Before considering the biology of dry skin and the dry skin cycle, it is important to review the effect of environmental conditions on the SC, as these are the primary initiating events for the precipitation of the condition. In studies conducted in the different seasons of the year in the U. K., Rogers et al. (62) demonstrated that there was a significant reduction in the levels of SC ceramides and fatty acids, together with linoleate-containing CER EOS in subjects in winter. Similar differences in scalp lipid levels have been observed between the wet and dry seasons in Thailand (63). Nevertheless, more importantly, Declercq et al. (64) have reported an adaptive response in human barrier function, where subjects living in a dry climate such as Arizona (compared with a humid climate in New York) had much stronger barrier function and less dry skin due to increased ceramide levels and increased desquamatory enzyme levels (SCCE and SCTE).
Several animal studies have been conducted that support these findings. TEWL was reduced by approximately 30% in animals exposed to a dry (! 10%RH) environment due to increased lipid biosynthesis, increased lamellar body extrusion, and a slightly thicker SC layer, whereas, in animals exposed to a high humidity environment (80%RH), this induction of lipid biosynthesis was reduced (65). However, abrupt changes in environmental humidity
can also influence stratum corneum moisturization (66). After transferring animals from a humid (80%RH) to dry (< 10%RH) environment, a six-fold increase in TEWL occurred. Barrier function returned to normal within seven days due to normal lipid repair processes. These changes did not occur in animals transferred from a normal to dry humidity environment. These changes in barrier function have also recently been reported in a group of Chinese workers who are exposed to very low humidity conditions. However, the changes in barrier function take longer to reach equilibrium than anticipated from the animal studies (Fig. 15) (67).
Similarly, findings were reported for the water-holding capacity and free amino acid content of the SC. Katagiri et al. (68) demonstrated that exposure of mice to a humid environment, and subsequent transfer to a dry one, reduced skin conductance and amino acid levels even after seven days following transfer; after transfer from a normal environment, however, decreased amino acid levels recovered within three days.
Exposure to low humidity conditions also increases epidermal DNA synthesis and amplifies the DNA synthetic response to barrier disruption (69). Equally, when in a dry environment epidermal IL-1 levels increased and increased levels of this cytokine were greater when the barrier was experimentally-challenged (70). More recently, the same group also reported increased numbers of mast cells and increased dermal histamine levels (but unchanged epidermal histamine levels) (71). These changes in barrier properties of the SC are attributable to changes in SC moisture content and provide evidence that changes in environmental humidities contribute to the seasonal exacerbation or amelioration of xerotic skin conditions which are characterized by a defective barrier, epidermal hyperplasia, and inflammation.