Abstract
Lead exposure is an unresolved pediatric health risk and disproportionately affects children in lower-income neighborhoods. Residences with children younger than age 5 years are the focus of mitigation policies; however, studies have shown that older children between the ages of 5 and 12 years also are at risk of central nervous system effects. Whether historically contaminated neighborhoods present ongoing risk to older children also is of concern. This study compared the blood lead levels (BLLs) of older children from an historically contaminated urban neighborhood to those of demographically matched children from a nearby rural locale and predicted significantly higher BLLs in the urban children. The study included 222 children aged 5–12 years, 111 from the urban neighborhood and 111 from local rural townships, matched for age, sex, race/ethnicity, and family income. Blood lead, cadmium, and mercury were measured using inductively coupled plasma mass spectrometry. General linear models tested whether geographic location (urban vs. rural) predicted child heavy metal levels, controlling for sex and age. Only location predicted only child BLL (R2= 0.36); children living in the urban setting had significantly higher BLLs as compared with matched rural township children (F = 125, df220,2, p <0.001). Neighborhoods with a history of lead contamination can present current risk of lead exposure for older children between the ages of 5 and 12 years, as well as for infants and toddlers. More studies are needed to better characterize the risk of lead exposure to older children, particularly in lower-income neighborhoods with a history of lead contamination.
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References
Adler T (2005) Questioning lead standards: even low levels shave points off IQ. Environ Health Perspect 113(7):A473–A474
Agency for Toxic Substances and Disease Registry (2018) Health consultation: analysis of risk factors for childhood blood lead levels El Paso, Texas, 1997–2002. Accessed 10 Jan 2018. https://www.dshs.texas.gov/epitox/consults/elppasblpbgisfinal4_23.pdf
Bose-O’Reilly S, McCarty KM, Steckling N, Lettmeier B (2010) Mercury exposure and children’s health. Curr Probl Pediatric Adolesc Health Care 40(8):186–215. https://doi.org/10.1016/j.cppeds.2010.07.002
Census: El Paso, Texas (2014) Accessed 10 Jan 2018. https://www.unitedstateszipcodes.org
Centers for Disease and Control Prevention (2013) Blood lead levels in children aged 1–5 years—United States, 1999–2010. MMWR. Morbidity and mortality weekly report 62, no. 13 (April 5, 2013): 245–248
Chinaro K, Yard E, Dignam T, Buchanan S, Condon S, Brown MJ, Raymond J et al (2016) Blood lead levels among children aged < 6 years—Flint, Michigan, 2013–2016. MMWR Morbid Mortal Weekly Rep 65:650–654. https://doi.org/10.15585/mmwr.mm6525e1
Chłopicka J, Zachwieja Z, Zagrodzki P, Frydrych J, Słota P, Krośniak M (1998) Lead and cadmium in the hair and blood of children from a highly industrial area in Poland. Biol Trace Elem Res 62:229–234. https://doi.org/10.1007/BF02783973
Gagan F, Gupta D, Tiwari A (2012) Toxicity of lead: a review with recent updates. Interdiscip Toxicol. https://doi.org/10.2478/v10102-012-0009-2
Goyer RA (1997) Toxic and essential metal interactions. Ann Rev Nutr 17:37–50. https://doi.org/10.1146/annurev.nutr.17.1.37
Hanna-Attisha M, LaChance J, Sadler RC, Schnepp AC (2016) Elevated blood lead levels in children associated with the flint drinking water crisis: a spatial analysis of risk and public health response. Am J Public Health 106:283–290. https://doi.org/10.2105/AJPH.2015.303003
Kostial K, Kello D, Jugo S, Rabar I, Maljković T (1978) Influence of age on metal metabolism and toxicity. Environ Health Perspect 25:81–86
Landrigan PJ, Baker EL (1981) Exposure of children to heavy metals from smelters: epidemiology and toxic consequences. Environ Res 25:204–224. https://doi.org/10.1016/0013-9351(81)90090-6
Landrigan PJ, Gehlbach SH, Rosenblum BF, Shoults JM, Robert PE, Candelaria M, Barthel WM et al (1975) Epidemic lead absorption near an Ore Smelter: the role of particulate lead. N Engl J Med 292:123–129. https://doi.org/10.1056/NEJM197501162920302
Lanphear BP, Hornung R, Ho M, Howard CR, Eberly S, Knauf K (2002) Environmental lead exposure during early childhood. J Pediatrics 140:40–47. https://doi.org/10.1067/mpd.2002.120513
Morales LS, Gutierrez P, Escarce JJ (2005) Demographic and socioeconomic factors associated with blood lead levels among Mexican-American children and adolescents in the United States. Public Health Rep 120:448–454. https://doi.org/10.1177/003335490512000412
Morrison D, Lin Q, Wiehe S, Liu G, Rosenman M, Fuller T, Wang J, Filippelli G (2013) Spatial relationships between lead sources and children’s blood lead levels in the urban center of Indianapolis (USA). Environ Geochem Health 35:171–183. https://doi.org/10.1007/s10653-012-9474-y
Morse DL (1979) El Paso revisited: epidemiologic follow-up of an environmental lead problem. JAMA 242:739. https://doi.org/10.1001/jama.1979.03300080037022
Pell MB, Schneyer J (2016) The thousands of U.S. locales where lead poisoning is worse than in Flint. Reuters website, December 19, 2016. https://www.reuters.com/investigates/special-report/usa-lead-testing/
Roberts EM, Madrigal D, Valle J, King G, Kite L (2017) Assessing child lead poisoning case ascertainment in the US, 1999–2010. Pediatrics 139:e20164266. https://doi.org/10.1542/peds.2016-4266
Romero M (1997) The death of Smeltertown: a case study of lead poisoning in a Chicano community. Chicano Stud Surv Anal 115:26–37
Sobin C, Gutierrez M, Alterio H (2009) Polymorphisms of delta-aminolevulinic acid dehydratase (ALAD) and peptide transporter 2 (PEPT2) genes in children with low-level lead exposure. NeuroToxicology 30:881–887. https://doi.org/10.1016/j.neuro.2009.08.006
Sobin C, Parisi N, Schaub T, Gutierrez M, Ortega AX (2011) δ-Aminolevulinic acid dehydratase single nucleotide polymorphism 2 and peptide transporter 2*2 haplotype may differentially mediate lead exposure in male children. Arch Environ Contamin Toxicol 61:521–529. https://doi.org/10.1007/s00244-011-9645-3
Sobin C, Flores-Montoya MG, Gutierrez M, Parisi N, Schaub T (2015) δ-Aminolevulinic acid dehydratase single nucleotide polymorphism 2 (ALAD2) and peptide transporter 2*2 haplotype (HPEPT2*2) differently influence neurobehavior in low-level lead exposed children. Neurotoxicol Teratol 47:137–145. https://doi.org/10.1016/j.ntt.2014.12.001
Acknowledgements
The authors thank Jesus Placencia, M.S., for creation of the map. Funding was provided by National Institute of Child Health and Human Development (Grant No. R21HD060120, CS PI), National Center for Research Resources (Grant No. 5G12RR008124) and J. Edward and Helen M.C. Stern Professorship in Neuroscience (CS).
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The studies followed all current standards for human subjects’ research and was approved by the University of Texas Institutional Review Board (IRB Protocol #564493-1 and #79085-14), by the El Paso Independent School District Research Board, and by the Canutillo Independent School District Board and Superintendent.
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Informed consent was obtained from all parents before children’s participation; child assent was obtained from each child immediately before study participation. The study methods and procedures underwent annual review by University Institutional Review Board.
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Alvarez, J., Del Rio, M., Mayorga, T. et al. A Comparison of Child Blood Lead Levels in Urban and Rural Children Ages 5–12 Years Living in the Border Region of El Paso, Texas. Arch Environ Contam Toxicol 75, 503–511 (2018). https://doi.org/10.1007/s00244-018-0549-3
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DOI: https://doi.org/10.1007/s00244-018-0549-3