|Year : 2017 | Volume
| Issue : 4 | Page : 97-98
Is PM2.5a double-edged sword?
Longfei Guan1, Raja Anand2, Yuchuan Ding1
1 China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
2 Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
|Date of Submission||05-Dec-2017|
|Date of Acceptance||07-Dec-2017|
|Date of Web Publication||22-Jan-2018|
Department of Neurosurgery, Wayne State University School of Medicine, 550 E Canfield, Detroit, MI 48201
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Guan L, Anand R, Ding Y. Is PM2.5a double-edged sword?. Environ Dis 2017;2:97-8
A recent article by Qui et al. revealed that exposure to airborne PM2.5 may yield the health benefits of reducing hepatic steatosis and hyperlipidemia in certain populations. The authors exposed normal chow (NC) and high fat (HF)-fed mice to 111.0 μg/m 3 of PM2.5 using a versatile aerosol concentration system. This concentration of PM2.5 exposure was nearly 10 times the concentration of ambient PM2.5 (15.8 μg/m 3) at the testing site in Columbus, Ohio. Following the 10-week period of exposure, the authors examined the molecular mechanism for PM2.5 activity and its effects in combination with a high-fat diet, on hepatic steatosis.
The study yielded numerous important findings [Figure 1]: (1) PM2.5 exposure promotes hypertriglyceridemia and hepatic steatosis in NC-fed mice, while PM2.5 exposure reduces hepatic injury, hyperlipidemia, and hepatic steatosis in obese, HF-fed mice; (2) The reduction in steatosis and hyperlipidemia was due to induction of autophagy by PM2.5; (3) The hepatic autophagy induced by PM2.5 is reliant upon myeloid differentiation primary response 88 (MyD88), the primary mediator of toll-like receptor-mediated inflammatory signaling. The results of this study are significant for better understanding the mechanistic basis by which ambient PM2.5 pollution, in combination with other stressors, can modulate pathophysiology.
|Figure 1: The effect of PM2.5exposure in promoting or reducing hepatic steatosis in NC- or HF-fed mice. (a) PM2.5exposure induces hepatic autophagy depending on the inflammatory pathway mediated through MyD88 and strongly represses lipid metabolism (FA oxidation and lipolysis) in the livers of mice under NC. NC diet-fed mice experienced increased hepatic steatosis since the suppression of lipolysis overweighed the anti-steatosis effect of hepatic autophagy triggered by PM2.5exposure. (b) PM2.5exposure promotes hepatic autophagy in addition to repressing lipid metabolic pathways in the livers of mice under HF diet. The anti-steatosis effect of hepatic autophagy triggered by PM2.5exposure overweighs the suppression of hepatic lipid metabolism. Thus, PM2.5-induced hepatic autophagy produces a measurable effect on alleviating hepatic steatosis in the HF-fed animals. NC: Normal chow, HF: High fat, FA: Fatty acid|
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The study revealed the underlying mechanism by which PM2.5 can reduce hepatic steatosis. Hepatic autophagy is activated by exposure to inhaled PM2.5. Autophagy has important protective metabolic functions, including maintenance of insulin sensitivity and degradation of intracellular lipids, under metabolic conditions, such as obesity or HF feeding., Obesity induced by a HF diet decreases hepatic autophagy. Decreased autophagy is a major factor involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD)., The study indicated that PM2.5 exposure also triggered hepatic autophagy in mice fed with NC. However, the NC mice displayed hepatic steatosis due to the repression of lipolysis and fatty acid oxidation by PM2.5. The anti-lipolytic and anti-fatty acid oxidative effects of PM2.5 exposure overrode the effect of hepatic autophagy in these mice. In contrast, the HF-fed mice experienced a reduction in hepatic steatosis because their initial levels of hepatic autophagy were reduced. In these mice, hepatic autophagy induced by PM2.5 negated the suppressive effect of HF feeding on autophagy and possibly, other metabolic pathways. The anti-lipolytic and anti-fatty acid oxidative effects of PM2.5 were overweighed by its induction of fat-reducing lipophagy. Therefore, PM2.5 exposure alleviated liver injury, reduced hepatic steatosis, and reduced hyperlipidemia in HF-fed mice.
This study raised an interesting question: Is PM2.5a double-edged sword? Does PM2.5 exposure promote or relieve hepatic steatosis under NC or HF diet? It may suggest that individuals with obesity or NAFLD resulting from HF diet or “Western-style” diet under clean air environments can gain health benefits by living in areas under high levels of ambient PM2.5 (such as China and India) for a designated period. However, future studies are required to determine if the proposed anti-hepatic steatosis and anti-hyperlipidemia effects are enough to overcome the detrimental health effects of exposure to airborne pollution. The mice in the study were exposed to 111.0 μg/m 3 of PM2.5. Recent studies have shown a decrease in 1.10 cardiovascular-related deaths per 100,000 individuals for every 1 μg/m 3 decrease in PM2.5. Studies in which varied concentrations of PM2.5 exposure are examined against hepatic steatosis in HF-fed mice may begin to elucidate the point at which PM2.5 effectively achieves the observed outcomes of this study. Furthermore, the ratio of prior-exposure PM2.5 level to experimental PM2.5 level may be useful in determining if a therapeutic relationship exists. Future studies may also analyze exposure time required to obtain the outcomes observed in the study. Specifically, does shorter exposure time yield similar benefits? How does longer exposure time affect hyperlipidemia and steatosis?
The study conducted by Qiu et al. was well considered and thought provoking. PM2.5 indeed proves to be a double-edged sword in determining how therapeutic benefits might be obtained from a current public health dilemma.
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