## 1 Introduction  
Perturbations of oxidant levels, such as reactive oxygen species (ROS), in the cellular matrix arise due to endogenous or xenobiotic processes that are either a cause or effect of various disease states. The oxidative stress (OS) related to such perturbations has been extensively studied and reported in the literature [1; 2; 3; 4; 5]. Redox imbalance is directly implicated in lung carcinogenesis; in particular, oxidative cleavage of lung tissue lipids is attributed either to systematic ROS or their presence in the lung organs [6]. Lipid peroxidation (LPO) is a widely accepted free radical process used to describe the oxidative destruction of unsaturated fatty acids. The products of such peroxidation have been confirmed in various biological matrices using a variety of techniques [7]. The wide interest in LPO-derived metabolites is due in part to the potential of these small, volatile organic products to serve as indicators of early-stage lung cancer [8].  
Lung cancer (LC) is the most common form of malignancy in the world. A reported 142,080 people died from LC in the United States in 2018 [9]. The advent of computedtomography (CT) scanning has allowed for the large-scale screening for lung cancer. The surveillance and early diagnosis of LC leads to timely treatment and higher survival rates [10]. However, the disadvantages of repeated exposure to radiation from CT or positron emission tomography (PET) scans, the high false positive rates associated with this primary modality of LC screening, and the need for subsequent, more invasive technologies to confirm diagnoses have limited the wider application of these tests. It is therefore imperative to evaluate alternative methods of LC detection. One promising alternate modality is to analyze the exhaled breath of patients to detect products of LPO and thereby diagnose the presence, extent, and possibly even the type of LC [11].  
While the existence of volatile LPO products in exhaled breath have been known since the 1970s, reports differ in terms of assigning the origin of the volatilome, the mechanism of oxidative breakdown, and the predictive value of exhaled markers for the clinical diagnosis of disease [12]. We have therefore examined the reports that correlate exhaled volatile organic compounds (VOCs) with incidences of LC. This study is aimed to investigate the reports of LPO products while also providing an explanation for the existence and predictive efficiency of individual markers in breath as they relate to lung cancer detection. Although systemic LPO is well established in the literature [13], our focus in the present review was to evaluate the aldehyde volatilome originating in the lungs. Other LPO-derived VOC families, such as alkanes, alkenes, and alcohols, have been discussed elsewhere and are not addressed in this review [14; 15]. Limiting our study to aldehydes allowed us to focus on the particular species of markers that is expected in higher concentrations in exhaled breath, namely volatile aldehydes generated from the oxidative cleavage of mono-, di- and polyunsaturated lipids, which constitute nearly 69% of all phosphatidylcholines--the major lipid class in lung tissue [16]. The LPO products generated within the lungs are expected to better survive the endogenous environment compared to those originating systemically because they can rapidly exchange across the liquid-air interface within the alveoli as they are generated and then be exhaled.  
To enumerate the source and predict potential aldehyde candidates of LPO due to lung disease, we followed a systematic approach:  
1. identify common unsaturated fatty acids found in lung tissue;
2. based on the free radical mechanism of LPO, simulate oxidative cleavage of the identified panel of unsaturated lipids;
3. list potential aldehyde products of LPO generated by the simulation;
4. conduct a literature search for reports of the LPO products in exhaled breath and document the analytical techniques used to detect them.