Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts

Topic: Brain proteins, microglia and lab models

Air pollution is a risk factor for cardiovascular and respiratory morbidity and mortality. A growing literature also links exposure to diverse air pollutants (e.g., nanoparticles, particulate matter, ozone, traffic-related air pollution) with brain health, including increased incidence of neurological and psychiatric disorders such as cognitive decline, dementia (including Alzheimer's disease), anxiety, depression, and suicide. A critical gap in our understanding of adverse impacts of pollutants on the central nervous system (CNS) is the early initiating events triggered by pollutant inhalation that contribute to disease progression. Recent experimental evidence has shown that particulate matter and ozone, two common pollutants with differing characteristics and reactivity, can activate the hypothalamic-pituitary-adrenal (HPA) axis and release glucocorticoid stress hormones (cortisol in humans, corticosterone in rodents) as part of a neuroendocrine stress response. The brain is highly sensitive to stress: stress hormones affect cognition and mental health, and chronic stress can produce profound biochemical and structural changes in the brain. Chronic activation and/or dysfunction of the HPA axis also increases the burden on physiological stress response systems, conceptualized as allostatic load, and is a common pathway implicated in many diseases. The present paper provides an overview of how systemic stress-dependent biological responses common to particulate matter and ozone may provide insight into early CNS effects of pollutants, including links with oxidative, inflammatory, and metabolic processes. Evidence of pollutant effect modification by non-chemical stressors (e.g., socioeconomic position, psychosocial, noise), age (prenatal to elderly), and sex will also be reviewed in the context of susceptibility across the lifespan.

Key findings

• Recent experimental evidence has shown that particulate matter and ozone, two common pollutants with differing characteristics and reactivity, can activate the hypothalamic-pituitary-adrenal (HPA) axis and release glucocorticoid stress hormones (cortisol in humans, corticosterone in rodents) as part of a neuroendocrine stress response.

Why it matters

This paper proposes that air pollutants such as particulate matter and ozone can activate the stress hormone system, which may contribute to brain conditions including dementia. It is a conceptual review of a possible pathway, not evidence that reducing pollution treats or prevents Alzheimer's disease.

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Study details

• Evidence strengthLow

Read the original

• DOI: 10.3233/jad-190015
• PubMed: 31127781
• Original source →
• Free full text: Journal of Alzheimer s Disease →

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

@article{thomson2019-31127781,
  author  = {Thomson, E. M.},
  title   = {{Air Pollution, Stress, and Allostatic Load: Linking Systemic and Central Nervous System Impacts}},
  journal = {Journal of Alzheimer's disease : JAD},
  year    = {2019},
  doi     = {10.3233/jad-190015},
  pmid    = {31127781},
  url     = {https://doi.org/10.3233/jad-190015}
}

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• Exposure to ambient air pollution and the incidence of dementia: A population-based cohort study Environment international · 2017-09-13 · usefulness score 66/100 · Getting a diagnosis
• Association of Insulin Resistance With Cerebral Glucose Uptake in Late Middle-Aged Adults at Risk for Alzheimer Disease JAMA neurology · 2015-09-01 · usefulness score 63/100 · Brain tissue and pathology
• Neurodegenerative and neurological disorders by small inhaled particles Neurotoxicology · 2016-07-19 · usefulness score 47/100 · Inflammation and the immune system

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