Asphalt fumes are complex mixtures of particulate and organic compounds. Field studies report an increased incidence of mucus membrane irritation and workshift decline of peak flow for road pavers. The objective of the present study was to characterize the acute pulmonary responses in rats after AFC exposure. AFC was collected from a paving asphalt storage tank. Rats received a single intratracheal instillation (IT) of saline, 0.1 or 0.5 mg AFC and were sacrificed 1- or 3-day later. Another set of rats were exposed by IT to saline, 0.1, 0.5, or 2 mg AFC for 3 consecutive days and were sacrificed the following day. Differential cell counts, acellular protein and lactate dehydrogenase (LDH) were measured in bronchoalveolar lavage fluid (BALF) to monitor inflammation and damage. Chemiluminescence (CL) generated from alveolar macrophages (AM) was measured and tumor necrosis factor-a (TNF-alpha) and interleukin-l (IL-I) in AM-conditioned media were assayed to monitor AM function. The results show that AFC exposure did not induce significant neutrophil infiltration or alter LDH and protein content in BALF. CL and nitric oxide-dependent CL generated from APC-exposed AM were not different from control at rest or in response to zymosan stimulation. Likewise, AFC exposure did not induce increased TNF-alpha or IL-1 secretion from AM at rest or in response to LPS. These results suggest that exposure of rats to APC did not cause acute pulmonary inflammation or injury. Furthermore, AFC exposure did not alter AM functions such as the release of oxidants or inflammatory cytokines by AM at rest or in response to stimulants.
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