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Year : 2017  |  Volume : 6  |  Issue : 3  |  Page : 158-162

The assessment of systemic inflammatory response in apparently healthy adult smokers in Nnewi, South East Nigeria

1 Department of Medical Laboratory Science, College of Health Sciences, Nnamdi Azikiwe University, Nnewi, Anambra, Nigeria
2 Department of Haematology, Faculty of Medicine, College of Health Sciences Nnamdi Azikiwe University, Nnewi, Anambra, Nigeria

Date of Web Publication25-Sep-2017

Correspondence Address:
John C Aneke
Department of Haematology, Faculty of Medicine, College of Health Sciences, Nnamdi Azikiwe University, PMB 5001, Nnewi, Anambra
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Source of Support: None, Conflict of Interest: None


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Background: Induction of systemic inflammation is thought to underlie major organ dysfunction in cigarette smokers.
Objective: The objective of the study is to estimate the levels of inflammatory markers (the leukocyte count and C-reactive protein [CRP]) in adult smokers in Nnewi metropolis, South East Nigeria.
Subjects and Methods: A total of 120 adults, comprising of 60 smokers and age-matched nonsmokers, respectively were recruited. Five millilitre of venous blood was collected from each participant, of which 2 ml was used for full blood count estimation, using the Sysmex NX® hematology analyzer, while 3 ml was dispensed into plain tube and serum was extracted for CRP measurement, using the ELISA technique. Statistical analysis was done using SPSS (version 20), the students t-test was used for the comparison of means, and level of statistical significance set at (P < 0.05).
Results: The serum CRP level was significantly higher in smokers compared with controls (P < 0.001) and the neutrophil count, neutrophil/lymphocyte ratio (NLR), and CRP were significantly higher in study individuals with smoking history of >5 years, compared with those whose smoking history was <5 years (P = 0.001, 0.001, and <0.001, respectively). The white cell count, eosinophil count, and serum CRP levels were significantly higher in individuals who smoked >5 sticks of cigarettes in 1 month (P = 0.023, 0.004, and <0.001, respectively).
Conclusion: Cigarette smoking is associated with a significant acute inflammatory response which becomes exaggerated with increasing duration and frequency of exposure.

Keywords: Cigarette smoking, C-reactive protein, leukocyte count, systemic inflammation

How to cite this article:
Ibeh NC, Aneke JC, Okocha CE, Mmaduka C. The assessment of systemic inflammatory response in apparently healthy adult smokers in Nnewi, South East Nigeria. J NTR Univ Health Sci 2017;6:158-62

How to cite this URL:
Ibeh NC, Aneke JC, Okocha CE, Mmaduka C. The assessment of systemic inflammatory response in apparently healthy adult smokers in Nnewi, South East Nigeria. J NTR Univ Health Sci [serial online] 2017 [cited 2021 May 11];6:158-62. Available from: https://www.jdrntruhs.org/text.asp?2017/6/3/158/215519

  Introduction Top

Tobacco use is said to cause as much as 6 million deaths globally each year; this has been postulated to increase to over 8 million annually by 2030, with 80% of these preventable deaths occurring in low- and middle-income countries.[1],[2] Smoking has been reported to be associated with an increase in serum levels of a variety of inflammatory markers such as C-reactive protein (CRP), fibrinogen, albumin, and leukocytes, with a consequent increase in plasma viscosity.[3] Leukocytes are an essential element of the inflammatory process and have been shown to be an independent predictor of coronary heart disease in smokers.[4],[5] A possible explanation for leukocytosis in smokers could be the so-called cell trafficking phenomenon, which involves cells moving from lymphoid organs to the peripheral blood and also a probable reduction in the fraction of these in the marginated pool.[6]

Cigarette smoking is a major risk factor for the development of a number of inflammatory conditions, the risk of which could be assessed by measuring serum high sensitive CRP (HSCRP) level.[7] In fact, low-grade inflammation, indicated by high serum acute phase reactants such as HSCRP and fibrinogen is thought to be a risk factor for developing future cardiovascular complications.[8],[9],[10] There is increasing evidence on the direct correlation between cigarette smoking and many cardiovascular and respiratory complications, including morphological changes of vessel walls.[11] Cigarette smoke contains many toxic components, such as carbon monoxide, hydrogen cyanide, benzopyrene, and oxygen radicals which could predispose to cardiac and pulmonary dysfunction and even a number of cancers.[12],[13]

Even though some studies have earlier observed increased markers of systemic inflammation among smokers, there is paucity of report on this, particularly in the South East Nigerian population. It was therefore based on this knowledge gap that the present study was designed, with a view to estimating the total leukocyte count/differentials and serum CRP level, as markers of systemic inflammation, in adult male smokers in Nnewi metropolis, South East Nigeria.

  Subjects and Methods Top

Research design

The research was cross-sectional, designed to measure the serum level of CRP, leukocyte, and differential count among adult male smokers in Nnewi, Anambra State, Nigeria. The study individualswere recruited by simple random sampling, prospective participants were administered a questionnaire which was structured to collect data on medical history to determine suitability for the research as well as individual lifestyle, including the duration and frequency of smoking.

Study population

The study population comprised of 120 adult males who reside in Nnewi North Local Government Area of Anambra state, aged between 18 and 40 years. They comprised of 60 smokers as test individuals and 60 nonsmokers who formed the control group. The inclusion criteria included smoking history of at least 6 months before the time of recruitment.

Individuals with medical condition which are known to be associated with systemic inflammation such as HIV, tuberculosis, diabetes mellitus, or who had a fever or indeed any form of ill health were excluded from the study.

Sample collection

Each participant had 5 ml of venous blood collected following standard protocol for venesection, 2 ml was dispensed into a potassium-ethylene diamine tetra acetic acid container for full blood count estimation, using the Sysmex NX® automated (five-part differential) hematology analyzer. The remaining 3 ml was dispensed into the plain tube, allowed to clot, spun at 5000 rpm, and the serum extracted (and stored at −20°C until batch testing) for CRP measurement, using an immunometric assay, based on the double-antibody sandwich technique. Each well of the immunometric microplate was supplied with the kit precoated with a monoclonal antibody specific for human CRP (mouse anti-human CRP) which will bind to any human CRP introduced into the well. Standards and samples were incubated on the antibody-coated plate, and horse radish peroxide-labeled CRP monoclonal antibody was added to detect any captured CRP, the two antibodies formed a sandwich by binding to different locations on the CRP molecule. The concentration of the analyte was determined by measuring the enzymatic activity of horseradish peroxidase using the chromogenic substrate, tetramethylbenzidine. The reaction was stopped after the formation of a product with a distinct yellow color, which was subsequently measured at 450 nm.

Ethical issues

Ethical approval was obtained from our institution ethic and research committee and written informed consent was obtained from all participants at the point of recruitment.

Statistical analysis

Statistical Package for Social Science, Version 20. 0 (SPSS Inc., Chicago, IL, USA) was used for all data analysis and results were presented as mean ± standard deviation (SD). The Student's t-test was used to compare two means while the level of statistical significance was set at P < 0.05.

  Results Top

The mean value of CRP was significantly higher in smokers compared with nonsmokers (9.66 ± 3.62 mg/L vs. 1.53 ± 0.18 mg/L, P < 0.001), while the lymphocyte and monocyte counts were significantly lower in smokers compared with nonsmokers (P = 0.02 and < 0.001, respectively), [Table 1].
Table 1: Comparison of Means±Standard Deviation of C-Reactive Protein, Leukocyte Count, and Differentials in Smokers and Nonsmokers

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Correspondingly, the neutrophil count, neutrophil/lymphocyte ratio (NLR), and serum CRP levels were significantly higher in study individuals with smoking history >5 years (P = 0.001, 0.004, <0.001, and 0.001, respectively) [Table 2].
Table 2: Comparison of Serum C-Reactive Protein, Leukocyte, and Differential Counts in Smokers Based on Duration of Smoking

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The white cell count, eosinophil count, and serum CRP levels were significantly higher in individuals who smoked >5 sticks of cigarettes in 1 month (P = 0.023, 0.004, and <0.001, respectively) [Table 3].
Table 3: Comparison of Serum C-Reactive Protein, Total Leukocyte, and Differential Counts in Smokers Based on Smoking Frequency (Per Month)

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There were no significant differences in serum CRP levels, leukocyte, and differential counts in study individuals with different age distributions (P > 0.05).

  Discussion Top

The present study considered the effect of smoking status on white blood cell and CRP levels in adult male smokers. The findings showed that the mean serum HSCRP level was significantly higher in smokers compared with nonsmokers (9.66 ± 3.62 mg/L vs. 1.53 ± 0.18 mg/L, respectively, P < 0.01), [Table 1] Siasos et al.,[14] had earlier implicated cigarette smoking as a risk factor for the development of systemic inflammation and end organ dysfunction in chronic smokers. Inflammation is associated with increased release of polymorphonuclear neutrophil from the bone marrow and consequent rise in secretion of pro-inflammatory cytokine interleukin (IL)-1b, IL-6, and tumor necrosis factor-α. These cytokines, in turn, bind to hepatocyte surface receptors and induce increased serum concentration of HSCRP.[14],[15]

This study equally noted that the mean values of total white blood cell count were higher in smokers than in nonsmokers, this difference approached statistical significance (P = 0.081), [Table 1]. Earlier independent studies had observed significantly higher white cell count in smokers compared with nonsmokers.[16],[17] The mechanism responsible for associated elevated leukocytes count is thought to be related to the occurrence of acute inflammatory response induced by particulates of cigarette smoke in smokers, which leads to increased release of white cells from the bone marrow, as well as a reduction in the marginated pool fraction.[18] In addition, nicotine may also produce smoking-induced leukocytosis through circulating catecholamine, as an increase in endogenous hormones levels such as epinephrine and cortisol have been reported, to increase total leukocytes count.[19] While leukocytosis may simply be a marker of smoking-induced tissue damage, the high count can promote cardiovascular diseases through multiple pathologic mechanisms that mediate inflammation, plugging of the microvasculature, induction of a hypercoagulability state, and promotion of infarct expansion.[20],[21]

Reports on differential counts in cigarette smokers have consistently shown that increased granulocyte count (particularly neutrophils) is associated with cigarette smoking.[22],[23],[24] The finding from this study is in keeping with this postulation; there was a significant increase in neutrophil count in smokers when compared to nonsmokers [Table 1], it may thus appear that cigarette smoking induces acute (and not chronic) inflammation in our population. The increased neutrophil count could alter blood rheology by causing an increase in endothelial-dependent dilatation and may contribute to the blocking of micro vessels which is a common prelude to overt cardiovascular complications.[25]

Significant differences were observed between total leukocyte and differential counts and duration and frequency of smoking. Study participants with >5 years smoking history had significantly higher neutrophil count, NLR and serum CRP levels (P = 0.001, 0.004, <0.001, and 0.001, respectively) [Table 2]. Similarly, higher frequency of smoking (>5 sticks per month) was associated with a significantly higher total leukocyte and eosinophil counts as well as serum CRP (P = 0.023 and 0.004, respectively) [Table 3]. This observation thus implies a dose dependent relationship, with a more pronounced inflammatory response seen in heavier smokers; these results are consistent with previous studies.[22],[26],[27],[28],[29] The authors equally find the increase in eosinophil count which occurred with increasing frequency of smoking in this study instructive [Table 3]. Since eosinophil counts become markedly increased in a number of hypersensitivity and allergic reactions,[30] the higher count in smokers may thus be related to allergic responses to components of cigarette smoke in chronic smokers. Indeed allergic responses (such as allergic rhinitis) may be a prelude to more serious adverse respiratory symptoms, such as bronchial asthma.[31]

There were also significantly lower lymphocyte and monocyte counts in smokers when compared to the control in this study (P = 0.002 and <0.001, respectively), [Table 1]. Since these 2 markers predominantly mediate chronic inflammatory response,[32] this finding may, therefore, put additional credence to our postulation that acute inflammation (as opposed to chronic inflammation) is a more predominant feature among cigarette smokers in our population. The increased NLR observed in the smokers in this study is in keeping with previous reports which all agree with the argument that cigarette smoking induces a pro-inflammatory state which becomes more prominent as the length of exposure increases.[22],[26],[27],[28],[29]

  Conclusion Top

Dose-dependent activation of significant inflammatory response as seen in our apparently healthy adult cigarette smokers is as previously reported in other parts of the world. This may well underlie the protean (mainly cardiovascular and respiratory) complications associated with this life style. The acute inflammatory response appeared to predominate in our data set, as evidenced by the more prominent increase in markers associated with acute (as opposed to chronic) inflammation in this study. These markers could become potential tools for risk stratification, particularly in chronic smokers (with high risk of end organ dysfunction) and for monitoring of participants on cigarette cessation programs.

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Conflicts of interest

There are no conflicts of interest.

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  [Table 1], [Table 2], [Table 3]


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