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The Impact of Early-Life Vitamin D Deficiency on Adverse Cardiopulmonary Responses to Atmospheric Smog in Mice
Citation:
Stratford, K., N. Coates, N. Kurhanewicz, Todd Krantz, C. King, J. Krug, Ian Gilmour, A. Farraj, AND M. Hazari. The Impact of Early-Life Vitamin D Deficiency on Adverse Cardiopulmonary Responses to Atmospheric Smog in Mice. Society of Toxicology, New Orleans, LA, March 14 - 17, 2016.
Impact/Purpose:
This abstract presents the effects of vitamin D deficiency on adverse cardiopulmonary responses to atmospheric smog in mice. It addresses the role of modifiable factors in the toxicological response. This study demonstrates that Vitamin D deficiency during development worsens the cardiopulmonary response to atmospheric smog.
Description:
Although it has been well established that air pollution contributes to cardiovascular morbidity and mortality, the role of nutrition in altering susceptibility has not been adequately addressed. Low levels of micronutrients like vitamin D in childhood can result in chronic problems into adulthood, including decrements in cardiovascular function, and may impact responsiveness to air pollution. We hypothesized that low vitamin D would alter the electrical and mechanical function of the heart and worsen the response to smog. Three-week old mice were fed a vitamin D deficient (VDD) or normal diet (ND) and then surgically implanted with radiotelemeters to continuously monitor electrocardiogram (ECG), heart rate (HR) and heart rate variability (HRV) at 17 weeks of age and exposed to atmospheric smog (1070 ug/m3 of PM2.5 and 97 ppb of ozone) or air 2 weeks later. Ventilatory function was assessed using whole-body plethysmography at specific points during the diet, before and after exposure while pulmonary function was measured after exposure. Tidal volume increased with age in ND mice but was significantly reduced by VDD, which also caused it to increase after smog when compared to air. There were no differences in the body weights or ECG parameters of any groups at any time point. Although HR was similar for all groups before exposure, smog caused a significant elevation in HR in ND mice, which persisted 24hrs later; this effect was further elevated by VDD. Smog significantly increased RMSSD, HF and arrhythmia in ND mice; this was further increased by VDD. There was no effect of diet on airway responsiveness however smog exposure in VDD mice showed a trend towards an increase. These data demonstrate that aside from subtle developmental physiological effects, VDD worsens the cardiopulmonary response to smog thus highlighting the importance of nutritional factors in determining an individual’s responsiveness to air pollution. (This abstract does not reflect USEPA policy)