Cardiopulmonary effects of inhaled concentrated ambient particulate matter (PM2.5) downwind of a heavily trafficked freeway intersection in 22-month old Fischer 344 rats

Associations between air pollutants and mortality and morbidity mostly in elderly individuals have been documented. To test the hypothesis that fine ambient particles could stimulate cardiac responses and affect lung redox and inflammatory status in an elderly population, we exposed 22-month-old rats, as an aging model, to concentrated ambient fine particles (CAPs) or filtered air. Rats were exposed, whole body, for 4 hours/day for 3 consecutive days in a mobile exposure facility downwind of a heavily trafficked freeway intersection. Cardiovascular parameters were collected before and after exposure. Rats were sacrificed 18-24 hours after the end of the third day of exposure. We observed decreased levels in IL6 and cell signaling kinases in lung homogenate in addition to plasma c-reactive protein (CRP) in PM2.5-exposed rats in comparison to rats which had received filtered air. Redox balance of the lung tissue assayed did not exhibit any group differences. With respect to cardiovascular responses, increased trends in the root mean square of the standard deviation (rMSSD) of heart rate variability (HRV), a parameter highly correlated with vagal activity in the heart were observed on the second and third days of exposure. The standard deviation of normal to normal beat (SDNN) domain of HRV, an overall indicator of HRV, exhibited a relative increase in CAPs-exposed rats in comparison to filtered air-exposed rats on day 2. The ratio of the low frequency (LF) to high frequency (HF) range of HRV (LF is strongly associated with sympathetic activity and HF with parasympathetic activity) produced no significant differences among groups and neither did heart rate. Rat core temperature was decreased on day 2 of exposure as was blood pressure in exposed versus control groups. In addition, two exposed and no control rats exhibited increases in arrhythmia frequency. Thus, PM-exposed animals responded differently than control animals receiving filtered air as was obvious with the changes in core temperature, rMSSD and SDNN in addition to arrhythmia induction. The biochemical responses observed indicate a suppressive effect on some pro-inflammatory markers and cell signaling processes in the lung, the result of which might not be favorable given the role these molecules play in cardiac protection, apoptosis and general cellular function.