Teaching with chalk is an ancient and economical method of teaching that is used in many areas of the world, especially in China. Chalk sticks and blackboard are the most common tools during chalk teaching. While writing and scraping on a blackboard, the chalk sticks release total suspended particulate (TSP), including coarse and fine chalk dust particles.
Because ambient fine particulate matter may be introduced into the human respiratory system and reach the lung alveoli, they have the potential for bioaccumulation in tissues/organs and oxidative damage on the respiratory system. Teachers spend approximately 6-8 h each teaching day, and for children, at least one-third of their day is spent in the classroom. Thus, it is not surprising that fine chalk dust in the classroom can exert some adverse effects on the human respiratory system.
Lung inflammation is central to the pathogenesis of airway disorders, including acute lung injury, chronic obstructive pulmonary disease (COPD), chronic bronchitis and asthma. The acute inflammation, as a transient and initial response to injury, is rapid in onset and is of short duration lasting for hours or a few days; it is characterized by the release of numerous chemical mediators and the migration of leukocytes, predominantly neutrophils.
The recruitment of pro-inflammatory cells such as neutrophils and macrophages are involved in the up-regulation of various signaling molecules, such as cytokines (TNF-α, IL-6), and adhesion molecules (ICAM) that amplify the inflammatory response and recruit additional cells. Activation of the endothelium at the sites of inflammation allows macrophages and neutrophils to attach to release cytokines, including ICAM-1 and other factors that propagate the inflammatory process often leading to bouts of inflammation.
In this study, the possibility was verified that exposure to fine chalk dust increased the TNF-α, IL-6, iNOS, and TGF-β1 gene transcriptions in vivo. Consequently, fine chalk dust may activate endothelium to increase neutrophils and macrophages to attach, leading to the increase of inflammatory cell infiltration and inflammatory injury on the lungs. Our data have shown that fine chalk dust exposure increases the activation of p38 and ERK MAPK in rat lung leading to inflammation effects.
Oxidative stress is related to the pathogenesis of inflammatory lung diseases. During inflammatory process, various ROSs are overproduced and released by the activated immune cells. The immune cells involved in this production are mostly macrophages and neutrophils. The ROS is able to kill pathogens, but also function as determinant signal transduction molecules that regulate inflammatory. Expectedly, oxidative stress occurred in rats exposed to fine chalk dust. These data support the fact that ROS actively participate in the inflammatory responses in the lung.
NAC serves as anti-inflammatory functions because it restores cellular redox status and can modulate the activity of redox-sensitive cell-signaling and transcription pathways; thereby, NAC regulates a variety of pro-inflammatory genes. NAC injection effectively inhibits oxidative stress-induced damage to the lung.
In summary, fine chalk dust can induce inflammatory responses, as measured by inflammatory cytokine gene expression and inflammatory cell infiltration. Also, these responses were attenuated by NAC administration and could be mediated via p38 and ERK MAPK pathway. The obtained data from our study suggests that fine chalk dust may induce lung injury in rat and the NAC supplement may be a viable protective strategy for fine chalk dust-associated lung inflammation.
This study, reporting that fine chalk dust induces inflammatory response via p38 and ERK MAPK pathway in rat lung, was recently published in the Environmental Science and Pollution Research.
These findings are described in the recently published article entitled Fine chalk dust induces inflammatory response via p38 and ERK MAPK pathway in rat lung, in the journal Environmental Science and Pollution Research. This work was led by Yuexia Zhang, Chuan Dong and Zongwei Cai from Shanxi University and Hong Kong Baptist University.
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