239J Contemp Med Sci | Vol. 8, No. 4, July-August 2022: 239–244 Original The Effect of Pollution Represented by Polycyclic Aromatic Hydrocarbons on the Levels of p53 and Some Antioxidant Enzymes in Baghdad Traffic Police Ashraf R. Salem1*, Estabraq A.R. Al-Wasiti2, Fahem A. Hasan3 1College of Nursing, University of Telafer, Telafer, Nineveh, Iraq. 2College of Medicine, Department of Chemistry and Biochemistry, Al-Nahrain University, Baghdad, Iraq. 3Al-Hussaini Medical City, Kerbala Health Directorate, Ministry of Health, Kerbala, Iraq. *Correspondence to: Ashraf R. Salem (E-mail: ashraf.r.salem@uotelafer.edu.iq ) (Submitted: 01 April 2022 – Revised version received: 22 April 2022 – Accepted: 18 May 2022 – Published online: 26 August 2022) Abstract Objectives: To ascertain the protective effect of p53 tumor protein by monitoring its levels in comparison with the levels of antioxidant enzymes, against any type of cancer that can be caused by chronic exposure of traffic policemen to air pollutants. Methods: This study comprises 140 participants, who have been divided into two groups (Traffic police and Office police). PAHs were analyzed for each participant by GC/FID while p53 protein and antioxidant enzymes were measured by the ELISA technique. Results: The concentrations of polycyclic aromatic hydrocarbons and p53 tumor protein were high in the blood of traffic police compared to office police, while higher levels of antioxidant enzymes (Catalase and G-Px) were observed in the blood of office police. Conclusion: Exposure to PAHs can cause oxidative stress, which can damage DNA and lead to cancer. However, because natural endogenous biomolecules like p53 protein can neutralize PAHs’ carcinogenic effects, their elevation has a beneficial anti-cancer effect by reducing oxidative stress and preventing tumorigenesis. Keywords: PAHs, p53 tumor protein, catalase, G-Px, DNA ISSN 2413-0516 Introduction All living things, including people, are subject to air pollution’s multiple detrimental consequences, and because of how it affects human life and health, this problem has gained promi- nence on the international political agenda. Air pollution is the number one environmental killer and the fifth-highest risk factor for total all-cause mortality.1 It’s a complex chemical mix- ture that contains various concentrations of gases such as nitrogen dioxide (NO2), ozone (O3), carbon dioxide (CO2), sulfur dioxide (SO2), carbon monoxide (CO), and carbon dioxide (CO2). Gaseous pollutants may have both immediate and long-term negative effects on health.2 Many of these gases have oxidizing properties, and one way they can be harmful to human health is by causing oxidative stress.1 Semi-volatile kinds including Benzene, Formaldehyde, Naphthalene, and polyaro- matic hydrocarbons occur as liquid droplets, but they may also move between the gaseous particle phases of air pollution.3 Numerous cancers and air pollution are related,4 and it is estimated that cancer causes 4.2 million early deaths world- wide and affects organs including the lung, mouth, bladder, kidney, breast, liver, prostate, and ovary. In addition, the International Agency for Research on Cancer has classed out- door air pollution as a category 1 human carcinogen (IARC).5 The liver is where PAHs are mostly processed and activated after being ingested through the lungs, skin, and intestines. Many polycyclic aromatic hydrocarbons are bioactivated to form phenols, epoxides, and dihydrodiol, which are mostly oxidized by cytochrome P450 monooxygenases (CYPs). 6 The two main mechanisms for the carcinogenicity of PAHs are the creation of reactive oxygen species and PAH-DNA asymp- totics, particularly those of diolepoxides, radical cations, and o-quinones7 (Figure 1). The gene encoding the p53 tumor protein is known as tumor protein (TP53). It’s a phosphoprotein containing 393 amino acids in its structure9 and ‘Guardian of the Genome’ is another name for it.10 The p53 tumor protein attaches to DNA in the nucleus directly and it is involved in the cell cycle, DNA repair, and apoptosis control, as well as regulating the repair process in reaction to damaging substances such as radiation, chemicals, and UV radiation from sunshine.9,11 This protein is crucial in deciding whether or not a dam- aged cell will undergo DNA repair or programmed cell death. If DNA damage can be repaired, p53 activates the genes needed to do it, while this protein inhibits the cell from prolif- erating and tells it to undergo programmed cell death if the DNA cannot be repaired.12 This means TP53 controls cell divi- sion by stopping them from expanding and dividing (repro- ducing) in an uncontrolled manner. In vertebrates, these p53-mediated responses are critical and decisive in preventing cancer recurrence.13 Under genotoxic stress, p53 can induce the production of p21WAF1/Cip1, a cyclin-dependent kinase inhibitor, which can briefly arrest the cell cycle at G1 or G2. This permits the cell to remove and repair damage while also preventing damaged cells from replicating. The action of p53, which causes irreversible G1 inactivation, can also cause aging. p53 may induce apoptosis in highly injured cells by increasing the transcription of genes like PUMA and NOXA14 (Figure 2). Materials and Methods One hundred and forty Iraqi policemen affiliated with the traffic police in the city of Baghdad within the Iraqi Ministry of Interior. Their ages range between (25–65 years), during the period from July 15, 2019 to March 25, 2020. Subjects were divided into two groups as indicated below: Group 1: 70 policemen of those who were performing their duty in the crowded squares and intersections in Baghdad (Traffic police). Group 2: 70 policemen of those who were serving inside the buildings of the various traffic directorates (Office police). mailto:ashraf.r.salem@uotelafer.edu.iq 240 J Contemp Med Sci | Vol. 8, No. 4, July-August 2022: 239–244 The Effect of Pollution Represented by PAHs Original A.R. Salem et al. Fig. 1 The BaP metabolites diolepoxides and o-quinones are potent reactive metabolites that can form adducts with DNA.8 Fig. 2 The mechanism of action of p53 protein to avoid the accumulation of genetic errors.15 Six milliliters of blood were collected from each partici- pant, and the blood samples were then centrifuged for 10 min- utes at 3000 rpm to separate the serum before being aspirated, separated into aliquots, and refrigerated at 20oC until they were used for PAH. 1. Determination of PAH concentrations in serum by gas chromatography coupled with a Flame Ionization Detector (GC/FID). 2. Determination of tumor protein p53 by Enzyme-Linked Immunosorbent assay (ELISA) Kit Catalogue No. MBS2514403. 3. Determination of the serum concentration of GPX1 (Glutathione Peroxidase), by ELISA. Kit Catalog Number. E-EL-H5410. 4. Determination of the serum concentration of catalase, by ELISA Kit Catalog Number. MBS703074. 241J Contemp Med Sci | Vol. 8, No. 4, July-August 2022: 239–244 A.R. Salem et al. Original The Effect of Pollution Represented by PAHs Results The mean ± SD of age for the two groups was shown in (Table 1). Mean concentration of PAHs, levels of human p53 pro- tein, and two antioxidant enzymes (Catalase and G-px) for the two groups are shown in (Table 2), the effect of the Table 1. The mean age among the groups Group No. (Mean ± SD) of Age, Year Office police 70 38.54 ± 5.49 Traffic police 70 40.15 ± 5.7 Table 2. The mean concentration of PAHs, p53, Catalase and G-px among the groups Parameter Group Mean ± S.E. P-value PAHs, (ppm) Office police 6.91 ± 0.12 0.0001 Traffic police 8.94 ± 0.09 p53, (pg/ml) Office police 1070.7 ± 19.57 0.0001 Traffic police 1431.6 ± 39.9 Catalase activity, (pg/ml) Office police 648.15 ± 15.3 0.0001 Traffic police 398.52 ± 16.58 G-Px activity, (pg/ml) Office police 55.74 ± 2.99 0.0001 Traffic police 34.34 ± 2.2 P-value <0.05 is significant. Table 3. Comparison of studied parameters according to exposure duration for the office police group Parameter Duration of exposure Mean ± S.E. P-value PAHs, (ppm) Less than 10 years 6.7 ± 0.31 0.599 More than 10 years 6.97 ± 0.12 p53, (pg/ml) Less than 10 years 1055.4 ± 45.2 0.440 More than 10 years 1075.64 ± 21.6 Catalase activity, (pg/ml) Less than 10 years 652.12 ± 43.3 0.995 More than 10 years 646.88 ± 15 G-px, activity (pg/ml) Less than 10 years 59.89 ± 6.18 0.703 More than 10 years 54.41 ± 3.44 P-value >0.05 is non-significant. Table 4. Comparison of studied parameters according to exposures duration for the traffic police group Parameter Duration of exposure Mean ± S.E. P-value PAHs, (ppm) Less than 10 years 8.80 ± 0.21 0.487 More than 10 years 9.01 ± 0.09 p53, (pg/ml) Less than 10 years 1353.5 ± 80.07 0.491 More than 10 years 1467.47 ± 44.8 Catalase activity, (pg/ml) Less than 10 years 394.49 ± 33.7 0.947 More than 10 years 400.36 ± 18.8 G-px activity, (pg/ml) Less than 10 years 35.27 ± 5.00 0.781 More than 10 years 33.91 ± 2.28 P-value >0.05 is non-significant. exposure period to pollutants from car exhaust and diesel engines on the traffic police who are in the offices as well as the traffic police deployed in the crowded intersections of the Baghdad city are summarized in the (Table 3) and (Table 4) respectively. Discussion Exposure to these harmful substances—known as PAHs— increases the chance of developing tumors16 because these poi- sons and their reactive byproducts, such as dihydrodiols and epoxides, may attach to cellular proteins and DNA causing dire consequences17 such as mutations, developmental prob- lems, and thus cancers that occur as a result of cell damage and biochemical disturbance.18,19 242 J Contemp Med Sci | Vol. 8, No. 4, July-August 2022: 239–244 The Effect of Pollution Represented by PAHs Original A.R. Salem et al. The results of this study showed the presence of high levels of polycyclic aromatic hydrocarbons in the blood serum of the traffic police who are at the busy street intersections of the city of Baghdad, relative to the levels in the blood serum of the office police group. Since 2003, the number of passenger auto-mobiles., trucks, buses, and household generators have skyrocketed in Iraq, posing serious environmental concerns. Research was carried out by Chaichan et al.20 on and around the Muhammad Al-Qasim roadway close to the University of Technology in Baghdad, to assess the connection between the level of activity, the movement of cars with various engines, and the pollution that comes from exhaust pipes, and its was discovered that pollutants such assulfur and Polycyclic aro- matic hydrocarbons, increase during the start and end periods of the working hours of state departments. Moreover, Iraqi inhabitants employ hundreds of thousands of tiny electric generators in their houses,21 which use heavy oil or gasoline to create electricity, resulting in large quantities of soot, carbon deposits, and sulfur oxides.22 A recent study that measured air pollutants around Iraq, it showed that the highest number was recorded in Al-Diwaniyah, followed by Baghdad, specifically the Dora area.23 Our results are in agreement with several previous studies, such as24 of PAHs released by vehicles, which found that street cops have high exposures, much higher than chefs, and their exposure levels are comparable to coke fac- tory workers. Another study in China found that traffic cops have a higher risk of PM2.5 pollution in the workplace than office cops who are considered a control group.25 Among the objectives of this research is to study the impact of polycyclic aromatic hydrocarbons on the levels of p53 protein, and the results showed that the levels of this protein are affected by polycyclic aromatic hydrocarbons, as its level increased significantly in the traffic police group located in the crowded intersections of Baghdad city com- pared to the office police group, indicating that the amount of PAHs changed in direct proportion to the change in the concentration of p53 protein. On the other hand,26 discov- ered a substantial link between plasma levels of p53 and urine 1-hydroxypyrine, which is an acceptable biomarker of Polycyclic aromatic hydrocarbons exposure. Another study conducted in Saudi Arabia on professional workers during the Hajj season to appreciate the effect of intense exposure to polycyclic aromatic hydrocarbons on the cancer bio- marker proteins p53 and p21 discovered a positive engage- ment between short-term PAHs exposure and blood concentrations of p53 and p21.27 In another study, carried out by Yu et al.28 to explore the influence of prolonged expo- sure to PAHs on cellular processes occurring in mouse lung fibroblasts (mLFCs), this study concluded that long-term exposure to B a A and B a P increased the protein expression levels of p53 and p21. In most cell types examined, p53 is a short-lived nucleoprotein with a half-life of 5–20 minute. The half-life of p53 rises several times once the DNA is dam- aged.29 The activation of p53 is caused by the generation of DNA damage by a range of factors, including polycyclic aro- matic hydrocarbons and oxidative stress. This tumor sup- pressor gene encodes a protein that acts as a crucial mediator of cell cycle arrest, allowing DNA repair or starting an apop- totic cascade, and thereby preventing mutations from being passed on to daughter cells.11,30 The p53 protein’s activity may also be increased when healthy tissues experience pathophysiological alterations that cause oxidative or redox stress, such as damage from ischemia and reperfusion to the heart, brain, and other tissues. Thus the oxidative stress gen- erated by hydrogen peroxide appears to be a potent stimu- lator of p53 activity.29 Many occupational persons, such as workers in coke plants and food processing plants, are exposed to contami- nants, as are traffic policemen who are exposed to PAHs through vehicle exhaust and road dust.31 PAHs activation can be categorized into 3 paths: (1) cytochrome P450 enzymes and epoxide hydrolase catalyzes the formation of dihydrodiol epoxides (CYP/EH pathway), (2) cytochrome P450 peroxidase activity generates a polycyclic aromatic hydrocarbons reac- tive cation in metabolic oxidization, and (3) ortho-quinones are produced by dihydrodiol dehydrogenase, a member of the Aldo-ketoreductase family, oxidizing catechols (AKR pathway). Quinone redox cycling could result in the creation of ROS, which could lead to carcinogenesis through oxida- tive DNA damage.32 Defects in the p53 protein, on the other side, maybe the cause of its high levels. Faulty mutations in the gene that encodes for the p53 protein, or point mutations in this site, can disrupt the construction of a tetramer, ulti- mately in the transformation of wild-type p53 into a mutant kind and decreased function. The formation of the p53 muta- tion elongates its half-life to many hours in humans.33 Various studies regarding antioxidant enzymatic and non-enzymatic have been done in clinical investigations of different Iraqi patients.34,35 Our study chose two types of anti- oxidant enzymes (catalyze and glutathione peroxidase), to study their levels in the blood serum of the two study groups and their relationship with the levels of PAHs for both groups, found low levels in the levels of both catalase and glutathione peroxidase enzymes in the blood serum of traffic police per- sonnel deployed in Baghdad city intersections compared to the levels of the two enzymes were in the control group repre- sented by the office police, and the levels of these enzymes were inversely proportional to the levels of pollutants in the blood serum represented by polycyclic aromatic hydrocar- bons. Also, some studies conducted to evaluate the effects of occupational exposure to pollutants on oxidative stress in the body have indicated a decrease in the levels of antioxidant enzymes. In a study of pollution-exposed taxi drivers,36 reported a decrease in CAT and GSH-Px activities compared to the occupationally unexposed group. Cohort research done before, during, and after the Beijing Olympics has reported that when air pollution levels increased, indicators of total antioxidant status-declined.37 The production of a siz- able quantity of ROS by particulate matter in traffic exhausts is one theory for the reported negative health impacts. Aero- sols in the environment contain smaller, more ROS-rich par- ticles. Polycyclic aromatic hydrocarbons are also present in fine particles from vehicle exhaust (PAHs). Antioxidants have been shown to have a key part in the catalysis of the dismuta- tion of (O2) to H2O2 and the breakdown of H2O2 to H2O, respectively. When the presence of reactive oxygen species overcomes the antioxidant buffering capability, oxidative stress happens. Once antioxidant enzymes are depleted, the cell is more vulnerable to the harmful effects of xenobiotics, which can lead to cell harm or death. As a result, frequent exposure to gasoline vapors has the potential to cause oxida- tive stress by lowering the body’s antioxidant defenses’ cel- lular functions.38 243J Contemp Med Sci | Vol. 8, No. 4, July-August 2022: 239–244 A.R. Salem et al. Original The Effect of Pollution Represented by PAHs Poor nutritional status can also contribute to oxidative stress, for example, selenium deficiency, which is associated with increased oxidative stress; optimization of nutritional status of Se may result in higher G-Px activity. Small amounts of antioxidants have been associated with a greater risk of cancer in epidemiological research studies. G-Px loss resulted in endothelial dysfunction, decreased angiogenesis, and increased infarction severity and vascular permeability in experimental animals,39 as seen the activity of catalase, super- oxide dismutase, and glutathione peroxidase have a substan- tial negative relationship with the risk of coronary artery disease in patients.40 In response to oxidative stress, prolonged antioxidant enzyme deficiency enhances tissue sensitivity and severity.41 Conclusion Exposure to air pollutants like PAHs can result in lower levels of antioxidant enzymes and oxidative stress, which can damage DNA and cause a variety of cancers. However, natural biomol- ecules such as p53 protein can reverse these carcinogenic effects of PAHs. Its high levels are thus necessary to serve as an anticancer agent, reducing the effects of oxidative stress and preventing the formation of cancers in traffic cops.  References 1. Miller, M. R., (2020). 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