Despite these important results, many questions remain. First, of the thousands of toxic chemicals in cigarette smoke, what is the molecular mechanism of reduced eNOS and increased nuclear factor-κB expression in smokers and individuals exposed to SHS? Are there therapeutic targets that could be used to minimize cardiovascular risk among exposed individuals? Second, do similar toxicities exist for other forms of smoking (eg, do electronic cigarettes [e-cigarettes]) also affect vascular risk for the willing recipient as well as innocent bystanders? Recent data suggest that e-cigarettes may have unique toxicities to airway cells and may affect bacterial pathogenesis, suggesting the need for independent study of each injurious agent.10 Third, what is the difference in chemical delivery to the lungs of various different exposed individuals? Sidestream smoke may be more toxic than mainstream smoke because it is unfiltered, and it generates more toxins when it mixes with room air for 0.5 to 2 h.11 Moreover, carbon monoxide (CO) concentrations in the exhaled breath of cigarette smokers are higher compared with individuals exposed to SHS; in theory, inhaled CO may have potential benefits in very low concentrations. Inspired CO is entering clinical trials in various inflammatory lung diseases, due to its antiinflammatory, antiapoptotic, antiproliferative, and vasodilatory effects, although the clinical benefits remain unclear.12 We congratulate Adams et al7 on the provocative findings and for informing public policy with a strong scientific foundation. Clearly, any discussion around the civil liberty of smoking cigarettes is complex when the broader population is considered.