Impact of Reduced Tobacco Smoking on Lung Cancer Mortality in the United States During 1975–2000

Program in Biostatistics and Biomathematics, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave North, Seattle, WA 98109, USA.
Journal of the National Cancer Institute (Impact Factor: 12.58). 03/2012; 104(7):541-8. DOI: 10.1093/jnci/djs136
Source: PubMed

ABSTRACT Considerable effort has been expended on tobacco control strategies in the United States since the mid-1950s. However, we have little quantitative information on how changes in smoking behaviors have impacted lung cancer mortality. We quantified the cumulative impact of changes in smoking behaviors that started in the mid-1950s on lung cancer mortality in the United States over the period 1975-2000.
A consortium of six groups of investigators used common inputs consisting of simulated cohort-wise smoking histories for the birth cohorts of 1890 through 1970 and independent models to estimate the number of US lung cancer deaths averted during 1975-2000 as a result of changes in smoking behavior that began in the mid-1950s. We also estimated the number of deaths that could have been averted had tobacco control been completely effective in eliminating smoking after the Surgeon General's first report on Smoking and Health in 1964.
Approximately 795,851 US lung cancer deaths were averted during the period 1975-2000: 552,574 among men and 243,277 among women. In the year 2000 alone, approximately 70,218 lung cancer deaths were averted: 44,135 among men and 26,083 among women. However, these numbers are estimated to represent approximately 32% of lung cancer deaths that could have potentially been averted during the period 1975-2000, 38% of the lung cancer deaths that could have been averted in 1991-2000, and 44% of lung cancer deaths that could have been averted in 2000.
Our results reflect the cumulative impact of changes in smoking behavior since the 1950s. Despite a large impact of changing smoking behaviors on lung cancer deaths, lung cancer remains a major public health problem. Continued efforts at tobacco control are critical to further reduce the burden of this disease.

Download full-text


Available from: William D Hazelton, Sep 26, 2015
24 Reads
  • Source
    • "Lung cancer is the leading cause of cancer mortality for men and women [1,2]. Despite smoking prevention and cessation programs [3] and advances in early detection [4], the 5-year survival rate for lung cancer is only 16% with current therapies [1]. Although lung cancer incidence rates have recently declined in the United States [1], more lung cancer is now diagnosed when considered together in former- and never-smokers than in current smokers [5]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background New pharmacologic targets are urgently needed to treat or prevent lung cancer, the most common cause of cancer death for men and women. This study identified one such target. This is the canonical Wnt signaling pathway, which is deregulated in cancers, including those lacking adenomatous polyposis coli or β-catenin mutations. Two poly-ADP-ribose polymerase (PARP) enzymes regulate canonical Wnt activity: tankyrase (TNKS) 1 and TNKS2. These enzymes poly-ADP-ribosylate (PARsylate) and destabilize axin, a key component of the β-catenin phosphorylation complex. Methods This study used comprehensive gene profiles to uncover deregulation of the Wnt pathway in murine transgenic and human lung cancers, relative to normal lung. Antineoplastic consequences of genetic and pharmacologic targeting of TNKS in murine and human lung cancer cell lines were explored, and validated in vivo in mice by implantation of murine transgenic lung cancer cells engineered with reduced TNKS expression relative to controls. Results Microarray analyses comparing Wnt pathway members in malignant versus normal tissues of a murine transgenic cyclin E lung cancer model revealed deregulation of Wnt pathway components, including TNKS1 and TNKS2. Real-time PCR assays independently confirmed these results in paired normal-malignant murine and human lung tissues. Individual treatments of a panel of human and murine lung cancer cell lines with the TNKS inhibitors XAV939 and IWR-1 dose-dependently repressed cell growth and increased cellular axin 1 and tankyrase levels. These inhibitors also repressed expression of a Wnt-responsive luciferase construct, implicating the Wnt pathway in conferring these antineoplastic effects. Individual or combined knockdown of TNKS1 and TNKS2 with siRNAs or shRNAs reduced lung cancer cell growth, stabilized axin, and repressed tumor formation in murine xenograft and syngeneic lung cancer models. Conclusions Findings reported here uncovered deregulation of specific components of the Wnt pathway in both human and murine lung cancer models. Repressing TNKS activity through either genetic or pharmacological approaches antagonized canonical Wnt signaling, reduced murine and human lung cancer cell line growth, and decreased tumor formation in mouse models. Taken together, these findings implicate the use of TNKS inhibitors to target the Wnt pathway to combat lung cancer.
    BMC Cancer 04/2013; 13(1):211. DOI:10.1186/1471-2407-13-211 · 3.36 Impact Factor
  • Source
    • "This might be explained that there were many lung cancer patients included in NCRC-LM. As known to all, lung cancer is a disease closely associated with smoking (Moolgavkar et al., 2012; Rosenberg et al., 2012). Otherwise, alcohol consumption was found different between CRC groups with and without liver metastasis. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: The liver is the organ to which colorectal carcinomas (CRCs) most commonly metastasize, and surgical resection has been established as the most effective and potentially curative treatment for CRC with liver metastasis (LM). Therefore, surveillance of LM is vital for improvement of prognosis of CRC patients. In this study, we aimed to explore the potential value of carbohydrate antigen 19-9 (CA 19-9), carcinoembryonic antigen (CEA), and marker enzymes in indicating LM with CRC. Methods: Three groups of eligible patients with metastatic cancers were retrospectively included: CRC patients with LM (CRC-LM) or without LM (CRC- NLM), and non-CRC patients with LM (NCRC-LM). All metastatic lesions were identified by CT or MRI. Data on characteristics of the patients, the primary site, the locations of metastasis, CA 19-9, CEA, and biochemical parameters were collected for analysis. Results: A total of 493 patients were retrospectively included. More alcohol consumption was found in CRC-LM than CRC-NLM. Some biochemical enzymes were found to be significantly higher in groups with LM than without (CRC-LM or NCRC-LM v.s CRC-NLM). Both CEA and CA 19-9 were much higher in CRC-LM than CRC-NLM or NCRC-LM. For CRC patients, CA 19-9, γ-glutamyl transpeptidase, CEA and alcohol consumption were identified as independent factors associated with LM. Conclusion: Our analysis suggested the CA 19-9 might be a potential valuable indicator for LM of CRC in the clinic.
    Asian Pacific journal of cancer prevention: APJCP 02/2013; 14(2):909-13. DOI:10.7314/APJCP.2013.14.2.909 · 2.51 Impact Factor
  • Source
    • "Nicotine appears in both phases (Connolloy et al., 2007). Cigarette smoking has now been positively and strongly associated with increased morbidity and mortality due to a number of diseases, the most recognized of which is lung cancer (Moolgavkar et al., 2012). In addition, the various substances contained in cigarette smoke are partly responsible for malignant tumours of the oral cavity and the pharynx (United States Department of Health and Human Services, 1984) and are a main risk factor for arteriosclerosis, cerebral thrombosis, myocardial infarction, and chronic obstructive pulmonary diseases (COPD) such as chronic bronchitis and emphysema (Wipfli and Samet, 2009; Grief, 2011). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Tobacco use is a leading cause of preventable morbidity and mortality from non-communicable diseases. The objectives of the study were to determine the percentage of annual income used to purchase tobacco-related products and treat tobacco-related illnesses, and assess the characteristics of smokers and their awareness of the health-related risks of smoking. Method: Stratified and snowball sampling methods were used to obtain information (via a 17-item, close-ended questionnaire) from 85 adult respondents (49 males and 36 females). The instrument comprised of demographic characteristics, smoking behavioural/lifestyle, health, and micro socio-economics. Results: There were no significant differences between individuals who were affected by chronic obstructive pulmonary disorder (COPD) (14.1%) and cardiovascular disease (18.8%). It was found that respondents spend 30-39% of their annual income on tobacco-related products. Forty percent (40.0%) and 41.7% of respondents with lung cancer and COPD respectively spend more than 50% of their annual income to treat these diseases. The majority (80%) of those who continues to consume tobacco-related products were uncertain as to why they were doing it. Not all the smokers were aware of the dangers of tobacco consumption despite their level of education. Conclusion: The majority of the respondents who had tobacco-related illnesses such as lung cancer and COPD spend a significant amount of their income on their health care. Not all the smokers were aware of the dangers of tobacco consumption despite their level of education. This suggests the need for increase public awareness where both smokers and non smokers are being fully or adequately informed about the dangers or health risks of tobacco consumption.
    Asian Pacific journal of cancer prevention: APJCP 09/2012; 13(9):4733-8. DOI:10.7314/APJCP.2012.13.9.4733 · 2.51 Impact Factor
Show more