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  1. There is so much noise around BPA. It is understood now that 'BPA-free' doesn't mean safe, it even can be more toxic than 'with BPA'. But what are the reasons behind that? I lack a comprehensive knowledge about this and at the same time I found no good article written in layman terms about 'BPA free' still causing problems to public health. I think this is the topic that many people would like to read.
  2. Bisphenol A, a known endocrine disrupting chemical, is now banned in baby bottles. But as you may already know, BPA-free means that BPA was replaced by other sister toxins, that are as harmful as BPA, but still not banned, e.g. BPF, BPS, etc. I believe it is worthy to write an article about this so to make as many as possible people informed. Article should explain what are these chemicals, why they are dangerous and how to avoid them. 
  3. The last few decades have seen a decrease in the age of onset of puberty, particularly in girls.[1] [2] This is a potential health concern, as it has been observed that the earlier a girl begins puberty, the greater risk she has of developing certain cancers later in life.[3]  There are several reasons suggested for increasingly early puberty onset (also called ‘precocious puberty’), including alterations in the levels of hormones that trigger for puberty to commence. Certain foods such as beef contain steroid hormones (in the USA), while others contain endocrine disrupting chemicals (EDCs) which, at certain doses, can interfere with our endocrine (hormone) systems. These disruptions can cause numerous health concerns, including cancerous tumours, birth defects, and other developmental disorders. EDCs are present in countless foods and personal products that we come into contact with every day. They include chemicals such as Bisphenol A (commonly used in the production of plastics and epoxy resins, the latter of which often form the lining of food cans)[4] and phthalates (found in many plastics, but also in personal care products such as hair care, body wash and sunscreen)[5]. EDCs can be found in literally thousands of products that we come into contact with every day, including our food and the materials used in its packaging,[6] our toiletries and pharmaceuticals,[7]  and even our furniture in the form of commonly used fire-retardants and water repellents.[8] [9] We are therefore unknowingly exposed to these toxic chemicals every day, and literally any system in the body that is controlled by hormones can potentially be derailed by EDCs.[10][11] [12][13] The contents of our diet, including EDCs, can be involved in what is termed ‘precocious puberty’. Childhood obesity is a known prompt for puberty onset, with current observational studies suggesting notable associations between dietary intake and pubertal timing.[14] These associations are beyond simple contributions to an energy imbalance; children with the highest intakes of vegetable protein experience pubertal onset up to 7 months later than those with average consumption, while those with the highest consumption of animal protein enter puberty up to 7 months earlier than those with average consumption. Furthermore, girls with a high intake of isoflavones (phytoestrogens with similar effects on the body to oestrogen) from soy products may experience delayed onset of breast development and reduced height.[15][16]   In addition, in the USA, the FDA (Federal Drug Agency) allows the administration of six different steroid hormones to ‘beef up’ cattle, despite the use of these hormones for this purpose being prohibited in Europe.[17] [18] Poultry growth, however, is not affected by steroid hormones and as such they are not routinely used in poultry production, making this food relatively safe in terms of hormone ingestion.[19] Due to the increased cancer risks associated with early onset puberty, in addition to a whole host of other potential health concerns now linked to meat consumption, limiting the intake of meat, particularly in children, may be a wise choice. It is not always possible to know which food item, household products or personal care items contain EDCs, but eating fresh, rather than tinned food, using glass rather than plastic to store and microwave food, and sourcing natural personal products and household items is a positive approach.    [1] Aksglaede, L. et al. (2009) Recent decline in age at breast development: the Copenhagen Puberty Study. Pediatrics. 123(5). e932-9. [2] Biro, FM. et al. (2010) Pubertal assessment method and baseline characteristics in a mixed longitudinal study of girls. Pediatrics. 126(3). e583-90. [3] Robbins, CL. et al. (2009) Influence of reproductive factors on mortality after epithelial ovarian cancer diagnosis. Cancer Epidemiol Biomarkers Rev. 18(7). 2035-41. [4] Rogers, JA. et al. (2013) Review: Endocrine disrupting chemicals and immune responses; a focus on bisphenol-A and its potential mechanisms. Mol Immunol. 53(4). 421-30. [5] FDA (2013) Phthalates. Retrieved April 2016 from,  [6] Cwiek-Ludwicka, K. & Ludwicki, JK. (2014) Endocrine disruptors in food contact materials; is there a health threat? Rocz Panstw Zaki Hig. 65(3). 169-77. [7] Bledzka, D. et al. (2014) Parabens. From environmental studies to human health. Environ Int. 67. 27-42. [8] Vested, A. et al.(2013) Associations of in utero exposure to perfluorinated alkyl acids with human semen quality and reproductive hormones in adult men. Environ Health Perspect. 121(4). 453-8. [9] Waring, RH. & Harris, RM. (2005) Endocrine disrupters: a human risk? Mol Cell Endocrinol. 244(1-2). 2-9. [10] Aksglaede L. et al. (2006) The sensitivity of the child to sex steroids: possible impact of exogenous estrogens. Hum Reprod Update. 12(4). 341-9. [11] Fenton, SE. et al. (2012) Perinatal environmental exposures affect mammary development, function and cancer risk in adulthood. Annu Rev Pharmacol Toxicol. 52. 455-79. [12] Fenton SE. & Birnbaum, LS. (2015). Timing of Environmental Exposures as a Critical Element in Breast Cancer Risk. J Clin Endocrinol Metab. 100(9). 3245-50. [13] WHO (2016) Global assessment of the state-of-the-science of endocrine disruptors. Retrieved April 2016 from,  [14] Kaplowitz, PB. (2008) Link between body fat and the timing of puberty. Pediatrics. 121(3). S208-17. [15] Cheng, G. et al. (2012) Beyond overweight: nutrition as an important lifestyle factor influencing timing of puberty. Nutr Rev. 70(3). 133-52. [16] Kim, SH. & Park, MJ. (2012) Effects of phytoestrogen on sexual development. Korean J Pediatr. 55(8). 265-71. [17] FDA (2015) Steroid Hormone implants Used for Growth in Food-Producing Animals.Retrieved April 2016 from, [18] European Commission. (2016) Hormones in Meat. Retrieved April 2016 from, [19] Vasilatos-Younken R. (1999) Absence of growth hormone-induced avian muscle growth in vivo. Poult Sci. 78(5). 759-68.