Endotoxin (lipopolysaccharide, LPS), widely distributed in the atmospheric environment with strong immunogenicity, is an important biological component of ambient particulate matter. However, whether LPS participates in atmospheric chemistry and how its biological health impacts change with the relevant processes are poorly understood. In this study, we employed the rat model to investigate the impact of ozone oxidation on the biological toxicity of LPS and used Fourier transform infrared spectroscopy and high-resolution electrospray mass spectrometry to study the underlying reaction mechanisms. The results show that the LPS can be oxidized by ozone and the resulting reactant greatly enhanced inflammatory anemia with a 177% capacity increase despite a minor influence on its immunogenicity. In contrast to the control, rats exposed to oxidized LPS were observed to release characteristic exhaled biomarkers, indicating that the formed reactant indeed altered the biological effects of LPS. Mechanistic investigation reveals that ozone oxidation of the hydroxyl group in the key toxic part of LPS, kdo2-lipid A, can cause dysregulation of iron homeostasis in rats, which is the mechanism of oxidized LPS-enhanced anemia. Unfortunately, these chemical structure changes and the resulting health impacts cannot be detected by the conventional LPS analysis method. This study highlights the changes in the toxicity of LPS and its health impacts when oxidized by ozone and the need to broadly consider the involvement of bioaerosol in atmospheric chemistry.
