Newsdesk Hair products and cancer risk: good and bad news A new study which analysed cancer risk among hairdressers, has shown that hair dye use is linked to an increased risk of skin cancer in the scalp and neck (Int J Cancer 2003; 105: 108–12). The study also found that male hairdressers, who had an increased risk of bladder cancer in the 1960s, now have virtually normal risk.
Harri Vainio, International Agency for Research on Cancer (Lyon, France), comments: “This report is one of the first studies which is informative in terms of cancer risks at various sites. Previous studies have been mostly mortality studies, which are not very informative in terms of non-melanoma skin cancer.” Asked about what makes hair dye dangerous, Hemminki explains: “There
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A cohort of 38 866 female and 6824 male hairdressers were assessed for 39 years and information about all types of cancer was collected. This information was compared with population data from the Swedish Cancer Registry. The researchers found that male hairdressers had increased risks for cancers of the upper aerodigestive tract, lung, and colorectal system, and women had increased risks for cancers of the pancreas, lung, and cervix, and in situ squamous-cell carcinoma of the skin, which mainly affected the scalp and neck. Senior-author Kari Hemminki (Karolinska Institute, Huddinge, Sweden), believes that the scalp and neck cancers occur because hairdressers are heavy users of hair dyes themselves. He also notes that brilliantine (which contains the animal carcinogen pdimethylaminoazobenzene) is probably responsible for the 1960s incidence of male bladder cancers because the product was then widely used by barbers. “It is not possible to say whether the other cancers are linked to occupational exposure”, says Hemminki, “but there is no way of excluding that either”. THE LANCET Oncology Vol 4 May 2003
Claudia Orellana
Topo II may underlie acid-induced cancer
Stone/Bob Thomas
Hairdressers have an increased risk of several cancers.
are hundreds of different ingredients and some of them are the manufacturer’s secret, so we don't even know what is in there.” He considers cosmetic products to be insufficiently regulated in Europe. “In USA and Australia cosmetics are as regulated as pharmaceutical products”, he says, but in Europe, “there are compounds that are under no regulation whatsoever”.
Acidic pH may induce DNA damage through activation of topoisomerase II (topo II)—an enzyme involved in DNA duplication—according to new research. This finding could help explain why patients with acid reflux have an increased risk of oesophageal cancer. When gastric juices flow back into the oesophagus, the acidic pH causes changes to the epithelial lining. If this damage accumulates, the oesophagus can develop a metaplastic, intestinaltype lining, a condition known as Barrett’s oesophagus, which predisposes to oesophageal cancer. Although the link between acid reflux and cancer is well established, little is known about the molecular events that drive this process. However, new research by Leroy Liu and colleagues at the University of Medicine and Dentistry of New Jersey, USA, suggests that acid can cause damage by interfering with topo II (published online 11 April, 2003 Proc Natl Acad Sci USA doi/10.1073/pnas.0935978100). Topo II has an important role in DNA transcription, replication, and recombination: it produces transient breaks in both strands which release tension built up by excessive coiling. Several widely used antitumour drugs, including doxorubicin and etoposide, work by disrupting this process. They stop topo II from rejoining the broken strands, thus increasing the number of DNA breaks in the cell. Liu and colleagues found that acid can stimulate cancer development through a mechanism that is similar to the actions of topo II-targeting drugs. Using a model of cancer in mice, the
researchers observed that acid could promote tumour formation. After investigating the molecular basis of this effect, Liu and colleagues were convinced of topo II’s involvement. They found that in breast-cancer cells, acidic pH upregulated p53 and other molecules that signal DNA damage; and that acid also increased the frequency of DNA mutations. These effects were absent or reduced in topo II-deficient cells, thus implicating this enzyme in mutagenesis. Liu speculates that acid may need the help of another substance to induce carcinogenesis because acid primarily causes rearrangements in DNA sequence, rather than point mutations. “You need both types of mutation to induce carcinogenesis”, he says. “This is an interesting study”, comments Stuart Jon Spechler at the University of Texas Southwestern Medical Center at Dallas (TX, USA). “It suggests a mechanism whereby acid reflux might result in DNA damage.” However, he points out that there are many other ways by which an acidic pH could cause cancer. “It is hard to know how important this mechanism is. This study establishes that in culture, an acidic pH can induce topoisomerase IImediated DNA damage. Whether that occurs in vivo, or if it is biologically important, is not clear.” Liu agrees that other studies have suggested alternative mechanisms for acid-induced damage, including oxidative stress and inflammatory responses. “This is just a very basic finding”, he concludes. Martina Habeck
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