Five grades of tungsten specimens with different purity levels (resistivity ratios R of 5 × 10 4, 1.5 × 10 4, 50, 15 and 5) were irradiated in situ with 30 keV W + ions to a dose of typically 5 × 10 12 ion cm −2 at 18 K. Examination with a low-temperature field-ion microscope (FIM) showed the isochronal-annealing spectra of the specimens to result from a large self-interstitial atom (SIA) flux at ~ 38 K, followed by significant SIA flux from ~ 50 to 80 K and a small amount of additional recovery up to 120 K. The spectra for these five different R value specimens were essentially identical between 18 and 120 K. High-purity W specimens ( R = 5 × 10 4) doped with 5 × 10 −5 to 1 × 10 −4 atom fraction carbon showed only a small reduction in the amount of recovery observed for the long-range migration peak at 38 K. The isochronal recovery spectra for WRe alloy specimens (5 × 10 −3 and 3 × 10 −2 atom fraction Re) were radically different from the isochronal recovery spectra of pure W specimens. For both alloys the recovery of the Stage I long-range migration peak at 38 K was strongly suppressed; for the 3 × 10 −2 atom fraction alloy, all recovery from 18 to 120 K was virtually eliminated. This result indicated that during the long-range migration substage at 38 K tightly-bound, immobile SIA-Re complexes were formed that suppressed the SIA-SIA reaction. However, this effect was only observed at these high Re atom concentrations. The lack of any significant differences for the annealing spectra of the five purity-levels of undoped tungsten and the appearance of impurity effects only in the extremely concentrated W alloys (i.e. 5 × 10 −3 to 3 × 10 −2 atom fraction Re) indicated that the early Stage II recovery (45–120 K) observed in the FIM isochronal-annealing spectra of self-ion irradiated high-purity W was intrinsic in nature. Because of the highly inhomogeneous SIA distribution of the W + ion damage, the SIA-SIA interaction during Stage I long-range migration at 38 K appeared to be the dominant trapping mechanism. The early Stage II SIA recovery was therefore attributed to the migration or dissolution of these SIA clusters.