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basis for evaluating levels of soluble markers of neuroinflammation in peripheral blood is that inflammatory mediators released from glial activation cross the BBB and enter the systemic circulation, promoting proliferation of peripheral immune cells. On the other hand, cytokines originating from peripheral immune cells also enter the brain parenchyma and act on glial cells, while proinflammatory mediators also modify the permeability of the BBB. Hence, neuroinflammation may follow systemic inflammation. 25 , 32 MCP-1 is a chemokine that promotes monocyte

missions and may be exposed to additional flight-related hazards, including toxic materials and elevated levels of ionizing radiation above baseline, with significant health-related implications for fetal development. 2 – 4 Animal models and human cohort studies have previously reported that flight-related occupational exposures are associated with disruptions in fetal development and increased risk of adverse health outcomes. In vivo animal models of intermittent hypoxia during pregnancy have found an association with neonatal neuroinflammation. 5 Animal models have