Measurements of Gross α- and ß-Activities of Archived PM2.5 and PM10 Teflon Filter Samples.

The adverse effects of ambient particulate matter (PM) on human health have been well demonstrated, but the underlying properties responsible for its toxicity are still unclear. We hypothesized that particulate radioactivity, which is due to the attachment of radioactive nuclides on particle surfaces, may be responsible for part of PM toxicity. We measured the gross α- and ß-activities for daily PM2.5 and PM10 filters collected at the Harvard Supersite in downtown Boston from 2005 to 2006 and calculated the radioactivities at the time of air sampling retrospectively based on a previously established formula. We examined the relationship between different radioactivities and compared our measurements to those measured at the Boston EPA RadNet Station. The results showed that the majority of PM10 radioactivity is associated with that of PM2.5 samples for both α-activity (98%) and ß-activity (83%). A strong linear relationship was observed between the α- and ß-activities for both PM2.5 [slope = 0.47 (±0.03); p-value < 0.0001] and PM10 [slope = 0.46 (±0.09); p-value < 0.0001] samples. Measurements at the Harvard Supersite and at EPA RadNet sites are highly correlated for both α-activities [slope = 0.17 (±0.02), p-value < 0.0001] and ß-activities [slope = 0.30 (±0.05), p-value < 0.0001]. Additionally, we identified several significant predictors for PM2.5 α-activities. This novel method we developed to measure α- and ß-activities from archived filters will make it possible to assess the retrospective particle radioactivity exposure for future epidemiological studies.

Secondary particles formed from the exhaust of vehicles using ethanol-gasoline blends increase the production of pulmonary and cardiac reactive oxygen species and induce pulmonary inflammation.

BACKGROUND: Ethanol vehicles release exhaust gases that contribute to the formation of secondary organic aerosols (SOA). OBJECTIVE: To determine in vivo toxicity resulting from exposure to SOA derived from vehicles using different ethanol-gasoline blends (E0, E10, E22, E85W, E85S, E100). METHODS: Exhaust emissions from vehicles using ethanol blends were delivered to a photochemical chamber and reacted to produce SOA. The aerosol samples were collected on filters, extracted, and dispersed in an aqueous solutions and intratracheally instilled into Sprague Dawley rats in doses of 700 µg/0.2 ml. After 45 min and 4 h pulmonary and cardiac chemiluminescence (CL) was measured to estimate the amount of reactive oxygen species (ROS) produced in the lungs and heart. Inflammation was measured by differential cell count in bronchoalveolar lavages (BAL). RESULTS: Statistically and biologically significant differences in response to secondary particles from the different fuel formulations were detected. Compared to the control group, animals exposed to SOA from gasoline (E0) showed a significantly higher average CL in the lungs at 45 min. The highest CL averages in the heart were observed in the groups exposed to SOA from E10 and pure ethanol (E100) at 45 min. BAL of animals exposed to SOA from E0 and E85S had a significant increased number of macrophages at 45 min. BAL neutrophil count was increased in the groups exposed to E85S (45 min) and E0 (4 h). Animals exposed to E0 and E85W had increased BAL lymphocyte count compared to the control and the other exposed groups. DISCUSSION: Our results suggest that SOA generated by gasoline (E0), followed by ethanol blends E85S and E85W, substantially induce oxidative stress measured by ROS generation and pulmonary inflammation measured by the recruitment of white blood cells in BAL.