Airway epithelial cells (AECs) and airway macrophages (AMs) represent primary cellular targets of infection by seasonal influenza A virus (IAV). IAV infection of AECs results in productive replication, defined as the release of newly synthesised infectious virus. In contrast, infection of mouse macrophages is blocked at a late-stage in replication where infectious virus is not released (abortive replication). IAV infection outcomes are not as well-defined for human macrophages. Herein, we infected two sources of primary human macrophages isolated from matched donors (AMs from bronchoalveolar lavage and monocyte-derived macrophages (MDMs) from peripheral blood). Despite similar levels of IAV infection in AMs and MDMs at 8-hours post-infection, infectious virus was released from MDMs, but not AMs, at 24- and 48-hours post-infection. These data suggest that while IAV infection of AMs is abortive, productive replication occurs in MDMs. Indeed, abortive replication in AMs and productive IAV replication in MDMs was observed for a broad range of H1N1 and H3N2 IAV strains. Interestingly, only a small subset of recent H1N1 IAV strains (2009 to 2016) abortively replicated in MDMs. Comparison of sequences of all eight genes from closely related strains that underwent abortive vs. productive replication in MDMs mapped key differences in the haemagglutinin (HA), neuraminidase (NA), matrix (M) and non-structural (NS) genes. These findings provide novel insight into both host and viral determinants that influence IAV infection outcomes in human macrophages. We propose that resident lung macrophages (AMs) could play a key role in limiting the severity of influenza A virus-induced disease by blocking viral replication to contribute to an effective innate response. In contrast, MDMs share similarities with macrophages recently recruited from the blood to the airways during infection, but whether these cells contribute to protective innate host responses during IAV infection is the focus of ongoing studies.