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Fine particulate matter (PM 2.5 ) is able to pass through the respiratory barrier to enter the circulatory system and can consequently spread to the whole body to cause toxicity. Although our previous studies have revealed significantly altered levels of phosphorylcholine-containing lipids in the lungs of rats after chronic inhalation exposure to PM 2.5 , the effects of PM 2.5 on phosphorylcholine-containing lipids in the extrapulmonary organs have not yet been elucidated. In this study, we examined the lipid effects of chronic PM 2.5 exposure on various organs and serum by using a rat inhalation model followed by a mass spectrometry-based lipidomic approach. Male Sprague-Dawley rats were continuously exposed at the whole body level to nonfiltered and nonconcentrated ambient air from the outside environment of Taipei city for 8 months, while the control rats inhaled filtered air simultaneously. After exposure, serum samples and various organs, including the testis, pancreas, heart, liver, kidney, spleen, and epididymis, were collected for lipid extraction and analysis to examine the changes in phosphorylcholine-containing lipids after exposure. The results from the partial least squares discriminant analysis models demonstrated that the lipid profiles in the PM 2.5 exposure group were different from those in the control group in the rat testis, pancreas, heart, liver, kidney and serum. The greatest PM 2.5 -induced lipid effects were observed in the testes. Decreased lyso-phosphatidylcholines (PCs) as well as increased unsaturated diacyl-PCs and sphingomyelins in the testes may be related to maintaining the membrane integrity of spermatozoa, antioxidation, and cell signaling. Additionally, our results showed that decreased PC(16:0/18:1) was observed in both the serum and testes. In conclusion, exposure to chronic environmental concentrations of PM 2.5 caused lipid perturbation, especially in the testes of rats. This study highlighted the susceptibility of the testes and suggested possible molecular events for future study., Competing Interests: Declaration of competing interest All authors declare no known competing financial interests or other relationships in the submitted work., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Recent studies have illustrated an association between ambient fine particulate matter (PM 2.5 ) exposure and neuronal toxicity in epidemiological studies and animal models. However, the possible molecular effects on brains under real-world exposure to PM 2.5 remain unclear. In this pilot study, male spontaneously hypertensive rats were whole-bodily exposed to ambient air from the outdoor environment of Taipei City for 3 months, while the control rats inhaled HEPA-filtered air. The PM 2.5 -induced phosphatidylcholine and sphingomyelin profiles in the hippocampus, cortex, medulla, cerebellum, and olfactory bulb were assessed by mass spectrometry (MS)-based lipidomics. Partial least squares discriminant analysis (PLS-DA) and the Wilcoxon rank sum test were used to examine the lipid changes between the exposed and control groups. The PLS-DA models showed that phosphatidylcholine and sphingomyelin profiles of the PM 2.5 exposure group were different from those of the control group in each brain region except the cortex. More lipid changes were found in the hippocampus, while fewer lipid changes were observed in the olfactory bulb. The lipid alteration in the hippocampus may strengthen membrane integrity, modulate signaling pathways, and avoid accumulation of lipofuscin to counter the PM 2.5 -induced stress. The lipid changes in the cortex and medulla may respond to PM 2.5 -induced injury and inflammation; while the lipid changes in the cerebellum were associated with neuron protection. This study suggests that the MS-based lipidomics is a powerful approach to discriminate the brain lipid profiles even at the environmental level of ambient PM 2.5 and has the potential to suggest possible adverse health effects in long-term PM 2.5 exposure studies., (Copyright © 2018. Published by Elsevier B.V.)