Department of Pharmaceutical Sciences, University of New Mexico, Albuquerque, New Mexico, USA.
Curr Opin Pulm Med. 2012 Mar;18(2):155-60. doi: 10.1097/MCP.0b013e32834f210a.
Recent discoveries in the field of air pollution toxicology highlight the potential impact of specific sources of air pollution, especially related to roadway emissions, on acute and chronic cardiovascular disease. This review covers potential mechanisms, both in terms of biological pathways and chemical drivers, to explain these observations.
Air pollution is associated with chronic progression of cardiovascular disease. Roadway exposures appear to have a strong correlation to these adverse outcomes. Controlled toxicological studies highlight potential interactions between vehicle-source emissions and adverse vascular outcomes. Mechanistically, a role for both innate and adaptive immune responses is emerging, with important recent findings demonstrating that immunomodulatory pattern-recognition receptors such as Toll-like receptor-4 and lectin-like oxidized LDL receptor-1 may play a role in communicating airway exposures to cardiovascular outcomes.
An improved understanding of the sources and mechanisms underlying adverse cardiovascular health outcomes of air pollution would enhance our ability to manage vulnerable populations and establish precise, effective regulatory policies.
空气污染毒理学领域的最新发现强调了特定空气污染源（特别是与道路交通排放有关的空气污染源）对急性和慢性心血管疾病的潜在影响。本综述涵盖了潜在的机制，包括生物学途径和化学驱动因素，以解释这些观察结果。
空气污染与心血管疾病的慢性进展有关。道路暴露似乎与这些不良后果密切相关。受控的毒理学研究强调了车辆源排放与不良血管结局之间的潜在相互作用。从机制上讲，先天和适应性免疫反应都发挥了作用，最近的重要发现表明，免疫调节模式识别受体，如 Toll 样受体-4 和凝集素样氧化型 LDL 受体-1，可能在将气道暴露与心血管结局联系起来方面发挥作用。
更好地了解空气污染对心血管健康不良影响的来源和机制，将提高我们管理脆弱人群和制定精确、有效的监管政策的能力。
