Evaluation of lipid profile and high sensitive C reactive protein levels among cigarette smokers in East Gojjam, Ethiopia

Abstract

Introduction

Cigarette smoking is a well-recognized independent risk factor for numerous cardiovascular disorders and contributes to the increasing morbidity and mortality associated with chronic heart diseases (CHD). This study aimed to evaluate how cigarette smoking affects lipid metabolism and inflammatory processes, along with other related mechanisms, in order to better understand the potential cardiovascular risks faced by smokers.

Objectives

To evaluate and compare the serum lipid profile and high-sensitivity C-reactive protein levels between cigarette smokers and non-smokers.

Methods

A hospital-based comparative cross-sectional study was conducted from December 2023 to May 2024 in East Gojjam, Ethiopia. The study included 150 cigarette smokers and 150 non-smokers. Independent t-tests and ANOVA were used to compare the mean lipid profiles and high-sensitivity C-reactive protein levels between smokers and non-smokers. A p-value of <0.05 was considered statistically significant.

Result

The mean serum levels of total cholesterol, low-density lipoprotein, triglycerides, high-density lipoprotein, and high-sensitivity C-reactive protein in cigarette smokers were 178.46 ± 76.34 mg/dL, 112.36 ± 73.58 mg/dL, 138.80 ± 61.88 mg/dL, 38.33 ± 7.99 mg/dL, and 6.26 ± 5.53 mg/L, respectively. These values were significantly different from those of non-smokers (p-value <0.05).

Conclusion

Serum mean levels of total cholesterol, low-density lipoprotein, triglycerides, and high-sensitivity C-reactive protein were significantly higher in cigarette smokers compared to non-smokers. In contrast, the mean serum level of high-density lipoprotein was significantly lower in smokers. These changes—elevated TC, LDL-C, TG, and hsCRP, along with decreased HDL-C—may increase the risk of cardiovascular diseases among cigarette smokers.

1. Introduction

Every year over 8 million people around the world die due to tobacco epidemic, making it one of the biggest public health threats we face. About 1.3 million of these deaths are linked to secondhand smoke exposure for nonsmokers, while more than 7 million are directly caused by tobacco use [1].

There is no safe level of tobacco exposure, and all forms of tobacco use are harmful. The most common type of tobacco use worldwide is cigarette smoking [2].

In low- and middle-income countries, where tobacco-related illnesses and deaths are common, over 80 % of the world's 1.3 billion smokers live. For instance, tobacco smoking rates are 60.2 % in Bangladesh, 30.1 % in Cameroon, 20.2 % in India, 14.7 % in Malaysia, 13.7 % in Nigeria, and 10.7 % in Yemen and Pakistan [1].

Around 2.9 million adults in Ethiopia smoke cigarettes. Among them, one-third are exposed to secondhand smoke in public places, which significantly contributes to preventable illness and death [3].

A study conducted in India on the effects of cigarette smoking on lipid profile, high-sensitivity C-reactive protein (hs-CRP), and malondialdehyde levels found that the concentrations of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein (VLDL), and hs-CRP were significantly higher in smokers compared to non-smokers. In contrast, high-density lipoprotein (HDL) levels were lower among smokers [4]. Similarly, a study carried out in Arba Minch, Ethiopia reported elevated levels of total cholesterol, LDL-C, triglycerides, and hs-CRP in smokers compared to non-smokers [5]. A study conducted in Iran found that in cigarette smokers, the risk of cardiovascular diseases was positively associated with high-sensitive CRP, LDL-C, total cholesterol (TC), and triglycerides (TAG). Conversely, HDL-C showed a negative association with the risk of cardiovascular diseases [6]. Cigarette smoking is a significant modifiable risk factor for atherosclerosis, contributing to the rising morbidity and mortality associated with Chronic Heart Diseases (CHD) [7]. Tobacco smoke contains various chemicals such as nicotine, carbon monoxide, and oxidant chemicals that induce numerous biochemical changes, including alterations in lipid profiles [8], increased levels of oxidized LDL-C [9], reduced availability of nitric oxide (NO), endothelial dysfunction, heightened insulin resistance, changes in fibrinolysis, platelet dysfunction, elevated blood viscosity, persistent inflammation with rising inflammatory markers, and, more recently, oxidative stress mediated by free radicals commonly implicated in the pathogenesis of cardiovascular disease [10,11].

Increased plasma catecholamines from cigarette smoking cause lipolysis and the production of free fatty acids, which will be taken by the liver. Cigarette smoking affects various lipids, including high-density lipoprotein (HDL—C), which helps protect against coronary atherosclerosis. In contrast, low-density lipoprotein (LDL-C) and very low-density lipoprotein (VLDL) can promote atherosclerosis [4,12,13].

One way smoking cigarettes can increase the risk of cardiovascular disease is by fueling the inflammatory process, which plays a crucial role in atherosclerosis at every stage [14].

In particular, smoking is believed to cause an inflammatory response, most likely in the pulmonary bronchi and alveoli, which results in chronic low-grade systemic inflammation [15]. This inflammation may cause cytokines like interleukin (IL)-l, tumor necrosis factor a (TNFa), and IL-6 to be produced in greater amounts, which in turn cause hepatocytes to produce more C-reactive protein (CRP), an acute-phase reactant that is a marker of inflammation and has been shown to be a significant predictor of future cardiovascular disease risk [4,16,17].

In response to inflammation, the liver produces C - reactive protein (CRP), which is one of the most widely used hematology tests to measure non-specific inflammation. When there is no acute phase of inflammation, the level of CRP remains relatively constant, and an elevated baseline inflammatory status as indicated by CRP level has been linked to an increased risk of a number of chronic conditions, such as lung cancer, colorectal cancer, and cardiovascular diseases [18,19].

Many organs in the body have been shown to be negatively affected by smoking, which has been identified as a contributing factor in a wide range of disorders. It has long been recognized that smoking cigarettes is a traditional and significant risk factor for the onset of atherosclerosis and cardiovascular disease (CVD). Additionally, smoking has been linked to a number of other chronic inflammatory disorders, such as Crohn's disease, rheumatoid arthritis, systemic lupus erythematosus, and chronic obstructive pulmonary disease (COPD) [20].

The effects of cigarette smoking on host immunity are extensive and include changes in adaptive immunity at the systemic level as well as changes in innate immunity in the mucosa of the mouth, nose, and airways [21]. Many harmful effects of cigarette smoking, particularly the development of cancer, are caused by direct genetic or epigenetic changes that alter the activity of genes involved in the cell cycle, DNA repair, and tumor suppression [10].

A burning cigarette generates thousands of reactive oxygen species (ROS), which damage the epithelial cells that line the airways. This occurs by peroxidizing lipids and other components of the cell membrane, activating oxidative-sensitive cellular pathways, and harming DNA [22]. The chemicals found in cigarettes, especially reactive oxygen species (ROS), activate intracellular signaling pathways in epithelial cells. This activation leads to the expression of inflammatory genes such as interleukin-6 and tumor necrosis factor-alpha (TNFα), which subsequently affect the liver's production of hsCRP [23]. In particular, interleukin-6 (IL-6) stimulates hepatocytes, which is essential for the creation of acute-phase proteins [16].

Cigarette smoking is well-known independent risk factors for various kinds of cardiovascular disorders, however smoking induce those cardiovascular disorders by various mechanisms. Therefore, the aim of this study was to assess the role of cigarette smoking on lipid metabolism and inflammatory process to predict potential cardiovascular risks by evaluating serum levels of lipid profile and hsCRP levels among cigarette smokers.

2. Materials and methods

A hospital-based cross-sectional study was carried out at Bichena Primary Hospital, Yeduha Primary Hospital, Motta General Hospital, and Lumamie Primary Hospital from December 2023 to May 2024 in East Gojjam, Ethiopia. To estimate the difference in means between two independent populations, we calculated the required sample size for each comparison group using the formula:

$$\mathrm{ni}=2\left(\mathrm{Z}\mathrm{\sigma }/\mathrm{E}\right)2$$

where ni is the sample size required in each group, Z is the value from the standard normal distribution reflecting the confidence level, usually, 95 % confidence level is used = 1.96; E is the desired margin of error, assume to be not more than 5 mg/dL and σ reflects the standard deviation of the outcome variable (TG, HDL—C, LDL-C, and TC). For our study, we determined the maximum sample size based on total cholesterol, using a pooled standard deviation (σ) of 22 mg/dL obtained from a prior study [24].

The study involved 150 cigarette smokers and 150 non-smokers, selected from the outpatient department (OPD) during health check-ups, using purposive sampling to meet the inclusion criteria. Cigarette smokers included in this study are individuals who have smoked daily for at least the past one year. All willing participants visiting the four hospitals during the data collection period were included, while individuals with liver disease, renal dysfunction, obesity, diabetes, cardiovascular disorders, alcohol use, previous smoking history, malignancies, inflammatory conditions (such as Crohn's disease, rheumatoid arthritis, gouty arthritis, and systemic lupus erythematosus), chronic obstructive pulmonary disease (COPD), and those taking antihyperlipidemic drugs were excluded. After obtaining informed consent, 5 mL of blood was collected from each participant. The blood was allowed to clot for 30 min, then centrifuged at 3000 rpm for 15 min to separate the serum, which was stored at −70 °C until analysis. Normality of the data was assessed using the Shapiro-Wilk test, which confirmed that the data were normally distributed.

2.1. Laboratory tests

The serum levels of low-density lipoprotein (LDL-C) were calculated using the Friedwald formula, while the Cobas C 501 chemical analyzer (Roche Diagnostic, USA) was employed to measure total cholesterol, high-density lipoprotein (HDL—C), triglycerides (TG), and high-sensitivity C-reactive protein (hs-CRP). All biochemical analyses were conducted at the Amhara Public Health Institute in Bahir Dar, Ethiopia. The reference ranges for adults were as follows: HDL-C (40–60 mg/dL), TG (<130 mg/dL), total cholesterol (TC) (<200 mg/dL), LDL-C (<130 mg/dL), and hs-CRP (<5 mg/L).

2.2. Data processing and analysis

Data analysis was conducted using version 26.0 of the SPSS software suite. Socio-demographic information was summarized using basic descriptive statistics. The relationships between variables were assessed using Pearson chi-square and Pearson correlation tests. Continuous variables with a normal distribution were represented as mean ± standard deviation. An independent Student's t-test and ANOVA were used for variable comparison. A p-value of less than 0.05 at a 95 % confidence level was considered statistically significant.

3. Result

3.1. Socio-demographic data

This study was conducted on 150 cigarette smokers and 150 non-smokers participants. The average age of cigarette smokers and non-smokers was 32.99 ± 9.3 and 43.32 ± 11.9 years respectively. Among the total cigarette smokers included in this study, 116 participants were male and the remaining 34 participants were female. The majority of cigarette smokers were urban residence. A summary of these findings is presented in Table 1.

Table 1.

Socio-demographic data of cigarette smokers and non-smokers.

Variables	Category of variable	Smokers (n = 150)		Non-smokers (n = 150)		P- value
		Frequency	%	Frequency	%
Sex	Males	116	77.3	86	57.3	0.000
	Females	14	22.7	64	42.7
Educational status	Illiterate	31	20.7	44	29.3	0.25
	Primary education	53	35.3	53	35.3
	Secondary education	41	27.3	36	24
	College/university	25	16.7	17	11.3
Residency	Urban	126	84	71	47.3	0.000
	Rural	24	16	79	52.7
Income	Low	41	27.3	36	24	0.72
	Medium	85	56.7	86	57.3
	High	24	16	28	18.5
Age		32.9 ± 9.3		42.22 ± 11.3	50	0.000

Keynote: All categorical variables are determined by number and percent. The average age of the study participant is presented as mean ± SD.

3.2. The mean serum lipid profile and hs-CRP levels among cigarette smokers and non-smokers

The mean serum lipid profile for cigarette smokers was as follows: total cholesterol (TC) 178.46 ± 76.34 mg/dL, low-density lipoprotein (LDL-C) 112.36 ± 73.58 mg/dL, triglycerides (TG) 138.80 ± 61.88 mg/dL, and high-density lipoprotein (HDL—C) 38.33 ± 7.99 mg/dL. Additionally, the mean serum hs-CRP level for cigarette smokers was 6.26 ± 5.53 mg/L.

An independent t-test was conducted to compare mean serum hs-CRP levels and lipid profiles (TG, TC, HDL—C, and LDL-C) between cigarette smokers and non-smokers. The results showed significant differences in all serum lipid profiles and hs-CRP levels, with P-values less than 0.01. A summary of these findings is presented in Table 2.

Table 2.

The comparison of serum lipid profile and hs-CRP between cigarette smokers and non-smokers.

Variables	Smokers (n = 150)	No-smokers (n = 150)	p-value
TC mg/dL	178.46 ± 76.34	155.21 ± 31.9	0.001
LDL mg/dL	112.36 ± 73.58	86.11 ± 25.13	0.000
TG mg/dL	138.80 ± 61.88	113.14 ± 101.38	0.009
HDL mg/dL	38.33 ± 7.99	46.52 ± 6.56	0.000
hs-CRP mg/L	6.26 ± 5.53	1.38 ± 0.85	0.000

Keynote: Serum hs-CRP and lipid profiles are presented as mean ± SD. TC, total cholesterol; LDL, low-density lipoprotein; TG, triglyceride; HDL, high-density lipoprotein; hs-CRP, highly sensitive c-reactive protein.

3.3. Comparison of serum lipid profile and hs-CRP levels among cigarette smokers based on the amount of smoking

From the total cigarette smokers 39, 66 and 45 participants were mild smokers (1–10 cigarettes /day), moderate smokers (11–20 cigarettes /day), and heavy smokers (>20 cigarettes /day) respectively. One way ANOVA test was conducted to compare mean serum lipid profiles and hs-CRP levels among cigarette smokers based on the amount of smoking per day. The results showed that, when the amount of cigarette smoking increases, both lipid profiles and hs-C reactive protein levels significantly altered with P-values less than 0.01. The summary of this finding are presented in Table 3.

Table 3.

Comparison of serum lipid profile and hs-CRP levels among cigarette smokers based on the amount of smoking (N = 150).

Variables	Amount of smoking			P-value
	Mild smokers (1–10 cigarettes/day)	Moderate smokers (11–20 cigarettes/day)	Heavy smokers >20 cigarettes/day
TC in mg/dL	155.54 ± 35.61	175.00 ± 106.77	203.38 ± 26.02	0.014
LDL in mg/dL	87.32 ± 33.65	109.13 ± 102.53	138.79 ± 23.19	0.005
TG in mg/dL	118.94 ± 46.22	141.13 ± 72.23	152.61 ± 53.50	0.041
HDL in mg/dL	44.43 ± 5.42	37.64 ± 7.59	34.07 ± 7.31	0.000
hs-CRP in mg/L	4.07 ± 0.85	5.83 ± 5.65	8.77 ± 6.70	0.000

Keynote: Serum hs-CRP and lipid profiles are presented as mean ± SD. TC, total cholesterol; LDL, low-density lipoprotein; TG, triglyceride; HDL, high-density lipoprotein; hs-CRP, highly sensitive c-reactive protein.

3.4. Comparison of serum lipid profile and hs-CRP levels among cigarette smokers based on gender

From the total cigarette smokers in our study, 116 participants were male whereas 34 participants were female. An independent t-test was conducted to compare the mean lipid profiles and serum hs-CRP levels between male and female cigarette smokers. The results showed insignificant differences in all serum lipid profiles and hs-CRP levels between males and females, with P-values greater than 0.05. A summary of these findings is presented in Table 4.

Table 4.

The comparison of serum lipid profile and hs-CRP levels among cigarette smokers based on gender (N = 150).

Variables	Sex of participants		P-value
	Males (n = 116)	Females (n = 34)
TC in mg/dL	181.13 ± 84.83	169.32 ± 33.41	0.42
LDL mg/dL	114.90 ± 82.34	103.67 ± 26.70	0.43
TG in mg/dL	138.02 ± 56.84	141.50 ± 77.60	0.77
HDL in mg/dL	38.62 ± 7.59	37.35 ± 9.28	0.41
hs-CRP in mg/L	6.31 ± 5.59	6.06 ± 5.40	0.81

Keynote: Serum hs-CRP and lipid profiles are presented as mean ± SD. TC, total cholesterol; LDL, low-density lipoprotein; TG, triglyceride; HDL, high-density lipoprotein; hs-CRP, highly sensitive c-reactive protein.

4. Discussion

In our study gender was a significant predictor of cigarette smoking. Our findings showed that majority (77.3 %) of cigarette smokers were male. This is in line with the study conducted in Thailand [25], Sudan [2] and Ethiopia [3,26]. This may be attributed to the greater social acceptance of cigarette smoking among males compared to females in Ethiopia. Additionally, strong family ties, caregiving roles, and involvement in family-related responsibilities may offer protective factors that reduce cigarette use among females. Our findings revealed that cigarette smoking was more prevalent among urban residents compared to those living in rural areas. This difference may be attributed to the socio-cultural variations between urban and rural communities in the East Gojjam Zone. In rural areas, smoking is often discouraged and smokers tend to face social stigma. Similar findings were reported by Idris et al. [27], Guliani et al. [28], and Niels Schoenmaker et al. [29]. In contrast, studies by Doogan, N. J. et al. [30] and Mengesha, S. D. et al. [26] presented differing results. These discrepancies may stem from variations in sampling methods, sample sizes, and study locations.

We have found that serum levels of TG, TC and LDL-C were significantly higher among cigarette smokers as we compared with non-smoker participants. However, serum levels of HDL-C were significantly lower among cigarette smokers than non –smoker participants'. Similar findings were reported in studies conducted by Wendy Y Craig et al. [7]; Linda K. Gossett et al. [9]; Mahdieh Momayyezi et al. [11]. This similarity may be explained by the fact that smoking is linked to increased fat metabolism and the release of lipids. This lipolysis effect mainly stems from nicotine, which triggers the release of catecholamines. As a sympathomimetic substance, nicotine boosts the release of catecholamines and other neurotransmitters, influencing both central and peripheral systems. The increase in circulating catecholamines from smoking enhances lipolysis, leading to a greater rate, concentration, and delivery of free fatty acids (FFAs) to skeletal muscle [13,31].

Nicotine influences lipolysis by engaging the classical adrenergic pathway, which involves the release of catecholamines that activate beta-adrenoceptors. Additionally, it directly stimulates a nicotinic cholinergic lipolytic receptor in adipose tissue, and this effect can be inhibited by adrenergic blockers [32].

Another way that cigarette smoking impacts lipid metabolism is through nicotine's effect on adipocyte lipoprotein lipase (LPL) activity, which decreases in adipose tissue while increasing in heart and skeletal muscle [11,13]. Additionally, although the precise molecular mechanism is not fully understood, smoking reduces LDL receptor (LDLR) protein levels in the liver, resulting in higher LDL cholesterol levels. The LDLR protein, found on the surface of hepatocytes, is crucial for regulating LDL cholesterol levels in the bloodstream [33].

Our findings revealed that the mean serum levels of high-sensitivity C-reactive protein (hsCRP) in cigarette smokers were significantly higher than those in non-smokers. Additionally, heavy smokers exhibited even higher mean serum hsCRP levels. These results align with studies conducted by Silvano Gallus et al. et al [18], Jennifer O'Loug et al [14], and Thomas Dietric et al. [17] One possible explanation for the link between smoking and inflammatory process is that cigarettes contains various reactive oxygen species that oxidize low-density lipoprotein (LDL-C). This oxidation prompts macrophages to engulf the oxidized LDL-C, leading to vascular inflammation [21]. Additionally, smoking increases the expression of intercellular adhesion molecule-1 (ICAM-1), which facilitates the infiltration of inflammatory cells into blood vessel walls. It also elevates serum levels of interleukin-1 (IL-1) and interleukin-6 (IL-6), stimulating hepatocytes to produce more C-reactive protein [10]. Consequently, cigarette smoking emerges as a significant risk factor for chronic inflammation, which can trigger the onset of various diseases, including cardiovascular disease (CVD) [16].

There are several ways in which smoking cigarettes contributes to cardiovascular problems. Most often, the pathophysiology of cardiovascular disease is linked to the chemical components of cigarettes, including nicotine, carbon monoxide, oxidant gases, and toxin compounds. Cigarette chemicals are linked to hemodynamic changes, insulin resistance, endothelial dysfunction, inflammation, dyslipidemia, and hypercoagulability. These pathophysiologic pathways all work together to cause cardiovascular problems in cigarette smokers [12,21,34].

4.1. Limitation of the study

The data on job and age at first cigarette use was not included in our study, which could influence the results. Additionally, the control group was not matched with the study (case) groups regarding age, gender, and residence, which may affect the outcomes and should be addressed in future studies.

5. Conclusion

Cigarette smoking is a significant risk factor for cardiovascular diseases (CVDs) and contributes to their development through various mechanisms. Our study specifically examines the impact of smoking on lipid metabolism and inflammation by evaluating lipid profiles and levels of the inflammatory marker (hsCRP). Based on our findings, we observed that serum levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL-C), and high sensitive C reactive protein (hsCRP) were significantly higher in smokers compared to non-smokers. Conversely, high-density lipoprotein (HDL-C) levels were notably lower in smokers, which may increase the risk of cardiovascular diseases.

CRediT authorship contribution statement

Gelagey Baye: Methodology, Investigation, Funding acquisition, Data curation. Bayu Wondmneh: Investigation, Funding acquisition, Conceptualization. Baye Ashenef: Writing – review & editing, Writing – original draft, Software. Mohammed Jemal: Writing – review & editing, Writing – original draft, Validation. Temesgen Baylie: Methodology, Data curation, Conceptualization. Enyew Fenta Mengistu: Validation, Software, Formal analysis. Adane Adugna: Methodology, Investigation, Data curation.

Ethics approval and informed consent

This study was conducted in accordance with the Declaration of Helsinki. The ethical clearance with reference number (RCSTT/395/07/17) was obtained from Research and Community Service Coordinating office of Medicine and Health Science College, Debre Markos University. We collect data after we obtain written informed consent from each study subject.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.