Persistent immune injury induced by short-term decabromodiphenyl ether (BDE-209) exposure to female middle-aged Balb/c mice.

Decabromodiphenyl ether (BDE-209), widely used in various industries for its excellent flame-retardant performance, could be enriched in humans and is closely associated with immune impairment. In addition, immune system is gradually declined and becoming more sensitive to environmental pollutants in the ageing process. Therefore, the immunotoxicity of BDE-209 (4, 40, and 400 mg/kg/day) to middle-aged mice and its recovery and susceptibility was first to be comprehensively investigated in this study. The results showed that BDE-209 exposure could lead to oxidative injury to immune organs (spleen, thymus, and liver), impair humoral (immunoglobulins), cellular (lymphopoiesis), and non-specific immunity, and disturb the expressions of the genes related to Th1/Th2 balance (T helper cells) in the middle-aged mice. In addition, Integrated Biomarker Response (IBR) indicated that BDE-209-induced immune impairment was challenging to self-regulated, and even exacerbated after 21 days of recovery and oxidative injury in immune organs could be the main reason. Furthermore, factorial analysis showed that middle-aged mice exposed to BDE-209 suffered from greater immune impairment than adult mice, and the immune impairment in aged mice is more difficult to be self-repaired than that in adult mice. It can be seen that the aged tend to suffer from BDE-209-induced persistent immune impairment and health threats.