Data from the present study indicate that young, novice smokers (pack-year history of 3 ± 4) have a lower plasma antioxidant capacity and exhibit a greater degree of lipid peroxidation compared to nonsmokers, despite having similar dietary intake. These data suggest that the act of cigarette smoking may independently promote such negative changes, with the number of years spent smoking contributing most to these findings. While dietary intake, as well as other genetic and environmental factors not determined in this investigation may contribute to these results, it appears that smoking plays a major role in promoting these changes.
It is known that exogenous antioxidant intake from whole food and nutritional supplements may influence both the antioxidant capacity of blood  as well as oxidative stress biomarkers . It has been independently reported that smokers consume less antioxidant rich foods compared to nonsmokers [11–13] and have suppressed blood levels of certain antioxidants such as ascorbic acid , tocopherol, and superoxide dismutase , which may influence the degree of oxidative stress. As such, many investigators have reported elevated levels of oxidative stress biomarkers in smokers compared to nonsmokers [7–9]. However, no previous study has determined the independent and combined contribution of smoking and dietary antioxidant intake on blood antioxidant capacity and oxidative stress biomarkers, in particular within a population of young, novice smokers. Previous studies have included older, more established smokers, as in the work of Dietrich and coworkers  in which subjects had a mean age of 43 years and a mean pack history of 27 years. In contrast, our participants had a mean age of 24 years and a mean pack history of only 3 years. While these findings are interesting, they are highly specific to young, novice smokers. Future studies with larger sample sizes, inclusive of smokers of different ages and smoking histories, are needed to extend these findings. In this way, smokers could be classified by age, as well by smoking habit (e.g., light, moderate, and heavy). Using this approach, data would better be able to be generalized to the population at large.
We chose to measure blood antioxidant capacity as well as two common markers of lipid peroxidation, MDA and oxLDL. A great deal of focus has been placed on the oxidative modification of lipids, and in particular LDL and the causal role of oxLDL in the pathophysiology of atherosclerosis [23, 24]. Oxidized LDL is more atherogenic than native LDL and is taken up by the scavenger receptor system ultimately leading to the generation of foam cells and the development of early lesions . Atherosclerotic lesions in both animal and man have been reported to contain significant oxLDL , while antibodies to oxLDL have been found to correlate with the progression of atherosclerosis . Oxidized LDL is also cytotoxic and has the ability to promote endothelial dysfunction, as well as the induction of genes such as interleukin-1 that can induce smooth muscle cell proliferation and promote a procoagulant state . Furthermore, oxLDL may promote platelet adhesion, trigger DNA strand breaks, and promote apoptosis, all of which contribute to the development of atherosclerotic disease . Based on the above, we believe that oxLDL is an important marker to focus on in relation to oxidative stress research. Although we failed to note statistical significance between smokers and nonsmokers with regards to oxLDL, values were more than two-fold higher in smokers and our effect size calculation for this marker was moderate. It is likely that we were underpowered statistically to detect significance in oxLDL. Future studies with larger samples are needed to corroborate our findings.
It should be noted that despite no differences in dietary variables between smokers and nonsmokers, mean vitamin C, vitamin E, and vitamin A intake was lower than the recommended Dietary Reference Intakes for both groups of participants. The current recommended daily intake of vitamin C is 75 mg per day for women and 90 mg per day for men 19–50 years of age. Daily vitamin E intake is suggested at 15 mg per day for both men and women, while vitamin A intake is suggested at 700 μg per day for women and 900 μg per day for men 19–50 years of age. It is possible that the lower than recommended intake of these vitamins could have promoted a lower antioxidant capacity and higher lipid peroxidation. However, because we found no statistical difference between groups for these variables, we have no reason to believe that one group was affected more than another in this regard. While participants were instructed to record all food and drink consumed during the reporting period, it is possible that underreporting could have occurred. If so, the analyzed values may have been lower than what participants habitually consume. This is indeed a limitation of the present investigation and of using dietary records within a free living environment to determine nutrient intake.