Pyrogallol is an ingredient in hair dye. Its concentration in hair dye is managed at less than 2.0% in Korea. There have been no reports on the dermal absorption rate of pyrogallol. The two purposes of this study were to develop an analytical method and determine the dermal absorption rate of pyrogallol. An analytical method was developed and validated by high-performance liquid chromatography (HPLC) analysis of various matrices including swabs (SWAB), skin (SKIN, dermis + epidermis), stratum corneum (SC), and receptor fluid (RF). Linearity (r² = 0.9993–0.9998), accuracy (92.1–108.2%), and precision (0.5–9.5%) met the validation criteria in guidelines. A Franz diffusion cell was used to determine the dermal absorption of pyrogallol using the skin of mini pigs. Pyrogallol (2.0%) was applied to the skin (10 μL/cm²). For the actual hair dye conditions, the skin was wiped with a swab 30 min after application. Twenty-four hours later, it was wiped with a swab again and the SC was collected using tape stripping. All samples were extracted with water and analyzed. RF was recovered at 0, 1, 2, 4, 8, 12, and 24 h. The total dermal absorption rate of pyrogallol was determined to be 26.0 ± 3.9%.

Sulforaphane is an isocyanate abundantly present in cruciferous vegetables. In the present study, we aimed to investigate the effects of sulforaphane on secondhand smoking (SHS)-induced pulmonary damage in mice. Additionally, a metabolomic study was performed to identify biomarkers associated with pulmonary disease using proton nuclear magnetic resonance (¹H-NMR) analysis. Male C57BL6J mice were divided into a control group, an SHS exposure group (positive control group, PC), and a sulforaphane treatment group exposed to secondhand smoke (SS) (n = 5 per group). The PC and SS groups were exposed to secondhand smoke in a chamber twice daily for four weeks. Mice in the SS group were orally administered sulforaphane (50 mg/kg) for four weeks during secondhand smoke exposure. Histopathological examination of the lungs revealed pulmonary damage in PC mice, including loss of bronchial epithelial cells, bronchial wall thickening, and infiltration of macrophages. In contrast, mice in the SS group showed little or no epithelial thickening, thereby exhibiting reduced lung damage. Mouse serum and lung tissues were collected and analyzed to determine changes in endogenous metabolites using ¹H-NMR. After target profiling, we identified metabolites showing the same tendency in the serum and lung as biomarkers for SHS-induced pulmonary damage, including taurine, glycerol, creatine, arginine, and leucine. As a result of histopathological examination, sulforaphane might inhibit SHS-induced lung damage, and metabolite analysis results suggest potential biomarkers for SHS-induced pulmonary damage in mice.