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      Effects of Short-Term Exposure to Particulate Air Pollutants on the Inflammatory Response and Respiratory Symptoms: A Panel Study in Schoolchildren from Rural Areas of Japan

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          Abstract

          The relationship between particulate air pollutants and respiratory symptoms in children has not been consistent among studies, potentially owing to differences in the inflammatory response to different particulate air pollutants. This study aimed to investigate the effect of particulate air pollutants on respiratory symptoms and the inflammatory response in schoolchildren. Three hundred-and-sixty children were included in the study. The children recorded daily respiratory symptom scores for October 2015. In addition, the daily amount of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α production was assessed in THP1 cells stimulated with suspended particulate matter (SPM), which was collected every day during the study period. Generalized estimating equation logistic regression analyses were used to estimate the associations among respiratory symptoms and the daily levels of SPM, IL-6, IL-8, and TNF-α. Daily SPM levels were not associated with respiratory symptoms or the daily IL-6, IL-8, and TNF-α levels. Conversely, there was a significant association between respiratory symptoms and the daily IL-6, IL-8, and TNF-α levels. These results suggested that the effects of particulate air pollutants on respiratory symptoms in schoolchildren might depend more on the pro-inflammatory response to them than on their mass concentration.

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          Clearing the air: a review of the effects of particulate matter air pollution on human health.

          The World Health Organization estimates that particulate matter (PM) air pollution contributes to approximately 800,000 premature deaths each year, ranking it the 13th leading cause of mortality worldwide. However, many studies show that the relationship is deeper and far more complicated than originally thought. PM is a portion of air pollution that is made up of extremely small particles and liquid droplets containing acids, organic chemicals, metals, and soil or dust particles. PM is categorized by size and continues to be the fraction of air pollution that is most reliably associated with human disease. PM is thought to contribute to cardiovascular and cerebrovascular disease by the mechanisms of systemic inflammation, direct and indirect coagulation activation, and direct translocation into systemic circulation. The data demonstrating PM's effect on the cardiovascular system are strong. Populations subjected to long-term exposure to PM have a significantly higher cardiovascular incident and mortality rate. Short-term acute exposures subtly increase the rate of cardiovascular events within days of a pollution spike. The data are not as strong for PM's effects on cerebrovascular disease, though some data and similar mechanisms suggest a lesser result with smaller amplitude. Respiratory diseases are also exacerbated by exposure to PM. PM causes respiratory morbidity and mortality by creating oxidative stress and inflammation that leads to pulmonary anatomic and physiologic remodeling. The literature shows PM causes worsening respiratory symptoms, more frequent medication use, decreased lung function, recurrent health care utilization, and increased mortality. PM exposure has been shown to have a small but significant adverse effect on cardiovascular, respiratory, and to a lesser extent, cerebrovascular disease. These consistent results are shown by multiple studies with varying populations, protocols, and regions. The data demonstrate a dose-dependent relationship between PM and human disease, and that removal from a PM-rich environment decreases the prevalence of these diseases. While further study is needed to elucidate the effects of composition, chemistry, and the PM effect on susceptible populations, the preponderance of data shows that PM exposure causes a small but significant increase in human morbidity and mortality. Most sources agree on certain "common sense" recommendations, although there are lonely limited data to support them. Indoor PM exposure can be reduced by the usage of air conditioning and particulate filters, decreasing indoor combustion for heating and cooking, and smoking cessation. Susceptible populations, such as the elderly or asthmatics, may benefit from limiting their outdoor activity during peak traffic periods or poor air quality days. These simple changes may benefit individual patients in both short-term symptomatic control and long-term cardiovascular and respiratory complications.
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            Ischemic Heart Disease Mortality and Long-Term Exposure to Source-Related Components of U.S. Fine Particle Air Pollution

            Background: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. Objectives: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society’s Cancer Prevention Study-II cohort. Methods: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source–associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000–2005. Results: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic–related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-μg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality. Conclusions: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5–mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources. Citation: Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785–794; http://dx.doi.org/10.1289/ehp.1509777
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              Acute effects of particulate air pollution on respiratory admissions: results from APHEA 2 project. Air Pollution and Health: a European Approach.

              The APHEA 2 project investigated short-term health effects of particles in eight European cities. In each city associations between particles with an aerodynamic diameter of less than 10 microm (PM(10)) and black smoke and daily counts of emergency hospital admissions for asthma (0-14 and 15-64 yr), chronic obstructive pulmonary disease (COPD), and all-respiratory disease (65+ yr) controlling for environmental factors and temporal patterns were investigated. Summary PM(10) effect estimates (percentage change in mean number of daily admissions per 10 microg/m(3) increase) were asthma (0-14 yr) 1.2% (95% CI: 0.2, 2.3), asthma (15-64 yr) 1.1% (0.3, 1.8), and COPD plus asthma and all-respiratory (65+ yr) 1.0% (0.4, 1.5) and 0.9% (0.6, 1.3). The combined estimates for Black Smoke tended to be smaller and less precisely estimated than for PM(10). Variability in the sizes of the PM(10) effect estimates between cities was also investigated. In the 65+ groups PM(10) estimates were positively associated with annual mean concentrations of ozone in the cities. For asthma admissions (0-14 yr) a number of city-specific factors, including smoking prevalence, explained some of their variability. This study confirms that particle concentrations in European cities are positively associated with increased numbers of admissions for respiratory diseases and that some of the variation in PM(10) effect estimates between cities can be explained by city characteristics.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Environ Res Public Health
                Int J Environ Res Public Health
                ijerph
                International Journal of Environmental Research and Public Health
                MDPI
                1661-7827
                1660-4601
                30 September 2016
                October 2016
                : 13
                : 10
                : 983
                Affiliations
                [1 ]Department of Respiratory Medicine and Rheumatology, Faculty of Medicine, Tottori University, 36-1 Nishi-cho, Yonago 683-8504, Japan; junkurajun@ 123456gmail.com (J.K.); degujirefu@ 123456med.tottori-u.ac.jp (D.H.); eiji@ 123456med.tottori-u.ac.jp (E.S.)
                [2 ]Department of Data Science, Institute of Statistical Mathematics, 10-3 Midori-cho, Tachikawa, Tokyo 190-8562, Japan; noma@ 123456ism.ac.jp
                [3 ]Department of Respiratory Medicine and Allergology, Faculty of Medicine, Kinki University, Ohnohigashi 377-2, Osakasayama 589-0014, Japan; hsano@ 123456med.kindai.ac.jp
                [4 ]Center for Promoting Next-Generation Highly Advanced Medicine, Tottori University Hospital, 36-1 Nishi-cho, Yonago 683-8504, Japan; masaruueki@ 123456gmail.com
                [5 ]The Board of Directors, Tottori University, 36-1 Nishi-cho, Yonago 683-8504, Japan; hkitano@ 123456med.tottori-u.ac.jp
                Author notes
                [* ]Correspondence: watanabm@ 123456grape.med.tottori-u.ac.jp ; Tel.: +81-859-38-6537; Fax: +81-859-38-6539
                Article
                ijerph-13-00983
                10.3390/ijerph13100983
                5086722
                27706066
                3e66a774-408f-4af6-a265-5cd3ee77d263
                © 2016 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 30 August 2016
                : 21 September 2016
                Categories
                Article

                Public health
                particulate air pollutants,pro-inflammatory cytokine,respiratory symptom,schoolchildren

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