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Alsharairi, N. Supplements for Smoking-Related Lung Diseases. Encyclopedia. Available online: https://encyclopedia.pub/entry/6101 (accessed on 06 May 2024).
Alsharairi N. Supplements for Smoking-Related Lung Diseases. Encyclopedia. Available at: https://encyclopedia.pub/entry/6101. Accessed May 06, 2024.
Alsharairi, Naser. "Supplements for Smoking-Related Lung Diseases" Encyclopedia, https://encyclopedia.pub/entry/6101 (accessed May 06, 2024).
Alsharairi, N. (2021, January 05). Supplements for Smoking-Related Lung Diseases. In Encyclopedia. https://encyclopedia.pub/entry/6101
Alsharairi, Naser. "Supplements for Smoking-Related Lung Diseases." Encyclopedia. Web. 05 January, 2021.
Peer Reviewed
Supplements for Smoking-Related Lung Diseases
This is a peer-reviewed entry published in Encyclopedia Journal, full entry can be found at 10.3390/encyclopedia1010010

Supplements for smoking-related lung diseases are considered as nonfood products and thought to improve health. Multivitamins and antioxidants are the most commonly dietary supplements used by cancer and asthma patients. There are currently no clear regulatory guidelines that include dietary supplements and their effect on lung cancer and asthma patients, particularly in smokers. Several countries have taken steps to overcome challenges in regulating dietary supplements in the marketplace. These challenges include inadequate assurance of safety/efficacy, inaccuracy of product labeling, misleading health claims, and lack of analytical techniques for dietary supplements. There is a need to establish standards and regulation of dietary supplement use in patients with lung cancer and asthma. The aim of this entry is to expand knowledge on dietary supplements use and smoking-related lung diseases (lung cancer and asthma). 

asthma lung cancer supplements smokers nonsmokers
Smoking is known as one of the main causes of lung cancer and the most common cause of cancer mortality in men and women worldwide [1]. It has been estimated that around 7 million global deaths per year were caused by smoking [2][3][4]. Cigarette smoke is comprised of thousands of chemical compounds, most of which are toxins [5]. Lung cancer is classified into small cell lung cancer (SCLC) and non-small-cell lung cancers (NSCLCs), with the latter accounting for 85% of lung cancer cases, which is divided into three common subtypes-associated smoking, including large-cell carcinoma, squamous-cell carcinoma, and adenocarcinoma [6]. Reviews of published systematic reviews and meta-analyses have confirmed that the risk of lung cancer is increased in current and former smokers [7][8][9][10][11]. In fact, tobacco smoke is the largest contributor to adenocarcinoma and small-cell and squamous cell carcinoma, with over 76% of lung cancer deaths in men and 37–42% of lung cancer deaths in women aged ≥50 years attributable to tobacco use [12]. The link between smoking and lung cancer risk varies significantly by sex. A number of systematic reviews and meta-analyses examined the sex differences in smoking-related risk of lung cancer. One previous systematic review and meta-analysis showed that currently smoking men had higher susceptibility to lung cancer than women [13]. In a recent meta-analysis, currently/formerly smoking men and women had an increased risk of lung cancer, with no significant sex differences observed [14]. Another recent meta-analysis showed that passive smoking/secondhand smoking (SHS) increased the risk of lung cancer in nonsmoking women [15]. A few studies that have examined the sex differences in histological types of lung cancer have shown that lung adenocarcinoma incidence was higher in women than in men [16][17]. Although a declining prevalence of smoking among women was noted, the risk of mortality from smoking continues to rise [18].
Epidermal growth factor receptor (EGFR) mutations have emerged as a key player in lung tumor development. EGFR stimulates two main downstream signaling pathways; the phosphoinositide 3-kinase (PI3K) and the Ras–Raf–mitogen-activated protein kinase kinase (MEK)–mitogen-activated protein kinase (MAPK) [19]. Kirsten rat sarcoma viral oncogene homolog (KRAS) is identified as the most predominantly mutated oncogene, with mutations occurring at codons 12 and 13 in NSCLCs [19], particularly among smokers rather than nonsmokers in patients with lung adenocarcinoma [20][21], and affects cellular processes, including tumor angiogenesis, gene transcription, and cell proliferation [22][23][24]. By contrast, the tyrosine kinase (TK) domain mutations of the EGFR gene are more frequently found in patients with lung adenocarcinoma in nonsmokers than in smokers [25]. Deregulation of EGFR signaling in all histological types may contribute to lung pathogenesis. In fact, aberrant EGFR signaling pathways in most NSCLCs are activated by stimulating EGFR gene mutation, enhancing receptor–ligand binding and increasing the EGFR gene copy number via polysomy/amplification [23][24].
Asthma is one of the major prevalent chronic inflammatory diseases among young adults, the prevalence of which has been shown to be higher in developed countries than developing countries [26], and higher in females than males [27]. Asthma mortality rates were lower than other chronic diseases [28]. However, asthma mortality rates increased with increasing age, and the highest mortality rate was seen in adults aged 65 and over [29]. Asthma mortality data reported that the Netherlands and South Africa had the highest asthma mortality rate globally [26]. Adult-onset asthma may increase the risk of comorbid conditions such as dyspepsia, fluid and electrolyte disorders, chronic obstructive pulmonary disease (COPD), hypertension, congestive heart failure, and diabetes [30].
Asthma is characterized by airway hyperresponsiveness, which results in episodes of shortness of breath (dyspnea), coughing, chest tightness, and wheezing [31]. The type 2 immune responses (Th2) are associated with asthma and mediated by IgE-producing B cells, basophils, type 2 innate lymphoid cells (ILC2s), cytokines, mast cells, and eosinophils [32][33]. A number of environmental factors, including smoking, are associated with the development of asthma in children and adults [34]. Tobacco smoking is reported to cause nearly 10% of asthma mortality worldwide [12]. Tobacco smoke provokes asthma exacerbations and causes other allergy symptoms to worsen in adults [34]. There is also unequivocal evidence that SHS exposure is the main contributor to asthma and lung cancer risk in nonsmokers, disproportionately affecting women [7]. Smoking is able to trigger Th2 inflammation and increase the production of pro-inflammatory cytokines, including interleukin (IL)-4, IL-5, IL-6 IL-13, IL-17A, interferon-γ (IFNγ), and tumor necrosis factor α (TNF-α) [34]. A few studies showed higher levels of total immunoglobulin E (IgE) [35][36], sensitive C-reactive protein (hs-CRP), and malondialdehyde (a marker of oxidative stress) [36], in current and passive smokers than never-smokers. Other studies showed increased white blood cell (WBC) counts, and blood monocytes, lymphocytes, neutrophils, and leukocytes in current smokers in comparison to nonsmokers [37][38]. Cigarette smoking stimulates nasal epithelial cells, resulting in increased lipopolysaccharide (LPS) binding, neutrophil chemotaxis, Toll-like receptor (TLR) 4 expression and reactive oxygen species (ROS) production [39]. Cigarette smoking has shown to decrease CD83+ (a surface expression for mature dendritic cells) counts in smoker patients with asthma [40].
Dietary supplement use among adults is rising, but there is a substantial heterogeneity between supplement users depending on the type, consumption frequency, duration, and reason for supplements used [41][42][43]. Dietary supplement use differs by lifestyle and sociodemographic factors and geographical location among adults [44][45][46][47]. Supplement use also varies according to smoking status. Previous studies have shown that ex-and nonsmokers are more likely to be users of supplements than current smokers [45][46].
There is controversy over the role of dietary supplements in reducing or treating lung cancer in smokers and nonsmokers. There is also much uncertainty about its effectiveness and the consequences in asthmatic smokers and nonsmokers, and our understanding of whether dietary supplements can reduce lung cancer risk in asthmatic smokers and nonsmokers remains unclear in the absence of clinical trials [48]. In order to evaluate the safety and effectiveness of dietary supplement use by asthmatic smokers and nonsmokers before, during, and after lung cancer treatment, realistic and reliable studies worldwide are needed.

References

  1. Barta, J.A.; Powel, C.A.; Wisnivesky, J.P. Global epidemiology of lung cancer. Ann. Glob. Health 2019, 85, 8.
  2. Schane, R.E.; Ling, P.M.; Glantz, S.A. Health effects of light and intermittent smoking: A review. Circulation 2010, 121, 1518–1522.
  3. West, R. Tobacco smoking: Health impact, prevalence, correlates and interventions. Psychol. Health 2017, 32, 1018–1036.
  4. GBD 2015 Tobacco Collaborators. Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: A systematic analysis from the Global Burden of Disease Study 2015. Lancet 2017, 389, 1885–1906.
  5. Talhout, R.; Schulz, T.; Florek, E.; van Benthem, J.; Wester, P.; Opperhuizen, A. Hazardous compounds in tobacco smoke. Int. J. Environ. Res. Public Health 2011, 8, 613–628.
  6. Molina, J.R.; Yang, P.; Cassivi, S.D.; Schild, S.E.; Adjei, A.A. Non-small cell lung cancer: Epidemiology, risk factors, treatment, and survivorship. Mayo Clin. Proc. 2008, 83, 584–594.
  7. Jayes, L.; Haslam, P.L.; Gratziou, C.G.; Powell, P.; Britton, J.; Vardavas, C.; Jimenez-Ruiz, C.; Leonardi-Bee, J.; Tobacco Control Committee of the European Respiratory Society. SmokeHaz: Systematic reviews and meta-analyses of the effects of smoking on respiratory health. Chest 2016, 150, 164–179.
  8. Skaaby, T.; Taylor, A.E.; Jacobsen, R.K.; Paternoster, L.; Thuesen, B.H.; Ahluwalia, T.S.; Larsen, S.C.; Zhou, A.; Wong, A.; Gabrielsen, M.E.; et al. Investigating the causal effect of smoking on hay fever and asthma: A Mendelian randomization meta-analysis in the CARTA consortium. Sci. Rep. 2017, 7, 2224.
  9. Santillan, A.A.; Camargo, C.A., Jr.; Colditz, G.A. A meta-analysis of asthma and risk of lung cancer (United States). Cancer Causes Control 2003, 14, 327–334.
  10. Rosenberger, A.; Bickeböller, H.; McCormack, V.; Brenner, D.R.; Duell, E.J.; Tjønneland, A.; Friis, S.; Muscat, J.E.; Yang, P.; Wichmann, H.E.; et al. Asthma and lung cancer risk: A systematic investigation by the International Lung Cancer Consortium. Carcinogenesis 2012, 33, 587–597.
  11. Qu, Y.L.; Liu, J.; Zhang, L.X.; Wu, C.M.; Chu, A.J.; Wen, B.L.; Ma, C.; Yan, X.Y.; Zhang, X.; Wang, D.M.; et al. Asthma and the risk of lung cancer: A meta-analysis. Oncotarget 2017, 8, 48525.
  12. Institute for Health Metrics and Evaluation. Global Burden of Disease. 2017. Available online: http://vizhub.healthdata.org/gbd-compare/# (accessed on 26 December 2020).
  13. Yu, Y.; Liu, H.; Zheng, S.; Ding, Z.; Chen, Z.; Jin, W.; Ying, K.; Zhang, R.; Ying, F.; Wang, Z.; et al. Gender susceptibility for cigarette smoking-attributable lung cancer: A systematic review and meta-analysis. Lung Cancer. 2014, 85, 351–360.
  14. O’Keeffe, L.M.; Taylor, G.; Huxley, R.R.; Mitchell, P.; Woodward, M.; Peters, S.A.E. Smoking as a risk factor for lung cancer in women and men: A systematic review and meta-analysis. BMJ Open 2018, 8, e021611.
  15. Kim, A.S.; Ko, H.J.; Kwon, J.H.; Lee, J.M. Exposure to secondhand smoke and risk of cancer in never smokers: A meta-analysis of epidemiologic studies. Int. J. Environ. Res. Public Health 2018, 15, E1981.
  16. Kabir, Z.; Connolly, G.N.; Clancy, L. Sex-differences in lung cancer cell-types? An epidemiologic study in Ireland. Ulster Med. J. 2008, 77, 31–35.
  17. Barrera-Rodriguez, R.; Morales-Fuentes, J. Lung cancer in women. Lung Cancer 2012, 3, 79–89.
  18. Allen, A.M.; Oncken, C.; Hatsukami, D. Women and smoking: The effect of gender on the epidemiology, health effects, and cessation of smoking. Curr. Addict. Rep. 2014, 1, 53–60.
  19. Riely, G.J.; Marks, J.; Pao, W. KRAS mutations in non-small cell lung cancer. Proc. Am. Thorac. Soc. 2009, 6, 201–205.
  20. Kempf, E.; Rousseau, B.; Besse, B.; Paz-Ares, L. KRAS oncogene in lung cancer: Focus on molecularly driven clinical trials. Eur. Respir. Rev. 2016, 25, 71–76.
  21. Ferrer, I.; Zugazagoitia, J.; Herbertz, S.; John, W.; Paz-Ares, L.; Schmid-Bindert, G. KRAS-Mutant non-small cell lung cancer: From biology to therapy. Lung Cancer 2018, 124, 53–64.
  22. Wang, Z.D.; Wei, S.Q.; Wang, Q.Y. Targeting oncogenic KRAS in non-small cell lung cancer cells by phenformin inhibits growth and angiogenesis. Am. J. Cancer Res. 2015, 5, 3339–3349.
  23. Gazdar, A.F.; Minna, J.D. Deregulated EGFR signaling during lung cancer progression: Mutations, amplicons, and autocrine loops. Cancer Prev. Res. 2008, 1, 156–160.
  24. Gazdar, A.F. Epidermal growth factor receptor inhibition in lung cancer: The evolving role of individualized therapy. Cancer Metastasis Rev. 2010, 29, 37–48.
  25. Shigematsu, H.; Lin, L.; Takahashi, T.; Nomura, M.; Suzuki, M.; Wistuba, I.I.; Fong, K.M.; Lee, H.; Toyooka, S.; Shimizu, N.; et al. Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. J. Natl. Cancer Inst. 2005, 97, 339–346.
  26. Enilari, O.; Sinha, S. The global impact of asthma in adult populations. Ann. Glob. Health. 2019, 85, 2.
  27. Shah, R.; Newcomb, D.C. Sex bias in asthma prevalence and pathogenesis. Front. Immunol. 2018, 9, 2997.
  28. Dharmage, S.C.; Perret, J.L.; Custovic, A. Epidemiology of asthma in children and adults. Front. Pediatr. 2019, 7, 246.
  29. Baptist, A.P.; Busse, P.J. Asthma over the age of 65: All’s Well That Ends Well. J. Allergy Clin. Immunol. Pract. 2018, 6, 764–773.
  30. Kaplan, A.; Szefler, S.J.; Halpin, D.M.G. Impact of comorbid conditions on asthmatic adults and children. NPJ Prim. Care Respir. Med. 2020, 30, 36.
  31. Quirt, J.; Hildebrand, K.J.; Mazza, J.; Noya, F.; Kim, H. Asthma. Allergy Asthma Clin. Immunol. 2018, 14 (Suppl. 2), 50.
  32. Fahy, J.V. Type 2 inflammation in asthma- present in most, absent in many. Nat. Rev. Immunol. 2015, 15, 57–65.
  33. Dunican, E.M.; Fahy, J.V. The role of type 2 inflammation in the pathogenesis of asthma exacerbations. Ann. Am. Thorac. Soc. 2015, 12 (Suppl. 2), S144–S149.
  34. Strzelak, A.; Ratajczak, A.; Adamiec, A.; Feleszko, W. Tobacco smoke induces and alters immune responses in the lung triggering inflammation, allergy, asthma and other lung diseases: A mechanistic review. Int. J. Environ. Res. Public Health 2018, 15, 1033.
  35. Kim, Y.S.; Kim, H.Y.; Ahn, H.; Sohn, T.S.; Song, J.Y.; Lee, Y.P.; Lee, D.; Lee, J.; Jeong, S.C.; Chae, H.S.; et al. The association between tobacco smoke and serum Immunoglobulin E levels in Korean adults. Intern. Med. 2017, 56, 2571–2577.
  36. Ahmed, N.J.; Husen, A.Z.; Khoshnaw, N.; Getta, H.A.; Hussein, Z.S.; Yassin, A.K.; Jalal, S.D.; Mohammed, R.N.; Alwan, A.F. The effects of smoking on IgE, oxidative stress and haemoglobin concentration. Asian Pac. J. Cancer Prev. 2020, 21, 1069–1072.
  37. Fernández, J.A.F.; Prats, J.M.; Vicente, J.; Artero, M.; Mora, A.C.; Fariñas, A.V.; Espinal, A.; Méndez, J.A.G. Systemic inflammation in 222.841 healthy employed smokers and nonsmokers: White blood cell count and relationship to spirometry. Tob. Induc. Dis. 2012, 10, 7.
  38. Pedersen, K.M.; Çolak, Y.; Ellervik, C.; Hasselbalch, H.C.; Bojesen, S.E.; Nordestgaard, B.G. Smoking and increased white and red blood cells. Arterioscler. Thromb. Vasc. Biol. 2019, 39, 965–977.
  39. Pace, E.; Ferraro, M.; Vincenzo, S.D.; Gerbino, S.; Bruno, A.; Lanata, L.; Gjomarkaj, M. Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells. Toxicol. In Vitro 2014, 28, 292–299.
  40. Tsoumakidou, M.; Elston, W.; Zhu, J.; Wang, Z.; Gamble, E.; Siafakas, N.M.; Barnes, N.C.; Jeffery, P.K. Cigarette smoking alters bronchial mucosal immunity in asthma. Am. J. Respir. Crit. Care Med. 2007, 175, 919–925.
  41. Barnes, K.; Ball, L.; Desbrow, B.; Alsharairi, N.; Ahmed, F. Consumption and reasons for use of dietary supplements in an Australian university population. Nutrition 2016, 32, 524–530.
  42. Gahche, J.J.; Bailey, R.L.; Potischman, N.; Dwyer, J.T. Dietary supplement use was very high among older adults in the United States in 2011–2014. J. Nutr. 2017, 147, 1968–1976.
  43. Kuczmarski, M.F.; Beydoun, M.A.; Shupe, E.S.; Pohlig, R.T.; Zonderman, A.B.; Evans, M.K. Use of dietary supplements improved diet quality but not cardiovascular and nutritional biomarkers in socioeconomically diverse African American and white adults. J. Nutr. Gerontol. Geriatr. 2017, 36, 92–110.
  44. Kim, J.; Lee, J.; Shin, A.; Kang, M.; Shin, D.; Chung, H.; Kim, W. Sociodemographic and lifestyle factors are associated with the use of dietary supplements in a Korean population. J. Epidemiol. 2010, 20, 197–203.
  45. Kofoed, C.L.F.; Christensen, J.; Dragsted, L.O.; Tjønneland, A.; Roswall, N. Determinants of dietary supplement use-Healthy individuals use dietary supplements. Br. J. Nutr. 2015, 113, 1993–2000.
  46. Burnett, A.J.; Livingstone, K.M.; Woods, J.L.; McNaughton, S.A. Dietary supplement use among Australian adults: Findings from the 2011–2012 National Nutrition and Physical Activity Survey. Nutrients 2017, 9, 1248.
  47. Cowan, A.E.; Jun, S.; Gahche, J.J.; Tooze, J.A.; Dwyer, J.T.; Eicher-Miller, H.A.; Bhadra, A.; Guenther, P.M.; Potischman, N.; Dodd, K.W.; et al. Dietary supplement use differs by socioeconomic and health-related characteristics among U.S. adults, NHANES 2011–2014. Nutrients 2018, 10, 1114.
  48. Alsharairi, N. The effects of dietary supplements on asthma and lung cancer risk in smokers and non-smokers: A review of the literature. Nutrients 2019, 11, 725.
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Naser Alsharairi
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