Maternal cocaine use and mother-toddler aggression

This study examined the direct and indirect associations between maternal cocaine use during pregnancy and mother-toddler aggression in an interactive context at 2 years of child age. We hypothesized that in addition to direct effects of cocaine exposure on maternal and child aggression, the association between maternal cocaine use and mother-toddler aggression may be indirect via higher maternal psychiatric symptoms, negative affect, or poor infant autonomic regulation at 13 months. Participants consisted of 220 (119 cocaine exposed, 101 non-cocaine exposed) mother-toddler dyads participating in an ongoing longitudinal study of prenatal cocaine exposure. Results indicated that mothers who used cocaine during pregnancy displayed higher levels of aggression toward their toddlers compared to mothers in the control group. Results from model testing indicated significant indirect associations between maternal cocaine use and maternal aggression via higher maternal negative affect as well as lower infant autonomic regulation at 13 months. Although there were no direct associations between cocaine exposure and toddler aggression, there was a significant indirect effect via lower infant autonomic regulation at 13 months. Results highlight the importance of including maternal aggression in predictive models of prenatal cocaine exposure examining child aggression. Results also emphasize the important role of infant regulation as a mechanism partially explaining associations between cocaine exposure and mother-toddler aggression.     

Effects of prenatal cocaine exposure on infant reactivity and regulation

The purpose of this study was to examine the role of prenatal cocaine exposure and associated risk factors on infant reactivity and regulation at 7 months of infant age. Participants consisted of 167 mother-infant dyads participating in an ongoing longitudinal study of prenatal cocaine exposure, who completed the arm restraint procedure at the 7-month assessment (87 cocaine exposed, 80 non-cocaine exposed). We hypothesized that cocaine exposed infants would display higher arousal or reactivity and lower regulation during a procedure designed to arouse anger/frustration. Results indicated that cocaine exposed infants were more reactive to increases in the level of stress from trial 1 to trial 2 but exhibited no change in the number of regulatory strategies as stress increased, unlike the control group infants. Infant birth weight moderated the association between cocaine exposure and infant regulation. Among cocaine exposed infants, those with lower birth weight displayed higher reactivity compared to those with higher birth weight. Contrary to expectations, there were no indirect effects between cocaine exposure and infant reactivity/regulation via environmental risk, parenting, or birth weight. Results are supportive of a teratological model of prenatal cocaine exposure for infant reactivity/regulation in infancy.     

Physiological regulation in cigarette exposed infants: an examination of potential moderators

The primary purpose of this study was to examine pathways from prenatal cigarette exposure to physiological regulation at 2 months of age. Specifically, we explored the possibility that any association between prenatal cigarette exposure and infant physiological regulation was moderated by fetal growth, prenatal or postnatal environmental tobacco smoke (ETS) exposure or maternal depressive symptomatology during pregnancy. We evaluated whether exposed infants who were also exposed to ETS after birth, were small for gestational age (SGA) or had mothers with higher depressive symptoms during pregnancy had the highest levels of physiological dysregulation. Respiratory sinus arrhythmia (RSA) was obtained from 234 (166 exposed and 68 nonexposed) infants during sleep. As expected, cigarette-exposed infants had significantly lower RSA than nonexposed infants. This association was not moderated by prenatal or postnatal ETS exposure, or maternal depressive symptomatology during pregnancy. However, small for gestational age status did moderate this association such that nonexposed infants who were not small for gestational age had a significantly higher RSA than nonexposed small for gestational age infants and exposed infants. These findings provide additional evidence that prenatal cigarette exposure is directly associated with dysregulation during infancy.     

Maternal cocaine use and caregiving status: group differences in caregiver and infant risk variables

This study examined differences between cocaine and non-cocaine-using mothers, and between parental and non-parental caregivers of cocaine-exposed infants on caregiver childhood trauma, psychiatric symptoms, demographic, and perinatal risks. Participants included 115 cocaine and 105 non-cocaine mother-infant dyads recruited at delivery. Approximately 19% of cocaine mothers lost custody of their infants by 1 month of infant age compared to 0.02% of non-cocaine mothers. Mothers who used cocaine during pregnancy had higher demographic and obstetric risks. Their infants had higher perinatal risks. Birth mothers who retained custody of their infants had higher demographic risks and perinatal risks, higher childhood trauma, and higher psychiatric symptoms compared to birth mothers who did not use cocaine and non-parental caregivers of cocaine-exposed infants. Results highlight the importance of addressing childhood trauma issues and current psychiatric symptoms in substance abuse treatment with women who engaged in substance use during pregnancy.     

Influence of prenatal cocaine exposure on full-term infant neurobehavioral functioning

This study investigated infant neurobehavioral functioning during the newborn period in 334 full-term, African American neonates (187 cocaine exposed, 147 non-cocaine exposed) enrolled prospectively at birth, with documentation of drug exposure status through maternal interview and urine and meconium toxicology assays. Infants were assessed using the Brazelton Neonatal Behavioral Assessment Scale (BNBAS) during the newborn period (0–6 postnatal days). Findings from multivariate profile analyses support a consistent, modest effect of prenatal cocaine exposure on neurobehavioral functioning in full-term neonates. All of the BNBAS cluster scores, with the exception of abnormal reflexes, were similarly affected, sharing a common slope (D=−0.14; 95% CI=−0.27, −0.003; P=.046) representing a −0.14 point difference between cocaine-exposed and non-cocaine-exposed infants after controlling for prenatal exposure to alcohol, tobacco, and marijuana (ATM); maternal age, education, employment, primigravida status, and prenatal care visits; and infant sex and postnatal age in days. Fetal growth was also related to neurobehavioral functioning and, in part, mediated the relationship between cocaine exposure and the BNBAS cluster scores. Cocaine exposure during each trimester similarly influenced infant neurobehavioral profiles, with cocaine-associated deficits most pronounced in infants with exposure in all three trimesters. Results from qualitative and quantitative urine and meconium bioassay indicators further substantiated these results. Findings, while significant, represent modest effect sizes in full-term infants.     

Prenatal cocaine exposure and small-for-gestational-age status: effects on growth at 6 years of age

Objective

To evaluate the impact of prenatal cocaine exposure and small-for-gestational-age (SGA) status on childhood growth.

Study design

Cocaine exposure was defined by history or meconium metabolites. Hierarchical linear modeling was used to examine cocaine exposure and SGA status on growth, while controlling for exposure to other drugs and alcohol use.

Results

At birth cocaine-exposed infants (n = 364) had significantly lower growth parameters compared to non-exposed children (n = 771). At 6 years, weight was similar between exposed and unexposed children. SGA infants continued to be growth impaired. There was a significant interaction between prenatal cocaine exposure and SGA status at 6 years. The negative effects of cocaine on weight and height were greater among non-SGA than SGA children (432 vs. 280 gm, and 0.7 and 0.5 cm, respectively) while negative effects of SGA status on weight and height were larger in non-cocaine exposed compared to the exposed children (2.3 kg vs.1.6 kg and 2.2 and 1.0 cm).

Conclusions

Children exposed to prenatal cocaine were similar in weight to non-exposed children at 6 years of age. Cocaine had an unexplained greater detrimental effect on non-SGA than SGA children. SGA status at birth has an independent detrimental effect on childhood growth.     

Prenatal cocaine use and maternal depression: effects on infant neurobehavior

OBJECTIVE: The present study examined the impact of both perinatal maternal depression and cocaine use on infant neurobehavior at 1 month of age in a large, multi-site study. METHODS: Infant neurobehavior was examined in 1053 infants at 1 month of age using the NICU Network Neurobehavioral Scale (NNNS). Mothers were interviewed using The Addiction Severity Index to determine present and past psychiatric history. Four groups were derived from the total sample: 385 prenatally cocaine-exposed infants, 76 whose mothers reported current postpartum depression (DEP/COC) and 309 without current postpartum depression (nonDEP/COC); 668 infants were not exposed to cocaine, 104 whose mothers reported current postpartum depression (DEP/nonCOC), 564 without current postpartum depression (nonDEP/nonCOC). A 2x2 Analysis of Covariance was used with covariates (birthweight, maternal age, SES, nicotine, alcohol, and research site) to examine infant neurobehavior in these four conditions. Secondary analyses were conducted to examine the effects of amount and timing of prenatal cocaine exposure. RESULTS: DEP group by COC exposure status interactions were significant; there was only a DEP effect in the nonCOC infants. Infants in the nonCOC/DEP group had poorer self-regulation and more stress signs, excitability, and arousal than infants in the other groups. CONCLUSIONS: Postpartum maternal depression has negative effects on infant neurobehavior at 1 month of age. Prenatal cocaine exposure may serve to suppress or buffer the effects of postpartum depression on infant neurobehavior. Maternal mood could explain some of the inconsistencies found in the prenatal cocaine exposure literature.     

Prenatal cocaine exposures and dose-related cocaine effects on infant tone and behavior

BACKGROUND: In experimental models, prenatal cocaine exposure has been found to perturb monoaminergic development. In humans, numerous studies have sought clinical correlates, but few have focused on dose-related effects, especially as regards neurologic function beyond the neonatal period. OBJECTIVE: To assess whether prenatal cocaine exposure has adverse effects on infant neurologic, developmental and behavioral outcomes and whether any effects are dose-dependent. DESIGN/METHODS: Infants (398) were enrolled at birth from an urban hospital. Drug exposure was ascertained with biomarkers in hair (n=395), urine (n=170) and meconium (n=109). Children were followed prospectively and 286 (72%) were evaluated blind to drug exposure at 6 months of age with the Bayley scales, Fagan Scale of Infant Intelligence and a standardized neurological examination. RESULTS: Certain neurological findings increased significantly by the amount of cocaine detected in maternal hair, e.g. abnormality of tone, as indicated by extensor posture was detected among 28% of cocaine-unexposed infants, 43% of infants exposed to lower and 48% exposed to higher cocaine levels in maternal hair (p<0.009). Persistent fisting increased in a similar dose-dependent manner. These associations persisted in adjusted analyses. Prenatal cocaine exposure was not associated with developmental scores (mental, motor or novelty preference) but was associated with lower orientation scores in adjusted analyses. CONCLUSIONS: At 6 months of age, prenatal cocaine exposure was associated with abnormalities of tone and posture and with lower orientation scores. Perturbations in monoaminergic systems by cocaine exposure during fetal development may explain the observed neurological and behavioral symptoms. Whether such findings in infancy increase the risk of later neurobehavioral problems requires further study.     

Prenatal exposure to bisphenol A and phthalates and infant neurobehavior

Objective

To examine the association of prenatal exposure to bisphenol A and select common phthalates with infant neurobehavior measured at 5 weeks.

Methods

We compared the concentration of maternal urinary metabolites of bisphenol A and phthalates at two distinct time points in pregnancy (16w, 26w) with scores on the NICU Network Neurobehavioral Scale (NNNS) at 5 weeks of age in a cohort of 350 mother/infant pairs.

Results

Prenatal exposure to BPA was not significantly associated with neurobehavioral outcomes at 5 weeks. Significant associations between prenatal exposure to measured phthalates and infant neurobehavioral outcomes differed by type of phthalate and were only seen with exposure measured at 26 weeks. Higher total di-butyl phthalate (DBP) metabolites at 26w were associated with improved behavioral organization evidenced by decreased arousal (p = .04), increased self-regulation (p = .052), and decreased handling (p = .02). In males, higher total di-2-ethylhexyl phthalate (DEHP) metabolites at 26w were associated with more nonoptimal reflexes (p = .02).

Conclusion

The association between prenatal phthalate exposure and infant neurobehavior differed by type of phthalate and was evident only with exposure measured at 26w. Prenatal exposure to DBP was associated with improved behavioral organization in 5-week-old infants. Prenatal exposure to DEHP was associated with nonoptimal reflexes in male infants. There was no evidence of an association between prenatal BPA exposure and infant neurobehavior.     

Cocaine abuse in pregnancy: effects on the fetus and newborn

The outcome of infants born to cocaine-using drug dependent women was compared to that of infants of non-cocaine using drug dependent and non-drug dependent women. The study population included 150 pregnant women: 50 women used heroin and methadone plus cocaine, 50 used heroin and methadone minus cocaine, and 50 were non-drug dependent women. Significant differences were found between the cocaine and drug-free groups in infant birth weight, length, head circumference and Apgar scores, with the cocaine group having lower values for each variable. Average gestational age did not vary between the 3 groups. The cocaine group included 1 spontaneous abortion and 4 fetal deaths; non-cocaine drug dependent women had 2 fetal deaths, with none in the control group. Mean abstinence scores for 19 of the physiological and behavioral parameters were lower in the cocaine group than in the non-cocaine drug dependent women with the exception of vomiting and convulsions. These data suggest that: (1) infants born to drug dependent women have a poorer general outcome than those born to non-drug dependent women; (2) maternal cocaine use does not appear to increase the incidence of severe neonatal abstinence symptomatology; (3) pregnancies complicated by cocaine abuse have a greater chance for fetal loss resulting from both spontaneous abortions and fetal death; (4) infants born to cocaine abusing women had infants with decreased birth weight, head circumference, length and Apgar scores.     

Maternal cocaine use and infant behavior

We hypothesized that prenatal cocaine exposure results in less optimal infant behavior and more impaired maternal-infant interaction in healthy term infants. Infants were evaluated with the Neonatal Behavioral Assessment Scale (NBAS) at days 1-3 and 11-30 of age, and mother-infant pairs with the Nursing Child Assessment of Feeding Scale (NCAFS) at 7-16 weeks of age. Drug use was determined from confidential interviews, urine assays and medical records. Cocaine-exposed infants (N = 51) were no different than unexposed comparison infants (N = 60) on the first NBAS exam. On the second NBAS exam, 20 cocaine-exposed infants had slightly lower motor cluster scores compared with those of 32 unexposed infants (p = 0.01), but this difference was reduced after control for several confounding variables. The NCAFS detected no differences between groups in maternal or infant behavior. Infants in this population showed no clinically meaningful effects of cocaine exposure on behavior or maternal-infant interaction.     

Paternal alcoholism, negative parenting, and the mediating role of marital satisfaction

Given the documented association between paternal alcoholism and negative parenting behaviors, the purpose of this study was to examine longitudinally whether marital satisfaction mediates this relationship. Participants consisted of 197 families (102 without an alcoholic father, 95 with an alcoholic father) who were assessed at three time points: when children were 12, 24, and 36 months old. Results indicated that paternal alcoholism at 12 months was associated with decreased marital satisfaction at 24 months for both mothers and fathers. Marital satisfaction at 24 months in turn was associated with decreases in parental warmth and sensitivity at 36 months. Furthermore, marital satisfaction mediated the association between paternal alcoholism and parental warmth and sensitivity for both mothers and fathers. The implications of these findings for interventions for alcoholic families are discussed.     

Birth to age 7 growth of children prenatally exposed to drugs: a prospective cohort study

Prenatal exposure to cocaine, alcohol, and cigarettes has been linked to decreased birth weight and length. Unclear, however, is whether growth deficits persist into childhood. Women who were pregnant, African-American, not HIV-positive, and who delivered singleton infants were extensively screened throughout pregnancy for cocaine, alcohol, cigarette, and other illicit drug use. Of the approximately 1100 eligible subjects, 665 families were located at a 7-year postbirth follow-up and 540 participated. After appropriate control for potential confounders and prenatal exposures, prenatal exposure to cocaine, alcohol, and cigarettes each independently predicted birth weight and length. At age 7, prenatal cocaine exposure was significantly related to height deficits after accounting for other prenatal exposures and significant confounders. Children at age 7 exposed to cocaine in utero were up to 1 in. shorter and twice as likely to fall below the 10th percentile in height as the control children after accounting for other significant confounders including other prenatal exposures. Maternal age moderated the relation between prenatal exposures and child growth. Children born to women over 30 and exposed to cocaine were up to 2 in. shorter and four times more likely to have clinically significant height deficits at age 7. Children of older women and exposed to moderate-to-high levels of alcohol prenatally were up to 14 lb lighter and five times more likely to fall below the 10th percentile in weight. Similar growth restriction was not associated with prenatal exposures for children born to younger mothers. These outcomes add to the growing body of literature detailing long-term effects of prenatal drug exposure, suggesting differential effects for cocaine and alcohol, and indicating that maternal age may moderate these effects. Mechanisms for growth restriction and failure of catch-up under conditions of prenatal exposures are presented, suggesting further study of these developmental outcomes.     

Changes in children hair-Hg concentrations during the first 5 years: maternal, environmental and iatrogenic modifying factors

Children are exposed to Hg from mothers (via placenta and lactation), environment (food), and in many parts of the world by thimerosal-containing vaccines (TCV) during immunization. Neurodevelopment studies based on infant hair-Hg (HHg) have been designed without explicit attention to the factors associated with changes in infant physiology and Hg sources of exposure. A longitudinal study of changes in HHg concentrations from birth to 5 years was done in a sample of children from Porto Velho (Rondonia), Brazilian Amazonia. The study extracted information from the asymmetry associated with maternal and infant HHg changes at specified sampling: birth (fetal exposure), 6 months of exclusive breastfeeding, 36 months (weaning) and 60 months (pre-school). The distribution of HHg in breastfed infants followed a pattern different from their mothers. While mothers had the highest HHg concentrations at childbirth, infants showed the highest HHg values at 6 months after the recommended full schedule (six shots) of immunization with TCV; after that, the downward trend in HHg shown by children coincided with both weaning and less frequent vaccination period (5 years). Extended lactation (up to 36 months) was not significantly associated with HHg of infants or mothers; however, significant association (Spearman's r) between maternal and infant HHg concentration was seen at birth (r=0.3534; P=0.001), 6 months (r=0.4793; P<0.0001), 3 years (r=0.0122; P=0.012) and 5 years (r=0.0357; P=0.005). Maternal postpartum metabolic changes, infant development and transitional diets and possibly Hg from TCV contribute to the asymmetry of HHg changes between mothers and children.     

The effects of prenatal cocaine exposure and gender on inhibitory control and attention

Children exposed prenatally to cocaine show deficits in emotion regulation and inhibitory control. While controlling for the measures of medical complication in the perinatal period, environmental risk, and prenatal polydrug exposure (alcohol, tobacco, and marijuana), we examined the effects of prenatal cocaine exposure and gender on attention and inhibitory control in 203 children at ages 6, 9, and 11. Cocaine exposure affected the performance of males, but not females. Heavily exposed males showed deficits in the attention and the inhibition tasks. In addition, a significantly greater proportion of heavily exposed males (21%) than unexposed males (7%) or heavily exposed females (7%) failed to complete the task (p < 0.01). Even without those poorest performing subjects, the overall accuracy for heavily exposed males (81%) was significantly reduced (p < 0.05) compared to lightly exposed males (87%) and unexposed males (89%). The findings highlight the importance of considering gender specificity in cocaine exposure effects. Processes by which cocaine effects may be specific to males are discussed.     

The effects of prenatal cocaine use on infant development

This study examined the effect of prenatal cocaine use on infant physical, cognitive, and motor development, and temperamental characteristics, controlling for other factors that affect infant development. Women were, on average, 26.8 years old, had 12 years of education, and 46% were African American. During the first trimester, 18% were frequent users of cocaine (≥ 1 line/day). The infants were, on average, 14.6 months old at this follow-up phase. Women who used cocaine during pregnancy rated their infants as more fussy/difficult and unadaptable than did women who did not use cocaine. Cocaine use in the second trimester was associated with significantly lower motor scores on the Bayley Scales of Infant Development (BSID) [N. Bayley, Manual for the Bayley Scales of Infant Development, Psychological Corporation, New York, 1969.]. There was no effect of prenatal cocaine use on BSID mental performance or on growth. These findings are consistent with other reports in the literature and with the hypothesis that prenatal cocaine exposure affects development through changes in neurotransmitter systems.     

Neurobehavioral outcomes of cocaine-exposed infants

The present study investigated the neurobehavioral outcomes of fetal cocaine exposure. Attempts were made to control, by design or statistical analysis, for significant confounders. Timing and amount of drug exposures were considered, and biologic measures of exposure were quantified to classify exposure severity.One hundred sixty-one non-cocaine and 158 cocaine-exposed (82 heavily and 76 lightly exposed) infants were seen at a mean-corrected age of 43 weeks post-conception and administered the Neurobehavioral Assessment (NB Assessment). Heavily cocaine-exposed infants had more jitteriness and attentional problems than lightly and non-exposed infants. They also had more movement and tone abnormalities, and sensory asymmetries than non-exposed infants. Heavily exposed infants were more likely to be identified with an abnormality than non-exposed infants and there was a trend toward heavily exposed infants being more likely to be identified with an abnormality than lightly exposed infants. Furthermore, there was a trend for heavily exposed infants to be less likely to be testable than non-exposed infants. After the confounding and mediating factors were considered, heavily cocaine-exposed infants were four times as likely to be jittery and nearly twice as likely to demonstrate any abnormality than lightly and non-exposed infants, but all other effects were no longer significant. Higher concentrations of the cocaine metabolites of cocaine, cocaethylene, and benzoylecgonine (BZE) were related to higher incidence of movement and tone abnormalities, jitteriness, and presence of any abnormality. Higher cocaethylene levels were related to attentional abnormalities and higher meta-hydroxybenzoylecgonine (m-OH-BZE) was related to jitteriness. Drug effects on attention were mediated by maternal psychological distress, suggesting that this factor should be considered in future studies of drug exposure effects.     

Level of prenatal cocaine exposure and infant-caregiver attachment behavior

The objective of this longitudinal prospective cohort study was to determine whether level of prenatal cocaine exposure, or the interaction between level of prenatal cocaine exposure and contextual risk variables, was associated with a higher rate of infant-caregiver insecure attachment and disorganized attachment, or with alterations in infant crying or avoidant behavior, after controlling for prenatal exposure to alcohol, tobacco, and marijuana, the quality of the proximal caregiving environment, and other covariates. Subjects were 154 full-term 12-month-old infants (64 unexposed, 61 with lighter cocaine exposure, 29 with heavier cocaine exposure) and their primary caregivers from low-income, urban backgrounds. Exposure status was determined in the maternity ward by biologic assay (infant meconium and/or maternal or infant urine) and maternal self-report. At the 12-month follow-up visit, infants were videotaped with their primary caregiver in Ainsworth's Strange Situation. Reliable coders masked to exposure status scored videotapes for attachment variables, amount of crying, and level of avoidance. Contrary to popular perceptions, level of prenatal cocaine exposure was not significantly related to secure/insecure attachment status, disorganized attachment status, or rated level of felt security. Foster care status also was not associated with attachment status. However, heavier prenatal cocaine exposure, in interaction with maternal contextual variables (public assistance or multiparity) was associated with alterations in infant socio-affective behavior, including a higher level of behavioral disorganization, more avoidance of the caregiver, and less crying.     

Motor and cognitive outcomes through three years of age in children exposed to prenatal methamphetamine

Background

Methamphetamine (MA) use among pregnant women is an increasing problem in the United States. The impact of prenatal MA exposure on development in childhood is unknown.

Objective

To examine the effects of prenatal MA exposure on motor and cognitive development in children at 1, 2, and 3 years of age.

Design/methods

IDEAL enrolled 412 mother-infant pairs at four sites (Tulsa OK, Des Moines IA, Los Angeles CA, and Honolulu HI). MA subjects (n = 204) were identified by self report or GC/MS confirmation of amphetamine and metabolites in infant meconium. Comparison subjects (n = 208) were matched (race, birth weight, maternal education, and type of insurance), denied amphetamine use, and had a negative meconium screen. Both groups included prenatal alcohol, tobacco and marijuana use, but excluded use of opiates, lysergic acid diethylamide, phencyclidine or cocaine only. The Peabody Developmental Motor Scales (PDMS-2) were administered to the infants at the 1 and 3 year visits. This analysis includes a subsample (n = 350) of the IDEAL study with completed 1 and/or 3 year visits (n = 330 and 281, respectively). At each annual visit we also conducted the Bayley Scales of Infant Development (BSID-II) as a general evaluation of mental and motor development. The BSID-II analysis includes a subsample (n = 356) of the IDEAL study with completed 1, 2, and/or 3 year visits (n = 331, 288, and 278 respectively). GLM analysis conducted on the PDMS-2 and BSID-II examined the effects of MA exposure and heavy MA exposure (≥ 3 days of use/week), with and without covariates. Longitudinal analyses were used to examine the effects of MA exposure on changes in motor and cognitive performance over time.

Results

Heavy MA exposure was associated with significantly lower grasping scores than some and no use at 1 year (P = 0.018). In longitudinal analysis, lower grasping scores associated with any MA exposure and heavy exposure persisted to 3 years. There were no effects of MA exposure, including heavy exposure, on the Bayley Mental Development Index (MDI) or Psychomotor Development Index (PDI) at any or across age.

Conclusions

There were no differences in cognition as assessed by the BSID-II between the groups. There was a subtle MA exposure effect on fine motor performance at 1 year with the poorest performance observed in the most heavily exposed children. By 3 years, no differences in fine motor performance were observed. These findings suggest MA exposure has modest motor effects at 1 year that are mostly resolved by 3 years.     

Maternal fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring

Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal fenvalerate exposure on testicular development. The present study investigated the effects of prenatal fenvalerate exposure on testicular development and spermatogenesis. The pregnant mice were administered fenvalerate (30 mg/kg) by gavage daily from gestational day (gd) 13 to gd 18. The weights of testes and epididymides were significantly decreased in mice whose mothers were exposed to fenvalerate during pregnancy. Importantly, maternal fenvalerate exposure during pregnancy markedly decreased the number of mature seminiferous tubules (stages VII and VIII) in testes of adult male offspring. In addition, maternal fenvalerate exposure during pregnancy significantly reduced the number of epididymal spermatozoa in adult male offspring. Additional experiments showed that the level of serum testosterone (T) was significantly decreased in male fetuses whose mothers were exposed to fenvalerate during pregnancy. Correspondingly, mRNA and protein levels of P450_17α, a T synthetic enzyme, were significantly decreased in fetal testes. Moreover, the disruptive effect of prenatal fenvalerate exposure on testicular T synthesis was irreversible. In conclusion, prenatal fenvalerate exposure irreversibly impairs testicular development and spermatogenesis at least into early adulthood.