Traffic congestion, a prevalent urban issue characterized by slower speeds, longer trip times, and increased vehicular queuing, has implications for several Sustainable Development Goals (SDGs). Firstly, it is directly related to SDG 11 (Sustainable Cities and Communities), as alleviating traffic congestion can enhance urban livability, economic productivity, and transportation efficiency. Congestion also ties to SDG 3 (Good Health and Well-being), as it can result in increased pollution leading to respiratory diseases, as well as stress from long commutes. It impacts SDG 9 (Industry, Innovation, and Infrastructure) since robust, efficient transport infrastructures can help reduce congestion. Moreover, by encouraging more sustainable transport modes like cycling or public transit to alleviate congestion, we can contribute to SDG 13 (Climate Action) by reducing greenhouse gas emissions.
Background: Individuals with COPD have increased sensitivity to traffic-related air pollution (TRAP) such as diesel exhaust (DE), but little is known about the acute effects of TRAP on exercise responses in COPD. Research Question: Does exposure before exercise to TRAP (DE titrated to 300 μg/m3 particulate matter < 2.5 μm in diameter [DE300]) show greater adverse effects on exercise endurance, exertional dyspnea, and cardiorespiratory responses to exercise in participants with mild to moderate COPD compared with former smokers with normal spirometry and healthy control participants?
Transportation is a basic social need, but most trips are done by private vehicles, which is not environmentally sustainable with growing urban populations. Micromobility (e.g., shared bikes) represents a significant opportunity to replace short private vehicles trips (0–3 miles) and reduce transportation sector emissions. This paper uses Seattle as a case study and estimates that up to 18% of short car trips could be replaced by micromobility.
Traffic emission is responsible for most small-sized particulate matter (PM) air pollution in urban areas. Several recent studies have indicated that traffic-related PM may aggravate kidney disease. Furthermore, exposure to particulate air pollution may be related to the risk of chronic kidney disease (CKD). However, the underlying molecular mechanisms have not been adequately addressed. In the present study, we studied the mechanisms of renal damage that might be associated with exposure to PM.
