Depleted Housing Elicits Cardiopulmonary Dysfunction After a Single Flaming Eucalyptus Wildfire Smoke Exposure in a Sex-Specific Manner in ApoE Knockout Mice.

Although it is well established that wildfire smoke exposure can increase cardiovascular morbidity and mortality, the combined effects of non-chemical stressors and wildfire smoke remains understudied. Housing is a non-chemical stressor that is a major determinant of cardiovascular health, however, disparities in neighborhood and social status have exacerbated the cardiovascular health gaps within the United States. Further, pre-existing cardiovascular morbidities, such as atherosclerosis, can worsen the response to wildfire smoke exposures.

Enriched housing differentially alters allostatic load and cardiopulmonary responses to wildfire-related smoke in male and female mice.

Living conditions are an important modifier of individual health outcomes and may lead to higher allostatic load (AL). However, housing-induced cardiovascular and immune effects contributing to altered environmental responsiveness remain understudied. This investigation was conducted to examine the influence of enriched (EH) versus depleted housing (DH) conditions on cardiopulmonary functions, systemic immune responses, and allostatic load in response to a single wildfire smoke (WS) exposure in mice.

Depleted housing elicits cardiopulmonary dysfunction after a single flaming eucalyptus wildfire smoke exposure in a sex-specific manner in ApoE knockout mice.

Although it is well established that wildfire smoke exposure can increase cardiovascular morbidity and mortality, the combined effects of non-chemical stressors and wildfire smoke remains understudied. Housing is a non-chemical stressor that is a major determinant of cardiovascular health, however, disparities in neighborhood and social status have exacerbated the cardiovascular health gaps within the United States. Further, pre-existing cardiovascular morbidities, such as atherosclerosis, can worsen the response to wildfire smoke exposures.

Do Storage Conditions Affect Collected Cookstove Emission Samples? Implications for Field Studies.

Cookstove emissions are a significant source of indoor air pollution in developing countries and rural communities world-wide. Considering that many research sites for evaluating cookstove emissions and interventions are remote and require potentially lengthy periods of particulate matter (PM) filter sample storage in sub-optimal conditions (e.g.

Mutagenicity- and pollutant-emission factors of pellet-fueled gasifier cookstoves: Comparison with other combustion sources.

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 role of fuel type and combustion phase on the toxicity of biomass smoke following inhalation exposure in mice.

The characteristics of wildland fire smoke exposures which initiate or exacerbate cardiopulmonary conditions are unclear. We previously reported that, on a mass basis, lung toxicity associated with particulate matter (PM) from flaming smoke aspirated into mouse lungs is greater than smoldering PM. In this study, we developed a computer-controlled inhalation system which can precisely control complex biomass smoke emissions from different combustion conditions.

Douglas-Fir ( Pseudotsuga menziesii (Mirb.) Franco) Transcriptome Profile Changes Induced by Diesel Emissions Generated with CeO Nanoparticle Fuel Borne Catalyst.

It is important to understand molecular effects on plants exposed to compounds released from use of products containing engineered nanomaterials. Here, we present mRNA sequencing data on transcriptome impacts to Douglas-fir following 2 weeks of sublethal exposure to 30:1 diluted airborne emissions released from combustion of diesel fuel containing engineered CeO nanoparticle catalysts (DECe). Our hypothesis was that chamber exposure to DECe would induce distinct transcriptome changes in seedling needles compared with responses to conventional diesel exhaust (DE) or filtered DECe Gas Phase.

Inhalation of Simulated Smog Atmospheres Affects Cardiac Function in Mice.

The health effects of individual criteria air pollutants have been well investigated. However, little is known about the health effects of air pollutant mixtures that more realistically represent environmental exposures. The present study was designed to evaluate the cardiac effects of inhaled simulated smog atmospheres (SA) generated from the photochemistry of either gasoline and isoprene (SA-G) or isoprene (SA-Is) in mice.

Evaluation of an Air Quality Health Index for Predicting the Mutagenicity of Simulated 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 (O), 321 ppb NO, and 1007 μg/m PM; or isoprene to produce SA-O, which had a high ozone (O) concentration: 415 ppb O, 633 ppb NO, and 55 μg/m PM.

Comparative Cardiopulmonary Effects of Particulate Matter- And Ozone-Enhanced Smog Atmospheres in Mice.

This study was conducted to compare the cardiac effects of particulate matter (PM)- (SA-PM) and ozone(O)-enhanced (SA-O) smog atmospheres in mice. Based on our previous findings of filtered diesel exhaust we hypothesized that SA-O would cause greater cardiac dysfunction than SA-PM. Radiotelemetered mice were exposed to either SA-PM, SA-O, or filtered air (FA) for 4 h.

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-O (high ozone) decreased cholesterol levels immediately after a 4-h exposure, whereas only SA-O increased airflow limitation.

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.

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).

Mutagenicity and Lung Toxicity of Smoldering vs. Flaming Emissions from Various Biomass Fuels: Implications for Health Effects from Wildland Fires.

Background: 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.

Objectives: 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.

Regulating temperature and relative humidity in air-liquid interface systems eliminates cytotoxicity resulting from control air exposures.

VITROCELL systems permit cell exposures at the air-liquid interface (ALI); however, there are inconsistent methodologies in the literature for their operation. Some studies find that exposure to air (vehicle control) induced cytotoxicity relative to incubator controls; others do not mention if any cytotoxicity was encountered. We sought to test whether temperature and relative humidity (temp/RH) influence cytotoxicity with an unmodified (conditions A & B) and modified (condition C) VITROCELL 6 CF with temp/RH controls to permit conditioning of the sampled air-flow.

Chemical composition and source apportionment of size fractionated particulate matter in Cleveland, Ohio, USA.

The Cleveland airshed comprises a complex mixture of industrial source emissions that contribute to periods of non-attainment for fine particulate matter (PM) 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.

The effects of B0, B20, and B100 soy biodiesel exhaust on aconitine-induced cardiac arrhythmia in spontaneously hypertensive rats.

Context: Diesel exhaust (DE) has been shown to increase the risk of cardiac arrhythmias. Although biodiesel has been proposed as a "safer" alternative to diesel, it is still uncertain whether it actually poses less threat.

Objective: We hypothesized that exposure to pure or 20% soy biodiesel exhaust (BDE) would cause less sensitivity to aconitine-induced arrhythmia than DE in rats.

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

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/m(3), 4 h/day for 2 days or 4 weeks (5 days/week).

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

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/m(3).

Generation and characterization of diesel engine combustion emissions from petroleum diesel and soybean biodiesel fuels and application for inhalation exposure studies.

Biodiesel made from the transesterification of plant- and animal-derived oils is an important alternative fuel source for diesel engines. Although numerous studies have reported health effects associated with petroleum diesel emissions, information on biodiesel emissions are more limited. To this end, a program at the U.

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.

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.

Inhaled diesel emissions generated with cerium oxide nanoparticle fuel additive induce adverse pulmonary and systemic effects.

Diesel exhaust (DE) exposure induces adverse cardiopulmonary effects. Cerium oxide nanoparticles added to diesel fuel (DECe) increases fuel burning efficiency but leads to altered emission characteristics and potentially altered health effects. Here, we evaluated whether DECe results in greater adverse pulmonary effects compared with DE.

Use of novel inhalation kinetic studies to refine physiologically-based pharmacokinetic models for ethanol in non-pregnant and pregnant rats.

Ethanol (EtOH) exposure induces a variety of concentration-dependent neurological and developmental effects in the rat. Physiologically-based pharmacokinetic (PBPK) models have been used to predict the inhalation exposure concentrations necessary to produce blood EtOH concentrations (BEC) in the range associated with these effects. Previous laboratory reports often lacked sufficient detail to adequately simulate reported exposure scenarios associated with BECs in this range, or lacked data on the time-course of EtOH in target tissues (e.

Cardiopulmonary toxicity of peat wildfire particulate matter and the predictive utility of precision cut lung slices.

Background: 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.