To investigate the concentrations of rare earth elements in cereals and assess human health risk through cereal consumption, a total of 327 cereal samples were collected from rare earth mining area and control area in Shandong, China. The contents of 14 rare earth elements were determined by Inductively Coupled Plasma—Mass Spectrometry (ICP—MS). The medians of total rare earth elements in cereals from mining and control areas were 74.22 μg/kg and 47.83 μg/kg, respectively, and the difference was statistically significant (P < 0.05). The wheat had the highest rare earth elements concentrations (109.39 μg/kg and 77.96 μg/kg for mining and control areas, respectively) and maize had the lowest rare earth elements concentrations (42.88 μg/kg and 30.25 μg/kg for mining and control areas, respectively). The rare earth elements distribution patterns for both areas were characterized by enrichment of light rare earth elements. The health risk assessment demonstrated that the estimated daily intakes of rare earth elements through cereal consumption were considerably lower than the acceptable daily intake (70 μg/kg bw). The damage to adults can be neglected, but more attention should be paid to the effects of continuous exposure to rare earth elements on children.

Vitiligo (VIT) is caused by loss and degradation of functional epidermal melanocytes. Studies have indicated that melanocyte destruction may be associated with an imbalance between regulatory T cells (Treg cells) and effector T cells (Teff cells). The current study aimed to investigate the molecular mechanism through which Treg/Teff balance affects VIT pathogenesis. To explore this, peripheral blood mononuclear cells were isolated from patients with VIT and healthy individuals. The present study revealed that the proportions of CD4 + T cells, Treg cells and T helper 1 (Th1) cells were decreased in patients with VIT, but those of Teff cells (Th17 and Th22 cells) were increased; additionally, Foxp3 expression was decreased, but the expression levels of interferon-γ, interleukin (IL)-17A and IL-22 were increased. Furthermore, in patients with VIT, microRNA (miR)-21-5p expression was decreased, while that of STAT3 was increased. Further in vitro experiments in CD4 + T cells revealed that STAT3 was targeted by miR-21-5p. Functional analysis further indicated that miR-21-5p overexpression in Th17-polarized CD4 + T cells decreased the proportion of Teff cells and associated cytokines, such as IL-17A and IL-22, but increased the proportion of Treg cells and Foxp3. However, the effects of miR-21-5p overexpression were partly reversed by STAT3 overexpression. Increased apoptosis of melanocytes was detected after co-culture with Th17-polarized CD4 + T cells in the presence of a miR-21-5p mimic. However, this indirect effect of the miR-21-5p mimic on melanocytes was decreased via STAT3 overexpression. Therefore, miR-21-5p may protect melanocytes via targeting STAT3 and regulating Treg/Teff balance. The current findings may provide a possible treatment method for managing VIT.

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