In general, the possibility of vitamin A toxicity for swine is remote. However, of all vitamins, vitamin A is most likely to be provided in concentrations toxic to swine. Excessive vitamin A has been demonstrated to have toxic effects in most species studied. Presumed upper safe levels are four to 10 times the nutritional requirements for nonruminant animals, including swine (NRC, 1998). Most of the harmful effects have been obtained by feeding more than 100 times the daily requirements over time. Thus, small excesses of vitamin A for short periods should not exert any harmful effects. Recommended upper safe levels of vitamin A for swine are 20,000 IU per kg (9,091 IU per lb) of diet for growing pigs and 40,000 IU per kg (18,182 IU per lb) of diet for breeding animals.
The most characteristic signs of hypervitaminosis A are skeletal malformations, spontaneous fractures, and internal hemorrhage (Anderson et al., 1966; NRC, 1998). Other signs include loss of appetite, slow growth, loss of weight, skin thickening, suppressed keratinization, increased blood-clotting time, reduced erythrocyte count, enteritis, congenital abnormalities and conjunctivitis. Degenerative atrophy, fatty infiltration and reduced function of liver and kidney are also typical. A variety of effects of chronic hypervitaminosis A in weanling pigs were reported by Hurt et al. (1966). Dobson (1969) documented the effects of massive induced hypervitaminosis A on newborn pigs. In addition to reduced growth; high plasma, liver and kidney vitamin A levels; and a characteristic gait, Pryor et al. (1969) reported pathologic changes in the bones of pigs subjected to levels of vitamin A sufficient to produce hypervitaminosis A.
Bone abnormalities may include extensive bone resorption and narrowing of the bone shaft, bone fragility and short bones because of retarded growth. Wolke et al. (1968) reported the effects of excessive vitamin A on endochondral and intramembranous bone formation in the pig. Abnormalities in bone modeling are the essential causes of fractures, and the cartilage matrix of bone may be destroyed.
The effects of supplementing the diets of weanling pigs with up to 100 times the NRC (1988) estimated requirements for vitamin A have been investigated (Blair et al., 1989, 1992). Blair et al. (1989) indicated that a level of only 10 times the requirement even over just over four weeks may induce osteochondrosis. The allowable range of vitamin A set out in the Canadian Feeds Regulations (1983) was found to be appropriate for practical pig production (Blair et al., 1992). Hidiroglou (1996) reported that an intramuscular dose of 2.5 x 106 IU produced livers with levels of vitamin A high enough to be considered hazardous to health.
Another area of attention has focused on whether or not excessive vitamin A can affect vitamin E status. Blair et al. (1996) reported a significant depressing effect of vitamin A on vitamin E status. Blair et al. (1996) indicated that a tolerable dietary range of vitamin A for young pigs in the range of 10 to 30 kg is up to 10 times the requirement. Fuhrmann et al. (1997) reported that 20,000 IU per kg of vitamin A reduced plasma and tissue vitamin E levels, which in turn led to an increase of lipid peroxidation as indicated by a higher production of hydrocarbons. Blair et al. (1996) considered that this raised concern about further increases of vitamin A supplementation in early-weaned pigs. However, Anderson et al. (1997) concluded that during early gestation, the vitamin E status of gilts was not detrimentally influenced by three 350,000 IU injections of vitamin A shortly before, at and shortly after breeding. Anderson et al. (1995) reported that feeding a high level of retinyl acetate (20,000 IU/kg) did not influence animal performance or blood serum and tissue alpha-tocopherol concentrations in growing-finishing pigs. Weaver et al. (1989) reported a significant interaction for vitamin A and vitamin E for plasma tocopherol. Higher levels of vitamin A when supplied with a high level of vitamin E lowered plasma tocopherol concentrations. Hoppe et al. (1992) indicated that dietary retinol at up to up to 10,000 IU per kg does not affect alpha-tocopherol concentrations in plasma or in tissues selected with the exception of cardiac muscle. Alpha-tocopherol levels in heart and liver displayed an inverse relationship with levels (5,000, 10,000, 20,000 or 40,000 IU per kg) of dietary retinol, while dietary retinol had no effect on levels of alpha-tocopherol in Longissimus muscle or backfat. Zomborszky-Kovacs et al. (1998) reported a numeric decrease in plasma vitamin concentration in unsupplemented versus carotene-supplemented weaned pigs. Beginning one week prior to weaning, the supplemented group received 855 mg beta-carotene per kg diet (10 times the NRC [1988] recommendation). The carotene-supplemented pigs and control pigs had vitamin E concentrations in plasma of 2.12 and 5.58 mg/dl, respectively.
