Neurotoxicology · 2009
Association of high body lead store with severe intracranial carotid atherosclerosis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lee Tsong-Hai, Tseng Mei-Chun, Chen Chi-Jen, Lin Ja-Liang
Аннотация
OBJECTIVE: Lead is involved in the pathogenesis of atherosclerosis and hypertensive disease and may be related to cerebrovascular disease. We studied the association of body lead level with stroke subtypes and severity of cerebral atherosclerosis in order to identify the significance of lead exposure to cerebrovascular disease.
METHODS: From April, 2002 to March, 2005, we studied the lead level in all patients receiving digital subtraction angiography. Diameter stenosis at extracranial carotid, intracranial carotid and vertebrobasilar system was calculated according to the NASCET criteria. A blood sample and a mobilization test of 72-h urine sample were collected for lead measurement.
RESULTS: In a total of 213 subjects, 19 were free of stroke (blood lead level=4.62+/-2.41 microg/dL, body lead store=39.04+/-20.91 microg) and 194 were stroke patients (4.89+/-2.75 microg/dL, 45.13+/-29.8 microg; all stroke vs. non-stroke, P>0.05). In the 153 subjects with atherosclerotic origin, body lead store but not blood lead level in the intracranial carotid system was significantly higher in > or =50% group than <50% group (blood lead: 5.61+/-3.02 microg/dL vs. 4.80+/-2.50 microg/dL, Student's t-test, P=0.129; body lead store: 51.7+/-27.0 microg vs. 41.9+/-23.5 microg, Student's t-test, P=0.038, multivariate logistic regression, odds ratio=1.02, 95% CI: 1.00-1.03, P=0.043). However, there was no significant association between lead level and stenotic severity in extracranial and vertebrobasilar systems (P>0.05).
CONCLUSION: Our study demonstrated that long-term lead exposure as measured by body lead store might carry a potential risk of intracranial carotid atherosclerosis.
METHODS: From April, 2002 to March, 2005, we studied the lead level in all patients receiving digital subtraction angiography. Diameter stenosis at extracranial carotid, intracranial carotid and vertebrobasilar system was calculated according to the NASCET criteria. A blood sample and a mobilization test of 72-h urine sample were collected for lead measurement.
RESULTS: In a total of 213 subjects, 19 were free of stroke (blood lead level=4.62+/-2.41 microg/dL, body lead store=39.04+/-20.91 microg) and 194 were stroke patients (4.89+/-2.75 microg/dL, 45.13+/-29.8 microg; all stroke vs. non-stroke, P>0.05). In the 153 subjects with atherosclerotic origin, body lead store but not blood lead level in the intracranial carotid system was significantly higher in > or =50% group than <50% group (blood lead: 5.61+/-3.02 microg/dL vs. 4.80+/-2.50 microg/dL, Student's t-test, P=0.129; body lead store: 51.7+/-27.0 microg vs. 41.9+/-23.5 microg, Student's t-test, P=0.038, multivariate logistic regression, odds ratio=1.02, 95% CI: 1.00-1.03, P=0.043). However, there was no significant association between lead level and stenotic severity in extracranial and vertebrobasilar systems (P>0.05).
CONCLUSION: Our study demonstrated that long-term lead exposure as measured by body lead store might carry a potential risk of intracranial carotid atherosclerosis.