Skip to main content

CHRONIC MUCUS HYPERSECRETION AND CHRONIC OBSTRUCTIVE LUNG DISEASE THE MOST DISABLING HEALTH EFFECTS OF TOBACCO

Pharma courses

GPAT courses

Apollo Pharmacy hiring

pharma courses

pharma courses

Apollo Pharmacy hiring

About Authors:
Chinedu Enegide*, Mr. Kennedy I. Amagon
Department of Science Lab. Tech.
(Physiology/Pharmacology Tech.),
University of Jos, Nigeria
chinex.snow@gmail.com

Abstact
The use of tobacco have been in existence for long and have also been widely abused. Tobacco is now the leading cause of preventable death in the world today. An estimate of more than 5 million deaths  are recorded world-wide, yearly. Prediction also shows that deaths caused by tobacco may escalate to about 8 million by 2030. Statistics have shown that one out of every five deaths annually is caused by cigarette smoking. This statistics reveals about 440,000 smoking-related deaths yearly, and about 49,000 of these deaths are due to passive smoking. Both voluntary and involuntary (passive) smokers are at risk of the effects of tobacco. The effects of tobacco includes increased stress, alteration of brain cells chemistry, alteration of lipid profile, facilitation of atherosclerosis, increase in heart-rate and blood pressure, gastroesophageal reflux disease, peptic ulcer disease, micro-nutrient disorders, oxidtive damage, bronchospasm, chronic mucus hypersecretion and chronic obstructive lung disease. But however, chronic mucus hypersecretion and chronic obstructive lung disease stands out to be the most disabling effect of tobacco. As these effects are known to reduce one's physical performance, breathing capacity as well as fitness (both present and future). It is therefore advised that better measures for controlling tobacco usage especially in public places should be employed. As this will help to reduce the treat it currently posess on public health (especially the high rate of chronic mucus hypersecretion and chronic obstructive lung disease occurrence caused by tobacco).

[adsense:336x280:8701650588]

Reference Id: PHARMATUTOR-ART-1970

Introduction
Tobacco is a product from the dried leaves of tobacco plant (Nicotiana sp.). The dried leaves are usally treated with chemicals (like carbon monoxide, ammonia, toluene, acetone, arsenic, cadmium, butane, hydrogen cyanide etc) before being converted into cigarettes. The use of tobacco have been in existence for long and have also been widely abused. Though consuption is usually by smoking, other methods include  chewing and suffing. Tobacco constituets (such as nicotine and tar) and the chemicals used in processing it are however known to ellicit a number of harmful effects in the body. [1] Tobacco is now the leading cause of preventable death in the world today. An estimate of more than 5 million deaths are recorded world-wide, yearly. Prediction also shows that deaths caused by tobacco may escalate to about 8 million by 2030. [2] Statistics have shown that one out of every five deaths annually is caused by cigarette smoking. This statistics reveals about 440,000 smoking-related deaths yearly, and about 49,000 of these deaths are due to passive smoking. [3, 4] Therefore, this inidicates that both voluntary and involuntary (passive) smokers are at risk of the effects of tobacco. Passive smokers are usually nonsmokers who are exposed to second-hand smoke from the tobacco of voluntary smokers. This may be at the places of work, shopping centres, public transports, eateries and other public places. Hence tobacco poses a serious treat to pubic health. [5] The effects of tobacco are enomous with severe implications.

[adsense:468x15:2204050025]

Some Effects of Tobacco

1 Effect on the brain

  • Increase stress: It has been shown that smokers have increased stress levels more than non-smokers, and this is contrary to the common belief that it eases stress. A feel of relaxation felt after smoking is a mere return to the normal unstressed state of non-smokers. [6-8]
  • Alteration of brain cells chemistry: It has been proven that there are fewer dopamine receptors in the brain cells of smokers when compared to those in the brain cells of non-smokers. [8, 9]

2 Effect on the cardiovascular system

  • Alteration of lipid profile: Tobacco alters the lipid  profile due to its nicotine component. It decreases high density lipoprotein (HDL) and increases low density lipoprotein (LDL), triglyceride and cholesterol levels in the blood. This increses the risk for the ocurence of heart failure. [10]
  • Facilitates atherosclerosis: It has been shown that tobacco hastens the occurence of atherosclerosis, this have been backed-up by the increase of its occurence in smokers more than non-smokers. [10]
  • Increases heart rate and blood pressure:Literature have shown that tobacco increases heart rate and this may lead to the over-working of the heart which may lead to heart failure. [11] It has also been proven that tobacco increases blood pressure above the normal range. This increase may lead to damage in organs like the kidney. [12]

3 Effect on gastrointestinal system

  • Causes gastroesophageal reflux disease: Tobacco smoking causes an alteration in the esophageal acid-base balance (favouring acidity) in smokers. There is also loosening of the lower eophageal sphinter (which is the muscle separating the esophagus and stomach), and this allows the reflux of acidic contents in the stomach into the esophagus. These effects may lead to heart-burn, inflammation of the esophagus and barretts esophagus. [13-15] This may latter escalate into esohageal cancer. [16]
  • Causes peptic ulcer disease: Tobacco smoking increases acid seretion in the stomach and esophagus. It also decreases the secretion of mucus in this region. There is also an apparrent reduction of blood flow to the esophagus, stomach and intestines due to smoking. All these factors put together prevents wound-healing in the gastrointestinal region when it occurs. The unhealed wounds then develop into peptic ulcer if not treated. [17]
  • Halitosis (bad breath): Tobacco smoking causes bad breath, and this is also accompanied by smelling hair and teeth colouration. These effects are the  immediate, but unreactive effects of tobacco smoking. [18]

4 Effect on the metabolic system

  • Micro-nutrient disoders: Tobacco smoking interfers with the absorption of some micro-nutrients (like vitamins B, C and E) from the gastro-intestinal system leading to their deficiency. The deficincy of vitamin B may lead to prolonged diarrhea, anemia and swelling of the tongue. Deficiency of vitamin C results results to scurvey, while vitamin E deficiency causes red blood cells degradation, irreversible nerve damage and eye disease. [19]
  • Oxidative damage: Tobacco smoking alters the oxidant and anti-oxidant balance in the body. This is due to the degradative effect of tobacco on the anti-oxidants in the body. This leads to an increase in oxidative activities in the body. This can result in cell damage, blood vessels damage, heart disease and cancer. [20, 21]

5 Effect on respiratory system

  • Bronchospasm: This is the abnormal tightening of the lungs airway. This normally leads to the narrowing of the airways and this causes wheezing which is similar to that experinced in asthmatic attacks. This reaction is common with smokers even when they do not have asthma. [22] The condition is however worsened in ashtmatics when they participate voluntarily in smoking or involuntarily (passively) by inhaling second-hand cigarette smoke from the environment. [23]
  • Chronic mucus hyperseretion and chronic obstructive lung disease:
    The lungs (goblet cells) secretes mucus and its function is to filter-out toxic substances from the air passing through the lungs. Cillia (finger-like hair) present on the lung surface produces a kind of rhythmic movement which helps to clear-the mucus and the substances trapped by it. Tobacco smoke promotes the growth of the goblet cells of the lungs, leading to an increase in secretion (hypersecretion) of the mucus. [24] Tobacco smoke also immobilizes the cillia and this hinders the elimination of the mucus and the substances trapped by it. This phenomenom coupled with the hypersecretion of mucus, leads to an obstruction of the lungs airway. [25] It is usually called obstructive lung disease. When these effects are prolonged, they are now referred to as chronic mucus hypersecretion and chronic obstructive lung disease. Chronic mucus hypersecretion generally causes persistent productive cough and this is aimed at clearing the accummulated mucus and substances trapped by it from the air passing the lung.  However, chronic obstructive lung disease causes diffiulty in breathing and it is irreversible. This complication ones it escalates may lead to death. [26] Chronic obstructive lung disease is now wide spread in both developed and developing countries all over the world, and occurence have largely been attributed to tobacco use age. [27, 28, 29] Statistics have shown that about 80-90% chronic obstructive disease occurence in developed countries  are caused by tobacco. [28] Of the numerous effects caused by tobacco, chronic mucus hypersecretion and chronic obstructive lung disease are the most disabling effects of tobacco. A combination of both effects have been proven to reduce one's physical performance, breathing capacity as well as fitness (both present and future), [8] hence disabling and preventing such individual from participating in most normal life's activities.

NOW YOU CAN ALSO PUBLISH YOUR ARTICLE ONLINE.

SUBMIT YOUR ARTICLE/PROJECT AT articles@pharmatutor.org

Subscribe to Pharmatutor Alerts by Email

FIND OUT MORE ARTICLES AT OUR DATABASE

Conclusion
It is now very glaring that there are enomous adverse effects of tobacco smoking both to voluntary smokers and passive smokers. With chronic mucus hypersecretion and chronic obstructive lung disease being enlisted as one of these effects and also the must disabling effects. It is therefore advised that better measures to control and restrict the smoking of tobacco especially in public places should be developed. As this will help to reduce the treat it currently posess on public health ( especially the high rate of chronic mucus hypersecretion and chronic obstructive lung disease occurrence caused by tobacco).

Referenes:
1. Drug and Alcohol Services South Australia (DASSA ). Tobacco and Its Effects, 2010. dassa.sa.gov.au/site/ [accessed 2013 August 20].
2. World Health Organization. WHO Report on the Global Tobacco Epidemic, 2011. Geneva: World Health Organization, 2011 [accessed 2013 August 20].
3. Centers for Disease Control and Prevention. Smoking-Attributable Mortality, Years of Potential Life Lost, and Productivity Losses—United States, 2000–2004. Morbidity and Mortality Weekly Report  2008;57(45):1226–8.
4. U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2011.
5. Fielding, JE and Phenow, KL. New England Journal of Medicine 1988; 319: 1452-60
6. Caumo, W, et al, “Risk factors for preoperative anxiety in adults,” Acta Anaestheiologica Scandinavica 45(3):298-307, March 2001.
7. Parrott, AC, “Does Cigarette Smoking Cause Stress?,” American Psychologist 54(10):817-20, October 1999.
8. Campaign for Tobacco free Kids. Smoking's Immediate Effect on the Body. tobaccofreekids.org/facts_issues/fact_sheets/toll/products
9. Trauth, JA, “An animal model of adolescent nicotine exposure: effects on gene expression and macromolecular constituents in rat brain regions,” Brain Research, 867(1-2):29-39, June 2000
10. Mitchell, B, et al., “Tobacco Use and Cessation: The Adverse Health Effects of Tobacco and Tobacco-Related Products,” Primary Care: Clinics in Office Practice 26(3):463-98, September 1999.
11. Primatesta, P, et al., “Association between smoking and blood pressure,” Hypertension 37:187-193, 2001.
12. Righetti, M & Sessa, A, “Cigarette smoking and kidney involvement,” Journal of Nephrology, 14(1):3-6, January-February 2001
13. Fitzpatrick, TM & Blair, EA, “Smoking and pulmonary and Cardiovascular Disease: Upper Airway Complications of Smoking,” Clinics in Chest Medicine 21(1):147-157, March 2000;  Kadakia, SC, et al., “Original contributions: Effect of Cigarette smoking on Gastroesophageal Reflux Measured by 24 h Ambulatory Esophageal pH Monitoring,” American Journal of Gastroenterology  90(10):1785-1791, October 1995; Kahrilas, PJ, “Mechanisms of acid reflux associated with cigarette smoking,” Gut 31(1):4-10, January 1990
14. Brodish, PH, “The Irreversible Health Effects of Cigarette Smoking,” The American  Council on Science & Health, June 1998; Fitzpatrick, TM & Blair, EA, “Smoking and pulmonary and Cardiovascular Disease: Upper Airway Complications of Smoking,” Clinics in Chest Medicine 21(1):147-157, March 2000; Kadakia, SC, et al., “Original contributions: Effect of Cigarette smoking on Gastroesophageal Reflux Measured by 24 h Ambulatory Esophageal pH Monitoring,” American Journal of Gastroenterology  90(10):1785-1791, October 1995; Karilas, 1990; Wo, JM and Waring, JP, “Medical Therapy of Gastroesophageal Reflux and Management of Esophageal Strictures,” Surgical Clinics of North America 77(5):1041-62, October 1997.
15. Fitzpatrick, TM & Blair, EA, “Smoking and pulmonary and Cardiovascular Disease: Upper Airway Complications of Smoking,” Clinics in Chest Medicine 21(1):147-157, March 2000; Katz, PO, “Gastroesophageal Reflux Disease,” Journal of the American Geriatrics Society 46(12):1558-65, December 1998.
16. Falk, GW, “Barrett’s esophagus,” Gastroenterology 122(6):1569-91, May 2002.
17. Mitchell, B, et al., “Tobacco Use and Cessation: The Adverse Health Effects of Tobacco and Tobacco-Related Products,” Primary Care: Clinics in Office Practice 26(3):463-98, September 1999; Cotran, Robbins Pathologic Basis of Disease, 6th Edition, 499-503, 1999; Coroll, Primary Care Medicine, 3rd Edition, 1995; Sabiston, 1997
18. Katz, PO, “Gastroesophageal Reflux Disease,” Journal of the American Geriatrics Society 46(12):1558-65, December 1998; Belfiglio, G, “’Breath Mint’. Two words are the centerpiece of HealthPartners’ successful anti-tobacco campaign, the winner of AAHP’s Community Leadership Award,” Healthplan 38(4):46-52,54, July-August 1997; Lamkin, L & Houston, TP, “Adolescent Medicine: Nicotine Dependency & Adolescents: Preventing & Treating,” Primary Care, 25(1):123-35, March 1998; U.S. Preventive Services Task Force, Guidelines from Guide to Clinical Preventive Services, Second Edition,1996.
19. Goldman, Cecil Textbook of Medicine, 21st Edition, 2000; Feldman, Sleisenger and Fordtrans’ Gastrointestinal & Liver Disease, Sixth Edition, 1998.
20. Goldman, Cecil Textbook of Medicine, 21st Edition, 2000.
21. Gidding, SS, “Pediatric Cardiology; Preventive Pediatric Cardiology- Tobacco, Cholesterol, Obesity, and Physical Activity,” Pediatric Clinics of North America 46(2):253-262, April 1999.
22. Behrman: Nelson Textbook of Pediatrics, Sixteenth Edition, Copyright 2000 W.B. Saunders Company; Brodish, PH, “The Irreversible Health Effects of Cigarette Smoking,” The American Council on Science & Health, June 1998.  
23. Behrman: Nelson Textbook of Pediatrics, Sixteenth Edition, Copyright 2000 W.B. Saunders Company; Brodish, PH, “The Irreversible Health Effects of Cigarette Smoking,” The American Council on Science & Health, June 1998; Mitchell, B, et al., “Tobacco Use and Cessation: The Adverse Health Effects of Tobacco and Tobacco-Related Products,” Primary Care: Clinics in Office Practice 26(3):463-98, September 1999; U.S. Department of Health & Human Services (HHS), Preventing Tobacco Use Among Young People: A Report of the Surgeon General, 1994. 16 Behrman: Nelson Textbook of Pediatrics, Sixteenth Edition, Copyright
24. Behrman: Nelson Textbook of Pediatrics, Sixteenth Edition, Copyright 2000 W.B. Saunders Company; HHS, Preventing Tobacco Use Among Young People: A Report of the Surgeon General, 1994.
25. Takeyama, K, et al, “Activation of epidermal growth factor receptors is responsible for mucin synthesis induced by cigarette smoke,”   American Journal of Physiology:  Lung Cellular & Molecular Physiology, 280(1):L165-72, January 2001.  Maestrelli, P, et al, “Remodeling in response to infection and injury. Airway inflammation and hypersecretion of mucus in smoking subjects with chronic obstructive pulmonary disease,” American of Respiratory & Critical Care Medicine 164(10 Pt 2):S76-80, November 15, 2001
26. Laurence D.R, Bennett P.N and Brown M.J. Clinical Pharmaclogy, Eight Edition, Churchill Livingstone, 1998.
27. Barnes PJ. Chronic obstructive pulmonary disease. New England Journal of Medicine 2000;343.269-280.
28. Chen JC, Mannino DM. Worldwide epidemiology of chronic obstructive pulmonary disease. Current Opinion in Pulmonary Medicine 1999;5.93-99.
29. Hurd S. The impact of COPD on lung health worldwide. Chest 2000;117 (suppl):1S-4S

NOW YOU CAN ALSO PUBLISH YOUR ARTICLE ONLINE.

SUBMIT YOUR ARTICLE/PROJECT AT articles@pharmatutor.org

Subscribe to Pharmatutor Alerts by Email

FIND OUT MORE ARTICLES AT OUR DATABASE