Toxic Beauty Extracts: Cosmetics and Cancer

July 21, 2009 by DawnM  
Filed under Cancer

Cosmetics and Cancer

Cosmetics and Cancer

Cancer is the second leading cause of death in America, after heart disease and around one in four deaths in the EU are as a result of cancer. Cancer can be characterised as a cluster of diseases where normal cells multiply beyond normal growth mechanisms, generating millions of similar self-multiplying cells that become cancerous when they spread beyond their normal area (metastasis). There are over 100 types of cancer.

It is thought that every cancer develops from one altered cell, which fails to respond to normal attempts to control its growth, inheriting or aquiring DNA damage. Its offspring may develop and multiply to create a tumour. In most cells acquired damage is repaired and cells return to normal, or if it is not repaired, the cell does not divide, but in instances of cancer there are cell cycle errors.1

Before cancer appears two steps are believed to take place. In the initiation step a genetic change occurs in a cell and only culminates in cancer if promotion follows. This genetic change may be something that you are born with or may be created by initiators such as viruses, hormones, chronic inflammation within the body, or exogenous (external) agents such as radiation, carcinogens (cancer-causing chemicals, biological or physical agents). Promoters instigate rapid cell growth before the cell has had the chance to repair the DNA damage. Cancer promoters include chronic inflammation, radiation, hormones and environmental chemicals. Research has also suggested that extremely low frequency eletromagnetic fields (ELF-EMFs) may play a part in cancer promotion2, as does a high-fat diet and excess calorie intake.

It can take up to 20 years for cancer to appear after exposure to an initiator. If an individual is not exposed to many promoters, it may never materialise. Once the cancerous growth no longer requires exposure to a promoter, it grows independently (the progression phase). Synergism takes place when two or more substances interact, heightening each other’s effects, leading to more cancers than would be produced by the total sum of the substance’s individual effects. Exposure to certain occupational chemicals and smoking would be an example of this, or alcohol consumption and smoking.

Environmental or Genetic?

Studies have shown that environmental factors play a huge part in the onset of cancer, with only around five per cent being genetically predisposed.3 Environmental factors from this perspective can incorporate anything that people are exposed to, such as substances consumed, smoking, natural and medical forms of radiation, including exposure to the sun, workplace exposures, drugs, social and economic factors and substances existing in the air, water and soil.4 In addition, aging, alcohol, infections, hormonal factors, pollution, lack of exercise, sexual behaviour that elevates exposure to particular viruses and consumer products are all implicated in various types of cancers, to different degrees.

Chemicals and Breast Cancer

Did you know? Breast cancer is the most common cancer in women and incidences are highest in North America, Northern Europe and Australia. 5

Experts have estimated that only around 47 per cent of breast cancer incidences can be attributed to well-established risk factors (such as later age at first birth, higher family income and family history of breast cancer).6 According to Professor Andreas Kortenkamp, head of the Centre for Toxicology at the University of London, most women do not acquire breast cancer through genes but during their lifetime and although high alcohol consumption, high fat diets and other such lifestyle factors contribute to the risk of developing breast cancer, they cannot account for the huge number of newly diagnosed cases.7

Experts have estimated that only around 47 per cent of breast cancer incidences can be attributed to well-established risk factors (such as later age at first birth, higher family income and family history of breast cancer).6 According to Professor Andreas Kortenkamp, head of the Centre for Toxicology at the University of London, most women do not acquire breast cancer through genes but during their lifetime and although high alcohol consumption, high fat diets and other such lifestyle factors contribute to the risk of developing breast cancer, they cannot account for the huge number of newly diagnosed cases.7

As the Breast Cancer Fund notes in its recent report, State of the Evidence, “the increasing incidence of breast cancer over the decades following World War II paralleled the proliferation of synthetic chemicals…An important body of scientific evidence demonstrates that exposure to common chemicals and radiation may contribute to the staggering incidences of breast cancer.”8 Exposure to natural oestrogen present in the body during a lifetime is associated with breast cancer. Endocrine disrupting Compounds (EDC), which interfere with the actions of natural oestrogens, androgens and other hormones in the body, may present an increased breast cancer risk.9 Scientists at the Silent Spring Institute in Massachusetts compiled scientific data linking chemicals with breast cancer and identified, in total, 216 chemicals that have been associated with increased mammary gland tumours in animals including, industrial chemicals, chlorinated solvents, products of combustion, pesticides, dyes, radiation, pharmaceuticals, hormones, natural products and research chemicals. Almost all of the chemicals were mutagenic and the majority caused tumours in multiple organs and species.10
Some of the compounds found in personal care products that are associated with breast cancer include:

  • 1,2-propylene oxide – Used as a fragrance.
  • 1,3-butadiene – Plasticiser used in rubber sponges for cosmetic application. Cosmetic’s containers may contain this substance and it can be an impurity in butane – a propellant added to aerosol personal care products.
  • 1,4-dioxane – Petroleum derived byproduct of the ethoxylation process that can be present in shampoos, body wash and other foaming cosmetics as an impurity.
  • 2,4-diaminoanisole sulphate – An aromatic amine used in hair dyes.
  • Benzene and other organic solvents (such as toluene and formaldehyde) – Used in nail polish, nail polish remover and perfumes.
  • Bisphenol A – Synthetic chemical used in the production of epoxy resins and polycarbonate plastics, used for food, drink and cosmetic packaging.
  • Ethylene oxide – Non-ionic surfactants used in cleansing products are produced from ethylene oxide, traces of this volatile chemical may remain.
  • Synthetic musks - Synthetic chemicals commonly used in a range of fragranced consumer products, including, perfumes, aftershaves, cosmetics and personal care products as fragrances and fixatives.
  • n-nitrosamines – Nitrosamines can be formed in cosmetic products in the presence of nitrosating agents.
  • Nonylphenol – Organic compound belonging to alkylphenol family. Nonylphenols can be found in various cosmetic products (nonylphenol and nonylphenol ethoxylates banned for this purpose in the EU where they are classified as a hazard to health and environmental safety).
  • Parabens – Preservative and antimicrobials commonly used in cosmetic products.
  • Phthalates – Used as plasticisers in a range of personal care and other consumer products.
  • Placental extract – Refers to extracts from human and cow placenta found in hair conditioners, shampoos and other grooming products
  • Polycyclic aromatic hydrocarbons (PAHs) – common contaminants in petrolatum found in petroleum jelly, lipsticks, baby lotions and oils; tobacco smoke (active and passive exposures).
  • Titanium dioxide – White pigment used in sunscreens, mineral make-up and other cosmetics.
  • Triclosan – Organochlorine used as an antibacterial in soaps, toothpastes, mouthwash etc.
  • Urethrane (ethyl carbamate) – Ester of carbamic acid used as a co-solvent in hair care products, sunscreens, nail polish, mascara, foundation.

Campaigners Push for Ban on Chemicals Linked to Breast Cancer

In the EU campaigners have urged MEPS to strengthen chemicals legislation, following a report suggesting that some chemicals may be associated with rising incidences of breast cancer. Professor Andreas Kortenkamp, head of the Centre for Toxicology at the University of London, has pointed to significant evidence that the rise in breast cancer is linked to environmental exposures to substances such as hormone disruptive chemicals that mimic oestrogen. In the report commissioned by the health and environmental alliance HEAL and Chem Trust, Professor Kortenkamp said,

“There is overwhelming evidence that oestrogens are strong determinants of breast cancer risks…Given that natural oestrogens and man-made oestrogens used as pharmaceuticals have a role in breast cancer, concerns arise about the potential contribution of industrial chemicals and pesticides with hormonal activity.”11

Oestrogens are required for breast development but they also play a role in the development of breast cancer. Natural oestrogens act on the ‘end buds’ of the epithelial ducts in mammary glands to promote growth through elongation and branching of the duct system. This takes place initially during the foetal stage and then again at puberty and finally during pregnancy. It is this growth of the end buds that links oestrogens to breast cancer. Oestrogens cause an increase in cells that can be prone to cancerous growth. The breast is most susceptible to cancer causing influences during periods of growth, such as during puberty. In the womb, the mother’s oestrogen levels affect the number of end buds that develop in the foetus, with higher levels of oestrogen causing more end buds to grow, this effectively increases the cell pool from which cancer cells can be drawn.

Although Professor Kortenkamp acknowledges that numerous factors play a role in breast cancer, he continues, “There is a case for relinquishing the dominant view of breast cancer as a life-style and genetic disease and for reappraising the role of environmental factors, including chemical exposures. With UK breast cancer incidence at an all time high, risk reduction will not be achievable without considering preventable causes, particularly exposure to chemicals.”12

As well as prohibited industrial chemicals such as PCBs, still being detected in human tissues, there are a host of chemicals used in consumer products that have hormone disrupting properties, including phthalates, bisphenol A, UV filters, commonly used preservatives such as parabens, and numerous others. Many of these have been found to act in a similar way to the sex hormone oestradiol, although much higher concentrations are required to cause as pronounced effects. Environmental pollutants such as PCBS and certain pesticides do not act alone, but in combination with natural oestrogens and other hormonally active chemicals in a woman’s body, including chemicals released during the preparation of food, man-made chemicals including environmental pollutants (dioxins, pesticides, PCBs), synthetic cosmetic constituents (such as some synthetic fragrances, UV filters, antioxidants) and plant derived oestrogens present in some foods. Although the hormonal strength of these chemicals in much lower than natural or pharmaceutical oestrogens, research has shown that quite a significant number of chemicals can enhance the effects of natural oestrogens.13

Professor Kortenkamp presented evidence that whilst low levels of certain individual chemicals have no detectable impact on breast cancer, the combined additive effect of mixtures of these chemicals (even at low concentrations that would not usually present an observable effect), has a much greater impact. Testing a combination of 11 xenoestrogens (man-made chemicals that behave like oestrogen in the human body) on the actions of the hormone oestradiol, Professor Kortenkamp found that the combined effect of the xenoestrogens led to a dramatic enhancement of the hormone’s action, even when each agent was present at levels that do not individually generate measurable effects.14

Other research demonstrated than four organochlorines acted together to enhance the proliferation of human breast cancer cells, suggesting again that mixtures of certain chemicals produce a combined effect even when each agent is present at concentrations that individually produce insignificant effects. The combination effects of the mixture were stronger than the effects of the most potent individual component (thus the combined effects were synergistic).15

As well as discussing the issue of chemical mixtures, Professor Kortenkamp also noted the importance of exposure levels at different times in a woman’s life, such as development in the womb and puberty. Human studies have demonstrated that the daughters of women who took diethylstilboestrol (DES) to avoid miscarriages had an increased risk of breast cancer16 and studies on laboratory animals have suggested that exposure to synthetic oestrogenic compounds in the womb can result in persistent alterations of the mammary gland, signifying that these compounds may increase susceptibility to breast cancer 18. Professor Kortenkamp commented that the EU has funded a great deal of research on the subject but also said to CORDIS News, “this is not entirely matched by an equally well founded and well thought out regulatory approach to complement this, to act on the basis of scientific evidence.”19

This report is being examined by MEPs in Brussels who are presiding over whether Europe-wide legislation could help stall the rising incidences of breast cancer, which have increased by 50 per cent in some European countries over the last 20 years.20

Carcinogens in Cosmetics

Mainstream beauty products contain a variety of known carcinogenic or potentially carcinogenic ingredients such as p-phenylenediamine, diethanolamine (DEA), acetaldehyde, certain azo and coal tar dyes, butylated hydroxyanisole (BHA), adipic acid, ethyl acrylate, organic solvents (such as formaldehyde, benzene and toluene) and lead acetate. Additionally they may contain impurities in the form of nitrates which can react with other ingredients in the product to form carcinogenic substances, for example, nitrosodiethanolamine. Chemicals such as diazolidinyl urea, Imidazolidinyl urea, DMDM Hydantoin and quaternium 15 degrade to release the suspected carcinogen formaldehyde, and polyethylene glycol (PEG) can be contaminated with the carcinogens, 1,4-dioxane and ethylene oxide, to name but a few.

Carcinogenic or potentially carcinogenic chemicals may only be used in cosmetic products at low concentrations, but we commonly use a myriad of cosmetic products and numerous other consumer products containing cancer-causing ingredients. We are also exposed to many other carcinogens in our environment. Our exposure to cosmetic products is over a prolonged period of time and even prior to birth we are exposed to carcinogenic agents, through our mother’s use of cosmetic and other consumer products.

The skin is highly permeable to toxic substances. According to Dr Samuel Epstein, chairman of the Cancer Prevention Coalition and author of The Safe Shopper’s Bible and Unreasonable Risk, evidence presented at a 1978 Congressional hearing, suggested that skin absorption of nitrosodiethanolamine (NDELA) is 100 times greater than absorption by mouth.21 Dr Epstein points out that carcinogens taken in by mouth are absorbed from the intestines and transported to the liver, where they can be detoxified to different degrees, depending on the substance, but carcinogens absorbed through the skin reach can enter the bloodstream without this prior protective detoxification by the liver.22

In addition, numerous substances, known as penetration enhancers, increase the skin’s absorption of toxic ingredients, these include: sodium lauryl sulphate, polyethylene glycol (PEG), propylene glycol (PPG), acetone, cetereath compounds (including cetereath-12 and cetereath-20), cocoyl sarcinosine, ethanol, limonene, lactic acid and disodium EDTA.

Many studies have found that the risk of cancer developing is elevated if exposure to carcinogens begins in infancy, rather than later on in life. Young children have a greater susceptibility to carcinogens because the cells rapidly divide during childhood and if they are rapidly dividing following exposure to a carcinogen, any genetic mutation that has occurred is more likely to be fixed.23 There are various other reasons why babies, young infants and children are at greater risk. For instance, children take in more oxygen per kilogram of body weight than an adult and therefore more air pollutants, low molecular weight compounds can readily cross the placenta, newborn babies have more absorbative skin because it is not fully keratinised (therefore without one of the skin’s main protective barriers) until several days after the baby is born and various organs such as the lungs and brain are still developing. Children have different exposures, pathways of absorption, tissue distribution and responses to environmental exposures, and they also eliminate chemicals in different ways.24 This all needs to be considered when looking at the potential adverse health effects of environmental exposures.

The U.S. National Toxicology Program (NTP), an interagency program that evaluates agents of public health concern, produce a report on carcinogens (ROC), which currently contains 246 listings of known and reasonably anticipated human carcinogens.25 Our households and other external environments play host to a variety of known and potential carcinogens. Some of those listed substances we may commonly encounter that are known or suspected of causing cancer, according to the U.S. National Toxicology Program, include:

  • Tobacco
  • Red and preserved meats
  • Salt
  • Salt-preserved foods
  • Alcoholic beverages
  • UV radiation from the sun
  • Sunlamps or tanning beds
  • Viruses and bacteria
  • Ionising radiation - from sources such as radon
  • Radioactive substances - released by atomic bombs or nuclear weapons, and x-rays
  • Pesticides - such as ethylene oxide, DDT, amitrole, hexachlorobenzene, lead acetate and lindane
  • Medical drugs - such as cyclophosphamide and chlorambucil used to treat cancer
  • Oestrogens - long-term users of combined oestrogen and progesterone oral contraceptives may have an increased risk of early-onset breast cancers and liver cancer; tamoxifen may also increase the risk of developing endometrial cancer
  • Solvents - such as benzene, chloroform, methylene chloride and trichloroethylene
  • Fibres
  • Fine particles and dust - such as asbesto fibres, ceramic fibres, wood dust and silica dusts
  • Dioxins
  • Polycyclic aromatic hydrocarbons
  • Metals - such as arsenic, beryllium compounds, cadmium metal and cadmium compounds, chromium, lead and nickel
  • Diesel exhaust particles
  • Toxicants from fungi
  • Vinyl chloride
  • Benzidine.

  • Known and potentially carcinogenic ingredients in cosmetics include among other things:

  • Acetaldehyde
  • Acrylates
  • Butylated Hydroxyanisole (BHA)
  • Butylated Hydroxytoluene (BHT)
  • Coal tar
  • Hydroquinone
  • Synthetic musks (used in fragranced consumer products)
  • Teflon
  • Organic solvents (e.g. toluene, formaldehyde, xylene)
  • Phthalates
  • UV filters in sunscreens (e.g. padimate O, para-aminbenzoic acid (PABA), oxybenzone, avobenzone).
  • Cosmetic grade lanolin
  • Hair dyes
  • Parabens
  • Talc
  • Silica
  • Diethanolamine (common ingredients containing diethanolamine (DEA) include: cocamide DEA, cocamide MEA, Lauramide DEA, Myristamide DEA, Oleamide DEA etc)
  • Artificial colours

Some carcinogenic impurities (not listed on the label)

  • Acrylamides
  • 1,4-dioxane
  • Nitrosamines
  • Ethylene oxide
  • Formaldehyde
  • Polycyclic Aromatic Hydrocarbons (PAHs)

For more info Toxic Beauty is available from Amazon and book stores nationwide.

1. Klatz, R., Goldman, B., The Science of Anti-Aging Medicine, The American Academy of Anti-Aging Medicine, January 2003, p10.
2. Tenenbaum, D.J., A New View of ELF-EMFs: Are they Linked with Cancer Promotion?, Environmental Health Perspectives, October, 2000: 108 (10): 469.
3. ‘Cancer Facts and Figures 2004: Basic Cancer Facts,’ American Cancer Society (ACS); accessed September 25, 2008; online at: www.cancer.org.
4. ‘Assessment of Technologies for Determining Cancer Risks From the Environment,’ OTA (Office of Technology Assessment), U.S. Government Printing Office, Washington, DC, June, 1981; online at: http://govinfo.library.unt.edu.
5. Brody, J.G., Rudel, R.A., Environmental Pollutants and Breast Cancer, Environmental Health Perspectives, June 2003: 111 (8): 1007-1019.
6. Madigan, M.P. et al, Proportion of Breast Cancer Case in the United States Explained by Well-established Risk Factors, Journal of the National Cancer Institute, 1995: 87 (22): 1681-1685.
7. Kortenkamp, A., ‘Environmental Contaminants and Breast Cancer: The Growing Concerns about Endocrine Disrupting Chemicals,’ Produced for The World Wildlife Fund (WWF), October 2006; online at: www.wwf.org.uk.
8. ‘State of the Evidence: The Connection Between Breast Cancer and the Environment,’ Fifth Edition, Breast Cancer Fund, 2008; online at: www.breastcancerfund.org.
9. ‘State of the Evidence: The Connection Between Breast Cancer and the Environment,’ Fifth Edition, Breast Cancer Fund, 2008; online at: www.breastcancerfund.org.
10. Rudel, R.A. et al, Chemicals Causing Mammary Gland Tumours in Animals Signal New Directions for Epidemiology, Chemicals Testing, and Risk Assessment for Breast Cancer Prevention, Cancer, June, 2007: 109 (12): 2635-66.
11. Kortenkamp, A., ‘Breast Cancer and Exposure to Hormonally Active Chemicals: An Appraisal of the Scientific Evidence’, A Background Briefing Paper for the Health and Environmental Alliance (HEAL) and CHEMTrust, April, 2008: online at: www.chemtrust.org.
12. Kortenkamp, A., ‘Breast Cancer and Exposure to Hormonally Active Chemicals: An Appraisal of the Scientific Evidence’, A Background Briefing Paper for the Health and Environmental Alliance (HEAL) and CHEMTrust, April, 2008: online at: www.chemtrust.org.
13. Kortenkamp, A., ‘Environmental Contaminants and Breast Cancer: The Growing Concerns about Endocrine Disrupting Chemicals,’ Produced for The World Wildlife Fund (WWF), October, 2006: online at: www.wwf.org.uk.
14. Rajapakse, N., Silva, E., Kortenkamp, A., Combining Xenoestrogens at Levels below Individual No-Observed-Effect Concentrations Dramatically Enhances Steroid Hormone Action, Environmental Health Perspectives, September 2002: 110 (9): 917-921.
15. Payne, J., Scholze, M., Kortenkamp, A., Mixtures of Four Organochlorines Enhance Human Breast Cancer Cell Proliferation, Environmental Health Perspectives, April, 2001: 109 (4): 391-397.
16. Palmer, J.R. et al, Prenatal Diethylstilbestrol Exposure and Risk of Breast Cancer, Cancer Epidemiology, Biomarkers and Prevention, August, 2006: 15 (8): 1509-1514.
17. Munoz-de-Toro, M. et al, Perinatal Exposure to Bisphenol-A Alters Peripubital Mammary Gland Development in Mice, Endocrinology, 2005: 146 (9): 4138-4147.
18. Maffini, M.V., Endocrine Disruptors and Reproductive Health: The case of Bisphenol-A, Molecular and Cellular Endocrinology, 2006: 255-254: 179-186.
19. ‘Campaigners Urge Politicians to Act on Chemicals-Breast Cancer Link,’ CORDIS News, April 3, 2008; online at: http://cordis.europa.eu/news/home_en.html.
20. Batty, D., ‘Campaigns Urge Ban on Cancer-Link Chemicals,’ The Guardian, April 2, 2008; online at: www.guardian.co.uk.
21. Epstein, S.S., Unreasonable Risk: How to Avoid Cancer and Other Toxic Effects, from Cosmetics and Personal Care Products: The Neway’s Story, Second Edition, Environmental Toxicology Inc, 2005, p41.
22. Epstein, S.S., Unreasonable Risk: How to Avoid Cancer and Other Toxic Effects, from Cosmetics and Personal Care Products: The Neway’s Story, Second Edition, Chicago: Environmental Toxicology Inc, 2005, p43.
23. ‘Intolerable Risk: Pesticides in our Children’s Food, Natural Resources Defense Council, February 27, 1989; online at: www.tobaccodocuments.org.
24. Bearer, C.F., How are Children Different from Adults?, Environmental Health Perspectives, 1995: 103 (6): 7-12.
25. ‘Report on Carcinogens: Eleventh Edition,’ U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program (NTP), Research Triangle Park, NC; accessed September 25, 2007; online at: http://ntp.niehs.nih.gov. And email from C.W. Jameson, Ph.D., Director, Report on Carcinogens, DHHS, NIH, NIEHS, September 25, 2007.

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