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Context: Epidemiological studies show positive associations between increased ambient air pollutant levels and adverse cardiopulmonary effects. These studies suggest that the elderly and those with certain genetic polymorphisms are susceptible to adverse air pollution-associated health events. Hypothesis/objective: We hypothesize that physiological responses to air pollutants vary with age and are genetically influenced. Materials and methods: To test this hypothesis, we exposed mice from three inbred strains (C57BL/6J, B6; C3H/HeJ, HeJ; C3H/HeOuJ, OuJ) to ozone (O3) and carbon black (CB) at two ages, (5 months, 12 months), for 3 consecutive days, to either filtered air (FA), CB particles, or O3 and CB sequentially (O3CB) (CB, 550 µg/m3; O3, 600 ppb). Heart rate (HR), HR variability (HRV), breathing, and core temperature (Tco) responses were analyzed. Results: We observed time-dependent physiological changes in response to O3CB exposure in each strain, relative to FA exposure for both age groups. Each mouse strain showed distinct adaptation profiles to repeated acute exposures to O3. In younger mice, several time-dependent effects (decreased HR and increased HRV) were prominent in HeJ and OuJ mice but not B6 mice. We also observed variability in adaptation in older mice. However, responses in older mice were generally attenuated when compared to the younger mice. In addition, cardiac-respiratory interactions were affected with CB and O3CB exposures albeit with patterns differing by age or exposure. Discussion/conclusion: Our results suggest that age considerably attenuates physiological responses to O3 and O3CB exposures. Age-related physiological changes such as increased oxidative stress in mouse tissue may be involved in this attenuation. [ABSTRACT FROM AUTHOR]

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: 1) 2 hr-filtered air (FA) + 3 hr-FA; 2) 2 hr-FA + 3 hr-carbon black (CB); and 3) 2 hr-ozone (O3, 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 O3CB (7.5%±6) independent of HR changes in the B6 mice. Correlations between HR and VO2 were also examined. The C3 mice did not exhibit obvious coupling of HR and VO2 (r²=0.16±0.06) at baseline or with treatment. The B6 animals, however, appear to inherently possess a high association between HR and VO2 (r²= 0.40±0.08) and this association changed dramatically with exposure: i.e., FACB (r²=0.13±0.06) and O3CB (r²=0.60±0.01) exposures. Thus, these results suggest that HR and VO2 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. [ABSTRACT FROM AUTHOR]