The composition of airborne particulate matter (PM) varies widely depending on its source, and recent studies have suggested that particle-associated adverse health effects are related to particle composition. The objective of this study was to compare the biological/toxicological effects of different source-related PM. Specifically, we investigated the biological/toxicological effects of standard reference materials (SRMs): non-ferrous dust (PD-1, industrial), urban PM (UPM, SRM1648a), and diesel PM (DPM, SRM2975), and ambient PM(2.5) (PM with an aerodynamic diameter <2.5 µm) collected at an urban site (Toronto, Canada). The dithiothreitol assay was used to measure the redox activity of the particles. Human alveolar epithelial cells (A549) were exposed to a range of concentrations (10-1000 µg/ml) of total PM, and the respective water-soluble and insoluble fractions, for 24 h. Biological responses were then evaluated in terms of cytotoxicity and interleukin (IL)-8 release, and compared with the PM composition and redox activity. We demonstrated that transition metal-enriched PD-1 exhibited the greatest cytotoxic effect (LD(50) values of 100-400 µg/ml vs. >1000 µg/ml for the SRM1648a, SRM2975, and ambient PM(2.5)). Similarly, the PM-induced release of IL-8 was greatest for PD-1 (~6-9 ng/ml vs. ~1.5-3 ng/ml for others). These endpoints were more responsive to metals as compared with compared with secondary inorganic ions and organic compounds. Interestingly, we demonstrated a high degree of adsorption of IL-8 to the various SRMs and ambient PM(2.5), and subsequently derived a new correction method to aid in interpretation of these data. These characteristics likely impart differential effects toward the toxic and immune effects of PM.
Occupational exposures to combustion emissions were examined in Ottawa Fire Service (OFS) firefighters. Paired urine and dermal wipe samples (i.e., pre- and post-event) as well as personal air samples and fire event questionnaires were collected from 27 male OFS firefighters. A total of 18 OFS office workers were used as additional controls. Exposures to polycyclic aromatic hydrocarbons (PAHs) and other organic mutagens were assessed by quantification of urinary PAH metabolite levels, levels of PAHs in dermal wipes and personal air samples, and urinary mutagenicity using the Salmonella mutagenicity assay (Ames test). Urinary Clara Cell 16 (CC16) and 15-isoprostane F (8-iso-PGF) levels were used to assess lung injury and overall oxidative stress, respectively. The results showed significant 2.9- to 5.3-fold increases in average post-event levels of urinary PAH metabolites, depending on the PAH metabolite (p < 0.0001). Average post-event levels of urinary mutagenicity showed a significant, event-related 4.3-fold increase (p < 0.0001). Urinary CC16 and 8-iso-PGF did not increase. PAH concentrations in personal air and on skin accounted for 54% of the variation in fold changes of urinary PAH metabolites (p < 0.002). The results indicate that emergency, on-shift fire suppression is associated with significantly elevated exposures to combustion emissions.
Windsor (Ontario, Canada) experiences trans-boundary air pollution as it is located on the border immediately downwind of industrialized regions of the United States of America. A study was conducted in 2007 to identify the potential regional sources of total gaseous mercury (TGM) and investigate the effects of regional sources and other factors on seasonal variability of TGM concentrations in Windsor. <br><br> TGM concentration was measured at the University of Windsor campus using a Tekran® 2537A Hg vapour analyzer. An annual mean of 2.02±1.63 ng/m<sup>3</sup> was observed in 2007. The average TGM concentration was high in the summer (2.48±2.68 ng/m<sup>3</sup>) and winter (2.17±2.01 ng/m<sup>3</sup>), compared to spring (1.88±0.78 ng/m<sup>3</sup>) and fall (1.76±0.58 ng/m<sup>3</sup>). Hybrid receptor modeling potential source contribution function (PSCF) was used by incorporating 72-h backward trajectories and measurements of TGM in Windsor. The results of PSCF were analyzed in conjunction with the Hg emissions inventory of North America (by state/province) to identify regions affecting Windsor. In addition to annual modeling, seasonal PSCF modeling was also conducted. The potential source region was identified between 24–61° N and 51–143° W. Annual PSCF modeling identified major sources southwest of Windsor, stretching from Ohio to Texas. The emissions inventory also supported the findings, as Hg emissions were high in those regions. Results of seasonal PSCF modeling were analyzed to find the combined effects of regional sources, meteorological conditions, and surface re-emissions, on seasonal variability of Hg concentrations. It was found that the summer and winter highs of atmospheric Hg can be attributed to areas where large numbers of coal fired power plants are located in the USA. Weak atmospheric dispersion due to low winds and high re-emission from surfaces due to higher temperatures also contributed to high concentrations in the summer. In the winter, the atmospheric removal of Hg was slow, but strong winds led to more dispersion, resulting in lower concentrations than the summer. Future studies could use smaller grid sizes and refined emission inventories, for more accurate analysis of source-receptor relationship of atmospheric Hg
Epidemiological and toxicological studies have suggested that the health effects associated with exposure to particulate matter (PM) are related to the different physicochemical properties of PM. These effects occur through the initiation of differential cellular responses including: the induction of antioxidant defenses, proinflammatory responses, and ultimately cell death. The main objective of this study was to investigate the effects of size-fractionated ambient PM on epithelial cells in relation to their physicochemical properties. Concentrated ambient PM was collected on filters for three size fractions: coarse (aerodynamic diameter [AD] 2.5–10 μm), fine (0.15–2.5 μm), and quasi-ultrafine (<0.2 μm), near a busy street in Toronto, Ontario, Canada. Filters were extracted and analyzed for chemical composition and redox activity. Chemical analyses showed that the coarse, fine, and quasi-ultrafine particles were comprised primarily of metals, water-soluble species, and organic compounds, respectively. The highest redox activity was observed for fine PM. After exposure of A549 cells to PM (10–100 μg/ml) for 4 h, activation of antioxidant, proinflammatory and cytotoxic responses were assessed by determining the expression of heme oxygenase (HMOX-1, mRNA), interleukin-8 (IL-8, mRNA), and metabolic activity of the cells, respectively. All three size fractions induced mass-dependent antioxidant, proinflammatory, and cytotoxic responses to different degrees. Quasi-ultrafine PM caused significant induction of HMOX-1 at the lowest exposure dose. Correlation analyses with chemical components suggested that the biological responses correlated mainly with transition metals and organic compounds for coarse and fine PM and with organic compounds for quasi-ultrafine PM. Overall, the observed biological responses appeared to be related to the combined effects of size and chemical composition and thus both of these physicochemical properties should be considered when explaining PM toxicity.
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