Mercury exposure in high school chemistry teachers

To assess whether high school chemistry teachers had higher urinary mercury concentrations than other high school teachers, 24 high school teachers from nine schools in northeastern Ohio were studied. First morning voided urine samples and air samples from the teachers' classrooms were analyzed for total mercury content by cold vapor atomic absorption. The median adjusted urinary mercury concentration in the 12 chemistry teachers was 4.6 g/g creatinine (range 2.2–8.2 g/g creatinine) and it was 6.3 g/g creatinine in the 12 non-chemistry teachers. All classroom air samples contained mercury levels below detection limits. No evidence was provided that high school chemistry teachers are at increased risk of chronic mercury exposure from their teaching activities compared to other high school teachers.     

Sublethal Effects of Trace Metals (Cd,Cr, Cu,Hg) on Embryogenesis and Larval Settlement of the Ascidian <Emphasis Type="Italic">Ciona intestinalis</Emphasis>

Toxicity of Cadmium (Cd), Chromium (Cr), Copper (Cu), and Mercury (Hg) on the early developmental stages of Ciona intestinalis was investigated. Developmental defects of larvae after exposure of gametes throughout their development to the larval stage were assessed. Gamete exposure to increasing metal concentrations resulted in a significant decrease of the percentage of normally hatched larvae, showing median effective concentrations (EC₅₀) of 721 g/L (6.42 M) for Cd, 12772 g/L (226 M) for Cr, 36.6 g/L (0.576 M) for Cu, and 44.7 g/L (0.223 M) for Hg. Larval attachment was significantly affected when gametes were exposed to the metals throughout development. The EC₅₀ reducing larval attachment by 50% were 752 g/L (6.7 M) for Cd, 15026 g/L (289 M) for Cr, 67.8 g/L (1.607 M) for Cu, and 78.1 g/L (0.389 M) for Hg. Therefore, on a molar basis Hg is three times more toxic than Cu, 20–30 times more than Cd, and 700–1000 times more toxic than Cr, for both responses.     

Long-term mercury excretion in urine after removal of amalgam fillings

The long-term urinary mercury excretion was determined in 17 28- to 55-year-old persons before and at varying times (up to 14 months) after removal of all (4–24) dental amalgam fillings. Before removal the urinary mercury excretion correlated with the number of amalgam fillings. In the immediate post-removal phase (up to 6 days after removal) a mean increase of 30% was observed. Within 12 months the geometric mean of the mercury excretion was reduced by a factor of 5 from 1.44 g/g (range: 0.57–4.38 g/g) to 0.36 g/g (range: 0.13–0.88 g/g). After cessation of exposure to dental amalgam the mean half-life was 95 days. These results show that the release of mercury from dental amalgam contributes predominantly to the mercury exposure of non-occupationally exposed persons. The exposure from amalgam fillings thus exceeds the exposure from food, air and beverages. Within 12 months after removal of all amalgam fillings the participants showed substantially lower urinary mercury levels which were comparable to those found in subjects who have never had dental amalgam fillings. A relationship between the urinary mercury excretion and adverse effects was not found. Differences in the frequency of effects between the pre- and the post-removal phase were not observed.     

Chronic toxicity of dietary disodium arsenate heptahydrate to juvenile rainbow trout (Oncorhynchus mykiss)

Juvenile rainbow trout were fed semi-purified diets containing graded levels of disodium arsenate heptahydrate (DSA) for 12–24 weeks under standard laboratory conditions to define the maximum acceptable toxicant concentration (MATC) and to correlate signs of toxicity with diet and tissue arsenic concentrations. The MATC for DSA was between 13 and 33 g As/g diet or 0.281–0.525 mg As/kg body weight/day. The most sensitive and reliable indicator of chronic dietary DSA toxicity in rainbow trout was chronic inflammation of the gallbladder wall. Chronic inflammatory changes in the sub-epithelial tissues of the gallbladder wall were evident in 71% of rainbow trout exposed to 33 g As/g diet for 24 weeks, and 100% of rainbow trout exposed to 65 g As/g diet for 24 weeks or 49 g As/g diet for 12 weeks. No fish exposed to 13 g As/g diet or less for up to 24 weeks showed any demonstrable gallbladder lesions or any other ill effect of arsenic exposure. Other signs of chronic dietary DSA toxicity to rainbow trout included decreased growth rate, mild to moderate anemia, and, at higher levels of exposure, active feed refusal leading to decreased feed consumption. Mild nephrocalcinosis was noted in one experiment where kidney arsenic residues exceeded 14 g As/g tissue dry weight.Supported by the Natural Sciences and Engineering Research Council of Canada and the Ontario Ministry of Agriculture and FoodPortions of this material were presented at the 29th Annual Meeting of the Canadian Federation of Biological Societies, June 16–20, 1986, Guelph, Ontario, and the 14th Annual Aquatic Toxicity Workshop, November 2–4, 1987, Toronto, Ontario, Canada     

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.     

Mercury concentrations in hair from populations in Wau-Bulolo area, Papua New Guinea

Total mercury (Hg) concentrations were determined in scalp hair from the populations in the Wau-Bulolo area, eastern Papua New Guinea (PNG), where humans are exposed to large quantities of Hg through gold-mining activities by Hg amalgamation processes. Humans living upstream and not engaged in gold mining had a mean hair Hg concentration of 0.55 g g^–1 (range: 0.19–1.1 g g^–1) (n=80), which was recognized as the background level in this area. In contrast, the populations involved in gold-mining activities had a significantly higher level of hair Hg (mean: 1.2 g g^–1, range: 0.39–3.0 g g^–1) (n=86) than the background level, indicating direct or indirect exposure to Hg from gold mining. The hair Hg level in populations downstream of the gold-mining area was significantly higher than the background level, due to the consumption of Hg-contaminated fish. Mercury concentrations were significantly higher in males than in females, regardless of location properties.     

Response of a freshwater bacterial community to mercury contamination (HgCl2 and CH3HgCl) in a controlled system

An experimental study was made on the effects of inorganic mercury (HgCl₂) and methylmercury (CH₃HgCl) on freshwater aerobic heterotrophic bacterial population. The experimental system was based on two-compartment biotopes: natural sediment, from the Garonne River, and dechlorinated tap water. The response of bacterial communities to mercury additions (to the water column) was monitored by determining total Hg in water and enumerating the total number of bacteria and the evolution of the mercury resistant community. Isolation was carried out by plate count method. Enumeration of mercury resistant strains was made with a general medium (Iron-Tryp-tone agar) amended with 10 g Hg/ml of HgCl₂. The response to 2 g Hg/L (HgCl₂) was fast approximately 50% of the maximum percentage of mercury resistant bacteria being reached after one hour (21.7% after 17 h exposure). Spikes of CH₃HgCl (2 g Hg/L) in the water column caused an initial inhibition of growth of Hg-resistant and sensitive bacteria followed by a complete recovery of the background microbial population after 84 h. Seven mercury resistant bacterial strains were isolated from the experimental systems and each of them was checked for HgCl₂ and CH₃HgCl transformation. All were able to volatilize HgCl₂ by producing elemental mercury, but none was able to degrade methylmercury. Additions of different concentrations of HgCl₂ (0.02 g Hg/L to 2 g Hg/L) to the water column caused a proportional increase in the percentage of mercury-resistant bacteria. Low concentrations (<0.6 g Hg/L) of CH₃HgCl also induced the Hg-resistant community, whereas 2 g Hg/L of CH₃HgCl inhibited the growth of both Hg-sensitive and Hg-resistant heterotrophic bacteria.     

Short-term exposure of zooplankton to the synthetic pyrethroid,fenvalerate, and its effects on rates of filtration and assimilation of the alga,Chlamydomonas reinhardii

In acute tests of toxicity, two cladocerans,Daphnia galeata mendotae andCeriodaphnia lacustris, and the calanoid,Diaptomus oregonensis, were more sensitive to fenvalerate thanDaphnia magna, the organism used in standard laboratory bioassays. The 48-hr EC₅₀s for each species/stage in order of increasing sensitivity were adultD. magna — 2.52 g/L;D. magna (48-hr old) — 0.83 g/L; adultD. galeata mendotae — 0.29 g/L; adultC. lacustris — 0.21 g/L;D. galeata mendotae (48-hr old) — 0.16 g/L; adultDiaptomus oregonensis — –0.12 g/L. No toxicity was observed when these organisms were exposed to a range of concentrations of the emulsifiable concentrate without fenvalerate (the EC blank).Rates of filtration of the¹⁴C-labelled alga,Chlamydomonas reinhardii byD. galeata mendotae, C. lacustris andD. oregonensis were decreased significantly at sublethal concentrations of fenvalerate after only 24-hr exposure.Ceriodaphnia lacustris showed the greatest sensitivity with rates of filtration significantly decreased at 0.01 g fenvalerate/ L. Concentrations of fenvalerate 0.05 g/L resulted in decreased rates of filtration byD. galeata mendotae. A concentration of 0.10 g fenvalerate/ L caused rates of filtration to increase inD. oregonensis. whereas 0.05 and 0.5 g/L resulted in a decrease in these rates.Rates of assimilation of algae byD. galeata mendotae, C. lacustris andD. oregonensis exposed to similar concentrations of fenvalerate were decreased at concentrations 0.05 g fenvalerate/L. Changes in rates of assimilation were not as sensitive a parameter of toxicity as changes in rates of filtration. The EC blank had no significant effects on rates of filtration or assimilation for all three species.     

Copper/Metal Ratios in the Gills of Rainbow Trout (Oncorhynchus mykiss) Provide Evidence of Copper Exposure Under Conditions of Mixed-Metal Exposure

Previous work has suggested that the ratio of copper residues to zinc in the gills of rainbow trout may indicate short-term exposure to increased levels of waterborne copper. However, the effect of exposure to a combination of increased copper and zinc concentrates in the water column was unknown. We exposed rainbow trout to 8 ± 2 g L^–1, 40 ± 2 g L^–1 and 90 ± 9 g L^–1 of waterborne copper and 21 ± 3 g L^–1, 129 ± 40 g L^–1, and 202 ± 40 g L^–1 of waterborne zinc in a 2-factor experiments and gill copper and zinc residues were examined. Other gill parameters analyzed included the concentrations of calcium, magnesium, sodium, and potassium, liver copper and zinc concentrations and plasma copper, calcium, sodium, and potassium are also reported here. Copper residues in the gill filaments were significantly higher in the highest level of copper exposure (high Cu, 4.06 g g^–1; low Cu 2.41 g g^–1; 0 Cu 2.01 g g^–1; P = 0.001), whereas no differences were seen in zinc concentrations at any treatment level. Gill sodium and plasma calcium concentrations were also decreased at the highest waterborne copper concentrations. Although copper–zinc ratios in the gills were significantly different between the highest and lowest copper treatments (P = 0.002, F = 6.59), copper–sodium and copper–magnesium ratios were more sensitive to waterborne copper exposure (P = 0.001, F = 17.91 and P = 0.002, F = 15.45, respectively). These copper–metal ratios may be better indicators of copper loading in the water column.     

Effects of methylmercury on neurodevelopment in Japanese children in relation to the Madeiran study

Objectives: A cross-sectional study was carried out to assess the effects of methylmercury exposure on neurodevelopment in Japanese children, in relation to the Madeiran cross-sectional study, and to estimate benchmark dose (BMD) levels using the data of two studies. Methods: Mercury levels in hair samples obtained from 327 Japanese mothers and their 7-year-old children, and methylmercury levels in the umbilical cord, were determined. Neurodevelopmental examinations, including the brainstem auditory evoked potential (BAEP), were performed on the children. Results: The medians of hair mercury were 1.63 (0.11–6.86) g/g for mothers and 1.65 (0.35–6.32) g/g for children, and a significant correlation was seen between the hair mercury levels in mothers and children. The maternal hair mercury was significantly correlated with the methylmercury in the umbilical cords obtained from 49 children. In 210 children whose mothers had not changed their dietary habits since pregnancy, most of the neurodevelopmental variables were not significantly related to hair mercury levels. The BAEP latencies were significantly shorter in the Japanese children than in the 113 Madeiran 7-year-old children, whose mothers had hair mercury of 1.12–54.5 (median 10.9) g/g. Significant relationships between the maternal hair mercury level and BAEP latencies (peaks III and V, and interpeak I–III) were found only in the merged data of Japanese and Madeiran children. When the lower 95% confidence limit of BMD (BMDL) was calculated, the BMDLs of mercury exposure for BAEP latencies in the merged data were between 6.9 and 10.5 g/g, and lower than those in the Madeiran children. Conclusions: It is suggested that Japanese children may ingest similar doses per body weight of methylmercury to their mothers. If maternal hair mercury was used as a proxy for mercury exposure at birth, no significant dose–effect associations with the BAEP latencies were observed in Japanese children with exposure levels below 6.9 g/g of hair mercury, but only when higher-level exposures from Madeiran children were included. The BMDL was lower for the merged data than for Madeiran children alone.     

In vitro susceptibility of mycelial and yeast forms of Penicillium marneffei to amphotericin B,fluconazole, 5-fluorocytosine and itraconazole

The mycelial (25°C) and yeast-like (37°C) forms of Penicillium marneffei clinical and type strains were investigated for their in vitro susceptibility to amphotericin B (AmB), 5-fluorocytosine (5-FC), fluconazole (FLU) and itraconazole (ITZ), using Bacto antibiotic medium 3, yeast-nitrogen, Sabouraud's dextrose (pH 5.7) and high resolution (pH 7.1) broth media (1ml/tube), respectively. Results indicated that the minimal inhibitory and minimal fungicidal concentrations (MICs and MFCs) for the mycelial cultures of P. marneffei to AmB were in the range 0.78–1.56 and 0.78–3.125 g/ml, respectively, as against 3.125–25 g (MICs) for the yeast form cultures. The MFCs to AmB for the yeast form were one dilution higher. The MICs to FLU were generally lower for the yeast form (6.25–25 g) than the mycelial form (25–50 g/ml), whereas MFCs for the mycelial cultures were > 100 g as compared to 6.25–100 g for their yeast form. The MICs for the mycelial form to 5-FC ranged from < 0.195–0.39 g. Higher MICs (6.25 g) were recorded for their yeast form. The MFCs to 5-FC for the yeast form were 25–100 g/ml. The MICs for the mycelial form to ITZ ranged from < 0.195 to 3.125 g/ml. Higher values (< 0.195–50 g) were recorded for their yeast-like form. The MFCs to ITZ for mycelial and yeast forms ranged from < 0.195–0.39 and 25–100 g/ml, respectively. Results indicate that P. marnefei's yeast form is more sensitive to FLU and ITZ (8 of 10 strains) while the mycelial form displayed greater susceptibility to AmB and 5-FC. The MICs for ITZ remained steady in SD medium, pH 5.7 to 7.1. However, some strains gave higher MIC values (0.39–1.56 g/ml) when tested in the HR.     

Comparative Embryonic and Larval Developmental Responses of Estuarine Shrimp (<Emphasis Type="Italic">Palaemonetes pugio</Emphasis>) to the Juvenile Hormone Agonist Fenoxycarb

Grass shrimp (Palaemonetes pugio) were reared separately through both embryonic and total larval development during exposure to fenoxycarb at measured concentrations of <2.2 to 888 g L^–1. A fenoxycarb concentration of 888 g L^–1 significantly (p < 0.05) inhibited embryonic development to larval hatching and extended the embryonic developmental period from 11.9 to 12.7 days. Exposure to fenoxycarb concentrations 502 g L^–1 had no significant (p > 0.05) effect on complete embryonic development. Significantly fewer shrimp successfully metamorphosed to postlarvae when exposed through complete larval development to fenoxycarb concentrations 4 g L^–1. Larval development of grass shrimp was therefore >2 orders of magnitude more sensitive to this juvenile hormone agonist than was embryonic development. Viability of larvae developing in fenoxycarb was concentration dependent. Development beyond third zoeal stage was significantly inhibited at fenoxycarb concentrations 190 g L^–1, whereas development beyond fourth zoeal stage was inhibited by a concentration of 45 g L^–1. Fenoxycarb exposure of developing larvae did not alter either the duration of total larval development or the total number of larval stages before metamorphosis. Rearing of fenoxycarb-exposed embryos through larval development without further exposure had no significant effect on number of larval stages, larval development rate, or metamorphic success of larvae. Similarities in the sensitivity of grass shrimp larvae and mosquito larvae to fenoxycarb suggests that the use of a bioassay protocol measuring the metamorphic success of crustacean larvae would be a valuable adjunct to the hazard assessment of newly developed pesticides that target endocrine control of metamorphosis in insects and possibly other endocrine-disrupting xenobiotics as well.     

Chronic ecotoxicity of copper and cadmium to the zebra mussel Dreissena polymorpha

In order to evaluate ecological consequences of the long-term presence of metals in aquatic ecosystems, we investigated the filtration rate and survival of zebra mussels (Dreissena polymorpha) during chronic exposure to Cu and Cd. The filtration rate was measured once a week in laboratory experiments lasting 9–11 weeks. The lowest Cu concentration tested (13 g/L) did not affect the filtration rate and survival of D. polymorpha, but the lowest Cd concentration (9 g/L) did affect the filtration rate, but had no effect on survival. The EC₅₀ for Cd decreased markedly from 388 g/L to 27 g/L when the exposure time was lengthened from 48 hours to 10 weeks. The largest decrease in EC₅₀ for Cd was observed during the first week of exposure. In contrast, the EC₅₀ for Cu did not decrease with increasing exposure time (chronic EC₅₀: 43 g/L). Since the chronic LC₅₀ for Cd was 130 g/L, the filtration rate appeared to be a far more sensitive endpoint for ecotoxicological laboratory experiments than mortality. D. polymorpha was capable of regulating the body concentration of the essential metal Cu at low concentrations in the water (13 g/L). Cd was accumulated at every Cd concentration in the water, suggesting that Cd could not be regulated by D. polymorpha. It is concluded that the relation between short-term and long-term ecotoxicity was different for each metal and could not be predicted from the results of the short-term experiments.     

Indoor air mercury concentrations following application of interior latex paint

Mercury vapors are released from paint containing mercury compounds used to prolong the shelf-life of interior latex paint. To determine whether homes recently painted with paint containing mercury had elevated indoor-air mercury concentrations, we studied 37 Ohio homes. Twenty-one homes painted with mercury-containing paint a median of 86 days earlier were compared with 16 homes not recently painted with mercury-containing paint. Paint samples from the exposed homes contained a median of 210 mg Hg/L (range 120–610 mg/L). The median air mercury concentration was higher in the exposed homes (0.3 g/m³; range nondetectable-1.5 g/m³) than in the unexposed homes (nondetectable; range nondetectable-0.3 g/m³, P < 0.0001). Among the exposed homes there were seven in which paint containing <200 mg/L had been applied. In these homes, the median air mercury concentration was 0.2 g/m³ (range nondetectable-1 g/m³). Six (33%) exposed homes had air mercury concentrations >0.5 g/m³, the acceptable indoor concentration recommended by the Agency for Toxic Substances and Disease Registry. Elemental mercury was the form of mercury released into the air. These data demonstrate that potentially hazardous mercury exposure may occur in homes recently painted with paint that contains mercury concentrations <200 mg/L.     

Contaminant levels in harbor seals from the northeastern United States

The concentrations of polychlorinated biphenyls (PCBs), organochlorine pesticides, polycyclic aromatic hydrocarbons (PAHs), polychlorinated dibenzofurans (PCDF), polychlorinated dibenzo-p-dioxins (PCDD), and mercury (Hg) were determined in blubber and liver tissues of harbor seals (Phoca vitulina) collected along the northeast coast of the U.S. Average PCB concentrations in seal blubber (sum of congeners) were 12.0 g/g (wet weight) with a range of 7.30 to 24.3 g/g in 1980 and 6.66 g/g (wet weight) with a range of 2.61 to 11.3 g/g in 1990–1992. Comparisons between blubber data from this study and previous work indicated that the concentration of PCBs along the northeast coast of the U.S. may have decreased over the past twenty years.The average p,p-DDE concentrations in seal blubber were 10.9 g/g (wet weight) in 1980 with a range of 6.95 to 21.9 g/g and 4.12 g/g (wet weight) with a range of 1.83 to 7.84 g/g in 1990–1992. Only trace amounts of PCDFs and PCDDs were found in a few blubber samples; levels in most tissues were below detection (3–5 pg/g) (wet weight). Trace amounts (<30 ng/g) of phenanthracene, anthracene, and alkylated MW-178 compounds were found in some seal samples; all other PAH compounds were below the detection level (5–15 ng/g).Toxic equivalents (TEQ) of selected coplanar and mono-ortho PCB congeners and relative toxic equivalents (RTE) (pg total TEQ/g total PCB) were calculated, using recently proposed dioxin toxic equivalent factors (Ahlborg et al. 1994). The TEQs ranged from 41 to 315, and the RTEs ranged from 2.25 to 16.3. The RTEs for seal blubber indicated that the present values were in the midrange of those reported in the literature. Toxic equivalents calculated on the basis of the concentrations of the coplanar PCBs, PCDDs, and PCDFs indicated that coplanar PCBs, rather than PCDDs and PCDFs, may pose a more important toxic threat to harbor seals.Mercury levels in liver tissue averaged 70.0 g/g (wet weight) and 44.1 g/g (wet weight) in the 1991 and 1980 samples, respectively, and are similar to those found in relatively polluted waters of the British Isles.     

Toxicity of mercury,copper, nickel,lead, and cobalt to embryos and larvae of zebrafish,Brachydanio rerio

The toxicity of mercury (HgCl₂), copper (CuCl₂: 5 H₂O), nickel (NiSO₄: 6 H₂O), lead (Pb(CH₃COO)₂: 3 H₂O) and cobalt (CoCl₂: 6 H₂O) was studied under standardized conditions in embryos and larvae of the zebrafish,Brachydanio rerio. Exposures were started at the blastula stage (2–4 h after spawning) and the effects on hatching and survival were monitored daily for 16 days. Copper and nickel were more specific inhibitors of hatching than cobalt, lead, and mercury. Nominal no effect concentrations determined from the dose-response relationships (ZEPs, Zero Equivalent Points) for effect on hatching time were 0.05 g Cu/L, 10 g Hg/L, 20 g Pb/L, 40 g Ni/L and 3,840 g Co/L, and those for effect on survival time were 0.25 g Cu/L, 1.2 g Hg/L, 30 g Pb/L, 80 g Ni/L, and 60 g Co/L. The no effect concentrations for Ni, Hg and Pb are consistent with previously reported MATC values for sensitive species of fish. The no effect concentrations for copper are 1–2 orders of magnitude lower than previously reported values. The major reason for the latter discrepancy was considered to be the absence of organics that can complex copper ions in the reconstituted water that we used, which had a hardness of 100 mg/L (as CaCO₃) and a pH of 7.5–7.7. Unexposed controls were started with embryos from different parental zebrafishes and the parental-caused variability in early embryo mortality, median hatching time and median survival time were estimated.     

Hazardous exposure of ground-living small mammals to cadmium and lead in contaminated terrestrial ecosystems

The dietary exposure to cadmium and lead of two ground-living species of small mammals,i.e., shrewsSorex araneus (Insectivora) and volesMicrotus agrestis (Rodentia), was investigated and related to metal loads in target organs (kidneys and liver). The study was done in two natural areas polluted with cadmium and lead originating from urban and industrial metal sources. The average intake of cadmium by the herbivorous voles varied between 0.1 and 0.4 g/g/day and of lead between 2 and 10 g/g/day. The carnivorous shrews showed a considerably higher metal intake rates,i.e., cadmium 3 to 16 g/g/day and lead 19 to 53 g/g/day, which was largely due to the consumption of contaminated earthworms (Oligochaeta). An average cadmium intake of 15 g/g/day or a lead intake of 20 g/g/day corresponded with critical renal metal loads of 120 g/g for cadmium and 25 g/g for lead, which are indicative of adverse health effects. The renal metal loads in shrews reached the critical level, but they remained far below this level in voles. The results indicate a greater risk of toxic exposure to cadmium and lead in soricine shrews than in microtine rodents.     

Biological monitoring of isocyanates and related amines

Summary Five men were exposed to toluene diisocyanate (TDI) atmospheres for 7.5 h. The TDI atmospheres were generated by a gas-phase permeation method, and the exposures were performed in an 8-m3 stainless-steel test chamber. The mean air concentration of TDI was ca. 40 g/m³, which corresponds to the threshold limit value (TLV) of Sweden. The inhaled doses of 2,4- and 2,6-TDI were ca. 120 g. TDI in the test chamber air was determined by an HPLC method using the 9-(N-methyl-aminomethyl)-anthracene reagent and by a continuous-monitoring filter-tape instrument. After hydrolysis of plasma and urine, the related amines, 2,4- and 2,6-toluenediamine 2,4-, and 2,6-TDA), were determined as pentafluoropropionic anhydride (PFPA) derivatives by capillary gas-chromatography using selected ion monitoring (SIM) in the electron-impact mode. The urinary elimination of the TDAs showed a possible biphasic pattern, with rapid first phases for 2,4-TDA (mean t _1/2 for the concentration in urine, 1.9 h) and for 2,6-TDA (mean t _1/2 for the concentration in urine, 1.6 h). The cumulative amount of 2,4-TDA excreted in urine within 28 h ranged from 8% to 14% of the estimated dose of 2,4-TDI, and the cumulative amount of 2,6-TDA in urine ranged from 14% to 18% of the 2,6-TDI dose. The average urinary level of 2,4-TDA was 5 g/l in the 6 to 8-h sample (range 2.8–9.6 g/l), and the corresponding value for 2,6-TDA was 8.6 g/l (range, 5.6–16.6 g/l). Biological monitoring of exposure to 2,4- and 2,6-TDI by analysis of 2,4- and 2,6-TDA in urine is feasible.     

Estimation of mercury dose by a novel quantitation of elemental and inorganic species released from amalgam

Amalgam fillings constitute, after food, the main source of exposure to mercury for the general population. An evaluation of potential health risks has to be based on the dose of mercury released from the fillings. This dose is estimated by a new procedure of mercury speciation which elutes the released elemental and inorganic mercury with solvents of different polarity (paraffin and saline). In vitro tests with spherical amalgam pellets have shown that mercury release into the solvents is linearily correlated to time and amalgam surface area. Doses estimated in volunteers by this method average 4.5 g/day (range 0.3–13.9), as compared to a dose of 3.4 g/day (range 0.1–11.8) measured conventionally in the oral air. The aforementioned dose, combined with the nearly equal mercury uptake from food, is below the acceptable daily intake of 40 g for all forms of mercury.German patent nr. 4323072     

Cytogenetic examination of leucocytes of workers exposed to mercury vapour

Summary Cytogenetic observations have been performed on male subjects occupationally exposed to elemental mercury in a plant where mercury is amalgamated with zinc and in a chloralkali plant [n=22; average level of mercury in urine was 117 g/g creatinine and of mercury in blood 3.1 g/100 ml; mean duration of Hg exposure 4 years (range: 0.3–15.3)]. The exposure to mercury vapour did not result in an increased yield of structural chromosomal aberrations in peripheral blood lymphocytes of the workers. These negative results are in agreement with the findings reported for other eukaryotic systems and confirm that population monitoring based on cytogenetic examination of peripheral blood lymphocytes does not always represent a good indicator of damage to genetic material produced by a chemical.