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The Pregnancy Research on Inflammation, Nutrition, & City Environment: Systematic Analyses Study (PRINCESA) cohort was set up to evaluate associations between air pollution and birth outcomes among pregnant persons in Mexico City. Specifically, the study was designed to improve air pollution exposure assessment and elucidate biological mechanisms underlying associations between maternal exposures and adverse pregnancy outcomes. Pregnant persons (all women) (N = 935) between ages 18–45 who lived and/or worked in metropolitan Mexico City, Mexico, from 2009 to 2015 and liveborn singleton infants (N = 815) of participants who completed follow-up were enrolled in the cohort. We followed participants monthly from enrollment to delivery and the following categories of data were obtained: demographic, medical and obstetric history, geo-referenced data, repeated measures on daily activity patterns, reported food intake, anthropometric, clinical and obstetric data, 20 serum and 20 cervicovaginal cytokines, and lower reproductive tract infection. Repeated ultrasound measures of fetal parameters and infant birth data are also included in the study's database. In addition, PRINCESA investigators calculated air pollution exposure measures for six pollutants measured by the Mexico City Atmospheric Monitoring System (SIMAT). These estimates utilize participants' addresses to account for spatial variation in exposure (nearest monitor, inverse distance weighting, and kriging) and are available daily during pregnancy for participants. To date, associations between environmental and nutritional impacts on maternal and child health outcomes have been evaluated. PRINCESA has a comprehensive database of maternal and infant data and biological samples and offers collaboration opportunities to study associations between environmental and other factors, including nutrition and pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Background: Endocrine disrupting chemicals (EDCs) such as metals have been reported to alter circulating reproductive hormone concentrations and pubertal development in animals. However, the relationship has rarely been investigated among humans, with the exception of heavy metals, such as Pb and Cd. Our aim was to investigate measures of in utero and peripubertal metal exposure in relation to reproductive hormone concentrations and sexual maturation and progression among boys from the Early Life Exposure in Mexico to Environmental Toxicants (ELEMENT) cohorts.Methods: Our analysis included 118 pregnant women and their male children from the ELEMENT study. Essential and non-essential metals were measured in urine collected from the mothers during the third trimester of pregnancy and their male children at 8-14 years. Reproductive hormone concentrations [serum testosterone, estradiol, dehydroepiandrosterone sulfate (DHEA-S), inhibin B, and sex hormone-binding globulin (SHBG)] were measured in blood samples from the children at 8-14 years. We also assessed Tanner stages for sexual maturation (genital, pubic hair development, and testicular volume), at two time points (8-14, 10-18 years). We used linear regression to independently examine urinary metal concentrations in relation to each peripubertal reproductive hormones adjusting for child age and BMI. Generalized estimation equations (GEEs) were used to evaluate the association of in utero and peripubertal metal exposures with sexual maturation and progression during follow-up based on Tanner staging and testicular volume.Results: In utero and prepubertal concentrations of some urinary metals were associated with increased concentrations of peripubertal reproductive hormones, especially non-essential metal(loid)s As and Cd (in utero), and Ba (peripubertal) as well as essential metal Mo (in utero) in association with testosterone. More advanced pubic hair developmental stage and higher testicular volume at the early teen visit was observed for boys with higher non-essential metal concentrations, including in utero Al and peripubertal Ba, and essential metal Zn concentration (peripubertal). These metals were also associated with slower pubertal progression between the two visits.Conclusion: These findings suggest that male reproductive development may be associated with both essential and non-essential metal exposure during in utero and peripubertal windows. [ABSTRACT FROM AUTHOR]

Abstract: Globally, organophosphate (OP) pesticide usage and exposure is widespread. Studies have found that fetuses and infants are more sensitive than adults to environmental toxicants and that prenatal exposure to low levels of OPs has been associated with Attention Deficit Hyperactivity Disorder-Like Phenotypes (ADHD-LP). Paraoxonase 1 (PON1) is an enzyme involved in detoxifying some OPs and its polymorphisms influence enzyme activity and quantity. The objective of this study was to examine whether maternal and/or child PON1 genotypes (PON1R192Q and PON1L55M) were associated with ADHD-LP in a Mexico City, Mexico birth cohort. PON1R192Q and PON1L55M genotypes in mothers (PON1R192Q: N=531; PON1L55M: N=458) and children (PON1R192Q: N=532; PON1L55M: N=478) from blood DNA were determined. We assessed ADHD-LP for children between the ages of 6 and 13 using Conners׳ Parent Rating Scales-Revised (CRS-R), Conners׳ Continuous Performance Test (CPT), and the parent scores for Behavior Assessment System for Children-2 (BASC2). Multivariable linear regression models were used to test relationships between ADHD-LP and PON1 polymorphisms. In these models, significant associations were observed with maternal genotypes but not with the child genotypes. A higher DSM IV Hyperactivity/Impulsivity score (β=3.27 points; 95% CI (0.89, 5.65)) and a 2.17 higher score in child DSM IV Total (95% CI (0.05, 4.29)) were observed for maternal PON155MM in comparison to PON155LM+LL. The childattention problems score was 2.27 points higher (95% CI (0.002, 4.53) for maternal PON1192QQ in comparison to PON1192QR+RR. Because maternal PON1 polymorphisms were associated with child ADHD-LP, this may be a viable biomarker of susceptibility for ADHD-LP. [Copyright &y& Elsevier]

Abstract: Attention Deficit Hyperactivity Disorder (ADHD) is the most commonly diagnosed and studied cognitive and behavioral disorder in school-age children. The etiology of ADHD and ADHD-related behavior is unclear, but genetic and environmental factors, such as pesticides, have been hypothesized. The objective of this study was to investigate the relationship between in utero exposure to chlorpyrifos, chlorpyrifos-methyl, and/or 3,5,6-trichloro-2-pyridinol (TCPY) and ADHD in school-age Mexican children using TCPY as a biomarker of exposure. The temporal reliability of repeated maternal urinary TCPY concentrations across trimesters was also explored (N =21). To explore associations with ADHD-related outcomes in children, third trimester urinary TCPY concentrations in were measured in 187 mother-child pairs from a prospective birth cohort. Child neurodevelopment in children 6–11 years of age was assessed using Conners’ Parental Rating Scales-Revised (CRS-R), Conners’ Continuous Performance Test (CPT), and Behavior Assessment System for Children-2 (BASC-2). Multivariable linear regression models were used to test relationships for all children combined and also stratified by sex. Intraclass correlation coefficients (ICC) calculations were based on a random effects model. The ICC was 0.41 for uncorrected TCPY, and ranged from 0.29 to 0.32 for specific gravity-corrected TCPY. We did not observe any statistically significant associations between tertiles of maternal TCPY concentrations and ADHD-related outcomes in children. However, compared to the lowest tertile we found suggestive evidence for increased ADHD index in the highest TCPY tertile in boys (β =5.55 points; 95% CI (−0.19, 11.3); p =0.06) and increased attention problems for the middle tertile in girls (β =5.81 points; 95% CI (−0.75, 12.4); p =0.08). Considering the continued widespread agricultural and possible residential use of chlorpyrifos and chlorpyrifos-methyl in Mexico and the educational implications of cognitive and behavior deficits, these relationships deserve further study. [Copyright &y& Elsevier]

Background There is need to assess the developmental neurotoxicity of fluoride. Our knowledge of prenatal fluoride exposure is challenged as few population-based studies have been conducted and these generally date back several decades, provide incomplete data on sociodemographic variables, and have methodological limitations. Objective To measure urinary and plasma fluoride levels across three time points in pregnant mothers who were enrolled in the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) birth cohort study. Methods Fluoride levels were characterized in archived urine and plasma from 872 pregnant mothers sampled from the ELEMENT cohort. Various statistical methods were used to analyze the fluoride data with particular consideration for changes across three stages of pregnancy and against sociodemographic variables. Results All samples had detectable levels of fluoride. The mean urinary and plasma fluoride levels were 0.91 and 0.0221 mg/L respectively, and these were not statistically different across three stages of pregnancy. Fluoride levels correlated across the stages of pregnancy studied, with stronger correlations between neighboring stages. Urinary fluoride changed as pregnancy progressed with levels increasing until ~23 weeks and then decreasing until the end of pregnancy. For plasma fluoride, there was a decreasing trend but this was not of statistical significance. Creatinine-adjusted urinary fluoride levels did not associate consistently with any of the sociodemographic variables studied. Conclusions This study provides the most extensive characterization to date of fluoride exposure throughout pregnancy. These results provide the foundation to explore exposure-related health outcomes in the ELEMENT cohort and other studies. [ABSTRACT FROM AUTHOR]

Particulate matter ≤10 μm in aerodynamic diameter (PM 10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM 10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts. To evaluate the independent and joint effects of PM 10 and energy-adjusted DII (E-DII) on PTB risks. PM 10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM 10. We assessed for potential non-linear associations using natural splines. In adjusted models, PM 10 exposure was associated with increased risks of PTB for a range of values (58–72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55–65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM 10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM 10 and E-DII and the risk of preterm birth. Associations between PM 10 and PTB in Mexico City varied over time and across levels of PM 10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM 10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM 10 from shorter exposure windows may play a more proximal role in initiating preterm labor. • Average PM 10 concentrations decreased significantly during the study period. • E-DII scores were different between trimesters, except for second vs. third trimester. • Trimester or broad exposure periods may lead to inaccurate associations. • Exposures closer to birth may play a more important role in initiating preterm labor. [ABSTRACT FROM AUTHOR]