Your husband has voted, no CF children, but I don't see anything saying he doesn't want another child. In one way or another, from IVF to terminating a pregnancy, all the current tools end up testing an embryo and keeping one or two and destroying those with CF genes. The importance of this is how you and the two of you feel about this topic.
Long ago a friend and his wife were considering a second child. Their first child was born with a rare and horrible genetic disease called Osteogenisis Imperfecta. Every bone in her body was broken during childbirth and just depressing a computer key bent her finger to breaking when she was five. The fear of having another OI child was consuming. In spite of everything, they wanted another child and then magically, his wife was pregnant. Now they were terrified, and he was asking me about having an amniocentesis. This was an established procedure but it wasn't widely used and most weren't well informed on the subject.
After listening to the details of the situation, he asked what I thought about amnio. He and I belonged to the same church and very deliberately, the Synod had no official position on the termination of an embryo/fetus so any religious reasons were theirs. I was about to ask if abortion was the reason he was so fusticated when it struck me, he might not understand what and why he's considering doing.
Rather than explain the mechanics of the procedure, I asked what they planned to do with the results of the test. Suddenly he realized what the endgame of an amniocentesis can be. They couldn't and wouldn't terminate a pregnancy, their beautiful, intelligent daughter was proof that the life of a child is more than the sum of their genes.
My personal belief is to support the individual's choices regarding when and how to have a baby. You and your husband have some issues to negotiate. I doubt there's a CFer who truly wishes they'd never been born. CF is a part of me and it holds both bad and good influence over who I am. I also doubt any parent begrudges their child or children for having CF. And, though no parent should feel responsible for their child having CF, many harbor deep, irrational guilt.
Look into current drug trials for your mutation and your husband's. It's looking so bright, you'll have to wear shades. Genetic medicine, as in a medicine that modifies the action of each cell's nucleus to act as if there were no CFTR mutations are now targeting the most common mutations and some are near to panacea drugs. It's not the strongest argument for having a no-worry kid but it is valid.
One other item has to do with your 1 in 4 odds with each pregnancy. This statistical model assumes the same mutation in mom and dad. The fact that you carry ∆F508, you said you are a carrier, is good and bad news. You may still have CF as complete testing for all ~1900 hasn't been done on everyone involved. For the statistical model to work, hubby should carry ∆F508 as well. Toss out the model if you don't share the same mutation. ∆F508 is responsible for about 66% of all CF patients so it's a known harmful CFTR gene mutation. About a year ago, somebody cited a recent scientific paper hailing another 160 or so CFTR mutations that had been discovered to be CF causing, raising the total to something like 300. What? Only a fraction of the mostly harmless ~1900 CFTR mutations have been thoroughly scrutinized. And the matrix of possible combinations of mutations far exceeds the number of CF patients alive in the world.
What this means in short. His mutation is nothing to be blasé about, if it is known for virulence. Come back with some research on both mutations and ask us if anybody has ∆F508 and ........your husband's mutation. At this point in CF research, anecdotal evidence is as good as you'll get. You can read what is known about his mutation but even technical papers play word games. Note the difference between 'mutation "X" has not been proven to interfere with chloride ion exchange' and 'mutation "X" has been proven to not interfere with chloride ion exchange'.
I'd be generally unconcerned about having a CF baby. It is relatively new information that so many potential combinations of mutations could result in CF or CRMS. In our general population as high as 1 in 25 adults (Ireland) are carriers resulting in a staggering 1 in 1400 births with CF. Admittedly, you're not 1:1400 because you're both carriers and ∆F508 is usually nasty. Until you know more about dad's mutation, it could be as frightening as the standard 1:4, 2:4, 1:4 or more likely a 1:4 chance of some mild CF symptoms. The autosomal recessive bit of this equation works when both mutations are the same. Two different but non working mutations could act just like two identical bad mutations or they could do something that we don't understand in some arcane biochemical process.
Hope that helps.
LL
Best of luck with your journey!