Background-Second-hand smoke (SHS) accelerates atherogenesis and impairs va
scular function. The role of nicotine in this process has not been defined.
Methods and Results-To examine the potential effects of nicotine on atherog
enesis and vascular function, 48 rabbits receiving a 0.5% cholesterol diet
were randomized to control (cholesterol diet only), SHS from nicotine- stan
dard research cigarettes (SHS-ST), and SHS from nicotine-free research ciga
rettes (SHS-NF). The SHS rabbits were exposed to 48 nicotine-standard (12 a
nimals) or nicotine-free (12 animals) cigarettes/d, 5 d/wk for 10 weeks. Ai
r carbon monoxide and particulates and plasma carboxyhemoglobin were signif
icantly higher in the 2 SHS groups than the control group (P <0.001). The S
HS-ST group had significant increases in plasma nicotine and cotinine compa
red with the other groups (P <0.001). There was no difference in serum lipi
ds. Lipid lesions were increased in both SHS groups (54 +/-5% [SEM] aorta a
nd 66 +/-4% pulmonary artery, 53 +/-7% and 69 +/-4%, and 39 +/-4% and 43 +/
-3% in the SHS-ST, SHS-NF, and control groups, respectively; P=0.049 aorta
and P <0.001 pulmonary artery).
Conclusions-SHS exposure increased arterial lipid lesions, but nicotine did
not contribute significantly to this effect. This effect is presumably due
to other combustion products in the smoke.