IBCL-349 Veterans With Agent Orange Exposure Have a Shorter Latency From Exposure to Diagnosis of Indolent B-Cell Lymphoid Malignancies Compared to Unexposed Veterans.

CONTEXT: There is an increased risk of developing lymphomas after Agent Orange (AO) exposure, but specific information on lymphoma subsets is lacking.

OBJECTIVE: To identify differences in latency and outcomes among Veterans with AO exposure who develop indolent B-cell lymphoid malignancies (IBCL) compared with unexposed Veterans during the same period of military enlistment.

DESIGN: Retrospective case-case study Setting: National Veteran Health Administration Patients: Veterans with IBCL who served between January 1962 and May 1975.

MAIN OUTCOME MEASURE(S): 1) Median age at diagnosis of IBCL. 2) Latency from exposure to AO or enlistment to the development of IBCL. 3) Parameters that impact survival.

RESULTS: There were 17,175 Veterans identified (5,233 with AO exposure and 11,942 with no AO exposure). Shorter latencies were identified from exposure to diagnosis for chronic lymphocytic leukemia (CLL), follicular lymphoma (FL), mantle cell lymphoma (MCL), marginal zone lymphoma (MZL), and hairy cell leukemia (HCL), with respective median latencies for AO-exposed and AO-unexposed Veterans of 43 (range 10-57) vs. 45 (10-60) years [p<0.0001], 41 (12-59) vs. 44 (2-59) years [p<0.0001], 43 (range 25-54) vs. 45 (21-59) years [p=0.0004], 44 (26-55) vs. 45 (15-59) years [p=0.017], and 37 (11-54) vs. 42 (17-59) years [p=0.0021]. There was no difference in the latency to developing lymphoplasmacytic lymphoma (LPL): 47 (24-53) vs. 46 (18-59) years (p=0.4583). No differences in median age of diagnosis were identified for CLL (66 vs. 65 years), FL (65 vs. 64 years), MCL (67 vs. 66 years), MZL (66 vs. 66 years), LPL (68 vs. 66 years), or HCL (63 vs. 63 years). Using a Cox proportional hazard model, parameters associated with higher risks of death included age at diagnosis (HR, 1.067; 95%CI, 1.04-1.09), tobacco use (HR, 2.112; 95%CI, 1.739-2.565), more advanced stage (HR, 1.158; 95%CI, 1.098-1.220), and worse performance status (HR, 1.512; 95%CI, 1.382-1.655). AO exposure was not associated with a significantly higher risk of death (HR, 1.069; 95%CI, 0.885-1.291).

CONCLUSIONS: AO exposure was associated with a shorter latency from exposure to diagnosis of IBCL subtypes but was not associated with worse overall survival than no AO exposure.