## 6 Toxicity and Health Risk Assessments  
The toxicity mechanisms of IVOCs can be broadly categorized into carcinogenic and non-carcinogenic pathways (Figure 6). Certain IVOCs undergo metabolic activation in the body, generating reactive metabolites, such as epoxides, which are carcinogenic. These metabolites bind to DNA to form adducts, causing DNA damage, mutations, and, ultimately, cancer. Additionally, IVOC metabolites may interfere with DNA transcription, replication, and protein synthesis, disrupt gene expression related to cell growth and differentiation, and increase cancer risk. IVOCs can also induce oxidative stress, producing reactive oxygen species (ROS), damaging cellular antioxidant systems, and causing lipid peroxidation, protein oxidation, and DNA oxidative damage, further promoting carcinogenesis. In terms of non-carcinogenic risks, prolonged exposure to high concentrations of certain IVOCs can lead to acute toxicity, manifesting as nausea, vomiting, diarrhea, or skin inflammation, and, in severe cases, may impair immunity and damage vital organs. IVOCs can also induce DNA damage through mechanisms such as single- or double-strand breaks, base loss, guanine oxidation, thymine dimer formation, DNA adducts, and DNA crosslinking, potentially causing gene mutations and chromosomal abnormalities. Immune function may be suppressed by IVOCs, affecting immune cell activity and cytokine production, leading to immune suppression or imbalance. In regard to the reproductive system, IVOCs may disrupt hormone secretion (e.g., estradiol and testosterone), causing infertility or fetal malformations. The neurotoxic effects of IVOCs are associated with increased risk of anxiety, depression, and attention deficits, and may correlate with abnormal brain structure. Finally, certain IVOCs exhibit enhanced toxicity under UV or visible light exposure, converting into more toxic configurations, generating ROS, and causing cell membrane rupture, DNA strand breaks, and tissue damage in skin and eyes [102; 103]. As representative IVOC species, Nap and BaP exhibit distinct toxicity profiles, as shown in Table 3. According to carcinogenicity classifications by the International Agency for Research on Cancer (IARC), BaP is definitively categorized as carcinogenic to humans (Group 1), whereas Nap is classified as possibly carcinogenic to humans (Group 2B), indicating stronger evidence for BaP's carcinogenicity. In terms of long-term exposure risks, the reference concentration (RfC) for inhalation of BaP (\(2.0\times 10^{-6}\) mg m\({}^{-3}\)) is three orders of magnitude lower than that of Nap (\(3.0\times 10^{-3}\) mg m\({}^{-3}\)), and its inhalation unit risk (IUR, \(6.0\times 10^{-4}\) (ug m\({}^{-3}\))\({}^{-1}\)) is 17.6-fold higher than that of Nap (\(3.4\times 10^{-5}\)), highlighting the substantially higher carcinogenic potential of BaP as a result of low-dose chronic inhalation exposure. Similarly, for oral toxicity parameters, BaP's reference dose (RfD, \(3.0\times 10^{-4}\) mg kg\({}^{-1}\) day\({}^{-1}\)) represents only 1.5% of Nap's value (\(2.0\times 10^{-2}\) mg kg\({}^{-1}\) day\({}^{-1}\)), while its oral slope factor (CSFo, \(1\) mg kg\({}^{-1}\) day\({}^{-1}\)) is 8.3 times greater than that of Nap (0.12), further confirming BaP's significantly elevated carcinogenic risk via the oral route. In contrast, acute toxicity data reveal an opposing trend: the median lethal dose (LD50) for the intraperitoneal administration in mice demonstrates that Nap (\(150\) mg kg\({}^{-1}\)) exhibits stronger acute toxicity than BaP (\(250\) mg kg\({}^{-1}\)), suggesting that Nap may pose greater direct toxic effects in high-dose short-term exposure scenarios. Although both compounds share identical maximum contaminant levels (MCLs) in drinking water (\(0.2\) ug L\({}^{-1}\)), combined analysis with oral slope factors indicates that BaP's actual carcinogenic risk at equivalent concentrations far exceeds that of Nap.