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Quantitative Assessment of Serum C - Reactive Protein Levels among
Smokers and Non Smokers
1
Dr. Vegendla Swathi.,
2
Dr. Ruttala Sai Praveena.,
2
Dr. Perupaga Sudheera.,
2
Dr. Manem Bala Murali
Krishna.,
3
Dr. K. Lalith Prakash Chandra.,*
4
Dr. Kiran Kumar Kattappagari
1,2
Postgraduate student, Department of Oral & Maxillofacial Pathology, Sibar Institute of Dental
Sciences, Takellapadu, Guntur – 522506, India
3
Professor, Department of Oral & Maxillofacial Pathology, Sibar Institute of Dental Sciences,
Takellapadu, Guntur – 522506 Andhra Pradesh, India
4
Professor & HOD, Department of Oral & Maxillofacial Pathology, Sibar Institute of Dental Sciences,
Takellapadu, Guntur – 522506 Andhra Pradesh, India
*Corresponding Author
DOI: https://doi.org/10.51244/IJRSI.2025.120800154
Received: 01 Aug 2025; Accepted: 07 Aug 2025; Published: 16 September 2025
ABSTRACT
Background: Recent progress in the comprehension of intricate tumor interactions has resulted in the
identification of a link between inflammation and cancer. A high level of pro-inflammatory cytokines within
the tumor microenvironment can stimulate angiogenesis, thereby promoting neoplastic proliferation. Serum C-
reactive protein serves as a sensitive indicator of inflammation and could possess considerable prognostic
significance as an early biomarker for cancer diagnosis. Aims and Objectives: To quantitatively measure
serum C-reactive protein levels in both smokers and non-smokers, as well as to assess its role in cancer
development. Materials and Methods: The study included a sample of 25 non-smokers and 25 smokers. All
samples underwent C-reactive protein testing using immunoturbidimetry. The observations were analyzed
statistically. Statistical analysis: The data was entered into the database management system of SPSS version
20.0. An independent t-test and Mann-Whitney U test were utilized to compare the C-reactive protein levels
between two groups. For pairwise comparisons, Tukey's multiple post hoc procedure was employed. Results:
The average C-reactive protein level in non-smokers was 55.24±12.0312, while in smokers, it was
55.88±11.76. In smokers, the C-reactive protein level was slightly higher compared to non-smokers. The
comparison between non-smokers and smokers regarding C-reactive protein values showed statistical
significance, with a p-value of ≤0.05. Conclusion: Our results indicate that the concentration of serum C-
reactive protein was higher in smokers and is linked to an increased risk of developing oral cancer, potentially
serving as a biomarker.
Key words: C reactive protein, Smokers, Non – smokers, Cancer
INTRODUCTION
The link between smoking and the rise in morbidity and mortality is well-established, and current statistics
suggest that out of the one billion smokers globally, 500 million are likely to die prematurely due to smoking-
related illnesses. Smoking has been proven to adversely affect many organs, and the array of diseases
associated with smoking as a contributing factor is vast. C-reactive protein (CRP) is a well-recognized
biomarker indicating systemic inflammation, synthesized by the liver in reaction to pro-inflammatory
cytokines, especially interleukin-6 (IL-6). Elevated levels of CRP correlate with a higher risk of cardiovascular
diseases, diabetes, and various other chronic health issues. As a highly sensitive marker of inflammation, CRP
is frequently utilized in both clinical and research environments to evaluate an individual’s inflammatory
condition.
4
Tobacco smoking is a significant modifiable risk factor for several illnesses, such as several
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
ISSN No. 2321-2705 | DOI: 10.51244/IJRSI |Volume XII Issue VIII August 2025
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malignancies, coronary artery disease, and chronic obstructive pulmonary disease (COPD).
5
Additionally, it
causes systemic inflammation via oxidative stress and the activation of inflammatory pathways. According to
numerous studies, smokers often have higher CRP levels than nonsmokers, which may be a sign that the
body is continuously reacting to the hazardous components of tobacco smoke with inflammation.
6
There are two theories that explain how CRP functions within cages during inflammation. The first is referred
to as the induction hypothesis, which suggests that acute or chronic inflammation raises SRB levels, resulting
in excessive cell growth and permanent DNA damage. The second theory focuses on the host's immune
response and is termed the "response hypothesis."
7
This theory posits that the immune response to cancer
triggers an increase in CRP levels. However, it remains unclear how SRB levels rise at the onset of cancer, and
whether they should be regarded as a potential risk factor for cancer development is consistently highlighted.
8
The aim of the study was quantitative assessment of serum C reactive protein levels in potentially malignant
disorders (PMDS) and to evaluate their significant role as a prognostic marker.
MATERIALS AND METHODS
The cross-sectional study involved individuals who visited the department of Oral & Maxillofacial Pathology
and Oral Microbiology for hematological assessments. This study received ethical approval
(132/IEC/SIBAR/2023) from the Institutional Ethics Committee. The sample size was calculated using
G*Power 3.1.9, with an α of 0.05, an effect size of 0.060, and a power level of 0.08, corresponding to a p-
value of 0.05, resulting in a total of twenty-five samples in each group. The study included twenty-five non-
smokers and twenty-five smokers, with the inclusion criteria requiring participants to be individuals attending
for oral prophylaxis, with a history of smoking or no smoking habits. The exclusion criteria encompassed
individuals with systemic illnesses or those on long-term medication. Informed consent was obtained from all
individuals willing to participate in the study. Blood samples of 5 ml were collected from all fifty participants,
and serum was separated. The serum levels of C-reactive protein were measured using immunoturbidimetry
methods (Bio Majestry R JCA-BM), with the normal reference range defined as ≤ 10 mg/dl.
Statistical analysis
Data entry and analysis was performed using the software SPSS version 20.0. Descriptive statistics was used to
determine the frequency, percentage, mean, median, SD and range. The mean C reactive protein in both the
groups was done using independent t-test and pair wise comparisons of two groups with respect to C- reactive
protein values was done by Mann-Whitney U test.
RESULTS
The total number of individuals who participated in this study was fifty, consisting of twenty-five non-smokers
and twenty-five smokers. Within the non-smoker group, there were twelve males and thirteen females, while
all twenty-five individuals in the smoker group were male. When comparing non-smokers and smokers
regarding mean age using an independent t-test, the non-smokers had a mean age of 55.24 ± 12.03, compared
to 55.88 ± 11.76 for smokers. The maximum age range for non-smokers was 56-65 years, whereas for smokers
it was 46-55 years. The comparison of mean ages between non-smokers and smokers using an independent t-
test did not yield statistically significant results (p ≥ 0.05) (Graph 1). When examining C-reactive protein
levels between non-smokers and smokers using the Mann-Whitney U test, smokers exhibited higher levels at
55.88 ± 11.76, while non-smokers had levels of 55.24 ± 12.03. The comparison of C-reactive protein values
between non-smokers and smokers was statistically significant with p ≤ 0.05 (Table 1). The normality of C-
reactive protein values in both non-smokers and smokers, assessed by the Shapiro-Wilk test, showed a highly
statistically significant result with p ≤ 0.05 (Table 2). The receiver operating characteristic curve (ROC)
graphical plot illustrates the predictive capabilities of C-reactive protein values for identifying smokers (Graph
2).
DISCUSSION
The connections between smoking and higher rates of illness and death are well documented, and current
INTERNATIONAL JOURNAL OF RESEARCH AND SCIENTIFIC INNOVATION (IJRSI)
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projections suggest that out of the one billion smokers globally, 500 million will suffer premature deaths due to
tobacco-related illnesses
.1
Smoking has harmful effects on various body organs, and a comprehensive list of
diseases associated with smoking is extensive.
2
It has been widely recognized that cigarette smoking is a
significant and traditional risk factor for the onset of cardiovascular disease (CVD) and atherosclerosis.
10,5
Recently, it has been acknowledged that CVD has an inflammatory component and is even referred to as an
inflammatory condition.
11
Furthermore, a connection has been established between smoking and several
chronic inflammatory conditions, including chronic obstructive pulmonary disease (COPD), rheumatoid
arthritis, systemic lupus erythematosus, and Crohn’s disease.
12,13,14
While the precise mechanisms that link
smoking to these conditions are not fully understood, there has been a growing interest in exploring the
relationship between smoking and inflammatory markers as a means of uncovering smoking-related disease
explanations. One such marker, C-reactive protein (CRP), can be measured easily and sensitively in various
clinical contexts to track disease progression.
4
The incidence of smoking-related illnesses has been rapidly
increasing in our country over the past twenty years, primarily due to habits like tobacco use in forms such as
chewing or smoking. Numerous researchers are actively working to combat this deadly addiction.
15
The current research quantitatively measured serum C-reactive protein (CRP) levels in both non-smokers and
smokers to investigate the inflammatory effects of tobacco consumption. Our results indicate that smokers
have notably higher C-reactive protein levels than non-smokers, which supports the idea that smoking leads to
a persistent low-grade inflammatory condition. These results align with the findings of Black S et al. from
2004. The increase in CRP levels in smokers is consistent with existing research that shows tobacco smoke
contains various pro-inflammatory agents, such as reactive oxygen species (ROS) and other harmful
substances, which contribute to endothelial dysfunction and systemic inflammation
16
Notably, nicotine and
carbon monoxide are known to trigger the release of cytokines like interleukin-6 (IL-6), which is a key
promoter of hepatic CRP production. Various population-based studies, including the National Health and
Nutrition Examination Survey (NHANES) and the Framingham Heart Study, have also found a positive
association between smoking status and elevated CRP levels. Our research supports these findings and
provides quantitative evidence relevant to our demographic population.
17
Elevated CRP serves as an independent indicator of cardiovascular disease, which may help clarify the
heightened cardiovascular issues and mortality rates observed in smokers. Testing for high-sensitivity CRP
(hs-CRP) has been suggested as a method for assessing cardiovascular risk, making it particularly beneficial
for identifying individuals at risk within the smoking population.
18
Our findings also indicate a potential dose-
response correlation between daily cigarette consumption and CRP levels; however, additional studies with
larger participant groups and longitudinal approaches are necessary to validate this link. The potential for CRP
levels to decrease with smoking cessation is an encouraging avenue for research, as there is some evidence that
systemic inflammation may reduce after quitting tobacco.
CONCLUSION
The quantitative evaluation of CRP levels underscores the inflammatory burden associated with smoking.
These results highlight the need to incorporate inflammatory biomarkers into the risk evaluation of smokers
and further support the public health message regarding the comprehensive harm of tobacco use. Future studies
should aim to track CRP changes following smoking cessation and explore its possible role in informing
intervention strategies.
Financial support: Nil
Conflict of Interest: None
REFERENCES
1. World Health Organization. WHO Report on the Global Tobacco Epidemic, 2008: The MPOWER
Package. Geneva: World Health Organization; 2008.
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2. Centers for Disease Control and Prevention. 2004 Surgeon General’s Report – The Health
Consequences of Smoking. Atlanta, GA: Centers for Disease Control and Prevention, National Center
for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2004.
3. Mannino DM, Buist AS. Global burden of COPD: risk factors, prevalence, and future trends. Lancet.
2007; 370:765–73.
4. Casas JP, Shah T, Hingorani AD, et al. C-reactive protein and coronary heart disease: a critical review.
J Intern Med. 2008; 264:295–314
5. Smith SC, Jr, Milani RV, Arnett DK, et al. Atherosclerotic Vascular Disease Conference: Writing
Group II: risk factors. Circulation. 2004;109:2613–6.
6. Siemes C, Visser LE, Coebergh JW, Splinter TA, Witteman JC, Uitterlinder AG, Holfman A , Pols
HA, Stricker BH. C – reactive protein levels, variation in the C – reactive protein gene and cancer risk:
the Rotterdam study. J Clin Oncol 2006; 24:5216-5222
7. Coussens LM, and Web Z. Inflammation and cancer. Nature 2002; 420:860-867.
8. Baron JA. Epidemiology of non – steroid inflammatory drugs and cancer. Prog Exp Tumor Res 2003;
37:1-24.
9. Baron JA. Epidemiology of non – steroid inflammatory drugs and cancer. Prog Exp Tumor Res 2003;
37:1-24.
10. Ockene IS, Miller NH. Cigarette smoking, cardiovascular disease, and stroke: a statement for
healthcare professionals from the American Heart Association. American Heart Association Task Force
on Risk Reduction. Circulation. 1997; 96:3243–7.
11. Ross R. Atherosclerosis-an inflammatory disease. N Engl J Med. 1999; 340:115–26.
12. Mannino DM, Buist AS. Global burden of COPD: risk factors, prevalence, and future trends. Lancet.
2007 Sep 1;370(9589):765-73.
13. Majka DS, Holers VM. Cigarette smoking and the risk of systemic lupus erythematosus and
rheumatoid arthritis. Ann Rheum Dis. 2006 May;65(5):561-3.
14. Lakatos PL, Szamosi T, Lakatos L. Smoking in inflammatory bowel diseases: good, bad or ugly?
World J Gastroenterol. 2007 Dec 14;13(46):6134-9.
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Biochem 1990; 5:139-44.
16. Black S, Kushner I, Samols D. C-reactive Protein. J Biol Chem. 2004 Nov 19;279(47):48487-90.
17. Wong ND, Pio J, Valencia R, Thakal G. Distribution of C-reactive protein and its relation to risk
factors and coronary heart disease risk estimation in the National Health and Nutrition Examination
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Tables and Graphs
Graph 1: Comparison of non – smokers and smokers with mean age
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Table 1: Comparison of non-smokers and smokers with C-reactive protein values by Mann-Whitney U test
Groups
Mean
SD
Mean rank
U-value
Z-value
P-value
Non-smokers
55.24
12.03
20.22
Smokers
55.88
11.76
30.78
180.50
-2.5515
0.0107*
*p≤0.05
Table 2: Normality of C-reactive protein values in non-smokers and smokers by Shapiro-Wilk test
Group
df
p-value
Shapiro-Wilk
df
p-value
Non-smokers
25
0.0500*
0.8500
25
0.0020*
Smokers
25
0.0001*
0.6370
25
0.0001*
*p≤0.05
Graph 2: ROC curve in prediction of smokers by -reactive protein values