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 gen- erated 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 con- ducted 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 bring- ing about widespread monitoring and regulation of air quality. In the past few decades, epidemiologic studies delineated an association be- tween 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 ef- fects of air pollution include both pulmonary and extra-pulmonary morbidity and mortality. In addition to PM, studies support ozone (O 3 ) 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 investiga- tion into mechanistic pathways underlying the biological effects of air pollution. Ozone is a major component of air pollution responsible for decre- ments in pulmonary function, respiratory inflammation, airway hyper- reactivity, and bronchoconstriction. Bromberg describes O 3 to have an affinity for C = C bonds [1]. In the lower respiratory tract, molecular tar- gets of this oxidizing gas include phospholipids and cholesterol which react to generate ozonides. Inflammation following its exposure is me- diated by an activation of NF- kappa B and release of pro- inflammatory mediators by respiratory epithelial cells. Potential mechanisms underlying the biological effects of air pollu- tion are delineated by Bai et al. [2]. Following exposure of lung epithelial cells to air pollution particles, oxidative damage, surfactant protein ex- pression, and indices of autophagy are all impacted. Evidence suggests that inflammation after air pollution exposure can be related to the ac- tivity of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an en- zyme that degrades the endogenous nitric oxide synthase (NOS) inhibitor dimethylarginine. An influence of this pathway on oxidative 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 un- precedented spatiotemporal resolution optimal for redox studies in- cluding 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 expo- sure. Yan et al. defines major signaling pathways triggering inflamma- tion 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 inter- ventions. The effects of air pollution on cell signaling show a depen- dence on oxidative stress. The macrophage is a cell resident in the respiratory tract with a ca- pacity to impact defense against tissue damage and orchestrate the ini- tiation and resolution phases of both innate and adaptive immunity. Zhao et al. demonstrate that air pollution particles enhance the inflam- matory 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 macro- phages (M1) and anti-inflammatory responses of alternatively activat- ed macrophages (M2). In air pollution, ultrafine particles reflect anthropogenic emission sources, i.e. combustion engines and power plants. As a result of the ex- tremely small size, these particles are thought to play a major role in the adverse impact of air pollution on human health including cardiovascu- lar 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 environmen- tal and health effects of biodiesel and observes that these emissions can Biochimica et Biophysica Acta 1860 (2016) 2769–2770 ☆ 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. Contents lists available at ScienceDirect Biochimica et Biophysica Acta journal homepage: www.elsevier.com/locate/bbagen