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efsa-opinion-chromium-food-drinking-water

efsa-opinion-chromium-food-drinking-water efsa-opinion-chromium-food-drinking-water

damienvanherp
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16.04.2014 Views

Chromium in food and drinking water The most critical Cr(VI)-induced non-neoplastic effects in the NTP 2-year long term studies (NTP, 2008) were haematological effects (microcytic, hypochromic anemia), histiocytic cellular infiltration in the liver, mesenteric lymph node and duodenum in rats. In mice they were hyperplasia in duodenum, and hystiocytic cellular infiltration in the liver and mesenteric lymph nodes. In the NTP 2-year studies (NTP, 2008) microcytic, hypochromic anemia characterized by decreased mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), hematocrit and hemoglobin was observed in rats and mice from 22 days to 6 months. The severity of the haematological effects was dose-dependent, with maximum effects observed after 22-23 days of exposure, showing that with time, the animals adapted to exposure. Effects were less severe in mice than those observed in rats. The erythropoietic tissues were able to respond to the anemia, but there was some ineffective erythopoiesis resulting in production of increased number of smaller erythrocytes. The lowest LOAELs for haematological effects were 0.77 mg Cr(VI)/kg b.w. per day in male rats and 0.38 mg Cr(VI)/kg b.w. per day in female mice. The NOAEL in rats was 0.21 mg Cr(VI)/kg b.w. per day and a NOAEL was not established in mice. The LOAELs for liver toxicity were 0.77 mg Cr(VI)/kg b.w. per day in rats and 0.38 mg Cr(VI)/kg b.w. per day in mice. Chronic inflammation appeared to be more severe than in control animals at 7 and 8.8 mg Cr(VI)/kg b.w. per day in female rats and mice, respectively. The LOAELs for effects on the mesenteric lymph nodes were 0.77 and 0.38 mg Cr(VI)/kg b.w. per day in rats and mice, respectively. The LOAEL for histiocytic cellular infiltration in the duodenum in rats was at 0.77 mg Cr(VI)/kg b.w. per day and for hyperplasia in the duodenum in mice was 0.38 mg Cr(VI)/kg b.w. per day. Effects on the kidney have been reported in a gavage study in rats exposed for 20 days to 50 mg potassium chromate/kg b.w. per day (corresponding to 13.4 mg Cr(VI)/kg b.w. per day). The effects were increased accumulation of lipid, triglycerides and phospholipids in different regions of the kidney compared to controls, and inhibition of kidney membrane enzymes (alkaline phosphatase, acid phosphatase, glucose-6-phosphatase and lipase) (Kumar and Rana, 1982). Toxic effects on the kidney were also reported in male and female Wistar rats exposed for 22 weeks to 25 mg potassium dichromate (corresponding to 0.8 mg Cr(VI)/kg b.w. per day) via drinking water: degeneration of basement membrane in Bowman’s capsule and renal tubular degeneration (Chopra et al, 1996; Acharya et al, 2001). Thompson et al. (2011b) performed a 90-day drinking water study using similar exposure conditions as in a previous cancer bioassay (NTP, 2008) as well as lower concentrations. Female B6C3F1 mice were exposed to 0, 0.3, 4, 14, 60, 170 and 520 mg sodium dichromate dihydrate/L (corresponding to 0, 0.03, 0.3, 1.1, 4.7, 12.2, 31 mg Cr(VI)/kg b.w. per day). No treatment-related gross lesions were observed after 90 days of exposure. There were no microscopic lesions observed in the oral cavity. Following 90 days of exposure, significant increases in chromium were observed at ≥ 60 mg/L in the oral cavity, glandular stomach, jejunum and ileum. Total chromium concentrations in the duodenum were significantly elevated at ≥ 14 mg/L. Intestinal lesions including villous cytoplasmic vacuolisation were observed at concentrations ≥ 60 mg/L and atrophy, apoptosis and crypt hyperplasia were seen at ≥ 170 mg/L. Multinucleated syncitia (fused cells) in the villous lamina propria were present in mice exposed to 520 mg/L. Similar histopathological lesions were observed in the jejunum. The NOAEL was 14 mg sodium dichromate dihydrate/L (corresponding to 1.1 mg Cr(VI)/kg b.w. per day). A similar 90-day drinking water study was performed on rats. Female F344 rats were exposed to 0, 0.3, 4, 60, 170 and 520 mg sodium dichromate dihydrate/L (corresponding to 0, 0.02, 0.2, 3.6, 8.7, 24 mg Cr(VI)/kg b.w. per day mg Cr(VI)/kg b.w. per day). Statistically significant increases in total chromium concentrations occured in the oral cavity, duodenum and jejunum at ≥ 60 mg/L. Significant increases in the glandular stomach and ileum occured at ≥ 170 mg/L and 520 mg/L, respectively. No treatment-related gross lesions were observed after 90 days of exposure. There were no microscopic lesions observed in the oral cavity. In the duodenum, apoptosis was observed at ≥ 60 mg/L and crypt EFSA Journal 2014;12(3):3595 82

Chromium in food and drinking water cell hyperplasia at ≥ 170 mg/L. histiocytic infiltration was present in almost all animals at ≥ 60 mg/L. Apoptosis, crypt cell hyperplasia and villous atrophy were observed in the jejunum at concentrations as low as 4 mg/L (incidences not statistically different from control animals and in many instances the lesions were not observed at higher concentrations). There were concentration-dependent increases in histiocytic infiltration beginning at 60 mg/L. The NOAEL was 4 mg sodium dichromate dihydrate/L corresponding to 0.2 mg Cr(VI)/kg b.w. per day (Thompson et al., 2012b). Table 16 summarised the NOAELs and LOAELs for the critical non-neoplastic toxic effects of Cr(VI) observed in relevant 90 days and 2 year studies for critical endpoints (excluding cancer). EFSA Journal 2014;12(3):3595 83

Chromium in <strong>food</strong> and <strong>drinking</strong> <strong>water</strong><br />

cell hyperplasia at ≥ 170 mg/L. histiocytic infiltration was present in almost all animals at ≥ 60 mg/L.<br />

Apoptosis, crypt cell hyperplasia and villous atrophy were observed in the jejunum at concentrations<br />

as low as 4 mg/L (incidences not statistically different from control animals and in many instances the<br />

lesions were not observed at higher concentrations). There were concentration-dependent increases in<br />

histiocytic infiltration beginning at 60 mg/L. The NOAEL was 4 mg sodium dichromate dihydrate/L<br />

corresponding to 0.2 mg Cr(VI)/kg b.w. per day (Thompson et al., 2012b).<br />

Table 16 summarised the NOAELs and LOAELs for the critical non-neoplastic toxic effects of Cr(VI)<br />

observed in relevant 90 days and 2 year studies for critical endpoints (excluding cancer).<br />

EFSA Journal 2014;12(3):3595 83

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