Outdoor wood furnaces create significant indoor particulate pollution in neighboring homes

Abstract

Context: The use of outdoor wood furnaces (OWFs) is common in many parts of the United States. Little published information exists on the concentrations of outdoor and indoor fine particulates found near OWFs.

Objective: To compare PM_2.5 (cts) and PM_0.5 (cts) particle concentrations inside four Connecticut homes located 30.5–259?m from OWFs, and inside six Connecticut control homes located more than 2?km from the nearest OWF.

Materials and methods: PM_2.5 (cts) and PM_0.5 (cts) measurements were made with a Dylos light-scattering particulate counter.

Results: Mean PM_2.5 (cts) concentrations were 4.21 times as great in the four OWF exposed homes than the six control homes (0.302?×?10⁶ counts/m³ versus 0.0718 counts?×?10⁶/m³ p?<?0.001). The mean PM_2.5 (cts) concentrations inside the four OWF exposed homes roughly corresponds to a mass PM_2.5 of 37?µg/m³, which is above the US EPA 24-h PM_2.5 limit of 35?µg/m³. Mean PM_0.5 (cts) concentrations were 3.44 times as great in the four OWF exposed homes than in the six control homes (0.657 versus 0.191?×?10⁶/m³ p?<?0.001). Mean PM_2.5 (cts) and PM_0.5 (cts) concentrations were significantly higher in the house 259?m from an OWF as compared with the mean of the six control homes.

Conclusion: Existing regulations, such as the present Connecticut law requiring a 61 meter distance between an OWF and neighboring homes, are not adequate to protect the health of neighboring residents.     

Dose and Time Dependency of Inflammatory Responses in the Mouse Lung to Urban Air Coarse,Fine, and Ultrafine Particles From Six European Cities

We investigated the dose and time dependency of inflammatory and cytotoxic responses to size-segregated urban air particulate samples in the mouse lung. Coarse (PM_10?2.5), fine (PM_2.5?0.2), and ultrafine (PM_0.2) particles were collected in six European cities (Duisburg, Prague, Amsterdam, Helsinki, Barcelona, Athens) in selected seasons using a modified Harvard high-volume cascade impactor. Healthy C57Bl/6J mice were intratracheally exposed to the particulate samples in a 24-h dose-response study (1, 3, and 10 mg/kg) and in 4-, 12-, and 24-h time course studies (10 mg/kg). After the exposures, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: total cell number, cell differential, total protein, and lactate dehydrogenase (LDH) and cytokine (tumor necrosis alpha [TNF-α], interleukin-6 [IL-6], and keratinocyte-derived chemokine [KC]) concentrations. In general, PM_10?2.5 samples had higher inflammatory activity than PM_2.5?0.2 samples. PM_0.2 samples showed negligible inflammatory activity. PM_10?2.5 and PM_2.5?0.2 samples caused large increases in BALF cytokine concentrations at 4 h, but not at 12 or 24 h, after exposure. The BALF total cell number and total protein concentrations increased significantly at 12 h for both the PM_10?2.5 and PM_2.5?0.2 samples, but only PM_10?2.5 samples produced consistent, significant increases at 24 h after exposure. There was more heterogeneity in BALF cytokine and neutrophil cell number responses to PM_2.5?0.2 samples than to PM_10?2.5 samples between the sampling campaigns. Thus, particle size, sources, and atmospheric transformation processes affect the inflammatory activity and response duration of urban air particulate matter in the mouse lung.     

Exposure assessment of workplaces manufacturing nanosized TiO2 and silver

With the increased production and widespread use of nanomaterials, human and environmental exposure to nanomaterials is inevitably increasing. Therefore, this study monitored the possible exposure to nanoparticles at workplaces that manufacture nano-TiO₂ and nano-silver. To estimate the potential exposure of workers, personal sampling, area monitoring, and real-time monitoring using a scanning mobility particle sizer (SMPS) and dust monitor were conducted at workplaces where the workers handle nanomaterials. The gravimetric concentrations of TiO₂ ranged from 0.10 to 4.99?mg/m³, which were lower than the occupational exposure limit 10?mg/m³ set by the Korean Ministry of Labor or American Conference of Governmental Industrial Hygienists (ACGIH). Meanwhile, the silver metal concentrations ranged from 0.00002 to 0.00118?mg/m³, which were also lower than the silver dust 0.1?mg/m³ and silver soluble compound 0.01?mg/m³ occupational exposure limits set by the ACGIH. The particle number concentrations at the nano-TiO₂ manufacturing workplaces ranged from 11,418 to 45,889 particles/cm³ with a size range of 15–710.5?nm during the reaction, although the concentration decreased to 14,000 particles/cm³ when the reaction was stopped. The particle concentrations at the TiO₂ manufacturing workplaces increased during the reactor and vacuum pump operations, and during the collection of the synthesized TiO₂ particles. Similarly, the particle concentrations at the silver nanoparticle manufacturing workplaces increased when the sodium citrates were weighed or reacted with the silver nitrates, and during the cleaning of the workplace. The number of silver nanoparticles in the samples obtained from the workplace manufacturing silver nanoparticles using induced coupled plasma ranged from 57,789 to 2,373,309 particles/cm³ inside the reactor with an average size of 20–30?nm and 535–25,022 particles/cm³ with a wide range of particle sizes due to agglomeration or aggregation after the release of nanoparticles into the workplace air. In contrast, the silver nanoparticles manufactured by the wet method ranged from 393 to 3526 particle/cm³ with an average size of 50?nm. Thus, when taken together, the TiO₂ and silver nanoparticle concentrations were relatively lower than existing occupational exposure limits.     

Chemical Compositions Responsible for Inflammation and Tissue Damage in the Mouse Lung by Coarse and Fine Particulate Samples from Contrasting Air Pollution in Europe

Inflammation is regarded as an important mechanism in mortality and morbidity associated with exposures of cardiorespiratory patients to urban air particulate matter. We investigated the association of the chemical composition and sources of urban air fine (PM_2.5?0.2) and coarse (PM_10?2.5) particulate samples with the inflammatory activity in the mouse lung. The particulate samples were collected during selected seasons in six European cities using a high-volume cascade impactor. Healthy C57BL/6J mice were intratracheally instilled with a single dose (10 mg/kg) of the particulate samples. At 4, 12, and 24 h after the exposure, the lungs were lavaged and the bronchoalveolar lavage fluid (BALF) was assayed for indicators of inflammation and tissue damage: cell number, total protein, and cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-6, and KC). Dicarboxylic acids and transition metals, especially Ni and V, in PM_2.5?0.2 correlated positively and some secondary inorganic ions (NO₃^-, NH₄⁺) negatively with the inflammatory activity. Total organic matter and SO₄^2- had no consistent correlations. In addition, the soil-derived constituents (Ca²⁺, Al, Fe, Si) showed positive correlations with the PM_2.5?0.2-induced inflammatory activity, but their role in PM_10?2.5 remained obscure, possibly due to largely undefined biogenic material. Markers of poor biomass and coal combustion, i.e., monosaccharide anhydrides and As, were associated with elevated PAH contents in PM_2.5?0.2 and a consistent immunosuppressive effect. Overall, our results support epidemiological findings that the local sources of incomplete combustion and resuspended road dust are important in urban air particulate pollution-related health effects.     

Effects of copy center particles on the lungs: a toxicological characterization using a Balb/c mouse model

Abstract

Context: Printers and photocopiers release respirable particles into the air. Engineered nanomaterials (ENMs) have been recently incorporated into toner formulations but their potential toxicological effects have not been well studied.

Objective: To evaluate the biological responses to copier-emitted particles in the lungs using a mouse model.

Methods: Particulate matter (PM) from a university copy center was sampled and fractionated into three distinct sizes, two of which (PM_0.1 and PM_0.1–2.5) were evaluated in this study. The particles were extracted and dispersed in deionized water and RPMI/10% FBS. Hydrodynamic diameter and zeta potential were evaluated by dynamic light scattering. The toxicological potential of these particles was studied using 8-week-old male Balb/c mice. Mice were intratracheally instilled with 0.2,?0.6,?2.0?mg/kg bw of either the PM_0.1 and PM_0.1–2.5 size fractions. Fe₂O₃ and welding fumes were used as comparative materials, while RPMI/10% FBS was used as the vehicle control. Bronchoalveolar lavage (BAL) was performed 24 hours post-instillation. The BAL fluid was analyzed for total and differential cell counts, and biochemical markers of injury and inflammation.

Results: Particle size- and dose-dependent pulmonary effects were found. Specifically, mice instilled with PM_0.1 (2.0?mg/kg bw) had significant increases in neutrophil number, lactate dehydrogenase and albumin compared to vehicle control. Likewise, pro-inflammatory cytokines were elevated in mice exposed to PM_0.1 (2.0?mg/kg bw) compared to other groups.

Conclusion: Our results indicate that exposure to copier-emitted nanoparticles may induce lung injury and inflammation. Further exposure assessment and toxicological investigations are necessary to address this emerging environmental health pollutant.     

Synergistic effects of exposure to concentrated ambient fine pollution particles and nitrogen dioxide in humans

Context: Exposure to single pollutants e.g. particulate matter (PM) is associated with adverse health effects, but it does not represent a real world scenario that usually involves multiple pollutants.

Objectives: Determine if simultaneous exposure to PM and NO₂ results in synergistic interactions.

Materials and methods: Healthy young volunteers were exposed to clean air, nitrogen dioxide (NO₂, 0.5 ppm), concentrated fine particles from Chapel Hill air (PM_2.5CAPs, 89.5?±?10.7 µg/m³), or NO₂+PM_2.5CAPs for 2?h. Each subject performed intermittent exercise during the exposure. Parameters of heart rate variability (HRV), changes in repolarization, peripheral blood endpoints and lung function were measured before and 1 and 18?h after exposure. Bronchoalveolar lavage (BAL) was performed 18?h after exposure.

Results: NO₂ exposure alone increased cholesterol and HDL 18?h after exposure, decreased high frequency component of HRV one and 18?h after exposure, decreased QT variability index 1?h after exposure, and increased LDH in BAL fluid. The only significant change with PM_2.5CAPs was an increase in HDL 1?h after exposure, likely due to the low concentrations of PM_2.5CAPs in the exposure chamber. Exposure to both NO₂ and PM_2.5CAPs increased BAL α1-antitrypsin, mean t wave amplitude, the low frequency components of HRV and the LF/HF ratio. These changes were not observed following exposure to NO₂ or PM_2.5CAPs alone, suggesting possible interactions between the two pollutants.

Discussion and conclusions: NO₂ exposure may produce and enhance acute cardiovascular effects of PM_2.5CAPs. Assessment of health effects by ambient PM should consider its interactions with gaseous copollutants.     

Effects of Concentrated Ambient Particles on Heart Rate,Blood Pressure,and Cardiac Contractility in Spontaneously Hypertensive Rats During a Dust Storm Event

Epidemiological studies have suggested that cardiovascular mortality and morbidity increased during Asian dust events. The findings were still inconclusive though. We have shown an increased pulmonary toxicity in diseased animals during a dust storm event. However, the toxicity nature of dust storm particles remains unclear. It is our objective in this study to further investigate the cardiovascular effects of concentrated PM_2.5 on spontaneously hypertensive rats during the same dust storm event. Four spontaneously hypertensive rats were implanted with radiotelemetry transmitters at the age of 10 wk. Baseline heart rate, mean blood pressure, and cardiac contractility (measured as QA interval, QAI) data were collected 4 wk before. Exposure group received concentrated ambient particles inhalation for 6 h during a dust storm event, while the control group received room air inhalation at the same time. Self-control data were collected 4 wk after the event during the same clock hours while there was no dust storm. Gravimetric analysis showed a particle mass concentration of 315.55 μg/m³ during the 6 h of exposure. A linear mixed-effects model revealed sigmoid increases in heart rate (to a maximum of 93.8 ± 18.8 bpm) and mean blood pressure (to a maximum of 14.8 ± 5.4 mm Hg), and a sigmoid decrease of QAI (to a maximum of ? 3.5 ± 1.5 ms) during the exposure after an initial incubation period. We conclude that concentrated dust storm particles, which are different from products of automobile combustion process, may cause adverse cardiovascular effects on diseased animals.     

The role of pro-/anti-inflammation imbalance in Aβ42 accumulation of rat brain co-exposed to fine particle matter and sulfur dioxide

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO₂) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SO₂ and fine particulate matter (PM_2.5). Rats were exposed alternately to PM_2.5 with different dosages (1.5, 6.0 and 24.0?mg/kg body weight) and SO₂ at the level of 5.6?mg/m³. The results showed that the combined exposure to PM_2.5 and SO₂ enhanced the mRNA expression and protein level of TNF-α and IL-6 in rat cortex and hippocampus relative to the control, SO₂ and PM_2.5 alone. Instead, TGF-β1 mRNA and protein level were down-regulated in the brain. Additionally, PM_2.5 at medium and/or high dose caused marked increase in Aβ42 level and PM_2.5?+?SO₂ induced further increase of Aβ42 level in the cortex and hippocampus. It suggests that SO₂ and PM_2.5 can synergistically exert inflammation responses and induce Aβ42 accumulation in the brain. Also, it is notable that the Aβ42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PM_2.5 and SO₂ can induce the imbalance of pro-/anti-inflammatory cytokine, resulting in Aβ42 accumulation of rat brain cortex and hippocampus.     

Effects of Ambient Air Particulate Exposure on Blood–Gas Barrier Permeability and Lung Function

Particulate air pollution is associated with increased risk of pulmonary diseases and detrimental outcomes related to the cardiovascular system, including altered vessel functions. This study's objective was too evaluate the effects of ambient particle exposure on the blood–gas permeability, lung function and Clara cell 16 (CC16) protein release in healthy young subjects. Twenty-nine nonsmokers participated in a randomized, two-factor crossover study with or without biking exercise for 180 min and with 24-h exposure to particle-rich (6169–15,362 particles/cm³; 7.0–11.6?μg/m³ PM_2.5; 7.5–15.8?μg/m³ PM_10?2.5) or filtered (91–542 particles/cm³) air collected above a busy street. The clearance rate of aerosolized ^99mTc-labeled diethylenetriamine pentaacetic acid (^99mTc-DTPA) was measured as an index for the alveolar epithelial membrane integrity and permeability of the lung blood–gas barrier after rush-hour exposure. Lung function was assessed using body plethysmography, flow-volume curves, and measurements of the diffusion capacity of carbon monoxide. CC16 was measured in plasma and urine as another marker of alveolar integrity. Particulate matter exposure had no significant effect on the epithelial membrane integrity using the methods available in this study. Exercise increased the clearance rate of ^99mTc-DTPA indicated by a 6.8% (95% CI: 0.4–12.8%) shorter half-life and this was more pronounced in men than women. Neither particulate matter exposure nor exercise had an effect on the concentration of CC16 in plasma and urine or on the static and dynamic volumes or ventilation distribution of the lungs. The study thus demonstrates increased permeability of the alveolar blood–gas barrier following moderate exercise, whereas exposure to ambient levels of urban air particles has no detectable effects on the alveolar blood–gas barrier or lung function.     

Source category-specific PM2.5 and urinary levels of Clara cell protein CC16. The ULTRA study

Introduction: We have previously reported that outdoor levels of fine particles (PM_2.5, diameter <2.5 μm) are associated with urinary CC16, a marker for lung damage, in Helsinki, Finland, but not in the other two ULTRA cities (Amsterdam, The Netherlands, and Erfurt, Germany). We here evaluated whether PM_2.5 from specific source categories would be more strongly associated with CC16 than (total) PM_2.5. In addition, we compared two source apportionment methods.

Methods: We collected biweekly spot urinary samples over 6 months from 121 subjects with coronary heart disease for the determination of CC16 (n?=?1251). Principal component analysis (PCA) was used to apportion daily outdoor PM_2.5 between different source categories. In addition, the multilinear engine (ME) was used for the source apportionment in Amsterdam and Helsinki. We analyzed associations of source category-specific PM_2.5 and PM_2.5 absorbance, an indicator for combustion originating particles, with logarithmized values of CC16 adjusting for urinary creatinine using multivariate mixed models in STATA.

Results: In the pooled analyses, CC16 was increased by 0.6% (standard error 0.3%) per 1?×?10^?5 m^?1 increase in the same-day levels of PM_2.5 absorbance. Source category-specific PM_2.5 concentrations were not consistently associated with the levels of CC16 in the three cities. Correlations between source category-specific PM_2.5 determined using either PCA or ME were in general high. Associations of source category-specific PM_2.5 with CC16 in Amsterdam and Helsinki were statistically less significant when ME was used.

Conclusions: The present results suggest that PM_2.5 from combustion sources increases epithelial barrier permeability in lungs.     

Activated iRhom2 drives prolonged PM2.5 exposure-triggered renal injury in Nrf2-defective mice

Abstract

Research suggests that particulate matter (PM_2.5) is a predisposing factor for metabolic syndrome-related systemic inflammation and oxidative stress injury. TNF-α as a major pro-inflammatory cytokine was confirmed to participate in various diseases. Inactive rhomboid protein 2 (iRhom2) was recently determined as a necessary regulator for shedding of TNF-α in immune cells. Importantly, kidney-resident macrophages are critical to inflammation-associated chronic renal injury. Podocyte injury can be induced by stimulants and give rise to nephritis, but how iRhom2 contributes to PM_2.5-induced renal injury is unclear. Thus, we studied whether PM_2.5 causes renal injury and characterized iRhom2 with respect to TNF-α release in mice macrophages and renal tissues in long-term PM_2.5-exposed mouse models. After long-term PM_2.5 exposures, renal injury was confirmed via inflammatory cytokine, chemokine expression, and reduced antioxidant activity. Patients with kidney-related diseases had increased TNF-α, which may contribute to renal injury. We observed up-regulation of serum creatinine, serum urea nitrogen, kidney injury molecule 1, uric acid, TNF-α, MDA, H₂O_2, and O₂^– in PM_2.5-treated mice, which was greater than that found in Nrf2^?/? mice. Meanwhile, increases in metabolic disorder-associated indicators were involved in PM_2.5-induced nephritis. In vitro, kidney-resident macrophages were observed to be critical to renal inflammatory infiltration and function loss via regulation of iRhom2/TACE/TNF-α signaling, and suppression of Nrf2-associated anti-oxidant response. PM_2.5 exposure led to renal injury partly by inflammation-mediated podocyte injury. Reduced SOD1, SOD2, Nrf2 activation, and increased XO, NF-κB activity, TACE, iNOS, IL-1β, TNF-α, IL-6, MIP-1α, Emr-1, MCP-1, and Cxcr4, were also noted. Long-term PM_2.5 exposure causes chronic renal injury by up-regulation of iRhom2/TACE/TNF-α axis in kidney-resident macrophages. Overexpression of TNF-α derived from macrophages causes podocyte injury and kidney function loss. Thus, PM_2.5 toxicities are related to exposure duration and iRhom2 may be a potential therapeutic renal target.     

Inflammatory response and endothelial dysfunction in the hearts of mice co‐exposed to SO2, NO2, and PM2.5

SO₂, NO₂, and PM_2.5 are typical air pollutants produced during the combustion of coal. Increasing evidence indicates that air pollution has contributed to the development and progression of heart‐related diseases over the past decades. However, little experimental data and few studies of SO₂, NO₂, and PM_2.5 co‐exposure in animals exist; therefore, the relevant mechanisms underlying this phenomenon are unclear. An important characteristic of air pollution is that co‐exposure persists at a low concentration throughout a lifetime. In the present study, we treated adult mice with SO₂, NO₂, and PM_2.5 at various concentrations (0.5 mg/m³ SO₂, 0.2 mg/m³ NO₂ 6 h/d, with intranasal instillation of 1 mg/kg PM_2.5 every other day during these exposures; or 3.5 mg/m³ SO₂, 2 mg/m³ NO₂ 6 h/d, and 10 mg/kg PM_2.5 for 28 d). Blood pressure (BP), heart rate (HR), histopathological damage, and inflammatory and endothelial cytokines in the heart were assessed. The results indicate that co‐exposure caused endothelial dysfunction by elevating endothelin‐1 (ET‐1) expression and repressing the endothelial nitric oxide synthase (eNOS) level as well as stimulating the inflammatory response by increasing the levels of cyclooxygenase‐2 (COX‐2), inducible nitric oxide synthase (iNOS), tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6). Additionally, these alterations were confirmed by histological staining. Furthermore, we observed decreased BP and increased HR after co‐exposure. Our results indicate that co‐exposure to SO₂, NO₂, and PM_2.5 may be a major risk factor for cardiac disease and may induce injury to the hearts of mammals and contribute to heart disease. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1996–2005, 2016.     

Alteration of cardiac function in ApoE−/− mice by subchronic urban and regional inhalation exposure to concentrated ambient PM2.5

Ambient PM_2.5 (particulate matter with an aerodynamic diameters of less than 2.5 μm) is associated with alterations in the autonomic nervous system and cardiac function, but there are significant response variations. The authors simultaneously studied the effects of concentrated PM_2.5 (CAPs) in Sterling Forest (SF; dominated by long-range transported PM) and at the Mount Sinai School of Medicine (MS; rich in Ni and elemental/organic carbon [EC/OC]) in Manhattan, NY. ApoE^?/? mice (n?=?8/group) were exposed to filtered air or CAPs (average 133 and 123 μg/m³ in SF and MS, respectively) for 6?h/day, 5 days/week for 6 months. Electrocardiogram (ECG) tracings were monitored using telemetry. At MS, current day CAPs mass was negatively associated with short-term changes in heart rate (HR), and positively with HR variability (HRV). At SF, CAPs mass was positively associated with HR, and negatively with HRV. At MS, HR and HRV changes were associated with PM_2.5 components associated with redisual oil combustion?>?long-range transport?>?traffic?>?FeMn?>?incineration?>?soil, and fireworks had no associations. At SF, HR and HRV were associated with long-range transport?>?Ni refinery?>?soil?>?residual oil combustion/traffic. At both sites, there were cardiac function associations with PM_2.5, but not EC. At MS, there were associations with Ni and P, whereas at SF, they were with a mixture of long-range transported PM, crustal material, and combustion products. Thus subchronic CAPs exposures at locations with different particle compositions produced different effects on cardiac function in ApoE^?/? mice.     

Treg responses are associated with PM2.5-induced exacerbation of viral myocarditis

Abstract

The adverse cardiovascular events induced by ambient fine particles (PM_2.5) are paid more attention in the world. The current study was conducted to explore the mechanisms of T regulatory cells (Treg) responses in PM_2.5-induced exacerbation of viral myocarditis. The male BALB/c mice were administered an intratracheal (i.t.) instillation of 10?mg/kg b.w. PM_2.5 suspension. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100?μl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, serum, splenetic, and cardiac tissues were examined. The results showed that pre-exposure to PM_2.5 aggravated the cardiac inflammation in the CVB3-infected mice along with an increase of Treg cells in the spleen. The mRNA expressions of interleukin-6 (IL-6), TNF-α, transforming growth factor-β (TGF-β), and Foxp3 were up-regulated in the PM_2.5-pretreated mice than that in the CVB3-treated mice. Similar results were found in the sera. In addition, compared with the CVB3-treated mice, the cardiac protein expression of TGF-β increased in the PM_2.5-pretreated mice. These results demonstrated that preexposure to PM_2.5 exacerbated virus-induced myocarditis possibly through the depression of the immune response and increase of inflammation in myocardium through the Treg responses.     

Inflammation and tissue damage in mouse lung by single and repeated dosing of urban air coarse and fine particles collected from six European cities

The authors have previously demonstrated heterogeneities in the inflammatory activities of urban air fine (PM_2.5–0.2) and coarse (PM_10–2.5) particulate samples collected from six European cities with contrasting air pollution situations. The same samples (10?mg/kg) were intratracheally instilled to healthy C57BL/6J mice either once or repeatedly on days 1, 3, and 6 of the study week. The lungs were lavaged 24?h after the single dose or after the last repeated dosing. In both size ranges, repeated dosing of particles increased the total cell number in bronchoalveolar lavage fluid (BALF) more than the respective single dose, whereas cytokine concentrations were lower after repeated dosing. The lactate dehydrogenase (LDH) responses increased up to 2-fold after repeated dosing of PM_2.5–0.2 samples and up to 6-fold after repeated dosing of PM_10–2.5 samples. PM_10–2.5 samples evoked a more extensive interstitial inflammation in the mouse lungs. The constituents with major contributions to the inflammatory responses were oxidized organic compounds and transition metals in PM_2.5–0.2 samples, Cu and soil minerals in PM_10–2.5 samples, and Zn in both size ranges. In contrast, poor biomass and coal combustion were associated with elevated levels of polycyclic aromatic hydrocarbons (PAHs) and a consistent inhibitory effect on the inflammatory activity of PM_2.5–0.2 samples. In conclusion, repeated intratracheal instillation of both fine and coarse particulate samples evoked enhanced pulmonary inflammation and cytotoxicity compared to single-dose administration. The sources and constituents of urban air particles responsible for these effects appear to be similar to those encountered in the authors’ previous single-dose study.     

Particle-associated organic compounds and symptoms in myocardial infarction survivors

Context: The aerosol components responsible for the adverse health effects of the exposure to particulate matter (PM) have not been conclusively identified, and there is especially little information on the role of particulate organic compounds (POC).

Objective: This study evaluated the role of PM and POC with regard to daily symptoms.

Methods: One hundred and fifty-three myocardial infarction survivors from Augsburg, Germany, recorded daily occurrence of different symptoms in winter 2003/2004. Ambient concentrations of PM with a diameter <2.5 μm (PM_2.5), particle number concentration (PNC), PM_2.5-bound hopanes, and polycyclic aromatic hydrocarbons (PAH) were quantified. Data were analyzed using generalized estimating equations adjusting for meteorological and other time-variant confounders.

Results: The odds for avoidance of physically demanding activities due to heart problems increased immediately associated with most POC measures (e.g. 5% per 1.08?ng/m³ increase in benzo[a]pyrene, 95%-confidence interval (CI):1–9%) and tended to a delayed decrease. After a 2-day delayed decrease associated with hopanes, the odds for shortness of breath increased consistently after 3 days with almost all POC measures (e.g. 4% per 0.21?ng/m³ increase in 17α(H), 21β(H)-hopane, CI: 1–8%). The odds for heart palpitations marginally increased immediately in association with PNC (8% per 8146?cm^?3 increase in PNC, CI: 0–16%).

Conclusions: The study showed an association between PM, particle-bound POC, and daily symptoms. The organic compounds may be causally related with cardiovascular health or act rather as indicators for traffic- and combustion-related particles.     

Pulmonary Retention of Particulate Matter is Associated with Airway Inflammation in Allergic Rats Exposed to Air Pollution in Urban Detroit

A collaborative research study was conducted in order to improve our understanding of the source-to-receptor pathway for ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μ m; PM_2.5) and subsequently to investigate the identity and sources of toxic components in PM_2.5 responsible for adverse health effects in allergic humans. This research used a Harvard fine particle concentrator to expose Brown Norway rats, with and without ovalbumin-induced allergic airway disease, to concentrated air particles (CAPs) generated from ambient air in an urban Detroit community where the pediatric asthma rate was three times higher than the national average. Rats were exposed to CAPs during the exposure periods in July (mean = 676 μg/m³) and September (313 μg/m³) of 2000. Twenty-four hours after exposures lung lobes were either lavaged with saline to determine cellularity and protein in bronchoalveolar lavage fluid (BALF), or removed for analysis by inductively coupled plasma–mass spectrometry (ICP-MS) to detect ambient PM_2.5-derived trace element retention. PM_2.5 trace elements of anthropogenic origin, lanthanum (La), vanadium (V), manganese (Mn), and sulfur (S), were recovered from the lung tissues of CAPs-exposed rats. Recovery of those pulmonary anthropogenic particles was further increased in rats with allergic airways. In addition, eosinophils and protein in BALF were increased only in allergic animals exposed to CAPs. These results demonstrate preferential retention in allergic airways of air particulates derived from identified local combustion sources after a short-term exposure. Our findings suggest that the enhancement of allergic airway responses by exposure to PM_2.5 is mediated in part by increased pulmonary deposition and localization of potentially toxic elements in urban air.     

Cardiomyopathy confers susceptibility to particulate matter-induced oxidative stress,vagal dominance,arrhythmia and pulmonary inflammation in heart failure-prone rats

Abstract

Acute exposure to ambient fine particulate matter (PM_2.5) is tied to cardiovascular morbidity and mortality, especially among those with prior cardiac injury. The mechanisms and pathophysiological events precipitating these outcomes remain poorly understood but may involve inflammation, oxidative stress, arrhythmia and autonomic nervous system imbalance. Cardiomyopathy results from cardiac injury, is the leading cause of heart failure, and can be induced in heart failure-prone rats through sub-chronic infusion of isoproterenol (ISO). To test whether cardiomyopathy confers susceptibility to inhaled PM_2.5 and can elucidate potential mechanisms, we investigated the cardiophysiologic, ventilatory, inflammatory and oxidative effects of a single nose-only inhalation of a metal-rich PM_2.5 (580?µg/m³, 4?h) in ISO-pretreated (35 days?×?1.0?mg/kg/day sc) rats. During the 5 days post-treatment, ISO-treated rats had decreased HR and BP and increased pre-ejection period (PEP, an inverse correlate of contractility) relative to saline-treated rats. Before inhalation exposure, ISO-pretreated rats had increased PR and ventricular repolarization time (QT) and heterogeneity (Tp-Te). Relative to clean air, PM_2.5 further prolonged PR-interval and decreased systolic BP during inhalation exposure; increased tidal volume, expiratory time, heart rate variability (HRV) parameters of parasympathetic tone and atrioventricular block arrhythmias over the hours post-exposure; increased pulmonary neutrophils, macrophages and total antioxidant status one day post-exposure; and decreased pulmonary glutathione peroxidase 8 weeks after exposure, with all effects occurring exclusively in ISO-pretreated rats but not saline-pretreated rats. Ultimately, our findings indicate that cardiomyopathy confers susceptibility to the oxidative, inflammatory, ventilatory, autonomic and arrhythmogenic effects of acute PM_2.5 inhalation.     

Host and environmental factors affect pulmonary responses measured in bronchoalveolar lavage

Abstract

Context: Bronchoscopy with bronchoalveolar lavage (BAL) is used to measure pulmonary effects in inhalational exposure studies.

Objectives: To determine how host and background environmental factors may affect pulmonary responses in BAL.

Materials and methods: We retrospectively analyzed 77 healthy non-smoking volunteers (38 males and 39 females, age 18–35) who participated in a bronchoscopy study to donate cells for in vitro studies. BAL was performed by lavaging one subsegment of both the lingular segment of the left upper lobe and the right middle lobe with 250?ml of sterile normal saline each. We obtained temperature, relative humidity, ambient O₃, PM_2.5 and PM₁₀ levels from monitor stations in Durham area in North Carolina. We correlated concentrations of leptin, adiponectin, monocyte chemotactic protein-1 (MCP-1), interleukin (IL)-8, ferritin and total lavaged cells in BAL samples with body mass index (BMI), age, ambient O₃, PM_2.5, PM₁₀, temperature and relative humidity.

Results: Increased BMI was associated with higher lavage leptin. Males had higher MCP-1 and total lavaged cells than females. Average PM_2.5, PM₁₀ and O₃ concentrations before bronchoscopy were 13.7?µg/m³, 21.2?µg/m³ and 0.029?ppm, respectively. Using stepwise multiple linear regression, we found positive associations of MCP-1 with BMI, and of total lavaged cells with humidity and O₃. There were inverse associations of IL-8 and total lavaged cells with temperature.

Discussion and conclusions: Background environmental and host factors may affect some pulmonary responses to ambient pollutants. Interpretation of pulmonary effects in inhalational exposure studies may need to consider the effects of some host and environmental factors.     

Derivation of PM10 size-selected human equivalent concentrations of inhaled nickel based on cancer and non-cancer effects on the respiratory tract

Abstract

Nickel (Ni) in ambient air is predominantly present in the form of oxides and sulfates, with the distribution of Ni mass between the fine (particle aerodynamic diameter <?2.5?µm; PM_2.5) and coarser (2.5–10?µm) size-selected aerosol fractions of PM₁₀ dependent on the aerosol's origin. When deriving a long-term health protective reference concentration for Ni in ambient air, the respiratory toxicity and carcinogenicity effects of the predominant Ni compounds in ambient air must be considered. Dosimetric adjustments to account for differences in aerosol particle size and respiratory tract deposition and/or clearance among rats, workers, and the general public were applied to experimentally- and epidemiologically-determined points of departure (PODs) such as no(low)-effect concentrations, for both cancer and non-cancer respiratory effects. This approach resulted in the derivation of threshold-based PM₁₀ size-selected equivalent concentrations (modified PODs) of 0.5?µg Ni/m³ based on workers' cancer effects and 9–11?µg Ni/m³ based on rodent respiratory toxicity effects. Sources of uncertainty in exposure extrapolations are described. These are not reference concentrations; rather the derived PM₁₀ size-selected modified PODs can be used as the starting point for the calculation of ambient air reference concentrations for Ni. The described approach is equally applicable to other particulates.