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PubMed1997

Pregnancy outcome and neurodevelopment of children exposed in utero to psychoactive drugs: the Motherisk experience.

This paper presents an overview of the Motherisk Program data on pregnancy outcome and neurodevelopment of children exposed in utero to selected psychoactive drugs. First, the use of cocaine during pregnancy has been associated with increased risk of spontaneous abortions, abruptio placenta, premature labor, and stillbirth. Twenty-three adopted children exposed in utero to cocaine demonstrated an 8-fold increase in risk for microcephaly compared with controls. Global intelligence quotients (IQ) did not differ between the 2 groups, but the cocaine-exposed children achieved significantly lower scores on the Reynell language test. Second, the long-term neurobehavioral effects of fetal alcohol syndrome (FAS) were studied in 384 children to show that alcohol-induced brain insults, which consist of attention and memory deficits together, and poor adaptability and organization are not attenuated with age. Third, the rates of major malformations in children exposed in utero to fluoxetine, tricyclic antidepressants, and nonteratogenic drugs did not differ or exceed the expected rates in the general population. A 2nd phase of this study established the safety of antidepressants during pregnancy by demonstrating that the mean IQ and language scores are comparable in the 3 groups. A level 2 ultrasonography is recommended in cases of in utero exposure to lithium and carbamazepine because of an increased risk of cardiac malformations and spina bifida, respectively.

Developmental Disabilities↗

PubMedDate not supplied

Relationship between gestures and words in children with Down's syndrome and typically developing children in the early stages of communicative development.

BACKGROUND: Previous research has emphasized the importance of gesture in early communicative development. These studies have reported that gestures are used frequently during the first two years of life and may play a transitional role in the language acquisition process. Although there are now numerous descriptions of the relationship between gesture and the developing language system in typically-developing (TD) children, relatively little is known about the nature and early development of the gesture-language system in children with developmental disorders involving specific profiles of language delay and/or impairment. PRIMARY OBJECTIVE: The aim of this study is to compare early word and gesture use in children with DS and in typically-developing children to investigate potential differences in the relationship between gestural and verbal communication in early language development. METHODS AND PROCEDURES: Ten children from upper-middle class families participated in the study. The five children with DS (3 boys and 2 girls) had an average chronological age of 47.6 months, an average mental age of 22.4 months, and an average language age of 18 months. Each child with DS was matched to a typically developing child on the basis of gender, language age, and observed expressive vocabulary size. Children were videotaped for 30 minutes as they interacted spontaneously with their mothers. All communicative and intelligible gestures and words produced by the children were transcribed from the videotapes. Data analyses focused on: a) overall production of gestures and words (i.e., gesture and word tokens); b) the size of children's gestural and verbal repertoires (i.e., gesture and word types); and c) production and informational content of gesture-word combinations. MAIN OUTCOMES AND RESULTS: Although children with DS had significantly smaller gestural repertoires than their language age-matched peers, there was no reliable difference between the two groups in the overall use of gesture. In addition, with DS produced two-element combinations (primarily gesture-word combinations) and did so at a rate comparable to that observed among their TD counterparts. However, no two-word combinations were observed among children with DS, and there were also group differences in the information contained in children's gesture-word combinations. CONCLUSIONS: Taken together, these findings suggest that in addition to the well-documented global delays in early communicative development, children with DS may exhibit additional pockets of delay, specifically in making the transition from one- to two-word speech. Results are further discussed in terms of their implications for understanding the organization of the developing gesture-language system and for the assessment of gesture in young children with communicative delays and disorders.

Child, Preschool↗

PubMed2005

[Iron deficiency anemia in infants. Preliminary development results at five years].

INTRODUCTION: Research, mostly conducted in developing countries, have suggested short and long term developmental delay in children who had iron-deficiency anemia (IDA) in their early life. This study aims to evaluate the development of 5-years old children who were diagnosed IDA at 9 months of age. METHODS: 27 children with IDA diagnosed at 9 months of age and 28 non-anemic controls were followed-up until they were 5 years old. At 9 months of age and at 5 years of age, blood samples were collected for blood count, iron, transferrin and ferritin. Children with hemoglobin < 110 g/l and ferritin < 12 ng/ml were diagnosed with IDA and received iron treatment for IDA correction. C Reactive Protein and antibody to hepatitis A virus were also studied at 5 years of age. At this age, children's motor and cognitive development were accessed using Griffith's test. RESULTS: At 9 months of age, IDA children had [mean (SD)] 102.5 g/ l (5.9) g/l of hemoglobin and 5.6 ng/l (3.1) ng/ml of ferritin. At 5 years of age all children were healthy and without anemia. One child had positive antibody to hepatitis A virus. The results of Griffith's test at five years--anemic/non-anemic at 9 months of age. The mean (sd)-p: general coefficient--100.8 (6.6)/99.5 (7.1)-0.48; locomotor 110.2 (6.9)/109.3 (6.5)-0.62; personal-social--99.1 (11.4)/95.7(11.6)-0.28; hearing-speech--93.8 (9.1)/95.3 (13.7)-0.64; hand-eye--98.2 (13.2)/99.1 (14.3)-0.79; performance--97.5 (17.6)/96.9 (13.6)-0.88; practical reasoning--89.8 (9.1)/86.3(7.1)-0.21. CONCLUSIONS: As only one child had positive antibody to hepatitis A virus, the study population may be considered as belonging to a developed region. These results suggest that, at least in developed regions, infants who receive an early treatment for their mild IDA may not be affected in global development at the age of five.

Anemia, Iron-Deficiency↗

PubMed1998

Specificity of neurobehavioral outcomes associated with prenatal alcohol exposure.

A current issue in alcohol research is whether a "neurobehavioral profile" can be identified for prenatal alcohol exposure, even when dysmorphic features are not present, or whether comparable neurobehavioral deficits are detected when damage is incurred by numerous neurotoxicants to which the fetus is exposed during a common developmental period. Failure to detect such differences may, in part, be an artifact of the global developmental tests used to assess outcome. Cognitive effects of prenatal exposure to three different teratogens [polychlorinated biphenyls (PCBs), alcohol, and cocaine] are examined to determine whether exposure to each substance results in a common or different pattern of impairment on the same set of newer, more narrow band infant tests. Comparison of findings from three independent cohorts indicate that PCB exposure was related to poorer recognition memory on the Fagan Test of Infant Intelligence (FTII) in Michigan infants exposed prenatally to PCB-contaminated fish, whereas prenatal alcohol exposure was unrelated to recognition memory but to slower processing speed on a new FTII measure and slower reaction time on Haith's Visual Expectancy Paradigm (VExP) in our Detroit alcohol-exposed infants. Preliminary findings from a new study of infants recently born to Taiwanese women accidentally contaminated with sizable amounts of PCBs indicate recognition memory deficits, confirming our Michigan findings, but no processing speed effects on the FTII. Recent findings from our Detroit cohort suggest that heavy prenatal cocaine exposure is related to poorer recognition memory on the FTII, but faster reaction times on the VExP, a pattern different from that seen for either PCBs or alcohol.

Brain Damage, Chronic↗

PubMed2000

Health risks to infants from exposure to PCBs, PCDDs and PCDFs.

Global contamination by a variety of anthropogenic persistent organic chemicals, such as dioxins and PCBs, has resulted in human exposure throughout all phases of development. Detectable concentrations of PCBs and dioxins have been found in amniotic fluid, placenta and foetal tissue samples while infants who are breast-fed can obtain blood levels greater than those of their mother's. In two separate food poisoning episodes where infants were exposed in utero to elevated levels of heat-degraded PCBs (PCBs, PCQs, PCDFs), a variety of adverse mental and physical developmental abnormalities have been observed. In additional human cohorts where exposure could be considered as environmental or background, more subtle effects, including lower birth weights, alterations in thyroid hormones and lymphocyte subpopulations and detriments in neurological development, have been consistently seen. In most instances, negative associations were made between in utero exposure to contaminants compared with lactational. Although the observed neurodevelopmental deficits have been described as subtle, there could be unknown consequences related to future intellectual functionality. Current regulatory efforts should focus on identification and control of environment and food chain contamination as in utero exposure is a direct consequence of the accumulated maternal body burdens.

Accidents↗

PubMed2004

Global gene expression analysis identifies molecular pathways distinguishing blastocyst dormancy and activation.

Delayed implantation (embryonic diapause) occurs when the embryo at the blastocyst stage achieves a state of suspended animation. During this period, blastocyst growth is very slow, with minimal or no cell division. Nearly 100 mammals in seven different orders undergo delayed implantation, but the underlying molecular mechanisms that direct this process remain largely unknown. In mice, ovariectomy before preimplantation ovarian estrogen secretion on day 4 of pregnancy initiates blastocyst dormancy, which normally lasts for 1-2 weeks by continued progesterone treatment, although blastocyst survival decreases with time. An estrogen injection rapidly activates blastocysts and initiates their implantation in the progesterone-primed uterus. Using this model, here we show that among approximately 20,000 genes examined, only 229 are differentially expressed between dormant and activated blastocysts. The major functional categories of altered genes include the cell cycle, cell signaling, and energy metabolic pathways, particularly highlighting the importance of heparin-binding epidermal growth factor-like signaling in blastocyst-uterine crosstalk in implantation. The results provide evidence that the two different physiological states of the blastocyst, dormancy and activation, are molecularly distinguishable in a global perspective and underscore the importance of specific molecular pathways in these processes. This study has identified candidate genes that provide a scope for in-depth analysis of their functions and an opportunity for examining their relevance to blastocyst dormancy and activation in numerous other species for which microarray analysis is not available or possible due to very limited availability of blastocysts.

Animals↗

PubMed1999

Commentary on Annett, Yeo et al., Klar, Saugstad and Orr: cerebral asymmetry, language and psychosis--the case for a Homo sapiens-specific sex-linked gene for brain growth.

Annett, Yeo et al. and Klar have each proposed theories that relate the genetics of cerebral lateralization to predisposition to psychosis. These theories are considered in relation to the central paradox that psychosis is associated with a substantial biological disadvantage. Annett's heterozygote advantage hypothesis critically identified lateralization as a major determinant of ability, but it appears that what is inherited is degrees (as suggested by Yeo et al.) rather than (or as well as) direction of lateralization. Relative hand skill has been shown (Crow, T.J., Crow, L.R., Done, D.J., Leask, S.J., 1998. Relative hand skill predicts academic ability: global deficits at the point of hemispheric indecision. Neuropsychologia 36, 1275-1282.) to be a powerful predictor (interacting with sex) of academic ability but the greatest region of vulnerability (that includes reading disability and predisposition to psychosis) is close to the point of equal hand skill ('hemispheric indecision'). In contrast with Annett's single locus, Yeo's polygenic and Klar's strand-segregation hypotheses, each of which postulates an autosomal locus or loci, the hypothesis of a single gene for asymmetry located in a sex-specific region of homology on both X and Y chromosomes can account for sex differences, as observed in age of onset, and premorbid precursors of psychosis, as well as differences in the general population in relation to degrees of hand skill, verbal ability and cerebral asymmetry. The evolutionarily recent transposition to, and subsequent paracentric inversion in, the Y chromosome short arm of a 4-Mb block from Xq21.3 (the proximal long arm of the X) are candidates for speciation events in the lineage that led to Homo sapiens. A gene associated with a range of variation (that may be due to a high mutation site, or perhaps to epigenetic modification) on the Y that overlaps with, but differs quantitatively from, that on the X may explain the sex differences associated with psychosis, and may be relevant to its persistence. Such a gene could be the principal determinant in Man of the rate of brain growth, as suggested by Saugstad and by the findings of a recent study of adolescent onset psychosis (James, A., Crow, T.J., Renowden, S., Wardell, M., Smith, D.M., Anslow, P., in press. Is the course of brain development in schizophrenia delayed? Evidence from onsets in adolescence. Schizophr. Res.).

Biological Evolution↗

PubMed2001

Altered gene profiles in fetal rat testes after in utero exposure to di(n-butyl) phthalate.

Di(n-butyl) phthalate (DBP) has antiandrogenic-like effects on the developing reproductive tract in the male rat and produces regions of interstitial cell hyperplasia and gonocyte degeneration in the developing fetal testes at maternal doses of 100-500 mg/kg/day. Neither DBP nor its primary metabolites interact with the androgen receptor in vitro. The present study was performed to examine gene expression in the fetal rat testes following in utero DBP exposure. Pregnant Sprague-Dawley rats received corn oil, DBP (500 mg/kg/day), or flutamide (reference antiandrogen, 50 mg/kg/day) by gavage daily from gestation day (GD) 12 to 21. Dose levels were selected to maximize fetal response with minimal maternal toxicity. Testes were isolated on GD 16, 19, and 21. Global changes in gene expression were determined by microarray analysis. Selected genes were further examined by quantitative RT-PCR. DBP, but not flutamide, reduced expression of the steroidogenic enzymes cytochrome P450 side chain cleavage, cytochrome P450c17, and steroidogenic acute regulatory protein. Testicular testosterone and androstenedione were decreased on GD 19 and 21, while progesterone was increased on GD 19 in DBP-exposed testes. Testosterone-repressed prostate message-2 (TRPM-2) was upregulated, while c-kit (stem cell factor receptor) mRNA was downregulated following DBP exposure. TRPM-2 and bcl-2 protein staining was elevated in GD 21 DBP-exposed Leydig and Sertoli cells. Results of this study have led to the identification of several possible mechanisms by which DBP can induce its antiandrogenic effects on the developing male reproductive tract without direct interaction with the androgen receptor. Our results suggest that the antiandrogenic effects of DBP are due to decreased testosterone synthesis. In addition, enhanced expression of cell survival proteins such as TRPM-2 and bcl-2 may be involved in DBP-induced Leydig cell hyperplasia, whereas, downregulation of c-kit may play a role in gonocyte degeneration. Future studies will explore the link between these identified gene expression alterations and ultimate adverse responses.

Androgen Antagonists↗

PubMedDate not supplied

Potential developmental toxicity of anatoxin-a, a cyanobacterial toxin.

Some 2000 species of cyanobacteria (blue-green algae) occur globally in aquatic habitats. They are able to survive under a wide range of environmental conditions and some produce potent toxins. Toxin production is correlated with periods of rapid growth (blooms) and 25%-70% of blooms may be toxic. Anatoxin-a is an alkaloid neurotoxin that acts as a potent neuro-muscular blocking agent at the nicotinic receptor. Acute toxicity, following consumption of contaminated water, is characterized by rapid onset of paralysis, tremors, convulsions and death. Human exposures may occur from recreational water activities and dietary supplements, but are primarily through drinking water. The current studies were conducted to examine the effect of in utero exposure on postnatal viability, growth and neurodevelopment, to evaluate the potential of in vitro embryotoxicity, and to explore the synergistic relationship between anatoxin-a and the algal toxin microcystin-LR by the oral route. The results of preliminary studies on amphibian toxicity are also reported. Time-pregnant mice received 125 or 200 microg kg(-1) anatoxin-a by intraperitoneal injection on gestation days (GD) 8-12 or 13-17. Pup viability and weight were monitored over a 6-day period. Maternal toxicity (decreased motor activity) was observed at 200 microg kg(-1) in both treatment periods. There were no significant treatment-related effects on pup viability or weight on postnatal day (PND) 1 or 6. The GD 13-17 pups were evaluated on PND 6, 12 and 20 for standard markers of neurodevelopmental maturation (righting reflex, negative geotaxis and hanging grip time). No significant postnatal neurotoxicity was observed. In vitro developmental toxicity was evaluated in GD 8 mouse embryos exposed to 0.1-25 microm anatoxin-a for 26-28 h. Perturbations in mouse yolk sac vasculature were noted from the 1.0 microm concentration in the absence of significant embryonic dysmorphology. Potential algal toxin synergism was tested in mice receiving either 0, 500 or 1,000 microg kg(-1) microcystin-LR by gavage and approximately 50 min later receiving either 0, 500, 1,000 or 2,500 microg kg(-1) anatoxin-a by the same route. No deaths occurred at any dose and no definitive signs of intoxication were observed. Stages 17 and 25 toad embryos (Bufo arenarum) were exposed to 0.03-30.0 mg l(-1) of anatoxin-a for 10 days. Adverse effects included a dose-dependent transient narcosis, edema and loss of equilibrium. Most notable was the occurrence of 100% mortality at the high dose in both groups 6-13 days post-exposure. The observed delay between initial exposure and death is highly unusual for anatoxin-a.

Animals↗

PubMed2026

Prenatal exposure to particulate matter (PM) and autism spectrum disorder (ASD) among children: a systematic review and meta-analysis.

The global surge in Autism Spectrum Disorder (ASD) cases, coupled with evidence linking prenatal Particulate Matter (PM) exposure to developmental disruption, demands a comprehensive review to design targeted health interventions. This systematic review and meta-analysis aim to evaluate the strength and consistency of evidence linking prenatal PM exposure to ASD across studies, quantifying this relation to identify actionable environmental risk thresholds. This study employed PRISMA protocols to systematically extract and evaluate evidence from PubMed, Web of Science, Scopus, and ScienceDirect (2010-2024), and screened 4,013 articles to identify qualified case-control and cohort studies (n=29). Data synthesis employed random-effects modeling, accompanied by comprehensive assessment through I2 statistics, Q-tests, funnel plots, Duval and Tweedie's trim-and-fill analysis, and Egger's regression, to ensure validity. A meta-analysis of 16 case-control studies revealed a 34 % increased risk of ASD associated with prenatal PM exposure (pooled OR=1.34; 95 % CI: 1.13-1.54), despite substantial between-study heterogeneity (I2=94.02 %, p<0.001). Publication bias was not significant (Egger's test p value=0.114). Critical trimester-specific analysis uncovered that third-trimester exposure significantly increased ASD risk (OR=1.17; 95 % CI: 1.01-1.34), while first-trimester (OR=1.02; 95 % CI: 0.92-1.11; I2=49.18 %, p<0.10) and second-trimester exposures (OR=1.13; 95 % CI: 0.88-1.38; I2=92.59 %, p<0.001) showed non-significant associations. This review identified prenatal and early life exposure to PM as a risk factor for ASD, indicating a trimester-specific vulnerability. It highlighted the necessity of focused air quality interventions and targeted guidance to reduce prenatal PM exposure to alleviate ASD risk during the critical-window.

Child↗

PubMed1994

Increasing melanoma incidence: putatively explainable by retrotransposons. Experimental contributions of the xiphophorine Gordon-Kosswig melanoma system.

The worldwide accelerating increase of neoplasia in humans is difficult to explain. We use the Xiphophorus tumor model to approach this problem by melanoma provocation with X-rays. Melanoma develops following inappropriate expression of x-erb B-conducted developmental genes and their controllers. These oncodeterminants are inherited according to Mendelian rules. We detected a new type of oncodeterminants that, following a single treatment of embryos with X-rays, generates a self-generating non-Mendelian melanoma transmission and accelerating increase of its incidence in succeeding generations (e.g., 0-->18-->33-->52%). To localize these oncodeterminants, we crossed nonirradiated fish having half of their chromosomes irradiated with nonirradiated fish having none of, half of, or all of their chromosomes irradiated. Because tumor rate and expression in the following generations correspond to the rates of treated chromosomes, we conclude that the new oncodeterminants are distributed over the chromosomes of the fish, where they may increase in the changing generations. By means of xiphophorine-specific retroviral DNA, we isolated two retrotransposons that behave hereditarily like the new transgenerational oncodeterminants. Sequence analysis revealed three ORFs flanked by LTRs containing motives of regulatory sequences typical for known retroviral and retrotransposal LTRs. Pol- and env-resembling sequences are lacking. Southern and in situ hybridization showed their multiple and repetitive nature distributed throughout the chromosomes and indications for their capability to increase in number without further treatment. Their transcripts are expressed in concert with those of most of the other known xiphophorine tumor determinants. Their expression is extremely high in cell cultures from tumorous embryos derived from ancestors treated as embryos with X-rays.

Animals↗

PubMed2024

The effect of low birth weight as an intrauterine exposure on the early onset of sarcopenia through possible molecular pathways.

Sarcopenia, a musculoskeletal disease characterized by the progressive loss of skeletal muscle mass, strength, and physical performance, presents significant challenges to global public health due to its adverse effects on mobility, morbidity, mortality, and healthcare costs. This comprehensive review explores the intricate connections between sarcopenia and low birth weight (LBW), emphasizing the developmental origins of health and disease (DOHaD) hypothesis, inflammatory processes (inflammaging), mitochondrial dysfunction, circadian rhythm disruptions, epigenetic mechanisms, and genetic variations revealed through genome-wide studies (GWAS). A systematic search strategy was developed using PubMed to identify relevant English-language publications on sarcopenia, LBW, DOHaD, inflammaging, mitochondrial dysfunction, circadian disruption, epigenetic mechanisms, and GWAS. The publications consist of 46.2% reviews, 21.2% cohort studies, 4.8% systematic reviews, 1.9% cross-sectional studies, 13.4% animal studies, 4.8% genome-wide studies, 5.8% epigenome-wide studies, and 1.9% book chapters. The review identified key factors contributing to sarcopenia development, including the DOHaD hypothesis, LBW impact on muscle mass, inflammaging, mitochondrial dysfunction, the influence of clock genes, the role of epigenetic mechanisms, and genetic variations revealed through GWAS. The DOHaD theory suggests that LBW induces epigenetic alterations during foetal development, impacting long-term health outcomes, including the early onset of sarcopenia. LBW correlates with reduced muscle mass, grip strength, and lean body mass in adulthood, increasing the risk of sarcopenia. Chronic inflammation (inflammaging) and mitochondrial dysfunction contribute to sarcopenia, with LBW linked to increased oxidative stress and dysfunction. Disrupted circadian rhythms, regulated by genes such as BMAL1 and CLOCK, are associated with both LBW and sarcopenia, impacting lipid metabolism, muscle mass, and the ageing process. Early-life exposures, including LBW, induce epigenetic modifications like DNA methylation (DNAm) and histone changes, playing a pivotal role in sarcopenia development. Genome-wide studies have identified candidate genes and variants associated with lean body mass, muscle weakness, and sarcopenia, providing insights into genetic factors contributing to the disorder. LBW emerges as a potential early predictor of sarcopenia development, reflecting the impact of intrauterine exposures on long-term health outcomes. Understanding the complex interplay between LBW with inflammaging, mitochondrial dysfunction, circadian disruption, and epigenetic factors is essential for elucidating the pathogenesis of sarcopenia and developing targeted interventions. Future research on GWAS and the underlying mechanisms of LBW-associated sarcopenia is warranted to inform preventive strategies and improve public health outcomes.

Humans↗

PubMed2005

A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures.

Inner-city minority populations are high-risk groups for adverse birth outcomes and also more likely to be exposed to environmental contaminants, including environmental tobacco smoke (ETS), benzo[a]pyrene B[a]P, other ambient polycyclic aromatic hydrocarbons (global PAHs), and residential pesticides. The Columbia Center for Children's Environmental Health (CCCEH) is conducting a prospective cohort study of 700 northern Manhattan pregnant women and newborns to examine the effects of prenatal exposure to these common toxicants on fetal growth, early neurodevelopment, and respiratory health. This paper summarizes results of three published studies demonstrating the effects of prenatal ETS, PAH, and pesticides on birth outcomes and/or neurocognitive development [Perera FP, Rauh V, Whyatt RM, Tsai WY, Bernert JT, Tu YH, et al. Molecular evidence of an interaction between prenatal environment exposures on birth outcomes in a multiethnic population. Environ Health Perspect 2004;12:630-62; Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, et al. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol 2004;26:373-85; Whyatt RM, Rauh V, Barr DB, Camann DE, Andrews HF, Garfinkel R, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environ Health Perspect, in press]. To evaluate the effects of prenatal exposure to ETS, PAHs, and pesticides, researchers analyzed questionnaire data, cord blood plasma (including biomarkers of ETS and pesticide exposure), and B[a]P-DNA adducts (a molecular dosimeter of PAHs). Self-reported ETS was associated with decreased head circumference (P = 0.04), and there was a significant interaction between ETS and adducts such that combined exposure had a significant multiplicative effect on birth weight (P = 0.04) and head circumference (P = 0.01) after adjusting for confounders. A second analysis examined the neurotoxic effects of prenatal ETS exposure and postpartum material hardship (unmet basic needs in the areas of food, housing, and clothing) on 2-year cognitive development. Both exposures depressed cognitive development (P < 0.05), and there was a significant interaction such that children with exposure to both ETS and material hardship exhibited the greatest cognitive deficit (7.1 points). A third analysis found that cord chlorpyrifos, and a combined measure of cord chlorpyrifos, diazinon, and propoxur-metabolite, were inversely associated with birth weight and/or length (P < 0.05). These results underscore the importance of policies that reduce exposure to ETS, air pollution, and pesticides with potentially adverse effects on fetal growth and child neurodevelopment.

Child↗