Hair Dyes: Do They Cause Cancer and Other Health Problems?

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Article: Hair Dyes - Do They Cause Cancer?

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Introduction

Hair Dyes have been linked by scientist as being a possible cause of several different cancers. While there is some debate over the 'real' danger to humans, this research spells danger to people who are frequently exposed to particular hair colous and dyes.

Do Hair Dyes Cause Cancer?

 

 

 

 

An Interview with Susan Siegenthaler from Wildcrafted Herbal Products

Research into the toxicity of hair dyes by Japanese researchers has demonstrated that certain hair dyes are carcinogenic and present a serious threat to users of permanent hair colouring products. Their findings list several chemicals which were responsible in causing a number of different cancers in rats, including ovarian, bladder and other cancers (Read Abstract).

They warn hair dressers in particular and women who frequently use permanent hair dyes about unwittingly increasing their risk of developing cancer through frequent, long term use. A natural hair dye is henna, which was found to be safe for use as a hair dye and poses no genotoxic risk to consumers (Read Abstract).

These and similar finding is why we at Wildcrafted Herbal Products, an Australian, manufacturer of natural skin and personal care products, continuously scan the scientific literature for new findings related to ingredients used by the beauty, cosmetics, skin care and personal care industries.

There is an ever increasing demand by customers for products that are totally natural and are safe to use. "Our aim is to identify potentially harmful substances in order to keep our products as pure as nature intended", said Susan Siegenthaler, director of R & D at Wildcrafted Herbal Products. "As scientific investigation techniques are becoming more sophisticated, more chemicals both natural and synthetic are receiving increased scrutiny by the scientific community as to their safety and effectiveness", said Susan.

"At Wildcrafted we look for scientifically validated information on a wide range of ingredients, in terms of their actions, effectiveness and safety, as a pro-active measure to avoid using any questionable ingredients in our products. We just want our customers to know they are not slowly poisoning themselves when using any of our range of products", states Susan.

"I think consumers have the right to know what is in the products they are using and whether or not these ingredients have the potential to cause them harm," insists Susan. "I am very surprised that the finding from the Japanese research team has not made major headlines in news and current affair programs, and I have to wonder, Why?", asks Susan.

 

Abstracts referred to in the above article (in order of referring to them):

Oxidative DNA damage induced by hair dye components ortho-phenylenediamines and the enhancement by superoxide dismutase.

Murata M, Nishimura T, Chen F, Kawanishi S.

Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.

There is an association between occupational exposure to hair dyes and incidence of cancers. Permanent oxidant hair dyes are consisted of many chemical components including ortho-phenylenediamines. To clarify the mechanism of carcinogenesis by hair dyes, we examined DNA damage induced by mutagenic ortho-phenylenediamine (o-PD) and its derivatives, 4-chloro-ortho-phenylenediamine (Cl-PD) and 4-nitro-ortho-phenylenediamine (NO(2)-PD), using (32)P-labeled DNA fragments obtained from the human p16 and the p53 tumor suppressor gene. We also measured the content of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), a marker of oxidative DNA damage, in calf thymus DNA with an electrochemical detector coupled to a high performance liquid chromatograph. Carcinogenic o-PD and Cl-PD caused Cu(II)-mediated DNA damage, including 8-oxodG formation, and antioxidant enzyme superoxide dismutase (SOD) enhanced DNA damage. o-PD and Cl-PD caused piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at cytosine and guanine residues respectively in the 5'-ACG-3' sequence, complementary to codon 273, a well-known hotspot of the human p53 tumor suppressor gene. UV-vis spectroscopic studies showed that the spectral change of o-PD and Cl-PD required Cu(II), and addition of SOD enhanced it. This suggested that SOD enhanced the rate of Cu(II)-mediated autoxidation of o-PD and Cl-PD, leading to enhancement of DNA damage. On the other hand, mutagenic but non-carcinogenic NO(2)-PD induced no DNA damage. These results suggest that carcinogenicity of ortho-phenylenediamines is associated with ability to cause oxidative DNA damage rather than bacterial mutagenicity.

An assessment of the genotoxicity of 2-hydroxy-1,4-naphthoquinone, the natural dye ingredient of Henna.

Kirkland D, Marzin D.

Covance Laboratories Ltd., Otley Road, Harrogate, North Yorkshire HG3 1PY, UK. david.kirkland@covance.com

2-Hydroxy-1,4-naphthoquinone (HNQ; Lawsone; CAS 83-72-7) is the principal natural dye ingredient contained in the leaves of Henna (Lawsonia inermis). Published genotoxicity studies on HNQ suggested it was a weak bacterial mutagen for Salmonella typhimurium strain TA98 or was more clearly mutagenic for strain TA 2637, both in the presence of metabolic activation. HNQ was unable to induce sex-linked recessive lethal mutations in Drosophila melanogaster. However, a small increase in micronucleus frequency was reported in the bone marrow of mice at a single mid-range dose level, 24h after intraperitoneal injection. In view of the wide use of Henna hair dyes it was deemed necessary to conduct a thorough investigation, under Good Laboratory Practice conditions, of the genotoxicity of HNQ. HNQ was non-mutagenic in bacterial (Ames test) or mammalian (V79 hprt) assays. It was borderline positive in a mouse lymphoma tk mutation assay and a chromosome aberration test (CHO cells), results that may reflect a similar clastogenic mechanism. Negative in vivo genotoxicity results were noted in the rat hepatocyte in vivo/in vitro UDS test, in peripheral lymphocytes (chromosome aberrations) of rats receiving repeated oral doses of HNQ at the MTD for 28 days, and in mouse and hamster bone marrow chromosome aberration tests. However small, but statistically significant increases in the incidence of bone marrow micronuclei were observed in two out of five tests at 72 h after dosing, but not at 24 or 48 h. There was evidence of haematotoxicity at 72 h, which may have been enhanced by the vehicle (DMSO) used in the positive tests. As erythropoiesis and administration of haematotoxic agents are known to induce small increases in the frequency of bone marrow micronuclei, typically at delayed sampling times, the data suggest that the positive 72 h response produced by HNQ is consistent with stimulation of haematopoiesis subsequent to haematological toxicity of HNQ, and not due to a DNA-reactive mechanism. Overall, the weight of evidence suggests that Henna and HNQ pose no genotoxic risk to the consumer.

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