The impact of environmental and occupational exposures of manganese on pulmonary, hepatic, and renal functions

Abstract

Manganese (Mn) is an essential trace element for humans, but long‐term environmental or occupational exposures can lead to numerous health problems. Although many studies have identified an association between Mn exposures and neurological abnormalities, emerging data suggest that occupationally and environmentally relevant levels of Mn may also be linked to multiple organ dysfunction in the general population. In this regard, many experimental and clinical studies provide support for a causal link between Mn exposure and structural and functional changes that are responsible for organ dysfunction in major organs like lung, liver, and kidney. The underlying mechanisms suggested to Mn toxicity include altered activities of the components of intracellular signaling cascades, oxidative stress, apoptosis, affected cell cycle regulation, autophagy, angiogenesis, and an inflammatory response. We further discussed the sources and possible mechanisms of Mn absorption and distribution in different organs. Finally, treatment strategies available for treating Mn toxicity as well as directions for future studies were discussed.

The association between blood manganese and liver stiffness in participants with chronic obstructive pulmonary disease: a cross-sectional study from NHANES 2017–2018

“…Excessive manganese exposure could cause a severe liver burden, as the liver is the main organ responsible for storing and metabolizing manganese in the body [ 5 ]. Manganese toxicity has the potential to induce oxidative stress, exacerbate mitochondrial dysfunction, dysregulate autophagy, promote apoptosis, and ultimately lead to neurodegeneration [ 1 ]. Oxidative stress can disrupt the balance between the rate of removal of reactive oxygen metabolites by enzymes and non-enzymatic antioxidants [ 25 ].…”

“…As one of the essential trace elements [ 1 ], manganese is present in most tissues and plays an important role in maintaining intracellular homeostasis and normal growth and development of the human body, and insufficient or excessive manganese can lead to serious consequences [ 2 ]. For example, manganese ions are the active centre of manganese superoxide dismutase in the body, which has the ability to digest harmful free radicals, but can be counterproductive when overexposed [ 3 ].…”

“…Oxidative stress is an important feature of the pathogenesis of COPD and has a significant impact on several factors of lung physiology and COPD pathogenesis [ 12 ]. Excess manganese induces oxidative stress, exacerbates mitochondrial dysfunction, dysregulates autophagy, promotes apoptosis, and leads to neurodegeneration [ 1 ]. Therefore, it is of great interest to measure serum manganese indicators in people with COPD.…”

Relationship of Blood and Urinary Manganese Levels with Cognitive Function in Elderly Individuals in the United States by Race/Ethnicity, NHANES 2011–2014

“…The half-life of urinary Mn is believed to be about 30 h, while it is only about 2 h in the blood [38,39]. This difference may explain why there was no significant association found between blood Mn and urinary Mn levels as the renal route of excretion is only responsible for up to about 5% of Mn excretion [38,40]. The biologic half-life of Mn in the brain has been previously reported to be between 51-74 days, also suggesting that blood and serum levels may not be reflective of the total concentration of Mn in the body [41].…”

“Assessing exposure of printing factory workers in thailand to selected heavy metals using urine and hair as non-invasive matrices”

“…As, Ni, Cd, and Cr are Group 1 human carcinogens according to the International Agency for Research on Cancer (IARC) [2]. Ni, Co, Mn, and Cr can irritate the respiratory tract and impair lung function [3][4][5]. As, Hg, Pb, Cd, and Mn are nephrotoxic metals [6][7][8][9].…”