Called “one of the greatest public health catastrophes” of the 20th century in the Surgeon General’s semicentennial report, smoking has had profound health consequences that continue to be felt even as its North American prevalence decreases. For vascular surgeons in particular, the association with aneurysm formation and arterial occlusive disease means that smoking remains one of the most critical modifiable risk factors.

Epidemiology

Smoking is the foremost cause of preventable morbidity and mortality in the United States. Annually, more than 480,000 premature deaths and more than $300 billion in lost productivity and direct costs are attributed to smoking.

Although the prevalence of smoking in the United States has decreased by more than half since the Surgeon General’s seminal report on smoking in 1964, it remains significant. Based on the National Health Interview Survey of almost 27,000 Americans at least 18 years of age, 14.0% smoked regularly in 2017, the lowest ever since measurement began in 1965. The prevalence was higher in males than females (15.8% vs. 12.2%). Adults aged 45 to 64 years had the highest rate of 16.5% compared with the lowest rate of 8.2% in those who were 65 years or older. There were also differences based on racial groups, education, and economic status. Namely, cigarette use was highest among American Indian/Alaska natives (24.0%) and lowest among Asians (7.1%). Non-Hispanic Whites had an intermediate rate of 15.2%. Americans with graduate degrees had a mere 4.1% use compared with 36.8% in those with a general equivalency diploma. Finally, people with an annual household income of less than $35,000 had a use rate of 21.4% versus 7.6% in those with corresponding incomes greater than $100,000 living above the poverty line.

It is important to recognize that patients may use tobacco products besides cigarettes. The 2017 National Health Survey demonstrated that the following products were used daily or some days: cigars, cigarillos, filtered little cigars (3.8%); electronic cigarettes (2.8%); snuff, dip, and other smokeless tobacco (2.1%); pipes, water pipes and hookahs (1%).

A recent increasingly popular cigarette alternative is the electronic cigarette or e-cigarette. E-cigarettes, while tobacco-free, are battery-operated devices that deliver aerosolized nicotine (“vaping”). They are marketed both as cigarette alternatives and as smoking cessation tools. Although more than half of smokers who attempted to quit had used e-cigarettes in 2014, no such device has been FDA-approved for smoking cessation, and the United States Preventative Services Task Force has found inadequate evidence to support e-cigarettes as cessation tools. As a corollary, data regarding potential long-term harms from inhaling nicotine vapors are also absent. Finally, there is concern that e-cigarette use in minors may translate into long-term nicotine addiction for future generations.

Biologic Effects of Smoking on the Vasculature

Cigarette smoke has adverse effects on vascular biology through a variety of mechanisms. First, it creates endothelial dysfunction, including reduction of the availability of nitric oxide, and activation of enzymes leading to the increased production of reactive oxygen species. Flow-mediated dilation, a common measure of endothelial function, is diminished in active smokers and even nonsmokers exposed to secondhand smoke for less than 1 hour.

Second, smoking creates a prothrombotic environment. Smoking leads to the increased production of thromboxane A 2 and decreased levels of prostacyclin, thus overall promoting platelet aggregation. Smoking is also associated with elevated levels of prothrombotic substances such as von Willebrand factor, thrombin, and fibrin, while simultaneously reducing antithrombotic and fibrinolytic substances such as tissue plasminogen activator and plasminogen activator inhibitor-1. Smokers also have higher markers of platelet activation, which decline after smoking cessation. ,

Last, smoking promotes an inflammatory state, which has been associated with vascular disease. Compared with nonsmokers, smokers have higher levels of leukocytes, C-reactive protein, interleukin-6, tissue necrosis factor-α, interleukin-1-β, and other inflammatory markers. ,

It should also be noted that nicotine itself plays an important role in known drivers of vascular disease. Not only does it act as a sympathomimetic substance that raises blood pressure, but it is also associated with insulin resistance, altered lipid metabolism, and endothelial dysfunction. Finally, vascular surgeons have for generations passed on the observation of differential disease distribution patterns between patients who smoke versus those with diabetes. Smokers tend to have aortoiliac and superficial femoral disease, while occlusive atherosclerosis generally strikes the profunda and tibials in diabetic patients. However, rigorous documentation of these broad and frequently variable differential disease patterns is sparse.

Nonvascular Clinical Effects

Smoking has causal links with numerous diseases across several organ systems. Most prominently, smoking is associated with cancers of the lungs, oropharynx and larynx, esophagus, stomach, pancreas, kidney, bladder, and cervix. More recently, it has been implicated in liver and colorectal cancers as well.

Cigarette smoking also has been linked to diabetes, cataracts, macular degeneration, chronic obstructive pulmonary disease, asthma, and rheumatoid arthritis, among others.

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