Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).     

Body burdens of lead in hypertensive nephropathy

Chronic lead exposure resulting in blood lead concentrations that exceed 1.93 mumol/l (40 micrograms/dl) or chelatable urinary lead excretion greater than 3.14 mumol (650 micrograms) per 72 h has been associated with renal disease. A previous study had found greater chelatable urine lead excretion in subjects with hypertension and renal failure than in controls with renal failure due to other causes, although mean blood lead concentrations averaged 0.92 mumol/l (19 micrograms/dl). To determine if chelatable urinary lead, blood lead, or the hematologic effect of lead (zinc protoporphyrin) were greater in hypertensive nephropathy (when hypertension precedes elevation of serum creatinine) than in other forms of mild renal failure, we compared 40 study subjects with hypertensive nephropathy to 24 controls having a similar degree of renal dysfunction due to causes other than hypertension. Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l). We conclude that subjects from a general population with hypertensive nephropathy do not have greater body burdens of lead than renal failure controls.     

Lead exposure and radiator repair work.

In 1986, the ambient air for lead in radiator repair shops in the Minneapolis-St. Paul metropolitan area exceeded the Occupational Safety and Health Administration (OSHA) action level in nine of 12 shops sampled by Minnesota OSHA. We therefore sought to determine the prevalence of lead exposure/toxicity in this industry. Thirty-five radiator shops were identified, 30 were visited, and 53 workers were studied. The mean blood lead level was 1.53 (range 0.24-2.80). Seventeen individuals had blood lead levels greater than or equal to 1.93 mumol/L (40 micrograms/dl). The mean zinc protoporphyrin level (ZPP) was 0.55 mumol/L (range 0.16-1.43). No single worksite or personal characteristic was a strong determinant of either blood lead or ZPP level.     

An analysis of occupational blood lead trends in Manitoba, 1979 through 1987.

BACKGROUND: While regulations for workplace lead exposure become more strict, their effectiveness in decreasing blood lead concentrations and the method by which this is attained have not been evaluated. METHODS: An analysis was conducted of 10,190 blood lead samples from employees of 10 high-risk workplaces collected in Manitoba, 1979-87, as part of regulated occupational surveillance. RESULTS: A significant decrease in blood lead concentrations was observed overall as well as for each individual company. A 1979 government regulation to reduce blood lead to below 3.38 mumol/L (70 micrograms/dl) was followed by a drop in blood lead concentrations; a 1983 order to reduce blood leads to below 2.90 mumol/L (60 micrograms/dl) was not followed by such a drop. Longitudinal analysis by individual workers suggested that companies were complying by use of administrative control, i.e., removing workers to lower lead areas until blood lead levels had fallen, then returning them to high lead areas. CONCLUSION: Focusing upon blood lead as the sole criterion for compliance is not effective; regulations must specifically require environmental monitoring and controls. Biological surveillance serves as "back-up" to environmental surveillance and this database illustrates the usefulness of a comprehensive centralized surveillance system.     

Assessment of the body burden of chelatable lead: a model and its application to lead workers.

A hypothetical model was introduced to estimate the body burden of chelatable lead from the mobilisation yield of lead by calcium disodium ethylenediamine tetra-acetate (CaEDTA). It was estimated that, on average, 14 and 19% of the body burden was mobilised into the urine during the 24 hours after an injection of 53.4 mumol (20 mg) and 107 mumol (40 mg) CaEDTA per kg bodyweight, respectively. The body burden of chelatable lead ranged from 4 mumol (0.8 mg) to 120 mumol (24.9 mg) (mean 37 mumol (7.7 mg) in lead workers with blood lead concentrations of 0.3-2.9 mumol/kg (6-60 microgram/100 g) (mean 1.4 mumol/kg (29 microgram/100 g)). There were linear relationships between blood lead concentrations and body burden of chelatable lead on a log scale.     

Correlation between maternal and cord blood lead levels

Whole blood lead levels were estimated by atomic absorption analysis in 226 blood samples from 113 mothers of 23 different nationalities. Samples were collected before delivery, and from cord blood from their respective neonates. The concentrations of blood lead were within the expected range of occupationally unexposed populations. Mean maternal blood lead levels were 0.72 0.10 mumol/l (14.9 2.14 mug/dl), range 0.32-1.34 mumol/l (6.6-27.8 mug/dl) and mean cord blood levels were 0.64 0.12 mumol/l (range 0.29-1.46 mumol/l). Sixteen percent of the mothers and nearly 10% cord blood samples were found to have blood lead level greater than 0.97 mumol/l (20 mug/dl). Very high levels, in excess of 1.21 mumol/l (25 mug/dl), were detected in 3.5% of mothers as compared to 2.6% of cord blood samples. Out of 113 infants, 65 (58%) were males with a mean cord blood lead level of 0.63 mumol/l and 48 (42%) were females with a mean level of 0.66 muol/l. The lowest maternal blood lead levels 0.68 mumol/l were observed in ages 20 to 25 years old, and lowest cord blood levels 0.58 mumol/l were seen in maternal age of less than 20 years old. On the other hand, the highest maternal and cord blood lead levels (0.82 and 0.75 mumol/l, respectively) were observed in maternal ages of greater than 35 years old. The results show a direct correlation of blood lead level between mothers and umbilical cord as seen in the linear regression distribution curve.     

铅中毒筛选指标的再评价

目的 评价铅中毒筛选指标的准确性。方法 连续收集１５７名铅接触工人的血标本,同时测定血铅,红细胞游离原卟啉（ＦＥＰ）,锌卟啉（ＺＰＰ）,尿铅,尿δ－氨基－酮戊酸（δ－ＡＬＡ）,红细胞嘧啶５′核苷酸酶（Ｐ５′Ｎ）的活性。以血铅≥１．９３μｍｏｌ／Ｌ,≥２．９０μｍｏｌ／Ｌ为金标准,用受试工作特征（ＲＯＣ）,曲线下的面积评价上述指标在血铅≥１．９３μｍｏｌ／Ｌ,≥２．９０μｍｏｌ／Ｌ的准确性,用ＲＯ     

Neurobehavioural effects of occupational exposure to lead

A set of neurobehavioural tests selected on the basis of information processing theory was used to study the effect of low level occupational lead exposure on 59 lead workers compared with a matched control group of the same number. Only one of the lead exposed group had a blood lead concentration above the current threshold limit value of 3.81 mumol/l at the time of testing (mean 2.36 mumol/l, range 1.19-3.92 mumol/l) and none had been detected above that level in the previous three years. Nevertheless, most neurobehavioural functions tested showed some impairment in the lead workers. Visual sensory function was affected and, perhaps as a consequence, sustained attention and psychomotor tasks were performed more slowly by the lead exposed group. Cognitive functions were also impaired, with sensory store memory, short term memory, and learning abilities all showing deficits in lead workers. Such cognitive deficits may also be partly due to initial degradation of the visual input. Long term memory performance compared equally with control levels possibly because of development of a compensatory strategy such as rehearsal by the lead exposed subjects. Multiple linear regression analysis relating to lead workers test performance and their lead exposure showed that performance on the sensory store memory test alone was significantly related to exposure. This was probably due to the homogeneity of the lead exposed group with regard to blood lead concentrations and the use of blood lead as a measure of chronic lead exposure.     

Neurobehavioural effects of occupational exposure to lead.

A set of neurobehavioural tests selected on the basis of information processing theory was used to study the effect of low level occupational lead exposure on 59 lead workers compared with a matched control group of the same number. Only one of the lead exposed group had a blood lead concentration above the current threshold limit value of 3.81 mumol/l at the time of testing (mean 2.36 mumol/l, range 1.19-3.92 mumol/l) and none had been detected above that level in the previous three years. Nevertheless, most neurobehavioural functions tested showed some impairment in the lead workers. Visual sensory function was affected and, perhaps as a consequence, sustained attention and psychomotor tasks were performed more slowly by the lead exposed group. Cognitive functions were also impaired, with sensory store memory, short term memory, and learning abilities all showing deficits in lead workers. Such cognitive deficits may also be partly due to initial degradation of the visual input. Long term memory performance compared equally with control levels possibly because of development of a compensatory strategy such as rehearsal by the lead exposed subjects. Multiple linear regression analysis relating to lead workers test performance and their lead exposure showed that performance on the sensory store memory test alone was significantly related to exposure. This was probably due to the homogeneity of the lead exposed group with regard to blood lead concentrations and the use of blood lead as a measure of chronic lead exposure.     

Relationship between blood lead levels and renal function in lead battery workers

OBJECTIVES: The aim of this study was to investigate the correlation between blood lead (PbB) levels and renal function indices of blood-urea nitrogen (BUN), serum creatinine (SC) and uric acid (UA) among lead battery workers with exposure to lead. METHODS: A total of 229 workers of both genders from two lead battery factories were recruited in this cross-sectional study. The personal airborne and blood samples were collected on the same day. The airborne lead (PbA) and PbB levels, and individual renal function parameters were measured and statistically analyzed. RESULTS: A positive correlation between PbB levels and individual renal function index of BUN, SC, and UA was found ( P<0.01). The PbB levels and renal function indices showed significant difference between male and female workers. Based on a multiple regression model, an increment of 10 micro g/dl PbB produced an increase of 0.62 mg/dl BUN, after being adjusted for work duration and age, and an increase of 0.085 mg/dl UA, after being adjusted for gender and body weight. Workers with PbB 60 microg/dl showed a positive dose-effect relationship with significant difference in BUN ( P<0.001) and UA ( P<0.05), and the percentage of workers with BUN and UA over the reference value also showed an increasing trend. CONCLUSION: Blood-urea nitrogen and uric acid could be considered as suitable prognostic indicators of renal dysfunction in lead-exposed workers. Our results showed that PbB levels higher than 60 micro g/dl had increasing chances of inducing adverse renal effects.     

Lead-induced anemia: dose-response relationships and evidence for a threshold.

We conducted a cross-sectional epidemiologic study to assess the association between blood lead level and hematocrit in 579 one to five year-old children living near a primary lead smelter in 1974. Blood lead levels ranged from 0.53 to 7.91 mumol/L (11 to 164 micrograms/dl). To predict hematocrit as a function of blood lead level and age, we derived non-linear regression models and fit percentile curves. We used logistic regression to predict the probability of hematocrit values less than 35 per cent. We found a strong non-linear, dose-response relationship between blood lead level and hematocrit. This relationship was influenced by age, but (in this age group) not by sex; the effect was strongest in youngest children. In one year-olds, the age group most severely affected, the risk of an hematocrit value below 35 percent was 2 percent above background at blood lead levels between 0.97 and 1.88 mumol/L (20 and 39 micrograms/dl), 18 percent above background at lead levels of 1.93 to 2.85 mumol/L (40 to 59 micrograms/dl), and 40 percent above background at lead levels of 2.9 mumol/L (60 micrograms/dl) and greater; background was defined as a blood lead level below 1.88 mumol/L (20 micrograms/dl). This effect appeared independent of iron deficiency. These findings suggest that blood lead levels close to the currently recommended limit value of 1.21 mumol/L (25 micrograms/dl) are associated with dose-related depression of hematocrit in young children.     

Occupational lead exposure in Denmark: screening with the haematofluorometer.

The zinc protoporphyrin/haemoglobin (ZPP/Hb) ratio was measured in the field with a haematofluorometer. A significant increase in ZPP/Hb ratio with advancing age was found in 1295 men who denied any excess exposure to lead. Ninety-seven per cent of the results were below 110 mumol ZPP/mol Hb(Fe) (4.4 microgram ZPP/g Hb). The ZPP/Hb ratio was determined in a lead-exposed population of 2275 men, and in 305 a blood lead analysis was also performed. A blood lead limit of 2.9 mumol/l (60 microgram/100 ml) corresponds to about 500 mumol ZPP/mol Hb(Fe) (20 microgram/g). This limit was exceeded in workers engaged in secondary lead smelting, storage battery manufacture, car radiator repair, crystal glass manufacture, storage battery repair, ship breaking, metal foundries, the ceramic industry, scrap metal handling, and PVC plastic manufacture. Other occupations caused lower lead exposures with ZPP/Hb ratios between 110 and 500 mumol ZPP/mol Hb(Fe): such ratios were found in men from shooting ranges, in leaded pane manufacturers, gunsmiths, car paint sprayers, type setters, steel rolling mill workers, shipbuilders and welders, car mechanics, lead pigment handlers, and solderers. Increased ZPP/Hb ratios and blood lead levels in 210 workers were associated with a decrease in haemoglobin concentration in the blood. Thus, the haematofluorometer has proved to be very useful for screening purposes. A blood lead determination should be performed if the ZPP/Hb ratio exceeds 300 microgram ZPP/mol Hb(Fe) (12 microgram/g).     

Occupational lead exposure in Denmark: screening with the haematofluorometer.

The zinc protoporphyrin/haemoglobin (ZPP/Hb) ratio was measured in the field with a haematofluorometer. A significant increase in ZPP/Hb ratio with advancing age was found in 1295 men who denied any excess exposure to lead. Ninety-seven per cent of the results were below 110 mumol ZPP/mol Hb(Fe) (4.4 microgram ZPP/g Hb). The ZPP/Hb ratio was determined in a lead-exposed population of 2275 men, and in 305 a blood lead analysis was also performed. A blood lead limit of 2.9 mumol/l (60 microgram/100 ml) corresponds to about 500 mumol ZPP/mol Hb(Fe) (20 microgram/g). This limit was exceeded in workers engaged in secondary lead smelting, storage battery manufacture, car radiator repair, crystal glass manufacture, storage battery repair, ship breaking, metal foundries, the ceramic industry, scrap metal handling, and PVC plastic manufacture. Other occupations caused lower lead exposures with ZPP/Hb ratios between 110 and 500 mumol ZPP/mol Hb(Fe): such ratios were found in men from shooting ranges, in leaded pane manufacturers, gunsmiths, car paint sprayers, type setters, steel rolling mill workers, shipbuilders and welders, car mechanics, lead pigment handlers, and solderers. Increased ZPP/Hb ratios and blood lead levels in 210 workers were associated with a decrease in haemoglobin concentration in the blood. Thus, the haematofluorometer has proved to be very useful for screening purposes. A blood lead determination should be performed if the ZPP/Hb ratio exceeds 300 microgram ZPP/mol Hb(Fe) (12 microgram/g).     

Intrauterine lead exposure and preterm birth

The objective of this study was to determine the risk of preterm birth in relation to umbilical cord blood lead levels (UCL) among primiparous and multiparous women. A case-cohort study was performed in Mexico City during 1995. A total of 459 full-term births was compared with 161 preterm births (before 37 gestational weeks). Mothers were interviewed before the delivery about their reproductive histories and other related factors of preterm birth. Lead was determined by atomic absorption spectrophotometry. Lead levels were higher in primiparous women who had a preterm birth than in primiparous women with a full-term birth (9.77+/-2.0 microgram/dl vs 8.24+/-2.15 microgram/dl); this difference was marginally significant. After adjusting for other known preterm birth risk factors, the frequency of preterm birth was almost three times higher among women who had UCL levels greater or equal to 5.1 microgram/dl compared to those who had UCL levels lower than 5.1 microgram/dl. This difference was not observed among multiparous women. Our results suggest that intrauterine lead exposure may be associated with preterm birth in first deliveries but not in subsequent ones.     

Screening for lead toxicity among autobody repair workers

Fifty-one workers in 10 small, neighborhood autobody repair shops were screened for lead toxicity using blood zinc protoporphyrin (ZPP) levels and work history questionnaires. Those with high ZPP levels (greater than 50 μg/dl) had further studies, including blood lead determinations. The shops were dusty with ground putty dust (lead-free) and paint spray (lead content range 0–40%). Thirteen (26%) workers had mildly elevated ZPP levels (all were full-time sander/sprayers) though few had symptoms and none had elevated blood lead levels. Eighteen controls, workers in other occupations, had normal ZPP levels. Air monitoring during inactive periods failed to reveal high lead levels (range 0–28 μg/m²). These data suggest that workers in autobody repair shops are at risk of lead toxicity but the exposure and biologic effects are less than in many other industries that utilize lead.     

Effects of lead on the endocrine system in lead smelter workers.

In this study of the effects of lead on the endocrine system, 77 secondary lead-smelter workers (i.e., 62 active and 15 retired) were compared with 26 referents. Lead concentrations were determined in plasma with inductively coupled plasma mass spectrometry (i.e., index of recent exposure), in blood with atomic absorption spectrophotometry, and in fingerbone with K x-ray fluorescence technique (i.e., index of long-term exposure). In addition, pituitary hormones were determined in serum by fluoroimmunoassay, and thyroid hormones and testosterone in serum were determined with radioimmunoassay. Nine lead workers and 11 referents were challenged with gonadotrophin-releasing hormone and thyrotrophin-releasing hormone, followed by measurements of stimulated pituitary hormone levels in serum. Median levels of lead in plasma were 0.14 microg/dl (range = 0.04-3.7 microg/dl) in active lead workers, 0.08 microg/dl (range = 0.05-0.4 microg/dl) in retired lead workers, and 0.03 microg/dl (range = 0.02-0.04 microg/dl) in referents (1 microg/dl = 48.3 nmol/l). Corresponding blood lead concentrations were 33.2 microg/dl (range = 8.3-93.2 microg/dl), 18.6 microg/dl (range = 10.4-49.7 microg/dl), and 4.1 microg/dl (range 0.8-6.2 microg/dl), respectively. Respective bone lead levels were 21 microg/gm (range = -13 to 99 microg/gm), 55 microg/gm (range = 3-88 microg/gm), and 2 microg/gm (range = -21 to 14 microg/gm). Concentrations of basal serum hormone (i.e., free thyroid hormones, thyrotrophin, sex hormone binding globulin, and testosterone) were similar in the 3 groups. There were no significant associations between the hormones mentioned herein and blood plasma, blood lead, and bone lead levels. In the challenge test, stimulated follicle-stimulating hormone levels were significantly lower in lead workers (p = .014) than in referents, indicating an effect of lead at the pituitary level. Also, there was a tendency toward lower basal stimulated follicle-stimulating hormone concentrations in lead workers (p = .08). This effect, however, was not associated with blood plasma level, blood lead level, or bone lead level. In conclusion, a moderate exposure to lead was associated with only minor changes in the male endocrine function, particularly affecting the hypothalamic-pituitary axis. Given that sperm parameters were not studied, the authors could not draw conclusions about fertility consequences.     

Critical dose of lead affecting delta-aminolevulinic acid levels

To estimate the critical dose of the association between the blood lead concentration (BPb) and delta-aminolevulinic acid (ALA) levels, ALA levels in plasma (ALA-P), blood (ALA-B), and urine (ALA-U), and the activity of delta-aminolevulinic acid dehydratase (ALAD) were determined in 186 Japanese lead workers, aged 18-62 yr, with BPb levels of 2.1-62.9 g/dl. For this purpose, the benchmark dose (BMD) method, recently used in the environmental health field in place of the no-observed-adverse-effect level, was introduced into this study. The BMD was defined as the BPb level that resulted in an increased probability of abnormal change in ALA-related parameters by an excess risk (BMR) of 5% in exposed workers i.e., from P0 (abnormal probability of 5% in unexposed workers) to P0+BMR for exposed workers at the BMD. ALA-related parameters were significantly correlated with BPb. The BMDs computed from the 186 workers, after controlling for age, were 15.3-20.9 microg/dl for ALA levels, and 2.9 microg/dl for ALAD; likewise, the BMDs from the 154 workers with BPb levels of less than 40 microg/dl were 3.3-8.8 microg/dl for ALA levels, and 2.7 microg/dl for ALAD. Since the cutoff value of ALA-P, computed from the latter workers, seems to be closer to the upper normal limit in unexposed adults than does that from the former workers, it is suggested that the critical dose of BPb causing the increased levels of ALA is below 10 microg/dl. Such critical doses are necessary to promote preventive activities of adverse effects of lead.     

Relation between blood lead levels and childhood anemia in India

Lead pollution is a substantial problem in developing countries such as India. The US Centers for Disease Control and Prevention has defined an elevated blood lead level in children as > or = 10 microg/dl, on the basis of neurologic toxicity. The US Environmental Protection Agency suggests a threshold lead level of 20-40 microg/dl for risk of childhood anemia, but there is little information relating lead levels <40 microg/dl to anemia. Therefore, the authors examined the association between lead levels as low as 10 mug/dl and anemia in Indian children under 3 years of age. Anemia was divided into categories of mild (hemoglobin level 10-10.9 g/dl), moderate (hemoglobin level 8-9.9 g/dl), and severe (hemoglobin level <8 g/dl). Lead levels <10 mug/dl were detected in 568 children (53%), whereas 413 (38%) had lead levels > or = 10-19.9 microg/dl and 97 (9%) had levels > or = 20 microg/dl. After adjustment for child's age, duration of breastfeeding, standard of living, parent's education, father's occupation, maternal anemia, and number of children in the immediate family, children with lead levels > or = 10 microg/dl were 1.3 (95% confidence interval: 1.0, 1.7) times as likely to have moderate anemia as children with lead levels <10 microg/dl. Similarly, the odds ratio for severe anemia was 1.7 (95% confidence interval: 1.1, 2.6). Health agencies in India should note the association of elevated blood lead levels with anemia and make further efforts to curb lead pollution and childhood anemia.     

Elevated blood lead levels among construction workers in the Massachusetts Occupational Lead Registry.

Although the construction industry until recently was exempt from the Occupational Health and Safety Administration General Industry Lead Standard, including its medical monitoring provisions, periodic blood lead tests have been required for residential "deleaders" and structural painters in Massachusetts. Sixty-three percent of the 381 registrants in the Massachusetts Occupational Lead Registry with blood lead levels of 1.93 mumol/L or higher are construction workers. This proportion is much higher than that reported by registries of several states selected for comparison. These data highlight the need for better protection from lead exposure and the effectiveness of mandatory medical surveillance in identifying elevated blood lead levels among construction workers.     

Abdominal pain in lead workers

Thirty-four lead smelter workers with excessive lead absorption were evaluated and followed. Abdominal pain was present in 27 patients. Fifteen patients who had left the site of lead exposure experienced persisting abdominal pain for as long as 29 months; some of these demonstrated acceptable levels of lead in blood. There is no correlation between lead levels and persisting pain. Twenty-three patients developed abdominal pain with blood lead lower than 80 microgram/100 ml while working. Four out of 15 patients with persisting abdominal pain had blood lead between 40 and 60 microgram/100 ml while working. Typical lead-induced abdominal pain is a sensitive symptom of intoxication and may be a criterion for removal from exposure regardless of blood lead levels.