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Short course gamma tocopherol did not mitigate effects of ozone on airway inflammation in asthmatics.
Burbank, AJ, Hernandez, ML, Robinette, C, Wang, T, Zhou, H, Alexis, N, Bennett, WD, Peden, DB
Inhalation toxicology. 2020;(7):279-281
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Abstract
INTRODUCTION Exposure to elevated ambient ozone levels has been associated with exacerbation of asthma, likely mediated by oxidative stress. We have shown that supplementation with the antioxidant vitamin E isoform, gamma tocopherol, mitigates the inflammatory effects of inhaled endotoxin exposure, a key component of ambient air particulate matter. OBJECTIVE The objective of the current study was to assess the efficacy of gamma tocopherol for mitigating pulmonary effects of ozone, using an abbreviated dosing regimen that could be rapidly begun when high ozone days are anticipated. MATERIALS AND METHODS We conducted a randomized, double blind, placebo-controlled crossover study of adults with mild asthma who were pre-treated with gamma tocopherol-enriched supplement and exposed to 0.25 ppm ozone for 3 hours. Induced sputum samples were obtained before and after ozone exposure to measure airway inflammation. Mucociliary clearance was estimated using gamma scintigraphy. RESULTS With the short course of gamma tocopherol pre-treatment, we found no significant effect on ozone-induced airway inflammation. A transient slowing of clearance in the large airways was seen following ozone exposure in the placebo treatment period that was not present during gamma tocopherol treatment. DISCUSSION Short course gamma tocopherol did not protect against ozone-induced airway inflammation. Future work will focus on the efficacy of longer courses of gamma tocopherol supplementation for mitigating pollutant-induced health effects. The early transient ozone effect on airway clearance as well as the impact of gamma tocopherol on this effect will be further explored in future studies.
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Associations between urinary biomarkers of oxidative stress and air pollutants observed in a randomized crossover exposure to steel mill emissions.
Pelletier, G, Rigden, M, Kauri, LM, Shutt, R, Mahmud, M, Cakmak, S, Kumarathasan, P, Thomson, EM, Vincent, R, Broad, G, et al
International journal of hygiene and environmental health. 2017;(2 Pt B):387-394
Abstract
The effects of industrial air pollution on human health have not been as thoroughly investigated as those of urban air pollution which originates mostly from automotive transport. To better assess the health impacts of point sources of industrial air pollution, a randomized crossover exposure study was conducted. Sixty one young and healthy volunteers were randomly assigned to spend five consecutive eight-hour days near a steel mill or at a location five kilometres away. After a nine or sixteen-day washout period, volunteers spent another five consecutive days at the second site. Meteorological conditions and air pollutants were monitored at both exposure sites. On each exposure day, the first morning urine was collected along with a second urine sample obtained immediately before leaving the exposure site at the end of the day. Urinary levels of biomarkers of oxidative stress 8-hydroxy-2'-deoxyguanosine (8-OHdG, a biomarker of oxidative DNA damage), malondialdehyde (MDA, a biomarker of lipid peroxidation), 8-isoprostane (8-IsoP, a bioactive metabolite resulting from the peroxidation of arachidonic acid) and Vascular Endothelial Growth Factor (VEGF, involved in response to oxidative stress) were measured. According to mixed-effects linear regression models, intra-individual variations in 8-OHdG urinary levels were significantly associated with exposure site, but surprisingly, lower levels were observed at the steel mill site. Delayed, temporally-defined associations with specific air pollutants were observed for 8-OHdG, 8-IsoP and VEGF. However, these associations were subtle, presented complex patterns and their biological consequences remain unclear.
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Influence of exposure to coarse, fine and ultrafine urban particulate matter and their biological constituents on neural biomarkers in a randomized controlled crossover study.
Liu, L, Urch, B, Szyszkowicz, M, Speck, M, Leingartner, K, Shutt, R, Pelletier, G, Gold, DR, Scott, JA, Brook, JR, et al
Environment international. 2017;:89-95
Abstract
BACKGROUND Epidemiological studies have reported associations between air pollution and neuro-psychological conditions. Biological mechanisms behind these findings are still not clear. OBJECTIVES We examined changes in blood and urinary neural biomarkers following exposure to concentrated ambient coarse, fine and ultrafine particles. METHODS Fifty healthy non-smoking volunteers, mean age 28years, were exposed to coarse (2.5-10μm, mean 213μg/m3) and fine (0.15-2.5μm, mean 238μg/m3) concentrated ambient particles (CAPs), and filtered ambient and/or medical air. Twenty-five participants were exposed to ultrafine CAP (mean size 59.6nm, range 47.0-69.8nm), mean (136μg/m3) and filtered medical air. Exposures lasted 130min, separated by ≥2weeks, and the biological constituents endotoxin and β-1,3-d-glucan of each particle size fraction were measured. Blood and urine samples were collected pre-exposure, and 1-hour and 21-hour post-exposure to determine neural biomarker levels. Mixed-model regressions assessed associations between exposures and changes in biomarker levels. RESULTS Results were expressed as percent change from daily pre-exposure biomarker levels. Exposure to coarse CAP was significantly associated with increased urinary levels of the stress-related biomarkers vanillylmandelic acid (VMA) and cortisol when compared with exposure to filtered medical air [20% (95% confidence interval: 1.0%, 38%) and 64% (0.2%, 127%), respectively] 21hours post-exposure. However exposure to coarse CAP was significantly associated with decreases in blood cortisol [-26.0% (-42.4%, -9.6%) and -22.4% (-43.7%, -1.1%) at 1h and 21h post-exposure, respectively]. Biological molecules present in coarse CAP were significantly associated with blood biomarkers indicative of blood brain barrier integrity. Endotoxin content was significantly associated with increased blood ubiquitin C-terminal hydrolase L1 [UCHL1, 11% (5.3%, 16%) per ln(ng/m3+1)] 1-hour post-exposure, while β-1,3-d-glucan was significantly associated with increased blood S100B [6.3% (3.2%, 9.4%) per ln(ng/m3+1)], as well as UCHL1 [3.1% (0.4%, 5.9%) per ln(ng/m3+1)], one-hour post-exposure. Fine CAP was marginally associated with increased blood UCHL1 when compared with exposure to filtered medical air [17.7% (-1.7%, 37.2%), p=0.07] 21hours post-exposure. Ultrafine CAP was not significantly associated with changes in any blood and urinary neural biomarkers examined. CONCLUSION Ambient coarse particulate matter and its biological constituents may influence neural biomarker levels that reflect perturbations of blood-brain barrier integrity and systemic stress response.
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[Establishment and application effect appraisement of community chronic obstructive pulmonary disease integrated management system].
Zhao, DX, Chen, SY, Zhou, YM, Li, XC, Zou, WF, Chen, XM, Ran, PX
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases. 2017;(2):102-107
Abstract
Objective: To establish the COPD community integrated management system suitable for our national situation and assess its effects in the prevention and treatment for COPD. Methods: The COPD community integrated management system based on the electronic management system was established, including the functional modules of preliminary screening for COPD, electronic health record, grading management and dual referral system, ect. Two townships were randomly selected from the rural areas in north Guangdong as Observational Community and Control Community, respectively. Resident families were randomly selected from the two communities. One resident aged 40 or higher who was selected randomly from each family was enrolled in the trial and followed up for 2 years.Of a total of 460 participants from the Observational Community, 340 participants accomplished the two-years the follow-up, among whom there were 45 COPD patients, 117 high risk population, 178 common population. Of a total of 380 participants from the Control Community, 212 participants accomplished the follow-up, among whom there were 39 COPD patients, 68 high risk population, 105 common population.According to the COPD community integrated management system, the health cares including preliminary screening for COPD, grading management and dual referral, ect. were implemented in the Observational Community. Essential diagnosis and treatment services were performed in the Control Community. The effects of the system were appraised by comparisons of the pulmonary function change, acute exacerbation, quality of life and change of risk factors, ect. between the two communities. Results: After the intervention, the follow-up rate, smoking-quitting rate, the proportions of decline in current smoking, passive smoking and switching to clean energy for cooking in the Observational Community were significantly greater than those in the Control Community(73.9% vs. 55.8%, 70.8% vs. 9.1%, 24.2% vs. 7.1%, 32.6% vs. 3.5%, 67.8% vs. 3.2%, respectively, P<0.05). COPD knowledge rates of residents in the Observational Community, including "knowing about COPD" , "knowing about the symptoms of COPD" , "Whether COPD can be prevented and treated" and "lung function test" were significantly greater than before (84.7% vs.30.0%, 76.4% vs.7.6%, 71.5% vs.6.8%, 72.1% vs.27.4%, respectively, P<0.05) and greater than those in the Control Community(84.7% vs.73.6%, 76.4% vs.9.4%, 71.5% vs.7.1%, 72.1% vs.32.5%, P<0.05). In the Observational Community, FEV(1) and FEV(1) %Pred were significantly greater than before (1.88±0.71 vs. 1.74±0.64, 75.6±25.0 vs. 69.4±20.5, respectively, P<0.05). The values of the difference before and after the experiment in the patients of GOLD 1 grade COPD in the Observational Community were greater than those in the Control Community(P<0.05). In the Control Community, FEV(1)、FEV(1) %Pred had no significant difference before and after experiment(P>0.05). In the Observational Community, 6MWD, standard treatment rate and exercises>3 days per week were significantly greater than before(550.5±76.0 vs. 474.7±75.9, 64.4% vs. 8.9%, 100% vs. 22.2%, respectively, P<0.05) and greater than those in the Control Community(550.5±76.0 vs. 404.5±56.7, 64.4% vs. 10.3%, 100% vs. 30.8%, respectively, P<0.05), acute exacerbation was significantly less than before (4.4% vs. 17.8%, P<0.05). In the Control Unit, 6MWD was significantly less than before (404.5±56.7 vs. 469.8±58.5, P<0.05). Conclusions: The COPD community integrated management system can play a great role in community integrated prevention for COPD.
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A Randomized Cross-over Air Filtration Intervention Trial for Reducing Cardiovascular Health Risks in Residents of Public Housing near a Highway.
Padró-Martínez, LT, Owusu, E, Reisner, E, Zamore, W, Simon, MC, Mwamburi, M, Brown, CA, Chung, M, Brugge, D, Durant, JL
International journal of environmental research and public health. 2015;(7):7814-38
Abstract
Exposure to traffic-generated ultrafine particles (UFP; particles <100 nm) is likely a risk factor for cardiovascular disease. We conducted a trial of high-efficiency particulate arrestance (HEPA) filtration in public housing near a highway. Twenty residents in 19 apartments living <200 m from the highway participated in a randomized, double-blind crossover trial. A HEPA filter unit and a particle counter (measuring particle number concentration (PNC), a proxy for UFP) were installed in living rooms. Participants were exposed to filtered air for 21 days and unfiltered air for 21 days. Blood samples were collected and blood pressure measured at days 0, 21 and 42 after a 12-hour fasting period. Plasma was analyzed for high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), tumor necrosis factor alpha-receptor II (TNF-RII) and fibrinogen. PNC reductions ranging from 21% to 68% were recorded in 15 of the apartments. We observed no significant differences in blood pressure or three of the four biomarkers (hsCRP, fibrinogen, and TNF-RII) measured in participants after 21-day exposure to HEPA-filtered air compared to measurements after 21-day exposure to sham-filtered air. In contrast, IL-6 concentrations were significantly higher following HEPA filtration (0.668 pg/mL; CI = 0.465-0.959) compared to sham filtration. Likewise, PNC adjusted for time activity were associated with increasing IL-6 in 14- and 21-day moving averages, and PNC was associated with decreasing blood pressure in Lags 0, 1 and 2, and in a 3-day moving average. These negative associations were unexpected and could be due to a combination of factors including exposure misclassification, unsuccessful randomization (i.e., IL-6 and use of anti-inflammatory medicines), or uncontrolled confounding. Studies with greater reduction in UFP levels and larger sample sizes are needed. There also needs to be more complete assessment of resident time activity and of outdoor vs. indoor source contributions to UFP exposure. HEPA filtration remains a promising, but not fully realized intervention.
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Home interventions are effective at decreasing indoor nitrogen dioxide concentrations.
Paulin, LM, Diette, GB, Scott, M, McCormack, MC, Matsui, EC, Curtin-Brosnan, J, Williams, DL, Kidd-Taylor, A, Shea, M, Breysse, PN, et al
Indoor air. 2014;(4):416-24
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Abstract
UNLABELLED Nitrogen dioxide (NO2 ), a by-product of combustion produced by indoor gas appliances such as cooking stoves, is associated with respiratory symptoms in those with obstructive airways disease. We conducted a three-armed randomized trial to evaluate the efficacy of interventions aimed at reducing indoor NO2 concentrations in homes with unvented gas stoves: (i) replacement of existing gas stove with electric stove; (ii) installation of ventilation hood over existing gas stove; and (iii) placement of air purifiers with high-efficiency particulate air (HEPA) and carbon filters. Home inspection and NO2 monitoring were conducted at 1 week pre-intervention and at 1 week and 3 months post-intervention. Stove replacement resulted in a 51% and 42% decrease in median NO2 concentration at 3 months of follow-up in the kitchen and bedroom, respectively (P = 0.01, P = 0.01); air purifier placement resulted in an immediate decrease in median NO2 concentration in the kitchen (27%, P < 0.01) and bedroom (22%, P = 0.02), but at 3 months, a significant reduction was seen only in the kitchen (20%, P = 0.05). NO2 concentrations in the kitchen and bedroom did not significantly change following ventilation hood installation. Replacing unvented gas stoves with electric stoves or placement of air purifiers with HEPA and carbon filters can decrease indoor NO2 concentrations in urban homes. PRACTICAL IMPLICATIONS Several combustion sources unique to the residential indoor environment, including gas stoves, produce nitrogen dioxide (NO2), and higher NO2 concentrations, are associated with worse respiratory morbidity in people with obstructive lung disease. A handful of studies have modified the indoor environment by replacing unvented gas heaters; this study, to our knowledge, is the first randomized study to target unvented gas stoves. The results of this study show that simple home interventions, including replacement of an unvented gas stove with an electric stove or placement of HEPA air purifiers with carbon filters, can significantly decrease indoor NO2 concentrations.
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Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man.
Langrish, JP, Unosson, J, Bosson, J, Barath, S, Muala, A, Blackwell, S, Söderberg, S, Pourazar, J, Megson, IL, Treweeke, A, et al
Journal of the American Heart Association. 2013;(1):e004309
Abstract
BACKGROUND Diesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. We investigated the role of nitric oxide (NO) bioavailability in mediating these effects. METHODS AND RESULTS In 2 randomized double-blind crossover studies, healthy nonsmokers were exposed to diesel exhaust or filtered air. Study 1: Bilateral forearm blood flow was measured during intrabrachial infusions of acetylcholine (ACh; 5 to 20 μg/min) and sodium nitroprusside (SNP; 2 to 8 μg/min) in the presence of the NO clamp (NO synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA) 8 μg/min coinfused with the NO donor SNP at 90 to 540 ng/min to restore basal blood flow). Study 2: Blood pressure, arterial stiffness, and cardiac output were measured during systemic NO synthase inhibition with intravenous l-NMMA (3 mg/kg). Following diesel exhaust inhalation, plasma nitrite concentrations were increased (68±48 versus 41±32 nmol/L; P=0.006) despite similar l-NMMA-induced reductions in basal blood flow (-20.6±14.7% versus -21.1±14.6%; P=0.559) compared to air. In the presence of the NO clamp, ACh and SNP caused dose-dependent vasodilatation that was not affected by diesel exhaust inhalation (P>0.05 for both). Following exposure to diesel exhaust, l-NMMA caused a greater increase in blood pressure (P=0.048) and central arterial stiffness (P=0.007), but reductions in cardiac output and increases in systemic vascular resistance (P>0.05 for both) were similar to those seen with filtered air. CONCLUSIONS Diesel exhaust inhalation disturbs normal vascular homeostasis with enhanced NO generation unable to compensate for excess consumption. We suggest the adverse cardiovascular effects of air pollution are, in part, mediated through reduced NO bioavailability. CLINICAL TRIAL REGISTRATION URL: http://www.ClinicalTrials.gov. Unique identifiers: NCT00845767 and NCT01060930.
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Modulation of the metabolism of airborne pollutants by glucoraphanin-rich and sulforaphane-rich broccoli sprout beverages in Qidong, China.
Kensler, TW, Ng, D, Carmella, SG, Chen, M, Jacobson, LP, Muñoz, A, Egner, PA, Chen, JG, Qian, GS, Chen, TY, et al
Carcinogenesis. 2012;(1):101-7
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Abstract
Epidemiological evidence has suggested that consumption of a diet rich in cruciferous vegetables reduces the risk of several types of cancers and chronic degenerative diseases. In particular, broccoli sprouts are a convenient and rich source of the glucosinolate, glucoraphanin, which can release the chemopreventive agent, sulforaphane, an inducer of glutathione S-transferases. Two broccoli sprout-derived beverages, one sulforaphane-rich (SFR) and the other glucoraphanin-rich (GRR), were evaluated for pharmacodynamic action in a crossover clinical trial design. Study participants were recruited from the farming community of He Zuo Township, Qidong, China, previously documented to have a high incidence of hepatocellular carcinoma with concomitant exposures to aflatoxin and more recently characterized with exposures to substantive levels of airborne pollutants. Fifty healthy participants were randomized into two treatment arms. The study protocol was as follows: a 5 days run-in period, a 7 days administration of beverage, a 5 days washout period and a 7 days administration of the opposite beverage. Urinary excretion of the mercapturic acids of acrolein, crotonaldehyde, ethylene oxide and benzene were measured both pre- and postinterventions using liquid chromatography tandem mass spectrometry. Statistically significant increases of 20-50% in the levels of excretion of glutathione-derived conjugates of acrolein, crotonaldehyde and benzene were seen in individuals receiving SFR, GRR or both compared with their preintervention baseline values. No significant differences were seen between the effects of SFR versus GRR. Intervention with broccoli sprouts may enhance detoxication of airborne pollutants and attenuate their associated health risks.
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Particle traps prevent adverse vascular and prothrombotic effects of diesel engine exhaust inhalation in men.
Lucking, AJ, Lundbäck, M, Barath, SL, Mills, NL, Sidhu, MK, Langrish, JP, Boon, NA, Pourazar, J, Badimon, JJ, Gerlofs-Nijland, ME, et al
Circulation. 2011;(16):1721-8
Abstract
BACKGROUND In controlled human exposure studies, diesel engine exhaust inhalation impairs vascular function and enhances thrombus formation. The aim of the present study was to establish whether an exhaust particle trap could prevent these adverse cardiovascular effects in men. METHODS AND RESULTS Nineteen healthy volunteers (mean age, 25±3 years) were exposed to filtered air and diesel exhaust in the presence or absence of a particle trap for 1 hour in a randomized, double-blind, 3-way crossover trial. Bilateral forearm blood flow and plasma fibrinolytic factors were assessed with venous occlusion plethysmography and blood sampling during intra-arterial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil. Ex vivo thrombus formation was determined with the use of the Badimon chamber. Compared with filtered air, diesel exhaust inhalation was associated with reduced vasodilatation and increased ex vivo thrombus formation under both low- and high-shear conditions. The particle trap markedly reduced diesel exhaust particulate number (from 150 000 to 300 000/cm(3) to 30 to 300/cm(3); P<0.001) and mass (320±10 to 7.2±2.0 μg/m(3); P<0.001), and was associated with increased vasodilatation, reduced thrombus formation, and an increase in tissue-type plasminogen activator release. CONCLUSIONS Exhaust particle traps are a highly efficient method of reducing particle emissions from diesel engines. With a range of surrogate measures, the use of a particle trap prevents several adverse cardiovascular effects of exhaust inhalation in men. Given these beneficial effects on biomarkers of cardiovascular health, the widespread use of particle traps on diesel-powered vehicles may have substantial public health benefits and reduce the burden of cardiovascular disease.
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Endothelial function and chronic exposure to air pollution in normal male subjects.
Briet, M, Collin, C, Laurent, S, Tan, A, Azizi, M, Agharazii, M, Jeunemaitre, X, Alhenc-Gelas, F, Boutouyrie, P
Hypertension (Dallas, Tex. : 1979). 2007;(5):970-6
Abstract
Exposure to urban air pollution, ultrafine particles or gases, is associated with acute cardiovascular mortality and morbidity. We investigated the effect of ambient air pollution on endothelial function in 40 healthy white male nonsmokers spontaneously breathing ambient air in Paris, France. Air pollutant levels (nitrogen, sulfur and carbon oxides, and particulate matter) were averaged during the 5 days preceding arterial measurements. Brachial artery endothelium-dependent flow-mediated dilatation and reactive hyperemia induced by hand ischemia and endothelium-independent glyceryl trinitrate dilatation were measured using a radiofrequency-based echo-tracking device at 2-week intervals. Flow-mediated dilatation was independently and negatively correlated with the average levels of sulfur dioxide (P<0.001) and nitrogen monoxide (P<0.01). Sulfur dioxide levels explained 19% of the variance of flow-mediated dilatation. An increase in gaseous pollutants, 2 weeks apart, was significantly associated with a decreased in flow-mediated dilatation. No association was found between air pollutants and glyceryl trinitrate-induced vasodilatation. Reactive hyperemia was significantly and positively correlated with particulate matter with aerodynamic diameters <10 microm and <2.5 microm (P<0.0001 and P<0.001, respectively) and nitrogen dioxide (P<0.01). An increase in particulate matter, 2 weeks apart, was significantly correlated with an increase in reactive hyperemia. Endothelial function was impaired by ordinary levels of pollution in healthy young males, in an urban area, and may be reduced by 50% between the least and the most polluted day. Gaseous pollutants affect large artery endothelial function, whereas particulate matter exaggerates the dilatory response of small arteries to ischemia.