Particulate matter 2.5 – Muddling the healthy brain

Dear Editor, We write this letter to highlight the adverse effects of air particulate matter (PM) and its negative impact on cognitive functioning. Increased urbanization and industrialization have contributed to increased ambient air pollutants that could potentially increase the risk of both morbidity and mortality. This has become a cause of increasing community health concern, especially in India and other low- and middle-income countries. In particular, the association between chronic air pollution and cognitive decline has recently become a prominent area of interest. According to the Lancet Commission’s report on the prevention, intervention, and care of dementia (2020), the contamination of air accounts for a 2% increase in dementia prevalence.[1] Among the different types of dementia, the association between PM2.5 and Alzheimer’s disease (AD) is most studied. AD is found to have a prominent association with PM2.5 as it stimulates the increase of AD biomarkers such as amyloid-beta and hyperphosphorylated-tau.[2] Animal studies suggest that particulate air pollutants can accelerate the process of neurodegeneration through Aβ deposition and alterations in amyloid precursor protein processing.[3] Therefore, this issue must be addressed urgently in order to prevent or delay the accelerated cognitive decline and progression to neurodegenerative disorders, such as dementia, especially in the aging population. Among various pollutants, PM2.5 can have deleterious effects on brain health. PM2.5 is a type of air pollutant which includes fine particles that are approximately 2.5 μ in diameter that can easily penetrate the blood–brain barrier (BBB) and enter the cerebral circulation.[4] The major chemical components of PM2.5 are water-soluble ions, such as ammonium ions, sulfate, nitrate, organic carbon, silicon and sodium ions, and heavy metals.[5] The sources of the different components of PM2.5 can either be indoor or outdoor. Indoor sources include kitchen smoke generated by the use of solid fuels and secondary generation of chemical gases from cleaning products. Outdoor sources include vehicle exhaust, locomotives, construction equipment, soil dust, combustion of fuels, coals, and natural sources such as forest fires. PM2.5 from outdoor air pollution can penetrate indoor, due to infiltration and improper ventilation.[6] Indoor PM2.5 is significant as it can increase the risk of cognitive decline due to the consistent exposure to the fine particles.[7] In northern parts of India, ambient air pollution is three to five times more in the rural population.[8] Domestic energy usage, cooking with solid fuels, coal factories, agricultural waste, power generation facilities, cottage industries, and agricultural stubble burning could be the contributing factors of increased emission of PM2.5 in rural areas.[9] The aging population of rural and urban areas, suffering from chronic diseases like cardiovascular diseases, can be at an increased risk of developing cognitive dysfunction.[10] In addition, prenatal exposure to PM2.5 can interfere with the white matter development and affect cognition in newborn.[11] PM2.5 can have various other harmful effects on human health. Different diseases caused by PM2.5 exposure include cardiovascular diseases, chronic obstructive pulmonary disease (COPD), lung cancer, and neurological diseases.[12–15] The fine PM primarily affects pulmonary functioning, which can result in COPD. This, in turn, can reduce the oxygen supply to the brain, thereby affecting either single or multiple domains of cognitive function.[13] They also can reach the brain through olfactory modality, enter the blood circulation to cause neuronal inflammation and oxidative damage. PM2.5 exposure is said to disrupt multiple brain regions including the hippocampus, visual vortex, frontal and temporal lobes, and corpus callosum.[16] The continuous exposure to PM2.5 can stimulate the activation of microglia, especially M1 phenotype which induces the inflammatory markers in the brain, including inducible nitric oxide synthase, interleukin-6 (IL-6), tumor necrosis factor-α, IL-1β, triggering receptor expressed on toll-like receptor 2/4, myeloid cells 2 (TREM2), and cyclooxygenase-2 in BV-2 microglial cells.[17] This, in turn, induces neurotoxicity and synaptic damage that may subsequently result in cognitive impairment. Thus, PM2.5 can influence brain functioning directly by traversing the BBB and indirectly by compromising the pulmonary function and by both above mechanisms. In order to reduce indoor PM2.5 levels, it is required to decrease outdoor as well as indoor air pollution. To tackle the former, industrial emission standards may be strengthened by implementing desulfurization of gas, selective catalytic reduction, or selective noncatalytic reduction systems.[18] Sulphur dioxide and PM filters may be installed in industrial boilers. Policy measures to reduce biomass burning may also result in a significant reduction in PM2.5 levels.[5] The indoor pollution can be controlled by avoiding smoking inside the house, ensuring proper ventilation, and using cleaning agents that are relatively eco-friendly. Reduction of indoor air pollution may be brought about by replacing indoor coal and firewood burning with natural gas and advanced stoves. Trees act as vegetation barriers that help in controlling pollution, especially the leaf structure which is said to have a major role in PM2.5 capture. Therefore, afforestation can be helpful in reducing air pollution impacts, especially from vehicles.[19] Therefore, considering a green corridor in the adjacent parts of the roads may help in controlling vehicle pollution to a greater extent. Importantly, urgent public awareness needs to be given on how air pollution can adversely impact human health and aggravate pulmonary diseases. Addressing pollution, which is a modifiable risk factor for cognitive impairment, could help in preventing or delaying the progression into dementia. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.