Characterization of Carbonaceous Aerosols Emitted from Outdoor Wood Boilers

This study examines the chemical properties of carbonaceous aerosols emitted from different outdoor wood-fired boiler (OWB) technologies including two cord wood heaters, a pellet heater, and a multistage gasifier/combustor. The effect of fuel type [red oak wood (Quercus rubra), white pine wood (Pinus strobes), and red oak with supplementary refuse] on aerosol composition was examined using a classic boiler unit. Aerosol particle emissions were captured using established filter-based sampling methodology and subsequently analyzed using thermal-optical analysis and gas chromatography–mass spectrometry (GC-MS) techniques. GC-MS was coupled with a novel reduced-volume solvent extraction technique for semivolatile organic compound (SVOC) analysis. GC-MS identified 9% w/w of the aerosol mass emitted from the OWBs on average. The OWB aerosols comprised 1–5% w/w levoglucosan, an important molecular marker of cellulose pyrolysis. Organic acid and methoxyphenol SVOC classes showed the highest average concentrations in the OWB aerosol. Polycyclic aromatic hydrocarbons (PAHs) accounted for between 0.1 and 4% w/w of the aerosol mass; PAH emissions from pine wood combustion in the classic OWB were notably high. Each of the original 16 EPA priority PAHs was detected in the OWB PM emissions. Wood combustion in the OWB released significantly more PAH per unit mass of fuel burned than either domestic fireplace or woodstove appliances; although, changes in PAH enrichment (μg/kg aerosol) among domestic wood combustion aerosols was less certain. Of the OWBs tested, the pellet heater showed the lowest SVOC emissions on a mass of fuel burned basis. However, OWB technology did not always significantly influence the SVOC composition of the particle emissions

Early-Life Persistent Vitamin D Deficiency Alters Cardiopulmonary Responses to Particulate Matter-Enhanced Atmospheric Smog in Adult Mice

Early life nutritional deficiencies can lead to increased cardiovascular susceptibility to environmental exposures. Thus, the purpose of this study was to examine the effect of early life persistent vitamin D deficiency (VDD) on the cardiopulmonary response to a particulate matter-enhanced photochemical smog. Mice were fed a VDD or normal diet (ND) after weaning. At 17 weeks of age, mice were implanted with radiotelemeters to monitor electrocardiogram, heart rate (HR), and heart rate variability (HRV). Ventilatory function was measured throughout the diet before and after smog exposure using whole-body plethysmography. VDD mice had lower HR, increased HRV, and decreased tidal volume compared with ND. Regardless of diet, HR decreased during air exposure; this response was blunted by smog in ND mice and to a lesser degree in VDD. When compared with ND, VDD increased HRV during air exposure and more so with smog. However, smog only increased cardiac arrhythmias in ND mice. This study demonstrates that VDD alters the cardiopulmonary response to smog, highlighting the possible influence of nutritional factors in determining responses to air pollution. The mechanism of how VDD induces these effects is currently unknown, but modifiable factors should be considered when performing risk assessment of complex air pollution atmospheres

Comparative cardiopulmonary toxicity of exhausts from soy-based biofuels and diesel in healthy and hypertensive rats

<p>Increased use of renewable energy sources raise concerns about health effects of new emissions. We analyzed relative cardiopulmonary health effects of exhausts from (1) 100% soy biofuel (B100), (2) 20% soy biofuel + 80% low sulfur petroleum diesel (B20), and (3) 100% petroleum diesel (B0) in rats. Normotensive Wistar–Kyoto (WKY) and spontaneously hypertensive rats were exposed to these three exhausts at 0, 50, 150 and 500 μg/m³, 4 h/day for 2 days or 4 weeks (5 days/week). In addition, WKY rats were exposed for 1 day and responses were analyzed 0 h, 1 day or 4 days later for time-course assessment. Hematological parameters, <i>in vitro</i> platelet aggregation, bronchoalveolar lavage fluid (BALF) markers of pulmonary injury and inflammation, <i>ex vivo</i> aortic ring constriction, heart and aorta mRNA markers of vasoconstriction, thrombosis and atherogenesis were analyzed. The presence of pigmented macrophages in the lung alveoli was clearly evident with all three exhausts without apparent pathology. Overall, exposure to all three exhausts produced only modest effects in most endpoints analyzed in both strains. BALF γ-glutamyl transferase (GGT) activity was the most consistent marker and was increased in both strains, primarily with B0 (B0 > B100 > B20). This increase was associated with only modest increases in BALF neutrophils. Small and very acute increases occurred in aorta mRNA markers of vasoconstriction and thrombosis with B100 but not B0 in WKY rats. Our comparative evaluations show modest cardiovascular and pulmonary effects at low concentrations of all exhausts: B0 causing more pulmonary injury and B100 more acute vascular effects. BALF GGT activity could serve as a sensitive biomarker of inhaled pollutants.</p

Photochemical Conversion of Surrogate Emissions for Use in Toxicological Studies: Role of Particulate- and Gas-Phase Products

The production of photochemical atmospheres under controlled conditions in an irradiation chamber permits the manipulation of parameters that influence the resulting air-pollutant chemistry and potential biological effects. To date, no studies have examined how contrasting atmospheres with a similar Air Quality Health Index (AQHI), but with differing ratios of criteria air pollutants, might differentially affect health end points. Here, we produced two atmospheres with similar AQHIs based on the final concentrations of ozone, nitrogen dioxide, and particulate matter (PM_2.5). One simulated atmosphere (SA-PM) generated from irradiation of ∼23 ppmC gasoline, 5 ppmC α-pinene, 529 ppb NO, and 3 μg m^–3 (NH₄)₂SO₄ as a seed resulted in an average of 976 μg m^–3 PM_2.5, 326 ppb NO₂, and 141 ppb O₃ (AQHI 97.7). The other atmosphere (SA-O₃) generated from 8 ppmC gasoline, 5 ppmC isoprene, 874 ppb NO, and 2 μg m^–3 (NH₄)₂SO₄ resulted in an average of 55 μg m^–3 PM_2.5, 643 ppb NO₂, and 430 ppb O₃ (AQHI of 99.8). Chemical speciation by gas chromatography showed that photo-oxidation degraded the organic precursors and promoted the de novo formation of secondary reaction products such as formaldehyde and acrolein. Further work in accompanying papers describe toxicological outcomes from the two distinct photochemical atmospheres

Soy biodiesel emissions have reduced inflammatory effects compared to diesel emissions in healthy and allergic mice

<p>Toxicity of exhaust from combustion of petroleum diesel (B0), soy-based biodiesel (B100), or a 20% biodiesel/80% petrodiesel mix (B20) was compared in healthy and house dust mite (HDM)-allergic mice. Fuel emissions were diluted to target fine particulate matter (PM_2.5) concentrations of 50, 150, or 500 μg/m³. Studies in healthy mice showed greater levels of neutrophils and MIP-2 in bronchoalveolar lavage (BAL) fluid 2 h after a single 4-h exposure to B0 compared with mice exposed to B20 or B100. No consistent differences in BAL cells and biochemistry, or hematological parameters, were observed after 5 d or 4 weeks of exposure to any of the emissions. Air-exposed HDM-allergic mice had significantly increased responsiveness to methacholine aerosol challenge compared with non-allergic mice. Exposure to any of the emissions for 4 weeks did not further increase responsiveness in either non-allergic or HDM-allergic mice, and few parameters of allergic inflammation in BAL fluid were altered. Lung and nasal pathology were not significantly different among B0-, B20-, or B100-exposed groups. In HDM-allergic mice, exposure to B0, but not B20 or B100, significantly increased resting peribronchiolar lymph node cell proliferation and production of T_H2 cytokines (IL-4, IL-5, and IL-13) and IL-17 in comparison with air-exposed allergic mice. These results suggest that diesel exhaust at a relatively high concentration (500 μg/m³) can induce inflammation acutely in healthy mice and exacerbate some components of allergic responses, while comparable concentrations of B20 or B100 soy biodiesel fuels did not elicit responses different from those caused by air exposure alone.</p

Effects of Simulated Smog Atmospheres in Rodent Models of Metabolic and Immunologic Dysfunction

Air pollution is a diverse and dynamic mixture of gaseous and particulate matter, limiting our understanding of associated adverse health outcomes. The biological effects of two simulated smog atmospheres (SA) with different compositions but similar air quality health indexes were compared in a nonobese diabetic rat model (Goto-Kakizaki, GK) and three mouse immune models (house dust mite (HDM) allergy, antibody response to heat-killed pneumococcus, and resistance to influenza A infection). In GK rats, both SA-PM (high particulate matter) and SA-O₃ (high ozone) decreased cholesterol levels immediately after a 4-h exposure, whereas only SA-O₃ increased airflow limitation. Airway responsiveness to methacholine was increased in HDM-allergic mice compared with nonallergic mice, but exposure to SA-PM or SA-O₃ did not significantly alter responsiveness. Exposure to SA-PM did not affect the IgM response to pneumococcus, and SA-O₃ did not affect virus titers, although inflammatory cytokine levels were decreased in mice infected at the end of a 7-day exposure. Collectively, acute SA exposures produced limited health effects in animal models of metabolic and immune diseases. Effects of SA-O₃ tended to be greater than those of SA-PM, suggesting that gas-phase components in photochemically derived multipollutant mixtures may be of greater concern than secondary organic aerosol PM