ACTION OF ANTIPERSPIRANTS 797 B. Aluminum .... Skin obtained from the areas of aluminum salt induced anhidrosis before the subjects were sweated was normal. No plugs or casts were seen, the ducts were not dilated and there was no evidence of inflammation. The secretory coil contained abundant gly- cogen. Following the hour of forced sweating, a striking picture had developed. A well formed infiltrate of polymorphonudear and lym- phocytic leukocytes localized in the periductal tissue about the epider- mal-dermal function, where the eccrine duct traverses the rete peg (Fig. 7). Occasionally the infiltrate involved the epidermis and duct wall, coincident with spongiotic changes. This represented incipient mili- arial lesions (see below). Glycogen disappeared from the secretory coil after the thermal stress, verifying normal glandular secretion. The above sequence of histologic events are interpreted as demon- strating that aluminum chloride produces anhidrosis by altering the permeability or resorptive function of the epidermal portion of the ec- crine duct. Under conditions of forced sweating the perspiration pours into the dermis faster than it can be cleared, inciting the periductal inflammatory reaction. This concept is supported by the demonstration of increased transductal permeation of iontophoresed methylene blue. It also explains why the stripping maneuver is ineffectual in restoring perspiration in aluminum anhidrosis. Finally, it is to be reported that 3 of the 20 subjects developed scat- tered erythematous papules in aluminum salt treated areas only. These lesions erupted beneath the patch and closely resembled prickly heat or miliaria mbra. This diagnosis was confirmed on biopsy, which showed intraepidermal vesicles about the sweat duct, with an acute inflamma- tory reaction (Fig. 8). Finding miliaria only in aluminum chloride treated skin also speaks for a mechanism whereby damage to the intra- epidermal duct, either anatomic or physiologic, permits transductal es- cape of sweat. DISCUSSION Superficial obstruction of the eccrine outlet has long been favored as an explanation of how spontaneous sweat disorders develop as well as how antiperspirants produce anhidrosis. The same mechanism has been indicted in sweat retention complication in the chronic dermatoses such as psoriasis and atopic dermatitis (13, 14). Such high level blockage, re- gardless of the cause, may be demonstrated by the following procedures: i, removal of the stratum corneum relieves the obstruction, bringing about an immediate return of sweating ii, occluded eccrine ostia prevent

798 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS development of the eccrine pore pattern produced by the iontophoresis of methylene blue and iii, forced sweating into the obstructed duets causes wide dilatation and the accumulation of PAS positive diastase resistant material. The actual nature of the occlusion is quite variable in the chronic dermatoses it is a hyperkeratotie or parakeratotie plug, in formalin produced anhidrosis an intraluminal mass resulting from the protein preeipitant properties of the chemical. In the sweat suppression by hydration, a functional poral closure alone is operative. Aluminum anhidrosis meets none of the requirements that demon- strate a high level blockage. Removal of the horny layer does not re- verse the sweat suppression and, rather than preventing formation of the methylene blue pattern, actually facilitates the staining. Forced sweating, rather than producing duetal dilatation, leads to periduetal inflammation and, in extreme instances, duetal disruption as in miliaria rubra. This total picture suggests that aluminum salts alter the epi- dermal duet and permit large amounts of sweat to pour into the sur- rounding tissue. Perspiration will not reach the skin surface, in the same way that a multi-punctured garden hose, regardless of the head of pressure, prevents water from reaching the nozzle. Interestingly, Sulzberger (5) had described the same histologie findings in his studies on aluminum salt anhidrosis. W•thout employing the sequential biopsy technique and forced sweating as above, he concluded that the leukoeytie infiltrate resulted from the "ehemotaxis" of aluminum or its products and that the inflammation then interfered with duetal transport of sweat. Finding miliarial lesions in several subjects parallels Shelley's experi- ence with aluminum salt anhidrosis (,3). This does not, however, mean that one should regularly expect to find rashes produced by underarm deodorants. As a matter of fact, these agents, primarily composed of aluminum salts, rarely cause such effects in practice. The explanation for this paradox rests in the fact that experimenters wisely choose gla- brous skin such as the forearm or back, not the axilla, to study eeerine anhidrosis. While aluminum efficiently prevents perspiration in these areas, its effects in the underarm area are reduced. Miliaria probably does not develop because the chemical does not exert its full effect. The reason for the failure is not dear. The forehead is another resistant area (1•), and it is interesting that both these regions (as well as the palmar surface) also do not permit easy development of eeerine pore patterns with methylene blue iontophoresis (8). It is necessary to state that these areas share a common difference which distinguishes them from the remainder of the body: The eeerine glands of the axilla, forehead, and