Early-life nutritional deficiencies can lead to increased cardiovascular susceptibility to environmental exposures. Thus, the purpose of the study was to examine the effect of early-life persistent vitamin D deficiency (VDD) on the cardiopulmonary response to a particulate matter-enhanced photochemical smog. Mice were fed a VDD or normal diet (ND) after weaning. At 17 weeks of age, mice were implanted with radiotelemeters to monitor electrocardiogram, heart rate (HR) and heart rate variability (HRV). Ventilatory function was measured throughout the diet, before and after smog exposure using whole-body plethysmography. VDD mice had lower HR, increased HRV and decreased tidal volume compared with ND. Regardless of diet, HR decreased during air exposure; this response was blunted by smog in ND mice and to a lesser degree in VDD. When compared with ND, VDD increased HRV during air exposure and more so with smog. However, smog only increased cardiac arrhythmias in ND mice. This study demonstrates that VDD alters the cardiopulmonary response to smog highlighting the possible influence of nutritional factors in determining responses to air pollution. The mechanism of how VDD induces these effects is currently unknown, but modifiable factors should be considered when performing risk assessment of complex air pollution atmospheres.
生命早期的营养缺乏会导致心血管对环境暴露的易感性增加。因此,本研究的目的是检验生命早期持续性维生素D缺乏(VDD)对心肺对颗粒物增强型光化学烟雾反应的影响。小鼠在断奶后被喂食VDD饮食或正常饮食(ND)。在17周龄时,小鼠被植入无线电遥测仪以监测心电图、心率(HR)和心率变异性(HRV)。在整个饮食期间,使用全身体积描记法在烟雾暴露前后测量通气功能。与ND组相比,VDD组小鼠心率较低,心率变异性增加,潮气量减少。无论饮食如何,在空气暴露期间心率都会下降;ND组小鼠的这种反应被烟雾减弱,VDD组小鼠的减弱程度较小。与ND组相比,VDD组在空气暴露期间心率变异性增加,在烟雾暴露时增加更明显。然而,烟雾仅增加ND组小鼠的心律失常。这项研究表明,VDD改变了对烟雾的心肺反应,突显了营养因素在确定对空气污染反应中的可能影响。VDD如何诱导这些效应的机制目前尚不清楚,但在对复杂的空气污染环境进行风险评估时,应考虑可改变的因素。