Elevated Exposures to Polycyclic Aromatic Hydrocarbons and Other Organic Mutagens in Ottawa Firefighters Participating in Emergency, On-Shift Fire Suppression.

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 F2t (8-iso-PGF2α) 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-PGF2α 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.

Comparative cardiopulmonary effects of size-fractionated airborne particulate matter.

CONTEXT: Strong epidemiological evidence exists linking particulate matter (PM) exposures with hospital admissions of individuals for cardiopulmonary symptoms. The PM size is important in influencing the extent of infiltration into the respiratory tract and systemic circulation and directs the differential physiological impacts. OBJECTIVE: To investigate the differential effects of the quasi-ultrafine (PM(0.2)), fine (PM(0.15-2.5)), and coarse PM (PM(2.5-10)) size fractions on pulmonary and cardiac function. METHODS: Female BALB/c mice were exposed to HEPA-filtered laboratory air or concentrated coarse, fine, or quasi-ultrafine PM using Harvard Ambient Particle Concentrators in conjunction with our nose-only exposure system. These exposures were conducted as part of the "Health Effects of Aerosols in Toronto (HEAT)" campaign. Following a 4 h exposure, mice underwent assessment of respiratory function and recording of electrocardiograms using the flexiVent® system. RESULTS: Exposure to coarse and fine PM resulted in a significant reduction in quasistatic compliance of the lung. Baseline total respiratory resistance and maximum responsiveness to methacholine were augmented after coarse PM exposures but were not affected by quasi-ultrafine PM exposures. In contrast, quasi-ultrafine PM alone had a significant effect on heart rate and in reducing heart rate variability. CONCLUSION: These findings indicate that coarse and fine PM influence lung function and airways responsiveness, while ultrafine PM can perturb cardiac function. This study supports the hypothesis that coarse and fine PM exerts its predominant physiologic effects at the site of deposition in the airways, whereas ultrafine PM likely crosses the alveolar epithelial barrier into the systemic circulation to affect cardiovascular function.

Cytotoxic and proinflammatory effects of ambient and source-related particulate matter (PM) in relation to the production of reactive oxygen species (ROS) and cytokine adsorption by particles.

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.

Polycyclic aromatic hydrocarbon (PAH) and metal contamination of air and surfaces exposed to combustion emissions during emergency fire suppression: Implications for firefighters' exposures.

This study examined occupational exposures of Ottawa firefighters to combustion by-products and selected metals. We measured exposures to polycyclic aromatic hydrocarbons (PAHs), antimony, cadmium, and lead using (1) personal air samplers worn by firefighters during emergency fire suppression; (2) wipe samples from skin, personal clothing, and personal protective equipment (PPE) collected before and after emergency firefighting (n = 29); and (3) air samples collected in three fire stations vehicle bays, truck cabs, and one administration office. We assessed OFS PPE decontamination procedures using wipe samples collected before and after laundering (n = 12). Air concentrations exceeded occupational exposure limits at two fire events for lead and nine for PAHs. After fire suppression, PAH concentrations were significantly higher on skin and PPE (p < 0.001), skin, clothing, and PPE for antimony (p < 0.001, 0.01, and 0.05, respectively), and skin and PPE for lead (p < 0.001). Air concentrations of PAHs and antimony were significantly higher in vehicle bays compared to the office (p < 0.05), but significantly lower compared to fire truck cabs (p < 0.05). Washing PPE was effective in removing, on average, 61% of PAHs, 55% of antimony, 97% of lead, and 90% of cadmium. These results indicate that firefighters are significantly exposed, via multiple routes, to combustion by-products during on-shift fire suppression.

The combined effects of physicochemical properties of size-fractionated ambient particulate matter on in vitro toxicity in human A549 lung epithelial cells.

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.