Significant quantities of long-lived radionuclides were released to the environment during the Chernobyl nuclear power plant accident in 1986. These radionuclides contributed to radiation doses due to ingestion of contaminated foods and external exposure from the ground deposition that resulted. The contributions of these exposure pathways to thyroid doses received by subjects of an epidemiologic study of children from Belarus are evaluated and presented. The analysis shows that ingestion of the long-lived radionuclides, primarily radiocesium, typically contributed a small percentage of the total thyroid dose received by the study subjects. The median and mean fractional contributions were 0.76 and 0.95%, respectively. The contribution of external exposure to the thyroid dose was generally larger and more variable, with median and mean contributions of 1.2 and 1.8% of the total thyroid doses, respectively. For regions close to the reactor site, where radionuclide deposition was highest, the contributions of radiocesium ingestion and external exposure were generally lower than those of the short-lived radioiodine isotopes (132I and 133I) and their precursors (132Te). In other areas, the contributions of these two pathways were comparable to those of the short-lived radioiodines. For all subjects, intakes of 131I were the primary source of dose to the thyroid.