Early-weaned pigs (n = 64) averaging 5.3 +/- 0.3 kg and distributed into two environments (dirty and clean) were used to evaluate effects of conjugated linoleic acid (CLA) on growth performance, immune competence, and empty body composition. A factorial (2 x 4) arrangement within a split-plot design, with four littermate pigs as the experimental unit for the environment, pig within litter as the experimental unit for dietary treatment, and d-0 body weight used as covariate, were used in data analysis. Diets were formulated to contain CLA at 0, 0.67, 1.33, or 2% and to exceed the NRC (1988) nutrient needs of pigs. Animals were given ad libitum access to feed for 7 wk in three phases (I, 1 to 2; II, 3 to 5; and III, 6 to 7 wk). Within phases, diets were isocaloric and isonitrogenous. In Phase I, as dietary CLA concentration increased, ADG and ADFI decreased linearly (P < 0.05 and P < 0.02, respectively). In Phase II, upon adaptation to dietary CLA supplementation, ADG increased quadratically (603, 623, 622, and 548 g/d; P < 0.01), ADFI decreased linearly (873, 840, 867, and 717 g/d; P < 0.02) and gain:feed ratio tended to increase linearly (691, 742, 715, and 763; P < 0.07). In Phase III, no differences in growth performance were attributed to either dietary or environmental treatments. The poor health status associated with the dirty environment induced a growth suppression; pigs in the clean room had a greater cumulative ADG (P < 0.01) and ADFI (P < 0.01) than pigs in the dirty room. In Phase I, lower plasma urea nitrogen levels observed in pigs found in the dirty room (P < 0.03) indicated a lower protein intake caused by a lower ADFI. The effects of dietary CLA on peripheral phenotypic profiles of lymphoytes did not appear until d 42. However, as indicated by the growth suppression of pigs in the dirty room, the negative effects of the environmental challenge on pig health and growth had already appeared during phase I. On d 42, CLA induced a linear increase in percentages of CD8+ lymphocytes (21.7, 22.3, 28.0, and 32.7%; P < 0.001). These data suggest that a 42-d dietary CLA supplementation preceding a disease challenge could have prevented disease-associated growth suppression. Also, CLA-mediated amelioration of particular infectious diseases will depend on which CD8+ T cell subset (i.e., CD8alphaalpha-immunoregulatory or CD8alphabeta-cytotoxic) is most influenced by dietary CLA supplementation.