How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma-0

<p><b>Copyright information:</b></p><p>Taken from "How Exposure to Environmental Tobacco Smoke, Outdoor Air Pollutants, and Increased Pollen Burdens Influences the Incidence of Asthma"</p><p>Environmental Health Perspectives 2006;114(4):627-633.</p><p>Published online 26 Jan 2006</p><p>PMCID:PMC1440792.</p><p>This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.</p

Wildfire Variable Toxicity: Identifying Biomass Smoke Exposure Groupings through Transcriptomic Similarity Scoring

The prevalence of wildfires continues to grow globally with exposures resulting in increased disease risk. Characterizing these health risks remains difficult due to the wide landscape of exposures that can result from different burn conditions and fuel types. This study tested the hypothesis that biomass smoke exposures from variable fuels and combustion conditions group together based on similar transcriptional response profiles, informing which wildfire-relevant exposures may be considered as a group for health risk evaluations. Mice (female CD-1) were exposed via oropharyngeal aspiration to equal mass biomass smoke condensates produced from flaming or smoldering burns of eucalyptus, peat, pine, pine needles, or red oak species. Lung transcriptomic signatures were used to calculate transcriptomic similarity scores across exposures, which informed exposure groupings. Exposures from flaming peat, flaming eucalyptus, and smoldering eucalyptus induced the greatest responses, with flaming peat grouping with the pro-inflammatory agent lipopolysaccharide. Smoldering red oak and smoldering peat induced the least transcriptomic response. Groupings paralleled pulmonary toxicity markers, though they were better substantiated by higher data dimensionality and resolution provided through -omic-based evaluation. Interestingly, groupings based on smoke chemistry signatures differed from transcriptomic/toxicity-based groupings. Wildfire-relevant exposure groupings yield insights into risk assessment strategies to ultimately protect public health

Wildfire Variable Toxicity: Identifying Biomass Smoke Exposure Groupings through Transcriptomic Similarity Scoring

The prevalence of wildfires continues to grow globally with exposures resulting in increased disease risk. Characterizing these health risks remains difficult due to the wide landscape of exposures that can result from different burn conditions and fuel types. This study tested the hypothesis that biomass smoke exposures from variable fuels and combustion conditions group together based on similar transcriptional response profiles, informing which wildfire-relevant exposures may be considered as a group for health risk evaluations. Mice (female CD-1) were exposed via oropharyngeal aspiration to equal mass biomass smoke condensates produced from flaming or smoldering burns of eucalyptus, peat, pine, pine needles, or red oak species. Lung transcriptomic signatures were used to calculate transcriptomic similarity scores across exposures, which informed exposure groupings. Exposures from flaming peat, flaming eucalyptus, and smoldering eucalyptus induced the greatest responses, with flaming peat grouping with the pro-inflammatory agent lipopolysaccharide. Smoldering red oak and smoldering peat induced the least transcriptomic response. Groupings paralleled pulmonary toxicity markers, though they were better substantiated by higher data dimensionality and resolution provided through -omic-based evaluation. Interestingly, groupings based on smoke chemistry signatures differed from transcriptomic/toxicity-based groupings. Wildfire-relevant exposure groupings yield insights into risk assessment strategies to ultimately protect public health

Wildfire Variable Toxicity: Identifying Biomass Smoke Exposure Groupings through Transcriptomic Similarity Scoring

The prevalence of wildfires continues to grow globally with exposures resulting in increased disease risk. Characterizing these health risks remains difficult due to the wide landscape of exposures that can result from different burn conditions and fuel types. This study tested the hypothesis that biomass smoke exposures from variable fuels and combustion conditions group together based on similar transcriptional response profiles, informing which wildfire-relevant exposures may be considered as a group for health risk evaluations. Mice (female CD-1) were exposed via oropharyngeal aspiration to equal mass biomass smoke condensates produced from flaming or smoldering burns of eucalyptus, peat, pine, pine needles, or red oak species. Lung transcriptomic signatures were used to calculate transcriptomic similarity scores across exposures, which informed exposure groupings. Exposures from flaming peat, flaming eucalyptus, and smoldering eucalyptus induced the greatest responses, with flaming peat grouping with the pro-inflammatory agent lipopolysaccharide. Smoldering red oak and smoldering peat induced the least transcriptomic response. Groupings paralleled pulmonary toxicity markers, though they were better substantiated by higher data dimensionality and resolution provided through -omic-based evaluation. Interestingly, groupings based on smoke chemistry signatures differed from transcriptomic/toxicity-based groupings. Wildfire-relevant exposure groupings yield insights into risk assessment strategies to ultimately protect public health

Characterization of Size-Fractionated Airborne Particles Inside an Electronic Waste Recycling Facility and Acute Toxicity Testing in Mice

Disposal of electronic waste (e-waste) in landfills, incinerators, or at rudimentary recycling sites can lead to the release of toxic chemicals into the environment and increased health risks. Developing e-waste recycling technologies at commercial facilities can reduce the release of toxic chemicals and efficiently recover valuable materials. While these e-waste operations represent a vast improvement over previous approaches, little is known about environmental releases, workplace exposures, and potential health impacts. In this study, airborne particulate matter (PM) was measured at various locations within a modern U.S.-based e-waste recycling facility that utilized mechanical processing. In addition, composite size fractionated PM (coarse, fine and ultrafine) samples were collected, extracted, chemically analyzed, and given by oropharyngeal aspiration to mice or cultured with lung slices for lung toxicity tests. Indoor total PM concentrations measured during the study ranged from 220 to 1200 μg/m³. In general, the coarse PM (2.5–10 μm) was 3–4 times more abundant than fine/ultrafine PM (<2.5 μm). The coarse PM contained higher levels of Ni, Pb, and Zn (up to 6.8 times) compared to the fine (0.1–2.5 μm) and ultrafine (<0.1 μm) PM. Compared to coarse PM measurements from a regional near-roadway study, Pb and Ni were enriched 170 and 20 times, respectively, in the indoor PM, with other significant enrichments (>10 times) observed for Zn and Sb, modest enrichments (>5 times) for Cu and Sr, and minor enrichments (>2 times) for Cr, Cd, Mn, Ca, Fe, and Ba. Negligible enrichment (<2 times) or depletion (<1 time) were observed for Al, Mg, Ti, Si, and V. The coarse PM fraction elicited significant pro-inflammatory responses in the mouse lung at 24 h postexposure compared to the fine and ultrafine PM, and similar toxicity outcomes were observed in the lung slice model. We conclude that exposure to coarse PM from the facility caused substantial inflammation in the mouse lung and enrichment of these metals compared to levels normally present in the ambient PM could be of potential health concern

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

Differential Effects of Particulate Matter Upwind and Downwind of an Urban Freeway in an Allergic Mouse Model

Near-road exposure to air pollutants has been associated with decreased lung function and other adverse health effects in susceptible populations. This study was designed to investigate whether different types of near-road particulate matter (PM) contribute to exacerbation of allergic asthma. Samples of upwind and downwind coarse, fine, and ultrafine PM were collected using a wind direction-actuated ChemVol sampler at a single site 100 m from Interstate-96 in Detroit, MI during winter 2010/2011. Upwind PM was enriched in crustal and wood combustion sources while downwind PM was dominated by traffic sources. Control and ovalbumin (OVA)-sensitized BALB/cJ mice were exposed via oropharyngeal (OP) aspiration to 20 or 100 μg of each PM sample 2 h prior to OP challenge with OVA. In OVA-allergic mice, 100 μg of downwind coarse PM caused greater increases than downwind fine/ultrafine PM in bronchoalveolar lavage neutrophils, eosinophils, and lactate dehydrogenase. Upwind fine PM (100 μg) produced greater increases in neutrophils and eosinophils compared to other upwind size fractions. Cytokine (IL-5) levels in BAL fluid also increased markedly following 100 μg downwind coarse and downwind ultrafine PM exposures. These findings indicate coarse PM downwind and fine PM upwind of an interstate highway promote inflammation in allergic mice

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

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