Annals of Clinical Biochemistry, 1977, 14, 297-300
Diagnostic value of urine mercury measurements *ANDREW TAYLOR AND tVINCENT MARKS From the Departments of Biochemistry, "St Luke's Hospital, Guildford and tUniversity 0/ Surrey, Guildford A review of referrals to a regional heavy metals centre for possible mercury poisoning was made. Samples were received either from subjects who were well but were known to have some contact with mercury or from patients with an illness under investigation but undiagnosed. The problems associated with diagnosis of mercury toxicity in the absence of known exposure are illustrated by two case reports. SUMMARY
Sporadic reports (Gledhill and Hopkins, 1972; exposure to inorganic mercury can lead to weakness, Eastrnond and Holt, 1975) of cases of mercury anorexia, loss of weight, tremor, and erethisrnf. poisoning illustrate that the health hazards of Thus, in the absence of a clear history of exposure, mercury cannot be ignored. Despite their toxicity, mercury toxicity may not immediately be suspected by a physician confronted by a patient complaining mercury and its compounds are still extensively used and are of great importance in some industries-for of such non-specific symptoms. Laboratory diagnosis and assessment of exposure example, the manufacture of scientific instruments, production of chlorine, manufacture and repair of is made by measuring mercury in urine. Urinary direct current meters (Bidstrup, 1964). Moreover, the excretion, preferably over 24 hours, is the best index introduction of certain preparations containing of exposure to mercury (Smith et al., 1970). 'Normal organic mercurials as fungicides-for example, wall- output' has been variably reported as less than 0'5 paper paste, seed dressings, and Phytodermine oint- fLmol/1 (Noe, 1960), less than 0·15 fLmol/1 (Nobel and ment-has extended the range of the population Leifheit, 1961), and less than 0'05 fLmol/1 (Wallach, potentially exposed to mercury to almost every 1972). Results obtained in this laboratory using cold vapour atomic absorption spectrophotometry are in household in the country. Acute poisoning caused by mercury vapour or agreement with the last figure (Taylor and Marks, inorganic mercury compounds is characterised by 1973). inflammation of the exposed mucous membranes. Thus stomatogingivitis, pneumonitis with respiratory Materials and methods distress, cough, fever and abdominal pain, vomiting and diarrhoea are typical symptoms. If there is over- The Heavy Metals Reference Laboratory at Guildwhelming exposure, death may result from haemor- ford receives specimens from clinical laboratories rhage and circulatory collapse or from renal tubular within the South-west Thames Regional Health Authority for a wide range of trace metal and necrosis. Alkylmercury compounds are extremely toxic. associated analyses. The total population served is Acutely, they produce blistering and ulceration of the approximately three million although not all skin. After ingestion gastrointestinal symptoms laboratories with access to the Guildford centre refer develop-i-stomatogingivitis, abdominal pain, anor- specimens there for analysis, preferring to deal with exia, vomiting and diarrhoea-which may be fatal. them themselves. With so many referring laboratories there is Permanent neural damage may also develop; constriction of the visual fields, ataxia, and difficulty inevitably considerable variation in the type and cleanliness of containers used for the collection of 24with vocal articulation are the classical signs. In contrast to the florid symptoms of massive hour urine specimens. There is little variation, howmercury intoxication, those caused by mild exposure ever, in the type of bottles used to send aliquots from LV organic mercury or by chronic inorganic mercury such collections to the Reference Laboratory. ocisoning may not be so obvious. Fatigue, memory oss, and poor concentration develop after limited tErethism: behaviour characterised by nervousness, irrrtaexposure to alkyl compounds, while chronic bility, shyness, irrational outbursts of temper, and depression. 297
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298
Andrew Taylor and Vincent Mark:
With only very few exceptions plastic universal containers (Sterilin Ltd) have been used by laboratories to send specimens for urine mercury analyses. This type of tube, which is free from contamination and does not adsorb mercury, was also used whenever random, instead of 24-hour, collections of urine were made. Specimens were received from 121 subjects from 20 different sources during 1973-75. Seventy-seven represented aliquots of 24-hour urine collections; the remaining 44 were 'random' specimens. In some cases the subjects were asymptomatic and tests were carried out as part of an occupational health screening exercise because It was known that there had been mercury spillages. Mercury was measured by cold-vapour atomic absorption spectrophotometry after overnight sulphuric acid-potassium permanganate digestion. The recovery of added mercury was 97 % and the precision of the method assessed by determination of the coefficient of variation was 5·2 % within batch and 8·1 % between batch (Taylor and Marks, 1973). The standard autoanalyser method using alkaline picrate reagent was employed for measuring urine creatinine concentration. Results of random urine samples were expressed as fLmol of mercury per mole of creatinine in order to minimise variations in urine osmolality (Smith et al., 1970). A mercury excretion ofmore than 0·075 fLmolf24h, or a concentration of more than 8 fLmolfmercury per mole of creatinine, was construed as excessive and when such a level was found, a second urine sample was requested either to confirm the original result or to indicate contamination of the first.
bO
50
40
"
Ci E
a
0- 30
"E
.0
:l
20
Z
10
a
a
0'15
0·30
0·45
Fig. 1 Mercury content of 24 hour urine collections from 77 subjects.
40
30
"
Ci E
a
-5-20 "
..c E
1q7 182 120 81
:l
Results
O·bO
Mercury /-lrnol/24 hours
Z 10
The results of initial analyses are shown in Figs I and
a
2.
Urine mercury levels exceeded 0·075 fLmolf24h or 8 fLmolfmol of creatinine in 34 of the 121 samples received (28 %) on initial analysis. Repeat samples were obtained from only 18 of the 34 subjects and in five of them (28 %) the results were normal. A summary of the samples received and the number of high results obtained is given in Table 1. An analysis of the data according to the nature of exposure and the clinical information is given in Table 2. Urine samples containing increased amounts of mercury derived from subjects who could be classified either as having had (a) recognised episodes of exposure to mercury at work or after an accidental spillage, or (b) a history of illness which was under investigation but still undiagnosed.
a
Ib
32
48
Mercury /-lmol/mol cre ctt nine
Fig. 2 Mercury content of random urine collections from 44 subjects.
CATEGORY
1
Specimens received from the University of Surrey Health Centre were in the first category; these originated from individuals working in departments using large amounts of metallic mercury. Inevitably under such circumstances there are rare occasions when some mercury is spilt. When this happened any person exposed, either at the time of the accident or during the cleaning-up process, was asked to submit a urine specimen for analysis. Of the 14 specimens
Downloaded from acb.sagepub.com by guest on June 5, 2016
299
Diagnostic value of urine mercury measurements Table 1
Samples with high urine mercury
Results
No.
Total no. of subjects Number With high result in first sample Submitting second sample Falsely elevated results (out of 18) Confirmed high results Unconfirmed high results
121 34 18 5 13
16
Table 2 Source of exposure to mercury, nature of employment, and clinical information Source Dental workers University technicians Thermometer manufacturers Broken mercury switch in home Mercury ointment for psoriasis Elevated urine mercury with no details and no follow-up Normal urine mercury-miscellaneous exposure rotal
No.
No. elevated 9 3
40 14 4 7 1
4
5
5
7 I
SO
121
29
mainly of albumin. Ear, nose, and throat swabs revealed nothing abnormal. Only after nephrotic syndrome had been diagnosed was the fact obtained that a mercury switch had been broken. The accident had taken place at home over a carpet which formed an ideal reservoir for the spilled mercury. The incident had not been considered relevant to the child's illness. Urinary mercury concentration was 50 p.mol/mol creatinine, confirming the diagnosis of mercury toxicity. The child was treated with corticosteroids and discharged well two weeks later. Had the diagnosis not been established in the child, others in the family might have been affected. Although symptom-free they were examined and all were excreting greater than normal amounts of mercury in their urine (range 12-5-45 p.mol/mol of creatinine). The patient and her family were followedup as outpatients; their urinary mercury levels gradually decreased although four months later they were still above 'normal'. Case 2
received under these circumstances, three showed slightly increased mercury levels. Dental workers constitute a large group of people who constantly use mercury but because the amounts are usually small, dentists seldom pay much attention to the possible health hazards. A few, however, have expressed concern and sought reassurance about their health. CATEGORY 2 Cases which came within the second category demonstrate the clinical importance of mercury toxicity and the problems associated with its diagnosis. These are illustrated by the following examples:
Case 1
A girl of 2t years was admitted to hospital with a three-day history of weight gain and oedema. Oedema of the face, sacrum, and legs was noted on examination but there were no other obvious abnormalities. There was no history of dysuria or infection. Laboratory investigations in the referring hospital showed: haemoglobin 12'8 g/dl, WBC 9'0 x 109/1 with normal differential, erythrocyte sedimentation rate 90 mm/h, serum sodium 133 mmol/l, potassium 3'8 mmol/l, urea 3'3 mmol/l, bilirubin 17 p.mol/l, serum alanine aminotransferase 13 IU/l, alkaline phosphatase 15 KA units/100 ml, total protein 30 g{l, albumin 13 g/I, cholesterol 10·7 mmol/I, creatinine 62 p.mol/I. There was gross proteinuria which on electrophoresis was shown to consist
A 45-year-old dental surgeon complaining of severe headache, diplopia and tremor of the hands, was referred to a consultant physician by his general practitioner. Clinical examination showed only slight muscular incoordination and moderate hypertension (blood pressure 170/120 mrn/Hg), Routine clinical and laboratory investigations-including electrocardiograms, intravenous pyelography, and urinary catecholamine measurements-were all normal. The dental surgeon observed that his assistant also had trembling hands, and he confirmed that he, too, had had severe headaches, difficulty in focusing, and bouts of nausea and diarrhoea. When questioned their receptionist opined that she had had mild headaches and a metallic taste in her mouth. Suspecting a leakage of halothane or methyl methacrylate monomer the surgery suite was searched and approximately 25 g of mercury was discovered under the cupboards, amalgamator, and sterilizer. A dental surgery assistant, who had worked there temporarily, some months previously, later admitted to spilling some 250 g of mercury while filling the amalgamator. She had collected all that was visible but had neglected to report the accident. Mercury toxicity, which until this discovery had not been considered by the patient or his physician, was confirmed by urine analysis (190 p.moljmol creatinine). Treatment with N-acetyl-D-penicillamine was begun and the urinary mercury levels were monitored over the next year during which time they gradually fell to normal. This incident has been reported in detail elsewhere (Merfield et al., 1976).
Downloaded from acb.sagepub.com by guest on June 5, 2016
300
Andrew Taylor and Vincent Marks
Discussion
Intoxication caused by metallic mercury which was once common as an occupational hazard (Carroll, 1865) is now rare in most parts of the world. Nevertheless, our experience suggests that at least one or two cases of suspected mercury poisoning will be seen every year in the typical district hospital serving a population of a quarter of a million people. During the same time probably between five and 10 cases of suspected lead toxicity will be seen, but only very rarely will other types of metal poisoning such as that caused by cadmium or manganese be suspected. On initial screening of the patients' urine for mercury, approximately 30% of the cases will appear to have received excessive exposure, but one-third or more of them will be spurious because of postcollection contamination. Thus, potentially harmful exposure to mercury may eventually be proved in about 20 % of the suspected cases. Although contamination is an ever present problem in urine mercury as in other trace metal determinations where samples typically contain at most a few micrograms of analyte, losses of mercury owing to adsorption on to the walls of the container are equally important. Recent investigations (Trujillo et al., 1974; Lo and Wai, 1975) have shown that acid washed glass containers are preferable to bottles made of polyethylene, and that the addition of an oxidising agent-such as, potassium dichromate or potassium persulphate-to the bottle is essential to prevent adsorption and volatilisation. Measurement of mercury should, with modern equipment, seldom present technical difficulties and, while urinary excretion of mercury is probably the best index of exposure to mercury, this measurement may not always correlate well with the development of symptoms. Wallach (1972), for example, described a patient in whom extremely high urine mercury levels (2·75-3'0 p.moljl) were observed after aspiration of approximately 5 ml of elemental mercury. Despite this evidence of considerable absorption of mercury through the alveolar walls, no symptoms attributable to mercury toxicity developed. On the other hand, Eastmond and Holt (1975) reported a case of
transient exposure to mercury vapour from broken thermometer, probably containing no more than 1 g of mercury, which was followed by nausea, salivation, slight albuminuria, and microscopic haematuria. Urine mercury excretion was never higher than 0·09 p.mol/24h even while the patient was undergoing chelation therapy. Nevertheless, as the cases described above illustrate, measurement of urine mercury is invaluable in confirming a diagnosis of mercury toxicity and should be carried out whenever the appropriate symptoms are present even in the absence of a history of exposure to mercury. References Bidstrup, P. L. (1964). Toxicity of Mercury and its Compounds. Elsevier: Amsterdam. Carroll, L. (1865). The Adventures of Alia in Wonderland. Macmillan: London. Eastmond, C. J., and Holt, S. (1975). A case of acute mercury vapour poisoning. Postgraduate Medical Journal, 51, 428430. Gledhill, R. F., and Hopkins, A. P. (1972). Chronic inorganic mercury poisoning treated with N-acetyl-D-penicillamine. British Journal of Industrial Medicine, 29, 225-228. Lo, J. M., and Wai, C. M. (1975). Mercury loss from water during storage: Mechanisms and prevention. Analytical Chemistry, 47, 1869-1870. Merfield, D. P., Taylor, A., Gemmell, D. M., and Parrish, J. A. (1976). Mercury intoxication in a dental surgery following unreported spillage. British Dental Journal, 141, 179-186. Nobel, S., and Leifheit, H. C. (1961). Mercury in Urine. Standard Methods of Clinical Chemistry, volume 3. Edited by D. Seligson. Academic Press: New York. Noe, F. E. (1960). Chronic mercurial intoxication: A review. Industrial Medicine and Surgery. 29, 559-564. Smith, R. G., Vorwald, A. J., Patil, L. S., and Mooney, T. F. (1970). Effects of exposure to mercury in the manufacture of chlorine. American Industrial Hygiene Association Journal, 31, 687-700. Taylor, A., and Marks, V. (1973). Measurement of urinary mercury excretion by atomic absorption in health and disease. British Journal of Industrial Medicine, 30, 293-296. Trujillo, P., Stein, P., and Campbell, E. (1974). The preservation and storage of urine samples for the determination of mercury. American Industrial Hygiene Association Journal, 35,257-261. Wallach, L. (1972). Aspiration of elemental mercury: Evidence of absorption without toxicity. New England Journal of Medicine, 287, 178-179. Accepted for publication 23 June 1977
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Diagnostic value of urine mercury measurements *ANDREW TAYLOR AND tVINCENT MARKS From the Departments of Biochemistry, "St Luke's Hospital, Guildford and tUniversity 0/ Surrey, Guildford A review of referrals to a regional heavy metals centre for possible mercury poisoning was made. Samples were received either from subjects who were well but were known to have some contact with mercury or from patients with an illness under investigation but undiagnosed. The problems associated with diagnosis of mercury toxicity in the absence of known exposure are illustrated by two case reports. SUMMARY
Sporadic reports (Gledhill and Hopkins, 1972; exposure to inorganic mercury can lead to weakness, Eastrnond and Holt, 1975) of cases of mercury anorexia, loss of weight, tremor, and erethisrnf. poisoning illustrate that the health hazards of Thus, in the absence of a clear history of exposure, mercury cannot be ignored. Despite their toxicity, mercury toxicity may not immediately be suspected by a physician confronted by a patient complaining mercury and its compounds are still extensively used and are of great importance in some industries-for of such non-specific symptoms. Laboratory diagnosis and assessment of exposure example, the manufacture of scientific instruments, production of chlorine, manufacture and repair of is made by measuring mercury in urine. Urinary direct current meters (Bidstrup, 1964). Moreover, the excretion, preferably over 24 hours, is the best index introduction of certain preparations containing of exposure to mercury (Smith et al., 1970). 'Normal organic mercurials as fungicides-for example, wall- output' has been variably reported as less than 0'5 paper paste, seed dressings, and Phytodermine oint- fLmol/1 (Noe, 1960), less than 0·15 fLmol/1 (Nobel and ment-has extended the range of the population Leifheit, 1961), and less than 0'05 fLmol/1 (Wallach, potentially exposed to mercury to almost every 1972). Results obtained in this laboratory using cold vapour atomic absorption spectrophotometry are in household in the country. Acute poisoning caused by mercury vapour or agreement with the last figure (Taylor and Marks, inorganic mercury compounds is characterised by 1973). inflammation of the exposed mucous membranes. Thus stomatogingivitis, pneumonitis with respiratory Materials and methods distress, cough, fever and abdominal pain, vomiting and diarrhoea are typical symptoms. If there is over- The Heavy Metals Reference Laboratory at Guildwhelming exposure, death may result from haemor- ford receives specimens from clinical laboratories rhage and circulatory collapse or from renal tubular within the South-west Thames Regional Health Authority for a wide range of trace metal and necrosis. Alkylmercury compounds are extremely toxic. associated analyses. The total population served is Acutely, they produce blistering and ulceration of the approximately three million although not all skin. After ingestion gastrointestinal symptoms laboratories with access to the Guildford centre refer develop-i-stomatogingivitis, abdominal pain, anor- specimens there for analysis, preferring to deal with exia, vomiting and diarrhoea-which may be fatal. them themselves. With so many referring laboratories there is Permanent neural damage may also develop; constriction of the visual fields, ataxia, and difficulty inevitably considerable variation in the type and cleanliness of containers used for the collection of 24with vocal articulation are the classical signs. In contrast to the florid symptoms of massive hour urine specimens. There is little variation, howmercury intoxication, those caused by mild exposure ever, in the type of bottles used to send aliquots from LV organic mercury or by chronic inorganic mercury such collections to the Reference Laboratory. ocisoning may not be so obvious. Fatigue, memory oss, and poor concentration develop after limited tErethism: behaviour characterised by nervousness, irrrtaexposure to alkyl compounds, while chronic bility, shyness, irrational outbursts of temper, and depression. 297
Downloaded from acb.sagepub.com by guest on June 5, 2016
298
Andrew Taylor and Vincent Mark:
With only very few exceptions plastic universal containers (Sterilin Ltd) have been used by laboratories to send specimens for urine mercury analyses. This type of tube, which is free from contamination and does not adsorb mercury, was also used whenever random, instead of 24-hour, collections of urine were made. Specimens were received from 121 subjects from 20 different sources during 1973-75. Seventy-seven represented aliquots of 24-hour urine collections; the remaining 44 were 'random' specimens. In some cases the subjects were asymptomatic and tests were carried out as part of an occupational health screening exercise because It was known that there had been mercury spillages. Mercury was measured by cold-vapour atomic absorption spectrophotometry after overnight sulphuric acid-potassium permanganate digestion. The recovery of added mercury was 97 % and the precision of the method assessed by determination of the coefficient of variation was 5·2 % within batch and 8·1 % between batch (Taylor and Marks, 1973). The standard autoanalyser method using alkaline picrate reagent was employed for measuring urine creatinine concentration. Results of random urine samples were expressed as fLmol of mercury per mole of creatinine in order to minimise variations in urine osmolality (Smith et al., 1970). A mercury excretion ofmore than 0·075 fLmolf24h, or a concentration of more than 8 fLmolfmercury per mole of creatinine, was construed as excessive and when such a level was found, a second urine sample was requested either to confirm the original result or to indicate contamination of the first.
bO
50
40
"
Ci E
a
0- 30
"E
.0
:l
20
Z
10
a
a
0'15
0·30
0·45
Fig. 1 Mercury content of 24 hour urine collections from 77 subjects.
40
30
"
Ci E
a
-5-20 "
..c E
1q7 182 120 81
:l
Results
O·bO
Mercury /-lrnol/24 hours
Z 10
The results of initial analyses are shown in Figs I and
a
2.
Urine mercury levels exceeded 0·075 fLmolf24h or 8 fLmolfmol of creatinine in 34 of the 121 samples received (28 %) on initial analysis. Repeat samples were obtained from only 18 of the 34 subjects and in five of them (28 %) the results were normal. A summary of the samples received and the number of high results obtained is given in Table 1. An analysis of the data according to the nature of exposure and the clinical information is given in Table 2. Urine samples containing increased amounts of mercury derived from subjects who could be classified either as having had (a) recognised episodes of exposure to mercury at work or after an accidental spillage, or (b) a history of illness which was under investigation but still undiagnosed.
a
Ib
32
48
Mercury /-lmol/mol cre ctt nine
Fig. 2 Mercury content of random urine collections from 44 subjects.
CATEGORY
1
Specimens received from the University of Surrey Health Centre were in the first category; these originated from individuals working in departments using large amounts of metallic mercury. Inevitably under such circumstances there are rare occasions when some mercury is spilt. When this happened any person exposed, either at the time of the accident or during the cleaning-up process, was asked to submit a urine specimen for analysis. Of the 14 specimens
Downloaded from acb.sagepub.com by guest on June 5, 2016
299
Diagnostic value of urine mercury measurements Table 1
Samples with high urine mercury
Results
No.
Total no. of subjects Number With high result in first sample Submitting second sample Falsely elevated results (out of 18) Confirmed high results Unconfirmed high results
121 34 18 5 13
16
Table 2 Source of exposure to mercury, nature of employment, and clinical information Source Dental workers University technicians Thermometer manufacturers Broken mercury switch in home Mercury ointment for psoriasis Elevated urine mercury with no details and no follow-up Normal urine mercury-miscellaneous exposure rotal
No.
No. elevated 9 3
40 14 4 7 1
4
5
5
7 I
SO
121
29
mainly of albumin. Ear, nose, and throat swabs revealed nothing abnormal. Only after nephrotic syndrome had been diagnosed was the fact obtained that a mercury switch had been broken. The accident had taken place at home over a carpet which formed an ideal reservoir for the spilled mercury. The incident had not been considered relevant to the child's illness. Urinary mercury concentration was 50 p.mol/mol creatinine, confirming the diagnosis of mercury toxicity. The child was treated with corticosteroids and discharged well two weeks later. Had the diagnosis not been established in the child, others in the family might have been affected. Although symptom-free they were examined and all were excreting greater than normal amounts of mercury in their urine (range 12-5-45 p.mol/mol of creatinine). The patient and her family were followedup as outpatients; their urinary mercury levels gradually decreased although four months later they were still above 'normal'. Case 2
received under these circumstances, three showed slightly increased mercury levels. Dental workers constitute a large group of people who constantly use mercury but because the amounts are usually small, dentists seldom pay much attention to the possible health hazards. A few, however, have expressed concern and sought reassurance about their health. CATEGORY 2 Cases which came within the second category demonstrate the clinical importance of mercury toxicity and the problems associated with its diagnosis. These are illustrated by the following examples:
Case 1
A girl of 2t years was admitted to hospital with a three-day history of weight gain and oedema. Oedema of the face, sacrum, and legs was noted on examination but there were no other obvious abnormalities. There was no history of dysuria or infection. Laboratory investigations in the referring hospital showed: haemoglobin 12'8 g/dl, WBC 9'0 x 109/1 with normal differential, erythrocyte sedimentation rate 90 mm/h, serum sodium 133 mmol/l, potassium 3'8 mmol/l, urea 3'3 mmol/l, bilirubin 17 p.mol/l, serum alanine aminotransferase 13 IU/l, alkaline phosphatase 15 KA units/100 ml, total protein 30 g{l, albumin 13 g/I, cholesterol 10·7 mmol/I, creatinine 62 p.mol/I. There was gross proteinuria which on electrophoresis was shown to consist
A 45-year-old dental surgeon complaining of severe headache, diplopia and tremor of the hands, was referred to a consultant physician by his general practitioner. Clinical examination showed only slight muscular incoordination and moderate hypertension (blood pressure 170/120 mrn/Hg), Routine clinical and laboratory investigations-including electrocardiograms, intravenous pyelography, and urinary catecholamine measurements-were all normal. The dental surgeon observed that his assistant also had trembling hands, and he confirmed that he, too, had had severe headaches, difficulty in focusing, and bouts of nausea and diarrhoea. When questioned their receptionist opined that she had had mild headaches and a metallic taste in her mouth. Suspecting a leakage of halothane or methyl methacrylate monomer the surgery suite was searched and approximately 25 g of mercury was discovered under the cupboards, amalgamator, and sterilizer. A dental surgery assistant, who had worked there temporarily, some months previously, later admitted to spilling some 250 g of mercury while filling the amalgamator. She had collected all that was visible but had neglected to report the accident. Mercury toxicity, which until this discovery had not been considered by the patient or his physician, was confirmed by urine analysis (190 p.moljmol creatinine). Treatment with N-acetyl-D-penicillamine was begun and the urinary mercury levels were monitored over the next year during which time they gradually fell to normal. This incident has been reported in detail elsewhere (Merfield et al., 1976).
Downloaded from acb.sagepub.com by guest on June 5, 2016
300
Andrew Taylor and Vincent Marks
Discussion
Intoxication caused by metallic mercury which was once common as an occupational hazard (Carroll, 1865) is now rare in most parts of the world. Nevertheless, our experience suggests that at least one or two cases of suspected mercury poisoning will be seen every year in the typical district hospital serving a population of a quarter of a million people. During the same time probably between five and 10 cases of suspected lead toxicity will be seen, but only very rarely will other types of metal poisoning such as that caused by cadmium or manganese be suspected. On initial screening of the patients' urine for mercury, approximately 30% of the cases will appear to have received excessive exposure, but one-third or more of them will be spurious because of postcollection contamination. Thus, potentially harmful exposure to mercury may eventually be proved in about 20 % of the suspected cases. Although contamination is an ever present problem in urine mercury as in other trace metal determinations where samples typically contain at most a few micrograms of analyte, losses of mercury owing to adsorption on to the walls of the container are equally important. Recent investigations (Trujillo et al., 1974; Lo and Wai, 1975) have shown that acid washed glass containers are preferable to bottles made of polyethylene, and that the addition of an oxidising agent-such as, potassium dichromate or potassium persulphate-to the bottle is essential to prevent adsorption and volatilisation. Measurement of mercury should, with modern equipment, seldom present technical difficulties and, while urinary excretion of mercury is probably the best index of exposure to mercury, this measurement may not always correlate well with the development of symptoms. Wallach (1972), for example, described a patient in whom extremely high urine mercury levels (2·75-3'0 p.moljl) were observed after aspiration of approximately 5 ml of elemental mercury. Despite this evidence of considerable absorption of mercury through the alveolar walls, no symptoms attributable to mercury toxicity developed. On the other hand, Eastmond and Holt (1975) reported a case of
transient exposure to mercury vapour from broken thermometer, probably containing no more than 1 g of mercury, which was followed by nausea, salivation, slight albuminuria, and microscopic haematuria. Urine mercury excretion was never higher than 0·09 p.mol/24h even while the patient was undergoing chelation therapy. Nevertheless, as the cases described above illustrate, measurement of urine mercury is invaluable in confirming a diagnosis of mercury toxicity and should be carried out whenever the appropriate symptoms are present even in the absence of a history of exposure to mercury. References Bidstrup, P. L. (1964). Toxicity of Mercury and its Compounds. Elsevier: Amsterdam. Carroll, L. (1865). The Adventures of Alia in Wonderland. Macmillan: London. Eastmond, C. J., and Holt, S. (1975). A case of acute mercury vapour poisoning. Postgraduate Medical Journal, 51, 428430. Gledhill, R. F., and Hopkins, A. P. (1972). Chronic inorganic mercury poisoning treated with N-acetyl-D-penicillamine. British Journal of Industrial Medicine, 29, 225-228. Lo, J. M., and Wai, C. M. (1975). Mercury loss from water during storage: Mechanisms and prevention. Analytical Chemistry, 47, 1869-1870. Merfield, D. P., Taylor, A., Gemmell, D. M., and Parrish, J. A. (1976). Mercury intoxication in a dental surgery following unreported spillage. British Dental Journal, 141, 179-186. Nobel, S., and Leifheit, H. C. (1961). Mercury in Urine. Standard Methods of Clinical Chemistry, volume 3. Edited by D. Seligson. Academic Press: New York. Noe, F. E. (1960). Chronic mercurial intoxication: A review. Industrial Medicine and Surgery. 29, 559-564. Smith, R. G., Vorwald, A. J., Patil, L. S., and Mooney, T. F. (1970). Effects of exposure to mercury in the manufacture of chlorine. American Industrial Hygiene Association Journal, 31, 687-700. Taylor, A., and Marks, V. (1973). Measurement of urinary mercury excretion by atomic absorption in health and disease. British Journal of Industrial Medicine, 30, 293-296. Trujillo, P., Stein, P., and Campbell, E. (1974). The preservation and storage of urine samples for the determination of mercury. American Industrial Hygiene Association Journal, 35,257-261. Wallach, L. (1972). Aspiration of elemental mercury: Evidence of absorption without toxicity. New England Journal of Medicine, 287, 178-179. Accepted for publication 23 June 1977
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