Traffic-derived metal bioaccumulation in bone tissue as a driver of osteoporosis

Long-term air pollution exposures, particularly to fine particulate matter, have been linked to a wide range of health issues, including cardiovascular and respiratory diseases. Recent studies have expanded this scope to include skeletal disorders, such as osteoporosis and bone fragility. This is particularly concerning given the global burden of osteoporosis, which affects 500 million people worldwide and causes 13.5 million fractures annually. While traditional air pollution sources like exhaust emissions have been extensively studied, the role of non-exhaust sources, such as brake and tyre wear, remains largely unexplored. These non-exhaust sources are becoming a critical environmental concern, especially with the adoption of heavier electric vehicles. We hypothesize that lifetime accumulation of metals from non-exhaust traffic emissions contributes to the development of osteoporosis. This hypothesis is supported by several lines of evidence: epidemiological studies showing associations between air pollution exposures and increased fracture risk, particularly in populations living near busy roads; clinical studies demonstrating metal accumulation in the bone of individuals with osteoporosis and molecular studies showing the disruptive effects of metals on bone remodeling processes, including bone formation and resorption. To investigate this further, we propose a research approach combining in vitro, in vivo, ex vivo and computational modeling techniques. By studying the effects of metals on bone cells, analyzing the impact of metal exposure in animal models and simulating long-term exposure scenarios, we aim to elucidate the mechanisms underlying air pollution-induced bone damage. This research could inform urban planning policies, vehicle design and public health interventions protecting bone health.