weaving a comprehensive story of the influences behind science policy.
What is this about?
Seventeen scientists who have criticized plans in Europe to regulate endocrine-disrupting chemicals have past or current ties to regulated industries. An investigation by Environmental Health News reveals that of 18 toxicology journal editors who signed a controversial editorial, 17 have collaborated with the chemical, pharmaceutical, cosmetic, tobacco, pesticide or biotechnology industries. Some have received research funds from industry associations, while some have served as industry consultants or advisors. The stakes are high in the controversy because it involves the European Union’s strategy to regulate hormone-altering chemicals – the first attempt in the world to do so. The new rules would have sweeping, global ramifications because all companies that sell a variety of products in Europe would have to comply.
Antiepileptic drugs may cause congenital malformations. Less is known about the effect on development in infancy and childhood. The aim of this study was to examine whether exposure to antiepileptic drugs during pregnancy has an effect on early child development.
From mid-1999 through December 2008, children of mothers recruited at 13-17 weeks of pregnancy were studied in the ongoing prospective Norwegian Mother and Child Cohort Study. Information on birth outcomes were obtained from the Medical Birth Registry (108,264 children), and mothers reported on their child’s motor development, language, social skills, and autistic traits using items from standardized screening tools at 18 months (61,351 children) and 36 months (44,147 children) of age. The relative risk of adverse outcomes in children according to maternal or paternal epilepsy with and without prenatal exposure to antiepileptic drugs was estimated as odds ratios (ORs), using logistic regression with adjustment for maternal age, parity, education, smoking, depression/anxiety, folate supplementation, and child congenital malformation or low birth weight.
A total of 333 children were exposed to antiepileptic drugs in utero. At 18 months, the exposed children had increased risk of abnormal scores for gross motor skills (7.1% vs. 2.9%; OR 2.0, 95% confidence interval [CI] 1.1-3.7) and autistic traits (3.5% vs. 0.9%; OR 2.7, CI 1.1-6.7) compared to children of parents without epilepsy. At 36 months, the exposed children had increased risk of abnormal score for gross motor skills (7.5% vs. 3.3%; OR 2.2, CI 1.1-4.2), sentence skills (11.2% vs. 4.8%; OR 2.1, CI 1.2-3.6), and autistic traits (6.0% vs. 1.5%; OR 3.4, CI 1.6-7.0). The drug-exposed children also had increased risk of congenital malformations (6.1% vs. 2.9%; OR 2.1, CI 1.4-3.4), but exclusion of congenital malformations did not affect the risk of adverse development. Children born to women with epilepsy who did not use antiepileptic drugs had no increased risks. Children of fathers with epilepsy generally scored within the normal range.
Exposure to antiepileptic drugs during pregnancy is associated with adverse development at 18 and 36 months of age, measured as low scores within key developmental domains rated by mothers. Exposures to valproate, lamotrigine, carbamazepine, or multiple antiepileptic drugs were associated with adverse outcome within different developmental domains.
Le Réseau Environnement Santé s’étonne de la tournure que prennent les discussions sur la future réglementation des perturbateurs endocriniens. Alors que se confirme le non-respect de l’échéance d’élaboration des critères d’identification des perturbateurs endocriniens, fixée par les règlements biocides et pesticides de 2009 à fin décembre 2013, il semble que tous les coups soient permis pour tenter de déstabiliser les fondements mêmes de l’action européenne contre ces substances chimiques dangereuses pourtant qualifiées de “menace mondiale” par les plus hautes instances internationales.
Selon une enquête d’Environmental Health News, la quasi totalité – dix-sept sur dix-huit – des auteurs d’un éditorial controversé sur le projet de réglementation européenne des perturbateurs endocriniens sont liés à l’industrie. Ces dix-sept rédacteurs et rédacteurs en chef de plusieurs revues de toxicologie ont collaboré avec l’industrie chimique, pharmaceutique, cosmétique, et celles du tabac, des pesticides ou des biotechnologies. Certains ont bénéficié de financements d’associations industrielles. D’autres ont travaillé comme consultants ou conseillers…
Synthetic Estrogens exposures induce epigenetic modifications for multiple generations
2013 Study Abstract:
Women are using estrogens for many purposes, such as to prevent pregnancy or miscarriage, or to treat menopausal symptoms. Estrogens also have been used to treat breast cancer which seems puzzling, since there is convincing evidence to support a link between high lifetime estrogen exposure and increased breast cancer risk. In this review, we discuss the findings that maternal exposure to the synthetic estrogen diethylstilbestrol during pregnancy increases breast cancer risk in both exposed mothers and their daughters. In addition, we review data regarding the use of estrogens in oral contraceptives and as postmenopausal hormone therapy and discuss the opposing effects on breast cancer risk based upon timing of exposure. We place particular emphasis on studies investigating how maternal estrogenic exposures during pregnancy increase breast cancer risk among daughters. New data suggest that these exposures induce epigenetic modifications in the mammary gland and germ cells, thereby causing an inheritable increase in breast cancer risk for multiple generations.
2013 Study Conclusion:
Women use estrogens for many purposes. During pregnancy, synthetic strogen DES was used to prevent miscarriage and promote healthy pregnancy, although it turned out to cause the opposite. During the reproductive years when a woman’s own estrogen levels are high, women use synthetic estrogens as contraceptives. Since estrogens play an important role in normal physiological functions in women, some menopausal and postmenopausal women use estrogen supplementation to regain the benefits of natural estrogens.
The effects of estrogens on breast cancer risk differ depending upon when during a woman’s life time they are used. Maternal exposure to DES during pregnancy increases breast cancer risk in mothers and their daughters. The adverse effects of synthetic estrogen exposure during pregnancy may not be limited to mothers and their daughters. Our preclinical study in rodents showed that maternal exposure to EE2 increases breast cancer risk in daughters, granddaughters, and great granddaughters. The first generation of OCs increased breast cancer risk at the time women were taking them, but the increase in risk was not permanent. The current, third generation contraceptives do not increase breast cancer risk. Menopausal and postmenopausal HT, if it contains both estrogens and progestin, increases a woman’s breast cancer risk, and recent data suggest that tumors developing during therapy are more aggressive than those in women not using HT. Estrogen-only HT does not increase breast cancer risk, and might even reduce it. However, due to other adverse effects of estrogen-only HT, it is not recommended beyond using it to control the most severe menopausal symptoms.
We are beginning to understand how the increase in breast cancer risk following in utero exposures to synthetic estrogens occurs. It most likely involves long-term epigenetic changes in genes that are important in determining the risk for breast cancer development, such as tumor suppressor genes, PcTGs and oncogenes. Briefly, an exposure to synthetic estrogens during the fetal period induces modifications in the epigenetic reprogramming of the genome, leading to changes in mammary gland morphology, and gene and protein expression. Some of these changes are transient, such as an increase in the number of TEBs in rodents, and some persist, such as an altered gene and protein expression involving tumor suppressor genes and oncogenes. Together, epigenetically induced modifications in the mammary gland morphology and gene expression increase the likelihood that environmental carcinogens and radiation induce malignant transformation, and evetually breast cancer. The next challenge is to determine whether the increase in risk can be reversed by reversing epigenetic changes that occur as a consequence of early life exposure to synthetic estrogens.
Call for ban on endocrine disrupting pesticides in Europe
In this short video clip, Lisette van Vliet (HEAL) and Hans Muilerman (PAN Europe) explain why endocrine disrupting pesticides and other endocrine disrupting chemicals (EDCs) in Europe should be banned, the goals of the multi NGO ‘EDC Free Campaign‘ and urge organisations to join them.
HEAL and PAN Europe are members of the EDC Free campaign, a coalition of public interest groups representing more than 25 organisations across Europe working to raise public awareness and urge quicker governmental action on hormone disrupting chemicals.
Interview met Maria Zwart, Directeur van het DES Centrum
“We werken hard aan een DES Centrum met een nieuwe organisatiestructuur”, zegt Maria Zwart, directeur van het DES Centrum. “Mensen gaan dat merken, bijvoorbeeld in onze bereikbaarheid. Maar ons streven is om de dienstverlening op pijl te houden. Tijden veranderen. Wij ook“
Association with breast cancer mortality more evident in trial participants who received high DES doses
DES Follow-up Study Summary
This analysis examined cause of death in women who were given Diethylstilbestrol (DES) during pregnancy. The mothers cohort has not been actively followed since 1994, so survival was assessed through a search of the National Death Index. The results suggested a modest increase in death from breast cancer in the DES exposed mothers, compared to the unexposed. We did not, however, see an excess of overall mortality in the DES-exposed mothers, or an excess of death from any specific cause other than breast cancer. In particular, DES was not associated with an increased mortality from gynecologic cancers.
2006 Study Abstract
We used Cox regression analyses to assess mortality outcomes in a combined cohort of 7675 women who received diethylstilbestrol (DES) through clinical trial participation or prenatal care. In the combined cohort,
the RR for DES in relation to all-cause mortality was 1.06 (95% CI = 0.98-1.16), and 1.11 (95% CI = 1.02-1.21) after adjusting for covariates and omitting breast cancer deaths.
The RR was 1.07 (95% CI = 0.94-1.23) for overall cancer mortality, and remained similar after adjusting for covariates and omitting breast cancer deaths.
The RR was 1.27 (95% CI = 0.96-1.69) for DES and breast cancer, and 1.38 (95% CI=1.03-1.85) after covariate adjustment.
The RR was 1.82 in trial participants and 1.12 in the prenatal care cohort, but the DES-cohort interaction was not significant (P = 0.15).
Diethylstilbestrol did not increase mortality from gynaecologic cancers.
In summary, diethylstilbestrol was associated with a slight but significant increase in all-cause mortality, but was not significantly associated with overall cancer or gynaecological cancer mortality. The association with breast cancer mortality was more evident in trial participants, who received high DES doses.
Mortality in women given diethylstilbestrol during pregnancy,NCBI, PMID: 16786044, 2006 Jul 3;95(1):107-11. Epub 2006 Jun 20. Full text Br J Cancer. Jul 3, 2006; 95(1): 107–111. PMCID: PMC2360488 link.
U.S. Panel Warns Hormone Replacement Therapy Is Too Risky
In their November 2002 recommendations, the U.S. Preventive Services Task Force confirmed that the risk of HRT outweigh its potential benefits.
The USPSTF recommends against the routine use of estrogen and progestin for the prevention of chronic conditions in postmenopausal women ; advising women to use HRT to treat symptoms of menopause for only short periods of time.