Organochlorine chemicals and children's health
2002; Elsevier BV; Volume: 140; Issue: 1 Linguagem: Inglês
10.1067/mpd.2002.121690
ISSN1097-6833
AutoresMary S. Wolff, Philip J. Landrigan,
Tópico(s)Effects and risks of endocrine disrupting chemicals
ResumoSee related article, p 33 . The organochlorine chemicals (OCs) are a large, environmentally important family of synthetic organic compounds that include dichlorodiphenyltrichloroethane (DDT) and polychlorinated biphenyls (PCBs), as well as halogenated dioxins and furans. Persistence, bioaccumulation, and lipid solubility are the hallmarks of these compounds, and since publication of Carson's Silent Spring1Carson R. Silent Spring. Houghton Mifflin Company, New York1962Google Scholar in 1962, they have come to be recognized as the archetypal persistent organic pollutants (POPS). Twelve OCs are now subject to an international ban on their production, under the terms of the 2000 Stockholm Convention.2Karlaganis G Marioni R Sieber I Weber A. The elaboration of the “Stockholm convention” on persistent organic pollutants (POPs): a negotiation process fraught with obstacles and opportunities.Environ Sci Pollut Res Int. 2001; 8: 216-221Crossref PubMed Scopus (45) Google Scholar OCs are toxic. In adults, exposures to OCs have been linked to cancer,3Vineis P D'Amore F. The role of occupational exposure and immunodeficiency in B-cell malignancies. Working Group on the Epidemiology of Hematolymphopoietic Malignancies in Italy.Epidemiology. 1992; 3: 266-270Crossref PubMed Scopus (30) Google Scholar, 4Moysich KB Shields PG Freudenheim JL Schisterman EF Vena JE Kostyniak P et al.Polychlorinated biphenyls, cytochrome P4501A1 polymorphism, and postmenopausal breast cancer risk.Cancer Epidemiol Biomarkers Prev. 1999; 8: 41-44PubMed Google Scholar, 5Bertazzi PA Consonni D Bachetti S Rubagotti M Baccarelli A Zocchetti C et al.Health effects of dioxin exposure: a 20-year mortality study.Am J Epidemiol. 2001; 153: 1031-1044Crossref PubMed Scopus (339) Google Scholar cardiovascular disease,6Steenland K Piacitelli L Deddens J Fingerhut M Chang LI. Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8- tetrachlorodibenzo-p-dioxin.J Natl Cancer Inst. 1999; 91: 779-786Crossref PubMed Scopus (239) Google Scholar, 7Kreiss K Zack MM Kimbrough RD Needham LL Smrek AL Jones BT. Association of blood pressure and polychlorinated biphenyl levels.JAMA. 1981; 245: 2505-2509Crossref PubMed Scopus (111) Google Scholar endocrine alterations,8Longnecker MP Klebanoff MA Zhou H Brock JW. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.Lancet. 2001; 358: 110-114Abstract Full Text Full Text PDF PubMed Scopus (357) Google Scholar, 9Longnecker MP Michalek JE. Serum dioxin level in relation to diabetes mellitus among Air Force veterans with background levels of exposure.Epidemiology. 2000; 11: 44-48Crossref PubMed Scopus (135) Google Scholar and curtailed lactation.10Gladen BC Rogan WJ. DDE and shortened duration of lactation in a northern Mexican town.Am J Public Health. 1995; 85: 504-508Crossref PubMed Scopus (100) Google Scholar In children, 2 important characteristics of the OCs are (1) their capacity for intergenerational transfer across the placenta and through breast milk, and (2) their capacity to cause fetal toxicity. An unresolved question is whether this fetal toxicity reflects low-dose exposure during early windows of exquisite sensitivity or is the result of cumulative exposure. In utero exposures to OCs have been linked to reductions in intelligence and behavior. The evidence for this developmental neurotoxicity is strongest and most consistent following in utero exposure to PCBs,11Ribas-Fito N Sala M Kogevinas M Sunyer J. Polychlorinated biphenyls (PCBs) and neurological development in children: a systematic review.J Epidemiol Community Health. 2001; 55: 537-546Crossref PubMed Scopus (151) Google Scholar, 12Brouwer A Longnecker MP Birnbaum LS Cogliano J Kostyniak P Moore J et al.Characterization of potential endocrine-related health effects at low- dose levels of exposure to PCBs.Environ Health Perspect. 1999; 107: 639-649Crossref PubMed Scopus (285) Google Scholar and cognitive and psychomotor decrements have been observed in investigations undertaken in North America, Asia, and Europe.13Rogan WJ Gladen BC Hung KL Koong SL Shih LY Taylor JS et al.Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan.Science. 1988; 241: 334-336Crossref PubMed Scopus (435) Google Scholar, 14Lai TJ Guo YL Guo NW Hsu CC. Effect of prenatal exposure to polychlorinated biphenyls on cognitive development in children: a longitudinal study in Taiwan.Br J Psychiatr Suppl. 2001; 40: s49-s52Crossref PubMed Scopus (42) Google Scholar, 15Gladen BC Rogan WJ Hardy P Thullen J Tingelstad J Tully M. Development after exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene transplacentally and through human milk.J Pediatr. 1988; 113: 991-995Abstract Full Text PDF PubMed Scopus (279) Google Scholar, 16Koopman-Esseboom C Weisglas-Kuperus N de Ridder MA Van der Paauw CG Tuinstra LG Sauer PJ. Effects of polychlorinated biphenyl/dioxin exposure and feeding type on infants' mental and psychomotor development.Pediatrics. 1996; 97: 700-706PubMed Google Scholar, 17Winneke G Bucholski A Heinzow B Kramer U Schmidt E Walkowiak J et al.Developmental neurotoxicity of polychlorinated biphenyls (PCBS): cognitive and psychomotor functions in 7-month old children.Toxicol Lett. 1998; 102-3: 423-428Crossref Scopus (134) Google Scholar, 18Darvill T Lonky E Reihman J Stewart P Pagano J. Prenatal exposure to PCBs and infant performance on the Fagan test of infant intelligence.Neurotoxicology. 2000; 21: 1029-1038PubMed Google Scholar Prospective epidemiologic studies of PCB-exposed children followed from birth through 11 years suggest that these neurodevelopmental effects are persistent at least to that age.19Jacobson JL Jacobson SW. Intellectual impairment in children exposed to polychlorinated biphenyls in utero.N Engl J Med. 1996; 335: 783-789Crossref PubMed Scopus (973) Google Scholar OCs can profoundly affect growth, and exposures in utero appear especially toxic.20Taylor PR Stelma JM Lawrence CE. The relation of polychlorinated biphenyls to birth weight and gestational age in the offspring of occupationally exposed mothers.Am J Epidemiol. 1989; 129: 395-406Crossref PubMed Scopus (118) Google Scholar, 21Vartiainen T Jaakkola JJ Saarikoski S Tuomisto J. Birth weight and sex of children and the correlation to the body burden of PCDDs/PCDFs and PCBs of the mother.Environ Health Perspect. 1998; 106: 61-66Crossref PubMed Scopus (90) Google Scholar Thus, early exposures to PCBs and related compounds are associated with lower birth weight and decreased body size.13Rogan WJ Gladen BC Hung KL Koong SL Shih LY Taylor JS et al.Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan.Science. 1988; 241: 334-336Crossref PubMed Scopus (435) Google Scholar, 22Patandin S Koopman-Esseboom C de Ridder MA Weisglas-Kuperus N Sauer PJ. Effects of environmental exposure to polychlorinated biphenyls and dioxins on birth size and growth in Dutch children.Pediatr Res. 1998; 44: 538-545Crossref PubMed Scopus (219) Google Scholar, 23Guo YL Lambert GH Hsu CC. Growth abnormalities in the population exposed in utero and early postnatally to polychlorinated biphenyls and dibenzofurans.Environ Health Perspect. 1995; 103: 117-122Crossref PubMed Scopus (98) Google Scholar Elevated maternal levels of dichlorodiphenyldichloroethylene (DDE) and PCB have been associated with preterm birth and smaller size newborns8Longnecker MP Klebanoff MA Zhou H Brock JW. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.Lancet. 2001; 358: 110-114Abstract Full Text Full Text PDF PubMed Scopus (357) Google Scholar, 24Fein GG Jacobson JL Jacobson SW Schwartz PM Dowler JK. Prenatal exposure to polychlorinated biphenyls: effects on birth size and gestational age.J Pediatr. 1984; 105: 315-320Abstract Full Text PDF PubMed Scopus (375) Google Scholar; DDE is the major metabolite of DDT. OCs are toxic to reproductive development. There are many experimental reports of premature and delayed puberty and of disruption of estrus in females exposed to OCs in utero.25Gellert RJ Heinrichs WL Swerdloff R. Effects of neonatally-administered DDT homologs on reproductive function in male and female rats.Neuroendocrinology. 1974; 16: 84-94Crossref PubMed Scopus (43) Google Scholar, 26Lundkvist U. Clinical and reproductive effects of Clophen A50 (PCB) administered during gestation on pregnant guinea pigs and their offspring.Toxicology. 1990; 61: 249-257Crossref PubMed Scopus (31) Google Scholar, 27Ottoboni A Bissell GD Hexter AC. Effects of DDT on reproduction in multiple generations of beagle dogs.Arch Environ Contam Toxicol. 1977; 6: 83-101Crossref PubMed Scopus (25) Google Scholar The human evidence here appears to follow the experimental data and suggests that intense exposures to antiestrogenic OCs delay puberty, whereas casual exposures to DDE, PCB, or polybrominated biphenyl (PBB) lead to earlier development. Thus, girls in Michigan with higher perinatal exposures to PBB had earlier ages at menarche.28Blanck HM Marcus M Tolbert PE Rubin C Henderson AK Hertzberg VS et al.Age at menarche and tanner stage in girls exposed in utero and postnatally to polybrominated biphenyl.Epidemiology. 2000; 11: 641-647Crossref PubMed Scopus (239) Google Scholar DDE has been associated with higher weight and height in boys during puberty, whereas PCB levels have been associated with increased weight in girls.29Gladen BC Ragan NB Rogan WJ. Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene.J Pediatr. 2000; 136: 490-496Abstract Full Text Full Text PDF PubMed Scopus (230) Google Scholar Exposure to hexachlorobenzene has been associated with undescended testes.30Hosie S Loff S Witt K Niessen K Waag KL. Is there a correlation between organochlorine compounds and undescended testes?.Eur J Pediatr Surg. 2000; 10: 304-309Crossref PubMed Scopus (126) Google Scholar Now comes the report in this issue of the Journal by Karmaus et al,31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar who find that DDE levels measured at 8 years of age are related to delayed growth throughout early childhood. Thus, girls with higher DDE levels at age 8 exhibited consistently shorter stature than their peers from 1 month through 9 years of age. Average growth was slower, by more than 1.0 cm each year, among girls in the highest versus the lowest half of DDE exposures at 8 of 10 observation points from birth to 10 years of age. The height difference between the upper and lower half of DDE levels was 2 to 3 cm annually until 8 years of age, a decrement that represented 3% to 5% of the higher growth curve. At ages 9 and 10 years, the trends were similar, but smaller and not significant. By this age, many girls have passed their peak growth period, and perhaps by then, the shorter girls have caught up with the less exposed; “catchup” is a well-known phenomenon. Boys in the oldest age groups exhibited a similar, though not significant, trend. It is possible that their growth may become affected at later ages (ie, beyond 10 years of age) because boys mature later. Boys may be less susceptible to growth arrest associated with DDE. Boys also have less body fat, which may in turn be linked to reduced DDE levels and increased height. No independent effect on growth was seen in this study for PCBs in either girls or boys. A strength of the findings of Karmaus et al31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar lies in the dose-response relationships he observes between higher DDE levels and lower height. Although the levels of OCs in these children at age 8 appear to be extremely low, 0.3 μg/L whole blood (median), equivalent to 0.6 μg/L in serum, levels in utero and at early ages were likely to have been several times higher. Thus, the perinatal exposures of the children examined by Winneke et al17Winneke G Bucholski A Heinzow B Kramer U Schmidt E Walkowiak J et al.Developmental neurotoxicity of polychlorinated biphenyls (PCBS): cognitive and psychomotor functions in 7-month old children.Toxicol Lett. 1998; 102-3: 423-428Crossref Scopus (134) Google Scholar may have been comparable to exposures seen in previously published studies of child development. Two unresolved questions in the report by Karmaus et al31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar are (1) the relative importance on growth retardation of in utero exposures to OCs versus postnatal exposures via lactation, and (2) the possibly confounding effects of body mass index (BMI) and of BMI change as children grow. Lactational exposures, while not so toxic gram-for-gram as exposures in utero, are responsible for a significant proportion of the organochlorine body burden in young children, and the quantities of OCs transferred from mother to infant in lactation far exceed those transferred across the placenta. At young ages, breast-fed babies may have several times the OC level of nonbreast-fed infants, and this difference remains discernible until late childhood.32Jacobson JL Humphrey HE Jacobson SW Schantz SL Mullin MD Welch R. Determinants of polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dichlorodiphenyl trichloroethane (DDT) levels in the sera of young children.Am J Public Health. 1989; 79: 1401-1404Crossref PubMed Scopus (127) Google Scholar, 33Anderson HA Wolff MS. Environmental contaminants in human milk.J Expo Anal Environ Epidemiol. 2000; 10: 755-760Crossref PubMed Scopus (70) Google Scholar, 34Lanting CI Patandin S Fidler V Weisglas-Kuperus N Sauer PJ Boersma ER et al.Neurological condition in 42-month-old children in relation to pre- and postnatal exposure to polychlorinated biphenyls and dioxins.Early Hum Dev. 1998; 50: 283-292Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar, 35Longnecker MP Rogan WJ. Persistent organic pollutants in children.Pediatr Res. 2001; 50: 322-323Crossref PubMed Scopus (17) Google Scholar In earlier data presented by Karmaus et al,36Karmaus W DeKoning EP Kruse H Witten J Osius N. Early childhood determinants of organochlorine concentrations in school-aged children.Pediatr Res. 2001; 50: 331-336Crossref PubMed Scopus (62) Google Scholar breast-fed children had 50% higher OC levels at age 7 years than children who were bottle-fed. In fact, most children in this study were breast-fed, and there was a strong positive correlation of OC levels at 8 years of age with breast-feeding; a very high proportion of the children in the upper quartile of DDE exposures appear to have been breast-fed. In their earlier report of these children, Karmaus et al36Karmaus W DeKoning EP Kruse H Witten J Osius N. Early childhood determinants of organochlorine concentrations in school-aged children.Pediatr Res. 2001; 50: 331-336Crossref PubMed Scopus (62) Google Scholar observed an inverse association between OC levels and BMI. This association was mainly because of lower OC levels at 7 years of age among children in the topmost quartile of BMI. For this reason, the height reductions observed in children who had simultaneously the lowest BMI and highest DDE levels may be caused, at least in part, by a variation in BMI. Does this imply that DDE in breastmilk or in the diets of young children overcomes the positive effect of breast-feeding on growth? Or do bottle-fed baby girls become fatter, have lower DDE levels, and grow more? Although the authors do adjust for BMI, lactation, and other potentially confounding variables, it is possible that statistical adjustment cannot completely separate the strong, common contributions of in utero and lactational exposures, gender, birth weight, and BMI to both DDE levels and growth. It would be helpful to study this question more closely, either in a prospective study, by stratifying on the duration of lactation or by removing the nonbreast-fed babies from the model. Controlling for breast milk DDE levels, if they were available, might also help clarify the issue. In addition, it may be useful to more closely examine the abundant literature on the relationship of early body size on development. For example, if we assume that only pre or very early postnatal OC exposures alter development, it would be predicted that early overnutrition would lead to exactly the same results seen here: higher childhood BMI, lower DDE, and greater height. Several recent reports have attempted to elucidate relationships among fetal, childhood, adolescent and adult body sizes. For example, in a recent Swedish study, children whose BMI increased during childhood (2-8 years of age) were approximately 3 cm taller at 8 years than children whose BMI decreased.37He Q Karlberg J. BMI in childhood and its association with height gain, timing of puberty, and final height.Pediatr Res. 2001; 49: 244-251Crossref PubMed Scopus (323) Google Scholar Just as in the current report by Karmaus et al,31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar no height differential was evident in those children, either at birth or in later adolescence. Also similar to the Swedish data,37He Q Karlberg J. BMI in childhood and its association with height gain, timing of puberty, and final height.Pediatr Res. 2001; 49: 244-251Crossref PubMed Scopus (323) Google Scholar in the current study, the girls with higher BMI were taller. It would be helpful to study weight gain in the new dataset, to establish parallels with the Swedish data. Another possible pathway to the association seen by Karmaus et al between reduced childhood height and DDE level could be through intrauterine growth retardation.8Longnecker MP Klebanoff MA Zhou H Brock JW. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.Lancet. 2001; 358: 110-114Abstract Full Text Full Text PDF PubMed Scopus (357) Google Scholar Reduced birth weight associated with higher in utero exposure to DDE could lead to smaller body size in childhood,38Persson I Ahlsson F Ewald U Tuvemo T Qingyuan M von Rosen D et al.Influence of perinatal factors on the onset of puberty in boys and girls: implications for interpretation of link with risk of long term diseases.Am J Epidemiol. 1999; 150: 747-755Crossref PubMed Scopus (168) Google Scholar which in turn would result in higher OC levels at 8 years of age. Why do Karmaus et al31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar see an effect of DDE, but not of PCB, on growth? If BMI alone were responsible for the findings, the same association should be seen for PCBs. The explanation may be that the PCB levels seen among 8-year-olds in this cohort reflect childhood exposures from nonmaternal sources, most likely fish consumption. Three observations support this hypothesis. First, the trends for PCBs with BMI and lactation are somewhat different than those for DDE. Second, the inverse association of BMI with PCB is stronger than that for DDE, suggesting more current exposure to PCB.33Anderson HA Wolff MS. Environmental contaminants in human milk.J Expo Anal Environ Epidemiol. 2000; 10: 755-760Crossref PubMed Scopus (70) Google Scholar, 39Wolff MS Anderson HA. Environmental contaminants and body fat distribution.Cancer Epidemiol Biomark Prev. 1999; 8 ([letter]): 951-952PubMed Google Scholar And third, nonbreast-fed children had PCB levels that were two thirds those of breast-fed children. Serious gaps exist in current understanding of the mechanisms by which OCs modulate growth and development. A better mechanistic understanding for these observations might enable us to better comprehend the implications to health and to resolve the results of apparent conflicting studies. For example, the inverse association of DDE with height seen in the data of Karmaus et al31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar contrasts with previous findings on the effect of DDE on body size in adolescence,29Gladen BC Ragan NB Rogan WJ. Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene.J Pediatr. 2000; 136: 490-496Abstract Full Text Full Text PDF PubMed Scopus (230) Google Scholar but it is consistent with negative effects of OCs on growth in other studies. A likely biologic mechanism for the findings of Karmaus et al is that DDE is antiandrogenic,40Kelce WR Stone CR Laws SC Gray LE Kemppainen JA Wilson EM. Persistent DDT metabolite p,p'-DDE is a potent androgen receptor antagonist.Nature. 1995; 375: 581-585Crossref PubMed Scopus (1339) Google Scholar, 41Baatrup E Junge M Gunier RB Harnly ME Reynolds P Hertz A et al.Antiandrogenic pesticides disrupt sexual characteristics in the adult male guppy Poecilia reticulata.Environ Health Perspect. 2001; 109: 1063-1070Crossref PubMed Scopus (161) Google Scholar and that androgens may control growth factors key to body size. If this hypothesis is true, we need to look at DDE/androgen/growth models in epidemiologic studies, such as those that are investigating racial/ethnic differences in androgens and development as they relate to the onset of puberty,42Girgis R Abrams SA Castracane VD Gunn SK Ellis KJ Copeland KC. Ethnic differences in androgens, IGF-I and body fat in healthy prepubertal girls.J Pediatr Endocrinol Metab. 2000; 13: 497-503Crossref PubMed Scopus (30) Google Scholar, 43Richards RJ Svec F Bao W Srinivasan SR Berenson GS. Steroid hormones during puberty: racial (black-white) differences in androstenedione and estradiol—the Bogalusa Heart Study.J Clin Endocrinol Metab. 1992; 75: 624-631Crossref PubMed Scopus (50) Google Scholar, 44Herman-Giddens ME Slora EJ Wasserman RC Bourdony CJ Bhapkar MV Koch GG et al.Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network.Pediatrics. 1997; 99: 505-512Crossref PubMed Scopus (1331) Google Scholar cardiovascular disease,45Morrison JA Sprecher DL Barton BA Waclawiw MA Daniels SR. Overweight, fat patterning, and cardiovascular disease risk factors in black and white girls: The National Heart, Lung, and Blood Institute Growth and Health Study.J Pediatr. 1999; 135: 458-464Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar and breast cancer.46Stoll BA Secreto G. New hormonerelated markers of high risk to breast cancer.Ann Oncol. 1992; 3: 435-438PubMed Scopus (46) Google Scholar PCDD/DFs, PCBs, and PBBs may all affect neuroendocrine function through thyroid, Ah, and hormone receptors. These mechanisms have been explored, but there is a need to consolidate the experimental and human data into a unified mechanistic basis for future epidemiologic research. Such research may also help to clarify the speculation that the in utero milieu may influence later disease risk.47Cooper C Kuh D Egger P Wadsworth M Barker D. Childhood growth and age at menarche.Br J Obstet Gynaecol. 1996; 103: 814-817Crossref PubMed Scopus (212) Google Scholar, 48Colditz GA Frazier AL. Models of breast cancer show that risk is set by events of early life: prevention efforts must shift focus.Cancer Epidemiol Biomarker Prev. 1995; 4: 567-571PubMed Google Scholar, 49Trichopoulos D. Hypothesis: does breast cancer originate in utero?.Lancet. 1990; 335: 939-940Abstract PubMed Scopus (442) Google Scholar For the future, it will be important to separate the effects of in utero from lactational exposure. Better understanding of the source and timing of exposures will clarify research findings and guide public health policy. Our long experience with human exposure to OCs, particularly to DDT, has found few acute health effects. But meticulous studies such as this report by Karmaus31Karmaus W Asakevich S Indurkhya A Witten J Kruse H. Childhood growth and exposure to dichlorodiphenyldichloroethene and polychlorinated biphenyls.J Pediatr. 2002; 140: 33-39Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar that have carefully measured exposures have documented a series of subclinical deleterious effects. As in the case of children exposed to levels of lead that were insufficient to cause acute toxicity, the individual deficits may be difficult to discern.50Bellinger D Leviton A Waternaux C Needleman H Rabinowitz M. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development.N Engl J Med. 1987; 316: 1037-1043Crossref PubMed Scopus (682) Google Scholar The population effects are, however, enormous, and have profound effects on societal productivity and even on the sustainability of the human species. Childhood growth and exposure to dichlorodiphenyl dichloroethene and polychlorinated biphenylsThe Journal of PediatricsVol. 140Issue 1PreviewObjectives: Dichlorodiphenyl dichloroethene (DDE) and polychlorinated biphenyls (PCB), toxic contaminants known to be persistent in the environment, may affect growth. We investigated whether growth from birth to 10 years of age is associated with blood concentrations of DDE and PCB taken at 8 years of age. Study design: We ambispectively followed up a cohort of 343 German children. DDE and PCB blood concentrations were determined in 1995. Height measurements were conducted prospectively between 1994 and 1997 and obtained retrospectively from each Child's Health Card. Full-Text PDF
Referência(s)