Urinary mercury levels in females: influence of skin-lightening creams and dental amalgam fillings

The influence of application of skin-lightening creams and dental amalgam fillings on the urinary mercury (Hg) level was evaluated in 225 females (ages 17 to 58 years) living in Riyadh, capital of Saudi Arabia. The arithmetic mean of the urinary Hg level was 6.96 +/- 20.43 micrograms 1(-1), in the range 0 to 204.8 micrograms 1(-1). The mean urinary Hg level adjusted by creatinine (Cr) was 11.22 +/- 37.23 micrograms g-1 Cr, in the range 0 to 459.37 micrograms g-1. No significant difference in urinary Hg was noted between the females regarding the use of skin-lightening creams. On the other hand, results showed that urinary Hg concentration was influenced by the use and number of dental amalgam fillings. No women were identified with symptoms or signs that could be attributed to Hg intoxication. Urine analyses for creatinine, urea, uric acid, phosphorus, magnesium, glucose and calcium showed significant correlation with urinary Hg. This suggests that chronic exposure to Hg may be associated with a deterioration of renal function.     

Association between the clastogenic effect in peripheral lymphocytes and human exposure to arsenic through drinking water

We describe the association between structural chromosome aberrations (CAs) and parameters of exposure to arsenic among 42 individuals exposed to arsenic through well waters in Finland. The median concentration of arsenic in the wells was 410 microg/l, the total arsenic concentrations in urine (As-tot) was 180 microg/l, and in hair 1.3 microg/g, for current users (n = 32) of contaminated wells. Urinary arsenic species and CAs were also analyzed in eight control individuals from the same village who consumed water which contained arsenic <1.0 microg/l (detection limit). Increased arsenic exposure, indicated best by increased concentrations of arsenic species (inorganic arsenic, methylarsonic acid (MMA), dimethylarsinic acid (DMA)) in urine, was associated with increased frequency of CAs. The increased urinary ratio of MMA/As-tot and the decreased ratio of DMA/As-tot were associated with increased CAs when all aberration types, including gaps, were considered. Associations between CAs and arsenic exposure indicators were stronger among current users than among persons who had stopped using the contaminated well water for 2-4 months before sampling (ex-users, n = 10). Furthermore, there was a positive but not statistically significant association between CAs and arsenic in hair among the current users, but not among the ex-users, who still had relatively high arsenic concentrations in hair. The results suggest that the effect observed in the present study reflects relatively recent arsenic exposure.     

Mercury exposure from dental amalgam fillings: absorbed dose and the potential for adverse health effects

This review examines the question of whether adverse health effects are attributable to amalgam-derived mercury. The issue of absorbed dose of mercury from amalgam is addressed first. The use of intra-oral Hg vapor measurements to estimate daily uptake must take into account the differences between the collection volume and flow rate of the measuring instrument and the inspiratory volume and flow rate of air through the mouth during inhalation of a single breath. Failure to account for these differences will result in substantial overestimation of the absorbed dose. Other factors that must be considered when making estimates of Hg uptake from amalgam include the accurate measurement of baseline (unstimulated) mercury release rates and the greater stimulation of Hg release afforded by chewing gum relative to ordinary food. The measured levels of amalgam-derived mercury in brain, blood, and urine are shown to be consistent with low absorbed doses (1-3 micrograms/day). Published relationships between the number of amalgam surfaces and urine levels are used to estimate the number of amalgam surfaces that would be required to produce the 30 micrograms/g creatinine urine mercury level stated by WHO to be associated with the most subtle, pre-clinical effects in the most sensitive individuals. From 450 to 530 amalgam surfaces would be required to produce the 30 micrograms/g creatinine urine mercury level for people without any excessive gum-chewing habits. The potential for adverse health effects and for improvement in health following amalgam removal is also addressed. Finally, the issue of whether any material can ever be completely exonerated of claims of producing adverse health effects is considered.     

Evaluation of the critical body burden concept based on inorganic and organic mercury toxicity to rainbow trout (Oncorhynchus mykiss)

Subadult rainbow trout (Oncorhynchus mykiss) were exposed to four waterborne concentrations each of 64-426 microg/L mercuric chloride (HgCl2) and 4-34 microg/L methylmercury chloride (CH3HgCl) until death to evaluate the critical body burden concept. Mean days to death for fish exposed to the highest and lowest concentrations of HgCl2 were 1 and 58 d, and 2 and > 100 d for fish exposed to CH3HgCl. Time to death was an important factor that influenced Hg tissue concentration, and was most evident among fish that died within a few days of exposure. Critical body burdens for Hg could be difficult to establish at the tissue level because no threshold concentrations were clearly indicated among the liver, kidney, spleen, brain, muscle, and gill that were monitored in this study. A critical burden for Hg was derived on a whole body basis for Hg in its organic form. An evaluation of this and other studies suggests whole body concentrations of 10-20 mg/kg Hg could be lethal to fish. Extrapolation from other studies indicate whole body concentrations of 1-5 mg/kg Hg could have chronic effects on fish and possibly other aquatic organisms. This concept could be used to assess the toxicological significance of chemical concentrations that are monitored in feral aquatic organisms. The tissue-based approach appears to have some advantages over current assessment protocols that focus on waterborne concentrations.     

Renal effects of environmental and occupational lead exposure

Environmental and industrial lead exposures continue to pose major public health problems in children and in adults. Acute exposure to high concentrations of lead can result in proximal tubular damage with characteristic histologic features and manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. A high incidence of nephropathy was reported during the early part of this century from Queensland, Australia, in persons with a history of childhood lead poisoning. No such sequela has been found in studies of three cohorts of lead-poisoned children from the United States. Studies in individuals with low-level lead exposure have shown a correlation between blood lead levels and serum creatinine or creatinine clearance. Chronic low-level exposure to lead is also associated with increased urinary excretion of low molecular weight proteins and lysosomal enzymes. The relationship between renal dysfunction detected by these sensitive tests and the future development of chronic renal disease remains uncertain. Epidemiologic studies have shown an association between blood lead levels and blood pressure, and hypertension is a cardinal feature of lead nephropathy. Evidence for increased body lead burden is a prerequisite for the diagnosis of lead nephropathy. Blood lead levels are a poor indicator of body lead burden and reflect recent exposure. The EDTA lead mobilization test has been used extensively in the past to assess body lead burden. It is now replaced by the less invasive in vivo X-ray fluorescence for determination of bone lead content.     

Effects of dental amalgam and its components of histamine release from human basophils and tissue mast cells

Recent studies have shown that metal ions can be released from dental amalgam or other dental materials, and can cause toxic effects on various cells. In this study, the effects of amalgam-conditioned culture medium (ACCM), components of amalgam (Ag+, Cu2+, Sn2+, Hg2+) and dental composite-conditioned culture medium (CCCM) on histamine release from human blood basophils (healthy subjects, n = 3) and tissue mast cells (n = 3) were analyzed. ACCM and CCCM were prepared using either fresh or 6-weeks-aged specimens. Of the metal ions tested, Ag+, and Hg2+ were found to induce histamine release from basophils (Ag+, 0.33 mM: 83 +/- 11% vs Hg2+, 0.33 mM: 100% vs control medium: 5 +/- 5%) and mast cells (Ag+, 0.33 mM: 91 +/- 16% vs Hg2+, 0.33 mM: 99 +/- 1% vs control: 2 +/- 1%), whereas no effects were seen with Cu2+ and Sn2+. Neither ACCM from freshly prepared amalgam nor ACCM from 6-weeks aged amalgam, produced histamine release in basophils or mast cells. Inductively coupled plasma atomic emission spectrometry (ICP) revealed that the Ag(+)- and Hg(2+)-concentrations in ACCM were below the range in which histamine release occurred. Similar to ACCM, no effects on basophils or mast cells were observed with CCCM. In summary, our data show that distinct metal ions present in dental amalgam, can induce (toxic) histamine liberation from basophils and mast cells. However, the amounts of metal ions released from amalgam apparently were too low, to cause histamine release.     

The future of dental amalgam: a review of the literature. Part 2: Mercury exposure in dental practice

This is the second article in a series of seven on the future of dental amalgam. It describes the means of exposure to mercury which can occur in dental surgeries from the storage of mercury, preparation and placement of dental amalgam restorations, polishing dental amalgam restorations, the removal of amalgam fillings and the storage of waste amalgam. It also reports on the monitoring of dental practices and studies on the mercury air levels in dental surgeries and blood and urine levels in dentists and their staff. Also, studies which compare these levels with the health and neurobehaviour of dentists and their staff are included. In addition, it discusses post-mortem studies of the mercury levels in body organs in dentists and controls. It then recommends methods for the safe handling of mercury and dental amalgam. Finally, it discusses the issues surrounding the release of mercury into the environment from dental practices and industry.     

Occupational exposure to mercury in dentistry and dentist mortality

In response to public concern, Health Canada recently conducted a review of amalgam safety and released a position statement entitled The Safety of Dental Amalgam. Essentially, the department has concluded that the levels of mercury absorbed by the body due to the release of mercury vapor from amalgam restorations, while detectable, do not approach those recognized to cause illness. It has therefore confirmed that amalgam restorations can be used safely in most patients, with some notable caveats. Despite Health Canada's position statement in support of amalgam, patient doubts about amalgam safety remain, including the tenuous hypothesized link between amalgam restorations and specific diseases. This article reviews the available studies of dentist mortality to identify possible links between mercury exposure and negative health effects. A lack of evidence to suggest a detrimental health outcome in dentists who are occupationally exposed to higher levels of mercury than their patients, and are known to have higher levels of mercury in their blood, provides an important reassurance concerning the safety of amalgam. The reviewed data indicates that the 10 leading causes of death in the United States and Canada are the same for both dentist and non dentist population groups, and that the percentage of deaths by the same cause are remarkably similar. By 1975, the year of the most recent U.S. study, the average age at death for white male dentists was about three years higher than for all adult white males. Although suicide standard mortality rates are known to be higher for dentists, suicide deaths have also been shown to be a factor in many other occupations, particularly those where there is easy access to drugs. Although updated actuarial data for dentist mortality are needed, the available data indicate no reduction in the life expectancy of practising dentists, nor any specific or disproportionate rates of disease associated with high mercury exposure. In fact, the available mortality studies are generally optimistic about the health of dentists, which should reassure patients about the safety of dental amalgam.     

Psychologic factors in the etiology of amalgam illness

Eleven patients with amalgam illness aged 33-50 years were investigated by psychodynamic methods. Six of them, all women, were dental nurses and hygienists exposed to amalgam/mercury both from their own dental fillings and occupationally. Four men and one woman were exposed only to amalgam/mercury from their own fillings. Assays of mercury in urine samples and in the ambient air during work routines involving the heaviest exposure indicated that the exposure was far below the levels at which even subclinical symptoms could be indicated by psychometric tests. The psychologic investigation indicated that the symptoms of amalgam illness were psychosomatic. All patients had experienced important psychic traumata in close connection with the first appearance of symptoms. It can be concluded from the psychodynamic dialogues that they had not been able to mourn for a loss in an adequate manner and that the body had been forced to symbolize the great pain in their souls.     

Dental care using silver amalgam

Dental amalgam is the most widely used filling material in dentistry. In our country there are an estimated 40 million amalgam fillings in place. The mercury present in these fillings has caused health concerns over the last 160 years that amalgam has been used in decayed teeth. The fears have always proven to be unjustified and no harmful effects have ever been demonstrated in dental patients. Mercury can be found in several forms. In dentistry, only the metallic form is used, while inorganic and organic compounds are also present in the environment. The metallic form is absorbed in the human body mostly through the lungs. Once mercury reaches toxic levels inside the body, it will interfere with cell metabolism. Most important among the target organs are the brain, the liver and the kidneys. Elimination occur through urine and feces. Mercury is universally found in blood and urine. The concentration depends on absorption by air, water, nutrition, medication (including dental fillings) and occupational hazards. There are four kinds of objectives to dental amalgam: oral galvanism, toxicity, allergenicity and ecological grievances. Disorders from oral galvanism are difficult and delicate to evaluate as the actual currents are very small. Furthermore, no significant difference can be found in current intensity between patients with and without complaints. Finally patients with complaints often present other oral disorders, the treatment of which most often eliminates all complaints that could be attributed to oral galvanism. Toxicity is dose dependent. Industrial safety rules indicate that the amount of mercury absorbed from dental amalgam fillings is far below the safety level. HgB and HgU levels in patients with amalgam fillings are situated well below the acceptable levels. Allergic disorders are observed in patients with amalgam fillings but far less than expected in view of the wide spread use of dental amalgam. The problem of mercury spilling from dental amalgam fillings into the environment will be resolved by strict legislation in the near future. In this context, it can be stated that the use of dental amalgam is safe and justified. Furthermore, it is also advisable as no other material can meet the actual dental needs as efficiently as can dental amalgam.     

DMPS-arsenic challenge test. I: Increased urinary excretion of monomethylarsonic acid in humans given dimercaptopropane sulfonate

The purpose of the present study was to evaluate in a novel manner the arsenic exposure of humans living in two towns in Northeastern Chile. Residents of one town drink water containing 593 microg As/l. Those in the control town drink water containing 21 microg As/l. Our hypothesis was that the administration of the chelating agent, 2,3-dimercaptopropane-1-sulfonic acid, Na salt (DMPS, DIMAVAL) would increase the urinary excretion of arsenic, alter the urinary profile of arsenic species and thus result in a better indication of the body load of arsenic and a better biomarker for arsenic exposure. The method used to evaluate these subjects was to give them 300 mg DMPS by mouth, after an overnight fast, and collect urine at specified time periods. The urine samples were analyzed for inorganic arsenic, monomethylarsonic acid (MMA), dimethylarsinic acid (DMA) and total arsenic by hydride generation and atomic absorption spectrophotometry. The results indicated that: 1) During the 2-hr period after DMPS administration, MMA represented 42%, inorganic As, 20 to 22% and DMA, 37 to 38% of the total urinary arsenic. The usual range of the MMA percentage in human urine has been 10 to 20%. The % MMA increased almost equally for both the arsenic-exposed and control subjects. 2) The exposed subjects had a greater urinary excretion of total arsenic, before and after DMPS administration, than the control subjects. 3) Although buccal cells were obtained only from a few subjects, the prevalence of mononucleated buccal cells, an indication of genotoxicity, was 5-fold greater for those who consumed drinking water with the higher arsenic content than among control subjects. Our conclusions are that 1) DMPS has a highly specific effect in humans on MMA metabolism and/or urinary excretion; 2) the human body stores substantial amounts of arsenic; and 3) the urinary arsenic concentration after DMPS administration may be more indicative of the body burden of arsenic because it was greater than that found before DMPS was given.     

Human exposure to mercury: a critical assessment of the evidence of adverse health effects

The ubiquitous nature of mercury in the environment, its global atmospheric cycling, and its toxicity to humans at levels that are uncomfortably close to exposures experienced by a proportion of the population are some of the current concerns associated with this pollutant. The purpose of this review is to critically evaluate the scientific quality of published reports involving human exposures to mercury and associated health outcomes as an aid in the risk evaluation of this chemical. A comprehensive review of the scientific literature involving human exposures to mercury was performed and each publication evaluated using a defined set of criteria that are considered standards in epidemiologic and toxicologic research. Severe, sometimes fatal, effects of mercury exposure at high levels were primarily reported as case studies. The disasters in Minamata, Japan, in the 1950s and in Iraq in 1971-1972 clearly demonstrated neurologic effects associated with ingestion of methylmercury both in adults and in infants exposed in utero. The effects were convincingly associated with methylmercury ingestion, despite limitations of the study design. Several well-conducted studies have investigated the effects of methylmercury at levels below those in the Iraq incident but have not provided clear evidence of an effect. The lower end of the dose-response curve constructed from the Iraq data therefore still needs to be confirmed. The studies of mercury exposure in the workplace were mainly of elemental or inorganic mercury, and effects that were observed at relatively low exposure levels were primarily neurologic and renal. Several studies have investigated effects associated with dental amalgam but have been rated as inconclusive because of methodologic deficiencies. In our overall evaluation, 29 of 110 occupational studies and 20 of 54 studies where exposure occurred in the natural environment provided at least suggestive evidence of an exposure-related effect.     

Equilibrium vapour pressure of mercury from dental amalgam under loading conditions

Earlier studies have failed to establish a consensus on the amount of mercury vapour released from dental amalgam restorations. The purpose of this study was to accurately and quantitatively measure the equilibrium mercury vapour pressure from dental amalgam. The vapour pressure was measured using a quartz crystal microbalance as a function of the load from 0-5.4 MPa. Auger spectra were collected of the as-formed and argon ion sputter cleaned dental amalgam surface. For the as-formed surface the mercury vapour density is zero with no load and increases to 0.6 microg m(-3) at 5.4 M Pa. Following cleaning the mercury, vapour density increased to a maximum value of 15 microg m(-3). The Auger spectra of the as-formed surfaces were dominated by features associated with carbon and oxygen. These spectral results in concert with the mercury vapour density measurements indicate that the oxide film on the as-formed surfaces inhibited the release of mercury vapour. The results of this experiment provide an upper limit for the amount of mercury vapour released by dental amalgams. Under conditions simulating the oral cavity this value would be reduced by oxides that form on the surface of dental amalgam restorations.     

Risk estimation of mercury intake from different sources

Biological monitoring of mercury (Hg) in blood, urine and hair was performed in volunteers with amalgam fillings, in subjects who consumed fish and in Hg-exposed workers. It was found that both amalgam fillings and the consumption of fish burden the organism with Hg in the same order of magnitude. The Hg concentrations in urine in the occupationally exposed group were higher by a factor of about 100 compared to the group with amalgam fillings. No pathological changes were found in the exposed workers. It seems safe to conclude that no health-related problems from Hg are to be expected from amalgam fillings.     

Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice: dose-response studies

Six groups of genetically mercury-susceptible female SJL/N (H-2s) mice were exposed to mercury vapor at a concentration of 0.3-1.0 mg Hg/m3 air for 0.5-19 hr/day 5 days a week for 10 weeks. The absorbed doses were calculated to be between 75 and 2365 micrograms Hg/week/kg body wt (micrograms Hg/week/kg). The correlation between the dose and the concentration of Hg in kidney, spleen, and thymus was highly significant (p < 0.0001; Spearman's rank correlation test). The lowest observed adverse effect level (LOAEL) for serum IgG antinucleolar antibodies (ANoA) was 170 micrograms Hg/week/kg, corresponding to a renal mercury concentration of 4.0 +/- 0.76 micrograms Hg/g wet wt. The correlation between the absorbed dose and the ANoA titer was highly significant (p < 0.0001; Spearman's rank correlation test), and all mice were ANoA-positive at a dose of 480 micrograms Hg/week/kg. High-titer ANoA targeted the nucleolar 34-kDa protein fibrillarin. The LOAEL for B-cell stimulation, measured as an increase in serum IgG2a and IgG1 concentrations, was 360 micrograms Hg/week/kg, but the increase was fivefold higher and also included IgE at a dose of 690 and 2365 micrograms Hg/week/kg. The serum Ig concentrations peaked after 2-4 weeks and then slowly declined but, except for IgE, remained significantly increased during the entire exposure time. Glomerular, mesangial IgG immune complex (IC) deposits, accompanied by systemic vessel wall IC deposits, were first detected at a dose of 480 micrograms Hg/week/kg. The mesangium also showed increased titers of IgM IC deposits and complement factor C3c. The correlation between the absorbed dose, and the individual titer of IgG, IgM, and C3c, was highly significant (p < 0.0001; Spearman's rank correlation test). In conclusion, mercury vapor efficiently induced an autoimmune syndrome in genetically susceptible mice, and the LOAEL for the adverse effects varied in the order ANoA < B-cell stimulation < IC deposits. Comparing the body burden of mercury in mice at the LOAEL for autoantibodies with the body burden in populations of occupationally exposed humans suggests that the safety margin may be narrow for genetically susceptible individuals.     

Acute exposure to mercury from amalgam: no short-time effect on the peripheral blood lymphocytes in healthy individuals

Mercury, released from dental amalgam, has been considered to adversely affect the human immune system. This study has been performed in order to evaluate if an acute low-dose mercury exposure, achieved by total amalgam removal in 10 healthy individuals, would affect the immunocompetent cells in human blood when the mercury level in blood and plasma was increasing. Induction of lymphocyte proliferation, measured as spontaneous de novo DNA synthesis, and total T cells, CD4+ T cells, CD8+ T cells, and B cells, was studied prior to and 7, 31, and 48 h after amalgam removal. In addition, the levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in serum/plasma were measured. Despite a significant increase of the plasma mercury levels within 24 h after intervention, no significant influence on the peripheral blood lymphocytes could be detected during the first 48 h. The serum IL-6 levels increased significantly within 48 h after intervention, but were still low and within normal range. No influence on the CRP levels up to 7 d after amalgam removal was detected.     

Effects of lifetime lead exposure on spatial and temporal visual function in monkeys

Detailed characterization of several aspects of visual function was performed in two groups of monkeys (Macaca fascicularis) exposed to lead continuously from birth. One group of four monkeys was dosed from birth onward with 500 microg/kg/day of lead as lead acetate, while another group of six monkeys was dosed with 2000 microg/kg/day. Blood lead levels peaked in the former group at 50 microg/dl early in life; the latter group had peak blood lead concentrations averaging 115 microg/dl during infancy. Blood lead concentrations decreased before one year of age to stable levels of 25 or 35 microg/dl in the low and high dose groups respectively. Spatial and temporal visual function was assessed using a psychophysical procedure at 7-9 years of age. Six age-matched controls were tested concurrently. Two treated monkeys had severe hyperopia: one was assessed on temporal vision only and the other was not assessed. Spatial data from a third monkey were considered suspect and excluded. Six of the nine treated monkeys in which temporal vision was assessed had thresholds below control values at low and/or middle frequencies under high luminance conditions. Low-luminance temporal vision was not affected. There was no evidence of impairment of spatial visual function in lead-exposed monkeys with normal refractive status at either high or low luminance. This study suggests that temporal visual function may be preferentially impaired as a result of lifetime exposure to a moderate body burden of lead, although these results require replication before definitive conclusions may be drawn.     

Lead exposure causes generation of reactive oxygen species and functional impairment in rat sperm

The relationships between blood lead, sperm lead, sperm reactive oxygen species (ROS) level, and sperm fertile capability were investigated to understand the effects of lead exposure on sperm function and the mechanism of these effects. Male Sprague-Dawley rats, 7 weeks old, were randomly divided into control group and lead-treated group. The controls and lead-treated animals received intraperitoneal injection of 10 mg sodium acetate and 10 mg lead acetate/kg body weight, respectively, weekly for 6 or 9 weeks. The blood lead and epididymal sperm lead were analyzed by graphite furnace atomic absorption spectrophotometer. Chemiluminescence was measured to evaluate the generation of sperm ROS. Sperm-oocyte penetration rate (SOPR) was measured to evaluate sperm function. After 6 weeks of lead exposure, the rats had average blood lead levels of 32 microg/dl, sperm lead levels of 0.67 +/- 0.11 microg/10(9) sperm, unchanged epididymal sperm counts, percent of motile sperms, and motile epididymal sperm counts compared with control animals. However, after 9 weeks of lead exposure, the rats had average blood lead levels of 48.0 +/- 4.3 microg/dl, sperm lead levels of 0.88 +/- 0.16 microg/10(9) sperm, statistically lower epididymal sperm counts, and lower motile epididymal sperm counts. There was a good correlation between the blood lead and sperm lead(r2 = 0.946, P < 0.001). The sperms of lead-exposed rats produced significantly higher counts ofchemiluminescence than did those from the control rats (P < 0.001). The chemiluminescence counts were positively associated with sperm lead level (r2 = 0.613, P < 0.001). Epididymal sperm counts, motility and motile epididymal sperm counts were negatively associated with sperm chemiluminescence (r2 = 0.255, 0.152, and 0.299; P < 0.01, 0.05, and 0.01, respectively). The SOPR were positively associated with epididymal sperm counts, motility and motile epididymal sperm counts (r2 = 0.136, 0.285, and 0.264; P < 0.05, 0.01, and 0.001, respectively). The sperm chemiluminescence was negatively associated with SOPR (r2 = 0.519, P < 0.001). It is concluded that lead exposure probably affected the sperm function by activating one of the pathways of ROS generation.     

Allylmercapturic acid as urinary biomarker of human exposure to allyl chloride

OBJECTIVE: To evaluate the use of urinary mercapturic acids as a biomarker of human exposure to allyl chloride (3-chloropropene) (AC). During three regular shut down periods in a production factory for AC, both types of variables were measured in 136 workers involved in maintenance operations. METHODS: Potential airborne exposure to AC was measured by personal air monitoring in the breathing zone. In total 205 workshifts were evaluated. During 99 workshifts no respiratory protection equipment was used. Mercapturic acid metabolites were measured in urinary extracts by gas chromatography-mass spectrometry (GC-MS). RESULTS: During 86 work shifts when no respiratory protection was used the air concentrations of AC were below the Dutch eight hour time weighted average (8 h-TWA) occupational exposure limit (OEL) of AC (3 mg/m3), whereas in 13 workshifts the potential exposure, as measured by personal air monitoring, exceeded the OEL (3.3 to 17 mg/m3). With the aid of GC-MS, 3-hydroxypropylmercapturic acid (HPMA) was identified as a minor and allylmercapturic acid (ALMA) as a major metabolite of AC in urine samples from the maintenance workers exposed to AC. The concentrations of ALMA excreted were in a range from < 25 micrograms/l (detection limit) to 3550 micrograms/l. The increases in urinary ALMA concentrations during the workshifts correlated well with the 8h-TWA air concentrations of AC (r = 0.816, P = 0.0001, n = 39). Based on this correlation, for AC a biological exposure index (BEI) of 352 micrograms ALMA/g creatinine during an eight hour workshift is proposed. In some urine samples unexpectedly high concentrations of ALMA were found. Some of these could definitely be attributed to dermal exposure to AC. In other cases garlic consumption was identified as a confounding factor. CONCLUSION: The mercapturic acid ALMA was identified in urine of workers occupationally exposed to airborne AC and the increase in ALMA concentrations in urine during a workshift correlated well with the 8 h-TWA exposure to AC. Garlic consumption, but not smoking, is a potential confounding factor for this biomarker of human exposure to AC.     

Cellular targets in response to dioxin exposure

Dioxins are contaminants present in a variety of environmental media. The 2,3,7,8-tetrachlorinated dibenzo-p-dioxin (TCDD) is biologically reactive at very low concentrations. This research is based on the use of innovative bioindicators able to evidence the exposure to TCDD by evaluating the biological effects on the embryonic development of the amphibious Xenopus laevis. TCDD exposure effects analyzed found that an Lc 50 value of 342 ng/l, TCDD concentrations up to 400 ng/l caused significative developmental delays. No significative teratogenic effects were found. X. laevis proved to be sensitive to the P-450 induction and alteration of glutathione levels at TCDD low doses (0.1-0.5 ng/l).