Originally published on EV Obsession.
Even just a single, sub-clinical exposure to extracts of particulate matter taken from the side of a roadway is enough to induce transient pulmonary stress (via oxidative and inflammatory pathways), according to new work from an international team of researchers from the University of Wisconsin-Madison, the Weizmann Institute of Science, and Ben-Gurion University of the Negev.
Much of this effect can be attributed to the metals found dissolved in roadside emissions, according to the researchers involved — heavy metals such as Ni, Mn, V, Cu, Fe, and Cr.
Interestingly, removal of soluble metals via the use of chelating agents very notably reduced the pulmonary response. That said, local response seemed to resolve on their own by 48 hours after exposure.
Here’s an except from the study:
The effect of near roadway air pollution on human health is especially significant in major cities, and respiratory and cardiovascular diseases are mostly implicated in response to continued/repeated exposure to air pollution. In an effort to limit roadway-related air pollution, the common regulations have focused on reducing tailpipe emissions. Among the various particulate matter (PM) constituents, some metals are potentially cytotoxic and can contribute to organ and tissue damage and injury. Yet, because tailpipe emissions from mobile sources are not major sources of these metals it is expected that their roadway emissions are largely associated with resuspended road dust that contains brake wear, tire wear, and crustal elements.
The heterogeneity of chemical species and different roadway sources presents a major challenge in identifying specific components that are most biologically active, lead to pathogenesis of disease, or both. Identifying these components is essential for appropriate mitigation policies that could reduce their public health impact.
The researchers speculate the self-resolution of the response is related to the activation of defense mechanism pathways — perhaps demonstrating why repeated low exposure to air pollution has been associated with morbidity and mortality by earlier work (the eventuality of potentially decompensated biological responses).
The new research was published in the ACS journal Environmental Science & Technology.