Abstract
Smoking is the largest preventable cause of morbidity and mortality in the world. Despite the development of numerous preventive and treatment interventions, the rate of daily smoking in the United States is still approximately 22%. Effective psychosocial interventions and pharmacologic agents exist for the prevention and treatment of smoking. Unfortunately, both approaches are hindered by our inability to accurately quantify amount of cigarette consumption from the point of initial experimentation to the point of total dependency. Recently, we and others have demonstrated that smoking is associated with genome-wide changes in DNA methylation. However, whether this advance in basic science can be employed as a reliable assay that is useful for clinical diagnosis and treatment has not been shown. In this communication, we determine the sensitivity and specificity of five of the most consistently replicated CpG loci with respect to smoking status using data from a publically available dataset. We show that methylation status at a CpG locus in the aryl hydrocarbon receptor repressor, cg05575921, is both sensitive and specific for smoking status in adults with a receiver operated curve characteristic area under the curve of 0.99. Given recent demonstrations that methylation at this locus reflects both intensity of smoking and the degree of smoking cessation, we conclude that a methylation-based diagnostic at this locus could have a prominent role in understanding the impact of new products, such as e-cigarettes on initiation of cigarette smoking among adolescents, while improving the prevention and treatment of smoking, and smoking related disorders.
Highlights
Smoking is the largest preventable cause of morbidity and mortality in the United States
But well characterized set of participants, we show that DNA methylation status at cg05575921, and to a lesser extent at three Chromosome 2 loci, can be used to accurately quantify the amount of smoking
In our experience with several large cohorts of subjects from longitudinal studies, we often find that participants who deny ever smoking cigarettes often have markedly elevated levels of cotinine in their serum and have medical illnesses, such as chronic obstructive lung disease (COPD), that are generally found in association with smoking
Summary
Smoking is the largest preventable cause of morbidity and mortality in the United States. In attempts to supplement self-report, objective measures of tobacco consumption, such as serum or salivary cotinine or exhaled carbon monoxide levels, are sometimes used Each of these approaches for determining smoking status has its limitations (Florescu et al, 2009). We have shown that the effects of smoking on DNA methylation are unique to smoking and are not affected by alcohol consumption, allowing smoking and alcohol consumption status to be assessed simultaneously from the same dataset (Philibert et al, 2014a) Taken together, these studies indicate that DNA methylation assessments hold considerable promise as a tool for supplementing self-report information in smoking prevention and smoking cessation efforts. As a first step in answering this question, in this study, we use publically available methylation data from a recently completed study and standard analytic approaches to test single and multiple locus approaches to the determination of smoking consumption
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