Silica particles induce the release of metalloproteases, free radicals, and pro-inflammatory mediators, such as: IL-1β and TNF-α through activation of the nuclear factor (NF)-κB pathway (Rimal et al., 2005; Greenberg et al., 2007), which is involved in the recruitment of more inflammatory cells to the site of the lesion—including neutrophils, which are involved in the lung fibrosis process (Maron-Gutierrez et al., 2011). Here, IL1B is linked to pulmonary fibrosis.