efsa-opinion-chromium-food-drinking-water
efsa-opinion-chromium-food-drinking-water
efsa-opinion-chromium-food-drinking-water
You also want an ePaper? Increase the reach of your titles
YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.
7.3.2.1. Acute oral toxicity<br />
Chromium in <strong>food</strong> and <strong>drinking</strong> <strong>water</strong><br />
Most studies identified on acute toxicity are case reports from intentional and accidental poisoning.<br />
Those case reports on the consequences of high doses of Cr(VI) allow the identification of the type<br />
and nature of possible effects of Cr(VI) in humans when describing a range of effects from mild to<br />
serious and life-threatening and lethal effects (see Appendix I1) Clinical effects included<br />
haematological, hepatic and renal injury as well as respiratory and gastrointestinal lesions.<br />
Accidental ingestion has been reported for Cr(VI) compounds including chromic acid (Fristedt et al.,<br />
1965; Saryan and Reedy, 1988; Loubières et al., 1999), potassium chromate (Goldman and Karotkin,<br />
1935; Partington, 1950; Kaufman et al., 1970; Sharma et al., 1978; Iserson et al., 1983; Clochesy,<br />
1984; Hanston et al., 2005), and ammonium dichromate (Reichelderfer, 1968; Hasan, 2007) resulting<br />
in a large variety of clinical presentations such as abdominal pain, nausea, and vomiting; hematemesis<br />
and bloody diarrhea; caustic burns of the mouth, pharynx, esophagus, stomach, and duodenum and GI<br />
hemorrhage; anemia, decreased blood Hb, abnormal erythrocytes, and intravascular hemolysis;<br />
hepatotoxicity (hepatomegaly, jaundice, elevated blood bilirubin, and liver enzymes activities); renal<br />
failure (oliguria and anuria); cyanosis; and metabolic acidosis, hypotension, and shock (see also<br />
ATSDR, 2012). Fatty degeneration in the liver and tubular degeneration and necrosis in the kidney<br />
were observed in biospies (Reichelderfer, 1968; Kaufman et al., 1970; Sharma et al., 1978; Loubières<br />
et al., 1999).<br />
Doses of Cr(VI) ranging 4 to 360 mg/kg b.w. were reported to be lethal (Kaufman et al., 1970; Iserson<br />
et al., 1983; Clochesy, 1984; Saryan and Reedy, 1988; Loubières et al., 1999).<br />
Paustenbach et al. (1996) investigated the kinetics of Cr(VI) in a male volunteer who ingested 2 L per<br />
day of <strong>water</strong> containing 2 mg/L for 17 consecutive days. Kerger et al. (1996) studied four adult male<br />
volunteers ingesting a single dose of 5 mg Cr (in 0.5 liters deionized <strong>water</strong>) in three choromium<br />
mixtures: (1) Cr(III) chloride (CrCl 3 ), (2) potassium dichromate reduced with orange juice (Cr(III)-<br />
OJ); and (3) potassium dichromate [Cr(VI)]. Kuykendall et al. (1996) report on four adult male<br />
volunteers ingested a bolus dose of 5000 micro <strong>chromium</strong> in a 0.51 volume of <strong>water</strong> (10 ppm),<br />
Corbett et al. (1997) examined the systemic uptake of <strong>chromium</strong> in four human volunteers immersed<br />
below the shoulders in <strong>water</strong> at 91 +/- 2.5 degrees F. following three hours of contact with <strong>water</strong><br />
containing Cr(VI) at a concentration of 22 mg/L. Finley et al., 1997 studied adult male volunteers<br />
ingesting a liter (in three volumes of 333 ml, at approximate 6-hr intervals) of deionized <strong>water</strong><br />
containing Cr(VI) at concentrations ranging from 0.1 to 10.0 mg/L. Kerger et al. (1997) investigated<br />
in adult male volunteers the oral exposure to 5 and 10 mg Cr(VI)/L in <strong>drinking</strong> <strong>water</strong> administered as<br />
a single bolus dose (0.5 L swallowed in 2 min) or for 3 days at a dosage of 1 L per day (3 doses of<br />
0.33 L each day, at 6-h intervals). None of these reports presented indications of clinical effects.<br />
In conclusion, at high doses Cr(VI) exerts acute health effects in the respiratory, haematological,<br />
hepatic and renal system and in the gastrointestinal tract where acute effects include abdominal pain,<br />
vomiting, ulceration, hemorrhage, necrosis, and bloody diarrhea.<br />
7.3.2.2. Subchronic and chronic toxicity excluding cancer<br />
Haematological effects have been inconsistently reported in the literature such that haemotoxicity after<br />
oral exposure cannot be assessed. It was suggested that those effects originate from primary exposure<br />
to Cr(VI) and its accumulation in erythrocytes and subsequent reduction to Cr(III) via the reactive<br />
intermediates Cr(V) and Cr(IV) and their binding to hemoglobin and other ligands. The Crhaemoglobin<br />
complex is relatively stable and remains sequestered within the cell over the life-span of<br />
the erythrocyte (Lewalter et al., 1985). Haematological effects observed in some cases of accidental or<br />
intentional ingestion of high doses Cr are detailed in Appendix I2. A cross-sectional study from an<br />
alloy plant in the People's Republic of China (summarised below) reports associations between Cr(VI)<br />
and the occurrence of leukocytosis and immature neutrophils.<br />
Gastrointestinal effects observed in occupational studies may occur due to exposure via mouth<br />
breathing or other means of ingestion of Cr (e.g., mucociliary clearance of inhaled Cr particles to the<br />
gastrointestinal tract and/or ingestion secondary to hand-to-mouth activity). In particular, epigastric<br />
EFSA Journal 2014;12(3):3595 98