A Role for Epigenetics in Broadening the Scope of Pediatric Care in the Prevention of Adolescent Smoking

Abstract

Adolescence presents a critical opportunity to support the development of healthy patterns of behavior and prevent future health problems. Unfortunately, there is not yet a well-developed prevention model that allows pediatricians to initiate and monitor prevention efforts for the substantial minority of individuals who engage in risky behavior during adolescence. We suggest that recently developed epigenetic technologies may provide a bridge to a new prevention paradigm in which pediatricians screen for indicated smoking prevention services. Specifically, since currently available tobacco use screening measures are insensitive to low levels of use, newly developed methylation based approaches may enhance the sensitivity of the initial screening for nascent smoking behavior as well monitoring of outcomes. We conclude that the incorporation of Next Gen screening technologies into standard pediatric evaluations may allow for more effective referral to prevention programming for tobacco use. In addition to the potential direct impact on long-term enhancement of health outcomes secondary to smoking prevention, well-established links between smoking and other risk behaviors suggest that expanded referral for nascent smoking may also create opportunities to address other risky adolescent behaviors, and so decrease several interrelated drivers of long-term health care costs.

Smoking-Related DNA Methylation is Differentially Associated with Cadmium Concentration in Blood

“…The cg05575921 site in AHRR showed hypomethylation in smokers, in accordance with previous studies (Zeilinger et al 2013 ; Dogan et al 2014 ; Lee et al 2017 ). These data support the suggestion that methylation levels of AHRR (cg05575921) may be used as an indicator of smoking intensity (Beach et al 2015 ). Our findings were consistent with those of previous studies on smoking-associated DNA methylation at other CpG sites as well.…”

“…These were under-methylated by > 10% in smokers compared to that in non-smokers. DNA methylation of cg05575921 in AHRR (Beach et al 2015 ) and cg03636183 in F2RL3 (Zeilinger et al 2013 ; Breitling et al 2011 ) is the putative indicator for smoking. Taken together, these CpG sites (cg05575921 and cg23576855 in AHRR , cg03636183 in F2RL3 , and cg21566642) may be differentially methylated by cadmium exposure due to smoking.…”

Nonsupportive parenting affects telomere length in young adulthood among African Americans: Mediation through substance use.

“…Accordingly, these results suggest the potential benefit of efficacious secondary prevention efforts focused on prevention of escalation of use among youth who have already tried alcohol and cigarette smoking (Brody, Yu et al, 2012). A secondary prevention model would attempt to detect early substance use and prevent both rapid escalation and subsequent health consequences (Beach, Gibbons, Gerrard, Brody, & Philibert, 2014).…”

Prenatal epigenetics diets play protective roles against environmental pollution

“…DNA methylation markers could be potential indicators of paternal smoking as methylation alteration of a series of genes has been shown to link to cigarette use. Among these genes, hypomethylation of AHRR , particularly at cg05575921 loci, was often found [104, 450–452]. In a recent study on African-American cohorts, smoking-induced DNA demethylation at AHRR was moderated by increased methylation of methylene tetrahydrofolate reductase ( MTHFR ), which is a key regulator in methyl metabolism [453].…”