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Preface: Special Issue on Air Pollution
Biochimica et Biophysica Acta 1860 (2016) 2769–2770
Contents lists available at ScienceDirect
Biochimica et Biophysica Acta journal homepage: www.elsevier.com/locate/bbagen
Editorial
Preface: Special Issue on Air Pollution☆
Suspended particulate matter (PM) has presented a challenge to the human respiratory tract for as long as the species has existed. This PM was initially of crustal and plant origin but later included particles generated from the burning of biomass for purposes of heating and food preparation. Only recently, in the past few hundred years, have humans been exposed to combustion products of coal, gas, and oil. Studies conducted during the past century showed that episodes of extremely high levels of air pollution originating from such combustion in both Europe and the United States increased human morbidity and mortality (e.g. London fogs). These air pollution debacles were instrumental in bringing about widespread monitoring and regulation of air quality. In the past few decades, epidemiologic studies delineated an association between exposures to ambient air pollution particles (at levels lower than those currently observed in many cities worldwide) and numerous indices of human morbidity and mortality. These findings were initially met with some skepticism, but both reevaluation of the initial studies and a plethora of new epidemiologic investigation provided concordant results thus confirming the validity of the observations. The adverse effects of air pollution include both pulmonary and extra-pulmonary morbidity and mortality. In addition to PM, studies support ozone (O3) as a major ambient air pollutant with the capacity to impact human morbidity and mortality. While epidemiology has identified adverse impacts of air pollution, mechanistic pathways remain to be described. Such pathways must be defined prior to appreciating prognosis of and developing therapies for air pollution-related disease. This special issue focuses on investigation into mechanistic pathways underlying the biological effects of air pollution. Ozone is a major component of air pollution responsible for decrements in pulmonary function, respiratory inflammation, airway hyperreactivity, and bronchoconstriction. Bromberg describes O3 to have an affinity for C=C bonds [1]. In the lower respiratory tract, molecular targets of this oxidizing gas include phospholipids and cholesterol which react to generate ozonides. Inflammation following its exposure is mediated by an activation of NF- kappa B and release of proinflammatory mediators by respiratory epithelial cells. Potential mechanisms underlying the biological effects of air pollution are delineated by Bai et al. [2]. Following exposure of lung epithelial cells to air pollution particles, oxidative damage, surfactant protein expression, and indices of autophagy are all impacted. Evidence suggests that inflammation after air pollution exposure can be related to the activity of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an enzyme that degrades the endogenous nitric oxide synthase (NOS) inhibitor dimethylarginine. An influence of this pathway on oxidative ☆ This article is part of a Special Issue entitled Air Pollution , edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
http://dx.doi.org/10.1016/j.bbagen.2016.09.007 0304-4165/© 2016 Published by Elsevier B.V.
stress and cell apoptosis following air pollution particle exposure is characterized by Wang et al. [3]. Modification of the expression of DDAH1 is shown to be protective in air pollution particle exposures. Changes in biological effect associated with varying DDAH1 expression were related to alterations in oxidative stress. Exposure to a variety of xenobiotics dysregulates cellular physiology by interfering with redox-dependent processes. Live-cell imaging for redox studies are reviewed by Wages et al. [4]. Such imaging using a new generation of small molecule and genetically encoded fluorophores is observed to have excellent sensitivity and specificity and to afford unprecedented spatiotemporal resolution optimal for redox studies including those into the biological effects of air pollution particles. A role for a disruption in iron homeostasis following exposures to air pollution has been supported by numerous studies conducted over the past decades. Ghio et al. suggest that a mechanism underlying biological effects of particles is a complexation of cell iron by surface functional groups resulting in a functional deficiency in the cell and tissue [5]. The loss of requisite iron after complexation of cell iron to PM initiates oxidative stress and inflammation. Activation of cell signaling networks and transcription factors is one of the initial events mediating inflammation after air pollution exposure. Yan et al. defines major signaling pathways triggering inflammation after exposure to air pollution particles and ozone [6]. Elucidation of these cellular signaling pathways initiated by air pollutants can assist in 1) revealing mechanistic pathways and 2) developing potential interventions. The effects of air pollution on cell signaling show a dependence on oxidative stress. The macrophage is a cell resident in the respiratory tract with a capacity to impact defense against tissue damage and orchestrate the initiation and resolution phases of both innate and adaptive immunity. Zhao et al. demonstrate that air pollution particles enhance the inflammatory capacity of macrophages through oxidant-sensitive pathways [7]. PM is shown to act directly on polarization of these cells affecting pro-inflammatory cytokine secretion by classically activated macrophages (M1) and anti-inflammatory responses of alternatively activated macrophages (M2). In air pollution, ultrafine particles reflect anthropogenic emission sources, i.e. combustion engines and power plants. As a result of the extremely small size, these particles are thought to play a major role in the adverse impact of air pollution on human health including cardiovascular disease. Composition, sources, oxidative effects, potential exposure routes and health risks of ultrafine particles included in air pollution are reviewed by Chen et al. [8]. Exposure to biodiesel combustion products has been considered not to induce either the biological effects or injury observed after exposure to other fuel combustion products. Madden evaluates the environmental and health effects of biodiesel and observes that these emissions can
2770
Editorial
induce biological effects [9]. Evidence of studies provide conflicting data but inflammatory, vascular, mutagenic, and other effects of biodiesel may approximate those of diesel exhaust. The function of numerous tissues in the human body can be affected by air pollution exposure. Kodavanti evaluates the neurohormonal stress response as a pathway mediating pulmonary and extrapulmonary effects of ozone [10]. The contributions of sympathetic and hypothalamus-pituitary-adrenal axis activation in mediating systemic homeostatic effects of ozone are addressed. Air pollution particles contribute to a development of atherosclerosis. Bai and Sun review mechanistic pathways whereby air pollution particles promote the development of atherosclerosis [11]. PMmediated enhancement of atherosclerosis is considered likely the product of pro-oxidant and pro-inflammatory effects, involving multiple organs and tissues, different cell types, and various mediators. Cascio proposes a pathophysiologic framework to explain the relationship between human exposure to air pollution particles and cardiovascular disease [12]. Systemic inflammation, vascular thrombosis, and electrical dysfunction after exposure to ambient air pollution exposure are thought to contribute to elevations in cardiovascular disease including myocardial infarction and arrhythmias. Potential interventional strategies to modify the impact of air pollution are reviewed by Tong [13]. On the basis of demonstrated involvement, such efforts focused on treatment and prevention have been directed toward either diminishing or inhibiting inflammation and oxidative after exposure. Dietary supplementation (e.g. antioxidant vitamins and polyunsaturated fatty acids) and medications are among the strategies proposed to mitigate air pollution-induced effects. References [1] P.A. Bromberg, Mechanisms of the acute effects of inhaled ozone in humans, Biochim Biophys Acta 1860 (2016) 2771–2781. [2] R. Bai, L. Guan, W. Zhang, J. Xu, W. Rui, F. Zhang, W. Ding, Comparative study of the effects of PM1-induced oxidative stress on autophagy and surfactant protein B and C expressions in lung alveolar type II epithelial MLE-12 cells, Biochim Biophys Acta 1860 (2016) 2782–2792. [3] H. Wang, Y. Guo, L. Liu, L. Guan, T. Wang, L. Zhang, Y. Wang, J. Cao, W. Ding, F. Zhang, Z. Lu, DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells, Biochim Biophys Acta 1860 (2016) 2793–2801. [4] P.A. Wages, W.Y. Cheng, E. Gibbs-Flournoy, J.M. Samet, Live-cell imaging approaches for the investigation of xenobiotic-induced oxidant stress, Biochim Biophys Acta 1860 (2016) 2802–2815. [5] A.J. Ghio, J.M. Soukup, L.A. Dailey, Air pollution particles and iron homeostasis, Biochim Biophys Acta 1860 (2016) 2816–2825. [6] Z. Yan, Y. Jin, Z. An, Y. Liu, J.M. Samet, W. Wu, Inflammatory cell signaling following exposures to particulate matter and ozone, Biochim Biophys Acta 1860 (2016) 2826–2834. [7] Q. Zhao, H. Chen, T. Yang, W. Rui, F. Liu, F. Zhang, Y. Zhao, W. Ding, Direct effects of airborne PM2.5 exposure on macrophage polarizations, Biochim Biophys Acta 1860 (2016) 2835–2843. [8] R. Chen, B. Hu, Y. Liu, J. Xu, G. Yang, D. Xu, C. Chen, Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution, Biochim Biophys Acta 1860 (2016) 2844–2855. [9] M.C. Madden, A paler shade of green? The toxicology of biodiesel emissions: Recent findings from studies with this alternative fuel, Biochim Biophys Acta 1860 (2016) 2856–2862. [10] U.P. Kodavanti, Stretching the stress boundary: Linking air pollution health effects to a neurohormonal stress response, Biochim Biophys Acta 1860 (2016) 2879–2889. [11] Y. Bai, Q. Sun, Fine particulate matter air pollution and atherosclerosis: Mechanistic insights, Biochim Biophys Acta 1860 (2016) 2863–2868. [12] W.E. Cascio, Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: Insights for public health translation, Biochim Biophys Acta 1860 (2016) 2869–2878. [13] H. Tong, Dietary and pharmacological intervention to mitigate the cardiopulmonary effects of air pollution toxicity, Biochim Biophys Acta 1860 (2016) 2890–2897.
Professor, Executive Dean College of Life Sciences, University of Chinese Academy of Sciences, No.19A YuQuan Road, Beijing 100049, P.R. China Tel: +8610-88256290, FAX: +8610-88256460 e-mail: [email protected] Wenjun Ding, MD & PhD, received his medical education from Tongji Medical University and High Energy Physics of the Chinese Academy of Sciences. After postdoctoral training in Yamanashi Institute of Environmental Sciences (Japan), the Institute of Physical and Chemical Research (Japan), and Colorado State University (USA), he joined the faculty in the College of Life Sciences, University of the Chinese Academy of Sciences (UCAS) from 2004 to the present. His research interests focus on the molecular mechanism of cytotoxicity and pathogenesis of diseases associated with particulate matters exposure.
Andrew J. Ghio, MD, received his medical education from Boston University. After training in internal medicine and pulmonary/critical care medicine, he joined the faculty in the division of Pulmonary and Critical Care Medicine at Duke University in 1988. He continued his investigation as a Research Medical Officer in the Human Studies Division at the United States Environmental Protection Agency in Chapel Hill, North Caroline, from 1995 to the present. Research and clinical interests include pathogenesis of lung injury after air pollution exposure. He is the author of numerous publications which focus on the mechanisms of biological effects by particles.
Weidong Wu, Bachelor in Public Health, Master in Occupational Health, PhD in Toxicology, Professor of Environmental and Occupational Health, School of Public Health, Xinxiang Medical University, P.R. China. Adjunct Professor at School of Medicine, University of North Carolina at Chapel Hill, USA. Research interest is in air pollution-induced health effects, mechanisms and intervention. He (as PI or co-PI) was awarded a US EPA STAR grant and a NIH RO1 grant, and three National Natural Science Foundation of China. He has been invited to chair many national and international academic conferences and give seminars. So far he has published 140 research papers in peer-reviewed journals.
Wenjun Ding Laboratory of Environment and Health, College of Life Sciences, University of Chines Academy of Sciences, Beijing, China Andrew J. Ghio National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, NC 27711 Corresponding author at: Human Studies Facility, Campus Box 7315, 104 Mason Farm Road, Chapel Hill, North Carolina 27599-7315. Tel.: +919 966 0670; fax: +919 966 6271. E-mail address: [email protected]. Weidong Wu School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China
Contents lists available at ScienceDirect
Biochimica et Biophysica Acta journal homepage: www.elsevier.com/locate/bbagen
Editorial
Preface: Special Issue on Air Pollution☆
Suspended particulate matter (PM) has presented a challenge to the human respiratory tract for as long as the species has existed. This PM was initially of crustal and plant origin but later included particles generated from the burning of biomass for purposes of heating and food preparation. Only recently, in the past few hundred years, have humans been exposed to combustion products of coal, gas, and oil. Studies conducted during the past century showed that episodes of extremely high levels of air pollution originating from such combustion in both Europe and the United States increased human morbidity and mortality (e.g. London fogs). These air pollution debacles were instrumental in bringing about widespread monitoring and regulation of air quality. In the past few decades, epidemiologic studies delineated an association between exposures to ambient air pollution particles (at levels lower than those currently observed in many cities worldwide) and numerous indices of human morbidity and mortality. These findings were initially met with some skepticism, but both reevaluation of the initial studies and a plethora of new epidemiologic investigation provided concordant results thus confirming the validity of the observations. The adverse effects of air pollution include both pulmonary and extra-pulmonary morbidity and mortality. In addition to PM, studies support ozone (O3) as a major ambient air pollutant with the capacity to impact human morbidity and mortality. While epidemiology has identified adverse impacts of air pollution, mechanistic pathways remain to be described. Such pathways must be defined prior to appreciating prognosis of and developing therapies for air pollution-related disease. This special issue focuses on investigation into mechanistic pathways underlying the biological effects of air pollution. Ozone is a major component of air pollution responsible for decrements in pulmonary function, respiratory inflammation, airway hyperreactivity, and bronchoconstriction. Bromberg describes O3 to have an affinity for C=C bonds [1]. In the lower respiratory tract, molecular targets of this oxidizing gas include phospholipids and cholesterol which react to generate ozonides. Inflammation following its exposure is mediated by an activation of NF- kappa B and release of proinflammatory mediators by respiratory epithelial cells. Potential mechanisms underlying the biological effects of air pollution are delineated by Bai et al. [2]. Following exposure of lung epithelial cells to air pollution particles, oxidative damage, surfactant protein expression, and indices of autophagy are all impacted. Evidence suggests that inflammation after air pollution exposure can be related to the activity of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an enzyme that degrades the endogenous nitric oxide synthase (NOS) inhibitor dimethylarginine. An influence of this pathway on oxidative ☆ This article is part of a Special Issue entitled Air Pollution , edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.
http://dx.doi.org/10.1016/j.bbagen.2016.09.007 0304-4165/© 2016 Published by Elsevier B.V.
stress and cell apoptosis following air pollution particle exposure is characterized by Wang et al. [3]. Modification of the expression of DDAH1 is shown to be protective in air pollution particle exposures. Changes in biological effect associated with varying DDAH1 expression were related to alterations in oxidative stress. Exposure to a variety of xenobiotics dysregulates cellular physiology by interfering with redox-dependent processes. Live-cell imaging for redox studies are reviewed by Wages et al. [4]. Such imaging using a new generation of small molecule and genetically encoded fluorophores is observed to have excellent sensitivity and specificity and to afford unprecedented spatiotemporal resolution optimal for redox studies including those into the biological effects of air pollution particles. A role for a disruption in iron homeostasis following exposures to air pollution has been supported by numerous studies conducted over the past decades. Ghio et al. suggest that a mechanism underlying biological effects of particles is a complexation of cell iron by surface functional groups resulting in a functional deficiency in the cell and tissue [5]. The loss of requisite iron after complexation of cell iron to PM initiates oxidative stress and inflammation. Activation of cell signaling networks and transcription factors is one of the initial events mediating inflammation after air pollution exposure. Yan et al. defines major signaling pathways triggering inflammation after exposure to air pollution particles and ozone [6]. Elucidation of these cellular signaling pathways initiated by air pollutants can assist in 1) revealing mechanistic pathways and 2) developing potential interventions. The effects of air pollution on cell signaling show a dependence on oxidative stress. The macrophage is a cell resident in the respiratory tract with a capacity to impact defense against tissue damage and orchestrate the initiation and resolution phases of both innate and adaptive immunity. Zhao et al. demonstrate that air pollution particles enhance the inflammatory capacity of macrophages through oxidant-sensitive pathways [7]. PM is shown to act directly on polarization of these cells affecting pro-inflammatory cytokine secretion by classically activated macrophages (M1) and anti-inflammatory responses of alternatively activated macrophages (M2). In air pollution, ultrafine particles reflect anthropogenic emission sources, i.e. combustion engines and power plants. As a result of the extremely small size, these particles are thought to play a major role in the adverse impact of air pollution on human health including cardiovascular disease. Composition, sources, oxidative effects, potential exposure routes and health risks of ultrafine particles included in air pollution are reviewed by Chen et al. [8]. Exposure to biodiesel combustion products has been considered not to induce either the biological effects or injury observed after exposure to other fuel combustion products. Madden evaluates the environmental and health effects of biodiesel and observes that these emissions can
2770
Editorial
induce biological effects [9]. Evidence of studies provide conflicting data but inflammatory, vascular, mutagenic, and other effects of biodiesel may approximate those of diesel exhaust. The function of numerous tissues in the human body can be affected by air pollution exposure. Kodavanti evaluates the neurohormonal stress response as a pathway mediating pulmonary and extrapulmonary effects of ozone [10]. The contributions of sympathetic and hypothalamus-pituitary-adrenal axis activation in mediating systemic homeostatic effects of ozone are addressed. Air pollution particles contribute to a development of atherosclerosis. Bai and Sun review mechanistic pathways whereby air pollution particles promote the development of atherosclerosis [11]. PMmediated enhancement of atherosclerosis is considered likely the product of pro-oxidant and pro-inflammatory effects, involving multiple organs and tissues, different cell types, and various mediators. Cascio proposes a pathophysiologic framework to explain the relationship between human exposure to air pollution particles and cardiovascular disease [12]. Systemic inflammation, vascular thrombosis, and electrical dysfunction after exposure to ambient air pollution exposure are thought to contribute to elevations in cardiovascular disease including myocardial infarction and arrhythmias. Potential interventional strategies to modify the impact of air pollution are reviewed by Tong [13]. On the basis of demonstrated involvement, such efforts focused on treatment and prevention have been directed toward either diminishing or inhibiting inflammation and oxidative after exposure. Dietary supplementation (e.g. antioxidant vitamins and polyunsaturated fatty acids) and medications are among the strategies proposed to mitigate air pollution-induced effects. References [1] P.A. Bromberg, Mechanisms of the acute effects of inhaled ozone in humans, Biochim Biophys Acta 1860 (2016) 2771–2781. [2] R. Bai, L. Guan, W. Zhang, J. Xu, W. Rui, F. Zhang, W. Ding, Comparative study of the effects of PM1-induced oxidative stress on autophagy and surfactant protein B and C expressions in lung alveolar type II epithelial MLE-12 cells, Biochim Biophys Acta 1860 (2016) 2782–2792. [3] H. Wang, Y. Guo, L. Liu, L. Guan, T. Wang, L. Zhang, Y. Wang, J. Cao, W. Ding, F. Zhang, Z. Lu, DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells, Biochim Biophys Acta 1860 (2016) 2793–2801. [4] P.A. Wages, W.Y. Cheng, E. Gibbs-Flournoy, J.M. Samet, Live-cell imaging approaches for the investigation of xenobiotic-induced oxidant stress, Biochim Biophys Acta 1860 (2016) 2802–2815. [5] A.J. Ghio, J.M. Soukup, L.A. Dailey, Air pollution particles and iron homeostasis, Biochim Biophys Acta 1860 (2016) 2816–2825. [6] Z. Yan, Y. Jin, Z. An, Y. Liu, J.M. Samet, W. Wu, Inflammatory cell signaling following exposures to particulate matter and ozone, Biochim Biophys Acta 1860 (2016) 2826–2834. [7] Q. Zhao, H. Chen, T. Yang, W. Rui, F. Liu, F. Zhang, Y. Zhao, W. Ding, Direct effects of airborne PM2.5 exposure on macrophage polarizations, Biochim Biophys Acta 1860 (2016) 2835–2843. [8] R. Chen, B. Hu, Y. Liu, J. Xu, G. Yang, D. Xu, C. Chen, Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution, Biochim Biophys Acta 1860 (2016) 2844–2855. [9] M.C. Madden, A paler shade of green? The toxicology of biodiesel emissions: Recent findings from studies with this alternative fuel, Biochim Biophys Acta 1860 (2016) 2856–2862. [10] U.P. Kodavanti, Stretching the stress boundary: Linking air pollution health effects to a neurohormonal stress response, Biochim Biophys Acta 1860 (2016) 2879–2889. [11] Y. Bai, Q. Sun, Fine particulate matter air pollution and atherosclerosis: Mechanistic insights, Biochim Biophys Acta 1860 (2016) 2863–2868. [12] W.E. Cascio, Proposed pathophysiologic framework to explain some excess cardiovascular death associated with ambient air particle pollution: Insights for public health translation, Biochim Biophys Acta 1860 (2016) 2869–2878. [13] H. Tong, Dietary and pharmacological intervention to mitigate the cardiopulmonary effects of air pollution toxicity, Biochim Biophys Acta 1860 (2016) 2890–2897.
Professor, Executive Dean College of Life Sciences, University of Chinese Academy of Sciences, No.19A YuQuan Road, Beijing 100049, P.R. China Tel: +8610-88256290, FAX: +8610-88256460 e-mail: [email protected] Wenjun Ding, MD & PhD, received his medical education from Tongji Medical University and High Energy Physics of the Chinese Academy of Sciences. After postdoctoral training in Yamanashi Institute of Environmental Sciences (Japan), the Institute of Physical and Chemical Research (Japan), and Colorado State University (USA), he joined the faculty in the College of Life Sciences, University of the Chinese Academy of Sciences (UCAS) from 2004 to the present. His research interests focus on the molecular mechanism of cytotoxicity and pathogenesis of diseases associated with particulate matters exposure.
Andrew J. Ghio, MD, received his medical education from Boston University. After training in internal medicine and pulmonary/critical care medicine, he joined the faculty in the division of Pulmonary and Critical Care Medicine at Duke University in 1988. He continued his investigation as a Research Medical Officer in the Human Studies Division at the United States Environmental Protection Agency in Chapel Hill, North Caroline, from 1995 to the present. Research and clinical interests include pathogenesis of lung injury after air pollution exposure. He is the author of numerous publications which focus on the mechanisms of biological effects by particles.
Weidong Wu, Bachelor in Public Health, Master in Occupational Health, PhD in Toxicology, Professor of Environmental and Occupational Health, School of Public Health, Xinxiang Medical University, P.R. China. Adjunct Professor at School of Medicine, University of North Carolina at Chapel Hill, USA. Research interest is in air pollution-induced health effects, mechanisms and intervention. He (as PI or co-PI) was awarded a US EPA STAR grant and a NIH RO1 grant, and three National Natural Science Foundation of China. He has been invited to chair many national and international academic conferences and give seminars. So far he has published 140 research papers in peer-reviewed journals.
Wenjun Ding Laboratory of Environment and Health, College of Life Sciences, University of Chines Academy of Sciences, Beijing, China Andrew J. Ghio National Health and Environmental Effects Research Laboratory, Environmental Protection Agency, Research Triangle Park, NC 27711 Corresponding author at: Human Studies Facility, Campus Box 7315, 104 Mason Farm Road, Chapel Hill, North Carolina 27599-7315. Tel.: +919 966 0670; fax: +919 966 6271. E-mail address: [email protected]. Weidong Wu School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, PR China