Histological and inflammatory effects of 26.5 GHz quasi-millimeter wave exposure on rat skin

TL;DR

This study examines how exposure to 26.5 GHz quasi-millimeter waves affects rat skin, finding that high exposure causes burn-like damage and inflammation.

Contribution

The study identifies a threshold for inflammatory responses in rat skin exposed to quasi-millimeter waves using absorbed power density as a reference.

Findings

Exposure to 500 W/m² caused burn-like tissue damage and elevated inflammation markers in rat skin.

The threshold for inflammatory responses was estimated between 370 and 500 W/m² APD.

Lower exposure levels (250 and 370 W/m²) did not cause significant morphological changes.

Abstract

Information regarding the biological effects of localized exposure to quasi-millimeter waves (qMMW) is limited. Given that qMMW exposure can elevate skin temperature and potentially induce thermal injury, further investigation is required. In this study, we aimed to evaluate histological changes and the expression of inflammation-related markers in rat skin tissue locally exposed to 26.5 GHz qMMW, as well as investigate the threshold for inflammatory responses.

The dorsal skin of rats was locally exposed to 26.5 GHz qMMW at absorbed power densities (APD) of 0, 250, 370, and 500 W/m2 for 18 min using a patch antenna. Histological changes and expression patterns of inflammation-related markers were examined in skin tissue sections exposed to qMMW. Furthermore, serum levels of prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) were measured at each post-exposure time point.

Histological analysis revealed burn-like tissue damage in the 500 W/m2 exposure group, characterized by subepidermal blister formation, epidermal thickening, and dermal edema, which increased in severity over time. Conversely, the lower exposure groups (250 and 370 W/m2) showed no distinct morphological changes, similar to the sham group. The 500 W/m2 group exhibited significantly elevated expression of inducible nitric oxide synthase (iNOS) and ionized calcium-binding adapter molecule 1 (Iba1), particularly in the dermis, dermal white adipose tissue, and sebaceous glands. Serum levels of PGE2 increased in a dose-dependent manner at 24 and 72 h; TNF-α and IL-6 remained undetectable. The skin temperature increased during qMMW exposure, reaching 39.0 ± 0.6°C, 42.4 ± 0.9°C, and 44.8 ± 1.2°C at APDs of 250, 370, and 500 W/m2, respectively.

Localized exposure of rat skin to qMMW induces burn-like tissue degeneration and triggers an inflammatory response. This effect may be thermally induced by qMMW irradiation, with the threshold estimated to range between 370 and 500 W/m2 APD under the present experimental conditions. Few studies have demonstrated MMW-induced inflammatory responses in the skin. To the best of our knowledge, this is the first study to clearly define the threshold using APD as a reference. These findings may contribute useful evidence for future revisions of exposure guidelines.

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