Juvenile fathead minnows ( Pimephales promelas) were exposed to fluoranthene (< 0.2, 6.1, and 12.5 μg l −1) in the presence of solar ultraviolet radiation (SUVR) for 6, 12, 24, 48, and 96 h. Ultrastructural pathology of the secondary gill lamellae was examined using transmission electron microscopy. Following 12 h of exposure to 12.5 μg l −1 fluoranthene and SUVR (UV-A = 49.5 μW cm −2, UV-B = 4.2 μW cm −2), the outer mucosal layer of epithelial cells exhibited cellular swelling and dilation of endoplasmic reticulum and mitochondria. At 48 h, additional morphological alterations in mucosal cells included hypertrophy, blebbing of the plasma membrane, and the presence of cytolysosomes, myelinoid bodies, and lipid droplets. The staining characteristics of these droplets were consistent with that of neutral unsaturated lipids, which suggested that their formation was the result of rapid lipid peroxidation reactions. In addition, a second physiologically distinct reaction occurred within the secondary lamellae following 24 h of exposure. This reaction was inflammatory in nature, and as the exposure progressed, was characterized by edema, leukocyte infiltration, and vasoconstriction. In those fish exposed to 6.1 μg l −1 fluoranthene and SUVR, a similar progression compared to 12.5 μg l −1 exposure of mucosal cell damage and inflammatory-type reaction was evident beginning at 24 h of exposure. The net result of mucosal cell hypertrophy and the inflammatory-type reaction was a significant increase in the water-blood diffusion distance of 294% and 285% for those fish exposed to SUVR and the 12.5 and 6.1 μg l −1 fluoranthene treatments, respectively, suggesting that lethality was a consequence of respiratory stress due to the decreased oxygen diffusion capacity of the gills. These observations demonstrate that the mode of action of photo-induced fluoranthene toxicity in fish is a disruption of mucosal cell membrane function and integrity.