Monocyte to High Density Lipoprotein Cholesterol Ratio in Smokers

e-ISSN: 0975-5160, p-ISSN: 2820-2651 Available online on www.ijtpr.com International Journal of Toxicological and Pharmacological Research 2024; 14(12); 203-207 Mamta V et al. International Journal of Toxicological and Pharmacological Research 203 Original Research Article Monocyte to High Density Lipoprotein Cholesterol Ratio in Smokers Rode Mamta V.1, Jaiswal Ankita2 1Associate Professor, Department of Physiology, Government Medical College, Nagpur, Maharashtra 2Associate Professor, Department of Physiology, Government Medical College, Nagpur, Maharashtra Received: 18-10-2024 / Revised: 21-11-2024 / Accepted: 26-12-2024 Corresponding author: Dr. Mamta Rode Conflict of interest: Nil Abstract: Background: smoking is a leading cause of mortality. Smoking has been linked to low grade inflammation. Recently the monocyte to high density lipoprotein cholesterol ratio (MHR) emerged as an indicator of inflammation. So we aimed to investigate the relationship between MHR and cigarette smoking. Material and Methods: this was Hospital based cross sectional study. 25-35 years old 200 males were included in the study & divided in two groups. Smoker group comprising 100 smokers having duration of smoking more than 3 years. 100 randomly selected non-smokers were included in the non-smoker group. Detailed history, smoking habits number of cigarette smoked per day and pack year was calculated. Complete blood count was done by procon PE 600 automated analyzer. Total cholesterol, HDL cholesterol, triglyceride was measured on AU 5800 Backmann coulter fully automated biochemical analyzer using enzymatic colorimetric assay. Statistical analysis was done by unpaired student 't' test. Correlation was determined by Pearson correlation Coefficient test. Result: MHR was significantly higher in smokers as compared to non-smokers (14.4 + 2.02, 11.1 + 1.98 respectively). Pearson's correlation analysis revealed significant positive correlation between pack years, number of cigarette smoked daily and MHR in smokers group. Monocyte to high density lipoprotein can be used as a surrogate marker of inflammation and endothelial dysfunction. Keywords: smoking, monocyte to high density lipoprotein cholesterol ratio (MHR) inflammation.. This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided original work is properly credited. Introduction Smoking is the most important public health problem according to WHO 2.4 billion people worldwide have consumed tobacco in the form of chewing sniffing or dipping. WHO estimates tobacco related deaths to 8.3 million in 2030 and 1 billion deaths during the 21st century [1]. Toxic ingredients in cigarette smoke circulate throughout the body causing damage in several different ways. The burning tobacco and paper produce more than 4000 chemical compounds in form of gases, vapors particulates like carbon monoxide hydrogen cyanide phenols Ammonia formaldehyde Benzene nitrosamines nicotine and tar [2] 194 million man and 45 million women use tobacco in smoke or smokeless form in India [3]. Smoking has been linked to low grade systemic inflammation as reflected in elevated white blood cell count a well established predictor of myocardial infarction cancer and chronic obstructive pulmonary disease. Cigarette smoke contains oxidant free radicals that are capable of initiating or promoting oxidative damage leading to degenerative pulmonary, cardiovascular disease and cancer [4]. Oxidative damage to unsaturated lipid is a wellestablished general mechanism for oxidant mediated cellular injury [5]. Smoking is associated with a more atherogenic lipid profile [6] several toxins present in cigarette smoke have immunomodulatory effects. Cigarette smoke constituents induce chronic inflammation at the mucosal surface and modify the host response to exogenous antigen [7]. The ratio of monocyte to high density lipoprotein cholesterol ratio was defined as a cardiovascular prognostic marker indicating the extent of inflammation and oxidative stress. [7,8,9] So we planned the study to analyze the effect of cigarette smoking and its intensity with the lipid profile and MHR ratio. International Journal of Toxicological and Pharmacological Research e-ISSN: 0975-5160, p-ISSN: 2820-2651 Mamta V et al. International Journal of Toxicological and Pharmacological Research 204 Material and Methods The study was approved by institutional ethical committee. study conducted at tertiary Health Care Centre. 200 male participants aged 25 to 35 years were included in the study. Participants were divided in two group: 1) smoker group comprised, 100 smokers having duration of smoking more than 3 years. 2) non-smoker group included 100 non-smokers selected randomly from the general population. Exclusion criteria. Patients with presence of chronic disease such as Diabetes mellitus, hypertension, coronary artery disease, heart failure, chronic lung disease, connective tissue disease, chronic kidney disease, metabolic syndrome, leukocytosis, leukopenia or other hematological biochemical or serological abnormalities were excluded. Subjects consuming lipid lowering drugs, steroids, hematinic were excluded. Detailed data about smoking habits was collected using structural interviewing questionnaires. Smoking characteristics such as the number of cigarettes smoked daily, Number of Pack year was calculated. Pack year represents a combined measure of dose and duration of smoking. Pack year was calculated as the number of cigarettes smoked per day * number of years smoked / 20. Standing height in centimeter was measured by asking the participants to stand bare feet against the wall on which the measuring scale was inscribed ( 10 ) Weight was measured in kilograms with KRUPS weighing machine in lightweight garments without footwear. Body mass index was calculated using Quetelet's formula - Body weight in kilogram / height meter squared. Blood pressure was measured with sphygmomanometer by the standard auscultatory Riva Rossi method. Random blood sugar was measured. Venus blood sample was collected after 12 hours of fasting from the antecubital vein with all aseptic precautions. Blood was drawn and transferred into EDTA and plain bulb equally. Hematological parameters were studied by Procan PE 600 three part differentiated automated hematology analyzer. Total cholesterol HDL cholesterol triglyceride was measured on AU 5800 Backmann coulter fully automated biochemical analyzer. LDL cholesterol was calculated by friedwald formula. Statistical analysis. Statistical analysis was done by software SPSS version 22. Continuous variables were expressed as mean and standard deviation. Analysis was done by unpaired 't' test and correlation by Pearson correlation test. Result The mean age, weight, height and body mass index was matched in both smoker and non-smoker group. There was no statistical difference in age, height, weight and body mass index of smoker and nonsmoker group. The study included 200 participants. It was observed that monocyte, High density lipoprotein Cholesterol ratio values for the smoker group was significantly higher in smokers than those of non-smoker group (Respectively14.4+/-2.02 and 11.1+/- 1.98). Triglyceride low density lipoprotein cholesterol, total cholesterol, leukocyte count monocyte values for the smoker group were significantly higher than those of the non-smoker group. High density lipoprotein cholesterol value was significantly less in smoker group than non-smoker group. There was significant positive correlation between pack year, number of cigarette smoked daily and monocyte to high density lipoprotein cholesterol ratio. There was positive correlation between Triglyceride, total cholesterol, low density lipoprotein cholesterol and pack year, the number of cigarette smoked daily in smoker group. There was negative correlation between high density lipoprotein cholesterol and pack years, the number of cigarette smoked daily in smoker group. Table 1: Anthropometric Characteristics of Smokers and non-smokers Variable Smokers Non Smokers P value Age (years) 29.38 + 1.95 28.44 + 1.25 NS Weight (kg) 57.68 + 5.07 56.67 + 4.71 NS Height (Cm) 158.58 + 5.03 156.57 + 4.75 NS BMI kg/m2 23.10 + 1.85 23.28 + 1.54 NS International Journal of Toxicological and Pharmacological Research e-ISSN: 0975-5160, p-ISSN: 2820-2651 Mamta V et al. International Journal of Toxicological and Pharmacological Research 205 Table 2: comparison of Hematological and lipid profile in Smokers and Non Smokers Variable Smokers Non Smokers P value WBC X 103/mm3 14.67 + 5.19 8.28 + 3.76 S Monocyte x 103/mm3 0.75 + 0.53 0.55 + 0.31 S Total cholesterol mg/dl 194.21 + 12.05 175.38 +11.32 S Triglyceride mg/dl 107.12 +25.21 96.12 + 14.25 S HDL Cholesterol mg/dl 49.01 + 5.47 53.34 + 3.14 S LDL Cholesterol mg/dl 123.4 + 10.32 106.81 + 8.85 S Monocyte to HDL Cholesterol Ratio ( MHR Ratio) 14.4 + 2.02 11.1 + 1.98 S Table 3: Correlation analysis between Smoking as pack years, MHR & Blood lipid profile Variable pack years r P Value MHR 0.254 S Monocyte x 103/mm3 0.203 S HDL Cholesterol (mg/dl) - 0.104 S Triglyceride (mg/dl) 0.231 S Total cholesterol (mg/dl) 0.195 S Low density Lipoprotein cholesterol(mg/dl) 0.198 S Table 4: Correlation analysis between the number of cigarettes smoked daily MHR and blood lipid levels. Variable The number of cigarettes smoked daily r P Value MHR 0.329 S Monocyte x 103/mm3 0.295 S HDL Cholesterol (mg/dl) -0.279 S Triglyceride (mg/dl) 0.293 S Total cholesterol (mg/dl) 0.105 S Low density Lipoprotein cholesterol 0.132 S Discussion In the present study we found that the monocyte to High density lipoprotein ratio was significantly higher in the smoker group than non-smoker group. Total cholesterol and Triglycerides was significantly higher in the smoker group. According to several recent studies exposure to cigarettes smoke impairs functional structure of endothelial cells. Nicotine and increase oxidative stress generated from smoking induce vascular endothelial dysfunction via the inhibition of endothelial nitric oxide synthase and decreasing generation of nitric oxide [10,11]. Nicotine increases the expression of adhesion molecules in endothelial cells such as E select and intracellular adhesion molecule because of enhanced attachment and transmigration of monocytes in the vessel wall. [12]. It is evident that these results suggest that smoking is an established risk factor for atherosclerosis through several underlying pathways. Monocytes are a distinct type of leukocytes which have a key role in inflammation and atherosclerosis process [13]. Activated monocytes interact with damaged or activated endothelium which result in over expression of pro inflammatory cytokines / adhesion molecules and intracellular adhesion molecule. There after monocytes differentiate into the macrophages that ingest oxidized LDL-C and form dangerous foamy cells[14]. In another study The Count of circulating monocytes was found to be a predictor for new plaque development as well. [15] however HDL-C features anti-inflammatory antioxidants and antithrombotic effect. [14.16.17] HDLC can prevent inflammatory response by acting directly on monocytes. Recent studies indicate the role of HDL -C in modulating monocyte activation adhesion and in controlling the proliferation of progenitor cells that differentiate to monocyte. HDL-C also prohibits oxidation of LDLC IN addition to inhibition of macrophages migration. It also removed oxidized LDL-C from foamy cells. [16,17,18,19,20]. Therefore monocytes show a pro inflammatory effect but HDL-C functions as reversal factor during the process. It has been suggested that MHR has a relationship with systemic inflammation and endothelial dysfunction and it is accepted as newly recognized inflammation based diagnostic and prognostic marker in cardiovascular disease [21,22,23,24]. Recently Acikgoz et all assessed International Journal of Toxicological and Pharmacological Research e-ISSN: 0975-5160, p-ISSN: 2820-2651 Mamta V et al. International Journal of Toxicological and Pharmacological Research 206 endothelial functions using flow and nitroglycerine mediated dilation technique and calculation of MHR. The study reported there was a strong inverse correlation between MHR and flow mediated dilatation. Therefore elevated MHR may be a useful marker reflecting impaired endothelial function and systemic inflammation[25]. The relationship between smoking systemic inflammatory response, vascular endothelial injury and atherosclerosis has been well defined MHR can be used as a surrogate marker of inflammation and endothelial dysfunction. Conclusion MHR is a simple easy cost-effective tool that should be used for predicting the systemic inflammatory response and possible endothelial dysfunction in smokers. Cases with high MHR can easily be identified during routine complete blood analysis and could possibly benefit from preventive treatment. Therefore more attention should be given to these indices in the examination of smokers. Declaration by Authors Ethical Approval : Approved Acknowledgement : None Source of funding : None Conflict of Interest : The authors declare no conflict of interest References 1. Ojtuna F, cellular effects of smoking, Lung Archieve 2000: 2: 111-6 2. Tirlapur VG, Gicheru K, Charalambous BM, Evans PJ, Mir MA Packed cell volume, haemoglobin and oxygen saturation changes in healthy smokers and nonsmokers Thorax 1983 oct: 38 (10):785-7 3. Sinha DN, Gupta PC Padnekar MS Tobacco use in rural area of Bihar Indian journal community medicine 2003: 28 (4): 10-12 4. Panda K, Chattopadhyay R Ghosh MK, Chattopadhyay DJ and Chatterjee IB Free Rad, Biol Med 1999: 27: 1063-1079 5. Yogi K Lipid peroxides and related radicals in clinical medicine AdvExo Med Biol1994: 366: 1-15 6. Luo HL Zang, W. J. Lu, J Yu, XJ Lin YX Cao YX The protective effects of Captopril on nicotine induced endothelial dysfunction in rat Basic Clin Pharmacol Toxicol 2006:99:237-245 7. Lee J, Taneja V, Vassal R Cigarette smoking and inflammation cellular and molecular mechanisms J Denta Res 2012:9:142-149 8. Compolet U, Cetin E. H, Cetin S, Aydin S, Akobga MK, Yayla C, Turak O, Aras D, A. Y Clogdu S association of monocyte to HDL cholesterol ratio with slow coeonary blood flow is linked to systemic inflammation. CliniapplthrombHenost 2019:22:476-482 9. Akboga MK, Balci KG, MadenoErtemAG, Kirbas O, Yayla C, Acar B, Arad D, Kisacik H, Aydogdu S. Usefulness of monocyte to HDL cholesterol ratio to predict high SYNTEX score in patients with stable coronary artery disease. Biomark. Med2016:10:375-383 10. National health and nutrition examination survey (NHANES): Anthropometry procedures manual, center for disease control and prevention 2007 11. Li H Shrinivasan SR, Chen W, Xu JH, Li S, Betensan GS. Vascular abnormalities in asymptomatic healthy young adult smokers without other major cardiovascular factors. The Bogalusa heart study Am J Hypertension 2005:18:319-324 12. Heeschen C, Weis M, Cooke JP. Nicotine promotes arteriogenesis. J Am cill.Cardiol 3003:41:488-496 13. Ancuta P Wang J. Gabuzda DCD 16+ monocytes produce IL-6, CCL 2, andmatrixmetalli proteinase -9 upon interaction with CX3CL1 expressing endothelial cells J LewkocBiol 2006:80:1156-1164 14. Ghattas A, Griffiths HR, Devitt A, Lip GY, shantilaE,onocytes in coronary artery disease and atherosclerosis, where are we now? J Am collcardiol 2013:62:1541-1551 15. Giratchev A Sobenin I, Orekhob A, Kzhyshkowaska J. Monocytes as a diagnostic market of cardiovascular disease immunobiology2012:217:476-482 16. Murphy AJ, Chindusting JP, Sviriclav F, Woodlard KJ. The anti-inflammatory effects of high-density lipoproteins. Curr. Mef. Chem 2009:16:667-675 17. Murphy A. J, Woodlard K. J. High density lipoprotein: A potent inhibitor of inflammation. Clin. Exp. Pharmacol, Physiol. 2010:37:710718 18. YvanCharvet J, Pagler T, Gautien EL, Avagyan S, Siry RI, Han S, Tall AIP binding cassette transporters and HDL suppression hematopoietic stem cell proliferation science 2010:328:1689-1693 19. Murphy AJ, Woodlard K. J, Hoang A, Mukhamedova N, Stirzaber R. A, Mccormick S P, Chin Dusting J high density lipoprotein reduces the the human monocyte inflammatory response Arteriosclet Thrombvasc Biol 2008: 28:2071-2077 20. Burke AP, Garb A, Malcom GT, Liang YH, Smialek J Virmani R Coronary risk factors and plaque morphology in men with corinary International Journal of Toxicological and Pharmacological Research e-ISSN: 0975-5160, p-ISSN: 2820-2651 Mamta V et al. International Journal of Toxicological and Pharmacological Research 207 disease, who died suddenly. N EngL J Med 1997:336:1276-1282 21. Kanbay M, Solak Y Unai HU Kurt YG, Gok M, Cellinkaya H, Covic A. Monocyte count/ HDL cholesterol ratio and cardiovascular events in patients with chronic kidney disease Int Urol. Nephrol 2014:46:1619-1625 22. Canpolat U, Aytemir K, Yorgun H, Sahner L, Kaya EB Kay S, Ota A The role of preprocedural monocyte ti high density lupi protein in prediction of atrial fibrillation recurrence after cryoballoon based catheter ablation Eurospace 2015:17:1807-1815 23. Celin EH, Celin MS, Canpolat V, Aydin D Topalogu S, Aras D, Aydogdu S. Monocyte / HDL cholesterol ratio predicts the definite stent thrombosis after primary per cutaneous coronary intervention after ST segment elevation myocardial infarction. Biomark Med 2015:9:967-977 24. Acikgiz N, Kurtoglu E, Yagmur J, Kapicisglu Y, Cansel M, Ermis N. Elevated monocyte to high density lipoprotein cholesterol ratio and endothelial dysfunction in Behcet disease. Angiology, 2018:69:65-7 25. Zhou MS, Chandipiralla K, Mendoz AJ, Jaimes EA, Silverstein RL, Webstin K Raij K Nicotine potentiates pathogenic effects of LDK by stimulating and upregulating macrophages CD36 signalling. Am J Physiol Heart circPhysiol 2013: 305:H563H574