Oak Ridge Institute for Science and Education, 1299 Bethel Valley Rd, Oak Ridge, TN 37830, United States.
Environmental Public Health Division, US EPA, 109 TW Alexander Drive, Research Triangle Park, NC, United States.
Sci Total Environ. 2018 Dec 1;643:378-391. doi: 10.1016/j.scitotenv.2018.06.089. Epub 2018 Jun 22.
Wildland fire emissions cause adverse cardiopulmonary outcomes, yet controlled exposure studies to characterize health impacts of specific biomass sources have been complicated by the often latent effects of air pollution. The aim of this study was to determine if postprandial responses after a high fat challenge, long used clinically to predict cardiovascular risk, would unmask latent cardiometabolic responses in rats exposed to peat smoke, a key wildland fire air pollution source. Male Wistar Kyoto rats were exposed once (1 h) to filtered air (FA), or low (0.36 mg/m particulate matter) or high concentrations (3.30 mg/m) of peat smoke, generated by burning peat from an Irish bog. Rats were then fasted overnight, and then administered an oral gavage of a HF suspension (60 kcal% from fat), mimicking a HF meal, 24 h post-exposure. In one cohort, cardiac and superior mesenteric artery function were assessed using high frequency ultrasound 2 h post gavage. In a second cohort, circulating lipids and hormones, pulmonary and systemic inflammatory markers, and circulating monocyte phenotype using flow cytometry were assessed before or 2 or 6 h after gavage. HF gavage alone elicited increases in circulating lipids characteristic of postprandial responses to a HF meal. Few effects were evident after peat exposure in un-gavaged rats. By contrast, exposure to low or high peat caused several changes relative to FA-exposed rats 2 and 6 h post HF gavage including increased heart isovolumic relaxation time, decreased serum glucose and insulin, increased CD11 b/c-expressing blood monocytes, increased serum total cholesterol, alpha-1 acid glycoprotein, and alpha-2 macroglobulin (p = 0.063), decreased serum corticosterone, and increased lung gamma-glutamyl transferase. In summary, these findings demonstrate that a HF challenge reveals effects of air pollution that may otherwise be imperceptible, particularly at low exposure levels, and suggest exposure may sensitize the body to mild inflammatory triggers.
野外火灾排放物会导致不良的心肺后果,但由于空气污染的潜在影响,控制暴露研究以描述特定生物质源对健康的影响一直很复杂。本研究旨在确定高脂肪挑战后的餐后反应是否会揭示暴露于泥炭烟雾(一种关键的野火空气污染源)后的大鼠潜在的心脏代谢反应,因为高脂肪挑战长期以来一直用于临床预测心血管风险。雄性 Wistar Kyoto 大鼠单次暴露于过滤空气(FA)或低浓度(0.36mg/m 颗粒物)或高浓度(3.30mg/m)泥炭烟雾中 1 小时,烟雾由爱尔兰沼泽地燃烧泥炭产生。大鼠随后禁食过夜,然后在暴露后 24 小时给予 HF 混悬液(60%来自脂肪的热量)口服灌胃,模拟 HF 餐。在一个队列中,使用高频超声在灌胃后 2 小时评估心脏和肠系膜上动脉功能。在第二个队列中,在灌胃前或灌胃后 2 或 6 小时评估循环脂质和激素、肺和全身炎症标志物以及循环单核细胞表型。单独给予 HF 灌胃会引起循环脂质增加,这是餐后反应 HF 餐的特征。在未灌胃的大鼠中,泥炭暴露后很少出现影响。相比之下,与 FA 暴露的大鼠相比,暴露于低浓度或高浓度的泥炭会在 HF 灌胃后 2 和 6 小时引起几种变化,包括增加的心脏等容舒张时间、降低的血清葡萄糖和胰岛素、增加的 CD11b/c 表达的血液单核细胞、增加的血清总胆固醇、α-1 酸性糖蛋白和α-2 巨球蛋白(p=0.063)、降低的血清皮质酮和增加的肺 γ-谷氨酰转移酶。总之,这些发现表明 HF 挑战揭示了空气污染的影响,否则这些影响可能是察觉不到的,尤其是在低暴露水平下,并表明暴露可能使身体对轻度炎症触发敏感。