title: Association between prenatal lead exposure and blood pressure in children.
abstract: BACKGROUND
  Lead exposure in adults is associated with hypertension. Altered prenatal nutrition is associated with subsequent risks of adult hypertension, but little is known about whether prenatal exposure to toxicants, such as lead, may also confer such risks.
  
  
  OBJECTIVE
  We investigated the relationship of prenatal lead exposure and blood pressure (BP) in 7- to 15-year-old boys and girls.
  
  
  METHODS
  We evaluated 457 mother-child pairs, originally recruited for an environmental birth cohort study between 1994 and 2003 in Mexico City, at a follow-up visit in 2008-2010. Prenatal lead exposure was assessed by measurement of maternal tibia and patella lead using in vivo K-shell X-ray fluorescence and cord blood lead using atomic absorption spectrometry. BP was measured by mercury sphygmomanometer with appropriate-size cuffs.
  
  
  RESULTS
  Adjusting for relevant covariates, maternal tibia lead was significantly associated with increases in systolic BP (SBP) and diastolic BP (DBP) in girls but not in boys (p-interaction with sex = 0.025 and 0.007 for SBP and DBP, respectively). Among girls, an interquartile range increase in tibia lead (13 μg/g) was associated with 2.11-mmHg [95% confidence interval (CI): 0.69, 3.52] and 1.60-mmHg (95% CI: 0.28, 2.91) increases in SBP and DBP, respectively. Neither patella nor cord lead was associated with child BP.
  
  
  CONCLUSIONS
  Maternal tibia lead, which reflects cumulative environmental lead exposure and a source of exposure to the fetus, is a predisposing factor to higher BP in girls but not boys. Sex-specific adaptive responses to lead toxicity during early-life development may explain these differences.
authors.affiliation: Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan 48109-2029, USA. aiminz@umich.edu
authors.forename: Aimin
authors.initials: A
authors.lastname: Zhang
authors.forename: Howard
authors.initials: H
authors.lastname: Hu
authors.forename: Brisa N
authors.initials: BN
authors.lastname: Sánchez
authors.forename: Adrienne S
authors.initials: AS
authors.lastname: Ettinger
authors.forename: Sung Kyun
authors.initials: SK
authors.lastname: Park
authors.forename: David
authors.initials: D
authors.lastname: Cantonwine
authors.forename: Lourdes
authors.initials: L
authors.lastname: Schnaas
authors.forename: Robert O
authors.initials: RO
authors.lastname: Wright
authors.forename: Hector
authors.initials: H
authors.lastname: Lamadrid-Figueroa
authors.forename: Martha Maria
authors.initials: MM
authors.lastname: Tellez-Rojo
mesh_terms: D000293:Adolescent; D001794:Blood Pressure; D001842:Bone and Bones / Q000737:chemistry*; D002648:Child; D015331:Cohort Studies; D004785:Environmental Pollutants / Q000633:toxicity*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000453:epidemiology*; D007854:Lead / Q000633:toxicity*; D008137:Longitudinal Studies; D008297:Male; D008800:Mexico / Q000453:epidemiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000453:epidemiology*; D011446:Prospective Studies; D012737:Sex Factors; D014470:Umbilical Cord / Q000737:chemistry*
chemical_list: D004785:Environmental Pollutants; D007854:Lead