Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony

Unlike inorganic arsenic, inorganic trivalent antimony (Sb) is not methylated in vivo. It is excreted in the bile after conjugation with glutathione and also in urine. A significant proportion of that excreted in bile undergoes an enterohepatic circulation. In workers exposed to pentavalent Sb, the urinary Sb excretion is related to the intensity of exposure. It has been estimated that after eight hours exposure to 500 micrograms Sb/m3, the increase of urinary Sb concentration at the end of the shift amounts on average to 35 micrograms/g creatinine.     

Biliary excretion of diethyl lead after administration of tetraethyl lead in rabbits

In order to investigate into whether the large amount of inorganic lead excreted into the feces following intravenous injection of tetraethyl lead to rabbits is derived from the diethyl lead excreted into the bile, we administered 12 mg/kg of tetraethyl lead to rabbits which had been fistulated into the bile duct for taking the bile out of the body. The total lead excreted into the bile during the first 24 hours after the injection of tetraethyl lead amounted to about 8% of the injected amount of lead (with 97% of the excreted lead made up of diethyl lead). The amount of total lead contained in the cecal contents of unfistulated rabbits 24 hours after the injection of tetraethyl lead was equivalent to about 12% of the injected amount of lead (with inorganic lead accounting for about 90% of the excreted lead), but the counterpart of the fistulated rabbits was equivalent only to about 0.6%. The amount of lead excreted into the bile, when measured in terms of the total lead content of the liver, was slightly less in the fistulated rabbits than in the unfistulated ones. These findings indicated that the amount of total lead excreted into the bile of the fistulated rabbits was almost the same as that contained in the cecal contents of unfistulated rabbits, and that the major portion of the lead contained in the cecal contents or feces was composed of inorganic lead. From these results, we came to the conclusion that the large amount of inorganic lead detected in the feces after the injection of tetraethyl lead is derived from the diethyl lead excreted into the bile.     

Control Devices

Mercury transport pathways through the gastrointestinal tract were investigated to explain preferential inorganic mercury excretion in feces after exposure to methyl mercury salts. Mercury is excreted in bile predominantly as methyl mercury cysteine. Protein-complexed methyl mercury and protein-bound inorganic Hg are found less extensively. Methyl mercury cysteine is rapidly reabsorbed, not adding significantly to fecal Hg. Protein-bound inorganic Hg is not reabsorbed and comprises about 15% total fecal Hg the first days after methyl mercury chloride injection. A corresponding fecal Hg amount derives from protein-bound methyl mercury from bile. Intestinal cell shedding is the main fecal Hg source. These cells, however, contain less than 5% inorganic Hg, compared to about 50% in feces. Methyl mercury bound to structural proteins in these cells releases inorganic Hg, probably by lower-intestinal microbiological action.     

Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites.

The relation between exposure to As2O3 fumes and dust, and the urinary excretion of inorganic arsenic metabolites (monomethylarsonic acid, dimethylarsinic acid, unchanged inorganic arsenic) has been studied in 18 workers from a sulphuric acid producing plant. The concentration of arsenic in the breathing zone of each worker was measured during five consecutive days and urine samples were obtained after one shift and before the next. The collection efficiency of the air sampling system exceeded 95%. The time weighted average exposure (TWA) concentrations of As2O3 ranged from 6 to 502 micrograms As/m3 and were log normally distributed. Although exposure probably occurred by ingestion as well as inhalation, statistically significant correlations (log scales) were found between airborne TWA of As2O3 and the inorganic arsenic metabolites in urine collected immediately after the shift, or just before the next shift. For a TWA of 50 micrograms As/m3, the mean concentration of the sum of the three inorganic arsenic metabolites in a postshift urine sample amounted to about 55 micrograms arsenic/g creatinine (95% confidence interval (95% CI) 47-62). Higher estimates of urinary arsenic reported by other authors are probably due either to the influence of dietary organoarsenicals when total arsenic is measured in urine or to a low retention efficiency of the air sampling system for As2O3 in the vapour phase.     

Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites.

The relation between exposure to As2O3 fumes and dust, and the urinary excretion of inorganic arsenic metabolites (monomethylarsonic acid, dimethylarsinic acid, unchanged inorganic arsenic) has been studied in 18 workers from a sulphuric acid producing plant. The concentration of arsenic in the breathing zone of each worker was measured during five consecutive days and urine samples were obtained after one shift and before the next. The collection efficiency of the air sampling system exceeded 95%. The time weighted average exposure (TWA) concentrations of As2O3 ranged from 6 to 502 micrograms As/m3 and were log normally distributed. Although exposure probably occurred by ingestion as well as inhalation, statistically significant correlations (log scales) were found between airborne TWA of As2O3 and the inorganic arsenic metabolites in urine collected immediately after the shift, or just before the next shift. For a TWA of 50 micrograms As/m3, the mean concentration of the sum of the three inorganic arsenic metabolites in a postshift urine sample amounted to about 55 micrograms arsenic/g creatinine (95% confidence interval (95% CI) 47-62). Higher estimates of urinary arsenic reported by other authors are probably due either to the influence of dietary organoarsenicals when total arsenic is measured in urine or to a low retention efficiency of the air sampling system for As2O3 in the vapour phase.     

Biological monitoring of workers exposed to 4,4′-methylene-bis-(2-orthochloroaniline) (MOCA)

OBJECTIVES: The objectives of the study were to investigate the best urinary marker of exposure to MOCA in urine samples of exposed workers and to study its applicability in exposure evaluation in polyurethane resin production plants. In addition, our intention was to contribute to the question of biological target value in order to reduce exposure levels. METHODS: Urinary MOCA markers were measured in urine samples collected at the end of the workshifts. 40 workers from four factories were observed for three consecutive days in the same week. "Free" MOCA in non-acid-stabilized urines, "total" MOCA in urines after alkaline hydrolysis, "acid-labile" MOCA in sulfamic or citric acid-protected urines were measured in all urine samples. MOCA liberated by heating the non-acid-stabilized urines ("heat-labile" MOCA) was also measured in 17 urine samples of exposed workers. RESULTS: The median value of "free" MOCA was lower than that of "sulfamic acid-labile" MOCA: 6.0 and 12.5 micrograms/l respectively. The difference between "free" and "total" MOCA was statistically significant (Mann-Whitney test, P = 0.023) for the urine samples collected without acid. Correlations between urinary MOCA concentrations in hydrolysed and non-hydrolysed urine samples were high (r = 0.984, 0.966 and 0.950; P < 0.001) for urine samples with sulfamic acid, with citric acid and without acid respectively. For all the factories, the postshift urinary MOCA concentrations ranged between 1 microgram/l (detection limit) and 570 micrograms/l; 25% of "sulfamic acid-labile" MOCA concentrations exceeded 50 micrograms/l. Workers handling crystallized MOCA excreted the highest amounts of MOCA in urine. The urinary MOCA concentrations (median) were: 84.0 micrograms/l (mixer), 15.5 micrograms/l (moulder). 59.0 micrograms/l (maintenance) and 3.0 micrograms/l (others). CONCLUSIONS: MOCA measured in sulfamic acid-protected urine samples without hydrolysis provides a more practical and reliable biomarker than "total" MOCA (after hydrolysis) or "free" MOCA. A biological guiding value of 20 micrograms/l expressed as "sulfamic acid-labile" MOCA is proposed.     

People with high mercury uptake from their own dental amalgam fillings.

OBJECTIVES--To describe people with high mercury (Hg) uptake from their amalgam fillings, and to estimate the possible fraction of the occupationally unexposed Swedish population with high excretion of urinary Hg. METHODS--Three case reports are presented. The distribution of excretion of urinary Hg in the general population was examined in pooled data from several sources. RESULTS--The three cases excreted 23-60 micrograms of Hg/day (25-54 micrograms/g creatinine), indicating daily uptake of Hg as high as 100 micrograms. Blood Hg was 12-23 micrograms/l, which is five to 10 times the average in the general population. No other sources of exposure were found, and removal of the amalgam fillings resulted in normal Hg concentrations. Chewing gum and bruxism were the probable reasons for the increased Hg uptake. Extrapolations from data on urinary Hg in the general population indicate that the number of people with urinary excretion of > or = 50 micrograms/g creatinine could in fact be larger than the number of workers with equivalent exposure from occupational sources. CONCLUSION--Although the average daily Hg uptake from dental amalgam fillings is low, there is a considerable variation between people; certain people have a high mercury uptake from their amalgam fillings.     

Elevated urinary excretion of beta-aminoisobutyric acid and exposure to inorganic lead

beta-Aminoisobutyric acid (beta-AIB), a normal degradation product of thymine, a constituent of DNA and, to a lesser extent, of transfer RNA, is excreted in low levels in human urine. We found that a group of iron workers occupationally exposed to inorganic lead excreted high levels of urinary beta-AIB. Elevated urinary excretion of beta-AIB was also observed in marmosets, Callithrix jacchus, that received lead acetate in drinking water. Our results suggest that increased urinary excretion of beta-AIB could stem from damage to DNA on exposure to lead.     

A comparison between health effects of cadmium and cadmium concentration in urine among inhabitants of the Itai-itai disease endemic district.

The relationship between urinary cadmium concentration (micrograms/g creatinine) and the health effects of cadmium exposure was studied in 406 inhabitants who lived in and around the Jinzu River basin. Cadmium concentration in urine was employed as the index of cadmium exposure. Total protein, glucose, calcium, and phosphorus in urine and calcium, inorganic phosphorus, and alkaline phosphatase in serum served as indices of health effects. On a group basis a close relationship was found between cadmium concentration in urine and health effects. Prevalence rates of indices of health effects increased proportionally with increasing cadmium concentrations in urine. It was concluded that cadmium concentration in urine expressed as micrograms/g creatinine is a useful parameter in estimating the health effects of cadmium exposure from the environment.     

Biological monitoring of occupational exposure to inorganic arsenic

OBJECTIVES: This study was undertaken to assess reliable biological indicators for monitoring the occupational exposure to inorganic arsenic (iAs), taking into account the possible confounding role of arsenicals present in food and of the element present in drinking water. METHODS: 51 Glass workers exposed to As trioxide were monitored by measuring dust in the breathing zone, with personal air samplers. Urine samples at the end of work shift were analysed for biological monitoring. A control group of 39 subjects not exposed to As, and eight volunteers who drank water containing about 45 micrograms/l iAs for a week were also considered. Plasma mass spectrometry (ICP-MS) was used for the analysis of total As in air and urine samples, whereas the urinary As species (trivalent, As3; pentavalent, As5; monomethyl arsonic acid, MMA; dimethyl arsinic acid, DMA; arsenobetaine, AsB) were measured by liquid chromatography coupled with plasma mass spectrometry (HPLC-MS) RESULTS: Environmental concentrations of As in air varied widely (mean 84 micrograms/m3, SD 61, median 40) and also the sum of urinary iAs MMA and DMA, varied among the groups of exposed subjects (mean 106 micrograms/l, SD 84, median 65). AsB was the most excreted species (34% of total As) followed by DMA (28%), MMA (26%), and As3 + As5 (12%). In the volunteers who drank As in the water the excretion of MMA and DMA increased (from a median of 0.5 to 5 micrograms/day for MMA and from 4 to 13 micrograms/day for DMA). The best correlations between As in air and its urinary species were found for total iAs and As3 + As5. CONCLUSIONS: To avoid the effect of As from sources other than occupation on urinary species of the element, in particular on DMA, it is proposed that urinary As3 + As5 may an indicator for monitoring the exposure to iAs. For concentrations of 10 micrograms/m3 the current environmental limit for iAs, the limit for urinary As3 + As5 was calculated to be around 5 micrograms/l, even if the wide variation of values needs critical evaluation and application of data. The choice of this indicator might be relevant also from a toxicological point of view. Trivalent arsenic is in fact the most active species and its measure in urine could be the best indicator of some critical effects of the element, such as cancer.

 

     

A comparative study of biliary and urinary 2-hydroxylated metabolites of [6,7-3H]17 alpha-ethynylestradiol in women

The biliary and urinary metabolites of [6,7-3H]17 alpha-ethynylestradiol (EE2) in women were studied with reference to the possibility of estimating EE2 2-hydroxylation by analysing urinary metabolites alone. Five subjects received 50 micrograms of 3H-EE2 orally. Bile was obtained by either endoscopy or T-tube drainage. The metabolites excreted in bile and urine were largely glucuronides and arylsulphates, but in variable proportions. The glutathione adduct of 2-hydroxyethynylestradiol was not observed in bile. EE2 was the predominant component of the glucuronide fractions of bile and urine. Additionally, the proportion of glucuronylated EE2 in a subject's urine quantitatively paralleled that in bile. HPLC analyses indicated that the proportions of EE2 and 2-methoxy-EE2 in urine are predictive of EE2 2-hydroxylation in most women. With some subjects, however, urinary analysis alone considerably underestimates the extent of 2-hydroxylation.     

Comparison of measures of lead exposure, dose, and chelatable lead burden after provocative chelation in organolead workers.

OBJECTIVES--To describe 6 h urinary lead excretion (6 h PbU) after 1 g intravenous ethylene diamine tetraacetic acid (EDTA) in organolead manufacturing workers with mixed exposure to organic and inorganic lead; to determine the predictors of lead excretion (PbU); and to determine the extent to which internal lead stores and ongoing external exposure govern blood concentrations of lead (PbB). METHODS--A case series of 21 active workers were studied. Personal industrial hygiene data, grouped by 29 exposure zones, in combination with personal interviews about work location and times were used to derive several measures of recent and cumulative exposure to organic and inorganic lead. The average exposure intensities assigned to the 29 zones ranged from 4 to 119 micrograms/m3 (0.02-0.57 mumol/m3 as lead) for organic lead and from 1 to 56 micrograms/m3 (0.004-0.27 mumol/m3) for inorganic lead. RESULTS--After controlling for age, 6 h PbU was significantly and positively correlated with summary measures of PbB--for example, lifetime peak PbB, time weighted PbB--and zinc protoporphyrin concentrations--for example, lifetime peak zinc protoporphyrin, time weighted zinc protoporphyrin--but not with measures of estimated external exposure--for example, duration of exposure and cumulative exposure to inorganic or organic lead. Among workers with higher chelatable lead burdens (6 h PbU > or = 212.4 micrograms (1.03 mumol) divided at the median), there was no apparent relation between recent inorganic lead exposure and PbB at the time of chelation. Among workers with lower chelatable lead burdens (6 h PbU < 212.4 micrograms (1.03 mumol) however, there was a significant relation between exposure and effect between recent exposure to inorganic lead and PbBs. CONCLUSION--These findings are consistent with the concept of physiological dampening. The high chelatable lead burden, a source of internal exposure, dampens the effect of external exposure on PbBs. The data suggest that in organolead workers with high chelatable lead burdens, PbBs may be more influenced by internal lead stores than by variations in airborne exposure to organic and inorganic lead.     

陕西省部分地区人群血和尿中镍、锡、锑、铊的水平分析

目的 调查陕西省部分地区人群全血和尿液中镍、锡、锑、铊内暴露水平,分析人群分布特征.方法 2017年在陕西省采用多阶段分层随机抽样的方法选取5个县(区)720名人员为研究对象,采集研究对象的血液和尿液样品并检测镍、锡、锑、铊含量,分析不同性别、年龄和区域之间的分布差异.两独立样本的比较采用Mann-WhitneyU检验...     

Application of the urinary S-phenylmercapturic acid test as a biomarker for low levels of exposure to benzene in industry.

Recently, the determination of S-phenylmercapturic acid (S-PMA) in urine has been proposed as a suitable biomarker for the monitoring of low level exposures to benzene. In the study reported here, the test has been validated in 12 separate studies in chemical manufacturing plants, oil refineries, and natural gas production plants. Parameters studied were the urinary excretion characteristics of S-PMA, the specificity and the sensitivity of the assay, and the relations between exposures to airborne benzene and urinary S-PMA concentrations and between urinary phenol and S-PMA concentrations. The range of exposures to benzene was highest in workers in chemical manufacturing plants and in workers cleaning tanks or installations containing benzene as a component of natural gas condensate. Urinary S-PMA concentrations were measured up to 543 micrograms/g creatinine. Workers' exposures to benzene were lowest in oil refineries and S-PMA concentrations were comparable with those in smoking or nonsmoking control persons (most below the detection limit of 1 to 5 micrograms/g creatinine). In most workers S-PMA was excreted in a single phase and the highest S-PMA concentrations were at the end of an eight hour shift. The average half life of elimination was 9.0 (SD 4.5) hours (31 workers). Tentatively, in five workers a second phase of elimination was found with an average half life of 45 (SD 4) hours. A strong correlation was found between eight hour exposure to airborne benzene of 1 mg/m3 (0.3 ppm) and higher and urinary S-PMA concentrations in end of shift samples. It was calculated that an eight hour benzene exposure of 3.25 mg/m3 (1 ppm) corresponds to an average S-PMA concentration of 46 micrograms/g creatinine (95% confidence interval 41-50 micrograms/g creatinine). A strong correlation was also found between urinary phenol and S-PMA concentrations. At a urinary phenol concentration of 50 mg/g creatinine, corresponding to an eight hour benzene exposure of 32.5 mg/m3 (10 ppm), the average urinary S-PMA concentration was 383 micrograms/g creatinine. In conclusion, with the current sensitivity of the test, eight hour time weighted average benzene exposures of 1 mg/m3 (0.3 ppm) and higher can be measured.     

Cognitive functioning in lead workers

In a cross sectional study of occupational exposure to inorganic lead 91 men performed a series of microcomputer based tasks assessing sensor motor reaction time, memory, attention, verbal reasoning, and spatial processing. Performance on the tasks was studied in relation to three ranges of blood lead concentration (low, less than 20 micrograms/dl; medium, 21-40 micrograms/dl; and high, 41-80 micrograms/dl) and exposure response correlations for blood lead concentration, zinc protoporphyrin (ZPP) (range 7-210 micrograms/dl), and urinary aminolaevulinic acid (ALA) (range 0.5-22.0 mg/l). The results show that the high group were impaired on most of the tasks used and, in general, the magnitude of the impairment correlated better with blood lead concentration than ZPP or urinary ALA. An examination of the patterns of task impairment indicated a general slowing of sensory motor reaction time which was relatively independent of the nature of the cognitive functions being tested. There was some evidence, however, suggesting mild impairment of attention, verbal memory, and linguistic processing. In general, workers with high blood lead concentrations showed clear impairment of sensory motor functions in the absence of correspondingly strong evidence for impaired processing and memory functions. It is argued that a general slowness in responding may underlie many previous reports of widespread cognitive impairment in lead workers.     

Cognitive functioning in lead workers.

In a cross sectional study of occupational exposure to inorganic lead 91 men performed a series of microcomputer based tasks assessing sensor motor reaction time, memory, attention, verbal reasoning, and spatial processing. Performance on the tasks was studied in relation to three ranges of blood lead concentration (low, less than 20 micrograms/dl; medium, 21-40 micrograms/dl; and high, 41-80 micrograms/dl) and exposure response correlations for blood lead concentration, zinc protoporphyrin (ZPP) (range 7-210 micrograms/dl), and urinary aminolaevulinic acid (ALA) (range 0.5-22.0 mg/l). The results show that the high group were impaired on most of the tasks used and, in general, the magnitude of the impairment correlated better with blood lead concentration than ZPP or urinary ALA. An examination of the patterns of task impairment indicated a general slowing of sensory motor reaction time which was relatively independent of the nature of the cognitive functions being tested. There was some evidence, however, suggesting mild impairment of attention, verbal memory, and linguistic processing. In general, workers with high blood lead concentrations showed clear impairment of sensory motor functions in the absence of correspondingly strong evidence for impaired processing and memory functions. It is argued that a general slowness in responding may underlie many previous reports of widespread cognitive impairment in lead workers.     

Contribution of dietary protein and inorganic sulfur to urinary sulfate: toward a biomarker of inorganic sulfur intake

BACKGROUND: Sulfiting agents are widely used as food additives. Limits are set on their use in foods because they may adversely affect health. Sulfiting agents are excreted in urine as sulfate, which is indistinguishable from sulfate derived from sulfur amino acids. OBJECTIVE: The objective was to assess the contribution of inorganic sulfur to urinary sulfate excretion and of dietary protein to urinary sulfate and nitrogen excretion with the aim of developing a urinary biomarker of inorganic sulfur intake. DESIGN: Nine healthy men were fed a sequence of 3 diets for 15 d (n = 7), 5 diets for 10 d (n = 6), or both. The diets contained 51-212 g protein/d (0.43-1.71 g S/d) and 0.17-0.27 g inorganic S/d; p-aminobenzoic acid-validated 24-h urine samples (n = 47) were analyzed for sulfate and nitrogen. RESULTS: Dietary inorganic sulfur was efficiently excreted as sulfate in urine. Urinary sulfate derived from protein correlated strongly (r(2) = 0.86) with urinary nitrogen. Urinary recovery of protein sulfur and nitrogen decreased from 84% at average protein intakes (72 g/d) to 70% at high protein intakes (212 g/d). The nitrogen:sulfur ratio (in g) of the protein in the study diets was 18.9, which was maintained in urine (18.4 +/- 0.1) after dietary inorganic sulfur intake was subtracted from urinary sulfate. Therefore, inorganic sulfur intake (g/d) = urinary sulfur (g/d) - 0.054 x urinary nitrogen (g/d). For typical UK intakes of inorganic sulfur (0.25 g/d), this biomarker should produce mean (+/- SD) values of 0.24 +/- 0.10 g S/d. CONCLUSION: Twenty-four-hour urinary nitrogen and sulfate values can be used to predict inorganic sulfur intake.     

Estimation of individual dermal and respiratory uptake of polycyclic aromatic hydrocarbons in 12 coke oven workers.

Twelve workers from a coke plant in The Netherlands participated in an intensive skin monitoring programme combined with personal air sampling and biological monitoring during five consecutive eight hour workshifts. The purpose of the study was to make a quantitative assessment of both the dermal and respiratory intake of polycyclic aromatic hydrocarbons (PAHs). Pyrene was used as a marker compound for both dermal and respiratory exposure to PAHs. The biological measure for the internal exposure to PAHs was urinary 1-OH-pyrene concentration. Measurements on exposure pads at six skin sites showed that mean total skin contamination of the 12 workers ranged between 21 and 166 micrograms pyrene a day. The dermal uptake of pyrene ranged between 4 and 34 micrograms/day, which was about 20% of the pyrene contamination on skin. The mean concentration of total pyrene in the breathing zone air of the 12 coke oven workers ranged from 0.1 to 5.4 micrograms/m3. The mean respiratory uptake of pyrene varied between 0.5 and 32.2 micrograms/day. Based on the estimates of the dermal and respiratory pyrene uptake it is concluded that an average 75% (range 28%-95%, n = 12) of the total absorbed amount of pyrene enters the body through the skin. Because of the difference in the pyrene:benzo(a)pyrene ratio between the air samples and the skin contamination samples, the dermal uptake of benzo(a)pyrene was also estimated. This was about 51% of the total absorbed amount (range 8%-92%, n = 12). The total excreted amount of urinary 1-OH-pyrene as a result of exposure to PAHs during the five consecutive workshifts varied between 36 and 239 nmol. A multiple regression model of the mass balance between pyrene dose (both dermal and respiratory) and 1-OH-pyrene excretion confirmed the relevance of the dermal exposure route. The variation in urinary 1-OH-pyrene excretion was determined more by the dermal pyrene dose than by the respiratory dose. The model showed an estimate of the percentage of the absorbed amount of pyrene that is metabolised and excreted as 1-OH-pyrene in urine. For the 12 workers this percentage varied between 13% and 49% depending on smoking habits and consumption of alcohol. The results of this study indicate that among coke oven workers, the skin is the main route of uptake of PAHs. Preventive measures to reduce exposure to PAHs should be focused more on the reduction of dermal contamination by PAHs than on the reduction of inhaled dose.     

Evidence of aluminium accumulation in aluminium welders

Using atomic absorption spectrometry the aluminium concentrations in blood and urine and in two iliac bone biopsies obtained from welders with long term exposure to fumes containing aluminium were measured. The urinary excretion of two workers who had welded for 20 and 21 years varied between 107 and 351 micrograms Al/l, more than 10 times the concentration found in persons without occupational exposure. Urinary aluminium excretion remained high many years after stopping exposure. Blood and bone aluminium concentrations (4-53 micrograms Al/l and 18-29 micrograms Al/g respectively) were also raised but not to the same extent as urine excretion. It is concluded that long term exposure to aluminium by inhalation gives rise to accumulation of aluminium in the body and skeleton of health persons, and that the elimination of retained aluminium is very slow, in the order of several years.     

Evidence of aluminium accumulation in aluminium welders.

Using atomic absorption spectrometry the aluminium concentrations in blood and urine and in two iliac bone biopsies obtained from welders with long term exposure to fumes containing aluminium were measured. The urinary excretion of two workers who had welded for 20 and 21 years varied between 107 and 351 micrograms Al/l, more than 10 times the concentration found in persons without occupational exposure. Urinary aluminium excretion remained high many years after stopping exposure. Blood and bone aluminium concentrations (4-53 micrograms Al/l and 18-29 micrograms Al/g respectively) were also raised but not to the same extent as urine excretion. It is concluded that long term exposure to aluminium by inhalation gives rise to accumulation of aluminium in the body and skeleton of health persons, and that the elimination of retained aluminium is very slow, in the order of several years.