RESUMO
Burn pits are a method of open-air waste management that was common during military operations in Iraq, Afghanistan, and other regions in Southwest Asia. Veterans returning from deployment have reported respiratory symptoms, potentially from exposure to burn pit smoke, yet comprehensive assessment of such exposure on pulmonary health is lacking. We have previously shown that exposure to condensates from burn pit smoke emissions causes inflammation and cytotoxicity in mice. In this study, we explored the effects of burn pit smoke condensates on human airway epithelial cells (HAECs) to understand their impact on cellular targets in the human lung. HAECs were cultured at the air-liquid interface (ALI) and exposed to burn pit waste smoke condensates (plywood, cardboard, plastic, mixed, and mixed with diesel) generated under smoldering and flaming conditions. Cytotoxicity was evaluated by measuring transepithelial electrical resistance (TEER) and lactate dehydrogenase (LDH) release; toxicity scores (TSs) were quantified for each exposure. Pro-inflammatory cytokine release and modulation of gene expression were examined for cardboard and plastic condensate exposures. Burn pit smoke condensates generated under flaming conditions affected cell viability, with flaming mixed waste and plywood exhibiting the highest toxicity scores. Cardboard and plastic smoke condensates modulated cytokine secretion, with GM-CSF and IL-1ß altered in more than one exposure group. Gene expression of detoxifying enzymes (ALDH1A3, ALDH3A1, CYP1A1, CYP1B1, NQO1, etc.), mucins (MUC5AC, MUC5B), and cytokines was affected by several smoke condensates. Particularly, expression of IL6 was elevated following exposure to all burn pit smoke condensates, and polycyclic aromatic hydrocarbon acenaphthene was positively associated with the IL-6 level in the basolateral media of HAECs. These observations demonstrate that exposure to smoke condensates of materials present in burn pits adversely affects HAECs and that aberrant cytokine secretion and altered gene expression profiles following burn pit material smoke exposure could contribute to the development of airway disease.
Assuntos
Células Epiteliais , Fumaça , Humanos , Fumaça/efeitos adversos , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/metabolismo , Células Cultivadas , Sobrevivência Celular/efeitos dos fármacos , Citocinas/metabolismo , Linhagem Celular , Queima de Resíduos a Céu AbertoRESUMO
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. Male and female C57BL/6J mice were divided into EH or DH for 22 weeks, and cardiopulmonary assessments measured before and after exposures to either one-hr filtered air (FA) or flaming eucalyptus WS exposure. Male and female DH mice exhibited increased heart rate (HR) and left ventricular mass (LVM), as well as reduced stroke volume and end diastolic volume (EDV) one week following exposure to WS. Female DH mice displayed significantly elevated levels of IL-2, IL-17, corticosterone and hemoglobin A1c (HbA1c) following WS, while female in EH mice higher epinephrine levels were detected. Female mice exhibited higher AL than males with DH, which was potentiated post-WS exposure. Thus, DH increased susceptibility to extreme air pollution in a gender-dependent manner suggesting that living conditions need to be evaluated as a modifier of toxicological responses.
Assuntos
Abrigo para Animais , Camundongos Endogâmicos C57BL , Fumaça , Incêndios Florestais , Animais , Feminino , Masculino , Camundongos , Fumaça/efeitos adversos , Alostase , Poluentes Atmosféricos , Fatores Sexuais , Frequência CardíacaRESUMO
OBJECTIVE: Inhalation of smoke from the burning of waste materials on military bases is associated with increased incidences of cardiopulmonary diseases. This study examined the respiratory and inflammatory effects of acute inhalation exposures in mice to smoke generated by military burn pit-related materials including plywood (PW), cardboard (CB), mixed plastics (PL), and a mixture of these three materials (MX) under smoldering (0.84 MCE) and flaming (0.97 MCE) burn conditions. METHODS: Mice were exposed nose-only for one hour on two consecutive days to whole or filtered smoke or clean air alone. Smoldering combustion emissions had greater concentrations of PM (â¼40 mg/m3) and VOCs (â¼5-12 ppmv) than flaming emissions (â¼4 mg/m3 and â¼1-2 ppmv, respectively); filtered emissions had equivalent levels of VOCs with negligible PM. Breathing parameters were assessed during exposure by head-out plethysmography. RESULTS: All four smoldering burn pit emission types reduced breathing frequency (F) and minute volumes (MV) compared with baseline exposures to clean air, and HEPA filtration significantly reduced the effects of all smoldering materials except CB. Flaming emissions had significantly less suppression of F and MV compared with smoldering conditions. No acute effects on lung inflammatory cells, cytokines, lung injury markers, or hematology parameters were noted in smoke-exposed mice compared with air controls, likely due to reduced respiration and upper respiratory scrubbing to reduce the total deposited PM dose in this short-term exposure. CONCLUSION: Our data suggest that material and combustion type influences respiratory responses to burn pit combustion emissions. Furthermore, PM filtration provides significant protective effects only for certain material types.
Assuntos
Poluentes Atmosféricos , Camundongos , Animais , Poluentes Atmosféricos/análise , Incineração , Poeira , Pulmão/química , Respiração , Material Particulado/toxicidade , Material Particulado/análiseRESUMO
A weighted chemical coexpression network analysis (WCCNA) was utilized to identify chemicals co-modulated to variable burning of anthropogenic materials and to link chemicals to biological responses (lung toxicity and mutagenicity). Polyaromatic hydrocarbons (PAHs) were co-modulated with increased concentrations in flaming smoke particulate matter (PM) from the burning of plastic-containing materials and showed significant association with increased neutrophil influx, cytokine levels, and mutagenicity. Inorganic elements were co-modulated with increased concentrations in flaming plywood and cardboard smoke PM and showed significant association with increased protein and albumin levels. This study shows the potential for using a computational network analysis to identify and prioritize hazardous chemical components within complex environmental mixtures and provides guidance on key chemical tracers required for intervention research to protect public health from the exposure.
Assuntos
Poluentes Atmosféricos , Material Particulado , Material Particulado/toxicidade , Fumaça/efeitos adversos , Fumaça/análise , Poluentes Atmosféricos/análise , Nicotiana , Mutagênicos/toxicidadeRESUMO
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.
Assuntos
Incêndios Florestais , Feminino , Camundongos , Animais , Biomassa , Transcriptoma , Fumaça/efeitos adversos , Fumaça/análise , SoloRESUMO
BACKGROUND: Open burning of anthropogenic sources can release hazardous emissions and has been associated with increased prevalence of cardiopulmonary health outcomes. Exposure to smoke emitted from burn pits in military bases has been linked with respiratory illness among military and civilian personnel returning from war zones. Although the composition of the materials being burned is well studied, the resulting chemistry and potential toxicity of the emissions are not. METHODS: Smoke emission condensates from either flaming or smoldering combustion of five different types of burn pit-related waste: cardboard; plywood; plastic; mixture; and mixture/diesel, were obtained from a laboratory-scale furnace coupled to a multistage cryotrap system. The primary emissions and smoke condensates were analyzed for a standardized suite of chemical species, and the condensates were studied for pulmonary toxicity in female CD-1 mice and mutagenic activity in Salmonella (Ames) mutagenicity assay using the frameshift strain TA98 and the base-substitution strain TA100 with and without metabolic activation (S9 from rat liver). RESULTS: Most of the particles in the smoke emitted from flaming and smoldering combustion were less than 2.5 µm in diameter. Burning of plastic containing wastes (plastic, mixture, or mixture/diesel) emitted larger amounts of particulate matter (PM) compared to other types of waste. On an equal mass basis, the smoke PM from flaming combustion of plastic containing wastes caused more inflammation and lung injury and was more mutagenic than other samples, and the biological responses were associated with elevated polycyclic aromatic hydrocarbon levels. CONCLUSIONS: This study suggests that adverse health effects of burn pit smoke exposure vary depending on waste type and combustion temperature; however, burning plastic at high temperature was the most significant contributor to the toxicity outcomes. These findings will provide a better understanding of the complex chemical and combustion temperature factors that determine toxicity of burn pit smoke and its potential health risks at military bases.
Assuntos
Poluentes Atmosféricos , Material Particulado , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Animais , Feminino , Incineração , Pulmão , Camundongos , Testes de Mutagenicidade , Mutagênicos , Material Particulado/toxicidade , RatosRESUMO
Human exposure to wildfire-derived particulate matter (PM) is linked to adverse health outcomes; however, little is known regarding the influence of biomass fuel type and burn conditions on toxicity. The aim of this study was to assess the irritant potential of extractable organic material (EOM) of biomass smoke condensates from five fuels (eucalyptus, pine, pine needle, peat, or red oak), representing various fire-prone regions of the USA, burned at two temperatures each [flaming (approximately 640°C) or (smoldering approximately 500°C)] using a locomotor assay in zebrafish (Danio rerio) larvae. It was postulated that locomotor responses, as measures of irritant effects, might be dependent upon fuel type and burn conditions and that these differences relate to combustion byproduct chemistry. To test this, locomotor activity was tracked for 60 min in 6-day-old zebrafish larvae (25-32/group) immediately after exposure to 0.4% dimethyl sulfoxide (DMSO) vehicle or EOM from the biomass smoke condensates (0.3-30 µg EOM/ml; half-log intervals). All EOM samples produced concentration-dependent irritant responses. Linear regression analysis to derive rank-order potency indicated that on a µg PM basis, flaming pine and eucalyptus were the most irritating. In contrast, on an emission-factor basis, which normalizes responses to the amount of PM produced/kg of fuel burned, smoldering smoke condensates induced greater irritant responses (>100-fold) than flaming smoke condensates, with smoldering pine being the most potent. Importantly, irritant responses significantly correlated with polycyclic aromatic hydrocarbon (PAH) content, but not with organic carbon or methoxyphenols. Data indicate that fuel type and burn condition influence the quantity and chemical composition of PM as well as toxicity.
Assuntos
Poluentes Atmosféricos/efeitos adversos , Irritantes/efeitos adversos , Fumaça/efeitos adversos , Incêndios Florestais/classificação , Peixe-Zebra , Poluentes Atmosféricos/química , Animais , Biomassa , Irritantes/químicaRESUMO
Wildland fires (WF) are linked to adverse health impacts related to poor air quality. The cardiovascular impacts of emissions from specific biomass sources are however unknown. The purpose of this study was to assess the cardiovascular impacts of a single exposure to peat smoke, a key regional WF air pollution source, and relate these to baroreceptor sensitivity and inflammation. Three-month-old male Wistar-Kyoto rats, implanted with radiotelemeters for continuous monitoring of heart rate (HR), blood pressure (BP), and spontaneous baroreflex sensitivity (BRS), were exposed once, for 1-hr, to filtered air or low (0.38 mg/m3 PM) or high (4.04 mg/m3) concentrations of peat smoke. Systemic markers of inflammation and sensitivity to aconitine-induced cardiac arrhythmias, a measure of latent myocardial vulnerability, were assessed in separate cohorts of rats 24 hr after exposure. PM size (low peat = 0.4-0.5 microns vs. high peat = 0.8-1.2 microns) and proportion of organic carbon (low peat = 77% vs. high peat = 65%) varied with exposure level. Exposure to high peat and to a lesser extent low peat increased systolic and diastolic BP relative to filtered air. In contrast, only exposure to low peat elevated BRS and aconitine-induced arrhythmogenesis relative to filtered air and increased circulating levels of low-density lipoprotein cholesterol, complement components C3 and C4, angiotensin-converting enzyme (ACE), and white blood cells. Taken together, exposure to peat smoke produced overt and latent cardiovascular consequences that were likely influenced by physicochemical characteristics of the smoke and associated adaptive homeostatic mechanisms.
Assuntos
Poluentes Atmosféricos/toxicidade , Arritmias Cardíacas/induzido quimicamente , Barorreflexo/efeitos dos fármacos , Pressão Sanguínea/efeitos dos fármacos , Exposição por Inalação/efeitos adversos , Material Particulado/toxicidade , Fumaça/efeitos adversos , Animais , Masculino , Ratos , Ratos Endogâmicos WKY , Solo , Testes de Toxicidade AgudaRESUMO
OBJECTIVE: Previous studies have shown that air pollution exposure primes the body to heightened responses to everyday stressors of the cardiovascular system. The purpose of this study was to examine the utility of postprandial responses to a high carbohydrate oral load, a cardiometabolic stressor long used to predict cardiovascular risk, in assessing the impacts of exposure to eucalyptus smoke (ES), a contributor to wildland fire air pollution in the Western coast of the United States. MATERIALS AND METHODS: Three-month-old male Sprague Dawley rats were exposed once (1 h) to filtered air (FA) or ES (700 µg/m3 fine particulate matter), generated by burning eucalyptus in a tube furnace. Rats were then fasted for six hours the following morning, and subsequently administered an oral gavage of either water or a HC suspension (70 kcal% from carbohydrate), mimicking a HC meal. Two hours post gavage, cardiovascular ultrasound, cardiac pressure-volume (PV), and baroreceptor sensitivity assessments were made, and pulmonary and systemic markers assessed. RESULTS: ES inhalation alone increased serum interleukin (IL)-4 and nasal airway levels of gamma glutamyl transferase. HC gavage alone increased blood glucose, blood pressure, and serum IL-6 and IL-13 compared to water vehicle. By contrast, only ES-exposed and HC-challenged animals had increased PV loop measures of cardiac output, ejection fraction %, dP/dtmax, dP/dtmin, and stroke work compared to ES exposure alone and/or HC challenge alone. DISCUSSION AND CONCLUSIONS: Exposure to a model wildfire air pollution source modifies cardiovascular responses to HC challenge, suggesting air pollution sensitizes the body to systemic triggers.
Assuntos
Poluentes Atmosféricos/efeitos adversos , Carboidratos da Dieta/farmacologia , Eucalyptus , Fumaça/efeitos adversos , Administração por Inalação , Animais , Glicemia/efeitos dos fármacos , Pressão Sanguínea/efeitos dos fármacos , Líquido da Lavagem Broncoalveolar/química , Líquido da Lavagem Broncoalveolar/citologia , Débito Cardíaco/efeitos dos fármacos , Citocinas/sangue , Masculino , Líquido da Lavagem Nasal/química , Líquido da Lavagem Nasal/citologia , Período Pós-Prandial/fisiologia , Ratos Sprague-Dawley , Volume Sistólico/efeitos dos fármacos , Incêndios FlorestaisRESUMO
The rates of development of 2 tissues in mammary glands, parenchyma (PAR) and the mammary fat pad (MFP), in response to nutrition in early life might have a major bearing on lifetime milk production. Historical studies reported that feeding greater amounts of dietary nutrients from postweaning to puberty increased growth rates of heifers and stimulated the growth of MFP at the expense of PAR, which might suggest compromised mammary development and future milk production. The current study sought to determine if a higher volume of whole milk (8 vs. 4 L/d) offered to calves would increase rates of growth and development of PAR in mammary glands at weaning (1 to 12 wk). To measure these tissues, we developed 2 simple methods to assess the size of PAR and MFP at the time of screening using ultrasound. We report that calves offered 8 L/d of whole milk had greater rates of growth until weaning (0.86 ± 0.06 vs. 0.81 ± 0.09 kg/d), compared with calves offered 4 L/d. Ultrasonography showed that despite the faster rates of growth in calves offered 8 L/d of milk/d, the ratio of PAR:MFP depth was 40% less at weaning in the front glands (34%) compared with calves offered 4 L of milk/d. Rear glands were less impaired. The ultrasound methods developed here might be useful to monitor the development of mammary glands in response to different nutritional regimens during the preweaning period.
Assuntos
Ração Animal , Bovinos/crescimento & desenvolvimento , Glândulas Mamárias Animais/crescimento & desenvolvimento , Leite , Tecido Adiposo/crescimento & desenvolvimento , Ração Animal/análise , Animais , Peso Corporal , Dieta/veterinária , Feminino , Estado Nutricional , DesmameRESUMO
The biological response of bronchial epithelial cells to particles is associated with a sequestration of cell metal by the particle surface and a subsequent disruption in host iron homeostasis. The macrophage is the cell type resident in the respiratory tract that is most likely to make initial contact with inhaled particles. We tested the postulates that (1) silica, a prototypical particle, disrupts iron homeostasis in alveolar macrophages (AMs); and (2) the altered iron homeostasis results in both an oxidative stress and pro-inflammatory effects. Human AMs (1.0 × 106/mL) demonstrated an increased import of iron following particle exposure with nonheme iron concentrations of 0.57 ± 0.03, 1.72 ± 0.09, 0.88 ± 0.09, and 3.21 ± 0.11 ppm in cells exposed for 4 h to media, 500 µM ferric ammonium citrate (FAC), 100 µg/mL silica, and both silica and FAC, respectively. Intracellular ferritin concentrations and iron release were similarly increased after AM exposure to FAC and silica. Silica increased oxidant generation by AMs measured using both dichlorofluorescein diacetate fluorescence and reduction of nitroblue tetrazolium salt. Concentrations of interleukin (IL)-1ß, IL-6, IL-8, and tumor necrosis factor-α in macrophage supernatant increased following 100 µg/mL silica exposure for 24 h. Treatment of AMs with 500 µM FAC decreased both oxidant generation and cytokine release associated with silica exposure, supporting a dependence of these effects on sequestration of cell metal by the particle surface. We conclude that (1) silica exposure disrupts iron homeostasis resulting in increased import, accumulation, and release of the metal; and (2) the altered iron homeostasis following silica exposure impacts oxidant generation and pro-inflammatory effects.
Assuntos
Homeostase/efeitos dos fármacos , Inflamação/induzido quimicamente , Ferro/metabolismo , Macrófagos Alveolares/efeitos dos fármacos , Quartzo/toxicidade , Acetofenonas/farmacologia , Animais , Linhagem Celular Tumoral , Citocinas/metabolismo , Inibidores Enzimáticos/farmacologia , Compostos Férricos/farmacologia , Ferritinas/metabolismo , Humanos , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , NADPH Oxidase 2/genética , NADPH Oxidases/antagonistas & inibidores , Estresse Oxidativo/efeitos dos fármacos , Compostos de Amônio Quaternário/farmacologiaRESUMO
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. This system was used to examine the toxicity of inhaled biomass smoke from peat, eucalyptus, and oak fuels generated under smoldering and flaming phases with emissions set to the same approximate concentration of carbon monoxide (CO) for each exposure (60-110 ppm), resulting in PM levels of ~ 4 mg/m3 for flaming and ~ 40 mg/m3 for smoldering conditions. Mice were exposed by inhalation 1 h/day for 2 days, and assessed for lung toxicity at 4 and 24 h after the final exposure. Peat (flaming and smoldering) and eucalyptus (smoldering) smoke elicited significant inflammation (neutrophil influx) in mouse lungs at 4 h with the peat (flaming) smoke causing even greater lung inflammation at 24-h post-exposure. A significant alteration in ventilatory timing was also observed in mice exposed to the peat (flaming) and eucalyptus (flaming and smoldering) smoke immediately after each day of exposure. No responses were seen for exposures to similar concentrations of flaming or smoldering oak smoke. The lung toxicity potencies (neutrophil influx per PM mass) agreed well between the inhalation and previously reported aspiration studies, demonstrating that although flaming smoke contains much less PM mass than smoldering smoke, it is more toxic on a mass basis than smoldering smoke exposure, and that fuel type is also a controlling factor.
Assuntos
Biomassa , Exposição por Inalação/efeitos adversos , Fumaça/efeitos adversos , Poluentes Atmosféricos/toxicidade , Animais , Monóxido de Carbono/análise , Eucalyptus , Feminino , Pneumopatias/induzido quimicamente , Pneumopatias/patologia , Camundongos , Camundongos Endogâmicos BALB C , Infiltração de Neutrófilos/efeitos dos fármacos , Material Particulado/toxicidade , Quercus , Testes de Função Respiratória , Solo , MadeiraRESUMO
Background: Acute and chronic exposures to biomass wildfire smoke pose significant health risks to firefighters and impacted communities. Susceptible populations such as asthmatics may be particularly sensitive to wildfire effects. We examined pulmonary responses to biomass smoke generated from combustion of peat, oak, or eucalyptus in control and house dust mite (HDM)-allergic mice. Methods: Mice were exposed 1 h/d for 2 consecutive days to emissions from each fuel type under smoldering or flaming conditions (â¼40 or â¼3.3 mg PM/m3, respectively) while maintaining comparable CO levels (â¼60-120 ppm). Results: Control and allergic mice reduced breathing frequency during exposure to all biomass emissions compared with pre-exposure to clean air. Smoldering eucalyptus and oak, but not peat, further reduced frequency compared to flaming conditions in control and allergic groups, while also reducing minute volume and peak inspiratory flow in control mice. Several biochemical and cellular markers of lung injury and inflammation were suppressed by all biomass emission types in both HDM-allergic and control mice. Control mice exposed to flaming eucalyptus at different PM concentrations (C) and times (T) with the same C × T product had a greater decrease in breathing frequency with high concentration acute exposure compared with lower concentration episodic exposure. This decrease was ameliorated by PM HEPA filtration, indicating that the respiratory changes were partially mediated by biomass smoke particles. Conclusion: These data show that exposure to smoldering eucalyptus or oak smoke inhibits respiratory responses to a greater degree than peat smoke. Anti-inflammatory effects of CO may possibly contribute to smoke-induced suppression of allergic inflammatory responses.
Assuntos
Biomassa , Hipersensibilidade/fisiopatologia , Fumaça , Madeira , Alérgenos/imunologia , Animais , Antígenos de Dermatophagoides/imunologia , Líquido da Lavagem Broncoalveolar/citologia , Líquido da Lavagem Broncoalveolar/imunologia , Citocinas/imunologia , Eucalyptus , Feminino , Hipersensibilidade/imunologia , Hipersensibilidade/patologia , Pulmão/imunologia , Pulmão/patologia , Pulmão/fisiopatologia , Macrófagos/imunologia , Camundongos Endogâmicos BALB C , Neutrófilos/imunologia , Quercus , Testes de Função Respiratória , SoloRESUMO
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.
Assuntos
Poluentes Atmosféricos , Ozônio , Animais , Atmosfera , Exposição por Inalação , Camundongos , Material Particulado , SmogRESUMO
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.
Assuntos
Poluição do Ar , Deficiência de Vitamina D , Animais , Exposição Ambiental , Camundongos , Material Particulado , SmogRESUMO
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 (PM2.5). One simulated atmosphere (SA-PM) generated from irradiation of â¼23 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 PM2.5, 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 PM2.5, 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.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Dióxido de Nitrogênio , Material ParticuladoRESUMO
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.
Assuntos
Poluentes Atmosféricos , Ozônio , Animais , Atmosfera , Camundongos , Material Particulado , Ratos , Roedores , SmogRESUMO
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 â¼54% C â T and â¼46% C â A. Thus, the AQHI may have some predictive value for the mutagenicity of the gas phase of air.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Atmosfera , Testes de Mutagenicidade , Mutagênicos , Material ParticuladoRESUMO
BACKGROUND: There is an urgent need to provide access to cleaner end user energy technologies for the nearly 40% of the world's population who currently depend on rudimentary cooking and heating systems. Advanced cookstoves (CS) are designed to cut emissions and solid-fuel consumption, thus reducing adverse human health and environmental impacts. STUDY PREMISE: We hypothesized that, compared to a traditional (Tier 0) three-stone (3-S) fire, acute inhalation of solid-fuel emissions from advanced natural-draft (ND; Tier 2) or forced-draft (FD; Tier 3) stoves would reduce exposure biomarkers and lessen pulmonary and innate immune system health effects in exposed mice. RESULTS: Across two simulated cooking cycles (duration ~ 3h), emitted particulate mass concentrations were reduced 80% and 62% by FD and ND stoves, respectively, compared to the 3-S fire; with corresponding decreases in particles visible within murine alveolar macrophages. Emitted carbon monoxide was reduced ~ 90% and ~ 60%, respectively. Only 3-S-fire-exposed mice had increased carboxyhemoglobin levels. Emitted volatile organic compounds were FD ⪠3-S-fire ≤ ND stove; increased expression of genes involved in xenobiotic metabolism (COX-2, NQO1, CYP1a1) was detected only in ND- and 3-S-fire-exposed mice. Diminished macrophage phagocytosis was observed in the ND group. Lung glutathione was significantly depleted across all CS groups, however the FD group had the most severe, ongoing oxidative stress. CONCLUSIONS: These results are consistent with reports associating exposure to solid fuel stove emissions with modulation of the innate immune system and increased susceptibility to infection. Lower respiratory infections continue to be a leading cause of death in low-income economies. Notably, 3-S-fire-exposed mice were the only group to develop acute lung injury, possibly because they inhaled the highest concentrations of hazardous air toxicants (e.g., 1,3-butadiene, toluene, benzene, acrolein) in association with the greatest number of particles, and particles with the highest % organic carbon. However, no Tier 0-3 ranked CS group was without some untoward health effect indicating that access to still cleaner, ideally renewable, energy technologies for cooking and heating is warranted.