BIOCHEMICAL AND HAEMODYANAMIC ASPECTS OF SMOKE … 978-93-84648-81-7.pdf · 2017. 7. 30. · Sikkim 4 074 0.76 10 1.95 21 1.45 21 Tamil Nadu 15 118 0.57 4 0.50 8 0.48 2 West Bengal

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BIOCHEMICAL AND HAEMODYANAMIC

ASPECTS OF SMOKE (CIGARETTE)

INTOXICATION IN HUMANS

Dr.S.MOHAMMED GHOUSE, M.Sc., Ph.D, READER IN ZOOLOGY, OSMANIA COLLEGE, KURNOOL

2

BIOCHEMICAL AND HAEMODYANAMIC

ASPECTS OF SMOKE (CIGARETTE)

INTOXICATION IN HUMANS

Dr. S. MOHAMMED GHOUSE, M.Sc., Ph.D.,

READER IN ZOOLOGY

O S M A N I A C O L L E G E , K U R N O O L

2015

International E - Publication

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BIOCHEMICAL AND HAEMODYANAMIC ASPECTS OF SMOKE…………. iii

ACKNOWLEDGEMENTS

I take this opportunity to respectfully record a deep sense of gratitude to

my beloved teacher and Research supervisor Prof.P. INDIRA, Head of the

Department of Zoology, S.K.UNIVERSITY, Anantapur, for her invaluable

guidance, keen interest and affectionate encouragement through out the

progress of the work.

I express my heartfelt thanks to the principal, Prof. C .R .REDDY, Prof.

G. H. PHILIP, Chairman, Board of studies Zoology, Prof .K.

VENKATESWARULU, Dean of faculty of sciences, Anantapur, for their co-

operation and encouragement through out this work.

I thank the faculty members Prof. RADHA KRISHNAIH, ,and other

members of Department of Zoology, S.K. University, Anantapur for their co-

operation and encouragement throughout this work.

I am thankful to my dear friend A.Venkataswamy, Dr.Suresh M.D for their

kind help in this work.

I express my gratitude to the Management of Osmania College, especially

Joint secretary Correspondent Mrs. Azra Javed, M.A for the encouragement and

support through out this work.

I will fail in my duty if I do not express sincere gratitude to my parents,

brother, late sister, My wife and Children friends and all my relatives who stood

by me through out this work.



BIOCHEMICAL AND HAEMODYANAMIC ASPECTS OF SMOKE…………. iv

Index

Topic Page

1. Introduction 1

2. Effect of alcohol consumption on homocysteine

levels in chronic alcoholics in Kurnool district. 11

3. Effect of chronic smoking on plasma lipid profile

in male smokers of Kurnool district 17

4. Stress and serum mineral concentrations in

Male smokers of Kurnool district 22

5. Smoking cessation effects on body weight,

haemoglobin, total and HDL cholesterol and blood pressure 29

6. Cigarettes and Other Tobacco Products Act 49



BIOCHEMICAL AND HAEMODYANAMIC ASPECTS OF SMOKE…………. 1

INTRODUCTION

CIGARETTE SMOKING:

Tobacco has been used for many centuries dated back to more than 2000 years. It

was originally cultured in America and was brought to Europe in the 15th

century by

Columbus. Initially tobacco was used in pipes and cigars as snuff on chewing tobacco. In

the beginning of the 20th

century, tobacco in the form of cigarette rose dramatically.

Studies show that smoking not only increase the risk for lung cancer, but also the risk for

number of other diseases i.e., other types of cancers and cardio vascular diseases. Besides

the harmful effects of smoking on morbidity, quality, smoking also leads to poor health

related quality of life, this makes cigarette smoking the number one preventable public

health problem in India.

Various studies show that smoking cessation decreases the risk for tobacco related

diseases and also improves health related quality of life. The aim of this thesis therefore,

is to educate the public, the health benefits of smoking cessation. Furthermore, this

theses aims to give more insight in the impact of smoking cessation on health – related

quality of life.

Prevalence of smoking behaviour:

Smoking prevalence increased rapidly in the beginning of 20th

century and has

been declining for several decades. This trend started among the males and was followed

by females some decades later. Women generally take up smoking later than in men is

mainly due to socio-cultural factors.

In Western countries the trend of prevalence of smoking in males is low Sweden

(17%) and around 27% in Finland and United States, where as a high percentage is seen

in Japan (53%). Among females, the prevalence of smoking is low in Portugal (7%),

Japan and Italy (both below 20%) and high in Denmark. Germany and Ireland (30%)

more, in the second half of the 1990’s.

Smoking is more prevalent among younger age groups. Cigarette smoking is

associated with several unfavourable life factors, such as high intake of alcohol




beverages, a less healthy diet and lower physical activity level.

World wide, approximately 1:3 billion people currently smoke cigarette or other

products (almost one billion men, 250 million women) with the decline in tobacco use in

many industrialized countries, the geography of smoking countries to shift from the

developed to developing world. In 1995, more smokers lived in low-and middle- income

countries (933 million) than in high income countries (209 million). An estimated 4.9

million premature deaths from smoking occurred in the year 2000, more than 600,000

these smoking death occur in china alone.

Unadjusted prevalence of adults aged 18 and above who smoke or chew tobacco in

1998-99 by Indian State

Crude prevalence of adults aged 18 and above who smoke or chew tobacco in 1998-9, by Indian state. The

term “crude” means unadjusted prevalence and is computed as number of individuals who smoke and chew




tobacco divided by the total number of individuals, in each state, and expressed as percentages.

Courtesy : Patterns and distribution of tobacco consumption in India: cross

sectional multilevel evidence from the 1998-9 national family health survey.

Fig 2

Model based predicted proportion of adults aged 18 and above who smoke or chew tobacco in 1998-9 by

Indian state after controlling for demographic and socioeconomic markers at the individual level and for

variation in tobacco consumption between households, local areas, and districts. The term “model based”

means conditional prevalence and is based on model based, residual, state level differences in smoking and

chewing after accounting for between-individual differences in tobacco consumption that are due to age, sex,

marital status, caste, religion, education, standard of living, and urban and rural differences, and after taking

account of within-state variation attributable to the level of households, local areas, and districts, and

expressed as percentages.

Courtesy: Patterns and distribution of tobacco consumption in India: cross sectional

multilevel evidence from the 1998-9 national family health survey.

In India cigarette smoking increased up to 1970’s, remained stationary declined




during the 1980’s Bidi smoking has risen substantially during last three decades. It is

estimated that 65% of all men use some forms of tobacco (about 35% smoking 22%

smokeless tobacco, 8% both). It differs in women from 15% in Bhavnagar to 6-7% in

Andhra Pradesh. However, over all prevalence of bidi and cigarette smoking among

women is about 3%. Difference to tobacco use also vary among other groups, Sikhs do

not use tobacco at all, and Parsis use very little, while tobacco use is permissible among

Hindus, Muslims and Christians. Smoking rates tend to be higher in rural areas than urban

areas. Smoking is a status symbol among urban educated youth, but most appear to be

unaware of hazards of smoking.

Annual consumption of manufactured cigarettes declined between 1984 and 1992

from around 90 million to about 85 billion. In 1992, 61 % of World total unmanufactured

tobacco and 1.5% of total World total manufactured cigarettes were consumed in India.

Only about 20% of total tobacco is consumed in India is in the form of cigarettes, Bidis

account for about 40% tobacco consumption (above 675,000 million bidis) with the rest

divided among chewing tobacco, pan masala, snuff, hooka, hookli, chutta dhumti etc.,

Table

Odds ratios for smoking, chewing, and smoking and chewing for the different Indian

states, based on the state level residuals estimated from a five level multiple binomial

logit model

Smoking

Chewing

Smoking and chewing

States

Sample size

Odds ratio

Rank

Odds ratio

Rank Odds ratio

Rank

Andhra Pradesh

11 668

0.90 15

0.47 6 0.59 6

Assam

10 531

0.80 12

2.62 23 1.71 22

Bihar

21 260

0.61 6

1.42 18 0.78 13

Goa

5 397

0.67 9

0.52 10 0.54 3

Gujarat

12 514

0.63 7

0.74 13 0.66 9

Haryana

9 317

1.72 21

0.36 3 0.70 11

Himachal Pradesh

10 460

1.43 20

0.35 2 0.59 5

Jammu

10 595

2.26 23

0.31 1 0.76 12

Karnataka

14 580

0.61 5

0.65 12 0.63 8

Kerala

10 055

0.79 11

0.51 9 0.59 4




Smoking

Chewing

Smoking and chewing

States

Sample size

Odds ratio

Rank

Odds ratio

Rank Odds ratio

Rank

Madhya Pradesh

21 853

0.66 8

1.26 17 0.91 16

Maharashtra

19 488

0.35 1

1.43 19 0.87 15

Manipur

5 547

2.04 22

2.33 22 2.28 23

Meghalaya

3 519

2.44 24

1.26 16 2.61 24

Mizoram

4 335

8.11 26

29.83 26 18.43 26

Nagaland

2 961

0.94 16

1.83 20 1.01 18

Orissa

15 072

0.46 2

2.70 24 1.44 20

Punjab

10 232

0.54 3

0.39 4 0.35 1

Rajasthan

21 815

0.97 17

0.49 7 0.61 7

Sikkim

4 074

0.76 10

1.95 21 1.45 21

Tamil Nadu

15 118

0.57 4

0.50 8 0.48 2

West Bengal

14 891

1.09 18

0.82 14 0.94 17

Uttar Pradesh

29 489

0.88 14

1.05 15 0.86 14

New Delhi

9 222

1.13 19

0.54 11 0.70 10

Arunachal Pradesh

4 045

0.85 13

4.09 25 2.72 25

Tripura

3 946

2.45 25

0.43 5 1.05 19

The model additionally included the demographic and socioeconomic markers of

individuals or households in the fixed part and variance component at the level of

households, local areas, districts, and states, in addition to the dispersion variable.

The reference point for the calculation of the state odds ratios is the all India log of the

odds of smoking, chewing, and smoking and chewing.

Courtesy: Patterns and distribution of tobacco consumption in India: cross sectional

multilevel evidence from the 1998-9 national family health survey




CONSUMPTION OF MANUFACTURES CIGARETTE

Annual average per adult (15 + )

Cigarette Bidis Total

1970-72 170 840 1,010

1980-82 180 1,130 1,310

1990-92 150 1,22 1,370

CONTENTS OF CIGARETTE SMOKE:

Tobacco smoke consists of more than 4,000 different chemical components, of

which most are formed during the burning of tobacco product Nicotine is the principal

addictive component of smoke. Tar a mixture of all particles in smoke minus water and

Nicotine contains several carcinogenic compounds of which polycyclic aromatic hydro-

carbons (pah) including benzopyrene, N-nitro amines are most important carcinogens.

Other chemical components in cigarette smoke include carbon monoxide, carbon dioxide

nitrogen oxides and ammonia. The amount of these components in cigarette smoke

depends on the smoking conditions, the type of tobacco and the design of the cigarette,

such as presence of a filter. Shortly after inhalation of cigarette smoke, a part of these

components reaches the blood stream and may induce the development of tobacco-related

diseases, through several mechanisms

This is from Table 3-1, 1992 EPA Report, Respiratory Health Effects of Passive Smoking

Benzene

2-napthylamine

4-aminobiphenyl

Nickel

Polonium 210 (radioactive)

Nitrogen oxides

N-nitro sodimethylamine

N-nitro sodiethylamine

N-nitro sopyrrolidine

1,3-Butadiene

Analine

Formaldehyde




Hydrazine

N-Nitrodiethanolamine

Cadmium

Benzo(a)pyrene

Benz(a)anthracene

Y-Butyrolactone

Particulate matter

N-NitrosonorNicotine

NNK

Carbon monoxide

Carbon dioxide

Carbonyl sulfide

Toluene

Acrolein

Acetone

Pyridine

3-Methylpyridine

3-Vinylpyridine

Hydrogen cyanide

Ammonia

Methylamine

Dimethylamine

Nicotine

Anatabine

Phenol

Catechol

Hydorquinone

Cholesterol

Quinoline

Harman

Zinc

Benzoic acid

Lactic acid

Glycolic acid




Succinic acid

PCDDs and PCDFs (Dioxins,Dibenzofurans)

Formic acid

Smoking behaviour and health

Cigarette smoking is a strong risk factor for premature death. It is estimated that

smoking caused about 4-5 million deaths Worldwide by the end of the 1990’s, which is

expected to increase to at least to million each year by 2030 if current smoking pattern

remained .It is estimated that one cigarette may reduce life by eleven minutes.

Smoking behavour and cardio vascular diseases:

(Serum cholesterol, blood pressure, triglycerides)

Serum cholesterol, blood pressure and triglycerides together in smoking is a major

cause for Cardiovascular diseases (CVDS). It is estimated that, in 1995, 13% of all deaths

from CVD in developed countries could be attributed to smoking. Coronary heart disease

(CHD) among smokers is generally about twice the risk among non-smokers. In general,

CVD risk increases with the number of cigarettes smoked daily, the number of years

smoked, the age of initiation and the degree of inhalation.

Smoking cessation generally reduces the CVD risk. The risk of death from CHD

is halved, about year after smoking cessation.

Generally smoking accelerates atherosclerosis, the under laying process of CHD

and stroke. Smoking increases the levels of LDL (cholesterol), triglycerides and blood

pressure due to Nicotine and Co.

Smoking behaviour and health-related quality of life :

The health-related quality of life reflects the self-rated perception of several

aspects of physical and mental health, including limitations due to physical functioning,

pain, vitality, general health, mental health problems and related role and social

functioning. Results of several studies suggest that cigarette smoking is related to poor

health-related quality of life. In cross-sectional studies, smokers are reported to have less

favourable outcomes on physical functioning, general health and mental health or

depression when compared with non or never smokers. Wilson et al. Reported less

favourable outcomes for all aspects of health-related quality of life, which was more




Cigarette

Smoking

Metabolic

Activation

Persistence

Miscoding

pronounced among heavy and moderate than among light smokers.

↓

Excretion

Figure: Schematic view of the effect of tobacco smoke carcinogens on lung cancer.

The association between smoking and physical functioning and depression has

been confirmed in cohort studies.

More research is needed to establish the effect of smoking cessation on health-

related quality of life. Only a few studies examined this association. These studies

suggested that ex-smokers have more limitations in role functioning due to physical

problems, but also have more vitality and experience a better mental health and perceived

health than smokers. However, results were not consistent. The difference between ex-

and current smokers tended to be larger for mental health than for physical health.

Rationale:

Cigarette smoking and alcohol use is common in India with an adaptation to

Western culture. Cigarette smoking and alcohol consumption leads to many health related

problems especially among youth.. Homocysteine levels increase may be related to

increasing in the risk of CAD. The total Homocysteine levels in chronic alcoholics are

more than the controls and non alcoholics. Increase in the levels of Homocysteine is a

independent risk factor for Cardiovascular diseases due to malabsorption of folate and

Vitamin B12 in the gut of chronic alcoholics.

The effects of smoking cessation on body weight, total, LDL, HDL, VLDL

cholesterols and B.p were analyzed to examine the quality of life after smoking

cessation in comparison with smokers and nonsmokers .the lipid profiles, ascorbic acid ,

PAH

and

NNK

DNA adducts

Mutations in k-ras, p53 and

other critical genes

Lung Cance




serum mineral concentrations in nonsmokers and smokers indicates the risks of CAD is

more in smokers in comparison with nonsmokers. We can conclude that there is

overwhelming evidence that cigarette smoking causes morbidity and mortality from

several chronic diseases, independent of culture. Furthermore, there is widespread

agreement on the morbidity and mortality risk reduction due to smoking cessation. Based

on this knowledge, several projections have been published on the number of future

deaths attributable to smoking. These numbers strongly underline the worldwide

importance of smoking cessation interventions. Public health policy makers more and

more realize this and set targets to reduce the smoking prevalence and alcohol

consumption. It is now time to quantify the future public health effects of smoking

cessation, which are less well described. From a public health point of view, it is

important to have insight in the decline in morbidity and mortality following such

reductions in smoking prevalence, and alcohol consumption. Since this has great impact

on the allocation of health care and health care costs. For instance, smoking cessation

would decrease the burden of smoking-related diseases. Furthermore, this thesis aims to

give more insight into the impact of smoking cessation on health-related quality of life.

In order to quantify future public health benefits of smoking cessation, it is important

to have information on the association between smoking or smoking cessation and other

risk factors for tobacco-related diseases. For instance, other risk factors may have an

intermediate or a modifying effect on the relation between smoking cessation and disease.

Therefore, first, the associations between smoking or smoking cessation and the main risk

factors for the most important tobacco related diseases (Cardiovascular diseases) were

examined, cholesterol level and blood pressure due to smoking cessation are described.




EFFECT OF ALCOHOL CONSUMPTION ON HOMOCYSTEINE LEVELS IN

CHRONIC ALCOHOLICS IN KURNOOL DISTRICT

ABSTRACT

Homocysteine higher levels associated with the increase in the risk of coronary artery

disease is called Hyperhomocysteinemia. Hyperhomocysteinemia is one the major and

independent risk factor for the development of atherosclerotic coronary artery disease.

Coronary artery disease is a leading cause of death all over the world. The total

Homocysteine levels in chronic alcoholics were studied along with the other parameters

like vitamin B12, folate, blood pressure etc. Alcohol consumption destroys the lining of

the stomach which ` is responsible for the mal absorption of folate, and vitamin B12 which

in turn results in the increased levels of total Homocysteine levels in alcoholics than in

controls. Chronic alcohol consumption is associated with elevated homocysteine levels,

probably because of the effect of alcohol on vitamin levels. In contrast, moderate alcohol

consumption appears to be associated with low homocysteine levels.

Keywords: Homocysteine, Coronary artery disease, elevated, Chronic alcoholics, folate,

and vitamin B12.

INTRODUCTION

Cardiovascular disease is the leading cause of death in India. Homocysteine is a

sulphur containing amino acid, rapidly auto-oxidised in plasma to the disulfides,

homosysteine and cysteine – Homocysteine and to Homocysteine thiolactone.

Homocysteine is an intermediate that is generated in the metabolism of methionine (Nasir

K, Tsai M, Rosen BD, et al., 2007). The increase in the homocysteine level is called

hyper-homocystemia; it is due to several factors like methionine catabolism, dietary

intake of vitamin B12, folate, methionine, smoking and chronic alcoholism. People, who

have homocystinuria an autosomal recessive disorder, have severe hyper

homocysteinemia, premature atherosclerosis and thrombo-embolic complications.

Coronary artery disease is a leading cause of death all over the world (Boushey CJ,

Beresford SAA, Omenn GS, Ureland PM, Refsum H, Brattström L, et al) and plasma

total homocysteine level is a strong, graded and independent risk factor for coronary heart




disease (CHD). Furthermore, Homocysteine may promote the oxidation of low-density

lipoprotein cholesterol, vascular smooth muscle cell proliferation, platelet and

coagulation factor activation, and endothelial dysfunction. About 80% plasma

Homocysteine is a protein bound through disulfide links with plasma proteins, especially

albumin; less than 5% is free. Therefore, altered Homocysteine metabolism has become

the focus of increasing attention because of its potential role in the pathogenesis of

atherosclerosis and other conditions, such as venous thrombosis. Hyperhomocysteinemia

is one the major and independent risk factor for the development of atherosclerotic

coronary artery disease. The disease seems to follow an accelerated course in the

developing countries as compared to the developed world.

Several intriguing observations suggest a role of Homocysteine in the

development of vascular disease. The aim of these studies to examine the association

between homosysteine levels in chronic alcoholics.

MATERIALS AND METHODS:

The total Homocysteine levels in chronic alcoholics (15 men aged 29-67 years)

and controls (15 men aged 31-66 years), participants in the study completed a baseline

lifestyle questionnaire, including details on past medical history, occupation, smoking

alcohol consumption and exercise in Kurnool district in with the assistance of Elisa

diagnostic ltd. Physical examination included measurement of blood pressure, height and

weight. Homocysteine were assayed by high – performance liquid chromatography.

STATISTICAL ANALYSIS:

Systolic and diastolic blood pressures, body mass index, total serum cholesterol,

number of cigarettes smoked per day, alcohol consumed and vitamin B12 were analyzed

as continuous variables, and differences in means were estimated. .




HOMOCYSTEINE IN MALE ALCOHOLICS:

TABLE 1. Baseline Characteristics in Matched Cases and Controls

BMI Indicates body mass index; AT alpha-tocopherol; BC, beta-carotene

*Geometric mean.

Serum foliate and vitamin B6 were normally distributed but were log normal. Linear

regression was used to examine the relationship between the natural log of Homocysteine

and systolic diastolic blood pressures.

MEAN (SD)

n Alcoholics Controls Difference

(95% CI) P

Age, y 15 37.9(5.2) 37.8(5.3) 0.1(1.1-0.9) 0.9

Blood pressure, mm Hg

Systolic 15 146.7 (19.7) 142.6 (20.4) 2.1 (0.2-7.9) 0.04

Diastolic 15 89.1 (10.9) 86.8 (10.7) 2.2 (0.2-4.2) 0.03

BMI, kg/m2

15 25.4 (3.5) 25.2 (3.8) 0.2 (0.5-0.9) 0.6

Cholesterol mmol/L 15 6.5 (1.2) 6.3 (1.1) 0.2 (0.01-0.4) 0.07

Alcohol, g/d 15 21.1 (8.3) 20.9 (8.6) 0.2 (1.4-1.8) 0.8

Cigarettes smoked per day, n 15 22.1 (8.3) 21.9 (8.6) 0.2 (1.4-1.8) 0.8

Vitamin B12, pmol/L 15 343.3 (100.5) 334.8 (111.9) 8.4 (12.6-29.4) 0.4

tHcys,*µmol/L 15 13.2 (5.2) 12.5 (4.8) 0.05 (-0.009-0.12) 0.09

Folate,*nmol/L 15 10.4 (4.7) 9.7 (4.5) 0.02 (-0.05-0.09) 0.6

Vitamin B6, *nmol/L 15 25.6 (15.7) 27.1 (18.7) -0.04 (--0.2-0.07) 0.4




RESULTS:-

The geometric mean total Homocysteine was higher in alcoholics than in controls,

as were systolic and diastolic blood pressures, total serum cholesterol, daily consumption

of alcohol, number of cigarette smoked daily, and duration of smoking. Vitamin B6 was

slightly lower in cases than in the controls, but serum folate and vitamin B12 were slightly

higher in cases than in controls. Both systolic (B coefficient, 3.5; 95% CI, - 0.3 to 7.2; P

= 0.07) and diastolic (B coefficient, 2.1; 95% CI, 0.08 to 4.2; P = 0.04) blood pressures

were associated with increasing Homocysteine.

DISCUSSION:

Atherosclerosis is considered the primary cause of death in industrialized

countries as it represents the underlying path mechanism responsible for the majority of

cases of myocardial and cerebral infarction (McCully, et al.,1996).

Hyperhomocysteinemia is being recognized as a serious and independent risk factor for

the development of atherosclerosis and thromboembolism (Kang et al., 1993). Several

articles have demonstrated an association between elevated total homocysteine and

stroke. Homocysteine may simply be a non specific marker of vitamin deficiency.

Several studies identified an inverse relation between serum folate levels and CAD

(coronary artery disease) events on univariate analysis. The present study describes

quantitative importance of folate and vitamin B12 concentrations as determinants of total

Homocysteine concentration in as representative samples of healthy adults. Serum

vitamin B12 levels have no correlation to CAD. However, vitamin B6 may be an

independent risk factor. Homocysteine remained a significant predictor of CAD after

controlling for serum vitamin levels.

Whether lowering plasma homocyseine levels will prevent CAD events is unknown

because of the absence of longer randomized controlled trials with appropriate end points.

Some epidemiological data suggest that folate and vitamin B6 intake influence the

occurrence of major CAD. Many of the biochemical samples were inadequate for

biochemical analysis data, particularly vitamin B6. The analyses demonstrate the

importance of folate and vitamin B12 as determinants of total Homocysteine

concentrations at the population level. More than 60 of high total homocyteine

concentrations in the sample linked to low folate concentration. (With (or) without low




B12 concentrations). The important role of vitamin B12 in Homocysteine metabolism is

indicated by the high attributable risk percentage among persons with low vitamin B12

concentrations. Many people claim that up to 10% of cardiovascular events could be

prevented by a reduction in total homocysteine in patients with hyperhomocysteinaemia.

A high dietary intake of folate, low coffee consumption, cessation of smoking and an

increase in physical exercise can all contribute to a reduction in homocysteine. However,

vitamin B12 concentration is much less important than folate concentration in the general

population as a cause of high total Homocysteine concentration because low B12

concentrations are less prevalent.

Age seems to influence the association between high Homocysteine and vitamin

concentrations. Among the persons 12 to 39 years of age, approximately

75 of the cases of high Homocysteine concentrations were associated with low folate (or)

vitamin B12 concentrations. Homocysteine in human plasma is formed by demethylation

of dietary amino acid, methionine, the average dietary intake of which is > 1.8 g/d. It is

present only trace amounts in the diet; dietary Homocysteine does not, under normal

circumstances, appear to affect the plasma Homocysteine level. Intracellular

Homocysteine has a short half-life and rapidly excreted.

Moderate alcohol consumption is associated with improved vascular risk profile and

decreased mortality in the middle aged. An elevated Homocysteine concentration is an

independent risk factor for cardiovascular diseases. Alcohol consumption destroys the

lining of the stomach which is responsible for the mal absorption of folate and vitamin

B12, which in turn results in the increased levels of total Homocysteine levels in alcoholics

than in controls. It appears that a limited betaine-dependent remethylation of

homocysteine to methionine (BHMT pathway) also exists within mammalian brains

(Finkelstein, 2007) Chronic alcohol consumption is associated with elevated

homocysteine levels, probably because of the effect of alcohol on vitamin levels. In

contrast, moderate alcohol consumption appears to be associated with low homocysteine

levels.




References

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2. Finkelstein JD (2007). Metabolic regulatory properties of Sadenosylmethionine and

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3. Kang, S.S., Passen, E.L. and Ruggie, N., et al. Thermolabile defect of

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JAC, et al: (2007). Elevated homocysteine is associated with reduced regional left

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6. Ureland PM, Refsum H, et al: Plasma homocysteine, a risk factor for vascular disease:

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7.Ureland PM, Refsum H, Brattström L, et al: Plasma homocysteine and cardiovascular

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and Endothelial Function, New York, Dekker, pp. 183-236.




EFFECT OF CHRONIC SMOKING ON PLASMA LIPID PROFILE IN MALE

SMOKERS OF KURNOOL DISTRICT

.

ABSTRACT:

The aim of the present study was to assess the association between smoking and the

alteration in plasma concentration of lipid profile. Smoking is an escalating health

problem especially in developing countries such as India. By 2030, if current trends

continue, smoking will kill more than 9 million people annually. (Yanbaeva DG,

Dentener MA, Creutzberg EC , et al.,) . Every cigarette reduces the life span by about 5

minutes. In the present study male subjects were divided into different groups and their

lipid profile have been estimated by various tests i.e. Cholesterol, Triglyceride, HDL-C,

LDLC, VLDL-C. It was observed that in cigarette smokers HDL-C level decreased and

cholesterol, triglyceride, LDL-C, VLDL-C level increased as compared to the control i.e.

non- cigarette smokers .The variation in the level of lipid profile from normal values

causes several diseases such heart disease, and stroke and has numerous immediate health

effects on the brain and on the respiratory, cardiovascular, gastrointestinal, immune

systems.

Key words: Smoking, HDL- cholesterol, triglycerides, heath effects

INTRODUCTION

Cigarette smoking is the serious health problems and most important

avoidable cause of death in world. Every cigarette reduces the life span by about 5

minutes. Cigarette smoking remains the most important cause of the preventable

morbidity and the early mortality. Nicotine is highly addictive, it raises the brain levels of

dopamine and it produces withdrawal symptoms on its discontinuation. Smoking in

different forms is a major risk factor for atherosclerosis and coronary heart disease

(Wilhelmsen L. J . Mc Gill HC et al., 1988,).A one to threefold increase in risk of

myocardial infraction (MI) has generally been noted among current cigarette smokers 4. A

lipid profile is a direct measure of three blood components: cholesterol, triglycerides, and

high-density lipoproteins (HDLs). Cholesterol is a vital substance that your body uses to

produce such things as digestion-aiding material, hormones, and cell membranes.

cigarette/bidi leads to increase in the concentration of serum total cholesterol,




triglycerides, LDL-cholesterol, VLDL-cholesterol and fall in the levels of antiatherogenic

HDL cholesterol, as reported by various workers. (Carlson LA, Bottiger,, et al,1979,

MJOS OD et, al 1988, Rustogi R, Shrivastva SSI et al , 1989) . Tobacco is patho-

genetically a cholesterol dependent risk factor and it acts synergistically with other risk

factors for the causation of coronary heart disease. Thus, a strong synergistic interaction

exists between hyper cholesterolaemia and tobacco consumption in the genesis of

coronary heart disease Tobacco smoke also contains various types of nitrosamines. The

most important nitrosamines are: N-Nitroso nor nicotine (NNN), 4- (Methyl nitroso

amino) –1-(3 Pyridyl)-1 (Butanone (NNK), Nitroso anatabine, Nitroso anabasine. All

these nitrosamines are formed from various alkaloids which are present in tobacco, i.e.,

nictotine, nornicotine, anabasine and anatabine by nitrozation. These nitrosamines are

potential carcinogenic substances and they are capable of alkylating the DNA. The actual

content of nicotine in tobacco varies between 1-2%. The aim of the study was to find out

differences in the serum lipid profile between young smokers and nonsmokers in the

fasting state. While cholesterol is necessary for various bodily functions, too much

cholesterol is harmful, since excess cholesterol can be deposited in blood vessel walls.

These fat deposits can lead to atherosclerosis, or hardening of the arteries, and

cardiovascular disease. High levels of triglycerides are also associated with an increased

risk of heart disease. Plasma lipoprotein abnormalities are said to be the underlying major

risk factors and may even be essential for the common occurrence of atherosclerotic

vascular diseases .( Shai I, Rimm EB, Hankinson SE, et al,2004)

MATERIAL AND METHODS

40 healthy male smokers in the age group of 19- 39 years were recruited for the

study in Kurnool district, Andhra Pradesh, India after obtaining written informed consent

(group I). 40 healthy non obese, non-smokers, age and weight matched selected from the

patients attendants and hospital staff were recruited as controls (group II). Group I

(smokers) were divided into two different categories according to the number of

cigarettes/bidis/ smoked per day and the duration of smoking. A detailed physical

examination of the subjects of both groups was done.

The blood samples are collected after an overnight fasting for about 14 hours. 5 ml.

of whole blood was collected from each subject and the serum was separated. The serum

lipid profiles were studied and the lipid levels were calculated. The readings which were

obtained are shown in the tables. The complete lipid profile measures the serum total

cholesterol, HDL and the triglycerides. The persons abusing alcohol, ex-smokers,




diabetes mellitus, hypertension, renal disease, hepatic impairment, endocrine disorders

and obesity and on drugs like β-blockers, lipid lowering drugs, and thiazide diuretics are

excluded from the study.

RESULTS: Table I: Showing distribution of smokers in relation to duration and no. of

cigarettes/ bidis smoked/day.

Duration

In yrs.

Mean

No. of cigarettes/bidis smoked per day

Total

No. 10% II-No. 20%

1-5 3 8 13 5 5 11

6-10 8 15 22 15 32 36

11-15 13 4 5 6 7 7

Total 27 40 26 44 54

Most of the smokers (36) had been smoking for a mean duration of 8 yrs as shown in

table I

Table II : Showing lipid profile in non-smokers and smokers.

Lipid profile

Values (mg/dl)

Non-smokers

(n = 40)

Smokers

(n = 40)

P value

Mean HDL-C 47.65 ± 4.18 42.8 ± 4.12 < 0.01**

Mean LDL-C 89 ± 17.80 102.7 ± 29.16 < 0.05*

Mean VLDL-C 18.3 ± 1.5 26.7 ± 3.1 < 0.05*

Mean TC 162.1 ± 20.26 184 ± 28.10 < 0.05*

Mean TG 127.10 ± 32.60 175 ± 55.65 < 0.01 **

* Significant, ** highly significant

There was significant increase in the mean values of total cholesterol LDL-C VLDL-C




and triglycerides: while there was significant fall in mean HDL-C in smokers as

compared to that in non-smokers.

DISCUSSION

Smoking, or if we say more carefully, tobacco, has a very bad influence on the total

health system of the human beings, not only effecting the arteries or the lung but almost

all the functional systems of the body, from cell to cell. It has long been established that

tobacco contains nicotine and it has a considerable influence on increasing the level of

lipids in the blood. Smokers have significantly higher triglycerides, LDL-C, VLDL-C, TC

in comparison with the non smokers. The mean serum triglycerides levels in non-smokers

and smokers were 127.10 ± 32.60 mg/dl and 175 ± 55.65 mg/dl respectively. The total

cholesterol were higher in smokers i.e serum concentration 184± 28.10 mg/dl in

comparison with the non smokers i.e. 162.1 ± 20.26 mg/dl. The mean LDL-C and

VLDL-C values in nonsmokers were 89 ± 17.80 mg/dl and 18.3 ± 1.5 mg/dl respectively.

But these values were significantly higher in subjects smoking. The mean HDL-C in non-

smokers was 47.65 ± 4.18 and 42.8 ± 4.12 in smokers respectively. Smoking causes an

increase in oxidised LDL-cholesterol level which plays the key role for atherosclerotic

process. (Zimmerman M, Mc Geachie J A et al 1985) high level of LDL-C, VLDL-C and

triglyceride are strongly associated with development of coronary artery disease while a

low level of HDL-C remains a significant independent predictor of coronary artery

disease.

CONCLUSION

Once again, let us remember that old is gold; that prevention is better than cure.

This has a very applicable role as far as smoking is concerned. The nicotine in tobacco

causes a decrease in the HDL cholesterol level (good cholesterol) with an increase in the

LDL cholesterol level (bad cholesterol) and also an increase in the VLDL cholesterol

level, with an accumulation of lipids in the arterial wall. This is responsible for the greater

risk of developing atherosclerosis in the tobacco users than in the non-tobacco users. To

conclude smoking causes alteration in lipid profile. Cigarette smoking has been found to

increase the concentrations of triglycerides and lowers the concentration of HDL

cholesterol (Willett W, Hennekens CH, Castelli W, et al.1983, Ledwozym A, Michalak J,

Stepien A, Kadziolka A , et al.1986) . Amount and duration of smoking also influences

dyslipidaemia . Smokers excrete more ascorbic acid in urine as compared to nonsmokers

.Low plasma ascorbic acid in smokers might be due to increased excretion of ascorbic




acid in urine. Increased amount and duration of smoking causes more of dyslipidaemia

The serum anti-atherogenic HDL-C level is significantly low in chronic smokers

irrespective of the number of cigarettes smoked. The serum level of total cholesterol,

LDL-C and VLDL-C and TG are significantly increased in persons smoking in

comparison with non smokers therefore raising the cardiovascular disease risk.

References

1. Yanbaeva DG, Dentener MA, Creutzberg EC, Wesseling G, Wouters EFM . Systemic

Effects of Smoking. Chest ; 131:1557-156,(2007).

2. Wilhelmsen L. Coronary heart disease. Epidemiology of smoking & intervention

studies of smoking. Am Heart J 1988; 115: 242-7.

3. Mc Gill HC. Cardiovascular pathology of smoking. Am Heart J 1988; 115: 250-7.

4. Slone D, Shapiro S, Rosenberg L et al. Relation of cigarette smoking to myocardial

infraction in young women. N Engl J Med 1978; 298: 1273– 1276.

5. Carlson LA, Bottiger LE, Ahfeldt PE. Risk factors for myocardial infarction in the

Stockholm prospective study: A 14 year follow up on focusing on the role of plasma

triglycerides and cholesterol. Acta Med Scand 1979; 206: 315-60.

6. MJOS OD. Lipid effects of smoking. Am Heart J 1988; 115: 272-5.

7. Rustogi R, Shrivastva SSI et al. Lipid profile in smokers. JAPI 1989; 37 (12): 764-7. 8.

Austin MA. Plasma triglycerides and coronary heart disease. Arterio Throm 1991; 11: 2-

14.

8.. Shai I, Rimm EB, Hankinson SE, et al. Multivariate assessment of lipid parameters as

predictors of coronary heart disease among postmenopausal women. Potential

implications for clinical guidelines. Circulation 2004; 110: 2824– 2830.

9. Zimmerman M, Mc Geachie J. The effect of nicotine on aortic endothelial cell

turnover. Atherosclerosis 1985; 58: 39-47.

10. Willett W, Hennekens CH, Castelli W, et al. Effects of cigarette smoking on fasting,

triglyceride, total cholesterol, and HDL-cholesterol in women. Am Heart J 1983; 105:

417–421.

11. Ledwozym A, Michalak J, Stepien A, Kadziolka A. The relationship between plasma

triglycerides, cholesterol, total lipids and lipid peroxidation products during human

atherosclerosis. Clin Chem Acta 1986; 155: 275–284.




STRESS AND SERUM MINERAL CONCENTRATIONS IN

MALE SMOKERS OF KURNOOL DISTRICT

ABSTRACT:

Smoking has been accepted as a risk factor for many chronic diseases, including

cardiovascular diseases, respiratory diseases, cancer, ulcers and osteoporosis. Tobacco

smoke contains many oxidants and free radicals that can cause damage to lipids, proteins,

DNA, carbohydrates and other bio molecules. The purpose of this study is to examine the

effect of cigarette smoking on serum oxidative damage, antioxidant status, and mineral

concentrations in male subjects. Subjects were randomly chosen from different work

places in Kurnool city. Serum oxidative defense enzyme activities (CAT and glutathione-

s- transferase) and serum mineral (Zn, Cu and I) were evaluated. Serum zinc and copper

concentrations were similar in the two groups. These findings show that there is depletion

in the non enzymatic antioxidant change depending on their co factor concentrations in

tobacco smokers.

Keywords: Smoking, free radicals, , damage bio molecules, minerals , enzymes ,

cofactors, smokers.

INTRODUCTION

Smoking has been accepted as a risk factor for many chronic diseases, including

cardiovascular diseases, respiratory diseases, cancer, ulcers and osteoporosis. Tobacco

smoke contains many oxidants and free radicals that can cause damage to lipids, proteins,

DNA, carbohydrates and other biomolecules. Smoking is a widely accepted practice in

India men and is associated with socializing, sharing, and male identity. Although

smoking is a recognized risk factor for several diseases including emphysema, chronic

bronchitis, cardiovascular diseases, and cancer .very little is known about the nutritional

consequences of smoking. Each puff of a tobacco contains 104 oxidants in the tar phase

and 105 in the gas phase. It has been demonstrated that one of the prominent risk factors

for increased lipid peroxidation is smoking (Kocyigit A, Erel O, Gur S et al.

2001).Smoking may enhance oxidative stress not only through the production of reactive

oxygen radicals in smoke but also through a weak of the antioxidant defense systems.

Cigarette smoke may promote atherogenesis by producing oxygen – derived free radicals

that damage lipid s(Palanisamy pasupathi, G. Saravanan and Farook;et al. 2009).smoking

produces Reactive oxygen species (ROS) which involved in many cellular metabolic and




signaling processes and are thought to have a role in aging and smoking. Therefore, their

detoxification and elimination are necessary for normal physiologic cell activity and

survival. To defend themselves against these free radical attacks, cells have developed

various antioxidant systems. Several enzymatic systems can detoxify free radicals,

copper/zinc superoxide dismutase (SOD) catalyzes the conversion of the superoxide

anion to hydrogen peroxide and works concomitantly with hydroperoxide, removing

enzymes such as catalase and as elenoprotein, glutathione peroxidase (GPX).

The present study was conducted to determine the effect of cigarette smoking on

change in antioxidant status (glutathione , superoxide dismutase and catalase ) in smoker

healthy subjects and compared with non smokers healthy subjects. The potential damage

that can be caused by free radicals is normally minimized by a combination of biological

antioxidant systems including enzymatic and non-enzymatic reactions. Important

antioxidant enzymes include copper and zinc (CuZn SOD) and manganese (Mn SOD)

superoxide dismutase, catalase, selenium glutathione reductase (GSH-Red). Ascorbic

acid, a-tocopherol, and urate can also act to reduce the concentration of free radicals.

MATERIALS AND METHODS:

The patients who had a history of smoking 10 or more cigarettes per day were

considered smokers, and those who never smoked were controls. The study did not

include females in this study because smoking is not a norm among females in Indian

society. This study included only heavy smokers who smoked at least 10 sticks per day,

and excluded mild or casual smokers to leave a buffer zone of comparison between

smokers and non-smokers. Forty healthy, males ranging in age of 19-35 years, from

Kurnool, volunteered to participate in this study. Thirty six of the volunteers had never

smoked. None of the volunteers had any history of cardiovascular, endocrine or

gastrointestinal disorders, and none were receiving medication or taking any nutritional

supplement. The procedures of the study were approved by a research committee, and a

written informed consent was signed from all volunteers after careful explanation of the

purpose and procedures of the study. Blood pressure and anthropometric measurements

(weight and height) were done by well-trained staff. Blood pressure (mm Hg) was

measured on the same arm with a standard cuff while the participant was sitting and in a

relaxed position. Three separate measurements were taken and the average was recorded.

All anthropometric measurements were taken with the participant wearing light clothing,




standing relaxed and looking straight ahead, with arms at the sides, feet together and with

weight equally distributed over both legs (14.) The weighing scale was zeroed before and

after every measurement and standardized with a certified weight every day. Volunteers

were asked not to smoke for more than 10 hours before sampling to exclude the effects of

acute smoking on the blood parameters studied. Two overnight fasting blood samples

were collected from all volunteers. The first blood samples were centrifuged at 3000 g

for ten minutes at room temperature and then serum was stored at -80°C until analyzed

for the, zinc, copper and selenium. The second blood samples were centrifuged at 1700g

for twenty minutes at 4°C, then serum was stored at -80°C until analyzed for serum

vitamin C. Hemolyzed samples were excluded from the analysis. Serum concentrations of

trace elements were measured by an atomic absorption spectrophotometer. Zinc and

copper concentrations were determined after dilution with 6% 1- butanol solution by

using flame atomic absorption spectrophotometer (20). Serum selenium determination

was preformed after (1:4) dilution with 0.05% TritonX 100 in 0.125% (v/v) nitric acid by

atomic absorption spectrophotometer with a graphite furnace (21).

Data analysis: Analysis of data was performed using the Statistical Package for Social

Sciences version 11.0 (SPSS) computer software.

RESULTS AND DISCUSSION

Some of the chemicals in cigarette smoke generate a large number of free radicals, 22.

Recent studies have demonstrated that antioxidants, including vitamin C and some trace

elements such as selenium, zinc and copper, protect the body against reactive oxygen

species (ROS).

1. In the present study no statistical differences in body weight, height were observed

between smokers and nonsmokers. These results are similar to the results of Kim et al.

2003, who found that the slightly lower body weight of smokers was probably secondary

to a lower calorie intake in the smoking group compared to the non-smoking group. Kim

et al. reported that cigarette smoking was not associated with a reduction in height.

2. Regarding the effect of smoking on hypertension, the average blood pressure in

smokers and non-smokers was in normal range; however, the diastolic and systolic blood

pressures were significantly (P<0.05) higher in smokers than in non-smokers and ranged

to the upper limit of the normal range. This observation suggests that the hypertension,

typically reported in smokers, reflects the effects of chronic and long-term vascular




damage as mentioned by Kim et al.

3. These results were confirmed in the present study for the effect of cigarette smoking on

trace elements as shown in Table 3 which shows that smoking decreased serum zinc and

selenium, but increased copper concentrations attributed to the hormonal changes induced

by cigarette smoking, i.e., the increased release of corticosteroids and

catecholamine.(Dubick et al. 1991 and Kim et al.2003, have reported increased zinc.

concentrations in smokers)

4. The lower serum vitamin C concentrations due to cigarette smoking are consistent with

several investigators who have pointed out those smokers

Table: 1 Characteristics of the study subjects

Subjects (n) Age ( year) Number of

cigarette

smoked per

day

Duration of

smoking (year)

Smokers Non-

Smokers

Smokers Non-

Smokers

40 36 19 ± 16 21 ± 15 11.5 ± 1.9 10.2 ± 4.1

* Data are given as mean ± SD.

Table – 2

Comparison of height, body weight, blood pressure, and daily nutrient intakes between smokers and non-smokers*

Variable Smokers Non-smokers

Height (cm) 166±2|| 168 ±3

Body weight (kg) 59±4|| 62±5

Blood pressure(mmHg)

Diastolic 67± 2§ 79±2

Systolic 101±3‡ 107±2

Reported daily nutrient intake

Energy (kcl/d) 1850±80§ 2141±100




Ascorbic acid(mg/d) 27.2±3§ 71.1±7

Ascorbic acid intake/energy intake 0.02 0.03

Table 3: Comparison of plasma parameters of tobacco smokers and

non-smokers

Variable Smokers

(n= 40)

Non-smokers

(n=36)

P

Cu μg/dl 98.4 ± 21 92.1 ± 14.1 0.103

Zn μg/dl 68.4 ± 12.4 72.0 ± 12 0.484

Se μg/l 60.3 ± 12.9 88.9 ± 18.1 000

Fe μg/dl 106.2 ± 35 115.2 ± 34.6 0.443

Table : 4 Levels of serum lipids and antioxidant status in non smokers

and smokers subjects

Parameters

Smokers

Non-smokers

MDA ( u mol/L ) 2.11± 0.7* 1.13± 0.45

GSH ( u mol / L ) 39.18 ± 16.38** 66.64± 18.61

SOD ( u mol / L ) 27.0 ± 10.63** 75.54 ± 11.34

CAT ( u mol / L ) 39.84 ± 20.79** 75.54 ± 11.34

*Data are presented as mean ± standard error of the mean.

§P<0.001. || Not significant by t test at µ = 0.05. ‡ P<0.05. † n = 19/group

possess a lower level of plasma antioxidants, especially vitamin C. ( Mezzetti, A.,




Lapenna, D., Pierodomenico, S.D., Calafiore, A.M et al 1995, Halliwell, B. and

Gutteridge, J.M. et al. 1990).

5. The serum MDA levels were significantly higher (p< 0.05)in smokers compared with

non-smokers which indicate the oxidative damage of cigarette smoking . SOD along with

CAT preventive antioxidants , plays a very important role in protection against lipid

peroxidation . In this study, SOD and CAT activities were significantly lower smokers

than in non smokers. CAT has been suggested to play an important role in the protection

against oxidative stress (Valco, M., Leibfritz, D., Moncol, J. ,et al. 2007). Serum

glutathione levels are believed to be predicators of morbidity and mortality (Venkatesan,

A., Hemalatha, A., Bobby, Z., et al. 2006) . GSH plays a key role in protecting cells

against electrophiles and free radicals.GSH can act directly as a free radical scavenger by

neutralizing hydroxyl radicals, or indirectly by repairing initial damage to

macromolecules inflicted by hydroxyl radicals. It is essential in the maintenance of

protein and non protein SH group in reduced form ( Goraca A., Skibska B et al. 2005).

CONCLUSION:

Antioxidant defenses act as balanced and coordinated system and each relies on the action

of the other.(Evans, P and Halliwell, B. et al. 2001) The oxidative damage observed in

smokers can be associated with the direct effects of oxidants in cigarette smoke and the

consequences of lower antioxidant nutrition status associated with smoking. Although the

best medical advice for this population is to stop smoking, the present data also suggest

that this population has an increased requirement for dietary antioxidants. Consistent with

this concept, vitamin C supplements have been reported to reduce the extent of oxidative

damage in smokers. The potential value of antioxidant supplements for smokers is

underscored by the observation that dietary antioxidant intakes tend to be lower in

smokers than in non-smokers. Campaigns aimed at improving the antioxidant status of

this group should be mounted in conjunction with antismoking campaigns.

References

1. Dubick MA, Keen CL. Influence of nicotine on tissue trace element concentrations and

tissue antioxidant defense. Biol Trace Elem Res. 1991 Nov; 31(2):97-109.

2. Evans, P and Halliwell, B. : Micronutrients; Oxidant/ Antioxidant Status. British J. of

Nutrition, 85.Suppl. 2,567-574 2001

3.Goraca A., Skibska B.; Plasma antioxidant status in healthy smoking and non –




smoking men. Bratisl lek listy 2005; 106 (10): 301 -306.

4. Halliwell, B. and Gutteridge, J.M. 1990. Role of free radicals and catalytic metal ions

in human disease: An Overview. Methods Enzymol. 168:1- 85.

5. Kim, S.H., Kim, J.S. Shin, H.S. and Keen, C.L. 2003. Influence of smoking on markers

of oxidative stress and serum mineral concentrations in teenage girls in Korea. Nutrition

19:240-243.

6.Kocyigit A, Erel O, Gur S. Effects of tobacco smoking on plasma selenium, zinc,

copper and iron concentrations and related antioxidative enzyme activities. Clin

Biochem.2001 Nov; 34(8):629-633.

7. Mezzetti, A., Lapenna, D., Pierodomenico, S.D., Calafiore, A.M., Costantini, F.,

Riario-Sforza, G., Imbastero, T., Neri, M. and Cuccurullo, F. 1995. Vitamin E, C and

lipid peroxidation in plasma and arterial tissues of smokers and non-smokers.

Atherosclerosis 112:91-96.

8. Palanisamy pasupathi, G. Saravanan and Farook; Oxidative stress Bio Markers and

antioxidant status in cigarette smokers comparedto non smokers. J. Pharm. Sci. and

Res.2009 (2), 55-62.

9. Valco, M., Leibfritz, D., Moncol, J. ,et al.; Free radicals and antioxidants in normal

physiological functions and human disease. Int. J.Biochem. Cell Biol. 2007; 39: 44- 84.

Venkatesan, A., Hemalatha, A., Bobby, Z., et al ; Effect of smoking on lipid profile and

lipid peroxidation in normal subjects. India J. Physiol. Pharmacol. 2006; 50 (3) : 273-278.




SMOKING CESSATION EFFECTS ON BODY WEIGHT, HAEMOGLOBIN,

TOTAL AND HDL CHOLESTEROL AND BLOOD PRESSURE

ABSTRACT:

Tobacco use including both the smoking and the nonsmoking forms of tobacco is

common in India. The World Health Organization reported that tobacco smoking

killed 100 million people worldwide in the 20th century and warned that it could kill

one billion people around the world in the 21st century. The increase in body weight

may mediate between smoking cessation on the one hand and total cholesterol and blood

pressure change on the other hand. Hemoglobin concentration increases in smokers

because the inhaled carbon monoxide results in increased

carboxyhaemoglobin, which has no oxygen-carrying capacity Smoking intensity

also has been associated with small, statistically significant increases in low-density

lipoprotein cholesterol (LDL-C) and decreases in HDL-C. Some have described small

dense LDL particles among current smokers and improvements in lipids after smoking

cessation; however, these findings have been less consistent. This emphasizes that some,

at least, of the adverse effects of smoking appear to be rapidly reversible on quitting,

strengthening the argument for encouraging smokers to quit.

Keywords : smoking, quitting , haemoglobin, body weight, HDL cholesterol.

INTRODUCTION:

Tobacco use including both the smoking and the nonsmoking forms of

tobacco is common in India. (Jindal SK, Agarwal AN, Chaudhry K, Chhabra SK,

D'Souza GA, Gupta D et al., 2006) . The number of smokers in the population of the

Third World will increase from 4.5 billion to 7.1 billion by 2025. The World Health

Organization reported that tobacco smoking killed 100 million people worldwide in

the 20th century and warned that it could kill one billion people around the world in

the 21st century (WHO Report 2008). Each year, smoking contributes to more than

443,000 smoking related deaths in the United States and nearly 20% of all coronary heart

disease deaths can be attributed to smoking. (American Heart Association, 2009,. Center

for Disease Control and Prevention, 2009) . Tobacco smoking rates have decreased in

industrialized countries since 1975, but there has been a corresponding 50% increase

in smoking rates in low- income countries. (Yu JJ, Shopland DR. et al.,




1989) Although the strong relationship between smoking and cardiovascular disease

(CVD) has been well-documented. Several means by which smoking increases the risk of

cardiovascular disease have been postulated. First the. formation of carboxyhaemoglobin

in the blood result in anoxemia in the myocardium, thereby weakening it. Second,

smoking is known to increase vasoconstriction, platelet aggregation and adhesion, in

effect, increasing the blood's clotting ability. Third, nicotine may chemically induce

various cardiac arrhythmias. This effect may result directly from the elimination of the

harmful effects of cigarette smoke, such as increased heart rate and myocardial

contractility, decreased oxygen transport of the blood and increased blood coagulation. In

addition, smoking cessation may also have an effect on other risk factors for CVD, such

as serum total and HDL cholesterol level, blood pressure and body weight.

The blood haemoglobin estimation is one of the most frequently used

laboratory parameters in clinical settings. Hemoglobin values, however, vary with age,

sex, and stage of pregnancy, and they are also affected by ethnicity, altitude, and

smoking.

Alterations in blood pressure (BP), heart rate (HR), and autonomic nervous

function are thought to be at least in part responsible for the rapid reduction in the risk of

cardiovascular diseases after quitting. Ex-smokers may adopt a healthier lifestyle, which

may result in a decreased body weight, total cholesterol level or blood pressure. Changes

in body weight will consequently alter serum total and HDL cholesterol level and blood

pressure levels. Since CVD risk is associated with the duration of cessation and the

amount of smoking, changes in CVD-risk factors may also be associated with these

characteristics of smoking behaviour.

Arteriosclerotic lesions throughout the vascular system are more prevalent in

smokers than in non-smokers . Cigarette smokers have also been shown to have

significantly lower levels of high-density lipoprotein cholesterol (HDL-C) and higher

low-density lipoprotein cholesterol (LDL-C) levels in their blood than non-smokers

Smoking intensity also has been associated with small, statistically significant

increases in low-density lipoprotein cholesterol (LDL-C) and decreases in HDL-C. Some

have described small dense LDL particles among current smokers and improvements in

lipids after smoking cessation; however, these findings have been less consistent .To what

extent the reduction in CVD risk after smoking cessation is due to smoking-related

changes in other risk factors is not established yet in the general population. The effect of




smoking cessation on body weight, total and HDL cholesterol levels and blood pressure

was examined under controlled circumstances in several smoking intervention trials or in

several cohort studies among special groups of the population. This is a matter of

considerable importance, because smokers in the 21st century are significantly more

overweight than those studied previously.( Gossett LK, Johnson HM, Piper ME, et al,

2009, Campbell SC, Moffatt RJ, Stamford BA , et al , 2008, Center for Disease Control

and Prevention ,2009) Since smoking cessation is associated with weight gain.( Eisenberg

D, Quinn BC. 2006, Johnson HM, Gossett LK, Piper ME, et al. 2010, Flegal KM, Troiano

RP, Pamuk ER, et al ,1995) and weight gain affects lipoproteins ( Dattilo AM, Kris-

Etherton PM. et al ,1992, Hession M, Rolland C, Kulkarni U, et al. 2009 ) the effects of

smoking cessation on lipoproteins remains unclear. Results obtained from the general

population are of greater importance for public health policy makers, since they are

derived from a sample of the total population under natural and uncontrolled conditions.

In these general-population cohort studies, an unfavourable increase in body weight was

observed after smoking cessation.

Therefore, in the present study, we used longitudinal data from the general

population to study the change in body weight, serum total and HDL cholesterol level and

systolic and diastolic blood pressure in subjects who stopped smoking during follow up.

Furthermore, we studied the effect of amount of smoking before cessation and duration of

cessation on these changes in CVD risk factors. Finally, we examined whether these

changes were influenced by other factors, including body weight change.

MATERIAL AND METHODS:

Subject were examined on Cardiovascular Disease Risk Factors, of 20-59 year old

men from Kurnool. Weight change due to smoking cessation may not be distinguishable

from weight change due to a weight reducing diet or smoking-related chronic diseases,

such as CVD, or COPD. 210 never smokers, ex-smokers, 83 and 200 current smokers at

both examinations, quitters between baseline and re-examination, 137 ‘relapsers’ (ex-

smokers at baseline who smoked at re-examination) and 160 subjects who were

occasional smokers (less than 1 cigarette per day) or who had inconsistent smoking

information across the two examinations. All subjects gave their written informed

consent.

Measurements:

1. Subjects were classified as persistent smokers if they reported to smoke 1




cigarette or more per day at both examinations, as quitters if they smoked 1

cigarette or more per day at baseline and reported to have quit smoking at the

re-examination, and as never smokers if they did not smoke at both

examinations.

2. For persistent smokers and quitters, information on the number of cigarettes

smoked per day at baseline was collected and categorized as 1-9, 10-19 and >

20 cigarettes per day.

3. For quitters, the duration of cessation was established at the re-examination

and categorized as 0-1 years, 2-3 years and 4-6 years.

4. After taking antiseptic precautions blood samples were drawn from the

antecubital vein and collected into 3m1 EDTA vacutainers (Akuret,

eastern medkit limited). The EDTA blood samples were processed by

using MS-9 automated. hematology cell counter for Haemoglobin.

Samples were processed on the same day within 3-5 hours of collection.

Data collected was subjected to standard statistical analysis by SPSS

software.

5. Lipid profile was estimated by drawing 5ml of fasting blood sample. Serum

lipids and lipoproteins cholesterol fractions were measured on fasting state.

Total cholesterol and triglyceride level estimations are carried out using

enzymatic end point kit method. HDL cholesterol was estimated by

precipitation of non HDL lipoproteins and estimations done using

superannuant. Total and HDL cholesterol levels were determined at the

Clinical Laboratory.

6. Blood pressure was measured twice on the upper arm with the participant in

sitting position, with a random-zero sphygmomanometer. Systolic and

diastolic blood pressure were recorded at the first and fifth and fifth Korotk off

phase, respectively. The average of the two blood pressure measurements was

used in the analyses.

7. Height was measured with as wall-mounted stadiometer in subjects without

shoes who stood upright against the wall.

8. Body weight was measured in light indoor clothing without shoes, and 1 kg

was subtracted to correct for clothing. .




Information was obtained by means of a questionnaire. Educational level at

baseline, as an indicator of socio-economic status, was divided into three categories,

according to the highest achieved level of education: low (intermediate secondary

education or less), intermediate (intermediate vocational or higher secondary education)

and high (higher vocational or university education). Alcohol intake was reported in

number of glasses of beer, wine or spirits per week at both examinations. We transposed

this into the number of glasses alcohol per day, assuming equal amounts of alcohol intake

between the two examinations. Their previous history related with of myocardial

infractions, cerebro-vascular accident, diabetes mellitus or cancer etc., respiratory

symptoms, including chronic cough, chronic phlegm, and shortness of breath and

wheezing are taken in to consideration

STATISTICAL ANALYSIS:

Differences in characteristics between persistent smokers on the one hand and

quitters and never smokers on the other hand were tested by means of a t-test for

continuous variables or by means of x2 –test for categorical variables. Multivariate

analysis of variance was used to estimate changes in body weight, total and HDL

cholesterol and blood pressure level between baseline and re-examination. These changes

were estimated for persistent smokers, quitters and never smokers and for quitters in

categories of duration of cessation. Differences in changes between categories were

tested with the total group of persistent smokers as the reference group. Furthermore,

changes were estimated for persistent smokers and quitters in categories of amount of

smoking. In these analyses, differences in changes between quitters and persistent

smokers were tested in subgroups of amount of smoking with persistent smokers as the

reference group. A trend in amount of smoking with change in risk factors was tested

using linear regression modeling. Haemoglobin Data collected was subjected to

standard statistical analysis by SPSS software

Data were analysed using the GLM-procedure of SAS statistics version

6.12. Two-sided p-values below 0.05 were considered statistically significant.

RESULTS:

There were no significant differences in baseline characteristics between

persistent smokers and quitters, except for educational level and for body mass index




(BMI) among men and number of cigarettes per day among women (Table 1). At re-

examination, quitters reported a lower prevalence of asthma and COPD among men and

of cancer and COPD among women.

Table 2 reflects the age-adjusted changes in body weight, total and HDL

cholesterol level and blood pressure for categories of smoking behaviour. Compared to

persistent smokers, quitters experienced a larger age-adjusted increase in body weight,

HDL cholesterol and diastolic blood pressure (DBP) between baseline and re-examination

among both men and women (excess gain in quitters compared to persistent smokers:

body weight 3.4 kg among men and 3.8 kg among women; HDL cholesterol 0..7 mmol/L

among both men and women; DBP 2.8 mm Hg among men and 1.7 mm HG among

women). Furthermore, in men only, quitters experienced a larger age-adjusted increase in

total cholesterol and systolic blood pressure (SBP) (excess gain in quitters compared to

persistent smokers: total cholesterol 0.17 mmol/L; SBP 2.7 mm Hg).

Quitters who quit smoking 2-6 years before re-examination tended to gain more

weight than quitters who quit smoking within 2 years before re-examination, which was

most pronounced among women (Table 2). Furthermore, the gain in body weight showed

a positive trend with amount of smoking within quitters.




Table 1 Baseline characteristics of the study population (men (sd) or%).

Persistent

smokers

Men

Quitters

Never smokers Persistent

smokers

Women

Quitters

Never smokers

N 200 83 210 50 15 100

Age (years) 38.2(9.6) 37.0(10.3) 38.3(9.8)*** 37.4(9.2) 37.0(10.0) 42.7(11..0)***

Educational level(%):

Low 67.7 53.6 40.3 75.6 77.2 66.4

Intermediate 21.7 26.3** 33.8*** 16.1 10.4* 20.3***

High 10.6 20.1 26.0 8.3 12.4 13.3

Nr of cigarettes per day 16.9(7.9) 15.7(8.0) -- 13.2(6.9) 10.5(6.1)*** ---

Body weight (kg) 71.0(11.7) 74.5(10.2) 75.2(10.0) 62.6(10.1) 63.3(9.2) 66.9(10.6)***

BMI(kg/m2) 24.7(3.2) 24.3(2.7)* 24.5(2.9) 23.4(3.4) 23.5(3.3.) 24.4(3.8)***

Total cholesterol (mmol/l) 5.65(1.19) 5.48(1.10) 5.30(1.04)*** 5.41(1.06) 5.46(1.04) 5.32(1.00)




HDL cholesterol (mmol/l) 1.07(0.26) 1.10(0.26) 1.16(0.26)*** 1.30(0.31) 1.29(0.29) 1.39(0.28)***

Systolic blood pressure(mm Hg) 124.8(12.8) 123.5(12.6) 124.5(12.9) 115.3(13.5) 114.4(13.6) 117.6(13.8)***

Diastolic blood pressure(mm Hg) 77.5(9.8) 76.0(9.8) 77.3(9.8) 72.7(9.4) 71.8(9.4) 74.5(9.4)***

Alcohol intake:

% drinkers 73.5 75.8 62.2*** 47.5 43.2 37.2***

No of glasses/day among drinkers 2.3(1.8) 2.1(1.6) 1.4(1.2)*** 1.3(1.0) 1.1(0.9) 0.7(0.5)***

* p<0.05, **p<0.01, ***p<0.001 for a difference with persistent smokers.




Table 2 (Chapt Age –adjusted change () (95% confidence interval) between baseline and re-examination in body weight, total and HDL

cholesterol, and systolic and diastolic blood pressure for the total groups of persistent smokers. Quitters and never smokers, and for quitters in

categories of duration of cessation.

Body weight Total cholesterol HDL cholesterol

Systolic blood

pressure Diastolic blood pressure

(kg) (mmol/L) (mmol/L) (mm Hg) (mm Hg)

Men

Persistent smokers 3.2(2.8-3.4) -0.04(-0.10-0.02) 0.05(0.3-0.06) 2.3(1.1-3.0) 2.0(1.2-2.7)

Quitters 6.2(5.9-7.2) 0.13(0.01-0.24)* 0.12(0.10-0.15)*** 4.6(2.9-6.6)* 4.3(3.2-6.1)**

Never smokers 3.5(3.5-4.1)** 0.07(0.01-0.13)** 0.06(0.05-0.08) 2.4(1.6-3.5) 2.4(1.8-3.3)

Duration of cessation (years)a

0-1 5.3(3.9-7.1)*** 0.10(-0.12-0.32) 0.09(0.03-0.15) 2.6(-0.7-6.3) 2.2(-0.2-5.1)

2-3 6.8(5.4-8.8)*** 0.31(0.17-0.55)** 0.15(0.09-0.22)*** 4.1(0.5-8.2) 3.1(0.4-6.2)

4-6 6.5(5.5-8.0)*** 0.01(-0.17-0.18) 0.14(0.09-0.18)*** 6.6(4.1-9.8)** 6.7(4.8-9.1)***




Women

Persistent smokers 2.8(2.6-3.4) 0.05(-0.002-0.11) 0.12(0.10-0.14) 4.3(4.0-5.9) 2.7(2.2-3.6)

Quitters 6.5(6.1-7.5)*** 0.03(-0.08-0.14) 0.19(0.15-0.23)*** 5.3(3.8-7.7) 4.4(3.2-5.9)*

Never smokers 3.8.(3.7-4.4)*** 0.12(0.07-0.16) 0.12(0.10-0.14) 3.9(3.5-5.2) 2.6(2.2-3.4)

Duration of cessation (years)a

0-1 5.4(3.5-6.8)** -0.02(-0.23-0.20) 0.22(0.15-0.29)** 5.6(1.9-9.8) 3.9(1.3-6.9)

2-3 7.6(6.3-9.6)*** 0.02(-0.19-0.23) 0.19(0.13-0.26)* 4.9(1.4-9.1) 5.8(3.3-8.7)*

4-6 6.3(6.1-9.0)*** 0.04(-0.15-0.23) 0.17(0.11-0.23) 3.9(0.8-7.8) 2.9(1.2-6.1)

*P<0.05, **p<0.01, ***p<0.001 for difference with persistent smokers. a Among quitters.




Figure Age adjusted change in the body weight between baseline and re

examination, for persistent smokers and quitters in categories of amount of smoking

at base line *p for trend.

Figure Age-adjusted change in body weight between baseline and re-examination,

for persistent smokers and quitters in categories of amount of smoking at baseline. * p for

trend.<0.01), but no trend within persistent smokers, which implies that heavy smokers

who quit smoking gained more weight than light smokers who quit smoking (Figure). No

clear effect of duration of cessation and amount of smoking was observed on the change

in total and HDL cholesterol level and blood pressure between baseline and re-

examination. Among men, but not among women, the increase in HDL cholesterol level

tended to be largest after at least 2 years of cessation. Furthermore, in men, change in

both systolic and diastolic blood pressure seemed to be larger among long-term quitters

than among quitters who quit within 4 years before the re-examination, but this was not

observed in women (Table 2). Among women, but not among men, HDL change among

quitters tended to be largest from 10 cigarettes per day onward (data not shown).

So far, we expressed the change in risk factors as the age-adjusted, actual

observed change. This change in risk factors after smoking cessation may be explained




by several factors. We examined the effect of several demographic and lifestyle factors,

disease history, and weight gain, which are shown in Table 3. adjustment for age,

educational level, number of cigarettes per day at baseline, change in alcohol

consumption and disease history did not substantially alter our adjusted

results(Adjustment I).




Table 3 Change (95% confidence interval) between baseline and re-examination in body weight, total and HDL cholesterol, and systolic

and diastolic blood pressure, adjusted for several factors, a for persistent smokers, quitters and never smokers.

Body weight Total cholesterol HDL cholesterol Systolic blood pressure

Diastolic blood

pressure

(kg) (mmol/L) (mmol/L) (mm Hg) (mm Hg)

Men

Adjustment 1

Persistent smokers 2.9(2.6-3.5) -0.002(-0.08-0.07) 0.05(0.09-0.07 1.4(0.2-2.7 1.5(0.5-2.5)

Quitters 5.9(5.8-7.2)*** 0.14(0.02-0.26)* 0.12(0.09-0.15)*** 4.2(2.2-6.2)* 4.2(2.9-6.0)***

Never smokers 3.9(3.4-4.3)* 0.03(-0.05-0.11) 0.06(0.04-0.08) 3.0(1.7-4.3) 2.6(1.9-4.0)

Adjustment II

Persistent smokers 0.02(-0.05-0.10) 0.04(0.02-0.06) 1.9(0.7-3.01) 1.7(0.9-2.8)

Quitters - 0.04(-0.08-0.16) 0.15(0.12-0.18)*** 2.6(0.6-4.6) 3.1(1.6-4.8)

Never smokers 0.03(-0.05-0.11) 0.06(0.04-0.08) 3.0(1.7-4.2) 2.5(1.9-3.9)

Women

Adjustment I

Persistent smokers 2.6(2.2-3.3) 0.07(-0.01-0.15) 0.11(0.09-0.14) 4.2(2.8-5.6) 2.1(1.3-3.3)

Quitters 6.4(5.8-7.4)*** 0.14(-0.08-0.16) 0.18(0.14-0.22)** 5.3(3.2-7.4) 4.1(2.9-5.9)*




Never smokers 4.2(3.8-4.7)*** 0.11(0.04-0.18) 0.13(0.10-0.15) 4.7(3.5-5.9) 3.1(2.5-4.2)

Adjustment II

Persistent smokers 0.09(0.02-0.17) 0.10(0.08-0.13) 5.0(3.6-6.3) 2.6(1.8-3.8)

Quitters -0.02(-0.13-0.10) 0.20(0.17-0.24)*** 3.6(1.5-5.6) 3.1(1.8-4.7)

Never smokers 0.10(0.03-0.17) 0.13(0.11-0.15) 4.5(3.3-5.6) 3.0(2.3-4.0)

*p<0.05, **p<0.001 for difference with persistent smokers. a Adjustment I includes age, educational level and number of cigarettes per day

at baseline, change in alcohol consumption between baseline and re-examination and history of myocardial infarction, cerebrovascular

accident, diabetes, cancer, asthma and COPD at re-examination; adjustment II includes adjustment I plus changes in body weight between

baseline and re-examination.




Table 4 depicts the effect of smoking on haemoglobin concentration. The mean value of haemoglobin in smokers was 14.22±0.79,

while in non-smokers was 13.27±1.32 and the difference was statistically highly significant (p = 0.001).

Haemoglobin concentration of smokers and nonsmokers

Smoking Mean p-value

Haemoglobin

Smokers

14.22±0.79

0.001

Non Smokers 13.27±1.32

45

Pa

ge4

5

Pa

ge4

5

After adjustment for weight gain, the increase in total cholesterol level, systolic and

diastolic blood pressure among quitters tended to become smaller for both men and

women, and the difference in total cholesterol (among males) and blood pressure change

between quitters and persistent smokers lost significance (Adjustment II). The increase in

HDL cholesterol level tended to become slightly larger after adjustment for weight gain.

DISCUSSION:

In this general-population study, quitters experienced a larger increase than

persistent smokers in body weight,. Men experienced a large increase in total cholesterol

level and systolic blood pressure. Heavy smokers gained more weight after cessation

than light smokers. Weight gain largely explained the larger increase in total cholesterol

and blood pressure among quitters compared with persistent smokers and slightly

counteracted the favourable increase in HDL cholesterol among quitters.

Study, shows that age-adjusted, observed changes in CVD risk factors after

smoking cessation and examined to what extent confounding factors such as demographic

and lifestyle factors, were responsible for these changes.

Limitations of our study include the possibility that quitters may have adopted other

healthy lifestyle habits affecting body weight, cholesterol level and blood pressure, which

we were not able to account for. For instance, non-smokers usually are more physically

active than current smokers. Furthermore, non-smokers generally consume a healthier

diet compared to smokers, especially heavy smokers. Dietary intake at both baseline and

re-examination did not substantially differ between quitters and persistent smokers.

Information on intake of alcoholic beverages, which also differs between heavy smokers

and ex-smokers, was comparable between the two examinations and the change in

alcohol consumption between baseline and re-examination was included in our analyses.

Hemoglobin concentration increases in smokers because the inhaled carbon

monoxide results in increased carboxyhaemoglobin, which has no oxygen-

carrying capacity. Impaired tissue oxygen supply results from decreased oxygen

carrying capacity and increased oxygen-haemoglobin affinity caused by

carboxyhaemoglobin (COHb) .(Sagone Jr AL, Lawrence T, Balcerzak et al,. SP.

1973). To compensate, hemoglobin levels increase.

A gain in body weight following smoking cessation has been widely reported. On

average, male and female quitters gained 3.4 kg and 3.8 kg respectively more than



46

persistent smokers in our study with six years of follow-up, which did not substantially

change after adjustment for relevant variables. It is clear that smokers weigh less than

non-smokers after many years of smoking. However, among adolescents and young

adults, weight differences between smokers and non-smokers are small or non-existent,

and smoking initiation is not associated with weight loss. In contrast, smoking cessation

reliably produces weight gain. In several large prospective studies, weight gain

attributable to smoking cessation has averaged 2 to 4 kg, and has been greater in women

These excess gains were smaller than those found in a smoking cessation trial (6.3 kg and

6.8 kg for men and women respectively after 5 years of follow-up), but larger than those

found in other smoking cessation trials, in cohort studies among specific groups of the

population, or in other cohort studies among the general population, which reported

excess gains from around 2 kg to 3.8 kg after 4-16 years of follow up. Larger excess

gains in our study may be explained by the longer duration of follow-up in some other

studies, since it is suggested that, after an initial increase, body weight may decrease later

in the follow-up period. .

The Nicotine in tobacco smoke stimulates the adrenal cortex, leading to

consecutive releases of free fatty acids and very low density lipoprotein, which in turn

results in lower HDL cholesterol levels. The absence of Nicotine after smoking cessation

may reverse this process. HDL cholesterol has been identified as a protective factor

against cardiovascular diseases. It is estimated that the excess gain of quitters compared

to persistent smokers of 0.07 mmol/L, as was found in our study, would decrease CVD

mortality with around 5.5% among men and 8% among women. This indicates that this

post cessation change in HDL cholesterol may contribute to the positive effects of

smoking cessation on CVD.

Smoking cessation increased total cholesterol levels in men and systolic

(significant in men only) and diastolic blood pressure levels in both men and women.

Weight gain is known to increase total cholesterol and blood pressure levels. This

indicates that the increase in body weight may mediate between smoking cessation on the

one hand and total cholesterol and blood pressure change on the other hand.

These results suggest that quitters should prevent post cessation weight gain as

much as possible in order to gain the maximum health benefits from smoking cessation.

In this large, prospective, contemporary study of current smokers, smoking

cessation improved HDL-C, total HDL, and large HDL particle concentrations, despite



47

weight gain. These findings were especially strong in women. Smoking cessation, not

baseline smoking intensity, predicted increased HDL parameters. These findings suggest

that an increase in HDL may mediate some of the reduced CVD risk observed after

smoking cessation.

Quitting smoking is clearly associated with an increase in HDL-C

concentrations. Generally the increase occurs rapidly, in less than three weeks, with no

clear pattern of change thereafter. This emphasizes that some, at least, of the adverse

effects of smoking appear to be rapidly reversible on quitting, strengthening the argument

for encouraging smokers to quit. The high prevalence of an atherogenic lipid profile in

smokers makes them prone to develop premature atherosclerosis and the changes become

more marked with the number of cigarette/day smoked.

.

References:

1. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and

cardiovascular disease: an update. J Am Coll Cardiol. 2004;43:1731–37.

2. American Heart Association. Heart Disease and Stroke Statistics--2009 Update.

Dallas, TX: American Heart Association; 2009.

3. Campbell SC, Moffatt RJ, Stamford BA. Smoking and smoking cessation - The

relationship between cardiovascular disease and lipoprotein metabolism: A

review. Atherosclerosis. 2008; 201:225–35.

4. Center for Disease Control and Prevention. Smoking-Attributable Mortality,

Years of Potential Life Lost, and Productivity Losses - United States. 2002–2004

[accessed 2009 Apr 8] Morbidity and Mortality Weekly Report. 2008;57:1226–

28.

5. Center for Disease Control and Prevention. State-Specific Prevalence of Obesity

Among Adults--United States, 2007. Morbidity and Mortality Weekly Report.

2008;57:765–68.

6. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood lipids and

lipoproteins: a meta-analysis. Am J Clin Nutr. 1992;56:320–328.

7. Doll R, Peto R, Boreham J, et al. Mortality in relation to smoking: 50 years’

observations on male British doctors. BMJ. 2004;328:1519.



48

8. Eisenberg D, Quinn BC. Estimating the effect of smoking cessation on weight

gain: an instrumental variable approach. Health Serv Res. 2006;41:2255–66 .

9. Flegal KM, Troiano RP, Pamuk ER, et al. The influence of smoking cessation on

the prevalence of overweight in the United States. N Engl J Med. 1995;333:1165–

70.

10. Freund KM, Belanger AJ, D’Agostino RB, et al. The health risks of smoking.

The Framingham Study: 34 years of follow-up. Ann Epidemiol. 1993;3:417–24.

11. Gossett LK, Johnson HM, Piper ME, et al. Smoking Intensity and Lipoprotein

Abnormalities in Active Smokers. J Clin Lipidol. 2009;3:372–78.

12. Hession M, Rolland C, Kulkarni U, et al. Systematic review of randomized

controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the

management of obesity and its comorbidities. Obes Rev. 2009;10:36–50.

13. Jindal SK, Aggarwal AN, Chaudhry K, Chhabra SK, D'Souza GA, Gupta D et

al. Tobacco Smoking in India: Prevalence, Quit-rates and Respiratory Morbidity.

The Indian Journal of Chest Diseases & Allied Sciences 2006; 48:37-42.

14. Johnson HM, Gossett LK, Piper ME, et al. Effects of smoking and smoking

cessation on endothelial function: 1-year outcomes from a randomized clinical

trial. J Am Coll Cardiol. 2010;55:1988–95.

15. Sagone Jr AL, Lawrence T, Balcerzak SP. Effect of Smoking on Tissue

Oxygen Supply.Blood 1973; 41: 84551.

16. WHO Report: Tobacco Could Kill One Billion by 2100, Science Daily; Aug

2008; 24:71.

17. Yu JJ,Shopland DR. Cigarette smoking behavior and consumption

characteristics for the Asia- Pacific region. World Smoking Health

1989;14:7-9



49

Cigarettes and Other Tobacco Products Act

Cigarettes and Other Tobacco Products (Prohibition of Advertisement and Regulation of Trade and Commerce, Production, Supply and Distribution) Act, 2003

Cigarettes and Other Tobacco Products (Prohibition of Advertisement

and Regulation of Trade and Commerce, Production, Supply and

Distribution) Act, 2003

An act to prohibit the advertisement of, and to provide for the regulation of trade and commerce

in, and production, supply and distribution of, cigarettes and other tobacco products and for

matters connected therewith or incidental thereto.

Citation Act No. 32 of 2003

Enacted by Parliament of India

Date enacted 9 April 2003 (Rajya Sabha) 30 April 2003 (Lok Sabha)

Date assented to 18 May 2003

Date commenced 1 May 2004

The Cigarettes and Other Tobacco Products (Prohibition of Advertisement and

Regulation of Trade and Commerce, Production, Supply and Distribution) Act, 2003 or

COTPA is an Act of Parliament of India enacted in 2003 to prohibit advertisement and

regulation of tobacco business in India. The Act put restriction on tobacco products

including cigarettes, gutka, panmasala (containing tobacco), cigar, cheroot, Beedi, Snuff,

chewing tobacco, hookah, tooth powder containing tobacco.



50

Front of a Gold Flake Kings box, sold in India, displaying pictorial warning

• The Act prohibits smoking of tobacco in public places, except in special smoking zones in hotels, restaurants and airports and open spaces. Places where smoking is restricted include auditoriums, movie theatres, hospitals, public transport (aircraft, buses, trains, metros, monorails, taxis,) and their related facilities (airports, bus stands/stations, railway stations), restaurants, hotels, bars, pubs, amusement centres, offices (government and private), libraries, courts, post offices, markets, shopping malls, canteens, refreshment rooms, banquet halls, discothèques, coffee houses, educational institutions and parks. Smoking is allowed on roads, inside one's home or vehicle. The meaning of open space has been extended to mean such spaces which is visited by public, and includes open auditorium, stadium, bus stand.

• Advertisement of tobacco products including cigarettes is prohibited. No person shall participate in advertisement of tobacco product, or allow a medium of publication to be used for advertisement of tobacco products. No person shall sell video-film of such advertisement, distribute leaflets, documents, or give space for erection of advertisement of tobacco products. However, restricted advertisement is allowed on packages of tobacco products, entrances of places where tobacco products are sold. Surrogate advertisement is prohibited as well under the Act.

• Tobacco products cannot be sold to person below the age of 18 years, and in places within 100 metres radius from the outer boundary of an institution of education, which includes school colleges and institutions of higher learning established or recognized by an appropriate authority.

• Tobacco products must be sold, supplied or distributed in a package which shall contain an appropriate pictorial warning, its nicotine and tar contents. Cigarette packets are required to carry pictorial warnings of a skull or scorpion or certain prescribed pictorial warnings along with the text SMOKING KILLS and TOBACCO CAUSES MOUTH CANCER in both Hindi and English.

• The Act also gives power to any police officer, not below the rank of a sub-inspector or any officer of State Food or Drug Administration or any other officer, holding the equivalent rank being not below the rank of Sub-Inspector of Police for search and seizure of premises where tobacco



51

products are produced, stored or sold, if he suspects that the provision of the Act has been violated.

• A person who manufactures tobacco products fails to adhere to the norm related to warnings on packages on first conviction shall be punished with up to 2 years in imprisonment or with fine which can extend to Rs. 5000, in case of subsequent conviction shall be punished with up to 5 years in imprisonment or with fine which can extend to Rs. 10000.

• A fine up to Rs. 200 can be imposed for smoking in public place, selling tobacco products to minors, or selling tobacco products within a radius of 100 metres from any educational institution.

• A person who advertises tobacco products shall on first conviction shall be punished with up to 2 years in imprisonment or with fine which can extend to Rs. 1000, in case of subsequent conviction shall be punished with up to 5 years in imprisonment or with fine which can extend to Rs. 5000.

• The Act repealed The Cigarettes (Regulation of Production, Supply and Distribution) Act, 1975

• The owner/manager/in-charge of a public place must display a board containing the warning “No Smoking Area - Smoking here is an offence “ in appropriate manner at the entrance and inside the premises. In place where tobacco products are sold must display appropriate messages like “Tobacco Causes Cancer” and "Sales of tobacco products to a person under the age of eighteen years is a punishable offence”.

COURTESY: From Wikipedia, the free encyclopedia



52

ABOUT AUTHOR

Dr.S.MOHAMMED GHOUSE , I have completed

my M.Sc, Ph.D, in Zoology from Sri Krishna

Devaraya University , Anatapuramu, Andhra Pradesh,

India. .Joined as a lecturer in my parent college,

Osmania College, Kurnool where I was studied, from

1997 – till date. I have a teaching & research

experience of 17 years, teaching subjects: Zoology,

Biotechnology, , Cell biology, Cell biology & Genetics

etc.I have Investigated around 7 research problems in various fields of science .

1. Books published: 01

2. Papers published in National and International journals: 15

3. UGC minor project: 1 (4, 10,000)

4. National and International Seminars/Conferences’/Symposia/Workshop/ Chaired/

Attended: 70

5. Presently Working on Birds of Kurnool District.

6. Member of various professional bodies and in editorial board and reviewer of many

journals.

Life Member of The Indian Science Congress Association, Kolkata, India –10

December 2010,

Life Member of CELL INDIAN SOCIETY OF BIOLOGY, India 2010,

Life Member of ISCAP Tirupati, India –December 2010,

Member of ISSLR, 2010

Member of ISZS , CHINA 2010,

Documents

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