MRI and neuropathological validations of the involvement of air pollutants in cortical selective neuronal loss

Abstract

Vehicles are a major source of air pollution, especially particulate matter (PM) pollution, throughout the world and auto-rickshaws are considered main contributors to this air pollution. PM, in addition to causing respiratory and cardiovascular disorders, has potential to gain access to the brain and could induce neuroinflammation leading to different neurological disorders. Therefore, in the current project, MRI and immunohistochemistry techniques were adopted to ascertain the neurotoxic potential of the chronic exposure to different PM generated by two-stroke auto-rickshaws (TSA), four-stroke auto-rickshaws (FSA), and aluminum sulfate (AS) solution in rats. The results highlighted that all treated groups followed a pattern of dose-dependent increase in pure cortical neuronal loss, selective neuronal loss (SNL), nuclear pyknosis, karyolysis, and karyorrhexis. Mild to moderate areas of penumbra were also observed with increase in the population of activated microglia and astrocytes, while no alteration in the intensities of T2W MRI signals was perceived in any group. When comparing the findings, TSA possess more neurotoxic potential than FSA and AS, which could be associated with increased concentration of certain elements in TSA emissions. The study concludes that chronic exposure to PM from TSA, FSA, and AS solutions produces diverse neuropathies in the brain, which may lead to different life-threatening neurological disorders like stroke, Alzheimer's, and Parkinson's disorders. Government and environmental agencies should take serious notice of this alarming situation, and immediate steps should be implemented to improve the standards of PM emissions from auto-rickshaws.

The Effects of Air Pollution on the Brain: a Review of Studies Interfacing Environmental Epidemiology and Neuroimaging

“… WMH, cerebral microbleeds T1, T2 weighted, and FLAIR ROI-based analysis/volumetric measurements Adjusted for age, sex, education, income, smoking status, diagnosis (dementia or other), diabetes, statin, hypertension, and stroke history. 74 (12) years MADRC BPF Near roadway exposure In rats [ 29 ] n = 60 L PM (collected in Lahore, Pakistan). MRI 4.7 T Visual inspection No changes in the hyperintense signal nor any cortical atrophy of brain hemisphere detectable with MRI (even in the group treated with high PM concentrations that showed obvious selective neuronal loss in the cortical areas and glial activations histopathologically).…”

“…Our review also included a study conducted in rats experimentally exposed to PM collected in Lahore, Pakistan [ 29 ]. This study represents the advantage to combine and compare the in vivo MRI findings detected with a visual inspection with the cerebral air pollution-related anatomopathological lesions observed directly on brain sections after animals were sacrificed.…”

“…Results were more inconsistent when studies focused on GM. In rats, while a positive-dose relationship was observed postmortem between PM exposure and severity of neuronal loss on representative brain sections (predominantly in motor cortex and primary somatosensory cortex), no changes in the hyper intense signals nor any cortical atrophy were visually detectable on T2-weighted images [ 29 ]. In the birth cohort study conducted in New York City, prenatal exposure to PAHS did not correlate with cortical thickness anywhere across the cerebrum in children [ 19 ].…”

Reduced gray matter volume and cortical thickness associated with traffic-related air pollution in a longitudinally studied pediatric cohort

“…Early life TRAP exposures pose a substantial risk for interfering with normal brain development as constituent exposures may permanently harm the maturing cortex. Ejaz, Anwar [78] observed with histopathology and immunohistochemistry a positive dose-response relationship between PM exposure and severity of neuronal loss, predominately in the motor cortex and primary somatosensory cortex in rat models. Allen, Oberdorster [79] studied mice with an exposure models employing concentrated ambient ultrafine (UFP) particles with two exposure periods: postnatal day (PND) 4-7 and 10-13 (human 3rd trimester equivalent).…”

Association between exposure to air pollution and thalamus volume in adults: A cross-sectional study

“…neuronal loss [42], and mitochondrial dysfunction in a mouse model possibly could have mediated part of the association between cognitive dysfunction and NO 2 [37]. Further, air pollution can result in neuroinflammation, oxidative stress [28], and prefrontal vascular damage [5], factors that could influence thalamic gray-matter volume.…”