Environmental Lead Exposure and Chronic Renal Disease

2003 ◽  
Vol 348 (18) ◽  
pp. 1810-1812 ◽  
2011 ◽  
Vol 2011 (1) ◽  
Author(s):  
Maitreyi Mazumdar ◽  
David Bellinger ◽  
Matthew Gregas ◽  
Kathleen Abanilla ◽  
Janine Bacic ◽  
...  

Author(s):  
Lily D. Yan ◽  
Vanessa Rouzier ◽  
Jean Lookens Pierre ◽  
Myung Hee Lee ◽  
Paul Muntner ◽  
...  

Cardiovascular disease is the leading cause of death in lower-income countries including Haiti. Environmental lead exposure is associated with high blood pressure and cardiovascular mortality in high-income countries but has not been systematically measured and evaluated as a potential modifiable cardiovascular risk factor in lower-income countries where 6.5 billion people reside. We hypothesized lead exposure is high in urban Haiti and associated with higher blood pressure levels. Blood lead levels were measured in 2504 participants ≥18 years enrolled in a longitudinal population-based cohort study in Port-au-Prince. Lead screening was conducted using LeadCare II (detection limit ≥3.3 µg/dL). Levels below detection were imputed by dividing the level of detection by √2. Associations between lead (quartiles) and systolic blood pressure and diastolic blood pressure were assessed, adjusting for age, sex, obesity, smoking, alcohol, physical activity, income, and antihypertensive medication use. The median age of participants was 40 years and 60.1% were female. The geometric mean blood lead level was 4.73µg/dL, 71.1% had a detectable lead level and 42.3% had a blood lead level ≥5 µg/dL. After multivariable adjustment, lead levels in quartile four (≥6.5 µg/dL) compared with quartile 1 (<3.4 µg/dL) were associated with 2.42 mm Hg (95% CI, 0.36–4.49) higher systolic blood pressure and 1.96 mm Hg (95% CI, 0.56–3.37) higher diastolic blood pressure. In conclusion, widespread environmental lead exposure is evident in urban Haiti, with higher lead levels associated with higher systolic and diastolic blood pressure. Lead is a current and potentially modifiable pollutant in lower-income countries that warrants urgent public health remediation. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03892265.


2014 ◽  
Vol 140 ◽  
pp. e170-e171 ◽  
Author(s):  
Antonio Pascale ◽  
Cristina B. Bares ◽  
A. Sosa ◽  
M.J. Moll ◽  
S. Couto ◽  
...  

2010 ◽  
Vol 143 (1) ◽  
pp. 97-102 ◽  
Author(s):  
Hua Shi ◽  
Yong-mei Jiang ◽  
Jia-yuan Li ◽  
Fang Liu ◽  
Hong Wang ◽  
...  

Mutagenesis ◽  
2007 ◽  
Vol 22 (3) ◽  
pp. 201-207 ◽  
Author(s):  
L. Kapka ◽  
A. Baumgartner ◽  
E. Siwinska ◽  
L. E. Knudsen ◽  
D. Anderson ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Jintana Sirivarasai ◽  
Winai Wananukul ◽  
Sming Kaojarern ◽  
Suwannee Chanprasertyothin ◽  
Nisakron Thongmung ◽  
...  

A number of studies suggested that lead is related to the induction of oxidative stress, and alteration of immune response. In addition, modifying these toxic effects varied partly by GST polymorphism. The objectives of this study were to assess the association between the lead-induced alteration in serum hs-CRP, with GSTM1, GSTT1, and GSTP1 Val105Ile genetic variations and the health consequence from environmental lead exposure. The 924 blood samples were analyzed for blood lead, CRP, and genotyping of three genes with real-time PCR. Means of blood lead and serum hs-CRP were 5.45 μg/dL and 2.07 mg/L. Both CRP and systolic blood pressure levels were significantly higher for individuals with blood lead in quartile 4 (6.48–24.63 μg/dL) compared with those in quartile 1 (1.23–3.47 μg/dL,P<0.01). In particular, in men with blood lead >6.47 μg/dL the adjusted odds ratio (OR) of CRP levels for individuals with GSTP1 variants allele, GSTM1 null, GSTT1 null, double-null GSTM1, and GSTT1 compared with wild-type allele was 1.46 (95% CI; 1.05–2.20), 1.32 (95% CI; 1.03–1.69), 1.65 (95% CI; 1.17–2.35), and 1.98 (95% CI; 1.47–2.55), respectively. Our findings suggested that lead exposure is associated with adverse changes in inflammatory marker and SBP. GST polymorphisms are among the genetic determinants related to lead-induced inflammatory response.


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