Heart Rate (HR) and Oxygen Consumption (VO2) Changes After Inhaled Ozone (O3) and Particulate Matter (PM) in Two Mouse Strains

O3 is a principal pollutant that coexists with PM in urban ambient air. Studies associate O3 and PM exposure with adverse health effects; however the mechanisms of action remain unclear. We implanted radiometers to measure HR, and then exposed two mouse strains (i.e. C3H/HeJ, C3 and C57Bl/6J, B6 [n=3/strain]) to three different protocols for 3 consecutive days as follows: 2 hr‐filtered air (FA) + 3 hr‐FA; 2 hr‐FA + 3 hr‐carbon black (CB); and 2 hr‐ozone (O 3 , 550 ppb) + 3 hr‐CB HR and VO2 were collected simultaneously on the mornings before and after exposure. We observed relative increases in O2‐pulse,(VO2/HR) with FACB (4.9%±2.4), and O 3 CB (7.5%±6) independent of HR changes in the B6 mice. Correlations between HR and VO 2 were also examined. The C3 mice did not exhibit obvious coupling of HR and VO 2 (r 2 =0.16±0.06) at baseline or with treatment. The B6 animals, however, appear to inherently possess a high association between HR and VO 2 (r 2 = 0.40±0.08) and this association changed dramatically with exposure: i.e., FACB (r 2 =0.13±0.06) and O 3 CB (r 2 =0.60±0.01) exposures. Thus, these results suggest that HR and VO 2 coupling varies between inbred strains and among different pollutants. In terms of hemodynamic control, HR regulation is altered by air pollutant exposures such that a greater O2 delivery is required with each stroke of the heart. Future studies will aim to elucidate genetic factors that may modify individual responses and susceptibility to these air pollutants. Support: AG 021057