## 2 Lipid Composition of Lung Tissue  
To understand the origin of exhaled LPO products, it is first important to understand the source of these oxidative byproducts--the lipidome. The lipid composition of lung tissue is well understood [17]. The human lung is composed of a variety of cell types, and each cellular membrane contains a signature combination and high percentage of phospholipids [17]. The variations in phospholipids arise from a multitude of possible configurations involving different polar headgroups and types of fatty acid (FA) hydrophobic domains. FAs are incorporated in the cellular membranes and may be either saturated, monounsaturated, or polyunsaturated depending on the biochemical pathway activated for their de novo synthesis. The activation of such pathways may be triggered in response to endogenous or xenobiotic stimulus and may vary widely between individuals. Consequently, the resulting biosynthesis of lipids and the incorporated FAs vary accordingly. While there are abundant studies on the activation of biochemical pathways that result in the selective, enzymatic incorporation of specific FAs in the phospholipid framework, it is outside the scope of this review. We focused on the most common FAs reported in the lung tissue for the further evaluation of their respective LPO products [18]. Unlike other organs, lung epithelium (alveolar type II cells) also secretes a surfactant, composed mainly of lipids (90%) and protein (10%), that lines the surface and promotesalveolar stability by lowering surface tension [16]. Lung surfactant may be further classified based on its physical form; namely, tubular myelin, a monolayer at the air-liquid interface, or micellar lipid form. The levels of fatty acids in surfactant are also in a state of constant flux and vary from person to person. Lung surfactant has no unique phospholipids (PL); however, the combinations of fatty acids vary extensively. The PL composition of surfactant is more than three-quarters phosphatidylcholine (PC), and half of these PC lipids are polyunsaturated [19]. Due to the fact that excess ROS also react with surfactant lipids, leading to a weakened surface tension and the breakdown of lung surfactant as well as LPO products [20], the composition of surfactant lipids will have a bearing on the aldehyde volatilome. The commonly reported FAs found in human lung tissue and lung surfactant are provided in Table 1[18], and the breakdown of lipids comprising lung tissue is shown in Figure 1[16]. \begin{table}
\begin{tabular}{l l l l l} \hline \hline \multicolumn{1}{c}{**Saturated FA**} & \multicolumn{3}{c}{**Monounsaturated FA**} & \multicolumn{1}{c}{**Polynsaturated FA (PUFA)**} \\ \hline
12:0 \({}^{a}\) & Lauric acid & 16:1 & Palmitoleic acid & 18:2 & Linoleic acid \\
14:0 & Myristic acid & 18:1 & Oleic acid & 18:3 & Linolenic acid \\
16:0 & Palmitic acid & 20:1 & Eicosenoic acid & 20:2 & Eicosadienoic acid \\
18:0 & Stearic acid & & & 20:3 & Eicosatrienoic acid \\  & & & & 20:4 & Arachidonic acid \\  & & & & 22:6 & Docosahexaenoicenoic acid \\ \hline \hline \end{tabular} \({}^{a}\) XX:Y = number of carbons comprising the FA: number of double bonds in FA.  
\end{table} 
Table 1: Commonly reported FAs in lung tissue and lung surfactant [16; 21]. Figure 1: Lipid composition of lung tissue. (**A**) Neutral lipid breakdown; (**B**) phospholipid breakdown and relative fatty acid compositions (treemap charts) for the major phosphatides phosphatidylcholine (PE) and phosphatidylcholine (PC). For a key to abbreviations, see list at end of article. To determine the potential aldehyde volatilome that could be generated as a result of LPO in lung tissue, we applied the free radical oxidative cleavage mechanism of LPO to the relevant FAs (Table 1) as described in the next section [14; 22]. This simulation generated a number of saturated aldehydes, \(\alpha\),\(\beta\)-unsaturated aldehydes, and hydroxylablehydes.