
Cigarette smoking strongly contributes to the development of cardiovascular (CV) disease, with a recent study showing dose-response relationships of smoking-relevant parameters across three domains of subclinical markers of CV harm.
Of the 182,364 participants in the study, 15.3 percent were current smokers (mean 16.7 cigarettes/day, mean 30.0 pack-years) and 34.6 percent were former smokers (median 19.0 years since quitting, mean 22.4 pack-years).
Compared with nonsmokers, participants with a history of smoking had higher levels of all subclinical markers. Stronger associations were noted among current smokers.
Among participants who currently smoke, smoking intensity demonstrated a dose-response association with all markers, except for D-dimer. An increase of 1 percent to 9 percent in the levels of subclinical markers was observed per 10 cigarettes. After 20 cigarettes, the patterns seemed to plateau for blood markers but continued to rise for atherosclerosis markers.
Among those with have ever smoked, strong dose-response associations were seen for pack-years with all subclinical markers, with an increase of 1 percent to 9 percent per 10 pack-years. These effects persisted after 20 pack-years for all markers, but with a milder slope.
“Among participants who smoked formerly, there were substantially lower levels of biomarkers with longer time since quitting, and most markers were not different compared with those who have never smoked by 30 years, except for the coronary artery calcium score, which remained 19-percent higher even beyond quitting after 30 years,” the researchers said.
“The sensitivity of the tested subclinical markers to small increments in cigarette exposure suggests potential value in the regulation of new and existing tobacco products,” they added.
This study identified participants (mean age 58.3 years, 69.0 percent female) from 22 cohorts of the Cross Cohort Collaboration with self-reported smoking status. Researchers categorized markers into three domains, namely inflammation, thrombosis, and subclinical atherosclerosis.
Multivariate regression models and restricted cubic splines were used to examine the associations of smoking status, intensity, pack-years, and time since cessation with subclinical markers.