Back to Authors

Neri, Monica

https://orcid.org/0000-0003-4796-3675

Mayo Clinic

Vita-Salute San Raffaele University

Citations 3

Secondhand Tobacco Smoke Exposure and Lung Adenocarcinoma In Situ /Minimally Invasive Adenocarcinoma (AIS/MIA)
Kim, Claire H., Lee, Yuan-Chin Amy, Hung, Rayjean J., Wampfler, Jason A. , Chang, Shen-Chih, Ugolini, Donatella, Neri, Monica , Schwartz, Ann G. , Morgenstern, Hal, Zhang, Zuo‐Feng , Hung, Rayjean J. , Xie, Dong , Hung, Rayjean J., Boffetta, Paolo , Coté, Michele L. , Marchand, Loı̈c Le , Christiani, David C. , Yang, Ping , Hung, Rayjean J

Cancer Epidemiology, Biomarkers & Prevention | October 26, 2015 | Volume: 24 | Issue: 12 | Pages: 1902-1906

10.1158/1055-9965.epi-15-0436 Get It

Abstract The aim of this study was to estimate the effect of exposure to secondhand tobacco smoke on the incidence of lung adenocarcinoma in situ/minimally invasive adenocarcinoma (AIS/MIA). Data from seven case–control studies participating in the International Lung Cancer Consortium (ILCCO) were pooled, resulting in 625 cases of AIS/MIA and 7,403 controls, of whom 170 cases and 3,035 controls were never smokers. Unconditional logistic regression was used to estimate adjusted ORs (ORadj) and 95% confidence intervals (CI), controlling for age, sex, race, smoking status (ever/never), and pack-years of smoking. Study center was included in the models as a random-effects intercept term. Ever versus never exposure to secondhand tobacco smoke was positively associated with AIS/MIA incidence in all subjects (ORadj = 1.48; 95% CI, 1.14–1.93) and in never smokers (ORadj = 1.45; 95% CI, 1.00–2.12). There was, however, appreciable heterogeneity of ORadj across studies (P = 0.01), and the pooled estimates were largely influenced by one large study (40% of all cases and 30% of all controls). These findings provide weak evidence for an effect of secondhand tobacco smoke exposure on AIS/MIA incidence. Further studies are needed to assess the impact of secondhand tobacco smoke exposure using the newly recommended classification of subtypes of lung adenocarcinoma. Cancer Epidemiol Biomarkers Prev; 24(12); 1902–6. ©2015 AACR.
Abstract 4826: International Lung Cancer Consortium: Pooled analysis of previous lung diseases and lung cancer risk
Brenner, Darren R. , Bickeböller, Heike , Wichmann, Erich, Schwartz, Ann G. , Friis, Søren, Field, John K. , McLaughlin, John R., Lan, Qing , Park, Bernard J. , Hung, Rayjean J., Boffetta, Paolo , Duell, Eric J. , Rosenberger, Albert , Muscat, Joshua E. , Yang, Ping , Tjønneland, Anne , Marchand, Loı̈c Le , Zhang, Zuo‐Feng , Lazarus, Philip J. , McLaughlin, John R., Wiencke, John K. , Neri, Monica , Orlow, Irene , Hung, Rayjean J., Field, John K , Bickeböller, Heike

Cancer Research | February 25, 2011 | Volume: 70 | Issue: 8_Supplement | Pages: 4826-4826

10.1158/1538-7445.am10-4826 Get It

Abstract To clarify the role of previous lung diseases (PLDs) (chronic bronchitis, emphysema, pneumonia, tuberculosis, asbestosis and silicosis) in the development of lung cancer we conducted a pooled analysis in the International Lung Cancer Consortium (ILCCO). Data from 16 studies (9 population based case-control, 4 hospital based case-control, 2 mixed case-control and 1 cohort - 10 from North America, 5 from Europe and 1 from Asia) were pooled, including 24044 cases and 81256 controls. Study-specific effect estimates were derived using logistic regression models for case-control studies and Cox proportional hazards models for cohort studies adjusted for age, sex, education and pack-years of smoking. Effect estimates were then pooled using random effects models where summary effects for each of the PLDs were evaluated separately. Stratified analyses were conducted based on smoking status, histology and study design or control source. Heterogeneity was evaluated using the Cochrane Q statistic and Galbraith plots, and publication bias was evaluated using funnel plots as well as the Begg test. A previous history of emphysema conferred a relative risk (RR) of 2.17, 95% confidence interval (CI): 1.67-2.82 (from 15 studies, p-het<.001). A previous history of chronic bronchitis conferred a RR of 1.49, 95% CI: 1.33-1.60 (from 12 studies, p-het.=0.434). Tuberculosis was associated with a RR of 1.54, 95% CI: 1.19-1.99 (from 15 studies, p-het.=0.001). Both asbestosis (RR 2.51, 95% CI: 1.53-4.12 (from 7 studies, p-het=0.379)) and silicosis (RR 1.70, 95% CI: 1.15-2.54, (from 3 studies, p-het. p=0.476)) were also associated with lung cancer risk. When the outlying studies were removed, effect estimates changed minimally and heterogeneity was reduced. Findings were consistent in subgroup analyses by smoking status and histology (adenocarcinoma, squamous cell carcinoma and small cell lung cancer). Effect estimates among never smokers were for emphysema a RR of 2.21, 95% CI: 0.99-4.90 (from 8 studies), for chronic bronchitis 1.12, 95% CI: 0.78-1.62 (from 9 studies), for pneumonia 1.37, 95% CI: 1.10-1.70 (from 10 studies) and for tuberculosis 1.54, 95% CI: 0.99-2.39 (from 9 studies). In this analysis of data from multiple continents, PLDs were associated with an increased risk of lung cancer. The evidence among never smokers supports a direct relationship between previous lung diseases and lung cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4826.