6. Emphysema results from loss of elasticity (elastic fibers and other connective tissue proteins) in alveolar walls of the lungs, so CO$_{2}$ can't be exhaled effectively, so there isn't room for inhaling much fresh air (O$_{2}$). Neutrophils (white blood cells that engulf invading bacteria) secrete elastase. The excess elastase in blood plasma can hydrolyze elastic fibers in alveolar walls of the lungs and resulting in emphysema. To prevent elastase from running amok in plasma, liver makes and secretes a plasma protein, $\alpha_{1}$-antiproteinase (also sometimes referred to by its old name, $\alpha_{1}$-antitrypsin), which in blood plasma keeps elastase inhibited, protecting lungs from damage.
Components of cigarette smoke oxidizes a Met residue in $\alpha_{1}$-antiproteinase that's required for binding to elastase (oxidation $\rightarrow$ non-functional inhibitor). Smokers continually inactive $\alpha_{1}$-antiproteinase in the blood plasma in their lungs and thus are also much more likely to develop emphysema.
Consider if there would be a mutant $\alpha_{1}$-antiproteinase that would be more resistant to oxidation than the naturally occurring inhibitor, and thus might make an individual with that mutation less susceptible to emphysema? What kind of amino acid substitution might have that effect, and why?