Lead exposures

Ideally, markers of human lead exposure should reflect past and current exposures of both a chronic and an acute nature. Realistically, no single 

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Because of the toxicity of lead, special care must be taken when working with lead ahoys. Lead and its inorganic compounds are neurotoxias which may produce peripheral neuropathy. Eor an overview of the effects of lead exposure, see Occupational Exposure to Lead, Appendix A (29 CRE 1910.1025) (see... 

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

However, if air sampling estabHshes that the lead exposure concentration is excessive, engineering controls (such as improved ventilation), adrninistrative controls (such as job rotation), and work practices (such as improved personal hygiene of workers) have to be appHed to comply with the permissible exposure limit (PEL) of the OSHA standard. 

Exposure to lead can occur from a variety of occupational or nonoccupational sources. A comprehensive treatise on human lead exposure is available (3). 

Operating under contract to EPA, the TCSA Hotline provides technical assistance and information about programs under the Toxic Substances Control Act (TSCA), including the Asbestos School Hazard Abatement Act (ASHAA), the Asbestos Hazard Emergency Response Act (AHERA), and the Lead Exposure Reduction Act. Hours 8 30 a.m. - 5 00 p.m. EST weekdays. 

When the Dixie site is compared to the reference area, proximity to the smelter (within 0.5 mile) contributed 1.85 pg/dl to the mean blood-lead level. The potential contribution of traffic density could not be determined because of the configuration of the roadway and the distance of the roadway from the smelter site. Although an elevated mean blood-lead level was found for children living close to the Dixie site, the increase was not as great as observed in the RSR site and the few children found to have lead toxicity, as defined previously, appear to have lead exposure due to occupation of parents. 

Burger J. 1990. Behavioral effects of early postnatal lead exposure in herring guU (Lams argentatus) chicks. Pharmacol Biochem Behav 35 7-14. 

Pyrimidine 5 -nucleotidase (P5N) is a unique enzyme that was recognized from studies of families with relatively common hemolytic disorders. The enzyme catalyzes the hydrolytic dephosphorylation of pyrimidine 5 -nucleotides but not purine nucleotides. The role of this enzyme is to eliminate RNA and DNA degradation products from the cytosol during erythroid maturation by conversion of nucleotide monophosphates to diffusible nucleosides. P5N is inhibited by lead, and its activity is considered to be a good indicator of lead exposure (PI). 

The third report was an unequivocal vindication of Patterson s work lead exposure was recognized to be among industrialized society s most important environmental health problems. . . Science and society have been remarkably slow to recognize and respond. . . but that is changing. The Centers for Disease Control s acceptable concentration of lead in children s blood had dropped from 60 to 10 lead had been removed from gasoline in the United States and average blood levels had improved by more than 95 percent. 

Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations. Washington, DC National Academy Press, 1993. 

FIGURE 38 Lead coffin. Lead coffin (first—third centuries c.E.) from Jerusalem, Israel. Lead, widely used in many ancient civilizations, was one of the first metals to be recovered from its ores. Lead objects date back from as early as the seventh century b.c.e. In Mesopotamia molten lead was used to fasten bolts and shafts into masonry. In Syria it was made into rods used as currency, and in Greece it was cast into coins. During the Roman Empire the use of lead become so widespread that the health hazards caused by lead exposure are suspected to have been one of the factors affecting the fall of the Roman Empire. Since it is very resistant to corrosion, lead was also used by the Romans, for making coffins as the one illustrated. 

The amount of total lead in the blood can be measured to determine if exposure to lead has occurred. This test can tell if you have been recently exposed to lead. Lead can be measured lead in teeth or bones by X-ray techniques, but these methods are not widely available. These tests tell about long-term exposures to lead. Exposure to lead can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high. However, the EP level is not sensitive enough to identify children with elevated blood lead levels below about 25 micrograms per deciliter ( ig/dL). For this reason, the primary screening method is measurement of blood lead. For more information on tests to measure lead in the body, see Chapters 2 and 6. 

OSHA regulations limit the concentration of lead in workroom air to 50 ig/m3 for an 8-hour workday. If a worker has a blood lead level of 50 ig/dL, then OSHA requires that worker be removed from the workroom where lead exposure is occurring. 

PbB concentrations reflect the absorbed dose of lead. However, the interpretation of PbB data depends on a knowledge of the past history of exposure to lead. This is because in the body, bone constitutes the major lead sink and this results in lead having a long body half-life. Thus, in the absence of intense exposure to lead for a considerable period up to its body half-life, the PbB concentrations reflect recent lead exposures. However, if intermittent exposure to lead is occurring in several distinct environments, the PbB concentration reflects both recent and past exposures to lead. Thus, biological effects for populations with the same PbB concentrations may not be the same since different exposure times scales may be involved. This is the reason why free erythrocyte protoporphyrin (FEP) and erythrocyte zinc protoporphyrin (ZPP) have been used as additional biological markers since their elevation is more related to chronic lead exposure than acute lead exposure (see Section 2.7). 

In summary, while no strong conclusions can be drawn based on these mortality studies, it is important to note that four of these studies (Fanning 1988 Malcolm and Barnett 1982 McDonald and Potter 1996 Michaels et al. 1991) reported some elevation in deaths due to cerebrovascular disease. No other studies reported increased mortality due to cerebrovascular disease caused by lead exposure. 

Respiratory Effects. The only information located regarding respiratory effects in humans associated with lead exposure was a case report of a 41-year-old man who was exposed to lead for 6 years while removing old lead-based paint from a bridge. At the time of the initial assessment, his PbB level was 87 pg/dL, and he complained of mild dyspnea for the last 2-3 years. No abnormalities in respiratory function were seen at clinical examination, so it is not possible to conclude that his respiratory symptoms were related to exposure to lead (Pollock and Ibels 1986). 

Cardiovascular Effects. There is currently considerable scientific debate as to whether there is a causal relationship between lead exposure and hypertension. Another area of controversy is whether African Americans are more susceptible to the cardiovascular effects of lead than are whites or Hispanics. The evidence from both occupational studies and large-scale general population studies (i.e., National Health and Nutrition Examination Survey [NHANES II], British Regional Heart Study [BRHS]) is not sufficient to conclude that such a causal relationship exists between PbB levels and increases in blood pressure. The database on lead-induced effects on cardiovascular function in humans will be discussed by presenting a summary of several representative occupational studies followed by a discussion of the findings from the large-scale general population studies. 

Another occupational study failed to reveal any significant correlation between occupational lead exposure and diastolic and systolic blood pressure (Parkinson et al. 1987). After controlling for known risk factors (e.g., age, education, income, cigarette usage, alcohol consumption, and exercise), the association between exposure and blood pressure was found to be small and nonsignificant when a group of randomly selected white battery plant workers (n=270) was compared to 158 nonexposed workers. 

Hypertension has also been associated with lead exposure in the general population. In a case-control study of clinically defined groups, 38 male cardiovascular patients were compared with 48 matched normotensive patients (Khera et al. 1980b). The cardiovascular patients were found to have higher PbB levels (mean, 44.9 ig/dL) than the normotensive patients (mean, 29.0 pg/dL). However, this study is limited by small sample size and incomplete control of confounding factors. 

Taken together, the results of both the occupational and general population studies do not provide conclusive evidence that lead exposure, as assessed by PbB levels, is positively associated with hyper-... 

Histopathological evidence of renal damage has been observed in lead-exposed workers. Renal ultrastructure and function were examined in five men with heavy occupational exposure to lead (Cramer et al. 1974). In addition, renal function was evaluated in two men from whom renal biopsies were not obtained. PbB levels ranged from 71 to 138 pg/dL. Renal function tests were normal in all except for a reduced glomerular filtration rate in one worker. Two subjects with relatively short exposure to lead (6 weeks and 8 months) and PbB levels of 89-129 pg/dL had intranuclear inclusions in the proximal tubules. Renal biopsies from workers with longer periods of lead exposure (4-20 years, PbB levels of 71-138 pg/dL) had diffuse interstitial or peritubular fibrosis. Glomeruli were normal in all subjects. 

Blood lead levels, urinary lead levels, serum creatinine, blood urea nitrogen (BUN), creatinine clearance (CCT), and NAG were measured in 158 male and 51 female workers in a lead battery factory or a lead smelting plant in Japan (Ong et al. 1987). Controls consisted of 30 professional and laboratory staff members with no history of renal disease or lead exposure. The length of exposure to lead averaged 10.8 8.0 years with a range of 1-36 years. Exposure levels were not available, but indicators of lead body burden in the exposed workers were PbB level = 3.0-80.0 pg/dL and urinary lead level =... 

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