Airborne particulate matter (PM) may lead to increased cardiac risk through an inflammatory pathway. Therefore, we investigated associations between ambient PM and markers of systemic inflammation among repeated measures from 44 senior citizens (≥ 60 years of age) and examined susceptibility by conditions linked to chronic inflammation. Mixed models were used to identify associations between concentrations of fine PM [aerodynamic diameter ≤ 2.5 μm (PM2.5)] averaged over 1–7 days and measures of C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cells (WBCs). Effect modification was investigated for diabetes, obesity, hypertension, and elevated mean inflammatory markers. We found positive associations between longer moving averages of PM2.5 and WBCs across all participants, with a 5.5% [95% confidence interval (CI), 0.10 to 11%] increase per interquartile increase (5.4 μg/m3) of PM2.5 averaged over the previous week. PM2.5 and CRP also exhibited positive associations among all individuals for averages longer than 1 day, with the largest associations for persons with diabetes, obesity, and hypertension. For example, an interquartile increase in the 5-day mean PM2.5 (6.1 μg/m3) was associated with a 14% increase in CRP (95% CI, −5.4 to 37%) for all individuals and an 81% (95% CI, 21 to 172%) increase for persons with diabetes, obesity, and hypertension. Persons with diabetes, obesity, and hypertension also exhibited positive associations between PM2.5 and IL-6. Individuals with elevated mean inflammatory markers exhibited enhanced associations with CRP, IL-6, and WBCs. We found modest positive associations between PM2.5 and indicators of systemic inflammation, with larger associations suggested for individuals with diabetes, obesity, hypertension, and elevated mean inflammatory markers.

A photoelectric aerosol sensor (PAS) was used to measure real-time indoor concentrations of polycyclic aromatic hydrocarbons (PAHs) at three residences. Semi-quantitative measurements of total indoor particle-bound PAH and temperature were collected continuously every minute for approximately 2 weeks at each location. The purpose of this study was to examine the effect of traffic on indoor concentrations of PAHs. This was accomplished by collecting indoor measurements at an urban, semi-urban, and suburban residential location with varying levels of, and proximity to, traffic. Since the homes were occupied, the effects of cooking, the dominant indoor source, were also examined among the three nonsmoking households. The results indicate that traffic was the main outdoor source of PAH concentrations measured indoors for all locations. In fact, a significant (p<0.001) traffic-related trend in weekday PAH concentration was detected with a geometric mean concentration at the urban location (31 ng/m 3 ) nearly two times that at the semi-urban location (19 ng/m 3 ) and over three times larger than the suburban location (8.0 ng/m 3 ), once adjusted for indoor sources. Hourly average concentration profiles also revealed weekday rush hour peaks of PAHs at all locations. No pronounced peaks and significantly lower concentrations (10, 10, and 4.9 ng/m 3 ) were seen during the weekends for all locations i.e., the urban, semi-urban and suburban locations, respectively. Indoor sources including frying/saute Âing, broiling, and candle-burning were characterized by peak concentration, duration of PAH elevation, and potential dose. This analysis suggests that cooking, and especially frying/saute Âing, may be an important source of indoor PAH concentrations.

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