Objective: This study examined the effects on mortality and cell death after biomass charcoal combustion, in which carbon monoxide (CO) emissions were reduced using a biomass combustion improver in mice. Methods: The biomass (glycerin) charcoal (Biomass CharCoal by Pusan National University, BCCP) was generated in the Power Generation System laboratory, Pusan National University. The effects and molecular mechanisms of biomass charcoal in carbon monoxide poisoning were examined by analyzing the mouse mortality, circulating leukocytes, carboxyhemoglobin (COHb), and expression of the inflammation-related genes, and cleaved capase-3 using enzyme-linkedimmunosorbent- assays, real-time polymerase chain reaction, or Western blotting. Results: The mortality rates were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. The circulating leukocytes were lower in the BCCP-exposed mice than in the raw charcoal-exposed mice. On the other hand, there was no significantly difference in the levels of COHb between both mice. Interestingly, the expression of the apoptosis-related gene, cleaved-capase 3, and the inflammation and tissue necrosis-related gene and receptor for the advanced glycation end products were reduced markedly in the BCCP-exposed mice compared to the raw charcoal-exposed mice. Decreased inflammation and tissue necrotic factors could be molecular mechanisms for the decreased mortality rates after BCCP burning. Conclusion: Biomass charcoal (BCCP) reduced the mortality rates and inflammation and tissue necrotic factors by 30%- 40%. These results suggest that the biomass charcoal (BCCP) could reduce the incidence of suicide and CO-associated delayed symptoms after charcoal burning. Furthermore, it could extend the time for rescue in suicide attempts using charcoal burning.