Epigenetic biomarkers to provide insights on measures of smoking & tobacco use

Tobacco use remains one of the most important risk factors for developing serious conditions such as heart disease, lung disease, and cancer. Due to its influence on health, underwriting places significant value on identifying tobacco exposure among life insurance applicants.

Accordingly, the life insurance industry widely screens for tobacco use by testing with the biomarker cotinine, a metabolite of nicotine, in an applicant’s clinical chemistry panel. The challenge with measuring cotinine biomarkers is its short half-life of approximately 16 to 19 hours. A life insurance applicant who can forgo tobacco use for a few days can pass a cotinine test as a “non-smoker” and significantly save on future annual premium payments. Within the industry this is known as “smoking amnesia,” which ultimately results in non-smokers picking up the cost.

Another challenge with the cotinine test is that it does not reflect the amount of tobacco smoked. In other words, beyond a self-report from an applicant, underwriters have no means to distinguish between whether an applicant is for instance a never-smoker versus a recent quitter who smoked two packs a day for the past twenty years; or distinguish between someone who smokes a pack a week versus someone who smokes a pack a day. The life insurance industry dichotomizes tobacco use between current and recent users versus past and never users. However, numerous studies have demonstrated a continuum of health and mortality impacts depending on how long and how much someone has been a smoker. Misclassifying long-time former smokers who quit merely a year or two prior to applying to life insurance could lead to substantial excesses in mortality risk that would not transpire until decades after the policy has already been issued. This presents problems in correctly assessing mortality risk and establishing premium rates for non-smokers, smokers, and former smokers.

Contrast this with the use of epigenetic biomarkers for detecting tobacco usage. Methylation markers associated with tobacco use persist years after smoking cessation and can, therefore, serve as a stable biomarker of lifetime exposure to tobacco. Furthermore, these epigenetic markers of smoking have been shown to be usage dependent and likely reversible, with smoking-induced demethylation reverting as a function of abstinence. The ability to quantitatively measure tobacco exposure through methylation markers opens the door to developing epigenetic tests that can discriminate more precisely between current, former, never, and heavy smokers.

Epigenetic biomarkers that provide further insights into an insurance applicant’s tobacco usage stand to provide improved insights for underwriting that traditional measures cannot. Thus, epigenetic biomarkers differ materially from cotinine biomarkers in that they are able to provide greater utility by more direct measurement of the core aspects of traditional measures of health (e.g., long-term tobacco use) by capturing new dimensions of tobacco use, which can enable more accurate segmentation of applicants based on mortality risk.