PHOTODEGRADATION OF HUMAN HAIR 109 Figure 3. FESEM micrographs of hair fibers after exposure to UV radiation. (a) control, 0 h (b) 100 h (c) 300 h and (d) 700 h UV exposure. FUSION OF THE CUTICULAR SHEATH We were also interested in exploring the changes in the physical nature of the cuticular sheath, which had shown such thinning and fusion of the surface cuticle cell during long-term UV exposure. Cross-sectional views of the freeze-fractured untreated hair fiber showed the individual layers of the cuticular sheath to be easily identifiable (Figure 5al,a2). However, after 300 hours of UV exposure, fusion of all cuticular layers into a monolithic, brittle unit had occurred preferentially on the side of the hair fiber oriented towards the damaging rays of the light source (Figure 5b). In that region of the fiber, individual cuticle cells were no longer identifiable. Also, fibers exposed to 300 hours of UV light exhibit deep radial cracks, which are parallel to each other and absolutely perpendicular to the fiber axis (Figure 6), fracturing easily under minimal amounts of stress during bending or extension. More drastic results were observed in hair fibers exposed for an even longer time (700 h) to UV light under similar conditions. Upon extension of hair fibers exposed for 700 hours to UV irradiation/humidification cycling, most fibers failed instantaneously at the start of extension. These fibers had become so brittle that they were incapable of extension due to loss of all original elastic properties. Upon failure, these hair fibers displayed an unusual fracture pattern. Figure 7 shows this fracture phenomenon, which occurs as the fibers snap apart. Fusion of the complete cuticula and possibly the outer

110 JOURNAL OF COSMETIC SCIENCE E 0.5 0.3 0.1 0.0 I I I I I I I 0 100 200 300 400 500 600 700 UV Irradiation (h) Figure 4. Progressive thinning and fusion of the surface cuticle cells as a function of exposure time to UV irradiation. layer of the cortex into one rigid unit causes brittle failure circumferentially and dis- places the stress of extension to those regions of the hair fiber that are still untouched by this progressive fusion. Multiple, successive fractures develop at individual sites along the cortical cell boundaries, then change direction and travel radially across individual cortical cells, and this pattern continues until it tapers off towards the core of the fiber, thereby creating what we call the "cathedral spire" fracture pattern (Figure 7a). The opposite, corresponding site of the "cathedral spire" fracture shows a hollow opening (Figure 7b), surrounded by a firmly fused wall. Higher magnification shows that this wall consists of a firmly fused cuticular sheath and possibly also the outer layer of cortical cells (Figure 7c,d). Some cuticular regions, preferentially those on the side of the fiber oriented towards the damaging light source, have become indistinguishable, rigid, and very brittle. The "cathedral spire" fracture pattern clearly shows primary levels of photodegradation in the fiber periphery (cuticular sheath) and a drop-off to lesser levels of degradation in the fiber interior. PHOTOCHEMICAL VERSUS CHEMICAL OXIDATION Differences between chemical and photochemical oxidation of hair proteins and melanins have been widely discussed in the literature. Robbins (9) reports that both chemical and photochemical oxidation attack both the hair pigments and proteins, and within the proteins, primarily the amino acid cystine. Up to 25 % of the disulfide bonds in human hair are degraded by "normal" bleaching, and 45 % of the disulfide bonds may be broken