A research team led by Kezhong Zhang, Ph.D., at the Wayne State University School of Medicine's Center for Molecular¹ Medicine and Genetics, has discovered that exposure to air pollution has a direct adverse² health effect on the liver and causes liver fibrosis, an illness associated with metabolic³ disease and liver cancer. Dr. Zhang, assistant professor of Molecular Medicine and Genetics and of Immunology and Microbiology, and his group have been studying the adverse health effects of air pollution from a unique perspective. While the major research efforts in the field were focused on the effects of air pollution on lung tissues and cardiovascular system, the Zhang lab studied the pathological effects and stress mechanisms⁴ of air pollution on the liver, the major organ of detoxification and metabolism⁵. Their work demonstrated that inhalation exposure to high-concentration airborne particulate⁶ matter PM2.5 has direct effects on the liver, triggering liver fibrosis, a pathological condition characterized by accumulation of the extracellular matrix protein collagen that occurs in most types of chronic⁸ liver diseases.

 

PM2.5 is fine airborne particulate matter with aerodynamic diameter smaller than 2.5 micrometers. It is a complex mixture of particles and gases from gasoline and diesel⁹ engines, together with dust from wear of road surfaces, tires and brakes. PM2.5 is the major and most toxic¹⁰ component¹¹ of air pollutants¹² in the real-world air environment of intensive traffic or industrial activity. Recent epidemiological studies confirmed that populations exposed to high-level PM2.5 are at a higher risk of developing heart disease and metabolic disease.

 

Dr. Zhang said that PM2.5 pollution has major impact on the public health for the general population in urban areas, such as Detroit, one of the most PM2.5-polluted cities in the United States, according to annual air quality reports by the American Lung Association.

 

Dr. Zhang's group, in collaboration¹³ with a research group at the Ohio State University College of Public Health led by Qinghua Sun, M.D., Ph.D., professor and assistant dean for Global Public Health, performed both short-time and long-term inhalation exposure of animal models to real-world PM2.5. After a 10-week exposure, the animals developed liver fibrosis. Utilizing¹⁴ molecular, cellular⁷ and pathological approaches, the team discovered the stress sensor¹⁵ on the cell membrane¹⁶ that initiates¹⁷ PM2.5-triggered stress signals and the mediators inside the cell that transduces the signaling. The PM2.5-triggered inflammatory stress responses promote collagen deposition¹⁸ -- a hallmark of fibrosis -- in the liver through activating¹⁹ the transforming growth factor β (TGFβ) signaling. This work will soon be published in the Journal of Hepatology.

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