Smoking Case Study

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Question 4 Answer:
Smoking damages the whole body, but for this answer, I am going to focus on smoking and the changes to our respiratory tract, skin blood vessels and antioxidant levels.
Respiratory tract: “(1) Nicotine constricts terminal bronchioles, which decreases airflow into and out of the lungs. (2) Carbon monoxide in smoke binds to hemoglobin and reduces its oxygen-carrying capability. (3) Irritants in smoke cause increased mucus secretion by the mucosa of the bronchial tree and swelling of the mucosal lining, both of which impede airflow into and out of the lungs. (4) Irritants in smoke also inhibit the movement of cilia and destroy cilia in the lining of the respiratory system. Thus, excess mucus and foreign debris are not easily
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Tortora, G. & Derrickson, B. (2017). Principles of Anatomy and Physiology, 15th ed. New York: John Wiley & Sons Inc. p 889.
2. Sela BA. Dermatological manifestations of smoking. Harefuah. 2002 Aug;141(8):736-40, 760. Review. Hebrew. PMID: 12222141
3. Powell J.T. (1998) Vascular damage from smoking: Disease mechanisms at the arterial wall. Vasc Med 3:21–28.

4. Alberg A. The influence of cigarette smoking on circulating concentrations of antioxidant micronutrients. Toxicology. 2002 Nov 15;180(2):121-37. Review. PMID: 12324189

Question 3 Additon:
Hi Emily,
I wanted to share something I found on thirdhand smoke. "Thirdhand smoke (THS) refers to components of secondhand smoke that stick to indoor surfaces and persist in the environment" (1). When I was a teacher, I would collect the student's homework folders daily and knew which children had a parent that smoked in the house. As the child opened their folder, I would smell the cigarette smoke coming off of the paper. I could only imagine the level of thirdhand smoke in their home if I was smelling it on their
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Zonulin is a protein with the ability to unzip the tight junctions of the cells lining the digestive tract causing leaky gut. “The two major triggers of zonulin release that have been described so far are bacteria and gliadin. It is well described that many enteric pathogens are able to produce enterotoxins that affect the intestinal tight junction of the host. In addition to enteroxins, several enteric pathogens, including commensal Eschericha coli, lab E. coli, virulent E. coli, and Salmonella typhi have been shown to cause a release of zonulin from the intestine when applied to the apical surface” (1). Gliadin is a protein found in gluten which stimulates zonulin release. Those suffering with celiac disease and also with nonceliac gluten sensitivity have been found to have a high level of serum zonulin which can cause leaky gut and inflammation. “Dysbiosis of the microbiome may cause the release of zonulin leading to the passage of luminal contents across the epithelial barrier causing the release of pro-inflammatory cytokines. The presence of cytokines eventually sustains the increased permeability causing massive influx of dietary and microbial antigens leading to the activation of T-cells”

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