AhR-mediated responses with dioxin and dioxin-like compounds are thought to contribute to asthma pathogenesis through increased expression of inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β, which in turn can induce mucin production, cell chemotaxis, and immunoglobulin E (IgE) production (Chiba et al. 2012). Here, AHR is linked to asthma.