Mexico City Metropolitan Area children chronically exposed to high 
concentrations of air pollutants exhibit an early brain imbalance in genes 
involved in oxidative stress, inflammation, innate and adaptive immune responses 
along with accumulation of misfolded proteins observed in the early stages of 
Alzheimer and Parkinson's diseases. A complex modulation of serum cytokines and 
chemokines influences children's brain structural and gray/white matter 
volumetric responses to air pollution. The search for biomarkers associating 
systemic and CNS inflammation to brain growth and cognitive deficits in the 
short term and neurodegeneration in the long-term is our principal aim. We 
explored and compared a profile of cytokines, chemokines (Multiplexing LASER 
Bead Technology) and Cellular prion protein (PrP(C)) in normal 
cerebro-spinal-fluid (CSF) of urban children with high vs. low air pollution 
exposures. PrP(C) and macrophage inhibitory factor (MIF) were also measured in 
serum. Samples from 139 children ages 11.91 ± 4.2 years were measured. Highly 
exposed children exhibited significant increases in CSF MIF (p = 0.002), IL6 (p 
= 0.006), IL1ra (p = 0.014), IL-2 (p = 0.04), and PrP(C) (p = 0.039) vs. 
controls. MIF serum concentrations were higher in exposed children (p = 0.009). 
Our results suggest CSF as a MIF, IL6, IL1Ra, IL-2, and PrP(C) compartment that 
can possibly differentiate air pollution exposures in children. MIF, a key 
neuro-immune mediator, is a potential biomarker bridge to identify children with 
CNS inflammation. Fine tuning of immune-to-brain communication is crucial to 
neural networks appropriate functioning, thus the short and long term effects of 
systemic inflammation and dysregulated neural immune responses are of deep 
concern for millions of exposed children. Defining the linkage and the health 
consequences of the brain / immune system interactions in the developing brain 
chronically exposed to air pollutants ought to be of pressing importance for 
public health.