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      Recirculating Air Filtration Significantly Reduces Exposure to Airborne Nanoparticles

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          Abstract

          Background

          Airborne nanoparticles from vehicle emissions have been associated with adverse effects in people with pulmonary and cardiovascular disease, and toxicologic studies have shown that nanoparticles can be more hazardous than their larger-scale counterparts. Recirculating air filtration in automobiles and houses may provide a low-cost solution to reducing exposures in many cases, thus reducing possible health risks.

          Objectives

          We investigated the effectiveness of recirculating air filtration on reducing exposure to incidental and intentionally produced airborne nanoparticles under two scenarios while driving in traffic, and while generating nanomaterials using gas-phase synthesis.

          Methods

          We tested the recirculating air filtration in two commercial vehicles when driving in traffic, as well as in a nonventilation room with a nanoparticle generator, simulating a nanomaterial production facility. We also measured the time-resolved aerosol size distribution during the in-car recirculation to investigate how recirculating air filtration affects particles of different sizes. We developed a recirculation model to describe the aerosol concentration change during recirculation.

          Results

          The use of inexpensive, low-efficiency filters in recirculation systems is shown to reduce nanoparticle concentrations to below levels found in a typical office within 3 min while driving through heavy traffic, and within 20 min in a simulated nanomaterial production facility.

          Conclusions

          Development and application of this technology could lead to significant reductions in airborne nanoparticle exposure, reducing possible risks to health and providing solutions for generating nanomaterials safely.

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          Most cited references25

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          Health effects of fine particulate air pollution: lines that connect.

          Efforts to understand and mitigate thehealth effects of particulate matter (PM) air pollutionhave a rich and interesting history. This review focuseson six substantial lines of research that have been pursued since 1997 that have helped elucidate our understanding about the effects of PM on human health. There hasbeen substantial progress in the evaluation of PM health effects at different time-scales of exposure and in the exploration of the shape of the concentration-response function. There has also been emerging evidence of PM-related cardiovascular health effects and growing knowledge regarding interconnected general pathophysiological pathways that link PM exposure with cardiopulmonary morbidiity and mortality. Despite important gaps in scientific knowledge and continued reasons for some skepticism, a comprehensive evaluation of the research findings provides persuasive evidence that exposure to fine particulate air pollution has adverse effects on cardiopulmonaryhealth. Although much of this research has been motivated by environmental public health policy, these results have important scientific, medical, and public health implications that are broader than debates over legally mandated air quality standards.
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            Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease.

            Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function. In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions. During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve). Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov].). Copyright 2007 Massachusetts Medical Society.
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              Exposure to traffic and the onset of myocardial infarction.

              An association between exposure to vehicular traffic in urban areas and the exacerbation of cardiovascular disease has been suggested in previous studies. This study was designed to assess whether exposure to traffic can trigger myocardial infarction. We conducted a case-crossover study in which cases of myocardial infarction were identified with the use of data from the Cooperative Health Research in the Region of Augsburg Myocardial Infarction Registry in Augsburg, in southern Germany, for the period from February 1999 to July 2001. There were 691 subjects for whom the date and time of the myocardial infarction were known who had survived for at least 24 hours after the event, completed the registry's standardized interview, and provided information on factors that may have triggered the myocardial infarction. Data on subjects' activities during the four days preceding the onset of symptoms were collected with the use of patient diaries. An association was found between exposure to traffic and the onset of a myocardial infarction within one hour afterward (odds ratio, 2.92; 95 percent confidence interval, 2.22 to 3.83; P<0.001). The time the subjects spent in cars, on public transportation, or on motorcycles or bicycles was consistently linked with an increase in the risk of myocardial infarction. Adjusting for the level of exercise on a bicycle or for getting up in the morning changed the estimated effect of exposure to traffic only slightly (odds ratio for myocardial infarction, 2.73; 95 percent confidence interval, 2.06 to 3.61; P<0.001). The subject's use of a car was the most common source of exposure to traffic; nevertheless, there was also an association between time spent on public transportation and the onset of a myocardial infarction one hour later. Transient exposure to traffic may increase the risk of myocardial infarction in susceptible persons. Copyright 2004 Massachusetts Medical Society.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                July 2008
                26 March 2008
                : 116
                : 7
                : 863-866
                Affiliations
                [1 ] Particle Technology Laboratory, University of Minnesota, Minneapolis, Minnesota, USA
                [2 ] Environmental Medicine, University of Rochester, Rochester, New York, USA
                [3 ] Woodrow Wilson Center for Scholars, Washington, DC, USA
                Author notes
                Address correspondence to D.Y.H. Pui, Mechanical Engineering Department, University of Minnesota, 111 Church St. SE, Minneapolis, MN 55455 USA. Telephone: (612) 625-2537. Fax: (612) 625-6069. E-mail: dyhpui@ 123456umn.edu

                The authors declare they have no competing financial interests.

                Article
                ehp0116-000863
                10.1289/ehp.11169
                2453152
                18629306
                91c02d28-6cfa-48b4-8a56-f906c2cfbbcc
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 13 December 2007
                : 19 March 2008
                Categories
                Research

                Public health
                workplace,automobile,filtration,prevention,nanoparticle exposure
                Public health
                workplace, automobile, filtration, prevention, nanoparticle exposure

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