Abstract

Exposure to particulate matter 2.5 (PM2.5) is detrimental to multiple organ systems. Given the factor that aging also alters the cellularity and response of immune system and dysfunction of hypothalamic‐pituitary‐adrenal, ‐gonad and ‐thyroid axes, it is imperative to investigate whether chronic exposure to PM2.5 interacts with aging in these aspects. In this study, two‐months‐old Sprague–Dawley rats were exposed to real world PM2.5 for 16 months. PM2.5 exposure diminished the relative numbers of CD4 + T cells and CD8 + T cells and increased the relative number of B cells in the peripheral blood of male rats. Conversely, only reduced relative number of CD4 + T cells was seen in the blood of female rats. These shifts resulted in elevated levels of proinflammatory factors interleukin‐6 and tumor necrosis factor‐ α in the circulatory systems of both sex, with females also evidencing a rise in interleukin‐1 β levels. Moreover, heightened interleukin‐6 was solely discernible in the hippocampus of female subjects, while increased tumor necrosis factor‐ α concentrations were widespread in female brain regions but confined to the male hypothalamus. Notable hormonal decreases were observed following PM2.5 exposure in both sex. These comprised declines in biomolecules such as corticotrophin‐releasing hormone and cortisol, generated by the hypothalamic‐pituitary‐adrenal axis, and thyroid‐releasing hormone and triiodothyronine, produced by the hypothalamic‐pituitary‐thyroid axis. Hormonal elements such as gonadotropin‐releasing hormone, luteinizing hormone, and follicle‐stimulating hormone, derived from the hypothalamic‐pituitary‐gonad axis, were also diminished. Exclusive to male rats was a reduction in adrenocorticotropic hormone levels, whereas a fall in thyroid‐stimulating hormone was unique to female rats. Decreases in sex‐specific hormones, including testosterone, estradiol, and progesterone, were also noted. These findings significantly enrich our comprehension of the potential long‐term health repercussions associated with PM2.5 interaction particularly among the aging populace.