The refining of silver from old silver ornaments,
articles and jeweller’s waste by smelting these with lead scraps for the
fabrication of new jewellery is an industry in India. The clinical
investigations have shown that 31 out of 50 silver refiners with blood lead,
32.84+1.78 mg/dL (20.3-64.9), decrease
in blood d-aminolevulinic acid
dehydratase (ALAD) activity and thiamine level and an enhanced urinary ALA were
suffering from lead poisoning. Most of these workers have shown anaemia,
abdominal colic, blue gum lining and muscular wasting indicative of lead toxicity.
Twentyfour workers with high blood lead were equally divided into two groups
and given either vitamin B1 (75 mg, once a day) or vitamin C (250
mg, twice a day) for a month. The treatments significantly lowered the blood
lead and reduced blood thiamine and copper deficiency. Vitamin C was also
effective in reversing the inhibition of blood ALAD activity while the effect
of B1 was marginal. The daily intake of these vitamins may prevent
the accumulation of lead and reduce its toxic effects in those regularly
exposed.
INTRODUCTION
Clinical surveys have been conducted to identify
cases of occupational lead poisoning among
workers of different lead occupations and population residing in their
vicinity. Lead poisoning in adults and children in a family of 18 has been
attributed to lead fumes and lead oxide dust emanating during processes of
extraction of gold and silver from jeweller’s waste (Joshua et al., 1971). In 8 out of 9 male
workers (25-65 yrs) and in 7 workers (25-70 yrs) involved in silver purification
by heating impure silver waste and old jewellery together with lead scrapes,
with an average blood lead, 120.8 mg/dL (40-210) (Behari et al.,1983) and 113.4 mg/dL (71-208) (Kachru et al., 1989) respectively were found to suffer from lead
poisoning. In another survey 23 out of 105 workers (13-60 yrs) engaged in
different work`shops of silver industry with blood lead, 60+36 mg/dL were identified on the
basis of altered lead sensitive parameters and clinical symptoms (Flora et
al.,1990).
The data on hematological investigations and
urinalysis of silver refiners and control are summarised in Table 1. Out of 50
silver refiners 31 with high lead, 32.84+1.78 mg/dL have shown an inhibition of blood ALAD
activity, a decrease in blood thiamine (indicated by an increase in pyruvic
acid) and copper and an enhanced urinary ALA as compared to control, were
suspected of lead poisoning. Most of these silver refiners have shown clinical
symptoms such as blue gum lining, abdominal colic, anaemia and muscular wasting
suggestive of lead poisoning. The remaining 19 silver refiners have also shown
significant alterations in lead sensitive parameters and shown separately in
Table 1 because of far lower blood lead
(12.66+1.11 mg/dL) and less clinical
symptoms. However, they seem to have a risk of developing lead poisoning. The
blood zinc and calcium levels in silver refiners and in control were similar
and not included in Table 1. The fact that blood levels of thiamine and
ascorbic acid decrease in lead intoxication (Bratton et al., 1981, Flora and Tandon, 1995), the administration of these
vitamins may reduce their deficiency and prevent lead toxicity. Therefore, 24
out of 31 silver refiners with high blood lead levels who were willing to
participate in the treatment programme, were divided equally into two groups.
Each worker of first group was given BENALGIS (thiamine propyldisulfide-vitamin
B1-Franco-Indian
Remedies Ltd, Chennai, India)-75
mg, once a day and that of second group VITAMIN C (Wings Pharmaceuticals Pvt.
Ltd, New Delhi, India)-250 mg twice a day for one month to investigate their
effect on the elevated blood lead and altered lead sensitive parameters. The
treatment of workers suspected of lead poisoning with Benalgis reduced blood
lead and thiamine and copper deficiencies and further elevated blood iron. The
treatment of workers with vitamin C lowered blood lead, reversed the inhibition
of blood ALAD activity and reduced thiamine and copper deficiencies. It also
elevated blood ascorbic acid and iron levels (Table 2).
The present findings are consistent with our earlier
surveys conducted among silver jewellery workers (Behari et al., 1983, Kachru et al.,
1989, Flora et al., 1990) and show
that atleast 31 out of 50 workers involved in silver refining were indeed
suffering from lead poisoning. The old silver ornaments and jeweller’s waste
are smelted with lead scrapes at high temperatures in congested workshops
without adequate exhaust system, ventilation and protective measures where
workers are exposed to lead fumes and lead oxide dust. Their clothing, hair and
food also get contaminated. Besides elevated blood lead, the decreased activity
of enzyme blood ALAD and enhanced urinary excretion of its substrate, ALA are
the earliest biochemical indicies of lead intoxication (Granick et al., 1972, Sakai et al.,1982 Ong et al.,1990). Apart from these, the
silver refiners have shown a definite lowering in blood thiamine and copper and
a decreasing trend in blood ascorbic acid as also the early toxic effects of
lead affecting the hemopoietic system. There has been a relationship between these biochemical
alterations and clinical symptoms of lead poisoning such as anaemia, abdominal
colic, blue gum lining and muscular wasting.
The selected silver refiners
with considerably high blood lead levels responded well to one month treatment
with vitamins B1 and C.
These vitamins significantly lowered blood lead and reversed lead sensitive
hematological alterations. The beneficial effect of thiamine in lead poisoning
may be attributed to the formation of their complex(es) followed by excretion.
Lead has high affinity for the thiol group (Barton, 1989). Thiamine may undergo
conformational transformation in vivo
resulting in thiazole open-ring conformation with sulfhydryl (SH) group capable
of complexing lead (Olkowski et al.,
1991). Ascorbic acid is a lactone containing an enediol group capable of
complexing lead to form a poorly ionized but soluble compound. The in vivo ability of ascorbic acid to
reduce disulfides to SH containing compounds that are capable of complexing
lead and are also required for the stimulation of heme synthetase activity (Kao
and Forbes, 1973). The intake of ascorbic acid and zinc in lead exposed workers
has been shown to lower blood lead and to protect against lead intoxication
(Papaioannoa et al., 1978). These
vitamins may have bifunctional role, i) to alleviate lead induced vitamin
deficiency or disturbance in their metabolism and ii) to act as potential
therapeutic complexing agents.
The occupational lead exposure is preventable if the
workers use protective clothing, such as face mask, gloves, respiratory filters
and refrain from smoking, eating and drinking in working areas. The workshops
should have proper ventilation and efficient exhaust system to reduce the
exposure. The daily intake of thiamine and ascorbic acid may prevent
accumulation of lead in the body system.
Barton, J.C. (1989) Toxicol.
Appl. Pharmacol. 99: 314-322. Behari, J.R., Singh, S. and Tandon, S.K. (1983) Ann.
Occup. Hyg. 27:107-109. Berlin, A.
and Schaller, K.H.. (1974) Z. Klin. Chem. Klin. Biochem. 12:389-390. Bratton, G.R., Zmudzki, J., Bell, M.C. and Laken, G.W.
(1981) Toxicol. Appl. Pharmacol. 59:164-172. Clegg, J.W. and King, E.J.
(1942) Brit. Med. J 2:329-333. Davis, J.R., Abrahams, R.H.,
Fishbein, W.I and Fabrega,E.A. (1968)
Archiv. Environ. Hlth. 17:164-171.
Flora, S.J.S., Singh, S. and Tandon, S.K. (1990) J. Environ. Sci. Hlth. A 25: 105-113. Flora, S.J.S. and Tandon
S.K. (1995) Tr. Elem. Electro. 12:
131-140. Friedmann, E. and Haugen, E.G. (1943)
J. Biol. Chem. 147: 415-442.
Granick, S., Sassa, S. Granick, J.L., Levere,R.D. and Kappas,A.(1972) Proc.
Nat. Acad. Sci. (USA) 69:
2381-2385. Joshua, G.E., Rathaiken, N. and Benjamin, V. (1971) Ind. J.
Med. Res. 59: 1496 -1507.
Kachru, D.N., Tandon, S.K., Misra, U.K. and Nag, D. (1989) Ind. J. Med. Sci. 43: 89-91. Kao, R.L.C. and Forbes, R.M. (1973) Archiv. Environ Hlth. 27:
31-35. Olkowski, A.A., Gooneratne, S.R. and Crestensen, D.A. (1991) Toxicol. Lett. 59: 153-159. Ong,
C.N., Kong, Y.M., Ong, H.Y and Teramoto, K. (1990) Pharmacol. Toxicol. 66:
23-26. Papaioannoa, R.A., Sohler, R.A. and Pfeiffer, C.C. (1978) J. Orthonol. Psyt. 7: 1-13. Parker, M.N., Humoller, F.L. and Mahler, D.J. (1967) Clin.
Chem. 13: 40-48.Roe, J.H.
(1954) Methods of Biochemical
Assays, ed. Vol. I, pp 115.
Interscience Publishers, New York. Sakai, T., Yanagihara, S., Kunugi, Y. and
Ushio, K. (1982) Brit. J. Indus. Med. 39: 382-387.
Table 1. Investigations on lead sensitive biochemical parameters in blood and urine of silver refiners.
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No. of subjects |
Age (year) |
Haematological investigations |
Urinalysis |
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Pb (mg/dL) |
Cu (mg/dL) |
Fe (mg/dL) |
Hb (gm/dL) |
d-ALAD (mmole d-ALA/min/L erythrocyte |
Ascorbic acid (mg/dL) |
Pyruvic acid (mg/dL) |
Pb (mg/L) |
d-ALA (mg/dL) |
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Control |
20 |
18-45 |
9.40±0.92 |
96.45±9.00 |
1.86±0.08 |
12.34±0.42 |
38.19±1.22 |
0.46±0.02 |
0.65±0.02 |
0.29±0.04 |
0.15±0.01 |
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(1.9-16.4) |
(59.0-225.0) |
(1.2-2.5) |
(10.0-16.8) |
(28.7-50.0) |
(0.40-0.58) |
(0.52-0.87) |
(0.07-0.76) |
(0.05-0.21) |
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Silver Refiners |
31 |
18-60 |
32.84±1.78* (20.3-64.9) |
60.39±3.64* (20.0-122.0) |
2.58+0.02* (1.4-5.4) |
11.68±0.31 (8.6-15.4) |
22.76±1.62* (10.1-47.1) |
0.39±0.03 (0.17-0.66) |
0.96±0.04* (0.53-1.23) |
0.37±0.06 (0.08-1.70) |
0.32±0.02* (0.05-0.56) |
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19 |
16-55 |
12.66±1.11*** |
63.50±7.62** |
2.36±0.18*** |
12.54±0.30 |
22.73±1.75* |
0.39±0.03 |
0.88±0.05* |
0.51±0.11 |
0.21±0.02 |
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(4.9-19.4) |
(7.5-155.0) |
(1.1-3.4) |
(10.1-14.9) |
(12.2-42.3) |
(0.21-0.75) |
(0.63-1.16) |
(0.12-1.84) |
(0.02-0.35) |
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Values represent mean + SE with range (in parenthesis). The student ‘t’ test was applied for determining the statistical significance between control and silver refiners, *p<0.001, **p<0.01, ***p<0.05
Table 2. Investigations on the reversal of lead sensitive haematological and biochemical parameters in silver refiners.
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Treatment |
No. of Subject |
Pb (mg/dL) |
Cu (mg/dL) |
Fe (mg/dL) |
Hb (gm/dL) |
d-ALAD (mmole d-ALA/min/L erythrocyte) |
Ascorbic acid (mg/dL) |
Pyruvic acid (mg/dL) |
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Pre Vit.B1 Post |
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38.50+3.48 |
61.63+3.82 |
2.47+0.16 |
11.98+0.54 |
25.53+3.48 |
0.47+0.05 |
0.93+0.05 |
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12 |
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23.58+2.86** |
86.63+6.59** |
4.20+0.11* |
11.99+0.22 |
29.29+3.19 |
0.50+0.04 |
0.59+0.03* |
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Pre Vit.C Post |
12 |
30.55+1.82 |
49.17+3.61 |
2.88+0.34 |
11.53+0.54 |
21.79+1.54 |
0.34+0.04 |
1.02+0.06 |
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20.21+1.94* |
71.93+6.17** |
4.18+0.14** |
12.20+0.27 |
28.38+1.47** |
0.53+0.03* |
0.79+0.04** |
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Values represent mean +SE with range (in parenthesis). The student ‘t’ test was applied for determining the statistical significance between pre- and post-treatment of silver refiners, *p<0.001, **p<0.01