Portal de Periódicos da CAPES

Cumulative Childhood Lead Levels in Relation to Sleep During Adolescence

2019; American Academy of Sleep Medicine; Volume: 15; Issue: 10 Linguagem: Inglês

10.5664/jcsm.7972

1550-9397

Erica C. Jansen, Galit Levi Dunietz, Aleena Dababneh, Karen E. Peterson, Ronald D. Chervin, Jonggyu Baek, Louise M. O’Brien, Peter X.‐K. Song, Alejandra Cantoral, Howard Hu, Martha María Téllez‐Rojo,

Air Quality and Health Impacts

Free AccessCaffeine - Sleep Quality - Insufficient Sleep - Sleep Duration - Adolescents - Education - Actigraphy - Behavior - Scientific InvestigationsCumulative Childhood Lead Levels in Relation to Sleep During Adolescence Erica C. Jansen, PhD, MPH, Galit Levi Dunietz, PhD, MPH, Aleena Dababneh, BS, Karen E. Peterson, ScD, Ronald D. Chervin, MD, MS, Jonggyu Baek, PhD, Louise O'Brien, PhD, MS, Peter X.K. Song, PhD, Alejandra Cantoral, ScD, Howard Hu, ScD, MS, MPH, MD, Martha M. Téllez-Rojo, ScD Erica C. Jansen, PhD, MPH Department of Nutritional Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, Michigan , Galit Levi Dunietz, PhD, MPH Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, Michigan , Aleena Dababneh, BS Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, Michigan , Karen E. Peterson, ScD Department of Nutritional Sciences, University of Michigan School of Public Health, Ann Arbor, Michigan , Ronald D. Chervin, MD, MS Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, Michigan , Jonggyu Baek, PhD Population and Quantitative Health Sciences, University of Massachusetts Medical School, Worcester, Massachusetts , Louise O'Brien, PhD, MS Division of Sleep Medicine, Department of Neurology, University of Michigan, Ann Arbor, Michigan , Peter X.K. Song, PhD Department of Biostatistics, University of Michigan School of Public Health, Ann Arbor, Michigan , Alejandra Cantoral, ScD CONACYT, National Institute of Public Health, Cuernavaca, Mexico , Howard Hu, ScD, MS, MPH, MD Department of Environmental and Occupational Health Sciences, University of Washington School of Public Health, Seattle, Washington , Martha M. Téllez-Rojo, ScD Center for Research on Nutrition and Health, National Institute of Public Health, Cuernavaca, Mexico Published Online:October 15, 2019https://doi.org/10.5664/jcsm.7972Cited by:3SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives:Lead exposure has been linked to adverse cognitive outcomes among children, and sleep disturbances could potentially mediate these relationships. As a first step, whether childhood lead levels are linked to sleep disturbances must be ascertained. Prior studies of lead and sleep are scarce and rely on parent-reported sleep data.Methods:The study population included 395 participants from the Early Life Exposure in Mexico to Environmental Toxicants project, a group of sequentially enrolled birth cohorts from Mexico City. Blood lead levels measured from ages 1 to 4 years were used to calculate a cumulative measure of early childhood lead levels. Average sleep duration, sleep fragmentation, and movement index were assessed once between the ages of 9 and 18 years with wrist actigraphs worn for a continuous 7-day interval. Linear regression models were fit with average sleep duration, fragmentation, or movement as the outcome and cumulative lead levels divided into quartiles as the exposure, adjusted for age, sex, and maternal education.Results:Mean (standard deviation) age at follow-up was 13.8 (1.9) years, and 48% of participants were boys. Median (interquartile range) cumulative childhood lead level was 13.7 (10.8, 18.0) μg/dL. Patients in the highest quartile of the cumulative childhood lead group had on average 23 minutes less sleep than those in the first quartile in adolescence (95% confidence interval [7, 39]; P, trend = .02). Higher cumulative lead level was associated with higher sleep fragmentation in younger adolescents (younger than 14 years) only (P, interaction = .02).Conclusions:Shorter sleep duration may represent an as-yet unrecognized adverse consequence of lead exposure in youth.Citation:Jansen EC, Dunietz GL, Dababneh A, Peterson KE, Chervin RD, Baek J,O'Brien L, Song P, Cantoral A, Hu H, Téllez-Rojo MM. Cumulative childhood lead levels in relation to sleep during adolescence. J Clin Sleep Med. 2019;15(10):1443–1449.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Lead exposure has been linked to cognitive outcomes among children. Insufficient and fragmented sleep have also been related to cognitive outcomes, yet the relationship between lead exposure and sleep has rarely been examined.Study Impact: In a cohort of youth from Mexico City, we found that children in the highest compared with the lowest quartile of cumulative childhood lead levels had a 23-minute shorter sleep duration in adolescence, whereas differences in sleep fragmentation were apparent only for younger adolescents. Shorter sleep duration conceivably could represent an as-yet unrecognized adverse consequence of lead exposure in youth.INTRODUCTIONLead exposure poses a risk to human health, as it is toxic to central and peripheral nervous systems.1 Children are particularly vulnerable, and lead exposure has been associated with developmental delays,2 as well as long-term cognitive and neurologic effects.3 Although it has now been phased out of gasoline and most other products, lead can still be found in certain indoor and outdoor environments, including within and surrounding older homes, and in water from contaminated pipes in many urban areas worldwide. Mexico is one country that still has high prevalence of lead exposure, mostly via cooking and eating with lead-glazed pottery.4,5Another salient risk factor for cognitive and neurologic outcomes in children is sleep. Children with consistent short sleep or disrupted sleep have behavioral and mental difficulties, problems with learning,6 and symptoms of attention deficit-hyperactivity disorder.7 This indicates the possibility that sleep disturbances might mediate the pathway between lead exposure and behavioral and mental difficulties in children. The first step toward understanding these relationships is to determine whether lead exposure is associated with sleep in children. Indeed, a few studies in adults and children have reported associations between lead and sleep disturbances. An Iranian study among workers from zinc-lead factories showed an association between blood lead level (BLL) and prevalence of sleep problems such as self-reported insomnia and excessive daytime sleepiness.8 In Chinese preschool children (ages 3 to 5 years), early lead levels were associated with parent-reported sleep disturbances during preadolescence.9 In addition, a cross-sectional study of Mexican children aged 6 to 8 years that examined micronutrients and lead found that BLL ≥ 10 µg/dL was associated with later parent-reported waking time and shorter sleep duration.10 Previous studies were limited by use of self- or parent-reported sleep duration or disturbances, which can be subject to measurement error11 as well as reporting bias. In addition, these studies used blood assessments of lead levels collected at one point in time. Finally, two of the three studies were cross-sectional, rather than longitudinal, meaning that whether or not elevated lead levels preceded the associated adverse outcomes could not be ascertained.In contrast to prior studies, the current study among Mexican youth used accelerometry to estimate sleep as well as a longitudinal study design that took into account multiple measures of blood lead during early childhood. Our primary aim was to evaluate whether cumulative lead levels from ages 1 to 4 years were associated with sleep duration and quality measured in adolescence (9 to 17 years). We hypothesized that higher cumulative lead levels would be associated with shorter sleep duration and lower sleep quality as assessed by sleep fragmentation and movement during sleep.METHODSStudy PopulationThe study sample included adolescent participants from two of three sequentially enrolled cohorts of the Early Life Exposure in Mexico to ENvironmental Toxicants (ELEMENT) study.12,13 Between 1997 and 2004, 1,012 mother/child dyads were recruited from prenatal clinics of the Mexican Social Security Institute in Mexico City, which serves low- to middle-income populations formally employed in the private sector. Of interest for this secondary analysis, children were followed annually from the ages of 1 to 4 years to measure BLL. Several other follow-up visits occurred over mid-childhood and adolescence. In 2015, a subset of 550 participants from the original birth cohorts two and three, who were undergoing the pubertal transition (ages 9 to 17 years), were selected to participate in a follow-up study that included 7 consecutive days of actigraphy in addition to pubertal assessments (described elsewhere)14. The analytic sample for this report comprised 375 children who had cumulative early childhood lead measures as well as adolescent sleep actigraphy measures (of 1,013 children with cumulative early blood lead measures, 375 also had sleep measurements in adolescence). The institutional review boards at the Mexico National Institute of Public Health and the University of Michigan approved the research protocols. Informed consent was obtained from parents for all participants, and beginning from age 7 years, assent was also received from the participants.Cumulative Childhood Lead LevelsBlood samples were taken annually during childhood from ages 1 to 4 years and stored in trace metal–free tubes by trained research assistants using standardized protocols. Lead levels were assessed using graphite-furnace atomic-absorption spectroscopy (model 3000; Perkin-Elmer, Chelmsford, Massachusetts, USA) at the research facility of the American British Cowdray Hospital in Mexico City as previously described.15,16 All BLLs were above the limit of detection and the precision of this instrument was within 1 μg/dL. Cumulative BLL from ages 1 to 4 years was calculated by estimating the area under each child's age-by-blood-lead curve from 12 to 48 months as previously described.17 We categorized this variable into quartiles, with the highest quartile representing highest cumulative BLL.Sleep MeasuresAt the clinic visit, adolescents were given an actigraph (ActiGraph GT3×+; ActiGraph LLC, Pensacola, Florida, USA) to wear on their nondominant wrist continuously for 7 days. Nightly sleep duration was estimated from the actigraphic and sleep diary data with the use of a fused Lasso (least absolute shrinkage and selection operator)-based calculator package developed in R (R Foundation for Statistical Computing, Vienna, Austria). The obtained estimates were highly correlated with manual sleep duration detection in a validation subset of 50 randomly selected participants (r = .95). We examined sleep duration (averaged over the wear period), as well as two measures of sleep quality: sleep fragmentation index and movement index. In accordance with the Actilife software (ActiGraph LLC) and used in previous research,18 sleep fragmentation index was calculated as the percentage of 1-minute (or shorter) periods of sleep out of the total number of sleep bouts of any length, with higher values representing more fragmented sleep. The sleep versus wake episodes (during the previously determined night-time sleep duration window) were identified with the Sadeh algorithm.19 Movement index was calculated as the percentage of minutes with movement count > 0 out of the total number of minutes in the nightly sleep period.Potential ConfoundersPotential confounders examined included sex, age, and maternal education. Maternal education was abstracted from questionnaires mothers completed during the original cohort enrollment visit. Maternal education was categorized as < 9 years, 9 to < 12 years, 12 years, or > 12 years.Statistical AnalysisFirst, associations between potential confounders and cumulative BLL from 1 to 4 years of age were examined by comparing the mean ± standard deviation (SD) cumulative BLLs between potential confounder-defined categories. Next, bivariate associations between cumulative BLL and sleep measures were evaluated by estimating the means ± SD sleep duration, fragmentation index, and movement index according to quartiles of cumulative blood lead. Value of P for trend (P, trend) were obtained from linear regression models with sleep measures as the outcome and a variable representing quartiles of cumulative lead levels. In multivariable analysis, linear regression models were run with continuous sleep measures (sleep duration, fragmentation index, and movement index each in separate models) as the outcome and indicator variables for quartiles of cumulative BLL as the exposure, adjusting for sex, age, and maternal education. Models for sleep fragmentation and movement index included sex, age, and average sleep duration, as sleep duration was correlated with fragmentation and movement, and did not include maternal education (it was not associated with either sleep fragmentation or movement index). In sensitivity analyses, additional covariates were added to the models (puberty, screen time, smoking, and caffeine intake), and analyses were restricted to adolescents whose sleep was not measured during summer vacation months. In post hoc analyses, we stratified all models by age (younger than 14 years and age 14 years and older) and evaluated the interaction with age in unstratified models. All analyses were conducted in Stata 14.0 (StatCorp LLC, College Station, Texas, USA).RESULTSAssociations between lead levels and sleep characteristics were examined in a sample of 375 adolescents, of whom 181 (48%) were boys. The overall mean age was 13.8 (1.9) years and most adolescents (close to 80%) had reached the latter stages of puberty (menarche for girls of testicular volume 15 mL or greater for boys).The median (interquartile range) cumulative exposure to lead was 13.7 (10.8, 18.0) μg/dL and 38% of the sample had average BLL >5 μg/dL (at any given point in time). Older age and lower maternal education were each associated with higher cumulative childhood lead levels (Table 1). Cumulative early childhood BLL did not differ with respect to sex or pubertal status.Table 1 Cumulative child lead measures of 375 youth from Mexico City, according to sociodemographic predictors.Table 1 Cumulative child lead measures of 375 youth from Mexico City, according to sociodemographic predictors.In bivariate analyses examining cumulative childhood lead in relation to sleep characteristics during adolescence, lead levels were inversely associated with sleep duration, but not with sleep fragmentation or movement during sleep (Figure 1). In multivariable analyses adjusted for sex, age, and maternal education, sleep duration remained linearly associated with early childhood lead levels (Table 2). In comparison to adolescents with the lowest childhood lead levels (median = 9.1 ug/dL), those with the highest cumulative lead levels (median = 23.3 μg/dL) had 23 minutes shorter sleep on average per day [β = −23 95% confidence interval (−39, −7); P, trend = .02]. Additional adjustment for sex, age, puberty, screen time, smoking, and caffeine consumption did not alter estimates. Similarly, results did not change when excluding participants whose sleep was evaluated during the summer.Figure 1: Bivariate associations between childhood lead exposure (cumulative from ages 1 to 4 years) and sleep in adolescence.1 Early childhood cumulative lead exposure levels were as follows: Quartile 1, median = 9.1 ug/dL; Quartile 2, median = 12.3 ug/dL; Quartile 3, median = 15.1 ug/dL; Quartile 4, median = 23.2 ug/dL.Download FigureTable 2 Adjusted associations between blood lead levels and sleep among 375 adolescents aged 9 to 17 years from Mexico City.Table 2 Adjusted associations between blood lead levels and sleep among 375 adolescents aged 9 to 17 years from Mexico City.In analyses stratified by age (younger than 14 years and age 14 years or older), there were stronger associations between cumulative childhood lead and shorter sleep duration among younger participants (Table 2), although there was not a statistically significant interaction. In contrast, there were statistically significant interactions for sleep fragmentation (P, interaction = .02), such that higher lead exposure was related to higher sleep fragmentation in younger participants only.DISCUSSIONIn a prospective cohort of adolescents from Mexico City, we have shown an inverse association between cumulative BLL in early childhood and actigraphy-derived sleep duration in adolescence. In particular, participants with the highest as opposed to lowest quartile of cumulative lead levels slept on average 23 minutes less. Cumulative BLL was also associated with higher sleep fragmentation, although only among younger adolescents. These longitudinal associations suggest lead in early childhood as a novel exposure that conceivably could reduce sleep in adolescence.Insufficient sleep duration in adolescents can have significant physical, emotional, and cognitive implications. Predictors of insufficient sleep among youth include delayed bedtimes and early wake time as a consequence of school and extracurricular demands, extensive daily screen use, and caffeine consumption.20 Increased childhood lead levels may represent a risk factor for insufficient sleep duration in populations vulnerable to lead exposure. The observed 23-minute lower sleep duration per night could have clinical relevance for children: even periods as short as a few nights of 30-minute nightly sleep deprivation demonstrably impair cognitive function.21 Further, although it was not the subject of the current investigation, it is possible that insufficient sleep is an intermediate variable on the pathway from lead exposure to cognitive and behavioral difficulties among pediatric populations.The current study corroborates two prior investigations on lead levels and sleep in children. These studies, one also among Mexican children10 and another among Chinese children,9 were distinct from ours in that they included younger children and relied on parent-reported sleep data. The Chinese study was similar to ours in the use of a prospective study design, and they found that children with higher BLL from ages 3 to 5 years had a higher probability of sleep problems, that is, longer sleep onset, shorter sleep duration, frequent night waking, and excessive daytime sleepiness, in preadolescence. Our findings suggest that the associations between early childhood lead exposure and sleep problems may persist even longer. Nonetheless, we cannot disentangle whether the associations were due to high lead exposure during early childhood per se or to the fact that children with high lead exposure in early childhood may have had continual high lead exposure over childhood and into adolescence.Several potential pathways may help explain the association between lead levels and sleep duration. One pathway linking lead levels and sleep duration could be through neurotransmitters; animal studies have shown that lead exposure alters serotonin, acetylcholine, and norepinephrine, neurotransmitters that are intricately involved in sleep/wake processes.22,23 Serotonin dysregulation is also implicated in mental health disorders including anxiety and depression, which are linked to insufficient sleep.24 Another plausible pathway between increased lead levels and insufficient sleep duration may be mediated by iron. Higher levels of lead have been associated with lower iron levels due to the inhibition of iron absorption by lead.25 The effect of iron deficiency on sleep duration has been rarely reported, although iron deficiency anemia has been linked to poor sleep quality in adults,26 and to sleep architecture differences among infants and children.27,28 Further, a randomized study of iron supplementation among infants at risk for iron deficiency anemia showed that daily iron supplementation for 12 months was associated with longer, less disrupted sleep duration.29 Iron deficiency has also been suspected to play a role in restless legs syndrome and periodic limb movements during sleep.30 Indeed, we found an association between higher childhood lead levels and sleep fragmentation in younger adolescents. These associations were not observed in older adolescents, perhaps due to changes in sleep timing and duration that occur during puberty.20Placing these findings within the context of Mexico City has public health relevance, as this pediatric population is unique in regard to both its overall lead exposures and sleep behaviors. First, these youth were highly exposed to lead during their childhood; 38% of the sample had an estimated average lead level > 5 μg/dL at any given point in time, which is an excessive lead level according to the Centers for Disease Control and Prevention, with known neurocognitive effects.31 Interestingly, from the perspective of sleep, these Mexican adolescents had on average longer sleep duration than their US counterparts.32 This finding is likely attributed to between-country differences in school start times. Yet, longer sleep duration has also been observed in Mexican Americans compared to non-Hispanic Caucasian Americans,33 which could suggest positive perceptions of sleep and its importance in Mexican culture.34Both the strengths and limitations of the current study are relevant to consider. This study utilized a prospective design and followed 375 children from early childhood to adolescence. Sleep data were recorded objectively for 7 days with wrist actigraphy. Lead data were collected annually between the ages of 1 and 4 years, which allowed the construction of cumulative lead levels to estimate chronic childhood exposure. Despite these strengths, this study has some limitations. First, sleep data that have been collected during 1 week may not represent sleep changes over a longer time period. However, sleep patterns collected via actigraphy for 1 week were highly similar to estimates averaged over 2 weeks in a sample of British adults.35 Second, actigraphy devices are unable to record perceived sleep quality, a self-report sleep measure that can be informative of the sleep experience and complement the objective data. Third, although sleep fragmentation and movement indices have been examined in adolescent populations in other studies,36 these indices were not specifically validated in this age group. Fourth, post hoc power calculations revealed that we may have been underpowered to detect associations, especially for sleep fragmentation and movement indices (post hoc power for sleep duration, sleep fragmentation, and movement index were 70%, 37%, 24%, respectively, based on standard post hoc power formulas37). Finally, the possibility of unmeasured confounding cannot be ruled out, such as potential confounding from household- or neighborhood-level factors that affected early childhood lead exposure and also accounted for differences in sleep during adolescence. Adjustment of models for maternal education is likely to have addressed some confounding from these influences.38In summary, these findings suggest a difference in adolescent sleep duration among those with higher lead exposure during childhood, a relationship rarely considered by health care clinicians. Findings are relevant for Mexico City as well as other urban areas where lead contamination persists.DISCLOSURE STATEMENTAll authors have seen and approved the manuscript. Work for this study was performed at the University of Michigan. Dr. Chervin reports grants from National Institutes of Health during the conduction of the study; his institution and collaborators have received grant support from the American Sleep Medicine Foundation; grant support from the National Multiple Sclerosis Society; financial and non-financial support from Michigan Medicine, other from International Pediatric Sleep Association, personal fees and non-financial support from American Academy of Sleep Medicine, personal fees and non-financial support from American Academy of Dental Sleep Medicine, personal fees from UpToDate, personal fees from Cambridge University Press, and non-financial support from Association of Professional Sleep Societies. In addition, Dr. Chervin developed questionnaires for childhood sleep problems (PSQ, PSQ-SRBD Scale) with copyright owned by University of Michigan, and patents or patents pending, for technology, tools, or agents relevant to diagnosis and treatment of sleep disorders. All of this support is outside of the submitted work and did not influence the design, interpretation, or writing of this work. Dr. Jansen reports support from National Institutes of Health/National Heart, Lung, and Blood Institute grant 5T32HL110952-05 during the conduct of the study. The other authors report no conflicts of interest.ABBREVIATIONSBLLblood lead levelELEMENTEarly Life Exposure in Mexico to ENvironmental ToxicantsSDstandard deviationREFERENCES1 Flora G, Gupta D, Tiwari AToxicity of lead: a review with recent updatesInterdiscip Toxicol2012524758 CrossrefGoogle Scholar2 Jansen EC, Zhou L, Song PXK, et al.Prenatal lead exposure in relation to age at menarche: results from a longitudinal study in Mexico CityJ Dev Orig Health Dis201894467472 CrossrefGoogle Scholar3 Reuben A, Caspi A, Belsky DW, et al.Association of childhood blood lead levels with cognitive function and socioeconomic status at age 38 years and with IQ change and socioeconomic mobility between childhood and adulthoodJAMA20173171212441251 CrossrefGoogle Scholar4 Pantic I, Tamayo-Ortiz M, Rosa-Parra A, et al.Children's blood lead concentrations from 1988 to 2015 in Mexico City: the contribution of lead in air and traditional lead-glazed ceramicsInt J Environ Res Public Health201815102153 CrossrefGoogle Scholar5 Acosta-Saavedra LC, Moreno ME, Rodríguez-Kessler T, et al.Environmental exposure to lead and mercury in Mexican children: a real health problemToxicol Mech Methods2011219656666 CrossrefGoogle Scholar6 Aishworiya R, Chan PF, Kiing JSH, Chong SC, Tay SKHSleep patterns and dysfunctions in children with learning problemsAnn Acad Med Singapore20164511507512 Google Scholar7 Baddam SKR, Canapari CA, van Noordt SJR, Crowley MJSleep disturbances in child and adolescent mental health disorders: a review of the variability of objective sleep markersMed Sci201862 Google Scholar8 Sadeghniiat-Haghighi K, Yousefian M, Aminian O, Najafi AAssociation between blood lead level and sleep quality in lead- zinc factories in Zanjan: a cross-sectional studyJ Sleep Sci2016111822 Google Scholar9 Liu J, Liu X, Pak V, et al.Early blood lead levels and sleep disturbance in preadolescenceSleep2015381218691874 CrossrefGoogle Scholar10 Kordas K, Casavantes KM, Mendoza C, et al.The association between lead and micronutrient status, and children's sleep, classroom behavior, and activityArch Environ Occup Health2007622105112 CrossrefGoogle Scholar11 Bianchi MT, Thomas RJ, Westover MBAn open request to epidemiologists: please stop querying self-reported sleep durationSleep Med2017359293 CrossrefGoogle Scholar12 Lewis RC, Meeker JD, Peterson KE, et al.Predictors of urinary bisphenol A and phthalate metabolite concentrations in Mexican childrenChemosphere2013931023902398 CrossrefGoogle Scholar13 Ettinger AS, Lamadrid-Figueroa H, Mercado-García A, et al.Effect of calcium supplementation on bone resorption in pregnancy and the early postpartum: a randomized controlled trial in Mexican womenNutr J2014131116 CrossrefGoogle Scholar14 Chavarro JE, Watkins DJ, Afeiche MC, et al.Validity of self-assessed sexual maturation against physician assessments and hormone levels.J Pediatr2017186172178 CrossrefGoogle Scholar15 Afeiche M, Peterson KE, Sánchez BN, et al.Prenatal lead exposure and weight of 0- to 5-year-old children in Mexico CityEnviron Health Perspect20111191014361441 CrossrefGoogle Scholar16 Hernandez-Avila M, Gonzalez-Cossio T, Hernandez-Avila JE, et al.Dietary calcium supplements to lower blood lead levels in lactating women: A randomized placebo-controlled trialEpidemiology2003142206212 CrossrefGoogle Scholar17 Hu H, Shih R, Rothenberg S, Schwartz BSThe epidemiology of lead toxicity in adults: measuring dose and consideration of other methodologic issuesEnviron Health Perspect20071153455462 CrossrefGoogle Scholar18 Chung S, Youn S, Lee C, et al.Environmental noise and sleep disturbance: night-to-night variability of sleep/wake patternSleep Med Res2016727881 CrossrefGoogle Scholar19 Sadeh A, Sharkey KM, Carskadon MAActivity-based sleep-wake identification: an empirical test of methodological issuesSleep1994173201207 CrossrefGoogle Scholar20 Owens JAdolescent Sleep Working Group Committee on AdolescenceInsufficient sleep in adolescents and young adults: an update on causes and consequencesPediatrics20141343e921e932 CrossrefGoogle Scholar21 Sadeh A, Gruber R, Raviv AThe effects of sleep restriction and extension on school-age children: what a difference an hour makesChild Dev2003742444455 CrossrefGoogle Scholar22 Mansouri MT, Naghizadeh B, López-Larrubia P, Cauli OBehavioral deficits induced by lead exposure are accompanied by serotonergic and cholinergic alterations in the prefrontal cortexNeurochem Int2013623232239 CrossrefGoogle Scholar23 Sprowles JLN, Amos-Kroohs RM, Braun AA, Sugimoto C, Vorhees CV, Williams MTDevelopmental manganese, lead, and barren cage exposure have adverse long-term neurocognitive, behavioral and monoamine effects in Sprague-Dawley ratsNeurotoxicol Teratol2018675064 CrossrefGoogle Scholar24 Willis TA, Gregory AMAnxiety disorders and sleep in children and adolescentsSleep Med Clin2015102125131 CrossrefGoogle Scholar25 Hegazy AA, Zaher MM, Abd El-Hafez MA, Morsy AA, Saleh RARelation between anemia and blood levels of lead, copper, zinc and iron among childrenBMC Res Notes201031133 CrossrefGoogle Scholar26 Murat S, Ali U, Serdal K, et al.Assessment of subjective sleep quality in iron deficiency anaemiaAfr Health Sci2015152621627 CrossrefGoogle Scholar27 Peirano PD, Algarín CR, Chamorro RA, et al.Sleep alterations and iron deficiency anemia in infancySleep Med2010117637642 CrossrefGoogle Scholar28 Peirano PD, Algarín CR, Garrido MI, Lozoff BIron deficiency anemia in infancy is associated with altered temporal organization of sleep states in childhoodPediatr Res2007626715719 CrossrefGoogle Scholar29 Kordas K, Siegel EH, Olney DK, et al.The effects of iron and/or zinc supplementation on maternal reports of sleep in infants from Nepal and ZanzibarJ Dev Behav Pediatr2009302131139 CrossrefGoogle Scholar30 Munzer T, Felt BThe role of iron in pediatric restless legs syndrome and periodic limb movements in sleepSemin Neurol2017374439445 CrossrefGoogle Scholar31 Advisory Committee on Childhood Lead Poisoning Prevention of the Centers for Disease Control and PreventionLow Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention. Atlanta, GA: CDCL: 2012 Google Scholar32 Wheaton AG, Jones SE, Cooper AC, Croft JBShort sleep duration among middle school and high school students — United States, 2015MMWR Morb Mortal Wkly Rep20186738590 CrossrefGoogle Scholar33 Kuo SI-C, Updegraff KA, Zeiders KH, McHale SM, Umaña-Taylor AJ, De Jesús SARMexican American adolescents' sleep patterns: contextual correlates and implications for health and adjustment in young adulthoodJ Youth Adolesc2015442346361 CrossrefGoogle Scholar34 Domino GSleep habits in the elderly: a study of three Hispanic culturesJ Cross Cult Psychol1986171 CrossrefGoogle Scholar35 Briscoe S, Hardy E, Pengo MF, et al.Comparison of 7 versus 14 days wrist actigraphy monitoring in a sleep disorders clinic populationChronobiol Int2014313356362 CrossrefGoogle Scholar36 Matthews KA, Hall M, Dahl RESleep in healthy black and white adolescentsPediatrics20141335e1189e1196 CrossrefGoogle Scholar37 Lenth RVPost Hoc Power: Tables and Commentary. Iowa City, Iowa: University of Iowa Department of Statistics and Actuarial Science; 2007 Google Scholar38 Desai S, Alva SMaternal education and child health: is there a strong causal relationship?Demography199835171 CrossrefGoogle Scholar Previous article Next article FiguresReferencesRelatedDetailsCited by Association between cumulative childhood blood lead exposure and hepatic steatosis in young Mexican adultsBetanzos-Robledo L, Cantoral A, Peterson K, Hu H, Hernández-Ávila M, Perng W, Jansen E, Ettinger A, Mercado-García A, Solano-González M, Sánchez B and Téllez-Rojo M Environmental Research, 10.1016/j.envres.2021.110980, Vol. 196, , (110980), Online publication date: 1-May-2021. Exposure to environmental neurotoxic substances and neurodevelopment in children from Latin America and the CaribbeanDórea J Environmental Research, 10.1016/j.envres.2020.110199, Vol. 192, , (110199), Online publication date: 1-Jan-2021. Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead NeurotoxicityRamírez Ortega D, González Esquivel D, Blanco Ayala T, Pineda B, Gómez Manzo S, Marcial Quino J, Carrillo Mora P and Pérez de la Cruz V Toxics, 10.3390/toxics9020023, Vol. 9, No. 2, (23) Volume 15 • Issue 10 • October 15, 2019ISSN (print): 1550-9389ISSN (online): 1550-9397Frequency: Monthly Metrics History Submitted for publicationFebruary 19, 2019Submitted in final revised formJuly 2, 2019Accepted for publicationJuly 2, 2019Published onlineOctober 15, 2019 Information© 2019 American Academy of Sleep MedicineKeywordssleep fragmentationsleep durationtoxicantleadACKNOWLEDGMENTSThe authors gratefully acknowledge the American British Cowdray Medical Center (ABC) in Mexico for providing research facilities.PDF download