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Essay / CPSE - 844
The authors of the article are Jesse D. Troy (and corresponding author), Brenda Diergaarde, Joel L. Weissfeld, Jennifer R. Grandis, and Ada O. Youk.Jesse D. Troy, Brenda Diergaarde and Joel L. Weissfeld work at the University of Pittsburgh in the Graduate School of Public Health's Department of Epidemiology and Cancer Institute. Jennifer R. Grandis works in the Department of Otolaryngology at the University of Pittsburgh School of Medicine. Ada O. Youk works in the Department of Biostatistics at the University of Pittsburgh Graduate School of Public Health. They are all in the United States (Troy et al, 2013, p. 417). This is original research to determine whether the carcinogenicity of passive smoke experienced during childhood passive smoke exposure (CPSE) causes head and neck squamous cell carcinoma (HNSCC). ) (p. 417). The research method involved designing a model to link CPSE, HNSCC, and other factors in individuals' direct environment that increase the risk of exposure to carcinogens. These confounders include frequency-matched factors (age, sex, race, recruitment period), smoking status, and alcohol drinking status. The study considered 858 HNSCC cases (104 never smokers) and 806 cancer-free controls (415 never smokers) as the study sample. Participants completed a questionnaire to provide data on demographics, risk factors, their history of CPSE, and other lifestyle factors related to HNSCC or cancer (pp. 417-418). They provided basic details such as frequency and cigarettes smoked per day by a smoking family. member and the duration of exposure to second-hand smoke (SHS) to estimate CPSE. Out of 806, 64% of controls had CPSE and the frequency of CSPE was 73.8%. The model was modified to study...... middle of paper ......s. Using questionnaires to collect data on risk factors limits the amount of information collected on the CPSE. For example, they observed that sibling smoking was associated with an increased risk of HNSCC among nonsmokers, but they were unable to further study the effects of their birth order. Finally, they did not have enough tumor samples to study the association between HPV and CPSE in oropharyngeal cases (p.421). In theory, the carcinogenic mechanisms of passive smoke exposure are similar to those of smoking since carcinogenic compounds (such as S-NNN) in cigarettes do not racemize. The conclusive results indicate that CPSE plays a role in the causation of HNSCC, especially oropharyngeal cancer in nonsmokers. Therefore, smoking household members should avoid smoking in the home to avoid exposing non-smoking members to the risks associated with SHS..