47 research outputs found
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Breast cysts and aluminium-based antiperspirant salts
On the basis that aluminium-based antiperspirant salts are designed to block apocrine sweat ducts of the axilla, and that breast cysts result from blocked breast ducts in the adjacent region of the body, it has been proposed that breast cysts may arise from antiperspirant use if sufficient aluminium is absorbed into breast tissues over long-term usage. This review collates evidence that aluminium can be absorbed from dermal application of antiperspirant salts and describes studies measuring levels of aluminium in breast tissues, including in breast cyst fluids. It is notable that breast cysts, as for breast cancers, start most frequently in the upper outer quadrant of the breast, which is the region closest to the site of underarm antiperspirant application. Mechanistic evidence is reviewed for a link between aluminium levels in breast tissue, cyst formation and development of breast cancer. If excessive use of antiperspirant is a cause of breast cysts, then reduction or cessation of use could provide a preventative or even treatment strategy. Furthermore, if cyst formation from antiperspirant use is an indicator of increased risk for breast cancer, then reduction in use of antiperspirant could also provide a strategy for reducing breast cancer risk
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Overview of air pollution and endocrine disorders
Over recent years, many environmental pollutant chemicals have been shown to possess the ability to interfere in the functioning of the endocrine system and have been termed endocrine disrupting chemicals. These compounds exist in air as volatile or semi-volatile compounds in the gas phase or attached to particulate matter. They include components of plastics (phthalates, bisphenol A), components of consumer goods (parabens, triclosan, alkyl phenols, fragrance compounds, organobromine flame retardants, fluorosurfactants), industrial chemicals (polychlorinated biphenyls), products of combustion (polychlorinated dibenzodioxins/ furans, polyaromatic hydrocarbons), pesticides, herbicides and some metals. This review summarises current knowledge concerning the sources of endocrine disrupting chemicals in air, measurements of levels of endocrine disrupting chemicals in air and the potential for adverse effects of endocrine disrupting chemicals in air on human endocrine health
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The potential for estrogen disrupting chemicals to contribute to migration, invasion and metastasis of human breast cancer cells
Estrogen disrupting chemicals are environmental compounds which mimic, antagonize or interfere in the action of
physiological estrogens. They occur naturally (plant phytoestrogens) but the majority are man-made compounds,
which, through their use in agricultural, industrial and consumer products, have become widely present in human
tissues including breast tissue. Since exposure to estrogen is a risk factor for breast cancer, estrogen disrupting chemicals may also contribute to breast cancer development. This review discusses evidence implicating estrogen disrupting chemicals in increasing migratory and invasive activity of breast epithelial cells, in epithelial-to-mesenchymal transition, and in growth of breast tumours at metastatic sites as well as the primary site. Mechanisms may be through the ability of such chemicals to bind to estrogen receptors, but unlike for proliferation, effects on cell migration and invasion are not limited to estrogen receptor-mediated mechanisms. Furthermore, whilst effects on proliferation can be measured within hours/days of adding an estrogen disrupting chemical to estrogen-responsive breast cancer cells, effects on cell migration occur after longer times (weeks). Most studies have focused on individual chemicals, but there is now a need to consider the environmentally relevant effects of long-term, low-dose
exposure to complex mixtures of estrogen disrupting chemicals on mechanisms of metastasis
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Chemical components of plastics as endocrine disruptors: overview and commentary
Bisphenol A and phthalate esters are used as additives in the manufacture of plastic materials, but their ability to leach out with age and heat has resulted in their becoming ubiquitous contaminants of the ecosystem including within
human body tissues. Over recent years, these compounds have been shown to possess endocrine disrupting properties with an ability to interfere in the actions of many hormones and to contribute to human health problems. Much
of the reported disruptive activity has been in relation to the action of estrogens, androgens, and thyroid hormones, and concerns have been raised for
adverse consequences on female and male reproductive health, thyroid function, metabolic alterations, brain development/function, immune responses, and development of cancers in hormone-sensitive tissues. A recurring theme
throughout seems to be that there are windows of susceptibility to exposure in utero and in early postnatal life, which may then result in disease in later life
without any need for further exposure. This commentary highlights key issues in a historical context and raises questions regarding the many data gaps
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Long-term exposure to triclosan increases migration and invasion of human breast epithelial cells in vitro
Extensive use of triclosan (2,4,40-trichloro-20-hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen-disrupting properties raise concerns for an involvement in breast cancer. Because metastatic tumour spread is the main cause of breast cancer mortality, we have investigated the effects of triclosan on cell migration and invasion using three human breast epithelial cell lines and using concentrations comparable with those in
human tissues. Long-term exposure to 10−7 M of triclosan resulted in increased migration and invasion as measured by xCELLigence technology for all three cell
lines, for the immortalized but nontransformed MCF-10F breast epithelial cells (after 28 weeks), the oestrogen-responsive MCF-7 breast cancer cells (after 17 weeks) and
the oestrogen-unresponsive MDA-MB-231 breast cancer cells (after 20 weeks). The effects were therefore not limited to cancerous cells or to oestrogen-responsive cells. This was paralleled in the MCF-10F and MCF-7 (but not MDA-MB-231) cells by a reduction in levels of E-cadherin mRNA as measured by reverse transcription–polymerase chain reaction (RT-PCR) and of E-cadherin protein as measured by western immunoblotting, suggesting a mechanism involving epithelialto-mesenchymal transition. This adds triclosan to the increasing list of ingredients of personal care products that can not only enter human breast tissue and increase cell proliferation but also influence cell motility. If mixtures of components in household and personal care products contribute to increasing cell migration and invasion, then reduction in exposure could offer a strategy for reducing breast cancer spread
Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology
Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety ‘Mode of Action’ framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology
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Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/ mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety ‘Mode of Action’ framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology
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Exposure to environmental oestrogenic chemicals and breast cancer.
The human population is now exposed on a daily basis to a multitude of environmental pollutant chemicals that would not have been present a century ago, and many of these chemicals have been detected in the human breast. The fatty nature of human breast tissue makes it a particular target for lipophilic as well as hydrophilic pollutant chemicals, which may enter the human body through oral, respiratory, or dermal routes. These chemicals possess a range of endocrine-disrupting properties and genotoxic activity, but from a breast cancer perspective the greatest concern has centered around their ability to mimic or interfere with the action of estrogen. The breast is an endocrine target organ and exposure to estrogen is a known risk factor for breast cancer
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