Correspondence Comment on “Emissions from Brake Linings and Tires: Case Studies of Stockholm, Sweden 1995/1998 and 2005” The paper by Hjortenkrans et al. (1), reporting on case studies of the city of Stockolm, Sweden, outlines that, in addition to petrol and diesel exhaust, brake linings and tires are major emission sources of PM to air. In particular, they showed that (1) brake linings still remain one of the major emission sources for metals, such as Cu, Zn, and antimony, whereas Pb and Cd emission have decreased to one tenth compared to 1998; and (2) tire debris still is one of the main sources of Zn and Cd emission in the city of Stockolm. Because Stockolm represents a rather average city, the results from this study may be relevant for many other urban areas (1). The aim of the article is restricted to the measurement of the metal components of brake linings and tire debris as a dangerous source of traffic-related pollutants. However, the general aims are broader, including the following: (1) trafficrelated emissions are not only related to diesel exhaust or petrol, but also to other components of the road traffic, such as brakes and tires; and (2) traffic-related pollution must be considered as a separate source of pollutants, capable of independent and severe adverse health effects, irrespective of the other components (heating, background pollution). In this larger sense, we would make some observations and comments. On one hand, we criticize that the overall approach to health damage from pollution is oversimplified, assuming that measurement of metals in a given city is sufficient to hypothesize health damage, strictly on the basis of their concentration or “toxic activity”. This is an oversimplification of a complex question, in which “host response”, that is mainly due to individual susceptibility, plays a greater role than pure “toxic effect” of pollutants, each of which is present in the atmosphere at an extremely low concentration, which is unable by itself to determine relevant health effects. On the other hand, we outline that, in addition to metal emission, organic compounds, namely by tire debris, play a basic role to determine adverse effects, which could be more relevant than those elicited by metal emissions. In addition, we also observed that tires are a major source of Zn (and less of Cd in our city) and S, due to traffic emission. But in our studies, either “in vitro” or “in vivo”, of pollutionrelated health damage, both metallic and nonmetallic components contributed to the final result. As Hjortenkrans et al. state, “the materials used in brake lining (and in tires) are of environmental relevance”. But this concerns both metallic and nonmetallic components. They stated that “emissions related to the road traffic were 50% or more of total emission depending on metal”. We observed that debris produced by friction of tires (tire debris TD) of motor vehicles, constitutes 5–7% of human inhalable particulate material (PM) and an even greater proportion of traffic-induced PM. Therefore toxicological data derived from TD and brake 2708
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linings could be particularly relevant for a better understanding of traffic-related specific toxicity or potential health damage. In particular, concerning tire debris, we have shown that in addition to metals, it also contains polycyclic aromatic hydrocarbons (PAHs) and a conspicuous proportion of TD extractable organic components (TDOE), including isoprene polymers, and other organic hydrocarbons, such as longchain alkanes. We have shown that, in addition to Zn leached by tire materials, the TD organic fraction was toxic for cells and organisms and the DNA structure and that these damages were detectable, at the highest doses of tire debris organic extract, already after 24 h of cell exposure (3, 4). In addition, TDOE has been proven to be a teratogen compound for X. laevis development (5). Moreover, it has been demonstrated that TDOE induced reactive oxygen species and heat shock proteins in the human alveolar cell line A549 (6), further documenting that not only diesel exhaust, but also tire debris is able to produce oxidative stress. Obviously, results from in vitro and animal studies cannot be transferred directly to humans. Our final comment is that reduction of PM is a main goal of governments and policies (7). In particular, reduction of traffic-related transition metals and PM represents a cost-effective measure to reduce health damage from airborne particles, regardless of background pollution (2). Therefore a better knowledge of which is of paramount importance, as well as a deeper insight into the pathophysiological mechanisms determining biological damage and clinical diseases in individuals (7, 8), because of PM, also including, among the various traffic-related components, brake linings and tire debris. This work is supported by Comune di Milano, Prolife Flagship Project.
Note Added after ASAP Publication There was an error in the author affiliations, and an acknowledgment was omitted in the version published ASAP February 2, 2008; the corrected version published ASAP February 28, 2008.
Literature Cited (1) Hjortenkrans, D. S. T.; Bergbäck, B. G.; Häggerud, A. V. Metal emissions from brake linings and tires: Case studies of Stockolm, Sweden 1995/1998 and 2005. Environ. Sci. Technol. 2007, 41, 5224–5230. (2) Gauderman, W. J.; Vale, H.; McConnell, R.; Berhane, K.; Gilliland, F.; Thomas, D.; Lurmann, F.; Avol, E.; Kunzli, N.; Jerrett, M.; Peters, J. Effect of exposure to traffic on lung development from 10 to 18 years of age: a cohort study. Lancet 2007, 369, 571–577. (3) Gualtieri, M.; Andrioletti, M.; Vismara, C.; Milani, M.; Camatini, M. Tire debris eluates affect living organisms. Environ. Intern. 2005, 31, 723–730. (4) Gualtieri, M.; Rigamonti, L.; Galeotti, V.; Camatini, M. Toxicity of tire debris extracts on human lung cell line A549. Toxicol. In Vitro 2005, 19, 1001–1008. (5) Mantecca, P.; Gualtieri, M.; Andrioletti, M.; Bacchetta, R.; Vismara, C.; Vailati, G.; Camatini, M. Tire debris organic extract affects Xenopus development. Environ. Int. 2007, 33, 642–8. (6) Gualtieri, M.; Mantecca, P.; Cetta, F.; Camatini, M. Organic compounds in tire particles induce reactive oxygen species 10.1021/es702664q CCC: $40.75
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and heat-shock proteines in the human alveolar cell line A549. Environ. Int. 2007, in press. (7) Cetta, F.; Dhamo, A.; Schiraldi, G.; Camatini, M. Particulate matter, science and European Union Policy. Eur. Respir. J. 2007, 30, 805–806. (8) Gianazza, E.; Allegra, L.; Bucchioni, E.; Eberini, I.; Puglisi, L.; Blasi, F.; Terzano, C.; Wait, R.; Sirtori, C. R. Increased Keratin content detected by proteomic analysis of exhaled breath condensate from healthy persons who smoke. Am. J. Med. 2004, 117, 514.
Francesco Cetta* and Armand Dhamo University of Siena, Surgery, viale Bracci, Siena, Tuscany, 53100, Italy
Gianfranco Schiraldi and Luigi Allegra University of Milan, Department of Pneumology, Milan, Italy ES702664Q
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