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Both medications can begin reducing appetite early in treatment

Inhalational toxins (e.g., cigarette-derived nicotine, tar, carbon monoxide, and heavy metals) elevate lung oxidative stress and permeability, promote ferroptosis and autophagy-dependent senescence of lung epithelial cells, elicit the recruitment of a large number of inflammatory cells, and ultimately establish a pro-inflammatory microenvironment, disrupt the normal structure and immune balance, and increase the risk of lung metastasis [25,26,27,28,29]