efsa-opinion-chromium-food-drinking-water

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Chromium in food and drinking water Decreased testes weight, disorganisation in seminiferous tubules, decreased sperm count and motility, sperm death, disrupted spermatogenesis and histopathological changes to the epididymis (ductal obstruction, development of microcanals, germ cell depletion, hyperplasia of Leydig cells and Sertoli cell fibrosis) have been reported in adult bonnet monkeys exposed to doses ≥ 1.7 mg Cr(VI)/kg b.w. per day as potassium dichromate in drinking water for 180 days (Aruldhas et al., 2004, 2005, 2006 and Subramanian et al., 2006). Effects increased in severity with dose and duration. The studies have also shown that potassium dichromate administered via drinking water caused reversible oxidative stress in the seminal plasma and sperm leading to sperm death and reduced sperm motility and damage to the epididymal luminal spermatozoa, as a consequence of which the principal cells phagocytosed dead sperm from the lumen. Cr(VI) has also been shown to alter weights of female reproductive organs, to have an effect on lengthening the oestrus cycle, to reduce the number of ovarian follicles and to induce changes in circulating levels of steroid and pituitary hormones (Murthy et al., 1996; Al-Hamood et al., 1998; Banu et al., 2008; Samuel et al., 2011). Atretic follicles and congestion in stromal tissue were observed in female mice receiving 750 mg Cr(VI)/L as potassium dichromate (equivalent to 135 mg Cr(VI)/kg b.w. per day, according to EFSA default values, 2012) for 20 days. Ultrastructural observations revealed disintegrated cell membranes of two layered follicular cells and altered villiform mitochondria in thecal cells of mice exposed to 5 mg Cr(VI)/L (corresponding to 0.8 mg Cr(VI)/kg b.w. per day) for 90 days (Murthy et al., 1996). A series of studies have examined the effects of Cr(VI) on oxidative stress in rat offsprings. Samuel et al. (2011) reported that maternal exposure to ≥ 6 mg Cr(VI)/kg b.w. per day as potassium dichromate in the drinking water on lactation days 1-21 resulted in dose-related reductions in antioxidant enzymes activities in uterine tissue from offspring measured on postnatal days 21, 45, and 65. This correlated with significant increases in lipid peroxidation and hydrogen peroxide in uterine tissue. Similar results were reported by Soudani and coworkers (Soudani et al. 2011a, b; Soudani et al., 2013) in the kidney, liver, and bone from 14-day-old pups born to dams exposed to 9.4 mg Cr(VI)/kg/day (only dose level tested) as potassium dichromate in the drinking water on gestation days 14-21 and postnatal natal days 1-14. This dose level also caused histological alterations in the tissues studied. In all of these studies, final body weight of the pups was significantly reduced, 25 % in the Soudani et al. (2011a, b) studies and 10-13 % at 6 mg Cr(VI)/kg per day and 26-33 % at 24 mg Cr(VI)/kg per day in the Samuel et al. (2011) study. Developmental toxicity (embryotoxicity: increase in pre- and post-implantation loss, and in resorptions, fetotoxicity: decrease fetal weight, number of fetuses, number of live fetuses, and increased frequency of gross, visceral and skeletal malformations) has been observed in rats or mice treated during gestation with potassium dichromate in drinking water. In mice effects were observed at doses of 250 mg/L (corresponding to 45-53 mg Cr(VI)/kg b.w. per day) (Trivedi et al., 1989; Junaid et al., 1995; Junaid et al., 1996a). In rats, effects have been observed at 50 mg/L (corresponding to 1.6 mg Cr(VI)/kg b.w. per day) (Elsaieed and Nada, 2002). No NOAELs have been established. Administration by gavage of 25 mg potassium dichromate/rat (corresponding to 36 mg Cr(VI)/kg b.w. per day during gestation days 1-3 (before implantation) result in absence of implantation and during gestation days 4-6 (during implantation) result in post-implantation loss, decreased number of viable fetuses and increased number of resorptions (Betaineh et al., 2007). Studies have shown that chromium passed the placental barrier and accumulate in fetal tissues (Trivedi et al., 1989; Junaid et al., 1995, 1996a, b; Kanojia et al., 1996, 1998; Elsaieed and Nada, 2002). In studies where dams have been exposed prior to mating to potassium dichromate in drinking water, Cr(VI) decreased mating and fertility indices, the number of corpora lutea and the number of implantations as well as it increased the number of resorptions, pre- and post-implantations loss, decreased fetal weight and reduced ossification. Effects were observed at doses of 250 mg/L (equivalent to 45 mg Cr(VI)/kg b.w. per day in rats and 31-52 mg Cr(VI)/kg b.w. per day in mice) (Junaid et al., 1996b; Kanojia et al., 1996, 1998; Elbetieha and Al-Hamood, 1997). No NOAELs have been determined by the authors EFSA Journal 2014;12(3):3595 86
Chromium in food and drinking water Delayed vaginal opening (delayed puberty) was reported in offspring of rats exposed to potassium dichromate (6-24 mg Cr(VI)/kg b.w. per day) during lactation (Banu et al., 2008; Samuel et al., 2011) or mice (76 mg Cr(VI)/kg b.w. per day) exposed from gestation to lactation D20 (Al-Hamood et al., 1998). Cr(VI) was also reported to alter mandibular growth and tooth eruption in rats (De Lucca et al., 2009). In this study, 4-day-old suckling Wistar pups received gavage doses of 0, 6.25 or 12.5 mg potassium dichromate/kg b.w. per day (corresponding to 0, 2.2 or 4.4 mg Cr(VI)/kg b.w. per day) for 10 consecutive days. Rats dosed at 4.4 mg Cr(VI)/kg b.w. per day showed a statistically significant reduction in mandibular length, base, height and area, and delayed eruption of the first molar. Delayed eruption of the second molar was observed in pups receiving the low-dose. These effects may have been secondary to a delay in body growth, as terminal body weight was reduced by 20 and 40 % in the low- and high-dose groups, respectively, relative to controls. Shorter tail length was also observed in high dose animals. The CONTAM Panel noted that some of the studies have methodological limitations that were already reported for Cr(III). The NOAELs and LOAELs from the relevant studies are reported in Table 17 and the studies are described in details in Table H6 (Appendix H). Table 17: Developmental and reproductive toxicity studies with Cr(VI) compounds. Parental: 30.3 Study NOAEL LOAEL Doses in mg Cr(VI)/kg b.w. Species per day (a) mg Cr(VI)/kg b.w. per day Multigeneration reproductive toxicity 2-generation (diet) mice Parental: 13.6 30.3/37 (b) potassium dichromate Reproduction: 30.3 (c) Reproduction:- F0/F1: 0, 6.9/7.9, 13.6/16.1, Male reproductive toxicity studies Reference NTP (1997) 9-week (diet) + 8-week recovery Potassium dichromate 0, 1.4, 4.6, 9.9, 40.7 (b) mice Reproduction: 40.7 (c) - NTP (1996a, 1997) 9-week (diet) + 8-week recovery Oral (diet) Potassium dichromate 0, 0.5, 1.6, 3.2, 12.7 (b) rats Reproduction: 12.7 (c) - NTP (1996a, 1997) 2-year (drinking water) mice Reproduction: 5.9 (c) - NTP (2008) F: 0, 0.38, 1.4, 3.1 and 8.7 (b) sodium dichromate dihydrate M: 0, 0.38, 0.91, 2.4 and 5.9 (b) 2-year (drinking water) sodium dichromate dihydrate M: 0, 0.21, 0.77, 2.1 and 5.9 (b) F: 0, 0.24, 0.94, 2.4 and 7.0 (b) rats Reproduction: 5.9 (c) - NTP (2008) EFSA Journal 2014;12(3):3595 87
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EFSA Journal 2014;12(3):3595 SCIENT
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