Extract
We read with great interest the work published by Yoon et al. [1]. The authors found that a high concentration of nitrogen dioxide at an individual's residential address is significantly associated with increased mortality in idiopathic pulmonary fibrosis (IPF) patients when all confounders are included in the health analysis model. However, an important question that remains unclear in the study is whether active or passive cigarette smoking-associated release of nitrogen dioxide or particulate matter plays a role in the clinical outcome of IPF patients. Consistent evidence reported in previous studies showing that smokers are at high risk of developing IPF and/or acute exacerbation of the disease underscores the relevance of smoking as a confounding factor in the clinical outcome of IPF patients [1–3]. Also, based on the literature, there is no doubt that tobacco smoke is a source and an important contributor to increased indoor levels of nitrogen dioxide and particulate matter [4]. In the study, the authors stratified their patients by age and sex for subgroup analysis and found a similar significant association between nitrogen dioxide and IPF mortality. However, subgroup analysis by the smoking history of the patients was not reported. Tobacco smoke exposure was included only as a confounder in the health analysis model (models 3 and 4) [1]. The effect of tobacco smoke in this study is of particular interest because of the person-focused research design used to measure the environmental pollutants. Theoretically, the person-centered approach would increase the power of the model to deny or confirm the influence on the outcome of a confounding factor closely associated with the patient's lifestyle. In addition to the active cigarette smoking history, the model would become even more powerful if the history of smoking by family members or neighbors is also included. Among all patients (n=1114) included in the study, the number of ever-smokers (n=846) was significantly higher than that of smokers. However, the population of patients with a history of smoking (n=268) was sufficiently large to negate or confirm the involvement of smoking-derived pollutants in the clinical outcome of IPF. Thus, we believe it would be appropriate and valuable to perform and provide the results of subgroup analysis by tobacco exposure. This information would help to design future epidemiological studies and therapeutic strategies to predict and prevent the effect of smoking-derived pollutants on mortality in IPF patients.
Footnotes
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Conflict of interest: Dr. Yasuma reports grants from Shionogi, outside the submitted work.
Conflict of interest: Dr. D'Alessandro-Gabazza reports grants from Shionogi Pharmaceutical Inc., grants from Astellas Pharmaceuticals Inc., grants from Asahi Kassei, outside the submitted work.
Conflict of interest: Dr. Hataji has nothing to disclose.
Conflict of interest: Dr. Kobayashi reports grants and personal fees from Chugai, grants and personal fees from Pfizer, grants and personal fees from ONO, grants from TAIHO, grants and personal fees from Boehringer Ingelheim, grants and personal fees from Eli Lilly, outside the submitted work.
Conflict of interest: Dr. Gabazza reports grants from Shionogi Pharmaceutical Inc., grants from Astellas Pharmaceuticals Inc., grants from Asahi Kassei, outside the submitted work.
- Received May 15, 2021.
- Accepted May 28, 2021.
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