Workers, lead

Lead is known to cause reproductive and developmental toxicity. Decreased sperm counts and abnormal sperm development have been reported in male workers heavily exposed to lead. Increased incidences of spontaneous abortion have been reported in female lead workers as well as in the wives of male lead workers (13). Lead crosses the placenta and has been found to cause irreversible neurologic impairment to the fetus at maternal blood levels as... 

Increases in ALAS activity have been observed in lead workers (Meredith et al. 1978). Leukocyte ALAS was stimulated at a PbB level of 87 pg/dL (Meredith et al. 1978), a level at which ALAD activity is already significantly inhibited. ALAD activity correlated inversely with PbB levels in occupationally exposed individuals (Alessio et al. 1976 Wada et al. 1973), as has been seen in subjects with no occupational exposure (Secchi et al. 1974). Erythrocyte ALAD and hepatic ALAD activities were correlated directly with each other and correlated inversely with PbB levels in the range of 12-56 pg/dL (Secchi etal. 1974). 

Inhibition of ALAD and stimulation of ALAS result in increased levels of ALA in blood or plasma and in urine. For example, in a case report of a 53-year-old man with an 11-year exposure to lead from removing old lead-based paint from a bridge, a PbB level of 55 pg/dL was associated with elevated urinary ALA (Pollock and Ibels 1986). The results of the Meredith et al. (1978) study on lead workers and controls indicated an exponential relationship between PbB and blood ALA. Numerous studies reported direct correlations between PbB level and log urinary ALA in workers. Some of these studies indicated that correlations can be seen at PbB levels of <40 pg/dL (Lauwerys et al. 1974 Selander and Cramer 1970 Solliway et al. 1996), although the slope may be different (less steep) than at PbB levels of >40 pg/dL. In a study of 98 occupationally exposed subjects (51 pg/dL, mean PbB) and 85 matched controls (20.9 pg/dL. mean PbB) it was found that log ZPP and log ALA in urine correlated well with PbB levels (Gennart et al. 1992a). In the exposed group, the mean ZPP was 4 times higher than in the controls, whereas urinary ALA was increased 2-fold. 

A dose-related elevation of EP or ZPP in lead workers has been documented extensively (Herber 1980 Matte et al. 1989). Correlations between PbB levels and log EP or ZPP indicate an apparent threshold for EP elevation in male workers at 25-35 pg/dL (Grandjean and Lintrup 1978 Roels et al. 1975) for FEP and a threshold of 30-40 pg/dL for EP (Roels and Lauwerys 1987 Roels et al. 1979). The threshold for EP elevation appears to be somewhat lower (20-30 pg/dL) in women than in men (Roels and Lauwerys 1987 Roels etal. 1975, 1976, 1979 Stuik 1974), regardless of whether exposure is primarily by inhalation (occupational) or oral (nonoccupational). These studies were controlled for possible confounding factors such as iron deficiency or age, both of which increase erythrocyte ZPP. 

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). 

In a study of lead workers, Wedeen et al. (1979) identified 15 who had no other risk factors for renal disease and who had previously unsuspected lead nephropathy (detected as reduced glomerular filtration... 

Taken together, these studies provide some evidence for the association of chronic nephropathy in occupationally exposed workers with PbB levels ranging from 60 to >100 pg/dL. It should be noted, however, that PbB levels measured at the time of renal function testing may not fully reflect the exposure history that contributed to the development of chronic nephropathy in lead workers. 

Behavioral Function in Adults. Neurobehavioral testing has revealed effects in adults at PbB levels (i.e., 40-80 pg/dL) below those causing encephalopathy (>400 pg/dL). Evaluations of occupationally exposed adults include several affected parameters at PbB levels between 40 and 80 pg/dL. Disturbances in oculomotor function (saccadic eye movements) in lead workers with mean PbB levels of 57-61 pg/dL were reported in a study by Baloh et al. (1979) with follow-up by Spivey et al. (1980) and in a study by Glickman et al. (1984). Deficits in hand-eye coordination and reaction time were reported in 190 lead-exposed workers (mean PbB level, 60.5 pg/dL) (NIOSH 1974). Most of the workers had been exposed for between 5 and 20 years. A similar study, however, reported no differences... 

One study has reported effects on neurobehavioral function in lead-exposed workers at mean PbB levels of 50 pg/dL (Williamson and Teo 1986). Neurobehavioral function was measured using tests that are based on information processing theory in 59 lead workers and 59 controls matched for age, type of job, time on the job, education level, smoking history, and alcohol consumption. Statistically significant decreases in the lead-exposed workers were seen for critical flicker fusion reaction, simple reaction time, tracking speeds, hand steadiness tests, and sensory store memory. Sensory store memory speed showed a low but statistically significant correlation with PbB concentrations. Measurements of neurobehavioral function seemed well chosen, and repeated measures with associated appropriate statistics were used. 

A marked interference with heme synthesis results in a reduction of the hemoglobin concentration in blood. Decreased hemoglobin production, coupled with an increase in erythrocyte destruction, results in a hypochromic, normocytic anemia with associated reticulocytosis. Decreased hemoglobin and anemia have been observed in lead workers and in children with prolonged exposure at higher PbB levels than those noted as threshold levels for inhibition or stimulation of enzyme activities involved in heme synthesis (EPA 1986a). 

Children 1-6 years of age N=32 0.008 Homes of lead workers housedust Baker et al. 1977... 

Immunotoxicity. The data in humans are limited to a few studies of immune function in lead workers and a study of firearm instructors. In both type of studies, inhalation is assumed to be the primary route of exposure. One study reported significant suppression of IgA levels (Ewers et al. 1982). Another study indicated that serum immunoglobulin levels were not significantly altered (Alomran and Shleamoon 1988). Another large study examined several parameters of immune function (serum immunoglobulins, PHA response, and natural killer cell activity) and found no differences in exposed workers and controls (Kimber et al. 1986b). The study of firearm instructors found functional impairment of cell-mediated immunity in subjects with PbB levels >25 pg/dL (Fischbein et al. 1993). A recent study that evaluated a... 

Schwartz BS John Hopkins University School of Hygiene Public Health, Baltimore, MD Study of the relations among BLLS, DMSA-chelatable lead, bone lead, and health effects (heme synthesis, renal early biologic effects and function, blood pressure, and CNS and PNS function) in lead workers in South Korea National Institute of Environmental Health Sciences... 

Cooper WC, Gaffey WR. 1975. Mortality of lead workers. J Occup Med 17 100-107. 

Ewers U, Stiller-Winkler R, ldel H. 1982. Serum immunoglobulin, complement C3, and salivary IgA level in lead workers. Environ Res 29 351-357. 

FanningD. 1988. A mortality study of lead workers, 1926-1985. Arch Environ Health 43 247-251. 

Hwang O-J, Lee B-K. 1988. [Biological indicators of lead exposure in female lead workers.] J Cathol Med Coll 41 85-92. (Chinese)... 

Lin S, Hwang S, Marshall EG, et al. 1996. Fertility rates among lead workers and professional bus drivers A comparative study. Ann Epidemiol 6 201-208. 

Milbum H, Mitran E. Crockford GW. 1976. An investigation of lead workers for subclinical effects of lead using three performance tests. Ann Occup Hyg 19 239-249. 

Oishi H, Nomiyama H, Nomiyama K, et al. 1996. Fluorometric HPLC determination of delta-aminolevulinic acid (ALA) in the plasma and urine of lead workers biological indicators of lead exposure. J Anal Toxicol 20(2) 106-10. 

Sata F, Araki S, Tanigawa T, et al. 1998. Changes in T cell subpopulations in lead workers. Environ Res 76(l) 61-64. 

Stollery BT, Banks HA, Broadbent DE, et al. 1989. Cognitive functioning in lead workers. BrJInd Med 46 698-707. 

Yeh JH, Chang YC, Wang JD. 1995. Combined electroneurographic and electromyographic studies in lead workers. Occup Environ Med 52(6) 415-419. 

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