Abstract
The authors reviewed human data related to motor development following exposure to a subset of chemicals thoroughly reviewed in Agency for Toxic Substances and Disease Registry (ATSDR) Toxicological Profiles and Addenda. The resulting dataset includes the following variables and confounders: chemical name, exposure route, exposure duration and frequency, study design, cohort name and/or geographic location, sex of cohort subjects, NOAEL, and LOAEL. This data summary can help validate motor development outcomes observed in animal exposure studies; it can also aid in determining whether these outcomes and corresponding exposure windows are relevant to humans.
Keywords: Windows of sensitivity, Motor function, Developmental effects, Human exposure effects, in utero exposure effects
Specifications table
| Subject area | Biology |
| More specific subject area | Epidemiology, Toxicology, Environmental Health |
| Type of data | Table |
| How data was acquired | Literature search |
| Data format | Filtered |
| Experimental factors | N/A (Literature review) |
| Experimental features | N/A |
| Data source location | N/A |
| Data accessibility | Data are with this article |
Value of the data
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The human epidemiological data provide researchers with a condensed reference of chemicals for which motor development effects have been observed and at which doses and exposure durations.
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They can be compared to animal data to help assess relevance to humans.
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They provide a list of chemicals for which researchers can design much-needed acute duration studies on motor development effects known to occur in humans.
1. Data
Table 1 presents motor development outcome and study design data extracted from epidemiological studies of chemicals reviewed in ATSDR’s Toxicological Profiles and Addenda. The data include: No Observed Adverse Effect Levels (NOAELs) and/or Lowest Observed Adverse Effect levels (LOAELs), exposure routes and durations assessed, cohort name and demographics [geographic location, sex(es)], and study design type. Agency for Toxic Substances and Disease Registry Toxicological Profiles (http://www.atsdr.cdc.gov/toxprofiles/index.asp), NCBI’s PubMed (http://www.ncbi.nlm.nih.gov/pubmed).
Table 1.
Summary of human NOAEL & LOAEL data for motor development outcomes.
| Chemical | Sex of offspring | Cohort (location) | Study design | Exposure duration/frequency | NOAEL (mg/kg/d) | LOAEL (mg/kg/d) | Reference |
| Motor activity | |||||||
| Ethanol | M & F | Birth Cohort (Grady Memorial Hospital, Atlanta, Georgia) | Prospective cohort | Gestation (entirety or first two trimesters) | Not established | 12 oz/week×entire gestation period, 14 oz/week×first and second trimesters (reduced motor maturity, increased activity) | [13] |
| DDE | M & F | Birth Cohort (Flix, Spain) | Prospective cohort | Gestation | Not established | Delay in psychomotor development observed at 13 months age; decreased locomotor performance on the Griffiths Mental Development Scales | [34] |
| ΣPBDEs | M & F | Menorca birth cohort/INMA (INfancia y Medio Ambiente [Environment and Childhood]) project (Spain) | Prospective cohort | Gestation (cord blood) and postnatal (4 years age) | 2.10(16.8) ng/mL (Median(max)) cord blood; 0.12(130.2) ng/mL serum at age 4 (hyperactivity via ADHD criteria of DSM-IV) | [23] | |
| Motor function | |||||||
| Arsenic | M & F | Maternal and Infant Nutritional Intervention at Matlab (MINIMat) study (Matlab, Bangladesh) | Community-based randomized trial | 8 or 30 weeks gestation | 81 (37–207) μg/L at 8 weeks of gestation; 84 μg/L (42–230 μg/L) at 30 weeks (PDI score) | [43] | |
| Arsenic | M & F | Children from Health Effects of Arsenic Longitudinal Study (HEALS) (Araihazar, Bangladesh) | Cross-sectional | Post-natal (8–11 years age; drinking water levels; blood levels) | Not established | Mean 6.3 μg/L in blood (decreased motor function – including motor coordination – via Bruininks–Oseretsky test) | [33] |
| Carbon monoxide | M & F | Birth Cohort (San Marcos, Guatemala) | Prospective cohort | Gestation, postnatal inhalation | Exposure during the first 9 postnatal months (fine motor function via Reitan-Indiana Finger tapping test, WRAVMA Pegboard test, and Bender-Gestalt-II connect the dots motor test); mean 3.8 ppm (fine motor function as measured by WRAVMA and Bender Gestalt-II tests) | Mean 3.8 ppm, range 0.62–12.52 ppm (decreased fine motor speed via Reitan-Indiana Finger tapping test: −5.7 (−9.7, −1.7)) with increasing maternal third trimester exposure level at age 6–7 years | [16] |
| Chlordecone | M & F | Timoun mother– child cohort (Guadaloupe) | Prospective cohort | Gestation | Median (range) <0.24 (0.07–3.91) μg/L F (fine motor function via Ages and Stages Questionnaire (ASQ) score converted to IQ score); M & F (gross motor function) | 0.24 μg/L M (impaired fine motor function via converted ASQ score) | [12] |
| Chlordecone | M & F | Timoun mother– child cohort (Guadaloupe) | Prospective cohort | Gestation+lactation (breast milk sample measured when infant reached 3 months age) | Median (range) 0.62 (0.2–4.2) μg/L M & F (fine and gross motor function (Ages and Stages Questionnaire (ASQ) score converted to IQ score)) | [12] | |
| Chlorodibenzofurans (CDFs) | M & F | Yu-Cheng rice oil contamination victims (Taiwan) | Field survey (retrospective) | Gestation | Not established | Decreased PDI score | [37] |
| Total CDDs/CDFs+PCBs | M & F | Duisburg Birth Cohort Study (Germany) | Prospective cohort | Gestation | Mean (range) 18.8 (4.0–51.2) pg/g blood lipids TEQs (motor development (PDI) assessed by the Bayley Scales of Infant Development (at ages 12 and 24 months)) | [45] | |
| DDE | M & F | Birth Cohort (Flix, Spain) | Prospective cohort | Gestation | Not established | Delay in psychomotor development observed at 13 months age; decreased locomotor performance on the Griffiths Mental Development Scales | [34] |
| DDT, DDE | M & F | Center for the Health Assessment of Mothers and Children of Salinas study (Salinas Valley, California) | Prospective cohort | Gestation | Not established | A decrease of ~2 points in the psychomotor developmental index score (PDI) with each 10-fold increase in maternal p,p′-DDT blood serum levels (geometric mean (95% CI): 22.0 (18.4–26.4) ng/g lipid) when the children reached 6 and 12 months of age (but not at 24 months) and maternal p,p′-DDE levels (geometric mean (95% CI): 1436.9 (1257.4–1642.1) ng/g lipid) at 6 months of age only) | [21] |
| DDT, DDE, DDD (except o,p′-isomers) | M & F | Perinatal Cohort (Morelos, Mexico) | Prospective cohort | Gestation (exposure at each trimester measured) | 6.8 (2.8) ng/mL (GM (GSD)) 2nd and 7.8 (2.8) (GM(GSD)) 3rd trimester exposure (PDI score at 3, 6 and 12 months age) | 6.4 (2.8) ng/mL (GM (GSD)) 1st trimester exposure (PDI score at 3, 6 and 12 months age) | [44] |
| DDT, DDE, DDD (except o,p′-isomers) | M & F | Groningen infant COMPARE (Comparison of Exposure-Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Improved coordination (via Touwen’s neurologic examination) | [41] |
| Ethanol | M & F | Birth Cohort (Grady Memorial Hospital, Atlanta, Georgia) | Prospective cohort | Gestation (entirety or first two trimesters) | Not established | 12 oz/week×entire gestation period, 14 oz/week×first and second trimesters (reduced motor maturity, increased activity) | [13] |
| Ethanol | M & F | Pregnant women seeking prenatal care (U.S.) | Prospective cohort | Gestation (exposure measured at 5 months gestation) | Not established | ≥.5 oz per day in early pregnancy (approximately 1 drink per day) decreased fine motor skill performance on the Wisconsin Fine Motor Steadiness Battery at 4 years age; | [2] |
| Decreased gross motor performance (includes motor coordination) on a battery adapted from the Gross Motor Scale developed by Crippled Chidren’s Division of the University of Oregon Medical School | |||||||
| Heptachlor epoxide | M & F | Oahu high school students exposed during gestation (Oahu) | Retrospective | Gestation | Not established | Impaired motor planning at high school age | [1] |
| Lead | M & F | Cincinnati Lead Study, Birth Cohort (Cincinnati, Ohio) | Prospective cohort | Gestation (first trimester, gestation+10 days (neonatal), gestation through age 6 (current level)) | 8.4 μg/dL (prenatal) (fine motor function) | Mean 4.8 (neonatal) and 10.1 μg/dL (current level)(decreased fine motor function) (Bruininks–Oseretsky Test of Motor Proficiency (BOTMP)); | [15] |
| 10.1 μg/dL (current level) (decreased motor coordination as per bilateral coordination subtest of BOTMP at age 6) | |||||||
| Lead | M & F | Birth Cohort (Cleveland, OH) | Prospective cohort | Gestation (cord blood measured on day of delivery) | Not established | Mean 5.8 (range, 2.6–14.7) μg/dL cord blood (neurological soft signs in newborn infants) | [17], [19], [18] |
| Lead | M & F | Birth Cohort (Cleveland, OH) | Prospective cohort | Gestation (maternal blood level measured on day of delivery) | Not established | Mean 6.5 (range, 2.7–11.8) μg/dL pre-natal maternal blood (altered Psychomotor Developmental Index) | [18] |
| Lead | M & F | Middle- and upper-class children (Boston, Massachusetts) | Prospective cohort | 10 years (from birth) | Mean 7 μg/dL PbB at 24 months (Psychomotor Developmental Index) | [3], [4], [5], [6], [7], [8], [9], [10], [11] | |
| Manganese | M & F | Mexican children (Chiconcoac and Tolago, Mexico) | Cross-sectional | Gestation+post-natal (lifetime exposure, elementary school aged) | Median 12.6 μg/g in hair (Motor function via finger tapping (Halstead-Reitan battery), grooved pegboard, and Santa Ana (motor coordination) tests); Median 9.5 μg/Lin blood (motor function via groove pegboard and Santa Ana tests) | Median 9.5 μg/Lin blood (decreased motor function via finger-tapping test (on-dominant hand only)) | [25] |
| Manganese | M & F | public school children (Province of Brescia, Italy) | Cross-sectional | Post-natal (11–14 years age; soil levels) | Not established | 958 ppm in soil (impairment of motor coordination (Luria–Nebraska test), hand dexterity (Pursuit Aiming)); | [30] |
| 10.99 μg/L in blood (increased tremor intensity); | |||||||
| 0.16 ppm in hair (increased tremor intensity) | |||||||
| Manganese | M & F | Children from Health Effects of Arsenic Longitudinal Study (HEALS) (Araihazar, Bangladesh) | Cross-sectional | Post-natal (8–11 years age; drinking water levels; blood levels) | Motor function – including motor coordination -- via Bruininks–Oseretsky test | [33] | |
| Mercury (organic) | M | Seychelles Child Development Study (Republic of Seychelles) | Prospective cohort | In utero exposure | Female arithmetic mean 6.9 ppm (<3–12 ppm) (performance on the grooved pegboard time for non-dominant hand) | Male arithmetic mean 6.9 ppm (<3–12 ppm) (decreased performance on the grooved pegboard time for non-dominant hand) | [31] |
| Mercury (organic) | F | Seychelles Child Development Study (Republic of Seychelles) | Prospective cohort | In utero+post-natal exposure, 107 months | Mean 6.6 ppm (6 months age), 4.8 ppm (66 months age), 6.9 ppm (107 months age); Male (performance on the grooved pegboard time for non-dominant hand) | Female mean 6.6 ppm (6 months age), 4.8 ppm (66 months age), 6.9 ppm (107 months age) (decreased performance on grooved Pegboard with the non-dominant hand test) | [32] |
| Mercury (organic) | M & F | Birth Cohort (Poland) | Prospective cohort | Prenatal exposure (maternal fish consumption) | Geometric mean 0.52 μg/mL maternal blood (MDI & PDI scores) | Geometric mean 0.75 μg/L maternal blood (reduced MDI & PDI scores) | [27] |
| Mercury (organic) | M & F | Mother-child pairs exposed during Iraqi poisoning incident (Iraq) | Prospective cohort? | Prenatal exposure (maternal consumption, measured in hair sample) | Not established | 0.0012 (delayed walking; abnormal motor scores (includes assessment of ataxia, abnormal reflexes, and athetoid movement)) | [14] |
| Methyl parathion | M & F | Children exposed during illegal spraying (Mississippi and Ohio, USA) | Cross-Sectional? | Post-natal (6 years age and under when homes sprayed with MP) | Integration of motor skills based on Pediatric Environmental Neurobehavioral Test Battery (PENTB) | [42] | |
| ΣPBDEs | M & F | Menorca birth cohort/INMA (INfancia y Medio Ambiente [Environment and Childhood]) project (Spain) | Prospective cohort | Gestation (cord blood) and postnatal (4 years age) | 2.10(16.8) ng/mL (Median(max)) cord blood; 0.12(130.2) ng/mL serum at age 4 (McCarthy Scales of Children׳s Abilities motor function score) | [23] | |
| ΣPBDEs | M & F | CHAMACOS cohort (Salinas, California) | Prospective cohort | Gestation (maternal blood at 26.7±2.6 weeks gestation or delivery) and postnatal (child serum at age 7 years) | Gestation and postnatal levels (Gross motor function via McCarthy Scales of Children׳s Abilities (MSCA)); postnatal levels (motor function via finger tap test, WRAVMA pegboard test, and MSCA gross motor test) | Gestational exposure (decreased motor function at ages 5 and 7) via WRAVMA pegboard test (non-dominant hand) | [20] |
| BDE 47 | M & F | Groningen infant COMPARE (Comparison of Exposure-Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Improved coordination (via Touwen’s neurologic examination), but the effect disappeared after correcting for SES, sex, and Home Observation for Measurement of the Environment (HOME) questionaire results | [41] |
| BDE 100 | M & F | Groningen infant COMPARE (Comparison of Exposure–Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Improved coordination (via Touwen’s neurologic examination), but the effect disappeared after correcting for SES, sex, and Home Observation for Measurement of the Environment (HOME) questionaire results | [41] |
| BDE 154 | M & F | Groningen infant COMPARE (Comparison of Exposure–Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Decreased fine manipulative abilities (via Touwen’s neurologic examination), but the effect disappeared after correcting for SES, sex, and Home Observation for Measurement of the Environment (HOME) questionaire results (p<0.1) | [41] |
| HBCDD | M & F | Groningen infant COMPARE (Comparison of Exposure–Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Improved coordination (via Touwen’s neurologic examination) | [41] |
| Pentachlorophenol (PCP) | M & F | Groningen infant COMPARE (Comparison of Exposure–Effect Pathways to Improve the Assessment of Human Health Risks of Complex Environmental Mixtures of Organohalogens) study | Prospective cohort | Gestation (35 weeks) | Not established | Decreased coordination (via Touwen’s neurologic examination) | [41] |
| Perfluoroalkyls | M & F | Danish National Birth Cohort (Denmark) | Prospective cohort | Gestation (maternal plasma) | Fine and gross motor function at ages 6 and 18 months (neurological consult) | [22] | |
| Polychlorinated Biphenyls (PCBs) | M & F | Birth Cohort (North Carolina) | Prospective cohort | Gestation | 1.8 ppm breast milk (lipid based) (Postnatal exposure to PCBs was not associated with the PDI at 6 or 12 months) | Median 9.06 ppb maternal serum; median <4.27 ppb cord serum (At 6 months, the PDI was estimated to decrease 0.96 points for every increase of 1 ppm in PCBs. This would mean a drop of 2.6 points if a child moved from the 5th to the 95th percentile of PCB exposure. At 12 months, the drop was estimated at 1.34 points/ppm) | [24], [29], [36], [35], [38], [40], [39] |
| Polychlorinated Biphenyls (PCBs) | M & F | Dutch PCB/Dioxin Study (Rotterdam, Denmark) | Prospective cohort | Gestation | 2.2 ppb maternal plasma, 0.45 ppb cord plasma (PDI at 7 and 18 months age) | 2.2 ppb maternal plasma, 0.45 ppb cord plasma (decreased PDI at 3 months age) | [28] |
| Polychlorinated Biphenyls (PCBs) | M & F | Dutch PCB/Dioxin Study (Rotterdam, Denmark) | Prospective cohort | Gestation+2 weeks lactation | Not established | Median 0.75 ppb child plasma, 0.046 ppb TEQ (decreased PDI at 7 months among infants who were breastfed for longer periods and had higher TEQ scores were associated with postnatal total TEQ exposure) | [28] |
2. Experimental design, materials and methods
As detailed in [26], the primary search utilized ATSDR’s Toxicological Profiles (n=173 chemicals) and Addenda (n=41 chemicals). We read through the profiles and addenda in search of data pertaining to motor function development in association with chemical exposure. In order to find human studies corroborating or challenging the results of the toxicological profile and addenda animal studies as well as assess additional chemicals known to affect motor development, further searches were done on PubMed using common text words and MeSH terms related to motor function development:
((((((((motor[All Fields] AND ("physiology"[Subheading] OR "physiology"[All Fields] OR "function"[All Fields] OR "physiology"[MeSH Terms] OR "function"[All Fields]))) OR (sensorimotor[All Fields] AND ("physiology"[Subheading] OR "physiology"[All Fields] OR "function"[All Fields] OR "physiology"[MeSH Terms] OR "function"[All Fields]))) OR (visual[All Fields] AND motor[All Fields])) OR graphomotor) OR gross motor function) OR (fine AND motor AND function))) AND ("developmental disabilities"[MeSH Terms] OR ("developmental"[All Fields] AND "disabilities"[All Fields]) OR "developmental disabilities"[All Fields]) and different chemicals.
Studies were not limited by date of publication, species, chemical, or study design; however, studies were limited to the English language. The following data from each study were extracted, when available: chemical name, exposure route, exposure duration and frequency, study design, cohort name and/or geographic location, sex of cohort subjects, NOAEL, and LOAEL.
Acknowledgments
SZ Ingber received funding from the Oak Ridge Institute of Science and Engineering (ORISE) Fellowship program when she completed this research.
Footnotes
Appendix A
Supplementary data associated with this article can be found in the online version at doi:10.1016/j.dib.2015.12.036.
Appendix A. Supplementary material
Supplementary material
mmc1.pdf (324.2KB, pdf)
References
- 1.Baker D. Neurobehavioral study of 18 year olds exposed to heptachlor epoxide during gestation. Neurotoxicology. 2004;25:700–701. [Google Scholar]
- 2.Barr H. Prenatal exposure to alcohol, caffeine, tobacco, and aspirin: effects on fine and gross motor performance in 4-year-old children. Dev. Psychol. 1990;26:339–348. [Google Scholar]
- 3.Bellinger D. Correlates of low-level lead exposure in urban children at 2 years of age. Pediatrics. 1986;77:826–833. [PubMed] [Google Scholar]
- 4.Bellinger D. Low-level lead exposure and children׳s cognitive function in the preschool years. Pediatrics. 1991;87:219–227. [PubMed] [Google Scholar]
- 5.D. Bellinger, et al. A longitudinal study of the developmental toxicity of low-level lead exposure in the prenatal and early postnatal periods, In: Proceedings of the International Conference on Heavy Metals in the Environment, vol. 1, 1985, pp. 32–34.
- 6.Bellinger D. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N. Engl. J. Med. 1987;316:1037–1043. doi: 10.1056/NEJM198704233161701. [DOI] [PubMed] [Google Scholar]
- 7.Bellinger D. Low-level lead exposure, social class, and infant development. Neurotoxicol. Teratol. 1988;10:497–503. doi: 10.1016/0892-0362(88)90084-0. [DOI] [PubMed] [Google Scholar]
- 8.Bellinger D. Lead Exposure and Child Development. Springer; 1989. Low-level lead exposure and early development in socioeconomically advantaged urban infants; pp. 345–356. [Google Scholar]
- 9.Bellinger D. Low-level lead exposure and child development: assessment at age 5 of a cohort followed from birth. Heavy Met. Environ. 1987;1:49–53. [Google Scholar]
- 10.Bellinger D.C. Early sensory-motor development and prenatal exposure to lead. Neurobehav. Toxicol. Teratol. 1984 [PubMed] [Google Scholar]
- 11.Bellinger D.C. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics. 1992;90:855–861. [PubMed] [Google Scholar]
- 12.Boucher O. Exposure to an organochlorine pesticide (chlordecone) and development of 18-month-old infants. Neurotoxicology. 2013;35:162–168. doi: 10.1016/j.neuro.2013.01.007. [DOI] [PubMed] [Google Scholar]
- 13.Coles C.D. Neonatal neurobehavioral characteristics as correlates of maternal alcohol use during gestation. Alcohol. Clin. Exp. Res. 1985;9:454–460. doi: 10.1111/j.1530-0277.1985.tb05582.x. [DOI] [PubMed] [Google Scholar]
- 14.Cox C. Dose-response analysis of infants prenatally exposed to methyl mercury: an application of a single compartment model to single-strand hair analysis. Environ. Res. 1989;49:318–332. doi: 10.1016/s0013-9351(89)80075-1. [DOI] [PubMed] [Google Scholar]
- 15.Dietrich K.N. The developmental consequences of low to moderate prenatal and postnatal lead exposure: intellectual attainment in the Cincinnati Lead Study Cohort following school entry. Neurotoxicol. Teratol. 1993;15:37–44. doi: 10.1016/0892-0362(93)90043-n. [DOI] [PubMed] [Google Scholar]
- 16.Dix-Cooper L. Neurodevelopmental performance among school age children in rural Guatemala is associated with prenatal and postnatal exposure to carbon monoxide, a marker for exposure to woodsmoke. Neurotoxicology. 2012;33:246–254. doi: 10.1016/j.neuro.2011.09.004. [DOI] [PubMed] [Google Scholar]
- 17.C. Ernhart, et al., Intrauterine lead exposure and the status of the neonate, In: Proceedings of the International Conference on Heavy Metals in the Environment, Athens, Greece, September, vol. 1, 1985, pp. 35–37.
- 18.Ernhart C.B. Low level lead exposure in the prenatal and early preschool periods: early preschool development. Neurotoxicol. Teratol. 1987;9:259–270. doi: 10.1016/0892-0362(87)90011-0. [DOI] [PubMed] [Google Scholar]
- 19.Ernhart C.B. Intrauterine exposure to low levels of lead: the status of the neonate. Arch. Environ. Health: Int. J. 1986;41:287–291. doi: 10.1080/00039896.1986.9936698. [DOI] [PubMed] [Google Scholar]
- 20.Eskenazi B. In utero and childhood polybrominated diphenyl ether (PBDE) exposures and neurodevelopment in the CHAMACOS study. Environ. Health Perspect. 2013;121:257. doi: 10.1289/ehp.1205597. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Eskenazi B. In utero exposure to dichlorodiphenyltrichloroethane (DDT) and dichlorodiphenyldichloroethylene (DDE) and neurodevelopment among young Mexican American children. Pediatrics. 2006;118:233–241. doi: 10.1542/peds.2005-3117. [DOI] [PubMed] [Google Scholar]
- 22.Fei C. Prenatal exposure to perfluorooctanoate (PFOA) and perfluorooctanesulfonate (PFOS) and maternally reported developmental milestones in infancy. Environ. Health Perspect. 2008;116:1391. doi: 10.1289/ehp.11277. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 23.Gascon M. Effects of pre and postnatal exposure to low levels of polybromodiphenyl ethers on neurodevelopment and thyroid hormone levels at 4 years of age. Environ. Int. 2011;37:605–611. doi: 10.1016/j.envint.2010.12.005. [DOI] [PubMed] [Google Scholar]
- 24.Gladen B.C. Development after exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene transplacentally and through human milk. J. Pediatr. 1988;113:991–995. doi: 10.1016/s0022-3476(88)80569-9. [DOI] [PubMed] [Google Scholar]
- 25.Hernández-Bonilla D. Environmental exposure to manganese and motor function of children in Mexico. Neurotoxicology. 2011;32:615–621. doi: 10.1016/j.neuro.2011.07.010. [DOI] [PubMed] [Google Scholar]
- 26.Ingber S., Pohl H. Windows of sensitivity to toxic chemicals in the motor effects development. Regul. Toxicol. Pharmacol. 2015 doi: 10.1016/j.yrtph.2015.11.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 27.Jedrychowski W. Effects of prenatal exposure to mercury on cognitive and psychomotor function in one-year-old infants: Epidemiologic Cohort Study in Poland. Ann. Epidemiol. 2006;16:439–447. doi: 10.1016/j.annepidem.2005.06.059. [DOI] [PubMed] [Google Scholar]
- 28.Koopman-Esseboom C. Effects of polychlorinated biphenyl/dioxin exposure and feeding type on infants׳ mental and psychomotor development. Pediatrics. 1996;97:700–706. [PubMed] [Google Scholar]
- 29.Longnecker M.P. Polychlorinated biphenyl (PCB) exposure in relation to thyroid hormone levels in neonates. Epidemiology. 2000;11:249–254. doi: 10.1097/00001648-200005000-00004. [DOI] [PubMed] [Google Scholar]
- 30.Lucchini R.G. Tremor, olfactory and motor changes in Italian adolescents exposed to historical ferro-manganese emission. Neurotoxicology. 2012;33:687–696. doi: 10.1016/j.neuro.2012.01.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Myers G.J. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Lancet. 2003;361:1686–1692. doi: 10.1016/S0140-6736(03)13371-5. [DOI] [PubMed] [Google Scholar]
- 32.Myers G.J. Postnatal exposure to methyl mercury from fish consumption: a review and new data from the Seychelles Child Development Study. Neurotoxicology. 2009;30:338–349. doi: 10.1016/j.neuro.2009.01.005. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Parvez F. Arsenic exposure and motor function among children in Bangladesh. Environ. Health Perspect. 2011;119:1665. doi: 10.1289/ehp.1103548. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Ribas-Fitó Núria. Breastfeeding, exposure to organochlorine compounds, and neurodevelopment in infants. Pediatrics. 2003;111:e580–e585. doi: 10.1542/peds.111.5.e580. [DOI] [PubMed] [Google Scholar]
- 35.Rogan W., Gladen B. Neurotoxicology of PCBs and related compounds. Neurotoxicology. 1992;13:27. [PubMed] [Google Scholar]
- 36.Rogan W.J., Gladen B.C. PCBs, DDE, and child development at 18 and 24 months. Ann. Epidemiol. 1991;1:407–413. doi: 10.1016/1047-2797(91)90010-a. [DOI] [PubMed] [Google Scholar]
- 37.Rogan W.J. Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan. Science. 1988;241:334–336. doi: 10.1126/science.3133768. [DOI] [PubMed] [Google Scholar]
- 38.Rogan W.J. Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) in human milk: effects of maternal factors and previous lactation. Am. J. Public Health. 1986;76:172–177. doi: 10.2105/ajph.76.2.172. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Rogan W.J. Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) in human milk: effects on growth, morbidity, and duration of lactation. Am. J. Public Health. 1987;77:1294–1297. doi: 10.2105/ajph.77.10.1294. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Rogan W.J. Neonatal effects of transplacental exposure to PCBs and DDE. J. Pediatr. 1986;109:335–341. doi: 10.1016/s0022-3476(86)80397-3. [DOI] [PubMed] [Google Scholar]
- 41.Roze E. Prenatal exposure to organohalogens, including brominated flame retardants, influences motor, cognitive, and behavioral performance at school age. Environ. Health Perspect. 2009;117:1953–1958. doi: 10.1289/ehp.0901015. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42.Ruckart P.Z. Long-term neurobehavioral health effects of methyl parathion exposure in children in Mississippi and Ohio. Environ. Health Perspect. 2004;112:46–51. doi: 10.1289/ehp.6430. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Tofail F. Effect of arsenic exposure during pregnancy on infant development at 7 months in rural Matlab, Bangladesh. Environ. Health Perspect. 2009;117:288. doi: 10.1289/ehp.11670. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 44.Torres-Sánchez L. Prenatal dichlorodiphenyldichloroethylene (DDE) exposure and neurodevelopment: a follow-up from 12 to 30 months of age. Neurotoxicology. 2009;30:1162–1165. doi: 10.1016/j.neuro.2009.08.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Wilhelm M. The Duisburg birth cohort study: influence of the prenatal exposure to PCDD/Fs and dioxin-like PCBs on thyroid hormone status in newborns and neurodevelopment of infants until the age of 24 months. Mutat. Res./Rev. Mutat. Res. 2008;659:83–92. doi: 10.1016/j.mrrev.2007.11.002. [DOI] [PubMed] [Google Scholar]
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