Polina B. Maciejczyk

Air pollution is a major environmental risk to health. Air pollution has been estimated to cause 6.7 million premature deaths worldwide annually (GBD, 2019). Fine Particulate Matter (PM2.5) is believed to be the largest contributor to the adverse health effects caused by air pollution, but the most toxic PM2.5 constituents and/or sources have not been definitively determined. In this chapter, we review the relevant scientific literature providing insights on health-related effects caused by inhalation of particulate metals, and their potential causal pathways. Based on both the available epidemiologic and toxicological evidence, we focus on the individual properties of metals commonly found in PM2.5 air pollution and their concentrations, sources, and adverse health effects. We also assess the possible involvement of metals in emerging occurrences of clusters of acute lung injury and mortality among e-cigarette users, as well consider the implications of particulate metals exposure effects to climate change mitigation efforts. While no single constituent is identifiable as causal to date, a central role by metals derived from fossil fuel combustion, in combination with acidic sulfur, is noted. In the future, with more ambient PM2.5 speciation monitoring, additional ambient source apportionment modeling, and additional toxicological studies involving PM2.5 component analyses (including of constituents, chemical form, and source-specific mixtures), the roles of specific metals and their coconstituent mixtures within PM can be expected to become clearer.

In this review, we elucidate the central role played by fossil fuel combustion in the health-related effects that have been associated with inhalation of ambient fine particulate matter (PM2.5). We especially focus on individual properties and concentrations of metals commonly found in PM air pollution, as well as their sources and their adverse health effects, based on both epidemiologic and toxicological evidence. It is known that transition metals, such as Ni, V, Fe, and Cu, are highly capable of participating in redox reactions that produce oxidative stress. Therefore, particles that are enriched, per unit mass, in these metals, such as those from fossil fuel combustion, can have greater potential to produce health effects than other ambient particulate matter. Moreover, fossil fuel combustion particles also contain varying amounts of sulfur, and the acidic nature of the resulting sulfur compounds in particulate matter (e.g., as ammonium sulfate, ammonium bisulfate, or sulfuric acid) makes transition metals in particles more bioavailable, greatly enhancing the potential of fossil fuel combustion PM2.5 to cause oxidative stress and systemic health effects in the human body. In general, there is a need to further recognize particulate matter air pollution mass as a complex source-driven mixture, in order to more effectively quantify and regulate particle air pollution exposure health risks.

Air pollution is a complex mixture of gaseous, volatile, and particulate matter (PM) containing inorganic and organic species. There is now abundant evidence in epidemiological and toxicological studies that air pollution contributes to the development and exacerbation of diseases of respiratory, cardiovascular, and other organs, and associated mortality. Studies showed that equal masses of PM could induce disparate health effects, suggesting that particle sizes and components may be at fault. The fine and ultrafine PM is considered to be particularly important because the small particles can be easily inhaled. Possible biological mechanisms of action leading to adverse effects include the production of inflammatory mediators in the lung causing systemic inflammation, interaction with neural receptors causing interference with the central nervous system regulation of cardiovascular function, and particle translocation via the bloodstream to other organs. This chapter reviews whether some components of the PM mixture are of a greater public health concern than others, and presents compelling evidence that trace elements are most strongly linked to the adverse effects. Air pollution has wide-ranging and harmful effects on human health and is a major issue for the global community. Further research should explore the effects of source-specific PM with more advanced approaches to exposure modeling, measurements, and statistics, which would lead to more effective legislation and interventions for greater benefits to public health.

In this study, factor analysis and mass regression were used to identify four fine particulate matter sources and estimate their contributions to the ambient air pollution in Beijing. The identified sources were traffic re-suspended soil, mixed industrial sources, oil combustion, and secondary sulfate. The estimated source contributions were then introduced into two models as exposure variables to explore the relationships between cardiovascular responses in mice and PM exposures. We observed that PM_(2.5) has a small negative acute effect on heart rate, but the individual source factors showed much more significant effects. Traffic re-suspended soil had the most significant effect on heart rate, with a positive contribution on the day of exposure and a negative one on day lag 1. Acute heart rate variability outcomes were better explained by the total PM_(2.5) than by the source components. Chronic effects were observed as a decreased heart rate but an increased number of heart rate variability outcomes.

This paper presents the first comprehensive investigation of particulate matter with an aerodynamic diameter less than or equal to 2.5 and 10 microns (PM2.5 and PM10) composition and sources in Saudi Arabia. We conducted a multi-week multiple sites sampling campaign in Jeddah between June and September, 2011, and analyzed samples by X–ray fluorescence (XRF). The overall mean mass concentration was 28.4±25.4μg m−3 for PM2.5 and 87.3±47.3μg m−3 for PM10, with significant temporal and spatial variability. The average ratio of PM2.5/PM10 was 0.33. Chemical composition data were modeled using factor analysis with Varimax orthogonal rotation to determine five and four particle source categories contributing significant amount of for PM2.5 and PM10 mass, respectively. In both PM2.5 and PM10 sources were (1) heavy oil combustion characterized by high Ni and V; (2) re-suspended soil characterized by high concentrations of Ca, Fe, Al, and Si; and (3) a mixed industrial source. The two other sources in PM2.5 were (4) traffic source identified by presence of Pb, Br, and Se; (5) other industrial source mixture; while in PM10 it was marine aerosol. To estimate the mass contributions of each individual source category, the PM mass concentration was regressed against the factor scores. Cumulatively, re-suspended soil and oil combustion contributed 77 and 82% mass of PM2.5 and PM10, respectively.

While many studies found associations between ambient particulate matter (PM) and morbidity or mortality outcomes, it is unclear whether these associations were dependent on the composition of PM, which varies with the source of that PM. We address this knowledge gap by conducting a time-series PM-health effects assessment that specifically investigates the role of source-apportioned fine PM (PM2.5) on the oxidant generation capacity that might be responsible for respiratory and cardiovascular health outcomes. Daily PM2.5 composition speciation and black carbon (BC) measurements, conducted in rural New York for 303 days between March 2003 and January 2005, were analyzed using factor analysis source-apportionment model, and five source categories (transported aerosol/secondary sulfate, resuspended soil, metals, residual oil combustion, and industrial/incineration) were identified. After the exposure of human epithelial cells (BEAS-2B) to these PM2.5 samples, cellular nuclear factor-κB (NF-κB) activation showed a relatively significant association Ni (concentration averaging 38 ng/m(3)), and weaker but still significant correlations with Ba (13 ng/m(3)), Mn (9 ng/m(3)), and Fe (500 ng/m(3)). The single-source regression analysis of NF-κB signal showed significant association with metal source only. Our results showed that metals in PM2.5 were the important source for cellular oxidant generation and may be responsible for subsequent health effects associate with particle air pollution.

We review literature providing insights on health-related effects caused by inhalation of ambient air particulate matter (PM) containing metals, emphasizing effects associated with in vivo exposures at or near contemporary atmospheric concentrations. Inhalation of much higher concentrations, and high-level exposures via intratracheal (IT) instillation that inform mechanistic processes, are also reviewed. The most informative studies of effects at realistic exposure levels, in terms of identifying influential individual PM components or source-related mixtures, have been based on (1) human and laboratory animal exposures to concentrated ambient particles (CAPs), and (2) human population studies for which both health-related effects were observed and PM composition data were available for multipollutant regression analyses or source apportionment. Such studies have implicated residual oil fly ash (ROFA) as the most toxic source-related mixture, and Ni and V, which are characteristic tracers of ROFA, as particularly influential components in terms of acute cardiac function changes and excess short-term mortality. There is evidence that other metals within ambient air PM, such as Pb and Zn, also affect human health. Most evidence now available is based on the use of ambient air PM components concentration data, rather than actual exposures, to determine significant associations and/or effects coefficients. Therefore, considerable uncertainties about causality are associated with exposure misclassification and measurement errors. As more PM speciation data and more refined modeling techniques become available, and as more CAPs studies involving PM component analyses are performed, the roles of specific metals and other components within PM will become clearer.

The objective of this study is to characterize the ambient air quality of the South Bronx, New York City (NYC), having high concentrations of diesel trucks and waste transfer facilities. We employed a mobile laboratory for continuous measurements of concentrations of fine particulate matter (PM2.5), black carbon (BC), and gaseous pollutants at 6 locations for three–four weeks each during the period of April 2001–February 2003. Integrated 24-hr PM2.5 samples were also collected for elemental and PAHs analyses. South Bronx PM2.5 and BC levels were compared to those at Bronx PS 154 (NYSDEC site) and at Hunter College in the Lower Manhattan. Although the median daily PM2.5 concentrations agreed within 20%, the median hourly BC concentrations were higher at all South Bronx sites ranging from 2.2 to 3.8μgm−3, compared to 1.0–2.6μgm−3 at Hunter College. Continuous Aethelometer measurements at additional 27 sampling sites in the South Bronx were conducted along major highways. BC concentrations varied within each site, depending on time-of-day, with a large spatial variability from site-to-site. Daily median BC concentrations varied from 1.7 to 12μgm−3 on the weekdays, and were lower (0.50–2.9μgm−3) on the weekends. Elemental concentrations were higher at all South Bronx sites than those at Hunter College for all measured elements but Ni and V, and at the Hunts Point, an industrial location, were approximately 2.5-fold higher. The average sum of 35 PAHs was 225ngm−3, which is 4.5 times larger than representative regional concentrations in Jersey City, NJ. Among the individual PAHs, 3,6-dimethylphenanthrene had the highest concentrations, and the overall PAH fingerprint differed from signal for Jersey City. Our data indicates that highways encircling the South Bronx are having a measurable adverse influence on residents’ exposure to pollutants compared to other NYC areas.