Dermody and Shiffman (2022) state that cigarette smoking is the predominant risk factor for chronic obstructive pulmonary disease (COPD) in the United States. Nevertheless, a risk factor does not imply that it is a causative element. Dermody and Shiffman (2022) assert that this phrase often denotes attributes linked to a phenomenon rather than serving as a direct causal factor. In the same research, the scientists examined the prevalence of chronic obstructive pulmonary disease (COPD) in both smokers and nonsmokers. They discovered that those who had ever smoked at any point in their lives and had been diagnosed with COPD had a prevalence rate of 17.8%. On the other hand, those who had never smoked had a prevalence rate of 6.4%.
Hill’s Guidelines & Causal Evidence
As per Aschengrau and Saege (2018), Hill has established nine criteria for evaluating causation: Strength of connection, consistency, specificity, timing, biological gradient, plausibility, coherence, experiment, and analogy. This criterion is often used to ascertain if an observed correlation is causal. Strength of association refers to the degree to which a link is considered more probable or believed to exist rather than being definitively proven as causative. Several research have extensively examined the correlation between COPD and smoking, which is why the degree of connection was selected as one of the four criteria to establish the causal link. Research conducted by Kreis et al. (2013) revealed a strong correlation between the duration of smoking and the occurrence of diagnosed COPD. As defined by Naramore et al. (2019), consistency pertains to similar results across various populations and research methodologies.
The investigation of the association between COPD and smoking included primarily three kinds of studies: systematic reviews, cohort studies, and experimental investigations. In a study conducted by the Office of the Surgeon General of the United States Health Service more than 35 years ago, approximately 7000 research articles on smoking and its many detrimental health consequences, including COPD, were examined, as reported by the CDC (2022). Naramore et al. (2019) define biological gradient as the change in intensity that directly affects the severity of the consequence. Another research discovered a significant rise in the risk of chronic obstructive pulmonary disease (COPD) associated with extended smoking duration, advanced age, and higher smoking intensity. The selection of this recommendation was based on its ability to strengthen the concept of causation in the correlation between COPD and smoking. Finally, the Hills guideline experiment investigates the impact of eliminating exposure, such as cigarettes, on the development of COPD. Tashkin (2015) suggests that the most efficient approach is to mitigate the course of COPD and decrease death rates. According to Wheaton (2019), the occurrence rate of COPD among those who have never smoked is 2.8%, but it is 15.2% in those who have smoked. This guideline elucidates the disparity in outcomes between the absence and presence of exposure.
Conclusion
There is substantial evidence supporting the causal association between smoking and the diagnosis of COPD. According to the CDC (2022), secondhand smoke is also recognized as a contributing factor to the onset of COPD. According to Naramore et al. (2019), smoking is the primary factor contributing to the development of COPD. Furthermore, smoking also leads to repeated exacerbations by causing damage to the air sacs and lining of the lungs. Multiple studies have shown that smoking is the primary causative factor for COPD. While Hill’s principles are often used, there is a contention that they do not sufficiently distinguish between causal and non-causal interactions. In order to establish a cause-and-effect relationship, it is necessary to have obvious connections between two variables rather than merely an association since various explanations might be used for this purpose.
References
Dermody, S., & Shiffman, S. (2022). The time-varying effect of alcohol use on cigarette smoking relapse risk. https://doi.org/10.32920/21618720.v1
Kreis, I. A., & Cromwell, D. A. (2013). Study designs for public health investigations: Basic concepts and practice. Essentials of Environmental Epidemiology for Health Protection, pp. 135–147. https://doi.org/10.1093/med/9780199663415.003.0014
Naramore, R., Wille, K., & Bhatt, S. (2019). Causes of mortality post single vs double lung transplantation for COPD. Chest, 156(4), A3. https://doi.org/10.1016/j.chest.2019.08.096
CDC. (2022). Smoking and COPD. Centers for Disease Control and Prevention. https://www.cdc.gov/tobacco/campaign/tips/diseases/copd.html
Tashkin, D. (2015). Smoking cessation in chronic obstructive pulmonary disease. Seminars in Respiratory and Critical Care Medicine, 36(04), 491–507. https://doi.org/10.1055/s-0035-1555610
Dugdale, D. (2021). Smoking and COPD. Medline Plus. https://medlineplus.gov/ency/patientinstructions/000696.htm
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