Environmental pollutant has long been evident to affect airway inflammation. Dechlorane 602, which is widely used as chlorinated flame retardant in many countries, is considered as potential persistent organic pollutant (POPs). Recent studies have demonstrated that Dechlorane 602 is accumulated in wildlife and detectable in human. Unlike its analog Mirex, which has been reported to significantly affect human health through damages to the immune, endocrine, developmental and reproductive system, little is known about the potential effects of Dechlorane 602 on human health and diseases. Here we revealed that exposure to Dechlorane 602 promoted the exacerbation of airway inflammation in house dust mite (HDM)-induced asthma in mice. Asthmatic mice exposed to Dechlorane 602 exhibited enhanced infiltration of eosinophils and macrophages in the lung, together with substantially increased expression of TNF-alpha, IL-6 and CCL11. We also found higher expression of Th2-related cytokines including IL-4, IL-5 and IL-13 in the same mice. Increased frequency of Th2 cells associated with GATA-3 up-regulation were observed in the asthmatic mice exposed to Dechlorane 602. Interestingly, we further found increased expression of IL-33 receptor in the Dechlorane 602 exposed asthmatic mice, suggesting that highly activated innate immune cells may also play important roles and contribute to the exacerbation of airway inflammation. Indeed, significantly primed group 2 innate lymphoid cells (ILC2) were observed in Rag-/- mice exposed to Dechlorane 602, indicating that both innate and adaptive type 2 immune responses were activated by this potential environmental pollutant. RNA-seq analysis further revealed that Dechlorane 602 strongly promoted the gene expressions that are required to sustain the development and function of ILC2 cells. Together, these findings for the first time indicate that chlorinated flame retardant Dechlorane 602 promotes both innate and adaptive type 2 immune responses and exacerbates airway inflammation.