Clinical evaluation and management of lead‐exposed construction workers

Levin, S. M.; Goldberg, Mark S.

doi:10.1002/(sici)1097-0274(200001)37:1<23::aid-ajim4>3.3.co;2-l

Cited by 9 publications

(16 citation statements)

References 90 publications

(100 reference statements)

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“…In addition to use in residences, lead paint was also used in commercial buildings and other structures, such as bridges. Workers who remove paint in these sectors are at extremely high risk for lead exposure (Levin and Goldberg 2000). Construction work is regulated under the OSHA construction lead standard that took effect in 1993 (OSHA 1993), and some states have additional standards that apply specifically to the painting and deleading of residences.…”

Section: Discussionmentioning

confidence: 99%

Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.

Weisskopf

Mulkern

et al. 2004

Environ Health Perspect

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Seventy-one-year-old identical twin brothers with chronic lead poisoning were identified from an occupational medicine clinic roster. Both were retired painters, but one brother (J.G.) primarily removed paint and had a history of higher chronic lead exposure. Patella and tibia bone lead concentrations measured by K-X-ray fluorescence in each brother were 5-10 times those of the general population and about 2.5 times higher in J.G. than in his brother (E.G.). Magnetic resonance spectroscopy (MRS) studies examined N-acetylaspartate:creatine ratios, a marker of neuronal density. Ratios were lower in J.G. than in his brother. Scores on neurocognitive tests that assess working memory/executive function were below expectation in both twins. Short-term memory function was dramatically worse in J.G. than in his brother. These results demonstrate some of the more subtle long-term neurologic effects of chronic lead poisoning in adults. In particular, they suggest the presence of frontal lobe dysfunction in both twins, but more dramatic hippocampal dysfunction in the brother with higher lead exposure. The MRS findings are consistent with the hypothesis that chronic lead exposure caused neuronal loss, which may contribute to the impairment in cognitive function. Although a causal relation cannot be inferred, the brothers were genetically identical, with similar life experiences. Although these results are promising, further study is necessary to determine whether MRS findings correlate both with markers of lead exposure and tests of cognitive function. Nevertheless, the results point to the potential utility of MRS in determining mechanisms of neurotoxicity not only for lead but also for other neurotoxicants as well.

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Section: Discussionmentioning

confidence: 99%

Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.

Weisskopf

Mulkern

et al. 2004

Environ Health Perspect

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“…However, it is also one of the most detrimental pollutants in the industrial environment in many countries. Occupational and environmental exposures to lead continue to be among the most significant public health problems [1][2][3]. Lead can have adverse effects on many organ systems, and various effects of lead on thyroid functions have been reported in the past 50 years [4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Effects of lead on thyroid functions in lead-exposed workers

et al. 2010

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AbstractLead exposure is a common public health problem. Exposure to the metal can cause hematological, gastrointestinal, rheumatological, endocrine, neurological and renal problems in humans. However, effects on the thyroid gland are controversial. We retrospectively investigated thyroid function parameters in 65 adult males who had been occupationally exposed to lead. We then compared the findings with those of 60 male patients who had no history of lead exposure or thyroid abnormalities, who served as the control group. The mean ages of the lead-exposed workers and the controls were 34.3 ± 7.9 and 32.9 ± 6.6 years respectively. Blood lead levels in the lead-exposed workers were significantly higher than in the control group. The lead-exposed workers were assigned to one of three groups according to their blood lead levels, as follows: 40–59 μg/dl, 60–79 μg/dl, or 80 μg/dl and above. Thyroid Stimulating Hormone (TSH) levels in the 80 μg/dl and above group were significantly higher than in either the 40–59 μg/dl group or the 60–79 μg/dl group. However, TSH levels in the 40–59 μg/dl group did not differ significantly from those in the 60–79 μg/dl group. These results suggest that high levels of lead in the blood may affect thyroid physiology. Clinicians should be aware of the potential hazardous effects of lead on the thyroid, especially in patients who have been occupationally exposed to lead.

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“…Therefore, usually all humans have lead in their organism as a result of exposure to exogenous sources (6). Some workers are exposed to high levels of lead in their activities.…”

mentioning

confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentrationresponse curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E + ), lead acetate increased maximal response (E max ) (control: 364.4 ± 36, Pb 2+ : 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD 2 ; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E -) lead had no effect but increased baseline perfusion pressure (E + : 79.5 ± 2.4, E -: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on E max and pD 2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenasederived vasoconstrictors and involving reactive oxygen species.

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Clinical evaluation and management of lead‐exposed construction workers

Cited by 9 publications

References 90 publications

Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.

Cognitive deficits and magnetic resonance spectroscopy in adult monozygotic twins with lead poisoning.

Effects of lead on thyroid functions in lead-exposed workers

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

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