The benzene metabolite 1,4-benzoquinone reduces regulatory T-cell function: A potential mechanism for tobacco smoke–associated atopic dermatitis

Exposure to environmental chemicals can contribute to the development or exacerbation of atopic dermatitis (AD). Benzene is one of the chemicals previously been implicated in the etiology of AD.1 Albeit a ubiquitous environmental chemical, nonoccupational exposure to benzene mainly results from active or passive tobacco smoke exposure in homes or public places. Exposure to benzene has been shown to exert diverse effects on blood cells, in particular on lymphocytes. Although chronic exposure to high levels of benzene may cause leukemia and probably other lymphohematopoietic cancers, already low levels of benzene have been described to decrease the number of peripheral lymphocytes2 in humans including circulating CD4+ T cells, CD4+/CD8+ ratios, B cells, neutrophils, and platelets.