Air pollution has been associated with metabolic disease and obesity. Adipokines are potential mediators of these effects, but studies of air pollution-adipokine relationships are inconclusive. Macrophage and T cells in adipose tissue (AT) and blood modulate inflammation; however, the role of immune cells in air pollution-induced dysregulation of adipokines has not been studied. We examined the association between air pollution exposure and circulating and AT adipokine concentrations, and whether these relationships were modified by macrophage and T cell numbers in the blood and AT. Fasting blood and abdominal subcutaneous AT biopsies were collected from 30 overweight/obese 18–26 year-old volunteers. Flow cytometry was used to quantify T effector (Teff, inflammatory) and regulatory (Treg, anti-inflammatory) lymphocytes and M1 [inflammatory] and M2 [anti-inflammatory]) macrophage cell number. Serum and AT leptin and adiponectin were measured using enzyme-linked immunosorbent assay (ELISA). Exposure to near-roadway air pollution (NRAP) from freeway and non-freeway vehicular sources and to regional particulate matter, nitrogen dioxide and ozone were estimated for the year prior to biopsy, based on participants’ residential addresses. Linear regression models were used to examine the association between air pollution exposures and adipokines and to evaluate effect modification by immune cell counts. An interquartile increase in non-freeway NRAP exposure during 1 year prior to biopsy was associated with higher leptin levels in both serum [31.7% (95% CI: 10.4, 52.9%)] and AT [19.4% (2.2, 36.6%)]. Non-freeway NRAP exposure effect estimates were greater among participants with greater than median Teff/Treg ratio and M1/M2 ratio in blood, and with greater M1 counts in AT. No adipokine associations with regional air pollutants were found. Our results suggest that NRAP may increase serum leptin levels in obese young adults, and this association may be promoted in a pro-inflammatory immune cell environment in blood and AT.

中文翻译：

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肥胖年轻人的道路附近空气污染、免疫细胞和脂肪因子

空气污染与代谢疾病和肥胖有关。脂肪因子是这些影响的潜在介质，但对空气污染与脂肪因子关系的研究尚无定论。脂肪组织 (AT) 和血液中的巨噬细胞和 T 细胞调节炎症；然而，尚未研究免疫细胞在空气污染引起的脂肪因子失调中的作用。我们检查了空气污染暴露与循环和 AT 脂肪因子浓度之间的关联，以及这些关系是否被血液和 AT 中的巨噬细胞和 T 细胞数量所改变。从 30 名超重/肥胖的 18-26 岁志愿者中收集空腹血液和腹部皮下 AT 活检。流式细胞术用于量化 T 效应因子（Teff，炎症）和调节因子（Treg，抗炎）淋巴细胞和 M1 [炎症] 和 M2 [抗炎]）巨噬细胞数量。使用酶联免疫吸附试验 (ELISA) 测量血清和 AT 瘦素和脂联素。根据参与者的居住地址，估计在活检前一年暴露于高速公路和非高速公路车辆来源的近道路空气污染 (NRAP) 以及区域颗粒物、二氧化氮和臭氧。线性回归模型用于检查空气污染暴露与脂肪因子之间的关联，并评估免疫细胞计数对效果的影响。活检前 1 年内非高速公路 NRAP 暴露的四分位数增加与血清 [31.7% (95% CI: 10.4, 52.9%)] 和 AT [19.4% (2.2, 36.6%)] 中较高的瘦素水平相关. 非高速公路 NRAP 暴露效应估计值在血液中 Teff/Treg 比率和 M1/M2 比率大于中位数以及 AT 中 M1 计数更高的参与者中更大。没有发现脂肪因子与区域空气污染物的关联。我们的研究结果表明，NRAP 可能会增加肥胖年轻人的血清瘦素水平，并且这种关联可能在血液和 AT 中的促炎免疫细胞环境中得到促进。