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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Policy & Risk Sign in to save

Pulmonary Fibrosis caused by Asbestos Fibers in the Respiratory Airway

Journal of Experimental & Biomedical Sciences/Biomedical Science Letters 2021 2 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 35 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Ji-Woo Jung, Ji-Woo Jung, Eung‐Sam Kim Eung‐Sam Kim Eung‐Sam Kim Eung‐Sam Kim Eung‐Sam Kim

Summary

This review discusses how inhaled asbestos fibers cause pulmonary fibrosis by generating reactive oxygen species and inflammation in the lungs. While asbestos is not plastic, the mechanisms of fiber-induced lung damage are relevant to understanding how inhaled plastic microfibers might affect lung health. Both types of fibers can become lodged in lung tissue and trigger chronic inflammatory responses.

Asbestos products had been widely used until 2007 in Korea since the 1930s. A total ban on their production and applications has been imposed because of the toxic effect of asbestos fibers on the human health. The inhaled asbestos fibers increase reactive oxygen species and inflammatory reactions in the respiratory airway including the alveolar sac, resulting in DNA damages and secretion of several inflammatory cytokines or chemokines. These paracrine communications promote the proliferation of fibroblasts and the synthesis of collagen fibers, thereby depositing them into the extracellular matrix at the interstitial space of alveoli. The fibrotic tissue hindered the gas exchange in the alveolus. This reviews describes not only the cytotoxic effects of asbestos fibers with different physical or chemical characteristics but also the interaction of cells that make up the respiratory airway to understand the molecular or cellular mechanisms of asbestos fiber-induced toxicity. In addition, we propose a pulmonary toxicity research technique based on the mini-lung that can mimic human respiratory system as an alternative to overcome the limitations of the conventional risk assessment of asbestos fibers.

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