There are 2 routes whereby tobacco smoke can hurt a patient's heart—by smoking directly or by inhaling someone else's smoke. When smoking rates were high, it was hard to avoid secondhand smoke, and it was also unclear that secondhand smoke was damaging because the assumption was that—as with smoking and lung cancer—sustained exposure was required for harm. But now that smoking is less common and smokers are increasingly marginalized (8- 9), evidence has emerged that secondhand smoke exposure is nearly as harmful to the heart as is chronic active smoking. Barnoya and Glantz (10) recently reviewed the many ways in which this harm occurs. Secondhand smoke exposure alters platelet function, causes endothelial dysfunction, increases arterial stiffness, decreases levels of high-density lipoprotein, increases markers of inflammation, increases arterial intima-media thickening, increases infarct size, causes oxidative stress and mitochondrial damage, decreases heart rate variability (thus increasing the risk of malignant arrhythmias), and increases insulin resistance (10). It is hard to imagine substances that would be more cardiotoxic. Furthermore, these adverse effects are observed at very low exposure doses (11).