Inhaled pollutants and neurological health via the lung-brain axis

Abstract

Background

The lung-brain axis is a communication network that links the lungs and the brain. Inhaled pollutants like tobacco smoke, asbestos, and nanoparticles can exploit this axis to cause neurological damage. They do this by triggering systemic inflammation, oxidative stress, and disrupting the blood-brain barrier (BBB), which can lead to neurocognitive decline, neurodegeneration, and cancer.

Objective

This review compares how two major types of inhaled pollutants, tobacco smoke and environmental chemicals, affect neurological health via the lung-brain axis. We evaluate their shared and distinct biological mechanisms, contrast their associated health outcomes such as neuropsychiatric disorders versus cancers, and identify critical gaps in current research.

Conclusion

Both smoking and chemical pollutants harm the brain through the lung-brain axis but via different primary mechanisms. Smoking primarily disrupts nicotinic acetylcholine receptor (nAChR) signaling, reinforcing addiction. In contrast, environmental chemicals often rely on the physical translocation of particles to cause genotoxicity and direct inflammation. Key research limitations include a lack of long-term human data and an incomplete understanding of the bidirectional nature of this axis. Future studies should use integrated multi-omics and advanced models like organ-on-a-chip to better understand these exposure dynamics. From a policy perspective, prioritizing smoking cessation, stricter pollution controls, and occupational safety is crucial. Future interventions must also account for genetic vulnerabilities and sex-specific differences to effectively reduce the global burden of pollution-related neurological diseases.