Urinary Arsenic Levels Research Articles

Exposure to environmental tobacco smoke in the household and urinary cotinine excretion, heavy metals retention, and lung function.

The relationship between urinary levels of cotinine (U-cotinine) and arsenic (U-As), blood levels of cadmium (B-Cd), blood levels of lead (B-Pb), lung function, and questionnaire data on smoking habits were studied in 107 parents and their 46 children (7-10 y of age). There was a statistically significant relationship between the reported amount of tobacco smoked and U-cotinine levels. Nonsmokers who were married to persons who smoked had three times higher U-cotinine levels than nonsmokers whose spouses did not smoke. There was a significant association between the number of parents who smoked in the family and the U-cotinine levels of children. If only one parent smoked, maternal smoking was of greater importance than paternal smoking. There was also an association between U-cotinine and B-Cd. A study of lung function in the children revealed that vital capacity and functional residual capacity (corrected for sex, age, and height) increased as the number of parents who smoked increased. Therefore, the present study showed that (1) U-cotinine was a useful index of active smoking and environmental tobacco smoke exposure in adults and children, (2) U-cotinine was associated with the blood concentration of cadmium, and (3) environmental tobacco smoke exposure was associated with changes in lung function of children.

Intake of different chemical species of dietary arsenic by the japanese, and their blood and urinary arsenic levels

AbstractWe calculated the intake of each chemical species of dietary arsenic by typical Japanese, and determined urinary and blood levels of each chemical species of arsenic. The mean total arsenic intake by 35 volunteers was 195±235 (15.8‐1039) μg As day−1, composed of 76% trimethylated arsenic (TMA), 17.3% inorganic arsenic (Asi), 5.8% dimethylated arsenic (DMA), and 0.8% monomethylated arsenic (MA): the intake of TMA was the largest of all the measured species. Intake of Asi characteristically and invariably occurred in each meal. Of the intake of Asi, 45‐75% was methylated in vivo to form MA and DMA, and excreted in these forms into urine. The mean measured urinary total arsenic level in 56 healthy volunteers was 129±92.0 μg As dm−3, composed of 64.6% TMA, 26.7% DMA, 6.7% Asi and 2.2% MA. The mean blood total arsenic level in the 56 volunteers was 0.73±0.57 μg dl−1, composed of 73% TMA, 14% DMA and 9.6% Asi. The urinary TMA levels proved to be significantly correlated with the whole‐blood TMA levels (r = 0.376; P<0.01).

Diagnostic Problems in a Case of Arsenic Encephalopathy in a Schizophrenic Patient Case Report and Review of the Literature

AbstractAlthough arsenic is the second most common cause of heavy metal intoxication in the United States today, its clinical presentation suggests a serious diagnostic challenge. A 58-year-old, chronic paranoid schizophrenic patient showed sudden clinical change heralded by flulike symptoms, followed by delirium, fever, scrotal candidiasis, and profound leukopenia. The presence of Guillain-Barre-like symptoms suggested a toxic polyneuropathy and the necessity of ruling out porphyria. Because of this suspicion, screening for heavy metals was performed, and revealed an urinary arsenic level of 124 u.g/L. The patient's wife had reporteclbeing frightened by the patient's threatening demeanor for years. She subsequently committed suicide. Eventual investigation into the patient's illness concluded that his wife had been poisoning him. Review of historical and current literature shows that encephalopathy is a relatively common presentation of arsenic poisoning. Furthermore, it is associated with distinctive cl...

Occupational and environmental exposure to arsenic — increased urinary arsenic level in children

The sum of concentrations of inorganic arsenic, methylarsonic acid (MMAA) and dimethylarsinic acid (DMAA) in urine from adults and children living in an unpolluted area was compared with the corresponding sum measured in urine from adults and children living in an area polluted with arsenic and in urine from persons occupationally exposed to arsenic. The median values for 22 adults and 10 children aged 3–10 years living in the unpolluted area were 9.3 and 19.8 nmol As/mmol creatinine, respectively. The corresponding ranges were 3.2–27.9 and 7.7–57.8 nmol As/mmol creatinine, respectively. The difference between adults and children was tested by Mann-Whitney's non-parametric test and found to be significant ( p < 0.0025). No significant difference was found in arsenic concentration in urine from 73 adults and 10 children living in the polluted area compared with the arsenic concentration in urine from those living in the unpolluted area. The arsenic level in urine from adult workers handling arsenic-treated wood was approximately four-fold higher ( p < 0.001), with a maximum recorded concentration corresponding to 814.9 nmol As/mmol creaunine. The arsenic levels in urine from two glass workers were nine- and two-fold higher, respectively. No significantly increased arsenic levels were found in urine from workers impregnating wood and in urine from lead accumulator workers.

The Effect of Variable Environmental Arsenic Contamination on Urinary Concentrations of Arsenic Species

Urinary arsenic species have been determined for approximately 3000 urine samples obtained from residents of a community surrounding an arsenic-emitting copper smelter. Levels of inorganic, monomethylated and dimethylated arsenic species ranged from less than 1 microgram/L (the instrumental detection limit) to 180 micrograms/L seen for dimethyl arsenic. Comparison of a subsample of this population that had the least environmental contamination with the subsample having highest environmental arsenic concentrations showed small but statistically significant differences in urinary arsenic levels for all species except dimethylated arsenic. However, for children under 7 years of age living in areas with increased environmental arsenic contamination, there was a larger and equally significant (p less than 0.001) increase in all urinary species. This effect was more pronounced in males (5-fold increase in median sum of species concentration over control group) than in females (2-fold increase in median sum of species concentration over control group) and was observed as a weaker effect in the next higher age group (7-13 years of age). Reported consumption of seafood also was significantly related to increased urinary dimethyl arsenic, but changes in distribution among the urinary arsenic species detected was not a sensitive indicator of recent seafood consumption.

The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species.

Urinary arsenic species have been determined for approximately 3000 urine samples obtained from residents of a community surrounding an arsenic-emitting copper smelter. Levels of inorganic, monomethylated and dimethylated arsenic species ranged from less than 1 microgram/L (the instrumental detection limit) to 180 micrograms/L seen for dimethyl arsenic. Comparison of a subsample of this population that had the least environmental contamination with the subsample having highest environmental arsenic concentrations showed small but statistically significant differences in urinary arsenic levels for all species except dimethylated arsenic. However, for children under 7 years of age living in areas with increased environmental arsenic contamination, there was a larger and equally significant (p less than 0.001) increase in all urinary species. This effect was more pronounced in males (5-fold increase in median sum of species concentration over control group) than in females (2-fold increase in median sum of species concentration over control group) and was observed as a weaker effect in the next higher age group (7-13 years of age). Reported consumption of seafood also was significantly related to increased urinary dimethyl arsenic, but changes in distribution among the urinary arsenic species detected was not a sensitive indicator of recent seafood consumption.

Pathways of human exposure to arsenic in a community surrounding a copper smelter

Several studies have found elevated levels of urinary arsenic among residents living near a copper smelter in Tacoma, Washington. To assess pathways of exposure to arsenic from the smelter, biological and environmental samples were collected longitudinally from 121 households up to 8 miles from the smelter. The concentration of inorganic and methylated arsenic compounds in spot urine samples was used as the primary measure of exposure to environmental arsenic. Urinary concentration of arsenic dropped off to a constant background level within one-half mile of the smelter in contrast to environmental concentrations, which decreased more steadily with increasing distance. Among all age-sex-specific groups in all areas, only children ages 0-6 living within one-half mile of the smelter had elevated levels of arsenic in urine. A separate analysis of data for these children suggests that hand-to-mouth activity was the primary source of exposure. Inhalation of ambient air and resuspension of contaminated soil were not important sources of exposure for children or adults.

Herbal Medicine as a Cause of Combined Lead and Arsenic Poisoning

1. Combined chronic lead and arsenic poisoning was diagnosed in a 33-year-old Korean woman following consumption of a Korean herbal medicine prescribed for haemorrhoids. 2. The patient had malaise, severe difficulty walking, arthralgia, oedema and abdominal pain with diarrhoea. 3. Investigation showed anaemia with basophilic stippling, fragmentation and a raised reticulocyte count. 4. Raised blood and urine lead levels and urine arsenic levels were found. 5. Analysis of the herbal medicine revealed a high lead and arsenic content. 6. Treatment with the newer chelating agent 2,3-dimercaptosuccinic acid was successful, with no detectable side-effects.

A statewide case registry for surveillance of occupational heavy metals absorption.

The New York State Heavy Metals Registry is a legislatively mandated program through which clinical laboratories, physicians, and health facilities report state residents 18 years of age and older with elevated levels of lead, mercury, arsenic, or cadmium in blood or urine. From 1982-86, the current employer was determined for 95.9 percent of 3,309 cases. Occupational exposures in 328 companies accounted for 82.8 percent of cases. The majority of companies were reported for lead (247 companies, 75.3 percent of total) or mercury (47 companies, 14.3 percent of total). Of the 247 companies reported to the Registry for lead, the Occupational Safety and Health Administration (OSHA) inspected 18 of 98 companies (18.4 percent) in the manufacturing sector, but only one of 149 companies (0.6 percent) outside the manufacturing sector. We conclude that the Registry effectively detects companies with heavy metals exposures, and is an especially useful adjunct to OSHA inspections outside the manufacturing sector.

Health status of copper refinery workers with specific reference to selenium exposure.

Copper refinery workers exposed to selenium were studied before, during, and after a shutdown period. Urine selenium levels were 83 +/- 30 mumol/mol creatinine and 69 +/- 27 mumol/mol creatinine when measured on two occasions during exposure compared with 56 +/- 17 mumol/mol creatinine when the workers had been free of exposure for 10 wk during a shutdown. The refinery workers reported more nose and eye irritation, indigestion, stomach pain, and fatigue than controls. "Garlic-like" breath odor was reported to be personally and socially offensive by many of the workers. Reporting of symptoms, pulmonary function indices, and laboratory test results did not change with exposure except for hemoglobin level, which rose during the shutdown. Hemoglobin levels were found to be inversely correlated with the urine selenium level, and there was a positive correlation noted for the interactive effect of urine selenium and urine arsenic levels on hemoglobin.

Urinary arsenic concentrations and speciation in Cornwall residents

Inorganic arsenic and its methylated metabolites were determined in urine from adults and children in Cornwall and from corresponding control groups in Glasgow. In the mineralised south-west of England, where it has been suggested that the highly enriched soil arsenic concentrations may at least be a cofactor in the increased incidence of skin cancer, urinary arsenic levels were, in general, only slightly elevated. The potential for increased intake of inorganic arsenic in Cornwall was, however, reflected in the more frequent occurrence of trivalent inorganic arsenic and monomethylarsonic acid in urine and, of especial significance, in two comparatively highly elevated sum of arsenic species concentrations of 48.7 and 20.8 μg g(-1) creatinine recorded for two pre-school children. These findings are discussed with reference to recommended limits and pathways of exposure to inorganic arsenic.

Toxic responses in F344 rats and B6C3F 1 mice given roxarsone in their diets for up to 13 weeks

Thirteen-week toxicity studies were conducted in groups of 10 F344 rats and B6C3F 1 mice of each sex fed roxarsone at 0, 50, 100, 200, 400, or 800 ppm in the diet. Arsenic levels in blood, urine, kidneys, and liver of rats were measured in additional animals of each sex dosed with 100 or 400 ppm roxarsone. Compound-related mortality occurred in both sexes of rats at 800 ppm and mice at 800 and 400 ppm. Significant body weight gain depression occurred in both sexes of rats at 200, 400, and 800 ppm and mice at 800 ppm. Clinical signs of toxicity (trembling, ataxia, and pale skin) were seen primarily in rats and mice at 800 ppm. Lesions associated with roxarsone administration were noted only in the kidney of rats and were characterized by tubular necrosis and mineralization at the corticomedullary junction. Arsenic levels in urine, blood, liver, and kidneys increased over time and were directly proportional to the level of roxarsone in feed. These levels were > 6 times higher in rats than in mice and were about 2 times higher in males than in females. The no-observable-effect level for roxarsone toxicity was estimated at 100 ppm for rats and 200 ppm for mice. No hematology or clinical chemistry effects were found in rats or mice of either sex.

Encephalopathy: An uncommon manifestation of workplace arsenic poisoning?

This report describes two cases of chronic encephalopathy associated with occupational exposure to arsenic fumes from hot pressurized impregnation of wood. Both cases displayed symptoms of cognitive impairment with onset 14-18 months after start of occupational exposure to arsenic fumes. Laboratory confirmation was provided by elevated urine arsenic levels. One patient was hospitalized for apparent psychiatric reasons. Neuropsychologic testing of one case showed typical and relatively mild impairments of new learning, recent memory, and concentration in addition to the psychological symptoms. Symptoms in both cases disappeared following cessation of exposure and return of urine arsenic excretion to normal levels. In future studies of workers exposed to arsenic, documentation of mild impairment of cognitive function should be sought using neurobehavioral test batteries.

Arsenic and Raynaud's phenomenon. Vasospastic tendency and excretion of arsenic in smelter workers before and after the summer vacation.

Occupational and environmental exposure to inorganic arsenic is associated with the occurrence of Raynaud's phenomenon and objectively registered abnormal finger systolic blood pressure at local cooling (FSP). A subnormal FSP during cooling indicates a vasospastic tendency. It is not known whether these phenomena are related to recent or historical long-term exposure to arsenic. Twenty-one workers from a Swedish smelter were selected on the basis of exposure to arsenic dust for more than 14 years and a previously (three years earlier) recorded subnormal FSP during local cooling. The workers were examined before and after a 4 to 8 week summer vacation. After this intermission in arsenic exposure the urinary excretion of arsenic decreased to normal values, whereas the vasospastic reaction in the fingers remained. Thus the vasospastic tendency seems to be unrelated to the most recent urinary arsenic levels. FSP levels on cooling were significantly increased as compared with the measurements made three years earlier. This suggests a gradual improvement in finger blood circulation caused by decreased exposure to arsenic as evaluated over a time period of several years. The data thus indicate that peripheral vascular disturbances caused by arsenic are dependent on long-term arsenic exposures and are independent of short-term fluctuations in arsenic exposure.

Urinary arsenic speciation by high-performance liquid chromatography/atomic absorption spectrometry for monitoring occupational exposure to inorganic arsenic

Total urinary arsenic determinations are often used to assess occupational exposure to inorganic arsenic. Ingestion of sea food can increase the normal background levels of total arsenic in urine by up to an order of magnitude, but this arsenic has relatively little toxicity; it is tightly bound as arsenobetaine. The excretion of inorganic arsenic and its metabolites dimethylarsenic acid (DMA) and monomethylarsonic acid (MMA) is not influenced by the consumption of arsenic from sea food. Specific measurements of DMA, MMA and inorganic arsenic provide a more reliable indicator or exposure than total urinary arsenic levels. An automated atomic absorption method involving high-performance liquid chromatographic separation of the arsenic species and continuous hydride generation is described for the determination of arsenite, arsenate, DMA and MMA at μg As l −1 levels. The method is used to study normal urinary arsenic levels in laboratory staff and arsenic excretion by exposed workers.

Diagnostic usefulness of trace arsenic in human urine, whole blood, hair and fingernails.

Because of rapid clearance of arsenic in the blood after an accidental exposure, it is important to check the blood arsenic level as soon as possible after exposure. In cases of chronic exposure, however, the blood arsenic level is usually so low that substantial analytical problems will probably be met. Blood arsenic level, therefore, cannot be regarded as an indicator of chronic exposure. Instead, urine arsenic level was used as an index of exposure, although a lot of factors, such as diets and the interval between exposure and urine sampling, might complicate it. For example, ingestion of sea food, which is rich in organic arsenic, often results in a high concentration of arsenic in urine. In the present study, the author tried to separate the organic and inorganic arsenicals in urine before assay, to prevent or to decrease the influence of dietary arsenic. Assessment of arsenic content in hair is another and still a better indication of arsenic long-term exposure. Hair is chemically an inert and homogeneous substance, so it is itself a continuous record of previous and present arsenic level in the body. Furthermore, the content of arsenic is higher in hair than in blood. Hence, hair is a good medium for monitoring body arsenic. The arsenic content in fingernails is also high. But , the value of the assessment of fingernail content as an indicator of chronic arsenic exposure remains to be determined.

Saccadic eye movements among copper smelter workers.

Saccade accuracy was studied in 87 copper smelter workers. Findings were compared with those obtained in 52 lead-exposed automobile production workers and 52 controls examined as part of a separate study. Both groups of workers showed a decrease in saccade accuracy compared to controls. Saccade accuracy was reduced in copper smelter workers over 50 years of age compared to automobile production workers in this age group. Decreased saccade accuracy was not correlated with blood lead (Pb-B), zinc protoporphyrin (ZPP), or urinary arsenic (As-U) levels among copper smelter workers, but was significantly correlated with both Pb-B and ZPP in the group of automobile production workers. Saccade accuracy decreased significantly with age and duration of exposure only in the group of copper smelter workers. Complex exposures to lead and other toxic agents present in the smelter may account for the reduction in saccade accuracy among copper smelter workers.

Distribution of blood lead, blood cadmium, urinary cadmium, and urinary arsenic levels in employees of a copper smelter

A cross-sectional medical examination of a copper smelter work force included determination of blood lead (Pb-B), zinc protoporphyrin (ZPP), blood cadmium (Cd-B), urinary cadmium (Cd-U), and urinary arsenic (As-U), since it was known that such metal impurities were present in the copper concentrate. A total of 776 copper smelter employees (680 active and 96 retirees and ex-employees) were examined. Another 144 men, never employed in the smelter, but who had worked in copper mines (and sometimes in gold mines) were also examined. Mean Pb-B, ZPP, Cd-B, and As-U were significantly higher in active copper smelter employees than in retirees or miners, indicating exposure and absorption in the copper smelter. Significant correlations between Pb-B and Cd-B, and Cd-U and As-U were present, confirming the common source of absorption. Although there was evidence for an increased lead absorption, this was very moderate, with practically no Pb-B levels in excess of 60 μg/dl. A marked effect of smoking on blood cadmium levels was present; nevertheless, for all smoking categories Cd-B levels were significantly higher in active employees, indicating the independent contribution of exposure to cadmium in the smelter. Cd-U did not exceed 10 μg/g creatinine, the generally accepted “critical” level for the kidney, but was higher than 2 μg/g creatinine, a level very rarely exceeded in the general population, in a sizable proportion of those examined. The highest Cd-U levels were found in retired copper smelter employees; age might have been a contributing factor, besides a longer duration of exposure in the smelter.

Urinary arsenic, chromium, and copper levels in workers exposed to arsenic-based wood preservatives.

Urinary excretion of arsenic, chromium, and copper in workers exposed to arsenic-based wood preservatives was examined to evaluate occupational exposure to these chemicals. Spot urine samples were collected from 89 wood treaters and a comparison group of 232 individuals with no known exposure to arsenicals. The results of urinalysis revealed that the wood treaters averaged 103 micrograms arsenic/L while the comparison group averaged 74 micrograms arsenic/L. The mean urinary chromium and copper levels of the wood treaters were 41 micrograms chromium/L and 191 micrograms copper/L compared with 63 micrograms chromium/L and 221 micrograms copper/L for the comparison group. Covariance analysis of urinary arsenic level between the exposed and comparison groups revealed that the adjusted mean arsenic levels of the exposed population (78 to 122 micrograms arsenic/L) were significantly higher than that of the comparison group (72 micrograms arsenic/L). The adjusted mean urinary arsenic levels of these wood treaters, however, were within published normal limits. Analysis of covariance allowed comparison of group means after statistical adjustments for possible confounding variables such as seafood intake and age. The results indicate that urinary arsenic values can provide a useful index of occupational exposure to chromated copper arsenate wood preservatives, when the effects of dietary arsenic are controlled statistically.

Occupational exposure to arsine. An epidemiologic reappraisal of current standards.

In an evaluation of chronic occupational exposure to arsine (AsH3), an epidemiologic survey was conducted at a lead-acid battery manufacturing plant. Personal (breathing zone) air samples were obtained for the measurement of exposure to arsine and particulate arsenic (As), and area air samples were also collected for the determination of arsenic trioxide (As2O3) vapor concentrations. For the quantification of arsenic absorption, total arsenic content was determined in duplicate 24-h urine samples. Arsine in 177 breathing-zone air samples ranged from nondetectable to 49 micron/m3. The highest levels were found in the battery formation area, where arsine is generated by the reaction of battery acid with lead-arsenic alloy. Exposures to particulate arsenic (maximum 5.1 micron/m3) and to As2O3 (maximum (20.5%) of 39 production workers had urinary arsenic concentrations (corrected to a specific gravity of 1.024) of 50 micron/1 (0.67 mumol/1) or above, indicating increased arsenic absorption. None of eight office staff had elevated urinary arsenic levels. A close correlation was found between urinary arsenic concentration and arsine exposure (N = 47; r = 0.84; p = 0.0001). Arsine levels above 15.6 micron/m3 were associated with urinary arsenic concentrations in excess of 50 micron/1 (0.67 mumol/1). No correlation was found between urinary arsenic content and exposures to particulate arsenic or to As2O3. Consumption of neither seafood, red wine, tobacco, nor contaminated drinking water accounted for urinary arsenic excretion. It was concluded that the current arsine exposure standard, 200 micron/m3, fails to prevent chronic increased absorption of trivalent arsenic from the inhalation of arsine.