Acute symptoms associated with asphalt fume exposure among road pavers.
ABSTRACT Although asphalt fume is a recognized irritant, previous studies of acute symptoms during asphalt paving have produced inconsistent results. Between 1994 and 1997, the National Institute for Occupational Safety and Health (NIOSH) evaluated workers at seven sites in six states.
NIOSH (a) measured exposures of asphalt paving workers to total (TP) and benzene-soluble particulate (BSP), polycyclic aromatic compounds, and other substances; (b) administered symptom questionnaires pre-shift, every 2 hr during the shift, and post-shift to asphalt exposed and nonexposed workers; and (c) measured peak expiratory flow rate (PEFR) of asphalt paving workers when they completed a symptom questionnaire.
Full-shift time-weighted average exposures to TP and BSP ranged from 0.01 to 1.30 mg/m(3) and 0.01 to 0.82 mg/m(3), respectively. Most BSP concentrations were <0.50 mg/m(3). Asphalt workers had a higher occurrence rate of throat irritation than nonexposed workers [13% vs. 4%, odds ratio (OR) = 4.0, 95% confidence interval (CI): 1.2-13]. TP, as a continuous variable, was associated with eye (OR = 1.34, 95% CI: 1.12-1.60) and throat (OR = 1.40, 95% CI: 1.06-1.85) symptoms. With TP dichotomous at 0.5 mg/m(3), the ORs and 95% CIs for eye and throat symptoms were 7.5 (1.1-50) and 15 (2.3-103), respectively. BSP, dichotomous at 0.3 mg/m(3), was associated with irritant (eye, nose, or throat) symptoms (OR = 11, 95% CI: 1.5-84). One worker, a smoker, had PEFR-defined bronchial lability, which did not coincide with respiratory symptoms.
Irritant symptoms were associated with TP and BSP concentrations at or below 0.5 mg/m(3).
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ABSTRACT: The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats. For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function. In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages. These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.Archive für Toxikologie 11/2000; 74(8):452-9. · 5.22 Impact Factor
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ABSTRACT: Asphalt fumes are complex mixtures of various organic compounds, including polycyclic aromatic hydrocarbons (PAHs). PAHs require bioactivation by the cytochrome P-450 monooxygenase system to exert toxic/carcinogenic effects. The present study was carried out to characterize the acute pulmonary inflammatory responses and the alterations of pulmonary xenobiotic pathways in rats exposed to asphalt fumes by inhalation. Rats were exposed at various doses and time periods to air or to asphalt fumes generated at paving temperatures. To assess the acute damage and inflammatory responses, differential cell counts, acellular lactate dehydrogenase (LDH) activity, and protein content of bronchoalveolar lavage fluid were determined. Alveolar macrophage (AM) function was assessed by monitoring generation of chemiluminescence and production of tumor necrosis factor-alpha and interleukin-1. Alteration of pulmonary xenobiotic pathways was determined by monitoring the protein levels and activities of P-450 isozymes (CYP1A1 and CYP2B1), glutathioneS-transferase (GST), and NADPH:quinone oxidoreductase (QR). The results show that acute asphalt fume exposure did not cause neutrophil infiltration, alter LDH activity or protein content, or affect AM function, suggesting that short-term asphalt fume exposure did not induce acute lung damage or inflammation. However, acute asphalt fume exposure significantly increased the activity and protein level of CYP1A1 whereas it markedly reduced the activity and protein level of CYP2B1 in the lung. The induction of CYP1A1 was localized in nonciliated bronchiolar epithelial (Clara) cells, alveolar septa, and endothelial cells by immunofluorescence microscopy. Cytosolic QR activity was significantly elevated after asphalt fume exposure, whereas GST activity was not affected by the exposure. This induction of CYP1A1 and QR with the concomitant down-regulation of CYP2B1 after asphalt fume exposure could alter PAH metabolism and may lead to potential toxic effects in the lung.Environmental Health Perspectives 08/2003; 111(9):1215-21. · 7.26 Impact Factor
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ABSTRACT: This study examines possible associations between asphalt fumes and workshift changes in lung function and symptoms among 170 workers exposed to asphalt fumes. The workers were from 5 segments of the asphalt industry, and most of them participated for 2 consecutive workdays. The primary response variables were changes in lung function (measured at the beginning and end of the shift) and incidence of symptoms (measured before, 3 times during, and at the end of the shift). Exposure was estimated from breathing-zone samples of total particulate (TP), respirable particulate (RP), the benzene-soluble fraction of the TP (BSF), volatile hydrocarbons collected on a charcoal tube (VHC), nitrogen dioxide, sulfur dioxide, formaldehyde, carbon monoxide, and hydrogen sulfide. Ozone and wet bulb/dry bulb temperature, as a measure of heat stress, were measured as area samples. In addition, daily cigarette smoking was determined by questionnaire. The exposure-response associations were assessed by both parametric and nonparametric statistical techniques. Overall, no consistent association was observed between an acute reduction in lung function or the incidence of symptoms and exposure to asphalt fumes. Concentrations in the neighborhood of the maximum levels constitute no-observed adverse effect levels: TP (<1.5 mg/m3 to maximum 6.2 mg/m3), RP (<0.6 mg/m3 to maximum 1.4 mg/m3), BSF (<0.6 mg/m3 to maximum 1.3 mg/m3), VHC (<8 mg/m3 to maximum 19.8 mg/m3). There were no exposure-response trends with ozone, heat stress, cigarettes smoked, or length of workday.Scandinavian journal of work, environment & health 07/1999; 25(3):186-206. · 3.78 Impact Factor