Neuroinflammation and Brain Health Risks in Veterans Exposed to Burn Pit Toxins

Abstract

Military burn pits, used for waste disposal in combat zones, involve the open-air burning of waste materials, including plastics, metals, chemicals, and medical waste. The pits release a complex mixture of occupational toxic substances, including particulate matter (PM), volatile organic compounds (VOCs), heavy metals, dioxins, and polycyclic aromatic hydrocarbons (PAHs). Air pollution significantly impacts brain health through mechanisms involving neuroinflammation. Pollutants penetrate the respiratory system, enter the bloodstream, and cross the blood-brain barrier (BBB), triggering inflammatory responses in the central nervous system (CNS). Chronic environmental exposures result in sustained inflammation, oxidative stress, and neuronal damage, contributing to neurodegenerative diseases and cognitive impairment. Veterans exposed to burn pit toxins are particularly at risk, reporting higher rates of respiratory issues, neurological conditions, cognitive impairments, and mental health disorders. Studies demonstrate that Veterans exposed to these toxins have higher rates of neuroinflammatory markers, accelerated cognitive decline, and increased risks of neurodegenerative diseases. This narrative review synthesizes the research linking airborne pollutants such as PM, VOCs, and heavy metals to neuroinflammatory processes and cognitive effects. There is a need for targeted interventions to mitigate the harmful and escalating effects of environmental air pollution exposures on the CNS, improving public health outcomes for vulnerable populations, especially for Veterans exposed to military burn pit toxins.

Keywords: Veterans; air pollution; brain–lung axis; burn pit toxins; mental health disorders; neurodegenerative disease; neuroinflammation; occupational health.

Figure 1

The relationships among air pollutants, the blood–brain barrier (BBB), and microglia. Particulate matter and metal nanoparticles are able to increase the permeability of the BBB by increasing intracellular adhesion molecules (ICAMs), vascular cellular adhesion molecules (VCAMs), and efflux transporters, which allow for peripheral inflammatory cytokines and reactive oxygen species (ROS) caused by the pollutants to enter the brain parenchyma and thus activate the microglia.

Figure 2

An overview of the lung–brain axis and diseases which are affected by it. Toxins inhaled cause increased cytokines and reactive oxygen species (ROS), along with endothelial cell damage, intracellular adhesion molecule/vascular cell adhesion molecule (ICAM/VCAM) upregulation, and increased permeability, all of which contribute to blood–brain barrier (BBB) damage. At the same time, these toxins that cross the BBB cause neuroinflammation through a number of pathways, including Rtp801 increase, inflammatory cytokine increase, and microglial activation. These neuroinflammatory mechanisms lead to neurodegeneration, depression, and anxiety.