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PubMed2003

Fume generation and content of total chromium and hexavalent chromium in flux-cored arc welding.

This study was performed to investigate the fume generation rates (FGRs) and the concentrations of total chromium and hexavalent chromium when stainless steel was welded using flux-cored arc welding (FCAW) with CO2 gas. FGRs and concentrations of total chromium and hexavalent chromium were quantified using a method recommended by the American Welding Society, inductively coupled plasma-atomic emission spectroscopy (NIOSH Method 7300) and ion chromatography (modified NIOSH Method 7604), respectively. The amount of total fume generated was significantly related to the level of input power. The ranges of FGR were 189-344, 389-698 and 682-1157 mg/min at low, optimal and high input power, respectively. It was found that the FGRs increased with input power by an exponent of 1.19, and increased with current by an exponent of 1.75. The ranges of total chromium fume generation rate (FGRCr) were 3.83-8.27, 12.75-37.25 and 38.79-76.46 mg/min at low, optimal and high input power, respectively. The ranges of hexavalent chromium fume generation rate (FGRCr6+) were 0.46-2.89, 0.76-6.28 and 1.70-11.21 mg/min at low, optimal and high input power, respectively. Thus, hexavalent chromium, which is known to be a carcinogen, generated 1.9 (1.0-2.7) times and 3.7 (2.4-5.0) times as the input power increased from low to optimal and low to high, respectively. As a function of input power, the concentration of total chromium in the fume increased from 1.57-2.65 to 5.45-8.13% while the concentration of hexavalent chromium ranged from 0.15 to 1.08%. The soluble fraction of hexavalent chromium produced by FCAW was approximately 80-90% of total hexavalent chromium. The concentration of total chromium and the solubility of hexavalent chromium were similar to those reported from other studies of shielded metal arc welding fumes, and the concentration of hexavalent chromium was similar to that obtained for metal inert gas-welding fumes.

Air Pollutants, Occupational↗
PubMed1991

Reaction of chromium(VI) with glutathione or with hydrogen peroxide: identification of reactive intermediates and their role in chromium(VI)-induced DNA damage.

The types of reactive intermediates generated upon reduction of chromium(VI) by glutathione or hydrogen peroxide and the resulting DNA damage have been determined. In vitro, reaction of chromium(VI) with glutathione led to formation of two chromium(V) complexes and the glutathione thiyl radical. When chromium(VI) was reacted with DNA in the presence of glutathione, chromium-DNA adducts were obtained, with no DNA strand breakage. The level of chromium-DNA adduct formation correlated with chromium(V) formation. Reaction of chromium(VI) with hydrogen peroxide led to formation of hydroxyl radical. No chromium(V) was detectable at 24 degrees C (297 K); however, low levels of the tetraperoxochromium(V) complex were detected at 77 K. Reaction of chromium(VI) with DNA in the presence of hydrogen peroxide produced significant DNA strand breakage and the 8-hydroxydeoxyguanosine adduct, whose formation correlated with hydroxyl radical production. No significant chromium-DNA adduct formation was detected. Thus, the nature of chromium(VI)-induced DNA damage appears to be dependent on the reactive intermediates, i.e. chromium(V) or hydroxyl radical, produced during the reduction of chromium(VI).

Animals↗
PubMed1981

[Studies on a specific chromium binding substance (a low-molecular-weight chromium binding substance) in urine (author's transl)].

The aim of this study was to identify a specific substance [a Low-Molecular-Weight Chromium binding substance (LMW Cr)] in normal urine and also to clarify the various factors affecting chromium to bind this substance in urine. The results obtained were as follows: 1. Normal human and rat urines contained unsaturated LMW Cr similar to that found in the liver or other organs of rabbits and dogs. The amount of chromium bound in vitro to the unsaturated LMW Cr in normal human urine was 14.81 +/- 1.84 microgram/ml urine when urine was incubated with trivalent chromium for 30 minutes at 37 degrees C. 2. Higher amounts of chromium were bound to LMW Cr in normal urine a 37 degrees C than at 24 degrees C, in acidic state of urine than in alkaline state, and when trivalent chromium was added to the incubation mixture than when hexavalent chromium was added. Chromium contained in LMW Cr was supposed to be trivalent. Furthermore, boiling urine at 100 degrees C for 10 minutes did not reduce the chromium binding capacity of LMW Cr in urine. These results indicate that LMW Cr in urine binds chromium by a chemical reaction. 3. Amounts of chromium bound to LMW Cr in urine obtained 3 hrs after intraperitoneal injection of 200 mumole K2Cr2O7 to a rat were much higher than amounts of chromium bound in vitro to LMW Cr in normal urine during 3 hrs incubation of the urine with K2Cr2O7. This suggests that most of excessively absorbed chromium is excreted into urine after being bound to LMW Cr in organs. 4. Urine from patients with chronic nephritis excreted a part of added chromium bound to high molecular weight fractions corresponding to peaks of UV absorption.

Adult↗
PubMed1998

Quantification of total chromium and hexavalent chromium in UHT milk by ETAAS.

Procedures for the quantification of total chromium and hexavalent chromium in UHT milk samples are presented. Total chromium was determined directly in milk with the addition of a surfactant and a mixture of Pd and Mg as a chemical modifier. For the selective separation of hexavalent chromium, the sample pre-treatment consisted in precipitation of proteins and elution of the supernatant through a Chromabond NH2 column. The metal was eluted with nitric acid. Both total chromium and hexavalent chromium were evaluated by atomic absorption spectrometry with electrothermal atomization using the same instrumental conditions. The detection limits were 0.2 and 0.15 microgram l-1 for total chromium and hexavalent chromium, respectively. The linearity ranges under the optimized conditions were 0.2-20 and 0.15-50 micrograms l-1. For total chromium the precision was 4.9 and 5.7% for the analytical and the over-all procedure, respectively, and for hexavalent chromium 4.3 and 4.9%, respectively. The validation of both procedures was performed by the standard additions method and the recoveries were higher than 93% in all cases. For total chromium, a certified reference material was also used to validate the methodology. The methods were applied to the determination of total chromium and hexavalent chromium in 60 UHT milk samples.

Animals↗
PubMed2001

A physiologically based model for the ingestion of chromium(III) and chromium(VI) by humans.

A physiologically based model of human chromium kinetics has been developed, based on an existing physiologically based model of human body and bone growth (O'Flaherty, 1993, Toxicol. Appl. Pharmacol. 118, 16-29; 1995a, Toxicol. Appl. Pharmacol. 131, 297-308; 2000, Toxicol. Sci. 55, 171-18) and an existing physiologically based model of chromium kinetics in rats (O'Flaherty, 1996, Toxicol. Appl. Pharmacol. 138, 54-64). Key features of the adapted model, specific to chromium, include differential absorption of Cr(VI) and Cr(III), rapid reduction of Cr(VI) to Cr(III) in all body fluids and tissues, modest incorporation of chromium into bone, and concentration-dependent urinary clearance consistent with parallel renal processes that conserve chromium efficiently at ambient exposure levels. The model does not include a physiologic lung compartment, but it can be used to estimate an upper limit on pulmonary absorption of inhaled chromium. The model was calibrated against blood and urine chromium concentration data from a group of controlled studies in which adult human volunteers drank solutions generally containing up to 10 mg/day of soluble inorganic salts of either Cr(III) (chromic chloride, CrCl(3)) or Cr(VI) (potassium dichromate, K(2)Cr(2)O(7)) (Finley et al., 1997, Toxicol. Appl. Pharmacol. 142, 151-159; Kerger et al., 1996, Toxicol. Appl. Pharmacol. 141, 145-158; Paustenbach et al., 1996, J. Toxicol. Environ. Health 49, 453-461). In one of the studies, in which the chromium was ingested in orange juice, urinary clearance was observed to be more rapid than when inorganic chromium was ingested. Chromium kinetics were shown not to be dependent on the oxidation state of the administered chromium except in respect to the amount absorbed at these ambient and moderate-to-high exposures. The fraction absorbed from administered Cr(VI) compounds was highly variable and was presumably strongly dependent on the degree of reduction in the gastrointestinal tract, that is, on the amount and nature of the stomach contents at the time of Cr(VI) ingestion. The physiologically based model is applicable to both single-dose oral studies and chronic oral exposure, in that it adequately reproduced the time dependence of blood plasma concentrations and rates of urinary chromium excretion in one of the subjects who, in a separate experiment, ingested daily 4 mg of an inorganic Cr(VI) salt in 5 subdivided doses of 0.8 mg each for a total of 17 days. The high degree of variability of fractional absorption of Cr(VI) from the gastrointestinal tract leads to uncertainty in the assignment of a meaningful value to this parameter as applied to single Cr(VI) doses. To model chronic oral chromium exposure at ambient or moderately above-ambient levels, the physiologically based model in its present form should be usable with urinary clearance set to a constant value of 1-2 liters/day and the gastrointestinal absorption rate constants set at 0.25/day for Cr(III) and 2.5/day for Cr(VI). The model code is given in full in the Appendix.

Administration, Oral↗
PubMed1997

Comparative induction of oxidative stress in cultured J774A.1 macrophage cells by chromium picolinate and chromium nicotinate.

The concentration-dependent effects of chromium picolinate and chromium nicotinate were assessed on the enhanced production of reactive oxygen species including superoxide anion and hydroxyl radicals, and lipid peroxidation and DNA fragmentation in cultured macrophage J774A.1 cells. The macrophage cells were incubated with 0-50 micrograms/ml [corrected] concentrations of these chromium (III) salts for 0 and 24 hrs at 37 degrees C. Concentration-dependent effects were observed. Lipid peroxidation increased by 1.3-1.5-fold following treatment of these cells with chromium picolinate while at these same concentrations of chromium nicotinate approximately 1.2-1.8-fold increases in lipid peroxidation were observed. Increases of 1.0-1.5-fold occurred in the production of superoxide anion as determined by cytochrome c reduction following treatment with chromium picolinate while with these same concentrations and conditions only 1.1-1.2-fold increases in cytochrome c reduction were observed following treatment with chromium nicotinate. Approximately 1.2-1.5-fold increases in hydroxyl radical production were observed following treatment of these macrophage cells with increasing concentrations of chromium picolinate and chromium nicotinate. Incubation of the cells with 30-50 micrograms/ml concentrations of chromium picolinate produced 1.2-1.6 fold increases in DNA fragmentation, while under these same conditions with chromium nicotinate 1.2-1.3-fold increases in DNA fragmentation occurred. No significant loss in cell viability was observed with either chromium salt. These results demonstrate that incubation of macrophage J774A.1 cells with these chromium salts induces low levels of oxidative stress as demonstrated by the biochemical assay techniques employed in this study.

Cells, Cultured↗
PubMed1999

In vitro metabolism and permeation studies in rat jejunum: organic chromium compared to inorganic chromium.

The purpose of these studies was to compare the in vitro absorption of two inorganic chromium(III) compounds: chromium chloride and chromium nitrate, with organic chromium(III)-picolinate; and to investigate if any in vitro metabolism of chromium(VI) takes place. The in vitro metabolism studies showed that chromium (VI) was reduced by artificial gastric juice. The reduction followed first order kinetics with a half-life of 23 min. The studies also showed that the chromium picolinate complex was stable in artificial gastric juice for 4 hours. By the rat everted gut sac technique, chromium chloride, chromium nitrate and chromium picolinate penetrated the rat jejunum with 165 +/- 59, 160 +/- 26 and 127 +/- 36 ng chromium per g rat jejunum, respectively, whereas the permeability coefficients (Papp) were 0.7 +/- 0.3, 1.0 +/- 0.4, and 9.6 +/- 2.2 microns/min, respectively. Absorption studies on pig intestine in Ussing chambers showed a nearly total adsorption of chromium(III) by the chambers, resulting in unreliable data.

Animals↗
PubMed1983

Purification and chromium-excretory function of low-molecular-weight, chromium-binding substances from dog liver.

From liver of dogs injected iv with potassium dichromate (38 mg/kg body wt), a low-molecular-weight chromium-binding substance (LMCr) was purified into two subfractions, LMCr I and LMCr II, which differ in physical and chemical properties. LMCr I was identified to be an anionic, organic chromium compound with a molecular weight of 1500. It contained glutamic acid, glycine, and cysteine as the predominant amino acids and firmly bound chromium in a ratio of one chromium(III) to one molecule of LMCr I. LMCr II was isolated in crystalline form and demonstrated to be a water-soluble, inorganic chromium(III) complex consisting of Na2HPO4 . 7H2O and Na2HPO4 . 2H2O. Although its crystallization reduced the chromium content, it had a maximum chromium-binding capacity as much as one chromium per one phosphorus in water. The mixture of LMCr I and LMCr II as approximated to be the natural composition showed a lower acute toxicity as measured by lethality in mice and had higher rates of urinary excretion and renal clearance in rabbits, accompanied by lower rates of renal tubular reabsorption and retention in kidney and liver than potassium dichromate(VI) and chromium(III) chloride. Pretreatment with chromium-free LMCr II remarkably reduced the mortality rates of mice acutely poisoned with chromium chloride. These results indicate that LMCr plays an important role in the detoxification and excretion of chromium in mammals.

Amino Acids↗
PubMed1994

Role of paramagnetic chromium in chromium(VI)-induced damage in cultured mammalian cells.

Chromium(VI) compounds are known to be potent toxic and carcinogenic agents. Because chromium(VI) is easily taken up by cells and is subsequently reduced to chromium(III), the formation of paramagnetic chromium such as chromium(V) and chromium(III) is believed to play a role in the adverse biological effects of chromium(VI) compounds. The present report, uses electron spin resonance (ESR) spectroscopy; the importance of the role of paramagnetic chromium in chromium(VI)-induced damage in intact cultured cells is discussed, based upon our studies with antioxidants including vitamin E (alpha-tocopherol), B2 (riboflavin), C (ascorbic acid), and so on. These studies appear to confirm the participation of paramagnetic Cr such as chromium(V) and Chromium(III) in chromium(VI)-induced cellular damage.

Animals↗
PubMed1995

Release of hexavalent chromium from corrosion of stainless steel and cobalt-chromium alloys.

Experiments were undertaken to determine whether hexavalent chromium was released during corrosion of orthopedic implants. Uptake of chromium (Cr) by cells and separation using amberlite resin were the methods used to determine that hexavalent Cr was present. We used salts of chromium as trivalent chromium (chromic chloride) and hexavalent chromium (potassium dichromate) to verify that the amberlite separation technique separates hexavalent Cr into the upper phase and trivalent Cr into the lower phase. The use of the salts also verified that only the hexavalent Cr became red blood cell-associated and that most of this was intracellular rather than membrane bound. The use of the amberlite separation technique demonstrated that the hexavalent Cr in the red blood cells was rapidly reduced to trivalent Cr. Cellular uptake of chromium was documented in red blood cells following corrosion of stainless-steel and cobalt-chromium implants in vivo, in the red blood cells of patients undergoing total joint revisions, and in fibroblasts subjected to products of fretting corrosion of stainless-steel and cobalt-chromium implants. Thus, corrosion of implants can lead to the release of the biologically active hexavalent chromium into the body. This chromium is rapidly reduced to trivalent chromium in cells.

Animals↗
PubMed1978

Relative chromium response as an indicator of chromium status.

Twenty-seven women ages 40 to 75 were divided into normal (n = 15) and hyperglycemic (n = 12) groups on the basis of 3-hr glucose tolerance tests. Each subject received 5 g of brewer's yeast extract containing 4 microgram of chromium daily for 3 months. Glucose, insulin, and chromium levels were analyzed by oxidase, radioimmunoassay, and radiochemical neutron activation analysis methods, respectively. The fasting and 1-hr serum chromium levels (ng/ml) changed from 1.67 and 1.43 to 1.46 and 1.86 in the normal group, and from 1.89 and 1.03 to 0.94 and 1.03 in the hyperglycemic group. Considerable changes occurred in the relative chromium response (RCR) at the 1-hr point. RCR is defined as (1-hr serum chromium level/fasting serum chromium level) X 100. Among the normal subjects, 73% showed an improved RCR after the supplementation: mean RCR was 107% before and 140% after. Among the hyperglycemic subjects, 75% showed an improved RCR: mean RCR was 81% before and 149% after the supplementation. The increased RCR was associated with decreased serum insulin and glucose levels. This is interpreted as reflecting an improved chromium status for the majority of individuals in both groups after the supplementation. The observations suggest that 1) in response to a glucose load, serum chromium levels drop in subjects with presumably inadequate chromium storage; 2) a low value of relative chromium response at the 1-hr point indicates a suboptimal chromium nutritional status.

Aged↗
PubMed1999

Thirteen-week subchronic rat inhalation toxicity study with a recovery phase of trivalent chromium compounds, chromic oxide, and basic chromium sulfate.

The toxicity of trivalent chromium compounds; chromic oxide and basic chromium sulfate, was investigated in rats in a 13-week nose-only inhalation study that included a 13-week recovery period. Nose-only exposures to insoluble chromic oxide dust at 4.4, 15, or 44 mg/m3 or soluble basic chromium sulfate dust at 17, 54, or 168 mg/m3 (trivalent chromium equivalent concentrations of 3, 10, and 30 mg/m3) were carried out for 6 h/day, 5 days/week. No compound-related mortality occurred. General toxic effects, only observed with high-exposure levels of basic chromium sulfate, included sporadic signs of labored breathing and depressed body weights. No apparent compound-related effects were noted for sperm motility or morphology, for any concentration of either test material. Bronchoalveolar lavage fluid evaluations showed test material in mononuclear cells with chromic oxide and increased neutrophils, protein, lactic dehydrogenase and cellular debris with basic chromium sulfate. The principle effects for both materials were primarily to the respiratory tract. Chromic oxide caused pathological changes in the bronchial and mediastinal lymphatic tissue and lungs, consisting of the presence of pigment-laden macrophages, lymphoid and septal hyperplasia, and interstitial inflammation similar to that observed with other inert dusts. Basic chromium sulfate produced more severe and widespread effects in the nasal cavity, larynx, lungs, and mediastinal lymph node. Effects were characterized by accumulation of foreign material, infiltration of alveolar macrophages, septal cell hyperplasia, and granulomatous and chronic inflammation. Pigment was still present in chromic oxide and, to a lesser extent, in basic chromium sulfate-treated animals after the 13-week recovery period, with partial recovery of the pathological lesions. A NOAEL was not established for either test material, but 4.4 mg/m3 was thought to be near the NOAEL level for subchronic exposure to chromic oxide. The results of this study indicate significant differences in toxicity to the respiratory tract between trivalent chromium compounds chromic oxide and basic chromium sulfate. These are likely related to differences in acidity and water solubility, rather than chromium concentration per se. This conclusion is substantiated by the lack of effect on other internal organs.

Administration, Inhalation↗
PubMed1983

Exceptional pharmacokinetics of trivalent chromium during occupational exposure to chromium lignosulfonate dust.

The excretion of chromium in the urine of workers exposed to chromium lignosulfonate was studied. The chromium in the dust was in the trivalent (III) oxidation state, and 30% of the particles were less than 5 micron in diameter. Chromium (III) lignosulfonate dust was rapidly absorbed, and a peak of urinary excretion was seen immediately after exposure. No appreciable accumulation of chromium occurred over 3 d, as evaluated by comparison with preshift urinary chromium concentrations. The addition of ethylenediaminetetra-acetate to the urine of exposed persons greatly enhanced the capacity of chromium to traverse a dialysis membrane; the same effect was seen with chromium (III) chloride. It is concluded that chromium (III) lignosulfonate yields chromium (III), which acts pharmacokinetically like water-soluble hexavalent chromium compounds.

Absorption↗
PubMedDate not supplied

Systemic uptake of chromium in human volunteers following dermal contact with hexavalent chromium (22 mg/L).

This study examined the systemic uptake of chromium in four human volunteers following three hours of contact with water containing hexavalent chromium [Cr(VI)] at a concentration of 22 mg/L. Volunteers were immersed below the shoulders in water at 91 +/- 2.5 degrees F. On the day prior to the experiment and for five days afterwards, samples of urine, plasma, and red blood cells (RBCs) were collected and analyzed for total chromium. Red blood cell chromium concentrations were used as a specific biomarker for systemic uptake of Cr(VI). Although total chromium concentrations in RBCs and plasma increased relative to historical background concentrations on the day of exposure, no sustained elevation of chromium concentrations was observed in RBCs or plasma of the volunteers tested. Since absorption of chromium in the hexavalent state would result in the irreversible binding of Cr(VI) to hemoglobin within the RBC (manifested as a sustained elevation of total chromium concentrations in the RBC), the pattern of blood uptake and urinary excretion observed was consistent with uptake and distribution of chromium in the trivalent state. Small increases were observed in the concentration of total chromium in urine within 48 h of exposure, indicating that some trivalent chromium [Cr(III)] may have penetrated the skin at a rate of about 3.3 x 10(-5) to 4.1 x 10(-4) micrograms/ cm2-h. In short, the data indicated that a 3-h contact with Cr(VI) at concentrations in water plausible for environmental exposure (e.g., swimming) was not expected to result in systemic uptake of measurable amounts of Cr(VI), although a small quantity of Cr(VI) may have penetrated the skin where it was subsequently reduced to Cr(III) prior to systemic uptake.

Adult↗
PubMed1988

Chromium in urine, serum and red blood cells in the biological monitoring of workers exposed to different chromium valency states.

Using personal air sampling exposure to hexavalent and trivalent chromium was measured in 22 workers mainly exposed to Cr(VI) and in 15 workers mainly exposed to Cr(III) as basic chromium sulphate. Determination of Cr(VI) in the urine of all the subjects using a selective technique by ETA-AAS and liquid anion exchangers failed to show detectable amounts of the hexavalent form, the detection limit of the technique being 0.05 micrograms/L. A clear relationship between exposure and postshift urinary total chromium was found in subjects exposed to Cr(VI), while urinary levels in workers exposed to chromic sulphate high concentration proved lower. Determination of total chromium in serum and red blood cells showed a significant increase of chromium levels in erythrocytes of workers exposed to Cr(VI) while in subjects mainly exposed to Cr(III) an increase of the serum fraction was observed. The results demonstrate that Cr(III) is absorbed through the respiratory tract, but its kinetics and distribution in the body are not the same as for Cr(VI), and are not adequately monitored by short-term urinary determinations. Oxidation states of chromium largely influence uptake, mechanism of absorption, transport and organ distribution as well as toxicity of chromium-containing compounds. In particular, hexavalent derivatives are known to induce adverse effects, both acute and chronic, in occupationally exposed subjects, while there is little conclusive evidence for toxic effects caused by trivalent chromium compounds. Biological monitoring of exposure to chromium(VI) has usually been performed by determining total chromium levels in urine, whereas biological monitoring data in subjects occupationally exposed to Cr(III) are still scanty.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromium↗
PubMed2003

Ageing of chromium(III)-bearing slag and its relation to the atmospheric oxidation of solid chromium(III)-oxide in the presence of calcium oxide.

Slag arising in ferrochromium and stainless steel production is known to contain residual levels of trivalent chromium. As the chromium is normally bound in the slag matrix in various silicate or spinel phases, and hence not easily mobilised, utilisation or controlled disposal of such slag is generally considered unproblematic. Experimental test work with a number of slag materials indicates, however, that very gradual oxidation of trivalent to hexavalent chromium does occur when the slag is exposed to atmospheric oxygen, rendering a quantifiable but small portion of chromium in this much more mobile and toxic form. Mechanisms and rates of the oxidation reaction were investigated in a number of long-term studies using both original slag materials and artificial mixes of chromium and calcium oxides. Powders of these materials, some of them rolled into balls, were left to age under different conditions for periods of up to 12 months. In the slag samples, which contained between 1 and 3 wt.% chromium, 1000-10000 microg Cr(VI) were found per gram of chromium within 6-9 months of exposure to an ambient atmosphere. The rate of the oxidation reaction decreased exponentially, and the reaction could generally be said to have ceased within 12 months. In mixtures of calcium and chromium oxides the oxidation reaction is presumed to occur at the boundaries between chromium oxide and calcium oxide phases through diffusion of oxygen along the grain boundaries and of Cr(3+) across the boundaries, resulting in the formation of calcium chromate. In the slags, where calcium and chromium oxide can form a solid solution, the oxidation is likely to occur at the exposed surface of grains containing this solution.

Atmosphere↗
PubMed1995

The effect of remediation of chromium waste sites on chromium levels in urine of children living in the surrounding neighborhood.

Exposure to chromium was assessed for 40 children living near chromium waste sites. Sampling was conducted in one Jersey City, New Jersey neighborhood during the summer and fall of 1991. Household dust samples from residences and urine samples from children living near chromium waste sites were collected and analyzed for chromium. During the summer and fall visits when the samples were collected, the children were also interviewed about lifestyle/activity patterns. Comparisons were made with similar samples collected from children and homes in other areas of New Jersey outside of Hudson County with no known chromium waste sites. Household dust masses and chromium loadings and concentrations in the dust showed a significant decline in this Hudson County neighborhood since the area was first sampled in 1990. Interim remediation of neighborhood sites and an active community education program in the interval between the first and second year of sampling may have contributed to the reduction in dust masses and chromium levels in dust. Children's urine chromium concentrations were consistent across the two sampling periods despite reported changes in activity patterns. Chromium concentrations in urine were found to be age-dependent and related to home location. In this sample of Jersey City children less than six years old, time spent playing outdoors was a weak secondary contributor to urine chromium levels.

Child↗