Hazardous Effect of Smoking on People’s Health


Please note! This essay has been submitted by a student.

Download PDF

Smoking is a health problem particularly in developing countries like Iraq. Cigarette smoking injure almost every organ in the body, and diminish the health of the smokers in general, its considered as a major reversible risk factor in relation with cardiovascular diseases morbidity and mortality.

Stopping smoking lowers the risk of smoking-associated disease and can add years to the life, smoking cessation reduce the risk for the coronary heart disease (CHD). Former smokers have a lesser CHD risk when compare with current smokers, and the changing increases with time since stopping smoking. However, the magnitude of harmful effects of cigarette smoking on cardiovascular health may vary between individuals.

Essay due? We'll write it for you!

Any subject

Min. 3-hour delivery

Pay if satisfied

Get your price

Various studies show the association between smoking and axial spondyloarthritis (axSPA) worse disease and demonstrate that ever-smoker is worse than never-smoker and current smoker is worse than ex-smoker in relation to the disease state. Smokers are more susceptible than non-smoker for developing heart disease, lung cancer and stroke. Estimation shows the increasing in the risk among smokers, about 2 to 4 times for coronary heart diseases, and 2 to 4 times for the stroke while for lung cancer the risk is 25 times in both men and women.

Smoking and atherosclerosis

Atherosclerosis is considered as a life-threatening disease, it characterized by a deposition of cholesterol, calcium, cellular waste, and other fatty substances along the lining artery walls of the body. These yellowish sticky, deposits, known as plaque, these plaque buildup with the time, leading to slow down the blood flow in the artery, it’s also demonstrated that atherosclerosis lead to damage of arterial epithelial cells, which followed by increased in the chemokines and adhesion molecules that cause aggregation and infiltration of monocytes, The monocytes then differentiate into macrophages which change into lipid-loaded foam cells through the uptake of lipoproteins, characteristic of the fatty streaks, in the beginning of atherosclerosis, and then develop to advanced atherosclerotic lesions.

Smoking, increased the risk of atherosclerosis, stroke, and heart attack. It was reported that cigarette smoking is one of the major risk factors for increasing the incidence of atherosclerosis and its associated diseases.

In the developing countries atherosclerosis was considered as a major cause of death. Atherosclerosis is considered as a chronic disease characterise by systematic inflammation that lead to the formation of plaques that cause obstruction of arterial lumen leading to atherosclerotic cardiovascular disease like myocardial infarction, coronary artery disease and ischemic stroke.

Cigarette smoking can enhance the progression of atherosclerosis by several aspects like oxidative stress responses, lipid deposition of foam cell, endothelial dysfunction and activation of macrophages. The injurious effects of cigarette smoking on atherosclerosis are conducted by pro-inflammatory matrix path way, this mediated through the damaging of the endothelial which enhance the movement of mononuclear cells and promote the attachments of leukocytes to sub endothelial layer leading to atherosclerosis, other studies suggested that the extract of cigarette smoking accelerate the remodelling genes of pro-inflammatory/matrix MMPs (matrix metalloproteinase), nuclear factor, tumor necrosis factor-Alfa and interleukin-1beta in culture cells. Recent study proposes that cigarette smoking enhance atherosclerosis by raised vascular inflammation and expression of NADPH oxidase and establish the significance of miRNAs in the pathogenesis of atherosclerosis induced by cigarette smoking.

Prevalence of smoking

The measured number of current smoker in the world exceeds 1.3 billion that means one third of the population in the world are smokers. The prevalence of smoking in Iraq according to surveys conducted between 1990 and 2009 ranged between 5% and 47% among males and 1% and 10% among females.

Other study showed that about 20.8% adolescence from Iraqi population are tobacco smokers, cigarette smoking is considered the major tobacco use practice in Iraq, its about (13.9%) then followed by shisha (4.8%).

A study conducted by health advocates in 2015 established that and average of 55 Iraqis die every day due to tobacco associated diseases. Since the Iran-Iraq War the prevalence of smoking in Iraq has elevated significantly. An estimation state that 1 in 4 Iraqis smoke. In Kurdistan region smoking are significantly lower with the rate being 25.1% for men and 2.7% for women.

In the United State cigarette smoking is considered the main cause of death, and causes more than 480,000 deaths every year, this mean one in five death. In Europe it was estimated that the prevalence of tobacco smoking among adults as 28% in 2015. In Sweden it was demonstrated that the prevalence of smoking was decreased from 14% in 2006 to11% in 2012.

Biochemical effect of cigarette smoking on the serum lipids levels

Cigarette smoking is associated with abnormal effects on serum lipids levels and result in increase the risk for atherosclerosis and heart disease. Cigarette smoking is related largely with lipid metabolism, represented by decrease in the serum levels of high density lipoprotein (HDL-C)( good cholesterol ) and increases the serum concentration of total cholesterol (TC), triglycerides (TG) and low density lipoprotein (LDL-C) (bad cholesterol) as reported in a large body literatures. Thus, smoking is considered as a predisposing risk factor for atherosclerotic cardiovascular disease and myocardial infarction. Smoking influences different mechanisms that may increase the rate of atherogenesis.

Mechanisms by which smoking cause abnormality in the serum lipids levels are:

(a) nicotine stimulate the release of catecholamine’s that lead to increase in the secretion of serum hepatic free fatty acids and increase secretion of hepatic cholesterol alone with hepatic secretion of very low density lipoprotein (VLDL) resulting in elevation of TG levels in the blood stream through stimulating sympathetic adrenal system, thus result in increased lipolysis.

(b) Cigarette Smoking affects estrogen levels leading to decrease in its levels and hence decreased HDL-C levels.

(c) Consumption of a diet enrich with cholesterol and fat but lacking in fiber and cereal content by smokers in comparison with non-smokers.

(d) Smoking also increases the resistance of insulin which leads to hyperinsulinemia and there were elevation in the level of LDL-C, VLDL and TG as a result of decreasing in the lipoprotein lipase activity.

(e) Smoking is known to be related with elevated plasma Homocysteine level which bring about oxidative modification of LDL-C and reduces HDL-C, various studies documented that homocysteine diminish Apo A-I protein expression thus reduced HDL- C.

Many hazard compound and their metabolites uptake through cigarette smoking. These metabolite may be electrophilic and when react with biological molecules give rise to oxidative stress and the formation of high concentration of free radicals or initiation of lipid peroxidation of polyunsaturated fatty acids (PUFA) that present in the cell membrane which destroyed easily by peroxidation

Cigarette smoking has been found to change plasma lipoprotein levels, this abnormalities are main risk factor for the incident of atherosclerotic vascular disease. It was demonstrated that smoking caused a reduction in the lipoprotein lipase activity (LPL). This was shown by the decrease in (LPL) activity in plasma of post- heparin smokers independently to their gender, age and BMI, and it was concluded that this disturbances in the LPL activity in the smokers individuals may contribute to the progression of the atherogenic lipoprotein phenotype in those individuals.

Genetic variation and smoking

Genetic variation is known to have an important role in association with the risk for several smoking complex disease, but the effects of cigarette smoking on the health are not completely explained through just genetic sequence variation, numerous recent studies have proposed that epigenetic mediation like DNA methylation have a role in smoking-related diseases.

In identifying the genetic variant that related to complex behaviors like cigarette smoking, Genome-wide association studies (GWAS) have conducted with success.The use of related biomarker in the estimation of behavioral phenotype provide precision measurement and improve the statistical power.

In the last years there was establish relationship between genetic variation of different population and atherosclerotic cardiovascular diseases especially coronary artery disease which was responsible for a large percentage of death every year in several countries and it has been well known that cigarette smoking was the classical risk factor for coronary artery disease. It was documented that smoking modifies the effect of the top SNP at the chromosome 9p21 locus, this locus is considered the strongest CHD-related locus.. Atherosclerotic cardiovascular diseases have been associated with lipid disorder but only a small percentage of patients have recognized with dysfunctional mutations in lipoprotein-related gene, therefore, it seems that an extra genetic and /or environmental factors was the cause of these polymorphisms.

Cigarette smoking has been mainly related to lipid metabolism and was considered one of the environmental factor that affect lipid levels among those extra genetic factors, the APO-CII gene. APO-CII was the activator of lipoprotein lipase and needed by lipoprotein lipase as a co factor for the hydrolysis of TG in VLDL and chylomicrons.

writers online
to help you with essay
banner clock
Clock is ticking and inspiration doesn't come?
We`ll do boring work for you. No plagiarism guarantee. Deadline from 3 hours.

We use cookies to offer you the best experience. By continuing, we’ll assume you agree with our Cookies policy.