Biochemical changes during the initial stages of industrial lead exposure.

Abstract

. (1976). British Journal of Industrial Medicine, 33,[29][30][31][32][33][34][35]. Biochemical changes during the initial stages of industrial lead exposure. Biochemical measurements were carried out on 20 workers entering employment in a lead industry. Blood lead (Pb-B), urinary 8-aminolevulinic acid (ALA), and coproporphyrin (CP) levels were determined before entry and then at approximately weekly intervals for the first 12 weeks of employment. Levels of blood lead began to increase in all men within one week rising from an average pre-employment figure of about I 1 t,mol/l (22 ,ug/100 ml) to a value of about 2-9 ,umol/l (60 ,ug/100 ml) at three weeks. Subsequently there was only a small increase and Pb-B values levelled for the rest of the period. There was no increase in urinary ALA and CP in most subjects during the first two weeks; thereafter there was a variable pattern of excretion although three main groups of response could be discerned. Urinary ALA and CP changes related well to each other but their correlation with the characteristic increase in Pb-B fell into three categories of relationship. The major finding of the study was the very contrasting response shown by some individuals. This emphasized the need for a reasonably comprehensive biochemical screen during the early stages of employment in the lead industry in order to assess the individual biological response of a new employee to this environment. The measurement of Pb-B and urinary CP or ALA was advocated for this purpose.

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

“…In contrast, lead is removed from bone tissue at a constant and extremely slow rate [23]. For this reason time integrals of body burdens of lead may well be diagnosed by determination of the lead content in bones and teeth [23][24][25][26][27][28][29][30][31], whereas momentary body burdens of lead should be derived rather from analyses of biochemical factors [32][33][34]. When lead ions are injected in the form of lead acetate, they not only interact with the calcified tissues [35,36], but they also induce ectopic calcification [37,38].…”

Indices of potential lead hazard.

“…The "normal range" found was about 5-40 ,ug/100 ml,t but the values obtained included 45,50,53,60, and 100 (New York City) ,ug/100 ml with, in all likelihood, more values in the latter range. The distribution was skewed as seen by the low median (18 ,g/100 ml) and mean (17 ,ug/100 ml).…”

“…Basophilic stippling is well known in lead toxicity but it is also caused by many other conditions. The percentage of reticulocytes is sometimes increased (28,(49)(50)(51)(52).…”

“…" Chisolm (15) found that FEP is a sensitive indicator of the "internal dose" of lead as long as iron deficiency and its concomitant anemia were mathematically corrected by a determination of Hct or Hb. "In children with hematocrit :36% and PbB <30 ,ug/100 ml, we have found that erythrocyte protoporphyrin levels are low and independent of PbB concentration ... ¢90% of children with PbB ¢50 ,tg/100 ml are positive reactors and that 50% response rate is associated with PbB in the [40][41][42][43][44][45][46][47][48][49][50] ,ug/100 ml range (15)." Elsewhere (89) it is stated that "significant numbers of children with blood lead levels of [30][31][32][33][34][35][36][37][38][39] ,ug/100 ml have shown evidence of metabolic impairment as detected by EP test-ing.…”

“…For Na+K+ATPase activity < 40 ,umole PJ/hr/mg tyrosine, [20][21][22][23][24][25][26][27][28][29] ,tg Pb/100 ml; for GSH < 58 ,g/100 ml of erythrocytes, 25-30 ,ug/100 ml. Anemia (decreased Hb) does not occur in otherwise healthy adults below 70-80 ixg/100 ml, and in socioeconomically poor children below [40][41][42][43][44][45][46][47][48][49][50] ,g/100 ml.…”