CPSE

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The authors of the article are Jesse D. Troy (and the 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 University of Pittsburgh in the Department of Epidemiology Graduate School of Public Health and The Cancer Institute. Jennifer R. Grandis works in the Department of Otolaryngology in University of Pittsburgh School of Medicine. Ada O. Youk works at the Department of Biostatistics, University of Pittsburgh Graduate School of Public Health. They are all in the United States (Troy et al, 2013, p. 417)

It is an original research aimed to investigate whether the carcinogenicity of passive smoke experienced through Childhood passive smoke exposure (CPSE) causes head and neck squamous cell carcinoma (HNSCC) (p. 417).

The research method involved designing a model to relate CPSE, HNSCC and other factors in individuals’ direct environment that increase the risk of exposure to carcinogens. These confounding factors include the frequency-matched factors (age, sex, race, recruitment period), smoking status, and drinking status. The study considered 858 HNSCC cases (104 being never smokers) and 806 cancer-free controls (415 being never smokers) as the study sample. The participants filled in questionnaire to provide data on demographics, risk factor, their history of CPSE and other lifestyle factors related to HNSCC or cancer (pp. 417-418).

They provided background details such frequency and cigarettes smoked per day by a smoking family member, and duration they were exposed to second hand smoke (SHS) to estimate CPSE. Of 806, 64% of the controls had CPSE and the frequency of CSPE was 73.8%. The model was modified to investig...

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...s. The use of questionnaires to gather risk factor data limits the amount of information collected about CPSE. For example, they observed that sibling smoking was associated with increased risk of HNSCC in never-smokers, but they could not further investigate the effects of their birth order. Lastly, they did not have enough samples of tumors to study the association between HPV and CPSE in oropharyngeal cases (p.421).

From theory, the carcinogenic mechanisms of passive smoke exposure are similar to that of cigarette smoking since the carcinogenic compounds (such as S-NNN) in cigarette do not racemize. The conclusive results indicate that CPSE has a role in HNSCC causation, particularly oropharynx cancer in never-smokers. Hence, smoking households members should avoid smoking in the house to avoid exposing non-smoking members to whatever risks associated with SHS.

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