Relationship between mercury levels in blood and urine and complaints of chronic mercury toxicity from amalgam restorations.

AIM: To determine whether patients complaining of oral and medical symptoms perceived to be associated with chronic mercury toxicity have elevated mercury levels in their blood and urine. METHODS: The study group in this audit were 56 patients presenting to an oral medicine unit with complaints perceived to be related to chronic mercury toxicity. Their symptoms and co-morbidity were charted and mercury levels in blood and urine were biochemically tested by atomic absorption spectrophotometry. RESULTS: None had elevated mercury levels in blood or urine above the normal threshold level. Subgroup analysis showed subjects with oral lesions, autoimmune disorders and multiple sclerosis had relatively and significantly higher mercury levels within this cohort, but within the threshold values. When tested by multiple logistic regression adjusted for age and gender, mercury levels in blood or urine, numbers of amalgams were not significant for multiple sclerosis or previously diagnosed autoimmune disease. CONCLUSION: Mercury levels in blood and urine of this cohort of patients with perceived chronic mercury toxicity were within the normal range in accordance with a national laboratory threshold value.

Adjusting copper concentrations for caeruloplasmin levels in routine clinical practice.

BACKGROUND: An investigation on copper metabolism usually includes the measurement of serum levels of copper and caeruloplasmin. Using these levels, some laboratories derive levels of non-caeruloplasmin-bound copper (NCC); however, a considerable number of patients may show negative values, which is not physiologically possible. AIM: To derive an equation for adjusted copper in a manner similar to that widely accepted for adjusted calcium. METHODS: A linear regression equation for the relationship between caeruloplasmin and copper was used: [copper] (micromol/l) = 0.052x[caeruloplasmin] (mg/l). An equation for copper adjusted for caeruloplasmin was derived using this equation and the reference interval of 10-25 micromol/l for copper. RESULTS: The derived equation was [adjusted copper] (micromol/l) = [total copper] (micromol/l)+0.052x[caeruloplasmin] (mg/l)+17.5 (micromol/l). The adjusted copper concentrations on the 2.5th and 97.5th centiles were 12.7 and 21.5 micromol/l, respectively, with the population having a gaussian distribution. The relationship between NCC and the adjusted copper concentrations is linear and independent of caeruloplasmin concentration. CONCLUSION: Calculation of copper adjusted for caeruloplasmin uses the same variables as those for NCC. Accordingly, the problems that are caused by the lack of specificity of caeruloplasmin immunoassays are the same as those identified for NCC. This calculation, however, overcomes the negative values that are found in a considerable minority of patients with NCC, as well as age and sex differences in the caeruloplasmin reference interval. As the concept is already familiar to non-laboratory healthcare professionals in the form of calcium adjusted for albumin, this method is potentially less confusing than that for NCC.

Should all patients with unexplained anaemia be screened for chronic lead poisoning?

The global prevalence of lead poisoning is declining. However, the prevalence of lead poisoning in patients with either microcytic or normocytic anaemia is unknown. Blood samples from anaemic patients residing in south-east London without an obvious cause for anaemia had their blood lead concentration (BLC) analysed. A batch of 988 samples was analysed for BLC using atomic absorption spectroscopy. Median haemoglobin was 10.3 g/dL (range: 4.2-10.9) in females, 10.6 g/dL (range: 5.2-11.4) in males and 10.7 g/dL (range: 6.7-10.9) in children. Median BLC was 2.63 microg/dL (0.21-24.0 microg/dL; 95th centile 7.54 microg/dL). Fifteen samples (1.5%) had a BLC > 10.0 microg/dL, five samples (1%) > 15.0 microg/dL and one sample (0.1%) > 20.0 micrg/L. In the 106 children, median BLC was 2.34 microg/dL (0.5-14.5 microg/dL; 95th centile 6.12 microg/ dL). Only one child (14.5 microg/L) had a BLC > 10.0 pg/dL. There was a poor correlation between haemoglobin and BLC (r2 = 0.08). Routine screening for lead poisoning cannot be justified in all patients with unexplained anaemia, unless there is a history or clinical features to suggest lead toxicity. Additionally, we have shown that in this former high-risk area for lead exposure, there is a low point prevalence of significant lead poisoning, even in an anaemic population.

Mercury contamination incident.

BACKGROUND: The aim of this paper is to describe an incident where elemental mercury led to widespread contamination and the exposure of 225 individuals and confirmed toxicity in 19 individuals. The paper describes the incident and difficulties found in trying to assess the risk to individuals and to identify and decontaminate the residences involved. METHODS: All individuals exposed to elemental mercury in the incident were followed up for 15 months. RESULTS: Thirty-seven individuals were found to be 'at risk' and 13 were symptomatic of mercury poisoning. Five patients required chelation therapy. The incident was closed when the risk of poisoning and re-exposure was minimized. CONCLUSION: Incident management depends on early effective communication and collaboration between all agencies involved.

A case of lead poisoning due to snooker chalk.

A 3 year, 9 month old child with pica presented with a blood lead concentration of 1.74 micromol/l (360 microg/l). The source of poisoning was snooker chalk (lead content 7200 microg/g). She was treated with intravenous calcium disodium edetate chelation. Thirty months later her blood lead was 0.39 micromol/l (80 microg/l). This case illustrates the need to be vigilant for more unusual causes of lead poisoning in the home.

Clinical lead poisoning in England: an analysis of routine sources of data.

OBJECTIVE: To examine the occurrence of clinical lead poisoning in England based on routine sources of data. METHODS: Three routine data sources were examined, over different periods according to availability of data: (a) mortality for England, 1981-96; (b) hospital episode statistics data for England, for the 3 years 1 April 1992-31 March 1995; (c) statutory returns to the Health and Safety Executive under the reporting of injuries, diseases, and dangerous occurrences regulations (RIDDOR), also for the period 1 April 1992-31 March 1995. Also, analyses of blood lead concentrations carried out by the Medical Toxicology Unit, Guy's and St Thomas' Hospital Trust in London during the period 1 January 1991-31 December 1997 were examined. The analyses were performed both for industrial screening purposes and in response to clinicians' requests where lead poisoning was suspected. This is one of several laboratories carrying out such analyses in the United Kingdom. RESULTS: One death, of a 2 year old girl, was coded to lead poisoning in England during 1981-96. Analysis of hospital episode statistics data identified 83 hospital cases (124 admissions) over 3 years with any mention of lead poisoning, excluding two with admissions dating from 1965 and 1969. For these 83 cases the median hospital stay per admission was 3 days (range 0-115 days). Five were coded as having received intravenous treatment. Further clinical details of these cases beyond what is routinely recorded on the hospital episode statistics database were not available, except for blood lead concentrations in cases also identified on the Medical Toxicology Unit database. Eighteen cases (22%) were below 5 years of age of whom 10 (56%) came from the most deprived quintile of electoral wards. There was evidence to suggest spatial clustering of cases (p = 0.02). Six occupational cases were reported under RIDDOR in England during the period of study, two of whom were identified on the hospital episode statistics database. One further occupational case was identified on hospital episode statistics. Blood lead analyses for 4424 people carried out by the Medical Toxicology Unit (estimated at about 5% of such analyses in England over 7 years) found that among 547 children aged 0-4, 45 (8.2%) had a blood lead concentration in excess of 25 micrograms/dl, the action level in the United Kingdom for investigation, or removal of environmental sources of lead. At all ages, there were 419 (9.5%) such people, including 106 adults with no mention of industrial exposure. CONCLUSIONS: Both mortality and hospital admission ascribed to lead poisoning in England are rare, but cases continue to occur and some, at least, seem to be associated with considerable morbidity. Lead poisoning was confirmed as a probable cause of clinical signs and symptoms in only a small proportion of those in whom a blood lead concentration was requested. Where indicated, appropriate remedial action for the safe removal of environmental sources of lead should be taken.

Concentration of blood lead and ethnicity in the United Kingdom.

The relation between concentration of blood lead and ethnic background in 779 children was examined with the analytical results from the trace element service at the Medical Toxicology Unit (MTU), Guy's and St Thomas's Hospital Trust for the period 1980-94. The ethnic identity was determined with the first and the second names of the investigated subjects. Of the patients of European origin (European) studied 72.8% v only 50.6% of the children with origins in the Indian subcontinent (Asian) had a concentration of blood lead < 100 micrograms/l. The percentage of subgroups with concentrations above the upper acceptable limit of 200 micrograms/l was significantly higher in Asian subjects (European 5% v Asian 26.5%), with the most pronounced difference in those with concentrations of blood lead of 500 micrograms/l (European 0.8% v Asian 10.5%). This study shows that a correlation exists between Asian ethnic background and concentration of blood lead in children. Factors such as cultural habits-for example, use of traditional remedies, cosmetics, diet- and socioeconomic status, may have contributed to this results.

Assessment of toxic metal exposure following the Camelford water pollution incident: evidence of acute mobilization of lead into drinking water.

Following the incident of acidic pollution of water by aluminium sulfate centred around Camelford in July 1988, we have carried out a retrospective analysis of the mobilization of toxic metals to residents of the area. An advanced nuclear technique was used to measure trace levels of elements within hair, thus, avoiding surface contamination. In contrast to controls, lead, but no other toxic metals, was consistently found within sections of hair that dated to mid-1988 from four residents; they must, therefore, have consumed this metal around the time of the incident. The source of this lead was probably local water pipe residue, and this was found on analysis to have a matrix specific to such soft-water areas that, prior to the incident, had slowly accumulated certain toxic metals such as cadmium and uranium and particularly lead. Lead is mobilized from such residues by acidic water and could, therefore, have heavily contaminated mains water after the incident. However, analyses of residents' plasma and whole blood, and of urine following a lead-chelation test, showed no evidence of either long-term increased body burdens of toxic metals or depletion of essential elements. In addition, we found no evidence of continued poor water quality in the area. In conclusion, during a short period following the pollution, some residents who consumed mains water would have been acutely exposed to lead and other toxic metals. Prediction of the scale of metal exposure to individuals was not possible owing to heterogeneity of the water distribution network, but long-term effects to residents from lead are not anticipated.(ABSTRACT TRUNCATED AT 250 WORDS)

Toxicological problems resulting from exposure to traditional remedies and food supplements.

The National Poisons Unit, London, carried out a pilot survey to investigate the frequency and severity of adverse effects/toxicity from exposure to traditional medicines and food supplements reported to the Unit. Enquiries related to suspected poisoning events were reviewed retrospectively from January 1983 to March 1989, and prospectively in 1991. Further information about cases identified by the prospective review was obtained, when appropriate, by follow-up questionnaire, clinical consultation by a consultant toxicologist, toxicological analyses of samples from patients and from products, and botanical identification of dried plant material. In total, 5536 enquiries were identified. Symptoms were reported in 657 (12%) of these. There was a large number of reports of accidental ingestion of vitamin preparations by children under 5 years. Appropriate assessment was possible in only relatively few cases, due to insufficient documentation, and poor labelling of certain products. A probable link between exposure and adverse effects was identified in 42 cases, and was highly probable in two. Heavy metal poisoning resulting from use of contaminated traditional remedies was confirmed in 5 cases. There was evidence that some patients took excessive doses of food supplements, without realising that this might result in toxic effects. The results of this pilot study suggest that there is a need for further surveillance to provide an appropriate risk assessment of food supplements and herbal remedies, improved quality control and labelling of these products, and increased awareness of their potential hazard.

Acute arsenic poisoning: absence of polyneuropathy after treatment with 2,3-dimercaptopropanesulphonate (DMPS).

Two men aged 19 and 21 years ingested 1 g and 4 g respectively from 3 kg of a white crystalline powder that they thought was a substance of abuse. It was later identified as almost pure arsenic trioxide. Both had nausea and vomiting and one developed acute renal failure. Each was treated with 2,3-dimercaptopropanesulphonate (DMPS), and made a full recovery with no evidence of prolonged renal or neurological impairment. The DMPS-arsenic complex is probably associated with lower penetration into the CNS and as a consequence treatment with DMPS may result in lower acute and chronic neurotoxicity than treatment with the currently standard recommended chelating agent dimercaprol (British Anti-Lewisite; BAL).

Thallium poisoning. Diagnosis may be elusive but alopecia is the clue.

Thallium is a heavy metal whose salts are used in some rodent poisons and in the manufacture of optical lenses, semiconductors, scintillation counters, low temperature thermometers, and switching devices, green coloured fireworks, and imitation jewelery, and as chemical catalysts. In clinical practice thallium isotopes are used in cardiac scanning, but the use of thallium salts to treat scalp ringworm was abandoned earlier this century because of their toxicity. The sale of thallium in Britain is strictly licensed because of its toxicity and potential for use in murder, which is helped by the fact that thallous salts are colourless, tasteless, and odorless. The more water soluble salts (such as thallium sulphate, acetate, or carbonate) have higher toxicity, and although the toxic dose is variable most deaths occur after the ingestion of 10-15 mg/kg of soluble salt. Most cases of thallium toxicity occur after oral ingestion but severe toxicity has been reported after inhalation of contaminated dust from pyrite burners, in zinc and lead smelting, and in the manufacture of cadmium, after dermal absorption through protective rubber gloves, and after snorting what was thought to be cocaine. The elimination half time of thallium is between 1.7 and 30 days depending on the time since, and chronicity of, ingestion. The elimination time phases are apparent and because of the long terminal elimination half time thallium may act as a cumulative poison. We present two cases of thallium poisoning with intent to kill.

Safety and efficacy of acetarsol suppositories in unresponsive proctitis.

In a prospective open study, 10 patients with intractable proctitis were treated with acetarsol suppositories (250 mg b.d. for 4 weeks) and were monitored clinically, biochemically and toxicologically. Proctitis resolved symptomatically and sigmoidoscopically within 2 weeks in nine patients; one patient was unaffected. The only side-effect was of transient thrombocytosis in a single patient. Maximal blood and urinary arsenic concentrations occurred after 1 week's treatment with a total inorganic arsenic in the hazardous range in six patients; subsequent concentrations fell despite continuing therapy and at 4 weeks potentially hazardous values persisted in only two patients. Continued renal excretion and diminished absorption across an improved rectal mucosa is thought to be responsible for this paradox. Arsenic levels fell rapidly when acetarsol was withdrawn and were indistinguishable from pretreatment values within 4 weeks. Short-term acetarsol therapy offers a useful additional measure when local steroids have failed to control ulcerative proctitis; it appears to be safe and formal controlled comparisons with other therapeutic options are therefore legitimate.