The link between traffic-related air pollution and neurologic disease?


Pamela Lein and Rhianna Morgan discuss organosulfates and the growing connection between air pollution and neurologic disease

The World Health Organization (WHO) estimates that traffic-related air pollution (TRAP) caused by gasoline and diesel emissions from automobiles, trucks, locomotives, ships and airplanes is responsible for more than 1 million premature deaths annually. It is widely accepted that adverse health consequences associated with TRAP include pulmonary disease (asthma, lung cancer and reduced lung capacity) and cardiovascular disease (myocardial infarction, hypertension). However, there is growing recognition that TRAP also has adverse impacts on the brain. Recent epidemiologic studies have identified a positive correlation between exposure to TRAP and increased occurrence of neurodevelopmental disorders, including autism spectrum disorders and attention deficit hyperactivity disorders (ADHD), and neurodegenerative disease, such as Alzheimer’s disease and Parkinson’s disease. Data emerging from toxicologic studies in animal models support a causal link between TRAP exposure and neurotoxic outcomes. However, which component(s) in TRAP disrupt normal brain development and/or promote neurodegeneration remain unknown.

TRAP is a complex mixture of pollutants. These include pollutants in tailpipe emissions from internal combustion engines, such as particulate matter (PM), gases (carbon monoxide, nitrogen oxides or NOx, and benzene), as well as evaporative emissions from vehicles that interact with chemicals in the air to form hazardous substances, such as ozone and NO2. TRAP also includes brake and tire debris, and road dust. Research on TRAP-associated neurologic disease has largely focused on PM. PM is classified according to particle size, and the particle sizes of particular health concern are those with diameters equal to or less than 2.5 micrometers (PM2.5).  When inhaled, PM2.5 readily crosses cell membranes into blood vessels whereupon these particles can access all organs of the body, including the brain. In addition, ultrafine particulate matter with particle diameters equal to or less than 0.1 micrometers, can be taken up by olfactory nerves that innervate the nasal cavity and transported directly to the brain. PM can trigger inflammatory responses in the brain, referred to as neuroinflammation, and because chronic neuroinflammation has been linked to neurologic disease, it is hypothesized that TRAP adversely impacts the brain by triggering sustained neuroinflammation. This hypothesis is being actively explored by a number of research laboratories around the world.

However, an ongoing collaborative study between research scientists at the University of California at Davis (UCD) and the University of Iowa (UI) suggests that organosulfates associated with PM2.5 may cause neurotoxicity independent of neuroinflammatory mechanisms. Organosulfates make up 4-30% of the overall PM2.5 mass. Their abundance reflects the fact that sulfur is a ubiquitous constituent of fossil fuels, and all fossil fuel combustion processes emit organosulfates. The concentrations of airborne organosulfates are, therefore, much higher in vehicle emissions, and by extension, in areas adjacent to heavy traffic. Analysis of TRAP samples by UI researchers identified hydroxyacetone sulfate, glycolic acid sulfate, 2-methyltetrol sulfate and hydroxyethyl sulfate as abundant organosulfates in TRAP. UI investigators synthesized these and other organosulfates commonly found in PM2.5 for UCD investigators to test for neurotoxicity using state-of-the-art in vitro screening methods. The UCD researchers observed that several organosulfates caused changes in neurons cultured from rat brains similar to those observed in the brains of humans with neurodevelopmental disorders and neurodegenerative diseases. These included concentration-dependent changes in apoptotic cell death, and in the morphology of dendrites, the neuronal processes that receive information from upstream cells in neural circuits. Overall, this collaborative study demonstrates that organosulfates may contribute to the neurotoxicity associated with TRAP exposures. The identification of specific neurotoxic constituents found in TRAP provides important insight regarding approaches for mitigating risks associated with TRAP, and will be important in guiding policy decisions to protect the developing and aging human brain.


Rhianna K. Morgan, PhD

Postdoctoral Scholar

University of California, Davis




Pamela J. Lein, PhD


University of California, Davis

Tel: +1 530 752 1970




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