302 JOURNAL OF COSMETIC SCIENCE CONCLUSION The microbiological method developed in the study may be considered an alternative method for photoprotective assessment that combines the greater reliability of a method using a living microorganism model and the simplicity and cost effectiveness of in vitro techniques. REFERENCES (1) U.S. Food and Drug Administration, Sunscreen drug products for over-the-counter human use: Final monograph, Federal Register, 64, 27666-27693 (1999). (2) COLIPA, Sun Protection Factor Test Method, Ref 94/289 (1994). (3) Australian/New Zealand Standard 2604, Standards Association of Australia, Sunscreen Products­ Evaluation and Classification (1998). (4) Japan Cosmetic Industry Association QCIA), Standard SPF Test Method, (1999). (5) G. A., Groves, P. P. Agin, and R. M. Sayre, In vitro and in vivo methods to define sunscreen protection, Austr.]. Derrnatol., 20, 112-119 (1979). (6) B. Herzog, S. Mongiat, K. Quass, and C. Deshayes, Prediction of sun protection factors and UVA parameters of sunscreens by using a calibrated step film model,]. Pharrn. Sci., 93, 1780-1795 (2004). (7) R. W. Jones, S. Smith, C. Boden, and B. G. Carpenter, A microbiological assay for the sun protection factor of sunscreen products,]. Pharrn. Pharrnacol., 50(Suppl. 9), S138 (1998). (8) M. Toyoshima, K. Hosoda, M. Hanamura, K. Okamoto, H. Kobayashi, and T. Negishi, Alternative methods to evaluate the photoprotective ability of sunscreen against photo-genotoxicity, Photochern. Photobiol. B, 73, 59-66 (2004). (9) A. J. Nataraj, J.C. Trent, and H. N. Ananthaswamy, p53 gene mutations and photocarcinogenesis, Photochern. Photobiol., 62, 218-230 (1995). (10) J. L. Zimmer and R. M. Slawson, Potential repair of Escherichia coli DNA following exposure to UV radiation from both medium-and low-pressure UV sources used in drinking water treatment, Appl. Env. Microbial., 68, 3293-3299 (2002). (11) B. S. Rosenstein and D. L. Mitchell, Action spectra for the induction of pyrimidine (6-4) pyrimidone photoproducts and cyclobutane pyrimidine dimers in normal human skin fibroblasts, Photochern. Pho­ tobiol., 45, 775-780 (1987). (12) J. Hildesheim, and A. J. Fornace, The dark side of light: The damaging effects of UV rays and the protective efforts of MAP kinase signaling in the epidermis, DNA Repair, 3, 567-580 (2004). (13) A. Besaratinia, T. W. Synold, H. Chen, C. Chang, B. Xi, A. D. Riggs, and G. P. Pfeifer, DNA lesions induced by UV Al and B radiation in human cells: Comparative analyses in the overall genome and in the p53 tumor suppressor gene, Proc. Natl. Acad. Sci. USA., 102, 10058-10063 (2005). (14) F. Modseen, J. D. Williams, and A. Secker, Standardization of inoculum size for disc susceptibility testing: A preliminary report of a spectrophotometric method,]. Antirnicrob. Chernother., 21, 439--443 (1988). (15) U. Citernesi, Photostability of sun filters complexed in phospholipids or [3-cyclodextrin, Cosrnet. Toiletr., 116, 77-78, 80-82, 84, 86 (2001). (16) D. L. Damian, G. M. Halliday, and R. S. Barnetson, Sun protection factor measurement of sunscreens is dependent on minimal erytherna dose, Br. J. Dermatol., 141, 502-507 (1999). (17) R. Wolf, B. Tuzun, and Y. Tuzun, Sunscreens, Derrnatologic Therapy, 14, 208-214 (2001). (18) W. Johncock. Sunscreen interactions in formulations, Cosmet. Toiletr., 114, 75-76, 78-82 (1999). (19) S. A. Wissing and R.H. Muller, A novel sunscreen system based on tocopherol acetate incorporated into solid lipid nanoparcicles, Int.]. Cosrnet. Sci., 23, 233-243 (2001). (20) J. Schulz, H. Hohenberg, F. Pflucker, E. Gartner, T. Will, S. Pfeiffer, R. Wepf, H. Gers-Barlag, and K. P. Wittern, Distribution of sunscreens on skin, Adv. Drug Deliv. Rev., 54(Suppl. 11), Sl57-Sl63 (2002). (21) F. Bohm, R. Edge, L. Lange, and T. G. Truscott, Enhanced protection of human cells against ultra­ violet light by antioxidant combinations involving dietary carotenoids,J. Photochern. Photobiol. B., 44, 211-215 (1998). (22) Y. O'Callaghan and N. O'Brien, The effect of carotenoids and tocopherols in the protection of human fibroblast cells against UVA-induced DNA damage, J. Dermatol. Sci., 34, 231-233 (2004).

J. Cosmet. Sci., 59, 303-315 Quly/August 2008) True porosity measurement of hair: A new way to study hair damage mechanisms YIN Z. HESSEFORT, BRIANT. HOLLAND, and RICHARD W. CLOUD, Nalco Company, 1601 West Diehl Road, Naperville, IL 60563. Accepted for publication February 20, 2008. Presented at the Annual Scientific Seminar of the Society of Cosmetic Chemists, Anaheim, CA, May 11, 2007. Synopsis This study employs a novel method, gas sorption (1), to quantify the porosity characteristics of hair by determining total pore volume, adsorption pore-size distribution, and the surface area of damaged hair. Damage mechanisms were studied by comparing the different pore volume and surface area resulting from two different types of damage: chemical and UV. Hair color measurement and tensile strength, both reflecting the changes in hair cortex, were also employed in this study. The results suggest that hair damage caused by oxidative bleach and UV oxidation follows different pathways. Chemical damage (oxidative bleach) nearly triples the hair surface area in the first minute of bleaching due to the increase in the number of pores, followed by a sudden drop after 10 min of bleaching from smaller pores breaking down into larger ones. In contrast, UV damage shows an immediate loss in surface area in the first 200 hr of exposure and a gradual increase as exposure time continues. INTRODUCTION Many studies show that hair damage caused by chemical processes and UV exposure will result in increased hair swelling. Although much of the literature uses the terms "swell­ ing" and "porosity" interchangeably, most of the methods developed to determine hair damage are geared toward measuring swelling rather than porosity. The techniques used to measure swelling include water uptake (2), hair diameter change (3 ), liquid retention (4), and a centrifuge method (5). There has been no study to date revealing the details of pore size, pore volume and surface area that precisely defines hair damage through the measurement of hair porosity. Gas sorption, the method we have developed recently, enables us to quantify the different porosity characteristics of damaged hair (1). Fur­ thermore, we have undertaken research to study the damage mechanisms. Bleaching and sun exposure (UV) are considered two major causes of oxidative hair damage. Several studies have concluded that chemical oxidation follows S-S fission, which generates two moles of cysteic acid (6,7), while photochemical oxidation of cystine follows the C-S scission pathway (8), where only one mole of cysteic acid is produced. 303