Dr Dingle's Blog / dangerous beauty

Environmental Estrogens and Endocrine Disrupting Chemicals (EDC's)

Environmental Estrogens and Endocrine Disrupting Chemicals (EDC's)

Since the 1980's, there has been a growing amount of research toward the potential interaction between these environmental estrogens and wild animals, with a number of reports detailing the emergence of 'feminised wildlife’ around the world, and a range of adverse effects in humans including decreased sperm count, increased cases of testicular cancer and testicular abnormalities, increased breast cancer in men and women and premature or precocious puberty. Other adverse health outcomes linked with EDC’s include headache, migraine, depression, gastrointestinal disturbances, insomnia, changes in breast tissue and in vaginal bleeding. More chronic symptoms affect the cardiovascular system, the skin (itching, rash, abnormal pigmentation), the gallbladder, and tumours particularly of the breast but also uterus, cervix, vagina and liver. While other studies have shown increases in the organ weight of estrogen-sensitive tissues such as the uterus, and calcium and bone metabolism are all examples of the estrogenic effects. Even how we age and age at menopause can be affected by these chemicals. In support of this at least one professional and very conservative group, the Endocrine Society, has concluded that sufficient evidence now exists linking endocrine disrupting chemicals (EDCs) to adverse human reproductive effects, including possible epigenetic and trans-generational effects.

Unfortunately, our babies are being born pre-polluted with chemicals detectable in their blood, in the placenta and in amniotic fluid because of exposure to these chemicals during pregnancy and throughout the mother’s life. The placental barrier has been shown to allow these chemicals to cross, as many of them have been measured in human fetal cord blood, fetal serum, human amniotic fluid and even newborn stools (meconium). Exposure to these chemicals before birth poses a serious health risks to developing fetus, infants and young children as shown by the increasing adverse effects including negative birth outcomes, childhood obesity and increasing intellectual disabilities. It is believed that current levels of environmental estrogen exposure results in lower birth weights, smaller head circumferences, poorer neuromuscular maturity and visual recognition, delays in psychomotor development, short term memory problems, and growth retardation in newborn babies. Fetal exposure to these environmental estrogens are suspected of disrupting thyroid functioning, sexual differentiation of the brain in foetal development and cognitive motor function and cause anxious behaviour. They are also able to bind to neurotransmitters such as epinephrine, neuroepinophrine and dopamine enabling estrogens to influence the body's central nervous system (CNS). Environmental estrogens have also been shown to effect the body’s immune system.

Studies have found strong links with exposure to excessive levels of estrogen in males with penis abnormalities, lower libido, congenital anomalies, failure of the testes to descend and testicular cancer, reduced penis size and increased embryo mortality.

What is most concerning regarding control of these chemicals is that there are no indications given or regulations set regarding the minimal age at which they should be used or exposed to them. Increasingly, pregnant mothers, infants, pre-pubescent and pubescent children are being exposed to a large number of products containing these chemicals, with no research to show that exposure is safe during these critical periods of development.

Equally strong is the evidence that these same chemicals can cause some of the most common cancers: prostate and testicular cancer in men and breast cancer in women. One of the most troubling is their association with breast cancer. Breast cancer is the major cancer affecting women in the Western world and one of the most disturbing and well documented current trends is the alarming increase in breast cancer incidence over the past few decades. Fifty years ago the risk rate was one woman in 20; today it is one in 8 and approximately two-thirds of breast tumors are estrogen receptive, and environmental estrogens like parabens, phthalates and BPA are known to bind to estrogen receptors. Estrogen-dependent cancers, such as breast cancer, are known to be highly responsive to estrogens for growth. Even more disturbing is the increase in numbers of young girls developing breast cancer.

 

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Common household disinfectants linked with birth defects, miscarriages and fertility.

Common household disinfectants linked with birth defects, miscarriages and fertility.

Quaternary ammonium compounds (QACs) are antimicrobial disinfectants commonly used in commercial and household settings and everyone is virtually exposed to these chemicals every day. Two common quaternary ammonium compounds, alkyldimethylbenzyl ammonium chloride (ADBAC) and didecyldimethyl ammonium chloride (DDAC), are combined in common cleaners and disinfectants.

In this study introduction of a cleaner containing ADBAC+DDAC in the living chambers caused neural tube defects (NTDs) in mice and rats. They found increased neural tube defects with exposure to the disinfectant combination in both rats and mice. The neural tube defects persisted for two generations after cessation of exposure.

They also found that male exposure alone was sufficient to cause neural tube defects. Equally significant, ambient exposure from disinfectant use in the cage they were kept in, influenced the levels of neural tube defects to a greater extent than oral dosing. So the ambient exposure through the air and surfaces had more impact than the feeding.

These results clearly demonstrate that ADBAC+DDAC in combination are teratogenic (birth defects) to rodents. Given the increased use of these disinfectants, further evaluation of their safety in humans and their contribution to health and disease is essential.

Quaternary ammonium compounds (QACs) are a large class of chemicals used for their antimicrobial and antistatic properties. They are common ingredients in cleaners and disinfectants, hand wipes, food preservatives, swimming pool treatments, laundry products, shampoos, conditioners, eye drops, and other personal care products. QACs have been in use for over 60 years, but the number of products containing QACs has increased recently as the versatility of these compounds is recognized. Over time, the chemical structure has been altered to increase antimicrobial and surfactant efficacy resulting in multiple generations of these products. Many products now contain a combination of two or more QACs. Extensive use of QACs results in ubiquitous human exposure, yet reproductive toxicity has not been evaluated.

Because chemical mixtures can act synergistically to produce greater toxic effects than the sum of the individual components, evaluation of common mixtures is essential in the evaluation of chemical risk.

This study was initiated because some laboratories which breed and test with mice and rats had noticed some anomalies. One laboratory noted abrupt declines in mouse colony productivity, along with declines in fetal health, that coincided with the introduction of disinfectants containing the QACs, alkyl dimethyl benzyl ammonium chloride (ADBAC) and didecyl dimethyl ammonium chloride (DDAC). Several years later, the laboratory encountered breeding problems and neural tube birth defects (NTDs) that began shortly after a change in room disinfectants. These experiences pointed to the QAC disinfectant but could not confirm toxicity because neither incident tested QACs under experimental conditions.

In an earlier study by the same team reproductive studies demonstrated that QACs adversely affect both male and female fertility and fecundity in rodents (Melin et al., 2014, 2016). Decreased reproductive performance in laboratory mice coincided with the introduction of a disinfectant containing both alkyl dimethyl benzyl ammonium chloride (ADBAC) and didecyl dimethyl ammonium chloride (DDAC). QACs were detected in caging material over a period of several months following cessation of disinfectant use. Breeding pairs exposed for six months to a QAC disinfectant exhibited decreases in fertility and fecundity: increased time to first litter, longer pregnancy intervals, fewer pups per litter and fewer pregnancies. Significant morbidity in near term dams was also observed. In summary, exposure to a common QAC disinfectant mixture significantly impaired reproductive health in mice.

 

Source 1

Ambient and dosed exposure to quaternary ammonium disinfectants causes neural tube defects in rodents. Hrubec TC et al 15 June 2017. http://onlinelibrary.wiley.com/doi/10.1002/bdr2.1064/full

Source 2

Exposure to common quaternary ammonium disinfectants decreases fertility in mice.

Melin VE1, Potineni H1, Hunt P2, Griswold J2, Siems B3, Werre SR4, Hrubec TC5.Reprod Toxicol. 2014 Dec;50:163-70. doi: 10.1016/j.reprotox.2014.07.071. Epub 2014 Aug 14.

 

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Common household disinfectants linked with birth defects, miscarriages and fertility.

Common household disinfectants linked with birth defects, miscarriages and fertility.

Quaternary ammonium compounds (QACs) are antimicrobial disinfectants commonly used in commercial and household settings and everyone is virtually exposed to these chemicals every day. Two common quaternary ammonium compounds, alkyldimethylbenzyl ammonium chloride (ADBAC) and didecyldimethyl ammonium chloride (DDAC), are combined in common cleaners and disinfectants.

In this study introduction of a cleaner containing ADBAC+DDAC in the living chambers caused neural tube defects (NTDs) in mice and rats. They found increased neural tube defects with exposure to the disinfectant combination in both rats and mice. The neural tube defects persisted for two generations after cessation of exposure.

They also found that male exposure alone was sufficient to cause neural tube defects. Equally significant, ambient exposure from disinfectant use in the cage they were kept in, influenced the levels of neural tube defects to a greater extent than oral dosing. So the ambient exposure through the air and surfaces had more impact than the feeding.

These results clearly demonstrate that ADBAC+DDAC in combination are teratogenic (birth defects) to rodents. Given the increased use of these disinfectants, further evaluation of their safety in humans and their contribution to health and disease is essential.

Quaternary ammonium compounds (QACs) are a large class of chemicals used for their antimicrobial and antistatic properties. They are common ingredients in cleaners and disinfectants, hand wipes, food preservatives, swimming pool treatments, laundry products, shampoos, conditioners, eye drops, and other personal care products. QACs have been in use for over 60 years, but the number of products containing QACs has increased recently as the versatility of these compounds is recognized. Over time, the chemical structure has been altered to increase antimicrobial and surfactant efficacy resulting in multiple generations of these products. Many products now contain a combination of two or more QACs. Extensive use of QACs results in ubiquitous human exposure, yet reproductive toxicity has not been evaluated.

Because chemical mixtures can act synergistically to produce greater toxic effects than the sum of the individual components, evaluation of common mixtures is essential in the evaluation of chemical risk.

This study was initiated because some laboratories which breed and test with mice and rats had noticed some anomalies. One laboratory noted abrupt declines in mouse colony productivity, along with declines in fetal health, that coincided with the introduction of disinfectants containing the QACs, alkyl dimethyl benzyl ammonium chloride (ADBAC) and didecyl dimethyl ammonium chloride (DDAC). Several years later, the laboratory encountered breeding problems and neural tube birth defects (NTDs) that began shortly after a change in room disinfectants. These experiences pointed to the QAC disinfectant but could not confirm toxicity because neither incident tested QACs under experimental conditions.

In an earlier study by the same team reproductive studies demonstrated that QACs adversely affect both male and female fertility and fecundity in rodents (Melin et al., 2014, 2016). Decreased reproductive performance in laboratory mice coincided with the introduction of a disinfectant containing both alkyl dimethyl benzyl ammonium chloride (ADBAC) and didecyl dimethyl ammonium chloride (DDAC). QACs were detected in caging material over a period of several months following cessation of disinfectant use. Breeding pairs exposed for six months to a QAC disinfectant exhibited decreases in fertility and fecundity: increased time to first litter, longer pregnancy intervals, fewer pups per litter and fewer pregnancies. Significant morbidity in near term dams was also observed. In summary, exposure to a common QAC disinfectant mixture significantly impaired reproductive health in mice.

 

Source 1

Ambient and dosed exposure to quaternary ammonium disinfectants causes neural tube defects in rodents. Hrubec TC et al 15 June 2017. http://onlinelibrary.wiley.com/doi/10.1002/bdr2.1064/full

Source 2

Exposure to common quaternary ammonium disinfectants decreases fertility in mice.

Melin VE1, Potineni H1, Hunt P2, Griswold J2, Siems B3, Werre SR4, Hrubec TC5.Reprod Toxicol. 2014 Dec;50:163-70. doi: 10.1016/j.reprotox.2014.07.071. Epub 2014 Aug 14.

 

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2017 Dr Dingle’s February Wellness Presentations.

2017 Dr Dingle’s February Wellness Presentations.

7.00 -9.00 PM. Wednesday nights

445 Charles St North Perth

$12 online/$20 at the door www.drdingle.com

February 1, 2017 : Probiotics, People and Poo 

http://tix.yt/probiotics   February 8, 2017 : Reducing Toxic Overload in our Kids 

http://tix.yt/toxic-kids February 15, 2017 : 7 Steps To Permanent Weight Loss 

http://tix.yt/7stepstoweightloss

February 22, 2017 : Living Longer, Ageing Well. The science of living a full life http://tix.yt/ageingwell

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Reducing toxic chemical exposure reduces the risk of diabetes

Reducing toxic chemical exposure reduces the risk of diabetes

New research suggests that a 25% reduction in exposure to just 4 chemicals commonly found in the home would reduce diabetes cases by around 13% which could save billions of dollars in annual health costs.
 
Increasing evidence suggests that synthetic chemicals commonly found in the environment contribute to metabolic disorders, especially obesity and diabetes. Previous publications have associated prevalent diabetes with polychlorinated biphenyls (PCBs), persistent chlorinated pesticides, phthalates and perfluoroalkyl substances (PFASs). Separate studies found similar connections between diabetes and exposure to DDT, PCBs and perfluoroalkyl.

In this study of 1,016 participants they found significant connections between the four chemicals investigated and a number of different diseases and found reduced exposure to all four chemicals would lead to a likely reduction 13% in diabetes cases. This study confirms substantial contribution, especially of mixtures of endocrine-disrupting chemicals, to adult type 2 diabetes, and large annual costs of medical care. A previous reported a significant positive relationship between phthalates in the blood and lowered insulin secretion, increased insulin resistance or both.
    
While this study supports efforts to reduce chemical exposures to reduce the burden and costs of diabetes there are many other disease states including cardiovascular disease and cancer that would also likely be reduced.

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Toxic chemicals cause weight gain

Toxic chemicals cause weight gain

Exposure to “obesogenic” chemicals has an important role in the obesity and diabetes pandemic. Studies dating back to the 1970s have shown that low-dose chemical exposures were associated with weight gain in experimental animals. Since then, a growing number of studies show links between toxins and weight gain, obesity and diabetes. Known or suspected culprits behind negative epigenetic changes include toxins such as heavy metals, pesticides, plastic compounds including BPA, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria and endocrine disrupting chemicals.

The main role of fat cells is to store energy and release it when needed. Scientists now know that fat tissue acts as an endocrine (hormone) organ, releasing hormones related to appetite and metabolism. Research to date suggests that different obesogenic compounds may have different mechanisms of action, some affecting the number of fat cells, others the size of fat cells, and still others the hormones that influence appetite, satiety, food preferences, and energy metabolism. Another mechanism through which these chemical obesogens can contribute to weight gain is through their impact on the gut microbiome, linking gut ecology and environmental chemicals to obesity and diabetes.

BPA, or bisphenol-A, a chemical found in everything from plastic bottles to metal food containers, may be partly to blame for our excess weight. BPA has been shown to alter the body’s metabolism, increasing weight gain and making it difficult to lose weight. In a study of 1,326 children, girls between ages 9 and 12 with high BPA levels had double the risk of being obese than girls with low BPA levels, validating previous animal and human studies. The chemical can alter the body’s metabolism and make it harder to lose weight. Girls with high levels of BPA, two micrograms per litre or more, were twice as likely to be obese as girls with lower levels of BPA in the same age group. Girls with very high levels of BPA, more than 10 micrograms per litre, were five times more likely to be obese, the study showed. In animal experiments, a mother’s exposure to BPA is producing the same outcomes that we see in humans born light at birth: an increase in abdominal fat and glucose intolerance. BPA affected rodent fat cells at very low doses, 1,000 times below the dose that regulatory agencies presume causes no effect in humans.

A growing body of evidence shows that the use of certain pesticides may also be associated with weight gain and diabetes risk. In animal experiments, mice fed high-fat diets gained about 30% more weight and had higher blood sugar than other mice eating the same high-fat diets when they also ingested doses of a brominated flame retardant, hexabromocyclododecane (HBCD), which is used in building materials and insulation. Perfluorooctanoic acid (PFOA) is a ubiquitous chemical, used in non-stick cookware, Gore-Tex™ waterproof clothing, Scotchgard™ stain repellent on carpeting and mattresses and is a potential endocrine disruptor. Researchers gave pregnant mice PFOA during pregnancy and when the offspring reached adulthood, they became obese, reaching significantly higher weight levels than controls. Phthalates are plasticizers that have been related to obesity in humans and occur in many PVC items as well as in scented items such as air fresheners, laundry products, and personal care products, and many plastics.
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Environmental Estrogens in cosmetics and personal care products. Breast Cancer and Toxicity

Environmental Estrogens in cosmetics and personal care products.  Breast Cancer and Toxicity

It is estimated that in the world today, there are at least 120,000 synthetic chemicals, or xenobiotics registered for commercial use and around 1,000 new chemicals are formulated each year. While many have been proven to be highly toxic and carcinogenic, little is known about the chronic effects particularly their potential to alter, or disrupt the function(s) of the endocrine system and our hormones. These synthetic chemicals are known as 'environmental estrogens', estrogen mimics, or xenoestrogens and have been found to affect hormonal functions by 'mimicking' the function of naturally occurring estrogen in the body.

Estrogens are a group of naturally occurring hormones present in both male testes and female ovaries, with females producing a considerably higher amount. They are particularly influential during puberty, menstruation and pregnancy; however they also assist in regulating the growth of bones, skin, liver and organs of the cardiovascular system. Estrogens, like all hormones, act as chemical signals and are important in helping cells in various organs to sense and respond to changing physiological conditions; therefore the right balance of hormones is critical in order to carry out the functions required of a healthy, strong body. Estrogen binds to a protein, or estrogen receptor, and the estrogen receptor complex can then bind to specific genes and by this, alter the way they are expressed, resulting in a change in cell programming 1.

Environmental estrogens, are now present in everyday products such as polycarbonate plastics, food packaging and cans. However the greatest source for many people is through cosmetics and personal care products and include chemicals such as triclosan, cyclosiloxanes, parabens and phthalates which are often left on the skin to absorb and accumulate 2. Women are disproportionately exposed to many environmental estrogens like paraben and phthalates because they use more personal care products on average than men 3 and teenage girls tend to use even more products than women, averaging 17 different products per day, compared with 12 for women 4.

Since the 1980's, there has been a growing amount of research toward the potential interaction between these environmental estrogens and wild animals, with a number of reports detailing the emergence of 'feminised wildlife’ around the world, and a range of adverse effects in humans including decreased sperm count, increased cases of testicular cancer and testicular abnormalities, increased breast cancer in men and women and premature or precocious puberty. Other adverse health include headache, migraine, depression, gastrointestinal disturbances, insomnia, mastopathia, changes in vaginal bleeding 5. More chronic symptoms affect the cardiovascular system, the skin (itching, rash, abnormal pigmentation), the gallbladder, and tumours, particularly of the breast but also uterus, cervix, vagina and liver 5.

One of the most troubling is their association with breast cancer 6,7,8. Breast cancer is the major cancer affecting women in the Western world 9 and one of the most disturbing and well documented current trends is the alarming increase in breast cancer incidence over the past few decades. Fifty years ago the risk rate was one woman in 20; today it is one in 8 and approximately two-thirds of breast tumors are estrogen receptive, and environmental estrogens like parabens are known to bind to estrogen receptors. Estrogen-dependent cancers, such as breast cancer, are known to be highly responsive to estrogens for growth. Even more disturbing is the increase in numbers of young girls developing breast cancer. Although many factors such as radiation, alcohol, smoking and diet, add to the risk of developing breast cancer, the predominant influencing factor has been identified as the exposure to estrogens throughout an individual's lifetime 9.

The breast is under hormonal control and a fine balance of hormones is what allows the cell to cell communication. Interaction between these cells and the surrounding fluid of the breast tissue is what controls differentiation and growth of the breast 9. If there is a disruption of those hormones, i.e. through the use of synthetic chemicals, the balance of hormonal control is thrown and the cells do not function normally which may lead to breast cancer. In support of this clinical studies show that estrogen has the capacity to drive breast tumours to grow in laboratory studies. Animal experimental studies have also shown the role of estrogen on the growth of breast cancer cells 9. While chemicals which mimic estrogen have been shown to promote and stimulate the proliferation of breast cancer cells 2,10,11, and activate other processes involved in breast cancer 2,11,12. Recent studies have also shown other factors can dramatically increase the the toxicity of Xenoestrogens and studies of individual estrogens may seriously underestimate their growth and spreading effects in breast tissue cells and their potency to promote breast cancer, particularly at lower doses 13.

Although the vast majority of studies on breast cancer are aimed towards women, men can also suffer from the disease, indicating that they have similar risk factors, with one case in a hundred diagnosed breast cancers being a male 14. Although this number is relatively small, the rate of incidence has increased by 25% in 25 years.

Sperm count of the average male in the US or Europe has been found to be declining continuously over the past four decades, dierectly linked with environmental estrogen exposure, and today it is less than 50% of what it was forty years ago15,16. One result of this lower count is the increased rate of male infertility; which is also the single most common cause of infertility. The rate of infertility has quadrupled in the past forty years, from 4% in 1965 to at least 16% today 15.

Other conditions including undescended testes caused by prenatal estrogen exposure to environmental estrogens have also been found in studies on mice and it has been suggested undescended testes increases the rate of testicular cancer 17. The incidence of testicular cancer, namely affecting males between the ages of 20 to 30, has also seen an increase worldwide. Studies have found strong links with exposure to excessive levels of estrogen with hypospadias (abnormal congenital opening of male urethra upon under surface of the penis) 18,19, lower libido 19, congenital anomalies, cryptorchidism and testicular cancer 20,21,22.

Environmental estrogens have also been linked to early puberty in girls and increasing number of girls experiencing precocious puberty in recent years 15. A study in the United States of 17, 000 girls indicated that 7% of white and 27% of black girls exhibited physical signs of puberty by age seven, and for girls aged 10 the percentages increased to 68 and 95 respectively 16. This trend for earlier puberty has been found to be widespread, with similar cases found in the United Kingdom, Canada and New Zealand (Trankina, M. V L., 2001).

Environmental estrogens are also suspected of disrupting thyroid functioning, sexual differentiation of the brain in foetal development and cognitive motor function 23. It is also believed that high levels of environmental estrogen exposure results in lower birth weights, smaller head circumferences, poorer neuromuscular maturity and visual recognition, delays in psychomotor development, short term memory problems, and growth retardation in newborn babies 24.

Prenatal exposure to environmental estrogens also poses a serious health risks to developing fetus and children as evidence of adverse effect on birth outcomes, childhood obesity, and intellectual disability are increasing 25. The placental barrier has been shown to allow these chemicals to cross as many of them have been measured in human fetal cord blood and tissue. More importantly, because organogenesis begins at the time when the fetus is solely dependent on maternal supply, early life exposure to environmental estrogens may lead to adverse short or long term health outcomes due to fetal reprogramming 26.

From testing on animals it has further been proposed that excessive estrogen levels could cause anxious behaviour 27,28, altered fecundency 29, reduced penis size 30 and increased embryo mortality 24. Environmental estrogens are not only capable of binding to estrogen receptors on cell membranes but are also able to bind to neurotransmitters such as epinephrine, neuroepinophrine and dopamine enabling estrogens to influence the body's central nervous system (CNS) 31. Environmental estrogens have also been shown to effect the body’s immune system 30. A large number of studies have also environmental estrogens to contributing to obesity and diabetes, independent of poor diet and physical inactivity; such chemicals including ingredients found in personal care products and cosmetics such as phthalates and phenols 32,33.

More recently studies have found effects of direct exposure to products instead of just individual chemicals. Extensive observational studies have indicated a relationship between certain hair product use and hormonally imbalances including early menache (puberty) 34,35 and uterine fibroids  36 as well as enlargement of breast tissue in boys and men 37.

 

However, estrogenic (or anti-estrogenic) effects of the personal care products as commercial mixtures have rarely ever been evaluated. In a study of eight commonly used hair and skin products four of the eight personal care products tested (Oil Hair Lotion, Extra-dry Skin Lotion, Intensive Skin Lotion and Petroleum Jelly demonstrated detectable estrogenic activity 38. The estrogenic activity of these products was not predictable by examining their listed ingredients. However, perhaps the most surprising finding about any one product was the estrogenic activity of SP4 (Petroleum Jelly). Petroleum jelly products are also often used on infants as low-cost therapies for common problems such as diaper rash and is manufactured by refinement of the crude petroleum product. While other studies have shown that hair oil use as a child was significantly associated with earlier menarche and hair relaxer use and uterine fibroids among participants in the 36. A third study found an elevated incidence of endometriosis and use of personal care products containing benzophenone-type UV filters 39.

 

Fortunately, studies have also shown it is relatively easy to reduce exposure by reducing personal care use or using safer products. In one study of around 100 girls they replaced their personal care products with safer alternatives for 3 days. The replacement products were chosen on the basis of whether their ingredient lists included triclosan, benzophenone-3, or parabens. Phthalates are not listed on ingredient lists, but they are often found in scented products. So the researchers avoided products that listed “fragrance” as an ingredient unless they were specifically labeled as phthalate free.  More than 90% of the participants had detectible levels of phthalates, parabens, and benzophenone-3 before they started using the replacement products. After using the alternative products for 3 days urinary concentrations of methyl and propyl paraben decreased by 43.9% and 45.4%, respectively, mono-ethyl phthalate decreased by 27.4%, and triclosan decreased by 35.7%. However, there were increases in concentrations of butyl and ethyl paraben, which were detected in about half the girls. These chemicals might have been unintentional contaminants or unlabeled ingredients in replacement products, which they acknowledge they were unable to ensure were paraben free 40.

 

 

  1. McLachlan, J. A. & Arnold, S. F., 1996
  2. Darbre, 2003
  3. February 2015
  4. 24 September 2008
  5. Ternes et al 2004
  6. Darbre and Harvey 2008;
  7. Vandenberg et al. 2012;
  8. Zoeller et al. 2012
  9. Darbe 2006
  10. Okubo et al. 2001;
  11. Wróbel and Gregoraszczuk 2013
  12. Gomez et al. 2005
  13. Pan S, et al 2016
  14. Williams, R. M., 2004
  15. Sax, L., 2001,
  16. Trankina, M. L., 2001
  17. Christiansen et al, 1996
  18. Paulozzi 1999
  19. Calzolari et al, 1986
  20. MeLachian et al, 1984)
  21. Rapp, 1996
  22. Bernstein, 1988
  23. Ayotte and Bonefeld‑Jorgensen, 2003
  24. Trankina, 2003
  25. Godoy, et al. 2014
  26. Skinner M. K., et al. 2011
  27. Arabo et al, 2005
  28. Caston et al, 2001
  29. Vos et al, 2000),
  30. Brooks et al, 2007
  31. Fuentes et al, 2000
  32. Song Y, et al 2014;
  33. Carwile JL, et al 2011
  34. James-Todd. 2011
  35. Tiwary CM. 1998
  36. Wise LA, 2012
  37. Gottswinter JM, 1984
  38. Myers et al 2015
  39. Kunisue T, et al. 2012
  40. Harley KG, et al. 2016

 

 

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Deadly deodorants

Deadly deodorants

In November 2008, a 12 year old boy, Daniel Hurley collapsed and died in his bathroom 'after using too much deodorant'. The hearing into his death found that “he was overcome by solvents in the Lynx Vice spray”. Unfortunately there were no repercussions for the company as the warnings are spelt out on the can. Despite the warning being there, my own research shows that around 1% of people actually read and understand the labels. However, this is not the first, nor is it the last. On July 12 1998, 10 years earlier a young boy in the UK, this time 16 years old who had an obsession with smelling nice died after months of spraying his entire body with deodorant. Jonathon Campbell had 10 times the lethal dose of propane and butane in his blood. While these are tragic outcomes, the real problems lies in the millions of kids (and adults) around the world who are slowly poisoning themselves. The warning signs on most cans reads something like “deliberately concentrating may be harmful or fatal” or for cans sold to kids “must be used in the presence of adults” and the company has no other responsibility to your health than these labels. If people really knew what was in these cans and read these labels closely I am sure they would have second thoughts about using them and giving them to their kids. Unfortunately, the ingredients are not listed and the warning is all in the small print on the back.

The problem with deodorants and antiperspirants is three fold. First the propellant gases like propane and butane are toxic and were implicated in the deaths of both boys. This associated with the fact that they are sprayed upward towards the armpit and headspace means you can’t help but breathe them in. The second is the long list of toxic ingredients used in the deodorants and antiperspirants which you don’t know about and which are absorbed through the skin and thirdly the blocking of our pores by the antiperspirants.

To highlight where the problem starts antiperspirants and deodorants are among the top six products causing adverse skin reactions, including itching, burning, dryness, irritant dermatitis and allergic contact dermatitis. They have become one of the most frequently purchased products worldwide, surpassed in market share only by soaps and hair care products. Unfortunately, they are also one of the most widely marketed products constantly playing on kids’ emotional health, sex and relationships to sell their toxic products.

Deodorants act to reduce, cover up, or eliminate the odour that develops when bacteria break down perspiration. This is achieved by the use of anti-microbial agents and fragrances. Antiperspirants are distinguished from deodorants by the presence of sweat retarding agents. These agents are based on aluminium complexes and may include aluminium chlorohydrate (ACH), aluminium zirconium chlorohydrate glycine complexes (AZAP) or aluminium zirconium tetrachlorohydroxy glycine. While the connection between aluminium in antiperspirants and Alzheimer's disease and epilepsy continue to be explored and debated they seem highly unlikely. Other problems such as a link with breast cancer are much more likely. The action of these chemicals limits the levels of perspiration produced in the underarm and other areas, by slowing the action of the sweat glands. Sweat production is reduced due to the fact that the chemicals produce an obstructive hydroxide gel inside the sweat gland ducts, limiting the amount of perspiration that can be excreted. However, we were meant to sweat. Sweating provides a valuable service to our body by eliminating waste products, and cooling down the body. As a result antiperspirants may lead to a build up of toxins in this area just near the breast.

Antiperspirant and deodorant ingredients include anti-microbials such as chlorhexidine d-1-gluconate and triclosan, odour eliminators such as zinc ricitioleate and various perfumes. Other ingredients which may cause contact allergies include formaldehyde, atranorm, evernic acid, fumarprotocetraric acid, cetalkonium chloride, fenticlor, gluteraldehyde, zirconium and dibutyl phthalate. Many of the same chemicals you would find in toilet deodorants. Starting to sound a bit smelly isn’t it. Formaldehyde is a skin irritant and thought to be carcinogenic, and phthalates are suspected of producing endocrine (hormone)‑disrupting effects as they are able to mimic the action of oestrogen and upset our hormone balance. In one study diethyl phthalate, which is a solvent, was detected in 2 out of 8 deodorants. The breast, as a result, is also exposed to a range of these oestrogenic chemicals applied to the underarm and breast area. These cosmetics are left on the skin in the appropriate area, allowing a more direct dermal absorption route for breast exposure to oestrogenic chemicals and allowing absorbed chemicals to escape systemic metabolism. It is also worth noting that the large increase in breast cancer over the last 30 years has been a result of an increase in oestrogen receptive cancers.

Research has shown that repeated application of deodorants permeate the skin resulting in accumulation of some of these chemicals. According to one study butyl paraben was systemically absorbed, metabolized and excreted in urine following application to the skin in a cream preparation. The study conducted over 2 weeks showed concentration peaked in urine 8-12 hours after application.  Isn’t it interesting to know that the chemicals you put on the outside of your body get in?

Then the problem is exacerbated even more when they are used in spray containers that we direct towards our face. If your lungs are a uniquely designed sponge for air, they are also a sponge for the contaminants that manage to evade all of your respiratory system’s defenses. All the ingredients and the propellants are rapidly absorbed into the body and detectable throughout the body within minutes to hours.

The safer option is to use roll on deodorant. Unfortunately, it does not look as sexy in the advertisements, but it is much safer. The next step is then to move toward natural products and organic when you can. We have evolved with natural plant products over millions of years and as a general rule they are much safer than synthetic products manufactured from petrol. I also think it is about time we stop overselling these products and teaching kids that too much fragrance can be toxic… and who would want to smell like a toilet block anyway?

 

 


 

 

 

 

 

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