Influence of chronic low-level exposure to lead on plasma immunoglobulin concentration and cellular immune function in man

Summary The immunological status of individuals occupationally exposed to low levels of inorganic lead has been examined and compared with that of non-exposed, age and sex-matched controls. At the time of testing the exposed population had a mean (± SD) blood lead concentration of 38.4 ±5.6 g · 100 ml^–1 (n = 39) compared witha mean value of 11.8 ±g · 100 ml^–1 (n = 21) for the control group. No differences in the serum concentrations of IgG, IgA and IgM between the populations were observed and there existed no correlation between blood lead concentration and serum immunoglobulin levels. In addition assessment was made of the capacity of peripheral blood mononuclear cells to respond to the mitogen phytohaemagglutinin (PHA), a correlate of T cell function, and to spontaneously lyse cells of the erythroleukaemic cell line K562, a measure of NK cell function. In neither case was there a difference between exposed and control populations and no correlation between reactivity and blood lead concentration. Although previous studies in rodents have indicated that exposure to inorganic lead resulting in similar blood lead concentrations may compromise immune competence our data suggest that no similar effect occurs in man.     

Increase in the amount of erythrocyte δ-aminolevulinic acid dehydratase in workers with moderate lead exposure

Summary The amount of ALA-D in human erythrocytes was determined directly by radioimmunoassay or calculated from the restored activity assayed in the presence of zinc and dithiothreitol, and a good correlation was observed between the RIA-based and the restored activity-based amounts.The RIA-based amount of ALA-D in the blood of 10 normal individuals (blood lead levels of 5.6 ± 2.3 g/100 ml: mean ± SD) and 19 lead-exposed workers (blood lead levels of 41.2 ± 10.2 g/100 ml) was 54.1 ± 11.8 g/ml blood and 92.3 ± 20.6 g/ml blood, respectively, indicating an apparent increase of the enzyme amount in lead-exposed workers.A significant increase in the amount of erythrocyte ALA-D calculated from the restored activity in lead-exposed workers was observed even in the low blood lead level of 10–20 g/100 ml, resulting in the range of blood lead level 20–40 g/100 ml. No significant difference was observed in hematocrit and hemoglobin content between lead-exposed and non-exposed groups. These observations suggested that the increase of erythrocyte ALA-D in lead exposure was not due to anemia, which might result in the increase of young erythrocytes in peripheral blood.This increase in the amount of ALA-D in human erythrocytes might be a result of the function to overcome the inhibition of the enzyme in bone marrow cells during lead exposure, and these findings may throw light on the danger to human health of low-level lead toxicity.Abbreviations ALA-D -Aminolevulinic acid dehydratase or 5-Amnoevulinic acid hydro-lyase, EC 4.2.1.24 - ALA -Aminolevulinic acid - Rc Reticulocyte - RIA Radioimmunoassay - DTT Dithiothreitol Supported in parts by Science Research Fund of the Ministry of Education, Science and Culture of Japan and by Research Grant of Fujiwara Foundation of Kyoto University     

Monitoring lead pollution near a storage battery recycling plant in Taiwan, Republic of China

This study presents the distribution of blood lead levels and lead in various environmental samples (water, sediments, soils, and air) near the Shing-Yie storage battery recycling plant in Taiwan before (July 1990 to June 1991) and after (July 1992 to June 1993) amelioration. Before amelioration, the average blood lead levels in the neighborhood of the plant were in the range of 10.55±5.7 to 12.28±7.9 g/dl. After amelioration, relatively lower average concentrations of blood lead (range 8.35±3.0 to 9.13±2.5 g/dl) were generally found; however, these averages were still higher than that (7.79±3.5 g/dl) from other lead-unpolluted areas of Taiwan. An exceedingly high geometric mean (GM) lead concentration (128 g/L) was found in the downstream river water of the Tawulum River passing by the plant. The concentrations of lead (GM=372 and 418 g/g) in the downstream river sediments were higher than those (GM=123 and 158 g/g) in the upstream river sediments before and after amelioration, respectively. Furthermore, lead species in river sediments were analyzed by a sequential leaching technique. The sum of phases I, II, and III accounted for 83.7% of total lead at station R₂ (nearest to the plant). Maximum lead concentration (GM=2402 g/g) in dust at the soil surface from station S₁ (nearest to the plant) was much higher than those from the other stations by about 18 times before amelioration. However, the maximum value dropped to 1,155 g/g after amelioration. On the whole, the geometric mean concentration of lead in dust at the soil surface nearest to the plant was >1,000 g/g and decreased to <100 g/g in the 15–30 cm depth soil about 2 km away from the plant. Before amelioration, the geometric mean lead concentration of 4.57 g/m³ (range 0.102–37.6 g/m³) in the air near the plant was higher than that at the background locations, the geometric mean value of which was 0.08 g/m³.     

Motor nerve conduction velocity in asymptomatic lead workers

Summary No difference was found between the nerve conduction velocities of the ulnar nerve of 32 lead exposed workers in the mill of a lead-zinc mine, compared to that of a control group of 14 persons. The lead exposure period was 2–37 months (mean: 12.9 months).The blood lead of the exposed group was as an average (± SD): 53 ± 16 g per 100 ml compared to 11 ± 4 g per 100 ml for the control group.Further studies are needed to establish a possible dose-time-response relationship for the possible, subclinical neuropathy found by some investigators.     

Effect of fire smoke on some biochemical parameters in firefighters of Saudi Arabia

Background

Lead exposure is common in automobile battery manufacture and repair, radiator repair, secondary smelters and welding units. Urinary Aminolevulinic acid has validity as a surrogate measure of blood lead level among workers occupationally exposed to lead. This study had therefore assessed the magnitude of lead exposure in battery repair workers of three transport service enterprises.

Methods

To this effect, a cross-sectional study was carried out on lead exposure among storage battery repair workers between November 2004 and May 2005 from Anbasa, Comet and Walia transport service enterprises, Addis Ababa, Ethiopia. Subjective information from the workers was obtained by making use of structured questionnaire. Other information was obtained from walkthrough evaluation of the repair units. Aminolevulinic acid levels in urine were used as an index of the exposure. This was coupled to measurements of other relevant parameters in blood and urine collected from adult subjects working in the repair units as well as age matched control subjects that were not occupationally exposed to lead. Aminolevulinic acid was determined by spectrophotometry, while creatinine clearance, serum creatinine, urea and uric acid levels were determined using AMS Autolab analyzer.

Results

Urinary aminolevulinic acid levels were found to be significantly higher in exposed group (16 μg/ml ± 2.0) compared to the non-exposed ones (7 μg/ml ± 1.0) (p < 0.001). Alcohol taking exposed subjects exhibited a significant increase in urinary aminolevulinic acid levels than non-alcohol taking ones (p < 0.05). Moreover, urinary aminolevulinic acid levels of exposed subjects increased with age (p < 0.001) as well as duration of employment (p < 0.001). Whereas serum uric acid levels of exposed subjects was significantly higher than non-exposed ones (p < 0.05), no statistically significant difference had been found in renal indices and other measured parameters between exposed and non-exposed subjects. From the questionnaire responses and walkthrough observations, it was also known that all the repair units did not implement effective preventive and control measures for workplace lead exposure.

Conclusion

Taken together, these findings indicated that workers in lead acid battery repair units of the transport service enterprises are not protected from possibly high lead exposure. Thus, strict enforcement of appropriate and cost effective preventive and control measures is required by all the enterprises.     

Effect of simultaneous exposure to toluene and xylene on their respective biological exposure indices in humans

Summary Studies that specifically address the influence of controlled human exposure to a combination of solvents on the biological monitoring of exposure are limited in number. The present study was undertaken to investigate whether simultaneous exposure of human volunteers to toluene and xylene could modify the respective metabolic disposition of these solvents. Five adult Caucasian men were exposed for 7 consecutive h/day over 3 consecutive days to 50 ppm toluene and 40 ppm xylene either separately or in combination in a dynamic, controlled exposure chamber (low-level exposure). The experiment was repeated three times at intervals of 2 weeks. In another experiment, three subjects were exposed to 95 ppm toluene and 80 ppm xylene or a combination of both for 4h (high-level exposure). The concentration of unchanged solvents in blood (B) and in end-exhaled air (EA) as well as the urinary excretion of hippuric acid (HA) and methylhippuric acids (MHAs) were determined. Simultaneous exposure to the lowest level of solvents did not alter the concentration of unchanged solvents in blood or in exhaled air (average of 3-weekly means; single vs mixed exposure at 6.5 h exposure): B-toluene, 77.1 vs 78.1 g/100 ml; B-xylene, 67.6 vs 77.8 g/100 ml; EA-toluene, 9.9 vs 9.5 ppm; EA-xylene, 5.3 vs 4.8 ppm. Similarly, mixed exposure did not modify the excretion of urinary metabolites during the 3- to 7-h exposure period: HA, 1.11 vs 1.11 g/g creatinine; MHAs, 0.9 vs 0.87 g/g creatinine. However, simultaneous exposure to higher levels did affect the concentration of unchanged solvents in blood and in exhaled air as measured at 3.5 h exposure (mean value for three subjects ± SD): B-toluene, 135.7 ± 26.7 vs 215.7 ± 34.9 g/100 ml; B-xylene, 114 ± 19 vs 127.6 ± 22.1 g/100 ml; EA-toluene, 16.6 ± 0.4 vs 20.5 ± 2.8 ppm; EA-xylene, 9.9 ± 0.6 vs 12.3 ± 1.2 ppm. Such effects were accompanied by a significant delay in the urinary excretion of HA but not of MHAs. These data suggest that there is a threshold level below which metabolic interaction between toluene and xylene is not likely to occur in humans.     

Urinary excretion of 1-pyrenol in automotive repair workers

Summary The urinary excretion of a pyrene metabolite was evaluated in 65 automotive repair workers whose skin was exposed to used mineral oils, and in 41 controls. Pyrene contents were determined in oily material taken from cloths used to clean various types of engines (n = 8) and were found to vary (mean ± SD) from 2.8 ± 0.4 ppm for dirty matter obtained from diesel truck engines to 9.3 ± 8.2 ppm for that from petrol car engines. Tobacco smoking and polycyclic aromatic hydrocarbon (PAH)-rich diets were considered as confounding factors. At both the beginning and the end of the working week, the values of urinary 1-pyrenol were slightly higher in exposed subjects (0.178 ± 0.150 and 0.194 ± 0.135 mol/mol creatinine on Monday and Friday, respectively) than in controls (0.124 ± 0.090 mol/mol creatinine) (Mann-Whitney test, z = 2.741, P < 0.01). The urinary 1-pyrenol values were higher in both smoking and non-smoking subjects than in controls. The highest values were found in urinary samples of smokers exposed to used mineral oils (0.259 ±0.201 mol/mol creatinine). In non-smoking workers (n = 40), post-shift 1-pyrenol values were 0.154 ± 0.105 ol/mol creatinine, as against 0.083 ± 0.042 mol/mol creatinine for the 19 non-smoking controls (Mann-Whitney test, z = 2.765, P < 0.01). In automobile repair workers, urinary 1-pyrenol values before the beginning of the weekly workshift did not differ substantially from those measured at the end of the week, not being related to the subjective degree of dirty skin as stated by workers. Multiple regression analysis between urinary metabolite levels and the three independent variables turned out to be statistically significant (r ² = 0.295, 0.246; F-test = 14.2, 11.1; P both < 0.01) for Monday and Friday urinary metabolite values and revealed that tobacco smoking had a greater influence (contribution to r ² = 16.1% and 18.3% on Monday and Friday, respectively) than occupational exposure (3.8% and 6.6%, respectively) on urinary levels of 1-pyrenol; the influence of PAH-rich foods on urinary pyrene metabolite levels was only detectable when subjects returned to work after the weekend (5.5%).Comparison between urinary excretion of 1-pyrenol in this group of workers and that found in professionally exposed subjects indicates that exposure to PAHs through contamination of the skin with used engine oil during automotive repair work is very low.     

Nitrous oxide in blood and urine of operating theatre personnel and the general population

Nitrous oxide (N₂O) was assayed in 676 urine samples and 101 blood samples provided after exposure by operating theatre personnel from nine hospitals. The blood and urine assays were repeated in 25 subjects 18 h after the end of exposure. For 80 subjects, environmental N₂O was also measured during intraoperative exposure. Mean urinary N₂O in the 676 subjects at the end of exposure was 40 g/l (range 1–3805 g/l); in 10 of the 676 subjects, urinary N₂O was in the range 279–3805 g/l (mean 1202 /l). The 98^th percentile was 120 g/l. Mean blood N₂O at the end of exposure, measured in 101 subjects, was 21 g/l (median 16 g/l, range 1–75 g/l). Blood and urine N₂O (1.5 g/l and 4.9 g/l, respectively) in 25 subjects, 18 h after exposure, was significantly higher than in occupationally non-exposed subjects (blood 0.91 g/l, urine 1 g/l). Environmental exposure was significantly related to blood and urinary N₂O (r = 0.59 andr = 0.64, respectively). Blood and urinary N₂O were significantly related to each other (r = 0.71), and were equivalent to about 25% of the environmental exposure level. The mean urinary N₂O of 1202 g/l in 10/676 subjects was not related to environmental exposure in the operating theatre. The highest urinary N₂O levels measured in these 10/676 subjects could be explained by an asymptomatic urinary infection.     

Histopathological progression of hemic neoplasms in the tropical crab Paratelphusa hydrodromous (Herbst) treated with sublethal cadmium chloride

Tropical crab Paratelphusa hydrodromous were exposed in the laboratory to five sublethal cadmium chloride concentrations (0.02, 0.05, 0.25 and 0.50M/L) for 30 days to evaluate the cellular inflammatory and chronic pathologic responses. The most frequent pathologic responses of hepatopancreas exposed to 0.25–0.50 M CdCl₂/L were atrophy of R-cells and the development of granulomatous reaction consisting of granulocytes and monomorphic basophilic cells. Coagulative necrosis was evident in the young oocytes at 0.05 M CdCl₂/L which was accompanied by the increased vitellophagia of follicle cells. Thirty-day exposure to 0.25–0.50 M CdCl₂/L shortened the reproductive life span of the crabs by inducing spontaneous atresia and granulocytosis. Eosinophilic granulocytes, the most numerous cell type found in the necrotic centers, phagocytosed the masses of cellular debris and yolk from cadmium-induced atretic oocytes. The widespread proliferation of basophilic cells related to hyalinocyte with high nucleocytoplasmic ratio would suggest the development of hemic neoplasia. Heavy granulocytic infiltration was the typical cellular inflammatory response during chronic pathological conditions.     

Measurement of manganese amelioration of cadmium toxicity inChlorella pyrenoidosa using turbidostat culture

Cadmium (Cd) toxicity and amelioration of Cd toxicity by Mn were measured inChlorella pyrenoidosa, using turbidostat culture. The responses were measured in terms of the maximum specific growth rate, _max, of the populations. In turbidostat culture _max is a dependent variable that can be measured continuously. Cd (as CdCl₂· 2.5 H₂O) was added to control populations at a concentration of 1.8 M Cd. Toxicity was expressed after a 5 generation lag and resulted in a _max steady state 62% lower than the initial control after 2 generations. With continued Cd exposure, Mn (as MnCl₂ · 6H₂O) was then added stepwise to a concentration of 10.4 M Mn which caused a rapid, immediate increase in _max followed by linear increase until a steady-state plateau was reached at a _max 90% of control. The ameliorative response spanned 20 culture generations. After addition of Mn (10.4 M), cellular Cd concentration did not change and cellular Mn concentration increased. Increase in mean cell size accompanied Cd exposure and was significantly decreased when supplemented with 10.4 M Mn. Possible mechanisms of the amelioration are discussed.     

Severe damage of cultured vascular endothelial cell monolayer after simultaneous exposure to cadmium and lead

This study evaluates the toxicity of lead in the presence or absence of cadmium on the maintenance of a monolayer of cultured bovine aortic endothelial cells. It was histologically shown that lead at 50 M or less induced a slight formation of de-endothelialized areas on the monolayer after a 24-h incubation. Although lead accumulated in endothelial cells in a dose-dependent manner, the cytotoxicity (evaluated by the [³H]adenine release assay) was not detected. However, cadmium (1.0 or 2.0 M)-induced de-endothelialized areas on the monolayer was considerably larger in the presence of lead at 10 M; the cytotoxicity of cadmium was significantly enhanced by lead. It was concluded that vascular endothelial cell monolayer is severely destroyed by a greater cytotoxicity of combination of cadmium with lead.     

A new HPLC fluorimetric method to monitor urinary delta-aminolevulinic acid (ALA-U) levels in workers exposed to lead

Summary A new sensitive HPLC method for the determination of urinary delta-aminolevulinic acid (ALA-U) was used to evaluate the relationship between blood-lead (Pb-B) and ALA-U levels in male workers exposed to lead. The differences between the ALA-U levels determined by this method (ALAU-HP) and by a colorimetric method (ALA-U-CL) are discussed. The HPLC method gave values similar to the ALA-U-CL values at high ALA-U level. However, at low blood-lead levels (58 ± 22 g/l, n = 23), the mean ALA-U-HP level corrected by urinary creatinine level was one-third of the corrected ALA-UCL level (0.83 ± 0.14 and 2.4 ± 0.5 mg/g creatinine, respectively). A significant increase of the mean corrected ALA-U-HP level was observed at 162 ± 22 g/l Pb-B (P < 0.05, n = 26), while that of ALA-UCL was observed at 245 ± 30 g/l Pb-B (P < 0.01, n = 37). The regression equation based on the logistic model fitted well to the relationship data between the Pb-B level and the percentage of the subjects with corrected ALA-U-HP above the cut-off point (1.12 mg/g creatinine) and the expected Pb-B level for 50% response was 270 g/l Pb-B, while it did not fit well to the relationship data between Pb-B level and the percentage of the subjects with corrected ALAU-CL above the cut-off point (3.5 mg/g creatinine). The maximum responses for the two sets of corrected ALA-U levels were both observed at 625 ± 25 g/l. The corrected ALA-U level by HPLC method seems to be a useful indicator for biological monitoring of exposure to lead at low levels (< 400 g/l Pb-B = health-based biological limit, WHO) as well as high ones.     

Passive smoking at work: biochemical and biological measures of exposure to environmental tobacco smoke

Summary Several biochemical and biological measures of tobacco smoke intake were used to evaluate exposure of restaurant personnel to environmental tobacco smoke as compared with active smokers and non-exposed non-smokers. All of the measured parameters — carboxyhaemoglobin (COHb), thiocyanate (SCN) and cotinine in plasma, cotinine and mutagenicity in urine, total white blood cell count (WBC), and sister chromatid exchange (SCE) frequency in cultured lymphocytes — were significantly elevated in the smoker group (n = 22) compared to the non-exposed group (n = 20). Work-related passive exposure (n = 27) was seen most clearly in the cotinine values, both from plasma (mean P-cot in passive smokers 10 ng/ml vs 5.2 ng/ml in non-exposed) and from urine (mean U-cot in passive smokers 56 ng/ml vs 8.3 ng/ml in non-exposed), but significant increases were also seen in the thiocyanate levels (mean P-SNC in passive smokers 58 mol/1 vs 46 mol/1 in non-exposed) and, as a preliminary finding, in total leucocyte count (in passive smokers 8.0 × 10⁹/1 vs 6.8 x 10⁹/1 in non-exposed). The results demonstrate that environmental tobacco smoke may be an occupational health hazard.     

Mercury and methylmercury in population risk groups on the Atlantic coast of Southern Spain

The presence of methylmercury and total mercury in the hair of high risk groups residing in the highly industralized South Atlantic coastal area of Spain were studied. In fishermen, total mercury and methylmercury content showed slight non-statistically significant differences among groups from two different coastal areas (geometric means: 10.41 and 8.36 g/g for total mercury; 8.28 and 6.72 g/g methylmercury). Mercury content in both groups differed significantly from controls (geometric mean 2.5 g/g total mercury, 4.50 g/g for methylmercury; p<0.05). In pregnant women, statistically significant differences were found in the three groups (two coastal areas and controls). Geometric means were 2.40, 5.94, and 0.94 g/g for total mercury and 1.93, 4.78, and 0.82 g/g for methylmercury. Results were compared with those obtained in other European countries in the Mediterranean area. Simultaneously, the same compounds were analyzed in fish and molluscs from those most consumed by people in the above-mentioned groups. The following results were obtained: sword fish, 1.57±1.27 g/g and 1.20±0.94 g/g for total mercury and methylmercury respectively; Scrobicularia plana, 0.07±0.052 and 0.053±0.039 g/g; Tapes decussatus, 0.046±0.20 and 0.039±0.018 g/g.     

Development of the surf clam (Spisula solidissima) following exposure of gametes,embryos, and larvae to silver

The gametes, embryos, and early larvae of the surf clamSpisula solidissima were exposed to silver at concentrations up to 65 g/L. All experiments were conducted at 20°C and 30 S, and lasted up to 48 hr after fertilization. Forty-five minute exposures of eggs to 16 g/L or more silver just prior to fertilization in non-silver seawater lead to production of abnormal larvae. Simultaneous exposures of eggs and sperm to silver concentrations up to 21 g/L for 45 min did not prevent fertilization but did produce abnormal larvae at silver concentrations greater than 6 g/L. Postfertilization treatments of zygotes, embryos, and larvae lead to fewer abnormalities than prefertilization or fertilization treatments of comparable exposure length and concentration. The greatest numbers of abnormalities and mortalities were observed in continuous exposures, from gametes through fertilization to 48 hr postfertilization. Variability in % normal development was greater in high than in low silver concentrations.     

Urinary hydroxy-metabolites of naphthalene,phenanthrene and pyrene as markers of exposure to diesel exhaust

Objective The objective of this study was to assess the exposure of bus-garage and waste-collection workers to polycyclic aromatic hydrocarbons (PAHs) derived from diesel exhaust by the measurement of levels of seven urinary PAH metabolites: 2-naphthol, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, 1+9-hydroxyphenanthrene, 4-hydroxyphenanthrene and 1-hydroxypyrene.Subjects and methods One urine sample from each of 46 control persons, and one pre-shift and two post-shift spot urine samples from 32 exposed workers were obtained in winter and in summer. The metabolites were analysed after enzymatic hydrolysis by high performance liquid chromatography (HPLC) with fluorescence detection.Results The sum of seven PAH metabolites (mean 3.94±3.40 and 5.60±6.37 mol/mol creatinine in winter and summer, respectively) was higher [P=0.01, degrees of freedom (df) =61.2 and P=0.01, df=67.6 in winter and summer, respectively] in the exposed group than in the control group (mean 3.18±3.99 and 3.03±2.01 mol/mol creatinine in winter and summer, respectively). The mean concentrations of 2-naphthol among exposed and controls ranged between 3.34 and 4.85 mol/mol creatinine and 2.51 and 2.58 mol/mol creatinine, respectively (P<0.01 in winter, P<0.03 in summer). The mean level of the hydroxyphenanthrenes in the samples of exposed workers was between 0.40 and 0.70 mol/mol creatinine and in the control samples 0.40–0.60 mol/mol creatinine. The concentration of 1-hydroxypyrene was higher among exposed workers in both pre-shift and post-shift samples (mean 0.10–0.15 mol/mol creatinine) than in control group (mean 0.05–0.06 mol/mol creatinine) in winter (P=0.002, df=78) and in summer (P<0.001, df=68).Conclusions The urinary hydroxy-metabolites of naphthalene, phenanthrene and pyrene showed low exposure to diesel-derived PAHs; however, it was higher in exposed workers than in control group. Urinary PAH monohydroxy-metabolites measured in this study did not correlate with the PAHs in the air samples, reported earlier, in 2002 and 2003.     

Assessment of thyroid,testes, kidney and autonomic nervous system function in lead-exposed workers

Summary The objective of the study was to assess whether moderate occupational exposure to lead may be associated with early changes in potential target organs (thyroid, testes, kidney, autonomic nervous system). Workers exposed to lead in a lead acid battery factory (n = 98; mean blood lead 51 g/dl, range 40–75 g/dl) and 85 control workers were examined. None of the indicators of kidney function (in urine: retinol-binding protein, ₂-microglobulin, albumin,N-acetyl--d-glucosaminidase; in serum: creatinine, ₂-microglobulin), endocrine function (follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, thyroxine, triiodothyronine) and autonomic nervous system (R-R interval variations on the electrocardiogram) were correlated with lead exposure (blood lead or duration of exposure) or showed significantly different mean values between the exposed group and controls. These results and an assessment of the published data suggest that compliance with the Directive of the Council of the European Communities on lead exposure (health surveillance in workers whose lead in blood exceeds 40 g/dl and removal from exposure when blood lead exceeds 70–80 g/dl) would prevent the occurrence of significant biological changes in the majority of lead-exposed workers.     

Hexahydrophthalic acid in urine as an index of exposure to hexahydrophthalic anhydride

Summary Post-shift and next-morning urine was sampled from workers exposed to hexahydrophtalic anhydride (HHPA), an epoxy hardener, sensitising at low exposure levels. Exposure levels of HHPA in air gas chromatography, GC) in the range of 30–270 g/m³ corresponded to urinary concentrations of 0.9–2.8 mol hexahydrophthalic acid (HHP acid; GC-mass spectrometry)/mmol creatinine. In the morning samples the concentrations were <0.04-0.3 mol HHP acid/mmol creatinine. In unexposed controls, the level was <0.1 mol/mmol creatinine. A correlation was found between the time-weighted levels of HHPA in air and HHP acid in the post-shift urine (r _s = 0.93; P < 0.023), indicating that the determination of HHP acid in urine is suitable for biologic monitoring of HHPA exposure.     

Blood acetone concentration in “normal people” and in exposed workers 16 h after the end of the workshift

Summary Acetone levels were measured by gas chromatography mass spectrometry (GC-MS) in environmental and alveolar air, blood and urine of 89 non-occupationally exposed subjects and in three groups of workers exposed to acetone or isopropanol. Acetone was detected in all samples from non-exposed subjects, with mean values of 840 g/l in blood (Cb), 842 g/l in urine (Cu), 715 ng/l in alveolar air (Ca) and 154 ng/l in environmental air (Ci). The ninety-fifth percentiles were 2069 g/l in Cb, 2206 g/l in Cu and 1675 ng/l in Ca. The blood/air partition coefficient of acetone was 597. Correlations were found in Cb, Cu and Ca. In specimens sampled at the end of the workshift from subjects occupationally exposed to acetone, a correlation was found in the blood, urine, alveolar and environmental air concentrations. The blood/air partition coefficient of acetone was 146. On average, the blood acetone levels of workers were 56 times higher than the environmental exposure level, and the concentration of acetone in alveolar air was 27% more than that found in inspiratory air. The half-life for acetone in blood was 5.8 h in the interval of 16 h between the end of the workshift and the morning after. The morning after a workshift with a mean acetone exposure of 336 g/l, blood and urinary levels were 3.5 mg/l and 13 mg/l, respectively, which were still higher than those found in normal subjects. It can be concluded that endogenous production of acetone and environmental exposure to acetone or isopropanol do not affect the reliability of biological monitoring of exposed workers, even 16 h after low exposure.     

Dislodgeability of pesticides from products made with recycled pesticide container plastics

Products containing high density polyethylene plastic from recycled pesticide containers were tested for levels of dislodgeable pesticide under dry and damp conditions. Trifluralin was found to be the pesticide released in largest quantity from plastic curbstops. Levels dislodged ranged from 0.18 g/100 cm² to 4.18 g/100 cm² for all plastics tested. Significantly higher dislodgeability occurred from products where low density polyethylene plastics were used to dilute pesticide container plastics, compared to products containing only pesticide container plastics. Amounts of trifluralin dislodged by wiping with dry cheesecloth for 15 min were 0.83±0.50, 3.52±0.40, and 2.53±0.56 g/100 cm² for products containing 100%, 50%, and 25% pesticide container plastics, respectively. Respective levels of trifluralin dislodged with saline-dampened cheesecloth were 2.00±0.71, 3.21±0.82, and 1.16±0.51 g/100 cm². Decreased amounts of trifluralin were released after product weathering, with levels dislodged under dry conditions of 0.007±0.002, 0.0083±0.001 and 0.0089±0.001 m/100 cm², respectively. Similar studies of asphalt products containing recycled pesticide containers found the average amounts of trifluralin and 2,4-D iso-octyl ester dislodged were 0.33 g/100 cm² and 1.35 g/100 cm², respectively. Pesticide levels dislodged from all products tested were within acceptable daily intake levels. Calculations of margins of safety showed exposure to products made with recycled containers would not present an unacceptable risk to individuals coming in contact with them.