{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T15:58:43Z","timestamp":1791388723729,"version":"4.3.3"},"reference-count":45,"publisher":"American Chemical Society (ACS)","issue":"3","license":[{"start":{"date-parts":[[2017,12,29]],"date-time":"2017-12-29T00:00:00Z","timestamp":1514505600000},"content-version":"vor","delay-in-days":2285,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>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.<\/jats:p>\n                  <jats:p>Objectives: We investigated the relationship of prenatal lead exposure and blood pressure (BP) in 7- to 15-year-old boys and girls.<\/jats:p>\n                  <jats:p>Methods: We evaluated 457 mother\u2013child pairs, originally recruited for an environmental birth cohort study between 1994 and 2003 in Mexico City, at a follow-up visit in 2008\u20132010. 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.<\/jats:p>\n                  <jats:p>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 \u03bcg\/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.<\/jats:p>\n                  <jats:p>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.<\/jats:p>","DOI":"10.1289\/ehp.1103736","type":"journal-article","created":{"date-parts":[[2011,9,26]],"date-time":"2011-09-26T23:37:44Z","timestamp":1317080264000},"page":"445-450","source":"Crossref","is-referenced-by-count":86,"title":["Association between Prenatal Lead Exposure and Blood Pressure in Children"],"prefix":"10.1021","volume":"120","author":[{"given":"Aimin","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"},{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"},{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brisa N.","family":"S\u00e1nchez","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrienne S.","family":"Ettinger","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"},{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"},{"name":"Division of Chronic Disease Epidemiology, Yale Schools of Public Health and Medicine, New Haven, CT, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung Kyun","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Cantonwine","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lourdes","family":"Schnaas","sequence":"additional","affiliation":[{"name":"Division of Public Health, National Institute of Perinatology, Mexico City, Distrito Federal, Mexico, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert O.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA"},{"name":"Channing Laboratory, Department of Medicine, Brigham and Women\u2019s 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