Background: Diesel exhaust (DE), which is emitted from on-and off-road sources, is a complex mixture of toxic gaseous and particulate components that leads to triggered adverse cardiovascular effects ...such as arrhythmias. Objective: We hypothesized that increased risk of triggered arrhythmias 1 day after DE exposure is mediated by airway sensory nerves bearing transient receptor potential (TRP) channels e.g., transient receptor potential cation channel, member A1 (TRPA1) that, when activated by noxious chemicals, can cause a centrally mediated autonomie imbalance and heightened risk of arrhythmia. Methods: Spontaneously hypertensive rats implanted with radiotelemeters were whole-body exposed to either 500 μg/m³ (high) or 150 μg/m³ (low) whole DE (wDE) or filtered DE (wDE), or to filtered air (controls), for 4 hr. Arrhythmogenesis was assessed 24 hr later by continuous intravenous infusion of aconitine, an arrhythmogenic drug, while heart rate (HR) and electrocardiogram (ECG) were monitored. Results: Rats exposed to wDE or fDE had slightly higher HRs and increased low-frequency: high-frequency ratios (sympathetic modulation) than did controls; ECG showed prolonged ventricular depolarization and shortened repolarization periods. Rats exposed to wDE developed arrhythmia at lower doses of aconitine than did controls; the dose was even lower in rats exposed to fDE. Pretreatment of low wDE—exposed rats with a TRPA1 antagonist or sympathetic blockade prevented the heightened sensitivity to arrhythmia. Conclusions: These findings suggest that a single exposure to DE increases the sensitivity of the heart to triggered arrhythmias. The gaseous components appear to play an important role in the proarrhythmic response, which may be mediated by activation of TRPA1, and subsequent sympathetic modulation. As such, toxic inhalants may partly exhibit their toxicity by lowering the threshold for secondary triggers, complicating assessment of their risk.
The increasing size and frequency of wildland fires are leading to greater potential for cardiopulmonary disease and cancer in exposed populations; however, little is known about how the types of ...fuel and combustion phases affect these adverse outcomes.
We evaluated the mutagenicity and lung toxicity of particulate matter (PM) from flaming vs. smoldering phases of five biomass fuels, and compared results by equal mass or emission factors (EFs) derived from amount of fuel consumed.
A quartz-tube furnace coupled to a multistage cryotrap was employed to collect smoke condensate from flaming and smoldering combustion of red oak, peat, pine needles, pine, and eucalyptus. Samples were analyzed chemically and assessed for acute lung toxicity in mice and mutagenicity in
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The average combustion efficiency was 73 and 98% for the smoldering and flaming phases, respectively. On an equal mass basis, PM from eucalyptus and peat burned under flaming conditions induced significant lung toxicity potencies (neutrophil/mass of PM) compared to smoldering PM, whereas high levels of mutagenicity potencies were observed for flaming pine and peat PM compared to smoldering PM. When effects were adjusted for EF, the smoldering eucalyptus PM had the highest lung toxicity EF (neutrophil/mass of fuel burned), whereas smoldering pine and pine needles had the highest mutagenicity EF. These latter values were approximately 5, 10, and 30 times greater than those reported for open burning of agricultural plastic, woodburning cookstoves, and some municipal waste combustors, respectively.
PM from different fuels and combustion phases have appreciable differences in lung toxic and mutagenic potency, and on a mass basis, flaming samples are more active, whereas smoldering samples have greater effect when EFs are taken into account. Knowledge of the differential toxicity of biomass emissions will contribute to more accurate hazard assessment of biomass smoke exposures. https://doi.org/10.1289/EHP2200.
This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O3)-enhanced (SA-O3) smog atmospheres in mice. Based on our previous findings of filtered diesel ...exhaust we hypothesized that SA-O3 would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O3, or filtered air (FA) for 4 h. Heart rate (HR) and electrocardiogram were recorded continuously before, during and after exposure. Both SA-PM and SA-O3 increased heart rate variability (HRV) but only SA-PM increased HR. Normalization of responses to total hydrocarbons, gas-only hydrocarbons and PM concentration were performed to assess the relative contribution of each phase given the compositional variability. Normalization to PM concentration revealed that SA-O3 was more potent in increasing HRV, arrhythmogenesis, and causing ventilatory changes. However, there were no differences when the responses were normalized to total or gas-phase only hydrocarbons. Thus, this study demonstrates that a single exposure to smog causes cardiac effects in mice. Although the responses of SA-PM and SA-O3 are similar, the latter is more potent in causing electrical disturbances and breathing changes potentially due to the effects of irritant gases, which should therefore be accounted for more rigorously in health assessments.
Emissions from solid-fuel burning cookstoves are associated with 3 to 4 million premature deaths annually and contribute significantly to impacts on climate. Pellet-fueled gasifier stoves have some ...emission factors (EFs) approaching those of gas-fuel (liquid petroleum gas) stoves; however, their emissions have not been evaluated for biological effects. Here we used a new International Organization for Standardization (ISO) testing protocol to determine pollutant- and mutagenicity-EFs for a stove designed for pellet fuel, the Mimi Moto, and for two other forced-draft stoves, Xunda and Philips HD4012, burning pellets of hardwood or peanut hulls. The Salmonella assay-based mutagenicity-EFs (revertants/megajouledelivered) spanned three orders of magnitude and correlated highly (r = 0.99; n = 5) with EFs of the sum of 32 particle-phase polycyclic aromatic hydrocarbons (PAHs). The Mimi Moto/hardwood pellet combination had total-PAH- and mutagenicity-EFs 99.2 and 96.6% lower, respectively, compared to data published previously for the Philips stove burning non-pelletized hardwood, and 100 and 99.8% lower, respectively, compared to those of a wood-fueled three-stone fire. The Xunda burning peanut hull pellets had the highest fuel energy-based mutagenicity-EF (revertants/megajoulethermal) of the pellet stove/fuel combinations tested, which was between that of diesel exhaust, a known human carcinogen, and a natural-draft wood stove. Although the Mimi Moto burning hardwood pellets had the lowest fuel energy-based mutagenicity-EF, this value was between that of utility coal and utility wood boilers. This advanced stove/fuel combination has the potential to greatly reduce emissions in contrast to a traditional stove, but adequate ventilation is required to approach acceptable levels of indoor air quality.
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•Pellet cookstoves can be a clean energy solution for those reliant on solid fuels.•Here, five pellet cookstove/fuel combinations were assessed for PM mutagenicity.•Mutagenicity emission factors spanned 3 orders-of-magnitude & correlated with PAHs.•Cleanest combination was similar to utility boiler; dirtiest to that of diesel PM.•Pellet stoves can greatly reduce emissions, but adequate ventilation is required.
Emissions from a large peat fire in North Carolina in 2008 were associated with increased hospital admissions for asthma and the rate of heart failure in the exposed population. Peat fires often ...produce larger amounts of smoke and last longer than forest fires, however few studies have reported on their toxicity. Moreover, reliable alternatives to traditional animal toxicity testing are needed to reduce the number of animals required for hazard identification and risk assessments.
Size-fractionated particulate matter (PM; ultrafine, fine, and coarse) were obtained from the peat fire while smoldering (ENCF-1) or when nearly extinguished (ENCF-4). Extracted samples were analyzed for chemical constituents and endotoxin content. Female CD-1 mice were exposed via oropharyngeal aspiration to 100 μg/mouse, and assessed for relative changes in lung and systemic markers of injury and inflammation. At 24 h post-exposure, hearts were removed for ex vivo functional assessments and ischemic challenge. Lastly, 8 mm diameter lung slices from CD-1 mice were exposed (11 μg) ± co-treatment of PM with polymyxin B (PMB), an endotoxin-binding compound.
On an equi-mass basis, coarse ENCF-1 PM had the highest endotoxin content and elicited the greatest pro-inflammatory responses in the mice including: increases in bronchoalveolar lavage fluid protein, cytokines (IL-6, TNF-α, and MIP-2), neutrophils and intracellular reactive oxygen species (ROS) production. Exposure to fine or ultrafine particles from either period failed to elicit significant lung or systemic effects. In contrast, mice exposed to ENCF-1 ultrafine PM developed significantly decreased cardiac function and greater post-ischemia-associated myocardial infarction. Finally, similar exposures to mouse lung slices induced comparable patterns of cytokine production; and these responses were significantly attenuated by PMB.
The findings suggest that exposure to coarse PM collected during a peat fire causes greater lung inflammation in association with endotoxin and ROS, whereas the ultrafine PM preferentially affected cardiac responses. In addition, lung tissue slices were shown to be a predictive, alternative assay to assess pro-inflammatory effects of PM of differing size and composition. Importantly, these toxicological findings were consistent with the cardiopulmonary health effects noted in epidemiologic reports from exposed populations.
The Cleveland airshed comprises a complex mixture of industrial source emissions that contribute to periods of non-attainment for fine particulate matter (PM2.5) and are associated with increased ...adverse health outcomes in the exposed population. Specific PM sources responsible for health effects however are not fully understood. Size-fractionated PM (coarse, fine, and ultrafine) samples were collected using a ChemVol sampler at an urban site (G.T. Craig (GTC)) and rural site (Chippewa Lake (CLM)) from July 2009 to June 2010, and then chemically analyzed. The resulting speciated PM data were apportioned by EPA positive matrix factorization to identify emission sources for each size fraction and location. For comparisons with the ChemVol results, PM samples were also collected with sequential dichotomous and passive samplers, and evaluated for source contributions to each sampling site. The ChemVol results showed that annual average concentrations of PM, elemental carbon, and inorganic elements in the coarse fraction at GTC were ∼2, ∼7, and ∼3 times higher than those at CLM, respectively, while the smaller size fractions at both sites showed similar annual average concentrations. Seasonal variations of secondary aerosols (e.g., high NO3− level in winter and high SO42− level in summer) were observed at both sites. Source apportionment results demonstrated that the PM samples at GTC and CLM were enriched with local industrial sources (e.g., steel plant and coal-fired power plant) but their contributions were influenced by meteorological conditions and the emission source's operation conditions. Taken together the year-long PM collection and data analysis provides valuable insights into the characteristics and sources of PM impacting the Cleveland airshed in both the urban center and the rural upwind background locations. These data will be used to classify the PM samples for toxicology studies to determine which PM sources, species, and size fractions are of greatest health concern.
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•PM sources in the Cleveland airshed varied across regions and with seasons.•Local industrial source impacts in the urban site were higher than the rural site.•Local industrial sources were mostly emitted from steel and coal-fired power plants.•Local industrial source impacts were associated with meteorological conditions.
The Cleveland airshed was enriched with local industrial sources but their contributions were influenced by meteorological conditions and emission source operation conditions.
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.
No study has evaluated the mutagenicity of atmospheres with a calculated air quality health index (AQHI). Thus, we generated in a UV-light-containing reaction chamber two simulated atmospheres (SAs) ...with similar AQHIs but different proportions of criteria pollutants and evaluated them for mutagenicity in three Salmonella strains at the air-agar interface. We continuously injected into the chamber gasoline, nitric oxide, and ammonium sulfate, as well as either α-pinene to produce SA-PM, which had a high concentration of particulate matter (PM): 119 ppb ozone (O3), 321 ppb NO2, and 1007 μg/m3 PM2.5; or isoprene to produce SA-O3, which had a high ozone (O3) concentration: 415 ppb O3, 633 ppb NO2, and 55 μg/m3 PM2.5. Neither PM2.5 extracts, NO2, or O3 alone, nor nonphoto-oxidized mixtures were mutagenic or cytotoxic. Both photo-oxidized atmospheres were largely direct-acting base-substitution mutagens with similar mutagenic potencies in TA100 and TA104. The mutagenic potencies (revertants/h)/(mgC/m3) of SA-PM (4.3 ± 0.4) and SA-O3 (9.5 ± 1.3) in TA100 were significantly different (P < 0.0001), but the mutation spectra were not (P = 0.16), being ∼54% C → T and ∼46% C → A. Thus, the AQHI may have some predictive value for the mutagenicity of the gas phase of air.
Background: Exercise "stress" testing is a screening tool used to determine the amount of stress for which the heart can compensate before developing abnormal rhythm or ischemia, particularly in ...susceptible persons. Although this approach has been used to assess risk in humans exposed to air pollution, it has never been applied to rodent studies. Objective: We hypothesized that a single exposure to diesel exhaust (DE) would increase the risk of adverse cardiac events such as arrhythmia and myocardial ischemia in rats undergoing a dobutamine challenge test, which can be used to mimic exercise-like stress. Methods: Wistar-Kyoto normotensive (WKY) and spontaneously hypertensive (SH) rats implanted with radiotelemeters and a chronic intravenous catheter were whole-body exposed to 150 ug/m 3 DE for 4 hr. Increasing doses of dobutamine, a ß₁ -adrenergic agonist, were administered to conscious unrestrained rats 24 hr later to elicit the cardiac response observed during exercise while heart rate (HR) and electrocardiogram (ECG) were monitored. Results: A single exposure to DE potentiated the HR response of WKY and SH rats during dobutamine challenge and prevented HR recovery at rest. During peak challenge, DE-exposed SH rats had lower overall HR variability when compared with controls, in addition to transient ST depression. All DE-exposed animals also had increased arrhythmias. Conclusions: These results are the first evidence that rats exhibit stress-induced cardiac dysrhythmia and ischemia sensitivity comparable to humans after a single exposure to a toxic air pollutant, particularly when in the presence of underlying cardiovascular disease. Thus, exposure to low concentrations of air pollution can impair the heart's ability to respond to stress and increase the risk of subsequent triggered dysfunction.
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.
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