TY - JOUR
T1 - Association of high body lead store with severe intracranial carotid atherosclerosis
AU - Lee, Tsong Hai
AU - Tseng, Mei Chun
AU - Chen, Chi Jen
AU - Lin, Ja Liang
N1 - Funding Information:
The authors would like to thank the National Science Council, Taiwan (Contract No. NSC 94-2314-B-182A-017) and Chang Gung Memorial Hospital under the Medical Research Project (Contract Nos. CMRPG331403, CMRPG350731 and CMRP 1150) for financially supporting this research.
PY - 2009/11
Y1 - 2009/11
N2 - 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 μg/dL, body lead store = 39.04 ± 20.91 μg) and 194 were stroke patients (4.89 ± 2.75 μg/dL, 45.13 ± 29.8 μg; 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 ≥50% group than <50% group (blood lead: 5.61 ± 3.02 μg/dL vs. 4.80 ± 2.50 μg/dL, Student's t-test, P = 0.129; body lead store: 51.7 ± 27.0 μg vs. 41.9 ± 23.5 μg, 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.
AB - 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 μg/dL, body lead store = 39.04 ± 20.91 μg) and 194 were stroke patients (4.89 ± 2.75 μg/dL, 45.13 ± 29.8 μg; 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 ≥50% group than <50% group (blood lead: 5.61 ± 3.02 μg/dL vs. 4.80 ± 2.50 μg/dL, Student's t-test, P = 0.129; body lead store: 51.7 ± 27.0 μg vs. 41.9 ± 23.5 μg, 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.
KW - Angiography
KW - Atherosclerosis
KW - Carotid artery
KW - Lead
KW - Stroke
UR - http://www.scopus.com/inward/record.url?scp=71349085779&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=71349085779&partnerID=8YFLogxK
U2 - 10.1016/j.neuro.2009.07.004
DO - 10.1016/j.neuro.2009.07.004
M3 - Article
C2 - 19616024
AN - SCOPUS:71349085779
SN - 0161-813X
VL - 30
SP - 876
EP - 880
JO - NeuroToxicology
JF - NeuroToxicology
IS - 6
ER -